DMSO and MND/ALS: separating the science from the hope
Before you read this
Dimethyl sulfoxide (DMSO) has attracted serious scientific interest because it does something genuinely unusual: a single compound interacts with several of the biological processes implicated in ALS, from the way cells handle oxidative stress to the way nerve fibres transmit pain. That convergence is why researchers keep looking at it, and it is why this article exists. No human clinical trial has established that DMSO improves symptoms, function, survival or disease progression in MND or ALS, and nothing here should be read as a treatment recommendation. What follows is an honest account of what the research shows, where it is genuinely interesting, and where the gap between laboratory and clinic remains wide.
What DMSO is and where it has been used
There is something almost paradoxical about DMSO. It is simultaneously one of the most studied and one of the least glamorous compounds in pharmacology: a simple sulphur-based organic liquid, produced naturally by marine algae, colourless, smelling faintly of garlic. Yet it does something remarkable. It passes through skin and cell membranes with a speed and ease that most molecules cannot match. Think of most substances as trying to cross a crowded room by pushing through the crowd: DMSO walks straight through the wall. For researchers and clinicians, that property is not just interesting in the abstract; it is practically useful.
DMSO has been in clinical and research use since the 1960s. Its one use approved by the US Food and Drug Administration (FDA) is the treatment of interstitial cystitis, a chronic bladder condition, administered by instilling a sterile 50 per cent solution directly into the bladder under medical supervision. A 2024 review confirmed it as the most widely used protective agent for freezing and storing stem cells, bone marrow and cellular therapies before transplantation (Fang and Vangsness, 2024). Both applications are tightly controlled and administered in clinical settings. The safety and dosing data established for these uses cannot be extended to oral ingestion, high-concentration topical self-application or intravenous use in any other condition, including ALS. That boundary holds throughout what follows.
Why ALS research has started paying attention
ALS (amyotrophic lateral sclerosis) and MND (motor neurone disease) refer to the same disease under two names: ALS is the standard in scientific literature and in North America; MND is the clinical standard in the United Kingdom (van Es et al., 2017). The disease is driven by several interconnected biological processes. Reactive oxygen species, unstable molecules that behave a bit like sparks inside a cell, accumulate and damage motor neurons when the body cannot neutralise them fast enough. Neuroinflammation, the nervous system’s equivalent of chronic swelling, amplifies that damage. Mitochondria, the tiny structures inside every cell that generate energy much like a battery, stop working efficiently, cutting off the fuel supply to the cells that need it most. And glutamate, a chemical messenger the brain uses to transmit signals between nerve cells, builds up to toxic concentrations when the transport proteins that should clear it away fail to do their job (Silva-Hucha et al., 2026; Wei et al., 2026).
What caught researchers’ attention is that DMSO has documented experimental activity across several of these pathways simultaneously. That is unusual. Most compounds interact with one target or one mechanism. A compound that appears in the experimental literature on oxidative stress, inflammation, mitochondrial function and nerve conduction is worth examining closely, even when the direct clinical evidence is limited.
A functional-medicine lens can help identify connections between biological pathways and generate clinically relevant questions. Those connections remain hypotheses until appropriate studies establish whether they translate into meaningful benefit for patients.
The claims in this blog are each accompanied by an evidence grade. At the strongest end sits human ALS/MND clinical evidence: direct findings from people with the disease. One step down is ALS animal-model evidence, drawn from genetically engineered mice or other recognised ALS models. Human evidence outside ALS covers findings from people with other conditions or from healthy volunteers. Below that, ex-vivo, cellular or non-ALS animal evidence refers to work done in tissue cultures, isolated preparations, or animal studies unrelated to ALS. At the base of the hierarchy sits theoretical or mechanistic inference: connections drawn from basic biology without direct experimental support in any disease model.
Inflammation: the pathway with the most evidence behind it
Evidence grade: ex-vivo human blood; mouse arthritis model. Not an ALS study.
Of all the biological properties DMSO has been tested for, its anti-inflammatory and immunomodulatory activity, meaning its ability to modify how the immune system responds, has accumulated the strongest experimental evidence. A 2020 review in the journal Immunobiology identified consistent effects across multiple laboratory models and noted growing interest in exactly how DMSO interacts with immune cell signalling (Huang et al., 2020). The mechanism, where it has been examined closely, points to something specific rather than a crude blunting of the immune response.
In stimulated human whole blood taken outside the body, DMSO at concentrations of 0.5 to 2 per cent was associated with substantially reduced production of a broad panel of inflammatory signalling molecules called cytokines and a related compound called prostaglandin E2. The way this happened gives it particular relevance: DMSO appeared to switch off specific signalling proteins, known as ERK1/2, p38 and JNK, inside monocytes, a type of white blood cell that plays a central role in driving inflammation. Rather than simply dampening the whole immune system, the compound seemed to interrupt a specific chain of chemical events, more like turning off a particular circuit than cutting the power to the whole building. A parallel experiment in the same study found that DMSO applied to the skin at 70 per cent reduced joint swelling in a mouse model of autoimmune arthritis (Elisia et al., 2016). Earlier work found dose-dependent reductions in several inflammation-driving proteins, including interleukin-6 (IL-6), MCP-1 and COX-2, in stimulated intestinal cells (Hollebeeck et al., 2011).
This is not evidence that DMSO reduces inflammation in the nervous systems of people with MND. Blood assays outside the body and mouse arthritis models do not replicate the neuroinflammatory environment of ALS. The Elisia study also found that monocyte viability was reduced at the 2 per cent concentration, meaning the cells themselves began to be harmed at that level, suggesting a narrow window between anti-inflammatory effect and harm to the cells. What the data do establish is that DMSO interacts with specific inflammatory signalling pathways that are directly relevant to ALS biology. That makes it a legitimate starting point for investigation in neurological models. It is not a clinical result.
Oxidative stress: following the most direct line of evidence
Evidence grade: established experimental chemistry; ex-vivo and cellular evidence for DMSO. Human Phase III randomised controlled trial for edaravone as mechanistic comparator only.
The case for oxidative stress as a therapeutic target in ALS is probably stronger than for any other single mechanism. Reactive oxygen species drive the abnormal behaviour of TDP-43 (TAR DNA-binding protein 43), a protein that in healthy cells helps regulate which genes are switched on. In ALS, TDP-43 migrates out of the cell nucleus into the main fluid-filled body of the cell and forms clumps that disrupt mitochondria and generate still more oxidative stress in a self-amplifying cycle: damage begetting more damage (Zuo et al., 2021). Separately, mutations in a gene called SOD1 (superoxide dismutase 1), found in some people with inherited ALS, cause the resulting protein to become actively harmful rather than simply losing its normal protective function (Guo et al., 2023). Both routes converge on the same outcome: damage accumulates faster than the body’s repair systems can handle it.
DMSO’s ability to neutralise a particularly destructive type of reactive oxygen species, called hydroxyl radicals, is among its most consistently documented properties. Researchers use it routinely as a reference standard in experimental work precisely because the activity is reliable and measurable (Madsen et al., 2019). Whether this translates to clinical benefit in ALS is answered most directly, not by DMSO itself, but by edaravone, a different compound that works through related mechanisms. The Edaravone (MCI-186) ALS 19 Study Group ran a rigorously designed randomised controlled trial, a type of study where neither patients nor clinicians know who is receiving the active drug until the study ends, in which edaravone was associated with significantly slower functional decline over 24 weeks in a carefully defined group with early-stage disease and preserved respiratory function (Edaravone (MCI-186) ALS 19 Study Group, 2017). A separate European programme evaluating an oral form of edaravone did not demonstrate equivalent benefit (Abrahao et al., 2026). Edaravone is not currently approved or available on the NHS (National Health Service).
The comparison with DMSO is mechanistic and no further. Two compounds that interact with oxidative pathways do not share their clinical evidence. Edaravone’s trial demonstrates that the oxidative stress pathway can, under specific conditions in a defined patient group, be modified by a free radical scavenger. It does not tell us what DMSO would do in the same situation.
Mitochondria: a story that depends on dose and cell type
Evidence grade: cultured heart muscle cells and cancer cells; cultured nervous system support cells. Not motor neurons. Not ALS models.
The mitochondrial picture around DMSO is instructive precisely because the evidence pulls in two directions depending on concentration and cell type, and both directions carry weight.
At concentrations below 0.5 per cent, DMSO was associated with improved mitochondrial efficiency in cultured heart muscle cells (cardiomyoblasts) and breast cancer cells: think of it as the engine running more cleanly at low doses. No harmful effects were observed at these low concentrations. At 3.7 per cent in the same cell types, the picture reversed, with mitochondrial dysfunction and increased cell death (Sangweni et al., 2021). These are laboratory observations with real dose-dependence. They were not conducted in motor neurons, ALS cell models or human subjects, and they cannot establish a therapeutic benefit in MND.
The second study is harder to set aside. In cultured astrocytes, the support cells of the nervous system that maintain the environment around neurons and are often compared to scaffolding holding a building together, DMSO at 1 to 5 per cent caused the mitochondria to swell, reduced the electrical charge across the mitochondrial membrane, and triggered a cascade of cell death processes (Yuan et al., 2014). Astrocytes are not peripheral to ALS; their dysfunction is specifically and centrally implicated in the disease. More striking still, DMSO at these concentrations also reduced the activity of EAAT2 (excitatory amino acid transporter 2), the protein responsible for clearing glutamate from the space around nerve cells. When EAAT2 is impaired, glutamate builds up like an overflowing drain and becomes toxic to motor neurons: this is one of the key processes driving nerve cell loss in ALS (Pajarillo et al., 2019; Dahlmanns et al., 2023; Yuan et al., 2014).
These findings do not mean that DMSO uniformly harms mitochondria. They mean that concentration and cell type are not peripheral details: they are the whole story. The concentration of any preparation applied to the skin also tells us nothing about what concentration actually reaches nervous system tissue deep inside the body. That data does not exist.
Pain and nerve conduction: intriguing but distant from the clinic
Evidence grade: isolated cat peripheral nerve preparation (foundational, 1993). One commentary on regeneration.
Neuropathic pain, often described as burning, stabbing or electric-shock sensations caused by damage or dysfunction of the nerves themselves, affects a proportion of people living with ALS and is frequently underrecognised. DMSO has documented pain-relieving effects in musculoskeletal conditions, and the experimental basis for them points directly at peripheral nerve physiology.
In foundational work now over thirty years old, DMSO applied directly to surgically exposed peripheral nerves in cats blocked conduction in C-type fibres, the small nerve fibres responsible for carrying pain signals, at concentrations of 9 per cent and above (Evans et al., 1993). No modern study has replicated or superseded this finding. The experimental conditions, direct application to surgically exposed nerve tissue, are a long way from applying a cream or solution to intact skin in people, and the finding does not establish whether clinically used preparations produce equivalent concentrations at nerve tissue or comparable pain-relieving effects.
A commentary in the Journal of Investigative Surgery identified DMSO as a compound of interest in peripheral nerve regeneration (Gkiatas and Gelalis, 2021). This is an opinion piece rather than an experimental study; it does not constitute clinical evidence. No clinical study has examined DMSO specifically for neuropathic symptoms in people with MND or ALS.
The ALS model study: The one direct test
Evidence grade: one unreplicated ALS mouse study. No human clinical trials exist.
One published study has examined DMSO directly in a recognised ALS model, and it deserves to be read carefully rather than either dismissed or overstated.
Transgenic mice carrying a specific genetic mutation known as SOD1-G93A, which causes a form of inherited ALS and is one of the most widely used animal models of the disease, were given DMSO at 5 per cent in their drinking water over the long term. The result was an association with improvements in some measures of movement and co-ordination, and a modest increase in mean survival compared with untreated animals (Park et al., 2022). This is not nothing. It is also not what it might appear. The study did not demonstrate any prevention of motor neuron loss in the spinal cord or the breakdown of connections between nerves and muscles: the underlying disease process continued even where some movement outcomes improved. And the findings have not been independently tested by another research group.
Animal models of ALS have a historically poor record of predicting what will happen in human trials (Wei et al., 2026). What improves mouse behaviour cannot be assumed to carry across to human quality of life or disease course. The study also flagged a broader concern: because DMSO is widely used as a carrier liquid in laboratory and animal research, its own biological activity may inflate the apparent benefit of whatever compound it is being used to deliver.
No human clinical trial has examined DMSO’s safety or efficacy in people with MND or ALS. No regulatory body in the United Kingdom, Europe or North America has approved it for this use.
Detoxification: where the popular claim parts from the evidence
Detoxification is the most frequently heard claim for DMSO, and it is the least supported by the published literature. DMSO’s documented biological properties are hydroxyl radical neutralisation, anti-inflammatory signalling and membrane penetration. None of these is the same as detoxification in any established scientific sense. Membrane penetration describes how DMSO moves through tissue, not how it extracts or neutralises harmful substances. Antioxidant and anti-inflammatory activity are real, documented properties of DMSO, but they are not the same as detoxification, and the two should not be used interchangeably.
A systematic review of human DMSO studies found no evidence base supporting detoxification as a clinical use (Madsen et al., 2019). No credible clinical evidence was identified in the published literature to support this claim. People living with MND deserve a straight answer: the detox rationale is not what the science points to.
Safety: The questions that remain open
DMSO is biologically active and not inert. The route by which it is taken, the formulation used, the concentration, the sterility of the product and the length of use each influence both its effects and its risks, and none of these has been studied in people with MND.
The best-known side effect is a strong sulphurous, garlic-like odour that develops when DMSO is absorbed into the body and released through breath and skin; this can be very noticeable to those nearby. A systematic review found that effects on the digestive system and skin were the most commonly reported side effects in human studies, generally mild and related to the dose used (Madsen et al., 2019). A separate study found that DMSO caused widespread cell death in the developing central nervous systems of mice, most severely in early life (Hanslick et al., 2009). This finding is most relevant to the developing nervous system, but it confirms that DMSO has biological activity in nerve tissue that cannot be assumed to be harmless.
One safety property that receives less attention than it deserves is DMSO’s ability to dramatically increase the absorption of other substances through skin and mucous membranes. Any impurities in a self-prepared product, or other preparations applied to the skin at the same time, may be absorbed at substantially higher levels than would otherwise occur. This is not a theoretical concern: it is a documented property of the compound.
The FDA-approved use directly into the bladder has defined safety data for that specific route and formulation. Those findings cannot be applied to oral ingestion, high-concentration topical self-application or intravenous use in ALS, for which no clinical safety or dosing data exist. Anyone with MND considering DMSO should discuss potential interactions with their ALS team, neurologist, pharmacist or prescribing clinician, particularly when taking riluzole, edaravone or other medications.
The laboratory findings on mitochondrial impairment and reduced glutamate-transporter activity in cultured astrocytes at 1 to 5 per cent are a specific consideration in ALS, given that astrocyte function and glutamate clearance are already compromised in the disease. This does not establish that any external application is harmful at any particular dose in a living person. It does confirm that the dose question is genuinely unresolved, and that clinical guidance is absent.
Where this leaves us
DMSO has documented activity across multiple experimental systems relevant to ALS biology. The anti-inflammatory data is the most robust, with specific named signalling mechanisms identified. The hydroxyl radical scavenging is chemically well-established. One mouse study in a genetic ALS model found modest improvements in movement outcomes and survival, though without halting the underlying neurodegeneration. Taken together, this body of evidence makes DMSO a scientifically coherent object of interest in ALS research. The biological hypothesis is not groundless.
What does not yet exist is human clinical evidence of any kind. No trial has tested whether DMSO slows progression, preserves function or improves quality of life in people with MND. The gap between biological plausibility and clinical proof is wide and real, and it cannot be closed by the coherence of the hypothesis alone, however strong that hypothesis is.
Living with ALS means navigating a great deal of information, and very little of it is written with the patience and honesty the situation calls for. At You Nutrition Clinic, our approach is to hold both parts of the picture honestly: what is scientifically interesting and what remains unproven. We assess nutritional status, support antioxidant defences through evidence-informed strategies, identify avoidable environmental factors, and work alongside your medical team at every stage.
Our dedicated MND/ALS programme, No Stone Unturned, is led by Dr Kirstie Lawton and supports people from early diagnosis through to advanced disease.
Supporting MND and ALS at You Nutrition Clinic
Dr Kirstie Lawton, PhD, MSc, FBANT, founder and Clinical Director of You Nutrition Clinic, leads a dedicated multidisciplinary team supporting people living with Motor Neurone Disease, Amyotrophic Lateral Sclerosis and Primary Lateral Sclerosis. Kirstie heads up the MND/ALS/PLS team alongside Kerry (RNTP), Deborah (RD) and Rachael (RN), with further support from Rae, our breath and movement practitioner. Together the team brings clinical nutrition, dietetics, nursing and movement support under one roof, with specialist experience in the particular nutritional and functional challenges that MND /ALS presents.
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Disclaimer: This article is for informational and educational purposes only and does not constitute medical advice. Always consult with a qualified, registered medical doctor (MD) for diagnosis and treatment decisions.
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