Chrysin

Chrysin at a Glance

Chrysin is a flavone from honey, propolis and passionflower, sold as a natural aromatase inhibitor and testosterone booster.

It is a genuinely potent aromatase inhibitor — in a test tube. In people it does nothing of the kind: human trials show no effect on testosterone or estrogen, and the reason is pharmacokinetic. Chrysin is almost entirely conjugated in the gut wall and liver before it reaches circulation, so the concentrations that inhibit aromatase in vitro are never achieved in a body.

It is one of the cleanest examples here of a real mechanism defeated by bioavailability.

What It's Used For

Chrysin (5,7-dihydroxyflavone) is a flavone from honey, propolis and passionflower, best known as a bodybuilding supplement sold as a “natural aromatase inhibitor” or testosterone booster. That reputation has a real root and a decisive flaw. The root: chrysin is a genuinely potent aromatase (CYP19) inhibitor in the test tube, among the more potent dietary flavones tested ^{3Reference 3Kao YC et al. · 1998Molecular basis of the inhibition of human aromatase (estrogen synthetase) by flavone and isoflavone phytoestrogensView study →}.

The flaw: in humans it does nothing to hormones, because oral chrysin is almost entirely destroyed by first-pass conjugation before it reaches the bloodstream — its oral bioavailability is under ~1% ^{1Reference 1Walle T et al. · 2001Disposition and metabolism of the flavonoid chrysin in normal volunteersView study →}, and a controlled trial found no change in testosterone ^{2Reference 2Gambelunghe C et al. · 2003Effects of chrysin on urinary testosterone levels in human malesView study →}.

Its other, better-founded pharmacology is preclinical and CNS-flavored: chrysin binds the GABA-A benzodiazepine site and is anxiolytic in rodents ^{4Reference 4Wolfman C et al. · 1994Possible anxiolytic effects of chrysin, a central benzodiazepine-receptor ligand isolated from Passiflora coeruleaView study →}, the mechanistic backbone of passionflower’s traditional sedative use.

Evidence by IndicationStrength of support · Beta

Support is an experimental score — weighted by study type (human > animal > in vitro) and volume. A beta, not a validated metric. The marquee supplement claim scores low because it is human-negative; the preclinical uses score low because they are animal-only. Each application links to its write-up.

01Anxiolytic / CNSShaky34%Rodent GABA-A behavioral pharmacology ^{4,5,6Reference 4Wolfman C et al. · 1994Possible anxiolytic effects of chrysin, a central benzodiazepine-receptor ligand isolated from Passiflora coeruleaView study →Reference 5Brown E et al. · 2007AnimalEvaluation of the anxiolytic effects of chrysin, a Passiflora incarnata extract, in the laboratory ratView study →Reference 6Filho CB et al. · 2015Chronic unpredictable mild stress decreases BDNF and NGF levels and the antidepressant-like effect of chrysinView study →}

02Anti-inflammatory / antioxidantShaky30%Rodent Nrf2/NF-κB models ^{9,10Reference 9Yao Y et al. · 2014AnimalChrysin protects against focal cerebral ischemia/reperfusion injury in mice through the Nrf2 pathwayView study →Reference 10Mani R · 2018Chrysin: sources, beneficial pharmacological activities and molecular mechanism of actionView study →}

03AnticancerShaky24%Cell-line / xenograft, review-level ^{8,12Reference 8Kasala ER et al. · 2015Chemopreventive and therapeutic potential of chrysin in cancer: mechanistic perspectivesView study →Reference 12Liu YL et al. · 1992Isolation of potential cancer chemopreventive agents from Eriodictyon californicumView study →}

04Aromatase / “testosterone booster”Shaky15%Potent in vitro ^{3Reference 3Kao YC et al. · 1998Molecular basis of the inhibition of human aromatase (estrogen synthetase) by flavone and isoflavone phytoestrogensView study →} but human-null ^{2Reference 2Gambelunghe C et al. · 2003Effects of chrysin on urinary testosterone levels in human malesView study →}

05MetabolicShaky14%Rodent diabetes models only ^{10,11Reference 10Mani R · 2018Chrysin: sources, beneficial pharmacological activities and molecular mechanism of actionView study →Reference 11Naz S et al. · 2019Chrysin: pharmacological and therapeutic propertiesView study →}

Mechanisms

Pharmacokinetics

This is the load-bearing caveat and the reason the aromatase claim collapses in humans. In the definitive human study, volunteers took a single 400 mg oral dose: peak plasma parent chrysin was only 3–16 ng/mL, chrysin sulfate ran ~30× higher, and most of the dose was recovered unabsorbed in the faeces — an estimated oral bioavailability of ~0.003–1% ^{1Reference 1Walle T et al. · 2001Disposition and metabolism of the flavonoid chrysin in normal volunteersView study →}. The cause is extensive first-pass glucuronidation and sulfation in both gut wall and liver, plus efflux of conjugates back into the intestine ^{1,10Reference 1Walle T et al. · 2001Disposition and metabolism of the flavonoid chrysin in normal volunteersView study →Reference 10Mani R · 2018Chrysin: sources, beneficial pharmacological activities and molecular mechanism of actionView study →}. The consequence: the potent in-vitro aromatase inhibition is pharmacologically inaccessible by oral dosing, because systemic parent-drug exposure sits far below any concentration active on CYP19 or GABA-A. Marketed products often add piperine to try to overcome this, but no human efficacy data exist for those combinations.

Clinical trials

Human data are thin and negative for the headline claim: a 21-day study of chrysin-containing propolis/honey found no change in urinary testosterone in men ^{2Reference 2Gambelunghe C et al. · 2003Effects of chrysin on urinary testosterone levels in human malesView study →}, and the only other human study is the pharmacokinetic disposition trial documenting near-absent bioavailability ^{1Reference 1Walle T et al. · 2001Disposition and metabolism of the flavonoid chrysin in normal volunteersView study →}. There are no RCTs for anxiety, inflammation, cancer or metabolic endpoints — all therapeutic evidence is preclinical.

Last checked: July 2026.

Toxicity & Safety

Chrysin has low apparent oral toxicity: single or short-term oral doses (up to 400 mg, and customary propolis/honey regimens) were tolerated without reported adverse events ^{1,2Reference 1Walle T et al. · 2001Disposition and metabolism of the flavonoid chrysin in normal volunteersView study →Reference 2Gambelunghe C et al. · 2003Effects of chrysin on urinary testosterone levels in human malesView study →}, and its own poor absorption limits systemic exposure and therefore systemic toxicity. The more substantive concern is a drug-interaction signal: chrysin strongly modulates conjugation enzymes, competing at UGT (glucuronidation) and SULT (sulfation) pathways and inducing intestinal UGT1A1 in vitro ^{1,10Reference 1Walle T et al. · 2001Disposition and metabolism of the flavonoid chrysin in normal volunteersView study →Reference 10Mani R · 2018Chrysin: sources, beneficial pharmacological activities and molecular mechanism of actionView study →}. That makes interactions with drugs cleared by glucuronidation or sulfation — acetaminophen, raloxifene, irinotecan/SN-38, thyroid hormone, some estrogens — mechanistically plausible, though none are clinically documented, so this is a caution rather than a proven event.

Dosage

Nothing here is a recommendation. Marketed supplement doses are commonly 500–3000 mg/day, frequently in “estrogen-blocker” stacks and often combined with piperine to try to overcome the bioavailability problem — but these doses are not supported by human efficacy data, and higher oral doses do not fix the first-pass conjugation ceiling. For research context, the human pharmacokinetic study used a single 400 mg oral dose ^{1Reference 1Walle T et al. · 2001Disposition and metabolism of the flavonoid chrysin in normal volunteersView study →} and the null hormone study delivered chrysin as propolis/honey at customary intakes ^{2Reference 2Gambelunghe C et al. · 2003Effects of chrysin on urinary testosterone levels in human malesView study →}.

References

1. Walle T, Otake Y, Brubaker JA, Walle UK, Halushka PV (2001). Disposition and metabolism of the flavonoid chrysin in normal volunteers. British Journal of Clinical Pharmacology. https://pubmed.ncbi.nlm.nih.gov/11259985/
2. Gambelunghe C, et al. (2003). Effects of chrysin on urinary testosterone levels in human males. Journal of Medicinal Food. https://pubmed.ncbi.nlm.nih.gov/14977449/
3. Kao YC, Zhou C, Sherman M, Laughton CA, Chen S (1998). Molecular basis of the inhibition of human aromatase (estrogen synthetase) by flavone and isoflavone phytoestrogens. Environmental Health Perspectives. https://pubmed.ncbi.nlm.nih.gov/9435150/
4. Wolfman C, Viola H, Paladini A, Dajas F, Medina JH (1994). Possible anxiolytic effects of chrysin, a central benzodiazepine-receptor ligand isolated from Passiflora coerulea. Pharmacology, Biochemistry and Behavior. https://pubmed.ncbi.nlm.nih.gov/7906886/
5. Brown E, et al. (2007). Evaluation of the anxiolytic effects of chrysin, a Passiflora incarnata extract, in the laboratory rat. AANA Journal. https://pubmed.ncbi.nlm.nih.gov/17966676/
6. Filho CB, et al. (2015). Chronic unpredictable mild stress decreases BDNF and NGF levels and the antidepressant-like effect of chrysin. Neuroscience. https://pubmed.ncbi.nlm.nih.gov/25592430/
7. Zanoli P, Avallone R, Baraldi M (2000). Behavioural characterisation of the flavonoids apigenin and chrysin. Fitoterapia. https://pubmed.ncbi.nlm.nih.gov/10930722/
8. Kasala ER, et al. (2015). Chemopreventive and therapeutic potential of chrysin in cancer: mechanistic perspectives. Toxicology Letters. https://pubmed.ncbi.nlm.nih.gov/25596314/
9. Yao Y, et al. (2014). Chrysin protects against focal cerebral ischemia/reperfusion injury in mice through the Nrf2 pathway. International Journal of Molecular Sciences. https://pubmed.ncbi.nlm.nih.gov/25402649/
10. Mani R, Natesan V (2018). Chrysin: sources, beneficial pharmacological activities and molecular mechanism of action. Phytochemistry. https://pubmed.ncbi.nlm.nih.gov/29161583/
11. Naz S, et al. (2019). Chrysin: pharmacological and therapeutic properties. Life Sciences. https://pubmed.ncbi.nlm.nih.gov/31472146/
12. Liu YL, et al. (1992). Isolation of potential cancer chemopreventive agents from Eriodictyon californicum. Journal of Natural Products. https://pubmed.ncbi.nlm.nih.gov/1593282/

View all 12 references▾