Mushrooms, Graded
What the human studies actually say about ergothioneine, UV-generated vitamin D2, beta-glucans, and the five best-known functional mushrooms. Enoki carries twenty times the ergothioneine of cremini.
Sofía moved in. She is training to be a chef, so the house now has someone in it who thinks about food for a living.
There were already two written nutrition plans in this house. Mine: 2,455 calories, 225 g of protein, twenty-five recipes. The children's is harder, because one of them eats almost everything and the other eats exactly seven foods and no fruit.
Her first lesson was mushrooms. I had been treating them as a texture. Then I went and read the literature, which is where it got interesting — one compound is better than I expected and most of the supplement aisle is worse.
Mushrooms are not a protein food. 200 g gets you 4–6 g of protein with mediocre digestibility. Count them as vegetables. This is the claim that dies first.
Ergothioneine is the reason to care. A compound your body has a dedicated transporter for, that it hoards in tissue, and that almost nothing else in the diet supplies. The epidemiology is good. The trials are still small.
Sunlight turns mushrooms into vitamin D. Fifteen minutes of direct sun on sliced mushrooms produced 704 IU per 100 g in one analysis. It is real, it is free, and it is D₂ — which is not the same thing as D₃.
"Immune boosting" is marketing. The dectin-1 receptor biology is genuine. Evidence that eating mushrooms prevents infections in healthy adults is not.
Four of the five famous functional mushrooms do not earn their price. Lion's mane is a defensible experiment. Chaga has a kidney risk and no efficacy trials.
Boiling throws 80% of the good part down the sink. The single highest-leverage thing in this article is a cooking method.
Not vegetables
Fungi are their own kingdom, and they are closer to us than to plants. They do not photosynthesise. They build cell walls from chitin — the same polymer as an insect shell — rather than cellulose, and they store carbohydrate as glycogen, like an animal.
Two consequences. They carry a distinct mix of compounds, ergothioneine and fungal β-glucans among them. And chitin is not digested by human enzymes, so it limits nutrient release — which is why cooking matters more here than with a vegetable.
What is in them
Per 100 g raw, from the USDA Foundation Foods dataset. Read these as representative rather than fixed — substrate, crop, maturity and assay method move several of these numbers by multiples, and the ergothioneine column especially so.
Two things. The cheap supermarket mushroom and the expensive one are not interchangeable — enoki carries twenty times the ergothioneine of cremini. And the protein column is where the popular story falls apart.
The protein claim
Mushrooms get sold as a protein source. They are not one. Look at the column again: roughly 2–3 g per 100 g. A generous 200 g portion is about 5 g of protein before you account for how much of it you actually absorb — and that part is worse than the raw number suggests.
A rat-balance study by Dabbour and Takruri found true protein digestibility around 73% for oyster mushroom and 81% for Agaricus macrosporus, but only 53–61% for two other fungi, with calculated PDCAAS values of 0.35–0.45 — sulfur amino acids limiting two of the four species, lysine limiting the other two. For comparison, whey scores 1.0. That is one rat-balance study of four fungi, not a general figure for all mushrooms; there are no robust whole-mushroom DIAAS values at all, and the numbers quoted for mycoprotein products like Quorn do not transfer to a portobello.
If you track protein for training, treat mushrooms as a low-protein side, not a protein source. A 200 g serving contributes about 5 g. Their value is in the far-right column.
Ergothioneine
Ergothioneine is a sulfur-containing amino acid derivative made almost exclusively by fungi and some soil bacteria. You cannot make it yourself. You get it from food or you do not get it.
The interesting part is not the molecule, it is the transport. Your body has a dedicated transporter for it — OCTN1, encoded by SLC22A4. Cells are otherwise nearly impermeable to it, so uptake depends almost entirely on that one highly selective transporter.
And it hoards it. In healthy people plasma ergothioneine averages around 1.28 µmol/L while whole blood averages 101 µmol/L — an eighty-fold difference, because red cells and tissues concentrate it. After dosing, less than 4% shows up in urine — it goes in and it stays in.
Bruce Ames proposed it in 2018 as a "longevity vitamin": a nutrient whose slow shortfall might drive age-related damage without ever producing an obvious deficiency disease. That was a hypothesis paper. It was not the recognition of a new vitamin, and it is not evidence that supplementing it extends anything.
What the epidemiology says
The Malmö Diet and Cancer cohort followed 3,236 people free of cardiovascular disease for a median of 21.4 years. Per standard deviation of higher plasma ergothioneine, adjusted hazard ratios came out at 0.85 for coronary disease, 0.79 for cardiovascular mortality and 0.86 for all-cause mortality.
Those are the numbers everyone quotes. Here is the part they leave out: ergothioneine was also strongly associated with a health-conscious dietary pattern. Which means the finding is equally consistent with ergothioneine protecting you, and with ergothioneine being an excellent biomarker for being the kind of person who eats mushrooms and vegetables and generally looks after themselves. Observational data cannot separate those two.
The trials are honest about their own limits. Cheah randomised 45 healthy men to placebo, 5 mg or 25 mg for seven days: uptake and retention were unambiguous, and most oxidative-damage and inflammatory markers did not move. A 2024 pilot in mild cognitive impairment showed learning improvements — in nineteen people, over a year. A 2025 16-week trial in 147 healthy older adults found <b>no effect on its primary outcome</b>, composite memory; exploratory measures of subjective prospective memory and sleep initiation favoured 25 mg, with plasma levels rising about sixfold at four weeks. Encouraging. Not conclusive.
What it costs in food
The species you choose matters more than the amount you eat. To hit 5 mg and 25 mg:
A hundred grams of enoki. That is the whole thing, and it costs about a dollar.
Distinctive uptake biology and encouraging observational data. Human outcome trials remain preliminary. "Mushrooms prevent dementia" does not hold up.
Vitamin D on a windowsill
Mushrooms contain ergosterol. Hit ergosterol with UV-B and it photoconverts to vitamin D₂ — the same reaction that happens in your skin, running the fungal version. It works well.
Urbain and Jakobsen put sliced white mushrooms in sunlight. After fifteen minutes they measured 17.6 µg per 100 g fresh — 704 IU. Over the first hour it rose roughly linearly to about 30 µg per 100 g. Past that it plateaued and eventually started degrading. An unexposed mushroom contains essentially none, so this is not a small enhancement; it is the difference between zero and a supplement dose.
1. Slice them, to increase the exposed surface area.
2. Single layer, outdoors. Not behind a window — ordinary glass blocks nearly all UV-B.
3. Fifteen to sixty minutes, near solar noon.
4. Cook or refrigerate promptly. Fresh mushrooms can lose about half the generated D₂ over a week in the fridge; dried and vacuum-stored in the dark they hold ~100% at three months.
The caveat is the one you would expect from a reaction driven by sunlight: latitude, season, cloud, UV index and slice thickness dominate the outcome, so this method cannot produce a reliable dose. A labelled UV-treated product is the answer if you need a number.
D₂ is not D₃
Five trials, including the ones that cut against mushrooms.
Mushroom D₂ works as D₂ — absorbed, raises 25(OH)D₂, not a myth. But several trials found 25(OH)D₃ falling as 25(OH)D₂ rose, and D₃ raises total 25(OH)D more reliably. If a blood test shows deficiency, treat UV mushrooms as food, not as a substitute for treatment.
Immune boosting
The mechanism is genuine and well characterised. Fungal β-glucans have a β-(1→3) backbone with β-(1→6) branches, and dectin-1 — a receptor on macrophages, neutrophils, dendritic and NK cells — recognises them and signals through Syk, CARD9 and NF-κB. That is real immunology, and it is not in dispute.
Three things get skipped between that receptor and the marketing. Orally consumed β-glucan is poorly absorbed intact, so whatever happens is happening through intestinal immune sampling and the microbiota rather than glucan circulating in your blood. Mushroom β-glucans are not interchangeable with oat β-glucan, which has a completely different linkage. And a cell experiment using purified or injected glucan tells you nothing reliable about a plate of shiitake.
The human trials are thin. A shiitake study showing a 60% rise in γδ-T-cell proliferation had no placebo group and was funded by mushroom-industry organisations. A trial in fifty elite athletes compared a proprietary oyster β-glucan product against a vitamin-C-matched placebo and did report fewer upper-respiratory symptoms — self-reported, never clinically confirmed, in a narrow population. A trial of 2.5 mg/day soluble shiitake β-glucan in older adults raised B-cell counts and moved almost nothing else. A 135-person reishi β-glucan trial changed T-cell counts and NK cytotoxicity — and measured no infection or clinical endpoint at all.
Almost all of these measured immune markers, not illness. The one that tracked symptoms tracked self-reported ones in fifty athletes. "Immune boosting" is not a defined outcome — and more immune activity is not automatically a good thing if you have an autoimmune condition or a transplant.
The five, graded
Grades reflect the quality of human evidence, not the marketing.
Lion's mane earns the C+. Mori randomised 30 adults with mild cognitive impairment to 3 g/day for sixteen weeks; scores improved during treatment and declined four weeks after stopping, and declined again during the four-week washout. Saitsu found MMSE improvement at 3.2 g/day — and no movement on two other cognitive measures in the same study. In 41 healthy younger adults, one acute Stroop result and a stress trend across many outcomes. Every one of these trials is small, and several have an author employed by a mushroom company.
Cordyceps results are inconsistent across small trials using different preparations and populations. Twenty adults aged 50–75 on 1 g/day for twelve weeks improved metabolic and ventilatory thresholds by about 10% — and VO₂max did not move. Twenty-two trained cyclists on 3 g/day for five weeks: nothing. A fourteen-day multi-ingredient trial: nothing. The one positive VO₂max signal comes from ten people who continued past a week in a study that showed no effect at the primary timepoint.
The supplement is probably not what the label says
Clean fruiting-body extracts test at 20–40% β-glucan. Mycelium grown on grain — most of what is on the shelf — routinely comes in under 10%, sometimes 1–2%.
A capsule sold as "reishi" that is actually myceliated grain can be well over half starch by weight, so most of what you swallow is spent grain. The phrase that hides it is "total polysaccharides": α-glucan from the starch inflates that number into something impressive while the fungal content stays small. In a 2017 analysis of 19 US reishi supplements, only five matched their labels across the study's chemical assays, and 13 contained starch-like polysaccharides.
The label should identify the species, the part of the fungus, and the β-glucan percentage — not "total polysaccharides", which can include starch. Independent batch assay if available.
Cooking and retention
Ergothioneine is thermally stable. Heat does not destroy it. What destroys it is water — it leaches out and goes wherever the water goes. So the cooking method is not a detail:
Retention varies by species and protocol, so read those as one enoki study and one shiitake study rather than universal constants. The direction is what holds: boil for five minutes and most of it leaves the mushroom — but almost all of it is recoverable in the cooking water. If you are making soup, fine, you eat the water. If you boil and drain, you have just paid for enoki and eaten cremini.
There is a second reason to cook them. The chitin cell wall is not something human digestive enzymes handle well. Cooking softens the tissue and improves nutrient release, and in Agaricus species it reduces — without necessarily eliminating — agaritine. Even then the wall is stubborn: in a randomised crossover study, 32 adults ate 226 g of roasted white mushrooms a day, split across two servings, for ten days, and some had visible undigested mushroom in stool.
Dry pan, hot, no crowding, no oil until they have released and re-absorbed their own water. Salt at the end — salt early and they steam in their own liquid, which is exactly the thing you are trying to avoid. Turns out the classical technique and the ergothioneine data want the same pan.
What we do
Whole mushrooms rather than powders or blends.
One of the children asks for the king oysters by name. The other eats seven foods and mushrooms are not one of them. That is a different problem.
Who should be careful
Concentrated extracts are not food, and the interaction profile changes accordingly. If you take immunosuppressants or are post-transplant, β-glucan products are the wrong direction on purpose. Anticoagulants and reishi have a plausible, if overstated, interaction. There are rare liver-injury case reports with powdered reishi. Chaga carries a documented oxalate-nephropathy risk that alone should end the conversation for anyone with kidney concerns. Wild mushrooms accumulate heavy metals and radiocaesium from their substrate. And the mannitol content makes a large serving a genuine FODMAP problem for some people.
Nearly all of the reported interaction and toxicity concerns involve concentrated products or unusually high intakes rather than food. Risk still depends on species, dose, product quality and the person.
For whole mushrooms the two practical variables are species and cooking method. The clinical evidence beyond that remains limited.
MONSTER 2.0 — The Kitchen — the plan this had to fit into: 2,455 kcal, 225 g protein, and why the deficit is deliberately moderate.
Seven Foods and a Signed Deal — the harder nutrition problem in this house: two children, one of whom eats exactly seven foods and zero fruit.
