Multiple Sclerosis and Supplements: What Was Measured, and What About Immune-Modulating Drugs

Multiple sclerosis (MS) is an autoimmune disease of the central nervous system, and the medicinal mushrooms offered for it online are mainly reishi (Ganoderma lucidum, the lingzhi of Chinese medicine) and lion’s mane (Hericium erinaceus). The honest answer: none of the four mushrooms we grow has been tested in a single person with multiple sclerosis. With glatiramer (Copaxone), interferon beta (Betaseron), fingolimod (Gilenya), teriflunomide (Aubagio), dimethyl fumarate (Tecfidera), natalizumab (Tysabri) or ocrelizumab (Ocrevus) — we found not one combination that has been measured. And in healthy adults, purified beta-glucan from reishi raised immune markers — exactly the system your drugs restrain.

The kinds of evidence that do exist, from closest to a person to furthest away: human trials in people with MS — on the drugs, on fatigue drugs, and on vitamin D, omega-3 and biotin (which we do not sell); human trials with mushrooms — in entirely different populations: healthy adults, mild cognitive impairment, neurasthenia, and Gulf War illness, where high-dose reishi did worse than placebo; and below those — mice with a model of multiple sclerosis, and brain cells in a dish. On the combination “mushroom × MS patient” we found not a single measurement. This page is built around the questions you are asking: what is allowed with your drug, and what was measured on the brain fog and fatigue you live with.

Do medicinal mushrooms help with multiple sclerosis — and what exactly was tested?

In humans — nothing. Not one trial, case series or observational study in people with MS on any of the four mushrooms we grow. What was tested: reishi in mice in the EAE model, reishi and lion’s mane in mice given a toxin that damages myelin, and cordycepin — an isolated molecule from cordyceps — again in mice. None of them is a person; only isolated cordycepin was also tested after disease onset — in mice.

The meaning is sharper than it looks. Out of 13 autoimmune diseases we scanned, only one randomized trial tested one of our mushrooms — reishi, together with a Chinese herbal formula, in rheumatoid arthritis: 65 patients, 24 weeks, and it missed its primary endpoint (ACR20: 15% versus 9.1%). Multiple sclerosis is not among them: here there is not even a failed trial. We gathered the broader picture across all autoimmune diseases on the medicinal mushrooms and autoimmune disease page. Here we deal with the narrow intersection: MS, the drug you take, and the symptoms you live with.

And one sentence before anything else: MS drugs were tested in large trials against placebo and against other drugs, and their purpose is to reduce relapses and accumulated damage. Even in the trial that tested omega-3 in 92 patients, what lowered disease activity on MRI was the interferon everyone received later on — “as expected”, in the researchers’ words — not the supplement. Nothing on this page is a reason to change, delay or stop treatment.

What was measured, in which system — and what came out?

The table sorts the questions you ask by what was measured on them and in which organism. The mushroom rows on the disease itself — all mice or a dish. The drug rows — 0 studies with mushrooms. And the only rows that contain randomized trials in people with MS belong to supplements we do not sell, and none of the three showed an effect on the disease.

“Mushrooms boost the immune system” — and what does that mean when your drug restrains it?

This is the central question of the page, and we found nobody who has tested it. In healthy adults, purified beta-glucan from reishi raised CD3, CD4, CD8 and NK cells versus placebo; in cancer patients — a rise of 2.02% to 3.91%. MS drugs restrain, divert or deplete immune cells. What happens when the two directions meet in a person with MS — not measured. That is not evidence of danger, and it is not evidence of safety.

What the market claims. “Mushrooms don’t boost — they balance, so they are suitable for autoimmune diseases.” The sentence is reassuring, but there is no measurement under it. The 2023 randomized trial in healthy adults aged 18–55 tested purified beta-glucan from reishi — not the whole mushroom — ran for 84 days and found a rise in CD3, CD4, CD8, the CD4/CD8 ratio and NK cells — one direction; plus a difference in IgA whose direction the abstract does not state. And in the Cochrane review of cancer patients: CD3 rose by 3.91%, CD4 by 3.05% and CD8 by 2.02%, from studies whose quality was described as “generally not adequate”. Conceptually, too, “modulating, not boosting” is a mistake: in the literature, “immunostimulant” is a kind of “immunomodulator”, not its opposite. We wrote about the language itself in reishi and the immune system: modulating or boosting?

Why this is especially sensitive in MS. In most autoimmune diseases the drug restrains inflammation in a joint or in the skin. In MS it acts on the cells that cross into the brain and spinal cord: some drugs trap lymphocytes in the lymph nodes, some block their passage, some deplete B cells. A supplement that raises immune-cell counts in a healthy person is at the very least a question worth testing against such a drug. But a rise of a few percent in a healthy person is not a relapse, and says nothing about what happens when the drug is working in the background.

And the direction is not fixed. Cordyceps, for example, was tested in kidney-transplant recipients precisely alongside immunosuppressants and in place of azathioprine: a 2015 Cochrane review, 5 trials and 447 transplant recipients — 4 of them compared a cordyceps preparation in place of azathioprine, one alongside low-dose cyclosporine; risk of bias was unclear in all, and the authors described the evidence on the secondary outcomes measured as “limited, low-quality”. In other words, the same family of supplements was tested once as a “stimulant” and once as a “restrainer” — depending on the mushroom, the preparation and the population. That is exactly why the question cannot be answered in advance.

What can be known today. We searched explicitly for a report of an autoimmune flare after reishi, lion’s mane, cordyceps or turkey tail — and found none. What exists is a 2004 series of 3 patients who flared — pemphigus and dermatomyositis — in close proximity to echinacea and spirulina, other immune-stimulating supplements. And even the absence of mushroom reports is limited: supplements are not required to report adverse effects, and a neurologist whose patient has a relapse will usually not suspect a supplement. What to ask the neurologist. “My drug acts on immune cells — is there a reason to avoid something that was measured as raising them?”

Taking glatiramer (Copaxone), interferon beta (Betaseron), natalizumab (Tysabri) or ocrelizumab (Ocrevus) — can you add mushrooms?

Not measured — 0 studies for each of them. All four are proteins or peptides given by injection or infusion, so the usual route by which a supplement changes a drug’s level — the liver enzymes — is barely relevant to them. The open question is immune, not enzymatic; and with interferon beta there is a liver question too. A question for the neurologist, not a decision to make alone.

Copaxone and Betaseron. Glatiramer (Copaxone) and interferon beta (Betaseron) are the veteran injectable drugs of MS. A search for reishi with interferon and multiple sclerosis returns 0 results. But on interferon beta there is one data point that does matter to you: an analysis of the FDA adverse-event reporting system, published in 2019, mentions “the expected hepatotoxic potential of interferon beta”. More on that in the liver chapter.

A trap worth knowing: “lion’s mane lowers interferon”. A 2023 study that circulates in this context tested extracts of Hericium coralloides — a relative from the same genus, not lion’s mane — and of turkey tail, in a test tube, on blood cells from older adults. In the presence of a virus, the levels of interferon the cells themselves produced went down. That is interferon the body makes against a virus, not the interferon beta drug you inject; it is a dish, not a person; and it is not lion’s mane. Anyone who cites it as evidence about an MS drug has not read it.

Tysabri and Ocrevus. Natalizumab (Tysabri) and ocrelizumab (Ocrevus) are monoclonal antibodies. They are broken down like any protein in the body, so an interaction through liver enzymes is less expected — but “less expected” is not “tested”: we found not a single study. And the question that remains is the one from the previous chapter: a drug that changes the movement of immune cells or depletes them, versus a reishi beta-glucan that was measured as raising them. The wording we can stand behind: not tested — neither “safe to combine” nor “dangerous to combine”.

And with fingolimod (Gilenya), teriflunomide (Aubagio), dimethyl fumarate (Tecfidera) or cladribine (Mavenclad)?

0 studies with mushrooms for each. For Gilenya there is a relatively reassuring pharmacological fact: it is cleared mainly through the enzyme CYP4F2, and CYP3A inhibitors affected it weakly or not at all — while reishi, in rat liver, inhibited the only three enzymes that were tested, CYP3A, CYP1A2 and CYP2E1; CYP4F2 was not tested. With Aubagio and Gilenya the real question is the liver: both carry a liver signal in FDA reports.

Gilenya. The 2012 pharmacokinetics review of fingolimod — by Novartis researchers, the manufacturer — describes oral bioavailability of over 90%, a half-life of 6–9 days, and clearance mainly through CYP4F2, “an enzyme through which few drugs pass”. Ketoconazole, which also inhibits CYP4F2, raised the drug’s concentration “moderately”; CYP3A inhibitors and inducers — a negligible or weak effect. A 2011 study in human liver microsomes showed that antibodies against CYP3A4, CYP2D6 and CYP2E1 did not meaningfully inhibit the drug’s breakdown. And what exists on reishi: in 2007, a reishi polysaccharide inhibited, dose-dependently, CYP3A, CYP1A2 and CYP2E1 — in rat liver microsomes, and MSKCC writes that the clinical relevance “is not known”. Only those three enzymes were tested; CYP4F2, the enzyme that breaks down Gilenya, has never been tested against reishi. That is not “tested and found safe” — it is “no known axis, and nobody has measured”.

Aubagio, Tecfidera and Mavenclad. Teriflunomide (Aubagio), dimethyl fumarate (Tecfidera) and cladribine (Mavenclad) — 0 studies with mushrooms. On their liver enzymes we found no data that intersects with what was measured on the mushrooms, so we will not invent an axis. What we did find is liver-safety data on the drugs themselves — that is the next chapter. What to bring to the pharmacist: the name of the drug, the name of the supplement, and any other drug you take. The wider list of what has and has not been measured — on the drug interactions page.

My drug requires liver tests — what does that mean for supplements?

It means anything new needs to be known to your neurologist. In a 2019 analysis of FDA reports, Aubagio and Gilenya had a liver-injury signal (ROR 2.31 and 2.53), and interferon beta — “the expected potential”. Reishi has two liver-injury reports and a D rating in the LiverTox database. And in one woman with MS, a different herbal supplement alongside interferon was documented with an ALT of 681.

The drugs and the liver. The researchers analyzed liver-injury reports in the FDA adverse-event database. Teriflunomide and fingolimod had a reporting odds ratio (ROR) of 2.31 and 2.53 for overall liver injury — including symptom-free enzyme elevations; fampridine (Ampyra) had a signal for severe injury as well; and between 26% and 90% of reports, depending on the drug, also included another hepatotoxic drug. Their conclusion: liver injury “may be a common feature” of MS drugs. It is important to read this correctly: this is a reporting system, not an incidence rate. But it explains why your neurologist checks your liver enzymes.

The case that illustrates the problem. In 2012 a case was described of a 23-year-old woman who had taken a melilot (sweet clover) supplement for 3 years, with 10 mg of coumarin a day. 14 days after she started interferon beta-1b, AST rose to 235 and ALT to 681. When both were stopped — the enzymes returned to normal; when she later started interferon beta-1a without the supplement — AST rose to only 61. The authors wrote that the combination “possibly caused” the injury. It is a single case, and it is not a mushroom. But this is what the question “do my supplement and my drug talk to each other” looks like when someone actually measures it — in a blood test.

And the mushrooms and the liver. Reishi has two reports worth knowing: in 2023, a 47-year-old man developed acute hepatitis after reishi powder taken with alcohol, and recovered within two weeks; in 2007, two patients were described (one new case and one from 2004) in whom liver injury appeared a month or two after switching from boiled reishi to powder — both had also taken other drugs, and one of them died. The NIH LiverTox database rates reishi D — “a possible rare cause”; cordyceps and lion’s mane — E. Of lion’s mane it adds that it “has not undergone prospective safety trials”. Our extract contains 32% alcohol; a daily serving of about 1.4 ml provides about 0.35 g of ethanol — arithmetic on the spec, not a measurement. None of this is evidence that the combination with MS drugs is dangerous — it simply was not measured. But anyone who has liver enzymes checked every few months needs the doctor to know about anything new, so that a rise is not attributed to the wrong cause. We expanded on this on the medicinal mushrooms and the liver page.

“Reishi protects myelin” — what exactly was seen in mice?

Two models, both in mice. In the EAE model — an autoimmune disease induced in the mouse — reishi given in advance reduced severity, inflammation and demyelination. In the cuprizone model — a toxin that destroys the cells that make myelin — reishi and lion’s mane powder in the feed suppressed demyelination, but only reishi improved movement. None of them is a person, and in both, reishi was given before the disease or together with the toxin — not as treatment of an existing disease.

What the market claims. “Reishi calms inflammation in the brain”, “mushrooms protect the nerve sheath”. These sentences rest on real studies — which are worth reading to the end.

What exactly was measured. In 2026, in mice with EAE — the accepted model of multiple sclerosis — reishi given preventively and early, before the disease developed, reduced disease severity, inflammatory infiltration, demyelination and the activation of microglial cells in the spinal cord; in a dish, in microglial cells, it lowered inflammatory cytokines by inhibiting NF-κB and STAT3. The dose does not appear in the abstract. In 2022, mice ate feed with 5% fruiting-body powder together with cuprizone for 5 weeks: reishi and lion’s mane prevented weight loss and suppressed demyelination; in motor function, on a rotating wheel, reishi and two edible mushrooms improved — and lion’s mane did not. And in the same EAE model, cordycepin — an isolated molecule from cordyceps — lowered inflammatory cytokines and eased symptoms, also when given after disease onset (2022), and a cordyceps preparation lowered the severity score to 2.26 and 2.69 versus 3.29 in controls, in a pilot of 15 female mice, 5 in each group (2017).

Why it does not carry over automatically to a person. First, the timing: in the main reishi study the supplement was given before the disease, and none of you starts treatment before diagnosis. Second, the model: cuprizone is a toxin, not an autoimmune disease, and EAE is induced by injection in a young mouse — two models that teach a great deal and do not replace a patient. Third, the substance: 5% of the feed is an enormous dose relative to body weight, and isolated cordycepin is not an extract. And fourth — and this you will not find on the sales pages — none of the studies was done in mice that also receive an MS drug. What can be known today: that there is a biological reason to research this, and that there is no evidence at all that it happens in a person. What to ask the neurologist. Not “does reishi protect myelin” — he has no data on that — but “is there a reason, in my case, with my drug, to avoid any supplement”.

“Lion’s mane regenerates myelin” — what was measured, and what was not?

Measured in a dish and in rat pups. In 2003, a lion’s mane extract accelerated myelination in cultured rat cerebellar cells; in 2021, a mycelium extract and erinacine molecules raised myelin protein in cells, and in day-old rat pups that received it for 7 days. No study has tested myelin regeneration in a person, and in the mouse model of myelin destruction lion’s mane did not improve movement.

This is the claim that brings most readers here from English, so we will go through it slowly. What was measured. The first study, from Ukraine, grew rat cerebellar cells with lion’s mane extract: myelination began earlier and ran at a higher rate, without toxicity. The second study, from Taiwan, used a mycelium extract — not fruiting body — and the molecules erinacine A, C and S: they promoted maturation of oligodendrocytes and raised the protein MBP in cells and in brain slices; in rat pups that received the extract for 7 days from the day of birth, more such cells were found. Among the authors are researchers from Grape King Biotech, a supplement manufacturer, and the context they themselves propose is developmental disorders, not disease.

Why it does not carry over to MS. The brain of a day-old pup makes myelin at a pace it will never reach again; in an adult brain with MS, the problem is that repair fails in the face of an ongoing immune attack. Cells in a dish are not a brain with a blood-brain barrier. And the adult-mouse model we found — cuprizone — found that lion’s mane suppressed demyelination but did not improve movement. What can be known: that the claim “regenerates myelin” rests on a dish and on pups, and that whoever writes it on a product for people with MS is skipping three steps. And what was measured on lion’s mane in humans — cognition, in the next chapter. On its safety — in who shouldn’t take lion’s mane.

What was measured on brain fog, memory and concentration?

Not in people with MS. Lion’s mane was tested in 30 Japanese adults aged 50–80 with mild cognitive impairment: the cognitive score rose at weeks 8, 12 and 16 — and fell 4 weeks after stopping. In 2019, out of three tests one improved. In healthy young adults — one speed test after a single dose. That is an entirely different population, and a different mechanism of “fog”.

“Lion’s mane for memory” and “for focus” are among Google’s common completions, and “brain fog” is a search in its own right. In MS, the fog is part of the disease — so it is worth knowing what exactly was measured, and in whom. Mild cognitive impairment. In 2009, 30 participants aged 50–80 (15 versus 15) took 3 grams of lion’s mane powder a day for 16 weeks: the cognitive function score rose versus placebo at weeks 8, 12 and 16, and fell significantly 4 weeks after stopping; laboratory tests showed no adverse effect. 2019. 12 weeks, fruiting body: out of three tests — MMSE, Benton and S-PA — only the first improved. Healthy young adults. In 2023, 41 young adults: a single dose of 1.8 grams shortened the time on the Stroop test after 60 minutes; after 28 days, the drop in subjective stress was not significant (p=0.051). Safety. In the longest trial — 49 weeks, in people with mild Alzheimer’s disease, 3 capsules of 350 mg of mycelium a day — 4 participants dropped out because of abdominal discomfort, nausea and rash.

Why it does not carry over to MS. Mild cognitive impairment in older age and “fog” in MS look similar from the outside, but the cause is different: in MS, lesions, fatigue, depression and drugs are intertwined. Nobody has tested lion’s mane on any of them in people with MS. What can be known. That the most positive data point — an improvement that disappeared after stopping — is in people aged 50–80, with mild impairment, in 30 people. What was measured on brain fog in general we laid out on the lion’s mane and brain fog page. What to ask the neurologist. Fog that worsens can come from the disease, from fatigue, from mood or from a drug — and that is checked before any supplement.

What was measured on fatigue — and on “reishi for sleep”?

On fatigue in MS something surprising was measured: amantadine, modafinil and methylphenidate — three drugs doctors prescribe for it — did no better than placebo, which itself lowered the fatigue score from 51.3 to 40.6. Reishi was tested for fatigue only in neurasthenia: 28.3% versus 20.1% on placebo. And on reishi and sleep there is not a single randomized trial in humans.

“Multiple sclerosis chronic fatigue” is the completion Google offers, and rightly so: it is one of the hardest complaints in the disease. What was measured on fatigue in MS. A 2021 double-blind crossover trial in 141 patients: each participant received, in turn, amantadine, modafinil, methylphenidate and placebo, for up to 6 weeks each. The fatigue score (MFIS) stood at 51.3 at baseline; on placebo — 40.6; on amantadine — 41.3; modafinil — 39.0; methylphenidate — 38.6. The difference between the treatments was not significant (p=0.20), and side effects were reported in 39%–40% on the drugs versus 31% on placebo. That is the bar: even real drugs could not beat placebo on fatigue in MS.

What was measured on reishi. The large trial, from 2005: 132 patients with neurasthenia, 1,800 mg three times a day, 8 weeks. The sense of fatigue fell by 28.3% — and on placebo by 20.1%. The net difference is about 8 percentage points, in a condition that is neither autoimmune nor neurological. Whoever quotes “28% less fatigue” without the second number is telling you half. In people with MS — not measured.

And sleep. “Reishi for sleep” is Google’s most common completion for “reishi for…” — 6 of 15. And we found not a single randomized trial in humans that tested reishi and sleep; the dedicated search returns one record, and it is actually an exercise study in fibromyalgia. We laid this out on the reishi for sleep page. What to ask the doctor. Fatigue in MS can come from the disease, from disrupted sleep, from depression, from anemia or from a drug — each of them is checked differently. That is the place to start.

Can reishi actually make symptoms worse?

Measured, as far as we found, once — in a different population: in 29 men with Gulf War illness — a condition of chronic fatigue, pain and a neuro-inflammatory component — symptom severity on high-dose reishi was higher than on placebo (p=0.012); on the low dose — no change. That is not multiple sclerosis and not an autoimmune relapse. It is the only trial we found in which symptom severity was higher on reishi than on placebo.

What exactly was measured. A 2021 crossover trial: each participant went through 30 days of baseline, 30 days of placebo, 30 days of low dose and 30 days of high dose, for three plants — reishi, stinging nettle and epimedium. At the low dose reishi did not differ from placebo (p=0.603); at the high dose symptom severity was higher than on placebo. The trial was pseudo-randomized. The authors wrote that “reishi may increase symptoms in some sufferers”, and alongside that — “small sample, preliminary results”. High-dose nettle, for comparison, lowered symptoms (p=0.048).

Why it is relevant, and why it is not. Gulf War illness is not MS and is not a demyelinating disease. What is shared is the experience — persistent fatigue, pain, and a neuro-inflammatory component — in other words, a human population with overlapping symptoms to a person with MS, in which reishi was measured against placebo over time. What it teaches: “natural” is not one direction, and the dose matters. The same finding stands at the center of the lupus page, a different autoimmune disease in which fatigue is the main complaint. What can be known: anyone who starts a supplement and feels a worsening — fatigue, weakness, new symptoms — stops, writes it down, and tells the neurologist. That data point of yours is worth more than any average.

Vitamin D, omega-3, biotin — what was actually measured as “natural treatment” for MS, which we do not sell?

All three were tested in randomized trials in people with MS — and all were negative on the disease. Vitamin D: 12 trials and 933 patients, with no effect on relapses, disability or MRI lesions. Omega-3: 92 patients, with no difference on MRI or relapses. High-dose biotin: 642 patients, 12% versus 9% — not significant. We do not sell any of them.

“Multiple sclerosis vitamin d” is Google’s only completion that connects the disease to a supplement, so it is worth knowing what was actually tested. Vitamin D. A 2018 Cochrane review: 12 randomized trials, 933 patients. Vitamin D3 had no effect on the annual relapse rate, on the EDSS disability score or on active MRI lesions, with “very low” quality of evidence. On fatigue — one trial in 158 patients found less fatigue after 26 weeks, and another in 71 patients found no effect after 96 weeks; the conclusion: “unclear”. At the doses tested it appears safe. Omega-3. The Norwegian OFAMS trial, 92 patients: 1,350 mg EPA and 850 mg DHA a day versus placebo; after 6 months everyone also received interferon beta for 18 months. MRI lesions, relapses, disability progression (70% free of progression in both groups), fatigue and quality of life — no difference. Biotin. The SPI2 trial, 642 patients with progressive MS, 100 mg three times a day: improvement in 12% versus 9% on placebo — not significant. And a worrying bonus: the high dose interfered with laboratory tests based on biotin-labeled antibodies. A supplement, in other words, can do harm without touching the disease at all — through the blood test your doctor reads.

Why this chapter is here: because this is what evidence on “natural treatment” in MS looks like when it is measured — randomized trials, hundreds of patients, and a negative answer. Mushrooms do not even have that. And the choice of such a supplement, if at all, belongs with the neurologist.

What we actually measure in our bottle

After a page that says “not measured” in almost every row, you deserve to know what was measured — and about what exactly. We grow the mushrooms ourselves, on a farm in the Galilee: fresh fruiting body, not mycelium grown on grain and not imported powder whose history cannot be known. The mushroom goes from harvest straight to extraction, with no drying step in between; as far as we know, we are among the few in the world who work this way. The extraction is triple, and its alcohol stage runs for 7 weeks. The extraction ratio of the reishi is 1:3, and of the lion’s mane 1:2, on a fresh-mushroom basis. Alcohol in the finished extract: 32% — the figure we wrote about in the liver chapter, and one worth bringing to the neurologist together with your list of drugs.

And the numbers are not ours to set. We sent the finished extracts for testing at TÜV Austria, and what came back is the beta-glucan percentage on a dry-matter basis — and alongside it alpha-glucan, meaning starch, which was not detected in any of them. Alpha-glucan not detected is the chemical proof that there is no grain in the bottle. To understand why that matters, it helps to know the market’s three-step ladder: mycelium grown on grain, where beta-glucan is usually below 7% and most of the weight is starch; imported dried fruiting body, whose quality depends on who dried it and when; and fresh fruiting body from the farm, which is what we do. And on a page that has dealt so much with beta-glucan and immune cells, it should also be said: this number describes what is in the bottle, not what it does in the body. Why beta-glucan and not “total polysaccharides” — we explained separately.

All our tests are public, and anyone who wants to read the report themselves will find our explanation of how to read a COA. Kosher certification — Mateh Yehuda Rabbinate, Rabbi Gad Atias. That is what we know how to measure and prove about what is in the bottle. What it will do for multiple sclerosis was not measured — so it is not written.

What this page does not say — and what we do not claim

We do not claim that reishi, lion’s mane, cordyceps or turkey tail improve multiple sclerosis, protect myelin, regenerate it, reduce relapses, ease brain fog or fatigue, or “balance the immune system” — all the evidence on the disease itself comes from mice and cells, and the cognition and fatigue data come from other populations. We do not claim the opposite either — that the mushrooms worsen MS: no such report was found, and the Gulf War illness trial is a different population. We do not claim that combining them with Copaxone, Betaseron, Gilenya, Aubagio, Tecfidera, Mavenclad, Tysabri or Ocrevus is safe — it was not measured; nor that it is dangerous — that was not measured either. We do not claim that vitamin D, omega-3 or biotin help — the trials on them were negative, and we do not sell them. And we do not deal here with disability benefits, disability ratings or entitlements — we have no expertise in those and no sources on them. What we do say: multiple sclerosis is managed by a neurologist, and its drugs were tested to reduce relapses and accumulated damage. Do not stop, delay or change them on your own, and anyone adding any supplement — including ours — tells the doctor before, not after. Under DSHEA, a dietary supplement may not claim to diagnose, treat, cure or prevent any disease. We sell mushroom extracts, and we are telling you explicitly not to buy them for multiple sclerosis.

The bottom line

On our four mushrooms and multiple sclerosis we found not a single study in humans — only mice that received reishi before they fell ill, mice that received a toxin, and cells in a dish. With Copaxone, Betaseron, Gilenya, Aubagio, Tecfidera, Mavenclad, Tysabri and Ocrevus — we found not one combination that has been measured; what is known is that in healthy adults purified beta-glucan from reishi raised immune markers, that several MS drugs carry a liver signal, and that Gilenya is broken down by an enzyme on which there is no mushroom data at all. On fog and fatigue there are data — in other populations, with a placebo that did almost the same. And there is one trial, in a different syndrome, in which high-dose reishi did worse than placebo. If someone sells you a mushroom “for multiple sclerosis” or “for myelin regeneration” — send them this page, and talk to your neurologist.

Frequently asked questions

Does reishi help with multiple sclerosis?

It has never been tested in humans. In mice with the EAE model, reishi given before the disease reduced severity, inflammation and demyelination; in mice given a toxin that damages myelin, reishi powder in the feed suppressed demyelination and improved movement. These are mice, and preventive dosing — not treatment of an existing disease, and not alongside an MS drug.

Does lion’s mane regenerate myelin?

It was measured in rat cerebellar cells in a dish and in day-old rat pups given a mycelium extract for 7 days. In adult mice given a toxin that destroys myelin, lion’s mane suppressed demyelination but did not improve movement. In people with multiple sclerosis — not a single study. “Regenerates myelin” is a jump of three steps.

Can I take medicinal mushrooms with glatiramer (Copaxone) or interferon beta (Betaseron)?

The combination was not tested — 0 studies that we found. These are injected proteins and peptides, for which the liver-enzyme route is barely relevant, so the question is mainly immune: purified beta-glucan from reishi raised immune markers in healthy adults — that is the measurement, not “every mushroom”. With interferon beta there is a liver question too. A question for the neurologist, with the supplement’s name in hand.

And what about fingolimod (Gilenya)?

Not measured. Gilenya is broken down mainly by the enzyme CYP4F2, and CYP3A inhibitors affected it weakly or not at all. Reishi, in rat liver, inhibited the three enzymes that were tested — CYP3A, CYP1A2 and CYP2E1; CYP4F2 was not tested, so there is no known axis — and no measurement either. But Gilenya has a liver signal in FDA reports, so any new supplement should be known to your doctor.

Mushrooms “boost immunity” — is that dangerous in multiple sclerosis?

Unknown. In healthy adults, purified beta-glucan from reishi raised CD3, CD4, CD8 and NK cells versus placebo, and MS drugs act precisely on immune cells. No report of an MS relapse after mushrooms was found — but supplements are not required to report. “Not measured” is neither “safe” nor “dangerous”.

Can lion’s mane help with brain fog in MS?

In people with MS — not measured. In 30 adults aged 50–80 with mild cognitive impairment, 3 grams a day improved a cognitive score at weeks 8–16, and the improvement disappeared 4 weeks after stopping. In healthy young adults — one speed test. Fog in MS comes from other mechanisms, and is worth investigating with your neurologist before any supplement.

Will reishi help with fatigue or sleep with multiple sclerosis?

In people with MS — not measured. In neurasthenia, fatigue fell by 28.3% with reishi versus 20.1% with placebo. In MS, even three fatigue drugs did no better than placebo. On reishi and sleep we found not a single randomized trial in humans. And in Gulf War illness, symptom severity on high-dose reishi was higher than on placebo.

Does vitamin D help with multiple sclerosis?

According to a Cochrane review of 12 trials and 933 patients — not on the disease: no effect on relapses, the disability score or MRI lesions, with very low quality of evidence. On fatigue — two contradictory trials. Omega-3 and high-dose biotin were negative too. We sell none of them, and the choice belongs with the neurologist.

Scientific sources (peer-reviewed)

• Reishi in the mouse EAE model, early preventive dosing: less severity, inflammatory infiltration, demyelination and microglial activation; in vitro — IL-1β, TNF-α, IL-6, COX2 and iNOS fell through NF-κB/STAT3 — Zhang L, et al. Chinese Medicine, 2026. View on PubMed
• Cuprizone model, 5% fruiting-body powder in the feed, 5 weeks: reishi and lion’s mane suppressed demyelination; motor function improved with reishi — not with lion’s mane — Yamashina K, et al. International Journal of Medicinal Mushrooms, 2022. View on PubMed
• Cordycepin (an isolated molecule) in the EAE model: less IFN-γ, IL-6, TNF-α and IL-17, symptom relief; mouse and human dendritic cells in vitro — Song YC, et al. Biochemical Pharmacology, 2022. View on PubMed
• A cordyceps preparation in the EAE model, pilot in 15 female mice (5 per group), 30 days: severity score 2.26 and 2.69 versus 3.29 in controls; less Th1 and demyelination — Zhong SS, et al. Chinese Medical Journal, 2017. View on PubMed
• Lion’s mane extract in cultured rat cerebellar cells: earlier and faster myelination, without toxicity — in vitro — Kolotushkina EV, et al. Fiziolohichnyi Zhurnal, 2003. View on PubMed
• Lion’s mane mycelium extract and erinacines: oligodendrocyte maturation and a rise in MBP in cells, in brain slices and in rat pups (7 days). Authors from Grape King Biotech — Huang HT, et al. Scientific Reports, 2021. View on PubMed
• Hericium coralloides (not lion’s mane) and turkey tail in vitro, blood cells from older adults: cellular type I and type II interferon fell in the presence of a virus — Williams LM, et al. Nutrients, 2023. View on PubMed
• Purified beta-glucan from reishi (not the whole mushroom) in healthy adults aged 18–55, 84 days, double-blind: a rise in CD3, CD4, CD8, the CD4/CD8 ratio and NK; a difference in IgA, direction not stated — Chen SN, et al. Foods, 2023. View on PubMed
• Cochrane, reishi in cancer patients: CD3 +3.91%, CD4 +3.05%, CD8 +2.02%; quality “generally not adequate” — Jin X, et al. Cochrane Database of Systematic Reviews, 2016. View on PubMed
• Three patients — pemphigus and dermatomyositis — who flared in close proximity to echinacea and spirulina (not mushrooms) — Lee AN, Werth VP. Archives of Dermatology, 2004. View on PubMed
• Cochrane, cordyceps preparations in kidney-transplant recipients: 5 trials, 447 participants — 4 in place of azathioprine, 1 alongside low-dose cyclosporine; unclear risk of bias; evidence on secondary outcomes “limited, low-quality” — Hong T, et al. Cochrane Database of Systematic Reviews, 2015. View on PubMed
• The only randomized trial of one of our four mushrooms in an autoimmune disease: 65 rheumatoid arthritis patients, reishi + San Miao San, 24 weeks: ACR20 15% versus 9.1%, not significant; immune cells and cytokines unchanged — Li EK, et al. Arthritis and Rheumatism, 2007. View on PubMed
• Fingolimod (Gilenya): oral bioavailability over 90%, half-life 6–9 days, clearance mainly through CYP4F2; ketoconazole raised concentration moderately; CYP3A inhibitors — a weak or negligible effect. Novartis — David OJ, et al. Clinical Pharmacokinetics, 2012. View on PubMed
• Human liver microsomes: only CYP4F2 (and CYP4F3B) break down fingolimod; antibodies against CYP3A4, CYP2D6 and CYP2E1 — no meaningful inhibition. Novartis — Jin Y, et al. Drug Metabolism and Disposition, 2011. View on PubMed
• FDA reporting system: overall liver injury — teriflunomide ROR 2.31, fingolimod ROR 2.53; fampridine — severe injury as well; expected hepatotoxic potential for interferon beta; another hepatotoxic drug in 26%–90% of reports — Antonazzo IC, et al. Multiple Sclerosis, 2019. View on PubMed
• Case report: a 23-year-old woman, melilot supplement (10 mg coumarin a day) + interferon beta-1b: AST 235, ALT 681 after 14 days; normalization on stopping; AST only 61 on beta-1a without the supplement — Tamura S, et al. Journal of Clinical Pharmacy and Therapeutics, 2012. View on PubMed
• A reishi polysaccharide dose-dependently inhibited CYP2E1, CYP1A2 and CYP3A in rat liver microsomes — Wang X, et al. Biological & Pharmaceutical Bulletin, 2007. View on PubMed
• A 47-year-old man, acute hepatitis after reishi powder with alcohol; recovery within two weeks — Guedikian R, et al. Cureus, 2023. View on PubMed
• Two patients (one new case + one from 2004): liver injury 1–2 months after switching from boiled reishi to powder; both had also taken other drugs; one — fatal fulminant hepatitis — Wanmuang H, et al. Journal of the Medical Association of Thailand, 2007. View on PubMed
• 30 people aged 50–80 with mild cognitive impairment, 3 grams of lion’s mane a day, 16 weeks: cognitive score rose at weeks 8, 12, 16 and fell 4 weeks after stopping; laboratory — no adverse effect — Mori K, et al. Phytotherapy Research, 2009. View on PubMed
• Lion’s mane (fruiting body), 12 weeks: of MMSE, Benton and S-PA — only MMSE improved — Saitsu Y, et al. Biomedical Research (Tokyo), 2019. View on PubMed
• Pilot, 41 healthy young adults: 1.8 grams — faster Stroop at 60 minutes; after 28 days subjective stress p=0.051, not significant — Docherty S, et al. Nutrients, 2023. View on PubMed
• Mild Alzheimer’s disease, 49 weeks, 3 × 350 mg of lion’s mane mycelium a day: 4 dropouts for abdominal discomfort, nausea and rash — Li IC, et al. Frontiers in Aging Neuroscience, 2020. View on PubMed
• 132 patients with neurasthenia, 1,800 mg ×3 a day, 8 weeks: fatigue −28.3% versus −20.1% on placebo — Tang W, et al. Journal of Medicinal Food, 2005. View on PubMed
• Fatigue in MS, 141 patients, double-blind crossover: MFIS 51.3 at baseline → placebo 40.6, amantadine 41.3, modafinil 39.0, methylphenidate 38.6 (p=0.20); side effects 39%–40% versus 31% — Nourbakhsh B, et al. The Lancet Neurology, 2021. View on PubMed
• 29 men with Gulf War illness, pseudo-randomized crossover: low-dose reishi — like placebo (p=0.603); high dose — symptom severity higher than on placebo (p=0.012). “Small sample, preliminary” — Younger J, et al. International Journal of Environmental Research and Public Health, 2021. View on PubMed
• Cochrane, vitamin D in MS: 12 trials, 933 participants; no effect on relapses, EDSS or MRI lesions; fatigue — “unclear”; very low quality — Jagannath VA, et al. Cochrane Database of Systematic Reviews, 2018. View on PubMed
• OFAMS: 92 patients, 1,350 mg EPA + 850 mg DHA a day, and later interferon beta-1a as well: no difference on MRI, relapses, disability or fatigue — Torkildsen O, et al. Archives of Neurology, 2012. View on PubMed
• SPI2: biotin 100 mg ×3 a day, 642 patients with progressive MS: improvement 12% versus 9%, not significant; interference with biotin-based laboratory tests — Cree BAC, et al. The Lancet Neurology, 2020. View on PubMed

Read next

• Medicinal mushrooms and autoimmune disease — the full picture
• Lupus and supplements
• Reishi and the immune system: modulating or boosting?
• How mushrooms modulate the immune system
• Lion’s mane and brain fog
• Who shouldn’t take lion’s mane
• Who shouldn’t take reishi
• Medicinal mushrooms and the liver
• Drug interactions
• Do medicinal mushrooms have side effects?
• Fibromyalgia and supplements
• Reishi for sleep — what was measured and what was not
• The science of reishi
• Lab results — beta-glucan

This page is educational and does not constitute medical advice, diagnosis or a substitute for professional care. Medicinal mushroom extracts are dietary supplements, not drugs, and are not intended to treat multiple sclerosis or any other medical condition. Multiple sclerosis requires diagnosis and follow-up by a neurologist. Do not stop, delay, replace or change the dose of an MS drug, steroids or any other medication without your physician’s guidance. It describes what published trials and case reports recorded — and what was not recorded; it is not a prediction of what any individual will experience, and it is not a recommendation to start, stop or combine any supplement with any medication — those decisions belong with your physician, especially if you take regular medication, are pregnant or breastfeeding, have surgery planned, or have liver or kidney disease. *These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.*