Compound Monograph
Enterodiol
Enterodiol is a mammalian lignan (enterolignan) — not a plant constituent but a product of gut bacteria acting on dietary plant lignans such as secoisolariciresinol and matairesinol. It is the immediate precursor that gut microbes further oxidize to enterolactone, and is almost always studied as the less-characterized half of the enterodiol–enterolactone pair. It is a weak phytoestrogen; there are no trials of the isolate.
Sources · 2
Where Does It Come From?
Enterodiol is a naturally occurring dibenzylbutanediol lignan (mammalian lignan / enterolignan), found in Not a plant constituent — produced in the gut from flaxseed lignans and 1 other source. It is well tolerated orally (low toxicity).
Concentration
Content by Source
Concentrations not reported. No percent-dry-weight or mg/g figures have been published for this compound in its source plants.
Enterodiol at a Glance
Enterodiol is a mammalian lignan — not a plant constituent at all, but a compound your gut bacteria make from dietary plant lignans such as secoisolariciresinol and matairesinol, found in flaxseed and sesame.
It is the immediate precursor that microbes convert further into enterolactone, the better-known enterolignan.
Because production depends on the microbiome, two people eating identical flaxseed can end up with very different enterolignan exposure — which is the central complication in interpreting lignan epidemiology.
What It's Used For
Enterodiol is a mammalian lignan (an “enterolignan”) — and, like enterolactone, it is not a plant constituent. It is produced in the colon by gut bacteria from dietary plant lignans (chiefly secoisolariciresinol, also matairesinol and lariciresinol) and is frequently oxidized further to enterolactone — so it is best understood as an intermediate on the way to enterolactone, and the less-studied half of the pair. Almost all human epidemiology measures enterolactone (sometimes both), not enterodiol alone, so its own evidence is thin and mostly shared or preclinical.
Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. Thin, mostly-shared evidence, so scores stay low by design.
Enterodiol is, with enterolactone, the endpoint of gut conversion of dietary lignans and is classed as a mammalian phytoestrogen 1Reference 1Mammalian phytoestrogens: enterodiol and enterolactoneView study →; in human-cell ER assays the enterolignans show weak, mixed agonist/antagonist activity on ERα and ERβ 5,
Gap: binding is weak and generally less characterized than enterolactone, and there are no clinical endpoints for enterodiol as an isolate — the phytoestrogen signal is measured on circulating enterolactone from mixed lignan intake 5Reference 5Phytoestrogens and their human metabolites show distinct agonistic and antagonistic properties on ERα and ERβ in human cellsView study →.
As a dihydroxy dibenzylbutane polyphenol, enterodiol has expected in-vitro radical-scavenging capacity, discussed at the enterolignan-class level 1,
Gap: in-vitro/class-level only, with enterolactone the more-studied and often stronger antioxidant of the pair, and no human antioxidant-outcome data for enterodiol 1,
Enterodiol is included among flaxseed-lignan metabolites reported to modulate proliferation in cancer cell models 7Reference 7Anticancer potential of flaxseed lignans, their metabolites and synthetic counterparts in relation to molecular targetsView study →.
Gap: all in-vitro, frequently at supraphysiologic concentrations, usually reported jointly with enterolactone, with no isolate clinical anticancer evidence 7Reference 7Anticancer potential of flaxseed lignans, their metabolites and synthetic counterparts in relation to molecular targetsView study →.
Mechanisms
| Target / pathway | Effect | Relevant to |
|---|---|---|
| ERα / ERβ | weak, tissue-selective SERM-like binding | phytoestrogen role; hormone-cancer rationale |
| Gut microbiota (dehydroxylation/demethylation → oxidation) | plant lignans → enterodiol → enterolactone | its precursor→product identity (an intermediate frequently oxidized onward) |
| Radical scavenging (phenolic H-donation) | antioxidant in vitro (class-level) | antioxidant |
| Tumor-cell proliferation pathways | anti-proliferative in cell models | preclinical anticancer |
Pharmacokinetics
Enterodiol is not ingested — it is produced in the colon by gut bacteria from dietary plant lignans (principally secoisolariciresinol, also matairesinol) 1,
Clinical trials
There are no interventional trials of enterodiol as an isolate. It is measured only as a diet-derived biomarker within enterolignan/phytoestrogen observational studies (which predominantly report enterolactone) 9,
| Completed | Planned | Terminated | Observational / preclinical |
|---|---|---|---|
| —(no isolate trial) | — | — | Modest(mostly shared with enterolactone) |
Last checked: July 2026.
Toxicity & Safety
Your gut already makes enterodiol every time you eat seeds or whole grains, so the dietary exposure is not the question — the open one is concentrated supplemental use of a weak phytoestrogen that has never been characterized in humans.
- A normal product of gut metabolism. Formed from ordinary lignan-containing foods, with a long history of everyday internal exposure and no toxicity signal at dietary intakes.
- Avoid the isolated supplement in pregnancy and lactation. Weak estrogenic activity plus no safety data.
- Theoretical caution in hormone-sensitive conditions. Isolated phytoestrogen use warrants care with ER-positive breast cancer or endometrial issues — precautionary, not evidence of harm at food levels.
- Antibiotics blunt formation. They markedly reduce enterolignan production — a microbiome interaction rather than a toxicity.
- No human isolate data. Concentrated or supplemental enterodiol has never been toxicity-characterized.
Full Safety & Interactions Detail
Enterodiol is an endogenous product of normal gut metabolism of ordinary lignan-containing foods (flaxseed, sesame, whole grains, seeds, vegetables), with a long history of everyday internal exposure and no toxicity signal at dietary intakes — hence low. There is no toxicity characterization of concentrated/supplemental enterodiol (no human isolate data). The phytoestrogen caution is theoretical: weak ER activity means isolated/supplemental phytoestrogen use warrants caution in hormone-sensitive conditions (ER-positive breast cancer, endometrial issues) — precautionary, not evidence of harm at food levels (a mouse study found the enterolignans did not promote MCF-7 xenograft growth 8Reference 8AnimalMammalian lignans enterolactone and enterodiol, alone and with genistein, do not promote the growth of MCF-7 xenografts in ovariectomised athymic nude miceView study →).
Note a microbiome interaction rather than a toxicity: antibiotics markedly reduce enterolignan formation.
Dosage
There is no established therapeutic dose and no validated human dose — enterodiol is not taken directly but generated internally from dietary lignan intake at a rate set by the individual’s gut flora (flaxseed is the richest common substrate; sesame, whole grains, seeds and vegetables also contribute). Any supplement figures would be research references, not recommendations.
References
- Wang LQ (2002). Mammalian phytoestrogens: enterodiol and enterolactone. Journal of Chromatography B. https://pubmed.ncbi.nlm.nih.gov/12270221/
- Heinonen S, et al. (2001). In-vitro metabolism of plant lignans: new precursors of the mammalian lignans enterolactone and enterodiol. Journal of Agricultural and Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/11453749/
- Zhu Y, et al. (2024). Bioconversion of lignans in flaxseed cake and isolation of an Enterococcus faecium strain converting secoisolariciresinol diglucoside to enterodiol. Food Chemistry. https://pubmed.ncbi.nlm.nih.gov/38905833/
- Baldi S, Tristán Asensi M, Pallecchi M, et al. (2023). Interplay between lignans and gut microbiota: nutritional, functional and methodological aspects. Molecules. https://pubmed.ncbi.nlm.nih.gov/36615537/
- Mueller SO, et al. (2004). Phytoestrogens and their human metabolites show distinct agonistic and antagonistic properties on ERα and ERβ in human cells. Toxicological Sciences. https://pubmed.ncbi.nlm.nih.gov/15084758/
- Rietjens IMCM, et al. (2017). The potential health effects of dietary phytoestrogens. British Journal of Pharmacology. https://pubmed.ncbi.nlm.nih.gov/27723080/
- Mueed A, Deng Z, Korma SA, et al. (2023). Anticancer potential of flaxseed lignans, their metabolites and synthetic counterparts in relation to molecular targets. Food & Function. https://pubmed.ncbi.nlm.nih.gov/36820797/
- Power KA, et al. (2006). Mammalian lignans enterolactone and enterodiol, alone and with genistein, do not promote the growth of MCF-7 xenografts in ovariectomised athymic nude mice. International Journal of Cancer. https://pubmed.ncbi.nlm.nih.gov/16152607/
- Zeleniuch-Jacquotte A, et al. (2004). Circulating enterolactone and risk of breast cancer: a prospective study in New York. British Journal of Cancer. https://pubmed.ncbi.nlm.nih.gov/15226762/
- Liu Z, et al. (2021). Lignan intake and enterolactone concentration and prognosis of breast cancer: a systematic review and meta-analysis. Journal of Cancer. https://pubmed.ncbi.nlm.nih.gov/33854638/
