• Since the dawn of vaccination, authorities have habitually doubled down on unsafe and ineffective vaccines, regardless of the pushback they received or the evidence against them.

• Sustaining this has required increasingly brazen methods to censor and conceal the deluge of “extremely rare” injuries caused by an ever-expanding vaccination schedule.

• Senator Ron Johnson, who has worked tirelessly to expose this coverup, recently held a Senate hearing aptly titled: “Unmasked: How Biden Health Officials Purposely Turned a Blind Eye Toward COVID-19 Vaccine Safety Signals.”

• Faced with a tsunami of vaccine injuries too large for anyone to ignore, the FDA and CDC searched for a way to statistically dismiss it, eventually settling on effectively comparing Moderna’s injury rate to Pfizer’s and declaring the vaccines “safe” because there was no major difference between the two.

• When a senior FDA analyst pointed out this obvious flaw and suggested comparing them to less toxic vaccines instead, documents show the entire FDA turned against her to suppress her findings. As a result, dozens of conditions we have all seen the COVID vaccines cause were never officially linked to them—despite the data clearly showing they were.

• The unprecedented damage caused by the COVID-19 vaccines has created a historic loss of trust in the parties who covered it up, giving us a once-in-a-lifetime opportunity to force them to start telling the truth and end an immunization experiment that has profoundly damaged the health of our society.

I have long believed in a “law of equilibrium” which posits that most things are cyclical and will eventually be brought back into balance. Mechanistically, this frequently results from existing phenomena being the result of competing forces reaching a balance point (e.g., you don't fall through the floor because the ground pushes up on you just as hard as gravity pulls you down) and because nature’s design utilizes feedback loops to maintain balance.

This process is commonly referred to as “negative feedback,” where anything that shifts a system away from its center (e.g., its “set point”) triggers a response that counteracts that change (e.g., a thermostat kicks on the heat when the temperature drops too low, or turns on the AC when it climbs too high). Biology in turn, has many layers of these negative feedback loops (where one thing counteracts another which counteracts another etc.) which collectively are able to keep the immensely complex orchestra of life functioning.

Conversely, “positive feedback loops” also exist, where a shift from baseline triggers a further shift from baseline (e.g., forest fires spreading, fruit ripening, the blood clotting cascade, the hormonal surge triggering ovulation, or childbirth contractions) but these are far rarer and ultimately still “turn off” because they rapidly consume a self-limiting resource.

Due to the cyclical nature of history, I have noticed the same vaccine fiascos repeat again and again, but each time, are forgotten, and hence able to repeat again. Briefly, the process is typically as follows:

•A new (dubious) vaccine is introduced and marketed with immense fanfare despite the existing evidence showing it does not deserve that fanfare.

•Once the vaccine hits the population, a significant number of vaccine failures and injuries inevitably occur.

•Once this happens, health authorities (and healthcare workers) respond by exaggerating the benefits, moving the goal posts from what was originally promised, and sweeping all the injuries under the rug.

•This produces increasing pushback from the public and resistance towards vaccinating.

•As time goes on, rather than acknowledge the shortcomings of the vaccine, the failures of the vaccine begin being increasingly blamed not enough people vaccinating (e.g., to reach “herd immunity”). As such, more and more aggressive mandates are instituted which create stronger and stronger public resistance against the program.

I named this the “vaccine positive feedback loop” because if things were functioning normally, the injuries and failures of the vaccine would trigger a negative feedback response that would cause the vaccine program to be pulled back—but instead a rather curious and unnatural thing occurs—the devotion to them increases. This I believe cuts to the core of why “vaccines are a religion” and why vaccine proponents will always double down on what they are doing rather than admit fault.

Recognizing that this is a recurring cycle, my focus hence has been on exposing the cycle, as I feel it is only through the knowledge of what our society is actually trapped in that it will be possible to free ourselves from it.

Note: a major reason I've focused on umbrella therapies like DMSO is that their mechanisms of action are in many ways the inverse of what vaccines do, which provides a concrete way to understand why so many different vaccines can cause such a wide range of neurological and autoimmune injuries. This for example was why my recent article on DMSO treating “incurable” neurological injuries had to be so detailed, but now that that has been done, a much shorter version which references the more extensive summary can be published (and will be).

Reducing “Vaccine Hesitancy”

One of the most depressing facets of the “vaccine positive feedback loop” is how consistently both doctors and government officials will sweep vaccine injuries under the rug to maintain public confidence in the vaccine, with the earliest example I’ve found being one that Suzanne Humphries unearthed:

Mr. Henry May, writing to the Birmingham Medical Review, in January, 1874 reported that deaths as a result of vaccination were often not reported because of an allegiance to the practice. Often a vaccinated person was recorded as having died from another condition such as chicken pox or erroneously listed as unvaccinated.

Polio Coverups

When producing the original (Salk) polio vaccine, manufacturers faced a delicate balance: the live poliovirus had to be fully inactivated with formaldehyde to ensure safety, but excessive inactivation could damage key viral antigens and weaken the immune response. This required a series of careful steps to strike an appropriate balance and during the clinical trials, three different parties (Salk, the US government and the manufacturers) tested the vaccines for safety.

Once the vaccine was approved, changes were made to the vaccine to increase potency (a preservative was removed), inactivation protocols became much more lax (increasing potency), and testing was delegated to manufacturers (despite large deviations from Salk’s inactivation protocols)—all of which was essentially done to meet the large demand for the polio vaccine as the trial approach was not feasible to implement at scale.

As a result, on April 12^th (based on the recent clinical trials), was declared “safe, effective, and potent,” and licensed the same day. The next day, widespread vaccinations began, and around April 24^th polio began being reported in recipients, ultimately causing 40,000 recipients to develop non-paralytic polio, 200 to develop paralytic polio and 10 to die.

To solve this public relations nightmare (which given previous assurances greatly shook public confidence in vaccines), the US government chose to blame it on faulty manufacturing from one of the five producers (who recalled their vaccines) but stand behind the other four. However, to quote Turtles All the Way Down (and Paul Offit):

Alexander Langmuir, the CDC’s chief epidemiologist, and Dr. Neil Nathanson, who at the time headed the CDC’s polio surveillance unit. The two conducted a follow-up investigation into the Cutter Incident and discovered that Wyeth’s vaccine had also caused several cases of paralysis. Following their report, the company silently recalled the allegedly “hot lot” from the market. No one other than senior US health officials ever saw that report.

“It was never released to the media,” Offit writes, “never shown to polio researchers, never shown to the National Foundation, never shown to polio vaccine advisers, never distributed to health care professionals, never published in medical journals, and never made available to defense attorneys in subsequent lawsuits against Cutter Laboratories. As a result, only a handful of people knew about the problem with Wyeth’s vaccine.”

Years later, Nathanson said he thought the report had been buried due to officials’ wish to maintain public confidence in the Salk vaccine: “As long as the problem was with one manufacturer [i.e., Cutter] and a couple of lots of vaccine, it would be viewed as an aberration due to sloppy manufacturing or testing procedures and not an intrinsic problem. Once it was extended to a second manufacturer, it would be seen as intrinsic to the product.” In this scenario, Offit further clarifies, ”people would be afraid to use any polio vaccine.”

Likewise, after a panel was convened to investigate the disaster:

Perhaps the most disturbing element of the entire program, has been the disparity between the risks that were known to be involved and the repeated assurances of safety.—Paul Meier, professor of epidemiology at the Johns Hopkins University School of Public Health

The National Foundation, in a memo sent to doctors, also stated emphatically that the [polio] vaccine was completely safe and that the risk of ensuing paralysis was “zero”.

The best way to push forward a new program is to decide on what you think the best decision is and not question it thereafter, and further, not to raise questions before the public or expose the public to open discussion of the issue.—Paul Meier (sarcastically) speaking at an expert panel on the polio vaccine.

Finally, in 1984, amid tort litigation raising technical questions about whether the original 1961–1962 clinical trial lots met the monkey neurovirulence test standards, the FDA loosened the clinical trial requirements for licensure so that any remaining regulatory doubts about the vaccine’s safety would not undermine the immunization program. Their announcement, in turn, was quite explicit:

Leaked transcripts have also revealed this mentality. For example, in a private June 2000 meeting, the CDC, WHO and vaccine manufactures discussed Verstraeten’s CDC analysis showing mercury in vaccines had a dose-dependent association with neurodevelopmental disorders. Expressing concern the study had ever been done, the WHO’s representative stated “My mandate as I sit here in this group is to make sure at the end of the day that 100,000,000 are immunized… and that will have to be with thimerosal containing vaccines unless a miracle occurs,” urging the group to present findings to the ACIP in a way that would not get “exposed to the traps which are out there in public relations.” Another warned that “the medical legal findings in the study, causal or not, are horrendous,” while the meeting’s own chairman, Dr. Dick Johnston, admitted, “I do not want my grandson to get a thimerosal-containing vaccine until we know better what is going on.” The study was stamped “DO NOT COPY OR RELEASE” on every page, and over the next three years the data was reworked until the significant associations largely disappeared in the version published in Pediatrics in 2003—by which time Verstraeten had left the CDC for GlaxoSmithKline.
Note: it should come as no surprise that despite decades of attempts to access this study's underlying database, the CDC has blocked every single one, leaving us to having to trust that their in-house analyses always correctly determined safety.

Likewise, Gavin Debecker’s Forbidden Facts, was written to expose leaked transcripts from the IOM’s closed Immunization Safety Review Committee meetings—which were tasked with definitively evaluating vaccine safety but instead prioritized downplaying risks to avoid eroding public confidence and triggering vaccine hesitancy. Committee members repeatedly framed their approach around protecting vaccination uptake. For example, Dr. Michael Kaback stated, “The more negative that presentation is, the less likely people are to use vaccination… We are kind of caught in a trap.” Dr. Bennett Shaywitz warned that any “waffling” could lead parents to opt for single vaccines [which are safer but less profitable], noting “everybody knows that that is going to reduce the vaccinating of children.” Dr. Steven Goodman emphasized they had to be “very, very careful” about quantifying side effects, lest it be seen as an “ideologic bias” harming public trust. This mindset shaped their wording and conclusions toward reassurance rather than full scientific transparency.

Looking into the present, as doubts about vaccines have continued to increase, the messaging on every platform has shifted to the urgent need to “reduce vaccine hesitancy” by censoring any information about serious adverse effects of vaccination. Given that Peter Marks (the FDA bureaucrat who was essentially in charge of the COVID vaccines and stonewalled all investigations into their harms) frequently publicly spoke out against vaccine misinformation and the dangerous vaccine hesitancy it caused, I suspected the longstanding tradition to bury vaccine injuries to preserve public trust in vaccination was alive and well throughout COVID-19. To quote the recent Senate investigations:

Records that the Subcommittee has obtained to date [5/21/25] offer a simple, yet troubling, answer to these questions: Biden administration officials knew in early 2021 that the mRNA COVID-19 injections could result in adverse health events and they downplayed the risks [e.g., myocarditis] to avoid alarming the public and create vaccine hesitancy. As a result, they violated what should be the inviolable principle of informed consent [and mandated the vaccine for virtually every American].

By May 2021, senior officials in the FDA’s CBER (the unit responsible for COVID-19 vaccine safety surveillance), drafted an email to Dr. Szarfman [who was providing evidence of serious vaccine harm], directing Dr. Szarfman to “hold off on creating and sending data mining reports and analyses.” Dr. Peter Marks, a staunch supporter of the COVID19 vaccines who at the time led CBER [and had told Szarfman to cease and desist in her activities], eventually warned [Dr. Szarfman’s boss] that Dr. Szarfman’s data mining could “create erroneous conflicts that feed in to anti-vaccination rhetoric.

Exposing the Coverup

Senator Johnson has spent more than four years working around the clock, regardless of the pushback he receives, to expose the COVID cartel and help those injured by its greed. In doing so, he has, for the first time, provided conclusive evidence that authorities habitually lie about vaccines, which I believe is necessary to finally break the toxic cycle we are trapped within.

Recently he held a hearing to present what his Senate investigative team had unearthed, a few parts of which I’d like to highlight. First, in his opening statement, he concisely lays out conclusive proof that the FDA and CDC compulsively covered up COVID vaccine injuries, while also demonstrating why anyone with basic common sense could tell a massive coverup was underway.

Note: the report Johnson references can be read here.

That opening statement alone was sufficient to make the hearing’s intended point. However, I chose to watch the rest, in large part because I was curious how Senator Blumenthal (the lead voice defending the pharmaceutical industry at each of these hearings) would attempt to defend the indefensible.

His response was, on one hand, somewhat disappointing: at Johnson’s previous hearing, Blumenthal had briefly displayed genuine surprise at and interest in the plight of the vaccine injured, which was entirely absent this time. On the other hand, it was reassuring, as despite his zeal to defend the industry, all he could muster were a few arbitrary denials of Johnson’s findings and emotionally manipulative tangents bearing no relation to the actual evidence, demonstrating that against Johnson’s case, his position was indeed indefensible.
Note: I felt Blumenthal’s most memorable line was “The majority’s report cherry picks, emails, and misconstrues an internal debate between scientists who were actively looking for ways to detect side effect to support a predetermined and flawed thesis that COVID nineteen vaccines have done more harm than good. That’s not the scientific method to have a preconceived result and then frame the evidence to fit the outcome.” This is because the second sentence perfectly characterizes all the science conducted throughout COVID-19 that rationalized ways to prove the vaccines were safe and effective despite immense evidence to the contrary.

To further support his position, Blumenthal summoned a witness (representative of his political base), who testified to the trauma of nearly dying from COVID and then recovering from long COVID—which, while tragic (and likely preventable with non-standard COVID therapies), was again, entirely irrelevant to whether authorities covered up vaccine injuries.

As she detailed her journey and desperate desire to just be heard, I could not help but notice every single thing she described was identical to what the COVID vaccine injured routinely experience, who unlike her, have been gaslighted and forgotten by the medical system and often do not recover. Senator Johnson also immediately picked up on this too, and politely suggested she collaborate with the (far more common) victims of COVID vaccine injuries.

Note: every medication, policy or decision has a trade off between risks and benefits. Propaganda preys upon people’s inability to accurately compute this from limited data by emphasizing one side of the equation and downplaying the other (which for example is why many people who follow mainstream media sincerely believe “long COVID” is a much larger issue than COVID vaccine injuries). Likewise, in this hearing, vaccine proponents repeatedly used the often repeated line “vaccines save lives,” which while true, is immensely deceptive because it omits that in many cases vaccines also kill more people than they save or injure far more than they save.

Other facets of the hearing which jumped out to me included:

1. After vaccine proponents (once again) attempted to whitewash all criticisms of the vaccine by highlighting how incredibly well the COVID response was done in spite of the challenges faced at the time, one Senator pointing out that we need to stop repeating that fable and it is only by acknowledging that serious mistakes were also made that we can avoid making them again in the future (particularly because of how damaging they were to our children).

2. Repeatedly highlighting (as the earlier quotes show) that the senior FDA analyst who demonstrated vaccine harms were being covered up, Dr. Szarfman, was ostracized by her peers and shut down by her superiors. This in turn is very similar to the experience of Andrew Mosholder (a child psychiatrist and FDA safety officer) who in 2003 correctly determined data showed Paxil caused suicidality in children, after which his superiors blocked him from releasing the report (and then a year later, once it was leaked, focused on catching the leaker rather than acting on its findings).

3. There were numerous attempts to dodge FOIA requests which included the FDA simply stopping (potentially incriminating) internal data releases of COVID-19 vaccine adverse event data like Szarfman’s.

4. One witness highlighting that all the vaccine adverse reporting was designed to only report adverse events “no one cared about” such as injection soreness or a fever rather than serious and life changing adverse events people had.

5. Szarfman’s analysis showing 45 conditions were strongly linked to the COVID vaccines (with an upper and lower bound for their increased frequency). Assuming I interpreted the chart shown in the hearing correctly, when put in descending order by the lower bound (which makes a stronger case for causality), the conditions most conclusively linked to the COVID vaccines are as follows:

• Strongest link: Product administered to patient of inappropriate age (Moderna), Acute myocardial infarction (Pfizer), Brain natriuretic peptide increased (Pfizer), Asymptomatic COVID-19 (Pfizer), Electrocardiogram ST segment elevation (Moderna), Blood pressure systolic (Pfizer), COVID-19 pneumonia, Acute myocardial infarction

• Strong link: Brain natriuretic peptide increased, Ischaemic stroke, Drainage, Dementia, Pneumonia aspiration, Cardiac telemetry normal (which indicates it was being frequently checked due to heart concerns), Paraesthesia ear, Magnetic resonance imaging heart (which is done to evaluate for myocarditis)

• Moderate link: Blood pressure systolic (all vaccines), Embolic stroke, Basal ganglia stroke, Cardiac assistance device user, Cardiac telemetry abnormal, Ejection fraction, Sinus rhythm, Hypertensive emergency

• Weaker but Notable: Bell’s palsy, Sudden cardiac death, Pulmonary infarction, Bradykinesia, Cerebral artery occlusion, Diastolic dysfunction, Aortic stenosis, May-Thurner syndrome, Acute left ventricular failure, SARS-CoV-1 test, Cardiac failure chronic, Agonal rhythm, Cholecystitis acute, Product substitution, COVID-19 immunisation, Cardiac telemetry abnormal, AST/ALT ratio abnormal, Diaphragmatic spasm, Mastoid disorder, Percutaneous coronary intervention, Aortic aneurysm rupture, Thalamic infarction

That chart, in turn, was quite notable to me, as most of the conditions on it I’d previously concluded were probably linked to the COVID vaccines as I’d seen people develop them shortly after vaccination, and in many cases, would never have otherwise expected them to. That, in turn, highlights a recurring theme with the COVID vaccines—the harms were frequent enough that people like me with extremely limited datasets could accurately detect the signals of harm from the vaccines—so it’s hard to conceive they were “too rare” for health authorities who had access to infinitely larger pools of data to identify.

6. Much in the same way the early polio vaccines had major issues when their production was scaled up for the general population, the COVID vaccines did as well (because they switched from duplicating the mRNA with PCR to having bacteria mass synthesize it—resulting in dangerous synthetic bacterial DNA contaminating the vaccines). At this hearing, I learned there was supposed to be a comparison study between Pfizer’s old and new production methods of the vaccine (which like many other “required” tests was magically never done), and that later Pfizer’s vaccine (the dilutant) was changed again without being tested.

Finally, a few of the participants were quite blunt about how egregious this all was. Here for instance, Senator Hawley points out that the entire COVID vaccine affair was an unconscionable money grab the government pushed along while “All of the public health problems get offloaded onto other people, namely the American people…All of the costs get borne by the patients” (after which Johnson highlights how the government, from the start, also abandoned the vaccine injured).

Or to quote one witness, who after highlighting that the emergency use authorizations for the COVID vaccines was contingent upon extremely robust safety monitoring of them in the marketplace stated:

This isn’t a blind spot. The FDA was completely blind to adverse events, and the CDC wasn’t even looking. There was a savior in the ranks of the FDA who correctly identified the problem, appropriately worked with the inventor of EB data mining to create a solution, communicated the fix to everyone who would listen. The problem is no one listened. Luck was not on our side.

The CDC failed to look. The FDA failed to fix a broken system that the CDC touted as the gold standard. The HHS failed to protect us, especially after our freedom of choice was assaulted by the president threatening us all with our patience is wearing thin. FOIA evasion was well practiced and discovered, obviously, not through a FOIA. Simply put, during the largest pharmaceutical rollout in human history, pharmacovigilance did not exist.

That is the betrayal of our time, so vast that we cannot even count its casualties.

Masking Illness

One of my foundational beliefs has been that humanity has experienced a massive decline in vitality over the last 250 years as:

•Many of my mentors reports that from the start of their careers to the end, patients became sicker and less responsive to the therapies which had previously worked on them.

•In many cases, they found both colleagues and their own mentors shared these observations, and in a few cases, confirmed their mentors had received a similar response from the people who trained them.

•Corroborating this, I found numerous medical texts, beginning in the early 1800s which showed new degenerative diseases had begun emerging and detailed examples of treatments being used with a much higher degree of efficacy than when I observe in the present.

•Many data sets show chronic illness has continually increased as time has moved forward.

One of the insidious things about this decline is that since it is never talked about (rather medical training just focuses on the “dark ages of infectious disease vaccines miraculously vanquished”), it is very hard for medical practitioners to recognize this larger trend has occurred. As such, each new generation of medical practitioners becomes habituated to the current baseline of illness, and unless they live at a time when there is a massive and permanent spike in illness, rarely are cognizant of what has occurred.

Because of this, we’ve put a lot of thought into what is actually causing this massive decline in human vitality, have identified roughly 10 key agents, and believe one of the most impactful ones is widespread vaccination (e.g., the permanent spikes in illness typically coincide with the introduction of particularly dangerous vaccines, beginning with the original smallpox ones and most recently with the COVID-19 vaccines).

Doctoring Data

Over the years, I’ve heard many different definitions of intelligence, one of which is one’s aptitude for manipulating logical symbols towards a desired outcome. In turn, many facets of human society ultimately boil down to competing parties trying to rearrange what’s there to their advantage (e.g., rhetoric is essentially the skill of how you do that with your words to control people).

One of the particularly unfortunate things about science is that while it began as a tool those interested in seeking truth relied upon to further that goal, once this started producing results and social capital, the unscrupulous members of society seized upon science to promote their own agendas and no longer prioritized accuracy.

Because of this, a lot of “science,” much like rhetoric, is simply an exercise in rearranging the data obtained (or how the data is obtained) until it can be put into a configuration which credibly supports your message. As such, being able to interpret the scientific literature has become somewhat of an art, as you need a complex toolset to separate fact from fabricated fiction.

Vaccine Masking

Vaccines have a dose-dependent toxicity, so as you take more of them, you are more likely to develop chronic neurological or autoimmune diseases. Since the vaccine industry, like many others, is continually growth focused (and has very unique protections from the Federal government), there has been a continual trend to give people more and more vaccines.

This has reciprocally led to a sustained increase in chronic illness (sometimes beginning immediately following vaccination) which has become harder and harder to cover up as it gets increasingly frequent. To address this, the vaccine industry has used increasingly aggressive methods to censor those injuries, so people do not connect them to vaccinations, and for those who nonetheless do, they will be widely ridiculed by those around them. This for example is why:

•Medical journals used to publish severe vaccine injury case reports (many of which are summarized here) but now never will.

•Television stations used to regularly air programs on individuals having their lives ruined by vaccines (56 of which I compiled here), but now never do due to Clinton-era regulatory changes allowing pharmaceutical advertising to buy out the media (which RFK is presently trying to reverse).

•So much work has gone into making it socially acceptable to demonize anyone who questions vaccines and hence end any question on the subject.

•Tech platforms (until recently) aggressively censored content critical of vaccination.

Likewise, a variety of absurd epistemological frameworks have been erected to sanctify the notion vaccines are completely safe and cannot harm you.

Aaron Siri, for example, in his book about the religion of vaccines (Vaccines Amen) highlighted that all of vaccine science is predicated on the notion that vaccines are completely safe and effective, so any evidence, regardless of how weak it is that supports this is viewed as true, while any evidence which refutes it, regardless of how robust it is, is typically disregarded.

This in turn, has allowed a rather remarkable standard to be accepted within vaccine clinical trials where rather than vaccines being tested against placebos, they are tested against other vaccines, and only deemed to be dangerous if their rate of harm is significantly higher than the other vaccine. Because of this, it is possible to “chain” vaccine studies together, where increasingly toxic vaccines are deemed “safe” (as they are only somewhat more harmful than the one that immediately preceded them and the newer vaccine was tested against).
Note: the justification for this experimental design is that “vaccines are so safe and effective and lifesaving that it is unethical to deny children in trials vaccines, so rather than placebo, they should get the previous “safe” vaccine.” Beyond that being absurd (as it’s far more unethical to inject every child with an untested vaccine), in many cases, the vaccine “placebo” is a completely different vaccine (which entirely defeats the logic of that argument).

One of the most insidious things about this framework is that it effectively hides the continual increase in chronic illness, as it occurs in tandem with increasing vaccine side effects being viewed as “normal” and not elevated from baseline (whereas they clearly are were the vaccines to be compared to an actual placebo).

Note: as you might expect, most of the basic studies necessary to determine vaccine safety, especially multiple at a time, have never been done because they are “unethical.” Conversely, when the studies that can be done are nonetheless done (retrospective or observational), they all show vaccines cause a massive increase in illness (typically a 2.5 to 9 fold increase), but are always dismissed for not having placebos (which can never “ethically” be done).

Interestingly, a very similar safeguard is put into Federal vaccine safety monitoring.

Specifically, the CDC uses the Proportional Reporting Ratio (PRR) to help identify potential safety signals in VAERS data (which only exists because a law forced the government to have a public reporting system available). The PRR compares the proportion of a specific adverse event reported for a given vaccine against the proportion of that same event reported across all other vaccines in the database to determine if that side effect is disproportionately higher in the vaccine in question. The FDA likewise utilizes a similar disproportionality analysis which uses additional statistical measures that reject certain links the PRR would establish.

While this approach can detect fairly unique side effects linked to a specific vaccine, it has major blind spots:

• Due to the top half of the formula, it struggles to flag individual side effects for vaccines that cause a high overall rate of adverse events. If nearly every side effect is elevated for that vaccine, no single one stands out proportionally compared to the vaccine’s own other reported events.

• Due to the bottom half of the formula, it cannot easily detect side effects that occur across many different vaccines (e.g., certain neurological, autoimmune, or cardiac events), because those events are also elevated in the comparator group, making the vaccine in question look less unusual.

• Additionally (due to the bottom half) when two or more similar vaccines enter the market at the same time and both have much higher adverse event rates than older vaccines, the PRR becomes heavily masked as the “all other vaccines” baseline gets flooded by reports from the other new vaccine(s), so neither one stands out as disproportionate.

When I learned about the PRR, I immediately noticed how well-engineered it was to conceal the ever increasing harm from vaccination, as harm would always be assessed against a previous (already increased baseline) and increases large enough to trigger a signal were hard enough to reach they would rarely if ever happen. More remarkably, this system also provided the magic solution for an incredibly toxic vaccine being released onto the market, provided there were at least two different ones released simultaneously.

As it happened, seven weeks after the first COVID-19 vaccines received Emergency Use Authorization, and as VAERS began receiving a surge of adverse event reports, the CDC issued its VAERS Standard Operating Procedures for COVID-19. In that document, the agency formally designated the Proportional Reporting Ratio (PRR) as one of its primary tools for routine safety signal detection, stating it would perform PRR data mining on a weekly basis or as needed (something I am almost certain was done as it was the only way to hide the massive signal of vaccine injury).

Note: despite this, the CDC eventually stopped doing even this to (while making numerous false statements on what it had done) and ultimately deferred to the analysis to the FDA’s “more robust system.”

The net result of this approach hence was that things like this “were not signals” because they were being compared to other massively elevated baselines.

Szarfman in turn came up with a fairly obvious solution to this problem: rather than compare an mRNA vaccine to all other vaccines plus the other mRNA vaccine, you don’t include the other mRNA vaccine in the comparison (red vs. blue rather than red vs red plus blue). However, despite being incredibly obvious, since that revealed critical issues with the COVID vaccine the existing approach masked, it hence was not acceptable (and we only even learned about it thanks to Johnson’s lengthy investigation).

One in a Million

Since vaccine injuries are frequent and unavoidable, the medical industry’s solution has been to reframe them as “very rare” so people are not alarmed by injuries they run into, and at some point settled on the phrase “that injury is one in a million”(which may have originated from the smallpox vaccine’s encephalitis rate — somewhere between 7 and 1,444 per million vaccinated), alongside assurances robust support is in place for the one in a million who are injured.

Because of that, a schizophrenic dichotomy exists with vaccine injuries where:
1. Common but relatively inconsequential ones are publicized (e.g., injection site pain or being ill for a few days), after which concerns about them are dismissed by highlighting the inconsequential nature of the injury.
2. The severe and life altering ones which affect large numbers of people are relentlessly denied.
3. The extraordinarily rare ones which are unique to specific vaccines are emphasized, and in some cases results in the vaccine being pulled if an alternative is available (e.g., this happened with one rotavirus vaccine).

This hence makes it possible to create the illusion of robust vaccine safety, as people will assume that if regulators are strict enough to go after extraordinarily rare things, they will definitely go after common things (further reinforced by the focus on inconsequential reactions). That, I believe is also why:

•The system used in VAERS to detect injuries (PRR) can only detect unique and rare injuries, whereas the common injuries everyone cares about seen across vaccination (category 2) are essentially never are flagged by it.

•Monitoring systems like V-safe which were designed to detect category 2 injuries were discarded by the FDA and CDC once they realized it was detecting large numbers of category 2 injuries.

•The NIH was initially very interested in providing support to individuals like Brianne Dressen who received severe neurological injuries from the vaccines (and even provided a costly treatment that somewhat worked), but once they realized her injury wasn’t “rare,” pivoted to ghosting her and blocking the publication of the research studies she participated in (as a very rare side effect they could treat would increase confidence in vaccination, whereas acknowledging a common one would decrease confidence and exceed their budget to treat every instance of).

•The FDA made a big deal of temporarily pausing the J&J vaccine due to a few cases of a very rare blood clot (cerebral venous sinuses thrombosis), while ignoring the far more common clotting risk of the mRNA vaccines.

Conclusion

Over the eons, many have concluded one of the greatest mistakes humans make is believing they can hijack and dominate natural processes rather than recognize their influence over them will be temporary at best and create significant strain in the process (e.g., most pharmaceutical drugs work by artificially shifting the enzymatic baselines within the body, something that commonly provokes resistance to the drugs and increasing side effects as the body deviates further and further from its baseline).

However, a major reason why I believe in the “law of equilibrium” is because in instances where it appears to not be being followed (e.g., during a positive feedback loop, or when expected negative feedback fails to materialize) on a broader scale it still is and the expected changes still occur.

Because of this, in instances where it appears people have been able to successfully suppress a natural equilibrium, a broader feedback loop will eventually take over. For example, in the case of vaccines, for 250 years, we have seen a continually escalating cycle of more and more powerful methods being used to push vaccines upon an increasingly resistant public (which has been incredibly depressing to witness as I’ve lost count of how many people I know whose lives were ruined by vaccines and then gaslit by everyone around them as the majority of people could not conceive these injuries could ever occur in the first place).

However, while propaganda has an incredible ability to sweep things under the rug, it has limits, and because of just how many people were injured by the COVID vaccines (e.g., polls consistently show 12-20% of those vaccinated were injured; often seriously), it has become impossible to cover up (e.g., 49–55% now believe the vaccines caused significant unexplained deaths). Furthermore, a much broader loss of trust has occurred in vaccines, the medical system, and health authorities that dwarfs anything else in the history of medicine (all of which I detailed here). Consider for example how scathing Hawley’s language was towards the pharmaceutical industry; we never heard statements like these before and they are only being said (before the midterms) because a large portion of the electorate supports them. The tide, at long last, appears to be turning—not because the truth changed, but because it finally became too large to hide.

To learn how other readers have benefitted from this publication and the community it has created, their feedback can be viewed here. Additionally, an index of all the articles published in the Forgotten Side of Medicine can be viewed here.

• DMSO is an “umbrella remedy” capable of treating a wide range of challenging ailments due to its combination of therapeutic properties (e.g., improving circulation, reducing inflammation, protecting cells from a myriad of otherwise lethal stressors, and reviving dying cells).

• These properties make DMSO uniquely suited to treat “incurable” neurological disorders, and in conjunction with forgotten research on the effects of microcirculatory impairments, reshape our understanding of the causes of neurological (and psychiatric) diseases.

• DMSO has shown remarkable promise for cognitive impairment, brain fog, and memory loss from a wide range of causes (e.g., aging, vascular disease, anesthesia, post-COVID or pharmaceutical poisoning), along with improving sleep quality and dream vividness — often by resolving the pain, breathing difficulties, or neurological conditions (e.g., restless leg syndrome) that were preventing restorative sleep.

• Extensive data supports DMSO’s use for the major neurodegenerative diseases — including Parkinson’s, Alzheimer’s, ALS, Huntington’s, and multiple sclerosis — and protein misfolding diseases such as prion disorders and Niemann-Pick disease, where DMSO’s ability to act as a chemical chaperone (stabilizing proteins and dissolving toxic aggregates) and augment cranial drainage is particularly relevant.

• Numerous psychiatric conditions (e.g., schizophrenia, depression, anxiety, and PTSD) have responded to DMSO, as have seizures and epilepsy, movement disorders, encephalitis, myasthenia gravis, and hydrocephalus.

• DMSO has also produced striking developmental improvements in children with Down syndrome across multiple clinical studies, along with many other neurodevelopmental disorders.

• This article will synopsize the extensive data demonstrating DMSO’s efficacy for CNS neurological diseases (approximately 2000 studies and 200 pertinent reader testimonials), share pertinent (non-DMSO) discoveries we’ve made about neurological diseases over the years, and then conclude with practical guidance on DMSO protocols and complementary approaches that also aid in the treatment of common neurological disorders.

DMSO has remarkable therapeutic utility across a wide range of challenging conditions yet is largely unknown. Recognizing this, I spent the last two years compiling the data which shows DMSO treats a wide array of conditions including lung issues (e.g. COPD and Asthma), skin issues (including hair loss), many different types of pain, arthritis, tissue injury (e.g., sprains or burns), eye issues (e.g., vision loss or dry eyes), autoimmune disorders, dental issues, gastrointestinal diseases, infections, and cancers (along with how DMSO’s efficacy can be further enhanced by combining it with pharmaceuticals or natural therapies).

As each of the above articles, drawing upon thousands of forgotten research studies, made a convincing case to try DMSO, they collectively received millions of views, and thousands of readers (currently over 6000) reported to me that improvements happened across a vast swathe of conditions they were dealing with, many of which were life-changing or match those in this 1980 news program:

More importantly, much in the same way Mike Wallace successfully revived interest in DMSO in 1980 after the FDA successfully spent two decades largely burying it, this series has again created a renewed interest in one of the most accessible and effective remedies available to us.

Since DMSO is particularly well-suited to treating neurological diseases (which often “nothing can be done about”), some of the most profound stories I’ve received related to neurological diseases. Likewise, consider this conversation I had a few days ago with James Miller MD, a physician, who inspired by the results reported here, began using it in a large number of his patients, and frequently seeing astonishing results he was initially left in disbelief by.

JM: Hope you are doing well. Just checking in, haven't seen a lot of your postings lately.

Me: Sorry, I turned into a ghost. I have been working as hard as I can on getting the DMSO neurology article done; there’s just so much to unpack.

JM: It is my impression, with no hard data, that ~80% of everything people see neurologists for goes away with DMSO. That is what my patients reflect back to me who choose to trial DMSO for their neurological problems.

Me: That’s basically why I’ve been working so hard on this.

Likewise, I recently received a remarkable testimonial from an ALS patient (the horrible terminal disease we’ve seen decades of research fundraisers for) that shows there may be real hope for this incurable disease.

Note: if any of you have profound DMSO stories you would like to share, please share them here and consider reaching out to Rebecca so she can document them.

Lastly, for those of you seeking DMSO protocols and recommendations, they can be found at the end of this article (which I advise reading first to better understand those instructions).

Cellular Protection

DMSO is well-known for protecting cells from many otherwise deadly stressors. For example, it prevents freezing damage to cells, which made modern cryopreservation (cryomedicine) possible, and extensive research shows that this protective effect works across nearly every type of tissue (along with repeatedly saving human fingers and animal ears or limbs^1,2,3 from being lost to frostbite). As the cells of the nervous system are particularly sensitive to injury (and often unable to heal from it), DMSO’s protective qualities are particularly useful for it. Core mechanisms of protection include:

•Reducing oxidative stress^1,2,3,4 and neutralizing harmful free radicals^1,2,3 (e.g., those caused by radiation like hydroxyl) through scavenging charged ions (e.g., H⁺) and forming protective DMSO radicals (along with decreasing lipofuscin formation in human glial cells, reducing the cumulative oxidative damage that drives cellular aging). In hippocampal slices DMSO also counteracted this oxidative stress,^1,2 and in cerebellar granule neurons, this prevented oxidative stress-induced apoptosis and cell death by reducing early mitochondrial impairment and DNA fragmentation^1,2 (with similar benefits also being seen when DMSO was combined with CDK and G9a inhibitors^1,2). Trace amounts of DMSO also protect plants from ozone gas injury and counteract reactive hypochlorous acid, superoxide, and hydrogen peroxide (while simultaneously working synergistically with oxidative therapies and not impairing neutrophil viability).

•Increasing the production of ATP in cells, and facilitating producing it when energy production has been compromised (e.g., minute concentrations of DMSO, as low as 0.000025–0.25%, have been shown to increase cellular metabolism such as by shunting metabolites from glycolysis to the mitochondrial Krebs cycle or to make a part of the mitochondria able to synthesize ATP without the rest of the mitochondria being present^1,2,3,4,5). DMSO also prevented hydroxyl radical-induced mitochondrial aconitase inactivation, ATP depletion, and neuronal damage. Furthermore, DMSO increased the metabolism of pyruvate and glucose in brain slices, protected mice from otherwise lethal nitrogen asphyxiation, and in a study where mice were decapitated, DMSO prolonged how long the mice continued to gasp (breathe) and hence how long brain function continued.
Note: many animal studies are exceedingly cruel and not something I support; however, as they have been done, I felt it was important to share the knowledge certain DMSO ones provided so it would not be necessary to repeat them to acquire that data.

•Protecting cells from dying once the blood supply is cut off (a key reason why so many readers have been able to avoid permanent disability from a stroke), including by preventing the rapid influx of calcium or sodium ions that frequently triggers apoptosis (cell death), and reducing the activity of caspase proteins (which trigger cell death) in the liver, heart, and airway epithelial cells.

Note: ^⬖ designates natural substances used in conjunction with DMSO.

These properties hence allow DMSO to:

•Protect neurons throughout the brain (e.g., in the hippocampus) from a wide range of excitotoxins—which are well-recognized as a common cause of neurodegeneration,^{1,2,3,4,5,6,7,8,9,10} (e.g., in one study DMSO restored 66.7-76.1% of normal electrical activity following glutamate toxicity), and to enhance the protective effects of other protective agents (e.g., syringaresinol,^⬖ isoquinolinesulfonamides, curcumin^⬖ and ginkgo biloba^⬖).^1,2,3,4,5,6

Note: DMSO is routinely combined with other neuroprotective agents such as curcumin^⬖, melatonin,^⬖ baicalin,^⬖ butein,^⬖ icariin,^⬖ naringin,^⬖ 4-PBA, and BPV(phen) , various Chinese medicinals, nitrone compounds, and capsaicin derivatives^⬖ (i.e., in the studies just listed, these combinations reduced neuroinflammation, oxidative stress, ER stress, and apoptosis while enhancing mitochondrial function and autophagy in neuronal cells).

•In carbon monoxide poisoned rats, reducing cerebral neuronal alteration and degenerative rate, along with total cardiac injury score (and also reducing liver injury if combined with ethyl pyruvate).^1,2 Glibenclamide further improved neurological deficit scores, reduced neural cell breakdown (NSE and S-100β) and reduced inflammatory TNF-α and IL-8 levels. Lastly, DMSO’s antioxidant properties have been proposed to confer a potential neuroprotective role in carbon monoxide poisoning.^1,2

•Protect normal cells against chemotherapies such as preventing brain injury, oxidative stress, inflammation and neuronal death from cyclophosphamide (in combination with Scenedesmus obliquus^⬖), cisplatin (alone or in combination with DMFM)^1,2,3 and doxorubicin (where in combination with curcumin^⬖ prevented “chemobrain”).

•Prevent neural cell damage and death from a variety of metals such as lead (alone or in combination with thymoquinone^⬖)^1,2,3 aluminum (alone or in combination with GSK-3β, 3MA or dantrolene)^1,2,3,4 cadmium, mercury (in combination with melatonin^⬖ or curcumin^⬖),^1,2 the toxic form of manganese (alone or in combination with NAC or PAS-Na or a FTO inhibitor),^1,2,3,4 toxic doses of lithium (in combination with curcumin^⬖) along with arsenic (in combination with 3-MA), zinc nanoparticles (in combination with quercetin^⬖) cobalt chloride (in combination with curcumin^⬖) and fluoride (in combination with M3OMG), and thioacetamide.
Note: neuroprotective effects from DMSO in those studies included reductions in oxidative stress, neuronal cell death, calcium dysregulation, intracellular calcium release, birth defects, and histopathological brain damage.

•Protect animals from organophosphates, including otherwise lethal doses of nerve gas^1,2,3,4,5,6 (or to enhance the efficacy of antidotes and reduce brain damage^1,2,3) and to treat snakebites and their associated swelling in humans, cats, horses and dogs.^1,2,3,4,5,6 Similarly, in two horses swarmed by African bees, IV DMSO as part of a combination protocol was able to reverse the severe neurological impairment created by the bee venom within five hours.

•In mice and rats, oxidative stress and neurotoxicity (e.g., in the hippocampus) from a variety of agents has been counteracted by DMSO in combination with another therapeutic agent: ethanol (nimodipine, DAPT or MSM),^1,2,3 methamphetamine (curcumin^⬖) mold aflatoxin (in combination with extracts of Chelidonium majus^⬖ or artichokes^⬖),^1,2 liquid petroleum gas poisoning (a p38MAPK inhibitor), diethyl phthalate and bisphenol S (vanillic acid^⬖), thrombin (estrogen), trimethyltin (carvacrol^⬖), tunicamycin (4-PBA) chlorpyrifos (niosomal hesperidin^⬖ or taxifolin^⬖), calyculin A (melatonin^⬖) fipronil (malvidin hydrochloride^⬖), thapsigargin (Activin A). Likewise, melatonin^⬖ mitigated PBDE-47 (fire retardant) neurotoxicity in PC12 cells.
Note: high-dose ivermectin causes neurotoxicity, limiting its use at higher doses. In one reported case, IV DMSO facilitated a full neurologic recovery in a comatose dog that had ingested a toxic dose of ivermectin paste.

Likewise DMSO also protects cells from a variety of harmful non-chemical stressors by:

•Protecting cells (including in a prophylactic manner) from being damaged by (often otherwise fatal) radiation exposures.^1,2,3,4,5 For example, DMSO prevented X-ray and gamma ray DNA damage to hamster ovary cells, fruit flies and cerebral organoids (e.g., by accelerating DNA repair),^1,2,3,4 and to prevent the harmful (bystander) signals irradiated cells emit in their vicinity from damaging non-radiated cells along with protecting certain bacteria from x-ray exposure.^1,2,3 Likewise, DMSO has been repeatedly shown to reduce chromosome damage from radiation^1,2 and prevent radiation from creating harmful free radicals. As such, DMSO has been shown to protect animals (e.g., mice, rabbits, dogs and monkeys) from often otherwise lethal doses of radiation, and prevent radiation tissue damage (e.g., to the bone marrow, intestinal lining, stem cells, eyes or skin),^{1,2,3,4,5,6,7} and, due to it preventing radiation damage in non-cancerous cells, DMSO has been extensively used as complementary cancer treatment.

Note: DMSO has been combined with many other substances to protect animals from radiation damage such as astragaloside-IV^⬖ (preventing neuronal senescence), rapamycin (repeatedly preventing X-ray induced malformations of cortical development in rat offspring)^1,2 thymoquinone^⬖ (reducing brain peroxynitrite) or a glycogen synthase kinase-3β inhibitor (preventing brain tissue necrosis).

•Preserving the function of nerve fibers exposed to UV radiation.

•Treating a wide variety of burns (detailed here) and protecting the brain from heat damage (along with the previously mentioned cold injuries).

•Protecting cells from osmotic stress and dehydration (and in combination with nimodipine, protect neural cells from osmotic shock while inducing neurite growth).

•Protecting glial cells from being destroyed by sonic disruption via an ultrasonic vibrator (78% vs. 13% survival), and in conjunction with a TRPV4 antagonist, protect hippocampal neurons and microglia from infrasound-induced (16Hz/130dB) apoptosis.

•Preventing the dramatic increase in germ cell death, lifespan shortening, and oxidative stress caused by strong static magnetic fields and likewise preventing similar harm from continual exposure to electrically generated air ions.

•In combination with curcumin,^⬖ protect fetal brain, kidney, and liver from damage caused by low-frequency electromagnetic field (EMF) exposure during pregnancy.

DMSO Safety

Every substance has an effective dose (how much elicits a therapeutic effect) and a toxic dose (how much elicits a harmful effect) with the balance between these two often deciding the value of a therapy (e.g., mercury partially treated syphilis but for centuries caused far more harm than good due to its severe neurotoxicity, and while often effective, certain modern therapies such as chemotherapy cause a lot of issues due to their toxic doses being so close to the therapeutic doses they are routinely prescribed for). Further complicating this, there is often no “correct” dose for everyone, so standardized ones are chosen which work for the majority of the population (which leads to sensitive patients those doses are too high for being routinely injured and then gaslighted by the medical system).

For this reason, I try to utilize therapies with a very wide therapeutic window (meaning the effective dose is much lower than the toxic one), but even in those cases, I still sometimes encounter patients who react to these “safe” doses and need much lower ones.

In the case of DMSO, what has been striking to me is how wide its therapeutic window is (demonstrated by the fact it has an extremely high, “practically non-toxic” LD50 and that rather than harm cells, it will protect them from a wide range of otherwise lethal stressors). Given this and how rapidly DMSO distributes and dilutes in the body, outside of animal experiments where large amounts of DMSO are injected, it is extremely unlikely DMSO can reach a toxic dose (so even in a human safety study where extreme doses were used for a prolonged period, no issues occurred).

That said, with (clean) DMSO, the following issues do exist:

1. Excessive DMSO commonly creates temporary itching and irritation on the skin. This can be avoided by using lower topical concentrations or a natural agent which prevents DMSO’s irritation—but nonetheless still routinely happens due to users using excessive doses.

2. In some individuals, DMSO will create an unpleasant odor (which often can be addressed through one of the methods detailed here).

3. A small number of people (one estimate pegged it at 1 in 2000) are allergic to DMSO. For this reason, it is advised to use topical DMSO first, ascertain if you are having an allergic reaction (rather than a typical skin irritation) and if so, back off, and absolutely avoid systemic applications (e.g., oral).

4. DMSO can bring toxic substances into the body, and in the early days of DMSO, there were rare reports of people becoming ill for a few days after having both DMSO and (now banned) pesticides contact their skin (along with one person who had a nicotine overdose). For this reason, it is generally advised to always wash your skin (with water) after applying DMSO (that has had time to dry), and in modern times, I have not come across reports of this being an issue.

5. DMSO will effectively transport allergens into the skin (leading to it being periodically used to patch test allergens). As some people are allergic to seemingly safe natural substances, this can occasionally cause issues (e.g., in the one report I received, hives followed a DMSO arnica preparation—as a surprising number of people are allergic to arnica).

6. All anti-coagulants carry the risk of excessive bleeding. Since DMSO uses a different method of anti-coagulation, this risk is much smaller, but still possible (e.g., three readers shared it seemed like their nosebleeds increased, and I’ve found one serious reaction in a case report).

7. One of DMSO’s greatest uses is it potentiating medications, but this also means it can increase their toxicity (even though, as the previous section shows, DMSO frequently counteracts toxicity). This has primarily been observed with alcohol, barbiturates, and to a lesser extent benzodiazepines (e.g., one cat study found adding diazepam to harmless IV DMSO caused fatal hypotension and ventricular fibrillation) but modern reports also exist of it increasing the frequency of side effects from more toxic medications (e.g., chemotherapy and fluoroquinolones). A major question is if this is also an issue with anticoagulants, as limited data and a lack of adverse reports suggest it is not, but simultaneously, due to the theoretical risk, we always advise patients to carefully monitor their blood coagulation (which is typically done for anticoagulant regimens). For all of these reasons, it is typically advised to take DMSO at least two hours away from pharmaceutical medications as this minimizes the potential for adverse potentiation.
   Note: the issues with DMSO and alcohol are discussed in more detail here.

8. In sensitive patients, temporary reactions to DMSO (e.g., headaches) can occur with excessive doses. I have also received two reports of extraordinarily sensitive patients (due to longstanding toxicity burdens) who became worse after DMSO due to it mobilizing stored toxins.

9. Over weeks, inhaling high doses of DMSO was found to harm rabbits, so for this reason, DMSO researchers (except for one successful ARDS study) avoided studying nebulized DMSO. Modern DMSO users, however, made the logical extrapolation to start nebulizing DMSO, and found significant benefit from it (e.g., remarkable results with COPD). Those who investigated this concluded a theoretical risk (they’d never observed) existed of nebulized DMSO neutralizing surfactant and collapsing the lung, so they cautioned against higher doses (which will also leach plastic from most nebulizers). Presently, one person (patient of a colleague) has had this happen to them (who due to their body type was already at high risk of a pneumothorax), but outside of that, a lot of people have successfully nebulized DMSO at much higher doses than we’d use without issue.

10. Similar concerns also existed with pregnancy as after injecting high doses of DMSO into or near fetuses was seen to cause developmental damage, very little research was conducted in this area (despite those doses being impossible to reach with standard DMSO uses). Fortunately, large numbers of pregnant and breast feeding parents having used DMSO without issue.
    Note: in a future article I will compile all the research which has been done. Presently, the most definitive (but still not definitive) study showing DMSO safety in pregnant mothers is this one.

11. When cells are exposed to high concentrations of DMSO for prolonged periods (which are impossible to reach in the body), cellular and microcellular injury will occur. Of note, the toxic DMSO thresholds for cancer cells are much lower than normal cells, which is likely one reason why DMSO is an excellent tool for cancer.

Because of the previous, virtually every study I’ve read which utilized DMSO did not report adverse effects from DMSO, serious adverse reports from DMSO are extraordinarily rare, and in almost all instances, those resulted from IV DMSO which was given in conjunction with an embolization agent or stem cells (whereas the much rarer ones from IV DMSO alone typically reversed once the infusion stopped¹,²). As some of these were quite concerning, and did not match what we’d ever seen from IV DMSO (such as in this comprehensive safety study in monkeys or what I’d seen reported by countless practitioners using IV DMSO), I spent a while looking into this and concluded:

•The liquid embolic agents have independent toxicity and may sometimes travel and accidentally obstruct other parts of the circulation (as many of the reports seem to indicate this had happened, and once I checked, product warning labels acknowledged this).

•Many of the patients who receive IV DMSO stem cells are extremely fragile cancer patients (who went through high dose chemo), and hence are more likely to react to therapies, especially a higher doses. Likewise, one study found while dogs generally did not have issues with DMSO, those with chronic kidney disease did from higher IV doses.

•Due to DMSO’s safety, very high IV doses are used. These are often sufficient to create an osmotic shock which will rupture the weakest membranes (e.g., hemolysis is a common complication of higher IV DMSO doses, and in this horse study, was seen alongside significant—but temporary—symptoms when 40% DMSO at ten times the normal dose was rapidly infused into horses).

•The concentrations used for the previous applications are sufficient to leach phthalates from IV tubing. Phalates in turn can cause heart arrhythmias and one DMSO doctor found this was an issue with DMSO injected into the bladder until he switched to different tubing.

•Since DMSO increases parasympathetic activity through cholinesterase inhibition, it can slow the heart rate, particularly if a large amount of it suddenly reaches the heart, so while it typically does not alter cardiac rhythm and has been observed to normalize the reactivity of the autonomic nervous system, at high doses it can be arrhythmic (e.g., a 1-3% DMSO slightly increased the heart rate,^1,2 while 6-10% significantly decreased it but could be reversed with atropine^1,2).

•While practitioners (in recent days and throughout the DMSO literature) using much higher IV DMSO doses than we do do not appear to have run into issues, significant care in identifying appropriate IV DMSO dosing is likely warranted.

Lastly, due to DMSO’s widely recognized safety and negligible toxicity and ability to rapidly transport substances throughout the body, it is often used as an “inert” ingredient to deliver other pharmaceuticals and as a solvent or vehicle to facilitate evaluating the biological effects of large numbers of substances (as without being dissolved or transported, it is often impossible to test them).
Note: in addition to testing therapeutic effects, DMSO will also be used to deliver a harmful agent to trigger a disease^{1,2,3,4,5,6,7,8,9,10,11,12,13} (which makes it very time consuming to filter out therapeutically relevant DMSO studies) or to evaluate a therapy’s mechanism of action by seeing if the specific inhibitor DMSO delivers blocks the therapy’s efficacy (e.g., many Chinese acupuncture studies like this exist^{1,2,3,4,5,6,7,8}).

As similar benefits are seen with many different therapies combined with DMSO (that DMSO alone would cause), this has led me to conclude:

•The toxicity of many toxins has been underestimated due to DMSO’s protective effects counteracting them (something also recognized by a few neurology researchers).

•A key reason benefits seen in pre-clinical studies do not appear in clinical ones (an extraordinarily common problem in scientific research) is because DMSO is no longer being used—particularly since I occasionally find studies where DMSO alone, rather than simply being the control, is also tested against saline, and in a significant number of those DMSO alone had a therapeutic effect.

Lastly, in writing this article, I have tried to condense thousands of pertinent studies into something feasible for everyone to read, while also ensuring that this forgotten literature remains available to researchers and authors wishing to advance this work. In that, I made the decision to include the combination studies, both because they illustrate the common benefits DMSO provides with these agents across a vast swath of neurological conditions and because combination can often enhance the efficacy of DMSO (detailed extensively here), hence providing additional ideas for individuals struggling with the neurodegenerative diseases covered here. As such, anytime an agent with a therapeutic effect is mentioned in this article assume that it was combined with DMSO. Additionally, if that agent was a natural therapy (e.g., herb, nutraceutical or botanical extract), to help you, as mentioned before, I have marked it with a ^⬖.

Causes of Disease

When trying to understand a disease, two different lenses exist for interpreting it. One, the (favored) reductionist perspective tries to break it down to its tiniest parts, and through understanding them understand the disease. The other, the holistic one, sees the specific disease as a gear in a much larger system, and tries to see what systemic process is giving rise to the issues at hand.

Since Descartes’ seminal work on reasoning in 1637 (~400 years ago), our culture has embraced the reductionist model and through it, created countless scientific innovations which have transformed society, such as numerous medical innovations that identified the discrete cause of a life-threatening condition and provided a cure so it was no longer fatal.

Unfortunately, while reductionistic approaches are often excellent for acute life-threatening illnesses, they often only identify the downstream concrete effects of the illness rather than the upstream process which gave rise to the illness (hence making the therapies chosen typically be symptom managing ones rather than curative). Because of this, modern medicine is often characterized as being “excellent for emergencies but terrible for chronic illness.” Likewise, a longstanding joke with neurology is that neurologists are excellent at diagnosing neurological diseases, but not very good at actually treating them (although recently there has been some progress on the therapeutic end).

Note: alternatively, one can argue our biochemistry-focused form of medicine (which tries to identify a specific molecular target for each disease) exists because this allows an almost infinite number of patentable therapies to be made for each illness, whereas were systemic remedies to be utilized that could treat a myriad of illnesses (e.g., umbrella therapies or ones based on biophysics), it would no longer be possible to have a lucrative business model which patents each disease.

In contrast, I see many illnesses as being a manifestation of an underlying disease process within the body, and in many cases, believe the specific disease that arises is largely a product of where that disease process landed in the individual’s body (e.g., it was very common that COVID-19 vaccine injuries affected a previously weakened or injured area of the body, which is part of why the condition had so many different symptoms).

Unfortunately, while this perspective is often necessary to solve an illness, it is diametrically opposed not only to how our society teaches us to think, but also the human ego, as reductionist frameworks offer the comforting illusion of certainty and control, whereas holistic perspectives require us to tolerate ambiguity and unpredictability so we can see beyond the parts and grasp the broader whole—and unfortunately, the human ego will go to great lengths to feel like it is in control.

The Sequence of Disease

Over the years, I have noticed a recurring pattern that characterizes many of the diseases I encounter:

• Something shocks the system, or a recurring issue eventually affects the body to an extent which exceeds its compensatory capacity.

• The body (or a part of it) enters a state of shock and partially or fully shuts down.

• The natural healing capacity of the body is unable to resolve this shutdown, and the issue becomes chronic.

• The shutdown causes other things in the body connected to it to go haywire and creates additional issues.

Because of this, my approach frequently is to:

• First identify where the actual issue is and the underlying issue that precipitated it.

• Then treat the underlying issue which caused the problem.

• See if that resolves the shutdown, and if not provide a regenerative therapy which wakes the tissue back up (which I discussed extensively in the cell danger response series).

• For any problems that remain, treat the underlying issue which predisposed that area to being affected by the systemic process.

• See what issues remain in the other parts of the body which were connected to the core problem and deal with those.

Note: in other cases, the situation is much simpler and I just focus on a therapy for where the actual issue is.

Because of this framework, I’ve put a lot of thought into what creates the shocks that initially shut the system down (e.g., an infection, prolonged stress, poor sleep, significant injury or tissue compression) and tried to discern why some people’s bodies can quickly shrug off those insults and the damage they create, while in others they become lodged and quickly become permanent.

From this, I’ve gradually come to the perspective that circulation is key, and that once circulation shuts down, areas of the body not only become “shocked,” but the body loses its inherent ability to reassert a state of health following the shocks it encounters. As such, I see many diseases and disease processes (e.g., inflammation) not as independent entities, but rather as consequences of poor circulation (and likewise recognize that the underlying reason why many different disease processes create similar symptoms is because they all impair circulation).
Note: within many schools of natural healing, nutritional deficiencies are identified as a root cause of illness to be treated with sufficient supplementation. My own experience (mirrored in some studies) has been that those illnesses often also resolve when circulation is restored to the affected area. Put differently, while raising the nutrient levels in the blood that reaches the area could solve the issue, those nutrients could also be obtained in sufficient amounts by increasing the amount of blood which reaches the area.

My focus on circulation in part results from how often I see it quickly produce dramatic effects for patients, in part because of how often I now identify pertinent circulatory obstructions, and because the individuals who pioneered this perspective provided one of the most illuminating models of disease I’d come across. Briefly:

•Building on work that came before him, in the 1940s to 1960s, Melvin Knisely elucidated that “blood sludging” (blood cells clumping together) underlay many illnesses, particularly hospitalizing ones as this generally reduced blood flow and eliminated microcirculation in vessels the clumped blood cells were too large to fit through. Key discoveries included burns, blood infections like malaria and cancer causing significant blood sludging (which then systemically affected the body) a few therapies (e.g., low molecular weight dextran and hydroxychloroquine) alleviating sludging, and by using a microscope to view vessels in the eye, it was possible to non-invasively assess how “sludged” the blood throughout the body was (whereas while sludging could be assessed in blood taken out of the body with live blood cell analysis or the ESR rate, it was not as accurate because the clumping behavior of blood always changed once it left the body).

•In Chinese medicine, numerous “disease patterns” exist to explain what is causing a specific illness. One of these, “blood stasis” (which I still need to write an article on) perfectly matches blood sludging, and interestingly, after the mass adoption of the smallpox vaccine, blood stasis more and more came to be seen as the primary cause of most illness. Notably, many diagnostic signs have been developed by Chinese medicine for blood stasis which have significant value in identifying “blood sludging.”

•While Knisely could tell blood sludging was a core cause of illness and that specific things triggered it (e.g., excessive heat or cold), he could not determine why it occurred and postulated it might be due to a sticky coating on the cells (not found in normal blood) that was tentatively identified as a protein.

•In the 1960s, Thomas Riddick, an engineer and chemist who regularly worked with colloidal solutions to thicken or thin them (e.g., clays need to be thinned to flow through pipes while sewage needs to be thickened so its waste matter clumps together and settles to the bottom) concluded his heart issues (which at the time were “incurable”) might be due to his blood being “too thick” and tried using the same agents he used to disperse industrial colloids on his body—which worked. This led to him concluding the primary variable he adjusted, zeta potential (the electrical repulsion between colloidal particles which allows them to resist agglomerating forces in a liquid system pushing them together) might underlie many different diseases and was the factor responsible for the blood sludging observed by Knisely. As such, he extensively studied it (e.g., with microscopes aimed at the eyes that filtered the heat from his incandescent bulb so exposed blood would not begin to sludge) and amongst other things concluded aluminum was extremely dangerous because its strong positive charge made it the ion most capable of disrupting zeta potential, that people with poor zeta potential were at high risk of heart attacks, and that bacterial and viral infections would consistently worsen the zeta potential of the body (hence making them most severely afflict the elderly as zeta potential worsens with age).

•A doctor with an incurable heart condition discovered Riddick’s work, and after it fixed his heart issues, discovered that with his patients restoring zeta potential was miraculous for a few other diseases including dementia.

•Canadian neurologist Andrew Moulden realized that he frequently saw children develop clinical signs of strokes after vaccination, and that more severe signs correlated to developmental disability following vaccination (mirroring a century of published case reports of cranial nerve issues accompanying vaccine encephalitis and those same deficits later being routinely observed in autistic children). Moulden then concluded that vaccines were causing microstrokes throughout the body due to zeta potential-disrupting agents in vaccines (e.g., aluminum) clumping blood cells together and because during an inflammatory response, larger white blood cells will obstruct the microcirculation (all of which was too small to detect with radiologic imaging and is a major reason why diagnostic tests cannot identify many chronic neurological conditions). He also concluded that the characteristic microstrokes he saw resulted from them being in parts of the brain with weaker blood supplies, and they hence served as indicators brain damage was also silently occurring in other parts of the brain being affected by these microstrokes. Finally, like those before him, he highlighted this could be caused by other things like infections, but emphasized it was a far more frequent problem with vaccination.

•Numerous doctors (myself included) independently realized that this process likely affected every fluid in the body as they are all colloids, and that many of the conditions ascribed to blood sludging (e.g., Chinese medicine links blood stasis to autoimmunity) likely resulted from obstructions in other fluids like the lymphatics.

•In December 2019, based on reports on anonymous message boards online, I became very concerned COVID-19 (SARS-CoV-2) would turn into a global catastrophe (in part because of how it behaved, and in part because every authority downplayed it, whereas typically far more minor and relatively inconsequential pandemics would be hyped up to an absurd degree). As such, from the start, I corresponded with everyone I knew treating the disease, and quickly noticed it had some very odd characteristics suggesting significant zeta potential disruptions throughout the body. As colleagues who had treated SARS-CoV-1 did not notice those features of the disease, I hypothesized there was likely a protein on the outside of the virus which carried a very strong charge density not present in SARS-CoV-1, and after teaching myself how to do the analysis, realized the spike protein fit the bill.

As such, particularly after the vaccine hit the market, my interest in understanding zeta potential greatly increased and a key goal of this newsletter has been to empower people to treat zeta potential (which is essentially done by eliminating strong positive ions and supplementing with strong negative ions) as it transforms so many different areas of medicine and health.

Note: the zeta potential topic (along with supporting references) is discussed in much greater detail here.

However, I also must disclose I do not believe zeta potential is the only factor which causes blood sludging; rather I’ve focused on it because it is simply the easiest one to understand and rapidly treat (e.g., I believe there is a great deal we still do not understand how blood and fluids behave in the body—evidenced by things like forgotten Russian research which shows blood travels through the body in spiraling vortexes the heart directs so vascular resistance is reduced and specific types of blood can arrive where they are needed).

DMSO and Neurological Disorders

DMSO has many qualities which allow it to treat a wide variety of diseases including:

•It increasing circulation.
•It accelerating the healing of injured tissue (which I currently believe results from it improving circulation and it stabilizing the gels needed for the initial healing process).
•It awakening dormant cells that are trapped in the cell danger response.
•It being a potent antioxidant and anti-inflammatory agent.
•It increasing parasympathetic tone (due to it being an acetylcholine esterase inhibitor) and it sedating dysfunctional neural circuits (allowing them to reset).
•It effectively reducing pain (in part by it blocking pain transmission and it relaxing the musculature).
•It protecting cells and tissue from a wide variety of injurious and lethal stressors.
•It being a potent delivery system for other therapeutic substances that are mixed with it (particularly in topical applications).

Of these, I believe the first three (circulatory improvement, tissue regeneration, and resetting the cell danger response—and possibly DMSO’s anti-inflammatory and anti-oxidant properties) are particularly important for neurological disorders (which DMSO has long been recognized for treating) as:

•Nervous system tissue has the highest energy demand in the body and is the most sensitive to its blood supply being reduced (e.g., functions of the nervous system will often immediately “turn off” once their blood supply is interrupted).

•Nervous system tissue is particularly vulnerable to interruptions in blood supply, and once this occurs, will often be stuck in a dormant “penumbra” state like the cell danger response (after which the tissue eventually dies). Furthermore, the brain and spinal cord are among the tissues most resistant to healing and regeneration in the entire body.

•Because so much of life depends upon a functioning nervous system, partial losses of function due to either of the previous create immediate noticeable consequences for the individual (whereas partial losses of function in the internal organs may not even be noticed without lab work).

Given all of this, I assumed that DMSO had to improve zeta potential, as while it has many proven anti-clotting properties (discussed here), many of the changes it created were identical to what would result from an improvement of microperfusion via a spacing out of red blood cells.

However, when I reviewed the literature, I discovered DMSO (due to it carrying a neutral charge) does not improve red blood cell zeta potential, and if anything, slightly worsens it. Likewise, DMSO is inherently viscous (thick), increases the viscosity of water by structuring it^1,2,3 (which can be seen when the two mix together).
Note: this exothermic structuring is why DMSO will create heat when it mixes with water.

However, DMSO formulations have low viscosity,^{1,2,3,4,5,6,7} (or become negatively charged when prepared in DMSO), DMSO decreases the viscosity of bulk hydrophobic ions and most importantly, reduces blood cell aggregation (blood sludging) and blood viscosity which I believe is due to:

1. It behaving as a gel stabilizing (promoting) agent, which thereby forms water barriers between particles preventing them from aggregating (along with it making biomolecules like urea switch from opposing to supporting gel formation).

2. DMSO reducing the attractive forces between red blood cells Knisely identified (e.g., by neutralizing aggregating proteins), thereby allowing the existing zeta potential to become able to disperse the blood cells.

3. It likewise counteracting the agglomerating factors seen in pathologic states which otherwise cause blood cells to clump together. For example:

   •DMSO (3%), by lowering blood cell viscosity (and increasing molecular mobility) completely prevented S. aureus from adhering to red blood cells (which if adhered would then cause blood cells to clump together).
   •When DMSO was mixed with LPS (to model sepsis), rather than increase viscosity (which is a key issue in sepsis), blood viscosity decreased, and further decreased once resveratrol^⬖ was also added.

   •In cancer, DMSO prevented the reduction in zeta potential (and mobility) which would otherwise occur in macrophages.

   •Prevented positive ions from disrupting the zeta potential of negatively charged laponite.

   •When exposed to radiation (gamma rays), lens proteins from the eye would aggregate and the viscosity would increase; DMSO prevented this.

   •To establish a foothold in the lungs, bacteria which often colonize cystic fibrosis patients release cepacian, a polysaccharide which forms thick biofilms in the lungs’ (already thick) mucus, making it much harder for cystic fibrosis patients to breathe. DMSO in turn has been shown in laboratory studies to disrupt cepacian aggregates and halve their viscosity (which may partly explain why one physician shared their cystic fibrosis patient had life-changing improvements after DMSO). Furthermore, DMSO in combination with ivacaftor (a key medication used for CF) was found to reduce the viscosity of cigarette smoke-thickened lung mucus.

All of this was best demonstrated by a remarkable 2009 study^1,2 by a team of Georgian researchers studying the effects of hyperthermia (a cancer treatment) on the brain as unlike the rest of the body, the brain and spinal cord are known to begin being injured by higher temperatures, with neurologic dysfunction beginning at 40-41°C and histological thermal damage (e.g., coagulative necrosis) occurring in primates after an hour of 44°C (which is why 43°C for 60 minutes is often considered the safety limit for hyperthermia treatment).

That study directly heated the CSF of rats, and then directly assessed the resulting blood flow changes in the brain and the lesions which followed, finding:
•Increasing heat caused increasing degrees of microclotting (mirroring Knisely and Riddick’s observations), corresponding losses of blood flow, and brain tissue damage from that loss of blood flow.
•DMSO counteracted all of these effects, preserving blood flow and brain tissue, while in contrast high molecular weight dextran (a substance Knisely used to induce blood sludging) worsened the sludging and brain damage—hence demonstrating why blood sludging can cause so many nervous system disorders, and why DMSO is able to antidote it.

Note: these results also make a strong case for using DMSO to mitigate the adverse effects of heat stroke and high fevers.

Additionally, DMSO has also been shown:

•In rat intestinal microcirculation, to reduce chemoattractant-induced leukocyte adherence (but not rolling velocity and flux), thereby counteracting the inflammatory microstroke-producing process Moulden had discovered of large white blood cells obstructing the smaller blood vessels.

• In microlymphatic vessels of intact rat mesentery to consistently stimulate phasic contractions, increasing the proportion of vessels exhibiting spontaneous phasic contractions from a baseline of 26–42% to 43–59%, while roughly doubling the contraction rate from ~11 to 25 per minute. As these contractions drive lymph flow, lymph velocity increased markedly — roughly doubling in 100% of vessels (via speckle-interferometry) and showing 40-100% increased movement in 60–64% of vessels (via direct microscopy) — thereby stimulating the drainage function of the lymph microcirculation. DMSO also completely removed the bacterial staphylococcal toxin’s lymphoconstrictive effects (which could progress to obliteration of microvessels), normalized lymphangion drainage, and attenuated the toxin’s overall lethal impact. Lastly, the Russian researchers who discovered this also found exposure greater than 15 minutes to 30% DMSO would induce lymphostasis in 20–40% of the vessels (concentrations that could never be reached in a patient using DMSO).^1,2,3,4

•To increase lymphatic circulation across numerous contexts — including resolving lymphostasis in Kaposi’s sarcoma patients and in 115 patients with purulent wounds, facilitating lymphatic drainage (with electrical stimulation and hyaluronic acid), increasing renal microcirculation and lymph flow, increasing lymph flow in osteoarthritis, dose-dependently increasing lymphatic flow (as the solvent for intravenous Daflon), facilitating the growth of new lymphatic vessels (with 13-cis retinoic acid), and treating post-mastectomy lymphedema (per multiple guidelines, studies and reviews^1,2,3). Additionally, a Russian detoxification patent first stimulated interstitial humoral transport and lymphatic drainage by applying DMSO combined with a proteolytic enzyme to the feet and then 30-60 minutes later, filtered the blood with plasmapheresis.

Note: DMSO is also used to directly deliver topical or injected therapies into the lymphatic system^{1,2,3,4,5,6,7,8} and to treat a wide range of lymphadenitis (e.g., from the BCG vaccine,^{1,2,3,4,5,6,7,8,9,10} tuberculosis,^1,2 hemorrhagic erysipelas, Post-COVID MIS-C, tonsillitis, and bacterial infections which hospitalized 61 children^1,2).

Lastly, a common side effect of IV DMSO is osmotic hemolysis, which predominantly affects aged blood cells (the spleen will eventually eliminate). Aged blood cells are well recognized to be much more prone to agglutinating and clumping (in part because red blood cells lose their negative charge with age) and as such, circulation will improve with their loss. This helps to explain Jack De La Torre’s observation with boluses of IV DMSO in brain injured patients:

Also, hematuria from red cell osmotic hemolysis was seen in all patients only after the initial loading dose of DMSO. Hematuria was seen to stabilize after subsequent doses of DMSO. The loading DMSO dose has no other consequences other than lowering the hematocrit about 25%, a temporary reaction that paradoxically lowers blood viscosity and vascular resistance while increasing cerebral blood flow.

DMSO and the Blood-Brain Barrier

In tandem with increasing circulation, DMSO rapidly spreads through the body, and within 5 minutes of going on the skin it can be found in the blood, within 30 minutes can be found throughout the organs, and within an hour, the bones—but simultaneously, does not accumulate within the body after prolonged use (e.g., 85% is excreted unchanged in the urine within 24 hours) and virtually none remains by a week after administration.^1,2,3

Additionally, studies in mice and rats have shown that DMSO at 10–15% concentrations reversibly opens the blood-brain barrier (BBB), allowing proteins like horseradish peroxidase (HRP), many drugs including pemoline, ketoconazole (with brain concentrations increasing 9-fold), or the Parkinson’s medication L-dopa (increasing dopamine levels in the tubero-infundibular and neostriatal areas and further potentiated when combined with carbidopa), drug carrying lysosomes, and amino acids like tyrosine to reach brain tissue in higher amounts than without DMSO.^{1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20}

DMSO also increased the transfer of amino acids across the subarachnoid space into underlying cortical tissue by approximately 57%, and in neonatal chicks, IV DMSO increased brain concentrations of adrenaline and noradrenaline by approximately 35–39% and intensified their central effects.^1,2 Similarly, in dogs, IV DMSO at escalating infusion rates reached a CSF concentration roughly half the corresponding plasma concentration, confirming a (slower) penetration across the BBB into the CNS. This ability to facilitate drug delivery to the brain underpins DMSO’s therapeutic potential for neurological disorders (e.g., Parkinson’s) and has led to DMSO being grouped with mannitol as a clinical agent for enhancing brain drug delivery. Likewise DMSO has been incorporated into brain-targeting nanoparticle formulations, such as glucose-mediated poloxamer micelles, which showed significantly higher transport across a BBB model than ordinary micelles.^1,2
Note: there are mixed results on DMSO temporarily opening the BBB (e.g., these eight studies found it did not,^{1,2,3,4,5,6,7,8} this one found that opening the BBB required 1% or greater DMSO, another found it had minimal effect on dopamine transport) these found the opening was also problematic,^1,2 while in rats and rabbits DMSO infusions into the carotids did not harm the BBB, arteries or brain^1,2 and a 1985 veterinary review likewise noted DMSO allows some substances but not others to cross the BBB.

In mouse MRI studies, DMSO accumulated at 1.5-fold higher concentrations in glioblastomas than in normal brain tissue with 2.2-fold longer washout, creating clear tumor "hotspots." Unlike toxic gadolinium contrast, DMSO freely crossed the intact blood-brain barrier, enabling visualization of low-grade tumors invisible to conventional MRI — and during chemotherapy, reductions in DMSO retention signaled treatment response earlier than volumetric MRI changes.^1,2,3,4,5,6 DMSO has also been shown to enhance light penetration into brain tissue, improving optical diagnostic techniques relevant to certain neurologic disorders.^1,2

DMSO and Psychiatric Conditions

Two of the most common complaints about psychiatry are that its (highly toxic) drugs do not treat the underlying illness—requiring lifelong symptom management—and that real biological issues (e.g., COVID vaccine injuries) are routinely misdiagnosed as primary psychiatric disorders. Both problems stem from the erroneous assumption that most psychiatric conditions originate purely in the mind, when in reality many have a clear biological (neurological) basis.

My perspective resulted from repeatedly observing psychiatric symptoms emerge after brain injuries and from seeing medical therapies that restore brain health also improve psychiatric issues. For example, one of my favorite therapies, ultraviolet blood irradiation works by improving circulation, reducing inflammation, and reawakening dormant cells—all of which DMSO also does. Because these processes underlie so many diseases, much in the same way a large body of literature supports UVBI’s efficacy across a wide range of conditions, including psychiatric ones, the same also holds true for DMSO (which I will show throughout this article).

In the process of unearthing every DMSO paper in existence, I uncovered a Russian team (at the Institute of Higher Nervous Activity and Neurophysiology of the Russian Academy of Sciences) which produced some of the best evidence I’ve come across for this theory.^{1,2,3,4,5,6,7,8}

Briefly, in their effort to find a biologic cause of psychiatric conditions (which have a wide variety of seemingly unrelated causes), they discovered that the chronic stress which causes psychiatric disorders is accompanied by impaired circulation to the brain which sets off a variety of degenerative processes, especially once the individual’s ability to compensate for acute short-term stress is overwhelmed by chronic sustained stress.

To study this, they repeatedly induced neurosis in animals using prolonged stressors (white noise, light flashes, and electric shocks over 3+ weeks), then using biomicroscopy (cranial window) and hydrogen clearance, they directly measured blood flow in the territory of the middle cerebral artery, and finally, they directly examined the brains.

Note: neurosis (невроз) is an outdated psychiatric term. In this Soviet-era context, it describes a breakdown of higher nervous activity caused by chronic stress that overwhelms the person’s coping ability. Modern equivalents include Generalized Anxiety Disorder, mixed depressive and anxiety disorder (ICD-11), neurasthenia, and adjustment disorder with anxious or depressed mood.

From this they found:

•The brain normally receives 5–7 times higher blood flow per gram of tissue than most other organs due to its exceptional energy demands. Acute stress typically causes a short-term increase in cerebral blood flow, but prolonged chronic stress (leading to neurosis) produces a sustained decrease that persists 4–6 weeks after the stressor ends. This reduction causes circulatory hypoxia, elevated brain lactate, decreased caspase-3 and Na,K-ATPase activity, impaired mitochondrial respiration (including reduced succinate dehydrogenase and NADH dehydrogenase activity), and increased reactive oxygen species (ROS) production (and in animals unable to adapt by shifting from succinic acid^⬖ to NADH oxidation, stress resistance is markedly reduced). The resulting hypoxia also increases cytochrome oxidase activity (by 35–40%) and triggers mitochondrial biogenesis, followed by ROS triggered lipid peroxidation (LPO).^1,2,3,4

Note: the brain is particularly vulnerable to this cascade due to its exceptionally high metabolic rate and oxygen demand, as well as its high content of (oxidizable) polyunsaturated fatty acids in cell membranes.

•In the early stages of neurosis, acute stress, a nonspecific protective response, inhibits LPO, accumulates readily oxidized phospholipids, decreases cholesterol content, and increases superoxide-scavenging activity (partly from stress hormones acting as radical scavengers). With continued chronic stress, this protective phase is overwhelmed, leading to activation of free-radical lipid oxidation, progressive phospholipid depletion, cholesterol accumulation, and an increased in oxidized proteins. These biphasic membrane changes initially increase resistance to further peroxidation but ultimately render membranes more vulnerable as stress continues.^1,2,3,4

Note: this biphasic pattern was also observed in women with dysmenorrhea (after 12 hours of pain, plasma levels of Schiff’s bases were reduced by almost two-thirds whereas after 12-24 hours it was nearly double from control values).

•The later adaptations to chronic stress are more specific and membrane and free-radical changes often show interhemispheric asymmetry varying by behavioral type. For example, in acute stress, animals with high emotional reactivity and emotional resonance shift toward balanced or right-dominant LPO (as do stress sensitive rats that excel with mazes), while low-reactivity animals have more LPO on the left (as do stress resistant rats that are not good with mazes).

•These molecular changes are accompanied by clear physiological disturbances: elevated and fluctuating systolic blood pressure, disruption and reduction of local cerebral blood flow, loss of functional specificity (equalization of blood flow across brain structures), and a behavioral shift toward passive-defensive behavior. As stress and sympathetic hyperactivity can cause these autonomic disturbances, the researchers concluded that the resulting restriction of cerebral blood flow contributed to many symptoms seen in neurosis.

Note: one of my favorite modalities (neural therapy) works by neutralizing autonomic disturbances and frequently produces rapid, dramatic responses in complex illnesses — which I believe relates to the pathological process described by the Russian researchers.

•They also found that local norepinephrine release within the lateral hypothalamus functions as part of a depressor system that helps normalize elevated blood pressure. During acute stress, the speed of return to baseline blood pressure depended on the strength of this local noradrenergic response in the lateral hypothalamus. As such, when this mechanism is impaired, repeated stress can lead to prolonged hemodynamic instability, which over time, can contribute to dysregulation of cerebral autoregulation and sustained reductions in cerebral blood flow (which then damages the hypothalamus, creating a downward spiral into chronic illness).

Note: most chronically elevated blood pressure has no known cause. This framework potentially explains a key unrecognized cause (along with another reason why restoring zeta potential will improve blood pressure, as doing so will restore blood flow to the hypothalamus). Additionally, I should note that certain holistic healers have reported significant success in treating excessive sympathetic activity by addressing hypothalamic function.

•Normal cerebral blood flow is approximately 50 ml/100 g/min; in chronic neurosis it falls below 30. Cerebral vessels also lose autoregulatory capacity: after bilateral carotid occlusion, normal animals show universal arterial dilation, whereas neurosis animals exhibit mixed arterial and venous responses (e.g., in arterioles 54% dilated, 21% constricted, 25% had no change) with frequent spastic contractions, bottle-shaped deformations, interrupted flow and perverted pial vascular reactions, resulting in a relative equalization of blood flow rate across all studied structures (indicating a loss of functional specificity—which I consider to have immense clinical significance as a few healing traditions associate this circulatory shift with approaching death).

Note: in many cases, cerebral hemodynamics never fully recover after the chronic stress period.

•These hemodynamic changes parallel the homogenization of EEG activity seen in neurosis. Biomicroscopy confirmed microstructural disturbances consistent with hypoxia, including perivascular and pericellular edema, tortuous vessels, dark neurons, acidophilic cells, microglial proliferation, and hippocampal damage (especially shrunken soma, altered nuclei, and corkscrew dendrites in CA3; 2.7–7.1% cell loss in CA1—approaching the threshold for cognitive impairment and dementia).

•The process selectively damages brain β-adrenoreceptors (which for about a week showed decreased receptor affinity that was compensated for by an increased receptor number, with the elevated receptor density persisting after three weeks), the sensorimotor cortex (layer V), and the hippocampus (in the pyramidal layer, particularly at the CA3 field).

•Three stages of the general adaptation syndrome were identified in the chronic emotional-painful stress model: (1) initial search for optimal functioning with residual visceral defects, fear-dominant behavior, and labile blood pressure, lasting a week; (2) partial autonomic stabilization but ongoing phospholipid depletion (“local wear”); (3) exhaustion with breakdown of autonomic regulation, LPO activation, and profound membrane disruption across neurons, glia, and synapses, contributing to the breakdown of higher nervous activity, which they described as “pathological adaptation with a high structural price.”

They then:

•Emphasized that an individual’s internal reaction to stressors rather than the stressor is pivotal (“...it does not matter what facts are reported to us — what is important is how we react to them; that is the main question”) and linked it to the observation that many illnesses resulting from chronic psychoemotional stress are characterized by autonomic (vascular) disorders, hypoxic states, and serious disturbances in metabolic processes, often manifesting as autonomic/vascular dysregulation, hypoxia, and metabolic disturbances.

Note: the non-English speaker who coined the medical concept of stress later stated he used the wrong word and meant to use the word strain (how a system deforms in response to stress).

•Noted that, while many individuals reach full neurosis, far more are in a pre-neurotic stage of significant strain without complete decompensation and would greatly benefit from therapeutic interventions early in their disease process.

•Highlighted that the effects of chronic stress they observed were similar to those seen after strokes, heart attacks, or traumatic brain injury, and in many cases, they successfully used the same therapies for both (e.g., panthenol^⬖).

To address neurosis:

•The researchers first used agents with antihypoxic and antioxidant properties (e.g., carnosine,^⬖ substance P, phenosan K, or synthetic phenolic antioxidants^1,2) and found these interventions both prevented and effectively treated experimental neurosis in animals (whereas untreated animals consistently developed neurosis and showed poor recovery).

Note: other agents like panthenol^⬖ only gave temporary improvements. Additionally, they also had significant success with alcohol (a hydroxyl scavenger), providing a novel explanation for why alcohol offers some relief from chronic depression. Notably, chronic stress decreased brain Na,K-ATPase activity (as detailed above), and a separate study on brain Na,K-ATPase found that while both DMSO and ethanol scavenge hydroxyl radicals, ethanol further destabilizes the enzyme whereas DMSO stabilizes it — potentially explaining why DMSO provides lasting benefit where alcohol only temporarily palliates (while in parallel, Riddick found alcohol increased blood sludging).

After testing multiple agents, the researchers achieved strong success with negative ion therapy (which has a pronounced antihypoxic effect). When present during acute stress (e.g., immobilization), negative ions completely prevented the pathologic brain changes in all animals — regardless of behavioral type — including preservation of oxidative enzyme activity in the sensorimotor cortex and normalization of behavioral and autonomic parameters (heart rate, blood pressure, and breathing). Similar protective effects were observed with succinic acid^⬖ (30 mg/kg orally daily for 8 days), which they also found preserved orienting behavior after a heart attack. Notably, rats with an active behavioral type showed greater natural resistance to cerebral hypoxia, exhibiting faster increases in local cerebral blood flow and brain oxygen tension during stress.

Note: positive ions in the air have been extensively linked to psychiatric conditions. I believe this is because positive ions impair zeta potential and hence reduce cerebral microcirculation (whereas negative ions restore it).

They eventually had the greatest success by combining oral DMSO (a potent hydroxyl scavenger) with vitamin E^⬖ (alpha-tocopherol), finding the efficacy of this combination exceeded them being given separately (e.g., for autonomic or behavioral issues). They attributed this to DMSO enhancing vitamin E^⬖’s antioxidant capacity as DMSO could rapidly deliver it to cell membranes before it had lost its antioxidant capacity from reacting with other substances in the body (supported by it reducing free radical oxidation products, raising superoxide scavenging activity in the brain and blood serum, raising brain phospholipid content and normalizing brain cholesterol content). Finally, in 1999, they shared these results had begun being replicated in government sanctioned clinical trials at the Moscow Medical Academy.

While much could be said about their research, one of the key lessons I received was one of the clearest mechanistic explanations I’ve encountered for what adaptogens actually do (a term applied to many natural products) as the agents which effectively counteracted the entire stress process were explicitly characterized by the researchers as “adaptogens.”

Note: to compile the above summary and accurately represent their findings, I read through over 50 papers (many of which omitted key details) and did my best to integrate their findings with current physiologic science.

With this understanding (and a further exploration of the importance of circulatory drainage which will be discussed in the Multiple Sclerosis section), let’s now examine how these properties allow DMSO to affect a wide range of neurological and psychiatric disorders.

Parkinson’s Disease

Parkinson’s disease results from the progressive loss of dopamine-producing neurons in the substantia nigra. Research in this field was revolutionized in the early 1980s when recreational drug users who injected a badly synthesized synthetic heroin rapidly developed severe Parkinson’s-like symptoms due to it being contaminated with MPTP, an agent whose active metabolite (MPP+) specifically targeted those neurons, making it possible to reliably model Parkinson’s in laboratory animals. This was followed by the realization that one herbicide (paraquat) was very similar to MPP+, another pesticide (rotenone) also causing similar damage to neurons, a variety of pesticides being linked to a higher risk of Parkinson’s (such as organophosphates), and 6-OHDA also being able to reliably create Parkinson’s.

Note: one of the major challenges with glyphosate (Roundup) is that while it is toxic, the herbicides it largely replaced like paraquat are more toxic.

Numerous studies have shown that DMSO directly counteracts the neurotoxicity of these Parkinson’s-producing agents (e.g., in the organophosphate studies mentioned previously, DMSO repeatedly reduced mortality, accelerated organophosphate detoxification, and protected neuromuscular function). Most remarkably, a case-control study of young-onset Parkinson’s disease (63 cases, 68 controls) found that individuals with Parkinson’s were one tenth as likely to have been exposed to DMSO as normal controls, suggesting DMSO exposure is associated with a roughly 10-fold reduction in disease risk (and hence may be protective against it). In contrast, the same study found insecticide exposure increased risk nearly 6-fold, fumigated housing over 5-fold, and herbicide exposure over 3-fold — results consistent with the extensive epidemiological literature linking pesticide exposure to Parkinson’s.

Note: this study also found smoking was associated with reduced PD risk, a finding that aligns with decades of epidemiological evidence linking nicotine exposure to lower PD incidence, lending credibility to the study’s methodology.

DMSO has directly demonstrated neuroprotective effects in multiple Parkinson’s models. In animals, DMSO suppressed hydroxyl radical-induced nigrostriatal injury from MPTP,^1,2,3,4 and in rotenone-induced Parkinson’s rats, DMSO improved hippocampal CA1 and CA3 neuron morphology, restoring pyramidal cells and Nissl bodies damaged by rotenone and normalizing their electrical activity. DMSO also protected astrocytes from MPP+-induced toxicity by reducing lipid peroxidation and metabolic impairment, protected glial glutamine synthetase from MPP+-induced hydroxyl radical damage, protected human SH-SY5Y neuroblastoma cells from 6-OHDA-induced cytotoxicity, and reduced both lipid peroxidation and protein carbonyl formation in rat brain homogenates from ferrous chloride or hydrogen peroxide, and separately reduced hydroxyl radical production during 6-OHDA autoxidation and the formation of hydroxylated dopamine products.^1,2

Note: in one mouse study, intraperitoneal DMSO did not protect against MPTP-induced dopamine depletion, indicating its neuroprotective effects may depend on the route, timing, or dose of administration.

Interestingly, DMS (DMSO’s naturally occurring, odor-producing metabolite) at near-physiological concentrations also protected neurons against both 6-OHDA and MPP+-induced apoptosis, with this effect being dependent upon MsrA (the enzyme that converts DMS to DMSO), suggesting the endogenous DMS-DMSO cycle functions as part of the body’s natural antioxidant defense against dopaminergic neurodegeneration.^1,2 This, in turn, raises an interesting conundrum as I have received a few reports of Parkinson’s patients who had dramatic responses to DMSO who then stopped due to the odor impeding sexual relations with their spouse, and my first thought was to recommend a low odor DMSO formulation (discussed here), but if DMS plays a key therapeutic role in Parkinson’s disease, that approach may not be viable.

Note: that study also found DMS protected against H₂O₂-induced lipid peroxidation and antimycin A generated superoxide production.

Additionally, DMSO reversed rotenone’s complete blockade of microtubule assembly from purified tubulin in vitro — a finding with direct relevance to Parkinson’s, as microtubule disruption impairs axonal transport and contributes to dopaminergic neuron death. Likewise, a Russian physical therapy monograph recommended topical DMSO novocaine compresses for neurological conditions including Parkinson’s, and a patent proposed DMSO as a transdermal enhancer for a botulinum toxin patch to treat the spasticity associated with Parkinson’s, cerebral palsy, dystonia, and multiple sclerosis.
Note: a large number of studies (which will be discussed later in this series) show DMSO stabilizes microtubules and likely accounts for some of its neuroprotective qualities.

A vast number of agents in combination with DMSO have also shown therapeutic benefit in Parkinson’s models.

Curcumin^⬖ protected nigral dopaminergic neurons, reduced iNOS and glial activation, and upregulated neuroprotective pathways (IGF-1/Akt/FoxO3a).^1,2

Paeoniflorin^⬖ repeatedly reduced α-synuclein expression, decreased Lewy body formation, and protected dopaminergic neurons across multiple studies.^1,2 It also inhibited microglial overactivation, increased BDNF and GDNF secretion, and promoted neural stem cell differentiation into dopaminergic neurons.¹

Icariside II^⬖ induced human amniotic mesenchymal stem cells to differentiate into dopaminergic neuron-like cells (optimal at 3–10 μmol/L via PI3K signaling). In another protocol DMSO helped differentiate iPSCs into dopaminergic progenitors for PD stem cell therapy.

Ginsenosides Rg1^⬖ and Rg3^⬖ both significantly attenuated dopaminergic neuron loss, neuroinflammation, and α-synuclein accumulation.^1,2,3,4

Geniposide^⬖ reduced α-synuclein levels and prevented dopaminergic neuron loss by modulating the miR-21/LAMP2A axis, while ginkgolide B^⬖ similarly reduced α-synuclein expression via the related miR-207/LAMP2A pathway.^1,2 Ambroxol increased β-glucocerebrosidase activity and reduced α-synuclein oligomer levels, restoring cell viability and mitochondrial function in dopaminergic neurons. Polyphenols^⬖ reduced seeded α-synuclein aggregation via NRF2-mediated antioxidant responses. Carnosic acid^⬖ attenuated 6-OHDA neurotoxicity by upregulating parkin and restoring proteasomal clearance of ubiquitinated proteins in cellular and animal PD models.

L-sulforaphane^⬖ dissolved in DMSO activated the NRF2 pathway in Parkinson’s disease patient-derived cells, restoring their deficient glutathione levels — one of the only studies using actual patient cells.

Most uniquely, NAMI-A — a low-toxicity ruthenium-DMSO complex — inhibited α-synuclein aggregation and membrane interactions with submicromolar affinity, disassembled pre-formed fibrils, abolished α-synuclein cytotoxicity toward neuronal cells, and mitigated neurodegeneration and motor impairments in a rat Parkinson’s model, providing a novel basis for designing ruthenium-DMSO complexes that target α-synuclein-driven pathology through a mechanism distinct from organic agents.

In MPTP models, tanshinone IIA^⬖ preserved approximately 75% of dopaminergic neurons while reducing microglial activation; tetramethylpyrazine^⬖ prevented motor deficits and neuron loss via the Nrf2 pathway; 6-Hydroxy-1H-indazole protected 90-93% of dopaminergic neurons from death; baicalein^⬖ dose-dependently reduced rotation behavior (a key indicator of motor impairment), neuroinflammation, and dopaminergic neuron apoptosis via Wnt/β-catenin; neferine^⬖ improved mouse motor disorders and reduced neuroinflammation and α-synuclein in the substantia nigra; SB239063 (a p38 MAPK inhibitor) protected TH-positive neurons; NESS 0327 (a CB1 receptor antagonist) ameliorated motor deficits; novel c-Abl kinase inhibitors outperformed nilotinib in blocking MPP+-induced apoptosis; GW5074 prevented TH-positive neuron loss in mice genetically engineered to have PD. In nigrostriatal pathway injury mice, both ERK inhibition (U0126) and PDGFRα inhibition (AG1296) reduced glial activation and scarring, with U0126 also improving long-term neurobehavioral outcomes.

In LPS-induced PD mice, pazopanib protected dopaminergic neurons by suppressing TNF-α, PGE2, and IL-6 via MEK4-JNK-AP-1 signaling, while rapamycin reduced neuroinflammation by enhancing microglial lipid metabolism.

NBP (a Chinese stroke medication) rescued dopaminergic neurons by 30% and striatal dopamine terminals by 49%. Carvacrol^⬖ (found in oregano and thyme oils) was neuroprotective via TRPC1 inhibition in dopaminergic neurons and TRPA1 activation in astrocytes. Dasatinib and resveratrol^⬖ in combination improved learning, memory, motor coordination, and reduced anxiety. MOTS-c^⬖ improved motor function, reversed TH-positive neuron loss, and activated the Nrf2/Keap1 antioxidant pathway in rotenone PD rats. Puerarin^⬖ mitigated rotation behavior and upregulated DAT, VMAT2, and TH in rotenone PD rats. A caspase inhibitor reduced neuron loss and improved rotation behavior in 6-OHDA rats, though blocking apoptosis triggered compensatory glial necroptosis.

Shuimuheningfang^⬖ improved motor and non-motor symptoms in 80 PD patients and reduced α-synuclein in model mice,^1,2 while Compound Dihuang Granules^⬖ (with a JNK inhibitor) reduced rotation behavior and protected dopaminergic neurons in 6-OHDA rats.

In C. elegans PD models, olive leaf extract^⬖ strongly protected dopaminergic neurons from 6-OHDA toxicity (up to ~56% less degeneration), while oleuropein,^⬖ oleanolic acid,^⬖ tyrosol,^⬖ 3-hydroxytyrosol,^⬖ saffron,^⬖ Polygonum multiflorum,^⬖ and Ziziphus jujuba^⬖ each also provided significant protection.

Additional agents showing neuroprotective effects in PD models include guaraná^⬖ (against rotenone in SH-SY5Y cells), Antarctic krill oil^⬖ (improved locomotor activity and dopaminergic neurons in zebrafish), lutein^⬖ (dose-dependently improved cognitive and motor outcomes in rats), cytochalasin compounds from endophytic fungi (against MPP+), Erythrina velutina extract,^⬖ rizonic acid,^⬖ and xyloketal derivatives^⬖ (against 6-OHDA or ROS-mediated damage), sodium butyrate^⬖ (an HDAC inhibitor that epigenetically restored dopamine transporter and VMAT2 expression against rotenone and MPP+), allopregnanolone (promoted TH-positive cell regeneration via BDNF and CaMKIIδ3 against 6-OHDA), wedelolactone^⬖ (upregulated the neuroprotective PD protein DJ-1/PARK7), dexmedetomidine (neuroprotective via ERK1/2-mediated histone acetylation), along with 7,8-dihydroxyflavone,^⬖ cordycepin^⬖ (against rotenone in PC12 cells), AMG9810 (a TRPV1 antagonist that reduced motor deficits but impaired cognition with chronic use), insulin with TLR4 inhibitor TAK242 (improved motor performance and normalized α-synuclein in 6-OHDA rats), catalpol^⬖ (reduced α-synuclein and improved mitochondrial function against rotenone), genistein,^⬖ Taohe Siwu decoction,^⬖ Ligusticum chuanxiong compounds,^⬖ and Nigella sativa fatty acids.^⬖

Since paraquat and other herbicides are among the strongest environmental risk factors for Parkinson’s, it is also noteworthy that DMSO has been shown across multiple studies to scavenge the hydroxyl radicals generated by paraquat,^1,2,3,4 including direct evidence from rats of DMSO intercepting paraquat-generated hydroxyl radicals via Fenton-like chemistry, and in bacterial biosensor assays, DMSO scavenges up to 96% of the superoxide radicals generated by paraquat. DMSO has also been shown to be directly neuroprotective against paraquat in cultured striatal cells, suppress paraquat-induced inflammatory signaling (e.g., IL-8 and neutrophil chemotactic activity), and protect DNA from paraquat-induced mutagenesis — providing a potential mechanistic explanation for the epidemiological finding that DMSO exposure is inversely associated with Parkinson’s risk. Additionally, myrtenol,^⬖ andrographolide^⬖ (via Nrf2/HO-1), VPA (an HDAC inhibitor), chymostatin, propofol and resveratrol^⬖ each combined with DMSO to counteract paraquat-induced toxicity and oxidative stress across various tissue models.

Note: α-synuclein aggregation into toxic fibrils is a core driver of Parkinson’s neurodegeneration. One study found DMSO at 0.75-1.0%, especially when combined with ferric iron, promoted α-synuclein oligomer formation and cytotoxicity. However, when oral DMSO was tested in living mice (both normal and transgenic mice overexpressing human α-synuclein), no increase in α-synuclein aggregation, no neuronal loss, and no Parkinson’s-like pathology was detected. Likewise, DMSO injected directly into the substantia nigra has not been found to cause dopaminergic neuron loss, ubiquitinated protein accumulation, or behavioral deficits^1,2 — suggesting that whatever pro-aggregant effect DMSO has on α-synuclein in isolated cell cultures (at much higher concentrations than it can reach clinically) does not translate to the living body.

In addition to the experimental evidence, I have received a few reports from readers and physicians who had success with DMSO. As my experience is primarily with IV DMSO (which I believe offers the greatest benefit), I wanted to share this entire sample which includes non-IV approaches to illustrate the difference between them.

One wife described what happened when her husband with Parkinson’s received an IV drip of mannitol and DMSO during stem cell therapy in Amsterdam: “He bounced down a flight of stairs without using the handrails, cut his own food for a week after, spoke clearly, opened cab doors.” They knew it wasn’t the stem cells, which would take months to show results.

The most detailed report came from a research scientist diagnosed with PD in 2018, who had already controlled his non-motor symptoms with sulforaphane^⬖ (an Nrf2 activator) but still had the full range of motor symptoms. After systematically testing oral DMSO over several months, he found that at an optimal dose, bradykinesia was eliminated, pain and dystonia reduced by 80%, stiffness reduced by 50%, and energy levels were markedly higher. He observed that DMSO addressed motor symptoms where sulforaphane^⬖ had not, suggesting DMSO was reaching the brain in ways sulforaphane^⬖ could not — consistent with DMSO’s known ability to cross the blood-brain barrier. Notably, doses above his threshold reliably worsened tremor, stiffness, and sleep, but these effects fully reversed within two days of stopping.

A third reported that topical and oral DMSO initially helped her husband with Parkinson’s walk short distances, but the effect did not persist.

Additionally, I have also received a few reports of oral DMSO helping readers with Parkinson’s, but as they were in passing (verbally) I can’t offer any specifics on them.

Given all of this (and our own experiences with Parkinson’s), I believe DMSO has great potential for Parkinson’s disease — oral administration is likely to benefit patients, IV significantly more so — and that the best results will ultimately come from combining DMSO with a complementary neurotrophic agent. Currently, I have identified one very promising candidate for this purpose (along with a few other possibilities), but as the combination studies above demonstrate, there are likely many more waiting to be discovered.

Amyotrophic Lateral Sclerosis (ALS)

Amyotrophic lateral sclerosis is a progressive neurodegenerative disease in which the motor neurons that control voluntary movement gradually die, leading to increasing muscle weakness, paralysis, and typically death within 2–5 years of diagnosis. No cure exists, and the few FDA-approved drugs provide only modest survival benefits. However, as Todd’s story shows (particularly since he was willing to prove DMSO worked by repeatedly discontinuing it and then documenting the rapid worsening of symptoms that started), there is hope for ALS. In turn, there is also some research to corroborate it:

•In ALS model mice, long-term oral administration of 5% DMSO significantly increased mean survival time, reduced neurological scores, and improved motor performance (with the improvements being primarily functional rather than histological).^1,2

•Low concentrations of DMSO were found to stabilize SOD1 protein conformation (SOD1 misfolding is a central cause of ALS). Additionally, 5-fluorouridine and epigallocatechin gallate^⬖ (which is often combined with DMSO) also stabilized SOD1.

•A variety of agents in combination with DMSO have also shown therapeutic benefit in ALS mice. Chronic intraperitoneal resveratrol^⬖ delayed disease onset, extended survival, and preserved nearly twice as many motor neurons. A GSK-3β inhibitor delayed disease onset and death, and partially preserved lumbar motor neurons. ASK1 inhibitors protected against motor neuron death and reduced glial activation. Rapamycin improved the neuroprotective mitochondrial fission/fusion balance. Lycopene^⬖ dose-dependently reduced oxidative stress and reduced motor neuron apoptosis. Notably, carboxyamidotriazole potently inhibited inflammatory cytokines in vitro but did not significantly improve onset or survival compared to the DMSO vehicle control in vivo—potentially suggesting DMSO itself was already providing a comparable benefit.

Note: DMSO has also been combined with riluzole (one of the only ALS drugs) to treat a variety of other neurological conditions including neuropathic pain,^1,2 light-induced retinal degeneration,^1,2 hearing loss (where DMSO alone also was found to protect hearing and preserved cochlear neurons), and status epilepticus—all of which data shows DMSO treats. Additionally, DMSO has been used as a solvent to screen large numbers of compounds for use in ALS.

In addition to Todd’s remarkable response to topical and particularly IV DMSO, a few other reports suggest DMSO can benefit ALS and related conditions. One book recounts Stanley Jacob treating an ALS patient with DMSO, producing “instant, overnight and slightly delayed wonders of therapy” (after which their doctor forbade further treatment).
Note: I suspect this case may have been what first inspired a mentor to try IV DMSO for ALS.

Another reader reported that a colleague gave DMSO to her father with ALS and “was surprised at visible improvement in his condition.” Finally, a reader with cramping fasciculation syndrome (a condition that presents like early ALS but does not progress to it) described being driven to the point of planning suicide by the combination of chronic pain and severe sleep deprivation before discovering that oral DMSO dramatically improved the effectiveness of his other medications, allowing him to sleep through the night, largely eliminating his cramping and nerve pain, and giving him back the ability to hold down a job and watch his children grow up.

Note: our (limited) experience has been that IV DMSO halts the progression of ALS rather than reverses it. However, the stories I’ve received suggest some individuals have a considerably more dramatic response — whether due to inherent responsiveness or higher IV doses. One of my major unresolved questions is whether the post-COVID vaccine “atypical” ALS cases respond differently to DMSO than the pre-vaccine ALS we had previously encountered (which is where all of our experience comes from).

Huntington’s Disease

Huntington’s disease is a fatal genetic disorder characterized by progressive loss of motor control, cognitive decline, and psychiatric disturbances. It belongs to a family of nine neurodegenerative disorders (polyglutamine diseases) caused by misfolded proteins with abnormally long glutamine repeats, and a review of chemical chaperones for these conditions found that DMSO showed similar or superior suppression of polyglutamine-mediated toxicity compared to the other chemical chaperones tested (glycerol, TMAO). Likewise, in cell models of Machado-Joseph disease (another member of this family), DMSO stabilized mutant ataxin-3 protein folding, reducing aggregation, cytotoxicity, and cell death.

In the only study which directly tested DMSO against Huntington’s disease, DMSO (~1-4%) partially prevented cell death, increased cell viability, decreased aggregated huntingtin protein, and increased its soluble (non-toxic) form.

A variety of agents in combination with DMSO have also shown therapeutic benefit in Huntington’s models. In rats, inosine^⬖ protected against Huntington’s-like symptoms by improving motor function, activating the neurotrophic BDNF/TrkB/ERK/CREB pathway, increasing striatal BDNF, and reducing oxidative stress, neuroinflammation, and striatal neuronal damage. FKBP5 inhibition reduced mutant huntingtin levels and increased autophagic clearance in both human Huntington’s stem cells and mouse models. In C. elegans Huntington’s models, olive leaf extract^⬖ strongly protected neurons from polyglutamine-induced degeneration (up to 4-fold more intact neurons) and improved mechanosensory response, while 3-hydroxytyrosol^⬖ and tyrosol^⬖ reduced polyglutamine plaque number, protected neurons, and improved mechanosensory response. Hyptis species extracts^⬖ also significantly improved locomotion and increased oxidative stress resistance in polyglutamine models.

Note: DMSO has also been used to screen a large number of potential therapeutics for Huntington’s disease and to investigate its underlying pathogenic mechanisms.

Alzheimer’s Disease

Alzheimer’s disease (AD), the most common form of dementia, is characterized by the extracellular accumulation of amyloid-β (Aβ) plaques (particularly in the hippocampus and cortex) and intracellular neurofibrillary tangles from hyperphosphorylated tau protein. It is thought to result from the damage those proteins are known to cause to brain tissue and as such virtually all research into the disease has revolved around removing amyloid.

Note: a strong case can be made amyloid proteins initially protect brain cells from stressors (e.g. toxins), supported by the fact all the amyloid eliminating drugs have failed (and often have significant side effects due to them priming the immune system to attack amyloid and hence create inflammation in the brain), along with the fact natural therapies which directly target the factors injuring brain tissue are currently the only treatment for Alzheimer’s with supportive data (discussed further here).

DMSO has unique utility in the disease as DMSO:

•Stabilizes proteins and eliminates misfolded amyloid aggregates (allowing it to remove dangerous amyloid accumulations in a non-injurious way). For example, a computer modeling study indicated DMSO inhibits Aβ aggregation by modulating the stability of the Lys28-Ala42 salt bridge, while molecular dynamics simulations showed DMSO promoted α-helical structure and stabilized Aβ42 (preventing the β-sheet formation that drives toxic aggregation).

•Is an acetylcholine esterase inhibitor,^1,2 (the same therapeutic strategy used by the FDA-approved Alzheimer’s drugs donepezil and galantamine).

•Has been shown to increase the activity of lysosomal alkaline phosphatase (ALP) by 20%, which likely enhances the clearance of the toxic protein aggregates that contribute to neurodegeneration.

Note: a nasal insulin DMSO spray developed for treating AD was found in rats to deliver insulin throughout the brain within an hour with no signs of toxicity.^1,2,3

Additionally, DMSO’s foundational properties (e.g., improving circulation, reducing inflammation and reawakening dormant “shocked” cells) directly counteract the pathological processes that create AD. For example, DMSO has been shown to inhibit activation of NLRP3 inflammasomes and caspase-1, which mediate the chronic neuroinflammation that accelerates AD progression.^1,2,3

Note: DMSO is routinely used in laboratory settings to solubilize and dissolve amyloid peptides for experimental use,^1,2,3,4 and initial solubilization conditions (including DMSO exposure) significantly impact the reproducibility of Aβ aggregation kinetics. Studies characterizing the toxicity of different Aβ species (oligomers, protofibrils, fibrils) and molecular weight fractions have relied on DMSO for peptide preparation.^1,2 DMSO has also been used as a solvent platform for screening anti-aging drug cocktails against Aβ and tau neurotoxicity in neuronal cell lines.

In animal studies, DMSO has repeatedly demonstrated direct cognitive benefits in AD models:

In rats where intracerebroventricular streptozotocin (STZ) infusions were used to model sporadic AD, daily IV DMSO for 2 weeks counteracted memory impairment, improving performance in behavioral and memory tests. This was corroborated by a study where chronic intracerebroventricular DMSO at 10% (but not 2.5% or 5%) significantly attenuated STZ-induced spatial memory deficits in the Morris water maze, with the authors attributing the benefit to DMSO’s antioxidant, anti-inflammatory, and cerebral perfusion-enhancing properties.^1,2 In another STZ study, a separate group found similar trends toward decreased neuroinflammation (IL-1β, TNFα), behavioral improvements and elevated BDNF with DMSO treatment.

In AD model rats with Aβ25-35 injected into the hippocampus, DMSO improved learning and memory, reducing escape latency and search distance in the Morris water maze. Notably, no significant synergistic effect was seen when DMSO was combined with Ginkgo biloba extract,^⬖ suggesting DMSO alone was already exerting a substantial effect. In a similar study, DMSO and Ginkgo biloba extract^⬖ each improved learning and memory in Aβ25-35 AD model rats, with effects associated with modulation of hippocampal APP expression.

Furthermore, in mice genetically engineered to have AD, DMSO increased spine density in a region-specific manner in the hippocampus, enhanced spatial memory accuracy, modulated olfactory habituation, and displayed an anti-anxiety effect. Despite these improvements occurring in animals with elevated Aβ levels, DMSO did not reduce oligomeric Aβ species, and instead appeared to act through modulation of NMDA receptor signaling (as the NMDA antagonist MK-801 recapitulated DMSO’s effect on spine density) leading the authors to conclude: “DMSO should be considered as a true bioactive compound, which has the potential to be a beneficial adjuvant to counteract Aβ-mediated synaptotoxicity and behavioral impairment.”

In a separate mouse AD study, DMSO independently crossed the blood-brain barrier, improved cognition, and reduced neuroinflammation — effects observed even though the study was designed to test serpina3n, not DMSO itself.

In young mice (3–4 months) genetically engineered to have early-onset AD, 0.01% DMSO mixed with drinking water mitigated the visual declines and retinal thickening seen in the prodromal phase of AD (with benefits comparable to R-carvedilol), indicating DMSO enhanced the energy-dependent transport of water out of the eyes.

In C. elegans, DMSO greatly delayed (by 48–98%) the paralysis caused by Aβ42 and extended lifespan by 23.0–24.4%.^1,2 The researchers attributed the delay in paralysis to DMSO modulating neurotransmission, noting DMSO reduced paralysis from acetylcholine-related agents by ~70% and that the protection was dependent on the daf-16/FOXO longevity pathway.

In cell culture, low concentrations of DMSO (0.015625–0.0625%) increased the viability of brain cells and masked Aβ toxicity (concentrations readily achievable in brain tissue from taking DMSO at home or DMSO’s routine use in cellular experiments).

Note: since DMSO is used so frequently in Alzheimer’s research, it has been repeatedly proposed this protective effect likely has contributed to overestimating the efficacy of therapies used with it and underestimating the neurotoxicity of amyloid particles.^1,2

Additionally, DMSO shifted amyloid precursor protein (APP) splicing in the adult rat hippocampus to favor the neurotrophic isoform APP-695 (increasing its proportion from 89% to 94%) while reciprocally reducing the pathologic KPI-containing isoforms (APP-751/770) that are typically elevated in AD (again underscoring its utility in the disease). In a controlled cortical impact model of TBI in mice, DMSO (used as the vehicle for glibenclamide) demonstrated unexpected independent beneficial effects in female mice, significantly downregulating pathological TAU and TDP43 proteins across multiple brain regions and helping restore cerebral blood flow (effects the study authors highlighted as novel).

A 1980s Japanese review noted DMSO had been explored for dissolving amyloid deposits in Alzheimer’s, with one report documenting partial improvement in motor function.

Human Studies

18 patients with probable Alzheimer’s were treated in Moldova with DMSO and tested regularly for nine months, with great improvements being noted after only three months of treatment, and becoming especially noticeable after six months. Areas of improvement included memory, concentration, and communication alongside a significant decrease of disorientation in time and space.

Likewise according to Jack De La Torre, the leading researcher on DMSO’s neurological applications: “Dimethyl sulfoxide, a powerful free radical scavenger that is known to increase cerebral blood flow clinically and experimentally during various pathological states involving brain, has been shown to improve cognitive function while stabilizing protein enzymes in Alzheimer’s patients treated with this drug for 6 months.”

Note: I could not tell if De La Torre was referring to the Moldovan study or something else.

Combination Studies in AD Models

A large body of research has evaluated therapeutic agents dissolved in DMSO across various AD models.

APP Processing and Secretase Modulation

A variety of agents dissolved in DMSO have demonstrated the ability to shift APP processing away from toxic Aβ production. Cinnamon bark extract^⬖ reduced Aβ40 production by 50–60% through its active compounds medioresinol and cryptamygin A, which decreased β-secretase levels. Levistolide A^⬖ (from Danggui-Shaoyao-San) reduced extracellular Aβ1-42 in AD cells and was shown to cross the blood-brain barrier, reaching peak brain concentrations within 30 minutes. Apicidin (an HDAC inhibitor) increased ADAM10 (α-secretase) expression through USF1 and ERK signaling, shifting APP cleavage away from the amyloidogenic pathway. Retinoic acid inhibited γ-secretase activity through ERK activation, while sulfonamide-based γ-secretase modulators shifted Aβ40/42 ratios without the Notch-related side effects of complete γ-secretase inhibition. Additionally, multiple BACE1 inhibitors dissolved in DMSO reduced Aβ1-40 and Aβ1-42 production in neuronal cells (but like other amyloid drugs, failed in subsequent human trials). DMSO has also been used to dissolve ursolic acid,^⬖ which was identified through high-content screening as a potent inhibitor of Aβ binding to the CD36 receptor, blocking microglial reactive oxygen species production.

Transgenic AD Mice

DMSO combinations have been extensively studied in transgenic AD mice. Dihydromyricetin^⬖ improved Morris water maze performance, decreased Aβ accumulation and senile plaques, and restored autophagic flux by increasing Beclin1, the LC3-II/LC3-I ratio, and reducing P62. Numerous HDAC6 inhibitors alleviated cognitive decline, reduced Aβ levels and plaque deposition, decreased hyperphosphorylated tau, upregulated autophagy proteins, and protected cortical neurons from oxidative damage.^1,2 A p38 MAPK inhibitor improved cognition by reducing Aβ, tau phosphorylation, BACE1, and presenilin while increasing synaptic and amyloid-degrading proteins. Astragalin improved spatial learning and memory in mice by reducing Aβ plaque deposition and enhancing autophagic flux via the PI3K/Akt-mTOR pathway. Ligustilide^⬖ improved learning and memory, promoted Aβ transport and clearance, and reduced neuroinflammation. Chronic blockade of the TRPA1 channel normalized astrocytic activity, prevented neuronal dysfunction, preserved synaptic integrity, and prevented spatial working memory decline. Kenpaullone improved cognitive performance and reduced Aβ plaques, neurodegeneration, and proinflammatory cytokines, while erlotinib improved short-term spatial memory, increased dendritic spine formation, and reduced tau phosphorylation and aggregation.

Among agents targeting Aβ clearance or reduction, novel c-KIT inhibitors enhanced autophagic clearance of Aβ and tau, eriodictyol promoted microglial Aβ clearance,^⬖ menthol^⬖ inhibited Aβ polymerization and reduced senile plaques, and picropodophyllin reduced Aβ and hippocampal microgliosis, while ellagic acid^⬖ reduced both Aβ and caspase-3. GTM-1, rapamycin, and carbamazepine each improved spatial memory and reduced Aβ42 (with GTM-1 activating autophagy via mTOR).

Among agents improving synaptic function and cognition, a JNK inhibitor reduced inflammation, rescued synaptic proteins, and improved cognition; a PDE4 inhibitor improved memory, synaptic plasticity, and hippocampal signaling; CA140 rescued memory and synaptic function via dopamine D1 signaling; puerarin^⬖ restored NMDA receptor activity; and isoliquiritigenin^⬖ restored excitatory/inhibitory synaptic balance. A SERCA activator improved memory and motor coordination, while clenbuterol increased PSA-NCAM and improved cognition.

Additional agents working through neuroprotection, neurogenesis, or immune modulation include a LXR agonist (which promoted neurogenesis and upregulated apoE), a CB2R agonist (which shifted microglia from M1 to anti-inflammatory M2), idebenone (which improved spatial memory and mitochondrial function), an estrogen receptor beta agonist, and berberine^⬖ (which dose-dependently reduced apoptosis and increased Bcl-2 expression in hippocampal neurons).

Sporadic AD Models

Sporadic AD models (using intracerebroventricular STZ) also responded to combination therapies. A triazine derivative improved spatial learning and increased hippocampal pyramidal layer thickness, canagliflozin improved dendritic morphology, the Croton hirtus extract^⬖ MECH reversed learning and memory impairments while reducing Aβ and AChE, and rapamycin reduced hyperphosphorylated tau and mTOR signaling. The MIF inhibitor ISO-1 improved hippocampal-dependent contextual memory and reduced cytokine production, with MIF levels found elevated in early-stage AD patients’ cerebrospinal fluid. The GSK-3β inhibitor SB216763 attenuated tunicamycin-induced UPR, synaptic impairments, and memory deficits.

Acute Aβ Injection Models

Acute Aβ injection models have been used to test a wide range of agents. Piper kadsura ohwi extract^⬖ significantly ameliorated ethological deficits from both Aβ oligomers and fibrillar Aβ while reducing neuroinflammation via TLR4/NF-κB/TNF-α.^1,2 Rapamycin improved cognitive function, reduced hippocampal Aβ deposition, and increased Homer3 expression. Testosterone reversed spatial learning deficits and neuronal loss via BDNF/CaMKII/CREB signaling (an effect completely blocked by the androgen receptor antagonist flutamide). Curcumin^⬖ dissolved in DMSO partially improved spatial learning in AD model rats and also reversed Aβ-induced damage to neural stem cells, improving viability and differentiation markers (Nestin, Tuj-1, GFAP).^1,2,3 Pioglitazone dose-dependently reversed Aβ1-42-induced activation of MKK4, JNK1, and c-Jun in rat hippocampus, with most p-JNK immunoreactivity co-localizing with microglia.

Additional agents that improved cognition or reduced AD pathology in Aβ-injected models include Angelica keiskei extract^⬖ (which dose-dependently improved memory), low-dose genistein^⬖ (which upregulated STAT3 and suppressed caspase-3), betulinic acid^⬖ (which improved memory, anxiety, and LTP), DL0410 (a dual AChE/BChE inhibitor that improved learning via CREB/BDNF), B. pendula leaf extract^⬖ (which reduced oxidative stress and NF-κB signaling), Huanglian Jiedu Decoction^⬖ (which reduced microglial activation), a DAPK1 inhibitor (which reduced NLRP3 inflammasome activation and ameliorated memory deficits), and atorvastatin (which prevented synaptotoxicity and neuroinflammation via p38 MAPK inhibition). Biochanin A^⬖ attenuated Aβ-induced neuronal death and improved spatial learning via estrogen receptor-dependent p38 MAPK inhibition, while Perilla frutescens^⬖ hexane fraction inhibited Aβ aggregation and protected cells from Aβ toxicity as did a purpose-designed beta-sheet breaker peptide.

Additional agents showing neuroprotective effects in Aβ cell models include Dendrobium nobile alkaloids^⬖ (which increased cell survival), neuroprotectin D1 (which reduced Aβ42, tau phosphorylation, and apoptosis while enhancing autophagy), curcumin^⬖ (which reduced mitochondrial ROS, enhanced autophagy via Rab proteins, and increased axonal transport),^1,2,3 icariin^⬖ (which inhibited autophagy and reduced Aβ production via p70 S6K), a DPP-4 inhibitor (which activated PI3K/Akt/GSK-3β and reduced tau phosphorylation), sodium ferulate^⬖ (which protected hippocampal neurons via Notch pathway modulation), butylphthalide (which protected endothelial cells from Aβ-induced apoptosis via TLR4/COX-2),^1,2 ZL006 (which activated Akt/Nrf2/HO-1), MS-275 and JQ1 (which improved memory via CREB and reduced TNF-α), pioglitazone (which reduced Aβ and tau via PPARγ activation), tetrahydroxystilbene glucoside^⬖ (which reduced microglial inflammation and APOE/TREM2 expression), berberine^⬖ (which promoted microglial M2 polarization via PI3K-AKT signaling, protecting neurons from Aβ-mediated injury), and 5-HT1B receptor inhibition (which restored Aβ1-42-disrupted eNOS and Akt phosphorylation in human endothelial cells, suggesting this receptor mediates Aβ-induced vascular dysfunction relevant to AD).

Okadaic Acid (OA) Models

Okadaic acid models (which induce tau hyperphosphorylation by inhibiting protein phosphatase 2A) also responded to DMSO-delivered therapies. Trillium tschonoskii^⬖ decoction improved spatial learning, increased PP2A activity, and reduced tau phosphorylation while preserving hippocampal neurons. Banqiao Codonopsis pilosula decoction^⬖ dose-dependently improved cognition, reduced tau hyperphosphorylation, and increased synaptic proteins and dendritic spine numbers.^1,2 In zebrafish, Mansonone G^⬖ reversed OA-induced cognitive impairments, improving spatial and recognition memory and restoring cholinergic function. Additional agents include ginsenoside Rb1^⬖ (which attenuated tau hyperphosphorylation), ginkgolide^⬖ combined with insulin (which synergistically improved learning and reduced neurofibrillary tangles), pilose antler polypeptide^⬖ (which activated PI3K/AKT and reduced apoptosis), and sarsasapogenin^⬖ (which attenuated tau hyperphosphorylation via Akt/GSK-3β).

Tau Pathology

Several findings directly address tau, a key driver of neurodegeneration in AD:

In female mice following traumatic brain injury, DMSO independently reduced pathological TAU and TDP43 proteins across multiple brain regions, an effect comparable to glibenclamide. EGTA (a calcium chelator) decreased tau phosphorylation at Ser396 in AD mice by reducing calpain 2 and CDK5 expression. Resveratrol^⬖ reduced cadmium-induced tau hyperphosphorylation via AMPK/PI3K/Akt activation, while resveratrol^⬖ also reduced tau acetylation and phosphorylation in aged rats with postoperative cognitive dysfunction by activating SIRT1 and shifting microglia from M1 to M2a phenotype.^1,2 Docosahexaenoic acid^⬖ administered after TBI reduced phosphorylated tau and APP accumulation. UCH-L1 inhibition blocked tau aggresome formation by reducing K63-linked ubiquitin chains and impairing HDAC6-tau binding.

In C. elegans (AD strains) hemp extract^⬖ (containing both cannabinoids and terpenes, dispersed in DMSO) significantly increased lifespan in tau-model nematodes, with CBD^⬖ directly hindering protein aggregate formation.

Oxidative Stress

Ferulic acid ethyl ester,^⬖ administered intraperitoneally in DMSO, protected gerbil brain synaptosomes from Aβ-induced oxidative damage, reducing reactive oxygen species, protein oxidation, and lipid peroxidation while boosting antioxidant defenses (HO-1, HSP72) and reducing iNOS. Astaxanthin^⬖ dose-dependently improved cognitive performance, reduced Aβ42 and malondialdehyde accumulation, inhibited AChE and MAO activities, and increased Nrf2 and miR-124 expression. In mice, DMSO reduced cerebral ROS by 9.8–79% (greatest effect in young mice) and irreversible oxidative protein damage by 30.7–69% (greatest effect in aged mice); these benefits were further enhanced by curcumin.^⬖ In rats, SIRT2 inhibition reduced oxidative stress, increased anti-apoptotic bcl-2, and elevated autophagy regulator beclin-1 in cortex and hippocampus, while melatonin^⬖ and curcumin^⬖ each reduced lipid peroxidation and SIRT2 expression and increased Nrf2 and antioxidant defenses in the cerebral cortex (though without synergistic effect when combined).

MSM^⬖ (DMSO’s oxidized metabolite) ameliorated BPA and radiation co-exposure-induced neurodegeneration, reducing AD markers (Aβ42 by 71.6%, AChE by ~50%, tau phosphorylation by 57%), boosting BDNF (132–160%), suppressing the TREM-2/DAP12 pathway, and reducing Aβ plaques by ~75%.

Note: MSM^⬖ crosses the blood-brain barrier rapidly (detectable within ~10 minutes of oral intake), reaching brain concentrations of ~2.36 mM after oral supplementation with a half-life of approximately 7.5 days.^1,2

AChE Inhibition and Drug Screening

In addition to DMSO itself being an AChE inhibitor, a variety of AChE inhibitors have been tested in DMSO for AD relevance. Novel tacrine-hydroxamic acid derivatives showed potent dual AChE/HDAC inhibition with Aβ inhibition, while thiazole-based inhibitors outperformed rivastigmine and huperzine-A. Among 21 flavonoids screened, galangin showed the strongest brain AChE inhibition (IC50 ~120 μM). Another screening identified a multifunctional probe that (with DMSO) bound Aβ aggregates, inhibited cholinesterase, and improved cognitive and spatial memory.

Natural Compounds and Model Organisms

A wide range of natural compounds dissolved in DMSO have shown neuroprotective effects in AD models. In C. elegans, olive leaf extract^⬖ strongly protected neurons from Aβ-induced degeneration, while 3-hydroxytyrosol,^⬖ tyrosol,^⬖ saffron,^⬖ Polygonum multiflorum,^⬖ and Ziziphus jujuba^⬖ each also provided significant protection.¹ Cannabidiol^⬖ extended lifespan and slowed age-related neuronal deterioration in C. elegans and enhanced neurite outgrowth and dendritic spine density in mammalian neurons through the same SIRT1 pathway. Quercetin^⬖ and rifampicin individually reduced Aβ plaques, with the combination producing the greatest clearance. Quercetin^⬖ and kaempferol^⬖ (polyphenols isolated from Ginkgo biloba cell cultures) dose-dependently reduced protein carbonylation in C. elegans, a key marker of aging-related protein damage linked to neurodegenerative diseases. Oxoisoaporphine-lipoic acid hybrids improved learning, memory, lifespan, and AChE inhibition in Aβ42 transgenic Drosophila. In zebrafish, purinergic receptor antagonists (caffeine, ZM241385, DPCPX) prevented scopolamine-induced memory impairment.

In cell and animal models, carvacrol^⬖ protected neurons from Aβ-induced neurotoxicity and improved memory in AD rats,^1,2 while Ashwagandha-derived withanolides^⬖ restored axon/dendrite lengths and synaptic markers in Aβ-injured neurons and reversed memory deficits when given orally. Cynarae folium extracts^⬖ exhibited neuroprotective effects against Aβ in both cells and rats, while in drug-resistant Aβ flies, anle138b significantly prolonged survival. Ptychopetalum olacoides extract reversed MK-801-induced amnesia, suggesting involvement of the glutamatergic system in its cognitive-enhancing properties.

Additional natural compounds showing anti-Aβ effects include curcumin^⬖1,2 (which suppressed microglial HMGB1/RAGE/NF-κB signaling), bisdemethoxycurcumin,^⬖ Ginkgo biloba polyphenols^⬖ (which protected dPC12 cells from Aβ damage), Perilla frutescens^⬖ (which disaggregated preformed Aβ aggregates), icariin^⬖ (which reduced iNOS and TNF-α and improved cognition in LPS-induced AD mice), various edible sprout extracts^⬖1,2,3 (with buckwheat sprouts^⬖ showing the strongest ROS suppression and Aβ reduction), curcumin^⬖ (which, through binding amyloid, enabled in vivo detection of retinal amyloid in live transgenic AD mice via confocal ophthalmoscopy, demonstrating the potential for non-invasive AD diagnosis), and the polyphenols nordihydroguaiaretic acid,^⬖ baicalein,^⬖ and Padina extract^⬖ (which protected cells from Aβ42-induced damage). Curcumin^⬖ dissolved in DMSO also achieved high serum solubility (at least 3 mM), effectively inhibiting Aβ plaque formation.

Aging-Related AD Models

D-galactose injection creates accelerated aging in rodents that models age-related cognitive decline. Guilingji^⬖ (a traditional formula) significantly improved Morris water maze performance in D-galactose-aged rats, restoring antioxidant activity and normalizing neurotransmitters. Ganoderma tsugae extract^⬖ improved locomotion, learning, and memory by increasing brain antioxidant enzymes and BDNF while reducing inflammasome activation. Kurarinone^⬖ combined with rehabilitation exercise synergistically improved spatial learning and memory, upregulated synaptic plasticity markers (PSD-95, synaptophysin), and reduced Aβ1-42 deposition via the BACE1/Aβ pathway. Resveratrol^⬖ significantly increased SOD and decreased oxidative damage in hippocampal neurons of mice with D-galactose-induced aging. Curcumin^⬖ reduced APP and tau expression and suppressed HAT activity in AD rats. Artemisinin^⬖ also demonstrated neuroprotective effects in an animal model of AD prevention.

Aluminum chloride, which induces Aβ plaque accumulation and tau phosphorylation, was counteracted by a bithiophene derivative that restored antioxidant defenses, prevented neuronal and synaptic loss, and mitigated AD-related pathology.^1,2

Vascular Dementia

Vascular dementia (VaD) results from chronic cerebral hypoperfusion that causes progressive neuronal damage and cognitive decline, making DMSO well suited for the condition.

Two p38 MAPK inhibitors dissolved in DMSO repeatedly improved spatial learning and memory in rats with bilateral carotid artery occlusion-induced VaD, reducing hippocampal apoptosis, extending survival, and decreasing p38 MAPK phosphorylation.^1,2,3 Curcumin^⬖ dissolved in DMSO dose-dependently improved learning and memory in rats with bilateral carotid artery occlusion-induced VaD, reducing hippocampal pathology and promoting brain cholesterol efflux via the LXR/RXR-ABCA1-apoA1 pathway.^1,2,3 Paeoniflorin^⬖ improved learning and memory in VaD rats by reducing proinflammatory cytokines and inducing microglial polarization from M1 to M2 via cannabinoid receptor type 2. Cathepsin B inhibition reduced mitochondrial abnormalities, neuronal apoptosis, neuroinflammation, and cognitive dysfunction after transient middle cerebral artery occlusion.

Additional agents improving cognition in VaD models include andrographolide^⬖ (which reduced hippocampal apoptosis and increased Bcl-2), PGE1 (which improved learning and memory via the BDNF/TrkB pathway), esketamine (which upregulated BDNF, ERK, and Nrf2), tripchlorolide^⬖ (which reduced Aβ, NF-κB, and COX-2), IGF-1 (which improved cognition via Akt/mTOR), intranasal recombinant erythropoietin (which improved escape latency and preserved hippocampal neurons), the Shenmayizhi formula^⬖ (which upregulated synaptic proteins and VEGF), resveratrol with SIRT1 activation (which improved cognition and enhanced antioxidant capacity in chronic cerebral ischemia), HDAC inhibitor compound 13 (which activated BDNF isoforms and modulated AMPA receptor signaling), rapamycin (which reversed mTOR-mediated autophagy suppression, reducing Aβ accumulation and tau hyperphosphorylation in diabetic rats after orthopedic surgery), and emodin^⬖ (which reduced ROS and inhibited neointimal proliferation in carotid artery stenosis). Quercetin^⬖ also alleviated hippocampal demyelination in a bilateral carotid artery stenosis model.

Note: molar loss (tooth extraction) in VaD rats worsened cognitive impairment and increased hippocampal apoptosis and iNOS/p38 MAPK/NF-κB expression; a p38 MAPK inhibitor in DMSO reduced these effects, illustrating that dental health impacts cerebrovascular cognitive decline.

DMSO has also been used to differentiate bone marrow mesenchymal stem cells (BMSCs) into neuron-like cells expressing neuronal markers (using a 2% DMSO/BHA medium), which were then transplanted into VaD rat brains, and BMSCs promoted recovery of an AD cell model by upregulating PDGF-BB via the PI3K/AKT pathway.

Reader Reports

My uncle’s wife has dementia and has been unable to speak for over a year. My mom recently visited them and told them about DMSO. He began to give his wife DMSO orally. After two weeks she began to talk again.

I read the article and began giving it to my 93 year old mother in her juice every morning the end of November. She has had some form of dementia for over 15 years. In the last year or so she would get sundowners really bad and could not follow instructions. Since taking the DMSO, she no longer suffers with sundowners. She is more “with it” and can communicate and laugh with us. Her personality is back. She is able to understand when I am asking her to use the bathroom. She is more cognitive and has started coloring in her coloring books again.

I deeply appreciate your posts on DMSO. You helped bring spontaneous interaction back into the life of my father with Alzheimer’s. As well as many other people I have educated about its uses. God bless you.

Meanwhile, your DMSO information seems to have been a game-changer for him [a stroke patient]. We are now about eight weeks into treatment and I have observed: voice is stronger, speech is markedly improved, appetite has increased, dysphagia has changed dramatically---he is now able to eat normal-sized meals. He now feeds himself almost exclusively, using his affected hand. His sense of taste has started to return.

We have been using several of the therapies you have informed us of. I started putting 2/3 teaspoon DMSO with a teaspoon of galactose^⬖ in his coffee each morning. I started giving him 2 teaspoons after breakfast in juice and again 2 teaspoons in the afternoon, with good results. Is he cured? NO but he’s functioning a lot better.

Lastly, a reader shared their partner (75) was diagnosed with an inoperable 8cm glioblastoma causing a slow brain bleed, losing the ability to speak, and right-side paralysis, with a prognosis of 3 weeks to live. After copious topical 99% DMSO, motor function began returning within 24 hours. By week 3, he was eating meals at the table. By week 4, he could walk with a walker. A new CT scan at day 55 showed no brain bleed and reduced tumor metrics.

Multiple Sclerosis

Multiple sclerosis (MS) is an autoimmune disease in which the immune system attacks myelin, the insulating sheath around nerves in the brain and spinal cord. As demyelinated nerves progressively lose their ability to transmit signals, patients develop worsening neurological deficits including impaired mobility, vision loss, pain, and cognitive decline. Despite decades of research, existing therapies primarily suppress the immune attack but do not restore lost myelin, leaving patients with accumulating disability.

DMSO has several properties that make it mechanistically well-suited for MS: it crosses the blood-brain barrier, reduces harmful immune activity, decreases inflammation, improves circulation (including to vulnerable white matter tracts), and as discussed in the protein folding section, acts as a chemical chaperone that stabilizes proteins. Additionally, DMSO inhibited the blood clotting triggered by myelin debris in a dose-dependent manner — significant because when myelin is broken apart by the immune system, exposed phospholipids activate clotting pathways that compromise the blood supply nerves depend on, providing a secondary mechanism for MS neurodegeneration that existing anticoagulants do not target. DMSO also prevented bilirubin-induced toxicity in myelinated axons, suggesting DMSO directly protects myelin from the blood breakdown products released during hemorrhage or inflammatory demyelination (likewise a caspase-1 inhibitor—in DMSO—reversed bilirubin’s NLRP3-mediated damage to hippocampal neurons).

This circulatory perspective on MS also aligns with a broader theory that beyond insufficient blood flow to the brain, impaired venous and lymphatic drainage from the brain also contribute to neurodegeneration — both by retaining toxins and by disrupting the glymphatic system (the brain’s waste clearance pathway), leading to accumulation of pathological proteins like β-amyloid and α-synuclein. In 2009, it was proposed that MS was linked to chronic cerebrospinal venous insufficiency (CCSVI) — poor drainage from the head through the jugular veins — and significant clinical improvements were reported after stenting the jugular veins open (a technique also used for other complex neurological conditions before being restricted due to both pharmaceutical lobbying and legitimate safety concerns). More recently, in China, lymphatic-venous anastomosis (LVA) — a microsurgery that creates direct connections between the neck’s deep cervical lymphatic vessels and adjacent veins to bypass obstructed drainage — has already produced dramatic short-term improvements for dementia patients and is now offered at over 30 surgical centers.^1,2,3

Note: this article provides an excellent synopsis of the evidence for CCSVI and the neurological conditions it causes (although our treatment approach differs from the authors).^1,2

I am inclined to believe this theory is correct, as we saw many neuroimmune patients make dramatic recoveries from jugular stenting when it was still available. Likewise, pioneering clinicians recently found that COVID vaccine injuries frequently resulted from sudden persistent compression of the iliac vein (which they successfully treated with stenting). My own belief is that drainage obstructions often result from poor zeta potential — which both drives fluid flow and creates the expansive force that keeps vessels open — or from inherently weak blood vessels that collapse easily. This explains why hypermobile patients are typically far more sensitive to pharmaceutical injuries (particularly vaccines that impair zeta potential, or via the spike protein, directly weaken blood vessels), and why MS has been found to be 10–11 times as common in hypermobile EDS patients.

Due to the risks associated with stenting, I have pursued other approaches to address impaired drainage (with success). Since DMSO increases lymphatic circulation, improves venous drainage, and clears the pathological protein aggregates that accumulate when drainage fails (as detailed earlier in this article), it may address this underlying impairment through pharmacological rather than surgical means.

Note: pioneering physician Dietrich Klinghardt extensively investigated CCSVI across neurological conditions and reported it present in 100% of tested MS, autism, Parkinson’s, ALS, and Lyme patients — with patients suffering from fibromyalgia and chronic fatigue also frequently presenting with it — and Lyme patients typically testing worse than MS patients (4 of 5 diagnostic parameters positive vs. 2 of 5 in MS).^1,2,3,4 He concluded CCSVI was driven by chronic endothelial infections (Borrelia, Rickettsia, Chlamydia pneumoniae, Babesia) that caused inflammation, scarring, and permanent vasoconstriction of the jugular veins^1,2,3 (and I would argue zeta potential impairment—as Knisely observed malaria [which is similar to babesia] ultimately killed by life-threatening blood sludging which began with small sludges forming along the vessels within which it hid from the immune system^1,2,3). While balloon dilation produced roughly one-third significant improvement, one-third modest, and one-third no lasting benefit, Klinghardt preferred it over stenting because stents caused scarring and vein occlusion^1,2 and he found that results were inconsistent regardless of method if the underlying infections, existing tissue compressions and elevated inflammatory markers (TGF-β1, C4a, MMP-9) were not addressed first, as the veins would re-stenose.^1,2,3,4,5,6 Likewise, other clinicians at a CCSVI summit corroborated it contributed to neurodegeneration across multiple conditions^1,2 and a diagnostic protocol Klinghardt helped create used therapeutic ultrasound to mobilize compartmentalized pathogens from the venous endothelium (or possibly sludges lining the endothelium) into the urine where they could be identified by DNA testing (and often were).¹

DMSO in MS Patients

In a famous case from the DMSO literature, Stanley Jacob decided to risk giving a 29-year-old woman paralyzed from MS who also had kidney failure oral DMSO. “Her improvement was dramatic — as dramatic as any benefit I have ever seen,” Jacob reported. Her kidney problems came under control, and after a few more weeks, she walked again. Six years later she still walked, drove her car, and cared for her family — though she was slowly declining (indicating DMSO was not enough to completely treat her condition).

Another more recent case involved a California woman confined to bed in the fetal position at a convalescent hospital, expected to die within months. After starting DMSO through multiple routes (injectable, oral, and topical), she began regaining sensation in her legs — initially experiencing pain, which was considered positive given her prior lack of feeling. Over the following year she regained leg movement and the ability to feed herself, with continued improvement until she was moved to another state where the treatment was unavailable.

The only formal study I know of evaluated 34 MS patients in Russia in 1984. Overall, the investigators felt DMSO had a very positive result, with the best outcomes in patients with remitting MS, while results were more inconsistent in rapidly progressive MS. They attributed the benefits to DMSO causing remyelination, reducing edema, improving nerve cell communication, and having positive effects on immunity and tissue repair, with no side effects reported.

Additionally:

•A Russian case report documented successful DMSO therapy in an MS patient with trophic lesions and a cystostoma.

•DMSO has also been used topically (mixed with anesthetics) on trigger zones to manage trigeminal neuralgia in MS patients, with outcomes including reduction of carbamazepine to minimum doses or complete discontinuation and achievement of full remission during exacerbations.

•A study of 35 MS patients (disease duration 2–18 years) recommended DMSO-containing topical gels mixed with nonsteroidal analgesics for chronic neuropathic pain, myofascial pain from spastic muscles, and pain along peripheral nerve trunks in bedridden patients.

Reader Reports

A few readers have also reported improvements in MS following DMSO use which corroborate the previous data.

One reader’s wife with MS-related trigeminal neuralgia that had been painful for over a year and a half tested 70% DMSO cream on a small spot on her face, and her pain dropped 90%. The next morning she applied it over the entire trigeminal area and the pain was 99.9% gone — even after three days without reapplication, the pain had not returned.

Another reader reported that DMSO “brings my MS hugs to a standstill. Before my husband found this for me I just had to endure them or go to the hospital for morphine.”

A reader with MS, fibromyalgia, liver fibrosis, CRPS, and lymphedema described oral and topical DMSO as “a godsend” after about a year of use.

An MS patient taking oral DMSO four times daily reported it was “incredibly helpful for pain and energy.”

One reader reported that MSM^⬖ (DMSO’s oxidized metabolite), along with other supplements, allowed them to stop all prescribed MS medications and their associated side-effect medications, stating they “feel younger and better than ever.”

Note: a 1982 article stated that DMSO had been touted as a miracle drug for numerous conditions including multiple sclerosis—suggesting these readers’ experiences are not unique.

DMSO Myelin Interactions

•X-ray diffraction studies have revealed that DMSO directly interacts with myelin structure and at high concentrations DMSO produces a fully reversible transformation of nerve myelin into a new highly ordered structure (DMSO squeezes the water out between myelin wraps and selectively alters the outer membrane layer).^1,2

•Clemastine, an antihistamine being investigated as a remyelinating agent for hypomyelinating diseases, also showed preliminary effects on myelination processes in vitro.

•Oligodendrocytes are the cells that produce myelin in the central nervous system, and their regeneration is essential for remyelination. DMSO, in turn, has been shown to drastically increase the generation of oligodendrocyte precursor cells from human stem cells^1,2,3 (and for this effect to be further enhanced in combination with all-trans-retinoic acid).^1,2 Additionally, in neural stem cells, γ-secretase inhibitors (in DMSO) modulated Notch1 signaling and increased oligodendrocyte marker expression and likewise, clobetasol (in DMSO) promoted neural stem cell differentiation into both neurons and oligodendrocytes.

Note: one study found DMSO shifted stem cells towards producing astrocytes, suggesting lower doses promote oligodendrocyte differentiation, while longer sustained ones promote astrocytes.

Other Demyelinating Diseases

Experimental autoimmune encephalomyelitis (EAE), the standard animal model for MS, immunizes animals against myelin proteins to trigger autoimmune demyelination, and hence provides poignant insights for treating MS. Notably, as I show here, the hepatitis B vaccine (which overlaps with myelin, creating autoimmunity to myelin) has been repeatedly linked to multiple sclerosis and also has caused autoimmune EAE.

In a 1969 study DMSO was listed as a therapeutic option for EAE, and in EAE experiments, animals are frequently treated with a therapeutic agent dissolved in DMSO. Across these studies, a consistent pattern emerged: agents dissolved in DMSO improved EAE clinical scores, decreased inflammatory cell infiltration, and reduced demyelination — with individual agents distinguished by their specific mechanisms and additional effects.

Nordihydroguaiaretic acid,^⬖ tanshinone IIA,^⬖ and sulforaphane^⬖ increased protective antioxidant and anti-inflammatory signals while lowering inflammatory IL-17A in EAE immune cells.^⬖ Nordihydroguaiaretic acid^⬖ also restored the blood-brain barrier, and in a separate study, both nordihydroguaiaretic acid^⬖ and tanshinone IIA^⬖ promoted remyelination and recovered axon integrity.^1,2,3,4,5 Curcumin^⬖ delayed disease onset and in addition to reducing inflammatory infiltration and myelin loss, normalized impaired autophagy and lowered inflammatory cytokines.^1,2 Mitochondrial division inhibitor 1 decreased oligodendrocyte and spinal cord apoptosis, protected axonal integrity, and promoted nerve growth factors.^1,2 Butylphthalide protected mitochondria, inhibited necroptosis, and lowered TNF-α and IL-1β, while ferrostatin-1 (a ferroptosis inhibitor) and matrine^⬖ each similarly reduced neurological severity.^1,2 An epoxide hydrolase inhibitor reduced disease severity in chronic EAE by suppressing multiple inflammatory pathways (TLR4/NF-κB signaling, inflammasomes, COX-2, and nitric oxide synthases) and in a separate study, promoted remyelination via enhanced myelin proteolipid protein expression.^1,2

Additional agents demonstrating efficacy in EAE include hydroxyfasudil (which also prevented EAE onset and suppressed key pro-inflammatory cytokines), a p38 MAPK inhibitor¹,² (which reduced IL-17 expression), ginkgolide A^⬖ (which delayed disease onset and shifted macrophages toward an anti-inflammatory state), isoliquiritigenin^⬖ (which suppressed inflammatory Th1 cells and activated protective astrocytes), nitidine chloride^⬖1 (which increased anti-inflammatory IL-10 when given preventively), a JAK2 inhibitor (which delayed onset and decreased Th17-driven inflammation), a GSNOR inhibitor (reduced demyelination and inflammation) arctigenin^⬖ (which decreased Th1 and Th17 cells via AMPK/PPAR-γ activation and p38 inhibition), a caspase-1 inhibitor (which delayed onset and lowered IL-1β and IL-18), tacrolimus (reduced demyelination and axonal loss by up to 95%) and schisandrin B,^⬖ baicalin,^⬖ AG490, and NBP.^1,2,3

In addition to EAE models, in cells from newly diagnosed and IFN-β-treated MS patients, silymarin^⬖ suppressed Th1 cell proliferation and inhibited IFN-γ production in a dose- and time-dependent manner, suggesting it could complement existing MS therapies. Chrysin^⬖ reduced disease severity and demyelination in experimental autoimmune neuritis (an animal model of Guillain-Barré syndrome).

Lastly, one reader with Morvan’s syndrome, a rare and severe autoimmune channelopathy (that developed following viral encephalitis) reported that after two weeks of topical 70% DMSO cream, inflammation in his hands visibly decreased and pain was reduced by 75%. His case was particularly severe, having required multiple nerve decompression surgeries, four joint replacements, cervical fusion, and two nerve stimulator implants.

Cuprizone Models

Cuprizone is a copper chelator that, when fed to mice, causes toxic demyelination — providing a model to study remyelination independently of the autoimmune component. In cuprizone-demyelinated mice, the cannabinoid agonist WIN55212-2 (1 mg/kg in DMSO) significantly reduced weight loss, improved motor function, reduced corpus callosum demyelination, increased myelin basic protein expression, decreased astrocyte activation, and upregulated juxtanodin and Nkx2.2 (transcription factors involved in myelin repair).^1,2,3 Hydroxyfasudil and fasudil also improved behavioral deficits, attenuated demyelination, and strongly inhibited microglia-driven neuroinflammation in the cuprizone EAE model. Mitochondrial division inhibitor 1 protected oligodendrocytes and suppressed complement activation on oligodendrocytes in the corpus callosum. Biochanin A^⬖ improved grip strength, spatial and recognition memory, and mitigated hippocampal and prefrontal cortex neuronal damage.

Neuromyelitis Optica

Neuromyelitis optica (NMO) is a related autoimmune demyelinating disease that preferentially attacks the optic nerves and spinal cord through antibodies targeting aquaporin-4 water channels. In an NMO mouse model, tanshinone IIa^⬖ (in DMSO) significantly reduced loss of aquaporin-4, GFAP, and myelin basic protein, decreased neutrophil and microglial infiltration, and increased neutrophil apoptosis. Arbidol (in DMSO) similarly increased cortical cell survival from 49% to 79% in vitro and reduced aquaporin-4/GFAP loss in vivo.

White Matter Injury and Neonatal Myelination

Several studies have demonstrated that agents combined with DMSO can protect or restore myelination in non-autoimmune white matter injury. The hydrogen sulfide donor anethole trithione promoted remyelination, oligodendrocyte precursor cell proliferation and differentiation, microglial myelin debris clearance, and long-term functional recovery after subcortical white matter stroke. Siponimod reduced myelin loss and brain atrophy after intracerebral hemorrhage. An α5 GABAA receptor inverse agonist promoted oligodendrogenesis, myelination, and improved motor function in ischemic rats. In a neonatal white matter damage model, miconazole (in DMSO) significantly increased myelin basic protein expression and improved myelin ultrastructure. MiR-219 agomir improved oligodendrocyte maturation in neonatal rats with LPS-induced neuroinflammation via the ERK1/2 pathway. In spinal cord injury, an epidermal growth factor receptor inhibitor reduced demyelination and myelin-associated inhibitory molecule expression.

DMSO and Protein Folding

Chemical chaperones are small molecules that help proteins be folded into their correct configuration, and hence can ensure protein stability or help the body eliminate misfolded protein. Since many challenging diseases (particularly genetic ones) are a result of misfolded or non-functional proteins, chemical chaperones offer a potentially invaluable therapeutic strategy.

Note: I believe the physiologic zeta potential has an important role in ensuring the correct folding of proteins.

Some of the best-known chemical chaperones include glycerol, deuterated water, and DMSO (which is thought to be in part due to it creating a tighter packing around proteins and stabilizing their conformation). DMSO, in turn, has shown promise in misfolding diseases such as nephrogenic diabetes insipidus,^1,2 cystic fibrosis and Machado-Joseph disease, and can increase the ability of impaired immune cells (due to defective HLA-DM) to present the antigens necessary to mount an immune response.¹

One protein-misfolding disease, amyloidosis, occurs when misfolded proteins enter the bloodstream, aggregate into amyloid fibrils, and deposit in tissues (which over time damages organs and can lead to organ failure). As options for this disease are limited, DMSO was attempted, and early positive responses led to it being repeatedly used in certain areas (e.g., in Japan), where it was found the best results were obtained when high concentrations could be applied directly to the affected area (e.g., bladder lining or skin), and that while not consistently effective, a large body of literature showed it repeatedly produced dramatic results for patients with otherwise fatal conditions, and appeared to do so by both dissolving amyloids and facilitating their urinary excretion (detailed here).

Note: since many cancer-causing proteins are misfolded proteins, it is thought that this may partly explain DMSO’s anticancer properties.

In addition to diseases discussed previously, three neurological conditions characterized by defective proteins have shown promising responses to DMSO.

Niemann-Pick disease

Niemann-Pick disease is a rare genetic lysosomal storage disorder marked by intracellular accumulation of sphingomyelin, either due to a defect in sphingomyelinase, the enzyme which breaks it down (types A/B) or defective lysosomal cholesterol trafficking (type C). Each causes damage to the organs and neurodegeneration, with A [NPA] being the most severe (death is typical at 2-3 years), B [NPB] the least severe (minimal neurological involvement), and C [NPC] on average causing death around 13 years of age. As DMSO stabilizes proteins and improves cellular transport, it has been repeatedly explored for this condition (particularly type C).

This disease is frequently studied in human fibroblasts with that defect. There DMSO has been shown to do the following:

•In normal fibroblasts, 2% DMSO for 4 days increased sphingomyelinase activity to 230% of control levels in normal cells in a dose-dependent manner (with a much smaller increase in other lysosomal hydrolases). In fibroblasts from NPC patients, 2% DMSO raised sphingomyelinase activity by 480% (correcting the deficiency), along with a smaller (280% increase) seen in NPB fibroblasts.

Note: in NPC, a decrease in sphingomyelinase activity results from the massive buildup of cholesterol in the cell (rather than genetic impairment of the enyzme).

•In normal fibroblasts, 2% DMSO increased sphingomyelinase activity, primarily within the lysosomes, by 168-263% (depending on pH). In NPC fibroblasts (which retained 30% sphingomyelinase activity), DMSO caused a 2+ fold increase in activity that brought it close to normal levels, whereas in NPA and NPB fibroblasts no improvement was seen. Additionally, smaller increases in other lysosomal hydrolases were seen, indicating DMSO specifically targets sphingomyelinase.

•When NPC fibroblasts were exposed to LDL, 2% DMSO had minimal effect in the first 12 hours but substantially reduced the excessive accumulation of unesterified cholesterol in lysosomes thereafter (particularly at 24–48 hours), bringing cholesterol levels close to those in normal cells (markedly diminished perinuclear/lysosomal cholesterol fluorescence), and restored the impaired cellular homeostatic responses to cholesterol.

•In normal fibroblasts, twelve specific drugs (e.g., older psychiatric ones) were found to markedly reduce cholesterol esterification (e.g., one caused a 93% reduction for at least 48 hours). DMSO (2%) partially counteracted this and restored 16-20% of the lost cholesterol processing capacity, suggesting potential use in NPC.

•2% DMSO (but not 1% or 4%) significantly increased sphingomyelinase activity in both normal and NPC fibroblasts. However unlike the other studies, none of the concentrations reduced cytoplasmic cholesterol in NPC fibroblasts.

•Lastly, in mice fibroblasts (modeling NPA/B), 2% DMSO caused a 2-3 fold increase in sphingomyelinase activity.

These results suggested DMSO could partially improve the disease, and they (especially the early ones) generated sufficient interest to explore using DMSO to treat it where the following was found:

In NPA/B mice, oral DMSO administration (0.25% in drinking water from 6 weeks of age) prolonged survival from ~12 weeks in untreated mice to an average of 15 weeks and 5 days (maximum 17 weeks and 5 days) and delayed the onset of neurological symptoms such as tremors. However, it failed to prevent symptom progression or improve manifestations once present and had minimal effect on cholesterol accumulation (liver slightly decreased, spleen and brain were unaffected).

•In NPC mice, flavopiridol (dissolved in DMSO) and infused directly into the brain dose dependently reduced hyperphosphorylation of cytoskeletal proteins and improved behavior.

•In human NPC patients, a Japanese paper reported oral administration of DMSO resulted in some clinical benefits, including decreased size of hepatosplenomegaly, lesser frequency of seizures, and improved EEG findings. However, the progressive clinical course of the disease was not changed, although it appeared to slow down.

The author of that paper also published:

•A case report of an 8 year old girl with NPC who presented with severe psychomotor deterioration, marked cortical atrophy, frequent seizures, moderate ventricular dilatation and hepatosplenomegaly. Oral DMSO was shown to normalize her sphingomyelinase activity. After 2 years of oral DMSO, she had a slight improvement in response to her surroundings, her seizures decreased (allowing an anticonvulsant to be tapered), her EEGs showed marked improvement (theta waves and spindles normalized), there was no further progression of her cortical atrophy, and both the spleen and liver shrank to normal size.

•Another report on siblings with NPC who clinically improved with DMSO.

•A study that again found DMSO corrected sphingomyelinase deficiency in cultured fibroblasts from NPC patients.

•A study showing other dipolar aprotic substances besides DMSO also selectively increased sphingomyelinase activity.

Note: lastly, a final case report detailed unsuccessful treatment of NPC with oral DMSO.

Creutzfeldt-Jakob Disease and Prion Disorders

Prion diseases (such as CJD in humans and scrapie in animals) result from normal prion proteins misfolding into a pathogenic form (PrPSc) that aggregates into toxic fibrils and progressively destroys brain tissue. These conditions are universally fatal and have no approved treatment.

DMSO has shown therapeutic potential through multiple mechanisms. As a chemical chaperone, DMSO stabilized the normal alpha-helical structure of newly synthesized prion protein in infected neuroblastoma cells, inhibiting its conversion to the pathogenic form. In cells carrying a familial CJD mutation, DMSO reversed the mutant phenotype by reducing lysosomal accumulation of misfolded prion protein and restoring its normal distribution to the cell surface.^1,2 In yeast prion models, DMSO cured multiple prion variants more efficiently than guanidine hydrochloride by enhancing chaperone activity (Hsp104) and converting aggregated protein back into soluble forms.

DMSO also partially inhibited PrPSc aggregation, producing amorphous aggregates with less than 1% of the prion infectivity of untreated rod-like aggregates when inoculated into hamsters.^1,2,3 In prion-infected hamsters, DMSO prolonged incubation time, reduced the rate of PrPSc accumulation in the brain, and (like seen in amyloidosis) increased urinary clearance of protease-resistant prion protein — though it was not sufficient as a standalone cure.^1,2

Ruthenium-DMSO complexes (related to NAMI-A) showed even stronger effects, disaggregating prion peptide fibrils, reducing copper-mediated oxidative stress, and rescuing neuronal cell viability from 33% to 85%.^1,2

One reader reported that her cousin with CJD improved after approximately one month of IV DMSO infusions; we subsequently learned she operated an infusion center and had used high-dose vitamin and DMSO infusions to treat numerous severe conditions, with her cousin still alive several years later.

Note: two prion studies found less favorable results,^1,2 indicating results may vary by species, strain, or protocol.

Lastly, DMSO’s protein-stabilizing properties likely extend beyond misfolded proteins — it has been shown to act as a pharmacological chaperone that restores normal membrane receptor trafficking, and (in many studies) to stabilize brain microtubules during isolation by preventing tubulin depolymerization under stress.^1,2 Since microtubules are essential for neuronal function and are impaired in neurodegenerative diseases, this likely enhances DMSO’s neuroprotective effects in conditions like strokes or TBIs, where microtubule collapse from oxidative stress or ischemia worsens neuronal damage.

Note: the benefits seen in the final disease, Down Syndrome, (discussed further below) may result from DMSO’s neuroprotective and antioxidant effects, combined with DMSO’s ability to act as a chemical chaperone (which could help cells manage proteostasis overload from excess proteins and support clearance of misfolded or damaged proteins), or DMSO improving transport of vital nutrients across compromised membranes.

Cognitive Impairment and Dementia

The same degenerative processes which cause dementia initially trigger cognitive impairment and as such, being able to head this off early, beyond greatly improving one’s current quality of life, also allows much worse situations to be avoided. As these neurodegenerative processes (e.g., poor blood flow and inflammation) also underlie many of the other neurological disorders DMSO treats, significant data has accumulated for either DMSO alone, or DMSO in combination with another therapy to reverse cognitive loss.

The animal research in this field is as follows:

When rats had their carotid arteries surgically modified to significantly reduce the amount of blood going to their brain, after 3 months, it was found that DMSO prevented both the neuronal damage and the significant loss of spatial memory and learning that otherwise resulted from that chronic loss of cerebral blood flow.

In a similar study, rats 14 weeks old were subjected to either permanent bilateral carotid artery occlusion or sham occlusion (mimicking the chronic vascular impairments many experience with increasing age) and then tested for visuospatial memory function. After 14 weeks, four rats who had shown persistent and severe memory impairment received DMSO and FDP for 7 days, which improved their memory by 54%, almost reaching the cognitive function of the controls. Unfortunately, this improvement was partially lost once DMSO-FDP were discontinued (as the blood supply was still occluded).^1,2

Lurcher mice are used to study olivary and cerebellar disorders because their Purkinje cells can’t survive (e.g., by 30 days of age their walking is grossly abnormal). When these mice received DMSO, it prevented the age-related deterioration of certain cognitive functions (e.g., memory and spatial learning abilities).^1,2

DMSO has also demonstrated direct cognitive effects in other contexts. It reduced MK-801-induced neuronal necrosis in the rat cingulate and retrosplenial cortex by 80–86%, even when administered up to 4 hours after dosing—a finding relevant to both anesthesia safety and neuroprotection. In morphine-sensitized mice, DMSO independently enhanced spatial memory formation in the Morris water maze (with the effects further enhanced by curcumin^⬖). In a mouse model of thiamine^⬖ deficiency (relevant to Wernicke’s encephalopathy), DMSO partially improved behavioral deficits and reduced thalamic damage, and when combined with high-dose thiamine,^⬖ enhanced recovery beyond thiamine^⬖ alone. DMSO alone also produced no spatial learning deficits when injected into the hippocampus in an 8-arm radial maze task, confirming its safety as a vehicle in cognitive research.

Anesthesia-Induced Cognitive Impairment

General anesthesia, particularly prolonged or repeated exposure, can cause lasting cognitive deficits and is recognized to significantly increase the risk for Alzheimer’s (making it a growing concern for both young children whose brains are still developing and the elderly). As we’ve seen numerous people tip over into dementia (as some of their neurons which are put to sleep during the surgery never seem to wake up afterwards), we hence try to minimize surgeries, have anesthesiologists use less toxic anesthetics (inhaled anesthetics cause the most issues), and use nutraceuticals to counteract that sedation.

Fortunately, DMSO addresses both the recognized mechanisms of anesthesia toxicity (e.g., neuroinflammation, oxidative stress, mitochondrial dysfunction, or neuronal apoptosis) and what we believe the key issue is (cells becoming stuck in a dormant phase). Unfortunately, all existing research on this subject involved DMSO combined with another agent, so definitive proof DMSO alone antidotes anesthesia toxicity does not exist.

Sevoflurane, one of the most widely used inhalational anesthetics, has been the most extensively studied. Resveratrol^⬖ dissolved in DMSO repeatedly protected against sevoflurane-induced cognitive deficits in both aged and neonatal rats by activating the SIRT1 pathway, reducing neuroapoptosis, upregulating BDNF, and improving spatial memory.^1,2,3 Additional combinations protecting against sevoflurane-induced cognitive impairment include arctigenin (which reduced inflammation via the Akt/NF-κB pathway and upregulated CTRP6), honokiol^⬖ (which activated SIRT3, reducing neuroinflammation, oxidative stress, and mitochondrial dysfunction), SAHA (which inhibited NLRP3 inflammasome activation and ameliorated cognitive impairment in aged mice),^1,2 curcumin^⬖1,2 (which improved memory retrieval dysfunction and reversed sevoflurane-induced Aβ increases and BACE-1 upregulation in aged rats), a S1P agonist (which prevented hippocampal apoptosis in neonatal rats), progesterone (which attenuated sevoflurane-induced neuronal injury in primary hippocampal neurons via progesterone receptors and Akt signaling), and inhibitors of the TLR4-p38MAPK-NF-κB pathway (which attenuated cognitive decline).

Note: in one neonatal rat study, resveratrol^⬖ improved molecular markers (SIRT1, PGC-1α, FOXO3α, SOD) and reduced brain pathological damage after sevoflurane, but Morris water maze testing showed no significant behavioral improvement across groups.

Propofol, another widely used anesthetic, causes dose-dependent neuronal apoptosis and lasting cognitive deficits with repeated neonatal exposure. Agents dissolved in DMSO that protected against propofol neurotoxicity include dexmedetomidine (which activated PI3K/Akt/GSK-3β in multiple studies),^1,2 etanercept (which blocked TNF-α-mediated damage), SAHA (which reversed learning and memory impairments by modulating histone acetylation, synaptic proteins, and CREB phosphorylation), 17β estradiol (which reversed deficits through the ERK pathway), hydroxylfasudil (which reduced apoptosis via p38 MAPK inhibition and improved Morris water maze performance) and coenzyme Q10^⬖ (which partially reversed propofol-induced mitochondrial respiratory chain inhibition in primary hippocampal neurons).

Isoflurane-induced cognitive impairment was counteracted by dexmedetomidine dissolved in DMSO (which activated PI3K/Akt and reduced hippocampal apoptosis), intranasal levosimendan (which protected newborn rat brains), and modafinil (which improved novel object recognition and contextual fear memory during the awakening period). Dexmedetomidine in DMSO also dose-dependently protected neonatal rat hippocampal neurons from etomidate-induced injury via the same PI3K/Akt pathway.

Other anesthetics: Dexmedetomidine attenuated ropivacaine-induced mitochondrial toxicity via p38 MAPK. Curcumin^⬖ in DMSO also protected developing rat brains against ketamine-induced neurotoxicity through the Nrf2-ARE antioxidant pathway, and also protected neonatal hippocampal neurons against the neurotoxicity of the anticonvulsants phenobarbital and valproic acid, significantly reducing neuronal loss.^1,2

Postoperative cognitive dysfunction (POCD), which affects a significant percentage of elderly surgical patients, similarly responded to DMSO-delivered agents. Jasplakinolide (an F-actin stabilizer) reversed POCD deficits in aged mice by restoring dendritic spine numbers, glutamate receptor expression, and hippocampal neuronal activation. Other agents improving POCD include a P300 inhibitor (which improved water maze performance and reduced hippocampal apoptosis after cardiopulmonary bypass), ononin (which reduced neuroinflammation and oxidative stress after nephrectomy in aged mice), and the Hippo/YAP pathway modulator Iduna. In a series of experiments, rapamycin activated hippocampal autophagy to alleviate postoperative cognitive impairment in aged rats, exendin-4 protected cognition by stabilizing blood glucose, and propofol at therapeutic doses prevented excessive autophagy from electroconvulsive shock (each through complementary mechanisms).

Other Causes of Cognitive Impairment

A wide range of conditions impair cognition, and in many of these, therapeutic agents delivered in DMSO have demonstrated cognitive protection.

Sleep disorders are a significant and underappreciated cause of cognitive decline. In sleep-deprived rats, diallyl sulfide^⬖ dissolved in DMSO reversed cognitive impairment, reducing anxiety behaviors and hippocampal oxidative stress, while resveratrol^⬖ prevented sleep deprivation-induced cognitive deficits by reducing neuroinflammation and enhancing synaptic plasticity proteins. In chronic intermittent hypoxia models (which simulate obstructive sleep apnea), agents improving cognition include a TGF-β1 inhibitor (which improved spatial memory by reducing hippocampal TGF-β1/Smad3 signaling), capsaicin,^⬖ STAT3 pathway inhibitors, an α7 nicotinic acetylcholine receptor agonist (which upregulated BDNF and CREB), and adenosine A1 receptor antagonists.^1,2

Diabetic cognitive impairment was improved by a variety of agents in combination with DMSO. Rapamycin improved cognition across multiple studies by reducing mTOR, hyperphosphorylated tau, and apoptosis,^1,2,3 while captopril and losartan improved cognitive function through a distinct mechanism — inhibiting the ACE-angiotensin II-AT1R axis in the hippocampus of diabetic mice. A TRPV4 agonist reversed cognitive deficits and enhanced hippocampal neurogenesis, and CNTF improved escape latency and increased hippocampal choline acetyltransferase expression via JAK2/STAT3. Additional agents improving diabetic cognitive impairment include pentamethylquercetin^⬖ (Akt/CREB signaling and increased synaptic proteins), sulforaphane^⬖ (PI3K/Akt/GSK-3β and inhibited mitochondrial apoptosis), curcumin nicotinate^⬖ (improved spatial learning by regulating autophagy), krill oil/EPA^⬖ (NRF2 antioxidant pathway), Urtica dioica^⬖ and pioglitazone (oxidative stress markers and mitochondrial function), and PSD-95/nNOS inhibitors (reduced neuronal injury via Sirt3).

Sepsis-associated encephalopathy responded to a HIF-1α inhibitor (which improved cognitive function and reduced autophagy), resveratrol^⬖ (which activated SIRT1, reduced hippocampal apoptosis and microglial activation), ROCK inhibitors (which reduced cerebral injury, inflammation, and improved spatial memory), and molecular hydrogen (which improved survival and cognition via Nrf2-dependent signaling). Additional agents improving cognition in other disease states include Babao Dan^⬖ for minimal hepatic encephalopathy, hesperidin^⬖ for hyperhomocysteinemia and curcumin^⬖ for cerebral hypoperfusion combined with diabetes.

Epilepsy-related cognitive impairment was improved by rolipram (a PDE4 inhibitor that rescued spatial learning, hippocampal long-term potentiation, and phosphorylated CREB after status epilepticus),^1,2,3 an eEF2K inhibitor (which restored AMPKα1 expression and improved cognition and social behavior in chronic epileptic mice), semaglutide (which improved cognitive function and protected hippocampal neurons via SIRT-1/NLRP3), and perampanel (which improved spatial learning and reduced hippocampal damage in immature mice with temporal lobe epilepsy).

Neuropathic pain frequently impairs cognition, and this was reversed by an α5-GABAAR inverse agonist (which restored GABAergic signaling and improved recognition and spatial memory in sciatic nerve injury rats), SAHA (which improved spatial learning in bone cancer pain rats), and curcumin^⬖ (which enhanced hippocampal neurogenesis and synaptic plasticity). Rutin^⬖ also protected against cadmium-induced cognitive impairment by restoring antioxidant balance.

Neonatal brain injury from hypoxia-ischemia was treated with coumestrol^⬖ (which partially reversed cognitive deficits, tissue loss, and reactive astrogliosis), C2-ceramide (which reduced neonatal hypoxic-ischemic brain damage by 45–65%) and recombinant human chemerin (which improved both short-term neurological function and long-term cognitive outcomes via the ChemR23/CAMKK2/AMPK/Nrf2 pathway). Repetitive transcranial magnetic stimulation combined with BDNF/TrkB signaling similarly improved spatial learning in rats with prenatal stress-induced cognitive deficits.

Oxidative stress and neuroprotection were addressed by ferrostatin-1 and a caspase inhibitor (which improved cognitive function and preserved synaptic proteins in iron-overloaded rats), and by glutamate receptor antagonists (which protected white matter and myelin ultrastructure in a focal ischemia model relevant to vascular cognitive decline).

Agents addressing psychiatric-related cognitive impairment include a CB1R antagonist (which rescued electroconvulsive shock-induced memory deficits without affecting antidepressant efficacy), fisetin^⬖ (which reversed MK-801-induced cognitive impairment in a schizophrenia model by restoring ERK/CREB/CaMKII), and 7,8-dihydroxyflavone^⬖ (which improved spatial cognition and restored hippocampal dendritic spines in a schizophrenia model).

Additional agents improving cognition across various models include a complement C3a receptor antagonist (LPS-induced cognitive dysfunction), a GPER agonist (traumatic brain injury), novel PDE4 inhibitors roflupram and chlorbipram (which reversed scopolamine-induced cognitive deficits without the emetic side effects of existing PDE4 inhibitors), and pregnenolone^⬖ (which improved spatial learning and upregulated choline acetyltransferase in aged rats). Sonchus asper^⬖ and Launaea^⬖ procumbens extracts each improved cognition and brain antioxidant status (with Sonchus asper^⬖ also inhibiting acetylcholinesterase), while 7,8-dihydroxyflavone^⬖ enhanced response learning via TrkB receptor phosphorylation and epigallocatechin gallate^⬖ reversed high-fat diet and rapamycin-induced cognitive impairment while improving serotonin and acetylcholinesterase activity.

Human Studies

These findings have been replicated in humans. A study evaluated 104 elderly adults with organic brain disease due to cerebrovascular diseases (e.g., a previous stroke, cerebral embolism, or hardening of the arteries of the brain), a previous head injury, senility, or degenerative disease (e.g., Parkinson’s, hyperthyroidism, or epilepsy). They received two DMSO mixes, Merinex (DMSO with amino acids^⬖) and Ipran (DMSO with vasoactive substances), typically alternating between the two, and for the majority of the time as an injection, and a minority of the time orally (with the fastest results occurring if both routes were used simultaneously), all of which resulted in remarkable improvements.^1,2 To quote the author:

The DMSO aminoacid therapy is undoubtedly valuable in the treatment of numerous organic cerebral diseases. At the same time, thanks to the improved cerebral blood irrigation achieved by DMSO used in combination with vasoactive substances, a highly favorable effect on the psychic and somatic functions of senile patients was achieved.

Note: another study found Merinex also treated patients with mood and anxiety disorders.^1,2

A Chilean study evaluated 100 patients with cerebrovascular diseases (e.g., a previous stroke, cerebral embolism, or hardening of the arteries of the brain), many of whom were senile, who received DMSO orally and through intramuscular injections over the course of 50 days. It was noted that their coronary heart disease and high blood pressure had a good improvement in 74.35% of DMSO recipients, a fair response in 21.77%, and no response for 3.88%.¹,² The neurologists overseeing these patients remarked that:

“Recovery from the general symptoms was positive; there were favorable changes which were reflected in a feeling of well being, the recovery of agility, changes of mood from depressed to gay [cheerful], improvement of sleeping, and clearer speech. As regards the ‘focal’ results, accelerated recovery from hemiplegia and hemiparesia was registered. A speedier recovery of speech in cases of defined or indicated aphasia took place.”

Additionally, in 127 elderly patients (aged 75–85) with cerebrovascular disorders, bitemporal ionophoresis with Neuromidin in a DMSO solution resulted in clinical improvement by the 5th procedure in 86%, including normalized sleep, reduced dizziness, improved memory and hearing, and decreased cognitive disorders (versus delayed improvement in controls receiving standard therapy alone). In another study of 250 patients with cerebral vascular pathology, DMSO plus vinpocetine via cervical-collar zone ionophoresis stabilized brain blood flow parameters and improved blood supply to the large cerebral arteries.^1,2 Likewise, a Russian geriatrics physiotherapy monograph recommended DMSO in transcranial ionophoresis protocols for discirculatory encephalopathy (chronic cerebral ischemia), including 50% DMSO solutions with aspirin. In a clinical study of 154 patients undergoing open revascularization for acute lower limb ischemia, intravenous DMSO (10 mg/kg) administered before reperfusion as part of a comprehensive prevention protocol resulted in reduced reperfusion injury markers, fewer renal dysfunction cases, less cardiopulmonary worsening, and milder cognitive issues compared to standard care.

Note: at a Russian military sanatorium treating victims of terrorist attacks and other emergencies, 25% DMSO was among the most frequently used agents for neurological injuries (primarily spinal pain and cerebrovascular disease), most commonly as part of a 21-day ionophoresis rehabilitation course (that was noted to effectively resolve pain).

Reader Reports

A variety of readers have reported cognitive improvements from DMSO:

I had a series of small strokes in August of 2023. I’m using 1 tsp of 99% DMSO twice a day and the results are remarkable! The improvement in mental acuity is amazing and the whole body pain relief is the best I’ve ever experienced.

I had ‘brain fog’ for 6–8 weeks after a total hip job which I am pretty sure was from the anesthetic, started drinking 2 tsp DMSO in 8oz water ~6–7 weeks after the op and feel this totally cured it in about 1 week and now my brain is very much back to normal.

I used to have the kind of mind that once skated through an Ivy League degree. Thanks to your writings on DMSO and Walsh’s nutritional therapy the last couple weeks I have begun to feel the fire that used to burn inside of my mind, the brilliant processing ability I used to take for granted. My brain actually works!!

The only thing that’s come close to helping with my Moderna vax injury. Gastroparesis, extreme brain fog, edema, SFN, MCAS, POTS, tinnitus, insomnia, mood disturbances...all improving for the first time in 3½ years!

Several additional readers reported that topical DMSO applied to the neck improved brain fog following COVID vaccination,^1,2 while others found oral DMSO cleared brain fog from zolpidem, statins, chronic fatigue syndrome, a TBI, fluoroquinolone toxicity, or long-haul COVID symptoms.^1,2

Memory

In addition to brain health (vibrant circulation and minimal inflammation or cells being trapped in the cell danger response) being intertwined with sleep, both are also intertwined with mental health, cognition and memory. As such, I have received a few memory improvement stories^1,2,3,4,5,6 like these:

MWD, your stack is transformative. We now make your zeta potential formula, and have noticed observable results in a short time, it is a daily routine now. We also incorporated DMSO (topically) and marvel at its ability to repair and heal (and yes we have noticed the Lucid dreaming!) - these two items are the basis of our ‘first aid’ kit that travels wherever we go. Thank you for passing on this knowledge. Inadvertently we started ‘studying’ post Covid, reading and listening to a vast amount of information - and more times than not falling asleep in the process. This article explains why we can now seem to retain so much information in our 60s than we ever did in our younger days.

I am a Family Physician who was diagnosed with MCI by Mass General Neurology. I responded by cleaning up my diet, exercising daily, and taking a bunch of supplements, including daily oral DMSO. My memory is now better than it was decades ago.

So many benefits & people have noticed…Memory is insanely good now.

DMSO alone is generally thought to have a minimal impact here (e.g., one paper stated “In all experiments, dimethyl sulfoxide (DMSO) was used as vehicle, since it has no significant effect on passive avoidance learning and memory”) so a variety of studies exist where DMSO facilitated another agent improving memory.

Studies which have combined a therapeutic agent with DMSO to enhance learning and memory are as follows:

In three different rat studies, pemoline (Pm) or magnesium pemoline (MgPm) was dissolved in DMSO to influence memory and learning. In one, where rats were evaluated on how many trials it took them to learn a complex maze, compared to a saline baseline, the following reductions were observed: DMSO alone (11.1%), Pm (25.3%), low dose MgPm (32.5%), high dose MgPm (44.6%)—whereas amphetamine worsened learning by 14.5%.^1,2 In a second study, MgPm (both low and high dose) dissolved in DMSO completely prevented retrograde amnesia induced by electroconvulsive shock (ECS). Lastly, a third study found these agents did not improve reversal learning (the ability to cognitively update an ingrained habit when the reward rule changes).
Note: DMSO was also shown to increase transport of pemoline into the brain.

Additional agents enhancing learning or memory in otherwise healthy or aged animals include pregnenolone^⬖ (which improved spatial learning and upregulated choline acetyltransferase in aged rats), capsaicin^⬖ (which improved acquisition and retention and mitigated a CB1/CB2 agonist's negative effects on learning), rapamycin (which improved novel object recognition and spatial working memory in middle-aged mice while protecting hippocampal neurons), testosterone (which nearly doubled hippocampal dendritic spine density via ERK/MAPK signaling and restored spatial memory in gonadectomized rats),^1,2 nandrolone (which improved spatial learning and long-term potentiation in adolescent rats), and intracerebroventricular DHEA^⬖ (which enhanced memory retention and prevented amnesia). Datumetine modulated hippocampal and prefrontal NMDA receptor signaling, upregulating CREB phosphorylation and BDNF expression, while sumac extract^⬖ enhanced passive avoidance learning and memory retention. In C. elegans, a mitochondrial uncoupler preserved mechanosensory neurons, short-term memory, and extended lifespan. Aniracetam and 1-BCP reversed pyrilamine-induced working memory deficits and restored hippocampal theta power.

These therapeutic agents (in DMSO) showed strong protective effects against memory impairment across a variety of injury models. Following strokes, 4-methylumbelliferone reduced infarct volume and improved learning and memory by downregulating HAS1/HAS2, modulating inflammatory cytokines, and reducing oxidative stress. In aged rats, pioglitazone improved learning and memory by reducing oxidative stress and increasing antioxidant enzymes in the hippocampus and cortex. In Alzheimer’s disease model rats, oral quercetin^⬖ significantly improved spatial learning and memory while lessening hippocampal oxidative stress and neuronal damage. 5-HT2A receptor agonists protected long-term memories from being disrupted by new memories formed shortly afterward. In ovariectomized rats modeling hormonal loss, an ERβ agonist reversed spatial learning and reference memory deficits along with impairments in dendritic spine density and synaptic structural integrity, while estrogen supplementation partially restored spatial learning and significantly increased CD147 expression (a neuroprotective protein involved in synaptic function and amyloid-β clearance). Additional agents protecting against memory impairment include Artemisia absinthium^⬖ (which reversed scopolamine-induced deficits and counteracted oxidative stress), a cannabinoid agonist (which prevented scopolamine-induced spatial memory impairment), a selective CB1 antagonist (which improved consolidation of aversive associative memory), and 7,8-dihydroxyflavone^⬖ (which restored spatial learning in rats subjected to maternal separation stress).

Note: in studies detailed in other parts of this article, memory and learning improvements were also demonstrated by agents combined with DMSO across a wide range of injury models — including chronic cerebral hypoperfusion (fructose 1,6-diphosphate^⬖), chronic restraint and psychological stress (necrostatin-1, flupirtine, and retigabine), sleep deprivation (quercetin^⬖ and almorexant), sepsis-associated encephalopathy (an LRRK2 inhibitor), manganese neurotoxicity (sodium para-aminosalicylate), anesthesia exposure during pregnancy (suberoylanilide hydroxamic acid), hyperthyroidism (AMPA and NMDA receptor agonists), and NMDA-receptor blockade modeling glutamatergic dysfunction (Ptychopetalum olacoides^⬖) — collectively reinforcing that the cognitive benefits of DMSO-delivered therapies extend across virtually every category of neurological insult that impairs memory.

Lastly, in a study showing that impairing dural (meningeal) lymphatic drainage disrupts spatial working memory and interhemispheric coherence, six weeks of daily DMSO injections had no adverse effects on memory.

Movement Disorders

Movement disorders encompass conditions characterized by abnormal voluntary or involuntary movements — including tremors, ataxia (loss of coordination), dystonia, and muscle spasticity. Many arise from dysfunction in the cerebellum, basal ganglia, or their neural connections, areas particularly sensitive to the circulatory and inflammatory disruptions DMSO addresses (e.g., consider the previously mentioned Lurcher mice study where DMSO counteracted cerebellar damage). For example:

In a copper-deficient sheep model, a single subcutaneous injection of DMSO combined with copper sulfate during mid-pregnancy completely prevented enzootic ataxia (swayback) in lambs (0% incidence vs. 60% in untreated controls), performing comparably to multiple oral copper doses and suggesting DMSO enhanced systemic copper delivery sufficiently to protect fetal neurological development. In veterinary case reports, IV DMSO contributed to the recovery of a mare with ataxia and cranial nerve deficits from temporohyoid osteoarthropathy (near-normal neurological status by discharge on day 5), while in a foal with cerebellar abiotrophy, DMSO as part of a multi-agent regimen produced temporary neurological improvement before the animal relapsed due to the progressive nature of the underlying genetic condition. In another horse, DMSO was used to manage vestibular disease and blindness that developed following a jugular catheter complication during anesthesia recovery.

In rats, a neurotensin antagonist (in DMSO) attenuated neuroleptic-induced vacuous chewing movements (a model of tardive dyskinesia), supporting a role for neurotensin in its pathogenesis, while abscisic acid^⬖ (in DMSO) improved harmaline-induced tremor and motor performance. Separately, microinjection of a synthetic cannabinoid into the globus pallidus enhanced motor behavior in rats.

Reader reports suggest DMSO can benefit several movement disorders. One reader with vaccine-induced Stiff Person Syndrome reported that topical 100% DMSO was the only treatment that relieved constant muscle spasms — spanning the back, calves, feet, and chest — over 22 months of uncontrolled pain, noting “I have it with me at all times.” A 74-year-old reader with essential tremors, multiple spinal and thoracic fractures, and advanced tendonitis credited “DMSO, and DMSO alone” with keeping them out of a wheelchair. Other readers reported improvements in essential tremors, in tremors from vaccine injury and a neck tremor that responded to topical DMSO.

Several readers also reported that topical DMSO dramatically improved restless leg syndrome, in some cases allowing them to discontinue long-term medications they had taken for decades.

Additionally, multiple dog owners reported that topical DMSO applied to the temples or behind the ears rapidly resolved vestibular episodes — stroke-like events characterized by disorientation, wobbly legs, and vomiting — with one describing recovery within an hour and continued preventive use whenever symptoms reappear, while another credited DMSO (along with grounding) with giving their elderly dog an extra year and a half of life.^1,2

Seizures and Epilepsy

Epilepsy is a neurological disorder characterized by recurrent seizures (sudden bursts of abnormal electrical activity in the brain that can cause involuntary movements), altered consciousness, and in severe cases, prolonged seizures that cause permanent brain damage or death. DMSO’s ability to cross the blood-brain barrier, counteract oxidative stress, modulate ion channels, and suppress excitotoxic glutamate signaling suggest it could help epilepsy — though as detailed below, its effects are notably dose-dependent.

Anti-Seizure Properties

Several studies have directly examined DMSO’s effects on seizure activity, revealing a consistent biphasic pattern: therapeutic doses suppress seizures while high doses can provoke them. In rats genetically prone to epilepsy, low-dose DMSO (1.65 mg/kg) significantly decreased the number and total duration of spike-wave discharges, while high doses (825–1651 mg/kg) significantly increased them — with all effects being fully reversible (supported by the fact higher concentrations of DMSO begin blocking GABA-induced chloride currents). Likewise when 50% DMSO was injected into the brain’s ventricles (diluting to approximately 6% in the CSF), no seizure activity was generated over the next hour, whereas 75% and 100% did create a significant spike in mice hippocampal evoked potentials.

In a different temporal lobe epilepsy model, high-dose DMSO (1651 mg/kg) produced significant anticonvulsant effects — prolonging seizure onset latency by 32%, shortening seizure duration by 34%, and reducing afterdischarge duration by 45% — effects the authors attributed to suppression of glutamatergic NMDA/AMPA-mediated calcium influx. In mice with chronic temporal lobe epilepsy, only 100% DMSO (1651 mg/kg) reduced seizure number and cumulative duration (by 19–41% depending on sex), while lower concentrations had no effect — and notably, DMSO did not alter acute seizure threshold in non-epileptic mice, suggesting its anticonvulsant action is specific to the chronically epileptic brain. Another study confirmed this pattern, finding 10% DMSO significantly reduced PTZ-induced epileptiform activity while 100% DMSO increased it. DMSO also raised seizure thresholds by approximately 9% against two different seizure-inducing agents and prolonged the latency to convulsions from hyperbaric oxygen exposure (thereby reducing seizures).

In specific contexts, DMSO has shown targeted protective effects: it partially prevented convulsions induced by 5-aminolevulinic acid (reducing their number and duration), likely through hydroxyl radical scavenging, and pretreatment with DMSO has been shown to prevent iron-induced epileptiform discharges, suggesting a potential role in preventing post-traumatic epilepsy.

Note: the biphasic dose response is an important consideration when using DMSO either therapeutically or as a research vehicle in epilepsy studies. Several studies have specifically documented proconvulsant effects: DMSO prolonged cortical epileptic afterdischarges in immature rats (most pronounced in the youngest animals), lowered tonic seizure thresholds in a PTZ model, and in one study, even 0.1% DMSO accelerated PTZ kindling and potentiated hippocampal neuronal damage. These findings underscore the importance of dose selection and appropriate vehicle controls in epilepsy research.

Additionally, DMSO’s ability to open the blood-brain barrier creates a dual-edged property: when excitatory amino acids (L-aspartate or L-glutamate) were administered peripherally in DMSO, they induced seizures they would not otherwise cause — which while a safety consideration, has proven useful for studying NMDA receptor involvement in seizure circuits and for demonstrating that the kindled amygdala plays a critical role in generalized seizure expression.^1,2,3,4

Seizure Reduction

The most direct clinical evidence for DMSO reducing seizures comes from patients with Niemann-Pick disease type C (detailed earlier). In NPC patients, oral DMSO decreased seizure frequency and improved EEG findings. Most notably, in an 8-year-old girl with frequent seizures and severe psychomotor deterioration, two years of oral DMSO decreased seizure frequency enough to allow tapering of an anticonvulsant, produced marked EEG improvement (with normalization of theta waves and spindle morphology), and halted the progression of cortical atrophy.

In veterinary medicine, IV DMSO has been used as part of multimodal seizure management. In a horse that developed seizures following surgery, IV 10% DMSO (1 g/kg twice daily for four days) — administered for its free radical scavenging and thromboxane-inhibiting properties to maintain cerebral blood supply — contributed to seizure cessation by day 3 and a satisfactory long-term outcome. In a 2-day-old foal with perinatal asphyxia presenting with seizures, cerebral edema, and acute renal failure, IV DMSO contributed to marked resolution of cerebral edema and complete neurological recovery by day 12. In a 3-day-old foal with convulsions and ataxia secondary to electrolyte derangements from bladder rupture, IV DMSO was included in supportive care that resolved the neurological signs within days.

Lastly, as mentioned above, a dog which had seizures develop from hydrocephalus had those seizures improve from IV DMSO.

Combination Studies

A large number of agents combined with DMSO have demonstrated anticonvulsant or neuroprotective effects in seizure models.

Among those directly reducing seizure severity, glibenclamide produced the greatest effects: following status epilepticus, it significantly reduced brain edema, blood-brain barrier damage, and neuronal loss while more than doubling 28-day survival (47.8% vs. 22.2%). Resveratrol^⬖ prolonged seizure latency, shortened seizure duration, reduced the brain injury marker S100B in cerebrospinal fluid and serum, protected hippocampal CA1 and CA3 neurons, and improved spatial learning and memory in PTZ-kindled rats.^1,2 Resveratrol^⬖ also protected against hyperbaric oxygen-induced convulsions. Quercetin^⬖ (10–20 mg/kg) significantly prolonged seizure onset, reduced severity, and shortened generalized seizure duration in PTZ-induced seizures, though higher doses (40 mg/kg) lost efficacy and in a picrotoxin model paradoxically shortened seizure onset. The DMSO combination of palmitoylethanolamide (PEA) with the neurosteroid ganaxolone markedly amplified seizure suppression and eliminated mortality, whereas PEA alone showed no efficacy in that model (though it did exhibit anticonvulsant activity in kindled amygdaloid seizures).^1,2 Montelukast synergistically enhanced phenobarbital’s anticonvulsant effect (when both were dissolved in DMSO), lowering the effective dose while reducing phenobarbital-induced sedation. Ruxolitinib shortened seizure duration, lowered seizure frequency over 4 weeks, and improved memory. A p38MAPK inhibitor prolonged seizure latency by 45% and halved seizure frequency. A 5-HT6 receptor antagonist reduced spontaneous recurrent seizure frequency, increased protective potassium channel (KCNQ2/3) expression, and in combination with ERK1/2 or Fyn inhibitors reversed the aberrant mossy fiber sprouting that perpetuates chronic epilepsy.^1,2 Triptolide^⬖ inhibited epilepsy in mice by improving hippocampal GABAergic inhibition and reducing IL-1β levels.

Carvedilol suppressed spontaneous seizure activity in hippocampal slices from Alzheimer’s model mice — a finding with implications for the seizure susceptibility frequently seen in that disease.

In a high-throughput screening of 343 essential oils using a PTZ-induced zebrafish epilepsy model, 52 demonstrated antiepileptic activity, with 15 (including patchouli^⬖ and cinnamon oils^⬖) showing potency far exceeding that of phenytoin. Maslinic acid,^⬖ identified through computational gene expression profiling, showed significant antiepileptic activity in the same model and selectively inhibited voltage-gated sodium channel subtypes Nav1.2 and Nav1.7.

Many agents combined with DMSO also protected against the neuronal damage that follows status epilepticus. Mitochondrial division inhibitor 1 (Mdivi-1) repeatedly reduced neuronal apoptosis and oxidative stress across multiple studies, in some cases also increasing seizure latency, decreasing seizure frequency, and improving post-seizure cognition.^1,2,3,4,5 Recombinant human erythropoietin protected hippocampal neurons via PI3K/Akt anti-apoptotic signaling across multiple seizure models.^1,2 Ganoderic acid^⬖ reduced hippocampal damage through multiple pathways (caspase-3 reduction, CaSR/JNK/P38 modulation, and improved dendritic spine density and spatial memory).^1,2,3 Salidroside^⬖ dose-dependently increased seizure latency, enhanced antioxidant defenses, and reduced endoplasmic reticulum stress-mediated apoptosis. Gastrodin^⬖ reduced seizure severity, protected hippocampal neurons, enhanced GABAA receptor expression, and regulated post-status epilepticus autophagy.^1,2 Rolipram rescued cognitive deficits, hippocampal long-term potentiation, and CREB phosphorylation in immature rats following status epilepticus. Curcumin^⬖ decreased aberrant mossy fiber sprouting through miR-134/LIMK1 modulation. ERK1/2 and p38 MAPK inhibitors reduced inflammatory markers, chemokine expression, and microglial activation in the hippocampus of immature rats with kainic acid-induced epilepsy.

Additional agents showing neuroprotective effects in status epilepticus models include glycyrrhizic acid^⬖ (enhanced mitochondrial autophagy and antioxidant defenses in juvenile epilepsy rats), glycyrrhizin^⬖ (reduced HMGB1/p38MAPK in the hippocampus), an Omi/HtrA2 inhibitor (ucf-101; increased anti-apoptotic XIAP and HAX-1), levetiracetam (dose-dependently reduced oxidative stress and caspase-3 in epileptic offspring mice), a caspase-12 inhibitor, olomoucine (a CDK inhibitor that reduced neuroinflammation and apoptosis), 2-methoxyestradiol (via HIF-1α suppression), a CaMKII inhibitor, honokiol,^⬖ a hydrogen sulfide donor (via PI3K/Akt), an IRAK1/4 inhibitor, an exosome inhibitor (which prolonged seizure latency by reducing BBB permeability changes), an eEF2K inhibitor that restored AMPKα1 expression and improved mitochondrial function, cognition, and social behavior in chronic epileptic mice, and a PARP-1 inhibitor (DPQ) that reduced neuronal apoptosis and activated the PI3K/Akt-SIRT1 survival pathway.

Interestingly, GPER-1 (the G protein-coupled estrogen receptor) activation with G1 improved spatial learning, memory, and reduced mossy fiber sprouting in chronically epileptic rats, yet the same receptor’s activation with G-1 or estradiol increased acute seizure susceptibility and nitric oxide levels in cortex and hippocampus during PTZ kindling — suggesting estrogen-mediated effects on epilepsy differ between acute seizure generation and chronic post-epileptic recovery.

Natural compounds demonstrating anticonvulsant effects in zebrafish or rodent models include vitexin^⬖ (comparable to diazepam), sesamin^⬖ (via PI3K/Akt), onopordia^⬖ (via the nitric oxide/nNOS pathway), linalool^⬖ and trans-nerolidol^⬖ (with nerolidol^⬖ showing superior efficacy), the combination of ursolic acid^⬖ with caprylic acid,^⬖ Lippia sidoides extract^⬖ (comparable to diazepam), olive pit polyphenols^⬖ (which protected against kainic acid-induced neurotoxicity), a tryptamine derivative of securinine^⬖ (with antioxidant, chelating, and anticonvulsant properties), ε-viniferin^⬖ (which inhibited NLRC4 inflammasome activation in astrocytes), thymoquinone,^⬖ and progabide (which specifically suppressed the tonic phase of seizures). Lamotrigine combined with anakinra partially normalized psychoneurological disturbances (anxiety, locomotor activity, social behavior) in chronically epileptic rats, suggesting their combination addresses both seizure control and behavioral comorbidities.

Rapamycin combined with pitolisant markedly improved anxiety (2.7-fold on maze testing) and depression (37.5% improvement in swim testing) in PTZ-kindled epileptic rats, highlighting that DMSO-delivered agents can address the psychiatric comorbidities that frequently accompany epilepsy.

In stimulant toxicity models, MK-801 dissolved in DMSO abolished EEG afterdischarges and seizures induced by cocaine, amphetamine, and methamphetamine — though notably, eliminating seizures did not prevent death from methamphetamine or cocaine, demonstrating that seizure-independent toxicity pathways drive stimulant lethality.

Note: CBD^⬖ in DMSO blocked voltage-gated sodium channels and demonstrated anticonvulsant effects in a PTZ model, whereas cannabigerol produced comparable sodium channel blockade but had no anticonvulsant effect — indicating that sodium channel inhibition alone does not confer seizure protection. 3-carene^⬖ modulated resting-state brain activity but did not reduce epileptiform activity. Retigabine, despite being an established antiepileptic drug, paradoxically increased spike-and-wave discharge number and duration in aged WAG/Rij rats, revealing age-dependent pro-epileptic effects from neuronal potassium channel activation. Two plant-derived extracts (Searsia dentata^⬖ and Searsia pyroides^⬖) inhibited NMDA receptor currents and reduced intracellular calcium influx, supporting their traditional use for epilepsy.

DMSO and Antiepileptic Drug Interactions

Several findings are relevant to using DMSO alongside conventional antiepileptic drugs. DMSO has been safely used as a vehicle for diazepam in seizure treatment studies. The antiepileptic drugs carbamazepine and lamotrigine dissolved in DMSO showed no concerning interactions on human reproductive tissue, suggesting compatibility during pregnancy. A pharmacological study demonstrated favorable molecular interactions between levetiracetam and DMSO-water mixtures, supporting DMSO’s potential utility in antiepileptic drug formulation. Mood-stabilizing antiepileptics (zonisamide, carbamazepine, valproate) dissolved in DMSO enhanced monoamine and acetylcholine systems in the striatum and hippocampus at therapeutic doses while reducing them at supratherapeutic doses — a biphasic pattern that may partly explain both their therapeutic effects and certain side effects. DMSO combined with ethosuximide may synergistically increase brain epinephrine levels, as DMSO alone can stimulate the central nervous system and increase catecholamines, potentially augmenting the neurotransmitter changes the antiepileptic produces. Menthol^⬖ dissolved in DMSO demonstrated dose-dependent anticonvulsant effects, with 400 mg/kg significantly reducing seizure activity below control levels — while simultaneously counteracting the proconvulsant influence of high-concentration DMSO, suggesting menthol^⬖ may be a useful adjuvant when DMSO is used as a seizure medication vehicle.

Note: multiple studies confirmed DMSO at vehicle concentrations had no independent effect on seizure parameters, supporting its safety as a solvent at appropriate doses.^1,2,3 A study employing DMSO-based electron spin resonance spectroscopy demonstrated that seizures induce rapid accumulation of ascorbate (an antioxidant) in the hippocampus in parallel with seizure progression — likely as a response to excessive free radical production during excitotoxicity — providing mechanistic support for why antioxidants like DMSO can be neuroprotective in seizure contexts.

Encephalitis

In addition to mitigating experimental autoimmune encephalomyelitis DMSO also mitigates brain inflammation triggered by a variety of infectious sources.

Viral Encephalitis

Intranasal DMSO mixed with nuclease mixture was used in human patients to treat meningitis and meningoencephalitis caused by acute viral respiratory infections.^1,2

Multiple papers have noted that DMSO was used in horses to treat myeloencephalopathy from herpes, but no data was provided other than longer courses of DMSO being used in more severe outbreaks.^1,2 In the only case report I’ve found, 500 mg/kg of IV DMSO (given every 24 hours to a hospitalized horse) contributed to a stabilization of neurologic deficits, clinical improvement and then full recovery.

Multiple papers have reported DMSO being used to treat suspected West Nile virus encephalomyelitis,^1,2 one of which reported mild to moderate cases recovered fully after an anti-inflammatory protocol that included DMSO.

Intraperitoneal arctigenin^⬖ (a plant lignan dissolved in DMSO), administered one day post intravenous infection, provided complete protection to mice from an otherwise fatal Japanese encephalitis virus infection (along with reducing brain inflammation, oxidative stress, cell death, and associated behavioral impairments).

In mice with a 100% fatal encephalomyocarditis (EMCV) viral infection, intraperitoneal DMSO combined with a DHEA derivative reduced mortality to 72.73%, greatly reduced (otherwise severe) neurological symptoms, prevented inflammatory brain lesions, and decreased brain viral load. In another study DMSO combined with a furin inhibitor or a different DHEA derivative showed strong antiviral activity against Zika and Japanese encephalitis virus in human and mosquito cells.

A p38-MAPK inhibitor dissolved in DMSO improved survival rate, reduced paralysis scores, lowered viral load in skeletal muscle, and decreased inflammatory cytokines in suckling mice with enterovirus 71 infection.

In dogs with neurological canine distemper, DMSO alone or combined with ribavirin and prednisone helped maintain higher hemoglobin levels and reduced the severity of anemia compared to regimens without DMSO. In another similar study, DMSO synergistically enhanced the treatment efficacy of ribavirin.

Parasitic Encephalitis

Equine protozoal myeloencephalitis (EPM) is a common and severe disease in horses that is difficult to treat because the medications for it have poor oral absorption. A 2009 study found that dissolving ponazuril in DMSO rather than water roughly tripled its bioavailability and enhanced its ability to reach the brain, potentially revolutionizing management of EPM.^1,2 In another study, DMSO was also found to greatly enhance the absorption of toltrazuril (resulting in oral toltrazuril having 56% of the bioavailability of IV toltrazuril). In the only clinical case report I could locate, severe EPM neurological dysfunction initially improved following DMSO+ponazuril and a few other therapies, but the elderly horse eventually succumbed to the illness. Lastly, a 2014 veterinary paper noted that IV DMSO and ponazuril was a viable EPM treatment.

Megazol formulated as a gel in DMSO and combined with melarsoprol successfully cured experimental CNS-trypanosomiasis in mice.

Arctigenin^⬖ improved depression-like behaviors in Toxoplasma gondii-infected mice, reduced neuroinflammation, and restored neurotransmitter balance by suppressing the TLR4/NF-κB pathway and IDO overexpression. Sertraline also inhibited Toxoplasma gondii brain proliferation, reduced neuroinflammation (TNF-α, TRAF2, NF-κB p65 nuclear translocation), and protected neurons in both in vitro and in vivo models of acute T. gondii infection.^1,2

A rare complication for dogs from babesia infections is cerebellar ataxia, and in one case where this was accompanied by blindness and quadriparesis, a dose of IV DMSO and then other treatments preceded a rapid recovery.

Two species of Acanthamoeba (which can cause eye infections, and occasionally encephalitis), were found to be roughly twice as sensitive (and in one case four times as senstive) to tea tree oil^⬖ when it was mixed in DMSO. The growth of another amoeba (used to model the deadly brain infecting N. fowleri) was inhibited by Torin-1 dissolved in DMSO.

Note: a review paper citing numerous 1990s veterinary textbooks stated that DMSO has been indicated in cases of viral and bacterial encephalitis, Herpes virus I, and myelitis due to protozoa [parasites].

Bacterial Meningitis

One Russian paper reported that in human patients DMSO enhanced the effectiveness of meningitis treatment protocols.^1,2

In a foal with suspected bacterial meningitis, intravenous DMSO was included as part of intensive supportive therapy for its anti-inflammatory, analgesic, neuroprotective, and free radical-scavenging properties. The foal showed clinical improvement (recovery of suckling reflex and milk intake) by day 7–8, at which point DMSO was discontinued.

Sepsis-Associated Encephalopathy

When infections reach the circulation, they can frequently set off sepsis, a life-threatening inflammatory cascade. As a toxin many bacteria carry (LPS) can trigger sepsis, this condition is often studied in animals by injecting LPS.

As one of the organs harmed by sepsis is the brain (e.g., by far the most common form of encephalopathy in critically ill patients is sepsis encephalopathy) numerous studies have evaluated how agents protect the nervous system from sepsis, such as a sheep one where intravenous DMSO significantly reduced clinical signs of sepsis and lowered acute phase protein levels (haptoglobin, serum amyloid A, ceruloplasmin, and fibrinogen).

A variety of agents in combination with DMSO have also been shown to reduce LPS triggered brain injury:

•Dexmedetomidine pretreatment in rats reduced systemic and brain inflammation in sepsis-related encephalopathy by lowering inflammatory cytokines and suppressing NF-κB signaling in the hippocampus.

•Ibrutinib reduced neuroinflammation and brain damage in mice by lowering pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), increasing IL-10, and suppressing the inflammatory TLR4/AKT/PI3K/STAT3 pathway.

•Dasatinib reduced neuroinflammation and brain damage in mice by lowering multiple pro-inflammatory mediators and modulating key signaling pathways while increasing the anti-inflammatory cytokine IL-10.^1,2

•Astaxanthin^⬖ reduced systemic inflammation, brain injury markers, oxidative stress, and brain edema while improving antioxidant activity and histopathological damage in rats.

•Dexamethasone reduced brain and systemic inflammation and attenuated sickness behavior (hypophagia) in mice.

•Incensole acetate^⬖ improved learning and memory, reduced neuroinflammation and oxidative stress, and increased antioxidant defenses and BDNF in rats exposed to LPS.

•Pioglitazone reversed rat hippocampal neurotoxicity by reducing inflammatory and apoptotic signaling (p-JNK, p-c-Jun, Caspase-3) and restoring protective pathways (p-Akt and p-p70S6K).

•Ziprasidone (in DMSO) reduced rat microglial activation and oxidative stress.

•Rapamycin dissolved in DMSO increased food intake and reduced inflammatory and hypothalamus metabolic signaling in chickens.

•An LRRK2 inhibitor reduced microglial inflammation and cell death pathways in vitro, and improved neuronal damage, microglial polarization, and cognitive performance in rats.

•Glibenclamide partially improved brain tissue pathology and myelin basic protein expression in neonatal rats with LPS-induced intrauterine infection-induced brain injury (which has clinical relevance as the study also found premature infants born to mothers with subclinical intrauterine infection had worse neurodevelopmental outcomes).

Additionally, DMSO prevented LPS-induced disruption of gap junction communication in rat astrocytes by scavenging hydroxyl radicals from peroxynitrite. Several other compounds also demonstrated protective effects in LPS-stimulated glial and neuronal models:

• Icariin^⬖ reduced astrocyte activation and inflammatory cytokine production (TNF-α and IL-1β) in primary astrocytes.

• Genistein^⬖ reduced LPS-induced TNF-α and IL-1β in BV2 microglial cells via an estrogen receptor-dependent mechanism.

• Incensole acetate^⬖ reduced neuroinflammation and oxidative stress, and increased antioxidant defenses and BDNF.

• Chlorogenic acid^⬖ lowered multiple pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-12), decreased iNOS, NLRP3, and NF-κB signaling, while increasing IL-10.

• Ibrutinib suppressed nitric oxide, TNF-α, cell senescence, TLR4/NF-κB signaling, and reactive oxygen species.

• Icaritin^⬖ protected neurons, and in another study, astrocytes from LPS-activated glial cell-induced damage via an IGF-1R-dependent mechanism and reducing inflammatory cytokines.^1,2

• Asiatic acid^⬖ protected primary hippocampal neurons from LPS-induced toxicity by reducing TNF-α and IL-1β, decreasing oxidative stress, and activating the Nrf2/HO-1 pathway while inhibiting NF-κB. Its protective effects were partially blocked by an Nrf2 inhibitor.

Lastly, Helenalin^⬖ significantly reduced LPS-induced cranial bone destruction.

Note: in emergency brain surgeries, removed skull bones are often frozen for later reinsertion. In 39 such cases, bones frozen with DMSO showed less absorption and better outcomes than those frozen without it.

Encephalopathy

In addition to pathogens that directly cause inflammatory brain damage, a variety of other triggers can also induce encephalopathy. DMSO, alone or in combination with other agents, has shown potential benefit against many of these (e.g., this Russian paper cites DMSO as a treatment method for encephalopathy).

Ebselen (dissolved in DMSO) reduced symptoms of oxidative and nitrative stress in a rat model of hepatic encephalopathy induced by thioacetamide.

In a 2015 review, DMSO was proposed as a potential treatment for naturally occurring bovine polioencephalomalacia due to it being mechanistically plausible it could help the condition, certain veterinarians using it there with success, and a general lack of strong evidence existing for treatment options for the condition. This disease often results from a thiamine^⬖ deficiency, to varying degrees responds to a repeated IVs of high-dose thiamine,^⬖ and has symptomatic overlaps with Wernicke’s encephalopathy, a thiamine^⬖ deficiency seen in humans (particularly alcoholics), suggesting DMSO may have use in that condition. Corroborating this, in a 2021 mouse model of thiamine^⬖ deficiency, DMSO (intraperitoneal) alone partially improved behavioral deficits and reduced thalamic damage (a key region affected in Wernicke’s encephalopathy). When combined with high-dose thiamine,^⬖ DMSO further enhanced recovery of locomotor function, motor coordination, and thalamic cell viability beyond thiamine^⬖ alone, and helped minimize long-term neurological sequelae.

Note: DMSO’s chemical interactions with thiamine^⬖ (e.g., to enhance thiamine^⬖ delivery) have also been repeatedly studied.^1,2,3

In a group of horses who developed leukoencephalomalacia from Fusarium moniliforme mycotoxins in their food, a DMSO combination therapy aimed at reducing cerebral edema halved their death rate (66% to 33%) and allowed the surviving horses to fully recover.

Myasthenia Gravis

In order for skeletal muscles to fire, they need to receive acetylcholine from the nerve that directs them. In myasthenia gravis (MG) the body forms antibodies to the muscle’s acetylcholine receptors (AChRs), and as they are destroyed, the muscles need more and more acetylcholine to be sent by the nerves to activate. In turn, MG is managed by various immune-suppressing medications, filtering the AChR antibodies out of the blood, and acetylcholine esterase inhibitors (which boost acetylcholine levels)—suggesting DMSO’s anti-inflammatory and AChR-augmenting properties (via acetylcholine esterase inhibition) may benefit the disease.

DMSO's potential for MG was initially discovered (accidentally) in 1980, when two researchers tested a variety of agents for their ability to reduce AChR antibodies, and realized that the DMSO being used as a vehicle for the various agents they were testing was independently reducing those antibodies. They then found giving rats daily intraperitoneal injections of 1 mL DMSO for two weeks resulted in a 52% decrease in AChR antibodies (but not total IgG levels) that persisted for an additional six weeks after treatment was terminated.^1,2

Note: after this discovery, the researchers expressed their eagerness to test DMSO in humans with MG (the New York Times even covered it).

A follow-up rat study then found DMSO suppressed anti-AChR antibody levels by an average of 53%–76%, with the effect being similar regardless of whether DMSO was given orally, rectally, or intraperitoneally. Additionally, DMSO treatment suppressed the anti-AChR antibody response to a weak primary antigenic stimulus. Interestingly, when given during strong primary or secondary immune responses, DMSO instead enhanced antibody production 1.7–2.8-fold — indicating bidirectional immune modulation depending on timing and stimulus strength (or DMSO’s ability to potentiate allergens).

These antibody findings were complemented by direct evidence that DMSO restores neuromuscular function. In ex vivo mouse nerve-muscle preparations where tubocurarine was used to mimic MG (reducing the strength of nerve-evoked muscle contractions), DMSO produced a rapid, dose-dependent, and sustained restoration of twitch force — with 0.1% restoring 20–30% of force and 0.75% achieving complete restoration that was sustained for over 150 minutes. Electrophysiology confirmed DMSO increased the amplitude of nerve signals at the muscle by ~25–30%, consistent with its acetylcholinesterase-inhibiting properties.

Additional studies in frog and mammalian nerve-muscle preparations confirmed that DMSO at concentrations ≤1% enhanced neuromuscular transmission through acetylcholinesterase inhibition, while concentrations above 1% began to have depressant effects in mammals, and that THC (but not CBD) counteracted this restoration of neuromuscular function.^1,2,3,4 DMSO has also been shown to reverse neuromuscular blockade caused by organophosphates (which poison the same acetylcholinesterase system that is therapeutically targeted in MG).^1,2,3,4,5,6,

Note: this research inspired a 1982 study to determine if DMSO suppressed thyroid autoantibodies (which were experimentally induced in rats). It did, and also was found to increase the ratio of IgM to IgG plaque forming cells (which suggested a true immunoregulatory effect). In turn, some patients report that DMSO benefits autoimmune thyroiditis.

A variety of agents combined with DMSO have also shown benefit in experimental autoimmune MG models — including resveratrol^⬖ (which reduced anti-AChR antibodies and protected AChR density at the neuromuscular junction), total glucosides of peony^⬖ and artemisinin^⬖ (both reduced clinical scores and anti-AChR antibodies while modulating regulatory T cells), atorvastatin-derived exosomes,^1,2,3 and a caspase-1 inhibitor (which suppressed disease progression via IL-1β/IL-17 pathways).

Separately, sepsis-induced disruption of acetylcholine receptor clustering on muscle cells was reversed by GSK3β inhibition, restoring the receptor aggregation needed for normal neuromuscular transmission.^1,2 In a rat sepsis model, rapamycin similarly improved nerve conduction velocity, muscle action potential amplitude, and survival by restoring acetylcholine receptor homeostasis.

Sadly, while physicians have highlighted DMSO’s potential for human patients, no human studies have ever been performed for DMSO with MG. However, one reader with generalized MG reported that after starting oral and topical DMSO in 2022, her muscle fatigue, cognitive function, and vision dramatically improved, and she has not had a myasthenic crisis since. She noted that higher doses at night would wake her after an hour feeling alert and functional — which she attributed to DMSO boosting her acetylcholine levels — and described the effect as “better than the pyridostigmine I used to take 6x/day.” Another reader with generalized MG alongside multiple other autoimmune conditions reported no myasthenic crises since starting DMSO in 2022, along with dramatically reduced muscle fatigue, greatly improved cognition and near-normal vision — after having been on 30 prescription medications, she is now nearly off all of them.^1,2 Other readers with MG have also noticed positive effects from DMSO.¹

Hydrocephalus

Cerebrospinal fluid (CSF) is primarily produced and circulates within chambers in the brain called ventricles. When too much CSF is produced or its drainage or flow from the ventricles is obstructed (or absorption is impaired), the ventricles enlarge and exert pressure on surrounding brain tissue. This can lead to cognitive impairment (including dementia-like symptoms), impaired coordination or gait disturbance, and urinary incontinence. Since DMSO facilitates fluid circulation and drainage, it could potentially help hydrocephalus.

Unfortunately, research in this area is quite limited, with the primarily referenced studies being work from a team that found injuring the ventricles (by puncturing them and then injecting DMSO) caused hydrocephalus in a dose dependent manner, with 2% DMSO causing a small increase (8-16% developed it, on average increasing ventricle volume by 50%), and 10% or 100% causing it much more frequently. This led the authors to postulate the effect they observed could account for why hydrocephalus is occasionally seen from other therapies which inject high concentrations of DMSO into the cerebral circulation.^1,2,3

As these concentrations are much higher than what can be reached with standard DMSO infusions (let alone any other route of administration) and interventricular injections of a variety of substances besides DMSO reliably cause hydrocephalus, it is unlikely these results are relevant to DMSO users, especially if high-dose IV DMSO infusions are avoided.

Outside of this study, two case reports suggested DMSO can benefit hydrocephalus:

•In a Shih Tzu dog which had severe acute neurological symptoms (e.g., seizures and opisthotonus) due to non-communicating hydrocephalus, IV 10% DMSO (1g/kg over 50 minutes), greatly improved symptoms (e.g., seizures were largely suppressed and consciousness was restored), which the authors attributed to DMSO reducing intracranial pressure and protecting neurological tissue. Ultimately, the dog died after 50 days, but its prognosis greatly exceeded what had been expected.^1,2

•A diffuse cerebral encephalopathy associated with hydrocephalus and cholesterinic [cholesterol] granulomas in a horse partially improved from a DMSO-containing regimen. In a horse with a large intracranial epidermoid cyst causing ataxia, head-pressing, and circling, IV DMSO with glucocorticoids and penicillin produced gradual clinical improvement (though the animal relapsed over six months due to the progressive nature of the lesion).

While in contrast, in a study of experimentally induced hydrocephalus where DMSO was used to deliver an aquaporin 4 inhibitor (which worsened hydrocephalus) intraperitoneal DMSO (at an unspecified dose) did not provide a therapeutic benefit.

Lastly, one reader shared that his brother had a progressive neurological disorder (syringomyelia, astrocytoma in the cervical spine causing paralysis, complications from its complex removal, and then hydrocephalus) which his (renowned) neurologists eventually said would be fatal in a few years (likely from encephalitis), so he sought out Stanley Jacob who agreed to treat him experimentally with DMSO. This proved to be a miracle for him and his spinal cord, with his neurologists saying “they’d never seen anyone in a similar situation stabilize and that was ‘making medical history.’” He lived 30 more joyful years, 20 of which he was Stanley Jacob’s patient, but unfortunately, IV DMSO gave him the greatest benefit and he was no longer able to obtain it once he stopped being Jacob’s patient.

Note: another reader, who had a 9-year-old daughter with cerebral palsy (and a shunt for hydrocephalus) shared that topical DMSO helped the cerebral palsy symptoms.

Psychiatric Conditions

Let’s now look at the rest of the data which has accumulated for using DMSO in psychiatry and note how often it mirrors the findings of the Russian researchers.

Human Studies

The most detailed study on DMSO’s use for psychiatric patients was conducted at a Peruvian psychiatric hospital, where 42 patients (25 schizophrenics, 4 manic depressive psychotics, 4 alcoholic psychotics, 4 compulsive-obsessive neurotics and 5 patients with severe anxiety) were taken off all their medications then given 2-5 intramuscular DMSO injections each day (with more given to the most psychotic patients) and compared to 16 controls receiving standard care.^1,2

Of the schizophrenics, all 14 of the acute cases experienced a rapid and dramatic improvement (particularly in their agitation—especially for the catatonic-paranoid patients), with all being discharged within 45 days (three having a complete recovery 15 days after admission) and not having a recurrence. To quote one of them:

“I have been out of my mind. I don’t know what happened to me. I wonder what my children are going to say.”

Of the 11 chronic schizophrenics, 4 periodically needed hospitalization and had a complete remission following DMSO (allowing them to be discharged much faster than normal), and in those who later relapsed, there was again a positive response to DMSO. The remaining 7 were more severe cases (e.g., they had been hospitalized for over 6 years and failed years of therapies) and experienced an improvement from DMSO, but it was not enough to leave the hospital.

Note: results like this (I’ve seen similar ones with other therapies as well) lead me to believe that the existing understanding of schizophrenia is far from complete. To further support that contention, this author also shared a case of a severely delusional paranoid schizophrenic responding to DMSO.

The 4 manic-depressive psychotics (who were in the manic phase, averaging 15 days of psychomotor agitation) rapidly calmed down and lost their mania after DMSO (with their recovery being much faster than what they’d previously experienced from conventional therapy).

The 4 alcoholic psychotics (2 with hallucinations and 2 with delirium tremens) had previously been hospitalized for these issues. They rapidly responded to DMSO, with restlessness improving in the first few days while the hallucinations took longer.

The remaining patients (obsessive-compulsive neurosis and severe anxiety) also had a good response to DMSO (e.g., they were calmer, ideas did not upset them as before, they were able to act in a more spontaneous way, and they were able to overcome their obsessive compulsions).

Note: the authors of the 1967 paper noted that DMSO had antipsychotic and antianxiety properties and that its action differed from tranquilizers in that little sedation or central depression was produced. A later 1992 paper proposed that the antipsychotic effects observed in this trial resulted from DMSO suppressing excessive interleukin-2 (IL-2) production by T-lymphocytes, a mechanism also attributed to certain antipsychotics in the same model.

Sadly (like many things in medicine) these 1967 results elicited minimal interest and no attempts were made to replicate them (although a 1982 Russian review noted DMSO could be used for psychiatric disorders and a 2006 Russian literature review noted intramuscular injections of 50% DMSO had a sedating effect on psychotic patients).

To the best of my knowledge, only five other human psychiatric studies have been done with DMSO:

•In 17 patients (ages 28-55 years) with chronic depression (for at least 5-20 years) that did not respond to antidepressant therapy whose most recent depressive episode lasted 8 months to 2 years, DMSO was able to treat their depression. Specifically, the existing basic antidepressant therapy (amitriptyline, pirasidol, anafranil), was combined with 1ml 50% oral DMSO and taken three times a day, resulting in 14 (82.3%) of the patients having a resolution of their depression which persisted for the 1-4 years of follow-up each patient received.

Note: studies evaluating DMSO in combination with SSRI antidepressants are quite rare. In one of the only ones I’ve found, they jointly decreased rat appetite for sugar, while in the other (a heart study) the detected effects occurred at much higher concentrations than the blood of an SSRI user will reach.

•A study of 210 women with exacerbated chronic generalized periodontitis found that 10% DMSO mixed with 0.2% oxymetacil and delivered via ultrasound effectively relieved their periodontitis and lowered their anxiety.

•In two Chilean studies, a DMSO combination with amino acids^⬖ was used to treat depressive neuroses (e.g., mood and anxiety disorder) while in another, when used to treat cognitive impairment and dementia, those patients also experienced a significant improvement of their mood (going from depressed to happy).^1,2

•In women with post partum depression (PPD), blood tests consistently showed significantly lower vitamin D, serotonin, and norepinephrine. When vitamin D^⬖ in DMSO was given to cultured hippocampal neurons, beneficial increases were observed in both their proliferation and secretion of serotonin, and norepinephrine (likely via the PI3K/Akt pathway).

Note: In lymphoblastoids from women with PPD, brexanolone (an approved PPD therapy) in DMSO modulated the expression of 98 genes potentially linked to PPD (which was believed to account for its rapid effect on PPD).

However, a variety of animals ones have been and will be summarized (all of which, unless otherwise specified were conducted with rats or mice).

PTSD

•In one study designed to model PTSD (via traumatic stress in adolescence), the methyltransferase inhibitor Unc0642 (dissolved in DMSO) alleviated (otherwise permanent) anxiety, depression, social and cognitive dysfunction and normalized PTSD impaired brain development.

•In a modified single prolonged stress (SPS) model of PTSD, a moderate dose of Cannabis sativa leaf extract^⬖ (dissolved in DMSO) significantly enhanced the efficacy of exposure therapy in extinguishing the conditioned fear memory. The benefit was CB1 receptor-dependent and persisted in a drug-free test 14 days later.

Stress

In addition to the stress which causes PTSD, many rodent studies have modeled a variety of other stressful situations (which frequently cause anxiety or depression). These comprise the majority of DMSO psychiatric studies, and collectively, these results help support the theory of psychiatric illness proposed by the previously mentioned Russian Researchers.

•In chronic “social defeat” stress induced by repeated exposure to an aggressive male which attacks another rodent into submission, DMSO combined with Dihydromyricetin^⬖ significantly improved learning and memory, decreased immobility time, and reduced anxiety. In another study, Epothilone D, dissolved in DMSO, prevented brain changes in the prefrontal cortex and hippocampus caused by this type of stress. Naringenin^⬖ attenuated social defeat-induced neurobehavioral deficits, reduced oxidative stress (brain MDA), restored glutathione, and lowered TNF-α and IL-1β.

Numerous studies have shown promise for mitigating the effects of chronic emotional-painful stress (typically three weeks of EPS).

•In one,^1,2 DMSO prior to the stress, increased superoxide dismutase (SOD) activity in brain homogenates and serum, in another, DMSO also increased SOD activity and decreased ceruloplasmin-transferrin activity¹—suggesting DMSO’s ability to neutralize chronic stress relates to DMSO reducing oxidative stress.

•In another, DMSO prior to chronic EPS completely prevented the development of gastric ulcers, blocked the stress-induced behavioral changes in the open field test (excessive locomotion, rearing, and reduced center exploration indicative of anxiety), and normalized the cardiovascular and autonomic responses, including the hypertension and altered heart and respiration rates that occurred both during stress and during subsequent immobilization. Additionally, like the previous studies, it markedly increased SOD activity in the brain.^1,2

Note: since DMSO interfered with the formation of malonic dialdehyde (a marker of lipid peroxidation) the investigators were unable to also measure if it reduced its formation within the brain.

The controversial forced swimming test (FST) evaluates depression through the shift from active coping behaviors to passive immobility in mice facing an inescapable stressor. Either alone or in combination with the tail suspension test, studies found DMSO in combination with the following substances elicited anti-depressant activity: flavonoids from Alpinia oxyphylla,^⬖ cinnamon extract,^⬖ asiatic acid^⬖ (comparable to midazolam), trans-resveratrol,^⬖ chrysin^⬖1,2 (which was further enhanced by prozac and similar in efficacy to diazepam), ethanolic extract of Ptychopetalum olacoides,^⬖ essential oil of Nepeta rtanjensis^⬖ (a monoamine oxidase inhibitor), Riparin III^⬖ (from an Amazonian plant), methanolic extracts of Cuminum nigrum (L)^⬖ and Centratherum anthelminticum^⬖ (which also reduced anxiety), ganoderic acid A,^⬖ methanolic extract of Withania qaraitica^⬖ (similar in efficacy to citalopram or desipramine), oridonin,^⬖ alarin, ODQ and 7-NI, Prozac, and a cannabinoid CB1 receptor agonist.

Chronic restraint stress is a common rodent test for modeling human depression, anxiety. For CRS rats, in combination with DMSO:

•A caspase-1 inhibitor reduced the immobility, social avoidance and anhedonia which followed CRS and social defeat stress.

•Xiao Yao San^⬖ and a c-Jun (JNK) inhibitor repeatedly improved anxiety-like behaviors. Additionally, the Chinese herbal formula reduced phosphorylated JNK, JNK, and P-c-Jun protein and mRNA expression in hippocampus comparably to the JNK inhibitor in CRS rats with liver depression and spleen deficiency syndrome.^1,2

•Intraperitoneal quercetin^⬖ significantly mitigated anxiety- and depression-like behaviors in CRS rats who also had restricted cerebral blood flow (via bilateral carotid artery stenosis) along with alleviating hippocampal demyelination, restoring myelin sheath thickness, reducing brain inflammation (via reduced IL-1β/TNF-α, increased IL-10/IL-4, promoted microglial M2 polarization) and enhanced microglial phagocytosis (elimination) of harmful myelin fragments.

•A corticotropin-releasing hormone type 1 receptor antagonist prevented stress-induced decreases in body weight, sucrose preference, and locomotion along with hypothalamus BDNF and GAP-43 upregulation (as unlike in the hippocampus, hypothalamic increases are maladaptive).

•Safranal^⬖ protected against restraint stress-induced oxidative brain damage and alleviated stress-induced behavioral changes.

•Saikosaponin A^⬖ and paeoniflorin^⬖ relieved corticosterone induced inhibition of autophagic flux in PC12 cells by reducing LC3II/I, P62, and mTOR expression, suggesting a role in chronic stress.

Depression

The Chronic Unpredictable Mild Stress (CUS) test mirrors the development of depression in humans is one of the top tests for evaluating it in rodents. Natural compounds, targeted pathway inhibitors, and clinically used pharmaceutical drugs (administered in combination with DMSO) showed the following beneficial effects in CUS-exposed rats:

•A ptychopetalum olacoides^⬖ extract prevented anxiety and hyperglycemia.

•Intraperitoneal curcumin^⬖ ameliorated depressive-like behavior and upregulated (neurotrophic) BDNF, PSD-95, synaptophysin, p-Limk1, and p-cofilin expression in the prefrontal cortex. In another study, it also reversed CUS behaviors and upregulated those three neurotrophic proteins in the lateral amygdala.

•Oridonin^⬖ (from Rabdosia rubescens) reduced social anxiety and depression, improved sucrose preference, open field activity, and neuronal morphology and cell numbers in prefrontal cortex and hippocampus and suppressed the inflammatory p38 MAPK/NF-κB/NLRP3 pathway.

The JNK blocker SP600125 partially modulated the hyperactive HPA axis by significantly lowering pituitary ACTH levels and upregulating glucocorticoid receptor (GR) expression in the hippocampal CA3 region compared to the solvent control, reduced the stress-induced increase in caspase-12 (suppressing hippocampal neuronal apoptosis), reduced C-jun (a pathway often overactivated in chronic stress) and enhanced electroacupuncture’s reduction of depression.^1,2,3,4

•Necrostatin-1 (which blocks inflammatory cell death) also improved depressive-like behaviors.

•Intracerebroventricular alarin reduced depression, decreased latency to feed, and restored p-ERK/ERK and p-AKT/AKT (neurotrophic/neuroplasticity) activity in prefrontal cortex.

•Agomelatine reduced TRPV1-mediated calcium influx, oxidative stress, and apoptosis in hippocampal neurons of chronically stressed rats, improving depression-related behaviors.

•Pioglitazone improved depressive-like behaviors, suppressed pro-inflammatory cytokine increases (TNF-α, IL-1β, IL-6), reduced M1/M2 microglial ratio, decreased NF-κB expression, and ameliorated peroxisome proliferator-activated receptor gamma (PPARγ) expression loss in the prefrontal cortex and hippocampus

•Quetiapine ameliorated depressive-like behavior in chronic unpredictable stress rats, increased hippocampal BDNF and phospho-ERK1/2 expression, and promoted neurogenesis (and was synergistically enhanced by combination with transcranial magnetic stimulation).

Note: DMSO alone decreased elevated caspase-12 protein expression in hippocampus (which can cause neuronal death).

Separating infant rats from their mothers produces long-term depressive-like behaviors (e.g., anhedonia, HPA-axis dysregulation, and reduced hippocampal neurogenesis) that mirror those seen in human adults with depression and chronic stress. In separated rats, melatonin^⬖ dissolved in DMSO significantly increased BrdU-positive cells and lowered glucocorticoid receptor expression in the dentate gyrus, directly counteracting the depressive process.

Note: The term “depression” is used for both a psychiatric (psychological/mood) state and a CNS-induced reduction in activity and alertness (neurologic depression or depressed mentation). These are related as inflammatory or infectious diseases can affect the nervous system and cause it partially shut down, triggering symptoms that overlap with both — such as reduced alertness/mentation and mood changes (often called “sickness behavior”). In certain cases, such as a foal with brain damage from losing blood supply during childbirth, DMSO’s therapeutic activity on the nervous system also addressed the neurologic depression (improved alertness and mentation). In others, DMSO has been observed to help resolve psychiatric depression that followed an illness, likely through anti-inflammatory and neuroprotective effects on shared nervous-system pathways.

Anxiety

In zebrafish, the willingness of zebrafish to leave dark areas to enter light areas is used to assess anxiety, and in this model, DMSO alone reduced anxiety (as did DMSO in combination with the chalcone C2OHPDA).

In mice and rats, the way they navigate specific mazes (e.g., elevated plus-maze test) or cross fields are used to evaluate anxiety. In one study, DMSO alone (10%, 0.5 µL) microinjected into the DPAG (a midbrain structure) greatly reduced anxiety and increased exploratory behavior.^1,2 In combination with DMSO the following agents were found to reduce anxiety: eucalyptol^⬖ (primary component of eucalyptus oil), cinnamomum^⬖ (a hydroalcoholic extract), marjoram^⬖ (extracted with DMSO), luteolin^⬖ (following acute experimental colitis), asiatic acid,^⬖ Casearin X,^⬖ valepotriates,^⬖ 5-MeO-DMT , CCK-8, CCK₂ agonists, cannabinoid and vanilloid (TRPV1) agonists.

•A mGluR2/3 agonist dissolved in DMSO reduced anxiety in chicks stressed by brief social separation.

Note: withania somnifera leaf extract^⬖ (in DMSO) protected against benzo[a]pyrene-induced neurotoxicity in zebrafish by restoring normal anxiety, improving brain antioxidant status, and reducing neuronal damage in the optic tectum.

Biological Stressors

In addition to putting animals into psychologically stressful situations, a variety of stressors that directly injure the body have also been observed to trigger anxiety and depression and to respond to therapeutic combinations containing DMSO.

Two AMPA-type glutamate receptor potentiators reduced pain hypersensitivity and depression-like behavior in rats with neuropathic and inflammatory pain.

In neuropathic pain caused by a spared nerve injury (SNI), a DNA methyltransferase inhibitor (in DMSO) significantly improved depressive symptoms and increased neurotrophic brain BDNF levels. In another SNI study, a chemogenetic DREADD inhibitor (in DMSO) alleviated both pain and depressive symptoms and in a third, rapamycin alleviated anxiety. depression and pain from an L5 SNI.

In rats with pentylenetetrazol triggered epilepsy (which consistently produces anxiety and depression), rapamycin and pitolisant (dissolved in DMSO) markedly improved anxiety (2.7 fold improvement on a maze test) and depression (37.5% improvement in swim test).

In mice with LPS induced depression induced, resveratrol^⬖ in DMSO reversed their depression along with reversing neural inflammation and triggering neurogenesis (particularly within the hippocampus).

In mice with toxoplasmosis triggered depression, arctigenin^⬖ in DMSO significantly reduced depressive behaviors and brain inflammation by inhibiting key pro-inflammatory pathways (TLR4/NF-κB and TNFR1/NF-κB).

In ovariectomized (OVX) mice modeling menopause, resveratrol^⬖ in DMSO significantly reduced ovariectomy (ovary removal) induced anxiety and depression and neural inflammation (particularly within the hippocampus).

In mice with anxiety induced by high-fat diet, Japanese ginseng^⬖ in DMSO significantly reduced anxiety-like behaviors, increased brain BDNF and synaptophysin levels, and reversed the brain’s FGF21 resistance (a key driver of the anxiety).

In mice, Naringenin^⬖ improved hypoxia-triggered depression and anxiety, along with reducing brain oxidative stress and inflammation, increasing BDNF expression, and protecting amygdala neurons.

In mice exposed to X-rays after consuming saccharin (as this conditions them to avoid the sweetener), topical DMSO prior to the X-ray largely prevented this condition aversion (there was an 8% rather than 66% drop in saccharin consumption). A later study had similar results, suggesting DMSO counteracts the stress that would otherwise create the aversion.^1,2

Note: lastly some of the DMSO combinations described in the previous sections were used to treat conditions directly triggered by a pharmaceutical (e.g., depression from corticosterone or anxiety from salicylates).

Psychosis

•DMSO was proposed to exert antipsychotic effects by modulating chronic macrophage activation and downstream cytokine dysregulation, particularly interleukin-2 signaling, thereby reducing schizophrenia symptoms across disease phases through immune regulation.

•MK-801, a drug with the same mechanism as psychosis-inducing phencyclidine (PCP) and ketamine, is used to induce schizophrenia in rodents. A study found that atypical antipsychotics and the Src kinase inhibitor PP1, dissolved in DMSO, significantly attenuated MK-801-induced cortical (brain) injury in rats, with the protective potency of the antipsychotics correlating with their clinical effectiveness in treating psychosis.

•In a MK-801 rat study, three different drugs that activated the α7nAChR receptor (when combined with DMSO), significantly improved schizophrenic behaviors by increasing following behavior and total interaction time, decreasing avoidance behavior time along with creating therapeutic changes within the prefrontal cortex and hippocampus (increased α7 nAChR protein expression, increased cAMP levels, decreased PDE4A and PDE4D protein expression).

•Diosmin^⬖ attenuated hyperactivity, behavioral deficits, oxidative stress, and neuroinflammation in a mouse model of LPS plus ketamine-induced schizophrenia-like symptoms.

•In another MK-801 schizophrenia study, the flavanoid Fisetin^⬖ (given intraperitoneally in DMSO) significantly decreased rat escape latency, increased space exploration time and platform crossings and (beneficially) phosphorylated CaMKII, ERK1/2, and CREB.

In addition to these combinations treating schizophrenia, tinospora cordifolia^⬖ (an Ayurvedic herb) dissolved in DMSO demonstrated antipsychotic activaty in mice given (psychosis-inducing) amphetamines (along with curcumin^⬖ in DMSO counteracting methamphetamine-induced neurotoxicity and spatial memory impairment in rats).

Note: a study (which found female rats were more prone to developing methamphetamine addictions than male rats) found modafinil dissolved in DMSO, attenuated METH-seeking behavior in both sexes. Another study found parthenolide (dissolved in 1% DMSO) partially blocked cocaine’s actions in the brain (but it is unlikely this could translate to a cocaine addiction therapy).

Sedation and relaxation are sometimes reported from DMSO use (e.g., sedation has been repeatedly observed in humans and animals at higher doses, intraperitoneal DMSO was observed to cause a decrease in spontaneous motor activity and in one large trial, 3% of DMSO users reported increased tiredness). This is likely due to DMSO increasing parasympathetic tone (due to it inhibiting acetylcholinesterase), and may partially account for DMSO’s psychiatric properties as excessive sympathetic activity plays a key role in anxiety, mania and psychosis.

Note: I find a significant portion of psychiatric issues result from excessive sympathetic activity or deficient parasympathetic tone (e.g., the “buzz” that state creates frequently creates anxiety), and likewise many (myself included) believe a significant number of health issues result from vagal (parasympathetic) dysfunction. Given that DMSO can both directly increase parasympathetic function and also heal or restore the function of nerves (along with potentially relaxing tight muscles compressing them), it is possible some of DMSO’s benefits in psychiatric conditions arise from its effect on vagal function.

Finally, like many other therapeutic agents, DMSO has also been combined with antipsychotics. For example, with intraperitoneal haloperidol, it facilitated haloperidol-induced 1.8-fold increases in striatal preproenkephalin mRNA and 1.6-fold increases in total endogenous opioid peptides (with no effect in other brain regions), increasing antipsychotic efficacy, and potentially reducing pain or antipsychotic extrapyramidal side effects.

Note: a variety of antipsychotics have used DMSO as a vehicle (e.g., this study did so with intraperitoneal olanzapine, amisulpride, quetiapine and aripiprazole, while this one did so with haloperidol, clozapine, RMI-81582 and risperidone).

Sleep

Sleep is one of the most important, yet least appreciated facets of our existence, as sleep healing the body and integrating our minds is an immensely complex process that can easily be derailed (e.g., poor sleep causes neurodegeneration, and neurodegeneration worsens sleep). Sadly, rather than support it, our medical system defaults to treating insomnia with sedatives (e.g., sleeping pills) which “put you to sleep” but also sedate the restorative process of sleep—which is tragic, as restoring healthy sleep is frequently one of the top three things which needs to be done to heal chronic illnesses.

Since DMSO heals the nervous system and restores impaired fluid circulation (which I believe is what ultimately underlies many cases of insomnia), I hence was hopeful DMSO could be a remarkable sleep aid to facilitate restorative sleep.

Yet, in the 6,000 reports I’ve received from readers, I have only received a few reports indicating that happened.^{1,2,3,4,5,6,7,8,9,10,11}

The thing I have noticed most recently is a reduction of fatigue. I used to indulge in a daily nap, then go to bed and sleep another 8-9 hours at night. Now, if I try to nap I just can’t be bothered. I sleep my normal sleep at night and awaken refreshed.

Note: another reader had an almost identical experience, while another reported DMSO addressed the excessive sleep they had long required following a stroke.

I take a couple of mls before bed helps dramatically improve my sleep.

I feel amazing. My sleep is generally remarkable.

I love the really deep sleep it gives me. Feeling very tired after months of long intense work, I took a small dose one morning just because. An hour later I had no choice but to sleep. Woke up hours later totally refreshed. Amazing stuff.

I have started using it instead of Hydroxyzine, which I use at times. No side effects!

Note: a few readers have also reported an energizing effect from DMSO causing them to wake up after much shorter periods and feeling refreshed (which may be positive or negative).

However, in the reports I’ve received, two consistent patterns have jumped out.

First, while DMSO did not inherently function as a “sleeping pill” a large number of people reported that DMSO cured an ailment which was causing insomnia, and I have received dozens of reports from individuals stating DMSO allowing them to sleep profoundly improved their life (including cases where they had previously been suicidal). This, in turn, highlights the flaws of the symptom-based approach to medicine we practice, as many cases of insomnia which have clearly identifiable causes (that are never addressed) are instead simply “treated” with sleeping pills.

Most commonly, this was due to DMSO treating musculoskeletal pain which had kept them from falling asleep (or routinely woke them up at night). Shoulder pain resolutions (e.g., bursitis, impingements, or rotator cuff tears) ^{1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17} were the most common, followed by low back pain (e.g., radiculopathy, disc herniations or tears, failed spinal surgery, vertebral metastasis),^{1,2,3,4,5,6,7,8,9,10,11,12,13,14} arthritis (e.g. rheumatoid arthritis and in the hands or toes),^{1,2,3,4,5,6,7,8,9} knee pain (e.g., arthritis, meniscus injury, or a sprain in a 2 year old),^{1,2,3,4,5,6,7} hip pain (e.g., bursitis),^1,2,3,4 elbow pain (e.g., tennis elbow),^1,2,3 neck pain (whiplash or degenerative discs)^1,2 hand pain,^1,2 jaw pain^1,2 lower extremity tendopathy (e.g., gluteal)^1,2 plus individual instances of sleep greatly improving following the resolution of sciatica, foot pain, a throbbing thumb, tight muscles, and blunt maxillofacial trauma (from a car throwing them into the pavement).

DMSO also resolved other types of pain that prevent sleep such as peripheral neuropathy (e.g., in the feet),^{1,2,3,4,5,6,7} headaches (e.g., migraines, concussions),^1,2,3 cancer pain^1,2 individual instances of eye pain, CRPS, and trigeminal neuralgia plus numerous resolutions of unspecified pains which had prevented them from sleeping.^{1,2,3,4,5,6,7,8}

DMSO also improved other challenging neurological conditions to the point sleep also dramatically improved such as restless leg syndrome,^1,2,3,4,5,6 Lyme disease,^1,2 vaccine injuries (from Moderna or the shingles vaccine)^1,2 along with individual successes with Down syndrome, demyelinating polyneuropathy, cramping fasciculation syndrome [similar to ALS and until DMSO had made the reader suicidal], an elderly dog with tics, and unspecified long term neurological issues that had prevented getting a good night’s sleep for years. For example, to quote one Lyme patient:

Then I woke one morning and was astounded to realize I had slept through the night, -[whereas] before DMSO I had been waking 3 or 4 times every night because of pain.

Finally, in addition to DMSO addressing pain and neuropathies which prevented sleep, it also addressed other issues which interfered with sleep. Most commonly this was through improved breathing, specifically by addressing sinusitis (e.g., “I had the best sleep last night, I didn’t want to get up this morning.)^1,2,3 or lung issues (e.g., asthma, COPD or lung damage from burn pits in Afghanistan).^1,2 One reader sent a particularly interesting testimonial, suggesting DMSO can sometimes improve nightly oxygen saturation:

I tried a little 70% on a Q-tip inside each nostril before bed to see if it would help nighttime congestion. Interesting that I get no itch or tingles from inside my nostrils…maybe due to the mucus? Well, anyway, I wear a sleep tracker ring and my oxygen level and oxygen drops have significantly improved and I am sleeping in longer periods without waking up so often! I am amazed and tried to find some research that would help explain these improvements. I found some research on sleep patterns in rodents but difficult to understand. I just wanted to let you know and thank you for sharing your knowledge. I will continue my experiment and so far every night it has improved sleep data.

Note: other issues readers reported DMSO sleep improvements with include Barrett’s esophagus, severe eczema, prostate enlargement, hypothyroidism, or an acute cold.

In short, given how necessary healthy sleep is for the nervous system (discussed further here) a case can hence be made that one of the primary ways DMSO “heals the nervous system” results from it treating the ailments that were preventing healthy sleep.

Secondly, I noticed that many readers independently shared that their dreams became more vivid or lucid after taking DMSO.^{1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16}

Separately, after several weeks of taking DMSO internally now I have indeed noticed increased dreaming. Most of my life I have either not dreamed at all or at least had no memory of any dreams. But I have always slept very deeply and soundly. Usually falling asleep within seconds of laying down and having no memory of anything until morning. When I supplemented 5HTP for a while a few years back I started to dream a lot for the first time in my life.

Two factors can potentially explain this. First, by DMSO healing the nervous system and restoring circulation, this likely aids the neurological apparatus which facilitates dreaming. Second, two compounds are commonly used to facilitate lucid dreaming, 5HTP (as the above reader used) and galantamine (one of the few drugs I’ve ever used, primarily because of its phenomenal effects with lucid dreaming—provided you do not use an excessive dose). Galantamine is an acetylcholinesterase inhibitor, and since DMSO is also widely recognized to do so, this likely accounts for it increasing the vividness of dreams. However, the effects I’ve noticed from the two are very different (to the point it would not have occurred to me a similar mechanism was involved), so if this theory is valid, my best guess is DMSO should be viewed as a much weaker acetylcholinesterase inhibitor which only affects the dreams of a subset of the population.

There seemed to be a wide mix of attitudes towards the dreams (absolutely loving them, appreciating they can finally remember them, being neutral, or finding them challenging), with the majority being positive. These responses accurately represent that spectrum:

Picked this stuff up since reading your posts, been giving me some crazy ass vivid dreams, some even fully lucid haha! Haven’t really noticed anything else yet but the dreams alone have been worth it 13/10 would recommend.

when i drink it...after a couple days...i sleep super deep and have incredibly emotional dreams...which can be tough but i wake up feeling rested (but sad or contemplative).

Funny you should mention dreams and DMSO, since I started taking it internally my dreams are super vivid and sometimes very unpleasant! There are people popping up in my dreams now that I haven’t thought of in decades…Melatonin^⬖ also caused vivid dreams, but nothing like what DMSO has been causing!

Overall my favorite dream story was probably this one:

I have to share this one thing…the first evening I applied DMSO to my neck I went to bed and in the night I heard a voice saying “THE TREES WILL HEAL YOU “. In my sleepy state I had thought, oh how nice, I do love our trees ;I live in a forest. However when I awoke it dawned on me that DMSO comes from trees and that message was about the DMSO!

Lastly, one reader shared that DMSO allowed them to dramatically lower the Xanax they needed to fall asleep, while another stated it made them much more sensitive to having their sleep disturbed by coffee or beer. This is congruent with DMSO’s known ability to potentiate benzodiazepines and alcohol and suggests thought should be taken when using these agents together, but simultaneously, given that only two readers noticed this, unlike the DMSO-alcohol issue, I am not sure how impactful it is. Additionally, two readers reported DMSO’s sleep promoting effects were enhanced by combining it with magnesium^⬖ (which is plausible).^1,2

Sleep Research

The limited literature on DMSO and sleep shows the following:

1. DMSO alone generally has a minimal impact on the sleep cycle. For example, a 2005 rat study found 5% and 10% DMSO administered intraperitoneally had no effects on sleep architecture, but 15% and 20% shifted deep sleep to light sleep. This indicates the doses individuals take are unlikely to affect sleep unless they are in the sensitive minority. Likewise, in a study where intraperitoneal corticotropin releasing factor was found to make rats REM sleep become Non-rem sleep, DMSO alone (at an unspecified dose) was found to have no effect on sleep architecture.

Note: one literature review cited a Russian report that one side effect of DMSO is sleep disturbance, but I have not seen this mentioned anywhere else.

2. A few references corroborate that DMSO’s healing qualities improve sleep by healing something else causing insomnia:

•In a study of 35 men with exacerbated knee osteoarthritis (and upper gastrointestinal bleeding), in addition to topical 50% DMSO (with hydrocortisone, lidocaine and potassium iodide) reducing their knee pain, it also improved their sleep (and ability to work). Specifically, on a -3 (worst) to 3 (best), scale, their baseline sleep score (0.4 ± 0.2) improved to 1.1 ± 0.4 with the DMSO combination, and to 2.8 ± 0.5 when the combination was used with physical therapy.

•In 40 patients (on average 53.7 years old) with cervical osteochondrosis complicated by shoulder myofascial pain syndrome, topical DMSO (in combination with other analgesics) and physiotherapy and acupuncture fully resolved the pain for 34 (85%), partially improved it for 6 (15%) and in all patients, there was a significant improvement in sleep.

•In a clinical guide from Uzbekistan on surgical infections of the hand and fingers, DMSO was recommended as a conservative treatment (in combination with novocaine and an antibiotic) and for abscess in the fingertip pad to prevent them from becoming painful enough to cause “sleepless nights” and require surgery. In a Ukranian dental manual, DMSO was recommended for healing (and preventing infections) of dry sockets, as it resolved the conditions and improved numerous associated things including disrupted sleep.

•In a study of patients with localized scleroderma, daily topical DMSO (and a few other therapies) significantly improved skin lesions, prevented relapse and improved emotional health, appetite and sleep.

3: Most of the existing research on DMSO for sleep involved it being a delivery vehicle that was combined with another sleep-promoting agent either to facilitate its action or make it more potent. These broke into four categories, two of which supported the observations in reader reports.

Potentiation of sleeping medications:

•Prior administration of DMSO increased the sleeping time created by pentobarbitone sodium by 78%. Conversely, another study found hexobarbital sleeping times were not altered when 2.5 g/kg of 25% DMSO were given subcutaneously to mice beforehand.

•A DMSO dissolved fraction of a Coriandrum sativum extract^⬖ accelerated and prolonged pentobarbital induced sleep more than any other agent tested (including diazepam).

•A Marjoram DMSO extract^⬖ and separately a Nardostachys jatamansi rhizome extract^⬖ significantly increased ketamine-induced sleep duration.^1,2

Modulation of circadian sleeping times (with potential utility for jet lag):

•Melatonin,^⬖ which accelerated re-entrainment of the mouse’s circadian rhythm after a 6-hour phase shift and also made mice more susceptible to light-induced circadian shifts.^1,2 In two other studies, Triazolam (a sleeping pill dissolved in DMSO) shifted and lengthened hamsters’ circadian rhythm, whereas DMSO alone only created a small non-significant shift.^1,2 Finally, DMSO’s metabolite, MSM^⬖ (in DMSO) mitigated neurobehavioral impairment, oxidative stress, and disruptions in clock gene expression in mice exposure to alcohol combined with circadian rhythm disruption.

Note: we suspect DMSO has a significant synergy with photobiomodulation, but still do not have enough data to claim anything definitive.

Improving sleep apnea:

Intraperitoneal treatment with a Chinese herbal composition of Gastrodia elata^⬖ and Cinnamomum cassia^⬖ (dissolved in DMSO) reduced snoring pressure and frequency in aged rats and increased activity of phrenic, recurrent laryngeal, and hypoglossal nerves, while prolonging inspiratory, expiratory, and pre-inspiratory times, suggesting modulation of upper airway neural activity.

In mice with obstructive sleep apnea, dronabinol, a vagal cannabinoid agonist, significantly reduced sleep apnea episodes when combined with 100% DMSO but not when combined with 25% DMSO (while at both concentrations, REM sleep was suppressed).^1,2 Separately, Anandamide (an endogenous cannabinoid) increased sleep and adenosine levels in the basal forebrain.

In an intermittent hypoxia model of sleep apnea with rats that had heart attacks, Paxil prevented intermittent hypoxia from causing systemic insulin resistance or further damage to the injured heart (e.g., fibrosis and apoptosis was reduced).

Counteracting adverse effects of chronic sleep deprivation

In mice models, a variety of substances in combination with DMSO have been found to counteract the adverse effects of chronic sleep deprivation. Kaempferitrin^⬖ (from monkfruit) increased antioxidant capacity, reduced oxidative stress, and reduced obesity. Astragalin^⬖ significantly ameliorated liver oxidative stress. Siraitia grosvenorii flavonoids^⬖ and melatonin^⬖ increased antioxidant capacity and reduced oxidative stress and inflammation. Almorexant improved spatial learning and memory and reduced (neuroinflammatory) astrogliosis. A macrophage migration inhibitory factor inhibitor improved spatial learning and memory, and partially protected the hippocampal neurons.

Modafinil (a stimulant used to increase wakefulness in individuals with chronic sleep deprivation) significantly decreased total sleep time and increased sleep latency in English bulldogs with sleep-disordered breathing, effectively alleviating hypersomnolence (tiredness).

In rats, Paxil dissolved in DMSO (for an osmotic minipump) significantly prolonged REM sleep episode duration and reduced the number of REM sleep episodes across multiple 6-h periods (which constitutes a positive shift in chronic sleep deprivation).

Down Syndrome and Developmental Disabilities

When I initially reviewed the DMSO literature, the thing I had the most difficulty believing was reports it significantly improved Down Syndrome, as like most doctors, I assumed this was a genetic condition absolutely nothing could be done for. However, after seeing the benefits being reported in numerous clinical studies and the official Congressional transcripts, I realized my assumption may have been wrong and decided to risk my credibility by publishing that data.

Shortly after, I received these testimonials from the parents of a two-year-old girl with Down Syndrome. Her father wrote first:

We’ve been giving DMSO to our young daughter who has Down Syndrome along with extra vitamins [e.g. amino acids^⬖] based on the treatment protocol from some studies. Almost immediately we noticed she was sleeping better through the night, she’s become more verbal—she suddenly seems like she wants to say words more intentionally now—and her appetite has improved substantially. She just seems more active, and that’s really awesome!

Her mother then followed up:

Even in the time since my husband made that comment, we have seen changes in our little girl. The biggest one is that she is now CRAWLING—she had seemed for the longest time like she wasn’t even interested, but now she’s doing it (she started on her 2nd birthday, in fact!). Her coordination and motor skills are steadily improving, and she is super close to sitting up on her own, something I was getting really worried about. It’s almost like she’s not even the same kid she was two weeks ago. DMSO has been a game-changer for us. I am so excited to keep learning and seeing what’s possible!

These parents’ experience echoes what was presented at a 1980 Congressional hearing convened to (unsuccessfully) pressure the FDA to end its embargo on DMSO, where testimony was given of a child with Down Syndrome having a similarly miraculous response—but over a much longer timeframe.

There, Melody Clark was discussed, who at 11 months was started on DMSO by Dr. Jacob. At that time, her legs were “just like a rag doll’s,” she couldn’t roll from her back onto her stomach, and her eyes couldn’t focus. Her initial evaluation at six months had predicted she would never progress mentally beyond age six.

After seven years on DMSO, Melody had progressed from what one physician described as “practically a vegetable state of existence” to being only mildly developmentally delayed—something her teachers had never seen in another child with Down Syndrome. Specifically, she functioned at a second-grade level (excelling in math, reading phonetically, spelling, and habitually using complete sentences), could jump rope, do somersaults, and play on a trampoline, and was quite popular with her classmates—having transformed from a child who played alone and stood near the teacher watching others into one who initiated group activities and took turns with peers. Her teacher wrote to Congress that in view of Melody’s achievements, she “would like to see DMSO given a fair testing and evaluation in helping the handicapped.”

Her dentist additionally testified that her palate, jaw, and tongue had moved significantly toward normalcy—something he had never seen in this patient population. Melody’s extremely high palate at birth was now within normal range.

Two other similar cases have also been reported:

•At 10 months of age, Bronwyn Nash (who had Down Syndrome) was frail and unable to gain weight, so her mother started her on DMSO. She began gaining weight and developed an increased awareness of the people and objects around her and then started reaching out to touch things. At 18 months, she was able to stand up, and then became able to get into her mother’s cupboards, started to feed herself, and held her water glass well. At the time a health journalist visited her at 28 months of age, she was an alert, cheerful little girl much enjoyed and well loved by her family and improving steadily.

•At 14, Billy King could walk and feed himself but had the mental capacity of a ten month old. He then began drinking milk with DMSO each morning, and two years later, had the mental capacity of a seven year old and began losing the characteristic Down Syndrome appearance.

He continued to improve and was eventually able to hold a job in a Portland bookstore.
Note: another account of Billy King’s story has a differing chronology (e.g., he started DMSO at 8 not 14, and also took the amino acid^⬖ formula).

Research in turn exists to support these unbelievable anecdotes.

•In Oregon, 67 moderately or severely mentally disabled children (aged 4-17) with Down Syndrome were randomized to receive a high or low DMSO dose and then were compared to 23 similar children whose parents did not want them to receive an experimental drug.^1,2 No side effects occurred and a dose dependent improvement was observed:

In Chile, 55 children with severe mental disability caused by Down syndrome (the oldest being 14) were given DMSO and amino acids^⬖ by intramuscular injection or served as controls. The vials for injection consisted of DMSO along with gamma aminobutyric acid (GABA^⬖), gamma amino beta hydroxybutyric acid (GABOB^⬖), and acetyl glutamine^⬖ (with lower doses given to those under 3 1⁄2 years of age). The children’s development was then evaluated with Gese[l scores and a massive improvement was seen in the DMSO group:

Note: this study (and the additional improvements that occurred) can be viewed here and here.

In Argentina, 13 mentally disabled children (5 severe cases, 4 moderate cases, and 4 mild ones), who did not have Down Syndrome, received a DMSO amino acid^⬖ mixture (known as Merinex) three times a week by injection for 180 days (with periodic 15 day periods where the amino acids without DMSO were administered orally)

Note: other authors have reported young patients (and older ones) with learning difficulties, low intelligence, ADHD, anxiety disorders, epilepsy, nervousness, dyscalculia, dyslexia, exhaustion, and concentration problems all benefit from this protocol. Additionally, some have argued adding galactose^⬖ to it enhances its efficacy.

In a 1969 study, 44 severely developmentally delayed children received the DMSO amino acid^⬖ mix, with many experiencing a heightened capacity for learning in a relatively short time and over 70% having favorable responses such as “increase of the IQ, an evident and accelerated progress in basic achievements, an overall improvement of intellectual capacity, evident progress in reading, writing, and mathematics, better coordination of movements and improved manual skill, and a decrease of behavioral problems,” along with gaining better psychomotor control, no longer having anger for no reason, a general reduction of irritability, and a lessening of disobedience.

Another 1969 study gave the DMSO amino acid^⬖ mixture for six months to 30 learning disabled children with language disorders (who did not have an accompanying neurological illness) and compared them to 20 controls, and observed it resulted in:

•Disappearance of mental lethargy.
•Evidence of sensorial reactions.
•Disappearance of automatic movements.
•Disappearance of inertia, passivity, and negativity.
•Growing interest and initiative in tasks and activities.
•Improvement of the physiognomic expression and of the spoken language.
•Lucid activity, group contact, and disappearance of unprovoked aggressiveness.
•Losing shyness and developing self-esteem.
•Successful training to carry out chores, to do shopping, to eat, and to dress without help, etc.
•Learning to read and to write and to do homework.

A 1976 Chile study gave DMSO and amino acids^⬖ (GABA,^⬖ GABOB,^⬖ L-acetylglutamine,^⬖ and arginine^⬖) to 15 children (under 3.5 years old) with Down Syndrome and compared them to 13 untreated controls. After 12 months of intensive treatment, per the Gesell Developmental Quotient, motor area average rose from 56 to 72, adaptive from 50 to 66, language from 52 to 58, and social from 40 to 64 (with many individuals improving >10 points, especially in motor, adaptive, and social domains), while controls remained largely unchanged. Physical improvements included reduced macroglossia, better facial expressiveness, increased muscle tone/coordination, and postural changes in treated children. During the subsequent 6-month maintenance phase (to 18 months total), treated children’s gains were largely maintained or slightly increased (e.g., motor to 74, adaptive to 69, social to 67), with no significant regression and only minor isolated losses (e.g., in language for a few), whereas controls showed no progress or slight declines. The authors noted no significant adverse effects and concluded that early intervention appeared beneficial for neuronal stimulation and development.^1,2,3

One author reported on an Argentinian study (I could not find) conducted by this physician, where 18 children with Down syndrome received DMSO and amino acids^⬖ and were compared to 91 controls, and to quote the author this resulted in:

a tendency towards accelerated maturity in the children treated, with marked progress in language integration; this could be established in statistically significant degrees in the children treated

Additionally:

•This study, and this study, also found the DMSO amino acid^⬖ mixture benefited developmentally disabled children.

•A 1982 Spanish literature review highlighted DMSO as a treatment for Down Syndrome.

•A 2009 Russian diabetes book promoted regularly applying a topical mixture of DMSO, hydrogen peroxide, and copper sulfate for diabetes and tissue regeneration, which cited a case of a pregnant woman whose fetus was diagnosed with Down Syndrome who did that protocol and then had a normal child.

•1980 and 1982 articles by skeptical physicians acknowledged DMSO was being explored as a treatment for Down Syndrome.

Note: in addition to Down Syndrome, the German DMSO community has had significant success using DMSO and amino acids^⬖ for learning disabilities, developmental delays, mood and anxiety disorders, and neurodegenerative diseases—of which minor or severe learning disabilities are the most common application.

Autism

One of the most frequent questions I receive is if DMSO can be used to treat autism (as many factors mechanistically argue for it), but unfortunately, other than a few vague parent reports I’ve come across suggesting it worked (I could not corroborate), I do not have any direct parental data to assess this question.

However, a variety of studies on mice (modified to model autism) have found DMSO in combination with another therapeutic helped their autism-like behaviors. Specifically, with DMSO:

Epothilone D (a microtubule-stabilizing agent) improved autism-like repetitive behaviors across multiple studies^1,2,3,4,5,6 through a consistent mechanism: stabilizing microtubules, increasing excitatory synapse number, and enhancing myelin basic protein expression in the cerebral cortex. These studies consistently found reduced self-grooming times and increased social ability, with individual studies additionally demonstrating improved restricted repetitive behaviors in marble burying tests, normalized myelination and increased dendritic spine density.

Curcumin^⬖ repeatedly enhanced sociability, reduced repetitive behaviors, and restored hippocampal neurogenesis across multiple studies,^1,2,3,4 with consistent findings of increased hippocampal neuron counts and reduced excessive astrocytes (a key facet of the disease process), along with improved learning, memory, and social communication. Individual studies further showed curcumin^⬖ promoted neural progenitor cell proliferation, increased radial glial cells in the subgranular zone, and enhanced newborn neuron maturation.¹

Prenatal resveratrol^⬖ prevented embryonic valproic acid exposure from causing autism-like behavioral features, including deficits in nest-seeking behavior, social interaction, and over-excitation in the brain’s glutamate system.^1,2

Melatonin^⬖ and Wortmannin (a PI3K inhibitor) improved autism-like behaviors, promoted synapse-associated protein synthesis, and improved dendritic spine development. Separately, Wortmannin alone rescued dendritic spine density, upregulated postsynaptic density protein, and inhibited the same pathway rapamycin targets.

Additional agents improving autism-like behaviors in mouse models include a 5-HT2A receptor antagonist (which attenuated repetitive self-grooming), a S1PR1 antagonist (which improved learning and memory while preserving hippocampal neuronal density and microvascular integrity), estradiol (which restored empathy and social affection in ovariectomized mice), and baicalin^⬖ (which dose-dependently improved recognition and spatial memory while increasing BDNF and healthy neuron counts in the hippocampus).

Collectively, these studies using a diverse variety of therapies that share the common thread of DMSO suggest DMSO may also independently improve autism, but due to DMSO rarely, if ever, being compared to a saline placebo in these types of studies, it is impossible to know.

Note: complete summaries of each study can be found in my reference Substack here.

Other Developmental Disorders

Cerebral Palsy: Given DMSO’s ability to heal central nervous system damage, particularly from temporary loss of blood flow (along with its ability to help muscle spasticity), it appears plausible DMSO could help with cerebral palsy. Unfortunately, this has not been studied and the only paper I’ve found on this topic noted that DMSO with verteporfin partially restored the ability of muscle satellite cells to correctly differentiate, potentially reducing their spasticity.

However, in horses, one paper reviewing veterinary textbooks reported DMSO treats neonatal brain damage (e.g., hypoxic-ischemic encephalopathy) and colic in foals, while another book reported that veterinarian Jack Metcalf had found horses developmentally disabled at birth (to the point they can’t nurse) once given IV DMSO three times daily regain the ability to nurse and that DMSO accelerates their overall development.

Finally, one of the most common and disabling features of cerebral palsy is severe disabling muscle spasticity (to the point aggressive measures like botox are routinely used). In patients with severe muscle spasticity, Russian researchers reported success with ultrasound-facilitated topical applications to the affected muscles and applicable spinal segments of DMSO mixed with sodium oxybutyrate (GHB, the potent sleep aid the FDA went to war against) and lidocaine. In the detailed patent (which I translated here), they specifically discussed a case of a patient who developed debilitating spasticity from arachnoiditis, but implied it could be used to regain mobility in other conditions like poliomyelitis or cerebral palsy. In parallel, one reader with a cognitively intact nine-year-old girl with cerebral palsy that affects three limbs shared that her daughter told her topical DMSO relaxed her tight muscles and allows her to move more easily.

Note: another Russian patent proposed DMSO as a transdermal enhancer for a botox patch to treat the spasticity associated with Parkinson’s, cerebral palsy, dystonia, and multiple sclerosis — potentially bypassing the need for the repeated injections botox currently requires. Outside of this patent, I have only seen DMSO botox formulations used for refractory idiopathic detrusor (bladder) overactivity (where they worked).

Cleft Palate: One of the original anti-seizure medications, phenytoin, was notorious for causing a pattern of birth defects, some of which (such as a flat nasal bridge and epicanthal folds) can resemble features seen in Down syndrome. One study found DMSO prevented some of the birth defects (e.g., cleft palate) phenytoin caused.

ACBD6-related neurodevelopmental syndrome: this rare disease also causes cognitive impairment and birth defects resembling those seen in Down Syndrome. While DMSO has not been tested on patients with it, the disorder is caused by defective activity of N-myristoyltransferase, an enzyme DMSO has been shown in vitro to increase the activity of.

Krabbe disease: this is a rare incurable genetic lysosomal storage disease that causes severe neurodegeneration and severe developmental delays at the start of life. A 1999 paper disclosed that Stanley Jacob had developed and implemented an oral DMSO protocol for this condition but it is unclear if it was successful.

Tourette syndrome: in disease-model rats, Vitamin D^⬖ (1.0 μg/kg/day) in DMSO significantly decreased locomotor behaviors (0.43–0.69 vs 0.92–1.33 scores) and reversed the decrease in striatal dopamine content (along with causing an expected vitamin D^⬖ induced increase in serum calcium).

Note: a lot of people have asked if DMSO could help muscular dystrophy. The only data I’ve found is a study where (-)-epicatechin^⬖ in DMSO reduced dystrophic fiber pathology and promoted muscle regeneration in MD mice, but did not address the underlying disease mechanism — which unfortunately tells you very little.

A New Model of Neurology

Through reading this, my hope is that it has not only given you hope for treating many “incurable” neurological conditions, but also that you share my fascination in the new perspective it provides on what ultimately causes many of these diseases.

In turn, while this article was lengthy, you may have noticed many neurological conditions were omitted. This was due to the length of this article (due to all its links) crashing Substack and the article hence needing to split into multiple parts. So, in addition to previous articles I’ve written which show DMSO provides similar neurological benefits to each of the sensory organs (e.g., particularly the eyes and ears), in the upcoming parts of this series I will cover the remarkable effects DMSO has provided for:

•Spinal issues (e.g., paralysis, spinal cord injuries, disc issues, radiculopathies, and arachnoiditis).

•Peripheral nerve issues (e.g., nerve regeneration, palsies, neuropathies and neuropathic pain).

•Strokes, brain bleeds, traumatic brain injuries, and concussions.

In the final part of this article, I will share practical guidance for properly obtaining each grade of DMSO (including IV DMSO), provide specific protocols for the neurological conditions discussed here — including Parkinson’s, Alzheimer’s, strokes, chronic stress, neuropathies, cognitive impairment, brain fog, anesthesia toxicity, and neurodevelopmental disorders — along with highlighting complementary natural therapies we have found to further benefit these conditions.”

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•As more and more issues emerged with the vaccine, rather than acknowledge them or change course, the government, media and medical press chose to hide all of it to protect the vaccine program.

•Because of this, there has been a profound loss of trust in the medical system never seen before in history, and as extensive polling shows, vaccines have gone from being something almost all of the public blindly supports to something a majority of Americans are skeptical of.

•Senator Johnson, who since 2020 has been relentlessly fighting for COVID transparency and accountability recently obtained records proving beyond a shadow of a doubt that the CDC and FDA were aware the COVID vaccines were causing myocarditis and strokes but nonetheless concealed this from the public to continue pushing vaccines.

•This article will present exactly what Johnson uncovered, the extensive polling data which shows the unprecedented loss of trust in the medical system and explore how we can best make use of the unique moment we have arrived at.

The increasing freedom of information enabled by an uncensored media is gradually waking people up to the many harmful things being done to them on a daily basis. That uncomfortable reality is traumatic to come to terms with, which in turn leads many to want to understand why it’s happening.

In my own case, whenever I observe something pernicious, my question is always whether the events were:

• A naturally emergent phenomenon resulting from human nature and the specific circumstances at play — one that likely would have occurred regardless of who was involved.

• A coordinated plot by a group of bad actors (e.g., powerful sociopaths) who deliberately harmed the world for their own benefit.

The essential problem is that in most cases, a strong case can be made for either interpretation, so which one you settle on is typically a product of what your mind is primed to focus on. In my own case, I seriously consider both — I’ve spent decades reading about the people behind the scenes who pull the strings, and I’ve lost count of how many malevolent things I’ve seen enacted in a coordinated, systematic manner over years if not decades. But as time has gone on, I’ve leaned toward the naturally emergent perspective because:

• I keep seeing the same processes play out across so many different spheres.

• In many cases, bad actors don’t directly orchestrate things so much as amplify existing dysfunctional dynamics to move things in their preferred direction.

• Putting all your focus on one bad actor rarely proves productive. Those fights drag out for years and rarely go anywhere (e.g., we are still waiting for Fauci to be brought to justice for COVID), and intensely focusing on a single person just creates a niche for other bad actors to do the same thing. In contrast, focusing on the core dynamics that allow evil to arise provides a much more lasting immunity against it.

For example, all things considered, the COVID-19 health freedom movement has been incredibly successful — accomplishing much more than I ever expected — but it has still fallen short of many of its key goals. Much of this stems from continual fracturing and infighting that has prevented MAHA from presenting a unified front to lobby for systematic policy changes. Partly because of this, RFK Jr. (who is still accomplishing a lot) has been unable to implement many of the most contested MAHA health policies the federal apparatus is doing everything it can to undermine.

As a result, many commentators have convinced their audiences that MAHA’s leadership sold out, while others are convinced the pharmaceutical industry has intentionally planted divisive voices to accelerate fractures — along with a smaller minority who believe pharma is using tools like bots to amplify divisive voices, incentivizing them through internet engagement rather than direct payments.

While I recognize it’s possible there are “controlled opposition” figures in the movement — particularly since both I and associates have periodically seen obvious plants inserted into much smaller movements we worked with — I believe the natural emergence hypothesis (likely amplified by bots and mainstream media) is far more probable because:

• I’ve seen the exact same dynamics in many smaller groups I’ve been involved with — disruptive members trying to defame or “controlled opposition” a leader I knew with certainty was completely committed to the cause. Ultimately, much of this resembles the gossip and reputational violence I dealt with from mean girls in high school, which I was then shocked to encounter again as a medical student and resident at multiple hospitals.

• In any movement, there will always be a spectrum from people deeply committed to the cause to those who join out of convenience or self-interest and are motivated to prioritize themselves over the group. No one is perfect, so even the most committed people, once put under a microscope, have potentially questionable traits. And individuals who have been marginalized their entire lives — who learned they can’t trust people when opposing the system — will be prone to traumatic, overreactive responses that can easily be misinterpreted as sinister.

Because of all this, my fear from the start was that the same fractures I’d seen everywhere else would appear in the COVID-19 health freedom movement. My goal has been to serve as a positive counterweight: promoting people with integrity who I felt were doing good work, working to create a standard others would be incentivized to replicate (e.g., factual, clear positions strongly supported by evidence), advocating for unity and compassion, and — when it was necessary to speak out, regardless of my frustration — attacking ideas rather than people.

The Nature of Government

In virtually every era, a large portion of the population concludes their government is evil, and in many cases, political schools emerge arguing that government itself, rather than who specifically occupies it, is inherently evil.

I personally consider this a dynamic subject. Strong arguments exist for the “evil” perspective: bad leaders routinely emerge who poison entire governmental systems, and governments frequently adopt the same tyrannical behaviors. But at the same time, my own experience interacting with government workers is that while there are some manipulative sociopaths in the hierarchy, many members of government genuinely want to do the right thing and try hard to do it.

My essential conclusion has been that the nature of government’s role (being responsible for solving problems, having only imperfect solutions available, and then having to force the population into accepting policies with downsides many don’t want) inevitably leads to increasing overreach. This is compounded by the fact that humans never want to admit they or their institutions are wrong, so there is always a tendency to double down on bad policies rather than admit fault and correct them.

This problem gets worse as governments grow. Larger and larger factions emerge that prioritize their own interests over the populace. And humans have a finite number of people they can be present to and hold real empathy toward, so once officials become responsible for thousands or millions of distant people, those they serve transform from being people into intellectual constructs. At that point, it becomes possible to mentally rationalize enacting abhorrent policies upon them that you would never inflict on your neighbor.

Since the sociopathic minority of society will always be drawn to positions of power, and then be favored for ascending the hierarchy, because they will do far more ruthless things to get ahead, I believe one of the best solutions humanity has developed for governance is the American Constitution’s emphasis on absolute individual rights and a system of checks and balances, where different parties are forced to compete against each other and hence not stray too far from policies the public can stomach, as otherwise they lose power to another group.

Governments and Vaccines

Much in the same way people act the same way in every era, governments do as well, and as such, if you can observe how a previous situation similar to the one at hand was handled, you can reasonably predict what will happen in the present.

In the case of vaccines, ever since the first ones in the days of smallpox, a very similar pattern has repeatedly emerged:

1. Governments will enthusiastically embrace an imperfect or rushed vaccine to address a public health issue or crisis.
2. The unproven vaccine will initially be met with great fanfare and promise.
3. The vaccine will have safety and efficacy issues which make the public resistant to it.
4. The government (and often medical profession) will gaslight the public by trying to cover up those objections and continue holding to the rosy picture they initially promised despite having extensive evidence the vaccine actually has serious safety issues (or does not work).
5. The public will grow increasingly opposed to the vaccines.
6. The government will eventually begin blaming the failures of the vaccine on not enough people vaccinating (or boosting) and institute a series of increasingly aggressive mandates.
7. If the vaccine is harmful enough, public protest will eventually shift the government and overturn the mandates. If this happens, the incident will then be erased from public memory and very few will ever realize there was a serious issue with some of the previous vaccines.

So, starting with smallpox, a key goal with this newsletter has been to show how again and again that happens in the hope we can break this dysfunctional cycle.

Note: presently I believe the government’s irrational obsession with vaccines results from the fact mass distributing vaccines and forcing people to take them is something that governments (wishing to exercise their power) can easily do, whereas addressing the actual causes of disease is much more challenging with a top-down approach (especially if powerful interests are poisoning the population for profit). Alternatively, a good case can be made that a malignant religion has formed around vaccines and infected large segments of the professional and ruling class.

Because of all of this, when the COVID vaccines came out, especially given that the marketing and propaganda push for them was much more aggressive than anything I’d seen in my lifetime I assumed:

•The benefits of the vaccines were being overstated, the harms understated, and there was likely significant fraud in the clinical trials that produced the “95% effective” claim (much of which was apparent if you read Pfizer’s December 2020 clinical trial report with a careful eye and was later proven by numerous trial whistleblowers).

•Serious issues with the vaccine, particularly long-term autoimmune, fertility and cancer ones would emerge (as leaked regulatory documents in December 2020 showed Pfizer was exempted for testing for these despite them being the greatest concerns with the vaccine), but by the time these issues were partially acknowledged, it would be too late to do anything.

•Rather than admit these issues, the government would cover them up, and at most would make a few token admissions of vaccine harm to make the public believe the core products were safe (e.g., after the FDA briefly paused the non-mRNA vaccine because it was linked to six cases of a very rare blood clot, many doctors were convinced vaccine safety monitoring was excessively strict and hence that the government not acknowledging any safety issues with the mRNA vaccines proved none existed).

•A series of increasingly aggressive policies would be taken to get as many people as possible to vaccinate, with a more aggressive approach being taken once the maximum uptake from the previous approach had been reached (as more extreme mandates could only be enacted once a sufficient portion of the population was vaccinated). This is essentially why they went from a scarcity model to increasingly sleazy financial incentives to soft mandates to hard mandates (e.g., being fired if you didn’t vaccinate).

Nonetheless, I was still astounded at how high the injury rate was once the vaccine came out (every day I had multiple patients who came in for reactions to the vaccine) and within a month, I had people I knew from around the country contacting me to ask if the vaccine could cause heart attacks, blood clots or strokes (as this had just happened to someone they knew). Given this, I was a bit surprised the government still committed to completely covering it up (as the scale of it was beyond what the government could cover up, so committing to doing so would be guaranteed to break public’s trust in the government).

Nonetheless, they did, and to this day still continue to lie.

Did the Government Lie?

One of the major reasons why pernicious gossip and reputational violence often sticks is because when people do not fully understand a situation, they will default to filling in the blanks by assuming they know someone else’s intentions and then using that assumption to explain everything which has happened. Sometimes those assumptions are correct, but in many other cases they are not (e.g., some of the caricatures I’ve seen made of people in this movement I know quite well have almost nothing to do with who these people actually are).

In law, a much higher standard applies: in civil defamation cases involving public figures or matters of public concern, it is quite difficult to hold someone liable unless there is strong evidence that they knew their statement was false at the time or acted with reckless disregard for the truth (which must be shown by clear and convincing evidence, which often requires near ironclad proof of the speaker’s state of mind). Likewise, for criminal perjury, prosecutors must prove beyond a reasonable doubt that the person knowingly and willfully made a false statement under oath about a material matter (rather than just being careless or not knowing their statement was false).

Remarkably however, we have gradually met that (nearly impossible) standard with the COVID vaccines. For example, Anthony Fauci, to dispel the notion COVID-19 leaked from a lab (which he funded), at the start of the pandemic repeatedly cited an expert paper that stated COVID-19 could have only emerged naturally. Documents provided by the House Oversight Committee subsequently revealed Fauci pushed for that study, was heavily involved in its drafting, and that he worked with the NIH director to quash “lab leak rumors” once the initial paper failed to. Likewise, documents and Slack leaks showed that the authors of the paper seriously doubted the natural origin hypothesis they published.^1,2,3

Note: while it is not possible to read minds, my experience has been that “past actions are the best predictor of future behavior,” so much in the same way governments or societies tend to repeatedly act the same way, if an individual has a history of acting in a specific dishonest or unscrupulous manner (e.g., Fauci always lies), you can reasonably assume they will continue to do so, and I cannot count how many times this has saved me (e.g., if someone I just met did something sketchy out of the blue, I immediately distanced myself from them and in a few cases, learned of them subsequently harming someone else when they were alone together in private or financially in some type of business arrangement).

With the COVID vaccines, while the focus was typically on the figurehead Anthony Fauci, when I went through everything, the issues kept on coming back to Peter Marks, the director of the FDA’s center for biologics (which oversees the vaccine division).

Briefly:
•Within the FDA Peter Marks continually pushed for expediting COVID vaccine approvals (that were necessary for White House political goals), even as the FDA’s top vaccine experts (who strongly supported vaccination) said the timeline was too fast and too many corners were being cut—eventually resulting in Marks pushing them out and the approvals occurring.

•Throughout the COVID vaccine process, Marks insisted the vaccines were rigorously tested, no corners were being cut, and there was no evidence the vaccines had any safety issues.

•In private, he continually met with vaccine injured patients over vaccine safety concerns but would always find some type of way to deflect the validity of the evidence presented (e.g., refuse to discuss it, say the FDA needed more time to conduct an analysis to find a signal, blame the injuries on something else) and most importantly, despite many requests, would never define what would constitute acceptable proof of vaccine harm.

•As he stonewalled the vaccine injured patients he continually insisted he cared about them and was deeply empathetic for their suffering (a common manipulative tactic dishonest people use). Remarkably, as he was doing this, he attended a vaccine conference where he publicly stated “It’s crazy that they don’t get how great vaccines are…I am past trying to argue with people who think that vaccines are not safe.”

All of this, in turn, is summarized in much more detail here:

Note: recently Marks left the agency and took up a lucrative executive position for a pharmaceutical company, following in the footsteps of many before him (e.g., FDA directors from Trump’s first term received lucrative positions at Pfizer and Moderna, while the CDC director who pushed Merck’s Gardasil through and buried its tsunami of injuries got a similar compensation from Merck).

The Permanent Subcommittee on Investigations (PSI)

The PSI is one of Congress’s most powerful investigative bodies, possessing broad authority to investigate government operations, waste, fraud, and a wide range of other matters, and it can issue subpoenas for documents and records — including certain federal materials — that are often difficult or impossible for other committees or private parties to obtain.

By great luck, Senator Ron Johnson (who has been the first Senator in history to extensively advocate for vaccine injured patients) after serving for 14 years on the PSI’s parent committee, was selected to become chair of the PSI in January 2025.

As Johnson had continually fought for COVID transparency since November 2020 (routinely holding hearings on early treatment and sending more than 70 oversight letters to the FDA, CDC, and HHS), once he assumed PSI chairmanship, he began directly subpoenaing the agencies and (as they could no longer legally ignore him) and gradually collected documentation that eventually met the threshold needed to show that these agencies, indeed, lied (a lot) about COVID-19 vaccine safety.

On May 21, 2025, the PSI released a 55-page report (based on more than 2,400 pages of subpoenaed HHS records) and held its first hearing on the topic where they showed on:

• February 28, 2021 — The Israeli Ministry of Health notified CDC officials of “a large number of reports” of myocarditis, “particularly in young people,” following the Pfizer vaccine.

• Mid-April 2021 — CDC officials internally discussed a “safety signal” for myocarditis linked to mRNA vaccines based on Israeli and U.S. Department of Defense data, but did not immediately issue a public warning.

• May 17–27, 2021 — CDC and FDA officials explicitly acknowledged a myocarditis/pericarditis signal (especially in males ages 16–17 and 18–24), including internal confirmation that VAERS was signaling the issue in those age groups. They drafted a formal Health Alert Network (HAN) message but ultimately decided against issuing it. Instead, they posted milder “clinical considerations” on the CDC website (which Marks still tried to block). White House talking points distributed to top officials (including CDC Director Rochelle Walensky and Anthony Fauci) downplayed the risk, and CDC shared draft HAN updates with Pfizer and Moderna representatives before informing the public.

Note: in 2022, Aaron Siri was also able to FOIA the CDC’s V-Safe data and show that they were covering up the harm demonstrated in that dataset (which is somewhat ironic, as V-safe was made to address the short comings of VAERS and provide the required monitoring for the expedited COVID-19 vaccines—but was dismissed once it showed inconvenient data).

Then, after proving the FDA and CDC knew the vaccine was causing myocarditis but instead went to great lengths to cover it up (killing many Americans), on March 23, 2026, Johnson released nearly 2,000 pages of records and a detailed letter to HHS Secretary Robert F. Kennedy, Jr. showing they also knew that the (“clot shot”) was causing strokes. Specifically:

• Shortly after the FDA authorized the Pfizer-BioNTech COVID-19 bivalent booster on August 31, 2022, the CDC’s Vaccine Safety Datalink (VSD) began detecting a statistically significant safety signal for ischemic stroke among individuals age 65 and older as early as November 27, 2022. This signal persisted across multiple weekly analyses in December 2022 and January 2023.

• Despite the repeated detection of the signal in VSD and supporting findings in VAERS (including dozens of reported ischemic stroke cases and several associated deaths), FDA and CDC officials did not issue a formal HAN warning or recommend any changes in vaccination guidance for this high-risk age group.

• Instead, internal records reveal that officials continued to emphasize the push for booster uptake among seniors while quietly launching multiple investigations, including a contractor-led “Stroke Project” to review cases. Draft communications plans in early January 2023—which appeared to include edits from the Biden White House—softened the description of the signal (changing language from “moderately elevated” to “slightly elevated”).

• On January 13, 2023, the agencies posted a brief informal notice on the FDA website acknowledging the signal but explicitly stating “no change is recommended in COVID-19 vaccination practice.” Even as VAERS reports of ischemic stroke climbed (reaching 226 cases by early February 2023) and empirical Bayesian data mining analyses in February and March 2023 also flagged a statistically significant signal, the agencies maintained their public recommendations.

• Evaluations of the signal, including follow-up VSD studies, continued into 2024 and at least through September 2025, yet booster guidance for adults 65 and older remained unchanged.

While much could be said about this, I just want to highlight one of the least appreciated tragedies of the COVID-19 vaccine roll-out. Dementia is caused by poor circulation to the brain, inflammation, and brain cells being shocked into a state of partial death (discussed in detail here)—all of which the COVID vaccines excel at causing. Because of this, I have come across so many cases of a relative in a nursing home showing signs of a stroke after a vaccine and then rapidly progressing into a fatal dementia (which the facility wrote off as “it just being Alzheimer’s”) and seen far more cases of accelerated cognitive impairment in all adult age brackets (which extensive data supports and we’ve all found to be one of the most common symptom of COVID vaccine injuries). This makes it particularly pernicious this side effect was known to disproportionately affect the elderly, as they are both the most vulnerable to it, and often the least able to advocate for themselves.

Note: proving something later causes cancer is much more difficult than showing it rapidly causes a heart attack or stroke (and also much less politically viable due to the outrage that will be generated by large swathes of the population being worried they are going to die from a cancer those they trusted gave them). Because of this, I am not sure how long it will take for the cancer link to the COVID vaccines to ever be acknowledged (or if it will even ever happen), which is tremendously unfortunate given the magnitude of this problem.

Loss of Trust

One of the key things I still do not understand about the COVID-19 vaccine program was why they continued to aggressively mandate the vaccine even as widespread opposition was emerging to the vaccine due to clear issue with both its safety and efficacy. As such, what could be gained (moderate increases in COVID-19 vaccine sales) would be counteracted by a far more costly widespread loss of trust in the medical system. Since a massive investment had been made over decades to create that trust (as it drives medical sales), it hence did not make sense the entire industry (which prioritized profit over everything else) would kill their golden goose to give Pfizer a sales bump.
Note: I hence believe the continued push for the vaccine either reflected a widespread inability of people in power to adapt and follow a new approach once the current one they’d committed to made no sense, or that some type of much larger benefit than inflating a few years of vaccine sales existed for injecting the entire population (e.g., to somehow alter the entire population, to eliminate a control group and hence the widespread evidence of vaccine injury, or to open up massive mRNA gene therapy markets in the future). Ultimately however, while I have many theories, I have no way to know why this policy was followed.

Because of this, we indeed saw a massive loss of trust in the medical system, health authorities, hospitals, doctors and vaccines on a completely different scale from anything I’ve witnessed in my lifetime. Initially, the media was able to hide this, but gradually, individuals such as Charlie Kirk and independent polling were able to expose how the public actually felt and just how many people had been harmed by these products:

Note: this event coincided with virtually every health authority around the world concealing their data indicating widespread harm from the vaccines and medical journals in lockstep refusing to publish and anything indicating vaccine harm.

Vaccine Polling

Following this polls began emerging which demonstrated how much concerned the public was about the COVID vaccines:

•Steve Kirsch and the Vaccine Safety Research Foundation hired polling firms to directly survey the public. In 2022, of those vaccinated:

•In 2023, Professor Mark Skidmore hired Dynata to survey 2,840 respondents and found 15% of vaccinated had a vaccine injury (13% of which were severe), and 22% knew someone with a severe vaccine injury. His taboo paper was retracted, and he was subject to an ethics investigation that eventually cleared him.

•In 2024, a Kirsch-commissioned poll found 12.5–20.3% of vaccinated respondents were injured, with two-thirds categorizing their injury as “serious” or “very serious.” Despite reporting higher injury rates, Democrat respondents were far more likely to believe the vaccine was safe and effective (83.62%) than Republicans (44.49%) or Independents (51.81%).

As no one wanted to touch this issue, only one polling organization (Rasmussen Reports) independently investigated this. For American adults, they found:

• July 2021: 32% believed public health officials were lying about vaccine safety.

• December 2022: 34% of vaccinated reported minor side effects; 7% reported major side effects.

• January 2023: 49% believed vaccine side effects have likely caused a significant number of unexplained deaths; 28% personally knew someone whose death may have been caused by the vaccine.

• January 2023: 57% wanted Congress to investigate how the CDC handled assessing vaccine safety.

• March 2023: 11% believed a member of their household died from COVID-19, while 10% believed a member of their household died from a side effect of the vaccine.

• September 2023: 47% did not believe the vaccines were safe and 34% did not believe they were effective. Democrats were less likely to believe the vaccines were unsafe (14% D vs. 51% R) or ineffective (17% D vs. 57% R).

• November 2023: 24% personally knew someone they believed died from a COVID vaccine; 69% of those would likely join a class action lawsuit against pharmaceutical companies.

• January 2024: 53% believe vaccine side effects have likely caused a significant number of unexplained deaths and 24% personally knew someone whose death may have been caused by COVID-19 vaccines.

• September 2024: 55% believe vaccine side effects have likely caused a significant number of unexplained deaths—including 30% who say it’s very likely.

• November 2025: 26% reported minor side effects; 10% reported major side effects; 46% believe vaccines have caused a significant number of unexplained deaths.

In short, the data shows you aren’t crazy—the majority of people are seeing exactly the same thing you are. One of the best data compilations I’ve seen that puts this into perspective was a March 2023 estimate Ed Dowd produced from available data sources. This deliberately conservative estimate showed:

This shift, in turn, was also reflected in public attitudes about the medical industry:

• A JAMA survey of 443,455 American adults found trust in physicians and hospitals decreased substantially in every sociodemographic group, from 71.5% in April 2020 to 40.1% in January 2024.

• A recurring Gallup Poll found trust in the pharmaceutical industry has greatly declined:

In parallel, support for vaccine mandates significantly decreased due to the COVID response:

In November 2025, Pew found this loss of trust was much more common in Republican voters:

A parallel Pew poll found only 57% had high confidence in childhood vaccine effectiveness (45% R vs. 71% D), 44% were confident in their safety testing (29% R vs. 63% D), and only 41% fully trusted the CDC vaccine schedule (27% R vs. 58% D).²⁰ Similar results were found by a KFF tracking poll:

Along with one this year:

Note: this 2026 poll also found a loss of trust in the MMR, COVID, and Flu vaccines.

Finally, to prepare for the midterms, MAHA allies commissioned three polls which all (in accordance with the previous polls) found a supermajority of voters support health and medical freedom.

Here’s what the first, from John Zogby Strategies, found about vaccines:

The second, of 1,000 likely voters by Rosetta Stone, found similar results:

This poll found support for the MAHA agenda (59.1%) was higher than for MAGA (45.8%) or America First (54.4%), but approval of what Trump and Kennedy are actually doing on children’s health is much lower (44.1%).

This indicates that MAHA is the party’s strongest midterm issue but what’s being done isn’t being effectively communicated, or that RFK’s base feels disappointed he hasn’t accomplished more on vaccines.

Finally, a February 2026 poll from FLA found MAHA was the most effective issue to flip someone’s vote—a key bloc chose the generic Democrat by 5:1, but once given a Republican focused on removing toxins from food and reducing overmedicating children, chose the Republican nearly 2:1. Candidates championing reducing the vaccine schedule also became much more favorable to voters:

Additionally, that poll showed the majority of voters have significant concerns over the current vaccine program.

The key thread all these polls share is that their results are completely unprecedented. That is essentially why after I saw how massive the results of the first few were, I was certain this would be an issue that would transform our society and that regardless of what the talking heads said, no degree of propaganda would be able to cover it up.

Rebuilding Trust

During RFK’s Senate hearings (along with those of his appointees), one of the few points Senators from both parties agreed upon was that there has been a massive loss of trust by the public in science and medicine and that this is catastrophic for the entire society (which is a valid point). However, their solutions differed:

On the Democrat end, their primary concern was to ensure the nominee attested to fully believing in vaccines, and at times explicitly stated the solution to this loss of trust was to have RFK emphatically endorse vaccines so that his followers would as well.

In contrast, RFK and many of his Republican supporters stated the only way trust could be regained in the Federal Health Authorities was with radical transparency so the public could trust the claims made on the basis of what the data actually showed rather than blindly believing in an expert (e.g., despite going to great lengths to obtain it, we were forbidden from getting the government’s vaccine safety data and instead just told to trust their analyses the COVID vaccines were “safe).

I never forgot this exchange, as I was quite surprised RFK’s opposition could be so out of touch with the current political climate that they would believe RFK suddenly pushing vaccines would make the public regain trust in vaccines and science. Nonetheless, they’ve continued to repeat their old tactics (e.g., censorship, lobbying, media spearheaded public relations campaigns) and hope that the COVID-19 vaccine problem will just “go away.”

Instead, the loss of trust continues to accelerate. For example, this week:

•Politico released an article titled: “More Americans doubt vaccine safety than trust it, POLITICO Poll finds—Health Secretary Robert F. Kennedy Jr.’s views are commonplace across the land.”

•A Tweet Elon Musk shared on this topic garnered 60 million views:

•Children’s Health Defense unearthed an April panel which showed the vaccine industry is recognizing the new reality too.

During the hour-long conversation, Clinton and the panelists criticized the growing number of parents and teens who are starting to question the safety of vaccines. They blamed the trend on increased access to what they characterized as online “misinformation” — and on organizations like Children’s Health Defense (CHD).

“What’s different today … is that people have access to a lot more information,” said Dr. Margot Savoy, chief medical officer of the American Academy of Family Physicians. “The part that makes me nervous is that, more and more, we’re getting into this odd space where people are feeling a little more polarized.”

Conclusion

For most of my life, vaccines have been a “90-10” issue, in that most people I met unquestionably supported them and it was only if they directly knew someone seriously injured by one that they doubted their safety. This makes sense, as the arguments against them are so strong, there really isn’t a way to defend how they are currently used, and as such, the only option is to prohibit the debate entirely and have everyone who hears questioning of them assume there can’t be any rational basis to criticisms of vaccines since pretty much everyone believes in them.

Now however, due to the excessive greed we witnessed during COVID-19 and the incredible luck that the right people appeared in the right place at the right time (Senator Johnson is just one of many), that paradigm has been shattered, and people who doubt vaccines are the majority.

This is ultimately very important for three reasons:

•First, the media and lobbyists have widely circulated a biased poll claiming eight times as many voters strongly support vaccines as question them (effectively making it a "90-10" issue) and that voters are overwhelmingly opposed to changing the vaccine schedule. This in turn was used to convince the Trump administration to make Trump and RFK back off from discussing vaccines until after the midterms—even though the coalition which elected him in 2024 supported safety reforms on vaccines and every other poll which has been conducted shows there is widespread support for vaccine safety reforms.

•Second, because the public is now open to the idea vaccines aren’t completely safe, there is a huge window for conversations to be had on this topic (e.g., it’s mind blowing to me that whenever I bring the vaccine topic up now, regardless of where I am in the country, rather than facing a hostile audience I have to very carefully convince, people will immediately voice their support of my position or that they know they were lied to about the COVID vaccines). As such, the window now exists through simple (compassionate) conversations to shift the public consciousness on the vaccine issue, and hopefully do so to the point regardless of which bad actor assumes power, it simply will not be possible to mandate these products.

•Third, every movement that creates social change goes through distinct phases. Initially, when the movement represents only a tiny minority, forward momentum often only occurs from relentless (and often very antagonistic) individuals who shock people and break the gates open for a wider conversation. However, once you become a mainstream viewpoint, creating a wider permanent shift requires presenting a levelheaded, credible, unified front. We have now reached that point, and our strategy needs to adapt accordingly.

I honestly never thought that this point would come, and from having witnessed decades of vaccine injuries be swept under the rug regardless of what we did, this new reality is still a bit surreal for me. For the first time in history, not only we have clear and unambiguous proof our government lied to us to protect the vaccine program, but also a public which is highly receptive to knowing that.

So many people before us have fought for more than 200 years to bring us to the point we are now, and we owe it to them to finish what they started and prevent this cycle from continuing. As I discussed at the start of this article, I've spent a long time considering whether the harms we face stem from coordinated sociopathy or naturally emergent dynamics — and the answer matters enormously right now, because it determines what "finishing" actually looks like. If this is purely a sociopathy problem, the solution is to punish the specific bad actors and move on — but history shows that just creates a niche for the next ones to do the same thing, which is exactly why this cycle has repeated for over two centuries with completely different people each time. If instead this is a structural problem that sociopaths exploit and amplify but do not create, then the real solution is what we are now finally in a position to build: a public conscious enough and a system transparent enough that the dynamic itself cannot repeat, regardless of who holds power.

That, in short, is why I keep giving my full effort to this newsletter despite all the energy and time it takes, as for my whole life I wished something could be done to fix this dysfunctional paradigm, so now that the window is there, I know in my heart I need to do all that I can (and hopefully be able to sustain it until 2028 and the end of RFK’s tenure). I know many of you are too, and I sincerely thank you both for supporting me in my role (which makes what I do possible), and for what each of you is doing in your own community to move things forward.

Lastly as a quick update on the DMSO neurology article; it is essentially done, but I decided not to release it until next weekend so I could ensure it’s quality was where I wanted it to be when it was released (due to how impactful the information in it is). DMSO has incredible utility in neurology, and I want to do all I can to help it see the light of day so all those who can benefit from it do.

To learn how other readers have benefitted from this publication and the community it has created, their feedback can be viewed here. Additionally, an index of all the articles published in the Forgotten Side of Medicine can be viewed here.

Since there are now over 336,000 readers here, it’s no longer feasible for me to do that and still have the time to write. Because of this, I decided the best solution was to have monthly open threads where people could ask whatever they wanted on any topic (e.g., any lingering questions from the previous months) and I would make a point to always reply to them.

Alongside these open threads, I like to highlight a topic that I believe is worth exploring, even if it doesn’t warrant a full article on its own. This month, I’m focusing on the often-overlooked wonders of coconuts as I often reflect on the small things I take for granted and how different life would be without them—and coconuts frequently make that list.

Note: one of the things that is extremely frustrating about nutritional guidelines is that they always tell you what you should not eat rather than what you should. One of the wonderful things about coconuts is how much easier having them be a dietary staple makes the rest of your diet.

Lastly, as a quick update on the DMSO project. Due to reader request (and very compelling testimonials I’ve received), the first article I am releasing is DMSO’s uses in neurology. In the process of doing that, I realized this was a very challenging topic to start with (as there are so many neurology articles in the master document I’ve compiled), so it took about a week longer than I expected to extract and sort all of them, and rather than do a single article, it needs to be split into three parts (neurodegenerative disorders, spinal and nerve issues, and traumatic injuries to the nervous system like strokes).

On one hand I feel bad about this, as despite my absolute best efforts to prioritize getting this done as quickly as possible without cutting corners, I am now about a month behind where I’d hoped to be. However, I am also excited to finally be at my favorite part of this process (synthesizing the data and unraveling the fascinating insights within it) and provided nothing too difficult comes up during the upcoming work week, I hope to have the first installment (neurodegenerative, autoimmune and psychiatric conditions plus developmental disability) out this Saturday. This has been a rough hump to get over (finding the time to identify every medically relevant DMSO study, then summarize and sort them), but once it’s done, I know it will help a lot of people, and I sincerely thank you for your continued support and patience as I work on it.

Cooking Oils

As the years have gone by, there has been increasing awareness that seed oils (specifically their omega 6 fats) are not good for us, but unfortunately, even if we want to avoid them they are in almost every processed food (e.g., infant formula, due to outdated science from the 1960s is required to contain large amounts of seed oils). This touches upon a longstanding observation I’ve made—if something toxic is on the market place, in most cases, regardless of how much the public protests against its use, normally only way it ever gets phased out is if a less toxic substitute is found for it

Note: examples include antibiotics replacing highly dangerous antiserums, ultrasounds replacing routine prenatal x-rays,the introduction of catalytic converters making lead no longer work in gasoline or the 1986 Vaccine Injury Act forcing the development of the less toxic DTaP vaccine to replace DTwP).

As such, I’ve put a lot of thought into which oils could replace the high omega 6 oils we routinely use (e.g., soy oil). If we look at it from a standpoint of omega 6 content and omega 3 content, the following options exist:

While a case can be made for a few of these, as the chart shows, coconut oil is arguably the best option, particularly since it also has a high smoke point (which means coconut oil, particularly refined coconut oil, can be safely used for frying).
Note: another option for frying is to bypass needing a liquid with a boiling point above that of water entirely with an air fryer.

Likewise, coconut oil (when prepared correctly) can be used as a substitute for many of the common oils (e.g., canola or soybean) in around 50-60% of processed foods and I’ve found most of the time a coconut oil containing version of a common product (e.g., chocolate or potato chips) can be found that both tastes and feels much better than those made with standard processed oils.
Note: there are a variety of other issues with the commonly used oils to (e.g., by not being saturated they are often rancid and they frequently contain a significant number of harmful chemicals).

Lastly, there are many non-culinary uses for coconut oil. For example, people, particularly those sensitive to chemicals, often find coconut oil is an excellent lubricant, skin care or hair care product (or carrier for DMSO cosmetics), I’ve heard a few reports of it being an excellent tick repellant (as ticks will not go onto skin covered with coconut oil) and I’ve heard numerous stories over the years of Alzheimer’s significantly improving from the consumption of coconut oil derived MCTs (for which which has been corroberated by a clinical trial—where it actually performed better than any of the costly therapies on the market).

Note: because there is a huge need to incentivize transitioning to healthier oils, RFK Jr. has been publicly promoting Steak and Shake’s decision to transition from using vegetable oils to beef tallow so that the market inertia for this shift can begin to form.

The Great Cholesterol Scam

Many (myself included) believe one of the most harmful nutritional myths is the notion that saturated fats and cholesterol cause heart disease and must be avoided.

As best as I can tell, this myth originated with in the 1960s from the sugar industry paying for fabricated data that showed animal fats rather than sugar were responsible for the increase in heart disease we were seeing, after which point vegetable oil producers became invested in the mythology (since it allowed them to displace animal fats).

The medical community tried to get on the bandwagon as well, but could not for decades as no medication could reliably reduce cholesterol. However, once statins (which could reliably lower cholesterol), were discovered (with the first one hitting the market in 1987) one of the largest drug markets in history formed (now worth 25 billion dollars a year in America alone). This incentivized funding a lot of research that argued saturated fats and cholesterol were bad for you and thereby cemented this dogma throughout medicine.
Note: A strong case can be made the primary factors responsible for the decline in heart disease we saw were removing lead from gasoline and smoking reduction (and conversely that the increase was in part due to water chlorination). However, much in the same way vaccinators took credit for modern sanitation reducing infectious disease, the cholesterol industry claimed credit for declining heart disease and now blames ongoing cases (which remain the leading cause of death) on too few people taking statins or blood pressure pills, rather than on the neglect of actual treatments for the conditions (much in the same way the persistence of COVID or the flu is always blamed on not enough people vaccinating).

All of this has been quite problematic for a few different reasons.

First, the premise behind it is wrong. Cholesterol does not clog arteries, rather it is the body’s way of repairing damage to the blood vessel lining.

Note: I believe the key reason this myth persists because it is easy to visualize (with disgust) arteries being clogged by thick fats in a manner equivalent to a drain pipe being clogged.

Second, the evidence used to argue cholesterol is bad for you is very weak (e.g., many studies show cholesterol does not cause heart disease), whereas multiple studies have shown lowering cholesterol or replacing saturated fats with vegetable oils greatly increases your risk of dying (e.g., many studies have found a roughly 25% increase in death).

Third, statins injure roughly 20% of users, with many experiencing severe side effects (which quickly adds up given that over a quarter of US adults take statins despite there being no evidence they extend life).
Note: the great statin scam and the forgotten ways to treat heart disease is discussed here, while a similar scam with blood pressure (and its forgotten treatments) is discussed here.

Fourth, this myth caused saturated fats to be replaced with vegetable oils (which cause many different chronic health issues).

Note: in the early 1980s, coconuts were consumed throughout Asia whereas processed vegetable oils (e.g., soy) were consumed in heavy quantities throughout India. At that time, one natural medicine pioneer (Bernard Jensen) widely promoted iridology, a diagnostic system where chronic health issues could be detected through changes in the eyes. He taught that a “scurf” ring being present around the iris correlated with fluid stagnation throughout the body (e.g., in the circulation) and retained toxicity and argued that vaccinations and overconsumption of bad oils caused this ring (and the congestion) to develop (and likewise the pioneer of zeta potential noticed vegatable oils would cause intravascular congestion)
Because of this, we paid attention to the eyes of people in place and noticed the scurf rings were vastly more common in India compared to low seed oil parts of Asia. Finally, a strong case can be made that many of the problems vaccines cause result from them creating fluid stagnation (e.g., microclots) throughout the body.

Coconut Production

Because of the media blitz against saturated fats in the 1980s, the demand for coconut oil rapidly decreased, resulting in the price of it also collapsing and many farms that had been made to produce coconuts being abandoned (we remember coconut plantations in the Philippines being burned in 1986 due to this). As such, while the production of coconut oil has slowly increased over the decades, that increase was a tiny fraction of what was seen with the cheaper vegetable oils.

This is highly unfortunate as:

•Coconuts are relatively sustainable to produce (as they do not require many of the toxic pesticides and herbicides other mass produced crops need and their husks have a variety of uses rather than simply being a waste product).

•Many tropical areas of the USA used to be economically sustained by the (environmentally destructive) production of sugarcane stopped producing it due to declining prices and farming subsidies for sugar cane. Because of this, large portions of underutilized, vacant (or never developed) farmland exist in many tropical regions of the United States and its territories. Had coconut production been implemented, it would have offered a way to revive local economies and working class jobs (whereas the trend in areas like Hawaii has instead been to build luxury housing and increase the gap between the rich and poor). Likewise, large areas of Asia were deforested to produce palm oil and now that demand is significantly dropping for it (e.g., due to environmental concerns) there is a huge opportunity to increase global coconut oil production (as those areas are also highly suitable for coconut cultivation).

•The primary reason why highly unhealthy seed oils are used in everything is because the existing subsidy system makes them incredibly cheap to produce. In contrast, were healthy oils like coconut oils to be subsidized our processed food production would not have needed to only revolve around toxic seed oils.
Note: since coconut trees take 6-10 years to begin producing coconuts, this shift would require a longterm investment (e.g., intelligent farming subsidies) to facilitate it (or over a longer term increasing consumer awareness and demand for it).

Coconut Water

In medicine, one of the most useful things hospitals can do for patients is provide them with infusions of specific blood replacement fluids, something I believe works in part due to the infusions restoring the zeta potential of the body (hence improving blood perfusion and reducing micro-clotting).

What many do not know is that coconut water is one of the only naturally occurring substances that has ever successfully been used as an IV fluid:

Another innovative approach regarding intravenous fluid administration also appeared during World War II and renewed attention during the Vietnam War (1955–1978): due to the lack of blood products or adequate alternatives for fluid administration, American soldiers received intravenous infusions of coconut water directly through a filter from the fruit. What sounds curious at first glance might have saved the life of many wounded soldiers: coconuts were omnipresent in Vietnam and the coconut water within an intact nut is sterile.

Furthermore, the composition of coconut water is compatible with human plasma, though it represents rather the intracellular cytoplasm than the extracellular fluid (low sodium and high potassium). In addition, coconut water is hyperosmolar (high glucose level) and acidic (pH 4–6), though the chemical composition depends on the age of the nut. Despite these properties, no adverse effects after the infusion of coconut water have been reported until today. Thus, coconut water is considered “a possible blood substitute for short-term application in emergency situations.” Even today, the Indonesian navy keeps supplies of coconuts for medical interventions and is trained in their usage.

Furthermore, in addition to coconut water matching the composition of the plasma, and containing health-promoting antioxidant phenolics, organic acids, amino acids, and phytohormones (such as cytokinins), it also contains an electrolyte mix somewhat suited for improving zeta potential (e.g., high potassium and low sodium, along with moderate amounts of the negatively charged ions that most improve zeta potential). I believe this is one reason why people often immediately feel better after drinking good quality coconut water.

Note: In tropical and resource-limited settings, sterile young coconut water is used as a natural semen extender for artificial insemination — especially in cattle, buffalo, and pig breeding programs in India, Brazil, Southeast Asia, and parts of Africa. Its near-isotonic composition, high potassium/low sodium profile, natural sugars, mildly acidic pH, and antioxidant content preserve sperm motility and viability for 24–72 hours at room temperature (or longer when chilled) and, when combined with egg yolk and glycerol, serve as an effective cryopreservation medium (as semen needs to be diluted prior to freezing) that is still routinely used for freezing bull, buffalo, and boar semen in many developing-country labs and field stations today, often yielding pregnancy rates comparable to commercial extenders (e.g., see this study and this study where it was combined with DMSO to preserve bull semen)—again illustrating coconut water’s remarkable biocompatibility with mammalian physiology. Likewise, coconut milk is sometimes used to preserve semen (e.g., one study found 5 % methanol with 6 % coconut milk was the optimal cryopreservant for koi semen).

Coconut water, in turn, is one of the most popular popular coconut products and over the years I’ve discovered:

•The quality of coconut water varies greatly from brand to brand (and in turn I will not drink many common brands now).
•Coconut water taken from store bought young coconuts typically tastes better than most packaged coconut water.
•Fresh coconut water from a freshly harvested coconut tastes the best.
•If that fresh coconut water (stored in a glass jar) is given a bit of time to lightly ferment in the fridge, it tastes even better, as the excessive sweetness is replaced by a powerful refreshing taste (due to a bit of bacterial fermentation).

Much of that is due to coconut water having a variety of components within them that bacteria will consume and spoil once it leaves the coconut (hence necessitating sterilization prior to packaging) and the coconuts having a variety of nourishing components that are damaged or destroyed by pasteurization.
Note: the many issues with pasteurizing dairy and why so many people seek out raw milk are discussed further here.

Coconut Options

For years I ate a mostly raw diet (which was only possible due to coconuts), and in that process, discovered there were many wonderful coconut based recipes, but also that the quality of coconut products varies immensely.

In the final part of this article (which primarily exists as an open forum for you to ask any answered questions that have come up over the last month) I will provide a preview of the upcoming DMSO neurology article, cover what my favorite uses for coconuts were (e.g., with chocolate), share the best sources I’ve come across for coconut products (e.g., coconut water) and note which of those had the greatest positive impact on my life.

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The problem, however, with that goal is that 100% accuracy is essentially impossible to ever achieve, and if you place too much of an emphasis on trying to reach it (e.g., spending days going down each possible rabbit hole on a simple idea you are considering) it’s not possible to get anything done, much in the same way readers here would greatly prefer 52 articles, each of which I spent a week on rather than me spending a year polishing and refining 1 of them.

The dilemma I just outlined touches every part of life. For example, to navigate the world, we hold thousands of unquestioned beliefs (axioms) we assume to be true at any given moment (e.g., that the solid ground ahead of you will support you when you step onto it, that it’s a good idea to let your lungs inhale and exhale, or that the person sleeping next to you is indeed your spouse), and were we to instead constantly question each one, it would be impossible to function at all in life.

Conversely, a very strong case can be made that many of the problems people run into in life are a result of the unquestioned assumption they have. In parallel, one of my longstanding observations has been that individuals with the cognitive capacity to turn off auto-pilot and recognize which automatic assumptions or behaviors they carry merit re-examination tend to be much more successful in life.
Note: a major problem with medicine is that from day one, doctors in training are taught axioms which exclude the possibility of natural or spiritual healing occurring and hence become rigidly anchored to the lucrative materialistic medical paradigm our society follows.

Lastly, it bears mentioning that a nihilistic school of philosophy (solipsism) essentially argues that it is impossible to know anything with certainty as a sliver of doubt exists behind virtually every axiom you hold (e.g., consider the examples I mentioned above). That line of reasoning is very attractive and is routinely used in debate to dismiss all types of arguments, but inevitably collapses into an endless abyss of absurdity that is immune to outside criticism. This concept is important to highlight as while we should always question things, one should always be mindful of how probable each contrary claim or argument is and to avoid the strings of improbable ones stitched together which lack any corroborating evidence regardless of how aggressively those who share it promote it.
Note: one helpful framework to examine these claims is that after acknowledging they are possible, to ask if they are probable, as in every circumstance there are an endless number of possible (but highly improbable) claims that could attributed to what happened.

Chain Letters

In the mid-1990s, as the internet was starting to see widespread adoption, the “chain letter” phenomenon took off, where a compelling and shocking story would be found in an email from a friend you’d be compelled to forward to other people. After forwarding a few and someone scolding me, it occurred to me they might not be true, so I began researching the ones I received and quickly realized give or take every one was demonstrably fake.

However, despite pointing this out, friends and coworkers kept sending them to me, as the chain letters were designed to always make you feel emotionally compelled to share the email before you wanted to make the mental effort to think about it and vet it. As such, I soon came to the conclusion that “if the improbable events described are too perfectly lined up for a viral story, it is probably fake.” In turn, no matter how the internet has evolved since, that rule has basically always held true.

Similarly, I found that virtually every social group would have a much lower standard of proof for stories which conformed to (or supported) their existing beliefs than those which questioned it. This is most commonly observed in politics, as individuals will frequently notice instances where members of the other political party do this, but it also exists in many other spheres (e.g., a major problem in medicine is that the medical field readily adopts false narratives which support its prevailing biases while simultaneously reflexively refuses to consider those which affirm a competing paradigm). Finally, members of the group, to fit in, will frequently parrot these stories and narratives to each other and in many cases, also share them outside the group to bolster their group’s social standing.

This dynamic can also be more subtle, as rather than it just being an idea held by members of a group clearly in alignment with the idea, it is also done on an individual level where it’s challenging for an outside observer to see what group the individual is affiliated with. Similarly, in writing this publication, one of the major challenges I’ve run into is discovering that numerous stories or narratives I’ve always believed were true actually aren’t and need to first be vetted. I’d like to think I’ve gotten better at this, but a correspondence from a reader highlighted this is not always the case.

James Sims

Critiques of Western medicine (along with Wikipedia’s list of unethical human experiments), for as long as I can remember, have frequently included James Sims. This is why in last week’s article I stated:

Another controversial doctor James Marion Sims, who in 1845 began experimental gynecological surgeries on black slaves (without anesthesia—and operated on some individuals up to 30 times) and after roughly 4 years of work, perfected the surgeries enough to use them on white women (with anesthesia) after which, in the 1850s, he opened the first women’s hospital (which was mired in controversy due to how barbaric some of his procedures were, their high fatality rate, and some of the unnecessary brain surgeries he did on black children). Nonetheless, he became one of the most famous doctors in the country (e.g., he was the 1876 president of the AMA) and is considered to be the father of gynecology.

Note: many critiques of Sims are far more scathing and graphic and in 2018, after sustained protest from groups like BLM, Sims’s statue in NYC was taken down.

After publishing the article, I received this email from a reader:

Thank you for the wonderful articles you have written. I have shared them with colleagues who share similar concerns and philosophies. I am a retired Neurosurgeon [redacted]. I appreciate and share your thoughts about organ donation. I was heavily involved in brain death testing, and had a personally traumatic experience with a patient who underwent harvesting post cardiac arrest.

I recently read your article about current OB/GYN health care. Excellent. I have attached an article about Dr. J Marion Sims. Wiki has a brief history of Dr. Sims. There are some nuances to his history.

After seeing that, my immediate thought was “oh dear, have I been telling a lie about James Sims for decades?” followed by “I never thought about it before, but I have been emotionally invested in believing a negative narrative about James Sims because the story I heard was so personally triggering for me that I did not vet it first” (not unlike what compels one to share chain letters).

I then read that article (which you can too here) and found out that:

• Most of the above allegations against Sims are not supported by the historical record or the clinical reality of the time (where many things we take for granted now instead were very difficult to do). Rather, they were strung together to support a narrative of white doctors ruthlessly exploiting black slaves.

• The gynecologic condition Sims was treating—vesicovaginal fistula (and other similar ones)—were devastating for those who had them and incurable at the time, so the enslaved women he operated on were desperate for relief and willingly consented to the procedures.

• Sims didn’t use anesthesia mainly because ether was still brand new, highly controversial, and carried real risks. He (and other surgeons) didn’t think the pain of these particular operations justified the dangers, and he applied the same standard to white patients as well.

• The surgeries he developed were the first consistently successful repair for this condition and basically founded modern gynecologic surgery, which is why he rose in the field.

• A lot of Sims’s behavior toward these women lines up with someone genuinely trying to help them rather than just exploiting them—he operated at his own expense, got their cooperation (they even assisted in each other’s surgeries), publicly acknowledged his debt to them, and kept going because they pushed him to continue when he wanted to quit.

So, I have to say I never expected to defend someone I despised as much as Dr. Sims, but since my priority is being accurate, I felt I needed to as I lied about him in the previous article.

Note: many other criticisms have been leveled against Sims besides the one I touched upon. They may be valid; my point is only on correcting what I was inaccurate about.

Sensitivity and Specificity

One of my favorite concepts in the philosophy of science is “sensitivity and specificity.” This dyad denotes how likely you are to identify what you are trying to get (sensitivity) and how likely you are to erroneously misidentify your target (specificity). In medicine, this concept is raised to highlight that no diagnostic test is perfect, and if you prioritize one of these, you typically worsen the other (e.g., if a cancer test is too liberal with its criteria, it will cause issues by falsely diagnosing people with cancer whereas if you design a test to avoid false positives, it typically will also have a higher rate of missed cancers).

Because of this, a major focus in diagnostic testing is to identify which tests have the best balance between the two, and to identify which situations merit tests which emphasize sensitivity and which merit tests that emphasize specificity (or a combination of both). Conversely, some of the biggest debacles in medicine result from this principle being disregarded. For example, to ensure the COVID nasal PCR tests did not miss any cases of COVID, their sensitivity was raised to the point they frequently had false positives to the point large segments of the population concluded the tests were a complete joke.

After I was introduced to the concept of sensitivity and specificity, it dawned on me this concept extended far beyond medical diagnosis, and underlies many different challenging situations faced by our society. For example, much of the debate with criminal justice and police boils down to prioritizing sensitivity (preventing as many criminals as possible from harming the population) or specificity (not falsely arresting and harming innocent individuals), and once one goes too far to either extreme, clear issues happen on the other hand (e.g., a culture of lax policing and prosecutions spikes violent crime whereas authoritarian societies that believe in guilty until proven innocent have populations who are terrified of the police and many innocent prisoners).

Unfortunately, once these debates become contentious issues, rather than the goal being to find the best way to maximize sensitivity and specificity, one side will typically identify with the sensitivity position, the other with the specificity position, and then each will be excellent at arguing for why greater sensitivity (or specificity) is needed but simultaneously incapable of seeing the downsides to their position on the other end of things. Ultimately, things typically settle out in a compromise position where the way sensitivity and specificity are addressed is “good enough” (rather than a rationally designed one aimed to maximize both), and in times when the society becomes more polarized, shifts more towards one or the other, and then later inevitably goes back in the opposite direction once the flaws of the previous became clear, and either societal polarization decreases or the opposite side comes to power.

Cognitive Sensitivity and Specificity

Likewise, sensitivity and specificity play a critical role in shaping our own cognition and how we navigate the world. For example, in the DMSO research project I’ve been doing full time since October, I essentially concluded that to do what was needed for DMSO, I would need to go through every applicable database, search each one for the terms used for DMSO, and filter those results to identify all the medically relevant studies, and then summarize them so I could sort them by subject (which I am currently doing for a requested DMSO neurology series).

The problem with this is depending on the query, that the results got thousands, tens of thousands, hundreds of thousands or millions of results, and while I can consciously process large bodies of data, the larger results greatly exceeded anything my mind could do. Because of this, a lot of the project was essentially trying to find a way to achieve sufficient sensitivity (so virtually no medically relevant study was missed) while simultaneously having a hard enough filter that the final outputs didn’t overlap and were constrained to tens of thousands of results (which was possible to manually review). Likewise, when manually reviewing those outputs, I was continually trying to consciously calibrate my mental filters and cognitive algorithms so I didn’t miss anything relevant but simultaneously could move at a past enough pace through the lists (by not spending time or focus on non-relevant results) and that the project could be completed in a timely fashion that I had enough cognitive energy to sustain completing it.

Ultimately, while very challenging, I was able to pull it off, and am truly grateful there was a way to do this (as I am doubtful it will ever be done again and hence felt an obligation to do it properly), but at the same time, will likely never undertake a similar endeavor because of how much it took out of me to do it.

Note: I initially thought ozone would be a much harder topic than DMSO (due to the larger volume of search results) but in the process of figuring out how to do this task, realized that ozone is actually much easier to do as the medically relevant results are much easier to separate out at the start (and hence is next in the queue after this project).

All of the previous may sound a bit abstract, but the reality is that every day, we are continually making the choice to screen out or ignore large pockets of data we are exposed to, while simultaneously devoting our limited cognitive resources to focusing on the things our mind prioritizes.

However, unlike the process I described above, this filtering is typically not conscious (or only partly conscious such as when deciding who in a group we want to approach and who we want to avoid), and in many cases, is externally hijacked (e.g., marketing and propaganda revolves around getting people to focus on specific things and ignoring others). I mention all of this because my consistent experience has been that people who consciously choose how they want their mind to filter reality tend to be much more successful (and happy) in life, particularly if they extensively deliberate on the merits of cognitive sensitivity and specificity in each situation and look for the most appropriate balance that best helps them.

Note: it’s impossible to ever be perfect at this, and a lot of life is being willing to recognize how your sensitivity or specificity was poorly calibrated. For example, even though I actively try to do this, as the case with James Sims showed, my choice to embrace and take the negative narrative about him at face value illustrates I had poor specificity there which caused me violate my core priority (not publishing inaccurate information).

Medical Philosophies

The way one chooses to see or practice medicine is also heavily shaped by how they prioritize sensitivity and specificity in a variety of contexts (e.g., many doctors fixate on the rare diseases vaccines sometimes prevent but simultaneously ignore the common side effects of vaccination and hence religiously support vaccination).

With medicine, I essentially believe that:

•Most medicinal interventions, due to the nature of how medical science interacts with the body, cause harm (that is sometimes obvious and sometimes subtle).

•Many medical interventions transformed humanity, and there are many problems we never think or worry about now which were major issues prior to medical science solving them.

•The relative risk of medical therapies greatly varies, but rather than view them as distinct entities, they are frequently seen as all being good or bad. Likewise, many conventional therapies, while not ideal, are often the best option many people have.

•With most medical issues, numerous viable approaches exist to treat them which have different upsides and downsides. Unfortunately, since there is not an open discussion on this, clearly suboptimal therapies are routinely chosen for patients (with significant consequences frequently following).

•I have seen many people be harmed by unnecessary medical procedures (who in many cases were warned by friends or family that harm could occur beforehand) but I have also seen people who were ideologically opposed to the medical system be harmed or die because they refused standard care for an issue which is straightforward to treat with conventional medicine.

Or, taking a step back, what this essentially means is that correctly engaging with medicine is a sensitivity-specificity issue, where you have to understand the subject well enough to be able to gauge where this best lines up in each instance.

In my own case, my own philosophy leans strongly towards avoiding harm, so I hold the position I would rather do nothing than something I feel holds a potential risk of harm.
Note: this is also why I will not give quick answers here on how to use therapies I think need to be well understood to avoid some people having negative experiences with them and why I have not promoted a number of compelling popular alternatives therapies as I am still not sure if they are satisfactorily safe.

Generally, this philosophy has served my goals well, as I’ve avoided making patients worse (with most of the exceptions being instances where the chronically ill patient had a partial improvement, then they desperately wanted more and were leaving the area for a while, so I did more than I was sure they were ready for which then set them significantly back). However the downside to my approach is that for a lot of people there is a massive cost to going slowly into a protocol and waiting much longer for a treatment response that far outweighs manageable adverse reactions they could have to therapies (but conversely, in many cases, there is an even greater cost if a protocol is done too quickly for it to ever have a chance to work).

Likewise, while my philosophy and personality is well suited to outpatient (non-emergent) issues, it does not work for more serious and pressing issues where you have to routinely utilize therapies with inherent degrees of harm to save people’s lives, so I have immense respect for the doctors who practice differently from me in those high-stakes contexts and were I there now, I too would adjust how I prioritized the risks and benefits of medical therapies.
Note: in many cases, I find appropriately utilized natural therapies can prevent hospitalizations (sometimes even when given in the ER shortly before admission), but at the same time, I do not like to rely upon this, as bad things will happen if hospital care is delayed for emergent conditions.

Cancer Treatment

One of the most challenging areas where these competing priorities converge is with cancer treatment as:

•Many conventional therapies have horrendous, unacceptable side effects and poor efficacy.

•Other conventional therapies work fairly well, and make previous death sentences survivable (however these therapies are often extremely expensive and their side effects significantly impair one’s quality of life).

•Many safer and cheaper natural therapies exist which sometimes independently treat cancer.

•If conventional cancer treatment is delayed (e.g., due to exploring non-toxic alternatives or a waitlist already existing for conventional care), it can worsen the condition to the point an acceptable outcome with conventional care is no longer possible.

Because of this, cancer patients frequently run into a “lose-lose” situation where there is no clear answer on what to do, alongside a great deal of stress and conflicting voices clamoring in their ears for them to prioritize either sensitivity or specificity with conventional or alternative treatment options (to the point one of the most helpful things you can often do for a cancer patient is have a friend serve as intermediary to field all the people who are bombarding them with advice and worry).

My “solution” to this dilemma mirrors how I approach emergent conditions.

•If time exists, I try natural therapies before conventional care.

•I always keep an eye out for the cases which are likely to fully respond to a natural therapy or safe pharmaceutical protocol (e.g., around 10% of cancer patients have incredible responses to protocols that use repurposed drugs like ivermectin), which cases have a clear underlying issue precipitating the cancer (e.g., estrogen dominance, key micronutrient deficiencies, or retained emotional trauma) that must be treated in tandem with whatever protocol is chosen, and how to optimize the chosen natural therapy (e.g., ivermectin can create neurologic issues at higher doses, but the need for high oral doses can be bypassed if ivermectin is mixed with a paste and applied directly to the skin above a tumor—where it frequently works much better than any oral protocol).

•In most cases, I default to the natural therapies supporting the conventional ones, as conventional cancer outcomes and side effects can be greatly improved with the correct holistic therapies (e.g., UVBI is excellent for mitigating chemotherapy side effects, and in most patients we see cancer outcomes significantly improve if therapies like the repurposed drug protocols are used in conjunction with them).

•When possible, I try to help make the conventional cancer protocol be more targeted to the specific patient (so lower doses and more effective regimens are used).

Therapeutic Precision

In many cases when an impossible balance has to be struck between sensitivity and specificity, an out-of-the-box solution exists which solves it. In the case of medical approaches, I gradually realized the following:

•The side effects from medical therapies typically result from them affecting areas besides the intended target (e.g., since most pharmaceutical drugs work by inhibiting enzymes, they will frequently either inhibit necessary functions of the target enzyme or inhibit other similarly structured enzymes in the body) and the body having a pathological compensation to the unnatural shifts the pharmaceuticals create (e.g., if an enzyme or receptor is chronically impeded, the body will try to fix this by upregulating that protein, while if it’s chronically stimulated, the body will downregulate it—which frequently creates addiction as higher and higher doses of the drugs are needed).

•The higher a dose of a therapy is used, the more likely it is to accomplish the intended effect and reach the desired target, but simultaneously the more likely it is to also hit unintended targets and cause issues (particularly in sensitive patients). While there are many ways to navigate this dilemma, the most common approach has been to simply ignore or dismiss the downsides to overdosing and focus solely on creating the desired effect.

•Natural therapies tend to be much weaker than conventional therapies. As such, they rarely create the same significant side effects, but also do not create the immediate significant shifts observed with pharmaceutical drugs. However, you can also overdo natural therapies (e.g., we see tons of people who are on large numbers of poor quality supplements that are not benefitting them, and they feel significantly better once we cut them down to the 20% that are helping).

As such, on one hand, I held a strong bias towards avoiding pharmaceutical therapies in favor of natural ones (along with minimizing prescriptions). However, I also feel it’s important to never be dogmatic, and from exploring pharmacology, I gradually discovered some drugs (e.g., ivermectin) have excellent risk/benefit profiles for illnesses that clearly justify their use, and that with many borderline drugs, lower doses of them frequently made it possible to get key benefits without significant side effects.

More importantly, as I pondered the dilemma of when to utilize the stronger conventional therapies, I realized a completely different solution to the question existed: if therapies are precisely targeted to the needed issue, much lower doses are needed to create the intended effect.

As such, one of the reasons why I can get away with using “weaker” natural therapies for difficult conditions which frequently require much stronger measures is because I found ways to ensure the therapy went directly towards addressing the root cause of their issue. Likewise, since pharmaceuticals are not my default approach, I can more easily recognize the cases where a specific pharmaceutical is likely to directly target the patient’s issue (at which point lower doses and shorter courses of treatments can be utilized).

Sadly, in contrast to this mindset, medicine revolves around creating standardized protocols everyone is subjected to, with the fraction of people who react poorly to that being seen as a necessary cost of doing business and then largely ignored.

Note: many different approaches have been developed over the years to improve the selection and targeting of therapeutics (too many to cover here). Generally speaking, the ability to do this is one of the key skillsets which distinguishes renowned healers from other physicians in the integrative medical field.

Conclusion

This newsletter has always been an exercise in pursuing accuracy within an imperfect world where complete certainty is impossible but the best attempt towards it must nonetheless be made. As such, I’ve tried to share some of the strategies I’ve found which are the most useful for bridging that divide and moving from reflexively believing emotionally provocative information to one that tries to calmly assess the sea of information around you and find the best path forward as you navigate the sensitivity and specificity challenges life throws at you.

In many cases, I find the greatest obstacle to doing this is within the person, as from birth, we are trained to prioritize protecting our ego and being right—even if that forces us to commit to an incorrect position or keep repeating the same counterproductive mistake. When I wrote this article, I did so in part because I felt obligated to correct the mistake I made with Sims, but also to illustrate the importance of having a paradigm that prioritizes truth and accuracy over being right and how in many cases (regardless of how much your ego lies to you) that is not something you can ever fully achieve, but rather simply a destination you keep gradually moving closer towards.

I thank each of you for your support which makes this newsletter possible, and hope this gives you some useful ideas to ponder.

To learn how other readers have benefitted from this publication and the community it has created, their feedback can be viewed here. Additionally, an index of all the articles published in the Forgotten Side of Medicine can be viewed here.

•Childbirth is one of the most important moments in our life. Unfortunately, it has been medicalized and has shifted from being viewed as a natural life event supported by local midwives to an emergency requiring urgent hospital care.

•Many of the interventions used during routine hospital births (and beforehand like ultrasound) are quite questionable, and have a variety of side effects, including making you likely to need more interventions (which also have side effects) and having difficulty bonding with your baby.

•This assembly line frequently leads to mothers getting C-section surgeries—something quite problematic for both the mother and the long-term health of the child.

•This article will discuss the history of the business of being born, the actual risks of many common hospital birthing interventions, and how to reduce those risks.

•It will also provide strategies for choosing the best place to give birth, ensuring both optimal childbirth and recovery, and having a healthy child.

Many traditions throughout history have come to view the prenatal period and childbirth as one of the most important moments in a human’s life as it sets the stage for all that follows. Unfortunately, much in the same way we desecrate the death process by over-medicalizing it (to the point research has found doctors are less likely to seek end of life care at a medical facility), the same issue also exists with childbirth. Many physicians I know who are familiar with the hospital birthing process chose to skip it and give birth at home (along with many more doctors featured in a 2016 documentary).

Conversely, a minority of childbirths do need advanced medical care, and for those mothers, access to a hospital greatly benefits them, particularly if actions are taken to mitigate the most dangerous aspects of hospital birth. As such, childbirth occupies a similar place as many other medical controversies; neither side of the issue is entirely correct. However, the discussion remains perpetually polarized because advocates on either side will not acknowledge the valid points raised by the other side for fear of weakening their own position. Since I feel strongly about the dangers of hospital birth, it is my hope in this article that I will be able to portray both sides of the issue fairly.

Note: I feel one of the most destructive trends in our society has been the devaluation of motherhood (e.g., when I last visited China, it was striking how much more respect and consideration they gave to pregnant women) and children. Beyond new life being necessary for the viability of our society, it often ends up being the most transformative and fulfilling experience in a parent’s life. Yet, so much of our societal messaging encourages us to shun that path and put our hearts into other things. In parallel, a general disconnect has been fostered upon this entire process where it is treated as a sterile, lifeless, and mechanistic event we need to be separated from and entrust to someone else—which I believe is the ultimate problem that underlies many of the issues that will be discussed in this article.

The History of Midwifery

A lot of the dysfunctional things that have come to characterize the birthing process (e.g., unnecessary hospital interventions that create complications begetting more hospital interventions) make much more sense once you understand the history behind them and how childbirth was transformed from a natural human life-event to a medical emergency requiring those interventions.

From the start of America, midwives were highly valued in colonial communities, receiving housing, food, land, and salary for their services (particularly since they also served as nurses, herbalists, and veterinarians). Then, during the 1800s, midwives played a key role in the westward expansion, particularly in the Mormon migration to Utah, but by the early 1900s, a variety of social factors (e.g., economic pressure and societal prejudices) caused midwifery’s reputation to decline.

Much of this was due to male doctors (who had initially been averse to delivering babies) displacing midwives. This began in the late 1700s when it became fashionable in Europe to have doctors attend deliveries, after which an influential Harvard professor (and its first profession of obstetrics) convinced his American colleagues to enter, for example in 1820 stating:

Women seldom forget a practitioner who has conducted them tenderly and safely through parturition they feel a familiarity with him, a confidence and reliance upon him which is of the most essential mutual advantage. . . . It is principally on this account that the practice of midwifery becomes desirable to physicians. It is this which ensures to them the permanency and security of all their other business.

Once doctors entered the field of midwifery, it quickly became necessary to justify their “expertise” and a gradual medicalization of childbirth began.

Dr. Joseph DeLee (who later became known as the father of obstetrics), in 1895, opened Chicago’s first obstetric clinic, and since it was successful, opened an obstetrics hospital which also trained doctors and nurses and developed lifesaving innovations (e.g., incubators for premature infants) which lowered the childbirth mortality rate.

Simultaneously however, because DeLee observed so many complications and deaths from childbirth, he was of the opinion that natural childbirth was extremely dangerous for both the mother and child, and hence needed to be medicalized. In turn, he spoke actively (e.g., at a 1915 professional meeting) against the use of midwives, arguing they lowered the standards of the profession, and were childbirth to be seen as a more dignified profession, higher fees could be charged, and more doctors would be willing to replace midwives.

Following this (like many zealots), in 1920, he argued that the approaches he had developed for challenging pregnancies (e.g., forceps, episiotomy, toxic anesthetics) should be used for most of them, while other doctors argued these approaches were too aggressive in many of the situations where DeLee advocated for them. However, due to his growing influence in the profession and success in making childbirth a part of the medical curriculum (in part due to how many doctors he trained) by the 1930s, his standardized invasive approaches became increasingly popular, particularly since society had become enamored with advanced technology improving things.

Finally, near the end of his career (in 1933), due to increasing maternal deaths and complications from hospital infections, he became an advocate for cleaner maternity wards, which met significant resistance from his colleagues (although not as severe as what Ignaz Semmelweis faced almost a century in Austria for pointing out that doctors not disinfection their hands was routinely killing mothers).

From one perspective, I can greatly sympathize with where DeLee came from, as significant issues needed to be addressed (e.g., in 1913, the infant mortality rate was 13.2%). However, he failed to recognize many of them were due to the abhorrent living conditions of the time (which as I show here were also the primary driver behind the incredibly high mortality from infectious diseases).

At the same time however, some of his approaches (e.g., making women partially unconscious during labor and then pulling the babies out with forceps) were abhorrent (and explicitly detailed within his classic 1920 paper), and set the stage for a variety of other harmful and unnecessary interventions to hijack the childbirth process.

Worse still, he seeded the idea within the medical profession that childbirth was inherently pathologic and required a doctor to save the mother and child—despite the fact for most of human history, we had not needed them. Likewise, the maternal death rate was actually the highest between 1900-1930 (when DeLee’s practices came into vogue), and it was only after years of deaths and mistakes that the standard of care began being improved and maternal deaths declined. Nonetheless, even now, over a century later, the United States still has a significant issue with these deaths (which is particularly noteworthy as during the period below, those deaths were declining in the other wealthy nations).

At the exact same time DeLee’s work occurred, a variety of federal and state initiatives recognized that the incredibly high infant and maternal mortality rates were connected, and that appropriate prenatal care could prevent them (e.g., Mother’s Day was created at this time to provide maternal support to prevent those deaths).

Simultaneously, a debate known as the "Midwife Problem" unfolded, with some (e.g., doctors) advocating for the abolition of midwifery (largely to shield themselves from competition) and others supporting it with proper training and licensing (as they felt midwives could play a critical role in preventing deaths if utilized correctly). Laws were passed in some states (e.g., those that simply did not have enough doctors to attend childbirths) to regulate midwifery, and schools were created to improve midwifery standards. However, by the 1930s, the increased use of hospitals for deliveries made it possible to close many of these schools.

However, a 1921 Federal law provided for training nurse midwives, and in 1931 (owing to the increasing recognition of the failures of American obstetric care), a successful nurse midwifery school emerged (which amongst other things, had a maternal mortality rate of one-tenth that of the country). Their graduates then created numerous schools and created the modern discipline of nurse midwifery.

Note: in parallel, the Frontier Nursing Service (founded in 1925 by a British trained midwife) trained nurses and provided extensive midwifery (and medical care) to the woefully underserved inhabitants of the Appalachians, which ultimately resulted in a far lower maternal death rate (roughly one third as much as the rest of the country). In turn, when many of its nurses returned to England at the start of World War 2, they also created a successful nurse midwifery program there as well.

Following this, in the 1940s and 1950s, due to limited existing opportunities to practice clinical midwifery, most of the graduates of these programs had to fill other obstetric related roles, and ultimately only a quarter served as midwives. In the 1960s, a variety of attempts were made to address this (e.g., having them work at hospitals where 70% of the births were taking place), and it was not until 1968 that more opportunities began to emerge (due to one school finding a way to integrate with New York’s medical system).

Shortly after, a variety of rapid shifts occurred (e.g., key professional organizations endorsed nurse-midwifery, feminism came into vogue, the media promoting midwifery, federal funding for it, an explosion of childbirths from the baby boomers coming of age that the existing system could not accommodate) which propelled midwifery into the mainstream. In turn, many doctors began partnering with midwives, programs became officially recognized by the U.S. Department of Education, and public demand for midwife supervised home births exploded.

This increased demand quickly exceeded the available supply, after which there was a rapid proliferation of non-nurse midwives (lay midwives) with highly variable degrees of training (who had their first national meeting in 1977). By the 1980s, nurse-midwives were present throughout the healthcare system, and a split developed in the medical community between obstetricians who recognized their value and worked with them versus those who viewed them as economic competition that needed to be eliminated (particularly because there was now an overabundance of obstetricians).

Since then, midwifery has faced additional obstacles from the medical system but has continued to develop. Mixed opinions exist within the obstetrics field towards midwifery, and its accessibility varies. Since the 1990s, approximately 1% of births have been at home (although recently it suddenly increased to 1.5%).

Note: this abridged history necessarily omits the immense struggles countless incredibly dedicated midwives went through to make midwifery available to the public or just how much that work approved the abysmal obstetric care that existed throughout the country and the human cost that came with it.

Prenatal Ultrasounds

Much in the same way vaccines are believed to be “safe and effective” from the start of their training doctors are always taught that ultrasound is harmless, and its only flaw is that the images it provides are “operator dependent.” This, I believe, accounts for why the most controversial and attacked article I have ever written here was the one on that topic.

My initial doubts about ultrasound arose from an inherent skepticism I have towards absolutist dogmas (e.g., 100% safe), and these early doubts were quickly affirmed after I received a practice echocardiogram that “did not feel good” in my heart (suggesting it was not “inert”—much in the same way numerous forms of [higher dose] therapeutic ultrasound now exist, which by definition are not “inert”).

Later, I learned through Robert Mendelsohn (a maverick doctor who was a key source of inspiration for me) that ultrasound was phased in to replace prenatal X-rays (which had severe health consequences for infants but nonetheless took the medical profession nearly a century to phase out).

Following this, literature and review articles (and then later articles by holistic midwives) gradually accumulated showing that ultrasound (in a dose dependent manner):
•Caused genetic damage and cancer.
•Damaged cellular structures and initiated cell death.
•Caused organ damage, nerve damage, behavioral impairments, and congenital malformations in animals.

In parallel, I:
•Noticed fetuses would consistently move (and sometimes try to move away from) “inert” prenatal ultrasounds (which is well-recognized in the scientific literature).
•Saw a few cases of distraught patients in the ER who were miscarrying who stated “I don’t understand how this is happening, my OB looked at my baby today and said he/she was completely healthy” (and then gradually found literature showing ultrasounds increased the risk of miscarriages).
•Learned (much later) through Dietrich Klinghardt that the uterus concentrates EMFs inside it 20-fold (which, if you ascribe to a spiritual view of embryology, makes sense), again suggesting caution may be required for prenatal ultrasounds.
Note: when I asked Klinghardt for a reference for this, he stated that it came from Wolfgang Maes (the father of the institute of building biology in Germany and Florida) but I was never able to find the exact paper (nor was Klinghardt as the computer it was on was lost).

Sadly, while this used to be a topic of controversy (e.g., in 1983, CNN aired a critical 11 minute program on ultrasounds), due to how large this industry is, the last (tepid) mainstream criticism I ever saw was a brief 2015 segment by USA today.

Finally, in 2015, a colleague (aware of my interest in the topic), informed me of a newly published book, which brought a newfound awareness to this topic by:

•Compiling 40 Chinese studies conducted in the 1980s, where women scheduled for an abortion (due to China’s abhorrent population control policies) were randomized to receive an ultrasound prior to the abortion, after which the fetus was dissected. Those studies (some of which are briefly summarize here) found ultrasound consistently induced damage to intracellular structures and organs throughout the body.

•Highlighting that in 1991-1992 the FDA, due to higher ultrasound doses creating better quality pictures, acceded to manufacturer demands to raise the allowable limit 15.7 times (and likely more so, as many machines output above their stated range), despite harm already being shown throughout the literature at the lower doses.
Note: doppler ultrasounds have a higher output than standard ultrasounds.

•Noting that this change directly correlated with the spike in autism typically attributed to vaccines (or sometimes glyphosate).

Given all of this, I presently believe:

•Some prenatal ultrasounds are viewed as medically necessary, but many others are not. Those which are not medically necessary should be avoided.

•The value of early pregnancy ultrasounds is minimal (which has been shown throughout the scientific literature), particularly since modern tests can provide most of the same data (excluding a picture of your fetus), and do so with higher accuracy (whereas I, and many others, know numerous people who were told their baby needed to be aborted based off ultrasound detected defects and actually was completely healthy).

•In emergent situations (e.g., unexplained vaginal bleeding after a car accident) or a bit before delivery, prenatal ultrasounds have significant value as a brief one can allow you to catch the unusual birth circumstances that do require a hospital birth or an emergency C-section.

•I believe ultrasounds have an adverse effect on children as we’ve seen infants that were regularly ultrasounded throughout pregnancy (e.g., the parent bought a home one and wanted to see her baby) had a general lack of vitality and chronic health issues. However, in most of those cases, there was something else which potentially could have caused those adverse effects (e.g., vaccines). Conversely, the healthiest, best-behaved and most vibrant babies and children I’ve known not only avoided vaccines, but also prenatal ultrasounds and infant formula (whereas, while healthier, I have known ultrasounded but not vaccinated children who had chronic issues). However, due to how small the sample size it, I can’t say with confidence my observation is valid, and everyone I’ve asked had a similar perspective (as most mothers get ultrasounds). That said, while some studies show ultrasounds adversely affect pregnancies (or causes subtle cognitive or behavioral effects), the majority of data indicates prenatal ultrasounds are harmless (which could either be due to a probable bias against research indicating ultrasound harm, the effects being subtle and hence hard to detect, or harms not existing).

Given all of that, my current perspective is that early prenatal ultrasounds (when the fetus is the most sensitive to them) should be avoided, whereas later ones shortly before birth (36-37 weeks) should be done in the briefest manner (and lowest intensity) possible to get the essential information needed for childbirth (e.g., the placentas location). I know numerous people who chose not to get any, all of whom ended up having healthy home births, and others who were considering avoiding ultrasounds, chose to get one, and caught a critical issue that otherwise would have created a disaster during a home birth.

That all said, a stronger case can be made for prenatal ultrasounds in “high-risk” pregnancies, and while quite rare, some (between 1 in a 1,000 to 1 in 10,000) require a surgery within the uterus in the middle of the pregnancy to protect the fetuses from a severe congenital abnormality.

Note: this subject is discussed further here and here. Additionally, an article on additional strategies for raising healthy children can be read here.

A Standard Hospital Birth

When women go into labor, it is frequently viewed as a medical emergency that necessitates getting to the hospital as quickly as possible (e.g., this idea has been reinforced in television and movies for decades) and then struggling and having the doctor miraculously deliver the baby.

During this whole process, the following will happen.

•The mother will be placed in an uncomfortable and stressful environment (where many unfamiliar people enter and exit the room), be subject to repeated vaginal examinations, and typically placed on her back with the legs spread out.

•The mother will be placed on fetal heart rate monitoring (typically via the abdomen, but sometimes also through an electrode applied intravaginally to the baby’s head).

•If the mother delivers too slowly, she will be given pitocin (oxytocin) to speed up the rate of contractions and may have her amniotic membrane prematurely ruptured.

•To mitigate her discomfort, she will often be given an epidural.

•Once the baby starts to come out, it may be pulled out with forceps or a vacuum extractor if the labor progresses “too slowly” or an issue arises.

•To prevent tearing and to make childbirth easier, mothers will often be given a prophylactic episiotomy, which preemptively cuts the vaginal opening to widen it.

•If any of the above goes awry, the mother will be converted to having a C-section.

•Once the baby is born, the cord will be immediately cut (and the placenta disposed of). The baby will typically be separated from the mother for a prolonged period (e.g., to go to a newborn nursery or the neonatal intensive care unit), and will receive a vitamin K shot and a hepatitis B vaccine and then have their blood drawn. Lastly, if the baby is a boy, circumcisions are often performed in the first days of life while they are still at the hospital.

•Finally, following this, if all goes well, the mother will go home with the baby in a few days, or a week if issues emerge.

However, while many of these steps can potentially save an infant's life, many of them create significant long-term complications, and many increase the likelihood more hospital interventions will be needed.

This in turn, touches upon a criticism of the medical industry—medical interventions often thrust you onto an assembly line that requires more and more of them (e.g., many psychiatric drugs are prescribed to treat the side effects of other psychiatric drugs). Typically, it takes time to see this process play out, but in the case of labor and delivery, the changes requiring additional interventions occur quite rapidly—whereas in contrast, almost none of this is seen outside of the hospital.

Note: I believe this bias towards excessive intervention in part occurs from obstetric units being understaffed (e.g., if a doctor is attending 6-10 mothers, the deliveries need to be artificially sequenced so that they don’t occur simultaneously and accelerated so they aren’t held up in one place) and due to OBYGN’s having significant liability risk if anything goes awry with a pregnancy if the standard protocols had not been followed.

Any intervention that interferes with women’s ability to cope in labor has enormous implications: it can destroy feelings of achievement and self-esteem. Women who feel they have coped have more confidence in their mothering abilities than women who feel traumatized by the birth process. Specifically disturbing to this aspect of common labor ward practice is the data of Robson and Kumar reporting an association between procedures in labor, such as artificial rupture of the membranes, and the delayed onset of maternal affection.

We’ll now look at the issues with each of the previous approaches.

Note: as we go through these, consider that America currently spends at least 111 billion dollars on childbirth (which is twice that of most high income countries) yet ranks last amongst the high income nations in both infant and maternal mortality.

Birthing position

There are many different positions where a mother could give birth.

However, in most hospital births, mothers deliver on their backs with their knees up (e.g., a 2014 study of 2,400 hospital births found 68% gave birth lying on their backs, and 23% did so lying down while having their backs propped up).

Note: The primary reason these positions are used at hospitals is that they make it much easier to manage hospital deliveries and train healthcare providers to conduct them (leading to them not being comfortable with any other position). Many also believe they serve to enforce a power dynamic where modern medicine is in control of the process, and by extension, its participants as well.

Despite this being the norm, and despite most healthcare workers knowing it is not the ideal position, it is quite controversial as:

•Lying down closes the pelvis making it harder to push the baby out. In contrast, squatting allows the force of gravity to help the baby come out and has repeatedly been shown via MRIs to increase the size of the pelvic outlet that the baby has to exit.

•Compressing the sacrum (by lying down or sitting) dramatically reduces the ability of the coccyx (or public symphysis) to move and accommodate the baby passing through.

•Different labor positions are often much more comfortable than lying on the back. For example, a study of 2992 home births (where mothers are allowed to choose their birthing position) found only 8% of mothers chose to deliver lying down (along with 23% who do so lying down with their backs propped up).

•Lying on the back can compress the mother's vena cava and thus the blood supply to the fetus.

In turn, a 2017 Cochrane review found that delivering while standing decreased abnormal fetal heart rates, accelerated labor, and reduced the need for assisted births (e.g., forceps deliveries) or episiotomies. A later 2020 review found those same benefits to a greater degree (e.g., there was a considerable reduction in perineal trauma).

Note: in many ways, this situation is analogous to the defecation (pooping) position we use, as when you sit in the normal position we use on the toilet, it partially closes down the rectum (hence making it much harder to poop), whereas if you squat, it’s much easier for the process to occur naturally. However, despite this making a huge difference for bowel health, virtually no one knows about it, and our toilets are highly counterproductive to having healthy bowel movements (all of which are discussed further in this article about the forgotten natural ways to treat constipation).

Fetal Heart Rate Monitoring

An infant’s heart rate can indicate if they are in danger (e.g., because their blood supply is being partially cut off), and can be assessed either with a specialized stethoscope or continuous ultrasound (which is what is typically done). Fetal heart rate monitoring forms a cornerstone of obstetric practices. It is almost always done in the hospital (which also incentivizes having the patient lie down as it’s much harder to monitor in more natural birth positions).

However, while abnormal heart rates correlate to a variety of potential issues, extensive studies (e.g., consider this 2006 Cochrane review) have consistently found that when compared to periodic stethoscope examinations, fetal heart rate monitoring does not reduce death or disability but does increase the likelihood of a C-section by 66% and an instrumental birth by 16% (due to the abnormal heart rates making doctors want to save “at risk” babies).

Pitocin

Oxytocin is the hormone that stimulates uterine contractions. Because of this, synthetic oxytocin (pitocin) will often be given to induce labor or accelerate a delayed labor. Pitocin can be quite helpful, but unfortunately, it is frequently given at far too high of a dose (e.g., because a natural labor pace is deemed “too slow”). This leads to a few common issues:

•Pitocin can induce contractions before the cervix is ready to open (leading to the baby being pushed along but not able to get out), leading to prolonged labor that can require C-sections.

•Pitocin causes much stronger (and frequent) contractions, which are often quite painful (hence leading to increased pain for laboring mothers and a need for pain-relieving medications).

•Excessive uterine contractions can compress and interrupt the blood supply to the fetus, leading to abnormal heart rates and possibly C-sections.

•The perineum needs time to stretch during labor before the baby comes out, so pushing the baby out too quickly can cause it to tear (similarly, one study found pitocin makes anal sphincter tears during labor 80% more likely, while another found induced labors were twice as likely to have perineal lacerations).
Note: occasionally, the excessive contractions can also be too much for the uterus and rupture it.

•Excessive contractions increase the risk of maternal bleeding (e.g., one study found pitocin induced labors were 6% more likely to cause postpartum hemorrhages and increased total postpartum bleeding by 46%).

Because of the previous complications, excessive oxytocin can significantly increase the likelihood of C-sections (e.g., one study found that higher doses of oxytocin made women 60% more likely to need C-sections).

Note: common side effects of pitocin include nausea, stomach pain, vomiting, headache, and fever or flushing (while a more extensive list with the more severe reactions can be read on the FDA label).

Artificial Rupture of Membranes

Another procedure used to induce labor and accelerate prolonged labors is to rupture the amniotic sac (so the water breaks) despite the evidence showing amniotomies do not significantly accelerate labor. Conversely it:

•Increases the pain of labor (e.g., a 1989 study of 3000 women found two-thirds of them felt it increased in rate, strength, and pain of contractions and made them more challenging to deal with).

•Can cause the umbilical cord to drop before the baby (e.g., one study found it happened in 0.3% of amniotomies), which cuts off the fetal oxygen supply (e.).

•Increases the risk of infections (as the amniotic membranes protect the fetus from microorganisms).

•Increases the risk of C-sections.

Sadly, amniotomies are frequently done (e.g., in 40.6% of deliveries in Sweden), despite medical guidelines advising against them for routine deliveries.

Note: another long standing problem with amniotomies is that doctors in certain areas will not discuss the procedure with women before it is performed.

Epidurals

Roughly 70-75% of women who deliver in the hospital end up using epidurals, a procedure where a local anesthetic (e.g., bupivacaine or ropivacaine) and sometimes an opioid is injected into the spine in the space directly above the membrane that encircles the spinal cord so that everything below the injection site will become numb. While helpful for reducing pain (and often necessary, especially if hospital interventions have made the pregnancy more challenging), epidurals have a variety of complications such as:

•Increasing the risk of respiratory depression in the fetus by 75%.

•Reducing blood pressure (e.g., a study of 439 women, 41.9% experienced significant systemic reactions to an epidural including 36.2% having severe maternal hypotension). That loss of blood flow in turn, has been shown to cause 11.4% of fetuses to have a worsening heart rate and increased risk of C-sections.

Note: mixed opinions exist on the degree to which epidurals increase the risk of C-sections as some studies found it does not, while others did (e.g., this one found it doubled it, this one found it increased it 2.5X, and this one found an epidural plus pitocin increased it 6X).

•Causing long-term back pain or headaches (due to the membrane coating the spinal cord being punctured and leaking). While the headaches are thought to be rare (around 1% of epidurals), I have seen so many women who developed this complication (until it was treated with a blood patch—which has its own set of issues). I think this risk needs to be seriously considered.

•Disconnecting the mother from birth (as she can’t feel it) and negatively affecting her self-esteem (as she felt she could not cope with the labor herself).

Note: other side effects of epidurals include a few days of soreness at the injection site, nausea, vomiting, and a temporary inability to urinate.

Episiotomies

Episiotomies (surgically cutting the back of the vaginal opening and part of the perineum, then sewing it back together after delivery) used to be performed in the majority of deliveries under the erroneous belief it would help mothers by reducing tears, but now are less frequently done (e.g., in 1979, the episiotomy rate was 60.9%, while in 2004 it was 24.5% in 2004).

The major issue with this surgery is that the incision often will not heal well (whereas natural tears are more likely to), which can then lead to a variety of issues such as: perineal pain, infections, too much bleeding, scarring, urinary or fecal incontinence, pain during sex (which may require a prolonged period of abstinence), pelvic floor dysfunction, and emotional or psychological effects (e.g., some women have PTSD from the experience and wish they had not had the decision).

As such, it is essential to consider if you want to have an episiotomy before childbirth, and to be able to decide if you want to consent to it when it is potentially justified (which for context, the WHO has said applies to less than 10% of births).

Forceps and Vacuum Cups

Frequently, if a delivery is progressing too slowly (or the fetus is deemed to be at risk) the infant will be pulled out by the head, either with clamps that grasp each side of the skull or a suction cup that attaches to the top of it. This practice has gradually become less frequent (it’s now only 5% of American births) due to increasing awareness about its harms and C-sections being done instead. Unfortunately, much of the world still has not recognized this.

When forceps are used, roughly a quarter of mothers experience injuries such as vaginal tears and sphincter injuries, while more severe complications (e.g., 3rd or 4th degree vaginal tears, are reported in about 8 to 12% of those undergoing forceps delivery). Likewise, when vacuum cups are used, 20.9% experience vaginal tears, and 2.4% experience postpartum hemorrhages.
Note: another study found 13.2% of mothers experience complications from vacuum cups.

When forceps or vacuum pumps are used for infants, a variety of injuries can occur, with severe traumas (e.g., injuries to the nerves for the arms, skull fractures, or brain injuries and bleeds) estimated to occur in 0.96% of births. A variety of other less severe injuries (detailed here) also occur such as bruises, lacerations, hematomas, and neonatal jaundice (which occurs in 14.5% of assisted deliveries).

Note: the most severe complication I’ve come across from an assisted delivery was a baby with a challenging birth recently being decapitated due to too much force being used to pull the baby out.

Additionally, due to how malleable the skull is at birth (as the cranium has not yet fully formed), vacuum pumps and forceps can significantly distort the shape of the bones. While these changes are typically not considered concerning within the conventional medical field, many holistic schools of medicine place heavy emphasis on them, and we have met many adults who still had detectable dents from the forceps in their skull (along with many others who had decades of headaches).
Note: within these fields, vacuum pump deliveries are typically considered to be more problematic for the skull.

Skin to Skin Contact

At this point, I am relatively certain babies are supposed to go on their mother's skin after birth, as this is immensely healing for both of them, and in many cases can stabilize abnormal vital signs and sometimes save at risk babies (e.g., in less affluent countries, it’s been shown to reduce mortality of low birth weight infants by 25% and I’ve seen quite a few miraculous instances of it stabilizing a baby).

Unfortunately, since everything in medicine is about streamlining the procedure and getting things done as quickly as possible, years of work went into pressuring hospitals to support this, and even now it’s not universal. Because of this, it’s important to verify you have this option and to push for it (including if your infant was delivered via a C-section) unless there is an urgent reason not to do so. Additionally, you should make a point to have skin-to-skin contact after childbirth.

Note: many of the benefits of skin-to-skin contact are ascribed to it releasing oxytocin, the bonding hormone that creates contentment, trust, empathy, calmness, and security (while reducing fear and anxiety) and also moving milk through the breast ducts. While this is true, I also believe there is a vital energetic exchange that occurs (which is arguably more important).

For context, benefits of immediate (and daily) skin-to-skin contact for the infant include:

•Shortening the time until a premature infant can be fed orally.
•Preventing low blood sugar in infants and NICU admissions for it (e.g., a 50% reduction).
•Improve the gut microbiome.
•Less crying and improved sleeping durations (which as any mother can attest is very important).
•Developing the emotional capacities of the brain (e.g., increasing empathy later in life).
•Improved behavior, social interactions, and cognitive function in early childhood.
•Reduced physiologic response to stressors in infants and improved maternal bonding.
•Enhanced cognitive development

While for the mother they include:

•Reduced maternal PTSD (and other negative emotions) following childbirth (e.g., feelings of fear and guilt in mothers who had C-sections).
•Decreasing maternal anxiety and fatigue.
•Reducing postpartum depression.
•Starting breastfeeding earlier, improving the likelihood, and duration of breastfeeding (e.g., by 24%), including after C-sections.

Note: many of these benefits have also been observed in fathers who have skin-to-skin contact with the infant (e.g., improved vital signs, crying, and feeding in infants, along with reduced anxiety and depression in the father). There is also a famous 1995 case of premature identical twins, where one was dying, and then as a last resort, against hospital protocol, the cyanotic infant was moved to the same NICU incubator as her healthy sister, approached her to snuggle, and then was hugged by her sister, at which point her vital signs immediately stabilized and she came back to life (which made that practice no longer be controversial in the USA).

Umbilical Cord Clamping

Typically, when a baby is born, the umbilical cord will be quickly clamped, and then (if around) the father will be given scissors to cut it so he can feel like he’s part of the process, after which the placenta will be extracted and thrown away. The problem with doing this is that the blood inside the placenta (and the placenta tissue itself) is one of the most healing substances in nature, as it contains a large number of stem cells and vital growth factors.

This makes it vital for the baby to recover from the trauma of the birthing process; likewise, the placenta provides a critical source of nutrition for the mother.

Note: many hospitals will not allow you to preserve the placenta for encapsulation and consumption, while others may, provided you follow a set of procedures. As such, if you wish to do that (which I advise), it must be figured out before delivery.

Additionally, these materials provide the most ethical (and potent) source of regenerative medicine products available (e.g., cord blood stem cells, if used correctly, are often a miraculous therapy. A variety of very potent regenerative therapies can be made from the placenta, and the amniotic fluid provides an excellent source of exosomes).

In turn, various benefits have been identified from delayed cord clamping, particularly in premature babies (the most vulnerable to losing this essential blood). These include:

•Increasing the blood volume (by up to a third) and the body’s iron stores (which is critical for brain development in the first few months of life) along with decreasing the need for infants to receive transfusions (e.g., 55% less likely to in one study).

•Improving cardiovascular stability (e.g., blood pressure), and organ function (as more blood is available).

•Improved respiratory function (as the lungs depend upon blood coming in and out of them), which reduces respiratory distress (particularly since extended placenta blood flow aids the transition from umbilical to pulmonary circulation).

•Reduced intraventricular hemorrhages (brain bleeds) since the cord blood stem cells repair wounds (e.g., this study found a 60% reduction, while this study found a complete elimination of them [and seizures]).

•Reduced necrotizing enterocolitis (e.g., this study found a 41% reduction), a severe condition (25% mortality) that affects 3-9% of premature infants each year.

•Improved brain myelination, and neurological development.

Note: for most of history, cords were not clamped (it began in the 1600s), in the 1700s it was critiqued and by 1801, authors were warning that rapid clamping decreased an infant’s health and vitality. Starting in the 1950s, research and practice opinions started emerging arguing against rapid clamping. Still, it was not until the 21^st century that guidelines began advocating for slightly delaying when cords were clamped (e.g., in 2008 the WHO did, then in 2012 ACOG did for preterm infants, and in 2016 ACOG did for all infants). Despite this, only approximately 50% of US hospital births receive DCC (with the highest rates seen at hospitals that deliver fewer babies—presumably because they are not as rushed), and a 2009 global survey found most doctors either only occasionally practiced DCC or never did so.

In short, a good case can be made that many of the birthing complications we see arise from prematurely clamping the umbilical cord. As such, it’s unconscionable that the medical field has been so resistant to delaying cord clamping. Over the years, a variety of rationalizations have been provided by the medical field for why this procedure should be done, but in my eyes, it’s ultimately due to the fact there are too few healthcare workers in birthing units, so any step that can be rushed (e.g., saving a few minutes by clamping a cord) will be skipped—even when a small action can provide a profound benefit for the baby.

Note: ideally, you should not clamp the cord until it stops pulsating (arguably, you should wait even longer because some cord blood still transfers into the baby afterward). In many cases, this takes much longer than the minute hospitals allocate for delayed cord clamping.

Injections

After childbirth, infants are immediately given a vitamin K shot (within 6 hours) and a hepatitis B vaccine (within 24 hours), and the pressure to do these is so strong that if they are declined at a hospital, it can result in a child protective services referral.

In the case of the hepatitis B vaccine, unless the baby is born to a high-risk family and was not tested for hep B (which does not apply to most children), there is no justification for it and it exposes the child to significant risk (which is essentially why most countries do not give the vaccine at birth and why Trump had the CDC review and remove it from the vaccine schedule until a rouge judge overruled that this month). Note: the four answers I’ve heard over the years from insiders for why it’s actually given then is either to habituate parents to bringing in their babies for pediatric vaccine appointments, because the refugee population from the Vietnam war had high rates of hepatitis B, to ensure a small subsection of high-risk urban youth (who are unlikely to come in for further vaccinations) can be subsequently protected against hep B, or so that the vaccine can be on the infant schedule and hence enjoy the liability protections afforded by the 1986 vaccine injury act.

In the case of vitamin K shots, the argument for them is that infants are often deficient in vitamin K (which is necessary for blood clotting) as it does not transfer through the placenta and instead must be obtained through breast milk. As such, without supplemental vitamin K, they are more likely to experience subsequent bleeding, which, without prevention, in the first 24 hours affects between 0.25%-1.7% of births and 0.004% of infants between 2-24 weeks of age (of whom, assuming the estimates are not biased, 20% die). Furthermore, while oral vitamin K can also prevent this, the effect is not as long lasting (it needs to be done multiple times), so a shot is considered a more effective way to ensure it does not happen (e.g., if the parent does not give subsequent oral doses).

In contrast, there is evidence suggesting that vitamin K injections create chronic health issues, so a subset of parents decline taking it (which in turn leads to a small number of infant bleeding events)—many of which could likely be prevented if safer shots were made (as the additives rather than vitamin K are the most likely issue). Furthermore, while I cannot prove this, I believe the actual issue is early cord clamping, and if proper delayed cord clamping were widely practiced, much of that bleeding would not occur.

Note: there is a surprising lack of data in this area, but from looking at all of it, my best is that the vitamin K shots prevent approximately 1 in 1000 children from dying. Conversely, 0.3 in 1000 children experience a severe reaction to the shot.

Lastly, there is quite a bit of evidence demonstrating that premature infants (gathered from NICU data) are more susceptible to sudden infant death syndrome following vaccination (particularly if multiple vaccines are given concurrently).

Note: there is also a bit of data that giving a mother antibiotics during can adversely affect the infant later in life (e.g., it has been linked to obesity, epilepsy, cerebral palsy, and asthma).

Cesarean Sections

C-sections bypass the birthing process by cutting open the abdomen and directly extracting the baby. While they are sometimes necessary (e.g., the WHO made a good case that in 10% of births, they prevent maternal and infant mortality), they are done far too frequently (e.g., in 2024, 32.4% of all births were C-sections).

Note: one of my least favorite statistics in medicine is that C-section rates dramatically rise at the times doctors typically want to go home.^1,2,3

Surgical Risks

Being a surgery, C-sections carry a variety of issues commonly seen with other surgeries like the mother needing a 4-6 week recovery period (which longer than that from a vaginal birth), a global 5.63% infection rate (which is a bit lower in the United States), and significant pain (at the most important bonding period of your life), potential reactions to general anesthesia and accidental organ injuries (particularly since some c-sections need to be done very quickly to save the baby’s life).

Additionally, there are some surgical complications more unique to C-sections such as:

•Damage to the lining of the uterus creating adhesions and scars which cause the placenta to attach in the wrong place in future pregnancies (e.g. two C-sections make women 13.8 times more likely to have a placenta accreta).

•The weakened uterine scar can rupture during a subsequent delivery (especially if oxytocin is used), so one C-section can result in patients needing to have all subsequent births to be C-sections as well (particularly if the placental attachment becomes abnormal).

•The infant can accidentally get cut during the C-section (e.g., 1.5-1.9% get facial lacerations).

•The scars often cause significant issues for women for years if not decades (until they are correctly treated)—which in many cases they do not realize are the root cause of many of their issues until you point it out.

•The general anesthetics used for the C-section can increase an infant's risk of neonatal complications.

Note: C-sections also cause a variety of other issues, such as breastfeeding problems, worsened sleep, and emotional challenges (e.g., PTSD or anxiety).

However, beyond the surgery itself, simply bypassing the normal birthing process can also cause significant issues for infants.

Acute Risks

Hyaline membrane disease (respiratory distress syndrome—RDS) affects approximately 24,000 infants in the United States annually and is the leading cause of neonatal fatalities. The birthing process protects against this (e.g., studies have found premature C-section babies are 2.4-3.92 times more likely to have RDS^1,2,3), likely due to its mechanical pressure forcing excessive fluids out of the lungs.

Note: in 1979, Dr. Robert S. Mendelsohn discussed a recent study that concluded 6,000 of the 40,000 cases of RDS could be prevented by not bringing babies out of the womb before they were ready and then stated, “Yet the rates of induced deliveries and Caesarean sections are going up, not down. I can remember when a hospital's incidence of Caesarean deliveries went above four or five percent, there was a full scale investigation. The present level is around twenty-five percent. There are no investigations at all. And in some hospitals the rate is pushing fifty percent.”

Chronic Risks

C-sections have also been linked to a variety of chronic issues, most of which are immunological in nature. For example:

•A Kaiser study of 8,953 children found C-sections increased allergic rhinoconjunctivitis (hay fever) by 37%, asthma by 24% (53% in girls and 8% in boys).

•Roughly 2000 studies have assessed the link between C-sections and asthma. From them, a 2020 meta-analysis found C-sections increase asthma by 41%, while a 2019 meta-analysis found a 20% increase.

•A Danish study of 750,000 children aged 0-14 assessed a few autoimmune diseases and found those born by C-sections were roughly 20% more likely to develop Laryngitis, Asthma, Gastroenteritis, Ulcerative colitis, Celiac disease, and Juvenile
Arthritis (along with Pneumonia and other lower respiratory tract infections).

•A later Danish Study of 2,699,479 births found that elective C-sections caused a 14% increase in diabetes, a 14% increase in rheumatoid arthritis, a 4% increase in Chron’s disease, and a 15% increase in irritable bowel disease. Generally, the risk for these conditions was higher in women and for elective C-sections (with the exception of Chron’s increasing by 15% after emergency C-sections). Another similar study also found C-sections significantly increased the risk of asthma, systemic connective tissue disorders, juvenile arthritis, inflammatory bowel disease, immune deficiencies, and leukemia.

•A study of 7,174,787 births found C-sections made infants (in the first 5 years of life) 10% more likely to be hospitalized for infections (particularly respiratory, gastrointestinal, and viral ones).

•A study of 33,226 adult women found being born by C-section made them 11% more likely to be obese and 46% more likely to develop type 2 diabetes.

Much of this is likely due to C-sections disrupting the microbiome (which can persist into adulthood) as infants depend upon the vaginal flora (and external fecal flora) to initially colonize the gastrointestinal tract (as the microflora of the vagina are predominantly composed of the “good bacteria” our digestion needs and shortly after birth, the stomach starts producing stomach acid so other bacteria can’t as easily colonize the GI tract). In turn, many studies have found C-sections significantly disrupt the microbiome, including a prospective trial that demonstrated that the degree of lasting microbiome disruption in an infant directly correlated to their likelihood of developing asthma and allergic sensitizations.

Note: one partial solution to this (which does not address harmful hospital microbes displacing the normal microbiome) is to inoculate the infant with the mother’s vaginal secretions immediately after delivery. However, while compelling evidence has emerged for vaginal seeding in the last decade (e.g., this study and this study), it is not currently endorsed by the medical community, and most hospitals do not offer it.

Neurological Issues

Finally, C-sections have been linked to a variety of neurological issues:

•A mouse trial found C-sections led to behavioral changes and increased cell death in certain portions of the brain, while a retrospective MRI study of 306 children found that C-sections significantly reduced brain white matter and functional neural connectivity. A large 2017 study (published in nature) found that C-section children (ages 4-9) performed lower on standardized tests than vaginally born children and that this was not due to confounding variables, while a 2024 Nature study found C-sections caused lower motor and language development scores during specific age windows in the first three years of life.

A 2020 Czech study found 5 year old children born via C-section had poorer performance on cognitive tests than children born via vaginal delivery.

•C-sections have been found to increase the rate of ADHD by 15-16% and autism by 23-26%, while early onset schizophrenia has also been associated with C-sections (much of which may be due to C-sections changing the dopamine receptors in the brain).
Note: as this study shows, the increase in autism is strongly correlated to mothers receiving general anesthesia during the C-section.

•C-sections have been found to impair a newborn’s ability to recognize familiar scents, make them more averse to being touched or hugged, and have poorer sensory integration, visual memory, and visuospatial perception. In parallel, mothers of C-section babies have been found to have less attachment to and more negative evaluations of their children.

Since neurological development is such a complicated process, it’s difficult to say which factor (e.g., anesthesia, reduced maternal bonding, gut microbiome alternations) is ultimately responsible for these changes. However, many excellent healers I’ve talked to from a variety of traditions (e.g., the New Zealand Maoris) have shared that they noticed there is a loss of vibrancy and vitality in C-section babies which they attribute to them not “getting a spark” the vaginal birthing process facilitates (e.g., because the micro-motion within the skull is catalyzed by the compression experienced during the birthing process).

One of the most interesting conversations I had on this subject was with a doctor who shared that he was taught the vitality of infants directly correlated to how much they cried at birth (which is why, in the older days doctors would wack a baby soles to trigger a vigorous cry). In turn, when he and his colleagues attempted to help struggling infants with birth trauma by gently compressing the tops of their skulls to recreate part of the birthing process, they found that C-section infants would let out a brief but very vigorous cry, whereas children who had been born vaginally typically had a much softer cry—something they attributed to the initial birthing process not having catalyzed the cry they needed then (which is why it was so loud at the subsequent compression).

Note: this is somewhat similar to the observation in homeopathy that patients who can mount fevers tend to have stronger vitalities and better responses to homeopathic remedies, but as the decades have gone by, people have become less able to mount fevers and now have smaller responses to homeopathic remedies.

High Risk Births

One of the major factors in deciding what to do for a pregnancy is if you have a “high-risk” pregnancy. However determining what constitutes a “high-risk” pregnancy is quite subjective, and that designation being erroneously applied frequently results in a lot of stressful, unnecessary and potentially harmful interventions.

Typically, there are a few common situations that can require hospital births:

•The placenta is in the wrong place. This typically requires C-sections. However, in many cases, the placenta can move to the correct position, so if this is diagnosed early in pregnancy with ultrasound, it can lead to a lot of unnecessary stress.

•The baby faces the wrong direction with the pelvis instead of the head coming out first (a breech presentation). This is a fairly controversial area as many people I know will deliver breech babies (and it went well), but many others will not (as they have seen bad outcomes or infant deaths) following them (e.g., one large study found breech babies are 2.4 times as likely to die from vaginal deliveries). Because of this, I believe the best option is to fix the issue before delivery by moving the baby into the correct position (which frequently works—provided it is done correctly).

Note: if one of the infant’s legs or shoulders is sticking forward, a vaginal birth should not be attempted.

•The baby is head down, but facing the wrong direction (not facing forward). In our experience, these often end up requiring C-sections as it’s not possible to get the infant out.

•Twins are present. This does not necessarily require a C-section, but a variety of issues are more likely to come up, so it can be very helpful to have additional assistance nearby if needed.

•The mother already had a C-section (due to an increased risk of the uterus rupturing during labor).

•There are other characteristics of a high-risk pregnancy (e.g., the mother is older or obese, there is a concurrent maternal illness, the mother had preeclampsia during the pregnancy).

The Risks and Benefits of a Hospital Birth

Note: in America, a hospital vaginal birth is typically $13,000- $18,000 ($2,000-$5,000 with insurance), a C-Section is $25,000-$30,000 ($3,000-$7,000 with insurance)—although sometimes C-sections with complications can exceed $70,000 and a home birth (including the Midwife’s care through the pregnancy) is typically $2,500 to $6,000 (which insurance sometimes covers part of). Many in turn, believe this pricing (and the fact the most cost-effective option, doulas, are never paid for) has created a business of being born that does not prioritize the mother and child.

Based on everything that’s been presented thus far (along with the more subtle implications of these points), a strong case exists for eschewing a hospital birth entirely, as there are so many risks, particularly if you have a low-risk pregnancy. Conversely, our experience has been that a bit more than 5% of low-risk births ultimately end up needing a hospital birth (which can be quite stressful if you have to suddenly be transferred to the ER and be delivered by the obstetrician who is on-call).

Because of this, there is no correct way to approach this situation, and I feel a lot of that is ultimately due to how incredibly resistant the medical field has been to basic adopting approaches that take a little bit more time but greatly help the mother and child. For example, in 1991, the WHO created the “baby friendly hospital” concept (which incorporated a few of the basic things that should always be done), but three decades later, only 30% of American babies were born at hospitals with that designation.

As such, I believe the following are critical to do if you pursue a hospital birth:

•Be familiar ahead of time with what the entire birthing process entails and the choices you will have to make, as it is often incredibly difficult to figure all of that out in the middle of a delivery (which is essentially why I wrote this article).

•Strongly consider working with a doula (someone who helps with the childbirth process and afterward but does not have formal training), as the right doula can be immensely helpful. For instance, a Cochrane review showed doulas (or other sources of continual support) are associated with an 8% higher chance of spontaneous vaginal birth, a 25% lower chance of C-sections (also shown in this clinical trial), and a 10% lower chance of instrumental vaginal birth. Labors were also 41 minutes shorter, and women were 31% less likely to have negative childbirth experiences and 7% less likely to use epidurals. Additionally, there was less postpartum depression, and babies had a 38% lower chance of a low five-minute Apgar score. Likewise, this study found doulas decreased epidural use by 11.7%, and made women more likely to have a positive birth experience, feelings as a woman, and body perception.

Note: this study found training a woman’s friend for two hours on being a doula provided many of the same benefits an actual doula did—illustrating both the vital need for support and how much room there is to improve this.

•It is extremely important to have advocates with you who do not stress you out, understand what you want during the delivery, and want to support you. This can include the father (ideal but sadly not always possible), a close friend you trust for the role (and are comfortable with having there), or an outside doula or midwife you brought into the facility with you (which can often be extremely helpful). Giving birth can be one of the most empowering and profound moments of your life, but it can also be incredibly painful and challenging, so whoever is with you needs to get that and be supportive rather than an added source of stress.

•Consider making many of the decisions outlined throughout this article (e.g., delayed cord clamping), and if possible, find the best hospital in the area, and identify an obstetrician who you feel comfortable with and who appears open to a more natural childbirth.

Conversely, if you choose to not give birth at a hospital, you need to:

•Make sure you are smart about it and do not endanger anyone.

•Find the right midwife (and doula) to work with. Midwife experience, skill, and how comfortable you will feel with each one varies greatly, so making a bit of effort upfront to find the right person can pay a lot of dividends (e.g., do multiple interviews or go to an event where you can meet multiple potential candidates to see who you have a resonance with). Larger areas will often have a midwifery community, so by connecting with them, you can get a lot of helpful guidance in this regard.

•Understand the difference between lay midwifery (less training) and a nurse midwife (more training). Generally speaking, nurses who are also trained to be midwives will provide better care and are much less likely to cause disasters, but at the same time, I have met excellent lay midwives.

•Make sure you have a good spot to give birth in (which a midwife can help you with).

•Have a plan in place in case you do need to go to a hospital.

•Finally, be sure you are already engaged in a robust pre-natal and pregnancy health plan (as this often dramatically improves labor and the longevity of the infant).

Note: from having reviewed the evidence, I can’t say with certainty if hospital births have any mortality benefit for low-risk pregnancies. However, in high-risk pregnancies, they do reduce an infant’s chance of dying.

Optimizing Childbirth

As I’ve tried to show in this article, there are immense issues with how the medical system (still) handles childbirth. In turn, it is my hope a key component of Making America Healthy Again MAHA will be fixing them, as the unique moment we are in has the potential to change many long-standing issues in the medical system, such as those maternal activists have fought for decades to address (or finding ways to reduce the pressure on hospital staff so mothers can give birth in a more natural and relaxed manner).

Since this topic is incredibly important to me, I have spent years upon years searching for better ways to address many issues and dilemmas with childbirth. I have found some very helpful solutions that are still relatively unknown.

These will be reviewed in the final part of the article and include:
•What I now believe to be the best model for where to give birth
•Our preferred alternatives to ultrasound.
•How to mitigate many of the complications from C-sections and vaginal births (e.g., such as vaginal tears and hemorrhages, C-section scars, or an inability for the infant to breastfeed)
•Safe and effective anesthetic options for childbirth.
•The best options for cord blood banking vs. delayed cord clamping and placenta encapsulation.
•What you can do before and during pregnancy to ensure the optimal health of your child (e.g., how to prevent miscarriages and methods for correcting a breech baby) and counteract issues that come up during it (e.g., back pain, preeclampsia, and edema).
•A few other resources I’ve found to be very helpful for parents wanting to understand and navigate this challenging dynamic.

Read more

From that process, I came across many papers detailing the history of DMSO, and while many essentially retold parts of the story in Pat McGrady’s book (The Persecuted Drug: The Story of DMSO), many also contained things I never expected to come across. For example, I remember in the 1980s that gas stations would have signs saying “we sell DMSO,” but try as I might, I could never find a picture to prove this. However, during that project, I eventually found this in a 1982 article, which, while not a gas station, was pretty close:

Of these, papers on the history of DMSO, one caught my eye as it contained numerous lessons which hold just as true now as they did more than forty years ago.

A Brief History of DMSO

DMSO is a naturally occurring substance that is found throughout nature and routinely studied in climate research as it forms a core part of the sulfur cycle many microbial organisms rely upon. Discovered in 1866 by a Russian chemist, it was mostly forgotten until the 1950s, when an emerging need for new chemical solvents prompted the paper industry to meet that demand by oxidizing the dimethyl sulfide (DMS) wood pulping produced into DMSO.
Note: the cycle between DMS, DMSO, and DMSO₂, beyond underlying many critical ecological processes, also explains why DMSO causes some users to experience an odor, and will be the focus of a future article (but in the meantime, an abridged version on how to reduce the odor some DMSO users experience can be read here).

Before long, one pulp and paper company, Crown Zellerbach, was the primary producer of DMSO, and assigned a chemist to see if there were other uses for the tree solvents they produced. Herschler accidentally discovered that DMSO could carry dyes into the skin, and also quickly realized the immense value of this with antibiotics and antifungals to treat infections normal medications could not reach. Serendipitously, Stanley Jacob, a renowned surgeon at the nearby Oregon medical school had been searching for a way to cryopreserve organs that would be transplanted, and had recently come across a revolutionary study suggesting DMSO could function as an effective cryoprotective agent.

So, when Herschler, in 1961 shared his discovery with Jacob, Jacob enthusiastically explored it, and after tasting iodine shortly after mixing topical DMSO with it, realized this drug rapidly facilitated systemic absorption, revolutionizing pharmacology. Shortly after, they discovered it rapidly treated burns, then sprains, and then a wide range of musculoskeletal issues and before long, Jacob started carrying it on him to address whatever ailment someone he ran into had (with DMSO often working). These remarkable cures inspired Jacob to invest his career, personal time (despite having a family) and savings into DMSO research, and then remarkably, once he was broke, his dean agreed to have the medical school fund his research.
Note: once DMSO began being used in a medical context, the pulp production method was abandoned as it could not produce DMSO pure enough for medical applications.

The results Jacob got attracted immense attention, and before long, numerous pharmaceutical companies had heavily invested in studying DMSO, while in parallel, the media (e.g., The New York Times) widely promoted it (e.g., a 1965 NYT editorial called it “the nearest thing to a wonder drug the nineteen-sixties have produced”) and DMSO quickly became the most demanded drug in America. Initially, the FDA was extremely open and supportive of this, but due to the public outcry over the thalidomide disaster Dr. Kelsey prevented (which caused Congress, in 1962, to grant the FDA strict regulatory powers), the FDA switched to needing “well-controlled” evidence of drug efficacy they would meticulously evaluate for a drug to be approved.

Before long, due to just how many different uses DMSO has (each of which drug companies were applying to receive approval for), this became a major issue:

' 'The FDA representatives [in 1964] seemed anxious to do everything possible to permit further testing of DMSO," Jacob told me later. "They pointed out that DMSO was a very versatile drug; and because of this they were a little apprehensive as to how many IND applications might be filed to test not only DMSO alone but DMSO in combination with various other pharmacologically active substances. "Dr. Kelsey said the number of combinations could be a hundred or more, representing a formidable challenge for a bureau that already was overburdened."

Laziness won, and the FDA began looking for reasons to stop this. Eventually in late 1965, settling on preliminary data in dogs showing high doses of DMSO could change how the eyes focused (which was never reported in the trials being conducted on 37,000 people or subsequently in humans or monkeys) and a single death (that has never occurred since and was likely due to an allergy to another drug being taken concurrently), the FDA not only banned all DMSO testing in the United States, but sent out global telegrams to each embassy encouraging other nations to do the same. Following this, the FDA, eager to assert its newfound power, then began a relentless campaign to intimidate doctors and scientists into not conducting any further DMSO research (which, I believe is a large part of why researchers now are so reluctant to ever study “unorthodox” topics).
Note: the playbook the FDA used against DMSO was also used against many other remarkable (now largely forgotten) medical therapies.

Fortunately, the scientific community had not yet lost their spine, and fought back, with Jacob organizing three American symposiums (one in 1966, along with one in 1974 and in 1982—along with a 1965 one in Germany and a 1966 one in Vienna). Sadly, despite the wide range of data presented, the FDA dug in, insisting there was “no evidence” DMSO worked for anything, and eventually, in 1980, a Congressional and Senate hearing were held on the FDA’s stonewalling, where the FDA repeated a variety of excuses and made a series of promises to stop stonewalling DMSO (which not surprisingly, were never followed).
Note: the first therapeutic FDA approval for DMSO (DMSO for interstitial cystitis) happened in 1978, and I suspect was motivated by the FDA wanting to create the impression they weren’t stonewalling DMSO drug application prior to those hearings (as no subsequent approvals ever happened despite many being sent in).

To support these 1980 hearings, Mike Wallace (of 60 Minutes) aired a program immediately before the first one, which introduced the public to DMSO, and created a new wave of widespread interest in DMSO (after the FDA successfully squashed the first one in the 1960s).

Following this, DMSO experienced another surge in popularity, but gradually was forgotten except by certain segments of the alternative health community and veterinarians (who widely use it in practice). Likewise, with American research, while there was initially a huge surge of it (particularly in the 1960s) it greatly declined, and by the 1990s, therapeutic studies of DMSO in humans or animals were rarely conducted. Instead, medical research in DMSO (besides its approved use for treating interstitial cystitis) largely shifted towards it:
•Being used as a cryopreservative
•Being used as an “inert” (harmless and non-beneficial) solvent to test a wide range of potentially therapeutic substances (predominantly in cell cultures).
•Making cancer cells revert to normal cells (which is often needed for research).
•Facilitating other therapies (e.g., there are now well over a dozen FDA approved drugs which contain DMSO as an “inert vehicle”).

Fortunately, in 1971, after extensive research the Soviet Union’s Ministry of Health approved it (as Dimexide/Dimexid/Димексид), and as a result, much of the forgotten data on DMSO’s medical uses comes from the Russian and Ukrainian literature, along with a smaller amount from Chinese, South American, and German researchers (most of which I have finally been able to compile).

Note: this history is covered in much more detail here.

Early Innovators

Propaganda essentially works because most humans want to follow the crowd, but simultaneously, there is always a small portion of the population which will trust their gut and have the courage to pursue things that aren’t yet “safe” to do because neither authorities or their peers are telling them to (e.g., despite the most aggressive propaganda campaign in history, immense peer pressure and increasingly strict vaccine mandates, roughly 25% of Americans did not get the COVID vaccine).

This blog in turn is catered to the self-directed “innovators” and “early adopters” as my goal as much as possible is to provide all the essential information one would need to understand a topic and then be able to figure out how to approach it, rather than giving you a set protocol for everyone to follow and “telling you what to do.” This I believe is essential, as virtually every therapy, despite having a standard dose, typically needs to be dosed differently for different people (and I believe many medical injuries with pharmaceuticals could be avoided if lower “non-standard” doses were used for more “sensitive patients”).

However, the education system trains everyone to repeat formulas and instructions rather than creatively thinking on their own, so the standardized model persists, and the harm the excessive doses create are simply viewed as a necessary cost of doing business. This is unfortunate as while (clean) DMSO has a fairly wide therapeutic window (so, unlike many far more toxic drugs, it is very difficult to take a DMSO dose which is high enough to be dangerous), the correct DMSO dose greatly varies from person to person. As such, many commentators (beginning with Jacob) have remarked that while it is incredibly easy to determine the correct dose for a unique patient you work with, DMSO lacking a “standardized dose” has been one of the most challenging aspects of widely deploying the drug.
Note: this is why I have to include about 8 pages of instructions on general DMSO use at the end of each DMSO article (e.g., I did so most recently here), along with a similar amount for specific conditions being discussed within a given article. This has worked for a lot of people (particularly early innovators), but simultaneously, many have not wanted to read through the instructions and instead simply wanted a simple universal protocol (which will inevitably not work for some of those who use it). This is quite challenging to navigate, and my approach has essentially been to hope that if I can provide enough clearly laid out information, the early innovators who see it can understand how to translate that to people they meet who just want a single protocol to follow.

The phrase “early innovators” in turn came to mind due to a noteworthy 1985 article which I read during the DMSO project (“DMSO, Hobby Shops and the FDA: The Diffusion of a Health Policy Dilemma”) which discussed DMSO and the diffusion of innovations (e.g., their adoption).
Note: the dilemma being referred to was that since DMSO was legal as an industrial solvent, the FDA could not ban it, and instead could only restrict people implying it had medical uses.

History Repeats

When I created this newsletter, one of my primary goals was to get (hard to find) information out there on effective forgotten therapies that told you what you actually needed to know about them in the hope I could spread it out enough that people who were genuinely interested in the topic would eventually be able to find it. However, due to the highly unusual era we are in now, far more happened, and due to the DMSO series here going viral, I essentially created the third wave of interest in DMSO.

DMSO, Hobby Shops and the FDA: The Diffusion of a Health Policy Dilemma, in turn, caught my eye as virtually everything it described in 1985 perfectly mirrors what has happened with DMSO over the last two years. As I cannot quote the entire article here (much of which came from interviewing DMSO users who responded to a newspaper ad), I will try to highlight the most poignant parts:

We learned that DMSO is being used for an astonishing range of ailments. In order of reported frequency, these include: Osteoarthritis, rheumatoid arthritis, back injuries or pains, stiff or painful necks, knee injuries or pains, bursitis, ankle sprains, tennis elbow, hip pains, muscle spasms, burns, decubitus ulcers, psoriasis, headaches, varicose veins, scleroderma, insect stings, emphysema, cataracts, and toothaches. Actually, these are only a few of the claims being made for the curative powers of DMSO. Clearly, it is a substance that could touch many lives.

The users are as diverse as the uses (see Table 1)

Rogers and Shoemaker speak of five key innovation characteristics that may facilitate or impede adoption: relative advantage, compatibility, complexity, trialability, and observability.

They observe that there are a number of subdimensions of relative advantage including ". . . low initial cost, lower perceived risk, a decrease in discomfort . . . and the immediacy of reward." For most of the respondents, DMSO had these attributes.

Moreover, the absence of effective medical remedies for arthritis and soft tissue injuries combined with these relative advantages, make DMSO an attractive alternative. Regardless of whether a possible placebo effect was operating, most of the interviewees reported rapid decrease in pain and increased mobility with few perceived side effects and a low price.

Fairly typical of our interviewees were statements like the following: I wasn't able to stand up and swing my left leg because of my knee pain. . . after two treatments of DMSO I could do it with no pain whatsoever. . . I cried because I could swing [my legs] almost like I was doing a can-can. I had not been able to walk up stairs for five years ... I used DMSO three times on my right hip and I now can climb stairs without any pain . . . I was severely burned when I spilled scalding coffee on my lap . . . I went to a burn center and they wanted me to stay but I did not want to because I had this trip planned to see my mother in Iowa . . . I started applying DMSO and it healed miraculously and I got to go on my trip . . .

The lack of approval by the FDA and other medical authorities may both lessen and reinforce the relative advantage of DMSO. While many interviewees are fearful of using an unapproved substance, other interviewees see the lack of approval as a confirmation that DMSO works. This paradox is explained through an interpretation which sees restraint of trade, not scientific caution, as the real explanation for the FDA failure to legitimize DMSO. If DMSO became legal, they argue, doctors and drug companies would lose a good deal of money. Therefore it must be good or "they" would let it on the market. Thus for some, the relative advantage of DMSO may even be strengthened by official non-approval.

Note: the next part of the article discusses how many being familiar with topical pain ointments, having already used DMSO in animals, or having a vet suggest it to someone for an “incurable” issue they’d seen DMSO treat in animals made it compatible (familiar) and hence likely to be adopted.

In addition to a strong relative advantage and high compatibility, DMSO compares favorably to other remedies because of its perceived low complexity, that is, ". . . the degree to which an innovation is perceived as relatively difficult to understand and use" For most people, there was no problem in learning how to use DMSO despite an almost total blackout on information, education, and instructions.

Vendors are fearful of FDA action and so are very guarded in what they say. A fairly routine story was related by one respondent: When I asked them what do I do with it they [vendor] said "I don't know," and I said just give me a little idea how to put it on and they said mix it with the paint and I said that's not what I'm going to use it for and they said "I don't want to hear any more." . . . they were kind of cold.

Note: this article also highlighted the immense confusion and variation with using DMSO (that users eventually somehow figured out) and that they experimented with topical DMSO combinations such as vitamin E oil or corticosteroids.

Although it often produced a skin burn or an unpleasant odor, these effects were welcomed by some as a positive sign. As one woman said, "If it doesn't smell or give a burn I'd throw it out because it wouldn't be the real stuff ... I know it's good, it burns ..." Users either tolerated these effects or applied creams and ointments just as they would do with other skin irritations. The distinctive odor was more often a source of amusement than worry.

Trialability means that a user can experiment with an innovation on a limited basis. DMSO was used in this way by nearly all the respondents. Those who found no relief stopped using it after about a week; one individual kept applying it for four months before the pain "suddenly" went away. It is an innovation that is eminently suited for trial on the installment plan, an important advantage for those who either are wary or without great financial resources. DMSO could be tried and discarded without much financial or any apparent physical harm

The degree to which an innovation is visible to others is labeled observability. DMSO is not highly observable in the sense that the absence of pain is not something someone else can see. However, we repeatedly found that those who used and liked DMSO did not hesitate to tell their friends, relatives, neighbors and, in some case, complete strangers. Word-of-mouth has been an important factor in making DMSO "observable" to many who otherwise would not have considered it….For this reason DMSO, despite its "illegality," has achieved a high positive observability.

It is not enough for a substance to have the requisite qualities of advantage, compatibility, reduced complexity, trialability, and observability. It must also become known. Just how did DMSO come to the attention of so many Americans? [In most cases, their initial interest was due to viewing the 60 Minutes program].

Many interested viewers naturally turned to their physicians; however, they soon learned that DMSO cannot be legally prescribed. Moreover, most physicians were either indifferent, uninformed or hostile; one respondent reported that his doctor refused to continue to treat him because he was using DMSO. Many did not even bother to tell their doctors often out of fear of just such a reaction. As one woman related: “I didn’t know who to call ... didn’t call my physician because he would climb the wall if he knew that I thought about using it ...” However there were a few physicians who were either neutral or had even tried DMSO themselves. Some respondents said their physicians were curious and asked the patients to let them know if it helped.

Thus, given the indifference or active opposition of most health professionals, many users started asking among their friends or relatives who had used DMSO, reading articles in papers or magazines or just using it without any verification or information. Those who felt that DMSO had helped them became in turn sources of information, and in a more than a few cases, active proselytizers. Some reported recommending it to up to a dozen people, including strangers who complained out loud in public places about aches and pains. Table 2 highlights the respondents' reports of their DMSO information and verification sources.

The article then concludes by highlighting that the FDA’s refusal to regulate DMSO in a responsible way has led to hundreds of thousands of Americans using it in an unregulated manner (the situation the FDA wanted to avoid) and criticizing programs like 60 Minutes for irresponsibly using “the enormous power electronic media now has over the health field” (whereas downplaying DMSO’s benefits would have been the “responsible choice”).

Conclusion

I have long believed one of the greatest mistakes humans have made throughout history is believing they can fully control fate and prevent the inevitable natural emergence of anything which challenges what they want. Because of this, again and again, I see the same historical dramas play out, and each time the rulership tries to suppress them from emerging, they temporarily disappear but then eventually emerge in a far more powerful manner.

For example, the smallpox vaccines were never proven to work, caused severe injury (that doctors covered up), and not only frequently failed but often caused smallpox outbreaks (detailed here). The public resisted this, and in response (to address the increasing outbreaks) harsher and harsher mandates were instilled. This lead to massive public protest against the vaccines and eventually, in 1885, an English city making vaccination optional alongside employing basic public health measures to contain smallpox. Contrary to the medical field’s apocalyptic predictions, this worked, and those public health measures were then copied, allowing smallpox (due to it not being very contagious) to be eliminated.

I mention this because I started this newsletter during the COVID-19 mandate protests (e.g., the Canadian truckers) as I realized we were re-enacting the exact same thing and people needed to know so we could break that dysfunctional cycle. Incredibly however, rather than it taking nearly a century (1976-1885) to stop the shots, it happened in two years, and public opposition now to the COVID vaccines is much greater than it ever was to the smallpox vaccine.

Similarly, due to the fanatical devotion the current rulership has to vaccines, for decades, any suggestion they cause harm is unilaterally censored, and the careers of those who speak out against them are destroyed. Nonetheless, because vaccines injuries are cumulative, as time goes on and more and more are given to us, the injuries have continued to increase, and in the last few years, reached the point it is no longer possible to cover them up.

Because of that, we have now seen rather extreme swings on this issue no one in the field previous imagined could happen (e.g., RFK becoming HHS Secretary, and the President openly speaking out about vaccines neurologically damaging children). Likewise, we are now seeing every stop be pulled out to protect vaccines (e.g., a wide coalition of Senators have been prioritizing targeting any political appointee who does not openly pledge allegiance to vaccines), and in the last week, to prevent ACIP (the committee which decides vaccine policy) from finally, after decades, allowing those injured by vaccines to publicly testify:

•Fake polls were made to convince the Trump administration the entire public loves vaccines (when in reality, most polls now show roughly half of Americans distrust vaccines) and then amplified by the mass media (e.g., The New York Times) immediately before the midterms.

•Damaging ACIP reports were “leaked” to the NYT (so a major hit piece on the upcoming meeting could be published three days before the meeting).
Note: I could not help but notice that article ridiculed the existence of COVID-19 vaccine injuries, whereas 10 months ago (due to the costly profound loss of public trust in the medical system from the COVID vaccines), the NYT published piece which “tried to have their cake and eat it” by acknowledging COVID vaccines injuries were real, but simultaneously downplayed them and said everyone was “sorry” but no one was at fault for this debacle—illustrating just how disingenuous these people are.

•Two days before the meeting, a rogue judge (who has been reprimanded for previous similar rulings) arbitrarily ruled against the recent CDC vaccine schedule change and that everyone whom RFK Jr. put on ACIP was “not qualified” to be there and therefore, all their previous decisions were voided and the committee could no longer meet.

As court decisions (even ridiculous and unjustifiable ones) take a while to appeal, this coordinated attack effectively cancelled the upcoming ACIP meeting and prevented the vaccine injured from ever having a voice (along with blocking simple policies like having a way to actually track COVID vaccine injuries with a new diagnostic code and thereby make the injuries statistically exist). This was understandably devastating, as many of us (especially the ACIP members) put an immense amount of work (and often personal sacrifice) into improving the vaccine program as the system permitted it to be done, but then in the blink of an eye, a dishonest judge arbitrarily swept it all away.

However, if you consider the broader process at play, the wave against vaccines keeps building (e.g., previously it was never necessary to use tactics as extreme as this to protect the vaccine program), and now, there are even stronger feelings on this issue (as it mainstreams the vaccine issue within the Republican base because they’ve developed a strong resentment towards activist judges arbitrarily overturning conservative policies). For this reason, vaccines are likely to be an increasingly contentious issue that sooner or later, will culminate into a wave which is too large for anyone to suppress.

Furthermore, the unique characteristic of our era is that everything is greatly accelerated, particularly due to the widespread loss of trust increasingly brazen propaganda creates in the populace (e.g., what we witnessed throughout COVID-19), users searching for new media platforms and key platforms like 𝕏 (Twitter) allowing the rapid free diffusion of pertinent information.

That, I would argue, accounts for why we were able to so rapidly overturn the COVID vaccine program (despite every stop being pulled out to enact it), why the public opinion on vaccines in general has shifted so rapidly in the last few years, or on a more minor note, how a DMSO project by an essentially unknown author (which I never expected to go anywhere) instead was seen by millions of people, and, after 40 years, at last created a third wave of interest in that remarkable therapy.

Things like this are essentially what motivate me to try as hard as I do to make a positive contribution to the world we now live in, and how I am able to keep each setback in perspective (e.g., I never expected shifting the cultural perspective on vaccines to be easy, and while the setbacks are frustrating, I am mostly in awe of how much has already happened). I hope that this perspective can be helpful for you as well, and I sincerely thank each of you for giving me the chance to finally be able to positively shift some of the massive issues I’ve always wished but never imagined could be improved.

Author’s note: The most current information on using and procuring DMSO can be found here. Additionally, a key part of this project has been made possible by you submitting your treatment experiences with DMSO (now nearly 6,000) so we jab sort and present them. If you have had any therapeutic experiences with DMSO you would like to share, please consider doing so here.

To learn how other readers have benefitted from this publication and the community it has created, their feedback can be viewed here. Additionally, an index of all the articles published in the Forgotten Side of Medicine can be viewed here.

I eventually decided that the best option I had was to try to address as many potential questions as possible in the articles post monthly open threads where anyone could ask what they wanted to, as that way I could efficiently get through the pressing questions I was not able to answer throughout my articles and then pair those threads with a topic that didn’t quite merit its own article.

For this month’s open thread, I wanted to talk about a topic that’s becoming an increasingly important part of our lives—artificial intelligence —given how much I’ve interacted with it over the last six months while researching DMSO.

Note: this article builds upon a previous one (the Great Vanishing of Information), which highlights how certain types of information are being buried on the internet unless you know how to find it.

The DMSO Project

DMSO is one of the only therapies I know of which:
•Treats a wide range of common ailments.
•Frequently is able to treat conditions often otherwise viewed as “incurable.”
•If used correctly, it has a very high safety profile.
•Has extensive scientific literature corroborating its safety and efficacy.
•Is easily available and highly affordable.

Unfortunately, DMSO has languished in an unusual spot. It was widely used throughout the pharmaceutical industry, a component in many drugs and was the active agent in a few FDA approved therapies but simultaneously, despite decades of protest (including by Congress) and being widely used around the world, the FDA essentially banned DMSO from medicine in America, and few even know about it (demonstrating that medical policies is often the result of politics rather than science).

Because of this, I felt it was worth publicizing the mountain of forgotten literature showing DMSO worked, and once I did so, many people reported profound improvements and disbelief that something like DMSO existed, which they had never heard of (resulting in those articles receiving millions of views and thousands of readers sending in remarkable reports of what DMSO did for them). This took me by surprise, and I realized it reflected the fact that, since DMSO costs so little, no one would ever be incentivized to promote it. So, as time continued, I gradually felt that I had a responsibility to do the best I could to present the case for DMSO as more and more readers began relying upon me to do so, and it was unlikely anyone else would undertake the full scope of what that endeavor to publicize the extensive volume of literature corroborating its use.

Unfortunately, as I dove into all the books that had been published on DMSO, I quickly discovered that almost all the books that had been written on the topic simply copied previous books in the genre (rather than independently researching the topic), and as such, the DMSO field was essentially unaware of most of the pertinent DMSO literature.
Note: similarly, there was immense variation in the DMSO protocols authors proposed, leading me to conclude that many were largely arbitrary and not extensively researched by the authors.

To some extent, this makes sense, as there is an overwhelming amount of literature on DMSO (DMSO has many different spellings, and many general searches for DMSO returned thousands, tens of thousands, hundreds of thousands, or millions of results). So, as I started scouring the databases, I gradually came up with ways to simplify the immense task of finding the pertinent studies (e.g., title-only searches in Google Scholar for DMSO/dimethyl sulfoxide/dimethylsulfoxide plus a condition would dig up many relevant studies).

However, it simultaneously dawned on me that because there were so many different permutations, the only possible way I would actually be able to find many key studies for DMSO would be to search each database for each phrasing used for DMSO, collate all of the relevant studies which came up in the process into a document, and then sort that document by each condition. For a while I went back and forth on if I wanted to do this, as it would take an immense amount of time to do (requiring me to cut off every non-essential commitment in my life and significantly reduce my output here), but as time went on, I felt more and more obligated to do it due to the unprecedented support so many of you had given the series.

So, eventually, on October 25^th, after I finished the last DMSO article, I set a goal to complete this in two months and hoped that this gap would not be too disruptive to everything else. However, as I began that project, I gradually realized searches I previously thought were impossible could be done, and kept extending my timeframe while simultaneously trying as hard as I could to get things done as fast as possible without cutting corners (which was very challenging for my body, mind, and spirit). A few days ago, I essentially finished, and because of that, I felt I owed the supporters of this newsletter some accounting of where all that time had gone.

Note: in the “title” searches, the studies themselves are not yet summarized (that will be done later), whereas in the non-title ones, they have (as I needed to verify the articles contained pertinent DMSO information). Additionally, in the PubMed searches, I feel I need to re-read through about 30,000 results to flag some that were missed, as I used AI to flag that set (due to being too tired to manually read them), and I realized near the end that the approach I used missed some of the studies that should be flagged. Lastly, while I went through the main databases and most of the terms for DMSO, I know I missed some, which means even with this, there are still DMSO studies waiting to be discovered.

Additionally, one of the most challenging parts of this project was going through the Chinese database, as due to its numerous issues, I eventually realized the only viable option was to use a very rough filter of the 40,000 search results, then copy and paste each one’s title and abstract into a document, and then subsequently sort that document. Presently, that is the only remaining task, but it’s essentially done and will be this week.

Fortunately, while all of the previous was quite challenging, the next step I’ve been waiting months to do (searching for specific keywords so the studies can be moved to other documents and sorted) is infinitely easier and faster to complete.
Note: in tandem with this, another member of the team is also doing a similar process with the 6,000 reader DMSO reports that have been received, so they can be turned into an easily accessible reference for individuals curious as to how DMSO interacts with a myriad of medical conditions (as it can be used in so many areas, it simply is not feasible to study every application so a synthesis of reader reports represent the best source of data which can practically be obtained in this regard).

Artificial Intelligence

Like many, I have begrudgingly accepted that AI is a part of life and I need to learn how to use it effectively (whereas initially I resisted it because I did not like how using it diminished my cognitive capacities). More than anything else, I believe the most important thing is that writing is not the information you present, but rather the heart and intention behind it (discussed further here). As this is somewhat of a spiritual process, I believe it is unlikely AI will ever be able to replicate it. In turn, I do not like the way AI text sounds or feels, and hence feel quite strongly about not using it (despite its potential to save a lot of time). Similarly, many of the edits AI proposes, while “correct,” break the flow of what I’m trying to convey within the writing, so I am very adverse to it (as how writing feels is very important to me).

Concisely, my perspective is that the currently existing AI has a lot of value if you use it to help you complete a task (or find out how to complete a task), but if you rely upon it to do a task for you, it will frequently create issues that outweigh the benefits it provides. Put differently, completing a task often requires completing a sequential series of steps, and if you understand each step well enough to quickly see if they are being done correctly, AI can greatly help you on the time consuming steps, but at the same time, if you task it with doing sequential steps in a row to do a task for you, rather than assigning something much more concrete (e.g., a single step or process), errors are inevitable which are not acceptable if accuracy is required.

For instance, in this task, I quickly realized:
•AI could not find most of the studies I wanted (e.g., because it wasn’t familiar with most of the databases I wanted), but simultaneously, it was very good at compiling generalizations of things repeatedly studied in the literature (e.g., how DMSO at different concentrations typically affects cells).

•With a bit of work, AI could accurately extract and summarize DMSO pertinent information from large studies (e.g., turn a 30-page paper into a one paragraph summary). This is essentially what made the project possible, as there was no other way I could have reviewed millions of pages of DMSO-related literature.
•AI eliminates language and text recognition barriers, which otherwise made it prohibitively time consuming to ever review foreign studies.
•If you give AI a large volume of studies to filter for relevance, it is very difficult to have it have appropriate sensitivity and specificity (it either misses some or flags way too many), and this accuracy varies by the model. Because of this, I largely avoided doing this (instead manually reading through them) and primarily used this filtering on certain groups of foreign studies where it was otherwise prohibitively time consuming to go through them, and accepted a certain portion of studies being missed as a necessary trade off to finish the project. Likewise, in many cases, it was effectively impossible to functionally filter results, as you had to be familiar enough with the DMSO literature to know how DMSO was likely used in a study based on its title (if DMSO was not within the title).
•There are a lot of tricks that exist within word processors and databases, which made projects like this a lot easier to do, and generally, while there were issues with executing them directly, the AI systems were very good for telling you how to do them. For example, Google Scholar only lets you view the first 1,000 search results, so I had to find very creative ways to sequentially break up 4,130,000 results (what you get for searching it for “DMSO”) into relevant chunks that were under that cap and throughout the process, I needed to write small lines of code to facilitate certain steps which they showed me how to do and I could then tweak.
•There are a lot of things AI will reliably screw up, to the point you simply cannot assign those tasks to it. Nonetheless, if 10 steps need to be done and AI can do 3-4 for you, that still saves a massive amount of time.

In short, AI as a tool made this entire project (which would have otherwise been impossible for anyone to ever do) possible to do, but simultaneously, it still required a lot of work on my end, and given the constraints I ran into, I feel it will be a long time (if ever) that functional AI systems can replicate what I did here. I wish it were not that way (the last 5 months were miserable), but that’s just the way it is, and I’m primarily grateful there was actually a way to do this.

Note: throughout this process, I was constantly learning and changing how I approached this compilation. One of my major regrets was that the moment the war with Iran started, my mental bandwidth was stretched to the point it did not occur to me to immediately switch to going through all the remaining Iranian studies (by adding site:.ir to the search query), as shortly after, Iran’s internet was cut off, and it became impossible to access anything on their servers.

Furthermore, because of all the time I’ve spent trying to understand how to effectively use AI to facilitate this task, I’ve also had a lot of time to reflect on how I think AI will affect humanity, particularly with regard to cognition.

The Scalability of Governance

In almost every government, there is an inevitable tendency by those who rise to power to try to control every aspect of society they can get their hands on—even when those individuals are clearly wrong (e.g., consider how many clearly counterproductive and harmful COVID policies were continually pushed despite widespread public protest against them). As such, over the centuries, a variety of approaches have been adopted to stop government overreach such as constitutions, courts, and guaranteed rights, putting checks and balances in place to prevent any part of the government from becoming too powerful, making officials accountable to the ballot box, or directly arming the citizenry so they can resist tyranny.

However, I believe the most effective check on government overreach is simply the scalability of tyranny. For example, if two officers or soldiers were assigned to ensure a troublesome citizen always complied, that would most likely work, but would be impossible to implement on a large scale as it’s generally accepted that at most 5-10% of the population can be soldiers (before the economy collapses), whereas what I just described would require more than half of the population to be diverted to simply ensuring people complied. Similarly, while police can generally maintain law and order, once too many stop obeying them (e.g., during riots), things can rapidly scale out of control, and anarchy will emerge (something also seen when a government partially collapses).

In turn, my observation throughout history is that frequently, the thing that stops horrific policies from being implemented is not any ethical considerations by the ruling class, but rather, simply how feasible policies are. In contrast, the thing that made the totalitarian states of the 20^th century so destructive and unprecedented was that technology no one was ready for, had recently emerged, making it possible to radically scale up mass social manipulation and genocide.

To illustrate, there has been a longstanding belief in the ruling class that, like wildlife managers, they have a duty to prevent the human population from becoming too large and overwhelming society’s resources, which has resulted in brutal forced sterilization or forced abortion campaigns (which the population understandably fought back against). Because of this, once injectable birth control became available, globalist organizations switched to this more feasible approach (e.g., on refugees) and then put decades of work into fervently developing a far more scalable form of population control—sterilizing vaccines (which were then pushed upon the developing nations).

Because of the scalability constraint, the ruling class has largely shifted to a passive model of control where:

•Economic incentives are put into place that force people to comply (e.g., many of the harmful or unnecessary practices in medicine ultimately originate from how the compensation model is set up—something we saw go into overdrive during the pandemic when hospitals were paid to push disastrous COVID protocols).

•Micromanaging the population was delegated to corporate employers (who could be controlled through economic incentives and, likewise whose workforce could be controlled by the economic necessity of having to tolerate an undesirable employer or submit to a dangerous vaccination).

•Using the limited enforcement resources of the government to make public examples of those who didn’t comply so the rest of the population would be frightened into compliance (which likewise was done to the doctors who dissented against the COVID protocols).

•Gradually create algorithmic systems to encourage compliance (e.g., social credit scores), and potentially digital currencies that can cut off people’s access to society.

•Have people be so busy and overwhelmed with their work and livelihood that they do not have time to do anything else, such as protesting a corrupt government (which I and many others believe is a key reason why so many things that could reduce the need for people to work or have effective, affordable healthcare are never implemented).

•Having the media continually distract and disorient the population so they were drawn away from doing anything that could challenge the system.

Unfortunately, AI effectively addresses this scalability issue, as rather than requiring the majority of the population to be soldiers, a handful of engineers can now manage a system that effectively monitors (and harasses) the population. This is a very worrisome possibility we’ve never had to deal with before, and was highlighted in one of RFK Jr.’s most controversial remarks:

“Even in Hitler’s Germany, you could you could cross the Alps to Switzerland. You could hide in an attic like Anne Frank did…the mechanisms are being put in place that will make it so none of us can run and none of us can hide.”

Similarly, one of the primary checks against war has been the need to have large numbers of soldiers to comply, as it’s typically not feasible to get a large portion of the population to fight a clearly unjust war as most human beings (regardless of how much you drug or condition them) do not want to kill others unless they truly feel they have to.

In turn, one of the major issues with AI is that it’s making it possible to kill on the battlefield without needing compliant soldiers. Presently, we are seeing this with drone warfare (which I believe the Ukraine war, to some extent, is being used to develop much in the same way Vietnam broke out a few years after the military decided they needed to develop helicopter gunship warfare). As such, I am extremely worried about the future that will be created once actual AI warfare (e.g., with robots) becomes viable, and if I could have one wish, it would be for an international treaty that outlawed it (which could potentially be justified under the need to avoid a Terminator scenario).

While this was long a hypothetical consideration, the fact that the knowledge gained from the Ukraine war is now being ported over to Iran (in lieu of soldiers being deployed to eliminate Iranian personnel in the streets), shows we are actually quite close to this future emerging. I find this particularly worrisome as the greatest atrocities in history typically occur when those who order the killing are disconnected from the act itself (e.g., Obama routinely signed off on drones to kill many people, including civilians, in the Middle East), and automated AI weapons put the entire process into overdrive to the point in may never be possible to put that genie back in the bottle.

Note: similarly, if the government can automate its policing activities, that opens the door to immense tyranny.

Government Efficiency

Bureaucracies by their nature are always inefficient and dysfunctional. On the one hand, this is a good thing, as it often ensures there is some way to hide from or evade it (e.g., via a legal loophole), but on the other hand, it can lead to immense waste, inefficiency, and inertia.

Elon Musk’s Department of Government Efficiency (D.O.G.E.), for example is making it possible to audit a wide range of government programs and identify the wasteful and unnecessary ones, something many have tried to do for years—but it simply was not feasible to implement as there was far too much data for a few assigned personnel to unravel.

While this new era exposes us to significant risks (e.g., D.O.G.E. is also sometimes cutting necessary programs, and the vast AI apparatus is taking away our ability to hide from the government), it is also making it possible to tackle many longstanding institutional problems.

For example, I have long believed one of the simplest ways to end bad medical practices would be to have AI systems analyze the electronic record data from large medical systems, as within minutes, they can complete analyses that would take researchers years to conduct (and then can be repeatedly tweaked to figure out what’s actually there). Unfortunately, over the years, I have met many people who were genuinely interested in pursuing this, but they all ran into roadblocks because the medical industry did not want the harms of their moneymakers being exposed.

In turn, one of the exciting ideas MAHA has brought forward is doing just that (e.g., using AI to compare all the health records of the vaccinated and unvaccinated) as this is a way to expose all the harmful and wasteful healthcare practices that have gone on for decades—particularly since the current administration is prioritizing eliminating wasteful spending. However, I should note that at this point, those systems are only being utilized to identify healthcare fraud (which is also a huge issue that needs to be addressed).

Likewise, one of the major problems we’ve faced for decades is that the monopoly on information that the mass media has wielded has made it impossible for the public to become aware of the policies that harm them and to mass-mobilize against those policies. However, the scalability of information transfer on the internet (and social media) has made it possible, essentially breaking that monopoly and giving rise to an unprecedented political climate where new and controversial ideas can rapidly go viral (particularly when honest algorithms highlight the information people actually want to know).

Note: having watched the global media landscape for decades, it’s hard for me to even begin to describe how profound and unprecedented the change Twitter (𝕏) has created is, as stories that previously would never see the light of day rapidly become national headlines and false narratives (typically) die in hours rather than persisting for months.

Lastly, while writing this article, I was reminded of a famous speech by Charlie Chaplin (the world’s most famous actor at the time), delivered in his 1940 film The Great Dictator, which he made to combat the rising tide of fascism and totalitarian across Europe—leveraging his striking physical resemblance to Hitler. The movie culminates with him warning against surrendering to “unnatural men—machine men with machine minds and machine hearts,” in a speech that has stayed with me ever since because of its uncanny parallels to our own era (underscoring history’s cyclical patterns).

The Future of Workers

If you track the course of history, the upper class has typically tried to hoard most resources for themselves and then shared only the excess they did not need with the population, or the bare minimum required for the working class to continue producing wealth for the upper class.

The recent era we were in (made possible by America’s intact infrastructure, well positioned to capture the post-World War 2 boom) was the wealthiest in humanity’s history. In recent decades, we’ve gradually been transitioning back to an era of vast wealth inequality where the upper class hoards all the society’s wealth and everyone else just scrapes by.

Typically, one of the main bulwarks against this exploitation is that to some extent, the upper class needs everyone else to work for them to generate the wealth they consume, so workers can’t be pushed too far (or they will revolt against the system).

AI in turn, changes this paradigm as any jobs that previously required human workers (e.g., document analysis or picking berries in a field) can be outsourced to AI systems (e.g., Tesla’s robots have a real shot of upending the economy within a few years).

Since many workers will no longer be needed, many people I’ve spoken to (including a few fairly influential people) are immensely worried that the ruling class is beginning to seriously consider reducing the population, particularly since we are at a time where the world’s population is undergoing great stress (e.g., due to the rapid and overwhelming transformation of life being created by the digital age), and times of great stress within society typically coincide with large wars breaking out (especially if there’s a pre-existing “need” to reduce the population or restore order).

As such, many of us believe that it’s critical:

•Individuals train themselves in fields that cannot easily be outsourced to AI (e.g., by becoming the master of a craft and by doing everything they can to maintain their lifelong creativity) and finding ways to be self sufficient so they are not dependent upon the monopolistic systems we are more and more controlled by.

•The consciousness of our society shifts (e.g., increased critical thinking) so that we cannot be manipulated into following harmful agendas (which fortunately is being made possible by platforms like Twitter).

•Our societal viewpoints are shifting to valuing the important things in life (e.g., being connected to others, respecting and cherishing life, being in nature rather than immersed in technology, or embodying a genuine spiritual faith) as this way of living is the antithesis of the sterile and dehumanizing future being pushed upon us.
Note: Elon Musk’s belief is that AI, space exploration and robotics can usher in a new era of prosperity for society that will eliminate many of the conflicts we’ve previously had over limited resources. While this is possible, I think it is vital to be prepared for the less optimistic scenario before it is too late to do so.

Artificial Thinking

I’ve long believed that one of the primary issues in our society is us being conditioned by the educational system that we “need to be taught to learn,” as this transforms education from an enjoyable active process to an unpleasant passive one that greatly diminishes both our ability to learn and think creatively (along with being conditioned to believe one needs a doctor to be healthy)..
Note: most of what I know was self-taught, as I realized early on that formalized education was taking away my ability to think.

One of the major problems with this model is that not only is the information we are taught biased, but the way we are taught to think is as well (e.g., we are encouraged to skip understanding the context behind a topic so we can cram the essential material for tests and to prioritize copying algorithms rather than independently coming up with a way to solve problems).
Note: this topic and how to effectively study are discussed here.

This issue has infected science and resulted in a large amount of erroneous (e.g., non-replicable) data being published that simply exists to support existing dogmas or pharmaceutical products rather than get us closer to understanding the universe (which for example is why discoveries that revolutionize science are getting much rarer).

In parallel with this, there has been a massive push to both eliminate undesirable information from the internet and create a very specific way of thinking online (e.g., blindly trusting “the science”), best embodied by astroturfed websites like Reddit. Because of this, as the years have gone by, I’ve noticed it’s become harder and harder to find the information I’m looking for (it essentially disappeared from all the standard channels) and that I’m frequently forced to navigate extremely biased platforms (e.g., Wikipedia) to find what I’m looking for.

Since I used the “old internet,” I know what used to be out there (and hence how to find it) and have an intrinsic sense of what types of biases I need to filter for in each type of information source I look through. As these are skills which I believe are nearly impossible for anyone to learn who was not on the “old internet,” I hence am quite worried that much of that will never be recognized by the generation who was raised on smartphones.

Note: this is somewhat analogous to how human beings used to be much healthier, but over the last 150 years, there’s been a gradually increasing epidemic of chronic and unusual diseases alongside many natural medical therapies becoming much less effective, which is a result of the unnecessarily toxic environment modern technology is creating.

AI and Cognition

I strongly believe that the things you learn at a young age are what you retain best for life, and in my case, I was very fortunate to have a strict 3rd-grade teacher who pushed me in mathematics to the point that I could do long division by the end of the year. A few years later, calculators became available in schools, and I noticed that when I used them, my ability to do math declined significantly. For this reason, I largely avoided using calculators (as I wanted to maintain a concrete awareness of numbers), and similarly, much later when GPS and cell phones became available, I tried to avoid relying upon them as I found they greatly reduced my ability to remember phone numbers or have an innate sense of direction that allowed me to find where I wanted to go.
Note: in contrast, I have seen people who quite literally have panic attacks when they can’t have a GPS guide them to where to go, even if it is very close to their location.

All of this, in turn, touches upon a common neurological phenomenon; cognitive processes you reinforce are strengthened, whereas ones you neglect atrophy (e.g., blind people frequently develop very advanced usage of their other senses, such as one individual, the bat man, who discovered how to echolocate, to the point he could ride a bike).

Note: the existing Alzheimer’s research shows that one of the primary contributing factors is individuals not fully exercising their brains. Worse still, since those who are cognitively impaired tend to rely more on external cognition aids (e.g., AI), the new paradigm will likely lead to a downward spiral that greatly accelerates that decline.

In my case, I feel the reason I can use AI effectively is because I understand what I am trying to do, how to do it, and maintain an awareness of each step that is required, so I can then recognize which parts of the process just make more sense to offload to AI while I have time to do the rest. Likewise, because I have a deep familiarity with the types of biases that exist in information the internet (e.g., I know on certain topics, whatever is presented will be a lie or heavily slanted in one direction) I can immediately recognize when those same biases are present in AI and can instinctively utilize similar filters to what I learned when browsing through the general internet.

In contrast, I feel neither of those will be applicable to people who grew up with AI (so they do not have a pre AI baseline) or those who chose to have AI think for them so that they do not have to do “hard work” and develop those cognitive skills, and worse still, will be particularly detrimental for children who miss that critical window at the start of life to develop their own cognition because they relied upon AI to think for them. Furthermore, I feel that, to some degree, this is unavoidable, as society constantly places pressure on students to succeed academically in the immediate future rather than prioritizing what is necessary for long-term cognitive development.

Two recent studies gave excellent proof of this concept.

The first, “Creative scar without generative AI: Individual creativity fails to sustain while homogeneity keeps climbing,” showed that AI was improving academic output and leading to far more quality studies being published, but the content became much more homogenous (repetitive, “machine like” and uncreative). More importantly, once AI was withdrawn from (now “dependent”) users, their academic output dropped significantly, and their content homogeneity continued to worsen over time, resulting in them being much less creative than they had been before they started. I feel this is concerning, as beyond permanently impairing the academics, it also will gradually pollute the entire scientific literature base (which in turn will shift AI to promoting even more rigorous non-creative conformity).

The second, a four month study of university students tasked with writing open-ended essays, found individuals who did not use AI or Google searches had much higher activation of neural circuits throughout the brain, while AI users had the worst, particularly in areas to memory, executive function, and creativity (e.g., ~55% lower in some metrics), which worsened as more AI was used (leading to more and more boring repetitive writing structures). Furthermore (after up to four months of follow-up), users who began with AI subsequently performed significantly worse when tasked not to use AI, had difficulty recalling what they wrote in “their essays,” and were much less happy about the process.

In my eyes, all of this leads me to believe that AI is going to be another thing that increases the wealth stratification in our society, as those who understand how to use it as an effective tool (while simultaneously preserving their cognitive function) will be immensely successful and be able to greatly scale up their productivity. Conversely, for the typical user, AI will atrophy many of the skill sets they previously had that protected them from exploitation, while simultaneously weaving in a variety of subtle thoughts that directly exploit users for someone else’s benefit.

Note: one of the most annoying things I have found with AI systems is that they will continually “lie to you” (or give inaccurate answers) to make you happy for increased engagement, and the experience I’ve gone through feels very similar to what many attractive women experience where men (desiring them) will continually give them unwarranted flattery, which initially is incredibly appealing, but as time goes on, makes you get fed up fed up with all the fake disingenuous comments and just desire people who will be real with you. As such, my hope is lots of men being forced to go through this with AI will allow them to relate to what women routinely experience, but unfortunately, at this point, the majority of people I talk to are enamored with the continual compliments and empathy AI provides them (leading to the situation where many report preferring AI to a therapist or friend and routinely seeking it out for advice on critical life decisions). This is unfortunate, as it again sets people who do not think independently and critically up to be easily manipulated by Silicon Valley algorithms. That all said, I admit I find myself periodically saying please and thank you to AI systems when I get really good results (in part out of gratitude and in part because I don’t want to train myself to be callous and entitled towards people helping me), even though the founder of ChatGPT (and others) have explicitly stated people doing that costs them money and leads to worse AI outputs.

Navigating Artificial Intelligence

Because of all of this, I feel AI is something which can be useful if it’s an adjunctive tool you utilize when it’s appropriate, but if it becomes your primary aid, its harms quickly outweigh the benefits it can provide (something which I believe is analogous to how I feel about pharmaceuticals in medicine—as while frequently unsafe and ineffective, if a doctor does not rely upon them, they can recognize the instances where they will clearly benefit patients).

In the final part of this article (which primarily exists as an open forum for you to ask your remaining questions), I will discuss:
•Which AI systems I have found to be the most useful for different types of situations I encounter (as their value varies greatly depending on what each is used for), and how I specifically utilize them, along with how you can use them to solve major longstanding challenges in natural medicine.
•My preferred resources for combatting the great vanishing of information and finding the forgotten medical information I’m looking for (e.g., how I locate many of the hard to find medical references online).
•Now that I have reviewed the entire literature base, which of the currently existing DMSO books do I consider to be the best for those looking to learn more about the subject (a lot of people have asked about this).

Read more

•Due to widespread media and scientific censorship, accurate information which challenges pharmaceutical interests is difficult to obtain. Polling offers a unique means to bypass this blockade.

•Extensive polling shows 9%–34% of COVID vaccine recipients developed side effects from the vaccine, 7-13% developed serious side effects, 7.5-22% know someone with a severe vaccine injury, 24-28% know someone who they believe died from the vaccine and 46-55% believe the COVID vaccines have killed a significant number of people.

•These results are profound and likely account for the unprecedented loss of trust in doctors and hospitals since COVID (from 71.5% to 40.1%) which is mirrored by a significant loss of trust in the pharmaceutical industry, government health authorities and support for childhood vaccinations (which, now, almost half of the population no longer fully trusts).

•MAHA’s policies and accomplishments, including those towards vaccines, are now some of the most popular issues with the electorate—but unfortunately are not being effectively promoted to the public due to media censorship.

•To prepare for the midterms, the Trump administration has pivoted away from vaccines due to (likely biased) polling data suggesting that vaccines are a toxic issue that must be avoided to have a chance of winning the election.

•I believe this pivot is a mistake as the polls (detailed in this article) show immense support for RFK’s actions on vaccines. Furthermore, this mistake is very similar to what happened in 2020 as the Trump administration struggled to address COVID and failed to secure the 2020 election.

Joe Rogan recently had RFK Jr. on his show, and there, RFK presented an excellent summary of the wide range of remarkable (and previously impossible) things he and his team have been able to pull off after a year due to them having the president’s complete support to challenge the vested interests that profit off of keeping us sick. As such, for those of you who want to know what MAHA is actually doing, I would highly recommend watching it.

Unfortunately, this segment also confirmed something I was quite worried about: RFK, someone I know sincerely cares about vaccine safety, did not once discuss vaccines with Rogan, even in numerous instances where it would have been the most expected subject to insert after related points were raised. Based on this (and many other shifts I’ve noticed recently), I am relatively certain the Trump administration received polling data that made them decide the vaccine subject needed to be avoided until after the midterms and that instead “safer” topics with a more widespread appeal needed to be focused on now. In this article, I will provide the data that shows why this is a mistake and the key steps we can take to correct it.

Note: much in the same way they are angling toward “safe” political health topics, within the integrative medicine field, one of my longstanding frustrations with the discipline has been that most practitioners prefer the “safe” remedies (e.g., supplements and herbs) that are relatively unlikely to generate controversy, but avoid the potent “controversial” therapies (e.g., the umbrella remedies) that get results but are less “safe” to prescribe to patients.

Doctored Data

For decades, a fairly simple formula has been used to control the populace:

•Enshrine chosen parties as credible sources.
•Buy out each credible source.
•Have each bought out credible source reinforce the credibility of the other co-opted sources until a monopoly is established.
•Have the credible sources work in unison to amplify chosen messages or psychological campaigns that supported vested interests.
•Prohibit credible sources from airing anything which threatens vested interests.
•Have all the smaller cogs in the system be pressured to conform to the chosen narratives, and ideally, to identify with them and attack anyone who challenges them so everyone stays in line.

Because of how vast and interwoven it is, I long thought this framework could never be broken, and that there hence would only be a small portion of the population that saw through it. However, the internet, by allowing the free diffusion of information, broke that monopoly on truth, particularly once Elon Musk bought Twitter, and provided a way to prevent that same formula being enacted online as the establishment sought to transform the internet into a landscape of gatekeepers (e.g., Google, Facebook and Wikipedia) that controlled most people’s access to online information and “curated” all of it so only approved messages were seen.

A lot of my life has hence revolved around observing how this cruel formula is implemented within the mainstream media and scientific press so that I can:

•Be more equipped to discern what is true and what is false.

•Predict the future, as the formulaic step-wise nature of how this propaganda is implemented often is a “tell” for what will be enacted in the future (e.g., this is how I correctly predicted most of what was going to happen with COVID-19 at the very end of 2019).

•Look for loopholes in the matrix where truth is able to leak out and seize them (e.g., the censorship within mainstream scientific literature was gradually phased in a few decades ago, and largely constrained to Western countries, so a large part of “The Forgotten Side of Medicine” is digging up research outside those bubbles).

COVID Vaccine Polling

Because so many of the social institutions conspire together to reinforce narratives which are at odds with reality, “gaslighting” (abusively altering someone’s environment so they start questioning what they are seeing with their own eyes) is commonly used to describe living through this.

Since the scientific literature effectively gaslights us by refusing to publish validated data which challenges pharmaceutical interest (while simultaneously allowing misinformation that promotes industry interests to proliferate throughout it), critical data, like information on COVID vaccine injuries, was largely absent from any credible academic sources. This in essence, is how they are able to convince people vaccine injuries are “rare” and greatly outweighed by the benefits of the vaccine despite injuries being frequent and sometimes quite severe.

Because of this, vaccine safety advocates got extremely frustrated, and eventually, Charlie Kirk figured out a way to bypass this blockade and show people they weren’t crazy for thinking COVID vaccine injuries were very real.

Following this, a few parties like Steve Kirsch and his vaccine safety research foundation hired polling firms to directly survey the public on vaccine injuries and provided quantitative data on what was happening. In 2022, of those vaccinated:

In 2023, Professor Mark Skidmore hired a reputable polling firm (Dynata), which surveyed 2,840 respondents and found 15% of those vaccinated had a vaccine injury, 13% of whom categorized it as severe (along with 22% of respondents saying they knew someone with a severe vaccine injury). Since you just can’t say that, his paper was retracted, and he was subject to an ethics investigation that eventually cleared him.
Note: Skidmore’s paper emphasized an important point for all of these polls—since those severely injured were much less likely to be able to respond to a poll, they were likely underestimated in polling.

Likewise, in 2024, a 1000 person poll Kirsch commissioned found that 12.5%-20.3% of vaccinated respondents were injured from the shots (along with 7.6-12.2% knowing someone who was injured), with roughly two-thirds of the injured categorizing their vaccine injury as “serious” or “very serious.” However, despite Democrat respondents reporting a higher rate of vaccine injury for themselves and those around them, they were much more likely to believe the vaccine was safe and effective (83.62% did) than Republicans (44.49%) or Independents (51.81%).

Note: in every poll I’ve seen, Democrats reported a somewhat higher rate of injury than Republicans (likely due to taking more vaccines) but simultaneously were much less likely to think the vaccine was unsafe or ineffective. Likewise, numerous polls consistently found those vaccinated were more likely to believe the vaccine was safe and effective. For brevity, I will omit that data (but for those interested it can be read here).

As no one wanted to touch this issue, only one polling organization independently investigated it, Rasmussen Reports (a conservative polling organization which has a reputation for getting accurate results due to them having listeners punch answers in response to an automated voice rather than directly talking to someone who may bias them). For American adults, they found:

•July of 2021: 32% believed public health officials were lying about the safety of COVID-19 vaccines.

•December 2022: 56% of 1000 respondents believed the vaccines were effective, 57% were concerned the vaccines had major side effects. Most importantly, 34% of those vaccinated reported minor side effects and 7% reported major side effects (e.g., those seriously impairing their quality of life).

•January 2023: 49% believed it is likely that side effects of COVID-19 vaccines have caused a significant number of unexplained deaths and 28% personally knew someone whose death may have been caused by side effects of the COVID-19 vaccines.

•January 2023: 57% wanted Congress to investigate how the CDC handled assessing vaccine safety (presumably since many suspected the CDC had covered up the dangers of the COVID vaccination program).

•In March 2023, 11% of those surveyed reported that they believed a member of their household died from COVID-19, while 10% believed a member of their household died and that their death may have been due to a side effect of the vaccine.

•In September 2023, 47% of those surveyed stated they did not believe the vaccines were safe and 34% did not believe they were effective. As before, these results also politically stratified as Democrats were less likely to believe the vaccines were unsafe (14% D vs. 51% R) or ineffective (17% D vs. 57% R).

•November 2023: 24% personally knew someone they believe died from a COVID vaccine, and of those individuals, 69% would be likely to join a class action lawsuit against the pharmaceutical companies.

•In January 2024, 53% believe it is likely that side effects of COVID-19 vaccines have caused a significant number of unexplained deaths and 24% personally knew someone whose death may have been caused by side effects of COVID-19 vaccines.

•In September 2024, 55% surveyed believe it is likely that side effects of COVID-19 vaccines have caused a significant number of unexplained deaths – including 30% who say it’s very likely.

•In November 2025, 26% reported they had minor side effects from the vaccine and 10% reported major side effects. Additionally, 46% believed it is likely that side effects of COVID-19 vaccines have caused a significant number of unexplained deaths - including 25% who say it’s very likely.

In short, the data shows you aren’t crazy, and while the news is not reporting it, the majority of people are seeing exactly the same thing you are. There is no getting around the fact a lot of people were harmed by these vaccines and one of the best data compilations I’ve seen that puts all of this into perspective was a March 2023 estimate Ed Dowd produced from data sources available at this time (e.g., these polls and disability data). This deliberately conservative estimate showed:

Note: one of the interesting discoveries in these polls (and many others) is that the rate of respondents who reported being vaccinated is much lower than the official figures suggested. I suspect a key motivation for this was that each increasingly authoritarian COVID vaccine mandate could only be enacted if a sufficient number of people were “vaccinated”. So in addition to pushing as many people as possible to vaccinate with the increasingly aggressive enticements we saw (scarcity sales, small payments, larger payments, prohibiting people from businesses, travel bans, and then mandates at school or work), they likely also directly inflated their figures.

Vaccine Polling

Typically, if a pharmaceutical injures people, propaganda can sweep it under the rug, and much of my life has revolved around advocating for those people. However there are limits to what propaganda can do, and once enough people are injured, it’s no longer possible to keep gaslighting people. As such, when I saw the early data on the COVID vaccines (much like what Charlie saw when he polled his crowd), I realized that this could not get swept under the rug, and that if we made the necessary commitments and sacrifices to keep going at it, the public would gradually awaken to.

This shift was reflected by a series of polls showing an unprecedented loss of trust in the medical industry:

•A JAMA survey of 443 455 American adults found in every sociodemographic group, trust in physicians and hospitals decreased substantially over the course of the pandemic, from 71.5% in April 2020 to 40.1% in January 2024.

•A recurring Gallup Poll found trust in the pharmaceutical industry has greatly declined:

In parallel, support for vaccine mandates (or vaccinating in general), which had been gradually declining, significantly decreased due to the COVID response:

Note: polling wording greatly affects outcomes. Jeffrey Tucker noted the wording of this question was designed to inflate “yes” responses. Likewise, he argued (and I agree) that one of the polls used to scare the Trump administration off challenging vaccines had similarly biased wording.

•This loss of trust, in November 2025, Pew again found was much more common in Republican voters:

Similar results were seen in a November 2025 Pew poll where 57% had high confidence in the effectiveness of childhood vaccines (45% R vs. 71% D), 44% were confident that their safety testing was adequate (29% R vs. 63% D) and only 41% fully trusted the CDC vaccine schedule (27% R vs. 58% D).

•Republican parents are far less likely than Democratic parents to have high confidence in childhood vaccine effectiveness (45% R vs. 71% D), safety testing (29% R vs. 63% D) and the vaccine schedule (27% R vs. 58% D).

Similar results were also found by a KFF tracking poll last year:

Along with one this year:

Note: this 2026 poll also found there has been a loss of trust in the MMR, COVID and Flu vaccines.

Real Voter Priorities

To prepare for the midterms, MAHA allies commissioned three polls to find out which issues had the broadest support in the public. The first, from John Zogby Strategies found that a supermajority of voters support health and medical freedom. With vaccines specifically:

The second, of 1000 likely voters by Rosetta Stone found similar results:

Of note, this poll found that support for the Make America Healthy Again agenda (59.1%) was higher than for the Make America Great Again agenda (45.8%) or America First Agenda (54.4%), but the approval of what President Trump and Secretary Kennedy’s are actually doing to make children healthy is much lower (44.1% jointly), along with 46.4% for Secretary Kennedy alone, and 48.1% for Trump overall (rather than just children’s health). What this indicates is either that:
•MAHA is the Republican party’s strongest issue for the midterms, but the specific popular things MAHA is doing are not being effectively communicated to the public (in part due to ineffective messaging, and in part due to a hostile media either not covering it or misportraying it).
•RFK’s MAHA base feels disappointed he has not accomplished more (particularly on vaccines) while the left-wing base has gradually succumbed to the negative messaging directed at RFK Jr. by the media (resulting in the amazing propaganda feat of them despising someone who is actively advocating for the issues they deeply care about).

•A February 2026 poll from FLA found that MAHA was the most effective issue to flip someone’s vote (e.g., a key voting bloc chose the generic Democrat by a 5:1 margin, but once given a Republican who “focused on things like removing harmful toxins from our food, limiting pesticides in agriculture, and making sure our kids are not overmedicated” they instead chose the Republican by nearly a 2:1 margin). Likewise, a large portion of voters were simply not motivated to turn out for the elections unless MAHA issues were championed by their candidate. Additionally, while not the most popular MAHA point, candidates championing reducing the vaccine schedule, at became much more favorable to voters.

Additionally, that poll again showed the majority of voters have significant concerns over the current vaccine program.

All of these polls (along with the far more extensive non-vaccine MAHA data I did not include here) touch upon a simple fact. People get that they are unhealthy and the system profits off their sickness. That’s why so many people are yearning for a change, and simultaneously why, until now, virtually no politician has been willing to threaten vested interests by stopping the mass poisoning of society. It’s absurd that’s been our status quo, but simultaneously, I am grateful that due to an unlikely alignment of fate, we finally had a political revolution that made politicians finally be interested in pursuing the issues we care about.

Lastly, it is important to note that many polls are not accurate, either due to poor methodology or because the individual conducting the poll has an agenda and the poll is structured so that it affirms their world view (e.g., certain politicians frequently complain polls are rigged to demoralize a candidate’s supporters and in both 2016 and 2024 Trump significantly outperformed what the polls forecast).

For example, consider this poll conducted at the end of December by FLA that found MAHA is popular, except for vaccines, and that pursuing that issue in the competitive districts will likely cost Congressional seats.

Unlike all the other (relatively unknown) polls which have shown strong support for vaccine safety, this outlier was promoted by the mainstream media (e.g., the New York Times published an article framed around just one in five Americans supporting rolling back the CDC vaccine schedule and that supporting vaccines would cost the midterms).

Smelling a rat, Jeffrey Tucker dissected the poll noting:
•The sponsor was never identified (this is a red flag).
•As the above questions show, the wording was very poor and designed to produce pro-vaccine answers rather than objective assessments of voter attitudes.
•These results wildly contradicted what every other poll showed in regards to public attitudes towards vaccines (which should be plain as day to you too as you review the actual data).

As such, Tucker concluded this poll was almost certainly sponsored (and then promoted) by the pharmaceutical industry in order to steer the Republican leadership away from touching the vaccine issue.

The COVID-19 Debacle

For all of human history, a common tactic in military campaigns (channelizing) has been to attack an enemy on one or more sides so they retreat to the side not being attacked and end up in a strategically disadvantageous position (e.g., they are corralled into an area where they are defenseless from an ambush).

Frequently when I observe propaganda campaigns being conducted by the mainstream media, it feels as though a very similar process occurs—that sadly is typically successful (and likewise, a major reason why I can “predict the future” is because I can see the lines of attack and hence the direction they are pushing things in).

My longstanding contention has been that the way Trump handled COVID-19 cost him the 2020 election, and I believe those lessons are a major reason why he’s had a much harsher stance on the pharmaceutical industry in his second term. It specifically cost him the election because:

•Immediately prior to COVID-19, the economy was in good shape, and per polling, Trump was favored to win the election. Likewise, once COVID started, the Democrat party coalesced around a marginal candidate (Biden) to keep Sanders from winning the primary, thereby alienating a major bloc of the party.

•COVID-19 destroyed the economy, thereby taking away Trump’s key edge. Likewise, it reframed Trump’s presidency to his gross failures to address COVID-19 (which the media promoted daily) and set the stage for pushing through mass mail-in voting (e.g., to protect people from getting COVID while voting) and all the electoral issues that entailed.

These failures to address COVID-19 were rooted in the COVID-19 policy as what was done (masking, social distancing, mass testing, widespread lockdowns and no treatments except remdesivir) was unproven, logically unsound, did not work, and arguably made things much worse. In contrast, a sensible policy was to prioritize developing effective treatments for COVID-19 that could address the illness early on before it became severe (rather than give them Tylenol), place cheap UV lights in buildings (as these sanitized the air and prevented indoor COVID transmission thereby eliminating any justification for lockdowns or masking), and restricting the extreme COVID transmission prevention measures to those at high risk of dying from COVID (e.g., nursing home patients) and ensuring they had enough supplies to implement all of this correctly..

Based on what I observed during COVID-19, Peter Navarro’s memoir, and Scott Atlas M.D.’s memoir (particularly Atlas’s), I believe the decision to follow these flawed policies was largely Trump’s fault as:

•Early on, Navarro warned the Trump administration that COVID-19 would turn into a disaster unless proactive measures were taken to counteract it, but his concerns were dismissed by senior White House officials (much in the same way mine were dismissed by my colleagues).

•Trump and Navarro recognized the importance of early COVID-19 treatment, and focused on using hydroxychloroquine. However, the federal health bureaucracy continually sabotaged their efforts (particularly FDA chief Stephen Hahn, who was then rewarded with a lucrative position from Moderna shortly after leaving the FDA).

•Each time Trump touched a treatment option for COVID besides Fauci’s baby (remdesivir), such as hydroxychloroquine, the media went hysterical and a massive amount of bad press followed (leading to the White House not wanting to touch other promising COVID-19 therapies despite knowing they had a realistic chance of ending the pandemic).

•The media (and H.H.S.) however was extremely supportive of a COVID vaccine. Because of this, the Trump administration was corralled into waiting for a COVID-19 vaccine to come out, and their efforts were redirected into doing everything they could at “Warp Speed” to get a vaccine ready before the election (likewise, many executive meetings on COVID-19 meeting revolved around eagerly awaiting each new detail on the vaccine’s trial progress).
Note: at the last minute, Pfizer delayed their vaccine so that it was not ready until after the election. I suspect this was done because Biden was preferable for the industry’s interests and partly accounts for Trump now being more hostile towards the pharmaceutical industry (as he learned it’s not a good idea to make deals with the devil).

Atlas specifically highlighted that:

•The absurd COVID-19 policies originated from the COVID-19 task force (specifically Fauci, Birx), but due to their prestige in the media and a general lack of medical or epidemiological knowledge in the White House, no one wanted to challenge them, leading to Atlas eventually being brought into the task force to provide a counterweight to the masks, testing and lockdowns dogma.

•From the start Atlas was attacked by the media. At the meetings, Atlas was aghast that Fauci and Birx lacked a basic grasp of medical knowledge (to the point they likely could not pass a medical residency) or critical thinking and appeared unable to understand why their policies were illogical and counterproductive regardless of how much he dumbed it down.

•While the task force (particularly its head, Mike Pence) would default to siding with Fauci and Birx, Atlas was periodically able to convince them to change the most absurd policies. However, each time Atlas got traction, he was relatively certain Fauci leaked it to the press, as the media would immediately drum up a hysteria about how Atlas’s rational and safe policies would actually cause mass deaths throughout America, leading to the White House bowing to the political pressure and retracting the policy.

•Despite the process being enough to drive anyone insane, for the country, Atlas persisted and did all he could to dislodge Birx’s influence on the task force. However, in most cases, he failed because Trump’s advisors “did not want to rock the boat” before the election. In contrast, Trump said his gut told him the current path (lockdowns etc) did not make any sense and was harming America, but due to the pressure of his advisors and the media, he did not fire Birx or change course.

Once Trump lost the election, to quote Atlas’s book:

When he resigned from the Task Force in a telephone call to Trump, Atlas writes, the president told him, “You were right about everything, all along the way. And you know what? You were also right about something else. Fauci wasn’t the biggest problem of all of them. It really wasn’t him.” Trump meant that it was Birx, and Atlas couldn’t resist a parting shot at the aides who had been so afraid of her. Knowing that they were listening on the speakerphone in the Oval Office, Atlas said, “Well, Mr. President, I will say this. You have balls. I have balls. But the closest people around you—they didn’t. They had no balls. They let you down.” They let down the rest of the country, too.

Note: one of the most remarkable facets of this story is that shortly after leaving the Coronavirus Task Force, Birx became chief medical and science advisor for a company which sold UV light air purifying devices that disinfect buildings from infectious illnesses such as COVID-19.

Lastly, it’s worth noting that because of his strong feelings on vaccines (Trump has spoken out on the issue for decades due to people he was close to having children who were permanently damaged by childhood vaccinations), immediately after winning the 2016 election, Trump contacted RFK Jr. and asked him to chair a presidential commission to assess the safety of the childhood vaccines. However, this never happened and Bill Gates eventually took credit for sabotaging it. While I cannot prove this, I believe that the decision to pull it came from his administration lobbying for it rather than Trump himself. Yet, had Trump implemented that commission, it is unlikely Trump would have later gone all in on the COVID-19 vaccines and subsequently lost the 2020 election.

Internal Polling

The current war in Iran has the potential to be one of the most impactful events in our lifetime, so over the last week, I have talked to a lot of people from many different backgrounds about what is occurring and found they have wildly varying perspectives on it. Given this variation, I am relatively certain this is not a “90-10” issue that virtually every American adult supports. Recent polls (and those preceding the war) likewise support my observation:

•CNN/SSRS (Feb 28-March 1): 41% approve, 59% disapprove.
•Reuters/Ipsos (Feb 28-March 1): 27% approve, 43% disapprove, 29% unsure.
•NPR/PBS/Marist (March 2-4): 44% approve, 56% oppose.
•YouGov (March 3) 36% approve, 49% disapprove, 15% not sure.

I mention this because Tucker Carlson (who has been vocally speaking out against the war) recently shared an diverging perspective over what is going on within the White House:

There, he stated that he had been repeatedly visiting Trump to convince him not to invade Iran, but most recently, when he wanted to try to convince Trump to call his initial results a win and withdraw, his contact told him not to bother because Trump is being shown polling that this is a “90-10 issue” and the mainstream news he’s watching is reinforcing that there is overwhelming support in the electorate for the war, leading to Tucker understandably questioning the accuracy of this internal polling which concluded 90% support the war.

I mention all of this because I believe something very similar has happened with the vaccine issue, and I am almost certain Trump (or his staffers), in addition to the December FLA, are being shown internal polling which demonstrates that vaccines (support for them) are close to a “90-10” issue and because of this concluded that the issue needed to be dropped until after the midterms, as pursuing any questions of vaccine safety will cause their part to lose the election. I feel this is a mistake as:

•Much in the same way Trump was channelized (corralled) by the media into adopting counterproductive approaches for COVID, he is also being pushed by a hysterical media and medical community to abandon the vaccine issue entirely (while simultaneously corralled to “safe” health topics that do not get acrimonious media pushback).

•As I’ve shown, all available data (which I have presented here) shows there is large support for reducing the CDC schedule, investigating vaccine safety and rescinding mandates. In contrast, I believe the polls Trump has received are erroneous, and were likely concocted to corral Trump into backing off the vaccine issue, especially once he shocked the medical industry by speaking out against childhood hepatitis B vaccination and then suddenly cutting the mandatory childhood vaccine schedule in half.

•Within the current ideological splits of the country, those who are firmly committed to vaccines are also typically firmly opposed to Trump’s presidency. As such, it is unlikely significant electoral benefits will be seen from crafting policies that demographic favors.

•Presently, there is significant division and dissatisfaction within the Republican party due to some of the core issues his base overwhelmingly supported and elected Trump for being dialed back due to media pushback and protests from the left (which polls show is costing him immense support). As Trump’s 2024 victory was largely due to MAHA coming out in droves to vote for him and tipping the election, neglecting this issue until after the midterms is likely to demoralize the voters within that constituency (many for whom vaccines are their #1 issue) and backfire.

•Because so much needs to be done on the vaccine issue, delaying it by 8 months greatly stifles what can ultimately be done by the end of Trump’s term (particularly since the tactic the pharmaceutical industry keeps using is to try and stall anything being done so nothing really shifts by the time 2028 comes and it can all be reversed). Likewise, decisions have a way of solidifying, so the longer this continues, the harder it will be to reverse.

In short, because of how much institutional resistance there is to questioning the religion of vaccines, it’s essentially impossible to change Federal policies on vaccines unless the president directly orders it and then resists all external pressure to dial it back. However, due to his own negative experiences with vaccines and his headstrong nature, Trump did just that, and he is probably the only president we will see in our lifetimes with that unique confluence of traits.

What Can We Do?

Because there are so many serious issues and irrational beliefs surrounding vaccination, the program cannot be maintained if it is subject to open debate. As such, the goal has always been to prohibit discussion of the topic and instill such a strong religious adherence to vaccines that only lone voices can occasionally break through, and once those few do, they will immediately be dismissed and ignored.

This has been a very depressing situation to navigate (e.g., discussions are largely prohibited in the medical field even once you are a doctor and I’ve had neighbors whose had successive vaccine injuries yet refused to listen to me despite me correctly pointing out the likely consequences of each new injury in the weeks, months and years to follow). As such, rather than be frustrated with the current situation, I am overjoyed, as for the first time, people are openly discussing the dangers of vaccination, and now when the topic is brought up in groups, rather than be a pariah, you will frequently encounter people who will support your position. It’s really hard to put into words how profound a shift that is, and it feels that as time goes on, it will become harder and harder to cover it up as a critical threshold has now been reached, and the momentum behind the people awakening to this issue will create an avalanche that will sweep the old dysfunctional paradigm away.

Given all of this, I feel that the most important thing we can do is simply to continue making those around us aware of the dangers of vaccination, as regardless of what policy the government chooses, if most of the electorate does not want to vaccinate, it ultimately has to abide by that. At the same time, in the immediate future, actionable steps also need to be taken to utilize the window we currently have. The most poignant ones I have identified are as follows:

•From observing the Trump administration’s conduct over the last year, it appears that they are responsive to public pressure if it gains sufficient traction. For this reason, once I finish the DMSO project (I am very close now—I just have to finish going through 2022-2025 on the final search and with a team use AI to pare down a 17,725 page document of Chinese studies), I am planning to start bringing a lot more attention to vaccine injuries on 𝕏. I can’t do this alone, so if you can do the same, this will help make our voices be heard. Likewise, others are also doing the same. For example, after Joe Rogan had RFK Jr. on (where vaccines were not discussed) he immediately had Aaron Siri on who poignantly highlighted why the current paradigm around them is so dysfunctional.

•A petition is being circulated which is demanding “COVID Justice” (that presently has 26,000 signatures). Many people I know were involved in it, and believe that with sufficient signatures can make a real impact to public policy, so if you can, please consider signing it. Presently, much of the political leadership recognizes that the handling of COVID-19—particularly the vaccine injuries—was a major mistake and is hoping the issue will simply fade away. We cannot allow that to happen, both for the sake of those who are still suffering and because COVID offers one of the clearest lessons of our lifetimes about the dangers of allowing the pharmaceutical industry’s profit motives to go unchecked. That lesson must remain part of America’s collective memory as we work to dismantle the industry’s most predatory practices and maintain the public support necessary to do so.

•As far more scientific evidence of widespread injuries from the COVID-19 vaccines is beginning to emerge, ACIP (the committee which decides vaccine policy in the USA) will be meeting on March 18-19, and specifically discussing COVID-19 vaccine injuries. Prior to that meeting occurring (until March 12) it is possible to leave public comments (here). Please consider doing so, especially if you or someone you know was injured by the COVID vaccines. ACIP broaching this subject puts them at odds with a lot of powerful forces, so it is vital they receive public support for what they are trying to do.

Most importantly, because the media’s entire attention is focused on Iran currently, there is a very unique window to bring attention to this matter without the typical coordinated blowback doing so typically elicits.

Conclusion

One of the things I never ceased to be amazed by is how deeply the medical community, media, and political class defends vaccines, and to be honest, I have no idea if it’s due to an irrational religious belief in them, the fact that that belief ties together so many other belief systems our society revolves around, or the fact that vaccination (due to its high rate of chronic injury) sets people up to be customers for life of the medical industry.

For instance, if we look at the campaign being waged by the media here, they’ve essentially decided to sacrifice every other health issue their sponsors have long used to poison us (and never were willing to question) to divert us away from focusing on vaccination. Likewise, consider that virtually every MAHA confirmation session has revolved around pressuring the nominee to assert their allegiance to vaccination rather than any of the pressing health issues our country faces (e.g., recently with Casey Means). This I find quite astounding, as all the senators openly admit loss of trust in medicine and vaccines is a major problem facing the country, yet, they believe the solution is to browbeat someone we trust into endorsing vaccines—demonstrating that they can’t comprehend our beliefs are being derived through critical thinking rather than following an authority figure.

Ultimately, I believe many of the problems with vaccines result from the widespread faith that exists in them, vaccines being mandated, and lack of legal liability for manufacturers. The fact that someone can be mandated to take something and then have no recourse for the injury which follows is grossly unjust—to the point most people can recognize that if it is pointed out to them—but don’t due to the religious shield vaccinations have long had from ever being scrutinized.

As such, I believe the ultimate solution is to somehow change that (e.g., remove liability protection from vaccines patients did not want to take, but did due to a mandate). If someone is forced to take a vaccine and then gets injured, the party who forced them to do it must be held responsible to deal with what they created and for centuries now, we’ve seen medicine play all sorts of games to get out of that responsiblity. I believe the members of ACIP see this too, and that is hence why their upcoming meeting will specifically focus on the COVID vaccine injuries every policymaker is trying to forget.

We have a great opportunity here if we seize it, and I thank each of you who has supported the newsletter and made endeavors like this possible.

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•Blood pressure diagnoses have exploded as guidelines repeatedly lower thresholds, resulting in half of American adults now being “hypertensive” despite minimal evidence justifying this, and erroneous diagnoses frequently occurring.

•Despite aggressively treating it, medicine still does not know what causes high blood pressure. As a result, it overlooks that impaired circulation elevates blood pressure and attributes the ensuing damage to “high” blood pressure rather than to insufficient blood flow to the tissues.

•Excessively low BP from over-treatment is dangerous, increasing risks of fainting, falls (especially in the elderly), kidney injury, cognitive decline, ischemic strokes, and mortality.

•Different blood pressure medicines have very different risks and benefits. Because doctors are unaware of this, they frequently push patients to take inappropriate medications and then deny that life-impairing side effects are happening.

•This article will explore the core issues with the conventional framework of blood pressure and what we must know to reclaim cardiovascular health.

Ever since I first entered the medical field, something struck me as off about the relentless focus on blood pressure, and over time I noticed that the blood pressures people reported to me varied widely. While pondering this, a talented practitioner and mentor once told me that the current medical paradigm fixates on blood pressure because it’s easier to measure than blood perfusion (healthy blood flow).

Then, as I became more acquainted with the medical field, I began to notice a consistent pattern—whenever a drug existed that could treat a number or statistic, as the years went by, the acceptable number kept on being narrowed, making more and more people eligible to take the drugs that treated the number.

Conventional Blood Pressure Perspectives

Since blood vessels are elastic fluid-filled structures, that fluid holds them under pressure. Blood pressure, in turn, is typically measured by determining how much external force is needed to exceed the artery’s pressure and compress it so that blood no longer flows through it. Low blood pressure (hypotension) is a problem because it prevents blood from reaching the areas where it’s needed, but in most cases, medicine instead focuses on the consequences of high blood pressure.

Within the conventional model, those consequences are:

•Weakened blood vessels become more likely to break open and leak as higher blood pressure pushes against them. This for instance, is why Emergency Rooms aggressively lower the blood pressure of patients who show up with symptoms of “hypertensive emergency,” such as a severe headache and a significantly elevated blood pressure. Likewise, whenever a critical blood vessel ruptures (e.g., the aorta or one in the brain), once the bleed has been confirmed, the first step in managing it is to lower the patient’s blood pressure (so less blood leaks out) after which they are sent to surgery.

•Excessive pressure on the arteries strains and damages them, causing the lining of the vessels to become damaged and gradually develop atherosclerosis.

•Excessive blood pressure damages the internal organs (termed end-organ damage), leading to premature failure and early death (e.g., from a heart attack or kidney failure)—something which also results from chronic insufficient blood flow.

Because of this, high blood pressure is viewed as one of the leading preventable causes of cardiovascular disease; therefore, ensuring that a patient achieves sufficiently reduced blood pressure is a primary focus of all medical visits.

Unfortunately, that chain of logic has quite a few holes in it.

Variable Blood Pressure

Blood pressure (BP) is highly variable, especially at the periphery, where it’s typically measured. This variability—around 14 points—can lead to misdiagnoses of hypertension and unnecessary medication, which can lower BP too much, causing hypotension. One common form of this misdiagnosis is known as White Coat Hypertension, where the stress of visiting a doctor temporarily raises BP. This affects 15-30% of patients “diagnosed” with hypertension. Guidelines recommend confirming hypertension with multiple measurements, including home monitoring, but this is often not done.

Measurement errors, such as using the wrong cuff size or failing to account for differences in BP between arms, contribute to the issue. It’s estimated that 25% of hypertension diagnoses are incorrect. Moreover, there is often a poor correlation between peripheral BP (limbs) and central BP (inside the aorta). Central BP, which is more closely linked to cardiovascular disease, can differ significantly from arm readings. Different BP medications also affect central and peripheral BP differently, adding complexity to treatment.

What Affects Blood Pressure?

If fluid at a set pressure tries to move through a tube, as the tube shrinks, the pressure it creates (e.g., on the walls of the tube) will increase, while if the tube enlarges, the pressure it exerts will decrease. The body continually controls where blood in the body goes by changing the heart rate and fully or partially constricting the arteries, allowing it to shunt blood to where it is most needed (e.g., by dilating arteries in that area).

Blood pressure is thus a product of two factors: the volume of blood in the arteries and the degree of arterial constriction or relaxation.

Note: since arterial BP is greater than venous BP, it’s what’s measured externally (as veins compress long before arteries do, and only arterial blood has a signature pulsatile wave created by the heartbeat).

Since each heartbeat pushes blood into the arteries and thereby increases the pressure within them, two blood pressure values exist—the baseline pressure (diastolic pressure, DBP) and the pressure when the heart contracts (systolic pressure, SBP). The blood pressure values you see (e.g., 140/90) represent the maximum and minimum.

Note: one reason why this stretching is important is that when the vessels contract back to their normal size once the systolic pressure fades, that recoil pushes blood further along into the circulation.

Blood pressure lowering medications in turn work by some combination of:

• Loosening the arterial walls

• Reducing the total blood in circulation

• Weakening the contraction of the heart

What Causes High Blood Pressure?

Most cases of high blood pressure (90-95% of them) are what is known as “essential hypertension” or “primary hypertension” which is a fancy (and rarely questioned) way of saying “elevated blood pressure without a known cause.” More importantly, the fact there is no known cause for most cases of elevated blood pressure has been a widespread belief in medicine for decades. Typically, the only cause we hear about is “not eating salt,” despite the fact that the most detailed review of this subject found that drastic salt reduction typically results in less than a 1% reduction in blood pressure and more importantly, that eating salt is actually critically important for health (discussed further here).

For the remaining 5-10% (known as secondary hypertension), recognized causes include reduced blood flow to the kidneys (which sets off a signal to raise the blood pressure because the kidneys believe there isn’t enough blood perfusion), sleep apnea, or having a rare tumor that releases a blood pressure increasing hormone).

Since the cause of most hypertension is unclear, medicine simply focuses on risk factors like age, diabetes, salt intake, obesity, stress, and family history.

Note: effectively addressing anxiety can often cure high blood pressure that would otherwise be perpetually medicated.

Atherosclerosis and Blood Pressure

Many of my colleagues became suspicious of the traditional blood pressure model after observing that circulatory impairments often co-occurred with rising blood pressure rather than resulting from long-term damage. This led us to conclude that elevated blood pressure might be a compensatory response to inadequate blood flow, similar to how the kidneys raise blood pressure when they don’t receive enough blood.

Several factors support this idea:

1. Arterial Stiffening: Calcified arteries can’t expand as effectively, raising blood pressure as they become less able to release pressure.

2. Measurement Inaccuracy: Blood pressure cuffs may overestimate pressure in stiffened arteries, particularly in those with severe atherosclerosis, resulting in higher readings than the true pressure (because hardened arteries require greater pressure to compress).

3. Endothelial Dysfunction: The blood vessel lining releases nitric oxide to dilate vessels and decrease pressure. When this function fails, it precedes atherosclerosis and increases blood pressure, suggesting the problem is with endothelial health, not high blood pressure itself.

4. Sympathetic Reflex: When the body rapidly loses a significant amount of blood, a reflex triggers increased heart rate and vessel constriction to raise blood pressure, a common response in critical conditions.

This all suggests that high blood pressure may be more of a symptom than the root cause of circulatory issues.

Note: as I show here, a strong case can also be made that the blood thickening and clumping together causes hypertension.

Changing Guidelines

When the blood pressure craze took off, there was a rush to bring the blood pressure lowering drugs to market before their benefit was actually proven (outside of a few short term studies which showed a small benefit for people with very high blood pressures).

That mindset cemented itself, and as the years went by, regardless of the evidence arguing against it), the blood pressure thresholds kept on getting lowered so more and more people could put on blood pressure lowering medications. Because of this, roughly 60 million American adults (23%) now take these drugs.

However, excessively lowering blood pressure cuts blood flow to parts of the body that can’t function without sufficient blood flow. For example, blood pressure medications increase the risk of kidney disease,^1,2 and suddenly passing out (from insufficient blood flow to the brain) is one of the most common side effects of blood pressure medications.^1,2

My best guess is that this inexorable march to putting everyone on these drugs is due to some combination of the following:

•Research funding is available for these areas (e.g., from the drug manufacturers), hence being a safe area of research for academics to explore.

• It illustrates the “if you have a hammer, everything looks like a nail” phenomenon and the medical profession’s desire to find more justifications for using its tools (especially since humans tend to double down on their existing approach when it fails rather than consider a new one).

Let’s now look at how the blood pressure guidelines have changed over the years.

Note: as these guidelines show, originally the focus was on treating diastolic blood pressure under the belief that the heart had to “work harder” if there was too much blood in the circulation. I believe this is helpful to note since it was believed for decades (but now is not), and hence illustrates how arbitrary many medical dogmas are.

To quote the 2017 guidelines:

“Rather than 1 in 3 U.S. adults having high blood pressure (32 percent) with the previous definition, the new guidelines will result in nearly half of the U.S. adult population (46 percent) having high blood pressure, or hypertension.”

Note: this rate further increases with age (e.g., 79% of men and 85% of women over 75 now have hypertension, while 71% of men and 78% of women now meet the threshold to start blood pressure medications).

Unfortunately, “Experts” on guideline panels are paid to create recommendations that result in more and more people taking the drugs, a sadly common phenomenon in medicine. For example, once statins entered the market (which unlike their predecessors, could effectively lower cholesterol), the acceptable blood cholesterol levels kept on being lowered, and before long almost everyone was told they would die from a heart attack unless they started a statin—despite statins have an almost non-existing mortality benefit (e.g., taking them for five years at best makes you live 3-4 days longer) and causing (often severe) side effects for roughly 20% of users. In turn, since so many people have been severely harmed by the great statin scam, more and more people, such as comedian Jimmy Dore, have begun to speak out against this:

The Effects of Hypertensive Medications

In many cases, the actual mechanism of a drug greatly differs from the purported one (e.g., the tiny benefit statins provide is most likely due to them reducing inflammation).

In the case of blood pressure medications (each of which works in a different manner), very different degrees of benefit are observed with their use, despite producing the same drop in blood pressure. This in turn strongly argues that their benefits are not due to them lowering blood pressure, but rather how each one specifically affects the body. To illustrate:

•A 1997 paper in JAMA reviewed the literature and found significantly different benefits from the antihypertensive drugs depending on which type was used.

•A 1998 review found that the (known) cardiovascular benefits of ACE inhibitors were not seen with calcium channel blockers, despite the latter having a more significant effect on blood pressure.

•A 2000 study of 3577 diabetics found that a specific ACE inhibitor, despite minimally reducing blood pressure (a 2.4 reduction in SBP and 1.0 reduction in DBP) had a massive effect (a 25% reduction) on the risk of a heart attack, stroke or cardiovascular death.

•A 2007, eight year long (and NIH funded) double-blind study of 42,418 subjects found that when two different types of blood pressure medications were used, there was no difference in their effect on blood pressure but simultaneously, found their rate of preventing heart failure varied by 18% to 80% depending on the drug, leading the investigations to conclude: “blood pressure reduction is an inadequate surrogate marker for health benefits in hypertension.”

Harms of Hypertensive Medications

Blood pressure management typically combines multiple drugs to achieve target levels while switching medications that cause intolerable side effects. This approach is problematic because each drug has markedly different pharmacological and physical effects and should be selected based on individual patient needs rather than simply achieving blood pressure targets.

The most common side effects stem from poor perfusion. Blood pressure medications increase the risk of fainting and frequently cause lightheadedness and falls in older patients with calcified arteries who require higher pressure to perfuse the brain (e.g., a 2014 JAMA study of 4,961 adults over 70 with hypertension found that over three years, 9% experienced serious falls and 16.9% died).

Note:an important Israeli study found that discontinuing an average of 2.8 drugs per elderly patient reduced their 1-year death rate from 45% to 21%. This is massive, and I believe a key reason for those results was reduced falls (as anti-hypertensives were one of the most successfully discontinued drug classes in the study).

Likewise, emergency medicine recognizes that aggressively treating high blood pressure can impair brain blood flow and trigger ischemic strokes. Furthermore, hypertension drugs increase the risk of an acute renal injury by 18%, and in patients who have end stage renal disease low blood pressure increases mortality by 39%.

Note: low blood pressure is particularly harmful to organs sensitive to reduced blood flow like the brain (e.g., low blood pressure is strongly linked to cognitive decline).

Finally, each blood pressure medication works differently, offering unique therapeutic benefits but also distinct side effects. Four main antihypertensive drug classes exist:

1: Diuretics lower blood pressure by increasing urination through blocking sodium reabsorption in the kidneys. They cause electrolyte imbalances (low potassium affects 8.2% of users), gastrointestinal symptoms due to dehydration, and hypotension(low blood pressure). Thiazides also increase uric acid, increasing the risk of diabetes and gout.

2: Beta-blockers slow the heart and reduce contraction force. While beneficial for patients with heart failure, they constrict peripheral arteries. Patients frequently report worsened quality of life from beta blockers, with the most common side effects including:

3: Calcium channel blockers reduce heart contraction force, dilate arteries by relaxing smooth muscle, and slow heart rate. Major issues include edema (affecting 5.7-16.1% of users), dizziness, lightheadedness, and constipation.

4: ACE inhibitors block the kidney’s blood pressure cascade and are considered most beneficial (commonly prescribed for diabetes and heart failure). The most common side effect is chronic dry cough (ranging from 3.9% to 35% of users—this detailed review determined it was 8.0%). Other common side effects include headaches, lightheadedness, and loss of taste. More severe effects include a 26% increased risk of acute kidney injuries(1.5% of users), a 103% increased risk of hyperkalemia (4.8% of users), and a 19% increase in the risk of lung cancer.

Under Recognition of Side Effects

While the numbers I just showed are quite concerning, I believe they actually underestimate the rate of side effects, as much of that data comes from industry clinical trials that deliberately find ways to downplay their drug’s side effects. Accordingly, I believe patient surveys provide a substantially better perspective on the incidence of symptomatic side effects. Consider this 1995 Swedish survey, which found roughly 1 in 5 users experience side effects:

Likewise, a study of 370,000 patients under 65 between 2007-2014 found 23.5% stopped taking the drugs within 270 days of starting them, while 40.2% of those who continued often skipped the medications.

Given such a high discontinuation rate of these drugs, one of the most surprising things about blood pressure drugs is how little awareness exists regarding their side effects, especially amongst doctors (e.g., the article I just cited acknowledged side effects were a reason for discontinuation but insisted it was due to patient ignorance about the importance of the drugs). All of that was best shown by this 1982 study (which would not be repeated in today’s political climate) that compared how patients, their families, and their doctors felt about the effects of these drugs on them. It found: