Blood Thinners and Supplements: What Was Measured on Medicinal Mushrooms, Platelets and Warfarin (Coumadin)

If you take an anticoagulant — warfarin (Coumadin), apixaban (Eliquis) or rivaroxaban (Xarelto) — or an antiplatelet drug such as low-dose aspirin or clopidogrel (Plavix), and you are considering a medicinal mushroom such as reishi (Ganoderma lucidum, the lingzhi of Chinese medicine), cordyceps or lion’s mane (Hericium erinaceus), you are asking a question that has numbers attached to it. The honest answer: two human studies on reishi and platelets contradict each other — inhibition of up to 31.49% in one, zero change in the other — and no study has tested any of our four mushrooms alongside an anticoagulant or antiplatelet drug.

The kinds of evidence that do exist, from closest to a person to furthest away: two human studies on reishi and platelets, and a third, small study in patients with hemophilia; a case report of bleeding after a tooth extraction in a patient who took cordyceps every day, and a single report of gastrointestinal bleeding with cordyceps, an antidepressant and two antiplatelet drugs; test-tube studies on human platelets and studies in mice; and, on the drugs themselves — interaction reviews, the EULAR recommendations and two trials in antiphospholipid syndrome. This page arranges them around what you are actually asking. For the wider picture on autoimmune disease, see the medicinal mushrooms and autoimmune disease page.

Do medicinal mushrooms thin the blood — and what is allowed with anticoagulants?

Unknown, and that is the precise answer. Reishi inhibited platelet aggregation in humans in one uncontrolled study, and changed no clotting measure at all in another, controlled trial. No study has tested any of our four mushrooms alongside warfarin (Coumadin), apixaban (Eliquis), rivaroxaban (Xarelto), aspirin or clopidogrel (Plavix). So this is a question for your doctor or pharmacist — before you start, not after.

“Blood thinner” is a confusing phrase, because it mixes two different mechanisms. Anticoagulants — warfarin (Coumadin), apixaban (Eliquis), rivaroxaban (Xarelto) — act on the clotting proteins in the blood. Antiplatelet drugs — aspirin, clopidogrel (Plavix) — act on the platelets, the small cells that stick to one another and form the first plug. Everything that has been measured on medicinal mushrooms, in humans and in the test tube, concerns mainly the second side: the platelets. That is why the practical question differs depending on your drug, and why each chapter here deals with a different drug.

This page is not about “mushrooms to prevent blood clots” — that is a claim no human study has tested, and anyone taking an anticoagulant takes it for a reason. It is about what you are asking: what was measured, what was not, and what to bring to your doctor. We have laid out the same question from the blood pressure angle on the medicinal mushrooms and blood pressure page.

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

The table arranges the questions by what was measured and in which organism. The only rows with humans are reishi’s alone — and they do not agree with each other. The drug rows contain no mushrooms at all: they hold what is known about the drug, not a measurement of the combination. The lion’s mane and cordyceps rows are test tube, mice and case reports.

Does reishi inhibit platelets by 31% — or change nothing? The two studies side by side

Both are correct, because they measured different things in different people. In 1990: 33 patients with atherosclerotic disease, 3 grams a day for two weeks, ADP-induced aggregation inhibited by up to 31.49% — with no control group. In 2005: 40 healthy volunteers, 1.5 grams a day for 4 weeks, double-blind — zero difference from placebo across five measures. Neither included people taking an anticoagulant.

The 1990 study. Researchers in Wuhan first added a water extract of reishi to the platelets of 15 healthy volunteers in a dish, and saw dose-dependent inhibition in both phases of aggregation. Then 33 patients with atherosclerotic disease took 1 gram three times a day for two weeks. The maximum inhibition rate of aggregation was 31.49% at one ADP concentration and 17.7% at a higher concentration (both P<0.01), and the length of the thrombus formed outside the body fell from 30.05 to 20.4 mm. That is the number behind every warning online. But there is no control group in it — only before and after — and the authors themselves write that the mechanism and the active substance “have not yet been studied”.

The 2005 study. Anesthesiologists in Hong Kong tested whether reishi — popular among cancer patients — impairs clotting, as earlier test-tube studies had hinted. 20 healthy volunteers received 1.5 grams of reishi a day and 20 received placebo, for 4 weeks, without anyone knowing who got what. They were tested at baseline, after 4 weeks and after 8: routine clotting tests, fibrinogen, von Willebrand factor, a platelet function analyzer (PFA-100) and thromboelastography. No difference between the groups, and all values stayed within the normal range. Their conclusion: using reishi before surgery “is not expected to increase the risk of surgical bleeding in healthy patients”. And a third, small study from the same year as the first: 5 HIV-positive patients with hemophilia A took a reishi extract, and the aggregation tests before and after did not change.

Why they do not really contradict each other. Four differences: double the dose (3 grams versus 1.5); a sick population versus a healthy one; a measure focused on ADP-induced aggregation versus a broad battery of measures; and no control group versus placebo. What can be known today: that at a dose of 1.5 grams, in healthy people, no impairment of clotting was found — and that this says nothing about someone who is already taking a drug that inhibits clotting. What to ask your doctor: “Is there a reason for a supplement that inhibited platelets in one study to be checked in my blood work after I start it?”

“Reishi thins the blood like aspirin” — what exactly was measured in the test tube and in animals?

In the test tube — a lot: ganodermic acid S from reishi inhibited 50% of human platelet aggregation at just 2 micromolar, and a protease isolated from reishi protected mice from thrombosis at a far lower dose than aspirin. But these are isolated substances, in a dish or in a mouse, and none of them was tested in humans swallowing an extract.

What the market claims. “Reishi thins the blood naturally”, “good for the heart because it prevents clots”, and on the other side “never, under any circumstances, with blood thinners”. What exactly was measured. In 1999, in gel-filtered human platelets, ganodermic acid S — a triterpene from reishi — inhibited 50% of aggregation in response to a substance that mimics thromboxane, and more than 95% at a higher concentration. In 2000 the same group found that the compound boosts an inhibitory signal in platelets (cAMP) 1.8-fold, and that together with prostaglandin E1 — the body’s own platelet-inhibiting substance — the two “inhibited additively”; that was measured only in that pairing. In 2011, a protease isolated from reishi protected mice from thrombosis at just 60 micrograms per kg, where aspirin needed 10–20 mg per kg. And in 2019, in a screen of eight edible mushrooms in a dish — reishi and lion’s mane among them — all eight extracts inhibited ADP-induced aggregation, and four of them outperformed aspirin in that test; the reishi extract inhibited both the ADP pathway and the arachidonic-acid pathway, but was also cytotoxic to platelets and white blood cells in the dish. No extract changed PT or INR. A 2003 review notes that reishi triterpenes both induce aggregation and inhibit it, depending on the compound.

And the other mushrooms? In lion’s mane, in 2010, isolated hericenone B inhibited aggregation — but only aggregation induced by collagen, not by ADP, thrombin or adrenaline — in rabbit platelets and in human platelets in a dish; whereas a hot-water extract of the whole mushroom, in the 2019 screen, did inhibit ADP-induced aggregation — an isolated compound and a whole extract are not the same thing. In cordyceps, in 2022, two polysaccharides from fermented mycelium inhibited human platelets in a dish, and in mice reduced thrombosis “without increasing bleeding risk”; a 2013 Chinese review sums up that the direction of cordyceps research is antithrombotic. In turkey tail — not one relevant platelet study.

Why this does not transfer automatically to a person. An isolated substance at micromolar concentration in a dish is not what reaches the blood after swallowing an extract; fermented mycelium is not fruiting body; and a mouse given a purified compound is not a person taking warfarin. What can be known: that the biological direction is consistent — medicinal mushrooms touch platelets — so the question is not theoretical. What to ask: not “does reishi thin the blood” — but “does my drug act on platelets, and what else am I taking that touches them”.

Taking warfarin (Coumadin), apixaban (Eliquis) or rivaroxaban (Xarelto) — can you combine them with mushrooms?

Not measured — no study has tested any of our four mushrooms alongside warfarin, apixaban or rivaroxaban; on maitake there is one case report of INR elevation with warfarin. It is known that warfarin is highly sensitive to food and supplements: a systematic review found 78 herbs, foods and supplements reported to interact with it. It is known that with the newer anticoagulants, an additional drug acting on platelets raises bleeding risk. This is a question for the pharmacist, with the supplement’s name in hand.

Warfarin (Coumadin). A 2021 systematic review gathered 149 articles on 78 herbs, foods and supplements reported to interact with warfarin: 45 of them (57.7%) enhanced its effect, 23 (29.5%) weakened it, and 10 had little effect. 20 of them were reported with bleeding events — from purpura (small bleeds under the skin) and gum bleeding up to fatal intracranial bleeding. The list the authors highlight includes goji, chamomile tea, cranberry, green tea, ginkgo, ginger, St John’s wort and spinach — there is no mushroom on it. Another review, from 2017, of 9 randomized trials on herbs and warfarin found that St John’s wort and echinacea changed the drug’s levels, and ginseng, ginger, garlic and cranberry did not — and again, not one mushroom was tested. What does exist on a mushroom — a different mushroom: a 2010 case report of INR elevation in an older man who took a maitake extract alongside warfarin. Maitake is not one of our four mushrooms, and it is a single case with no abstract — but it shows that the question “mushroom and INR” is not theoretical. The only record linking Ganoderma to warfarin is a 2000 Italian review that lists Ganoderma japonicum — a name whose relation to Ganoderma lucidum is unsettled — among the plants that “potentiate the effect of warfarin”, with no study and no number; the authors’ conclusion is that they should not be used in patients on an anticoagulant or an antiplatelet drug. The same review notes that the doctor is “usually not informed” about what the patient is taking.

Apixaban and rivaroxaban. A 2023 review, in atrial-fibrillation patients, describes the direct oral anticoagulants as substrates of CYP3A4, CYP2C9 and P-gp. Bleeding or embolism reports attributed to an interaction were found for 43 of the 171 drugs examined, most of them with antiplatelet and anti-inflammatory drugs; combining with a drug that affects platelets was “always” reported to increase bleeding risk, while the findings on CYP3A4 modulators were “inconclusive”. Reishi inhibited CYP3A — in rat liver microsomes, not in humans. A 2021 review adds that the newer anticoagulants were initially considered free of food interactions, “but observations from the field proved otherwise”. Apixaban or rivaroxaban with any mushroom: 0 studies.

What to bring to the pharmacist: the name and dose of the drug, the name of the supplement, and how much of it you take. On warfarin — ask when to check INR after starting a new supplement. In any case: not “dangerous to combine” and not “safe to combine” — not measured. The wider list of what was measured and what was not is on the drug interactions page.

Low-dose aspirin or clopidogrel (Plavix) — why is the question sharper here?

Because here the mechanisms meet. Clopidogrel (Plavix) belongs to the family of drugs that block the ADP receptor on platelets, and the 1990 reishi study measured exactly the inhibition of ADP-induced aggregation. That is a mechanistic connection, not a measurement of the combination: reishi with clopidogrel or with aspirin — 0 studies.

A 2013 review describes clopidogrel as the second generation of the drugs that inhibit the P2Y12 receptor — the receptor through which ADP activates platelets — and as the drug with the broadest clinical experience in the family. Aspirin acts on the same platelets, through a different pathway. Ganodermic acid S inhibited the thromboxane pathway in a dish, and in 1990 reishi taken by mouth inhibited the ADP pathway. In other words, each of the two drugs has a “neighbor” in the reishi research. And in the 2023 anticoagulant review the rule is clear: when you add something that affects platelets to an anticoagulant, bleeding risk rises. That was measured on drugs — not on supplements. The one human report we found that sits exactly on this axis is not about reishi but about cordyceps: a patient taking aspirin and ticagrelor — a P2Y12 inhibitor from the same family as clopidogrel — together with sertraline and cordyceps, who had a gastrointestinal bleed (next chapter).

What can be known: that anyone taking two drugs — for example aspirin and clopidogrel together after a catheterization, or aspirin alongside warfarin — is already in a scenario where the doctor has weighed bleeding risk against clot risk. A supplement that inhibited platelets in one study is one more variable in that calculation. What to ask: “Am I taking more than one drug that affects platelets, and if so — is there room for anything else?”

Cordyceps, bleeding and antidepressants — what exactly was reported?

Two reports, not studies. In 2018 a case was described of prolonged bleeding after dental surgery in a patient who took cordyceps every day as a “tonic”. And in 2023, out of 1,816 adverse-event reports in Poland, one report linked cordyceps with sertraline to upper gastrointestinal bleeding. Neither involved an anticoagulant — but the second patient was also taking aspirin and ticagrelor, an antiplatelet drug from the clopidogrel family.

The 2018 case report was published in an oral medicine journal, as part of a review of six traditional Asian remedies common among older Vietnamese-American adults in the US — and it is also the case that Memorial Sloan Kettering Cancer Center cites on its cordyceps page. It is important to know what it is: one person, a traditional preparation, no clotting measurement beforehand. A signal that justifies telling your dentist — not evidence that cordyceps causes bleeding.

The second report comes from a retrospective review in Kraków: adaptogens were involved in 9% of the adverse events reported with antidepressants, and 30 reports were judged to have a probable causal link. Cordyceps with sertraline — upper gastrointestinal bleeding, once: a 58-year-old man who, according to the case table, was also taking aspirin and ticagrelor — an antiplatelet drug from the clopidogrel family. The authors attributed the bleed to additive antiplatelet effects: of the mushroom, of the SSRI and of the two drugs. It is the one human report we found in which a mushroom sits squarely on the antiplatelet axis — which is why it belongs to the previous chapter as much as to this one. In the same review, another plant (eleuthero) was reported with three different bleeds with three antidepressants — and there too, in all three cases, the patients were taking an antiplatelet drug or an anticoagulant. This is relevant to you because antidepressants themselves raise bleeding risk with anticoagulants: a 2023 meta-analysis of 98,070 patients found that an SSRI alongside an oral anticoagulant raises the risk of major bleeding (HR 1.35), and with a direct anticoagulant — HR 1.47. Three layers — anticoagulant, antidepressant and supplement — are exactly where the pharmacist needs to see the whole list. We have also written about this report on the fibromyalgia page, and on the cordyceps safety page.

Bruising, bleeding gums and dental work — what do you do with the supplement before a procedure?

You tell them about it. The controlled reishi trial found that at 1.5 grams, in healthy people, use before surgery “is not expected to increase bleeding risk” — but someone taking an anticoagulant is not a “healthy person” in that sense. The accepted practice: report every supplement to your dentist, surgeon and anesthesiologist, and let them decide.

Mild bruising and bleeding gums are what many people on anticoagulants live with day to day, and in the 2021 warfarin review, purpura and gum bleeding are exactly the kinds of mild bleeding reported with herbs and supplements — alongside severe events. We found no study that measured bruising or gum bleeding in anyone who took a mushroom. What exists is one case of prolonged bleeding after an extraction with cordyceps, and one study in which reishi inhibited platelets. That is enough for the question to be asked, and not enough to answer it.

What you can do: if new bruises appear, nosebleeds or gum bleeding that was not there before, or black stools — that is data you are measuring on yourself, and it is worth more than all the literature: go to your doctor, and mention the supplement. And before dental work or surgery — the decision whether to pause the anticoagulant belongs to the doctor, and the decision whether to pause the supplement should be part of the same conversation.

Antiphospholipid syndrome (APS) — why warfarin, and why every supplement is measured by INR?

In antiphospholipid syndrome, autoantibodies raise the tendency to form clots, and the 2019 EULAR recommendations set long-term warfarin with a target INR of 2–3 after venous thrombosis. Medicinal mushrooms in this syndrome: 0 studies. What is known is that the choice of drug itself is especially sensitive here.

The European recommendations distinguish between situations: after a first venous thrombosis — long-term warfarin, INR 2–3; after arterial thrombosis — INR 2–3 or 3–4 depending on individual risk; low-dose aspirin for some carriers with no previous event, including some lupus patients; and the sharp sentence: “rivaroxaban should not be used” in patients positive for all three antibody types. The reason is the 2018 TRAPS trial: 120 high-risk patients were assigned to rivaroxaban or to warfarin, and the trial was stopped early — 19% events in the rivaroxaban arm versus 3% on warfarin, and 7 embolic events (stroke and heart attack) versus zero. At two-year follow-up, 2 of the 6 who stayed on a direct anticoagulant had an event, versus 6 of 109 on warfarin.

Why does this matter for the supplement question? Because an APS patient lives with a drug that is especially sensitive to food and other drugs, and with regular INR testing, and the disease itself shows that a small change in the drug can change the outcome. A new supplement is a variable that enters that measurement — so you mention it beforehand, and check INR afterwards, in coordination with the clinic. Antiphospholipid syndrome is common alongside lupus, and what was measured there is gathered on the lupus and supplements page.

ITP — low platelets: is the question reversed?

Yes, and it has been studied just as little. In ITP the immune system destroys platelets, and the problem is bleeding rather than clotting — so a supplement that inhibited platelets in one study is a relevant question here too, from the opposite direction. Reishi, cordyceps, lion’s mane or turkey tail in ITP: 0 studies. Nor did we find a study that tested whether any of them changes the platelet count.

ITP occurs in 2 to 4 of every 100,000 adults, according to a 2017 review in Blood, with bleeding symptoms that vary from person to person. In the I-WISh survey described in the fatigue chapter, 97% of patients reported having received treatment, most often steroids. “Low platelets diet” is one of Google’s autocompletes — but on our four mushrooms and platelet count we found not even a mouse study. What to ask: your hematologist — whether, at your current platelet count, there is room for any supplement that has touched platelets in research, and when to check a count after you start.

Mushrooms stimulate the immune system — what does that mean in APS and ITP?

Unknown. APS and ITP are autoimmune diseases, and in healthy people beta-glucan from reishi raised CD3, CD4 and CD8 cells and NK cells versus placebo over 84 days. In cancer patients, a Cochrane meta-analysis found a 3.91% rise in CD3. That is measurable stimulation. What it does to antiphospholipid antibodies or to platelet destruction — no one has measured.

The question is legitimate, and it must not be turned into either an alarm or a reassurance. In 2023, in a double-blind trial in Taiwan, healthy adults aged 18–55 received beta-glucan from reishi for 84 days, and their immune-cell measures rose — with no change in liver or kidney function. The 2016 Cochrane review found rises of 3.91%, 3.05% and 2.02% in CD3, CD4 and CD8 in cancer patients. That is the direction that was measured: a rise, not “balance”. We expanded on this on the reishi and the immune system page.

On the other hand, in our search we did not find a single report of an autoimmune flare after any of the four mushrooms. There is a 2004 series of three patients in whom pemphigus and dermatomyositis flared close in time to echinacea and spirulina — other immune-stimulating supplements, not mushrooms. And the absence of reports is not proof of safety either: adverse-event reporting for supplements is far sparser than for drugs. “Not tested” is neither “safe” nor “dangerous”. It is a data void.

What happened when reishi was tested in a population with chronic fatigue?

At the high dose, symptom severity was higher than on placebo (p=0.012); at the low dose — no change (p=0.603). That was in 2021, in a placebo-controlled crossover trial in 29 men with Gulf War Illness. This is not APS, not ITP and not an “autoimmune flare” — but it is one of the few controlled trials of reishi on symptoms in a fatigued population.

Gulf War Illness is a multi-system condition of chronic fatigue, pain and a neuro-inflammatory component in soldiers who served in that war. It has nothing to do with clotting. We bring it because it is one of the few controlled trials of reishi on symptoms; the only controlled trial we found in autoimmune patients — 65 rheumatoid arthritis patients, 2007 — gave reishi together with a Chinese herbal formula, and found no significant difference on the primary response measure. The design: 30 days of baseline, 30 days of placebo, 30 days of low dose and 30 days of high dose. The authors: “reishi may exaggerate symptoms in some GWI sufferers”; and in the same breath, the results are “from a small sample and are preliminary”. What this means for you: the sentence “at worst it just won’t help” does not hold up against the data. If you started a supplement and felt worse — stop, and tell your doctor.

Fatigue and sleep with anticoagulants or ITP — what was measured on reishi?

On sleep — nothing: there is not a single randomized trial in humans on reishi and sleep. On fatigue — one trial in neurasthenia: a 28.3% drop in the feeling of fatigue versus 20.1% on placebo, and 51.6% versus 24.6% “more than minimally improved” — and it is a different population. In a survey of ITP patients, 48% of patients reported that fatigue is common and problematic.

The fatigue is real and measured. In the 2026 I-WISh 2.0 survey — 1,018 ITP patients and 431 physicians in 15 countries, with the participation of a representative of the Israeli ITP association, and some of the authors from Novartis — 48% of patients, versus only 29% of physicians, reported that fatigue is common and problematic. In other words, physicians underestimate it. What was measured on reishi: in 2005, 132 neurasthenia patients received a reishi polysaccharide extract for 8 weeks; the feeling of fatigue fell by 28.3% — and on placebo by 20.1%; on the “more than minimally improved” measure — 51.6% versus 24.6%. The difference in the feeling of fatigue is about 8 percentage points, in a population without a blood disorder.

And sleep? “Reishi for sleep” is the most common search about reishi in Israel, and there is not a single randomized human trial behind it. A dedicated search returned one result — an exercise study in fibromyalgia. And insomnia actually appears as a side effect in the Cochrane review. Everything that was and was not tested is gathered on the reishi for sleep page.

What we actually measure in our bottle

After a whole page of “not measured”, 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 — like the preparation tested in mice in the chapter on test-tube studies — 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. Extraction ratios on a fresh-mushroom basis: reishi 1:3, cordyceps 1:2.5 and lion’s mane 1:2. Alcohol in the finished extract: 32% — and anyone taking warfarin should bring that figure to the pharmacist, together with the supplement’s name.

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 about clotting, this should also be said: we have not measured what a serving of our extract does to platelets or to INR, and no one has — so we will not write “has no effect”. 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 your clotting, your platelets or your INR 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, cordyceps, lion’s mane or turkey tail thin the blood, prevent clots or can replace an anticoagulant or an antiplatelet drug — at any dose and in any form. We do not claim they are dangerous alongside warfarin (Coumadin), apixaban (Eliquis), rivaroxaban (Xarelto), aspirin or clopidogrel (Plavix) — that was not measured; and we do not claim they are safe alongside them — that was not measured either. The study that found platelet inhibition was uncontrolled, and the controlled study was done in healthy people; neither one is the answer on its own. We do not claim that mushrooms affect antiphospholipid syndrome or ITP, in either direction — not tested. We do not claim that reishi improves sleep or fatigue in people on anticoagulants — on sleep there is no trial at all, and the fatigue trial was done in a different population. And we do not deal here with disability rights, social security benefits, pregnancy or diet with vitamin K — we have no sources on those. What we do say: an anticoagulant is prescribed and monitored by a doctor or an anticoagulation clinic; anyone taking one talks to the doctor or pharmacist before any supplement, including ours. 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 clotting.

The bottom line

On reishi and platelets there are two human studies, and they do not agree: inhibition of up to 31.49% in 33 patients with no control group, and zero change across five clotting measures in 40 healthy people in a double-blind trial. In the test tube and in mice the direction is consistent — medicinal mushrooms touch platelets — and on cordyceps there are two isolated bleeding reports — one of them in a patient who was also taking aspirin and ticagrelor. What does not exist: a single study of any of our four mushrooms alongside warfarin, apixaban, rivaroxaban, aspirin or clopidogrel, and any study of them in antiphospholipid syndrome or in ITP. The most sensitive axis is the antiplatelet drugs, because that is where the mechanisms meet. So: not “dangerous”, not “safe” — a question for the doctor and the pharmacist, with the supplement’s name, before you start, and a blood test afterwards. And if someone sells you a mushroom “for thinning the blood” — send them this page.

Frequently asked questions

Does reishi thin the blood?

It is not clear. In a 1990 study, 33 patients who took 3 grams of reishi a day for two weeks showed platelet aggregation inhibited by up to 31.49% — with no control group. In a 2005 double-blind trial, 40 healthy people who took 1.5 grams a day for 4 weeks showed no change at all across five clotting measures. Neither study included people taking anticoagulants.

Can I take medicinal mushrooms with warfarin (Coumadin)?

Not tested — there is not a single study of any of our four mushrooms alongside warfarin; on maitake, a different mushroom, there is one case report of INR elevation. Warfarin is highly sensitive to supplements: a systematic review found 78 herbs, foods and supplements reported to interact with it, 57.7% of them in the direction of enhancing its effect. This is a question for your doctor or anticoagulation clinic, including when to check INR after you start.

And what about apixaban (Eliquis) or rivaroxaban (Xarelto)?

Here too, 0 studies. The direct anticoagulants pass through CYP3A4 and P-gp, and reishi inhibited CYP3A only in rat liver microsomes. What was measured on the drugs: adding a drug that affects platelets raises bleeding risk. So — a question for the pharmacist, with the supplement’s name and dose.

I’m on clopidogrel (Plavix) or aspirin — is there a problem with reishi?

Not measured, but this is the most sensitive axis. Clopidogrel blocks the ADP receptor on platelets, and the 1990 reishi study measured inhibition of ADP-induced aggregation. That is a mechanistic connection, not a measurement of the combination. Anyone taking an antiplatelet drug — and especially two together — talks to their cardiologist before any supplement.

Should I stop medicinal mushrooms before dental work or surgery?

The decision belongs to the surgeon and the dentist, so tell them about the supplement. The controlled reishi trial found that use before surgery “is not expected to increase bleeding risk” in healthy people; on the other hand, there is one case report of prolonged bleeding after dental surgery in a patient who took cordyceps every day.

I have antiphospholipid syndrome — what about supplements?

Medicinal mushrooms have not been tested in this syndrome at all. The European recommendations set long-term warfarin with a target INR of 2–3 after venous thrombosis, and in the TRAPS trial rivaroxaban led to 19% events versus 3% on warfarin. Every new supplement is a variable measured by INR, so you coordinate it with your anticoagulation clinic.

I have ITP — do mushrooms raise or lower platelets?

Unknown: 0 studies on medicinal mushrooms in ITP, and no study has tested whether a mushroom changes the platelet count. What is known is that reishi inhibited platelet function in one uncontrolled study, and that mushrooms raise immune markers in healthy volunteers. This is a question for your hematologist, together with the question of when to check a count.

Does cordyceps cause bleeding?

Not proven. There are two isolated reports: prolonged bleeding after dental surgery in a patient who took cordyceps as a daily “tonic”, and a report of upper gastrointestinal bleeding with cordyceps combined with sertraline — in a patient who was also taking aspirin and ticagrelor, an antiplatelet drug. In the test tube, polysaccharides from cordyceps mycelium inhibited human platelets. Reports are not measurement — but they are a reason to tell your doctor.

Scientific sources (peer-reviewed)

• Reishi in the test tube inhibited platelet aggregation from 15 healthy volunteers; 33 patients with atherosclerotic disease who took 1 gram ×3 a day for two weeks — maximum inhibition of ADP-induced aggregation 31.49% and 17.7%, and ex vivo thrombus length fell from 30.05 to 20.4 mm; no control group — Tao J, Feng KY. Journal of Tongji Medical University, 1990. View on PubMed
• Randomized double-blind trial: 40 healthy volunteers, reishi 1.5 grams a day or placebo for 4 weeks — no difference in clotting tests, fibrinogen, von Willebrand factor, PFA-100 or thromboelastography; use before surgery “is not expected to increase bleeding risk” in healthy people — Kwok Y, et al. Anesthesia and Analgesia, 2005. View on PubMed
• 5 HIV-positive patients with hemophilia A who took a crude reishi extract — platelet aggregation tests with no significant change — Gau JP, et al. The American Journal of Chinese Medicine, 1990. View on PubMed
• Ganodermic acid S in human platelets in a dish: 50% inhibition of aggregation at 2 micromolar, more than 95% at 7.5 micromolar — Su CY, et al. Biochemical Pharmacology, 1999. View on PubMed
• Ganodermic acid S boosted the PGE1-induced cAMP rise in human platelets 1.8-fold, and together with it additively inhibited the platelet response — Su C, Shiao M, Wang C. Thrombosis Research, 2000. View on PubMed
• Review: reishi triterpenoids both induce platelet aggregation and inhibit it — Shiao MS. Chemical Record, 2003. View on PubMed
• A protease isolated from reishi: IC50 of 2.4 mg/ml for ADP-induced aggregation; in mice it protected against thrombosis at 60 micrograms/kg versus aspirin at 10–20 mg/kg — Kumaran S, et al. Medical Mycology Journal, 2011. View on PubMed
• Eight edible mushrooms in the test tube, reishi and lion’s mane among them: all eight inhibited ADP-induced aggregation, four more than aspirin; the reishi extract inhibited both ADP and arachidonic acid but was cytotoxic to platelets and white blood cells; none changed PT or INR — Poniedziałek B, et al. Nutrients, 2019. View on PubMed
• Lion’s mane: hericenone B selectively inhibited collagen-induced aggregation in rabbit and human platelets — not aggregation induced by ADP, thrombin or adrenaline — Mori K, et al. Phytomedicine, 2010. View on PubMed
• Two polysaccharides from fermented cordyceps mycelium inhibited human platelet activation in the test tube; in mice they reduced thrombosis without increasing bleeding risk — Mao YH, et al. International Journal of Molecular Sciences, 2022. View on PubMed
• Chinese review: cordyceps studies on blood viscosity, platelet aggregation and anticoagulant activity — Li XG, Xiao JH. Zhongguo Zhong Yao Za Zhi, 2013. View on PubMed
• Case report: prolonged bleeding after dental surgery in a patient who took cordyceps daily as a tonic, and a review of six traditional Asian remedies — Hatton MN, et al. Oral Surgery, Oral Medicine, Oral Pathology and Oral Radiology, 2018. View on PubMed
• 1,816 adverse-event reports: adaptogens in 9% of events with antidepressants; cordyceps with sertraline — upper gastrointestinal bleeding in a 58-year-old man also taking aspirin and ticagrelor; the authors — additive antiplatelet effects — Siwek M, et al. Frontiers in Pharmacology, 2023. View on PubMed
• Meta-analysis, 98,070 patients: an SSRI alongside an oral anticoagulant — HR 1.35 for major bleeding; with a direct anticoagulant — HR 1.47 — Rahman AA, et al. Thrombosis and Haemostasis, 2023. View on PubMed
• Systematic review: 149 articles, 78 herbs, foods and supplements interacting with warfarin — 57.7% enhanced, 29.5% weakened; 20 reported with bleeding events — Tan CSS, Lee SWH. British Journal of Clinical Pharmacology, 2021. View on PubMed
• Systematic review of 9 randomized trials on herbs and warfarin: St John’s wort and echinacea changed pharmacokinetic parameters; ginseng, ginger, garlic and cranberry did not — Choi S, et al. PLoS One, 2017. View on PubMed
• Italian review: Ganoderma japonicum (its relation to G. lucidum is unsettled) on the list of plants that “potentiate the effect of warfarin” — with no study or number; the authors’ conclusion: they should not be used in patients on an anticoagulant or antiplatelet drug — Argento A, et al. Annali Italiani di Medicina Interna, 2000. View on PubMed
• Case report: INR elevation in an older man who took a maitake extract alongside warfarin — a mushroom we do not grow; a letter with no abstract — Hanselin MR, et al. The Annals of Pharmacotherapy, 2010. View on PubMed
• Warfarin is “associated with extensive food and drug interactions”; with the newer anticoagulants few were reported — “it is still early” — Nutescu E, et al. Journal of Thrombosis and Thrombolysis, 2011. View on PubMed
• Direct oral anticoagulants and food and supplement interactions: “observations from the field proved otherwise” — Grześk G, et al. International Journal of Molecular Sciences, 2021. View on PubMed
• Direct oral anticoagulants — substrates of P-gp, CYP3A4 and CYP2C9; bleeding or embolism reports for 43 of 171 drugs; drugs that affect platelets always increase bleeding risk — Stöllberger C, et al. Expert Review of Clinical Pharmacology, 2023. View on PubMed
• Reishi polysaccharide inhibited CYP2E1, CYP1A2 and CYP3A in rat liver microsomes — Wang X, et al. Biological & Pharmaceutical Bulletin, 2007. View on PubMed
• P2Y12 ADP-receptor inhibitors: clopidogrel — the second generation, with the broadest clinical experience — Secco GG, et al. Cardiovascular & Hematological Agents in Medicinal Chemistry, 2013. View on PubMed
• EULAR recommendations for antiphospholipid syndrome: long-term warfarin, INR 2–3 after venous thrombosis; rivaroxaban should not be used in triple-positive patients — Tektonidou MG, et al. Annals of the Rheumatic Diseases, 2019. View on PubMed
• TRAPS trial: 120 high-risk APS patients — 19% events on rivaroxaban versus 3% on warfarin; stopped early — Pengo V, et al. Blood, 2018. View on PubMed
• Two-year follow-up after TRAPS: events in 2 of the 6 who stayed on a direct anticoagulant versus 6 of 109 on warfarin — Pengo V, et al. Journal of Thrombosis and Haemostasis, 2021. View on PubMed
• ITP occurs in 2 to 4 per 100,000 adults, with variable bleeding symptoms — Lambert MP, Gernsheimer TB. Blood, 2017. View on PubMed
• I-WISh 2.0 survey: 1,018 ITP patients and 431 physicians — 48% of patients versus 29% of physicians reported that fatigue is common and problematic — Cooper N, et al. American Journal of Hematology, 2026. View on PubMed
• Beta-glucan from reishi for 84 days in healthy adults: rise in CD3, CD4, CD8 and NK cells versus placebo — Chen SN, et al. Foods, 2023. View on PubMed
• Cochrane: reishi in cancer patients — CD3 +3.91%, CD4 +3.05%, CD8 +2.02%; minor side effects, including insomnia — Jin X, et al. Cochrane Database of Systematic Reviews, 2016. View on PubMed
• Three patients in whom autoimmune disease flared close in time to echinacea and spirulina — not mushrooms — Lee AN, Werth VP. Archives of Dermatology, 2004. View on PubMed
• 29 men with Gulf War Illness: low-dose reishi with no change (p=0.603), high dose with higher symptom severity (p=0.012) — Younger J, et al. International Journal of Environmental Research and Public Health, 2021. View on PubMed
• 132 neurasthenia patients, 8 weeks: fatigue fell 28.3% on reishi versus 20.1% on placebo; “more than minimally improved” 51.6% versus 24.6% — Tang W, et al. Journal of Medicinal Food, 2005. View on PubMed
• Randomized double-blind trial, 65 rheumatoid arthritis patients, 24 weeks: reishi together with a Chinese herbal formula versus placebo — no significant difference on the primary response measure; the only controlled trial we found of reishi in autoimmune patients — Li EK, et al. Arthritis and Rheumatism, 2007. View on PubMed

Read next

• Medicinal mushrooms and autoimmune disease — the full picture
• Lupus and supplements
• Who shouldn’t take reishi
• Who shouldn’t take cordyceps
• Drug interactions
• Do medicinal mushrooms have side effects?
• Medicinal mushrooms and blood pressure
• Fibromyalgia and supplements
• Medicinal mushrooms and the liver
• Reishi for sleep — what was measured and what was not
• Reishi and the immune system: modulation or boost?
• Medicinal mushrooms by goal — the hub
• Lab results — beta-glucan
• How to read a certificate of analysis (COA)

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 clotting disorders, antiphospholipid syndrome, ITP or any other medical condition, and they are not a substitute for an anticoagulant or an antiplatelet drug. Do not stop, replace or change the dose of warfarin, apixaban, rivaroxaban, aspirin, clopidogrel 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 anticoagulants or antiplatelet drugs, have surgery or dental work planned, are pregnant or breastfeeding, have liver or kidney disease, or have any existing medical condition. Triterra extracts contain 32% alcohol. *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.*