Red light therapy shows genuine biological promise for multiple sclerosis, but the honest state of the evidence is that it remains far from a proven treatment. Animal studies are encouraging, a few small human trials hint at benefits for fatigue and other symptoms, and the underlying biology makes a plausible case for why it could help. Yet no large, rigorous clinical trial has established that photobiomodulation (the technical name for red and near-infrared light therapy) changes the course of MS in people. What exists is a compelling hypothesis with early-stage support, not a treatment you can confidently rely on.
Why the Biology Makes MS a Plausible Target
Multiple sclerosis is driven by immune attacks on the myelin sheath that insulates nerve fibers. But a quieter process runs alongside that immune damage: the mitochondria inside neurons begin to fail. Multiple independent studies have found deficiencies in the mitochondrial respiratory chain in MS, particularly in complexes I, III, and IV of the electron transport chain, which are the molecular machinery cells use to generate energy.1PubMed Central. Mitochondrial Dysfunction and Multiple Sclerosis2PubMed Central. Impact of the Combination of Epigallocatechin Gallate and Ellagic Acid Supplemented with Ketone Bodies on Energetic Restoration of Mitochondrial Dysfunction and Metabolic Inefficiencies in Patients with Multiple Sclerosis This energy shortfall is especially damaging in progressive MS, where long nerve tracts like those running down the spinal cord lose their myelin and then need even more energy to keep firing signals. The neurons cannot meet that demand, and the result is irreversible nerve degeneration.3PubMed. Mitochondrial dysfunction and axon degeneration in progressive multiple sclerosis
Red and near-infrared light therapy works primarily by being absorbed by cytochrome c oxidase, a key enzyme sitting in that same mitochondrial respiratory chain. When photons at the right wavelength hit this enzyme, it becomes more active, which in turn boosts the cell’s production of ATP, its energy currency.4PubMed Central. Photobiomodulation Therapy on Brain: Pioneering an Innovative Approach to Revolutionize Cognitive Dynamics The logic connecting these two facts is straightforward: if MS creates an energy crisis in neurons and light therapy can boost mitochondrial energy output, then light therapy might help compensate for the deficit. That reasoning is why researchers have pursued this line of investigation, and it is more grounded than many alternative therapy claims. But having a plausible mechanism is not the same as having proof that it works in practice.
What Animal Studies Have Found
The most consistent evidence comes from experiments on mice with experimental autoimmune encephalomyelitis (EAE), a laboratory model that mimics key features of MS. Several teams have applied light at 670 nanometers (deep red) to these animals and seen real effects. In one study, treated mice showed less severe disease than untreated controls, and the researchers found that pro-inflammatory signaling molecules like interferon-gamma and tumor necrosis factor-alpha went down, while anti-inflammatory ones like IL-4 and IL-10 went up.5PubMed Central. Amelioration of experimental autoimmune encephalomyelitis in C57BL/6 mice by photobiomodulation induced by 670 nm light A follow-up study confirmed the clinical improvement and added an interesting mechanistic wrinkle: when the researchers used mice genetically lacking an enzyme that produces nitric oxide (iNOS), the light therapy stopped working. That suggests nitric oxide plays a role in how the treatment protects against damage.6PLoS ONE. Photobiomodulation Induced by 670 nm Light Ameliorates MOG35-55 Induced EAE in Female C57BL/6 Mice: A Role for Remediation of Nitrosative Stress
A more recent 2024 mouse study went further, applying light daily along the spine and finding that photobiomodulation prevented immune cells from infiltrating the central nervous system, reduced the overreactivity of glial cells (the brain’s support cells), and corrected abnormal hyperexcitability in spinal cord interneurons. The behavioral payoff was clear: treated mice had significantly less severe sensorimotor impairment.7PubMed Central. Dorsoventral photobiomodulation therapy safely reduces inflammation and sensorimotor deficits in a mouse model of multiple sclerosis That study also confirmed safety in healthy mice, addressing a reasonable concern about applying light energy to already-inflamed tissue.
A systematic review and meta-analysis pooling data from EAE studies found a statistically significant reduction in clinical severity scores, with a mean reduction of about 1.4 points on the clinical scale used for these animals. But the same review flagged an overall high risk of bias in all included studies and noted that very few studies met inclusion criteria. The authors concluded that more preclinical work is needed before jumping to human trials.8PubMed Central. The benefits of photobiomodulation in animal models of multiple sclerosis: a systematic review and meta-analysis Animal models of MS have a spotty track record of predicting what works in people, so even encouraging mouse data should be taken with a generous grain of salt.
Human Evidence Is Thin and Mostly About Fatigue
In people with MS, the research that exists has focused largely on fatigue, which is among the most disabling and common symptoms of the disease. One randomized trial compared bright white light therapy to dim red light (used as a sham control) in MS patients with significant fatigue. Both groups improved on fatigue scales, and there was no significant difference between them. The researchers noted that the improvement in the sham group likely reflected a strong placebo effect.9PubMed. Light therapy for multiple sclerosis-associated fatigue: a randomized, controlled phase II trial A separate sham-controlled trial of bright white light versus dim red light for MS fatigue found a similar pattern: fatigue scores dropped in both groups, and while the bright-light group trended toward more improvement, the difference between groups was not statistically significant.10PubMed Central. Bright light therapy as a non-pharmacological treatment option for multiple sclerosis-related fatigue
An exploratory crossover study using light therapy glasses found that both blue-enriched and standard light reduced fatigue scores, with blue light showing a clinically meaningful reduction on at least one of the measured days. Neither intervention, however, improved overall quality of life.11PubMed Central. Exploratory crossover field study indicates efficacy and feasibility of light therapy glasses to mitigate fatigue in multiple sclerosis It is worth noting that these light therapy studies used visible-spectrum bright light intended to affect circadian rhythms, which works through a different mechanism than the near-infrared photobiomodulation studied in the animal experiments. Fatigue in MS has multiple causes, including sleep disruption, and circadian light therapy may help with the sleep-related component even if it does nothing for the neurological one.
A 2024 systematic review of photobiomodulation specifically for MS concluded that the treatment has been associated with improvements in motor, sensory, and cognitive function in MS patients, and that no studies have reported adverse effects. But the same review stressed that future work needs to standardize treatment protocols, assess long-term outcomes, and identify which subgroups of patients are most likely to benefit.12PubMed Central. Systematic review of photobiomodulation for multiple sclerosis The word “associated” is doing heavy lifting there. The studies included were small, and the absence of adverse effects, while reassuring, is partly a reflection of how few people have been studied.
How Immune Modulation Fits the Picture
MS is fundamentally an autoimmune disease, so any treatment that claims to help needs to either suppress the harmful immune activity, protect tissues from its damage, or both. Photobiomodulation appears to touch the immune system in several ways. A comprehensive review of the immunomodulatory effects of light therapy found that it promotes the development of regulatory T cells, a population of immune cells whose job is to keep other immune responses in check and prevent autoimmune attacks. Several studies have reported increases in both the number and activity of these regulatory cells following light treatment.13PubMed Central. Immunomodulatory effects of photobiomodulation: a comprehensive review This aligns with the animal findings showing shifts from pro-inflammatory to anti-inflammatory immune signaling.
The appeal here is that most MS drugs work by broadly suppressing or altering the immune system, which is effective but comes with real risks including increased susceptibility to infection. If photobiomodulation could nudge immune balance toward tolerance rather than attack, without the blanket suppression, that would be genuinely valuable. But the immune effects seen so far have been measured in laboratory settings and animal models. Whether shining light on a person’s skin or scalp produces a meaningful enough immune shift to alter the course of MS is simply unknown.
The Penetration Problem
One of the biggest practical obstacles is getting light where it needs to go. The lesions in MS occur throughout the brain and spinal cord, which are well-protected by skin, bone, and layers of tissue. Research on near-infrared light penetration has found that at low power levels, essentially no light makes it through even a couple millimeters of skin and a few centimeters of skull and brain. At higher power levels around 10 to 15 watts, roughly 0.5% to 3% of 810-nanometer near-infrared light can reach a depth of three centimeters. Pulsing the light at 10 Hz cut the surface dose in half but still allowed about 2.4% to penetrate to the same depth.14PubMed Central. Near-infrared photonic energy penetration: can infrared phototherapy effectively reach the human brain?
Three centimeters into the brain covers some cortical tissue, but MS lesions can be scattered deep in the white matter, in the brainstem, or along the spinal cord. Getting therapeutic doses of light to those locations is a genuine engineering challenge. Some researchers have explored transcranial delivery for neurodegenerative conditions and reported positive impacts in both animal and human studies, but the doses that reach deeper structures are tiny fractions of what is applied at the surface.15PubMed Central. Transcranial near-infrared light in treatment of neurodegenerative diseases The 2024 mouse study that applied light along the spine found effects in both dorsal (near-surface) and ventral (deeper) areas, suggesting that even small amounts of penetrating light may trigger cascading effects. But a mouse spinal cord is far thinner than a human one, and scaling those results up is not straightforward.
The Dose Puzzle
Photobiomodulation follows a pattern that complicates dosing: a biphasic dose response, sometimes called the Arndt-Schulz curve. Low doses of light tend to stimulate cells, but higher doses can actually inhibit them or cause damage.16PubMed Central. Biphasic dose response in low level light therapy In cell culture experiments, researchers have found that lower energy densities produce the highest mitochondrial activity and cell viability, while higher doses reduce both.17PubMed. Biphasic Dose/Response of Photobiomodulation Therapy on Culture of Human Fibroblasts A study on human stem cells found the same pattern, with a specific dose level producing a more than sixfold increase in the secretion of extracellular vesicles (small signaling packages that cells release), while doses above and below that sweet spot produced weaker effects.18Journal of Photochemistry and Photobiology B: Biology. Exploring the biphasic dose-response effects of photobiomodulation on the viability, migration, and extracellular vesicle secretion of human adipose mesenchymal stem cells
This matters for MS because it means “more light” is not better, and the therapeutic window may be narrow. The optimal wavelength, power density, pulse frequency, treatment duration, and treatment location could all vary depending on the target tissue and the specific symptom being addressed. Right now there is no consensus on any of these parameters for MS. Every research group uses slightly different protocols, making it difficult to compare results across studies or to give practical advice about what settings someone should use.
The Home Device Problem
If you search for red light therapy devices online, you will find hundreds of products making sweeping health claims. A pilot study that tested several consumer-grade LED photobiomodulation devices found significant problems with reliability. Two of the devices tested lost roughly half their power output within just three minutes of operation, meaning the dose a user thinks they are getting may be dramatically different from what is actually being delivered.19PubMed Central. Photobiomodulation LED Devices for Home Use: Design, Function and Potential Only one device in that study maintained stable output for its full operating cycle. Given that the biphasic dose response means both too little and too much light can be counterproductive, an unstable device does not just reduce effectiveness; it makes it essentially impossible to hit the right dose consistently.
Most consumer devices also operate at far lower power levels than those used in research settings. The penetration studies mentioned earlier required 10 to 15 watts to push even small percentages of near-infrared light through a few centimeters of tissue. Many home panels and handheld devices operate at a fraction of that power, which raises questions about whether they deliver a biologically meaningful dose to anything deeper than the skin surface. For someone with MS hoping to affect lesions in the brain or spinal cord, a low-powered home device applied to the scalp is unlikely to deliver the kind of energy that produced results in the animal studies.
What This Means If You Have MS
The current state of the science puts photobiomodulation for MS in a frustrating middle ground. The biological reasoning is sound. Animal experiments show real effects on inflammation, nerve cell protection, and clinical symptoms. The treatment appears safe in the studies conducted so far. But the human evidence is sparse, the trials that do exist are small and often lack proper controls, and the question of whether enough light can actually reach the relevant areas of the human nervous system remains genuinely unresolved.
If you are considering trying red or near-infrared light therapy alongside your existing MS treatment, the lack of reported adverse effects is at least somewhat reassuring, though the small number of people studied means rare side effects could easily have been missed. The more practical concern is cost: clinical-grade devices and professional treatment sessions are not cheap, and insurance will not cover an unproven therapy. For fatigue specifically, the trials suggest that any light exposure, including ordinary bright light, may help, possibly through circadian rhythm effects rather than anything specific to the near-infrared wavelengths that the photobiomodulation research focuses on.
The therapy should not replace disease-modifying treatments. MS drugs have been tested in large trials involving thousands of patients and have well-established track records for reducing relapses and slowing disability. Photobiomodulation has nothing comparable. Viewing it as a potential complementary approach, something to explore alongside conventional treatment rather than as a substitute, is the responsible framing. Researchers in the field are openly calling for standardized protocols and larger trials, which suggests that even those most enthusiastic about the approach recognize how far it still has to go before it can be recommended with confidence.
Why MS Research Lags Behind Other Photobiomodulation Targets
Light therapy research has moved faster in other areas, including wound healing, musculoskeletal pain, and even some other neurological conditions like traumatic brain injury. MS presents unique challenges that help explain the slower pace. The disease is heterogeneous: two people with MS can have entirely different patterns of lesions, different rates of progression, and different balances of inflammatory versus degenerative damage. Designing a light therapy protocol that works across that variability is much harder than targeting, say, a specific joint or a localized wound. The autoimmune component also adds complexity, since the treatment would ideally need to suppress harmful immune activity without interfering with the beneficial immune functions that protect against infection. And the deep, diffuse distribution of MS lesions makes the penetration challenge far more daunting than for conditions affecting superficial tissues.
Funding is another factor. Photobiomodulation devices are relatively inexpensive compared to pharmaceutical development, which is good for eventual patient access but bad for attracting the kind of investment that powers large clinical trials. Drug companies have little incentive to fund studies on a therapy they cannot patent, and public research funding for light-based interventions has historically been modest. The result is a field populated by small, underfunded studies that produce suggestive but inconclusive results, which in turn makes it harder to justify the larger studies that would settle the question. It is a cycle that keeps the evidence base frustratingly thin.