By A Midwestern Doctor
The Forgotten Side of Medicine
August 31, 2026
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:
How DMSO Heals the Brain and Transforms Neurology
This article covers how circulatory impairments underlie many neuropsychiatric disorders and how DMSO:
• Biophysically eliminates microclots along with preventing immune cells from obstructing capillaries, facilitating lymphatic and venous drainage.
• Counteracts a broad range of inflammation and free radicals
• Shields cells from diverse lethal stressors and excitotoxins
• Protects ATP production, restarts dormant cells, and restores parasympathetic (vagal) tone (e.g., through acetylcholinesterase inhibition)
• Effectively delivers a variety of therapeutic agents to the central nervous system.
How DMSO Heals the Spine and Reverses Paralysis
This article also extensively covers:
• How DMSO facilitates neuronal regeneration by stabilizing microtubules and differentiating stem cells into replacement neurons.
• How DMSO's other established therapeutic mechanisms (e.g., muscle relaxation, tissue regeneration, and interruption of pain transmission) reduce or eliminate spinal pain.
How DMSO Heals The Nerves & Eliminates Pain
This article also extensively covers how:
• DMSO's biophysical effects on water temporarily shift the phase of cell membranes and the cytoskeleton, creating a reversible cellular reset that restores normal structure and function (along with uniquely enabling DMSO to transport substances across biological barriers without damaging them).
• DMSO selectively blocks the small nerve fibers that transmit chronic pain
• DMSO supports peripheral nerve regeneration (e.g., with membrane resealing)
• Through neuronal resets, DMSO can eliminate the source of chronic pain and autonomic dysfunction.
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 times 1, 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 radicals 1 blocks radical-mediated platelet activation 1 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, 2Note: because the clotting was prevented at a site of genuine vessel injury, these results 1 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.