Medicinal Mushrooms and Gout (Uric Acid): What the Research Has Actually Tested — and What It Hasn’t

In brief5 points · 1-minute read

• No human clinical trial has tested a medicinal mushroom extract on uric acid or gout flares, so no outcome can be promised.
• In large cohort studies, eating mushrooms did not raise gout risk, unlike meat, seafood and alcohol.
• Reishi and cordyceps lowered uric acid only in mice and rats, and such findings do not translate into a claim about a bottle.
• Anyone with gout, kidney disease or on urate-lowering medication should consult a physician before any supplement.
• Turkey tail has never been studied for uric acid, and absence of data is not evidence of safety.

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Gout is an inflammatory arthritis caused by uric acid — the end product of purine breakdown — crystallizing in a joint, and reishi (Ganoderma lucidum, lingzhi), lion’s mane (Hericium erinaceus, yamabushitake), Cordyceps (dong chong xia cao) and turkey tail (Trametes versicolor, yun zhi) are the medicinal mushrooms people ask about when their urate is high. Here is the answer before anything else: no randomized human trial has ever tested any medicinal mushroom, or any mushroom extract, on serum uric acid, hyperuricemia or gout flares. What exists is a set of large diet cohorts in which mushrooms did not raise gout risk, a handful of rodent and test-tube studies in which reishi and Cordyceps compounds lowered urate or inhibited xanthine oxidase, and three tiny or low-quality human data points. This page lays all of it out — study by study, with the number of participants or mice — and states plainly what none of it means for someone with gout.

Do medicinal mushrooms lower uric acid?

In humans, this has never been tested properly. There is no randomized controlled trial of reishi, lion’s mane, Cordyceps or turkey tail on serum uric acid or gout. In rodents, extracts and compounds from reishi and Cordyceps lowered urate and inhibited xanthine oxidase. That is a research lead, not an answer — and it cannot go on a bottle.

The gap between those two sentences is the whole page. Mechanism papers from Chinese laboratories show that reishi polysaccharide peptide, Cordyceps water extract, cordycepin and shiitake polysaccharides push mouse urate down by inhibiting the enzyme that makes it (xanthine oxidase) or by changing the kidney transporters that reabsorb it (URAT1, GLUT9, OAT1). Those papers are real and are listed below. What does not exist — we ran the search on August 30, 2026 through the NCBI database — is a single trial in which people took a mushroom extract and had their uric acid compared to placebo. A 2024 systematic review of mushroom consumption and cardiometabolic outcomes, covering five cohorts and four clinical trials, noted a “potentially beneficial connection” with hyperuricemia and then wrote, in the same abstract, that “drawing definitive conclusions is premature.” That is where the science stands, and where we stand too.

What are gout and uric acid — and why do mushrooms come up at all?

Uric acid is the end product of purine breakdown; purines come from your own cells and from food. Xanthine oxidase is the enzyme that makes it, and the kidneys excrete most of it. When production outruns excretion, urate crystallizes in a joint — that is gout. Mushrooms contain purines, and their compounds are studied on that enzyme.

Two points of the biology matter for everything below. The first is the enzyme: xanthine oxidase converts hypoxanthine to xanthine and xanthine to uric acid, and allopurinol and febuxostat work by blocking it. Any compound that inhibits xanthine oxidase in a test tube will therefore be described online as “natural allopurinol,” a leap this page refuses to make. The second is the kidney: a set of transporter proteins — URAT1 and GLUT9 pull urate back into the blood, OAT1 pushes it out — decide how much stays, and most of the rodent mushroom papers report changes in exactly these transporters. Hyperuricemia is the lab value (high serum urate); gout is the disease (crystals, flares, tophi). The two are not the same, and the epidemiology below mostly measured the lab value.

Does eating mushrooms raise the risk of gout?

The large cohorts say no. In 47,150 US men followed for 12 years, purine-rich vegetables were not associated with incident gout, while meat and seafood were. In 3,978 Shanghai men, purine-rich vegetables showed no association with hyperuricemia. In 19,830 Chinese adults, the highest mushroom intake carried a slightly lower hazard of hyperuricemia — an association, not a cause.

The cornerstone is the 2004 Health Professionals Follow-up Study in the New England Journal of Medicine: 47,150 men, 12 years, 730 confirmed new cases of gout. The highest fifth of meat intake carried a relative risk of 1.41 (95% CI 1.07–1.86) compared with the lowest; seafood 1.51 (1.17–1.95); dairy went the other way, 0.56 (0.42–0.74). The abstract’s own words on the plant side: “The level of consumption of purine-rich vegetables and the total protein intake were not associated with an increased risk.” Mushrooms are not itemized separately in that abstract — they sit inside the “purine-rich vegetables” group — so the honest reading is that the group in which mushrooms are counted did not raise risk, not that mushrooms were individually cleared. The 2012 Shanghai Men’s Health Study, 3,978 men, reached the same conclusion for hyperuricemia (“No associations between consumption of purine-rich vegetables or meat and prevalence of hyperuricemia were observed”), with seafood again positive (OR 1.34–1.56) and soy trending protective (p = 0.07).

The one cohort that measured mushrooms by themselves is the Tianjin TCLSIH study (2021): 19,830 adults, median follow-up 4.2 years, 4,260 new cases of hyperuricemia. Across quartiles of mushroom intake (under 1.76 g up to over 5.52 g per 1,000 kcal per day), the adjusted hazard ratios were 1.00, 0.93, 0.93 and 0.88 (95% CI 0.80–0.96), P for trend 0.007. That is a 12% lower hazard of a lab value, in people eating culinary mushrooms as food, in one Chinese population, observationally. It does not say mushrooms protect against gout, and it says nothing about extracts. For perspective on what does move dietary gout risk, a 2018 meta-analysis put alcohol at OR 2.58 (1.81–3.66) and coffee at 0.47 (0.37–0.59), with red meat, seafood and fructose raising risk and dairy and soy lowering it — mushrooms are not mentioned in it at all.

How many purines do mushrooms contain — and why do drying and cooking change the answer?

Fresh mushrooms are a moderate-purine food; the figure depends on species and preparation. Drying concentrates purines because water is removed. In shiitake, boiling raised measurable purines while freeze-drying lowered them. Among edible fungi analyzed by HPLC, reishi fruiting body had among the lowest nucleoside and nucleobase content — under 1 mg per gram of dry matter.

The Japanese reference work — a 2014 HPLC survey of 270 foodstuffs — anchors the clinical guideline of keeping purine intake below 400 mg per day and names the genuinely purine-dense categories: animal meats, fish, organs such as liver and fish milt, and yeast; it also flags hypoxanthine as the purine base most relevant to a rise in urate. The per-mushroom numbers sit in that paper’s tables rather than its abstract, so we do not quote them; what the literature does let us say is directional. A 2022 processing study of shiitake found that boiling increased total purine, driven by a rise in xanthine of 331.72 ± 50.07%, while freeze-drying decreased measurable purines — the authors recommend freeze-dried shiitake for people with hyperuricemia or gout. And a 2008 analysis measured seven nucleosides and five nucleobases across six edible fungi, tissue by tissue: totals ranged from 0.14 to 26.57 mg per gram of dry matter, above 10 mg/g in the gills and caps of shiitake and two other species, and below 1 mg/g in both the stipe and the cap of Ganoderma lucidum. Reishi is not eaten as a food, so the practical relevance is narrow — but the fruiting body we extract sits at the low end of that scale. What none of this tells you is the purine content of a tincture, which nobody, including us, has measured.

What has been tested on reishi and uric acid?

One human study and two rodent studies. In 10 healthy volunteers taking 0.72 g of lingzhi daily for 10 days, uric acid “tended to decrease, but changes were not statistically significant.” In rats, a mycelium culture lowered serum urate from 5.56 to 4.45 mg/dL; in mice, a polysaccharide peptide lowered it by up to 40.6%. No trial in gout.

The human record is a 2004 pilot from Hong Kong in which uric acid was one biomarker among many. Its result is the most quoted “human evidence” for reishi and urate, and the sentence deserves to be read whole: a downward tendency that did not reach significance, in ten healthy people, over ten days. The two animal papers are stronger on mechanism and weaker on relevance. In 2022, a Taiwanese group gave rats with potassium-oxonate-induced hyperuricemia 200–400 mg/kg of submerged-culture Ganoderma lucidum mycelium powder: serum uric acid fell from 5.56 ± 0.41 to 4.45 ± 0.46 mg/dL, hepatic xanthine oxidase from 841.29 ± 299.58 to 540.80 ± 199.20 μU per mg of protein, and blood urea nitrogen from 30.49 ± 4.71 to 21.16 ± 4.25 mg/dL. Note the material: liquid-culture mycelium, not fruiting body, and not a tincture. The same year, a Ganoderma lucidum polysaccharide peptide (GLPP) lowered blood uric acid in hyperuricemic mice dose-dependently by up to 40.6%, inhibited adenosine deaminase in liver and blood, and shifted the kidney transporters — GLUT9 down, OAT1 up. That is an isolated fraction, not a whole extract. Two further mouse papers often filed under “reishi” actually used Ganoderma applanatum, the artist’s conk — a different species — and we do not carry their results over to ours. The broader reishi literature is on our reishi science page.

What has been tested on Cordyceps and hyperuricemia?

The most rodent work of the four, and one Cochrane review in transplant patients. In mice, a Cordyceps water extract lowered serum urate from 306 to 162 μmol/L and cut renal URAT1 protein sharply; pure cordycepin did the same; in vitro, cordycepin’s xanthine-oxidase IC50 was 0.014 mg/mL. The human signal: “limited low quality evidence” in 447 transplant recipients.

The rodent series comes largely from one laboratory in Guangzhou. In 2016, mice made hyperuricemic with potassium oxonate and hypoxanthine received a Cordyceps water extract at 50, 100 or 200 mg/kg: serum uric acid fell from 306 to 189, 184 and 162 μmol/L (normal 184; P under 0.01), and renal URAT1 protein dropped from 93.45 to 28.15, 17.43 and 9.03 pg/mL. In 2018, the same group isolated the effect to cordycepin at 15, 30 and 60 mg/kg — serum urate 216, 210 and 203 μmol/L against 337 in untreated hyperuricemic mice and 202 in normal ones — and attributed it to URAT1 down-regulation. Earlier, in 2014, a fermentation exopolysaccharide at 200–800 mg/kg lowered urate dose-dependently, with the 400 mg/kg dose matching allopurinol on serum uric acid, BUN and liver xanthine oxidase. A 2024 paper screened seven medicinal fungi in vitro, then showed in mice that the Cordyceps extract and cordycepin lowered urate through xanthine-oxidase inhibition and reduced insulin resistance, with shifts in gut bacteria (fewer Oscillibacter and Alistipes). And a 2024 enzyme-kinetics study measured cordycepin’s IC50 against xanthine oxidase at 0.014 mg/mL and against COX-2 at 0.055 mg/mL, stronger than ergosterol, with both compounds bringing uric acid back to normal in a gouty-nephropathy mouse model.

The one human item is a 2015 Cochrane review of Cordyceps in kidney-transplant recipients: five studies, 447 patients, comparing Cordyceps with azathioprine (four studies, 265 patients) or Cordyceps plus low-dose cyclosporine with standard cyclosporine (one study, 182). The authors found “limited low quality evidence to suggest benefits in pulmonary infection, serum albumin, serum uric acid levels, CNI nephrotoxicity and hepatotoxicity,” and added that “given the limited number of small studies, and high risk of bias, results should be interpreted with caution.” No effect size for uric acid is given, and transplant patients on immunosuppressants are not people with gout — yet this is the closest thing to human urate data for any Cordyceps product. Two things worth stating: none of these mouse doses has been translated to an oral human dose, and several papers use allopurinol as a positive control — a laboratory comparator, not a claim of equivalence. More on the mushroom itself on the Cordyceps science page.

What has been tested on lion’s mane and uric acid?

One record, and a thin one. In a 2021 pilot, 13 healthy adults took Hericium erinaceus powder for 7 days; gut microbiota diversity rose, and the microbial shifts “were correlated with” blood indices including uric acid. No direction, no magnitude, no control group. That is the entire PubMed record for lion’s mane and urate.

It is worth being exact, because “lion’s mane and uric acid” produces a confident answer on many websites. The 2021 study was designed around the gut microbiome — it found higher alpha diversity and more Faecalibacterium prausnitzii — and reported correlations between those changes and a panel of blood values: alkaline phosphatase, LDL, uric acid and creatinine. A correlation in an uncontrolled seven-day pilot of thirteen people is not evidence that lion’s mane changes uric acid in either direction; the abstract does not even say which way the number moved. Everything else known about this mushroom — the hericenones, the NGF story, the cognition trials — is on the lion’s mane science page, and none of it touches urate.

And turkey tail?

Nothing. A PubMed search for Trametes versicolor or Coriolus versicolor together with uric acid returns zero records. We say this plainly because turkey tail appears on “mushrooms for gout” lists anyway. There is no human, animal or test-tube study on this mushroom and urate — so there is nothing to summarize, and nothing to claim.

The absence cuts both ways: no one has shown that turkey tail lowers uric acid, and no one has shown that it raises it or interacts with urate-lowering medication. Its research is almost entirely about polysaccharopeptides (PSK and PSP) in immunological contexts, summarized on the turkey tail science page. Our own turkey tail extract is a combined turkey tail and reishi tincture, and what applies to it here is what applies to reishi above — with the same limits.

Which mechanisms is the research examining — xanthine oxidase, URAT1, the gut–kidney axis?

Three routes recur across the rodent papers: inhibiting xanthine oxidase so less uric acid is made; lowering URAT1 and GLUT9 and raising OAT1 in the kidney so more is excreted; and, most recently, acting through the gut — restoring the microbiota and the intestinal barrier. The 2026 shiitake work shows the route depends on the polysaccharide’s structure.

The gut–kidney axis is the newest of the three and the most relevant to β-glucans, which are the main constituent class in all our extracts. In 2025, a shiitake polysaccharide–protein complex at 250–1,000 mg/kg per day reduced mouse serum uric acid from 281.62 to 109.42–138.12 μmol/L (p under 0.001), regulated renal urate transporters, and corrected gut dysbiosis and barrier disruption. In 2026, the same group separated two shiitake polysaccharides and found they work by different routes: LEP20, a (1→3)-β-D-glucan, through the gut–kidney axis; LEP50, a (1→4)-α-D-glucan, through systemic purine metabolism. That is the first clear sign that the specific β-glucan structure — not “polysaccharides” in general — determines the pathway, one reason we measure β-glucan rather than total polysaccharides. Other species studied in mice tell the same mechanistic story: honey mushroom (Armillaria mellea) extracts lowered urate through OAT1 and CNT2, and — an honest detail — its fermentation product outperformed the fruiting body, which the authors attributed to the fruiting body’s own purine load partly offsetting the effect. Two polypores, Sanghuangporus vaninii and Inonotus hispidus, reduced urate, xanthine-oxidase activity and joint swelling in a gouty-arthritis model. None of these is a mushroom we grow, and none is a human study.

What has actually been measured in humans?

Three records, none of them a trial in people with gout. The table below gives each one its size, duration, what was measured, the result in the authors’ own words, and what it does not show. Read the last column first: it is the reason this page cannot say “reishi lowers uric acid” and does not try to.

Set this beside the epidemiology and the shape becomes clear: tens of thousands of people were followed to see whether eating mushrooms hurts (it did not); 23 healthy volunteers and 447 transplant patients were measured to see whether a mushroom product helps, and none of those measurements is strong enough to say. A search for a randomized trial of a mushroom extract on serum uric acid in humans returned zero records.

What has been measured in rodents and test tubes — and what does it not show?

A lot, and it is consistent: urate down, xanthine oxidase inhibited, kidney transporters shifted. Every row below is a chemically induced hyperuricemia model (potassium oxonate, often with hypoxanthine), or an enzyme assay, at doses no one has translated to a human oral dose. Consistency across mice is a reason to study people — not a substitute for it.

Is a mushroom extract safe for someone with gout, or on allopurinol?

Unknown, in the strict sense. A search for interactions between medicinal mushrooms and allopurinol, febuxostat or colchicine returns no human report — only mouse papers using allopurinol as a comparator. Absence of data is not evidence of safety. Anyone with gout, kidney disease, or on urate-lowering medication should speak with their physician before adding any supplement, ours included.

Three honest specifics. First, the kidney. The one documented case of mushroom-supplement kidney harm in the literature is chaga (Inonotus obliquus) — a 69-year-old man taking 10–15 g per day for three months alongside 500 mg of vitamin C developed oxalate nephropathy with nephrotic syndrome, needed hemodialysis and high-dose steroids, and recovered within a month; a second man developed end-stage renal disease after about five years of chaga. That is a different species (we do not grow or sell it — see our chaga page) and a different mechanism (oxalate, not urate); we mention it because “mushroom supplement” and “kidney” belong in the same sentence at least once on a page about gout. No case report of reishi, lion’s mane, Cordyceps or turkey tail raising uric acid or precipitating a gout flare was found. Gout and chronic kidney disease travel together; our kidney-health post covers what has and has not been measured there.

Second, alcohol. Our extracts are about 32% alcohol, and in the 2018 meta-analysis alcohol was the strongest dietary risk factor for gout, OR 2.58. The daily dose of a tincture is about 1.4 ml — a very small amount of alcohol, a fraction of a milliliter of ethanol — but someone who avoids alcohol on medical advice should know it is there and decide with their physician. Third, medication. Several mouse papers put allopurinol in the same experiment as the mushroom compound; none tested them together, and no human study has. We do not know whether a mushroom extract adds to, interferes with, or does nothing beside allopurinol, febuxostat or colchicine. Our pages on side effects and drug interactions hold the rest of what is known — which for this drug class is nothing.

Why does a mouse study not become a claim on a bottle — and how do we write about it?

Because of three gaps the mouse papers cannot close: dose (mg per kg of mouse, no human equivalent), model (urate forced up chemically for days, not gout built over years), and breadth (most of the Cordyceps series is one laboratory). A rodent finding is described as a rodent finding — in the science section, never on a label.

Take the cleanest number on this page, cordycepin’s xanthine-oxidase IC50 of 0.014 mg/mL. It is a real measurement of a real compound in an enzyme assay. It says nothing about how much cordycepin reaches your blood after a dropper of extract, because that has not been measured; nothing about whether the enzyme in a human liver behaves like the enzyme in the dish; and the authors themselves did not translate the concentration into an oral dose. The same is true of “up to 40.6%” in mice and “306 → 162 μmol/L” — in animals whose urate was pushed up with potassium oxonate over days, a model built to test mechanisms quickly. The Armillaria paper adds an uncomfortable and useful detail: the fruiting body carried enough purine of its own to blunt its effect relative to a low-purine fermentation product. We grow and extract fruiting bodies. That is exactly the kind of finding a brand page omits, and the kind we think belongs here. So we write “studied in mice,” we write the numbers, and we write the limits — and we do not write “supports healthy uric acid levels” on a bottle, because no human study supports it.

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

We do not say that reishi, Cordyceps, lion’s mane or turkey tail lowers uric acid or helps gout — there is no human trial. We do not call any compound a “natural xanthine-oxidase inhibitor” as a product benefit. We do not say a mushroom extract is safe alongside allopurinol. And we do not say mushrooms are purine-free.

What we do say is limited to what we measure. Every extract we sell is tested at TÜV Austria on the finished product for β-glucan, on a dry-matter basis of the extract, and for α-glucan — the starch that betrays grain in a product. Those numbers describe what is in the bottle. They do not describe what the bottle does to your urate, and we do not measure purines in the tincture at all.

Tested at TÜV Austria on the finished extract, per extract; the certificates are open, and “How to read a mushroom supplement test report (COA)” explains each line. The rest of what we are responsible for — fresh fruiting body from our farm in the Galilee with no drying step, an extraction ratio of 1:2 to 1:3, three extraction phases with seven weeks in alcohol — is described on the transparency page. None of it is a statement about gout.

The bottom line

Eating mushrooms did not raise gout risk in 47,150 US men or 3,978 Shanghai men, and associated with a 12% lower hazard of hyperuricemia in 19,830 Chinese adults — but that is food, and association. In mice and test tubes, reishi and Cordyceps compounds lowered urate, inhibited xanthine oxidase and shifted the kidney’s urate transporters — but that is mice. In humans, the record is ten volunteers with a non-significant tendency, thirteen with a correlation, and 447 transplant patients with low-quality evidence — and no randomized trial at all. No study exists on turkey tail, and none on interactions with allopurinol, febuxostat or colchicine. Medicinal mushrooms are a legitimate research lead for uric acid and an unproven one for people — so we measure what is in the bottle, publish it, and leave gout to you and your physician.

Frequently asked questions

Does reishi lower uric acid?

Not according to any human trial. The only human data are ten healthy volunteers who took 0.72 g of lingzhi daily for 10 days; uric acid “tended to decrease” without reaching statistical significance. In rats and mice, a mycelium culture and an isolated polysaccharide peptide lowered urate (by up to 40.6% in mice). That is a mechanism lead, not a result you can expect.

Are mushrooms forbidden if you have gout?

The large cohorts say no. Purine-rich vegetables — the group mushrooms belong to — were not associated with gout in 47,150 US men or with hyperuricemia in 3,978 Shanghai men, while meat, seafood and alcohol were. In 19,830 Chinese adults, higher mushroom intake associated with a slightly lower hazard of hyperuricemia. Your physician’s diet plan still takes precedence over a cohort.

Does Cordyceps inhibit xanthine oxidase?

In a test tube and in mice, yes: cordycepin’s IC50 against xanthine oxidase was 0.014 mg/mL, and a Cordyceps water extract lowered mouse serum urate from 306 to 162 μmol/L, mainly through the URAT1 transporter. In humans, this has never been tested. “Natural xanthine-oxidase inhibitor” is a laboratory description, not a product benefit, and not an alternative to allopurinol.

Can I take a mushroom extract with allopurinol or febuxostat?

Nobody knows. A search for interactions between medicinal mushrooms and allopurinol, febuxostat or colchicine returns no human report — only mouse experiments that used allopurinol as a comparator. The absence of a documented interaction is not evidence that there is none. Discuss any supplement with the physician managing your urate-lowering therapy before starting it.

What about dried mushrooms — do they have more purines?

Per gram, yes: drying removes water, so purines are concentrated in the remaining mass. Processing matters too — in shiitake, boiling raised measurable purines (xanthine up 331.72%) while freeze-drying lowered them. Among edible fungi analyzed in 2008, reishi fruiting body had among the lowest nucleoside and nucleobase content, under 1 mg per gram of dry matter versus over 10 in shiitake.

Is a tincture different from a mushroom on a plate?

Different in what it delivers, and unmeasured on this question. A plate of mushrooms is a moderate-purine food; a tincture is an extract of a fruiting body in water and alcohol, taken in a dose of about 1.4 ml per day. No one has measured the purine content of a mushroom tincture, including us, and no trial has compared the two on uric acid.

Is there any risk to the kidneys?

The one documented mushroom-supplement kidney harm is chaga — two case reports of oxalate nephropathy after months to years of high daily intake, one requiring hemodialysis. Chaga is a different species we do not grow, and oxalate is a different mechanism from urate. No case report links reishi, lion’s mane, Cordyceps or turkey tail to kidney injury or gout. People with kidney disease should still consult their physician.

What do you actually measure in your extracts?

β-glucan and α-glucan on the finished extract, at TÜV Austria, on a dry-matter basis: Cordyceps 28.16%, reishi 25.65%, lion’s mane 23.93%, turkey tail + reishi 23.21%, with α-glucan not detected in any of them. We do not measure purines, cordycepin, or any uric-acid marker, and we make no claim about gout. The certificates are open on the lab-results page.

Scientific sources (peer-reviewed)

• Cohort — 47,150 US men over 12 years (730 gout cases): meat RR 1.41 and seafood RR 1.51 raised gout risk, dairy RR 0.56 lowered it; purine-rich vegetables were not associated — Choi HK, Atkinson K, Karlson EW, Willett W, Curhan G. The New England Journal of Medicine, 2004. View on PubMed
• Cross-sectional — 3,978 Shanghai men: no association between purine-rich vegetables or meat and hyperuricemia; seafood OR 1.34–1.56 — Villegas R, Xiang YB, Elasy T, et al. Nutrition, Metabolism & Cardiovascular Diseases, 2012. View on PubMed
• Cohort — 19,830 Chinese adults, median 4.2 years (4,260 hyperuricemia cases): highest mushroom intake HR 0.88 (0.80–0.96), P-trend 0.007 — Zhang T, et al. Food & Function, 2021. View on PubMed
• Systematic review — 5 cohorts and 4 clinical trials of mushroom consumption: a “potentially beneficial connection” with hyperuricemia, but “drawing definitive conclusions is premature” — Hong JY, et al. Nutrition Research and Practice, 2024. View on PubMed
• Meta-analysis of dietary factors and gout: alcohol OR 2.58 (1.81–3.66), coffee OR 0.47 (0.37–0.59); red meat, seafood and fructose raise risk, dairy and soy lower it; mushrooms not mentioned — Li R, Yu K, Li C. Asia Pacific Journal of Clinical Nutrition, 2018. View on PubMed
• Analytical — total purine and purine bases in 270 foodstuffs by HPLC; guideline of under 400 mg purine per day; meats, fish, organs and yeast the purine-dense categories — Kaneko K, Aoyagi Y, Fukuuchi T, Inazawa K, Yamaoka N. Biological and Pharmaceutical Bulletin, 2014. View on PubMed
• Analytical — shiitake processing: boiling raised total purine (xanthine up 331.72 ± 50.07%), freeze-drying lowered it — Xiao L, et al. Food Chemistry: X, 2022. View on PubMed
• Analytical — nucleosides and nucleobases in 6 edible fungi by tissue: 0.14–26.57 mg/g dry matter; over 10 mg/g in shiitake gills and caps, under 1 mg/g in Ganoderma lucidum stipe and cap — Yuan JP, Zhao SY, Wang JH, Kuang HC, Liu X. Journal of Agricultural and Food Chemistry, 2008. View on PubMed
• Human pilot — 10 healthy volunteers, 0.72 g/day lingzhi for 10 days: uric acid “tended to decrease, but changes were not statistically significant” — Wachtel-Galor S, Szeto YT, Tomlinson B, Benzie IF. International Journal of Food Sciences and Nutrition, 2004. View on PubMed
• Rats — submerged-culture Ganoderma lucidum mycelium, 200–400 mg/kg: serum uric acid 5.56 → 4.45 mg/dL, hepatic xanthine oxidase 841.29 → 540.80 μU/mg, BUN 30.49 → 21.16 mg/dL — Huang CH, et al. Metabolites, 2022. View on PubMed
• Mice — Ganoderma lucidum polysaccharide peptide lowered blood uric acid by up to 40.6%; adenosine deaminase inhibited, GLUT9 down, OAT1 up — Lin S, et al. Food & Function, 2022. View on PubMed
• Human pilot — 13 healthy adults, Hericium erinaceus powder for 7 days, uncontrolled: gut microbiota shifts correlated with ALP, LDL, uric acid and creatinine; no direction reported — Xie XQ, Geng Y, Guan Q, et al. Nutrients, 2021. View on PubMed
• Mice — Cordyceps water extract 50/100/200 mg/kg in potassium-oxonate + hypoxanthine hyperuricemia: serum uric acid 306 → 189/184/162 μmol/L; renal URAT1 protein 93.45 → 28.15/17.43/9.03 pg/mL; allopurinol as positive control — Yong T, et al. Journal of Ethnopharmacology, 2016. View on PubMed
• Mice — cordycepin 15/30/60 mg/kg: serum uric acid 216/210/203 μmol/L vs 337 in hyperuricemic controls (normal 202), via URAT1 down-regulation — Yong T, et al. Frontiers in Microbiology, 2018. View on PubMed
• Mice — Cordyceps fermentation exopolysaccharide 200/400/800 mg/kg lowered uric acid dose-dependently; 400 mg/kg matched allopurinol on serum uric acid, BUN and liver xanthine oxidase — Ma L, et al. Current Microbiology, 2014. View on PubMed
• In vitro screen of 7 medicinal fungi + mice — Cordyceps aqueous extract and cordycepin lowered uric acid via xanthine-oxidase inhibition, reduced insulin resistance, reduced Oscillibacter and Alistipes — Jiang Y, et al. Journal of Pharmaceutical and Biomedical Analysis, 2024. View on PubMed
• Enzyme kinetics + gouty-nephropathy mice — cordycepin IC50 0.014 mg/mL against xanthine oxidase and 0.055 mg/mL against COX-2; uric acid and inflammatory factors returned to normal in mice — Zhou HB, et al. International Journal of Biological Macromolecules, 2024. View on PubMed
• Cochrane review — Cordyceps in 447 kidney-transplant recipients (5 studies): “limited low quality evidence” of benefit in serum uric acid among other outcomes; high risk of bias, interpret with caution — Hong T, Zhang M, Fan J. Cochrane Database of Systematic Reviews, 2015. View on PubMed
• Mice — shiitake polysaccharide–protein complex 250–1,000 mg/kg/day: serum uric acid 281.62 → 109.42–138.12 μmol/L via the gut–kidney axis — Xiong X, et al. International Journal of Biological Macromolecules, 2025. View on PubMed
• Mice + structural chemistry — two shiitake polysaccharides act by different routes: a (1→3)-β-D-glucan through the gut–kidney axis, a (1→4)-α-D-glucan through systemic purine metabolism — Xiong X, et al. NPJ Science of Food, 2026. View on PubMed
• Case report — chaga 10–15 g/day for 3 months with vitamin C 500 mg/day: oxalate nephropathy with nephrotic syndrome in a 69-year-old man; hemodialysis, recovery within 1 month — Kwon O, et al. Medicine (Baltimore), 2022. View on PubMed
• Case report + review — end-stage renal disease in a 49-year-old man after about 5 years of chaga; oxalate intake 2× to 5× usual — Lee S, et al. Journal of Korean Medical Science, 2020. View on PubMed

Read next

• Medicinal Mushrooms by Goal — the hub
• Turkey Tail & Reishi for Immune Support
• Triterra Farm — home
• Medicinal mushrooms and joint health — what has been measured
• Medicinal mushrooms and kidney health
• Chaga — why we do not grow it, and what the case reports say
• Medicinal mushrooms and drug interactions
• Side effects of medicinal mushrooms: what’s important to know
• Reishi — the science
• Cordyceps — the science
• Beta-glucan vs “polysaccharides” — the number that actually matters
• How to read a mushroom supplement test report (COA)
• Full lab results
• The research hub
• Functional mushrooms — the complete guide

This page is educational and does not constitute medical advice. It summarizes what published studies measured on mushrooms, purines and uric acid; it is not a recommendation to start, stop or combine any supplement with a medication, and it is not a substitute for the medical treatment of gout, hyperuricemia or kidney disease. Our extracts are food supplements. *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.*