• Throughout the development, production and distribution of the COVID vaccines, whenever a choice had to be made between safety and efficacy, efficacy won—a pattern which can be traced through the antigen chosen, the nanoparticles used to deliver it, the modifications made to the mRNA, and the doses selected.

• Once the vaccines reached the public, a series of things happened which were not supposed to be possible, the most significant being that the spike protein kept being produced for months or years after injection, and that unvaccinated people around the vaccinated became ill in clear and reproducible patterns.

• For years I assumed this was simply the predictable result of a rushed and profit-driven product. However, while researching the existing vaccine designs, I learned that bringing foreign DNA into the nucleus of cells is already an established vaccine technology—which not only offers a far more feasible explanation for the persistence, but suggests those designs were chosen knowing what they would do.

• This matters because continual antigen production and spread through a population are not accidents of these platforms. They are the longstanding goals of vaccination itself, and are now being made explicit by the next generation of “replicon” vaccines which are designed to keep producing antigen long after injection.

• Spike protein injuries have consequently become one of the most widespread and complex illnesses the population currently faces, yet there is almost no mainstream research on them and no established protocols for treating them—which is why I am continually asked what can actually be done.

• This article is the result of a large project to answer that question. It covers the treatments which have consistently worked, why the far greater number of failures reveal so much about both the supplement industry and how chronic illness is approached in general, and everything we now know about shedding.

I have always been drawn to puzzles that contain large amounts of “unknown information” as this forces you to consider a wide range of possibilities, but simultaneously have the discernment to recognize which of those potential answers is the most probable and hence is less likely to backfire on you if you commit to it.

On one hand, many people have a total intolerance for anything uncertain or unsanctioned (which is why many medical professionals are unwilling to do anything slightly “unorthodox”—even if it is essentially a given that the existing conventional options will lead to a bad outcome for their patient (e.g., death from an “incurable” illness). On the other end of the spectrum, many people will be too eager to commit to unsubstantiated answers, and in many cases (due to confirmation bias), collect a body of highly questionable evidence that supports their chosen possibility (which in the case of the COVID vaccines, has resulted in numerous theories briefly going viral which are completely at odds with reality—and often basic science).

This, in turn, has been the lens I’ve observed the COVID vaccines through, as beyond the mRNA gene therapies still being in the experimental stage when they were given to the entire population, we saw a lot of very strange things occur which hence invited equally strange explanations for what was going on.

For example, since the vaccines came out, embalmers have been observing science fiction-like massive rubbery clots coming out of the bodies of deceased individuals who had been vaccinated. A few citizen researchers, in turn, have been trying to draw attention to this issue and have conducted numerous surveys of embalmers (which many professional organizations resisted) that were able to show those clots indeed were being found, and recently were able to have the 2022-2025 results be published in a medical journal—where across 808 responses, 66% to 83% of embalmers reported finding these clots in roughly 19% to 27% of embalmed bodies.

These disconcerting findings in turn met a variety of expected responses ranging from refusals to discuss the topic at all, to denials they existed (despite the extensive work the citizen journalists did to reveal that they did) to a variety of shocking explanations being put forward to explain what they were (e.g., alien parasites or nanotechnology).

While I was trying to make sense of this topic, I came across a largely unnoticed paper on COVID-19 that stated the spike protein causes fibrin (which the body uses to create long-lasting blood clots) to misfold. Since the body depends on a precise balance between enzymes creating and breaking down fibrin clots, if misfolded fibrin were to be formed, there was a high likelihood that the body's clot breaking enzymes would no longer match it, and hence that the body would not be able to break these clots, thereby allowing them to grow unchecked until they eventually became the massive clots embalmers were finding, particularly since the study modeling this was able to show (nowhere near as large) irregular fibrin clots formed by the spike protein that were resistant to the enzymes the body used to break down clots—all of which I detailed in this 2022 article. That model then became the accepted explanation and researchers were subsequently able to develop blood tests that showed the amyloid (misfolded) fibrin clots were present in the bloodstream.

Malice or Malfeasance?

Whenever something bad happens on a large scale, a case can normally be made that it was due to a deliberate desire to harm others, incompetence (and a tendency to double-down on one’s mistakes), or simply a complete lack of concern for the human cost of whatever they want to do. I tend to lean towards the latter explanation, as the strongest case frequently exists for it and it does not require ascribing (often ultimately unknowable) motives to someone else.

As such, from early on with the COVID-19 vaccines, I formed the impression that the vaccine industry (and to some extent the US government) felt they needed to get the vaccines to market as quickly as possible. For instance, leaders wanted a “working” vaccine to get to market as soon as possible (and ideally before the 2020 election) so the economy could be opened up, Operation Warp Speed was effectively a winner-take-all competition so whoever got the first vaccines to market would likely make most of the money in it and there was a real likelihood the population would develop herd immunity to COVID-19 before the vaccines came out (negating the need for them in the first place), which led not only to the vaccine being rushed along, but also federal health leaders trying to stall the virus enough for the vaccines to still have a market (e.g., HHS insiders admitted many of the 2020 "containment" measures were done to isolate the population so herd immunity could be delayed,¹ and Scott Gottlieb, a recent FDA commissioner who became a Pfizer board member in 2019—advocated for lockdowns and publicly gave statements we were much further away from herd immunity than what he privately told the CIA^1,2). In contrast, African nations which did nothing for COVID-19 rapidly developed herd immunity to COVID and had dramatically lower death rates than the Western Nations.
Note: one of the most appalling aspects of this strategy was not only was herd immunity delayed to protect the vaccines, but the unnatural “immunity” the vaccines gave prevented the population from being able to develop herd immunity to COVID-19, thereby turning a passing pandemic into a permanent seasonal infection. This was because the COVID vaccines created a very narrow immunity that locked the immune system onto the original strain (of a rapidly mutating virus), thereby both provoking the rapid evolution of variants but also making those locked onto the original virus less able to mount an immune response to the newer variants—shown by both Cleveland Clinic Research¹ and countless Reddit reports of individuals being more likely to catch COVID the more shots they’d gotten¹ (and in many cases catch COVID numerous times). While this was probably not intentional, it is notable that just two months after the COVID vaccines hit the market, vaccine CEOs were already talking about the COVID vaccine becoming an annual vaccination like the flu shot.^1,2,3,4,5

To expedite the vaccines, again and again, I identified how they appeared to have made the decision to cut as many corners as possible in each stage of its development, testing, production and distribution. As such, I long believed the fiasco we saw was simply due to a desire to make money and a complete lack of concern over the consequences the actions taken would create. However, while researching the existing vaccine designs for a recent article, I came across a rather surprising piece of information that has changed my perspective on what actually happened with the vaccines.

How Vaccines Work

When the body is exposed to a foreign invader, a series of defensive responses are mounted. Some of these are relatively non-specific and hence can initiate immediately, while others are specific to the microbe and, though often more protective later, initially require time to become effective (as the tiny fraction of your randomly generated immune cells which match the invader must encounter them and then after being activated, have time to reproduce enough that a sufficient amount of those cells are present to control the invader).

Note: life revolves around having DNA (or RNA equivalents in certain viruses) be transformed by cellular enzymes into corresponding mRNA sequences, which is then transformed into corresponding protein sequences. Because of this, most organisms contain unique protein sequences that give them a “molecular fingerprint.”

The theory of immunization, in turn, is that if you introduce the antigen (protein fingerprint) of the invader (without the invader also present), it becomes possible for the body to develop adaptive immunity to the antigen (and hence the pathogen which contains that antigen) without also having to survive a potentially dangerous infection. As such, a variety of different antigens are routinely injected under the belief doing so will create immunity to disease—even though in reality this frequently does not work or creates a host of problems from unintended off-target “immunity.” However, due to the religious fervor around vaccinations, the medical field essentially believes in the infallibility of this approach and continually tries to find every feasible way that can be done.

As such, over the years, a variety of methods have been created to develop these antigens.

Originally, the infectious microbe would either be cultured and then chemically inactivated (e.g., killed), filtered or selectively bred (via repeated passages through cellular mediums) so that the microbe was made less dangerous (e.g., no longer infectious) while still containing sufficient antigens to create an immune response (along with the microbe sometimes reproducing within the host and creating even more antigens to ensure the development of an immune response).

Later, once genetic engineering entered the picture, things would either be modified to produce the antigen so it could then be extracted (e.g., modified yeasts for Merck’s HepB and HPV vaccines or moth cells for Novavax), or a virus would be modified to carry the antigen and then mass produced outside of the body so those antigens could be delivered via the viruses (e.g., J&J or AstraZeneca’s COVID vaccines).

Later still, genetic engineering made it possible to instead have the vaccine recipient’s cells produce the antigen (thereby allowing a much lower initial dose of the vaccine to be used). Many public health officials, in turn, pushed for this approach as it takes much less time to create the synthetic mRNA which did that than producing traditional vaccine antigens, thereby making it possible to bring vaccines to market for a new infection much sooner (whereas with annual flu shots, they have to be produced before the flu season and frequently end up being for different strains than what is circulating).

Note: there are a variety of safety and efficacy issues with each of the vaccine designs (e.g., many of the “essential” ones on the market either provide almost no benefit or make their infections worse) and when I went through all the standard ones, I could only identify one you could make a good case provided a net benefit (along with a few non-standard ones like rabies after a bite). However, as mentioned before, due to the faith surrounding vaccines, every vaccine is assumed to be completely safe, effective and essential regardless of the actual data or logic underlying that assumption.

Designing the mRNA Vaccines

The vision of mRNA vaccines that was sold to the public is:

• A carefully crafted sequence of mRNA is created and then manufactured at scale.

• This mRNA is introduced into cells by injecting muscles with lipid nanoparticles containing the mRNA (which then travel into just the muscle tissue and the cells in them).

• Once in the cells, mRNA is transformed by the cellular machinery within the cytoplasm into a foreign antigen which gradually travels out of the cell and coats its surface, where the immune system can recognize the antigen and develop an immune response.

• Not long after, the immune system breaks the mRNA down and the entire process stops.

However, while that was the vision, it had major problems, and for decades attempts to find an acceptable balance between safety and efficacy failed (Dr. Malone, one of its pioneers, abandoned lipid-nanoparticle delivery in the 1990s after documenting its profound toxicity¹). This is best shown by Moderna, which raised billions from investors by selling the vision of life as software you could rewrite into health, yet could not deliver what was arguably the easiest mRNA therapy target on the market — a rare disease needing a single missing liver enzyme — because no dose was both low enough to be safe on repeat injection and high enough to work.¹,² According to former Moderna employees in 2017, this left vaccines as the only viable use of the technology, since a vaccine needs just one or two doses and the toxicity that made repeat dosing impossible never had a chance to accumulate.¹

So, by the time COVID-19 arrived, both companies that would bring mRNA vaccines to market were in trouble. Moderna had gone public in December 2018 in what was then the largest biotech IPO in history, raising $604 million at a $7.5 billion valuation—and then watched its stock fall more than 19% on its first day of trading.^1,2 It had no product, $60 million in revenue against $606 million in operating expenses, an accumulated deficit of $1.5 billion, and shrinking cash reserves, and it closed 2019 at $19.56 a share, below its $23 offering price.¹,² BioNTech was in a similar position: it had never taken a product past phase 2, its losses were widening, and its October 2019 IPO had to be cut from 13.2 million shares at $18–20 to 10 million at $15 before it could get done, closing its first day lower still.^1,2 One month before that IPO, the Bill & Melinda Gates Foundation had bought a $55 million equity stake in BioNTech (with up to $100 million in total funding pledged), reportedly at around $18 a share, meaning the foundation was underwater the day the company listed.^1,2 In other words, mRNA's two flagship companies entered 2020 needing exactly what a former Moderna employee had described three years earlier: a "miraculous, Hail Mary sort of save."¹

Given this, I felt it was a given they would take advantage of everyone’s desperation to get a viable vaccine to market by both cutting as many corners as possible and by leveraging the vast institutional support for the vaccine (e.g., liability protections, poor oversight of clinical trials, and zealous media support for the vaccine—particularly since Bill Gates, a key investor in the technology, had also cultivated a vast sphere of media influence through “donations” to many leading publications¹). As such, I was curious to see how they would solve the irreconcilable challenges with the mRNA technology and hypothesized whenever a balance needed to be found between efficacy and safety, efficacy would be chosen to expedite getting a COVID-19 antibody producing agent to market (since the widespread faith in vaccines makes robust antibody production one of the primary metrics regulators care about despite it often having a poor correlation to clinical benefit).

What follows is an (incomplete) list of how that balance was struck:

1. Choosing a toxic antigen: The easiest target for a vaccine was the COVID-19 spike protein since this was a novel part of the virus, needed for infection and highly immunogenic, so both Pfizer and Moderna’s vaccines were designed around causing cells to mass produce this protein (which was slightly modified so it could not fuse with cells and hence “safe” ¹) as this was by far the fastest way to reliably create an antibody producing vaccine. However, there were a few problems with this approach.

Chiefly, since the (positively charged) spike protein was inherently toxic in numerous ways (hence why it was so immunogenic), by mass producing it inside the body, an effect was created that was arguably worse than a COVID infection (particularly for the individuals whose bodies could not clear the spike protein—which was shown as the distinguishing factor in a January 2023 study comparing adolescent vaccine recipients with and without myocarditis, where those who developed myocarditis had free spike protein circulating in their blood for weeks despite having a normal antibody response, at levels equal to those seen in children hospitalized with the severe post-COVID inflammatory syndrome MIS-C).

Furthermore, this design was predisposed to creating off target immunity. For example, since the highly toxic antigen was expressed on the surface of cells, it was well-suited for provoking autoimmune responses—something made considerably more likely by the fact that the spike protein shares sequences with numerous human proteins.¹ A 2022 peer reviewed analysis identified a motif shared between the spike protein and thrombopoietin (where cross-reactive antibodies could produce the thrombocytopenia seen in these patients), along with another motif shared with PRKG1, which is involved in platelet activation, and with tropomyosin, which is linked to cardiac disease¹ (with the authors explicitly noting the implications of their findings for vaccine design).^1.

Note: beyond autoimmune disorders frequently being associated with the COVID vaccines, pathologists who examined the bodies of individuals who died after vaccination found unusual inflammatory infiltration and immune destruction of normal tissue expressing spike protein vaccine antigens (e.g., within the heart).^1,2

Likewise, by forcing the body to lock onto a single antigen (the original COVID-19 spike protein), pressure was made to rapidly mutate COVID to a different spike protein, thereby making immune systems locked onto the original strain less able to respond to the new ones (which as said before is why I believe the vaccines prevented us from developing herd immunity to COVID-19)—an issue sadly also seen with many other vaccines that use a small number of antigens.

Note: in 2022, I spoke to a few people who argued that China, knowing the US’s approach to vaccine development, may have designed COVID-19’s spike protein so that the likely vaccine for it would be highly dangerous. While it’s impossible to prove or disprove that hypothesis, it is noteworthy that China’s Sinovac instead used a traditional vaccine design (inactivating a COVID-19 virus), was significantly safer than the mRNA designs and debatably offered comparable efficacy to the mRNA vaccines^1,2 (which rather than proving malice could simply illustrate that the Chinese were intelligent enough not to pursue a bad vaccine strategy).

2. Choosing dangerous lipid nanoparticles: as mentioned before, one of the unsolvable challenges in mRNA technology was making the lipid nanoparticles which delivered them inside cells be both safe and effective (as since mRNA carries a strong negative charge, a strongly positive lipid is needed to package it, but nothing in the body is permanently positively charged, so those lipids damage whatever cell membranes they touch—and simultaneously, since most of the particles are digested before they release anything, far more of them have to be injected than the body can tolerate). Curious how this would be solved, I read through regulatory documents leaked from the EMA (Europe’s FDA) in December 2020, and noted that when the nanoparticle design chosen (ALC-0159) was discussed, only efficacy was highlighted as a rationale for it—indicating, again, that since there were so few viable ways to make these nanoparticles work, efficacy was prioritized over safety so the products could be brought to market (while the only concern regulators raised was that since its metabolite was an acetamide and certain acetamides have been linked to liver cancer, this could potentially be an issue). As such, I felt it was likely these nanoparticles would have toxicity and issues with spreading to unintended sites in the body which was indeed what happened (e.g., confidential Pfizer documents were obtained through a May 2021 Japanese FOIA showing the vaccine nanoparticles accumulated in the ovaries).
Note: there are a few potential explanations for the significant clotting seen with COVID-19 and the vaccines (e.g., the previously mentioned amyloid clots or our observation the vaccine causes a high rate of the rare but severe autoimmune clotting disorder antiphospholipid syndrome—likely due to it provoking the immune system into attacking the phospholipid coating of spike protein expressing cells). However, my observation from the start of COVID-19 is that the positive charges of both the spike protein and the lipid nanoparticles (which matter more acutely) appear to be what is causing the rapid clotting (and microclotting) seen with the vaccines and why so much of my focus since 2020 has shifted towards restoring the physiologic zeta potential.

3. Making mRNA resist degradation: Since foreign mRNA was rapidly degraded by cells, it was not possible to ensure enough would persist long enough to produce enough spike protein to generate the needed immune response. To address this, rather than using uridine (one of the four building blocks of RNA), the synthetic mRNA was manufactured with a modified version of it, pseudouridine, as RNA containing pseudouridine both resists degradation and hides from the immune sensors that would otherwise detect and destroy foreign RNA. In the body, this is a tightly regulated process where specific enzymes modify specific sites on specific mRNAs, and to this day it is not understood well enough to predict what a given modification will do. Rather than attempt to replicate that, the manufacturers simply replaced every uridine in the sequence and did so with N1-methylpseudouridine, a synthetic molecule more potent than the natural version which does not exist in the human body thereby guaranteeing enough was done for the mRNA to persist long enough to work.^1,2

This however led to two major problems. First, since the process was overshot, the mRNA no longer merely lasted long enough to produce an immune response—it persisted for months, continually producing spike protein the whole time. This was first shown by a 2022 Stanford study that found vaccine mRNA and spike protein still present in the lymph nodes of recipients 60 days after their second dose (the latest point at which they looked),¹ and corroborated by a Massachusetts General Hospital autopsy study that detected vaccine mRNA in the lymph nodes and heart muscle of patients who died within 30 days of vaccination,¹ another study which found mRNA persisted in the blood of 37% of recipients for at least two weeks after vaccination,¹ along with being found in human blood, placenta and semen in many cases over 200 days since vaccination.^1,2 Second, the key reason pseudouridine allows the mRNA to persist is that it hides it from the innate immune sensors (TLR7, TLR8, RIG-I and PKR) which exist to detect foreign RNA and destroy it.^1,2 The long term consequences of this immune suppression however were never tested, and hence may play a contributing role in the immune suppression and cancer being seen following COVID vaccination.

Note: Codon optimization (which increases protein production from mRNA) may have also caused the vaccine to excessively produce spike protein in the cells—once again illustrating that efficacy was chosen over safety.

4. Excessive dosing: with any substance, as greater amounts are taken, adverse reactions and severe ones become more common (to the point everything has a lethal dose). For something to be viable as a medicine, the dose needed to create a therapeutic effect has to be below its toxic dose, and generally, the greater that difference (the therapeutic window) is, the better the medication is (e.g., one of the main reasons why I’ve been able to promote DMSO is because the therapeutic window is so wide, most people who use it correctly have positive rather than negative effects), whereas the narrower it is, the more high risk the medication is and the more precisely its dosage has to be controlled (e.g., this is why chemo is frequently given at infusion centers). Further complicating this, the toxic dose (and effective dose) vary person to person, so frequently, the medication’s therapeutic window is narrow enough no optimal dose exists for everyone, which results in the medical system throwing the sensitive patients under the bus who can’t tolerate the standardized doses the medical system revolves around.

With the mRNA technology, as mentioned above, a major problem was that the therapeutic window was too small for it to be a viable therapy (as doses high enough to work were also toxic), and while the therapeutic window widened when vaccination (rather than addressing a genetic defect) was the goal, the fundamental issue still remained that there did not appear to be an optimal way to dose the therapy. As such, I was curious how this would be addressed, and immediately noticed Moderna used a dose which was 3.3x greater than what even Pfizer would use (something I attributed to Moderna at that point being desperate to bring a viable product to market). Remarkably, subsequent safety data showed Moderna’s vaccine indeed had a higher rate of side effects, but despite a dose toxicity relationship being demonstrated, regulators never did anything to address it.

Producing the mRNA vaccines

One of the greatest challenges with bringing a pharmaceutical to market is scaling up its production. So, as you might guess, a lot of corners were cut here as well to be able to bring a viable product to market. These included:

1. Vaccine mRNA rapidly degraded: This was one of the primary regulatory concerns with the vaccines (e.g., in the leaked EMA documents, numerous datasets were cited by regulators that showed the vaccine mRNA rapidly broke down into fragments), and is, I believe, why when the vaccines were first launched, a huge deal was made about keeping them ultra-frozen until injection (e.g., Pfizer shipped at -90°C to -60°C and Moderna shipped at -50°C to -15°C¹). However, once the launch happened, this gradually became forgotten (e.g., the vaccines were left out for long periods at vaccination clinics and they switched to just refrigerating them).
Note: when I initially learned about this, I was worried it would cause abnormal mRNA fragments to form that could be a potential safety risk, but I now believe this actually made the vaccine safer (as the more time they had to break down, the less active mRNA there was), and to some extent, this was supported by an adverse event reporting analysis that found vaccine lots distributed further away from Europe’s manufacturing site (and hence having longer to break down) had a lower rate of adverse events, as did ones taken further away from the date of manufacture.

2. Doctored Western Blots: To assess if an intended protein is present, Western Blots are one of the most commonly used tests, and in the pre-AI era, due to computer generated ones being much less amorphous than natural ones, authors would frequently get caught fabricating Western Blot tests (e.g., this caused billions of dollars and years of Alzheimer’s research to be wasted on the amyloid hypothesis and was only caught after the fact by an independent investigator who noticed the artificial blots). Given that it was a major question if the mRNA vaccines could actually work as promised (especially given their tendency to rapidly break down) when we looked into it, we realized the blots needed to assess what was being produced were likely fabricated.
Note: while I assumed this was done to gloss over the fact the vaccines had poor quality control (with many not producing the promised product), from looking at all the available blots, another reliable researcher made the case they showed something else which was not disclosed was in the vaccines too (and to this day, it has not been identified).

3. Vaccine contents varied lot by lot: in addition to numerous VAERS analyses (and published papers) showing the toxicity of COVID vaccine lots varied greatly, when Ryan Cole examined the COVID vaccines under a microscope (as detailed on The Highwire), he found what was present in the vaccines varied greatly (and likewise, Japan pulled 1.63M vials of Moderna’s vaccine after visible metal particles were found in them). Cole felt these observations indicated there were real quality control issues with the vaccines, that properly mixing the vaccines was challenging and that the process for the vaccines was very poor (resulting in some individuals getting excessive doses and others effectively getting saline shots—which mirrored our own experiences). Remarkably, when the UK’s MHRA was asked through a FOIA what testing had been done to look for contaminants in the COVID vaccines, they disclosed that some vials had been sent for a visual inspection test, which consisted of reviewing them against two monochrome backgrounds to observe particulate matter visible to the naked eye, and explicitly stated the composition of the vaccine was not examined.¹

Note: while Cole’s explanation for this is the most probable explanation, it is also possible saline was given because not enough vaccine product was available to meet the committed orders.

4. The production process was changed. When the original COVID vaccines were made for the clinical trials, in Process 1, they were produced by:

•Starting with a circular plasmid that had the vaccine sequence on it.
•Using PCR to copy that sequence and turn it into linear DNA.
•Having T7 RNA polymerase make the vaccine mRNA from those linear
•DNA templates.
•Purifying the result so that, for the most part, what you had left was the mRNA.

The problem with this approach, however, was that it did not scale anywhere close to the volume needed for the public roll-out. So when it came time to bring it to market, they cut corners and improvised a different way with Process 2:

•Starting with the same kind of circular plasmid and introducing them to E. coli bacteria.
•Growing E. coli that now had that plasmid in them.
•Using an antibiotic to eliminate E. coli in the culture that did not have the plasmid (as beyond producing a spike protein, the plasmid also contained a gene for antibiotic resistance).
•Once they had a pool of bacteria carrying the plasmid, they killed them and extracted the plasmids which were then cut into linear DNA.
•Having T7 RNA polymerase make the vaccine mRNA from those linear DNA templates.
•Purifying the result so that, for the most part, what you had left was the mRNA.

This shift, in turn, created a few key issues such as a different product being tested in the clinical trials than what was given to the public. Of these, the greatest one was that in Process 2, a different DNA plasmid was used, and that altered plasmid was not effectively purified from the final product. This, in turn, was discovered by Kevin McKernan, who having a background in genetic sequencing, decided to find out what was in the vaccines and discovered that not only was plasmid DNA present in them, but they contained an undisclosed SV40 virus promoter sequence (which included 72 base pairs that were repeated). These results were eventually published in a 2025 paper, that also showed the rate of adverse reactions to the COVID vaccines had a correlation to the presence of SV40 containing plasmids.

Note: McKernan’s sequencing found fragments up to 3.5 kb in length^.1 (which is many times the size of the SV40 promoter-enhancer region), and the same testing established that this DNA sits inside the lipid nanoparticles, which shields it from the enzymes that would otherwise break down loose DNA in the body.¹ Furthermore, the plasmid contamination he detected was corroborated by many other labs.¹

The switch to Process 2 also changed the methylation of that DNA, as Process 1 used PCR (which produces unmethylated DNA) whereas the bacterial strain used in Process 2 methylates the exact bacterial signature sites our innate immune system evolved to recognize as an invader. Industry is well aware of this, as CpG DNA deliberately used as a vaccine adjuvant is kept unmethylated—and McKernan suspects this is part of why Pfizer resisted removing the residual DNA, noting their product contains roughly ten times more DNA than Moderna’s at a third of the mRNA dose.¹

The presence of the SV40 promoter understandably drew significant concern—due to the virus this sequence comes from being strongly associated with cancer and potential cancer triggering effects being associated with the sequence,^1,2,3,4 along with the vaccine plasmids being discovered in unusual aggressive cancers,¹ and reports that raise the possibility vaccine plasmids integrated into the DNA of cancers.^1,2,3

Note: in 2004, Australia's TGA commissioned a review of the health consequences of SV40 contamination of the polio vaccines, which dismissed the cancer concerns by arguing that the SV40 sequences being detected in human tumors were most likely laboratory contamination, as many of the reported positives carried a deletion mutation found in experimental plasmids but not in the infectious virus. At the time this was a reasonable explanation, since there was no other conceivable source of those plasmids. It is not reasonable now, as the same logic dictates that a population injected with plasmids containing those sequences is a route by which they can reach human tissue.¹,²

Giving the benefit of the doubt to the industry, its presence was due to:

• The SV40 virus’s enhancer being established as a potent way to bring foreign DNA into the nucleus of many different mammalian cells and have the cells then turn that DNA into mRNA (which then created the intended protein). As a 1999 paper on the subject put it, the nuclear envelope is a major barrier to the uptake of plasmids and one of the most significant unsolved problems in non-viral gene delivery—and while various fragments of the SV40 region support nuclear import to some degree, it is the “72-bp repeats of the SV40 enhancer” which facilitate maximal transport.¹

• The SV40 enhancer being combined with a specific antibiotic-resistance gene, so that it could be ascertained if mammalian (e.g., human) cells were taking up lab-altered plasmids (as they became resistant to lethal antibiotic concentrations).

• This package often being bundled with the sequences needed to grow and select the same plasmid in bacteria, so that the same construct could be used for both mammalian and bacterial cell experiments without the cost of having to switch between the two (and hence is frequently used in biomedical research)

• BioNTech choosing to use this dual package (which already contained the SV40 part) as the backbone for creating the plasmids used to make their vaccine (despite not having any need for the SV40 part) because they already had easy access to the (well-established) dual package and wanted to use something as quickly as possible to scale up COVID-19 mRNA vaccine production rather than take the time to create a new backbone (much in the same way they did not take more robust measures to ensure residual DNA was consistently removed from the mRNA vaccines).

As such, while this is a bit jaw dropping, when I learned about it, I simply interpreted it as yet another example of speed and efficacy being prioritized over safety. Notably, Moderna’s vaccine plasmids did not contain SV40¹ (as they instead chose to use a backbone without it), which again illustrates that there was no real justification for Pfizer’s decision to keep it there.

Furthermore, later FOIAs revealed that five months after McKernan revealed the undisclosed plasmid contamination, Canada’s Health Agency deemed it inappropriate for the SV40 sequences to be included in the plasmids used to manufacture the vaccine and requested for them to be removed—a request Pfizer disregarded (and received no sanctions for).

Mysteries of the COVID Vaccines

After the COVID vaccines came out, a variety of odd things were observed that were hard to make sense of, and I spent a while investigating them. Some of these I felt were ultimately false (e.g., many of the alarming things individuals saw in the vaccines under the microscope were actually normal findings). Others I ultimately did not know what to make of (e.g., after many people online said the vaccines made them magnetic, I was able to find and evaluate one person who claimed this and noticed that his body appeared to magnetize paramagnetic metals until they became magnetic, I found a Luxermbourg study , where 29/30 vaccinated [with both mRNA and non-mRNA COVID vaccines] were magnetic while 0/30 unvaccinated were, but then also found a larger study James Thorp MD conducted which found about 60% of both vaccinated and unvaccinated individuals were magnetic, leading Thorp to conclude that humans have some degree of natural magnetism which had nothing to do with vaccination).

However, there were also a few inexplicable observations I became increasingly convinced of as time went on.

COVID Vaccine Persistence

When the COVID vaccines were originally pushed to the public, public health officials and the media promised a variety of things that were not supported by existing data (e.g., that the COVID vaccines would stop disease transmission).
Note: a common tell for a con is if legitimate objections are addressed with rhetoric rather than data—a pattern we saw through COVID-19.

As such, while reading through the Pfizer EMA leaks, I was very curious to see what was being said in private about the three largest safety concerns about the vaccine (autoimmunity, fertility issues and cancer). To my initial surprise, this is all that was discussed throughout the documents:

Genotoxicity: No genotoxicity has been provided. The components of the vaccine formulation are lipids and RNA that are not expected to have genotoxic potential. That being said, the novel lipids possess an acetamide moiety which is classified as possible human carcinogen (IARC Group 2B) with debated genotoxic mechanism, which should be discussed further (OC).

Vaccination with modRNA is expected to induce robust neutralising antibodies and a concomitant T cell response to achieve protective immunity. Nevertheless, no further discussion was provided regarding the risk of autoimmune responses induced by the modRNA. The Applicant is invited to further discuss the possibility that the mRNA vaccine can trigger potential autoimmune responses and how do it plan to possibly evaluate their occurrence

Given that these issues—especially genetic damage from an experimental gene therapy—were the largest concerns with the vaccines and hence most likely would have been tested, I formed the hypothesis (in December 2020) that internal testing had shown there were serious issues with all three, and Pfizer had concluded their best option was to pretend to have never tested it so they could claim plausible deniability once the issues were later discovered (or to sweep the independent evidence of it happening under the rug).

As the vaccines began to enter the market, I then began noticing countless media outlets state that the vaccines could not change your DNA and that anyone who thought so lacked a basic understanding of science. However, rather than provide evidence, they always referred back to “experts” like Paul Offit and Anthony Fauci who stated:^1,2

1. The vaccines cannot enter the nucleus of the cell

2. mRNA from the vaccines breaks down rapidly in the cell, so it does not have time to enter the nucleus and change your DNA.

3. mRNA is not DNA, and hence believing it can change DNA represents a fundamental lack of knowledge of biology.

Note: beyond the subsequently discovered SV40 plasmids, there were numerous other issues with these arguments such as the mRNA being deliberately modified to persist in the cytoplasm, and already published studies contradicting their statements (e.g., an August 2021 paper showing vaccine spike protein concentrated in the nucleus, a May 2021 study showing endogenous LINE-1 retrotranscriptases were integrating COVID-19 RNA into human DNA and a February 2022 cell study showing the Pfizer vaccine's mRNA was reverse transcribed into DNA inside human liver cancer cells within six hours, likely via the LINE-1 mechanism).

Beyond potentially causing cancer, one of the main reasons so many people were concerned about vaccine DNA integration was because this meant that the your body would perpetually produce the vaccine spike protein (rather than the process stopping once the mRNA broke down). In turn, we came across numerous clinical datasets suggesting this was happening such as:

•Autopsy studies showing the tissue (of people who had died unexpectedly up to six months after vaccination) was flooded with spike protein.

•Spike protein antibody bloodwork (in vaccinated individuals) studies showing elevated spike protein levels for months if not years after vaccination (the levels of which often roughly correlated with their clinical status) along with vaccine injured patients who clinically responded to spike protein binders months if not years after vaccination (who then often regressed if the binders were not continued, suggesting they were still being produced in the body).
Note: the only commercially available test (offered by Quest) measures existing antibodies to the spike protein receptor binding domain, and provides values anywhere from 0-25,000 (or higher than 25,000). Clinically, we’ve seen that long COVID patients rarely get levels above 4,000, whereas in those with vaccine injuries, it can be anywhere from 0-25,000 with many being over 25,000. In turn, a rough (but not precise) correlation exists between the antibody levels (which do not directly measure spike protein levels) and a patient’s illness (along with its levels improving or worsening generally correlating to a patient’s symptoms improving or worsening). Curiously, many patients do not have their antibody levels decline with time (which is what you typically see after a COVID infection), which again suggests spike protein is being produced within the body that then stimulates an immune response. Conversely however, some of these cases may instead have been from people who had antibody levels far above 25,000 who then had their antibody levels decline (but this cannot be detected as they are still above the 25,000 cut off). Additionally, these observations have been corroborated by others (e.g., Alex Berenson has also shared reports of vaccinated individuals who’ve had spike protein antibody levels over 25,000 for months after vaccination).

•When the spike protein could be directly measured (which requires specialized tests still not available to the public), long term persistence was observed. Currently, the longest dataset (Yale’s LISTEN study), showed it had persisted for over a year, with the longest case reaching 709 days of spike persistence at the time the study was finished (which sadly has remained a pre-print because no journal will publish anything critical of the vaccine program).

Because of this, a few schools of thought emerged on what was causing this persistence. These were:

•Genomic integration was happening (and hence that the nucleus was continually producing small amounts of vaccine mRNA).

•Rather than being due to a genomic integration (which would be rare enough it was unlikely to account for most of what was being seen) the persistence was due to the vaccine mRNA not breaking down and hence continually producing spike protein.
Note: the people I spoke to who I considered to be the most knowledgeable about mRNA technology tended to favor this explanation (as they felt it was by far the most probable).

•The actual issue is not continual cellular spike protein production, but rather a permanent dysregulation of the immune system (which can frequently happen after an autoimmune provoking stimulus). Numerous clinicians I know treating COVID vaccine injuries have gradually come around to this perspective (while others generally agree with it but feel a subset of vaccine injured people are still producing spike protein—mirroring the observations of Yale’s study).
Note: some have also postulated the “persistence” may have resulted from the gut microbiome (e.g., endogenous E. coli) being transfected by vaccine plasmids and then producing spike protein which travels into the body. That said, to the best of my knowledge, no one has ever tested if this is occurring. However, Pierre Kory spoke with researchers in Italy and Germany who developed a way to test for spike protein in the stools and urine and found that most people they tested (vaccinated or unvaccinated) had fragments in both which appeared to come from gut bacteria being transfected by the COVID virus (as it matched the virus rather than vaccine spike, and had bacterial modifications). Assuming this is true (and the data was collected and interpreted correctly), it indicates that there is widespread spike protein exposure in the population. This, in turn, argues that we are “in a post-spike world” and that the most prudent thing to do is to focus on is increasing your resilience to it, or in the cases of individuals who are sensitive to it (e.g., those affected by shedding), to figure out why—which I believe is likely due to their body’s not being able to effectively form neutralizing antibodies to it (as a 2023 study found this was the differentiating factor between adolescents who developed myocarditis after vaccination and those who did not).

Each of these explanations is compelling, and likely partially true. However, as I recently realized, there is actually a much simpler explanation for what is happening.

Vaccine Shedding

If a vaccine produces its antigens by replicating within the body, that vaccine has the ability to “shed” to others, as a tiny portion of it that reaches someone else can then reproduce into a much larger amount within the other person, thereby producing enough of an antigen there to also provide them with immunity. This, in turn, is viewed as one of the classic risks from using live viral vaccines (e.g., this is well recognized with the polio vaccine and a case can be made it is the source of many measles outbreaks) but simultaneously, by definition, is categorically assumed to not occur from any other vaccine type (with the exception of live bacterial ones—where it is much less of an issue than with viral ones).
Note: there has been some other work into self-spreading vaccines (primarily for wildlife but also theoretically for humans), but despite some pushing for it (so vaccination can reach difficult to un-vaccinate populations), there has thus far been a general restraint on using this technology.

Once the COVID vaccines came out, I began to hear numerous reports of individuals who had made a point not to vaccinate then becoming ill after being around someone who was vaccinated (particularly if they had recently been vaccinated or there was prolonged close contact with them) and I quickly noticed there was a clear and recognizable pattern to the symptoms experienced (e.g., menstrual abnormalities were one of the most common patterns, to the point quite a few of my post-menopausal friends began experiencing immediate and significant bleeding).

Since the COVID vaccines, by definition, could not shed, each time this point was raised, it was gleefully debunked much in the same way Fauci and Offit explained that it was impossible for the COVID vaccines to change your DNA. Given this, I felt it was essentially a lost cause to ever expect it to be investigated, so (with Pierre Kory’s help), I collected a lot of provider data that had accumulated on this phenomena, put out a call for readers to share shedding experiences (collecting over 2,000 of them), and searched the literature for everything known about this phenomenon.
Note: I ultimately received significantly more than 2,000 reports, but eventually stopped compiling them because they repeated the data seen in the earlier reports and our time to do projects like this is finite (currently that time is allocated to collecting reader DMSO testimonials at that point—of which 7,600 have been collected).

From this whole project (which can be read here), it then became evident that clear and reproducible events could be seen with:

•Who was affected by shedding.
•What situations triggered shedding symptoms (including that while rarer, “secondary shedding”—where someone exposed to a shedder then “shed” onto someone else and made them ill—did occur).
•What governed the severity of the symptoms experienced.
•How the symptoms could be prevented and mitigated.
•What symptoms were experienced—which resembled but had clear differences from COVID-19, long COVID or vaccine injuries.
Note: the most frequently reported shedding symptoms (in rough order of frequency) were abnormal menstrual bleeding (which far outnumbered everything else), headaches, rashes, flu-like illnesses, tinnitus, fatigue, dizziness, nosebleeds, unexplained bruising, shingles, a distinct odor around the vaccinated, palpitations, coughs, sinus congestion, muscle pain, gastrointestinal issues, and brain fog. Many others (e.g., swollen lymph nodes, hair loss, neuropathy, chest pain, and viral reactivations) were reported less often but still recurred throughout the reports. A few of these (e.g., nosebleeds) were unique to shedding injuries but not seen from other spike protein injuries. Additionally, many noticed “shedders” had a characteristic odor (and less frequently, a characteristic taste or feel), and a 2023 study a found that COVID vaccination produces a distinct exhaled VOC signature that can distinguish vaccine recipients from unvaccinated controls with high accuracy (as did a 2025 one which found the sweat VOC profile shifted after vaccination), providing a plausible chemical basis for the frequently reported odor around “shedders.”

It’s also worth noting that the shedding experiences were quite common. For example, after I described (in detail) everything which was known about shedding, readers here shared:

Since medical phenomena are almost never accepted without a mechanistic basis (and mRNA shedding was “mechanistically impossible”) I hence spent a long time looking for every possible mechanism, and from the many potential candidates I identified (each of which a case could be made for), I identified three I felt were the most probable to be true.

1. Exosome mediated shedding: Since the mRNA vaccines worked by causing the cells to produce massive amounts of spike protein that eventually came out on their surface, parts of the expanded cell membrane eventually blebbed off, causing exosomes (vesicles made from cell membranes) to be released which were studded with spike proteins that could then be exhaled or sweated out from the body and trigger reactions in others. Supporting this (in addition to it fitting numerous reports we received):

•COVID-19 infections were repeatedly shown to alter the exosome system,^{1,2,3,4,5,6,7,8} long COVID (and more severe acute COVID) is characterized by the presence of spike protein studded exosomes,^1,2 (which have been found circulating a year after infection¹) and at the start of the pandemic, it was discovered that using therapeutic (healthy) exosomes produced dramatic results from severe COVID-19^1,2,3 (something I and many colleagues also observed)—all of which led me to believe the spike protein “poisons” the exosome system.
Note: the spike protein has a high (heparin dependent) affinity for binding to the surface of exosomes. So, if it was not already there when the exosome initially formed, it can also attach to exosomes traveling in the bloodstream.

•One study showed the COVID vaccine’s spike proteins also altered the exosome system.

Note: a later case report detailed a man suffering from a significant COVID vaccine injury where spike protein coated exosomes were detected 1173 days post vaccination and vaccine mRNA containing exosomes were detected 1284 days post vaccination.¹

•A 2023 peer-reviewed study found that unvaccinated children who were around COVID-19 vaccinated parents developed an immune response to the spike protein that was not seen in children with unvaccinated parents and spike protein antibodies were found in surgical masks worn by the physicians. This led the authors to hypothesize that antibodies were being directly transferred through the parent’s breath to their children.

•Significant amounts of (RNA containing) exosomes can be found in your breath, and like exosomes from other tissues in the body, lung derived exosomes vary depending on the disease state of the lungs (“sicker” people have “worse” exosomes).^1,2,3 Exosomes from COVID patients, in turn, are highly inflammatory,^1,2 potentially clot forming¹ and are taken up by the lung cells.¹
Note: where the vaccine ends up in the body is highly dependent upon the charge of the lipid nanoparticles (essentially if they are negatively charged, they match the biodistribution data Pfizer provided, whereas if positively charged they go to the lungs—detailed here). As there was a significant subset of COVID-19 vaccine injured patients who developed lung issues, and a subset of recipients who were the primary "shedders," I suspect this was due to the wide variability in COVID vaccine production causing some to receive positively charged lipid nanoparticles which ended up at the lungs.

•Since spike coated exosomes trigger an immune response to the spike protein,¹ an inhaled vaccine was made from lung derived exosomes coated with spike proteins¹ (they were lung derived so the lung cells would be more likely to absorb them). These spike protein exosomes both generated an immune response and were absorbed into the body (and were repeatedly demonstrated, when injected, to effectively immunize at nano-gram levels¹,²). Once absorbed, those exosomes travel to other tissues and organs in the body, which (based on all the reports we’ve received and the patients we’ve seen) are known to be affected by shedding. Likewise, a 2021 review paper highlighted the feasibility of this approach and that numerous companies were developing exosome based COVID vaccines which contained either COVID-19 antigens (e.g., spike protein) or mRNA to create them.

Note: exosomes are very similar to the lipid nanoparticles used to deliver the mRNA vaccines (in fact, two studies detected vaccine mRNA within the breast milk exosomes of recently vaccinated mothers^1,2—potentially explaining the shedding reactions breast feeding infants developed), but to the best of my knowledge, their presence was never assessed in the breath of vaccine recipients. That said, I am doubtful they were the primary source of exhaled (or sweated) shedding because so little of the vaccine was given that it is unlikely enough would be available to be continually exhaled to a meaningful level.

2. Bacterial Transmission—if bacteria are transfected with the COVID-19 vaccine plasmids (and then reproduce), they will express the COVID-19 protein (and potentially be able to alter bacteria they come in contact with so that they too do the same)—a process which has been shown to occur in the gut with other plasmids.¹ This, in turn, provides a way that the COVID vaccine could behave like a traditional “live viral” or “live bacterial” vaccine that sheds. However, while this fits some of the observations reported, it has never been directly assessed (the closest was that vaccination caused a 41-73% decrease in one of the most beneficial gut bacteria species^1,2 — which potentially could have been caused by spike protein appearing on other bacteria). As such, I feel it’s worth raising the hypothesis (and have reached out to researchers who could evaluate this), but it remains a complete unknown. Something quite close to this was documented by accident in 2020, when four asymptomatic lab workers repeatedly tested positive for COVID on the nucleocapsid PCR but were negative for every other viral target—as what they were actually carrying was the plasmid they had worked with, which persisted in their nasal passages for up to three months after they stopped handling it, with the authors concluding either it had lodged in their nasal tissue or that E. coli containing it had colonized their noses (and a household member who never entered the lab also tested positive).¹

Note: one (oral) COVID vaccine was created which engineered E. coli bacteria with plasmids to either have spike protein on their surface (thereby creating both blood and mucosal immunity). Additionally, another was made which caused the bacteria to produce nanobodies (tiny antibodies that bind a single domain) against the spike protein which were expelled from the bacteria within exosome like vesicles that then traveled through the gut lining to the lungs and brain.^1,2

3. SARS-CoV-2 Shedding — In a significant number of the reports I looked at, after being exposed to an (asymptomatic) shedder, the individual (and often multiple other unvaccinated members of the group) became ill with one or more of the following:
COVID-19, a COVID-like illness, a flu which may have been COVID, a severe COVID infection that hospitalized and sometimes killed them.

Yet in contrast, before the vaccine rollout, they never had this issue (e.g., normally they never got sick, even around those they knew got COVID). This in turn means either that a remarkable coincidence keeps on happening, or that the vaccine increases your risk of transmitting COVID-19.

As it so happens, there are a few things that argue for the latter such as:

•The design of the vaccine does not create mucosal IgA immunity. This means it does not prevent COVID-19 from colonizing the respiratory tract and hence makes one still able to spread COVID-19. Rather, the vaccine’s design primarily reduces reactivity to the spike protein (i.e., COVID-19 symptoms). As such, vaccinated individuals can be infected with COVID-19 but not show symptoms of infection (which is also a major issue with the pertussis vaccine many are erroneously forced to take to see their grandchildren).

•The vaccine is immune suppressing. On one hand, this causes individuals who have a latent COVID infection to either start shedding the infection or become severely ill (which as I show here is a common but forgotten problem with vaccines). On the other hand, it causes individuals who have been vaccinated to be unable to develop permanent immunity and, hence, continually catch it.
Note: I have received numerous reports of vaccination causing an existing minor COVID infection to become life threatening,

In short, for some reason, individuals who do not get COVID will come down with it in the presence of a shedder, and in my assessment, this happens frequently enough for it not to be a simple coincidence.

Based on all of this, the possibility exists that vaccinated individuals with COVID infections either excrete higher concentrations of the spike protein than those with natural immunity, or have chronic infections they never clear (but show minimal symptoms of—leading to many being exposed to them). However, the existing data on the length of infectiousness and viral counts in the noses of those infected with COVID-19 (which may be biased) shows minimal differences between the vaccinated and unvaccinated. As such, while it seems that vaccination causes certain individuals to give others COVID, to the best of my knowledge data does not exist to support that claim and there may be some other process concurrently occurring which makes those around a shedder more susceptible to catching COVID-19 from them.

As you might guess, of these three models, I believe the strongest case exists for the first (exosome mediated transmission).

Note: Kevin McKernan stated that he was initially (and understandably) skeptical of the shedding phenomenon because he felt there could not be a high enough exhaled dosage for it to affect those who breathed it in (where I regularly encounter people who are that sensitive microdoses of a potent agent will still affect them). In turn, he shared that what changed his opinion was the potential presence of plasmids in exosomes, as these could serve as a self-replicating vector that allowed a small amount to noticeably affect those exposed to it.

DNA Vaccines

Since there is an irrational faith in vaccines, new designs are always being explored regardless of how unwise they are. Despite knowing this, I was quite surprised to learn “DNA vaccines” (which use synthetic DNA to create mRNA which creates the antigen cells then expel) existed, as this both seems to be a terrible idea, and directly contradicts all the messaging the vaccine industry has given that vaccines cannot change your genome.

Following this, I was then curious as to exactly how this technology worked (and once I found out, when it was developed). Briefly:

• Plasmids are created from a standard industry backbone (which contains a sequence that transports DNA into the mammalian nucleus) along with the DNA sequence that will become the target antigen.

• E. coli are transfected with that plasmid, the bacteria which took it up are bred, and the plasmids are then separated from the bacteria to become the vaccine product.

• The plasmids are injected into the body (typically with a jet injector or electroporation to force them into cells, but successful designs such as the first one brought to market simply injected the plasmid into muscle).¹

• Once inside a cell, the plasmid either enters the nucleus on its own (particularly when the cell divides and the nucleus is more porous), or the plasmid has a transport sequence that brings it into the nucleus regardless of which phase of the cell cycle it is in—where the cell’s own machinery turns it into vaccine mRNA (and from there into the antigen).^1,2,3

• This technology has been worked on for about 30 years¹ and there is now a human COVID-19 DNA vaccine¹ (licensed in India) along with several veterinary ones.^1,2 All of the licensed products use a CMV promoter (which was also used to produce J&J and AstraZeneca's adenovirus vector COVID vaccines)—however, the 72 bp SV40 enhancer has been added to many experimental DNA-vaccine plasmids both because it helps get the plasmid DNA into the nucleus and because it can also boost transcription once it is there.^1,2

Once I realized this, it cast two of the questions I’d pondered since the start in a completely different light.

First, it provides a completely different answer to the persistence problem, as if plasmids are being transported into the nucleus and then being transcribed to mRNA once there (but remaining separate from human DNA), this provides a much more feasible way for extensive production of the mRNA to occur, as it is effectively “in your DNA” but at the same time, does not have to meet the high threshold of integrating into the genome for this to happen (which is why many I spoke to had believed DNA changes could not account for the majority of the spike persistence being seen). More importantly, this is not merely theoretical, as delivering plasmid DNA into the nucleus is a licensed and working vaccine strategy,¹ and it was made to work with far cruder tools than the COVID vaccines had available, since those products rely on a CMV promoter and physical force rather than the two elements which most efficiently solve this problem (the SV40 enhancer—which the DNA vaccine literature identifies as the sequence producing maximal transport of plasmid DNA into the nucleus,¹,² and lipid nanoparticles). This is also McKernan’s assessment, as he considers the focus on genomic integration to be something of a limited hangout given that most plasmids operate episomally, and notes they can also be packaged into exosomes.

Second, while I still believe every bad choice made with the mRNA vaccines could be attributed to pursuing profit with a complete lack of concern for how others were harmed, it’s hard not to notice the chosen designs coincidentally mirrored existing vaccine designs (or that Pfizer refused to change them even when health regulators pushed them to and Moderna was using a SV40 free plasmid). Given that the chosen approaches were well-established vaccine production techniques, I feel it is reasonable to infer they were most likely aware of the expected effects of utilizing them. This is important as those “expected effects” dovetail with the core goals of a vaccination program.

Since the faith of vaccination revolves around provoking the body to produce a targeted immune response (e.g., antibodies), and since the profession has long sought to validate itself by eliminating infectious disease and claiming victory over nature, vaccine programs will inevitably err towards overstimulating that response to ensure as few people as possible have an insufficient one — which in turn requires ignoring or dismissing the consequences of that excessive stimulation, rather than trading a partial reduction in efficacy for a significant improvement in safety. The regulatory pathways are set up to support this, as the primary basis for approval is typically a consistently robust antibody response rather than a demonstration of safety.
Note: I believe a major issue with the HPV vaccine came from the fact its antigen had many overlaps with human tissue (which the immune system resisted forming an immune response to it), so a much stronger immune provoking adjuvant and massive antigen doses were needed for the vaccine to work (e.g., Gardasil 9 contains 270 micrograms of antigen whereas the recombinant hepatitis B vaccine contains only 20 micrograms^1,2). This resulted in the scale being heavily tipped to efficacy (rather than safety), and as a result, the HPV vaccine had an extraordinarily high rate of causing autoimmune disorders.

In this regard, one of the challenges vaccines face is that while natural immunity lasts for a long time (e.g., it is often lifelong), the body will typically “resist” the effects of a vaccine’s artificial stimulation of select parts of the immune system, so over time, vaccine derived immunity fades away (with the rate varying greatly depending on the vaccine). Boosters, in turn, are given either because the original vaccine derived immunity faded, or because the pathogen has mutated to a strain no longer covered by the vaccine (resulting in the immune system being “locked onto” the incorrect strain).

For this reason, one of the longstanding goals of the vaccine industry has been to effectively mimic what occurs in nature (a continual low level boosting of the population from individuals they encounter with minor infections).

One way to do this is to ensure the vaccine continually triggers a lighter immune response long after injection—which both the persistent mRNA and nuclear plasmids (which produce mRNA) accomplish by ensuring a steady supply of spike protein is produced after vaccination. This was recently explicitly illustrated by Japan’s next generation “replicon” COVID vaccine (approved in 2023 and deployed in October 2024), as it is designed to extend antigen production, so in addition to the mRNA coding for the spike protein, it contains mRNA coding for an enzyme which copies that mRNA, so that it is continually replicated as it is broken down and hence retained in the body far longer.¹ Its manufacturer’s selling point, in turn, is that the effect lasts, and in their Japanese trial, the antibody titer six months after the replicon vaccine was higher than the titer one month after Pfizer’s, with high titers still present at one year.¹ Yet their own pharmacokinetic data showed the mRNA was largely gone from the muscle within 15-30 days and the spike protein undetectable by day 15—leaving their head of R&D to admit the mechanism behind a year of elevated antibodies is not actually understood¹ (with a Japanese vaccine expert separately noting that the long term safety of this vaccine—which had already been given to 18,000 people was not yet possible to know¹).

In short, the same industry which insisted the original mRNA vaccines could not persist (despite the fact they do) has now built a product around making them persist, still cannot explain what its own product is doing, and has responded to the Japanese clinicians and nursing organizations raising these questions by threatening them with civil and criminal legal action.¹,²

This is a critically important point as the entire justification for a continually produced antigen assumes doing so is both safe and effective (when in reality, the antigens often have a cumulative toxicity, while simultaneously, it has been repeatedly shown that overstimulating the immune system to focus on one antigen reduces its ability to respond to other threats it encounters—which is why vaccines like the COVID shot have been repeatedly shown to increase one’s subsequent risk of catching disease). As such, a real possibility exists that the chronic illnesses seen after vaccine injuries persist because vaccine antigen production persists as well.

Note: Arkmedic (an excellent researcher) recently made the case that the COVID vaccines were not the first to be designed to get foreign DNA into cells.¹ Since every recombinant vaccine is manufactured with plasmids and residual plasmid DNA survives into the final product, what matters is whether anything in the vial can carry that DNA across the cell membrane — and aluminium, the most widely used adjuvant in vaccines, turns out to be exactly that (as do other widely used vaccine components). A 2007 paper from ETH Zurich found aluminium nanoparticles transfected human cells more efficiently than any other metal oxide tested, and were the only ones to do so at calcium concentrations approaching those found in the body.¹ This is not merely theoretical: in 2012, HPV DNA was found bound to the particulate aluminium adjuvant in Gardasil,¹ and the FDA has acknowledged the presence of residual DNA fragments in that vaccine since 2011 while maintaining they pose no safety risk.¹ Notably, Gardasil's competitor Cervarix uses a comparable aluminium-lipid adjuvant,¹ so this is not a quirk of one manufacturer's formulation.¹ The only study the industry has ever offered against this was a three-page 1999 communication co-authored by the Swiss vaccine regulator, which reported zero transfection from nine commercial vaccines — using a cell line with two publications in the entire PubMed database and no control to establish the assay could detect anything at all.¹ That said, some of this may simply be convergent chemistry, as a good transfection agent is a positively charged or amphiphilic particle which binds nucleic acid and disrupts membranes, while a good adjuvant is often a positively charged or amphiphilic particle which concentrates antigen and disrupts membranes so the innate immune sensors fire. If so, the situation is arguably worse rather than better, as it would mean the risk is inherent to adjuvanted recombinant vaccines rather than an avoidable formulation choice—and it still leaves the question of why it is disclosed nowhere

Another is to ensure the vaccine is able to spread in the population, both supplying a continual source of external boosting to those who already got the vaccine and to ensure those who did not vaccinate still are protected. The shedding observed with the COVID vaccines (and the 2023 study showing a transfer of COVID immunity) demonstrates this was indeed happening, and the fact that the strongest evidence exists for it being mediated through exhaled (or sweated) exosomes—which, like DNA plasmid transfection, was already an established vaccine technology—suggests this may have been an intentional feature of the mRNA vaccines rather than an accident (particularly since it is a given overproducing an antigen within a cell will cause the release of exosomes containing the antigen).

Note: the more speculative mechanism I touched upon (self-spreading plasmid transfection of bacteria), could have supported either goal (e.g., by having the gut microbiome produce spike, a continual internal production of it will repeatedly boost the recipient, while by having those bacteria travel to others—something which routinely occurs with the human microbiome—it would be possible for the vaccinated individual to stimulate the immune system of others). However, I must emphasize that this is a much more theoretical possibility as the research needed to critically assess it has never been done (at least publicly).

That said, everything I have described here is simply my best guess to make sense of all the inexplicable things we have observed the COVID vaccines do and it is quite possible some of the inferences I made here from the existing data (e.g., the exact mechanisms or motives at play) are entirely incorrect. What’s so frustrating is that none of it needs to be guessed at as each of the scientific points I’ve raised could be assessed with currently existing technology—but they likely never will be because too many parties have too much to lose if the wrong answer is arrived at. As such, I don't know the correct way to proceed, but I nonetheless feel real attention needs to be brought to these issues, as otherwise, the industry will continue hurtling forward with “safe” genetic technologies that have a wide range of known and unknown risks—that before long, we will be stuck with.

Mitigating The Disaster

A common metaphor used to describe how the predatory ruling class enacts their agenda is the boiling frog analogy (where a frog placed in hot water will jump out, but one placed in water that is slowly heated will stay in until it dies).

Note: this is actually an urban legend, as frogs will still leave if the temperature is raised slowly (something which unfortunately led to many cruel experiments that only “worked” when the frogs were unable to escape or had been surgically disabled). However, while the analogy does not hold for frogs, it does appear to hold for us, as again and again, changes which would have been fiercely resisted had they been implemented all at once were instead accepted without much protest once they were introduced gradually enough that no individual step seemed worth objecting to.

My longstanding view with the COVID vaccines, in turn, is that the industry had been counting on exactly that gradual acceptance, as a wide host of issues exist with the mRNA platform (and the DNA vaccines which may follow it) that had been slowly phased in over decades without much notice. What happened instead is that many longstanding agendas all rushed to use the pandemic to bring themselves to fruition at once, and because the antigen chosen to be mass produced by these injections was the spike protein (which is toxic to many different parts of the body), the problems with the platform were common and severe enough that it was no longer possible to sweep them under the rug. For example, had a less reaction provoking antigen been used, it is highly unlikely enough people would have noticed effects like shedding and demanded they be looked into. So, as horrific as the process was, it woke the public up to something being very wrong in the field of vaccinology in a way that another fifty years of incrementalism never would have.

If the Italian and German stool and urine findings hold up, spike protein exposure is now near universal rather than confined to the vaccinated, which means we are in a post-spike world and the relevant question has shifted from how to avoid exposure to how to become resilient to it. For the subset who clearly cannot tolerate it (e.g., those affected by shedding), the question then becomes why—and my best guess is that it comes down to their bodies not being able to effectively form neutralizing antibodies against it, as a 2023 study found this was the differentiating factor between adolescents who developed myocarditis after vaccination and those who did not.

I say “best guess” because that is all anyone can offer. A novel protein was introduced into essentially every human being on earth and is demonstrably capable of causing disease in a subset of them, so spikeopathy should by now be a recognized discipline with its own researchers, diagnostics and literature. Instead, as Kory put it to me, there are a handful of practitioners figuring it out independently while conventional medicine maintains the illness does not exist.

Nonetheless, while the injuries the COVID vaccines created brought long overdue attention to the dangers of this platform, they also created a disaster many of us have been struggling to fix ever since. In the final part of this article (which at reader request I have been working on for a few months), I will go through each of the approaches we have found work for the common subsets of vaccine injuries, how the use of supplements there mirrors the issues we see when they are used for many other conditions, along with some of the less appreciated aspects of the higher-end treatments now coming into vogue (e.g., plasmapheresis) which are necessary for getting the best outcomes from them, and address the questions I am most often asked about shedding (e.g., how do you counteract it, and what has been learned about shedding and sexual intimacy).

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• Throughout history, harmful products have rarely been removed because of the harm they caused consumers or the environment; they were removed once an equally profitable alternative existed. Here I will apply that principle to the largest deployment of capital in American history—the AI data center buildout.

• Roughly $800 billion is being spent on AI infrastructure this year, $1.4 trillion next year, and data centers now account for nearly a quarter of all nonresidential construction starts in the country. Because they need city-sized amounts of power, they are being placed next to communities, which are experiencing rising electricity bills, constant noise, and a cluster of health complaints that closely matches what electrically sensitive people have reported for decades.

• A Bloomberg analysis of 770,000 home sensors suggests why: data centers inject enormous amounts of “dirty electricity” back onto the grid, and the worst power distortion in the country clusters within 20 miles of them. Meanwhile, the administration’s response to the growing opposition (which has already recalled local officials and become a midterm issue) has been to override it rather than address it.

• The industry’s proposed alternative, data centers in space, fails on physics and economics, and even if it worked it would leave nothing behind for anyone on earth.

• A better option exists on U.S. soil, and the unprecedented need for power next to it creates the first real chance in fifty years to bring a cheap, safe, and abundant form of nuclear energy to market—one that was demonstrated at Oak Ridge in the 1960s but abandoned because it could not make weapons.

• The decisions that determine whether America builds this or buys it from China are being made now, and this article lays out how taking that path can not only protect communities across the country from the proliferation of data centers but also at last make affordable and abundant green energy.

Much of what is written here is guided by the fact I spend a lot of time thinking about the problems the world faces and what solutions could potentially address them, either now or in the future when cultural circumstances change. This year I realized a few longstanding issues were converging into a potential long-term solution that I wanted to have this newsletter help bring to light.

The Law of Displacement

One of the depressing things I have come more and more to terms with as I’ve gotten older is how so, so, many things ultimately come down to money (e.g., a lot of medicine is structured into sales funnels that ensure robust sales of medical services and many seemingly irrational ways the practice of medicine is structured finally make sense once you see it through that lens).

As such, all throughout history, you can cite examples of people being exploited for profit (e.g., for most of human history in most societies slavery was widely practiced). Once science entered the picture, this frequently resulted in profitable technologies being deployed which advanced the national wealth but harmed a significant portion of the population in the process (e.g., Monsanto’s profitable chemical plants poisoning their community’s water supply).

In all the case studies I’ve looked at, a recurring process occurred:

•Industry was aware of health issues from their product, but buried all of it (with this frequently being revealed in subsequent lawsuits).

•The profit margins for the products were typically larger than the cost of keeping it on the market (e.g., they could afford to fund doctored science that cast sufficient doubt on health issues with the product). Likewise, typically a small enough number of people were directly harmed (e.g., an isolated community or less than 1% of the people who took a pharmaceutical) that it was easy enough for the industry to sweep everything under the rug—especially since until recently, corporate news controlled the media landscape and was structured to support narratives from large corporate clients.

•Government typically sided with industry, due to some combination of lobbying (e.g., bribes), the industry effectively controlling the narrative (so government regulators thought the product was “safe”) or the government viewing the product as a strategic national asset which justified a certain degree of sacrifice to promote the national interest.

Because of this, you would again and again see things that were clearly toxic be able to stay on the market for decades despite those harmed by them doing all they could to bring attention to the issue (and supportive researchers providing the data to substantiate their claims).
Note: the most extreme example of this is likely the COVID vaccines, as the scale of harm they have done eclipses arguably any other product in history, there is widespread public opposition to them (to the point a clear majority now refuses to take them) and more researchers have come forward to expose their dangers than virtually any other product in history—but nonetheless—the FDA continues to advocate for them. Why? Because there is so much money to be made off mRNA technology too many parties are simply not willing to let it go.

Rather, what typically gets these products off the market is a commercially viable alternative to them being developed, as at that point, the same profit can be made, but it is no longer necessary to bear the additional cost of defending the old product to keep it on the market (which, for lack of a better term, I call the “law of displacement”).

For example, almost immediately once leaded gasoline was created in 1922, serious health concerns were raised about it—the Surgeon General questioned it before a gallon had been sold, workers making it began dying within months of its 1923 launch, and the engineer who invented it wrote the industry’s reassurances to the government while recovering from lead poisoning himself. However, since GM held the patent and collected a royalty on nearly every gallon of gasoline sold in America, rather than be ethical, GM wrote into its contract with the Bureau of Mines that the government’s safety findings required company approval before publication, then funded a university laboratory that produced essentially all of the “safety” data on lead for the next forty years. When Caltech’s Clair Patterson proved in 1965 that Americans carried roughly a hundred times the lead burden of their ancestors, the industry tried to buy him and then had his government contracts pulled. As such, all of the efforts to get lead out of gasoline were unsuccessful (which is truly remarkable given the massive health consequences of it such as 256,000 premature deaths from cardiovascular disease each year in America).

Rather, what did was the catalytic converter as automakers needed them to meet the 1970 Clean Air Act, lead destroys them on contact, and in 1970 GM (which had conveniently sold its stake in the lead business a few years earlier) announced it was switching away from leaded gas. As such, once the world’s largest carmaker needed unleaded fuel, refiners had a product that was just as profitable to sell, and the same machine that had defended lead for half a century quietly phased it out. Notably, a non-toxic alternative had existed the entire time (GM’s own researchers had tested ethanol blends before lead); it lost because it couldn’t be patented (whereas by 1970 other patentable additives existed).

Furthermore, this is not an isolated pattern. For example, DuPont fought the science linking CFCs to ozone depletion for fifteen years, then abruptly reversed its position in 1988—once it held the patents on the replacement refrigerants. The Montreal Protocol had been signed the year before, and the “impossible” phase-out proceeded on schedule.

Likewise, many things in medicine have fit this pattern:

• Seldane (terfenadine) was known from 1990 to cause fatal arrhythmias when taken with common antibiotics, but stayed on the market until 1998—eighteen months after the same company got Allegra approved (which is simply Seldane’s active metabolite without the cardiac risk). The FDA’s own withdrawal proposal stated the reasoning plainly: now that a safer alternative existed, Seldane’s risks were no longer acceptable.

• Rezulin (troglitazone) caused fatal liver failure and was pulled in Britain in 1997. The FDA kept it on the market until 2000, and when it finally withdrew the drug, explicitly cited the fact that Avandia (rosiglitazone) and Actos (pioglitazone) were now available to replace it.

• Bextra (valdecoxib) was withdrawn in 2005 for cardiovascular risk and rare, life-threatening skin reactions, with the FDA noting it offered no advantage over the NSAIDs already on the market—while Celebrex, Pfizer’s bigger-selling COX-2 inhibitor (with the same COX-2 class risk), was allowed to stay.

• Phenacetin was one of the most widely used painkillers in the world and was linked to kidney failure in the 1950s. It wasn’t banned in the U.S. until 1983, by which point Tylenol (phenacetin’s own metabolite) had already taken over its market.

• Barbiturates were known to be lethal in overdose and highly addictive by the 1930s, yet remained the default sedative for another thirty years until Librium and Valium (benzodiazepines) arrived in the 1960s with fresh patents and the same customers.

• Halothane hepatitis, a frequently fatal liver necrosis, was recognized within a few years of halothane becoming the standard anesthetic in the 1950s. It was tolerated for three decades until patented replacements (isoflurane, desflurane, sevoflurane) captured the operating room in the 1980s and 90s. Tellingly, halothane is still widely used in poorer countries where those patented pharmaceuticals are unaffordable.

• Tardive dyskinesia, an often irreversible movement disorder, was identified in patients on Thorazine and Haldol by the late 1950s and accepted as a cost of doing business for forty years. The older drugs were rapidly displaced once patented “atypical” antipsychotics arrived in the 1990s—which then turned out to cause diabetes and metabolic syndrome at rates that arguably made them no safer, only newer.

• The whole-cell pertussis (DTwP) vaccine had a high rate of causing encephalitis and nearly bankrupted the vaccine industry in lawsuits, leading to the 1986 National Vaccine Injury Act being passed (giving the industry immunity from lawsuits). As activists had begged for years for the safer but more expensive Japanese acellular (DTaP) vaccine to replace the DTwP vaccine (which the industry refused to spend the money to do), the 1986 Act was structured to require HHS to promote safer vaccines (leading to the necessary research being Federally funded) and a few years later DTaP quietly replaced DTwP (except in poorer nations where the WHO continues to promote DTwP).

• After the idea of X-raying a fetus throughout pregnancy was proposed in 1923, it was quickly taken up by the medical profession. Before long, evidence accumulated that this was very dangerous, but it was not until 1975 that the obstetric field shifted away from it—a shift that largely occurred because an alternative way (ultrasound) was found to conduct those routine exams.

• Cylert (pemoline), an ADHD drug, carried liver-failure warnings from 1996 onward but stayed on the market until 2005, once the stimulant market was fully covered by other products and it no longer filled a gap.

• OxyContin’s abuse potential was known to Purdue for a decade before it “solved” the problem in 2010 with a crush-resistant reformulation—which conveniently extended its patent protection and let the company argue the original (now unsafe) version should be blocked from generic competition.

So, while there are many harmful products on the market I believe should be banned, rather than continually emphasize how bad they are, I try to have my focus here be directed towards safer alternatives which can displace them, as I feel that is the most realistic way to get them off the market and have them stop harming people.

The AI Boom

One of the topics I’ve seen many people debate is how far AI is likely to go as on one hand, there are projections it will displace many people’s jobs and completely redo the economy, while on the other many argue that dystopian vision is simply hype the AI industry is creating to justify inflated stock values as the companies go public (and to obtain private investor funding prior to that).

Given the potential cultural implications of AI, I’ve hence put a lot of thought into how they actually generate their answers, the relative accuracy of the different types of responses they get, how AI can be a productivity increasing or decreasing tool, and the overall effects I expect them to create upon the society (e.g., a lot of the responses AI gives are terrible because its conversational style is tuned to please raters, which produces the same pretentious and obnoxious responses that dominates Reddit). From that, I’ve essentially concluded:

•A significant portion of the population prefers to follow the crowd, tends to defer to authority, and is somewhat averse to the hard effort it requires to think for oneself or deal with adversity. For these people, AI (as most currently understand it) will be irresistible, resulting in them being trapped in a bubble where they can’t grow or change (exemplified by the rising phenomenon of AI boyfriends and girlfriends) and it becoming increasingly easier for the system to manipulate them into compliance (in part because AI answers inevitably regress toward the orthodoxy of their training data and the preferences of the people who rate their answers).

•A smaller portion will recognize that AI provides a tool that allows them to greatly increase their productivity. This, I believe, will ultimately lead to a wealth explosion that will be concentrated in the upper classes (hence increasing the income division in society). However, I do not believe this benefit will be seen for many of the people pursuing it due to them failing to recognize what AI is and is not useful for. Put differently, AI will benefit users who make a point to keep their own agency while using it and harm those who hand it over.

•Since many of the things we are trained by the educational system to do are ultimately algorithmic (and hence possible for AI to do), AI will place an increasing pressure upon the population to shift to providing things which offer an inherent value that goes beyond what can be automated and trained (e.g., a genuine authentic human presence in medicine that is naturally therapeutic). However, I do not think many of the people who economically need to do this will do so, and as a result, AI will also amplify the income inequality in society from the opposite direction (by making the less wealthy poorer).

•A significant portion of the value of AI comes from things most users cannot see (AI interfacing with programs rather than individual users talking to chatbots), as this setup makes it possible for programs (or programs connected to physical systems) to do a lot of things that previously were not possible (e.g., to create a variety of highly profitable technologies or meticulously micromanage the population). Because of this, I suspect one of the main purposes of the chat bots (beyond creating positive PR for the AI industry) has been to provide free human training that can be used to develop these far more lucrative invisible systems.

To put all of that in more concrete terms; initially, I was strongly opposed to using AI as I felt it was highly inaccurate (due to it sharing the exact same subtle biases I was used to seeing on websites like Wikipedia) and found its pretentious and condescending style of conversation to be extremely obnoxious (until we realized you could stop a lot of that by telling the chatbots to stop “sounding like Reddit”). Later, I realized it was very useful for rapidly executing second and third order searches (e.g., I am going from point A to point B, based on my criteria, the possible routes I can take, and the time I am leaving, what is the optimal place for me to stop at midway) as it could quickly do all of that rather than requiring me to manually sort through each part of the decision tree (saving a lot of time).

Likewise, with writing, I was initially strongly opposed to using AI at all both because I could not tolerate the errors it continually introduced (e.g., AI hallucinations or regressions to the orthodoxy) and because I did not like the feel of AI writing (which beyond having a “Reddity tone” also just felt empty, which was a deal breaker as I am not willing to ask readers here to read things I myself would not want to read). I then switched to viewing AI as a good way to obtain “orthodox” perspectives (many of which are correct) and edit what you are working on (which for me works best by generating word document copies of articles with suggested edits highlighted so I can go through each one and manually add in the ones that make sense).

Later, I realized that while AI has a high rate of hallucination for anything it generates on its own (and pulls from fairly limited datasets), it’s fairly good with material you directly give it to process. So if you understand the entire pipeline that is required to create a finished output, it often makes sense to save a lot of time by having AI automate certain parts of the pipeline (rather than asking for the whole thing start to finish—which inevitably creates a highly erroneous and useless output). Because of this, one of the main things we’ve done over the last year has been to give them well over ten thousand studies (from all the databases AI systems do not look at) and have them process each one into a paragraph highlighting all the pertinent data in the study (and then sort those paragraphs by category and then sort those categories by overlapping information).

From doing this, it’s made it possible to compile a lot of information that simply was never accessible before and to do it in a very short timeframe (thereby making it actually possible to get all of this into the public domain while RFK is still HHS Secretary). For example, papers get exponentially harder to write the more sources they contain, and the capstone paper on DMSO for brain spine and heart injuries the top experts in the field wrote (after spending a decade researching the subject) contained 78 references—yet the four articles I released this year on this topic collectively contained nearly 5,000 references.^1,2,3,4 So while doing these four articles was immensely time consuming, with the help of AI (and very careful vetting of the outputs), it was possible to do orders of magnitude more than anyone ever has been able to do before, thereby, at last making that forgotten literature base accessible.

One of the main reasons I did all of this, in turn, was because I knew it was simply not feasible for independent researchers to ever uncover most of the actual research that had been done with DMSO. As such, my hope was that by making it all easily available, other researchers could copy my work and use it as a foundation for their own works on DMSO (as prior to me beginning this project, I’d realized almost every DMSO book in print rather than independently research the subject had just copied what was in the previously published books and hence all were collectively drawing from a very limited pool of scientific studies). So, if a much larger body of compelling literature was made available to everyone, it would effectively promote the therapy and make something that could help a lot of people widely available, thereby creating the pressure to shift us to a better model of medical care (which is why I chose to start by the writing the longer and far more difficult articles which make that critical literature available rather than jumping to the shorter ones that have more commercial appeal).

This has basically happened, and over the last two years, a lot of books and articles have started to be published on using DMSO which are incorporating many of those forgotten studies that have never before been seen in print. However (and this is the key point), what I’ve noticed is that most of them were AI generated summaries of what I wrote rather than the authors using them as a scaffolding to assist in developing their own DMSO content. On one hand, this has been problematic as the AI summaries introduce a significant amount of errors or misinterpretations (so in cases where authors who did this credited me, many people have asked me why I said something I never actually did but the AI summary erroneously concocted).

However, what I feel is far more important (and why I shared this story) is that even in cases where I’d already done the vast majority of the work for anyone who would want to broach the DMSO topic (and held off on writing the shorter DMSO pieces so an economic niche was created for other people to do it), when authors were faced with the choice between doing the last bit themselves or letting AI do it with the errors doing so inevitably entails, they chose the latter. I mention this because I do not think this issue is at all unique to DMSO, but rather that (as I alluded to in the first bullet point of this section) if AI provides an easier and faster way to do tasks at the expense of quality, human nature dictates that a lot of people will use AI to do that (which amongst other things is why the amount of content on the internet is rapidly increasing while in tandem its quality is rapidly declining).

So to summarize, I feel AI is a very useful tool which makes a lot of things previously not possible possible. However, my fear is that the majority of users will treat it as a crutch and not utilize it in a manner that productively enhances their own lives (or their personal development). In contrast, there will also be a sizable number of individuals who will grasp how to effectively leverage AI, but I think there is a high likelihood most of them will not have the ethics (or wisdom) to prevent their projects from harming humanity (e.g., one of the current AI enabled gold-rushes is AI facilitated mass surveillance while another is using mRNA to cure illnesses by "rewriting the programs your body runs on"—neither of which is likely to provide a net benefit to humanity). Put differently, the tool amplifies whatever its user brings to it, but most people instead rely upon AI to do everything for them.

Note: since America’s tech industry originates from a very left-wing area, it exists within a cultural ethos where presenting the appearance of aiming to benefit humanity is paramount. Because of this, many people I’ve spoken to have collectively seen more investor pitches than I can count from Silicon Valley tech companies over the years that claimed the company would help humanity but in reality were entirely about profit and often later created a negative impact on humanity (e.g., Facebook’s first president recently admitted he deeply regrets what they did to children’s brains). Because of this, I am fairly skeptical about all the (repackaged) utopian language I am seeing being increasingly wrapped around AI—particularly since more and more military spending is going towards developing AI weapon systems, which I feel is very dangerous for humanity (as once human beings are no longer held back by being confronted with the visceral reality of killing another person it opens the doors to unspeakable horrors occurring).

Datacenter Proliferation

Despite unresolved questions existing on the inherent worth of AI, leaders around the world (who seem unable to grasp AI is well suited for certain tasks but not others) have made the decision to go all in on creating robust national AI frameworks as AI dominance has been equated with economic supremacy and being a superpower in the 21^st century.

In America’s case, this has mostly meant the government clearing the way for private money rather than building anything itself. On his second day back in office (building on the precedent he established in his first term of expediting business projects he felt advanced America’s interests—such as Operation Warp Speed or obtaining massive amounts of ventilators and hydroxychloroquine), Trump hosted the launch of Stargate (a $500 billion, four-year private venture between OpenAI, SoftBank, Oracle, and MGX to build roughly 10 gigawatts of AI data centers—much of which has not yet come to fruition), and in July 2025 the White House released an “AI Action Plan” whose central pillar was “Build American AI Infrastructure.” The accompanying executive order designated any data center needing more than 100 megawatts of new power as a priority federal project, directed agencies to fast-track and narrow their environmental review, opened federal land (including contaminated Superfund sites) to them, and directed the Commerce Department to arrange loans and guarantees for qualifying projects with at least $500 million of private capital behind them. That same month's tax bill restored full immediate expensing for this type of investment,¹ which David Sacks (who ran AI policy for the White House until this year) has credited as a key driver of what followed.

What followed has no precedent—Sacks told the G20 on September 2, 2026 that about $800 billion is being invested in AI infrastructure in the United States this year, that the figure is expected to reach $1.4 trillion next year, that the estimates keep being revised upward, and that the only comparable buildout was the railroads in the 1800s¹ (it already exceeds the fiber-optic buildout of the internet era). The companies’ own numbers agree: Amazon, Microsoft, Alphabet, and Meta spent around $410 billion in 2025 and plan roughly $725 billion or more in 2026,¹ with analysts projecting their combined spending will pass $1 trillion in 2027 and Goldman Sachs expecting $5.3 trillion from those four companies alone by 2030.¹ In short, these are some of the most profitable enterprises in human history, and they are now spending so fast that Alphabet's (Google's) free cash flow went negative in the second quarter of 2026 for the first time since it became a public company.¹

Much of this shows up as physical construction. The Census Bureau only recently began tracking data centers as their own category, and when it did, it found they had overtaken traditional office construction in the country.¹ By July 2026 data center construction was running at an annual pace above $75 billion, up nearly 60% from a year earlier—during a month in which total U.S. construction spending fell (with residential construction down 7.3% from the previous year).^1,2 Data center construction projects now account for nearly a quarter of all nonresidential building in the country (and the buildings are only about a fifth of a data center's cost; the equipment inside is the rest), with nearly three times as much spent so far this year as in the same period last year¹ while nearly every other category of investment is flat or falling.¹ In turn, one analyst group estimates AI capital spending is adding roughly 1.4 percentage points to U.S. growth this year,¹ and Sacks has argued it accounted for about 75% of first-quarter GDP growth.¹

Note: this spending is not confined to America. China, for example, is preparing to spend around 2 trillion yuan ($295 billion) over the next five years on data centers,¹ the EU has announced a €200 billion "InvestAI" initiative,¹ Saudi Arabia is deploying hundreds of megawatts of Nvidia and AMD chips through a state-backed company,¹ and the UAE is building a 5-gigawatt AI campus in Abu Dhabi.¹ One analyst group, in turn, puts global data center capital expenditure (by a narrower definition than Sacks's) at roughly $800 billion per year in 2026 and projects $31.6 trillion will be spent on AI infrastructure through 2050.¹

Community Resistance

While understandable fears that AI will displace jobs have created public opposition to AI, the primary source of political pushback against the industry has actually come from communities AI data centers are being placed in. This is because:

•Data center processors require a massive amount of energy (a single facility can draw as much power as a mid-sized city), which in turn is spiking electricity demand¹ and hence electricity costs in the areas around them (as the grid upgrade costs get passed to residential ratepayers—so a key fight in most states is over who pays for those upgrades). That said, the extent to which data centers are raising electricity prices is hard to quantify as estimates vary widely (e.g., some have found none, one found a 10-20% increase and others found far more; the clearest documented case is the PJM grid serving the mid-Atlantic, whose independent monitor attributed most of a ten-fold jump in capacity prices to data center demand), but even in the most cited extreme cases, other pre-existing factors could explain some of the increases that occurred.
Note: those upgrades also mean new high-voltage transmission lines being run through communities, which raises residential exposure to the low-frequency magnetic fields that IARC classifies as a possible carcinogen and which have repeatedly been linked to childhood leukemia at exposure levels far below existing standards (an association IARC considers real but unexplained, as no [accepted] mechanism has been established).¹

•Since all that electrical usage creates heat, many facilities (particularly those using evaporative cooling) also require large amounts of water.¹ As such, ia March 2026 study estimated that $10–58 billion of new water infrastructure will be needed by 2030 to meet this demand (assuming the water is even available), with data centers' additional peak-day requirement by then roughly matching New York City's entire daily water use.¹ Presently, this translates to communities with robust water infrastructures being relatively unaffected, but smaller ones having challenges such as reduced water pressure and price increases, especially during surges (e.g., hot summer days). Furthermore, like the electrical cost increases, it’s hard to estimate exactly what degree of the increase can be attributed to data centers vs. pre-existing factors which were already increasing costs.
Note: evaporative cooling also produces blowdown (leftover water concentrated with salts, biocides, and corrosion inhibitors, plus traces of metals from pipes). This wastewater is usually sent to a municipal plant or a permitted discharge where poor handling can still stress a small treatment plant or creek.

•Data centers create a significant amount of constant noise (primarily due to the cooling systems, but also diesel generators during tests or outages, with some sites also having onsite turbines that run all the time). This noise makes it very unpleasant to live next to the centers and has resulted in many people who invested their lives into homes near the data centers wanting to move but having trouble doing so, with many saying the centers made their homes harder to sell (and as such, more and more heartwrenching documentaries are appearing on how communities have been negatively affected by data centers). Likewise, many are now reporting health effects from living in proximity to data centers (which is in part due to the air pollution their generators create¹).
Note: since data centers need a lot of power, land, and fiber, many newer ones are being placed in less affluent communities, including in the Midwest, so this is becoming an increasing problem in my region (which is a large part of why I wrote this article)—while in contrast, it’s easy for people in more affluent areas that don’t host them (but often profit off them) to not notice as cheaper regions are favored for new data center deployment.

Because of this, there is increasing community pushback against the data centers, which has led to local politicians who approved them despite vocal opposition in their communities subsequently being recalled¹ and data center opposition becoming one of the key issues in the midterms in certain affected districts.^1,2 More than 300 state bills targeting data centers were filed in the first six weeks of 2026 alone,¹ and in July New York's governor signed the nation's first statewide moratorium, pausing new hyperscale data center permits for a year."^1,2

In response to this, the industry has become increasingly aggressive in buying up land for the data centers (and pressing landowners to sell), while utilities use eminent domain for power lines across private land to serve those sites, and the industry has both lobbied politicians at every level and sued municipalities to push the projects through—all of which is expected given how much money is being invested.
Note: the industry is also beginning to work on innovations (e.g., onsite power generation and closed-loop cooling), which illustrates the displacement effect is already beginning.

Likewise in response to the pushback:

•President Trump has recently taken the position it is against one’s interest to oppose data centers:

•Individuals like Vice President Vance have tried to find middle ground positions like emphasizing the necessity of tech companies needing to build the power generation for the data centers rather than take it from the local grid and spike local electrical prices.

•Fox News originally aired data center concerns (and claimed they could be solved with deregulation, infrastructure improvements or developers absorbing some of the costs). However, as public opposition grew (e.g., in March 2026, 71% of Americans opposed data centers being constructed in their areas) Fox pivoted to the position that supporting data centers was necessary for US technological dominance, and that opposing data center proliferation helped China’s interests (e.g., “You’re against data centers, you are for China”). In tandem, Republican leaders have pressed the position that opposition to data centers is (at least in part) a Chinese campaign against America’s interests.
Note: as I discussed in a recent interview with Pierre Kory, dealing in absolutes is immensely problematic for society. So, while it is true opposition to data centers likely helps China, and that some of that opposition is probably being egged on by groups that benefit from the Trump administration’s AI attempts being derailed, that does not negate the fact that the thing motivating most of the opposition to the data centers is the impacts they are having on communities.

•The large conservative influencers have become split on the datacenter topic (e.g., Ben Shapiro has said opposition to them equates to working for China and Russia, others have linked opposition to existing left-wing groups, Matt Walsh has rejected both panic-bans and a no-questions buildout, arguing there are real problems with how centers are being rolled out that require a serious public debate before the country sprints further, and Tucker Carlson has come out strongly opposed, arguing communities are being stripped of the power to say no while paying the costs and getting no convincing public benefit).

Data Center Health Effects

Thus far, in this newsletter, I’ve focused on one half of this equation: some individuals are much more sensitive to toxicity, and hence are disproportionately injured by pharmaceutical drugs but then gaslighted by their doctors and community when they experience those inevitable injuries. The way I make sense of this is by viewing injuries as distributing on a bell curve, where the severe injuries (that are unmistakeable) are fairly rare, while the less severe (but harder to recognize ones) are fairly common.

This distribution pattern sadly makes it easy to dismiss the injuries, as the extreme ones are rare enough that they can be written off as spontaneous coincidences unrelated to the pharmaceutical, while the common ones are minor enough they are either not recognized or attributed to something else. In contrast, the way I interpret this curve is that if I see a cluster of severe events, I immediately assume the agent is dangerous and there will likely be a massive number of less severe effects, and likewise, if I see a high rate of people reporting moderate reactions to something (especially in different parts of the body), that means there are severe ones hiding in the background.

The COVID Vaccine Bell Curve

Since the COVID vaccine is fairly toxic and was given to a massive number of people, beyond this bell curve occurring, all of it was amplified to the point people who are not trained to spot it could still tell it was occurring. As such, when the COVID vaccine was approved, I had concerns it would have issues (which led to me advising people to hold off on it until more was known), but I initially expected the issues to primarily be chronic problems like delayed onset autoimmune diseases, increases in cancer a few years down the road and future fertility impairments (the potential risk of which I felt would most likely exceeded the meager benefit the vaccine was likely to offer).

However, the week it was released to the public, I began seeing distant colleagues post on social media they felt absolutely awful after vaccinating (but still intended to continue) and having multiple patients each day (in the demographics the vaccine had thus far been rolled out to) complaining about fairly significant (but not life-altering) reactions to the vaccines they’d never experienced from other shots (which most of the other doctors wrote off as not enough to justify skipping the second dose—despite reactions typically being worse from the second one).

As such, within a week I realized I had significantly underestimated the toxicity of the shot, and began pleading with people I knew to not get it as I was fairly certain the reactions I was seeing meant there were also going to be a lot of more severe ones that likely would take a while to show up (after which I had to watch quite a few of the people I cared about who didn’t listen to me develop much more severe chronic complications from the vaccine). Likewise, after about a month, I started having people around the country (many of whom I had not spoken to in years) reach out to ask if the COVID vaccines could cause sudden death as this had happened to a relative or friend.

I share all of this to highlight both why I have been so upset about the whole COVID vaccine program (as with the extremely limited data I had access to at the time, I could tell within a month of their rollout they were one of the most dangerous pharmaceutical products in history—yet the regulators with orders of magnitude more data than me could not at that time—and instead have continued to double down on their safety claim regardless of how much evidence mounts against the vaccines) but also to give an illustration of how this bell curve functions in real life.

However, that is only one half of the story. The other is simply that people are more sensitive to stimuli in their environment (which often goes hand in hand with them being predisposed to illness following a toxin exposure). For example, one of the projects with this newsletter has been to expose the COVID-19 mRNA vaccine shedding phenomenon, something we were told was impossible based on the design of the vaccine, but nonetheless we saw more and more cases of as time went on and eventually collected enough data to determine there were clear reproducible patterns in what was happening that elucidated what was actually occurring (all of which I detailed here). With the shedding phenomenon, I was originally clued into its reality because a few highly-sensitive patients I knew told me they could tell if someone had recently been vaccinated (as it made them ill and they shared overlapping sensory observations) and because numerous unvaccinated women (closer to the middle of the bell curve) had shared with me being around a vaccinated individual significantly disrupted their menstrual cycle (indicating that while shedding reactions were less severe than COVID vaccine reactions, there were likely still rarer severe reactions I would likely later come across and eventually did).

Note: when profitable projects are pushed through at the expense of the population, “sensitive” people normally bear the brunt of the human cost, but in almost all cases, are viewed as an acceptable sacrifice (since they are rare enough they can be swept under the rug) rather than as “canaries in the coal mine” that indicate larger but not yet detected issues will arise in the future.

The EMF Sensitivity Bell Curve

One of the areas where all these concepts best converge is with electromagnetic field sensitivity, as:

•A minority of people are “electrically hypersensitive” being both able to feel EMFs and becoming quite ill around them (which ultimately requires them to live in low EMF areas—which sadly are becoming increasingly rare).
•Some (myself included) are EMF sensitive (so we sometimes sense certain EMFs) and feel generally better in low EMF environments but can essentially tolerate everyday life (e.g., I will go to cities when I need to but prefer rural areas).
•Some don’t notice EMFs at all, but with careful deduction you can link certain symptoms they have to EMF exposure (which goes away once they go to low EMF environments or do things like turning off their wifi router at night and not keeping their phone by their bed).
•Many people really do not seem to be at all affected by them (but the data that would be needed to assess their longterm risks of things like cancer is not there).

As such, while a case can be made that EMF sensitivity is a primary contributing factor in many diseases (which has been observed by segments of the natural medicine field for decades), it’s also quite easy for someone who does not have a lived experience of the process to write it off—so that is what normally happens. Likewise, since so much of the economy revolves around EMF producing technologies, the necessary research in this area has been heavily suppressed (although a lot of it does exist if you know where to find it). Instead, the rebuttal typically is that EMFs are too weak to create ionizing radiation, so any biological effect they create must be thermal, and as all consumer devices are below the heating threshold, they are therefor harmless (whereas in reality the devices can still do many harmful things—particularly those in the microwave spectrum such as cellphones, bluetooth radar and wifi—which I suspect is due to their partial resonance with water). So as you might expect, the existing scientific consensus and mainstream research reject the notion of EMF sensitivity and the vast body of literature indicating it is harmful to life.
Note: two of the best books in print on the proven harms of EMFs are Devra Davis’s¹ and Arthur Fristenberg’s.¹ One of the most interesting studies I recently came across on this topic was one which discovered cell phones caused blood cells to clump together¹ (a process I believe underlies many diseases and which “sensitive patients” are predisposed to).

Given this, the symptoms many reported from living next to data centers (and attributed to the noise they made) caught my eye:

Note: a * means there is also decent scientific support that chronic environmental noise (or, for air items, combustion exhaust) can cause or worsen the reported effect.

What people notice from the site (exposures):

• Constant hum, high whine, or “vacuum left on,” indoors and outdoors* ¹ ² ³

• Vibration or rattling in windows, walls, floors, porch, or sometimes the body ¹

• A sense of pressure rather than an ordinary sound ¹

• A tone or hum that still seems audible after going inside ¹ ²

• Diesel, exhaust, “rotten,” or chemical odors when generators test or run ¹

• Construction dust, dirt, truck traffic, and early-morning work

• Bright site lighting / loss of darkness at night*

Most commonly reported effects:

• Sleep disruption — trouble falling asleep, nighttime awakenings, waking early and being unable to get back to sleep* ¹ ² ³

• Headaches or migraines* ¹ ² ³

• Stress, irritability, anxiety, or feeling constantly on edge* ¹ ² (including feeling agitated even with earplugs or headphones ³)

• Fatigue and poor concentration the next day* ¹ ²

• Avoiding or no longer using the yard, porch, patio, or open windows* ¹ ²

More often reported around very loud cooling or on-site power:

• Nausea ¹ ² ³

• Dizziness or vertigo ¹ ² ³

• Ear pressure, fullness, pain, or a “fluid” feeling ¹

• Perceived hearing problems or hearing deterioration ¹

• Feeling the sound or vibration in the head or chest ¹ ²

• Tinnitus, or a tone felt in the head, skull, or behind the eyes; some with pre‑existing tinnitus report worsening during high‑noise periods* ¹ ²
  Note: I have met a few EMF sensitive people who can hear EMFs and reported their tinnitus improves when they avoid EMFs (e.g., by turning off their house breakers at night).

Air and breathing:

• Closing windows because of fumes or noise* ¹ ²

• Asthma or breathing symptoms getting worse ¹ ² ³

Other common complaints:

• Can’t sit outside, garden, entertain, or enjoy the property* ¹

• Feeling like the house is no longer a quiet refuge* ¹ ²

• Feeling trapped in the house* ¹

• Worries about electricity bills, water, utilities, or infrastructure

• Concerns about property value ¹

• Pets becoming restless or behaving differently ¹

• Fewer birds or other wildlife changes ¹

The reason this list caught my eye is that beyond it being immensely unfortunate for the people who have to deal with it, many of these symptoms (e.g., headaches, sleep disruption, fatigue, brain fog, anxiety or feeling on edge, nausea, dizziness, tinnitus) also overlap with what individuals with electromagnetic hypersensitivity (EHS) report^1,2,3 and likewise, already EMF sensitive individuals report some of the other symptoms they experience (e.g., burning skin) near data centers.

This overlap in turn suggests:

•The same effects which trigger EHS are present with data centers, but, since they are stronger, rather than only the ends of the bell curve being affected, significantly more people (closer to the middle of the curve) are also being affected. So, much in the same way the COVID vaccines awakened the public to the dangers of the other vaccines (due to them being toxic enough large numbers of people were harmed the toxicity could no longer be covered up), the data centers could potentially do the same for the EMF issue.

•The overlap in symptoms is not due to strong EMFs being present by data centers, but rather due to the fact infrasound (sound below the typical threshold of human hearing which data centers generate and is a recognized hazard at high exposure levels) is a “harmful frequency,” and that some of the symptoms individuals experience from a variety of harmful frequencies have a significant overlap.

This hence made me curious about what was happening, as I did not see a reason why data centers would need to emit massive amounts of microwave radiation into their vicinity.

Note: with EMFs, the greatest effects individuals experience are typically from microwave sources. However, the fields generated by electrical wiring do also cause issues (particularly for more sensitive individuals) especially if “dirty electricity” (high-frequency electrical noise riding on household 50/60 Hz wiring) is present,^1,2,3,4 a process that often is due to devices within the home (e.g., solar power inverters or certain types of bulbs sometimes need to be removed to provide EHS individuals with relief).

From looking this up, I discovered the actual issue appears to be that data centers draw their power through enormous non-linear loads (tens of thousands of switched-mode server power supplies, uninterruptible power systems, and variable-speed cooling), which inject harmonics and high-frequency voltage distortion (dirty electricity) back onto the grid—however rather than a few low output devices creating it, something which draws 10,000 times as much power as a house is doing it and affecting everything.¹

Bloomberg News, in turn, in December 2024, published a remarkable study of 770,000 home power-quality sensors made by Whisker Labs (whose devices monitor the wiring inside homes to detect fire hazards, and which are dense enough that nearly 90% of American homes are within half a mile of one), cross-referenced against the locations of nearly 1,500 data centers.

Note: at the time this study was published there were far fewer data centers, far less pushback against them, and far less money behind them. As such, it is unlikely anything similar will be published again in the mainstream media despite the fact the issue Bloomberg highlighted has become much worse since late 2024.

Using the 8% total harmonic distortion threshold the Institute of Electrical and Electronics Engineers considers damaging to equipment, Bloomberg consistently found:

• More than three-quarters of the highly distorted readings in the country were within 50 miles of significant data center activity, and more than half of the households with the worst distortion were within 20 miles. The sensors with the cleanest power were typically at least 87 miles from any major data center. By the Census Bureau’s figures, about 3.7 million Americans live in the most affected areas.

• The pattern held in rural areas as well as cities. In big urban areas the median distance to a data center was 14 miles for the worst readings versus 51 for the best; in rural areas it was 49 miles versus 103.

• In Loudoun County, Virginia (home to “data center alley” and roughly 3,000 megawatts of capacity), the share of sensors exceeding the 8% threshold was more than four times the national average. In neighboring Prince William County, about 6% of sensors were over the limit, nearly all within 7 miles of a data center, with some readings reaching 12.9%. Around one newly opened Prince William facility, 78% of nearby sensors were above the limit in October. By contrast, in York County, Virginia, 80 miles from the nearest major data center, harmonics averaged under 3%.

• In the Chicago area, more than a third of sensors showed sustained high readings over nine months, and over 9,300 of the county’s 16,000 sensors had at least one monthly reading at or above 8%.

• The worst distortions occurred at night, when data centers make up a larger share of total demand (i.e., when everyone else is asleep and the servers are not).

• Bloomberg tested whether large solar installations could explain the pattern and found they did not. It concluded that while the sensor data alone cannot prove a single cause, the correlation with data center proximity was too strong to be coincidence. As you might expect, the utilities questioned these findings (e.g., one company said its 200 grid monitors showed nothing unusual), but Bloomberg stood by them as numerous sensors across the same neighborhoods replicated the findings.
  Note: this is also acknowledged within the industry itself, as data center engineering guides note that the harmonic disturbances these facilities generate can extend beyond the facility to anything connected to the same electrical infrastructure.¹ Likewise, a 2025 industry piece concedes that customer loads can distort power for their neighbors.¹

Bloomberg News also quoted a Bloom Energy executive explaining that AI workloads draw power in a sawtooth pattern of sudden swings rather than a steady line, which no grid was designed to absorb from one facility, let alone dozens (so given this and more importantly the massive demand being placed on the grid, a real risk exists our aging electrical infrastructure will not be able to handle the demands data centers are placing on them).

Notably, Bloomberg’s concerns centered on the health of electronics, highlighting that once AC power deviates from the ideal 60-cycle-per-second pattern, issues consistently emerge such as appliances running hot, motors in refrigerators and air conditioners rattling, lights flickering, increased fire risk during voltage surges, greater vulnerability to brownouts and blackouts, and billions of dollars in cumulative damage to home appliances and aging grid equipment.

However, as a limited body of research in dirty electricity has indicated, there are also consequences for the health of human beings, including many of the exact same symptoms individuals living by data centers have reported (e.g., sleep disruption, headaches or head pressure, irritability, anxiety or feeling on edge, fatigue, poor concentration or brain fog, dizziness or vertigo, tinnitus, worsened asthma or breathing, and nausea).^1,2,3
Note: animal studies also corroborate certain effects of dirty electricity (e.g., a study of 1,705 cows across 12 dairy farms found milk production fell in proportion to the number of transients and harmonics on the farms' power, that the cows' behavior tracked the voltage measured on their legs, and that the distortion was coming from the utility lines rather than the farms themselves).

Furthermore, many of the symptoms reported near data centers that are not classically associated with dirty electricity (e.g., ear fullness or pain, hearing deterioration, feeling the sound in the chest) have been extensively linked to infrasound exposure^1,2,3,4 (along with it being widely recognized certain animal species like elephants can hear infrasound or become more agitated when it is present).

Since Bloomberg’s data only showed what was reaching people’s homes, I also wanted to know what was actually coming out of the data centers themselves. It turns out this was measured in a 2026 study,¹ where researchers put a magnetometer inside the server room of a university’s data center and recorded the electromagnetic field continuously for a month (although this was a small facility with 250 servers running at about half capacity, so nothing like what is being built for AI).

What they found was that the field itself was not particularly strong (around 0.5 microtesla), but it was very distorted. On a typical day, the distortion averaged 36%, during working hours it rose to 65%, and 41 times during the month it spiked far beyond that (in one case to 330%, at which point the “noise” on the signal was three times larger than the signal itself). To put those (likely conservative) numbers in perspective, the same instrument in an office in the same building measured 5–7% during the day and 21–24% at night.

Finally, like Bloomberg, the authors of the 2026 study were only concerned with what this did to equipment (e.g., they noted the type of harmonics data centers produce don’t cancel out on the wiring but instead pile up in the neutral line, overheating wires and transformers), and the study had its limits (one sensor, one small facility, and it couldn’t measure the higher frequencies where computer power supplies emit the most). Nonetheless, it confirms that the electricity inside these facilities is far dirtier than what a normal building produces, and hence why homes twenty miles away from an AI data center drawing a thousand times more power are being affected (but again, the research needed to conclusively determine what is really happening has not been done).
Note: utilities typically only monitor dirty electricity harmonics up to about 2–3 kHz (as did both the Bloomberg report and the 2026 study), whereas the dirty electricity health studies focused on higher frequencies (the filters used in the school studies work between 4 and 100 kHz), which fall within the 2–150 kHz "supraharmonic" band that switching power supplies emit most strongly. That said, while they are almost never monitored on the grid, a 2023 study demonstrated that data centers also make emissions in these higher ranges.

Solving the Datacenter Dilemma

At this point, the AI sector appears to be facing a few critical bottlenecks:

•Shortages of chips and rare earth elements they need to function (much of which China currently controls the supply of but the United States is making an effort to create supply chains for).

•Insufficient energy to run the data centers (e.g., in a recent talk Musk stated the consensus estimate among analysts that follow the AI space very closely is that there will be at least a 15-gigawatt shortfall of power in 2027 for AI chips¹ and there is often a 2-5 year wait time for the major power components like generators and transformers data centers require¹ along with grid interconnection queues that commonly run two to three years).

•Inability of the electrical grid to sustain the power loads AI data centers requiring external power are creating.

•Increasing public pushback against data centers that has the potential to block new constructions or shift elections.

These constraints make the industry’s forecasted exponential growth (which has fueled their rapid rise in stock values) unlikely on the advertised timeline as the deployable capacity is likely to cost more than projected and take a while to arrive.

As such, a few (non-mutually exclusive) possibilities exist:

•First, AI encountering structural limitations that make it fail to live up to its hype will prevent it from taking over our society, or at least give us time to adapt to it.

•Second, to aid AI in overcoming the obstacles it faces, there will be increasing pressure to support it (e.g., consider how much Fox’s positions on the topic shifted over the last year). To this point, it must be emphasized that changing the party in power is unlikely to impede the AI roll-out as while certain Democrats are beginning to publicly oppose the datacenter push, the major tech companies primarily support the Democrat party, and hence will ensure the push continues if the presidency flips in 2028 (much as Biden, days before leaving office, signed his own order opening federal land to AI data centers, which Trump simply revoked and replaced with a more aggressive version; and not unlike how Kamala Harris cast doubt on “Trump’s COVID vaccine” in October 2020 and then pushed it onto the public once elected¹).

•Third, the pressures facing AI will force the industry to develop a better solution that allows the technology to scale without public pushback (which, given the law of displacement, I believe is the only realistic option to make things better here).

Since data centers need enormous amounts of power and are best placed where no one lives, Elon Musk has proposed an elegant solution that is very on-brand: use SpaceX’s launch capacity to put the data centers in orbit alongside Starlink and run them on solar power (which in the right orbit is nearly continuous and up to eight times more productive than on the ground). SpaceX, in turn, has filed with the FCC for up to one million data center satellites, Google is launching prototype satellites carrying its AI chips in early 2027, Nvidia announced a space-rated GPU, and China has already run an AI model in orbit on a small constellation.^1,2

However, while this could potentially solve many of the problems we are facing, I do not think this can be scaled to the degree needed as:

• Everything a data center does eventually turns electricity into heat. In vacuum that heat can be dumped to the environment only by thermal radiation. At temperatures chips can survive, each square meter rejects only a modest amount of power, so an orbital node is mostly solar arrays and radiators around a relatively small compute payload. However, getting that cooling to be light enough is a real jump from currently existing options (e.g., the international space station’s radiators are on the order of 13 watts per kilogram, while published orbital-data-center concepts assume something like 160–350) and nothing in that class of what will be needed has been built at data-center scale yet.

• Unlike on land, once in space, the hardware most likely cannot be fixed or upgraded (satellites in low orbit are almost never serviced; they are replaced), which is a major issue as AI chips go obsolete every three to five years (and possibly faster in space due to radiation shortening the chip’s life). Given the cost needing to replace all the data centers every few years adds (unless we have an inconceivable paradigm shift like say UFO antigravity technology being discovered or functional servicing robots being deployed to space) I am hence, doubtful this approach will ever be able to economically compete with the land based model (despite Musk’s knack for making the impossible possible).

• Getting large amounts of data down from orbit (or up to it) is much harder than sending the same data through fiber on the ground (making fiber much cheaper than space links).

• Beyond the sheer cost of launching all of that into space, scale itself is a manufacturing problem. A million satellites of the size SpaceX describes would take many years at build rates far beyond today’s Starlink production, and with the demonstrations being scheduled for late 2027, this likely puts any meaningful space data center capacity in the 2030s.

As such, I think this proposal realistically could be used for niche applications (space-native data, some batch training, or a future orbital data infrastructure for colonizing Mars), but I do not see a viable path for it to beat terrestrial facilities on general-purpose computing.

However, there is another approach I believe can displace the data centers flooding our communities.

The War on Climate Change

I care immensely about the health of the earth, so for a long time I was a fairly committed environmentalist. However, in the early 2000s, I distanced myself from that movement due to a more unfortunate occurrence of the law of displacement: one prong of the environmental movement (reducing carbon dioxide to prevent global warming) becoming a lucrative thing to promote (e.g., by selling expensive hybrid cars or carbon credits) and rapidly taking over the movement. I objected to this because:

•It caused the other legitimate environmental issues I cared about and had fought for to be pushed out of the discussion.

•It was highly debatable if carbon dioxide emissions were causing global warming (or even problematic), so I felt the dire predictions were unlikely to happen, and if they actually were going to occur as forecast, the changes were so rapid it was unlikely anything could be done to stop them.

•Reducing global warming was an extremely nebulous target, so it could never be falsified and the goal posts would be possible to continually shift on it. As such, once the inertia behind this orthodoxy became established, it would be immensely difficult to overturn it, so as time went on, it would inevitably consume more and more of the environmental movement.
Note: in 2009, a series of hacked emails indicated that global temperature data had been distorted by climate scientists¹ (with reactions, based on political leanings, ranging from it being treated as proof global warming was a hoax, to acknowledgments illegal scientific misconduct occurred but not questioning of the underlying consensus, to attempts to excuse everything).^1,2,3 Around this time, the environmental movement pivoted from global warming to the even more nebulous term “climate change” (something I suspected could likely be attributed, at least in part, to solar cycles and weather modification programs).

•The measures being implemented to stop global warming and carbon dioxide emissions skipped the options that could produce clear tangible results (e.g., stopping slash and burn farming practices in the rain forests) and instead focused on technologies with their own host of issues that primarily served to centralize power and make money.
Note: this is commonly analogized to how leaders in the new environmental movement would tell people not to drive cars but then fly on private jets to climate change conferences. Likewise, I have now see numerous memes highlighting that the same tech companies which cared so much about climate change and the environment threw it all to the wind once that got in the way of them building (far more profitable) data centers.

That said, I do think an argument exists for shifting away from fossil fuels due to the (non-carbon dioxide) emissions they create, so I’ve spent a while looking at every alternative energy option which exists, particularly since I’ve held the longstanding belief technologies which reduce the profitability of large markets inevitably get sidelined (e.g., this newsletter is devoted to showing how better and far cheaper medical alternatives have existed for decades but been largely kept off the market by the medical monopoly).
Note: I also hold the minority view (detailed here) that petroleum is not biological in origin but continually upwells from deep within the earth (and contains biological traces because it was the birthplace of the earliest lifeforms)

Because of this, over the years, I’ve spoken to numerous people researching “free energy” systems and seen a few which, when demonstrated, were quite compelling. From looking at the existing options, I eventually concluded “green nuclear power” was likely the most practical and viable option we had available to adequately address the energy needs of humanity, but then as the decades went by, much as I’ve seen with many transformative medical discoveries, I watched the promising nuclear designs go nowhere.

However, much in the same way the data center moment is finally creating the potential window to bring widespread attention to EMF toxicity, the unprecedented need for massive power generation in the immediate vicinity of data centers (along with the current Iran war) is finally creating the window to bring green nuclear power to market as more money can finally be made off a cheap and abundant energy source than the energy industry has made by locking the world into a limited and overpriced commodity.

Nuclear Power Designs

Every atom is composed of a nucleus of positively charged protons and neutrally charged neutrons (with the common isotope of hydrogen being the only one lacking neutrons) along with nearly massless negatively charged electrons which surround the atom’s nucleus. In most chemical reactions, while electrons shift, the nucleus never changes. But when it does, a nuclear reaction occurs, and the total mass of the nucleus shifts.

Anytime an atomic mass shift occurs, the collective mass of the resulting parts typically do not exactly total to what they were before, as some of that mass is converted to energy. The famous equation E=mc², in turn, quantifies this shift, illustrating that a tiny amount of mass being lost creates a massive amount of energy (as “c” equals the speed of light).

In stars, the immense heat and pressure primarily create these shifts by causing light nuclei to fuse together, whereas on Earth they occur naturally through radioactive decay. Very large nuclei (or those with the wrong number of neutrons to hold the nucleus together) are the least stable, so nuclear engineering focuses on the few heavy isotopes that can be made to split apart when struck by a neutron, releasing that stored energy on demand.

When the nuclear age began, uranium was identified as the optimal element for nuclear applications as beyond being intrinsically radioactive, one of its naturally occurring isotopes, U-235, could undergo fission (splitting into two much smaller nuclei), and the neutrons released when it split would trigger fission in adjacent U-235 atoms, thereby creating a chain reaction that quickly released a vast amount of energy. Nuclear power hence focused on using fuel with enough U-235 to sustain fission, plus neutron-absorbing control rods that could slow or stop the reaction so energy was released gradually enough to harvest for power rather than run away, while nuclear weapons (at least the early U-235 designs) focused on assembling a supercritical U-235 mass fast enough that the fission reaction ran away and exploded.
Note: a few natural nuclear reactors have been found in uranium deposits in Gabon, where two billion years ago, the ore still had enough U-235, and groundwater slowed the neutrons enough for a fission chain reaction. The reaction ran in pulses: heat boiled the water off, the reaction stopped, the deposit cooled, water returned, and it started again.

However, while U-235 is an optimal isotope to use for nuclear applications, it still has a few major problems.

First, only 0.72% of the earth’s uranium is U-235, whereas much higher uranium U-235 concentrations are needed for nuclear applications (typically 3–5% for nuclear reactors and around 90% for nuclear weapons).
Note: uranium enriched above 20% is called highly enriched uranium and is considered weapons-usable, whereas uranium enriched to 90% U-235 is called weapons grade uranium.

This, in turn, leads to two issues:

•In addition to uranium mining and milling creating large amounts of radioactive tailings to obtain uranium, since most of the uranium obtained is not U-235, concentrating the small fraction that is into usable fuel leaves the majority of it behind as "depleted" uranium. This waste is still radioactive, has piled up by the hundreds of thousands of tons, and some of it is used by the military for armor and ammunition, as uranium's density allows it to punch through other metals (but those rounds aerosolize into dust after hitting a target, which has been a major issue in many of the areas where these munitions were deployed).

•Concentrating the U-235 is challenging, as the uranium must first be converted into a fluoride gas (uranium hexafluoride) so its isotopes can be separated—originally through gaseous diffusion, and now with gas centrifuges, the difficulty of which has been a major barrier to smaller countries obtaining uranium-based nuclear weapons. The Iran conflict, in turn, was driven in large part by the fact Iran had developed centrifuges to enrich uranium for nuclear power and fears existed that this capacity could be pushed to the much higher enrichment required for nuclear weapons.
Note: many have wondered why something as toxic as fluoride is put into the water supply. The idea originated in the 1930s with the aluminum industry (Alcoa), which faced mounting lawsuits over fluoride pollution from its smelters and hence had a strong interest in the chemical being seen as beneficial. America’s Public Health Service was initially wary of it due to fluoride's toxicity. However, as documents declassified in the 1990s showed, the Manhattan Project needed enormous quantities of fluorine to enrich uranium, its workers were being injured and killed by it (deaths that were kept secret for fifty years), it was venting fluoride over the surrounding communities, and it was already being sued by farmers. So in 1944 the bomb program secretly organized and paid for a conference on fluoride's health effects while having the Public Health Service host it under its own letterhead, and its chief fluoride toxicologist, Harold Hodge, then chaired the advisory committee for the first water fluoridation trial at Newburgh, New York—which his classified program at the University of Rochester quietly monitored, collecting blood and placenta samples from residents to learn how much fluoride the body retains. Six years later, the official who endorsed fluoridation for the United States was Oscar Ewing, previously Alcoa's Wall Street lawyer (all of which is detailed in this 2004 book).

Second, once U-235 is obtained, the reactors still have a few key problems:

•The most well recognized is that both the chain reaction and the heat the fuel keeps producing after it is shut down have to be continuously controlled, so if the cooling or shutdown systems fail, the fuel can melt, destroy the reactor, and release radioactive material into the environment. This is what happened at Chernobyl in 1986 and Fukushima in 2011, nearly happened at Three Mile Island in 1979 (where the core partially melted but very little radioactivity escaped), and also occurred in a number of earlier military and experimental reactors that were barely reported at the time.
Note: these include a partial meltdown at a Canadian research reactor in 1952, another at the Santa Susana site outside Los Angeles in 1959 (whose extent was concealed for twenty years), a 1961 explosion at an Army reactor in Idaho that killed three operators, a partial meltdown at a breeder reactor near Detroit in 1966 (which most of the public only learned of from a book published nine years later), and several Soviet nuclear submarines whose reactors lost cooling at sea (most famously the K-19 in 1961, where crew members died of radiation sickness after improvising a repair), all of which were kept secret until the Soviet Union collapsed.

•The less recognized issue is that even “normally functioning” nuclear reactors release some radioactivity into their vicinity, and a number have had unplanned leaks of tritium and other material into local groundwater. The data I’ve seen, in turn, has led me to believe real health issues exist with this, but like many inconvenient things, the actual health effects on nearby residents have not been sufficiently researched and remain an open question.

Thorium Reactors

In addition to concentrated U-235 driving nuclear reactors, another alternative exists: exposing thorium to neutrons, which converts it into U-233, a uranium isotope that also undergoes fission (but being much shorter-lived than U-235, is much rarer in nature and cannot be procured through mining or enrichment). Thorium designs, in turn have a few major advantages over U-235 ones as:

•There is 3-4 times as much thorium in the earth as uranium,¹ mining it is cleaner than uranium, and since all of it is an isotope that can be used (rather than only 0.72%), beyond far less needing to be mined, large amounts of depleted nuclear waste are not created (though, as discussed below, the reactor still needs a small amount of fissile fuel to start it).
Note: once mined, thorium is usually mixed with rare-earth elements it must be separated from. That is both an advantage (those rare earths are strategically scarce) and a disadvantage (the separation is complex and uses harsh chemicals). As such, we already “mine” thorium, but it is presently disposed of as an unwanted radioactive waste from rare-earth processing.

•In the molten-salt designs usually paired with thorium, the fuel is already a liquid at low pressure, so there is no solid core to melt (reducing the risk of nuclear meltdown); if it overheats, the salt expands and the reaction slows, and it can be drained into a dump tank to shut down without pumps (the trade-off being that a leak anywhere in the system releases highly radioactive liquid, and the salts slowly corrode the reactor's plumbing, which remains the main engineering hurdle).
Note: some thorium designs instead use a particle accelerator to supply the neutrons (so the reaction stops the moment the accelerator is switched off, and the reactor can also burn existing nuclear waste). The concept has been pursued for over thirty years (most notably by a Nobel laureate at CERN in the 1990s), and Belgium and China are each currently building demonstration units, but none has yet operated, as the accelerator required to drive a commercial reactor is so expensive it costs about as much as the plant itself—which is why molten salt, rather than accelerators (which may ultimately be the superior technology), has become the focus of thorium development.

•Thorium reactors make far less long-lived non-uranium nuclear waste (plutonium, americium, curium) than conventional reactors, because thorium is lighter than uranium and does not climb the ladder of neutron captures as easily (but at the same time still produce ordinary fission-product waste).
Note: some thorium reactor designs (e.g., the accelerator ones) claim to further reduce the resulting nuclear waste.

•Thorium reactors greatly reduce (but do not eliminate) the risk of nuclear proliferation. Thorium itself cannot sustain a chain reaction, so a reactor needs a small amount of fissile material to start it, but once running it breeds its own fuel (U-233) from the thorium, which means a country does not need the standard enrichment plants that are also the path to weapons-grade uranium, and the reactor produces very little of the weapon’s grade plutonium formed in uranium reactors. Nuclear weapons can be made from U-233 (the United States tested this), but the U-233 a reactor produces is typically contaminated with U-232, whose decay products emit intense gamma radiation, making the material dangerous to handle, difficult to fabricate into a weapon in secret, and easy for detectors to spot.
Note: since Iran has been adamant it needs nuclear power to address the (real) rolling blackouts the country faces, during the war a former congressman proposed offering Iran American thorium reactor technology in exchange for permanently ending uranium enrichment, on the logic that this would give Iran electricity while making the weapons pathway harder to exploit rather than dependent on inspectors (although without additional safeguards nuclear weapons could still be made). As far as I can tell this never made it into the actual negotiations (which centered on enrichment limits, Iran's existing stockpile, and IAEA access), and in any case it could not have been implemented on any near-term timeline, as no commercial thorium reactor yet exists.

This then raises an obvious question: if thorium was the superior technology, why was it never adopted? Simply put, because the entire American nuclear complex was built as a weapons program with a civilian branch attached, and uranium was the fuel that made weapons. Enriching it produced bomb material directly, irradiating it produced plutonium, and so the enrichment plants, production reactors, and reprocessing facilities were all built around the uranium fuel cycle (with the civilian reactors that followed adapted from the Navy’s submarine designs and fed from that same infrastructure).¹ Thorium’s low proliferation risk, which is now its great selling point, at the time simply meant it did not offer what the nuclear establishment wanted. The decisive moment came in the early 1970s, when the Atomic Energy Commission (at Nixon’s direction) committed the country’s reactor future to a liquid-metal breeder that ran on plutonium, and its reactor chief pursued that program, in Weinberg’s words, “with Rickoverian dedication: woe unto any who stood in his way.” Weinberg kept arguing that his molten salt reactor was the safer path and was pushed out of Oak Ridge after eighteen years as its director; the program was cancelled in 1973.^1,2 Once that choice was made (and other factors reinforced it such as the Navy's light-water experience, abundant cheap uranium, and later cheap gas), the rest followed: the supply chain for uranium reactors was firmly established (making it difficult to justify creating an entirely separate one), regulatory requirements became far tighter after Three Mile Island (making it much harder for any new design to enter the market), and the existing industry became large enough to have the clout to keep competitors that would displace its plants, fuel mills, and licensing framework from getting off the ground (mirroring the pattern I have watched play out with countless forgotten medical technologies).

Notably, when the program was cancelled, Oak Ridge had already demonstrated the reactor itself worked, but simply had not yet built the remaining pieces (e.g., the chemistry for continuously processing the fuel salt, a solution to the slow corrosion of the reactor’s metal alloy by the fluoride salts, and a way to manage the tritium the salt produces)—all of which researchers believed could be solved but which have never been demonstrated at commercial scale, because the work was never funded.¹ After that, essentially no new reactor designs of any kind were built in America, and the regulatory framework hardened around the light-water reactors that already existed, so a design that used liquid fuel at atmospheric pressure did not fit any of the rules (and there is still no licensing framework for a thorium fuel cycle anywhere in the world).¹ Meanwhile, the original rationale for breeding fuel from thorium (a fear that uranium would run out) evaporated as uranium turned out to be abundant, and cheap natural gas removed any economic pressure to try something new.

The result is that the technology now requires an entire supply chain that does not exist, so Thorium, despite being abundant, currently has to be extracted from rare earth ores through costly processing, no facility exists to fabricate it into fuel, and a thorium reactor still needs a small amount of fissile material to start it,¹ which means either the high-assay uranium fuel America is only now beginning to produce or plutonium.¹ Finally, the fluoride molten salt these reactors run on requires lithium enriched to over 99.99% in a single isotope (lithium-7), and the United States has not produced enriched lithium since 1963—the only suppliers are China and Russia,^1,2 China has at times restricted exports to feed its own reactor program,^1,2 and a single molten salt reactor needs tens of tons of it (compared to the roughly 300 kilograms a year the entire existing American reactor fleet uses).^1,2 That said, the first serious commercial attempt to restart domestic production was a $7 million seed round recently closed (on 8/31/26).¹

What this essentially means is that for thorium technology to take off, two things are needed: a relaxing of regulatory restrictions (which has already begun: in May 2025, Trump signed four executive orders that set a goal of quadrupling U.S. nuclear capacity by 2050, ordered the NRC to decide new reactor applications within 18 months, created the Department of Energy test-reactor pathway described below, and invoked the Defense Production Act for the nuclear fuel supply chain¹) and a very large investment (which is now possible for the first time, as an industry has emerged that needs enormous amounts of power and is willing to pay almost anything for it). On the cost side, while no one can know the actual number until a commercial reactor is built, the published techno-economic models place thorium power among the cheapest sources of electricity ($20–55 per megawatt hour),^1,2,3 which is a fraction of what new conventional nuclear plants cost ($175–255)¹ and well below the roughly $110-115 that analysts estimate Microsoft agreed to pay for twenty years of power from a restarted uranium reactor at Three Mile Island (the contract price itself was not disclosed).¹

For this to happen, the regulatory opening and the money have to start now, because of how long every step takes. Building the early reactors under Department of Energy authorization rather than NRC licensing can get a test reactor running within a few years (this summer that path took four privately developed test reactors from construction to criticality, one in about eight months¹), but it does not license a commercial plant, and even the fastest program still needs years of operating data on salt chemistry, corrosion, and tritium before anyone will build the next size up. Likewise, the supply chain the reactors depend on (lithium-7 enrichment, fuel salt, thorium processing) does not exist at U.S. scale and has to be built alongside the reactor rather than after it works, which is why “a few billion dollars” is the entry price rather than the total. Put together, a serious American program could have a molten salt test reactor running by the end of this decade and first commercial power in the mid-2030s, with more money shortening the timeline by a few years but not skipping it. As such, thorium will not power the data centers going up this year—those will run on gas, restarted plants, and (if their schedules hold) the small uranium reactors now under construction, which at best can be sited away from people—but a decision now decides the second and third waves of data centers in the 2030s. China already has a molten salt reactor running and a public ladder toward a 10-megawatt demonstration around 2029–30, a larger one around 2035, and commercial units by 2040.¹ So if America waits until those are built to begin, it will be buying the technology from China rather than fielding it.

Note: thorium is not the only promising nuclear design to have been shelved for lack of permission and money. In the 1990s, Argonne’s Integral Fast Reactor—a sodium-cooled design that recycled its own fuel on site, consumed existing nuclear waste, and had been running as a prototype for decades—was cancelled by the Clinton administration in 1994 with roughly three years of work left, on the grounds that it had “no foreseeable commercial value” and undercut nonproliferation goals rather than for any technical failure.^1,2,3 Later, Bill Gates spent over a decade arguing that his company’s nuclear reactor design was ready and simply needed someone to fund the first plant (a partnership to build it in China collapsed under export restrictions in 2019); it finally received an NRC construction permit in March 2026, with federal cost-sharing, Meta (Facebook) as a customer, and a first unit targeted for around 2030.^1,2,3 That plant is one of a handful of small modular and advanced reactors now actually being built or licensed in America (the others include Google’s salt-cooled reactors in Tennessee, which broke ground this April but whose first unit has slipped to 2029, and a pebble-bed design for Dow in Texas expected to be permitted next year), and restarts of existing plants such as Three Mile Island (targeted for 2027) are closer still.^1,2,3,4 These are being funded in a way earlier reactor designs never were—the major technology companies have contracted for roughly ten gigawatts of nuclear capacity in two years, and the announced U.S. nuclear pipeline now stands near 74 gigawatts, much of it from data center buyers^1,2,3—and while much of that will slip, they are the most immediately viable nuclear option for data centers: slower than gas, but arriving around 2030, well before any thorium reactor, and building the licensing precedent and industrial base thorium will need (Google's salt-cooled uranium reactor developer, for example, is already building its own fluoride salt plant and lithium-7 enrichment—the very supply chain thorium requires).

The Space of Alaska

While space fits some of the requirements for America’s data center project, the ideal site would be cold (so the enormous cost of cooling largely disappears), on U.S. soil (which is why the Nordic countries and Greenland, despite coming up constantly, will never receive serious consideration for strategic data centers), sparsely populated (so the noise, water, and dirty electricity land on no one), rich in energy that can be used on site rather than pulled off a residential grid, wanted by its state government, and reachable by the transport and fiber needed to move equipment in and data out. Alaska meets all of these except the last, and that gap is both the entire problem and the reason this moment is different from every earlier attempt to industrialize the North Slope.

The climate case is straightforward: Alaska’s mean annual temperature is about 35°F against Texas’s 65°F (and Deadhorse on the North Slope averages 14°F), which the governor has been telling operators saves a one-gigawatt campus on the order of $150 million a year in cooling costs.¹ Likewise, Alaska’s low population density (740,000 people on a landmass larger than Texas, California, and Montana combined) aligns with data center needs and political support for the centers is already in motion—the Air Force is offering 4,700 acres at three Alaska bases for AI data centers, the state has issued a preliminary decision to lease a square mile of North Slope land to a company proposing a 1–3 gigawatt campus (disconnected from the grid and fueled by a new gas spur, with initial operations targeted for late 2028), and the governor has courted Meta, Amazon, and Microsoft for years with no state income, sales, or property tax to offer because Alaska has none.^1,2,3

Likewise, Alaska produces far more energy than it uses, and the North Slope holds 37 trillion cubic feet of proven natural gas that has been stranded for fifty years because no pipeline was ever built to move it, so the gas produced alongside oil is simply reinjected into the ground.¹ That fuel hence could be what the early data center campuses burn on site—which matters as Alaska does not have spare electricity in the grid state residents depend upon as the Railbelt serving Anchorage and Fairbanks peaks at about 750 megawatts, Cook Inlet gas is running out, and the utilities have already told the Air Force they cannot power large data centers at the bases from existing supply,^1,2 so a single AI campus’s demand would exceed the entire Railbelt (and residents are already protesting a planned data center). As such, the model that works in Alaska is the one the lower 48 states lack (and may need in the near future): generation built next to the servers, consumed behind the meter, and never touching a residential wire or threatening the power grid. This is also what makes Alaska the natural home for the reactors discussed above, as the upcoming modular designs (which could also eventually be done with thorium) are small enough to place next to the data centers. The state, in fact, rewrote its nuclear siting law in 2022 to accommodate microreactors, the Air Force’s first one is being built at Eielson (construction 2027, operation 2030), and villages across the state still burn diesel at electricity rates far above anything in the Lower 48, so Alaska has exactly the kind of customers that first-of-a-kind reactors have always needed but never had.^1,2,3 The North Slope has the gas; the rest of Alaska does not, and for sites away from it—the bases, the Interior, a Mat-Su industrial district—a reactor next to a data center is the only way to get gigawatt-scale firm power without a pipeline, and the data center is the only customer that will pay for the first ones.

Note: data latency, which is usually cited against Alaska, actually sorts the workload sensibly. AI training (the gigawatt-scale load causing most of the harm in the Lower 48) does not care about distance, since nearly all its traffic stays inside the building (training data is moved in once; it is not streamed). Inference that serves users does, and Alaska is far enough from Seattle to rule out the most latency-sensitive applications in the Lower 48. But Anchorage is closer to Tokyo than California is, and a planned trans-Pacific cable landing through Alaska would make it the shortest path between the United States and North Asia.^1,2 As such, Alaska could take the training load and Asian-facing inference, while the small inference sites the Lower 48 actually needs stay near their users at a fraction of the scale now being imposed on communities.

The state’s compensation structure is another piece the Lower 48 has never had. Alaska is already built on the principle that resource extraction pays the public: the Permanent Fund, funded by oil royalties, now supplies roughly 60% of the state’s general revenue and still pays every resident a dividend,¹ and the Native corporations created in 1971 own 44 million acres and are required to share 70% of their subsurface resource revenue across all twelve regions.¹ None of this applies automatically to a data center on state land, and the central dispute in the lease now under review for the North Slope campus is precisely whether the state collects a real royalty or leases a square mile of Arctic at pasture rates.¹ But the tools exist (whereas they do not in places like Virginia’s data center alley) and a lease written with a percentage of gross receipts flowing to the fund and, where the land or gas is Native, to the corporations, turns the host from a victim into a shareholder—which is the only arrangement under which “no one fights it” is actually true.

Infrastructure is the final constraint that decides whether Alaska could be a national solution or a press release, and the best candidate to start is Prudhoe Bay as the North Slope was built by barge and hence does not require connecting railways to be built (since 1968, the industrial plant has arrived by summer sealift during the six-to-eight-week window when the ice retreats, with modules the size of ten-story buildings offloaded at the West Dock causeway, and the heaviest equipment still moves there way).^1,2 Deadhorse, in turn already has the dock, the airport, the highway, fiber along the corridor, and a workforce accustomed to shift work at forty below, and it sits on top of gas with no other buyer. A pilot campus there does not have to invent an Arctic port or wait for an 800-mile export pipeline; it only has to prove the load, the lease, and the power. Fiber is the harder part: sea ice has cut the Arctic subsea cable twice, most recently in January 2025, when 20,000 residents from Utqiaġvik to Nome lost fiber for over seven months because repair ships could not reach the break until the ice cleared.¹ So the training-first, Asia-later sequence depends on the redundant routes now being built (an overland link to bypass the ice-prone segment, a second Arctic cable, and the trans-Pacific landing).^1,2 Rail comes after: a 471-mile extension of the Alaska Railroad from Fairbanks to Prudhoe Bay was studied before the oil pipeline was chosen and has been revived repeatedly at estimates of $8–11 billion (a fraction of the $40–55 billion gas line), and it would carry the transformers, modules, and eventually fiber and power that would turn an isolated camp into a district.^1,2 It does not need to exist for the first barge-fed campus; it needs to exist if that campus is going to become the second and third waves. Build the pilot on the dock that already works, then spend the billions to pin it to Fairbanks.

Note: other locations in Alaska would also likely make sense once additional railroads were developed—many of which have already been proposed or worked on (which amongst other things, would make it much easier to transport small modular nuclear reactors to them). To this point, in his first term, Trump attempted to begin (and permitted) the process of connecting Alaska’s railroads to Canada^1,2 something, which ever developed, would make it very feasible to move datacenter infrastructure (and small nuclear reactors) to Alaska.

That said, there are still real challenged with the initial Alaska deployment. The first campus’s own filings call for seven million cubic yards of gravel to build a pad on the permafrost (nearly twice what ConocoPhillips was permitted for its Willow oil project) and project 1,500 construction jobs but only 60 permanent ones,¹ everything (and everyone) has to be shipped or flown much farther than at a typical site in the Lower 48, gas generation still creates local air pollution even when it’s off the grid, and the “$500 million” figure being cited for the campus is only the first phase. Likewise, some Alaskans are already asking if the public will turn on data centers the way the Lower 48 has,.¹ which will be a valid concern if what gets built is a few gigawatts of gas turbines on a lease that pays the state almost nothing. However, provided the campuses are kept off the grid and the leases actually compensate Alaskans, this approach eliminates the main problems with the current model (forcing a massive electrical and acoustic load onto people who never asked for it), and more importantly, creates a customer for vital energy technologies that have never had one. A campus that starts on gas can then switch to a microreactor, then a small modular reactor, then a thorium plant, without ever raising anyone’s utility bills, and the rail and fiber built to support it will remain useful regardless of whether the AI boom lives up to its hype.

In short, Alaska shows that while no ideal solution exists to the data center problem, innovators are nonetheless coming up with viable options that are significantly better than what we currently have on the table (e.g., I was quite surprised to learn how much work the state had put into this once I began researching if Alaska could potentially work). That said, I can’t say with certainty if Alaska is the best solution we have for protecting the public from data centers, but I nonetheless felt it was important to layout exactly what the state attempted, as it provides a framework with the real potential to displace what is currently happening.

Conclusion

Throughout America’s history, “successful” industries have emerged that owed part of their success to exploiting the communities they resided in, and in most cases, regardless of how much the public fought it, nothing could be done to stop it. So, given that the finances behind the AI dwarf what’s happened in the past, it is unlikely protest alone with be sufficient to stop this—particularly since it is nearly guaranteed this push will continue regardless of who is in power.

However, while we can’t necessarily stop it (unless the AI business model collapses on itself), we can provide the public pressure to direct things towards a manageable compromise, and if we are savvy, simultaneously solve one of the greatest challenges humanity has faced—finding a clean source of energy which can affordably meet humanity’s civilizational needs far into the future. Likewise, while I never expected this, it’s quite possible giving people the language to explain why they are suffering from the data center push may, at last, be the thing that brings widespread attention to EMF toxicity—something I have long believe to be one of the most neglected foundational determinants of health.

Because of the timelines required to bring many of these options to market, decisions will need to be made in the near future to initiate them, and it is my belief the fundamentals behind them are strong enough that if we do not, competitors like China likely will.

The data center issue has been immensely upsetting for me, so I’ve tried my best to come up with realistic solutions to the crisis we are facing and I sincerely appreciate you taking the time to consider them. My hope, in turn, is that this article provided some insightful ideas on how we can tactically respond to the data center push to turn an appalling situation into something we can instead benefit from and I thank each of you for giving me the voice which makes this type of work possible.

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•DMSO is an “umbrella remedy” whose combination of therapeutic properties makes it uniquely suited to treat “incurable” conditions. This article will focus on the extensive evidence DMSO safely eliminates clots, protects the blood vessels, and restores circulation, as impaired blood flow is one of the most common causes of disease but challenging to manage with conventional options.

•DMSO revolutionizes the treatment of strokes, as it not only eliminates the stroke, but also can be started hours earlier than normal treatments and is able to heal the injured tissue that would otherwise be lost. Extensive evidence, and now reader reports show that were it to be widely adopted, millions could be spared from the disability or death they cause each year.

•DMSO is also uniquely suited to treating brain bleeds, traumatic brain injuries, and concussions, as it relieves pressure on the brain while restoring vital circulation and reviving dying brain cells. Extensive evidence and reader reports again show its utility here.

•Because the heart, like the brain, is exquisitely sensitive to its blood supply being cut off, many of DMSO’s properties have also been repeatedly shown to have immense value in heart attacks alongside many other severe heart conditions.

•DMSO has been extensively used for peripheral circulatory disorders, with hundreds of readers, mirroring the existing evidence, reporting it eliminating varicose veins present for decades, dissolving clots and DVTs, restoring color and sensation to blue, purple, or black ischemic limbs, healing venous, diabetic, and pressure ulcers, and resolving Raynaud’s, frostbite, and hemorrhoids, frequently within days.

•This article summarizes the extensive data demonstrating DMSO’s efficacy for circulatory and vascular conditions (approximately 1500 studies and 160 pertinent reader testimonials) and provides practical guidance on DMSO protocols and complementary approaches for the neurological and vascular conditions discussed throughout this series.

Decades ago, I learned that DMSO was an excellent therapy for strokes and then subsequently had numerous experiences where someone I told to take DMSO had their full stroke resolve on the way to the hospital (sparing them from a life of expected disability), after which I started also using DMSO for successful post-stroke recoveries. When you consider both how debilitating strokes typically are and that, for decades, there has been only piecemeal progress on reducing the suffering they cause, it’s hard to put into words how upsetting this has been for me.

So, once I realized I’d stumbled upon being the custodian of a widely read publication, one of my first major projects was to write “The Evidence DMSO Could Save Millions From Brain and Spinal Injury,” which struck the same chord in many readers that it had in me, and was seen by millions (many of whom subsequently shared DMSO saved them from a stroke).

In the process of researching that article and the reader requested ones which followed (on the myriad of other transformational uses for DMSO), I gradually realized that a massive volume of buried DMSO literature existed, and felt that due to the support I’d received from readership here, I had the obligation to make that lost knowledge (and the thousands of reader DMSO testimonials—currently 7,500) widely available.
Note: some of the most dramatic neurological recoveries readers shared (which can be viewed in filmed interviews) include from terminal ALS, terminal bulbar ALS, advanced CJD (the 100% fatal prion disease), sight that had been lost for nearly 75 years, and the same spinal cord injury that left Christopher Reeve on a vent for life.

The fastest way I could see to actually do that was to search the key English and foreign databases for each term for DMSO (rather than every possible keyword combination), then filter out the medically relevant studies and compile them and condense them into articles.

Given how much was there, I was initially unsure if this was possible, but over six grueling months (where I was forced to cut back on everything else and hence published less here), I learned a lot, and with the tools that have never before been available, eventually collected 15,000 summarized studies.
Note: in the process of doing the same for the medical ozone literature base, I recently discovered there is one large DMSO database I missed that will need to be done in the near future.

Once they were compiled, I polled the supporters here on which topics had the most interest, and the overwhelming answer was neurology. On one hand I supported starting there, as most of the therapeutic mechanisms which underlie how DMSO works are interwoven with neurology (and I believe laying out the mechanistic basis for how DMSO works is critical for the therapy’s adoption), but I was also hesitant as this was single most challenging part of the topic to synthesize (due to the ultimately 4,500 studies which would need to be incorporated).

Nonetheless, starting at the end of April, I was able to begin publishing them, and this article, at last, marks the final part of that series. The previous ones, which provided the mechanistic basis for much of what is discussed in this article are as follows:

In this article, I will cover one of DMSO most extensively studied mechanisms: how it works through several well-established anticoagulation pathways to reduce clotting, dilate vessels, protect blood vessels and improve circulation (which works synergistically with its biophysical ability to eliminate micro-clotting discussed in the first part of this series).

Note: if the information in the next section is too dense, you can skip ahead to the “Current Stroke Management” section.

Effects on Platelets

Platelets, the tiny cell fragments that clump together to initiate clotting, are one of the most common targets of blood-thinning medicines (e.g., aspirin) and likewise one of the most thoroughly studied targets of DMSO. Collectively, this evidence shows DMSO independently inhibits platelet aggregation, adhesion, and activation, and most importantly, does so through several converging mechanisms at once.

For example, one study examining the full panel of platelet agonists (the natural triggers that switch platelets on) found DMSO inhibited human platelet aggregation induced by ADP, adrenaline, arachidonic acid, collagen, and PAF, with the strongest effect against ADP. Multiple independent groups, in turn, have reproduced these results.^1,2,3

Likewise, across studies, DMSO has been found to inhibit platelet aggregation (clumping) triggered by ADP, epinephrine (adrenaline), arachidonic acid, collagen, thrombin, and platelet-activating factor, in a concentration-dependent manner, with ADP-induced aggregation typically the most sensitive to DMSO.^1,2,3 At the level of activation markers, DMSO-containing systems suppress the surface proteins that report a platelet has “switched on”—P-selectin (CD62P), PAC-1, GPIIb/IIIa, CD63, and platelet factor 4 (PF4)—and reduce the release of ATP and dense-granule contents.1 DMSO also directly binds platelet factor 4, disrupting its aggregation at the molecular level.

Note: these effects are concentration and time dependent. At the low-to-moderate concentrations relevant to therapeutic use, the antiplatelet effect reverses once DMSO is washed out—consistent with DMSO's rapid diffusion out of cells, which is why platelets cryopreserved in DMSO lose adhesion and aggregation during cold storage yet regain functionality once thawed and infused.^1,2 At the higher concentrations or longer exposures reached only outside normal use, the inhibition can persist even after removal,¹ reflecting a more durable structural change. However at the higher doses, such as the concentrations reached after a DMSO-cryopreserved cell infusion (0.2–0.6%), DMSO still measurably inhibits ADP, thrombin, and TRAP-induced platelet aggregation,^1,2 frequently causes transient circulating coagulation inhibitors and prolonged clotting times¹,² and at high topical doses can modestly lower the circulating platelet count.¹

•DMSO selectively inhibits cyclooxygenase-1 (COX-1) and thromboxane A₂ synthase,^1,2 (e.g., 0.5% DMSO reduced total COX activity by 36%¹) cutting production of thromboxane A₂ (the potent signal platelets use to recruit one another). Adding the synthetic thromboxane analogue U46619 restored platelet aggregation despite DMSO’s presence,¹ confirming that DMSO’s suppression of aggregation runs through the thromboxane pathway.

•DMSO raises intracellular cAMP and cGMP (the secondary messengers that hold platelets in the resting state) providing a thromboxane-independent brake on platelet activation.

•Because DMSO restructures the water in and around the cell membrane (detailed here), it alters membrane fluidity directly, desensitizing platelets to their agonists independent of COX-1—an effect visible under the microscope as a marked reduction in the filopodia platelets extend when activating.¹ This biophysical membrane action also likely explains DMSO’s suppression of shear-induced platelet activation,¹ where DMSO cut platelet adhesion under flow to roughly a fifth of control,¹ and connects to the same phase-transition effects DMSO exerts on the platelet membrane’s phospholipids.¹ A separate study of platelets forced through the non-physiological shear stresses generated by mechanical heart-assist devices found the same protection, and in a revealing pattern that mirrors the concentration-dependent membrane stages described earlier: low concentrations of DMSO sharply reduced shear-induced activation, while the effect reversed at higher concentrations as DMSO began permeabilizing the membrane—and DMSO-treated platelets, though shielded from mechanical activation, still responded normally to chemical agonists, confirming it desensitizes platelets to physical force rather than simply disabling them.¹ Notably, in that same body of work the conventional antiplatelet drugs, designed to block platelets through specific chemical pathways, were overwhelmed by these device-level physical forces, whereas DMSO, acting on the membrane itself, was not.¹ At higher concentrations this progresses to increased membrane permeability, at which point DMSO releases the platelet’s internal contents through a mechanism distinct from thrombin’s.¹

•DMSO reversibly inhibits platelet serotonin uptake, thereby (reversibly) reducing the amount of serotonin stored in (and later released from) dense granules that is available to amplify platelet aggregation.¹

•Since hydroxyl radicals trigger platelet serotonin release and aggregation, DMSO’s extensively documented scavenging of these radicals¹ blocks radical-mediated platelet activation¹ and thrombus (clot) formation.¹ In living microvessels, this was directly visualized: intraperitoneal DMSO more than doubled the time to platelet aggregation in injured mouse brain pial arterioles (117 vs. 57 seconds), and in the same vessels prevented the reactive arteriolar dilation that normally accompanies the injury (holding their diameter near baseline versus a 22% widening in controls).¹ As such, DMSO’s radical-scavenging action, in addition to reducing inflammation, also produces both an antiplatelet and a vasomotor effect simultaneously.

Note: as each of these effects is concentration dependent, not every study finds an effect on every pathway (e.g., one group reported DMSO did not inhibit thromboxane production in platelets and did not protect rabbits from arachidonic-acid–induced pulmonary thrombosis^1,2).

These effects, in turn have been demonstrated their utility in a variety of living systems:

•In a dog model of critical coronary stenosis (where platelets aggregating at a narrowed artery routinely cause cyclic drops in coronary blood flow) intravenous DMSO dose-dependently reduced (by up to 85%) those flow reductions without altering blood pressure, heart rate, or cardiac output, isolating the effect to platelet aggregation itself.¹

•In a rat carotid-injury model, IV DMSO (2 g/kg) virtually abolished thrombus formation despite clear endothelial damage, with electron microscopy showing only spherical, non-activated platelets where clots should have been.^1,2
Note: because the clotting was prevented at a site of genuine vessel injury, these results¹ are applicable to settings like microvascular and reattachment surgery, where a damaged vessel must stay patent long enough to heal.

Finally, DMSO’s effects on platelets (inhibition of aggregation and suppression of activation markers such as P-selectin, PAC-1, GPIIb/IIIa, and PF4) have also been observed when DMSO has been combined with a variety of natural compounds (which for reader ease I mark with ^⬖) such as xanthohumol,^⬖ wine polyphenols,^⬖ Ginkgolide B,^⬖ and vitexicarpin.^⬖

One of the more unusual reports came from a Russian practitioner combining DMSO with aspirin in "structured water," across a range from conventional doses down to ultra-low dilutions. Using nocturnal leg cramps in the elderly as a readout, he reported that conventional doses reliably prevented recurrence — cramps returned on withdrawal and stopped again on resumption — with the effect persisting even as aspirin was diluted roughly a thousandfold, becoming borderline around the nanogram range (~10⁻⁹) and disappearing by ~10⁻¹². He also described rapid relief in acute vascular events such as heart attack and stroke.¹

Anticoagulant & Fibrinolytic Effects

DMSO also acts directly on the coagulation cascade itself, and does so at nearly every level (the initiating trigger, the central enzyme thrombin, and the fibrinolytic system that dissolves clots once they form) giving DMSO a breadth of anticlotting activity that few single agents possess:

•Tissue factor (TF) is the key protein that ignites the entire clotting cascade (and is a critical link between inflammation and thrombosis). DMSO, in turn, suppresses TF expression and activity by inhibiting JNK and p38 MAP kinase signaling and prevents arterial thrombus formation in living animals, without detectable toxicity.^1,2 Because it simultaneously reduces the smooth-muscle overgrowth that causes stents to re-occlude, DMSO has been repeatedly proposed as a drug-eluting stent coating due to it being a rare agent that both lowers clotting risk and restenosis risk (unlike conventional stent drugs like sirolimus and paclitaxel, which reduce restenosis but increase TF expression and thrombosis risk).^1,2,3

•DMSO also acts on the coagulation enzymes themselves. It directly alters thrombin, the central clotting enzyme, changing its catalytic behavior through a conformational shift and—notably—reducing heparin’s ability to inhibit it.¹ In the invertebrate clotting systems used as sensitive models of the cascade, DMSO reversibly blocked the activation step that switches on the dormant clotting zymogen (enzyme precursor), without inhibiting the already-active enzyme, in both the Limulus and Carcinoscorpius systems (highly sensitive clotting cascades)^1,2—indicating DMSO acts on the trigger that starts the clotting cascade.

DMSO hence not only prevents clots from forming but, when applied topically, actively dissolves already-established venous thrombi while inhibiting arterial platelet thrombus formation. Finally, in a rat carotid-artery injury model intravenous DMSO eliminated thrombus formation at both crush and incision sites despite clear endothelial damage. Electron microscopy showed only minimal platelet-fibrin deposits and, spherical, non-activated platelets where clots should have formed (with DMSO’s antithrombotic effect statistically superior to the barbiturates and methylprednisolone tested alongside it).

Its ability to eliminate clots already present appears to be due to it augmenting the body’s natural clot removal pathways as DMSO activates streptokinase-initiated fibrinolysis across a wide concentration range (1.5–50%), stimulates production of tissue plasminogen activator (tPA), the body’s principal clot-dissolving enzyme and reduces plasminogen activator inhibitor-1 (PAI-1), the main physiological brake on that process.

This is cited so consistently that “fibrinolytic activity” appears as a standard listed property of DMSO throughout the clinical literature,^1,2,3,4 or as described by a Russian review: intravenous DMSO lengthens clotting time, suppresses platelet aggregation (initial clot formation), normalizes fibrin formation (clot solidification), and being fibrinolytic, normalizes fibrinolysis.¹

All of this touches on a key contrast I’ve noticed between pharmaceutical drugs and effective natural therapies. Pharmaceuticals tend to target a single pathway (or a few) as forcefully as possible, which produces both their immediately evident effects and, frequently, significant side effects. Time-tested natural agents instead often nudge many pathways at once toward a converging end, making them less immediately potent (their effect being distributed rather than concentrated) but also much better tolerated and often longer-lasting, since the body doesn’t develop the reflexive tolerance it mounts against a pathway being aggressively shifted in one direction.

Note: as with many of DMSO’s effects, its fibrinolytic action normalizes rather than simply pushing one direction—in cancer cells it suppressed urokinase-type plasminogen activator (uPA—which facilitates metastasis), the reverse of its tPA-stimulating effect in normal cells, consistent with DMSO restoring dysregulated systems toward baseline.

Clinically, this translates to DMSO improving coagulation across a broad range of situations. For example, in 42 patients with rheumatic diseases (including scleroderma and Raynaud’s), blinded thromboelastography showed DMSO normalized both fibrin formation, with accompanying improvement in microcirculation. Likewise, DMSO added to sepsis, endotoxemia, and disseminated-intravascular-coagulation models and paired with a long and chemically unrelated list of agents, has repeatedly reduced elevated fibrinogen and corrected the underlying coagulopathy.^1,2,3,4,5 Similarly, DMSO appears in numerous topical thrombosis and thrombophlebitis formulations where it both facilitates the delivery of and synergistically enhances the effects of the other anti-thrombotic agents present.¹

Note: DMSO’s broad range of effects also allows it to treat challenging clotting situations. For example, when the immune system breaks down myelin, the exposed phospholipids in the debris can trigger clotting that starves nerves of blood (a proposed secondary driver of multiple sclerosis) and while conventional anticoagulants don’t touch this pathway, a Russian study found DMSO inhibited myelin-triggered clotting dose-dependently.

DMSO and Blood Thinners

In medicine a balance often has to be struck between a therapeutic effect and the toxicity it entails, and getting it right can be quite challenging, such as in ensuring chemotherapy kills enough cancer cells without killing too many normal ones. Blood thinning poses another version of this problem: coagulation can predispose someone to severe complications (e.g., embolic strokes), but too little of it is also dangerous, since a minor injury can then produce a large hematoma and a blow to the head a lethal brain bleed.

For this reason, medicine typically reserves anticoagulants for those already at risk of clotting complications, as in atrial fibrillation, where the irregular rhythm lets clots form in the heart that can then travel to the brain and cause a stroke. It then tightly controls the degree of anticoagulation, doing enough to prevent the major event without raising bleeding risk any more than necessary. However, this is still far from perfect. Many individuals experience significant complications from anticoagulants each year, partly from incorrect dosing or monitoring, and partly because a perfect balance between preventing thrombosis and avoiding bleeding simply cannot always be achieved in the individual patient. All of this hence raises a few questions regarding DMSO.

First, can natural “anticoagulants” with a broader spectrum of action be used in lieu of the more potentially dangerous anticoagulants? Ultimately this is a difficult question to answer, as understandably, no clinician I know has taken the risk to attempt this in high risk situations (e.g., atrial fibrillation) and see if it suffices to stop the clotting (whereas gargantuan sums of data were needed to accurately assess the merit of pharmaceutical anticoagulants). However, in lower risk situations (e.g., preventing a heart attack over the next twenty years, or improving chronic illness symptoms resulting from excessive blood clotting), I have seen the natural alternatives perform extremely well without significant risk. Likewise, in acute situations (e.g., a heart attack or stroke), I have seen numerous cases where they (e.g., DMSO or a zeta potential restoration) resolved the incident prior to conventional options arriving. A few readers, in turn, have shared stories like quitting a problematic lifelong Eliquis prescription, noting DMSO not only prevented clots from forming but also dissolved existing ones and that “I’d be dead if DMSO didn’t work.”¹ I, however, do not think this is wise, as the data simply does not exist to determine if this is appropriate to do, and as such, I instead favor the natural anti-clotting approaches in cases where it seems likely someone would benefit from blood thinning but their inherent risk of a severe clotting complication is too low to justify conventional anticoagulation.
Note: while safer than conventional anticoagulants, many of the natural anticoagulants are still not completely safe (e.g., since mass consumption of generic nattokinase^⬖ came into vogue to counteract the spike protein, I have periodically come across cases of them causing a problematic bleed both within my social circle and from readers here).

Second, since DMSO potentiates the actions of pharmaceutical medications, is it safe to take with other anticoagulants? Presently, there is simply not enough data to answer this, but from everything I’ve been able to find, I lean to “yes,” with three major caveats: DMSO cannot be taken within at least two hours of the anticoagulant, coagulation must be carefully monitored to ensure excessive anticoagulation is not occurring (which should happen anyways) and IV DMSO should never be mixed with an anticoagulant in the same infusion. The limited datapoints I have to go off for this assessment are that:

•The German DMSO community, which has the most experience combining DMSO with conventional anticoagulants, considers this acceptable, citing patient reports, existing data that DMSO does not competitively inhibit clotting factors or irreversibly block platelet prostaglandins the way pharmaceutical anticoagulants do, and that in practice no meaningful changes in Quick-Wert (PT activity %) or INR values appear in patients on anticoagulants who use DMSO—although they did note DMSO can reduce the dose of aspirin (which targets platelets rather than the coagulation cascade), with multiple users “switching to 50 mg every other day and their coagulation values still being ‘as desired.’” That said, they still advise starting DMSO slowly, routinely checking coagulation values, and spacing it out from anticoagulants taken during the day.
Note: in the previously mentioned Russian study (where very limited information was provided), DMSO was reported to work synergistically with aspirin and no toxicity was mentioned from this combination.¹

•DMSO–heparin combinations have a long track record of safety in topical and oral formulations. DMSO enhances heparin’s anticoagulant action and, through its membrane-transport properties, can even render heparin orally absorbable when the two are formulated together (rather than via the injection typically required for heparin). Likewise, the commercial gel Dolobene (Долобене), which combined DMSO with heparin has been widely used for decades without issues (as has Phlebolan spray, although only certain Phlebolan formulations contained heparin).
Note: Jim McCann (the inventor who brought the DMSO hematoxylin cancer therapy to Ecuador) emphasized that he had seen serious bleeding issues when IV DMSO was combined with IV heparin.

•Due to the size of the readership of this newsletter, I've had a unique window for identifying rare complications of DMSO, so over the last two years, I've kept a careful eye out for bleeding incidents linked to DMSO, of which a few reported nosebleeds after DMSO, a reader who'd used topical DMSO and then had a shoulder surgery cancelled because their PTT was 71,¹ a friend on Eliquis whose small finger cut bled for two hours,¹ and a reader I reached out to after learning they developed a GI bleed, which we concluded may have been linked to them taking a high oral DMSO dose concurrently with a high dose of nattokinase^⬖ twice a day.
Note: conversely, many readers have also reported bleeding wounds healing with DMSO.

•The existing literature indicates at low doses (which is what can realistically be reached in the body from most uses), DMSO does not meaningfully affect standard clotting parameters at all (e.g. 1.1% did not affect clotting in a zebrafish model¹ and 0.1% had no effect on human plasma PTT¹). Conversely, at higher IV doses, according to one Russian review, DMSO (10–20%) lengthens clotting and bleeding time, decreases platelet aggregation and increases fibrinolysis,¹ while at even higher IV doses, promotes coagulation (e.g., ≥20% precipitates fibrin and consumes fibrinogen¹ and ≥50% in monkeys caused instant hemolysis and fibrinogen precipitation alongside transiently shortening PTT¹).
Note: due its safety, much higher doses of DMSO are routinely tested than most other agents, and as a result, toxicity often only shows up at DMSO concentrations orders of magnitude higher than most drugs. In tandem, because of how rapidly DMSO spreads through the body and dilutes, unless high IV doses are used or concentrated DMSO in ingested, it is quite difficult to reach DMSO’s toxic concentrations.

•Within the IV stem cell literature, complications are periodically reported from high dose DMSO infusions given to frail cancer patients, in the studies which looked at this, a small, transient increase in blood clotting was typically observed.^1,2 Conversely, one case report exists of two elderly patients receiving IV DMSO then developing shortened prothrombin and partial-thromboplastin times (where the clinicians concluded this was likely due to quinine, indomethacin, or a phenothiazine being taken concurrently as they had not seen anything similar in comparable patients receiving IV DMSO).¹ Additionally, from extensive review I was able to find three other cases exist where DMSO was linked to a problematic bleed,^1,2,3 which given their rarity, makes it difficult to determine if DMSO or another variable was the causative factor.
Note: while DMSO in general helps CNS (e.g., brain) conditions, IV DMSO produces the most dramatic improvements. I initially thought this was likely due to more DMSO being able to reach the CNS, but now suspect it might be due to direct anticoagulation occurring alongside DMSO’s other effects.

•At lethal or near-lethal doses (far above ordinary use), especially concentrated IV DMSO, animal studies often show hemolysis plus pulmonary or GI hemorrhage.¹ Much of the hemolysis and some fluid-shift injury is osmotic and can be produced by other strongly hypertonic infusions at similar osmolar loads. DMSO’s high LD50 (toxic doses) is why those concentrations are reachable at all, as typically a different toxicity of a drug would make it lethal far below the levels needed for osmotic damage to occur.

In short, excessive bleeding on DMSO appears to be rare and when it does occur, typically mild. Nonetheless, if anticoagulants are being taken, care must be taken to ensure coagulation parameters are routinely monitored and DMSO is not directly combined with any of them.

Note: the consistent finding across decades of animal safety studies is that diluted DMSO is remarkably well-tolerated, and that its one dose-dependent liability on the blood is transient hemolysis at high intravenous concentrations. Rhesus monkeys given intravenous DMSO at 3 g/kg (as a 40% solution) daily for nine consecutive days showed no significant or lasting changes in blood chemistry, hematology, urine, or ocular, neurological, and cardiovascular parameters over four months of follow-up. Cats given intravenous DMSO every other day across ten doses maintained normal hematology and biochemistry throughout, with no cumulative or delayed adverse effects, and a DMSO-containing mixture fed chronically at up to five times the therapeutic dose produced no adverse changes (if anything, hematologic parameters improved). The primary issue repeatedly seen is that highly concentrated intravenous DMSO has been associated in older toxicity reports with local vascular irritation and transient hemolysis (e.g., 10% intravenous DMSO given to horses produced a transient dip in red-cell and hemoglobin counts that recovered within 24–48 hours).

Effects on Prostaglandins & Thromboxane

Prostaglandins and thromboxane are the short-lived signaling molecules the body makes from arachidonic acid (via the cyclooxygenase, or COX, enzymes) to control clotting, vascular tone, and inflammation. The system has two opposing sides, thromboxane A₂ (TXA₂), which drives platelet aggregation and vasoconstriction and prostacyclin (PGI₂) and PGE₁, which do the reverse, dispersing platelets and dilating vessels. As such, the balance of these heavily influences whether blood clots and vessels constrict, or blood flows and vessels open.

DMSO is often described as a prostaglandin inhibitor (an aspirin-like agent that blocks COX) as for platelets, DMSO selectively inhibits COX-1 and thromboxane A₂ synthase,^1,2 cutting TXA₂ production and in cholesterol-fed rabbits, DMSO lowered arterial atherosclerosis, an effect attributed to its reduction in platelet thromboxane B₂ (a stable marker of TXA₂) while prostacyclin was untouched.¹ So, since DMSO raises PGE₁ and cAMP while decreasing thromboxane and fibrinogen,¹ it shifts the balance towards reducing clotting and dilating vessels.

Note: the fuller picture is more complex than “DMSO blocks COX,” as data shows DMSO is not uniformly a prostaglandin-synthesis inhibitor. In one study it increased arachidonic-acid oxidation rather than inhibiting it, didn’t suppress thromboxane, and led its authors to propose it acts as a reducing cofactor rather than a blocker.¹ Another found DMSO had no effect on thromboxane yet stimulated PGE₂ and concluded DMSO’s anti-inflammatory action doesn’t run through an arachidonic-acid metabolism at all.¹ On skin, DMSO releases prostaglandins and arachidonic acid into the tissue¹ (much as histamine does), while in cultured aortic endothelial cells it actually inhibited prostacyclin.¹ All of this argues that DMSO doesn’t switch the eicosanoid system off but rather rebalances it, with the net effect in platelets and vessels tilting toward the antithrombotic, vasodilatory side (consistent with DMSO’s broader tendency to normalize dysregulated systems rather than force them one way). Likewise, as we’ve seen before, the effect is also context-dependent, as in some models DMSO adds nothing, and did not improve sevoflurane’s cardioprotection when tested on its own.

Finally, DMSO has also been used to therapeutically deliver beneficial prostaglandins. In one report, topical PGD2 combined with DMSO was used to save digits (fingers or toes) that would otherwise be lost from acute inoperable thrombosis,¹ and has been used to deliver agents that act upon this system (e.g., tetrahydroxystilbene^⬖1 and curcumin^⬖1 to relax the superior mesenteric arteries and arterioles).

Raising cAMP & cGMP

Two closely related molecules cyclic AMP (cAMP) and cyclic GMP (cGMP), once elevated, in platelets, reduce their aggregation and in vascular smooth muscle trigger vessel relaxation and widening.

DMSO raises cAMP through both increasing its production and by slowing its breakdown. On one hand, DMSO directly stimulates adenylate cyclase,^1,2,3 the enzyme that synthesizes cAMP; in heart tissue this stimulation was maximal at around 10% DMSO, comparable in magnitude to the beta-agonist isoproterenol and additive with it—yet DMSO’s effect was unaffected by α- or β-adrenergic blockade, meaning it works independently of the adrenergic receptors those drugs act on.¹ DMSO also was found to inhibit cyclic AMP phosphodiesterase¹ (the enzyme that degrades cAMP), which would further raise cAMP levels.

As such, in platelets DMSO significantly raises both cAMP and cGMP (through a channel entirely separate from its COX-1 inhibition), further supporting its antiplatelet effects.¹ In blood vessels, DMSO likewise raises cGMP and relaxes the vessel wall through a nitric-oxide/cGMP-dependent pathway.¹

Note: like DMSO’s other effects, this one is concentration-dependent and not universal—at lower concentrations or in certain tissues DMSO showed no measurable effect on the cyclase system.^1,2,3

Opening Blood Vessels (Vasodilation)

Blood flow is controlled by smooth muscle surrounding the lining (endothelium) of the blood vessels, which tightens to restrict flow. As such, DMSO’s ability to relax that muscle provides another key way for it to restore tissue circulation. DMSO’s circulatory-promoting properties turn up across nearly every vascular bed studied (e.g., aorta, coronary, pulmonary, mesenteric, renal, cerebral, umbilical, and saphenous) both relaxing vessels by itself and serving as the medium through which other vasodilators are delivered without impeding their effect.¹,²,³,⁴

In the aorta, DMSO produced a concentration-dependent relaxation of contracted aortic rings through an endothelium-dependent pathway (via nitric oxide and cGMP), and an endothelium-independent one that inhibits calcium channels in the smooth muscle and reduces the muscle’s sensitivity to calcium (partly via Rho-kinase).^1,2 Likewise, in another study, DMSO relaxed aortic rings by 42-99% and renal arteries by 80% (in part through voltage-gated potassium channels),¹ in another DMSO relaxed mesenteric artery preparations, and in drug references, vasodilation is one of dimexide’s (DMSO) recognized pharmacological properties.¹
Note: since one of DMSO’s relaxing effects acts directly on smooth muscle, it likely can work on damaged vessels where the endothelium is no longer responsive to stimuli.

Additionally, part of DMSO’s local vasodilation is histamine-mediated—the same mechanism behind the warmth and flushing people often feel where DMSO is applied. Importantly, this is a controlled dilation rather than tissue injury, as when DMSO was injected into a limb, it markedly increased lymph flow while the protein content of that lymph fell (the opposite of what happens with a burn or a caustic agent, where protein rises) and tissue examination showed only vasodilation and occasional edema, but no cell necrosis (death).¹ DMSO hence opens vessels and shifts fluid without damaging the tissue.

Note: combined with hydrogen peroxide as an oxygen source, topical DMSO raised skin-flap survival to 92% versus 71% in controls, an effect the authors attributed partly to DMSO’s vasodilatory, histamine-like action.¹

DMSO and Nitric Oxide

The classic way a blood vessel dilates is that the endothelium produces nitric oxide, which diffuses into the surrounding smooth muscle and triggers relaxation there through cGMP. For this reason, many integrative cardiovascular health approaches focus on supporting endothelial nitric oxide production.

Much of DMSO’s own vasorelaxation runs through the nitric oxide/cGMP pathway as in isolated aorta, DMSO’s relaxation is blunted by removing the endothelium or by blocking nitric oxide synthase with L-NAME, while conversely, DMSO raises tissue cGMP the downstream marker of nitric oxide signaling¹ and at 10% redistributed intracellular nitric oxide into mobile membrane vesicles.¹

Furthermore, since DMSO effectively scavenges reactive oxygen species (which cripple the endothelium’s ability to make and use nitric oxide), DMSO is able to preserve the ability of blood vessels to dilate (e.g., protected against cigarette-smoke-induced impairment of nitric oxide production and vasodilation in rabbit aortas and human endothelial cells)¹ and, from the opposite direction, DMSO's radical scavenging restored an endothelium-dependent, nitric-oxide–mediated relaxation that iron had blocked in aortic rings.¹

Simultaneously, DMSO can counteract nitric oxide when it’s excessive, both by scavenging it directly (DMSO scavenges radicals including nitric oxide), as when IV DMSO in horses modestly raised systolic blood pressure,¹ and by throttling its production, as when 2.5–3.5% DMSO (but not 1%) cut endothelial nitric oxide output¹—an effect reversed by adding extra arginine (a common supplement used to enhance nitric oxide production).

Collectively, this suggests that DMSO normalizes nitric oxide function, both by preserving it when it would otherwise be impaired, but also by counteracting it if it becomes excessive and harmful (as at low doses, DMSO typically does not affect nitric oxide).

Finally, DMSO has also been used to deliver agents which preserved or restored nitric oxide mediated relaxation such as resveratrol,^⬖1,2 hesperidin,^⬖ (reducing hyperhomocysteinemia-induced cognitive deficits),¹ thymoquinone,^⬖1 red-clover isoflavones,^⬖1 genistein, ^⬖1,2,3,4 (e.g, for fructose-fed hypertension¹) methylated quercetin flavonoids and phenylbutanoids,^⬖1 Bacopa monnieri flavonoids and saponins,^⬖1 tetrahydroxystilbene glucoside,^⬖1 astragaloside IV,^⬖1 cinnamaldehyde,^⬖1 Jasminum sambac extract,^⬖1 ursolic acid,^⬖1 Acer okamotoanum sap,^⬖1 phloridzin,^⬖1 adenosine,^⬖1 a Periplaneta americana metabolite,^⬖1 a polyphenol nutraceutical,^⬖1 the soluble guanylate-cyclase activator cinaciguat,¹ the PPAR-γ agonist rosiglitazone,¹ 17β-estradiol,^1,2 a STAT3 inhibitor,¹ a selective adenosine kinase inhibitor,¹ a PPAR-α agonist,¹ and an angiotensin peptide analog.¹

Counteracting Oxidative Constriction

A large body of literature shows DMSO’s free-radical scavenging (discussed below) protects a wide range of blood vessels from the constriction and endothelial dysfunction caused by oxidative stress, hence keeping vessels from closing down:

• In the aorta, it nearly completely prevented ROS-induced vasoconstriction and preserved endothelial and contractile function¹ and attenuated hydroxyl-radical- and H₂O₂-induced contractions,¹ and it protected platelet-mediated, endothelium-dependent relaxation from hydroxyl-radical damage.¹

• In coronary arteries, it protected endothelium-dependent relaxation from radical-induced dysfunction,¹ and it preserved CGRP-mediated neurogenic relaxation of arteries under oxidative attack.¹

• In pulmonary and cerebral vessels, it reduced hypoxic pulmonary vasoconstriction by lowering oxygen-radical release,¹ and, as a reducing agent, inhibited and reversed the vasoconstriction that oxidizing agents such as peroxide and silver nitrate induce in rat aortas and dog basilar arteries.^1,2

Lastly, DMSO also shielded endothelial cells from the injury driven by infection and its toxins, including bacterial endotoxins¹ and Pseudomonas aeruginosa¹ products.

Note: DMSO’s direct vasorelaxation is concentration-dependent so at the higher concentrations DMSO reaches its own clear relaxing effect, but at the low concentrations used in many solvent experiments, it frequently shows no measurable effect on vascular tone.^1,2,3

Free Radical Scavenging

Free radicals are atoms or molecules that contain one or more unpaired electrons, which makes them highly reactive and potentially damaging to tissues such as fats, proteins, and DNA. DMSO’s most well-recognized property is its ability to scavenge (neutralize) free radicals—particularly the hydroxyl radical, one of the most damaging reactive species, of which DMSO is among the best-known scavengers (there are 135,000 results on Google Scholar for “DMSO radical scavenger”). Its reaction with the hydroxyl radical, in fact, is so reliable that DMSO is used as a standard molecular probe for detecting and quantifying hydroxyl radicals in biological systems as the hydroxyl converts DMSO into a stable, easily measured marker.^1,2

Note: two of the most commonly observed (and studied) scavenging effects of DMSO are its reduction of free-radical-induced lipid peroxidation and its preservation of the body’s own antioxidant enzymes.¹ Additionally, DMSO’s radical scavenging is dose dependent,¹ can directly suppress hydroxyl-radical production in solution,¹ and delivers vascular protection other approaches cannot—in a cobra-venom model of complement-driven vascular injury, it prevented the microvascular damage (capillary congestion and leukocyte plugging) that cyclooxygenase inhibitors, an iron chelator, and a thromboxane synthetase inhibitor all failed to touch.¹

Since the thin lining of the blood vessels (the endothelium) is highly vulnerable to oxidative damage, DMSO’s ability to scavenge radicals has shown a variety of key therapeutic effects including:
•Preventing endothelial dysfunction and preserving vessel dilation.¹
•Protecting aortic endothelial cells from radical-triggered programmed death.¹
•Blocking the reactive-oxygen signaling that switches on the adhesion molecules (ICAM-1, VCAM-1, E-selectin) endothelial cells use to catch and recruit inflammatory white cells (detailed here) largely by inhibiting the master inflammatory switch NF-κB—thereby preventing those white cells from sticking to the vessel wall, plugging the smallest vessels and causing the microstrokes which underlie many illnesses (e.g., vaccine injuries).
•Blocking the radical-driven stiffening of endothelial cells that would otherwise impair blood flow.¹

As such, many studies have shown DMSO protects the endothelium from oxidative stress and free radical injury.^{1,2,3,4,5,6,7,8,9,10, 11,12,13,14,15,16,17,18,19,20, 21,22,23,24,25,26,27,28,29,30, 31,32,33,34,35,36,37,38,39,40, 41,42,43,44,45,46,47,48,49,50, 51,52,53,54,55,56,57,58,59,60, 61,62,63,64,65,66,67,68,69,70, 71,72,73,74,75,76,77,78,79,80, 81,82,83,84,85,86,87,88,89,90, 91,92,93,94,95,96,97,98}

In addition to neutralizing the free radicals that constrict vessels and injure the vessel wall, DMSO protects against a second wave of radical damage: when a vessel’s blood flow is cut off and then restored, the oxygen-starved (ischemic) tissue converts the returning oxygen into a burst of radicals, creating a “reperfusion injury” that often exceeds the damage from the initial blood loss. As such, in virtually every part of the body (particularly the central nervous system), DMSO has been repeatedly shown to protect organs and tissue from oxidative stress and otherwise devastating reperfusion injuries.^1,2,3

For example, DMSO:
•Significantly reduced the microcirculatory vascular leakage caused by a radical-generating system in hamster cheek pouches.¹
•Reduced vascular permeability and edema in thermally burned skin.¹
•Protected dermal microvessels from burn injury.¹
•Reduced vascular permeability, edema, and tissue injury in gut and mesenteric ischemia-reperfusion, performing comparably to the antioxidant enzymes superoxide dismutase and catalase.^{1,2,3,4,5,6,7,8}
•Reduced damage in hemorrhagic shock and ischemic gastric injury.^{1,2,3,4,5,6,7,8,9,10}
•Protected the lung and pulmonary vasculature from radical injury.^1,2
•Prevented the secondary lung injury that radicals inflict on distant organs after a period of hind-limb ischemia.¹
•Reduced endotoxin- and shock-driven organ injury.¹
•Improved skin-flap and free-tissue survival by blunting reperfusion radical injury.^1,2
•Protected the liver during cold-ischemic preservation.^1,2
•Used to counteract the reperfusion radical injury implicated in equine laminitis.^1,2,3,4

Note: in many cases, these protective effects are dose-dependent (e.g., in a rat limb ischemia-reperfusion the dose used only gave partial protection,¹ while in a lung toxin model, a fairly high dose was needed to provide protection¹).

Protecting the Endothelium

The innermost surface of the endothelium is coated with the glycocalyx, a fragile, sugar-rich gel layer that regulates permeability, shields the cells from shear, and keeps clotting and inflammation in check. In shock, sepsis, and reperfusion, this layer is stripped away (”shed”), and its loss is now recognized as an early, pivotal event in vascular collapse.
Note: sulfates are one of the most effective biological molecules for restoring (vital) zeta potential. The glycocalyx is structured so that abundant sulfates on it form a (continually regenerating) liquid crystalline gel around the glycocalyx which repels other substances from entering the endothelium and independently drives blood circulation (all of which is detailed here)—making the glycocalyx one of the most critical components of cardiovascular health.

Many studies, in turn, show DMSO protects the glycocalyx along with the underlying endothelium:

•In a mouse model of LPS-induced acute respiratory distress, systemic DMSO preserved the pulmonary endothelial glycocalyx (staining intensity roughly four times that of untreated injury), cut protein leak into the airspaces, and reduced inflammatory cell counts; in human endothelial cells it prevented glycocalyx shedding by blocking the enzyme (a matrix metalloproteinase) that cleaves it from the cell surface.¹

•In a rat hemorrhage-resuscitation model, DMSO reduced glycocalyx shedding and the accompanying coagulopathy.¹

•At the level of the underlying matrix, DMSO restored the normal structure of heparan-sulfate proteoglycan in endotoxin-exposed endothelial cells,¹ and prevented endotoxin-induced lung protein leak while preserving the endothelium’s ability to relax.¹

•DMSO also inhibited apoptosis in nutrient-deprived human endothelial cells by promoting DNA replication and survival,¹ and protected them under oxidative stress by raising heme oxygenase-1 and reducing apoptosis through several cytoprotective pathways.¹

•In the equine ascending colon, DMSO protected against the capillary permeability changes caused by ischemia-reperfusion injury.1

Note: DMSO has also been used in combination with a variety of agents to promote endothelial growth and repair (e.g., in studies of endothelial proliferation, migration, tube formation, differentiation, and progenitor-cell-driven revascularization). Agents combined with DMSO to create these effects on the endothelium include: curcumin, ^⬖1 resveratrol,^⬖1 luteolin,^⬖1 kaempferol,^⬖1 diosgenin,^⬖1 icariin,^⬖1 arnebin-1,^⬖1 celastrol,^⬖1 dihydroartemisinin,^⬖1 alkannin,^⬖1 sulforaphane,^⬖1 ginsenoside Rg3,^⬖1 Illicium henryi extract,^⬖1 dracorhodin,^⬖1 onychin,^⬖1 Echinacea extract,^⬖1 13-cis retinoic acid,¹ fluvastatin,¹ simvastatin,¹ atorvastatin,¹ dihydrotestosterone,¹ recombinant proteoglycan-4,¹ sirolimus¹ rapamycin,¹ a demethylating agent,¹ a Kir2.1 blocker,¹ or a JAK2 inhibitor.¹

Current Stroke Management

Roughly 3.1% of adult Americans have experienced a stroke (a figure I expect to rise from the COVID-19 vaccines). Each year, this translates to about 800,000 people in the United States having a stroke, and in 2022, 165,393 died (making it the fifth most frequent cause of death in the United States), with between 20-40% of survivors experiencing long term disability from the stroke.

Because of the harm strokes pose to society, and the rate at which brain tissue deteriorates once its blood supply is lost, the medical system emphasizes doing everything that can be done to treat strokes as soon as possible. Unfortunately, there is a fundamental limitation to how strokes are addressed which makes it impossible to ever eliminate the immense toll strokes place upon society.

This is because three types of strokes exist, ischemic strokes (which are typically caused by a blood clot obstructing the artery), a brain hemorrhage (where bleeding is both directly toxic to sensitive brain tissue and creates large blood pockets that compress and damage the brain), and transient ischemic attacks (TIAs)—which are not classically considered strokes.
Note: TIAs occur when someone shows clinical signs of a stroke that resolves on its own (and typically does not have stroke imaging findings). I believe TIAs often represent microstrokes occurring (as the microclots are too small to be seen with conventional brain imaging and typically resolve on their own)—a subject I went into much more detail here as these visually detectable microstrokes frequently underlies vaccine injuries and many other chronic illnesses.

The essential challenge with managing strokes is that it’s nearly impossible to reliably differentiate an ischemic stroke from a hemorrhagic stroke without imaging (we’ve tried for a longtime, and while there are a few diagnostic signs that suggest one or the other, they are not reliable enough for the degree of certainty required). This matters because opposite approaches are taken to ischemic strokes and hemorrhagic strokes—with ischemic strokes a powerful clot busting medicine (tPA) is used to restore circulation, whereas with hemorrhagic strokes (13% of strokes in the developed world), a variety of steps are taken to reduce further bleeding in the brain (which can include brain surgery).

As such, when a stroke occurs, while it is urgent to treat it as soon as possible (as “time is brain”), the standard approach (tPA) cannot be used until a CT scan has ruled out a hemorrhagic stroke (as giving tPA for a hemorrhagic stroke is devastating or lethal). Because of this, definitive stroke treatment cannot begin until it has been recognized, an ambulance gets them to an ER, a CT scan has been completed, a diagnosis is made, and that diagnosis reaches the treating physician—all of which, despite the best efforts by the medical system to expedite the process, often takes hours.

Worse still, the statistics on tPA (approved in 1996 and still the only FDA approved treatment for ischemic strokes) aren’t actually that good. Presently, tPA is only approved to be given within 3 hours of a stroke starting (as its likelihood of benefitting a patient decreases with time), and in practice, it is often given up to 4.5 hours after symptoms start (since some degree of benefit still exists).

When that window is met (which only happens about 25% of the time and ultimately results in roughly 1.8%-8.5% of ischemic stroke patients receiving tPA), the existing data shows that only 13% percent of patients who receive tPA significantly benefit from it (39% return to normal, compared to 26% who would return to normal without treatment), with an additional 19% of tPA users experiencing some degree of improvement (but not a full recovery) from it.

Worse still, tPA can cause significant bleeding, which is sometimes minor (e.g., gum bleeding), but also carries a 6.4% risk of a symptomatic brain bleed, and a 1.6% risk of a serious systemic hemorrhage (along with other issues such as a 1.3% to 5.1% risk of angioedema and tPA frequently causing reperfusion injuries). In turn, many risk factors exist for the increased bleeding (e.g., a few common risk factors can lead to a 33% chance of tPA causing a fatal bleed), and there have been many lawsuits for either giving or not giving tPA to a stroke patient. Additionally, tPA is a poor choice for larger obstructions (e.g., one within the internal carotid artery), which instead must be physically removed. In short—many ICU doctors I know are quite hesitant to use tPA as they have seen cases where it dramatically improved patients, many where it did not do anything, and quite a few disasters (especially in the early days of the therapy where it was used for heart attacks and then often caused the patient to have a fatal or debilitating brain bleed).

Note: the best data exists for tPA being injected directly into the obstructed artery with interventional radiology. Unfortunately, while many premier institutions offer this, it is a specialized procedure that is not available at most hospitals.

Finally, there is essentially no therapy for recovery from stroke—which in short explains why stroke is the second leading cause of death and the third leading cause of disability worldwide.

DMSO and Stroke Management

As the previous section shows, there are insurmountable limitations to how strokes can be managed. DMSO, however, completely changes this equation as:

•It effectively treats ischemic strokes.
•It partially treats hemorrhagic strokes.
•It carries no known risk of worsening a hemorrhagic stroke.
•It can be easily administered at home or on an ambulance.
•In addition to addressing the circulatory issues, independently protects brain tissue from stroke damage.
•Prevents the reperfusion injuries which follow strokes.
•Can heal damaged brain tissue after a stroke.

As such, DMSO makes it possible to eliminate the multi-hour delay typically required for stroke treatment, often is a safer can be a more effective stroke treatment option than the conventional alternatives, and provides one of the only existing options to heal the permanent disability that follows a stroke.

This is why researchers like Jack de la Torre MD devoted their entire careers to producing a robust body of evidence DMSO could treat strokes, as they knew it was unlikely any other agent would ever be able to solve the ischemic-hemorrhagic stroke dilemma.

Note: many readers have reported to me successfully treating strokes at home or on the way to the ER with DMSO and hence, due to increasing skepticism towards hospital care,¹ have advocated for home DMSO in lieu of going to the hospital. This is extremely unwise, as if a significant hemorrhagic stroke is occurring, DMSO cannot work as the primary treatment. Rather, the correct course is to use DMSO on the way to the hospital, and then if the whole thing is written off as a TIA (which many people have shared happened to them after they used DMSO, it resolved the stroke midway to the ER, and ER could then not decide if a stroke had happened), simply be grateful you had the optimal outcome when things could have easily been much worse. In short, the existing management we have for strokes is correct, and DMSO should be viewed as way to improve the results it yields rather than a replacement for it.

Ischemic Stroke Data

Many stories like these two Archie Scott reported¹ exist throughout the DMSO literature:

A Los Angeles school teacher had a major stroke shortly after the start of the Christmas break. She was unconscious on her living room floor. DMSO treatment was started immediately after the stroke. The DMSO was first applied topically to her head within minutes of the stroke. Less than one hour after the stroke she was given DMSO by intramuscular injection. This patient was never taken to the hospital for this stroke. A prominent surgeon who was a family friend told the husband of this patient that it was important to keep her out of the hospital. The surgeon said that even though the treatment was completely legal, it would be difficult to get approval to give the DMSO especially by injection at his hospital.

This patient made a dramatic recovery. She regained consciousness later in the day in which she had her stroke. Treatment continued for the next week. Each day she received two topical applications of DMSO, one intramuscular injection of DMSO, and two doses of one teaspoonful of DMSO in juice. Her condition improved each day. When school resumed after the first of January, this teacher was back in the school teaching the students as if nothing had happened during the Christmas vacation. She continued teaching until she retired, healthy and with no disability.

A lady was in a coma in a convalescent hospital and had been in the coma since her stroke three months ago. She was given little chance of recovery and was expected to remain in a vegetative state until her death.

When I first observed this lady, there was no response to any type of stimulus. She was alive, but appeared lifeless. It was decided that her treatment should be topical DMSO daily….One month after the start of treatment, there were positive signs in the lady. Her brain was starting to respond to the DMSO. The treatment continued, and four months after treatment started this lady was able to return to her home [where treatment continued].

Three years after the start of DMSO treatment this writer returned to visit this patient. At this time the lady was living a normal life, not the life of a stroke victim. She was able to look after the house and walked normally.

The only lingering effect of the stroke was a slight speech defect. At this time she said that her memory was better than that of her husband who had not had a stroke and who was considered to be completely normal.

Note: there are also many reported cases of individuals who took DMSO for musculoskeletal or pain disorders (by far the most common use of DMSO) who then experienced a permanent improvement of stroke symptoms.

Extensive data, in turn, corroborates these remarkable stories.

Human Evidence

Due to the ethical issues with creating and then treating strokes in humans, most of the research in this field has been conducted in animals (which I hold many strong ethical objections to). As such, the only human study has been conducted in ischemic strokes was a 2002 trial, where IV DMSO given with fructose diphosphate twice daily to 11 patients (mean age 65) with acute or subacute ischemic stroke was well tolerated and, when started within 12 hours of stroke onset, left 63% “improved” or “markedly improved” versus 20% of those on standard care at three months, and the benefit held even when treatment began well after the stroke.

Note: animal studies further corroborate DMSO-FDP value. In rabbits whose brains were driven to flatlined (isoelectric) EEGs by combined hypoxemia, hypotension, and carotid occlusion, DMSO-FDP given after five minutes of electrical silence restored brain activity far faster and let all animals survive with minimal damage, versus only 22% survival (severely disabled) on saline, and in mice given head impacts (another area DMSO helps), DMSO-FDP was the most protective and DMSO alone the second, while FDP and the rest gave no benefit, confirming DMSO was therapeutic. Finally, when DMSO-FDP was given to rats with poor chronic blood flow to the brain (due to carotid obstruction), there was a 54% improvement in visuo-spatial memory^1,2 (which is corroborated by dementia patients who’ve improved from DMSO).

•A Russian patent treated perinatal hypoxic encephalopathy in newborns by daily electrophoresis of vitamin E^⬖ in DMSO. In three term infants 6–7 sessions produced disappearance of limb tremor (chin tremor remaining only with crying), normalization of muscle tone, return of tendon and support/automatic-walking reflexes, loss of the spontaneous Moro reflex, and restoration of the Babkin reflex, with faster clinical recovery than intramuscular vitamin E^⬖ plus standard care.

•One physician reported knowing of a patient of Stanley Jacob’s whose stroke was successfully treated with DMSO.¹
Note: I have corroborated through multiple sources that Stanley Jacob successfully treated numerous strokes with DMSO, but I have not been able quantify how many in total were treated or what the success rate was.

Additionally, numerous reviews support DMSO’s use in humans with strokes. These include:

•A 2009 pharmacology review by Jack de la Torre and Stanley Jacob of DMSO in cardiac and CNS damage (arguably the most detailed one in print) showed intravenous DMSO elevated cerebral blood flow, limited infarct volume after middle-cerebral-artery occlusion, preserved the vulnerable CA1 and dentate neurons and facilitated recovery from acute or chronic cerebral ischemia.¹
Note: de la Torre was publishing papers on DMSO treating strokes fifty years ago¹ and likewise, a 1982 paper¹ acknowledged DMSO was being used to treat strokes.

•A 1992 Chinese review that concluded DMSO protects ischemic brain tissue and blocks the secondary pathological processes that follow cerebral ischemia, outperforming mannitol, dexamethasone, and barbiturates as a neuroprotectant.¹

•A 2010 Chinese review of DMSO’s effects on the heart and central nervous system (which noted authors had identified over 10,000 articles on the biological effects of DMSO).¹

•A 2012 Chinese review classified DMSO as a classic antioxidant with therapeutic effects on ischemia reperfusion injury across many organs (and noted it had already been used clinically abroad for cerebral reperfusion injury).¹

•In a 2018 Ukrainian physical-rehabilitation review where DMSO appears as an iontophoresis solvent in post-stroke and disability rehabilitation protocols.¹

•A 2022 Russian review from Osh State University argued that drug electrophoresis (driving charged medication ions through the skin with direct current) is among the most valuable physiotherapy methods for cerebrovascular disease (stroke and TIA) and peripheral-nerve disorders. Within it, DMSO is used as a carrier that lets otherwise water-insoluble drugs dissociate and be pushed through the skin. In acute stroke in the early recovery period, this was applied to the eyelids and back of the neck with heparin added for ischemic stroke and iodine substituted for hemorrhagic stroke.¹

DMSO Alone in Stroke Models

DMSO has repeatedly been shown to reduce the core injury of an ischemic stroke:

•A rhesus monkey study blocked the MCA for 4 hours, gave DMSO, dexamethasone, or nothing, and then opened the MCA after it had been blocked for 17 hours. DMSO gave significant protection from the severe neurological deficits and loss of arterial blood flow the other two groups developed.

•A squirrel monkey study blocked the left MCA for 4 hours, after which the animals were given a variety of different treatments (e.g., saline, hemodilution, or hyperbaric oxygen at 2 atmospheres). Seven days after treatment, 8 of 10 DMSO treated monkeys were alive (with 2 having mild contralateral muscle weakness), while 75% of those receiving hyperbaric oxygen survived, and just 34% of those receiving hemodilution survived (with the last two groups also having more significant neurological deficits). Finally, combining either of these treatments with DMSO produced slightly worse results than just DMSO alone.

•In experimental canine middle cerebral artery embolectomy, DMSO (or low-dose methylprednisolone) extended the grace period to 6 hours following embolization and protected the cerebral tissue from the injury of ischemia and post-ischemic reperfusion (with no infarcted tissue in DMSO treated animals and a 1.45 cm³ area of infarction in untreated ones).^1,2,3,4

•In a canine model of severe cerebral ischemia (where blood flow was cut by 90% for an hour), DMSO given alone as pretreatment allowed EEG activity to re-emerge after recirculation where untreated animals showed none. In a second canine study, in brains subjected to 14 minutes of complete ischemia and then reperfused for an hour, DMSO added to the reperfusion blood lowered a marker of lipid peroxidation (TBAR) back to control levels, restored roughly three quarters of the lost energy stores (ATP and creatine phosphate), cut lactate accumulation by 60%, and produced a marked return of EEG and auditory evoked potentials that untreated brains entirely lacked. Adding a platelet-activating factor antagonist on top of the DMSO further improved mitochondrial energy markers, though the reduction in lipid peroxidation was attributable to DMSO alone.
Note: the first study also found vitamin E^⬖ restored brain function, mirroring forgotten Russian research on how to counteract the biological consequences of chronic stress on the brain with DMSO and vitamin E.^⬖

•In a canine model of pressure-induced focal ischemia worsened by ethanol exposure (done to model head trauma from a drunk driving car accident), DMSO significantly reduced brain lesion volumes under both normotensive and hypotensive conditions and scavenged the hydroxyl radicals generated from ethanol metabolism.

•When seven different therapies were compared head-to-head in a canine model of severe pressure-induced focal ischemia, intravenous DMSO produced the best neurobehavioral recovery scores and the smallest lesion volumes, with reduced edema, necrosis, and cavitation.

•In a rat transient focal ischemia model done with 90-minute middle cerebral artery occlusion followed by reperfusion (as the MCA is one of the most commonly sites of consequential strokes and hence often blocked to simulate strokes), DMSO given 30 minutes before ischemia dose-dependently reduced cortical and striatal infarct volumes (how much brain tissue was damaged), and at the higher dose also significantly improved neurological motor function (while a low dose produced no benefit).

•In rats, DMSO given 30 minutes prior to MCA occlusion significantly reduced the amount of permanently damaged brain tissue^1,2,3 In another, DMSO immediately after occluded MCA blood flow was restored reduced rat infarct size and blood-brain-barrier damage (as measured by MRI), with enhanced protection and reduced MMP-2/MMP-9 activity (enzymes that breakdown the blood–brain barrier) when combined with DPI. Additionally, oral DMSO with vitamins C^⬖ and E^⬖, given 12 hours after rat MCA occlusion, significantly reduced oxidative stress.

•In rats, DMSO one hour before or after MCA and carotid occlusion significantly reduced rat brain edema and infarct volume. In rats with focal cerebral ischemia DMSO reduced brain water content and lipid peroxidation, preserved Na⁺-K⁺-ATPase and superoxide dismutase activity relative to saline controls, and markedly improved brain edema and ischemic tissue damage.

•In rats subjected to four vessel occlusion (which cuts off almost all blood flow to the brain) DMSO partially reduced mitochondrial malondialdehyde and free fatty-acid accumulation after reperfusion.

•In neonatal (7 day old) rats with hypoxia-ischemia brain damage, DMSO injected into the brain reduced infarct volume and brain injury (particularly within the cortex) along with inhibiting the breakdown of MAP2 and fodrin, suggesting neuroprotection via calpain inhibition.

•In gerbils subjected to carotid ischemia-reperfusion, DMSO, significantly reduced delayed neuronal death and lowered markers of hydroxyl radical activity that accumulates after reperfusion.¹ In another study, intraperitoneal 10% DMSO before ischemia cut gerbil mortality from 60% to as low as 14%, reduced the proportion of ischemic hippocampal neurons (from 71% to 46% at the higher dose), and blunted neurological signs.^1,2

•In a thrombotic (clot) stroke mouse model, daily DMSO (given for five days after the infarction) prevented the shrinkage and nuclear condensation of injured neurons and, most strikingly, sharply reduced the excessive astrocytic scarring response (gliosis) in the damaged cortex and hippocampus, restoring the astrocytes toward their normal morphology.^1,2

•In decapitated mice (with blood flow hence being cut off to the brain), DMSO prolonged the time the animal continued to gasp for breath and produced a dose-dependent relaxation of pre-contracted vascular smooth muscle, pointing to a vasodilatory contribution to its anti-ischemic effect.¹ An earlier report found DMSO was protective experimental hypoxic respiratory depression.¹

•In a rat model of deep hypothermic circulatory arrest, the DMSO solvent-control group “unexpectedly” showed some of the same organ-protective effects as the active drug (ebselen) it was carrying.

Note: many of these results argue that giving IV DMSO beforehand could reduce the complications of many challenging surgeries (e.g., a coronary bypass). Unfortunately, much in the same way ultraviolet blood irradiation dramatically reduces bad surgical outcomes, neither has been adopted for this purpose.

Beyond reducing the core infarct, DMSO also protects the penumbra. Frequently in strokes, an area will form where blood has been impaired, but brain tissue has not yet died (known as the penumbra and the key target of most stroke management). In a rat stroke study where DMSO was administered an hour after brain blood flow had been permanently cut off, MRI imaging showed that DMSO stopped the region of dying brain tissue from continuing to expand, hence allowing a penumbra (rather than additional dead tissue) to form around the stroke site (particularly within the cortex).

Note: beyond the classic penumbra, groups of cells can also enter a shocked state where their normal functions cease (and they eventually die). As discussed here, this “penumbra” also responds to DMSO (which is one reason tissue often comes back to life following DMSO treatment and why the sooner DMSO is used after a brain or spinal injury, the better the results typically are).

•In guinea-pig hippocampal slices, 0.4% DMSO alone more than doubled the latency to irreversible ischemic depolarization (from 2.9 to 7.1 minutes) under combined oxygen-glucose deprivation while also reducing its amplitude, an effect further augmented when DMSO was combined with nimodipine.

•In rat hippocampal slices, 10 mM DMSO completely prevented the hypoxia-induced drop in serotonin (5-HT) release and directly increased spontaneous release under normoxia (indicating a direct stimulatory action on serotonergic neurons).

Finally, DMSO also potentiated hypoxic preconditioning on its own: given intraperitoneally or directly into the hippocampus, it increased rats’ resistance to severe hypoxia by roughly 79% and 111% respectively over controls (via α7-nicotinic receptors).

Note: a veterinary text¹ (along many with other parts of the veterinary literature¹) also highlighted DMSO’s edema-reducing, diuretic, and anti-inflammatory effects in cerebral ischemia. Likewise, in veterinary neurology, DMSO was used therapeutically or as a carrier in temporohyoid osteoarthropathy with acute neurological signs¹, post-anesthetic air embolism with neurologic sequelae in a horse¹, critically ill neonatal foals¹, a filly’s watershed cerebral infarction¹, and a 2-day-old filly with hypoxic-ischemic encephalopathy given IV DMSO.¹

How DMSO Protects the Brain

In addition to the extensive research showing that DMSO restores blood circulation and prevents reperfusion injuries in those (previously ischemic) tissues, numerous studies have shown DMSO mechanistically protects the brain from strokes:

•In anesthetized cats, DMSO significantly enhanced brain oxygenation (particularly in the caudate nucleus).

•DMSO was shown to preserve the neurological function of hippocampal brain tissue samples once their oxygen or glucose were withdrawn (with similar results seen in this study).

•When infused directly into the rat brain, DMSO alone reduced ischemia-induced (blood loss induced) extracellular glutamate (the excitotoxin that drives much of the neuronal death in a stroke) by 51% and modestly preserved the vulnerable hippocampal CA1 neurons relative to controls.

•DMSO down-regulated aquaporin-4 expression (a key driver of the brain swelling that follows an occlusion) after MCA occlusion in the rat.

•DMSO was found to protect the integrity of the blood-brain barrier integrity after MCA occlusion.

•Diazoxide and DMSO prevented the learning dysfunction and brain damage that follow carotid artery occlusion (with DMSO alone restoring) Morris-water-maze learning and preventing COX-2-positive neuron loss in the dentate gyrus.

Reader Stroke Reports

Corroborating DMSO’s benefits for strokes, numerous readers here shared the following with me:

•A medicinal chemist with a background in neuroscience, recognized his own stroke the moment it began: “Right after waking up I went to the toilet and noticed that I had lost control of my palm. I walked to bed and I froze, unable to lay down.” He had his wife get him diluted DMSO, drank most of it over the next hour, and went to the hospital—by which point he had lost speech (Polish entirely, English partially), leaving him, a Pole, to communicate in English in a Polish hospital. “I credit DMSO for not losing movement ability,” he wrote. His speech recovered well enough that he returned to full-time work as a scientist six weeks later, and he now drinks a small maintenance dose daily.¹

•One week after her husband’s stroke, which had left him with severe pain, vertigo, exhaustion, and partial paralysis of the left side of his face, arm, and leg, a reader discovered this series. She then applied undiluted DMSO to his face, neck, and shoulder two to three times a day; the pain, she reported, “went away almost instantly every time.” Within about two weeks he began walking short distances without a cane. “Only 3 months after the stroke he walked with me unassisted to a friend’s house carrying a guitar, and was able to play the guitar and sing flawlessly while standing with one foot on a chair. My jaw was on the floor... ‘You’re all witnessing a freakin’ miracle right now. This man had a stroke three months ago, and now he’s playing his guitar like nothing happened!’”¹

Thanks for saving my life. I had a stroke recently, and because of your article on dmso and strokes, was given some by my partner. Three minutes later I was OK again. I continue to read your articles daily.¹

I have been in health chats where twice now, folks were in the chat and were having a stroke, they both had DMSO on hand & took 1 oz it both were stopped within 10-15 min and reversed any damage.¹

I just recently had a stroke but used DMSO immediately ( I had my wife apply it in the hospital within hours of my stroke) and I’m about 95% back to normal and hoping to be 100% soon.¹

•A wife whose husband had atrial fibrillation and two microclot strokes in 2024 treated a recurrence herself the following year: when both his legs went numb with pins and needles, she applied DMSO and “Within two hours he was 70% better,” and after a second identical treatment “everything was cleared up and did not return” (months later she used the same protocol over his chest for a suspected pulmonary embolism, with the same result).

•Another wife, reported DMSO “Made a world of difference” for her husband’s entire-left-side deficit,¹ another reported their husband’s two mini-strokes cleared within a few hours,¹ another reported that when her husband woke up unable to speak and with numbness in his cheeks, she began DMSO, and there was “a huge improvement from a week ago” as he was speaking in complete sentences most times.¹

•A reader who saved her mother from a third stroke shared “It was miraculous!”¹; another reported it saving a family member from a stroke.¹ Likewise, a reader whose father began showing stroke symptoms wrote: “Thankfully I had some 99.9% DMSO on hand. The improvement was remarkable….“The Lord might have just used you to save my dad’s life.”¹

Interestingly, many readers have reported stories matching my own experience of giving someone DMSO and then having the ER be confused because they could not find any signs of stroke:

•After a reader woke at 4:30 a.m. and found his left side would not respond when he tried to walk stated he immediately knew to use his DMSO and over the next 4 hours “My walking returned to normal but my reach and grab with my left arm/hand would not allow me to pick green beans in my garden.” He hence called 911, walked down his own hill to greet the firemen, and talked the EMTs out of taking him; the next morning his clinic’s nurses sent him to the hospital by ambulance, where monitoring, a CT scan, and echocardiograms found “no evidence of stroke,” and his remaining left-hand impairment recovered over two weeks with self-directed therapy. His conclusion: “In every interaction with medical personnel I strongly recommended that DMSO should be the first/immediate action when stroke symptoms are detected. Waiting for an ambulance or an emergency room visit to respond is a tragic waste of time.”¹

•A 76-year-old man in excellent health had a nearly identical experience 36 hours after giving a double-red blood donation: he woke at 4 a.m. with trouble walking and gripping on his left side, and applied DMSO based on what he had read here. Hospital testing “has not found/confirmed stroke,” and he reported rehabbing himself until symptoms had “disappeared 97%.”¹

•Another reader who was already familiar with DMSO and kept it on hand took it during an apparent stroke: “The ER doc came in to tell me that I had not stroked, despite speech impairment and other signs. I told him I took DMSO.”¹

•The reports extend well beyond the acute window into recovery from established strokes. One reader’s husband, who had suffered eight strokes, takes DMSO three times a week; two years after his last stroke, in her words, “recovery great, he has some aphasia but still thinking great speaking to others although he’s an introvert and has lost some confidence in himself he is still living life to its fullest playing with grandkids gardening home renovations and going to the gym and doing a full work out which includes 30 chin ups!”¹ A caregiver eight weeks into treating a stroke patient (who noted the changes “began almost immediately, after the very first treatment”) observed a cascade of gains: stronger voice and markedly improved speech, dramatically improved swallowing (he could again eat normal-sized meals, and even swallow while the TV was on, previously a choking hazard), self-feeding with the affected hand; improved energy, strength, and balance; and, “the most recent and undeniable change,” the return of his sense of taste. On one lucid day he zipped up his own jacket—notable, she wrote, “because the fine motor skills in his right hand were quite impaired by the stroke” and “even he commented at the time that it was remarkable.”¹ Another reader watching his mother’s recovery described her damaged right side visibly “waking up”, regaining feeling and strength until one day she exclaimed, “Hey look, I’m sanding with my right hand!”¹

•Others report gains across the full range of stroke severity. One reader had a large stroke that “affected every joint on my right side” and used DMSO with CBD: “One year later? Only my knee and two fingers (pinky and ring) are still ‘lazy’ but each month I notice an improvement... I couldn’t write but I can now. I’ve learned to type with 8 fingers but the other two are still improving.”¹

•Another reader began giving her 72-year-old husband DMSO six weeks after his stroke; over two and a half weeks “he improved and slowly regained more function so that he could swim again,” and a later course brought further gains. She noted the oral route seemed to act faster, though its garlic-like odor kept him homebound—so he switched to applying DMSO nightly to his temples, forehead, and neck, on which he continued to slowly improve.¹

•A 65-year-old who’d had a series of small strokes reported that after starting DMSO the improvement in mental acuity was “amazing” alongside whole-body pain relief;¹ a physician who ran an IV chelation and ozone clinic recalled an “amazing recovery” in a stroke patient given IV DMSO;¹ and caregivers successfully treating loved ones after strokes (e.g. “a very bad stroke¹”) or an ischemic stroke and reporting steady, believable progress.^1,2,3

•A grandfather who nebulized DMSO for decades survived multiple strokes and “amazed doctors by how quickly he recovered,” living to 94.¹ Another reader stated flatly that DMSO saved him from a stroke a decade ago.¹

Finally, many readers describe using oral DMSO as ongoing stroke prevention. One was having strokes two or three times a week until he started DMSO (originally bought for sciatic nerve pain): “the strokes stopped happening... once it is in the blood stream it works everywhere.”¹ Another also reported DMSO stopped their strokes,¹ Likewise, a diabetic who’d had two strokes from clotting that monitoring his own blood under a microscope, found daily oral DMSO kept his red cells out of rouleaux formation and “the clots at bay.”¹
Note: these readers were almost certainly suffering from what would be diagnosed as “TIAs” and the fact that both DMSO prevented their recurrence and that one reader could link this to DMSO eliminating blood sludging argues for my theory many TIAs are actually microstrokes triggered by things like zeta potential disruption.

In short, I hope all of this (and what is to come) makes it clear why I feel so strongly about DMSO becoming a standard therapy for strokes. Nonetheless, as discussed earlier, it is absolutely critical you do not avoid emergency care just because DMSO is available and rather treat it as complementary therapy as you wait for conventional care.

DMSO Stroke Combination Therapies

Since DMSO is both a non-toxic solvent and able to deliver a variety of agents (e.g., through the skin), that rare combination results in it being used as a “vehicle control” in many studies. In these studies, DMSO is typically assumed to be inert (and hence not independently tested for an effect), but in some cases is tested, where it often yields a therapeutic effect (which I’ve noticed authors often do not disclose). As a wide number of agents combined with DMSO all yield therapeutic effects similar to those seen with DMSO, this suggests that DMSO plays a direct role in the effects observed, particularly since DMSO frequently potentiates the agents it is combined with. This dynamic I believe likely accounts for why many agents that succeed in preclinical studies (where DMSO is also used) fail in clinical studies where DMSO is not also used.

Note: replication failure is one of the largest problems in science.

As such, I include these combinations here (most of which were used for focal brain ischemia) both to highlight the shared effects seen across many agents (that potentially are due to DMSO) and to provide insights to readers looking for additional treatment strategies. To make these section easier to skim, all natural agents are marked with a ^⬖.

Natural agents

Polyphenols & flavonoids — curcumin^⬖ (reduced infarct size and cell death)^{1,2,3,4,5,6,7,8,9,10,11,12,13,14}; resveratrol^⬖ (reduced infarct size and preserved neurons, including in elderly and recurrent-stroke rats)^{1,2,3,4,5,6,7,8,9,10,11}; baicalein^⬖ (reduced infarct size and cell death)^1,2; chrysophanol^⬖ (reduced infarct size and cell death as a pre-treatment)^1,2; quercetin^⬖ (reduced infarct size)^1,2; chrysin^⬖ (improved movement and memory and reduced oxidative stress)^1,2; nordihydroguaiaretic acid^⬖ (reduced neurological deficits and infarct size)¹; apigenin^⬖ (reduced inflammation)¹; mangiferin^⬖ (reduced neurological deficits when given before ischemia)¹; shikonin^⬖ (reduced infarct size and oxidative stress)¹; trifluoro-icaritin (reduced neurological deficits and infarct size)¹.

Alkaloids & related plant compounds — berberine^⬖ (reduced infarct size and cell death)^1,2,3,4; evodiamine^⬖ (reduced infarct size)^1,2,3; rutaecarpine^⬖ (improved movement and raised neurotrophic factors)^1,2,3; cynandione A^⬖1; vinpocetine^⬖ (reduced infarct size and inflammation)¹; sinomenine^⬖ (reduced inflammation)¹; piperine^⬖ (reduced injury)¹; carvacrol^⬖ (reduced injury)¹.

Terpenoids, saponins & quinones — astragaloside IV^⬖ (protected neurons and reduced cell death)^1,2,3,4,5; celastrol^⬖ (reduced neurological deficits and infarct size)^1,2; the cembranoid 4R^⬖ (reduced infarct size and cell death)¹; ginsenoside Rb1^⬖ (reduced neuronal death)¹; bilobalide^⬖ (reduced neurological deficits and infarct size)¹; tanshinone IIA^⬖ (reduced infarct size when given after stroke)¹; sulforaphane^⬖ (reduced infarct size and inflammation)¹; triptolide^⬖ (reduced infarct size, swelling, and neurological deficits)¹; picroside^⬖ (protected mitochondria and reduced cell death)¹; ursolic acid^⬖ (reduced infarct size and improved neurological scores)¹; Z-guggulsterone^⬖ with boswellic acid^⬖ (improved neurological function and promoted new blood-vessel growth)¹; salvinorin A^⬖ (reduced inflammation and swelling and protected the blood-brain barrier)^1,2,3,4; herkinorin (reduced brain swelling and improved neurological function)^1,2.

Whole-herb & multi-herb extracts — kava extract^⬖ (reduced cell injury and inflammation)¹; Gastrodia elata extract^⬖ (reduced infarction by shifting immune cells toward healing)¹; Ptychopetalum olacoides extract^⬖ (protected brain tissue from oxygen deprivation)¹; Angelica sinensis extract^⬖ (improved neuronal survival and regrowth)¹; Ginkgo biloba extract^⬖ (prolonged survival and reduced injury)^1,2; Viola spathulata extract^⬖ (reduced infarct size)¹; Zhenbao Pill^⬖ (reduced inflammation and cell death)¹; Qing-Nao-Tong-Luo Recipe^⬖ (reduced infarct size and improved neurological function)¹; Tongxinluo^⬖ (protected the blood-brain barrier and circulation)¹; Shenmai injection^⬖ (reduced deficits and infarct size)¹.

Other natural compounds — stilbazulenyl nitrone^⬖ (was highly neuroprotective as an antioxidant)¹; docosahexaenoic acid^⬖ (protected brain cells from oxygen deprivation)¹.

Synthetic & pharmacological agents

Kinase & MAPK-pathway inhibitors — an ERK inhibitor (improved survival and protected mitochondria after cardiac arrest, and reduced infarct size)^1,2,3,4,5,6; a PI3K inhibitor (reduced injury in diabetic brain injury)¹; a p38 MAPK inhibitor (reduced cell death and swelling and improved neurological function)^{1,2,3,4,5,6,7,8}; a JNK inhibitor (protected neurons and improved survival)^1,2,3; rapamycin (reduced infarct size)^1,2,3,4; Mdivi-1 (reduced oxidative stress and cell death)^1,2; a STAT3 inhibitor (reduced injury)¹; anisomycin (improved neuronal survival)¹; a PTEN inhibitor (promoted neuronal repair)¹; HIF prolyl-hydroxylase inhibitors (induced protective autophagy)¹; bosutinib (reduced infarct size and inflammation)¹; a TAK1 inhibitor (improved neurological scores and reduced infarct size)¹; 5’-deoxy-5-iodotubercidin (reduced infarct size by up to 57%)¹; 2-Cl-MGV-1 (promoted new blood-vessel growth)¹.

Cell-death & protease inhibitors — caspase inhibitors (reduced infarct size and cell death)^1,2,3,4,5; cathepsin inhibitors (reduced infarct size and cell death)^1,2,3,4; a Notch/γ-secretase inhibitor (drove stem cells toward neurons and aided post-stroke regrowth)^1,2; necrostatin-1 (reduced necroptosis and improved myelination and memory)^1,2,3; cyclosporin A (protected neurons)¹; a calpain inhibitor (reduced cell death and injury)^1,2; a PARP inhibitor (reduced infarct size)¹; thalidomide (reduced infarct size and cell death)¹.

HDAC & epigenetic inhibitors — an HDAC inhibitor (trichostatin A) (reduced infarct size and inflammation)^1,2,3; an HDAC inhibitor (SAHA) (reduced infarct size by up to 57%)^1,2; an HDAC inhibitor (MS-275) (reduced infarct size)¹; an HDAC inhibitor (TSA) (reduced infarct size and inflammation)¹; an EZH2 inhibitor (improved coordination and reduced injury)¹.

Nuclear-receptor & metabolic modulators — pioglitazone (reduced neurological deficit, swelling, and inflammation)^1,2,3,4; all-trans retinoic acid (reduced infarct size as a post-treatment)^1,2,3; a PPARγ inhibitor^1,2; LXR agonists (reduced infarct size)¹; rosiglitazone (reduced infarct size, and in DMSO cut it by roughly half where DMSO alone was inert)¹; a thyronamine analog (induced protective hypothermia)¹; a PPARα agonist (bezafibrate)¹; an SGLT2 inhibitor (empagliflozin) (reduced microvascular injury)¹; an Nrf2 activator¹; an ALDH2 activator¹.

Receptor ligands & ion-channel modulators — an adenosine A1 agonist (improved outcomes and reduced injury)^1,2,3,4; an α7-nicotinic modulator (reduced damage after stroke)¹; dexmedetomidine (reduced mitochondrial fission and cell death)^1,2,3; octanol, a gap-junction blocker (reduced infarct size after longer ischemia (worsening it after brief ischemia))^1,2,3; a TRPC1 blocker (reduced calcium overload and cell death)^1,2; nimodipine (improved neuronal survival)¹; bumetanide (reduced swelling)^1,2; an LPA2 agonist (improved survival)¹; a GABAA α5 inverse agonist (promoted motor recovery)¹; a nucleoside-transporter inhibitor (reduced infarct size)¹.

Cannabinoid-system modulators — a CB1 agonist (acted through mitochondrial CB1 receptors)^1,2; a CB2 agonist (reduced injury)^1,2.

Hormones, steroids & vitamins — estrogen (reduced infarct size and cell death)^{1,2,3,4,5,6,7,8,9}; progesterone (reduced infarct size and improved recovery, less so in aged animals)^{1,2,3,4,5,6,7,8,9}; tamoxifen (reduced injury)¹; vitamin D3^⬖ (reduced infarct size and increased blood flow)¹; vitamin K2^⬖ (reduced swelling, cell death, and inflammation)¹; erythropoietin (reduced injury, including intranasal delivery)^1,2; leukemia inhibitory factor (protected neurons)¹.

Repurposed clinical drugs — 4-methylcyclopentadecanone (reduced infarct size and inflammation)¹; a norcantharidin MMP-9 inhibitor (improved scores and protected the blood-brain barrier)¹; modafinil (reduced infarct size and swelling)¹; cilostazol (protected brain blood vessels)^1,2.

Other synthetic / pharmacological agents — an nNOS inhibitor (reduced infarction by 70-92%)¹; an azulenyl nitrone (STAZN) (was neuroprotective)¹; Z-11 (reduced neurological deficits and infarct size)¹; a 12/15-LOX inhibitor (reduced infarct size and inflammation)¹; electroacupuncture with microRNA delivery (reduced deficits and promoted stem-cell regrowth).^1,2,3,4

Other injury models

The combination data also extend beyond focal ischemic stroke to the following models:

Neonatal & perinatal hypoxic-ischemic models — hesperidin^⬖ (reduced oxidative stress and improved survival)¹; baicalin^⬖ (cut neonatal infarct size roughly in half)¹; notoginsenoside R1^⬖ (improved survival)¹; melatonin^⬖ (reduced infarct size and improved brain metabolism)^1,2,3; a JNK inhibitor (reduced neonatal cell death)^1,2; dantrolene (reduced cell death and injury)¹; an adenosine A2A antagonist (reduced brain damage and cell death)^1,2,3; 2-methoxyestradiol (reduced swelling and cell death)¹; indomethacin (reduced infarct size and protected the blood-brain barrier)¹; miconazole (improved myelination in white-matter damage)¹; G-CSF (reduced neonatal cell death)¹; H2S donors (reduced injury and promoted remyelination)^1,2.

Cardiac-arrest & global-ischemia models — ellagic acid^⬖ (improved kidney function after global ischemia)¹; Gynostemma pentaphyllum^⬖ (improved outcomes after cardiac arrest)¹; necrosulfonamide (improved recovery by blocking programmed cell death)¹; a TLR4 inhibitor (reduced neuron loss after cardiac arrest)¹; oxcarbazepine (protected neurons after cardiac arrest)¹; WIN 55,212-2 (reduced infarct size and induced protective hypothermia that prolonged survival)^1,2,3,4,5; salubrinal (improved outcomes and preserved mitochondria after cardiac arrest)^1,2; glibenclamide (raised 7-day survival after cardiac arrest)¹; genistein^⬖ (increased neuron survival after cardiac arrest)^1,2; paclitaxel (protected neurons after cardiac arrest)^1,2.

Cerebral Blood Flow & Vascular Reactivity

Beyond protecting brain tissue once a stroke is underway, as highlighted previously in the endothelial data, DMSO also acts directly on the cerebral vessels themselves, changing their tone, their reactivity to constrictors and dilators, and the blood flow they carry.

Like many other properties of DMSO, its effect on cerebral vessel caliber (width) depends heavily on dose. In a cat study examining pial (brain) arterioles both in vitro and in vivo, DMSO concentrations from 0.0001% to 0.5% produced no significant change in arteriolar caliber, while 1% DMSO dilated them by 19%—and on isolated cerebral arteries, high-concentration DMSO reversed constriction induced by PGF₂α (85% reversal), serotonin (60%), and potassium (13%).¹ That study also found that intravenous 10% DMSO (1 g/kg) produced rapid, measurable brain shrinkage within 10–15 minutes, consistent with DMSO’s edema reducing properties.¹

Conversely, some of DMSO’s effects on cerebral vessels actually work by blocking dilation, and this too traces back to its radical scavenging. This is because hydroxyl radicals themselves dilate cerebral microvessels, so when acetaldehyde and xanthine oxidase were used to dilate mouse pial arterioles, free-radical scavengers including DMSO stopped that dilation.¹ Likewise, DMSO inhibited the pial arteriole dilation produced by a radical-generating xanthine oxidase acetaldehyde system while leaving carbon dioxide induced dilation untouched.¹ This selectivity (blocking only the radical-driven dilation) hence indicated DMSO was scavenging radicals rather than acting as a general vasomotor agent.¹ Likewise, in canine basilar arteries, DMSO reduced the Fe²⁺-mediated inhibition of endothelium-dependent relaxation by scavenging hydroxyl radicals.¹ DMSO hence does not push vascular tone in a fixed direction like a typical pharmaceutical, rather normalizes vascular function by removing the radical signal, so it dilates a vessel radicals were constricting and blocks a dilation radicals were driving.

DMSO also independently blocks ATP-sensitive potassium (KATP) channel mediated cerebral vasodilation, and it does so at very low concentrations (within the range routinely used just to dissolve a test compound). In anesthetized rats, DMSO dose-dependently inhibited pinacidil-induced dilation of pial arterioles at 0.01-0.2%, with significant inhibition at the very bottom of that range.¹ Notably, DMSO alone did not change the baseline vessel diameter, and the effect reversed within 15 minutes of washing the DMSO out.¹ A companion report found the same for very low dilutions of both ethanol and DMSO,¹ and in cats, DMSO inhibited the cerebral arteriolar dilation produced by hydrogen peroxide and KATP openers at under 1 mmol/L (which those authors attributed to potassium-channel blockade rather than radical scavenging).¹

That said, when perfusion is measured across the whole brain rather than in isolated vessels, DMSO consistently raises cerebral blood flow (e.g, this was a key focus of forgotten Russian research on reversing the effects of chronic stress). In a 1986 rabbit brain-edema study, a 20% DMSO bolus raised cerebral blood flow by roughly 75-77% in both hemispheres almost immediately, with flow still elevated an hour later.¹ Pretreating with indomethacin did not prevent this rise, which indicated the increase was not prostaglandin-mediated, and the intracranial pressure still fell despite the higher flow (as DMSO rapidly pulls water out of the brain).¹ Low-dose intravenous DMSO did much the same in a canine model of myocardial ischemia, raising both cardiac output and cerebral blood flow while lowering vascular resistance, with no adverse change in heart rate or blood pressure.¹ Likewise, when given an hour after an experimental brain hemorrhage, DMSO held brain oxygen and glucose consumption near baseline, curbed the excess lactate, stabilized or increased blood flow (partly by raising blood osmolarity), completely prevented the surge in lipid peroxidation, and eliminated the early mortality seen in the untreated animals (0% versus 25%).¹

Note: DMSO’s effect on central cardiovascular control has been found to be transient and local rather than systemic. Injected directly into the brainstem cardiovascular center (the NTS), 40% DMSO produced only a brief 1-2 minute drop in blood pressure and heart rate before returning to baseline, with no lasting change (consistent with DMSO’s rapid diffusion out of tissue).

Agents dissolved in DMSO have also been shown to dilate the cerebral vessels such as an activator of ATP-sensitive potassium channels,¹ various PDE5 inhibitors,¹ apigenin,^⬖1 (which relaxed the basilar artery), tetrahydroxystilbene glucoside,^⬖1 (which in rats relaxed the mesenteric artery while protecting carotid flow),¹ a gamma-secretase inhibitor (that reduced the vasospasm following a subarachnoid hemorrhage).¹

Finally, these cerebral-perfusion effects are often used as a rationale for clinical applications. For example, in a horse that developed seizures and blindness after surgery, intravenous DMSO was given specifically for its radical scavenging and thromboxane inhibition to maintain the brain’s blood supply, after which the seizures stopped by day 3 and the vision partially returned over the following months.¹ Likewise, the Russian clinical literature describes dimexide (DMSO) as relieving brain-tissue swelling, improving cerebral blood flow, and normalizing cerebral hemodynamics.¹ One unusual Russian diagnostic protocol even applied a DMSO, nicotinic acid,^⬖ and novocaine compress to the forehead to test whether increasing forehead blood flow improved a patient’s vision, using that result to predict who would benefit from surgery on the branches of the carotid artery.¹

Hemorrhagic Strokes

Hemorrhagic strokes are among the most difficult conditions in all of medicine to treat, and despite decades of work, there has been remarkably little progress in neurocritical care—particularly in preventing the long-term paralysis and disability that so often follow a brain bleed. This is because a hemorrhage sets off a cascade of injuries that conventional medicine has no single agent to address, whereas DMSO, remarkably, addresses each of them at once.

When blood escapes into the brain, three things happen more or less simultaneously. First, the swelling and accumulating blood raise the pressure inside the rigid skull (the intracranial pressure, or ICP), and brain tissue is exquisitely sensitive to being compressed—yet there is no good agent for lowering ICP (the most commonly used drug, mannitol, can produce a “rebound” in which pressure climbs higher than where it started). Second, the blood-brain barrier begins to break down, allowing still more fluid into the brain. Third, as the spilled blood cells die, the iron they release generates free radicals that destroy surrounding brain cells,1 while inflammatory processes triggered by the blood injure tissue further and drive additional cell death.

Remarkably, DMSO addresses each of these.¹ It rapidly lowers ICP without the risk of rebound,¹ and unlike most ICP-lowering agents it does not do so by cutting blood flow to the brain—instead it increases cerebral perfusion without raising blood pressure or heart rate,¹ which matters because brain cells die within minutes of losing their blood supply. That improved flow is also what clears the leaked blood, and DMSO is excellent at reducing the accompanying brain edema.¹

Note: I suspect rebound ICP is the brain’s attempt to restore its own blood supply; because DMSO already guarantees that supply, there is nothing to rebound from. Consistent with an osmotic rather than a direct vascular mechanism, one study in anesthetized cats found IV DMSO never constricted the cerebral arteries across an enormous concentration range, and only relaxed already-contracted vessels—while still shrinking the brain by pulling out excess fluid.

Beyond pressure and perfusion, DMSO lowers the inflammatory cytokines (IL-1α, IL-1β, IL-6) tied to stroke and tissue injury¹,² and calms overactive immune signaling.^1,2 It also directly counters the damage from blood breakdown products: its free-radical scavenging limits platelet aggregation at injured microvessels and prevents blood from flooding the injury site (reducing secondary ischemic injury).¹ At just 0.5% DMSO protected basilar-artery smooth muscle from oxyhemoglobin-induced contraction membrane blebbing, and cell death by scavenging hydroxyl radicals¹ and it reversed iron-mediated damage to vessel relaxation in canine basilar arteries.¹ DMSO likewise prevented bilirubin toxicity in myelinated axons, protecting nerve fibers from another toxic product of degrading blood.¹

In short, no comparable agent exists for lowering ICP—one of the greatest unsolved challenges in neurocritical care—and many drugs that succeeded in animals have failed in human trials.¹ Beyond removing edema, limited human work also suggests DMSO can somehow reduce the ongoing spilling of blood into the brain, through a mechanism that has not yet been definitively worked out.

Note: DMSO additionally lowers JAK2/STAT signaling,¹ suppresses neurotoxic NMDA/AMPA ion currents,¹ prevents iron-induced lipid peroxidation and focal edema,¹ and partially inhibits PARP-1.¹

De la Torre’s Discovery

The potential of DMSO here was recognized decades ago by Jack de la Torre, who when watching a near-dead experimental animal revive with DMSO recounted:

It was, as if the hand of God had somehow touched the animal’s forehead. “I don’t believe it,” I stammered. But it was true. I felt a tingling in my spine because this reawakening of a virtually dead animal had all the markings of a medical breakthrough.

Note: de la Torre’s observations were based partly on his repeated finding that animals with flatlined EEGs—which normally precede brain death—had their EEGs return within about ten minutes of receiving DMSO. As so often in this story, the discovery was never developed and was instead quietly laid to rest in the coffers of forgotten medicine.¹

Animal Hemorrhagic Stroke Studies

In experimental brain hemorrhages, DMSO given an hour after the bleed prevented the collapse of the brain’s antioxidant defenses and cut mortality to zero (vs. 25% in controls by three hours). In rats, it held lipid-peroxidation products at normal levels rather than letting them climb; in cats, it kept oxygen and glucose metabolism near baseline and blunted the flood of lactate an injured brain pours into the bloodstream. The authors doubted the improved flow was vasodilation as DMSO only widens vessels at 1%+ concentrations, well above those reached at 0.3 g/kg and attributed it instead to the compound’s antiedematous action: by raising blood osmolarity (335→352 mosm/L), DMSO drew fluid out of the swelling brain, an effect they compared to glycerol’s; the accompanying drop in brain lactate, they suggested, aided the same anti-edema process..^1,2

The protection reaches the molecular level too: in hemorrhagic shock, another state where the brain loses its blood supply, DMSO quieted the inflammatory driver NF-kappaB while boosting the survival protein HSP70.

Note: much of this foundational Russian work on DMSO in acute intracerebral hemorrhage is collected in a dedicated chapter (by M.B. Plotnikov) of a Russian monograph on DMSO in clinical practice.¹ Interestingly, much of Plotnikov’s later work (I just came across and need to read in detail) revolved around the hypothesis that increased blood viscosity (which included oxidized red blood cells clumping together, and after ischemia–reperfusion injuries occurred were further oxidized) was not only a marker but an amplifier of many diseases, particularly high blood pressure, chronic cerebrovascular disease, brain ischemia, and ischemic heart disease, and to a lesser extent venous insufficiency, diabetes, radiation injury, and shock—dovetailing with my understanding of the subject. As he worked in a Soviet/Russian cerebral-pharmacology and viscometry tradition he appears not to have engaged with the Western blood-sludging or zeta-potential or microstroke research, and hence arrived at a variety of different disease and treatment insights than what I’ve come across.

Human Hemorrhagic Stroke Studies

•In a study of 11 patients with dangerously high ICP and Glasgow Coma Scores of 4–6 following brain trauma, encephalitis or subarachnoid hemorrhage (patients on the verge of death for whom standard therapy had failed), IV DMSO (1 g/kg) promptly lowered ICP (mean drop ~23 mm Hg at 30 min) and produced a brisk diuresis. Three patients survived with good functional recoveries; the others died despite ICP control. Unlike barbiturates, which lower systemic arterial pressure and force patients into a coma, DMSO did neither—so cerebral perfusion pressure rose as ICP fell and patients remained clinically examinable.

•A second paper reported on nine patients who suffered partial or total paralysis after surgical repair of a ruptured aneurysm and had remarkable responses to DMSO:

• A 61-year-old man developed left-sided paralysis after surgery; within 30 minutes of starting DMSO his cerebral blood flow rose and he improved markedly. When DMSO was stopped on day 5 the paralysis and confusion rapidly returned—and resolved again once it was resumed, after which he fully recovered.

• A 67-year-old woman who lost speech and developed right-sided paralysis (and hadn’t responded to mannitol) became fully alert and regained her strength within 45 minutes of DMSO; her motor function permanently normalized within 12 hours.

• A 25-year-old woman who developed right-leg paralysis and speech difficulty 12 days after aneurysm surgery, again after mannitol failed, could lift her leg within 90 minutes of DMSO and had fully recovered by the next day.

• A 28-year-old woman with an MCA aneurysm and a severe carotid spasm unresponsive to standard care recovered completely on DMSO.

• The remaining five cases followed the same course, with all but one (who had severe complicating factors) making a full recovery. No adverse events occurred in any case.

In de la Torre’s own book,¹ IV DMSO for ruptured aneurysms in humans is likewise reported to reverse progressive hemiplegia, relieve vasospasm and the resulting low cerebral blood flow, and improve motor deficits.

Hemorrhages Elsewhere in the Body

That DMSO limits bleeding is not unique to the brain—it has been observed in other organs, indicating this is a general property of DMSO. In a pig model of myocardial ischemia-reperfusion, intracoronary DMSO essentially eliminated intramyocardial hemorrhage (0 of 8 DMSO animals vs. 7 of 7 controls by cardiac MRI, and 1 of 10 vs. 8 of 8 by pathology) and reduced microvascular obstruction by 45%, with no hemodynamic or arrhythmic side effects.¹ A Russian literature review likewise lists hemorrhages among the conditions DMSO (with antibiotics) is applied to directly, alongside bruises, sprains, and edema.¹ Finally, in children with hemophilia, topical DMSO has been used as part of physiotherapy protocols for acute joint bleeding (hemarthrosis)—applied for 2–4 days to relieve pain, prevent intra-articular clotting, and reduce the progression toward joint damage.^1,2

Hemorrhagic Stroke Combinations

As before, many agents have been combined with DMSO here and demonstrated efficiacy for intracerebral and subarachnoid hemorrhages, many of which targeting the same injury cascades DMSO itself acts on (e.g, oxidative stress, inflammation, blood-brain barrier breakdown, edema, vasospasm, and neuronal death).

Natural agents — curcumin^⬖ (reduced brain-cell death and mortality, protected the blood-brain barrier and reduced swelling, and outperformed nimodipine against vasospasm)^1,2,3; resveratrol^⬖ (improved neurological outcomes and reduced cell death, swelling, and inflammation)^1,2,3; 6-gingerol^⬖ (improved neurological function and reduced swelling, cell death, and inflammatory cytokines)¹; quercetin^⬖ (reduced oxidative stress, cell death, swelling, and vasospasm)¹; allicin^⬖ (improved neurological outcomes and protected the blood-brain barrier)¹; honokiol^⬖ (reduced cell death and improved cognition)¹; genistein^⬖ (reduced inflammation and improved neurological outcomes)^1,2,3; sulforaphane^⬖ (improved outcomes)^1,2; EGCG^⬖ (green-tea polyphenol; reduced oxidative injury and cell death)¹; naringenin^⬖ (improved neurological outcomes and reduced inflammation)¹; piperine^⬖ (relieved vasospasm)¹; triptolide^⬖ (reduced cell death and inflammation)¹; salvinorin A^⬖ (relieved vasospasm)^1,2; schisandrin A^⬖ (reduced pyroptosis, an inflammatory form of cell death) ¹; astragaloside (A and IV)^⬖ (improved neurological outcomes and reduced vasospasm)^1,2; anethole trithione (a hydrogen-sulfide donor; reduced inflammation) ¹; omega-3 polyunsaturated fatty acids^⬖ (improved outcomes and increased protective autophagy)¹.

A parallel set of targeted pathway inhibitors and drugs dissolved in DMSO also hemorrhagic reduced brain injury:

Cell-death pathway inhibitors — necroptosis inhibitor^1,2,3,4,5; caspase-1 inhibitor¹; caspase-3 inhibitor^1,2,3; ferroptosis inhibitor^1,2; necrosulfonamide¹; caspase inhibitor¹.

Kinase, signaling & channel inhibitors — ERK inhibitor^1,2,3; p38 MAPK inhibitor^1,2,3; JNK inhibitor¹; HIF-1α inhibitor^1,2,3,4; LRRK2 inhibitor^1,2; STING inhibitor¹; PTEN inhibitor ¹; PTP1B inhibitor¹; HDAC inhibitor¹; Drp1 inhibitor¹; IRE1α inhibitor¹; AP-1 inhibitor ¹; TRPC channel blocker¹; FAK inhibitor^1,2; aquaporin-regulating ERK inhibitor¹; valproate and related HDAC inhibitors (improved survival in hemorrhagic-shock and TBI models)¹.

Iron, heme & inflammatory-pathway agents — TLR4 blocker^1,2; heme oxygenase-1 inhibitor^1,2; iron chelator¹; mTOR inhibitor^1,2; tin-mesoporphyrin, a heme oxygenase inhibitor¹.

Receptor ligands, growth factors & neuropeptides — TSPO ligand^1,2; FGF-2¹; mitoNEET ligand¹; ghrelin¹; IGF-1¹; orexin-A¹; apelin-13¹; sufentanil¹; siponimod¹; recombinant neurotrophin-4¹.

Other drugs & compounds — mGluR1 antagonist¹; cyclosporine A^1,2; 2-methoxyestradiol¹; dabigatran¹; glibenclamide¹; tamoxifen¹; praeruptorin E¹; didymin¹; H₂S donor AP39¹; chelerythrine¹; Nur77 modulator¹; rosuvastatin and simvastatin (reduced tPA-related hemorrhage and infarct)¹

Note: an emodin^⬖ study in acute pancreatitis (DMSO alone as a solvent) reduced tissue hemorrhage scores as one marker.

DMSO in Interventional Neurosurgery

I have argued the reason many transformative medical therapies do not enter medical practice despite widespread public demand for them is because we exist within a “pay to play” system, where access to the mainstream medical marketplace can only be earned if massive amounts of money are spent to secure an FDA approval—which is problematic as approval is largely dependent upon the money spent, not the quality of the therapy (which is essentially why the medical medical marketplace is crowded with mediocre and harmful therapies).

A key piece of evidence for my contention is that while many of the transformative (but off-patent) therapies I have come across are effectively barred from mainstream care, once the therapy is repackaged into something far more expensive and proprietary, it is often a widely embraced therapy (e.g., while used globally with immense data behind it, ultraviolet blood irradiation is not permitted in American medicine, but UVBI combined with a photosensitizer—extracorporeal photopheresis—is a widely used and extremely expensive therapy here and likewise many proprietary DMSO containing drugs have been approved by the FDA).

So, while “unsafe” DMSO is not used for strokes despite fifty years of pleas and research—it simultaneously is. Specifically, a common way many blood vessel issues are addressed is by threading a catheter into an easy-to-reach artery (for example the groin or the wrist) and then guiding it through the vessels to the site of the problem and doing something there, such as placing a stent, so you do not have to open the body surgically to get to that spot.

One common reason this is done is to cut off blood flow in a vessel, for example a bleeding artery. One popular way to do that uses DMSO to dissolve a polymer that is not soluble in blood, thereby allowing it to stay liquid in the catheter, so it can be pushed to the target. However, once it is injected into the bloodstream, the DMSO diffuses away and the polymer precipitates into a cast that plugs the vessel and stops flow. As such, tens of thousands of published papers exist on this DMSO combination^1,2,3 (with numerous readers sharing they recognized DMSO because it was in one of those agents).

Note: while generally safe¹ (with an experienced operator), since very high concentrations of DMSO are used to dissolve the polymers, they have to injected slowly so the vessels and brain tissue are not injured by a highly concentrated burst of DMSO (whereas in contrast much lower DMSO concentrations are typically used in DMSO IVs). Additionally, since the polymer plugs can travel from the target site, side effects periodically happen (and comprise a significant portion of the small number of side effects which have been reported for DMSO—as all agents used at the time of an adverse event are typically reported).

Reader Hemorrhage Reports

My most impressive experience with DMSO has been post a hemorrhagic stroke my Father had due to anticoagulant use for atrial fibrillation. Free iron from hemorrhage, especially in the brain, is quite possibly the most inflammatory event that can happen and responds to DMSO.

After IV DMSO he was totally mentally restored in 4 hours, sitting up in bed asking what his Dr said about his condition and was discharged in 36 hours with NO complications!! — From a physician reader

Several readers have described applying DMSO in the immediate aftermath of an aneurysm or brain bleed. The most detailed came from a reader whose 84-year-old mother suffered a grade 3 brain aneurysm and subarachnoid hemorrhage: about 90 minutes after the event, as paramedics loaded her into the ambulance, the reader applied topical DMSO, with a smaller application in the ER hours later and small amounts perhaps six times over the next two weeks in the ICU. She went on to make a nearly complete—possibly complete—neurological recovery, with her remaining issues (weakness, UTIs) plausibly attributable to six weeks of bed rest. The reader described her recovering in sudden increments, as if her brain were “re-indexing” visual and motor skills and finding neural pathways that had been misplaced after the aneurysm.¹ In a follow-up roughly a year later, the same reader reported that despite a subsequent fall and subdural hematoma (during which DMSO was only applied several days late), his mother remained in assisted living with most of her cognitive function and mobility intact—an outcome he understood to be exceptional for someone her age.¹

Another reader described her own nonaneurysmal brain hemorrhage following an ice bath, three weeks after first buying DMSO on the strength of these articles. Her partner applied DMSO immediately; she went to the hospital, then resumed topical DMSO at home. At a follow-up scan, the neurosurgeon reportedly expressed surprise both that she had not developed cerebritis after the hemorrhage and that she had improved so markedly in such a short time.¹

A reader whose 93-year-old grandmother had suffered several brain injuries over eighteen months—including a stroke and two brain bleeds caused by a fall with a blow to the head—reported that treating her with DMSO “made her recovery much faster.”¹ Another reader survived a brain hemorrhage three weeks after buying DMSO on the strength of these articles; after the hospital misdiagnosed her, she applied it topically and then took it orally twice a day, and came through with “no inflammation and very little residual issues.” In her words, “without [@MidwesternDoc] I don’t think I would be alive today.”¹

A reader who purchased DMSO for her mother-in-law—who had suffered a brain aneurysm seven years earlier—noted improvements across a range of unrelated issues (plantar fasciitis, knee-replacement swelling, varicose veins, arthritic hands) and was watching to see whether cognition and brain fog would improve over time. In the same report, the reader’s husband, who suffered near-constant neck and head pain and worsening migraines, applied DMSO once and reported his headache and neck pain were “GONE.”¹

DMSO’s ability to relieve the pressure a mass places on neural tissue was also illustrated in a non-hemorrhage case. A clinician reader who shared he’d seen several glioblastomas resolve with mebendazole described one patient left virtually blind in one eye because the tumor had compressed the optic nerve; even after eight months of treatment fully eliminated the tumor, the blindness remained. After being shown DMSO eye drops, the patient used them once—and by the next morning his wife reported his vision had returned to normal.¹ Though the tumor was gone, the compressive injury to the nerve had persisted until DMSO addressed it, mirroring the way DMSO relieves the pressure and secondary injury that follow a brain bleed.

Likewise, another reader’s partner (aged 75) was diagnosed with an inoperable 8 cm glioblastoma causing a slow brain bleed, losing the ability to speak and developing right-side paralysis, with a prognosis of three weeks to live. After copious topical DMSO, motor function began returning within 24 hours; over the following weeks the partner regained the ability to feed himself, communicate using Google Translate, and perform basic activities, and by week four could walk with a walker. A new CT scan at day 55 showed no brain bleed and reduced tumor metrics.¹

Collectively, these reports mirror what was reported within DMSO literature and again suggest (provided another anticoagulant is not being taken), DMSO does not expose individuals with an active brain bleed to a serious risk. That said, the far smaller number of hemorrhagic testimonials makes me less confident in this assessment (e.g., if someone had used DMSO for a hemorrhagic stroke and died I would not have heard from them and within a sample that small that possibility can’t be excluded). However, given that hemorrhagic strokes are much rarer than ischemic strokes (13% vs. 87%), even if every case where a reader had used DMSO for either type of stroke was reported to me, I would still expect to receive far less hemorrhagic stroke reports. Notably, the ratio between all the ischemic and hemorrhagic stroke reports I’ve received here is fairly close to their expected distribution within the population, again suggesting there is not a significant (hidden) pool of readers with bad DMSO hemorrhagic stroke experiences.

Traumatic Brain Injuries and Concussions

While ischemic strokes are difficult to treat, hemorrhagic strokes and severe traumatic brain injuries are often more challenging still, and after decades, progress in neurologic intensive care has been limited, particularly in preventing the long-term paralysis and disability that follow a serious head injury.¹ The core problem is that the initial impact is only the beginning, as in the hours and days that follow, a secondary injury unfolds, as swelling raises the pressure inside the rigid skull, circulation to the injured tissue falls, free radicals are generated in large quantities, and cells that survived the initial trauma begin to die.

This secondary cascade, together with the impact itself, determines whether a patient lives, and whether they recover. DMSO addresses that cascade at almost every point at once. It rapidly draws off the excess fluid driving intracranial pressure, restores circulation to the compromised tissue, scavenges the free radicals generated by the injury, and directly protects neurons from dying. Because a traumatic brain injury requires all of these problems to be solved simultaneously (something conventional care attempts with a different intervention for each, with the therapies often having conflicting effects and hence requires careful balancing between them), an agent that does all of the needed actions together is uniquely suited to the task. What follows is the extensive and largely forgotten evidence that DMSO does here.

Note: conflicting evidence exists supporting the use of progesterone, hypothermia, and hyperbaric oxygen therapy for traumatic brain injuries, but none of these approaches are in widespread use. Strong evidence also supports the use of methylene blue but it also is rarely used. Finally, certain trials (e.g., with progesterone or with an adenosine kinase inhibitor) find those therapies work even better if combined with DMSO.

Severe Head Trauma

The most striking human evidence concerns DMSO’s ability to rapidly lower the dangerously high intracranial pressure (ICP) that follows severe head injury, an effect that repeatedly translated into improved survival and neurological recovery.
Note: typically agents that lower ICP also lower (necessary) cerebral perfusion. As DMSO instead protects both, it is hence uniquely suited for these situations (e.g., while pentobarbitone and DMSO lowered ICP comparably (a 66% versus 45% drop)—pentobarbitone dropped systolic pressure by an average of 20 torr while DMSO caused no such drop, preserving cerebral perfusion¹).

A pivotal study on this followed ten patients with closed head trauma and severely elevated ICP (40 to 127 mmHg, against a normal 5 to 13 mmHg) who received IV DMSO. In most cases ICP began dropping within 30 minutes, falling on average 28 mmHg after 24 hours and 58 mmHg after six days, with the reduction in brain swelling confirmed by CT scans. At a six-day neurological assessment, six patients had mild or no impairment and two had moderate impairment (two eventually died of their injuries), and by three months seven had minimal to no impairment. No adverse effects from DMSO were observed.^1,2,3 This study, in turn, built on an earlier report of ten patients with severe closed head injuries, where DMSO rapidly reduced ICP and increased cerebral perfusion without lowering systemic blood pressure, and again improved the neurological course and outcome.¹

These results were replicated across other studies. In a prospective study of 10 patients with severe closed head injury, marked brain swelling, and Glasgow Coma Scale (GCS) scores of 6 or below, IV DMSO (given whenever ICP reached 25 mmHg) dropped ICP markedly within 10 minutes (mean maximum reduction of 23.5 mmHg), raised cerebral perfusion pressure as ICP fell, and produced no rebound; seven of ten survived, six without gross deficits.¹ In 12 patients with traumatic brain injury and elevated ICP, IV DMSO (given on average twice) rapidly reduced ICP in 21 of 23 treatment sessions, with the non-responding sessions also failing to respond to mannitol or furosemide, and no effect on blood pressure or other side effects.^1,2 Likewise, a trial of 35 patients with severe head injury undergoing emergency cranial surgery found IV DMSO controlled ICP in 75% of cases (versus 53% with standard therapy), and controlled it in half of the patients who had already failed conventional treatment.¹

The speed of the effect impressed even DMSO’s contemporaries. At a 1980 Congressional hearing on DMSO,¹ Dr. Stanley Jacob discussed Oregon data (published in 1983¹) on 11 patients with intracranial hypertension from mixed causes, 5–6 of whom were already unresponsive to barbiturates and mannitol (3 of the barbiturate nonresponders after head trauma). IV DMSO dropped ICP to the normal range within 3–5 minutes in all 11 and was repeated as needed to keep ICP below 20 mmHg with three patients expected to die recovered well. A further five patients started on DMSO earlier did markedly better than those given it only after other measures had failed.

Finally, a report discussed by Dr. de la Torre¹ (which I could not locate) detailed five patients with closed head injuries and high ICP that rapidly fell with IV DMSO. A 1.5 year old with a GCS of 7 and ICP of 30 mmHg fully recovered over 3 weeks, and a 7 year old admitted with a GCS of 5 and ICP of 25 mmHg fully recovered after 8 weeks; the three others (aged 17 to 52 with GCS scores of 3 to 5, two with ICPs above 50 mmHg) initially responded but did not survive.

Note: an early and candid 1982 report by UC San Diego researchers captured both the promise and the practical problem with DMSO in this era. The authors found the drug “often initially successful in controlling ICP” and “occasionally effective when barbiturates have failed” (and noted the ICP drop was too rapid to be a simple diuretic effect, implying a distinct mechanism), but struggled with its administration, as concentrated DMSO could dissolve standard IV tubing and the large fluid volumes then used were poorly suited to a head-injured patient (making prolonged control of ICP challenging to calibrate). These were solvable problems as refined protocols were developed (e.g., later work used lower concentrations and different IV materials to avoid them), but at the time they blunted enthusiasm for a therapy that was otherwise working.^1,2,3 Likewise, a 1981 NIOSH report documented that staff at San Francisco General Hospital developed headaches and nausea (likely due to concentrated dimethyl sulfide) while working in rooms with patients receiving high-dose IV DMSO for an experimental cerebral-edema protocol, and that the problem resolved once room ventilation was improved¹—something which has required clinics offering IV DMSO to often have a “DMSO only day” and that could likely also be addressed with appropriate air filters.

DMSO’s use for traumatic high ICP is also recognized in veterinary medicine, where its edema and pressure-lowering effects have long been utilized in large animals. A 1991 veterinary review of IV DMSO for traumatic brain injury in horses describes its use to reduce cerebral edema, intracranial pressure, and anoxia (with a regimen used at Oregon State University given slowly, generally twice daily), noting that DMSO increases localized circulation and cortical vasodilation, reduces platelet aggregation and fibrin thrombus formation in small injured vessels, protects endothelium, and reduces elevated ICP.¹ Likewise, in equine clinical guidance, IV DMSO is indicated for acute head trauma resulting in high intracranial pressure and cerebral edema,¹ and in parallel, a broader review of DMSO in equine medicine covers its application to central nervous system trauma among other indications.¹ Similarly, in one case report, a 10-month-old filly presenting in coma after severe skull-brain trauma, IV DMSO was given as part of aggressive supportive therapy,¹ and an early proprietary DMSO formulation was evaluated in craniotomized (skull opened) dogs for its effects on cerebral edema and inflammation.¹ In another, a 2-day-old Quarter Horse filly with perinatal asphyxia and hypoxic-ischemic encephalopathy, given DMSO as part of supportive care, recovered fully by discharge,¹ and a goat with polioencephalomalacia treated with IV DMSO alongside corticosteroids and mannitol showed progressive neurologic improvement with MRI-confirmed resolution of the lesion.¹

Human Antioxidant Trials

A separate line of human research, largely published in the Ukrainian and Russian literature, approached DMSO from the angle of its free-radical scavenging rather than its pressure-lowering effect, and provides some of the strongest controlled human TBI data in this section.

The most substantial came from a 2003 dissertation at the Romodanov Neurosurgery Institute in Kyiv, which combined rat experiments with a controlled trial in 135 severe TBI patients. It established that lipid peroxidation, a key driver of secondary brain damage, activates within 3 hours of injury, peaks around days 3 to 7, tracks with injury severity, and persists for at least a year. In a controlled arm of 75 of those severe TBI patients, adding intravenous DMSO (first dose 3 to 5 hours after trauma and a second the following day) to standard therapy reduced lipid peroxidation markers by 22% by day 8 (versus a 15% rise in controls), raised the peroxide resistance of red cells by 71% (versus 13% in controls), and accelerated the regression of major neurological syndromes, with significant improvement in general cerebral (66.6%), meningeal (95.8%), asthenic (46.1%), and vegetative (95.6%) symptoms compared to standard therapy alone.¹ The parallel rat work found that the same intraperitoneal DMSO regimen significantly reduced lipid peroxidation products in brain and blood (TBARS by 8 to 34%, Schiff bases by 27 to 68%) and raised red-cell resistance to peroxide-induced hemolysis by 11 to 51%, with the antioxidant effect sustained out to 21 days.
Note: these results have many intriguing correlations to Plotnikov’s previously mentioned research and the Russian chronic stress discussed in the first part of the series all of which suggests DMSO can counteract primary causes of acute and chronic neurodegeneration.

Likewise, this antioxidant framing recurs throughout the Russian-language reviews, where DMSO is classified as a synthetic radical scavenger noted for trapping the highly damaging hydroxyl radical and for providing a “high and stable” antioxidant effect in severe craniocerebral trauma, raising the body’s antioxidant status and preventing secondary brain damage.¹

Animal Brain Injury Research

The human findings above have been reproduced and mechanistically dissected across a wide range of animal brain injury models.

•Compression and pressure injuries: Because any brain bleed or concussive impact risks putting pressure on part of the brain (for instance from an expanding clot), the models that mimic this are especially relevant. The most dramatic was a study in which an expanding balloon was placed in the brains of 40 rhesus monkeys to simulate a hematoma. All 10 saline-treated monkeys died, versus 10 of 15 surviving with urea (66.7%) and 14 of 15 with DMSO (93.3%), and among survivors neurological deficits occurred in 4 of 10 urea-treated animals versus only 1 of 14 given DMSO.^1,2 This study, in turn, was preceded by an earlier study of 30 monkeys with similar results.¹
Note: urea was previously regularly used as a diuretic,¹ and while it is now mostly (but not completely¹) forgotten. We have found one oral urea formulation to be very helpful for certain types of edema and swelling.

Pressure injuries in dogs told the same story. In dogs with reduced blood pressure, pressure was applied directly to the brain for an hour, cutting off cerebral blood flow and producing necrosis, cavitation, edema, and deficits on the opposite side of the body. Against a panel of agents (barbiturates, mannitol, dextran, methylprednisolone), DMSO was the most effective: compared to no treatment, it improved neurobehavioral scores by 220%, reduced lesion volume by 93%, and prevented death in 5 of 6 dogs. Since blood alcohol worsens the damage from a traumatic brain injury (as occurs in drunk driving), the experiment was repeated with high blood alcohol, where DMSO still reduced brain tissue damage by 60%.^1,2,3 In a related model, pressure-induced ischemia applied to the somatosensory cortex killed every untreated dog within days, whereas with IV DMSO five of six survived with no neurological or behavioral changes and preserved evoked potentials. A further comparison of seven therapies likewise found DMSO the most effective against pressure-induced focal ischemia. Likewise in rats with diffuse axonal brain injury, DMSO significantly reduced c-fos and c-jun gene expression in neurons across the cortex, white matter, brain stem, thalamus, and cerebellum, with the most pronounced reduction 2 hours post-injury compared to controls¹—which is noteworthy as these genes drive inflammation and neuronal cell death in the window immediately after traumatic brain injury.

Note: one of the more intriguing findings across these compression studies was that neurological function was frequently preserved even when injury was still present in the brain tissue itself, suggesting DMSO protects function above and beyond what its effect on visible damage would predict.

•Edema models: A large body of rabbit work established DMSO’s anti-edema effect. A rabbit study that created lethal brain edema by freezing part of the brain found DMSO significantly reduced ICP and edema within 5 minutes while raising cerebral perfusion and leaving central venous pressure unchanged.¹ This was reproduced repeatedly, including a follow-up with similar results,¹ one using slow infusion rather than a bolus,¹ another one that also found a 20% solution reduced ICP more reliably than 30% or 40% (at 1.0 to 2.0 g/kg),¹ two others showing a synergistic effect with a barbiturate (where DMSO enhanced the ICP reduction while counteracting the barbiturate’s reduction of brain blood flow),^1,2 one indicating the effect was mediated through sodium mobilization,¹ and a final set showing indomethacin partly blocked DMSO’s ICP reduction, implicating prostaglandins.^1,2,3

Note: highlighting DMSO’s normalizing properties, while DMSO lowers pathologically elevated ICP, in anesthetized rabbits with normal pressures, intravenous DMSO produced a prompt, significant rise in cerebrospinal fluid pressure (up to 66 mm H₂O, lasting under a minute)—and, unlike norepinephrine or epinephrine, it did so with no change in systemic blood pressure, respiration, or anything else, pointing to a local cerebral vascular or blood-CSF barrier effect.¹

A Chinese study likewise used DMSO for acute cerebral edema.¹ The effect held in other edema models too: in rabbits with brain edema induced by injecting pertussis vaccine into the carotid artery, IV DMSO effectively reduced ICP and edema,¹ and in rats with edema induced by injecting iron (FeCl₂) into the brain, intraperitoneal DMSO reduced edema by 23% initially and left treated rats with far less edema at 24 hours.¹ Similarly in cats exposed to standardized cortical freeze injury, DMSO reduced Evans blue extravasation—a marker of blood-brain-barrier disruption and vasogenic edema—acting as a hydroxyl-radical scavenger and grouped with deferoxamine as effective.¹ Finally in a rat frozen-brain-injury model, DMSO (0.4 g/kg*) significantly reduced brain water content and neuronal apoptosis, outperforming tetramethylpyrazine at relieving the edema.¹

Note: the older pertussis vaccine (which was notorious for causing severe brain injuries) contained a toxin that disrupted the blood-brain barrier and created brain inflammation. In that study, injecting it into the artery feeding the brain was used as a reliable way to induce brain damage.

•Missile and penetrating injuries: To simulate DMSO’s protective effects against gunshot wounds, missile injuries (frequently with BB pellets) were created in monkeys. Compared to mannitol, DMSO produced significantly better cerebral perfusion and oxidative metabolism along with an 86% survival rate (versus 75% for mannitol and 55% untreated).¹ These results were replicated in a more detailed follow-up¹ and by two other groups.^1,2 A direct comparison to mannitol in rhesus monkeys with a standardized occipitofrontal missile injury confirmed DMSO better preserved cerebral blood flow, perfusion pressure, and oxidative metabolism than mannitol,¹ and a further monkey study comparing 50% DMSO to mannitol for experimental brain gunshot wounds tested repeat dosing whenever ICP exceeded 20 mmHg.¹

•Impact and weight-drop models: Numerous studies simulate closed head trauma by dropping weights on the heads of animals, and DMSO consistently protected against the resulting damage. In injured rats it reduced neuronal apoptosis, increased anti-apoptotic Bcl-2 expression across 6 to 168 hours post-injury,¹ and raised Survivin and NF-κB expression in injured tissue, all reducing cell death.¹ Functionally, DMSO improved cognitive and locomotor performance (such as solving mazes) while reducing anxiety, oxidative stress, inflammation, necrosis, and axonal damage,¹ and separately reduced memory deficits by 62% a week after injury.¹ A particularly rigorous study found that DMSO significantly reduced secondary neuronal degeneration in the hippocampus, with a magnitude of neuroprotection statistically indistinguishable from curcumin^⬖ or alpha-tocopherol^⬖ tested alongside it, leading the authors to conclude DMSO itself acted as a neuroprotective agent.¹ In mice, DMSO combined synergistically with fructose 1,6-diphosphate (FDP) to protect motor function, survival, and cortical and hippocampal neurons from these injuries.¹

Note: in animal experiments simulating severe brain injury, DMSO has also been shown to strengthen respiration (which otherwise becomes shallow and may stop), and in both humans and animals it often significantly increases urination through its diuretic action.

•Free-radical scavenging: DMSO also attenuated free-radical-mediated neurotoxicity in traumatized rat hippocampal neuron cultures, reducing apoptosis in uninjured neighboring cells by scavenging reactive oxygen species,¹ providing a cellular-level mechanism to for its protective effects here.

Jacob and de la Torre’s capstone review of this literature,¹ summarized the whole picture: low-dose intravenous DMSO restores cardiac output and cerebral blood flow, inhibits tissue-factor expression, scavenges free radicals, suppresses platelet aggregation, and in CNS models and patients rapidly lowers intracranial pressure without rebound, reduces edema, raises cerebral perfusion pressure, limits infarct volume, and preserves vulnerable hippocampal neurons.

To put all of this into context:

A January 11, 1981, news report in the Ocala Star Banner [page 6] carried the headline “DOCTOR CLAIMS DMSO SAVED 11.” The story read:

SAN DIEGO (AP) - A doctor at the University of San Diego [UCSD] credits the controversial drug DMSO with saving the lives of 11 people who suffered severe head injuries.

Dr. Perry E. Camp, a UCSD Medical School neurosurgeon, said Friday that dimethyl sulfoxide was effective for 11 of 30 people judged near death and for which other lifesaving methods have proved useless.

“To take patients like that and have even one out of 10 survive is phenomenal,” Camp said. “The fact that we have any survivorship at all . . . doesn’t sound like much, but it is extremely encouraging,” Camp said.

Note: many of the same principles discussed above hold true for concussions, and the pioneers of DMSO felt DMSO was an essential treatment for athletes after they experienced one, particularly since concussions can predispose the athlete to long-term cognitive issues (e.g., both boxers and professional football players have a threefold risk of dementia).

Traumatic Brain Injury DMSO Combinations

Like many other neurological conditions, a variety of agents dissolved in DMSO have shown promise in treating traumatic brain injuries, and convergent effects seen suggest some of the effects arise from DMSO rather than the active agent.

For example, in a controlled cortical impact study using DMSO as the vehicle for glibenclamide, the authors reported “unexpected independent beneficial effects” of DMSO itself, particularly in female mice, in which DMSO alone significantly downregulated the neurodegeneration markers TDP43 and TAU and helped restore cerebral blood flow by 21 days post-injury, comparable to the drug it was merely supposed to be dissolving. The authors flagged these as novel, previously unrecognized protective effects.
Note: this response illustrates why the protective effects of DMSO are rarely recognized in combination studies as the authors frequently can’t even conceive they could be present to begin with (despite a vast body of evidence already showing it).

Traumatic Brain Injury Combinations

The TBI combinations were as follows:

Natural agents — curcumin^⬖ (reduced inflammation, oxidative stress, and seizure susceptibility)^1,2,3; tetrahydrocurcumin^⬖ (curcumin’s more absorbable form; enhanced autophagy and restored antioxidant enzymes)¹; resveratrol^⬖ (reduced cell death and modulated autophagy)^1,2,3,4; quercetin^⬖ (reduced swelling and cell death)¹; sulforaphane^⬖ (reduced swelling, contusion size, and oxidative stress)¹; alpha-lipoic acid^⬖ (improved neurological scores and reduced cell death)¹; honokiol^⬖ (from magnolia bark; protected the blood-brain barrier and reduced oxidative stress)¹; vitamin K₂^⬖ (reduced inflammation)¹; docosahexaenoic acid (DHA)^⬖ (the omega-3 fatty acid; improved autophagy and reduced inflammation)^1,2,3,4; erianin and the mangrove-fungus derivative C53N (from Dendrobium; reduced inflammation, oxidative stress, and cell death (isolated research compounds rather than accessible remedies))^1,2; Morin^⬖ with MK-801 (lowered dementia and inflammatory markers after repetitive TBI)¹; Auraptene^⬖ (reduced oxidative stress and inflammation)¹.

Note: the hormones progesterone and 17β-estradiol were also repeatedly delivered in DMSO and found protective after TBI, reducing swelling, oxidative stress, and inflammation while improving neurological outcomes. ^1,2,3 Notably, in one progesterone study the DMSO-only arm itself showed the same pattern of benefit¹ (reduced swelling and cell death and improved neurological scores over time), an ambiguity in the source data that again points to how independent DMSO effects get folded into the “vehicle” group.

A far larger set of studies used DMSO to deliver targeted pathway inhibitors and other synthetic compounds. Across these, the agents below repeatedly reduced brain swelling, cell death, oxidative stress, and neurological deficits, with the DMSO-only arm often following the same protective direction.

Oxidative-stress & Nrf2 agents — Nrf2 activators apocynin^1,2; and tert-butylhydroquinone¹.

HDAC & epigenetic inhibitors — HDAC inhibitors^1,2,3.

Cell-death & protease inhibitors — necroptosis inhibitors^1,2; a cathepsin, a calpain inhibitor¹ and a selective PAR-1 inhibitor (improved depression-associated behaviors, social interaction and hippocampal-associated cognitive impairment).¹

Autophagy & mTOR modulators — autophagy modulators^1,2,3; an Epac2 inhibitor¹; an mTOR inhibitor (rapamycin)¹.

Receptor ligands & agonists — an S1P1 agonist and a bile-acid-receptor agonist^1,2; a translocator-protein ligand¹; a histamine-receptor ligand¹.

Other pathway & enzyme modulators — a matrix metalloproteinase inhibitor^1,2; a PTEN inhibitor¹; an adenosine kinase inhibitor¹; mitochondrial uncouplers¹; a spinogenic agent¹; a CRMP2-derived peptide¹; cypin activators¹; an anti-inflammatory (ATB-346)¹; salubrinal (improved motor and cognitive function and reduced lesion size)¹; an ADAM inhibitor (reduced lesion size and axonal injury)¹.

Edema model combinations — curcumin^⬖ (reduced brain swelling and inflammation)¹; quercetin^⬖ (reduced oxidative stress, brain swelling, cell death, and vasospasm)¹; kadsura pepper stem extract^⬖ (reduced hematoma size)¹; a JAK2 inhibitor with dexmedetomidine (reduced brain swelling and cell death)¹; a KMO inhibitor¹.

TBI and Concussion Reader Reports

Within the DMSO literature, there are periodic cases of dramatic concussion recoveries following DMSO. For example, one author shared the case of a woman who had received a severe concussion from falling off a horse, after which she had trouble walking, would suddenly neurologically decompensate (e.g., dropping things), and had memory issues alongside foggy headaches. Thirteen years later, she received an injection of DMSO, immediately had a large improvement, and further improved with subsequent injections.

Readers recovering from traumatic brain injuries, concussions, and related head trauma have reported similar benefits from DMSO.

The most mechanistically intriguing report came from a reader who is post-traumatic brain injury since 2017 and lives with cervical instability and a CSF leak that leaves her with recurring concussion-like symptoms. Even at a low dose she could tolerate, she found DMSO noticeably lowered her intracranial pressure, along with reducing daytime fluid retention, improving her distance vision and bowel function, and lessening food reactivity. She noted this could be particularly helpful for others with raised intracranial pressure, since, as in her case, elevated ICP can itself produce CSF leaks.¹

Other readers reported briefer successes: one for sciatica and brain trauma¹ (”It works!”), and another for finger joints and a head injury.¹

Concussion Reports

Several readers have described using DMSO specifically for concussion. One with a concussion said it was “saving me and helping me to continue working,”¹ another used it for post-concussion and whiplash injury,¹ and another, recovering from fifteen concussions and a broken back after a 1992 Grand Canyon fall found success with castor oil^⬖ and DMSO.¹

Another reader described slipping on a wet floor and landing on her cheekbone with nothing but her glasses to break the fall—”I could feel my brain slam inside my head.” Within 30 minutes her cheek and eye had puffed up severely; she ingested DMSO and lathered it on her face, continuing for three days. By day five the bruising was already in its final yellowing stage. “I think had I not had DMSO in my house, I would be suffering from symptoms of concussion now,” she wrote, adding that she now keeps a bottle in her handbag at all times.¹

The most detailed concussion account came from a reader who said DMSO “gave me my life back” after a shoulder injury with a concussion of the upper back left everything from his neck to his left hand inflamed and painful, and left him feeling systemically ill for months. Standard anti-inflammatories were useless. Starting a topical DMSO once nightly, he felt “not sick for the first time in months” within about three weeks. He described the pain first being suppressed, then localizing to its true source (his neck rather than the shoulder), then resolving, alongside a range of incidental benefits (a chronic wrist problem, thumb inflammation, eye floaters, a fading scar, and body odor all improved). He also found an on-off strategy worked best, applying for several days then pausing, observing that each time he stopped, the pain would briefly spike and then settle to a new low, as though removing DMSO let the body “better see where the problems really are.”¹

One reader even tried it for a rare eye condition tied to an old concussion. He has superior oblique myokymia, a “twitch behind the eye” that makes his vision jump and occasionally double (alarmingly, sometimes while driving at speed), which had been attributed to a concussive injury from a serious car accident in which an airbag knocked him out. After a neuro-ophthalmologist offered only anti-convulsant drugs with “awful” side effects, he tried a 10% DMSO solution in distilled water as an eye drop, which temporarily “hit the off switch.” It didn’t cure the condition, but gave him, in his words, an actual tool in the toolbox.¹

Note: concussions are notoriously difficult to manage (e.g., I have only found one approach that seems to work consistently for them), so the possibility a simple and widely accessible option exists is immensely encouraging as it would benefit many. However, while the evidence strongly argues for DMSO’s use in severe traumatic brain injuries, there is much less data for typical concussions, and it is quite likely the results for DMSO on those injuries were will be highly variable with not everyone experiencing a noticeable benefit from DMSO.

The Heart

Because the heart, like the brain, is exquisitely sensitive to oxygen deprivation and to the flood of free radicals that accompanies the restoration of blood flow, DMSO’s protective and circulation-promoting effects have shown promise for many heart conditions (e.g., physiologic concentrations of DMSO enhanced respiratory control ratio and viability of heart cardiomyoblasts¹).

For example, DMSO’s scavenging ability has been shown to protect the heart from many stressors. These includes protecting heart-muscle contractility from iron-induced oxidative injury,¹ completely blocking radical-mediated damage to the calcium-handling machinery of cardiac cells,¹ preserving the sodium-potassium pump during ischemia-reperfusion,¹ protected the cultured chick embryo cardiac myocytes from injury caused by hydrogen peroxide,¹ and preventing lipid peroxidation of heart-cell membranes under bacterial-toxin stress.¹

Ischemia and Heart Attacks

As DMSO’s therapeutic properties in strokes directly translate to heart attacks, many studies have explored it here:

•When the heart’s blood supply is impaired, its ability to pump is as well (which is part of why heart attacks are a downhill spiral, as the heart loses the ability to give itself the blood it needs). When heart attacks were modeled (e.g., by ligating the coronary artery to impair the heart’s blood supply), DMSO was able to counteract this. For example, in a dog heart attack study, an IV bolus of DMSO raised cardiac output to 1.65 L/min by the third hour versus 1.15 L/min in untreated controls, alongside lowering systemic vascular resistance and increasing cerebral blood flow.¹ Likewise, in another dog study, intravenous DMSO (2 g/kg as a 50% solution*) transiently raised cardiac index from 4.56 to 6.91 L/min/m² and stroke index from 36 to 45 ml/beat/m² while dropping systemic vascular resistance.¹

•In addition to preserving the heart’s vital function, many studies have shown DMSO prevents damage to the heart itself. In isolated rat hearts subjected to global ischemia-reperfusion, three days of intraperitoneal DMSO pretreatment (550 mg/kg*) cut infarct size from 50.0% to 21.2% and improved post-ischemic left-ventricular function.¹ In rats where the coronary supply was cut for 30 minutes and then reperfused for 120 minutes, DMSO preserved coronary blood flow and reduced both the resulting necrosis (tissue death) by 57.6% and the ensuing left-ventricular dysfunction (an effect that was greater when DMSO was given for several days beforehand rather than immediately prior to occlusion).¹ In another rat study, DMSO reduced the damaged portion of the heart by 76.18%,¹ and in another it prevented contracture bands from forming in ischemic heart tissue (a common long-term complication of heart attacks).¹

•Similarly, in pigs, DMSO significantly reduced intramyocardial hemorrhages and gross pathological changes,¹ and in another study improved overall heart attack outcomes.¹ In rabbits, giving hydrogen peroxide (H₂O₂) concurrently with DMSO immediately after occlusion reduced the damage still further, presumably by supplying oxygen to the starved tissue.¹ Consistent with this, in models of heart attack DMSO reduced the oxidative markers and preserved the antioxidant enzymes that track myocardial injury.^1,2

Furthermore, a large part of the damage in a heart attack comes not from the loss of blood flow itself but from its restoration, and DMSO addresses this reperfusion injury directly. In perfused rat hearts, 10% DMSO attenuated the oxygen paradox, reducing reoxygenation creatine-kinase release from 25.3 to 7.2 IU/g and cutting calcium-paradox enzyme release from 134.1 to 54.9 IU/g,¹ and it likewise protected against the reperfusion injury caused by calcium-containing solutions.¹ In isolated cardiac muscle it preserved contractility during hypoxia,¹ an effect echoed in rabbit studies of preserved contractile strength¹ and maintained cardiac output and brain perfusion in dogs.¹

This same protection extends to hearts held for surgery or storage: in isolated rat hearts, 0.5% DMSO reduced post-storage contractile dysfunction during hypothermic ischemic storage,¹ and when added to cardioplegic solutions (used to stop the heart during surgery) at 0.55%, fully preserved mitochondrial respiration after two hours of global ischemia.¹ Combined with cardioplegia and alpha-tocopherol,^⬖ DMSO likewise improved rat-heart function through ischemia.^1,2 Beyond ischemia, it protected against endotoxin-induced myocardial injury,¹ improved survival in endotoxemic rats,¹ and shielded the heart from intravenous potassium (given at the dose used in lethal injections).¹ Most notably, with a cardiac enzyme that normally breaks down ATP (extracted from cow hearts) once mixed with DMSO, it instead synthesized ATP, suggesting DMSO can create a cellular environment that favors energy generation—particularly when the conditions cells normally rely on for it are absent (e.g., during a heart attack).¹

Reviews have accordingly proposed DMSO as an antioxidant therapy for myocardial ischemia reperfusion injury¹ and summarized its cardiac and CNS pharmacology,¹ and reviews of renal and organ protection in aortic surgery note that low-dose IV DMSO restored cardiac output after coronary ligation in dogs while scavenging free radicals, blocking Na⁺/Ca²⁺ influx, and suppressing platelet aggregation.¹

Note: as DMSO’s effects are dose and administration dependent, some studies found weaker results. For example, where DMSO served only as the solvent control, it sometimes protected on its own: in a rat deep-hypothermic-circulatory-arrest model testing ebselen, the DMSO solvent-control group itself showed partial protection on several markers, limiting attribution of the benefit to the drug.¹ Likewise, in a canine model of coronary occlusion and reperfusion, intravenous DMSO reduced infarct size but not to a statistically significant degree (43.7% vs. 53.4% in controls),¹ in two others the benefit was small^1,2 and in another heart attack study I located, DMSO provided no benefit (which was likely due to 50% DMSO being directly infused).¹ All of this indicates that while helpful, it is not guaranteed DMSO will be able to help every heart attack.

Lastly according to one of the main DMSO authors,¹ DMSO was used to treat angina pectoris, heart attacks and prevent heart attacks by physicians in Chile (likely at the dose of 2g/kg). However, despite my best efforts, I could not locate the published paper he referred to with the limited information provided, so it’s likely impossible to corroborate this claim.

Cardioprotective Combinations

Many agents delivered in DMSO reduced infarct size, apoptosis, or oxidative injury in myocardial ischemia-reperfusion and cardiac-arrest models.

Polyphenols & flavonoids — curcumin^⬖ (reduced inflammatory cytokines and oxidative stress) ^1,2,3,4,5; resveratrol^⬖ (reduced oxidative stress and inflammatory cytokines) ^1,2,3,4; quercetin^⬖ (shrank the infarct) ¹; lycopene^⬖ (reduced heart-cell death) ¹; propolis^⬖ (improved heart function) ¹; dihydromyricetin^⬖ (reduced inflammatory cytokines and cell death) ¹; eriocitrin^⬖ (improved cell survival and oxidative stress) ¹; danshensu^⬖ (reduced oxidative stress and cell death); Licochalcone A^⬖; curcumin^⬖; quercetin (with Ala-Gln)^⬖; eriocitrin^⬖; tanshinone IIA (PLGA nanoparticles)^⬖ (protected against oxidative damage); genistein^⬖ (reduced oxidative stress); flavonols^⬖ (preserved the heart’s pumping strength); mangiferin^⬖ (antioxidant protection against a chemically induced heart attack) ¹.

Alkaloids & terpenes — carvacrol^⬖ (reduced infarct size and cell death, and reduced mitochondrial fission)^1,2,3; higenamine^⬖ (reduced infarct size and improved heart function) ¹; notopterol^⬖ (improved heart function and reduced scarring)¹.

Saponins, terpenoids & other botanicals — ginsenoside Rh2^⬖ (reduced inflammatory cytokines) ¹; ginsenoside 20(S)-Rh2^⬖ (improved heart function)¹; ginsenoside Rd^⬖ (cut infarct size from 36% to 21%, and shifted immune cells toward healing)^1,2; magnolol^⬖ (reduced infarct size)¹; honokiol^⬖ (reduced infarct size) ¹; asiatic acid^⬖ (reduced cell death and oxidative stress)¹; curculigoside^⬖ (improved cell survival and reduced infarct size)^1,2; tanshinone IIA^⬖ (reduced cell death and inflammation)^1,2; astragaloside IV^⬖ (promoted new blood-vessel growth)^1,2; triptolide^⬖ (reduced inflammation and scarring)¹.

Anesthetic (pre-/postconditioning) agents — propofol (reduced cell death)^1,2; sufentanil¹; sevoflurane (reduced infarct size 36% vs 56%)^1,2; desflurane (reduced infarct size 48% to 19%) ¹; isoflurane¹.

Mitochondrial & metabolic-pathway agents — hydrogen sulfide donors (repeatedly reduced infarct size, including in diabetic hearts)^1,2,3,4,5; rapamycin (protected diabetic and normal hearts, cutting infarct size from 36% to 13%)^1,2,3,4; Mdivi-1 (reduced infarct size and cell death, including in diabetic and pre-diabetic hearts)^1,2; MOTS-c (reduced infarct size)¹; diazoxide (reduced oxidative stress and preserved mitochondria)^1,2; carbon monoxide-releasing molecules (reduced injury)^1,2,3.

Repurposed clinical drugs & metabolic agents — dapagliflozin (reduced inflammatory infiltration)¹; canagliflozin (improved heart function)¹; lovastatin¹; simvastatin (reduced infarct size 39%)¹; atorvastatin (reduced infarct size)¹; roxadustat (reduced infarct size and cell death)¹; ciglitazone (reduced infarct size and inflammation)¹; tert-butylhydroquinone (tBHQ)^⬖ (reduced oxidative stress); compound C^⬖; γ-secretase inhibitor^⬖ (reduced oxidative stress); nifedipine and diltiazem^⬖ (reduced inflammation and oxidative stress); pioglitazone^⬖; NS398 / Ca-channel blockers^⬖; sorafenib (toxicity model)^⬖; probucol^⬖ (reduced ferroptosis, a form of iron-driven cell death); allopurinol^⬖; DMOG (HIF-1α activator)^⬖; pioglitazone (PA/high-glucose)^⬖; agent (equal-volume ip DMSO vehicle)^⬖; netrin-1^⬖ (reduced oxidative stress and cell death); ferrostatin-1 (reduced ferroptosis)¹; 3-iodothyronamine (reduced infarct size)¹.

Hormones — 17β-estradiol (reduced microvascular damage)^1,2,3.

Cell-death & protease/lipoxygenase inhibitors — ilomastat (reduced infarct size)¹; MI-2 (restored the cell’s ferroptosis defenses)¹; necrosulfonamide (improved recovery after cardiac arrest by blocking programmed cell death)¹; ML355 (improved heart function in pigs and monkeys)¹; zVAD-FMK (reduced injury) ¹.

Receptor, kinase & other targeted agents — MMI-0100 (cut the loss of heart function by half and halved scarring)¹; MHBFC (reduced infarct size and inflammatory cytokines)¹; ginkgetin (reduced infarct size and inflammation)¹; IB-MECA (reduced infarct size by about 40% in dogs)¹; 9-phenanthrol (reduced infarct size from 38% to 9%)¹; LGK-974 (improved heart function 62% vs 41%)¹; ticagrelor (reduced inflammation)¹; MG132 ¹; L41 (reduced infarct size and spurred heart-muscle regrowth)¹; SEW2871 (shifted immune cells toward healing)¹; left-ventricular unloading¹; HU-210 (reduced infarct size).¹

Reader Heart Attack Reports

While CPR can produce miracles, the reality is that it typically doesn’t (e.g., 10.5% of people with heart attacks resuscitated out of the hospital by EMS survive¹ and 22-24% of those resuscitated in the hospital survive¹). Because of this, I’ve put quite a bit of thought over the years into how this can be improved, and in parallel, we’ve collectively had quite a few cases where something we expected to work (e.g., a natural agent which improves circulation or eliminates clotting) did, including a few cases with DMSO. Given DMSO’s properties described above, I’ve hence repeatedly wondered if injecting DMSO during a cardiac code (CPR protocol) could have saved the person—but due to how unorthodox this was, this was understandably impossible to test. Likewise, while I know of cases where DMSO has been used to treat a heart attack, the reality of the situations around heart attack make giving it quite difficult, so I have much less experience with this than DMSO for strokes. As such, while I suspect it would be lifesaving, that is nothing more than a guess without adequate clinical experience to begin corroborating it and hence not something I can stand behind.

For that reason, I did not previously broach this, but nonetheless a few reader tried it anyways and reported success in stopping heart attacks,^{1,2,3,4,5,6,7} along with two who stated it healed complications of COVID vaccine induced heart attacks.^1,2

Of these, the most interesting one that came from a woman who described her husband getting through what she characterized as a heart attack with a blockage and ischemia, using DMSO and aspirin at the onset and then frequent DMSO over the following days, and coming through it with no measurable heart damage and feeling nearly normal a week later.¹ Notably, she independently described the same three-stage structure this section lays out: an initial circulatory phase, in which she believed the DMSO and aspirin opened the blockage in the first minutes; then the oxidative-stress phase of the first few days, in which frequent DMSO was aimed at preserving the heart tissue that reperfusion would otherwise damage; and finally the fibrosis phase from roughly days three to seven, each of which she noted, called for a different approach.¹

Note: one reader also reported DMSO helping angina,^1,2 and another concerning chest pain.¹

Myocardial Necrosis and Fibrosis

DMSO also limits the death and scarring of heart muscle. In rats given isoproterenol (a standard chemical model of infarct-like injury), DMSO reduced fiber necrosis, prevented ventricular aneurysm formation and cardiac rupture, and left a smaller residual area of fibrosis,¹ an effect confirmed in a second isoproterenol study,¹ in further work showing reduced oxidative stress after isoprenaline,¹ and in dedicated work on DMSO and experimental myocardial necrosis.¹ Finally, DMSO reduced the several-fold rise in creatine kinase, LDH, and α-hydroxybutyrate dehydrogenase and reduced histologic damage after isoprenaline.1

In a D-galactose accelerated-aging model, subcutaneous 4% DMSO lowered TGF-β1, normalized cardiomyocyte diameter, and reduced fibrotic area to near-control levels, an anti-fibrotic effect the authors attributed to DMSO itself.¹ In a series of studies on copper deficiency (which drives cardiac hypertrophy), chronically administered DMSO inhibited the hypertrophy, anemia, and heart-copper depletion via hydroxyl-radical scavenging, attenuated the rise in heart weight and water content, and preserved mitochondrial and myofibrillar ultrastructure.^1,2,3 Consistent with a radical-mediated mechanism, DMSO also reversed the copper-induced impairment of force generation, calcium handling, and myosin-ATPase activity in cardiac muscle^1,2

Note: DMSO also protected older rat hearts from the stress caused by prolonged immobility and from dietary copper deficiencies.^1,2,3,4,5

Cardiac Fibrosis & Remodeling Combinations

In the fibrosis and remodeling literature, the same anti-fibrotic or anti-hypertrophic effects was seen with many agents delivered in DMSO.

•Natural agents — curcumin^⬖ (raised antioxidant defenses and reduced heart-muscle damage); curcumin^⬖ (protected against heart-muscle damage); genistein^⬖ (reduced hypertrophy, oxidative stress, and inflammation); atractylenolide III^⬖ (reduced post-heart-attack scarring); gCTRP9^⬖ (protected injured heart cells); RGS6 with DPI^⬖ (reduced remodeling); CRIF1 with NAC^⬖ (protected injured heart cells); Maresin 1^⬖ (protected heart cells); andrographolide^⬖ (reduced hypertrophy and scarring); baicalein^⬖ (reduced heart-muscle damage, scarring, and inflammation); β-carotene^⬖ (reduced inflammation and scarring); resveratrol^⬖ (reduced fibroblast overgrowth); tanshinone IIA^⬖ (reduced hypertrophy); asiaticoside^⬖ (reduced hypertrophy); salvianolic acid B^⬖ (improved heart function); anacardic acid^⬖ (blocked hypertrophy); colchicine^⬖ (reduced fibrosis); nimbolide^⬖ (reduced fibrosis in diabetic hearts); Buyang Huanwu Decoction^⬖ (reduced post-heart-attack cell death).

•Pharmaceutical & synthetic agents — valsartan (reversed chemotherapy-induced remodeling)¹; a JNK inhibitor (reduced fibrosis)¹; a LOXL2 inhibitor (reduced fibrosis and hypertrophy)¹; an EZH2 inhibitor (reduced fibrotic proteins)¹; a GCN5 inhibitor (reduced hypertrophy and fibrosis)¹; salubrinal (improved function in heart failure)¹; rapamycin (improved pressure-overload hypertrophy)¹; a Pannexin1 inhibitor (reduced hypertrophy and fibroblast activation)¹; an H2S donor (reduced remodeling and blood pressure)¹; dasatinib (reduced fat buildup and fibrosis in diabetic hearts)¹.

Cardiotoxicity, Sepsis, and the Diabetic Heart

In 42 severely ill patients with septic complications of post-resuscitation disease, intravenous DMSO was an effective therapy, including in cases where the sepsis arose from antibiotic-resistant bacteria.¹

Additionally, DMSO has been used with a wide variety of agents to protect chemically injured, septic, and metabolically stressed hearts where it frequently reduced cardiac enzymes, oxidative stress, inflammation, and apoptosis:

•Chemotherapy cardiotoxicity — Cissus verticillata^⬖; Irvingia gabonensis extracts^⬖ (reduced heart-injury markers); ursolic acid^⬖1,2 (improved heart function and reduced cell death); silibinin^⬖ (promoted protective autophagy); necrosulfonamide (restored antioxidant enzymes)¹; necrostatin-1 (reduced heart-injury markers and inflammation)¹; a PARP inhibitor (reversed apoptosis and remodeling)¹; azilsartan (reduced oxidative stress and cell death)^1,2; selenium^⬖ (reduced inflammation and cell death); avenanthramide-C^⬖ (reduced oxidative stress and inflammation); rutin^⬖ (raised antioxidant defenses and reduced inflammation).

•Sepsis-induced cardiac injury — Trimetazidine^⬖ (protected against sepsis heart injury); D3T^⬖ (raised antioxidant defenses); a pancreatitis-ascitic-fluid injury model (DMSO solvent control); paeoniflorin^⬖ (reduced vascular leakage and inflammation); astragaloside IV^⬖ (reduced oxidative stress and inflammation); astaxanthin^⬖ (reduced injury signaling); curcumin^⬖ (reduced heart-injury markers); luteolin^⬖ (enhanced protective autophagy); sulforaphane^⬖ (reduced inflammation); xanthohumol^⬖ (reduced inflammation and cell death); octreotide (reduced inflammation and raised antioxidant defenses)¹; simvastatin (reduced heart-injury markers and inflammation)¹.

•Diabetic cardiomyopathy — GLP-1 drugs^⬖ (reduced oxidative stress in heart blood vessels); tadalafil (protected mitochondria)¹; rapamycin (reduced oxidative stress)^1,2; ferrostatin-1 (reversed ferroptosis, a form of iron-driven cell death)¹; honokiol^⬖ (reduced high-glucose fibrosis); resveratrol^⬖ (reduced inflammation); EGCG^⬖ (restored cell-to-cell coupling).

Combinations for Additional Heart Conditions

In pulmonary hypertension and pulmonary embolism, where the right heart is strained by elevated pressures, DMSO delivered agents benefited right-ventricular function and pulmonary vascular remodeling:

•Myocarditis — A proteasome inhibitor (reduced inflammation and apoptosis);¹ an α7-nicotinic agonist^,1,2 (reduced inflammation and cell death); carbon monoxide-releasing molecules (reduced mortality and heart injury);¹ a 3C protease inhibitor (antiviral protection);¹ an androgen-receptor inhibitor (reduced inflammation and enhanced autophagy);¹ a tyrphostin (reduced inflammation).¹

•Arrhythmias — A calpain inhibitor (reduced atrial-fibrillation incidence); mexiletine (shortened repolarization in long-QT models); fisetin^⬖ (reduced atrial inflammation and fibrosis after heart attack); valsartan or an ERK inhibitor (reduced atrial fibrosis and remodeling).

•Pulmonary Hypertension (which also damages the heart)—Curcumin^⬖1,2 (reduced platelet activation and heart-injury markers); resveratrol^⬖ (reduced inflammation and heart strain); isoliquiritigenin^⬖ (reduced right-heart pressure and oxidative stress); icariin^⬖ (reduced inflammation); a fission inhibitor with 17β-estradiol (reduced right-heart enlargement and shifted immune cells toward healing); a TRAF6 inhibitor (improved right-heart function); a Pannexin-1 inhibitor (improved pulmonary artery flow).

Direct Effects on Heart Function

Several of DMSO’s standalone cardiac actions cut across all of the above. DMSO is a direct vasomotor agent, producing endothelium-independent relaxation of coronary and pulmonary arteries¹. As a hydroxyl-radical scavenger it also attenuated tempol-induced falls in blood pressure, heart rate, and sympathetic nerve activity¹. As discussed earlier, DMSO also protects coronary endothelium-dependent relaxation against oxidative injury, inhibits platelet aggregation, and suppresses tissue-factor expression and arterial thrombus formation—vascular protections equally relevant to the heart. A DMSO–aspirin preparation was likewise reported to reduce erythrocyte aggregation, normalize fibrin formation, lower peripheral vascular resistance, and improve microcirculation¹. In the vehicle-delivered atherosclerosis and vascular-injury literature the same effects recur, with cinnamaldehyde^⬖1 cutting serum lipids and raising heart antioxidant enzymes in atherosclerotic rats, hesperetin^⬖1 limiting diesel-exhaust cardiovascular oxidative damage, and kolaviron^⬖1 attenuating angiotensin-II/LPS-driven vascular smooth-muscle proliferation.

On the muscle itself it exerts direct, concentration-dependent effects on contractility, rate, and electrophysiology^1,2,3: at low doses positive inotropy¹—a moderate increase at 3% becoming marked at 6%¹—while potentiating the inotropic response to isoprenaline¹; still higher concentrations reversibly depress contractility¹ or produce a mild hyperpolarization that prolongs the action potential¹. These effects are independent of beta-adrenergic receptors¹ and typically do not alter cardiac rhythm¹, though the rate response is dose-dependent: 1–3% DMSO slightly raised heart rate while 6–10% markedly slowed it, an effect reversed by atropine¹ and thus mediated through cholinesterase inhibition.
Note: DMSO and colchicine were found to increase myocardial work output.¹

DMSO increased cardiac output during hypoxia¹ and, given IV to dogs, raised cardiac output, stroke volume, and central venous pressure¹. DMSO further protects cardiac t-tubules from stress-induced sealing¹. On the parasympathetic side it inhibits cardiac acetylcholinesterase, lowering the vagal threshold and potentiating acetylcholine’s slowing of the heart rate.¹

As discussed earlier, DMSO’s radical scavenging protects cardiac calcium handling, the sodium-potassium pump, and heart-muscle contractility against iron- and peroxide-driven injury making antioxidant protection equally relevant here. Beyond those, in cell-free and isolated-heart systems DMSO acts as a direct radical scavenger on its own: it neutralized electrolytically generated oxygen radicals in an enzyme-free buffer¹, protected rabbit hearts against radical-driven rises in coronary and end-diastolic pressure and albumin leakage¹, raised coronary release of protective uric acid in guinea-pig hearts¹, and served as the reactive-oxygen scavenger confirming the antioxidant basis of protection against ischemia-reperfusion injury¹. It also limits stress-induced lipid peroxidation in the myocardium¹ (most pronounced in aged hearts), and in H9c2 cardiomyocytes it upregulates heme oxygenase-1 via p38 MAPK and Nrf2 to protect against hydrogen-peroxide injury¹.

Differentiation of Heart Cells

DMSO has long been used to turn cancer cells back into normal cells and to steer stem cells into the cell types the body needs — a way to replace and repair damaged tissue, including the nervous system. A large body of work shows the same thing for the heart: DMSO alone reliably drives stem cells to become cardiomyocytes.

When stem cells are exposed to DMSO alone they are most often reported to become heart tissue, which points to a real role for DMSO in cardiac stem-cell protocols.

A very large literature has since used DMSO as a cardiomyocyte-differentiation inducer across many starting cell types, with the same result recurring: exposure to DMSO (typically 0.5 to 1 percent) drove the cells to switch on cardiac genes and structural muscle proteins and, in most reports, to form spontaneously beating cardiomyocytes.

By far the most studied model is the P19 (and P19CL6) embryonal carcinoma line, in which DMSO alone reliably produced beating cardiomyocytes and became the standard system for dissecting how it works.t^{1,2,3,4,5,6,7,8,9,10, 11,12,13,14,15,16,17,18,19,20, 21,22,23,24,25,26,27,28,29,30, 31,32,33,34,35,36,37,38,39,40, 41,42,43,44,45,46,47,48,49,50, 51,52,53,54,55,56,57,58,59,60, 61,62,63,64,65,66,67,68,69,70, 71,72,73,74,75,76,77,78,79,80, 81}.

The effect shows up across source cell type after source cell type. DMSO alone has turned bone-marrow mesenchymal stem cells^,2 into myocardial cells, adipose-derived stem cells into cardiomyoblast-like cells, and fetal liver stem cells into cardiomyocyte-like cells. It has also driven fetal cardiomyocytes to proliferate and boosted the direct reprogramming of fibroblasts into cardiomyocytes roughly five-fold.

The same DMSO-driven differentiation has been reported across species and stem-cell source: in goat embryonic stem cells, mouse embryonic stem cells^1,2,3,4,5, human embryonic stem cells^1,2,3,4,5, human bone-marrow stem cells, cardiac progenitor cells, and mouse embryonic fibroblasts.

Lastly, the same differentiation was also achieved when DMSO was combined with many other agents including 5-azacytidine, a cocktail of growth factors including BMP and FGF, retinoic acid with 5-azacytidine, oxytocin (which worked synergistically with DMSO) and many others.^1,2

Note: the effect is again concentration-dependent. At high concentration the picture reverses: a brief exposure to 10 percent DMSO disrupted muscle fibers and suppressed proliferation in cultured heart and cardiac endothelial cells,^1,2

Atherosclerosis

DMSO endothelial protective effects also allow it to prevent atherosclerosis itself. In rabbits fed a cholesterol-overloaded diet, oral DMSO reduced the resulting atherosclerosis by 30—40% and halved the cholesterol accumulating in the tissue.¹ Beyond limiting the damage, it also supported the vasculature’s ability to rebuild itself, as DMSO promoted the differentiation of human embryonic stem cells into endothelial, cardiac, and blood-cell precursors—the early cells the body draws upon to build new vessels and blood.¹

Finally, a series of studies in the cells lining human umbilical veins (a standard laboratory stand-in for the vessel wall) point to a protective and anti-inflammatory action there. Pretreatment with 2.5% DMSO reduced the neutrophil adhesion TNF-α normally triggers, which is one of the first steps of vascular inflammation and the initiating event in atherosclerosis.¹ In nutrient-starved cells it blocked programmed cell death by promoting DNA replication and enhancing survival,¹ and under oxidative stress it raised heme oxygenase-1 and reduced apoptosis through several anti-inflammatory and cytoprotective pathways.¹

Blood Pressure

As DMSO is a mild vasodilator which simultaneously increases parasympathetic tone and scavenges the radicals that stiffen and constrict vessels, there is a mechanistic basis for it reducing blood pressure. However, the direct evidence is quite limited and most of what exists is indirect.

For example, DMSO is used as a transdermal penetration enhancer for conventional antihypertensives such as diltiazem and labetalol, where it improves both how much of the drug crosses the skin and how far the pressure falls in hypertensive animals.^1,2 More importantly, it protects the vessels hypertension damages rather than merely the number on the cuff, as in rats made hypertensive with angiotensin II, DMSO reduced vascular hyperpermeability, smooth-muscle necrosis, and fibrin deposition in the small arteries by scavenging free radicals¹—guarding the vessel wall even in cases where it did not move the pressure at all.
Note: as I’ve shown throughout the series, the primary value of DMSO for cardiovascular disease is its ability to protect the tissue rather than meet a numerical blood pressure threshold (which is often not even healthy).

DMSO is not, however, a blood pressure drug in the way an ACE inhibitor is, and as with every other system, its effect is concentration dependent. At the low solvent-level doses used in most research it is close to neutral, as DMSO-alone control groups repeatedly show no meaningful change in mean arterial pressure.^1,2 Any lowering emerges only at the higher therapeutic concentrations where the vasodilation becomes pronounced, and at the far end of the range the direction reverses entirely—the same counter-current already seen when DMSO scavenged enough nitric oxide to nudge blood pressure up in horses. The clearest illustration of this is what happens when stem cell grafts cryopreserved in concentrated (10%) DMSO are infused rapidly, which produces a transient rise in blood pressure proportional to the DMSO dose¹—the same high-concentration ceiling described in the safety section above. In short, DMSO is a mild and dose-dependent vasodilator whose most consistent contribution in hypertension is protecting the blood vessels rather than driving down the number on the cuff.

Readers, in turn, have described exactly what the mechanism predicts, and frequently stumbled upon it by accident. One woman had been applying DMSO to her husband’s belly at night for a pulled muscle when a checkup found his blood pressure had normalized; months of magnesium and potassium had only brought him to 150/90, but he now read 125/80.¹

The pattern which recurs the most however is a rapid drop following a single oral dose. A 73-year-old found half a teaspoon in water took him from a usual 148/90 to 109/70 within thirty minutes, which he described as “way better than the meds I used to take.”¹ Another, who had been pushed up to 40 mg of lisinopril and was applying DMSO over his carotids, watched a pre-DMSO 159/95 fall to 106/75 on the first reading afterwards.¹ Others reported oral DMSO doing “more for my general inflammation and BP than aspirin or these days BP meds,”¹ blood pressure finally dropping after years of unsuccessful diet, exercise, and weight changes,¹ and a more modest shift from 160/90 to 150/80 which arrived alongside easier urination and sharper vision.¹

Consistent with this being vasodilation rather than something else, a few readers instead noticed it as mild low-pressure symptoms when they used DMSO aggressively, one describing feeling “rather unsteady” with unusually flat and invisible hand veins during heavy use¹ (which the German DMSO community believes accounts for why some people get temporary headaches from significant DMSO use). In others it was simply folded into a much broader recovery, such as the reader treating a vaccine injury with oral DMSO who listed normalized blood pressure among a long list of improvements,¹ and another who found his blood pressure and cholesterol returned to normal once DMSO allowed him to discontinue Humira.¹

Given all of this, I would expect DMSO to help certain kinds of blood pressure but not others (as many different things can cause the elevation). That said, blood pressure is not always a thing you want to treat (sometimes it being elevated is helpful)—although in the cases where it’s helpful to be elevated (to maintain perfusion through aging arteries), DMSO would likely at least somewhat bridge the gap due to its ability to promote circulation.

Note: because a few of these drops were both large and rapid, anyone already on blood pressure medication should monitor their pressure when starting DMSO rather than assume the two simply stack, as the reader above who was on 40 mg of lisinopril illustrates how quickly the combination can move things.

Peripheral Circulatory Disorders

In addition to protecting tissues from death, DMSO is remarkably effective at removing excess fluid from outside the bloodstream, increasing circulation, and clearing circulatory obstructions such as clots, along with many other conditions which result from impaired circulation (and microcirculation).
Note: numerous observations of the years have led me to believe blood congestion is a primary cause of many ailments including varicose veins and hemorrhoids.

The pioneering DMSO researchers documented this early. Stanley Jacob found¹ that half of Raynaud’s patients had their symptoms eliminated and that thrombophlebitis responded excellently, while two investigators using plethysmography demonstrated objective improvement¹ in peripheral-artery insufficiency in a large number of patients given topical DMSO. DMSO was also shown to relieve diabetic circulatory problems including peripheral neuropathy¹ and diabetic ulcers, where one study¹ of hundreds of patients reported over a 94% success rate — and to help prevent future amputations (data which has since been extensively corroborated).

The early clinical series were substantial. A study of 67 patients with varicose ulcers¹ (39 women, 28 men) found a remarkable response even in chronic ulcers that had been present for years and had failed other treatments. Likewise a larger early¹ study found:

DMSO’s vasodilatory action has long been invoked for frostbite, diabetic ulcers, and varicose ulcers¹, and over a hundred studies have since corroborated these results.

Venous disease and varicose veins. The most consistent modern use is topical, much of it centered on Dolobene — a gel of DMSO, heparin, and dexpanthenol in which DMSO both carries the heparin through the skin and adds its own analgesic and anti-inflammatory action. Dolobene has been evaluated across the venous disorders¹, used specifically for varicose vein disease¹, and ranked by vascular surgeons and pharmacists among the priority topical agents for varicose veins¹.²,³,⁴,⁵ An early double-blind study of 55 patients¹ tested topical DMSO for chronic venous insufficiency, and a 1975 New York Academy of Sciences report¹ documented its use across venous stasis, dermatosclerosis, and lymphedema. It recurs throughout the topical treatment of chronic venous insufficiency and post-thrombophlebitic disease¹ and appears in the formulation literature for antivaricose gels¹ and horse-chestnut/aescin preparations¹ as the penetration enhancer of choice.¹ This indicates DMSO may also play a wall-strengthening role (e.g., in a mouse model of venous hypertension¹ that reproduces varicose remodeling, agents delivered transdermally in DMSO prevented the pathological changes in vein structure and smooth muscle that drive the disease).

Thrombophlebitis, superficial venous thrombosis and hematomas. DMSO-based gels are commonly used here. A randomized, double-blind trial of a Phlebolan spray¹ and related studies¹,²,³ support topical DMSO-heparin (and the topical DMSO heparin gel Dolobene) for superficial thrombophlebitis.¹ Likewise Dolobene recurs as a standard thrombophlebitis and thrombosis therapy throughout the literature, including for combined deep and saphenous-vein thrombosis.^1,2,3 DMSO (alone) gels have also been used to treat acute thrombophlebitis¹, superficial-vein thrombosis¹, and chemotherapy-induced phlebitis.¹,²,³ Electrophoretic DMSO has also resolved intramuscular-injection hematomas in hemophilic children, clearing the bruising well enough to let their therapy continue.¹

Venous, trophic, and diabetic ulcers. DMSO’s ulcer record (e.g., the greater than 94% success rate and the 67-patient varicose-ulcer series above) are highlighted in many papers discussing the use of large DMSO containing wound-dressing for venous trophic ulcers and lipodermatosclerosis¹, chronic trophic leg ulcers¹, post-thrombophlebitic trophic ulcers¹, venous ulcers and chronic venous insufficiency (in one study a DMSO powder healed 95% of patients at 3 months versus 70% on placebo),^1,2 and trophic ulcers of atherosclerotic origin (with a DMSO powder)¹. In 58 patients with chronic purulent wounds from vascular disease or diabetic angiopathy, negative-pressure instillation of 20% DMSO produced faster cleansing, near-complete granulation in 76% by the first dressing change, and healing 1.5–3× faster than standard care.¹,² The diabetic-foot thread is distinct: in 80 diabetic patients with lower-extremity ulcers, DMSO dressings combined with an oxygen-carrying perfluorocarbon cut mean healing time to 17 days versus 47 for standard care, with faster bacterial clearance and a better microcirculatory index by day 22.¹ DMSO is also used as an antiseptic and penetration enhancer in diabetic-foot and gangrenous-wound protocols¹, in diabetic wound management with documented perfusion improvement¹, for necrobiosis lipoidica and other diabetic skin conditions¹, and as the vehicle in experimental diabetic-wound and angiogenesis models.¹

Scleroderma and Raynaud’s. In addition to the 50% Raynaud’s symptom-elimination figure from the original DMSO literature, DMSO is a standard component of scleroderma care specifically for its microcirculatory action. DMSO with nicotinic acid^⬖ has been used to treat systemic scleroderma,¹ and topical DMSO (often paired with heparin) is mentioned as a treatment throughout the scleroderma treatment literature¹, including pediatric localized scleroderma¹, explicitly to improve microcirculation and soften dermatosclerosis.¹,²,³,⁴,^5,6,7,8 (where in one study, blood flow was increased 20% by DMSO and 500% by DMSO with nicotinic acid^⬖1). It also appears in systemic lupus with acrocyanosis and Raynaud-type lesions¹, in vasculitis¹ with cutaneous circulatory involvement, and as the vehicle for vasoactive agents in scleroderma¹.²
Note: many more scleroderma studies are discussed here.

Tissue perfusion, flap and graft survival. The most objective experimental evidence that DMSO raises tissue blood flow comes from surgical flap models, where perfusion decides whether ischemic tissue lives. In 48 rats with abdominal island flaps¹, systemic DMSO significantly increased perfusion (by laser Doppler and perfusion fluorometry) and improved flap survival. In ischemic dorsal skin flaps¹, 5% DMSO reduced distal necrosis and produced greater neovascularization and earlier repair. The benefit recurs across independent models such as pedicle-flap necrosis¹,²,³,⁴ composite and vascular allografts¹, or nipple-areolar and penile tissue salvage¹.² The same perfusion gain runs through a large wound-healing literature, where DMSO (alone or as carrier) increases skin blood flow¹, normalizes capillary permeability and microcirculation¹, improves isolated-organ perfusion¹, and accelerates granulation and revascularization in trophic ulcers, burns, and other wounds.¹,²,³
Note: many additional DMSO skin flap studies can be read here.

Surgery. In addition to protecting skin flaps (a common challenge in plastic surgery), DMSO also addresses many other challenges. In breast reconstruction, applying topical 60% DMSO before each tissue-expansion session cut expansion time by roughly a third, allowed greater volume per session, and reduced pain¹, across two clinical series.¹ Topical DMSO salvaged (saved) an ischemic nipple-areola complex¹ after reduction mammoplasty by restoring perfusion, and as a trauma wound dressing used in nearly ten thousand cases it dilated capillaries and improved microcirculation¹. Finally, in 154 patients undergoing surgery to restore blood flow to an acutely ischemic leg, intravenous DMSO added before reperfusion reduced markers of reperfusion injury¹ ( lower peak lactate, faster normalization, fewer cases of kidney and cardiopulmonary dysfunction) though amputation and mortality were unchanged.

Hemorrhoids and frostbite. DMSO is used in topical mixtures for acute thrombosed hemorrhoids¹ and hemorrhoidal thrombosis¹, in a placebo-controlled trial of an MSM^⬖-containing gel¹ (MSM being DMSO’s oxidized metabolite), and in anorectal wound healing after hemorrhoid surgery¹.²,³ For frostbite, a peripheral cold-ischemic injury, DMSO appears in the treatment guidelines for local cold trauma¹, in military cold-injury research¹, and as a carrier delivering heparin into cold-injured tissue¹.²,³,^4,5
Note: Stanley Jacob (the pioneer of DMSO) treated hemorrhoids with DMSO,¹ other DMSO authors have advocated for using DMSO to treat them, and Merck (in their early clinical trials) reported that it improved recovery after their surgical removal.¹

Arterial and ischemic limb disease. The arterial side is thinner than the venous but present: DMSO has been used adjunctively for arterial disease of the extremities¹, for chronic purulent wounds from advanced peripheral arterial occlusive disease¹, with hyaluronidase for ischemic limb edema¹, and for vaso-occlusive hand-foot crises¹ where Dolobene relieved pain and edema. It also improved facial arterial blood flow after surgery¹.

Veterinary peripheral circulation. In veterinary medicine, where DMSO is a mainstream drug, it is used for equine laminitis to improve digital perfusion¹, distal-limb edema¹, and aorto-iliac thrombosis¹, in regional limb perfusion¹ and tendinitis¹, for bovine hoof and teat lesions¹, and as anti-endotoxemic support in colic and peritonitis¹ where circulatory collapse is the threat.¹,²

DMSO also completely abolished toxin-induced constriction of lymphatic microvessels¹, protecting lymphatic as well as blood-vessel tone.

Peripheral-Vascular Combinations

Many agents have also been combined with DMSO to topically treat the same conditions DMSO alone also treats.

Venous Disease, Trophic Ulcers & Wound Healing

Many agents combined with DMSO, like DMSO alone, speed cleansing, granulation, and closure of venous, trophic, diabetic, and traumatic wounds:

•Antiseptics & antibiotics (topical wound care) — furacillin + sensitivity-selected antibiotics (25% DMSO cleared monoflora by day 5–6 and healed varicose/post-thrombophlebitic ulcers in 16 days, 2.2x faster with phototherapy)¹; chlorhexidine (multimodal venous trophic-ulcer regimen; remission in 80–95% of 152 cases)¹; bactosin + sulbactam (DMSO antiseptic irrigation of contaminated vascular-trauma wounds; fewer thromboses, infections, amputations),¹ photoditazine plus photodynamic therapy (gunshot wound treatment aiding cleansing and microcirculation)^1,2.

•Anesthetics & anti-inflammatories (compounded dressings/ointments) — Anikol, a patented anilocaine ointment (~190-min surface anesthesia; infected wounds closed in 7 days, frostbite healed in 8)¹; splenic preparation splenodimexide (anorectal wounds; complications cut >1.5x, faster granulation)¹

•Free-radical scavengers & flavonoids (ulcer healing) — Quercetin^⬖ (10% DMSO vehicle showed no independent effect while quercetin-in-DMSO drove angiogenesis and closure in diabetic wounds)¹; loureirin A^⬖ (promoted vascularization and wound healing via miR-339-5p/Wnt).¹

Thrombosis, Clotting, Platelet Function & Vascular Tone

DMSO is frequently combined with other anti-clotting agents:

•Natural compounds — curcumin^⬖ (dose-dependently reduced platelet aggregation, CD63, GMP-140 in pulmonary embolism)¹; berberine^⬖ (prolonged mesenteric-artery occlusion time; reduced venous thrombosis and NET formation in colitis)¹; senkyunolide I (reduced platelet activation and NET formation in sepsis).¹

•Anticoagulants & other pharmaceuticals — rivaroxaban (suppressed leukocyte adhesion and microthrombus formation in diabetic microvasculature)¹; aspirin (DMSO + aspirin stopped nocturnal leg cramps within a day)¹. Nadroparin (15% DMSO carried this LMWH into tissue to prevent Nicolau syndrome skin necrosis after sclerotherapy)¹; hydrocortisone (90% DMSO potentiated hydrocortisone ~10-fold and, alone, prolonged arteriolar flow-stop time and sped flow restoration after venous thrombosis)¹; Procaine + heparin (corrected vascular tone and arterial-bed filling in chronic interstitial parotitis).¹

•Signaling-pathway inhibitors (thrombosis mechanism) — PI3K inhibitor wortmannin (malnutrition-driven venous thrombosis)¹; suberoylanilide hydroxamic acid(improved survival and clot quality in sepsis coagulopathy)¹; Tubastatin A (HDAC6) (reduced renal microcirculatory thrombin and NET formation in sepsis).¹

•Polyphenols & natural vasorelaxants — resveratrol^⬖ (near-complete relaxation of human intrapulmonary arteries, partly NO-dependent)¹; garlic diallyl trisulfide^⬖ (endothelium-independent relaxation of intrarenal arteries, Emax >91%)¹; tetrahydroxystilbene glucoside^⬖ (mesenteric relaxation via COX-2/TXA2 and K+/Ca2+ channels)¹; cannabidiol (potent inhibition of small-resistance-artery contraction, stronger in smaller vessels)¹; resveratrol ^⬖ + CAPE^⬖ silibinin^⬖ (concentration-dependent relaxation of human umbilical artery).¹

Endothelial Protection & Microvascular Barrier

Polyphenols & flavonoids — resveratrol^⬖ (raised hypoxic endothelial viability and SIRT1/PGC-1α; lowered inflammatory IL-6, ICAM-1, ROS)¹; resveratrol^⬖ plus atorvastatin (synergistically enhanced bone marrow stem cell endothelial differentiation and stent re-endothelialization beyond either alone)¹; kaempferol^⬖ (protected islet microvessel endothelium from fatty-acid injury)¹; astragaloside IV^⬖ (improved aortic-endothelial viability, migration, tube formation under hypoxia).¹

Endothelial-barrier disruption — ulinastatin (blocked endothelial hyperpermeability via p38)¹; HSPA12B pathway inhibitors (preserved endothelial barrier function),¹ thymoquinone^⬖ (sepsis) (improved mesenteric-artery blood flow and aortic function,)¹. resveratrol^⬖ (cut sepsis leukocyte/platelet adhesion, improved survival),¹ genipin^⬖ (reduced LPS-induced vascular hyperpermeability via SIRT1).¹

Neointimal Vascular Remodeling after Artery Injury — celastrol^⬖ (restored contractile VSMC markers)¹; ursolic acid^⬖ (also reduced NF-κB/PCNA)¹; YM201636¹; a Pol I inhibitor;¹ enalaprilat (DMSO alone demonstrated a modest reduction in remodeling).¹

Reader Reports

Since DMSO is easy to utilize for peripheral circulatory conditions, many readers have attempted it, and their testimonials mirror the successes for these conditions seen in the trials.

Varicose and spider veins. This is the single most common circulatory use readers describe, and the reports are strikingly consistent: repeated topical application (typically 70-100% DMSO,* often in aloe^⬖ or castor oil,^⬖ once or twice daily) shrinks, softens, fades, and in many cases eliminates the veins, frequently after they had been present for decades. One reader sprayed 100%* DMSO on varicose veins nightly and reported that “in 13 months they are entirely gone,”¹ another in New Zealand treated badly “varicosed” saphenous veins roughly half a dozen times over a week and found the change (documented in before-and-after photos) durable: “I am fairly sure that the applications are not maintaining the varicose vein recovery-they are fixed.”¹ A third watched veins that “stuck out about 1/2 inch” recede to “about 1/8 of an inch,”¹ and one posted a 24-hour before-and-after showing a large varicosity essentially gone.¹ Many more described veins that “just disappeared” along with the aching and end-of-day leg pain,¹ that faded or shrank steadily with continued use^{1,2,3,4,5,6,7} that became “much smaller, softer” with the previous sensation of “thickness” gone¹ or that improved only on the treated leg while the untreated leg served as an inadvertent control.¹ A woman treating her elderly relative’s chronic venous insufficiency tracked it week by week—roughly 20% improvement in the first week, 50% by the second, 75% by the third.¹ Several noted the veins returned when treatment stopped¹ and a minority saw little or no effect,¹,² but the dominant pattern was steady improvement of veins that conventional medicine treats only by stripping or ablation.^1,2,3,4,5,6
These are some of the many pictures I’ve received:

Blood clots and DVT. Readers reported both topical and oral DMSO dissolving existing clots and preventing new ones, often as a deliberate replacement for prescribed anticoagulants. One who had been told to take Eliquis for life stopped it and switched entirely to oral DMSO to dissolve clots in the legs and lungs: “I’d be dead if DMSO didn’t work.”¹ Another treated a bad DVT running from above the knee to the ankle with topical DMSO (plus lumbrokinase^⬖ and serrapeptase^⬖) and “dissolved the clot in 2.5 months,” declining the year of Eliquis doctors advised.¹ A mother whose son had hip-bone necrosis from a clot lodged in a small twisted vein reported that after starting DMSO “within 3 days he was able to walk without pain,” and that the hip healed without the scheduled surgery.¹ One reader whose arm had visible hardened clots from an IV reaction for months found “the clots were gone within three days” of applying DMSO gel,¹ and another watched a large hard lump on a calf vein resolve until “it is gone now and the area soft.”¹ Another described using DMSO to resolve a clot in an 89-year-old’s leg.¹

Raynaud’s and cold extremities. For Raynaud’s, the reported effect is often nearly immediate. One reader who came in from shoveling snow put DMSO on the fingertips and was “instantly warm”;¹ another applied it to the toes and it “changed the color of my toes back to normal.”¹ A regular user reported applying it two or three times daily to her hands with “great success, no longer needing to wear fingerless gloves around the house...It has been life changing,”¹ while another with cold hands happened to track the effect on a pulse oximeter and watched readings climb after each application.¹ Others described relief of the spasms, discoloration, and stiffness,^1,2,3 marked overall improvement in circulation alongside the Raynaud’s,¹ and one reported that five consecutive days of DMSO “cured Chilblains and Raynaud’s for the entire winter season.”¹ Several with autoimmune-associated Raynaud’s (lupus, scleroderma, rheumatoid disease) folded it into broader regimens with reported relief.^1,2,3

Ischemic and discolored limbs. Many reported normal color and warmth to feet and legs that had gone blue, purple, or black from poor perfusion. A daughter treating her 85-year-old mother’s severe foot neuropathy (toes and ankles “a blackish blue color,” numb, with nightly cramping) described the results after three weeks as “amazing” “the normal color has returned to her feet and legs...she now has feeling back in both of her heels.”¹ Another reader rubbing DMSO cream on the feet nightly found that “on the fourth morning I looked down at my feet and all the purple mottling was completely gone.”¹ One person watched an elderly mother’s “blue-black toes...from frostbite” return “to a healthy pink—permanently” after a single application of DMSO with magnesium.¹ An 84-year-old with a decades-old radiation wound near the bone that had never fully healed reported that once she applied DMSO gel, “the skin color has returned to normal and circulation is now almost normal, my foot does not swell from lack of circulation.”¹ Many others described impaired circulation, cold feet, leg swelling, and perfusion-related pain improving with topical or oral use^1,2,3,4,5,6 including a post-COVID reader whose cyanotic, “bluish purple” legs looked “a normal healthy colour...for the first time in 3 years.”¹

Frostbite and cold injury. Frostbite is a peripheral cold-ischemic injury, and readers reported DMSO restoring warmth and color to affected tissue, often within hours, particularly when applied promptly. One who “burned” a hand with liquid refrigerant until “half of my hand went numb and changed color” applied DMSO and reported the hand “back to normal” two days later, with only a little surface skin peeling.¹ A second described the same refrigerant injury (a hand “numb for 24 hours and changing color”) returning to normal in three days, adding that “immediate or even preemptive application is essential.”¹ Another reported that on a “almost frost bite,” DMSO “restored warm asap.”¹ These mirror the documented reports of frostbitten and blue-black toes regaining healthy color after DMSO.

Venous, diabetic, and pressure ulcers. DMSO’s reported effect on chronic wounds and ulcers is among the most consistent in this collection. A reader watched an elderly friend’s leg “a six inch diameter festering mess” that a year of medical treatment had failed to close, with surgeons wanting to cut “turn into clean skin” over a month of DMSO.¹ A 12-year user reported that DMSO “saved a 75-year-old woman’s leg” doctors wanted to amputate: “she walks now despite being bedridden before.”¹ Wives caring for diabetic husbands with chronic venous ulcers—one after a year of wound-care visits and twice-weekly home nursing—described the ulcers improving significantly within two weeks of switching to DMSO gel¹ and not recurring afterward.¹ A diabetic reader healed three foot ulcers with DMSO gel and pursued IV infusions to improve leg blood flow,¹ and a man given DMSO cream by an acquaintance saw “a 2 inch ulcer” on his arm heal over “in a couple of weeks.”¹ The same pattern appears with pressure sores: a family applied 80% DMSO to a bedbound 101-year-old’s bedsores and reported her skin “became normal in just a matter of days,”¹ and a caregiver treating early Alzheimer’s incidentally cleared his wife’s “horrid bed sores,” leaving her “with no sores or irritated pink skin.”¹ Others reported healing of diabetic leg ulcers, lupus-related skin ulcers, and assorted chronic sores, often in combination with iodine, silver, or chlorine dioxide.^1,2,3,4,5,6

Hemorrhoids. Because a hemorrhoid is essentially a swollen, clotted vein, readers repeatedly found it responded to DMSO the way varicosities did—often within days (to the great surprise of skeptical readers).¹ One applied “two drops of DMSO on a hemorrhoid I had for years” and reported that “after a single dose, it shrank to the size of a grain of sand.”¹ Another reported that two friends “had their hemorrhoids vanish after a single subcutaneous thigh injection of .5ml of DMSO,” including one who had had them for 15 years.¹ A reader whose doctor had diagnosed a hemorrhoid and written a prescription instead applied DMSO to the bulge and reported it “gone” after three days,¹ and another who makes DMSO-cocoa butter suppositories reported they “heal and relieve hemorrhoids immediately...Prep H is useless.”¹ Many more described hemorrhoids shrinking, clot release accelerating, and pain and itching resolving with topical gels, suppositories, or oral use, frequently after over-the-counter suppositories had failed.^{1,2,3,4,5,6,7,8,9,10,11}

Lastly, readers describe a number of adjacent circulatory and lymphatic uses that don’t fit neatly under a single heading. DMSO was credited with improving lymphedema and restoring sensation in a diabetic reader’s legs and feet (from roughly 20% to 85% feeling),¹ softening the “cord” of post-surgical axillary web syndrome until it “feels like a thin cotton string,”¹ and relieving lymphatic congestion in the neck and shoulders.¹ Two readers with pigmented purpuric dermatosis (capillaritis) reported the discoloration fading—one by “at least 50%” after months of oral DMSO following chemotherapy-induced capillaritis on both shins,¹ another finding that DMSO “drains blood from purpura in my older skin within 3-4 days.”¹ A reader with peripheral arterial disease found DMSO cream slightly eased claudication pain enough to resume treadmill walking,¹ and a post-COVID reader reported it changing “the micro clotting and total arterial blockage” of a popliteal artery.¹

Ending Fifty Years of Neglect

When I began this series nearly two years ago, I stated at the start the evidence showed DMSO could save millions from neurological disability or death. Now that I have been able to present that evidence, it should be clear there is something real here, and a lot of the suffering that happens doesn’t need to. I cannot begin to describe how much I wish DMSO could become the standard of care for strokes, and it is for that reason that I have tried so hard with pieces like this to effectively make the case for that to happen.

At the same time however, another one of DMSO’s unique characteristics is that even if the medical system wants to maintain its narrow paradigm of how medicine must be practiced, DMSO can still be used by anyone who has taught themselves how to do so. This is critical, both because it means an option exists now that can be taken to avoid these devastating outcomes, but also because the one type of pressure medicine does respond to is external economic ones (e.g., individuals shifting enough of their medical spending to a superior alternative that medicine is motivated to provide a service that is good enough to recapture those customers). So, since DMSO can address so many both common and rare “incurable” ailments, it not only provides an immediate and tangible benefit to those who use it, but also, through doing so, provides the critical grass roots pressure for it to shift the entire medical system.

As such, in the remainder of this article, I will provide:

• Practical guidance on sourcing each grade of DMSO (including what is needed for IVs) and detailed dosing protocols for topical, oral, and intravenous use.

• DMSO protocols for the urgent conditions discussed in this article such as strokes, heart attacks, and head injuries, including what to do on the way to the hospital along with other therapies we have seen work over the year for those conditions (e.g., heart attacks).

• Condition-specific protocols for the circulatory conditions covered here (e.g., varicose veins, clots, Raynaud’s, venous and diabetic ulcers, hemorrhoids, chronic wounds arrhythmias), along with the non-DMSO approaches we have found to further benefit them.

• Protocols for the neurological and spinal conditions covered earlier in this series (e.g., Parkinson’s, Alzheimer’s, cognitive impairment, brain fog, chronic stress, neuropathies, carpal tunnel syndrome, neuropathic pain, disc disease, and spinal cord injuries).

Read more

• For 50 years, medicine has waged a misguided war against critical sources of health like salt and sunlight while avoiding discussing the real causes of diseases. Because of this, the dangers of salt are relentlessly focused on despite evidence not supporting them.

• In parallel, the extreme dangers of consuming too little salt are rarely discussed in the medical field—despite dangerously low sodium being one of the most common conditions seen in hospitalized patients, and chronically low sodium greatly increasing one’s risk of dying.

• The war against salt originated from the belief salt raises blood pressure—despite the evidence showing it doesn’t.

• Many of the foundational beliefs around high blood pressure are not supported by the existing data, leading to situations where patients are routinely medicated to blood pressures far below what is safe, significantly reducing their quality of life and increasing their risk of severe injuries or death.

• Salt restriction creates many similar complications to dangerously low blood pressures (e.g., fatigue, lightheadedness, erectile dysfunction). Because of this, many find their health and energy dramatically improves once they start consuming healthy salts.

• This article will cover some of the key dangers associated with salt restriction and strategies for locating the healthiest natural salts.

This newsletter exists to help others, and as a result, I frequently receive correspondences from individuals with pressing questions I want to answer. Unfortunately, due to how long each article takes to write (e.g., I’ve spent most of the last two weeks finishing up the last part of the DMSO neurological series as I believe it’s vital that astonishing data becomes widely accessible), I simply no longer have the time respond to most of those correspondences.

The best solution I’ve been able to come up with is to have monthly open threads where anyone can ask whatever is needed (e.g., any lingering questions from the previous month) and I would make a point to always reply to them (as having them all in a single place makes it easier to get to them and also possible for others with the same question to see that answer).

Each time I do a monthly thread, I try to tag it to a topic I’ve wanted to write about but I do not quite feel is enough for its own article. In this article, I will focus on one my major frustrations with the medical system, the half a century war against salt (which began in 1977 when a Senate Committee published dietary guidelines arguing for reduced sodium consumption despite the existing evidence not supporting this). Since then, like many other bad government policies, it has developed a nearly unstoppable inertia of its own.

Note: in the recent interview I did with Pierre Kory, one of the key points I hoped to illustrate was that on highly contentious issues, middle ground positions often exist which achieve most of what both side is seeking and help everyone—but as things become increasingly politically polarized, both sides dig in and the common sense solutions fade into the background creating an irresolvable quagmire. For example, currently, there is a highly polarizing debate occurring over what should happen to a mother with postpartum depression who murdered her three children, as a large number of people are adamant the death penalty must be imposed while many others have made it clear they deeply emphasize with her stress and hence want an insanity defense to prevail. Yet, few have mentioned the violent psychosis inappropriate psychiatric medications cause (which may have played a key role here) or that much better non-pharmaceutical options exist for treating postpartum depression (e.g., decades ago William Walsh showed postpartum depression and psychosis was often caused by a copper overload that was highly responsive to treatment).

Is Salt Bad For You?

Many people you ask, particularly those in the medical field will tell you salt is bad, and one of the most common pieces of health advice given both inside and outside of medicine is to eat less salt.

Over the years, I’ve heard two main arguments for why salt is bad for you.

First, salt raises blood pressure, and high blood pressure is deadly, so salt is too and should be avoided.

Second, with individuals who have heart failure, eating too many salty foods will create exacerbations of their condition, and as a result, after holidays where people eat those foods (e.g., the 4^th of July) more heart failure patients will be admitted to hospitals for heart failure exacerbations.

Note: excessive sodium causes these exacerbations because an excess amount of fluid accumulates in the body (e.g., because the weakened heart can’t move enough blood to the kidneys to eliminate it), which then overloads other parts of the body (e.g., causing swelling and edema, which, if in the lungs, can be life threatening).

Because of these two things, many in the medical field assume that salt must be bad for you and hence strongly urge patients to avoid it (to the point you often see an elderly patient who loves her salt be aggressively pushed into abandoning it). Unfortunately, the logic behind those two arguments is much less solid than it initially appears.

Blood Pressure

Many things in medicine resulted from what approach to patient care was the most profitable, not the most helpful. In turn, since recurring revenue is a foundational principle of successful businesses, rather than cure patients, a key goal in medicine often ends up being to have as many patients as possible be on lifelong prescriptions.

In most cases, the drugs that are developed and approved have real value for specific situations, but those situations are not enough to cover the exorbitant cost it requires to get a drug to market. As a result, once drugs are approved, the industry will gradually come up with reasons to give them to more and more people (e.g., by relabeling a vast swathe of normal feeling as “depression”). As such, things quickly arrive at the point where many of the industry’s customers experience significantly greater harm than benefit from the pharmaceutical (e.g., while they harm the majority of users and providing minimal benefit to most patients, SSRI antidepressants are also very helpful for a subset of people who take them).

One classic way drug markets are expanded is by creating a drug that treats a number, asserting that the number has to be within a certain range for someone to be healthy, and then once that is enshrined, narrow and narrow the acceptable range so less and less people are “healthy” and hence need the drug (e.g., this happened with cholesterol once statins were invented). Likewise, this characterizes the history of blood pressure management:

Because of this, many people (particularly the elderly) are frequently pushed to excessively low blood pressures which reduces critical blood perfusion for the organs—which is particularly unfortunate as high blood pressure is often a symptom of poor circulation rather than its cause. As such, reducing the remaining circulation by lowering blood pressure then makes them significantly more likely to get a variety of significant issues (e.g., kidney injuries, cognitive impairment, macular degeneration), the most studied of which is lightheadedness or fainting leading to (often devastating) falls. Additionally, blood pressure medications also often greatly reduce one’s quality of life (e.g., by causing fatigue or erectile dysfunction).

Note: for those interested in learning more about the great blood pressure scam (a lot of what we’re taught about blood pressure is less than accurate), it can be read here.

Low Sodium

A corner stone of cementing the blood pressure market has been to make everyone terrified of salt (much in the same way making people terrified of the sun is a cornerstone of the lucrative skin cancer treatment market—despite the fact the deadly skin cancers are actually due to a lack of sunlight).

Remarkably, much like the great dermatology scam (which has been able to make a massive amount of money from removing cancers that almost never become life threatening) the link between blood pressure and salt consumption is actually quite tenuous.

For example, the most detailed review of this subject found that drastic salt reduction typically results in less than a 1% reduction in blood pressure. Likewise, doctors rarely recognize that patients in the hospital are routinely given large amounts of IV 0.9% sodium chloride, in many cases receiving ten times the daily recommended sodium chloride we are supposed to consume—yet their blood pressure often barely rises.

Note: much of the confusion with salt and blood pressure arises from the fact changes from salt-reduction are only seen in a minorities of the population (e.g., certain ethnicities), leading to the average change across everyone being very small. Likewise, a larger Cochrane analysis of this question found that cutting salt by roughly 4.4 grams a day lowered blood pressure by about 5.4/2.8 mmHg in hypertensives but only 2.4/1.0 mmHg in those with normal blood pressure (a rounding error you could achieve by relaxing for a few minutes).

Despite this, patients are often pushed to eliminate all (or almost all) salt from their life “to prevent them from dying.” Beyond this significantly reducing their quality of life (as people like salty foods) it can be dangerous. For example:

•A study of 181 countries found countries with lower salt consumption have shorter life expectancies.

•Low sodium levels (hyponatremia) are strongly correlated with a risk of dying (e.g., the salt consumption target we are recommended to follow increases one’s risk of dying by 25%). Likewise, a common reason for hospital admissions, are symptoms resulting from hyponatremia (as once sodium levels get too low, it can be very dangerous), and 15-20% of hospitalized patients have low sodium levels at admission.

Note: mild hyponatremia is also associated with an increased risk of death—even “mild” low sodium raises five-year mortality by 25%, and in a database of 2.3 million patients it independently predicted death. It also leaves the elderly nearly six times more likely to break a hip in a fall (which is frequently catastrophic).

•Reduced salt consumption, not surprisingly, increases one’s risk of hyponatremia (e.g., one study found salt restriction made hypertensive patients 9.9 times more likely to develop hyponatremia).
Note: in addition to dietary salt reduction, many blood pressure and psychiatric medications put you at risk for dangerously low sodium levels (e.g., SSRI antidepressants make you 3.16 times more likely to). Additionally, certain patients (e.g., those with autonomic nervous issues) are much more sensitive to salt restriction causing hypotension (low blood pressure).

• Low dietary sodium intake causes a 34% increase in cardiovascular disease and death.

•Rapidly lowering blood sodium levels reduces cardiac output and blood pressure in a manner resembling traumatic shock (which frequently raises the heart rate as the heart tries to compensate for insufficient blood). Low salt consumption, in turn, has been repeatedly linked to tachycardia (and atrial fibrillation).

Remarkably, while this is rarely prioritized in medicine, there is simultaneously a well-recognized physiologic mechanism for it. When the body senses insufficient sodium, it defends its blood volume by activating the renin-angiotensin-aldosterone system and the sympathetic nervous system—the same stress machinery that raises the heart rate (and patients take blood pressure medications to block). So, in exchange for a tiny blood pressure reduction, salt restriction was found to significantly raise plasma renin, aldosterone, adrenaline, noradrenaline, cholesterol, and triglycerides—trading a trivial drop in one number for a rise in the very hormones and lipids that drive cardiovascular disease. This is worse in the elderly, whose aging kidneys respond poorly to changes in blood sodium and are thus at greater risk for hyponatremia following sodium deprivation.

Note: three of the most common symptoms of hyponatremia (which lead people to go to the Emergency Room) are fatigue, confusion and difficulty concentrating.

•Chronic sodium depletion has been linked to fatigue and insomnia.

•Many readers have reported discovering low salt consumption was the cause of their fatigue and lightheadedness (which has also been proven in a clinical trial which treated postural orthostatic tachycardia syndrome with increasing dietary sodium).
Note: chronically low blood pressure (e.g., POTS) has been shown to be one cause of chronic fatigue syndrome,^1,2 and POTS is often treated with increased dietary sodium (e.g. the autonomic disorder consensus guidelines formally recommend it).

•A variety of other health issues (e.g., worsening of diabetes or a stomach hydrochloric acid deficiency) have also been linked to insufficient dietary sodium. For example, a review of 23 trials found low-salt diets consistently produced insulin resistance, and one study induced it in healthy people in as few as 7 days.

•Beyond the acute confusion of hyponatremia, there is now emerging evidence that chronically low sodium intake harms the aging brain. A 2025 longitudinal study of over 1,500 older adults found that those in the lowest sodium intake quintile (around 1,764 mg/day—right about where public health targets try to push people) experienced faster decline in global cognition, especially memory, compared to those eating a moderate amount. Likewise, low sodium intake was also associated with more tau tangles (a hallmark of Alzheimer’s pathology) on autopsy, while high sodium intake was not linked to faster decline in this cohort.
Note: the suppressed causes and treatments of Alzheimer’s disease are discussed further here.

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U-Shaped Curves

Much in the same way I have observed extreme positions on either side of a political issue will frequently cause problems for the society (as they prevent a healthy balance from ever being found), frequently in physiology, a number will be observed which, when improved, appears to correlate with improved health, leading to the assumption as much as possible should be done to improve that number. In many cases however, at some point, the effect reverses, and it becomes harmful to further increase or decrease that number.

For example, with blood pressure, a few data points showed that if it’s too high, it increases one’s risk of death, so this was used to create a linear model which extrapolated that trend to much lower blood pressure values.

Yet, in real life, once blood pressure gets too low, the trend reverses and one’s risk of dying increases rather than decreases.

Likewise, both high and low sodium diets have been shown to increase the risk of death. This U-shaped curve was best demonstrated in a study of chronic kidney disease and heart failure patients:

Further corroborating the U-shaped curve for sodium input, a study of 100,000 adults across 18 countries, found the same U-shape, with the lowest risk of death and cardiovascular events at a moderate intake of roughly 3–5 grams of sodium per day and rising risk at both lower and higher intakes (a pattern a follow-up study further corroborated), along with also finding that higher potassium and a lower sodium-to-potassium ratio predicted lower mortality.

The same U-shape even appears when sodium is measured directly in the blood, where a study of 32,666 patients found mortality was lowest at a serum sodium of 139–144 and rose at both lower and higher levels. Finally, most recently, a 2025 national Chinese cohort of nearly 271,000 adults confirmed the U-shape for cardiovascular mortality, with the lowest risk near 4.6–5.4 grams of sodium per day. Additionally, that study identified much of the increased risk of death from low sodium resulted from elevated heart rates and blood glucose—both well-known (but rarely discussed) effects of salt avoidance.

Sodium in Heart Failure

Due to excessive sodium consumption causing heart failure exacerbations, heart failure patients are often (dogmatically) told to avoid dietary sodium, despite there being many cases of them improving once they add some salt back into their diet (as they had been on the left side of this curve). While this has long been known within the integrative health field, in the last few years, data at last is emerging to support this (along with the U-shaped mortality curve in sodium consumption):

• A 2018 systematic review of 9 trials found no evidence that salt restriction reduced deaths, hospitalizations, or hospital stays in heart failure patients.

• The largest trial to date, (a 2022 one of 806 patients across six countries), found that cutting sodium to under 1,500 mg/day did not reduce deaths, hospitalizations, or emergency visits compared to usual care.

• A 2024 review concluded that across the randomized trials, restricting dietary sodium does not reduce clinical events in heart failure patients—and that strict restriction (1,500 mg/day) offers no advantage over moderate intake, with some data hinting a looser 2,000–3,000 mg/day may carry lower mortality.

• A 2026 meta-analysis of 16 randomized trials (roughly 2,260 heart failure patients) found sodium restriction associated with higher all-cause mortality (a 50% increase) and markedly higher cardiac mortality, with the harm most pronounced in the sickest patients and when restriction was combined with fluid restriction and diuretics.

In light of this data, while American medicine still clings to the low sodium dogma, Europe fortunately is beginning to rescind salt restriction recommendations for heart failure patients.

Zeta Potential Curves

When fluid contains suspended particles (which is true for most fluids in nature), those colloids can either have finely dispersed or clumped together particles. One of the primary determinants of this is the electrical repulsion or attraction between the particles, something quantified by a system’s zeta potential and heavily influenced by the charges present in a solution (e.g, too many positive charges will make fluid components like blood cells clump together and is why the aluminum in vaccinations frequently trigger microstrokes of varying severity). In turn, many diseases result from poor zeta potential, including poor circulation and fluid congestion or edema (e.g., that seen in heart failure).

One critical aspect of zeta potential is that it follows a U-shaped curve in relationship to the amount of a charged ion present, with both too little or too much of it being problematic.

Note: giving IV sodium infusions to hospital patients will frequently greatly improve their condition, something nonchalantly attributed to everyone being “dehydrated” but more accurately due to their blood sodium being too low to adequately support the physiologic zeta potential. Likewise, many people often feel much better after getting outpatient saline infusions at concierge hydration clinics.

This in turn helps to explain why too little salt (e.g., through intentional sodium restriction or unintentional sodium restriction through a diet that puts you into ketosis [which increases sodium excretion]) can be problematic while at the same time high salt diets can be problematic as well.

With high salt diets (the other end of the U-shaped curve), I believe a few points are particularly important to recognize:

1. I’ve had multiple cases where I ate fairly salty foods right before bed, then woke up feeling extremely dry throughout my body with a fast heart rate. Through trial and error I figured out drinking certain waters would help me feel better. Later, from reading Thomas Riddick’s work on zeta potential, I understood what was happening and measured the conductivity in my urine, showing that my kidneys indeed were trying to dump a large amount of sodium and restore my zeta potential. Riddick, tracked many cases where more severe versions of what I experienced resulted in cardiovascular incidents (as poor zeta potential causes blood to clot together and triggers heart arrhythmias as the heart struggles to push this congested blood).
Note: numerous readers here have reported zeta potential restoring protocols has fixed their atrial fibrillation.

2. Riddick (and those who followed him) found that processed foods and many restaurant meals tended to be problematic for zeta potential and hence advised reducing the frequency of their consumption (e.g., I try to minimize eating out because of the congestion I feel after restaurant meals).
Note: since there are so many other harmful things in processed foods, it is very possible many of the issues associated with salty foods are due to something else that is present in it (e.g., seed oils or questionable food additives).

3. Riddick believed one of our key issues with salt was that potassium was better for zeta potential than sodium, so by switching our potassium based sources of salt (e.g., vegetables) for highly salted foods, we were creating an unhealthy balance between the ions. Likewise, modern research has shown adequate potassium alongside sodium is critical for cardiovascular health (e.g., normalizing blood pressure), with a recent trial of 21,000 people finding that simply replacing ordinary salt with a 75% sodium / 25% potassium substitute (not reducing salt intake, just rebalancing it) led to 14% fewer strokes, 13% fewer major cardiovascular events, and 12% fewer deaths.
Note: potassium deficiency causes a variety of issues (e.g., fatigue and muscle cramps) and many practitioners over the years have found supplementary potassium greatly helps their patients.

4. In general, I noticed most of the salt overload issues individuals run into come from eating foods high in refined salt (e.g., salty processed foods) rather than those consuming natural salts. This has led me to suspect that a major issue with salt is either something else present in the processed foods or something specific to processed salts. At this point, my best guesses is that it is due to refined salts:
•Lacking minerals we otherwise need for homeostasis
•Containing other problematic additives (e.g., refined salt tends to clump together so it requires anti-caking agents, many of which adversely affect zeta potential).
•Having a refinement process that introduces unhealthy chemicals to the salt (e.g., sodium carbonate, sodium hydroxide, barium chloride or barium carbonate are used to remove minerals besides sodium from refined salt).
Note: salt bleaching or heating may also be problematic.

Healthy Salt

Since salt is such an integral part of our life, I frequently receive a variety of questions on which type of salt we should consume. In the last part of this article (which exists as an open forum for you to ask any questions you have), I will share what I’ve learned from years of exploration on this topic, which brands of salt we prefer, the other critical steps for ensuring salt is compatible with health and invite each of you to share what you have discovered from your own exploration of salt.

Read more

•No industry, organization, or cause tasked with solving a problem will actually solve it, because the problem disappearing threatens their economic livelihood or political power.

•The pharmaceutical industry has perfected this model: drugs are designed to be taken perpetually rather than cure, side effects create demand for additional drugs, and the entire regulatory apparatus is structured to suppress affordable natural therapies that challenge it.

•SSRIs epitomize this dynamic—massively overprescribed, frequently life-ruining, and nearly impossible to withdraw from—yet for decades, the industry successfully kept all criticism of them out of mainstream discourse.

•Kennedy announced a multiagency federal effort to combat inappropriate SSRI prescribing, train providers in how to correctly taper patients off antidepressants, and provide non-pharmaceutical alternatives.

•This marks the first time in memory a federal health initiative has aimed to help get patients off a major drug class rather than on one.

When I was in high school, I observed a few discouraging events which led me to postulate: “no industry, organization or cause tasked with solving a problem will actually solve it because the problem disappearing threatens their economic livelihood or political power.” Since that time, I have observed more examples than I can count in so many different spheres that I’ve accepted this dynamic is a common feature of society, and likewise, have come across many similar observations by others, my favorite of which was:

Nothing is so permanent as a temporary government program—Milton Friedman

Recently a noteworthy exampls of this principle came to my attention after I learned all of the online dating apps had switched from formats which allowed people to find suitable long term partners to ones which prevented people from matching, because if someone found a good match, they would stop paying for the service. Once one company figured this out, they bought out all competitors and shifted them to this predatory model as well (and all the profound consequences it entails).^1,2,3,4,5,6

Note: because online dating has now become so bad, the companies that monopolized the market are starting to lose a lot of users and money, signaling there may be a chance for this cycle to reset itself.¹

This article will focus on how that principle applies to medicine and why I believe beyond greed, complacency also plays a central role in the continual recurrence of this dynamic across societies.

Is Money The Root Of All Evil?

The love of money has long been recognized as one of the most powerful forces for twisting human hearts towards evil. However, I would argue the core issue is that for many people effectively, accumulating money becomes the foundational axiom used to navigate life, causing them to rationalize a variety of unethical positions because their internal algorithm will frequently default to the choice that acquires more money. Recognizing this provides an invaluable tool for understanding the world, as the motivations of others often become far clearer once you view things strictly through what and how they stand to profit from their actions.

Algorithms of Business

In the same way that a default behavior to seek the most profitable choice helps to explain individual actions, businesses also follow a relatively predictable set of behaviors aimed at optimizing profit. In general, most large businesses aim for the following, prioritizing whichever are most feasible:

• Continual growth

• High markups on their product

• The widest possible market

• Market exclusivity (to protect and maximize sales)

• Repeating sales far into the future

The pharmaceutical industry excels in all of these, which helps to explain why they have managed to sustain steady growth for decades, and why one-fifth of all money spent in the United States goes to healthcare despite our country receiving very poor returns on that investment.

Note: annual adult vaccines (which frequently do nothing, particularly because they are often for the wrong strain) are an excellent example of an unsafe, unproven and ineffective product that is pushed on everyone because it fulfills the need for perpetually recurring sales.

Lifelong Patients

A frequently shared meme highlights that members of the medical community frequently face the same dilemma dating companies do.

The more time I’ve spent in medicine, the more I’ve come to appreciate that many principles you see in business are not only replicated in medicine but inevitably will guide medical practice. The entire industry (and regulatory apparatus) is structured around this status quo, so anytime someone tries to deviate from it, countless stakeholders will emerge to oppose it.

This was best demonstrated by a 2018 report which provoked considerable public outrage when it was publicized by the mainstream media:

Note: while I can’t prove this, given how rarely the media will expose pharmaceutical misconduct, I believe the reason it did in this specific case was not to help the public but rather to send a message to the industry (and investors) to avoid curative genomic therapies.

All of this helps explain why the medical industry (and regulators) will only target competing therapies with the potential to meaningfully compete with their bottom line (e.g., we all saw what happened to the off-patent COVID-19 treatments like hydroxychloroquine and ivermectin).

Sadly, many even more consequential examples. For example:

•Ultraviolet blood irradiation cured a wide range of otherwise fatal bacterial and viral infections (and many autoimmune disorders), but as it was taking off across American’s hospitals, the American Medical Association tried to buy it, and once they couldn’t, successfully buried it (except in areas like Russia outside their monopoly).

•Sleeping medications have a wide range of issues which cause serious issues for their users, so once an effective (but un-patentable) one which restored people’s sleep and health (frequently to a profound degree) came into use, the FDA launched a relentless campaign that eventually outlawed it (detailed here).

•Oxidative therapies, like chlorine dioxide, when dosed appropriately, have shown remarkable efficacy against a variety of infectious diseases, along with certain ones (e.g., ozone) also showing significant efficacy against a variety of musculoskeletal issues, organ diseases and circulatory disorders. Yet, despite thousand of studies corroborating their use, the FDA treats them as toxic agents with no redeeming value, and any attempts to research these therapies (particularly chlorine dioxide) are obstructed.

•DMSO is safe and essentially free substance that rapidly heals injuries, cures a wide range of common debilitating problems (e.g., all types of pain, spine issues, most skin issues, most eye issues, gastrointestinal inflammation and many autoimmune disorders) along with addressing many otherwise incurable issues (e.g., stroke damage, paralysis, chronic lung disease, and many different neurodegenerative disorders). Yet, despite the life-changing properties of this substance, the FDA fought the public for decades (including at multiple Congressional hearings) to bury it, and as a result, few people know it is anything but an inert solvent widely used in research and to deliver pharmaceuticals (and an interstitial cystitis treatment).

While many other candidates exist too (e.g., many promising cancer therapies were blacklisted by the AMA and FDA), I believe DMSO’s story is likely the clearest case of the FDA suppressing something to maintain the status quo of profitable diseases being incurable (and requiring perpetual lucrative medical care). This is because roughly 15,000 studies (I am gradually compiling) show its efficacy across a wide range of illnesses and I have now received over 7000 thousand testimonials from readers who had a lifelong debilitating issue rapidly resolve with DMSO that are nearly identical to those the FDA received as the public begged them not to ban it.

Medical Sales Funnels

One of the most common critiques of the pharmaceutical industry is that the entire enterprise is a more sophisticated form of the addictive drug model: the drugs that are widely sold are designed to hook people for life and the immense lobbying the industry can afford effectively takes the place of cartel violence to maintain their market monopoly. Furthermore, unlike classic drug enterprises which have to market their products from the shadows, the state sanctioning of their business model makes it possible for them to publicly market the products to the entire society and buy out both the media and government so criticisms of their products are not allowed to be aired.

Note: other common criticisms include several of the largest pharmaceutical companies (e.g., Bayer via IG Farben) having been deeply entwined with Nazi Germany, and that many major pharma firms were once leading marketers and manufacturers of cocaine, methamphetamine, and heroin (Bayer famously marketed heroin as a “non-addictive” wonder drug¹).

Fittingly, the medical profession has largely moved away from the language of “cure.” For centuries, major medical dictionaries either omitted a clear definition of “cure” or defined it only minimally.^1,2 The word is also notably absent from the indexes of core references such as Merck’s Manual and Harrison’s Principles of Internal Medicine.^1,2 In practice, physicians are strongly discouraged from promising or even declaring a “cure” in many contexts.¹ You cannot be accused of failing to achieve something the profession rarely claims is possible.

Because of this, every successful pharmaceutical lies somewhere along a spectrum of being “addictive” to “ineffective.” Much of this results from the fact the body is designed to maintain homeostasis and resist unnatural alterations of physiology, so the human response to medications is frequently either: for the effect to be temporary, for progressively higher doses to be required, or for the body to shift to an unnatural baseline where it can no longer function without the artificial counterweight of the medication.

Note: sometimes additional steps are involved. For example, acid reflux frequently results from a lack of stomach acid (which prevents the top of the stomach from getting the signal to close) which argues for supplementing meals with stomach acid (that beyond frequently curing reflux, provides numerous other health benefits). However, rather than do this, the preferred approach is to completely suppress stomach acid production so nothing is there to reflux, making it very difficult to stop the medications because once small (insufficient) amounts of acid return, they will reflux and cause heartburn.

Beyond the design of pharmaceutical drugs inevitably producing side effects, those side effects are often actually an upside for the industry because they create additional problems that require other drugs to treat, hence creating a robust “sales funnel.” General practitioners not only provide a steady stream of patient referrals to more expensive medical services, but also give patients tests that convert a significant number into taking common lifelong drugs (which half of American adults are on at least one of¹).

SSRI Antidepressants

From the start, I decided to focus on SSRIs as while they significantly help a subset of patients, I also feel they are one of the worst offenders on the market. Beyond being massively overprescribed, they frequently ruin people’s lives (often in very cruel ways), are often nearly impossible to withdraw from, and have predatory sales funnels that affect large numbers of American women:

Unfortunately, SSRIs languished in the same place many other toxic drugs did: they harmed a significant number of people but the drugs made enough money (one in six adults take psychiatric medications¹) that it was possible for industry to corral the entire government and media into sweeping them under the rug.

To try to shift this, I decided to focus not on the common side effects, but rather the psychotic violence and mass shootings they occasionally cause. My theory was that since so much effort has gone into politicizing mass shootings and gun control, the right would be receptive to the fact SSRIs were triggering many of the shootings being blamed on inadequate gun control, and that this would spur interest into all the other far more common side effects SSRIs cause and make it finally an acceptable topic of discourse.

So, I tried to draft a very clear case for this (along with a follow up explaining the dangers of SSRIs and the corruption that allowed them to come to market) and then put them out immediately following a school shooting which was large enough to become the national media story. That article somehow made it to Tucker Carlson, who then, five weeks later, for the first time in the mainstream media, did a segment on the topic for Fox News.

Following this, as more and more political figures on the right were willing to broach the subject, it became a gradually acceptable topic to discuss (e.g., during his 2024 campaign, RFK Jr. shared that article stating: “Any conversation about gun violence is incomplete if it doesn’t touch on mental health and the suppressed evidence implicating SSRIs in suicide and homicide”).

The successive attention which bubbled up in the alternative media to the frequent side effects of SSRIs (and Secretary Kennedy’s public acknowledgment of it) has gradually brought mainstream attention to this, including at a recent May 4th panel (covered by the press) which began with victims of SSRIs sharing what they have experienced.^1,2

That panel concluded with Secretary Kennedy stating we need to do better, that withdrawing from SSRIs is significantly more difficult than withdrawing from heroin, and announcing that the Federal Government would begin combatting this. He laid out a multiagency national effort to educate health care providers in the dangers of SSRIs (particularly inappropriate prescribing), provide non-pharmaceutical mental health alternatives, and train providers in how to correctly taper off psychiatric medications (along with reimbursing them for doing this).¹

Since that May 4, 2026 announcement,¹ the multiagency effort has continued to advance rather than stall. HHS agencies issued the planned “Dear Colleague” letter emphasizing informed consent and non-drug options, CMS clarified reimbursement so clinicians can be paid for time spent helping patients taper, and SAMHSA began educational webinars and training modules on psychiatric medication risks, deprescribing, and alternatives. In early July a Technical Expert Panel of clinicians, patients, and professional societies met to shape formal clinical guidance on safe tapering of SSRIs and related drugs¹—the first such federal process focused on getting people off a major drug class rather than onto one.

Most remarkably, the profession is responding to these attempts—deprescribing has begun appearing as a formal topic at major psychiatry meetings, including sessions and consensus work at the American Society of Clinical Psychopharmacology’s 2026 gathering this week, where clinicians are now openly discussing when and how to taper patients off psychiatric medications rather than leaving them on them indefinitely.

Most remarkably, the profession is responding and deprescribing has moved into formal sessions at major psychiatry meetings. Shortly after RFK’s announcement, at the American Society of Clinical Psychopharmacology’s 2026 annual meeting, members of the society’s own Deprescribing Task Force held a detailed panel discussion on when and how clinicians should taper patients off psychiatric medications and on the importance of non-drug alternatives such as psychotherapy, lifestyle changes, and collaborative care rather than leaving patients on medication indefinitely:

Note: SSRIs are not the only psychiatric medication with major issues (e.g., there are many serious issues with benzodiazepines which are used for anxiety, insomnia and SSRI side effects).

Despite everything I’ve seen happen over the last four years, I still never believed something like this would happen. For context, in a period when the pharmaceutical industry had much less influence over the FDA, it took more than a decade of activism, leaks and Congressional hearings to simply get a warning label on SSRIs that they could cause suicide. This went miles beyond anything even the most optimistic activists had ever imagined, illustrating why it is so critical to shift the Overton window and make taboo subjects acceptable for regular discussion.

Additionally, it was quite notable that this entire effort goes contrary to the entire foundation of the medical system, as Secretary Kennedy’s ultimate goal was to decrease rather than increase pharmaceutical sales. As such, predictable criticisms of his completely reasonable approach emerged, such as this one from Senator Tina Smith (D-MN):

People I care a whole lot about rely on SSRIs to make their lives work. I don’t know where I would be without SSRIs. RFK Jr. can get his f***ing hands and crazy conspiracy theories out of our medicine cabinets”

Institutional Inertia

Most societies and institutions follow a similar trajectory: initially, they have to be as innovative and dedicated as possible to establish themselves. Once established, their focus shifts to maintaining their position rather than advancing their original mission (e.g., empires throughout history typically last seven generations because they all succumb to this cycle).

This shift commonly translates to the goal moving from solving the issue to providing an “indispensable service” by perpetually managing rather than fixing it. I’ve never forgotten one clip from a documentary²⁹ about soldiers injured by the (completely unnecessary) experimental anthrax vaccine, which much like the COVID vaccine, ended the careers of many promising soldiers despite widespread resistance against the shots.