Summary of Chrysin
Primary Information, Benefits, Effects, and Important Facts
Chrysin is a bioflavonoid compound found in high levels in propolis and in honey.
Chrysin is most well known for being a testosterone boosting plant compound, although this seems to be a misleading claim. While it has very good mechanisms of action that would lead to the conclusion that it could boost testosterone (as in, it sensitizes the testicles to produce more testosterone and inhibits the conversion of testosterone to estrogen) these both occur at significantly higher oral doses than are seen with oral supplementation. Chrysin appears to be poorly absorbed, and even then it is readily metabolized resulting in insufficient levels in the blood and testes to exert these beneficial effects.
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Things To Know & Note
Is a Form Of
Also Known As
Propolis, Honey extract, Passiflora caerulea Linn
Goes Well With
COX2 inhibitors (for the purposes of StAR upregulation)
StAR inducers like D-Aspartic Acid (as it potentiates the effects of cAMP induction)
Caution NoticeExamine.com Medical Disclaimer
How to Take Chrysin
Recommended dosage, active amounts, other details
Due to the poor bioavailability, the standard supplemental doses of chrysin (400-3,000mg) appear to be pretty much ineffective. Although enhancing absorption can theoretically aid in chryin's effects, this has not yet been demonstrated and thus supplementation of chrysin cannot be recommended for systemic purposes.
A supplemental dose of 400mg chrysin should be sufficient for intestinal related issues.
Human Effect Matrix
The Human Effect Matrix looks at human studies (it excludes animal and in vitro studies) to tell you what effects chrysin has on your body, and how strong these effects are.
|Grade||Level of Evidence [show legend]|
|Robust research conducted with repeated double-blind clinical trials|
|Multiple studies where at least two are double-blind and placebo controlled|
|Single double-blind study or multiple cohort studies|
|Uncontrolled or observational studies only|
Level of Evidence
? The amount of high quality evidence. The more evidence, the more we can trust the results.
Magnitude of effect
? The direction and size of the supplement's impact on each outcome. Some supplements can have an increasing effect, others have a decreasing effect, and others have no effect.
Consistency of research results
? Scientific research does not always agree. HIGH or VERY HIGH means that most of the scientific research agrees.
|-||- See study|
Scientific Research on Chrysin
Click on any below to expand the corresponding section. Click on to collapse it.
Like most bioflavonoids, chrysin suffers from poor bioavailability in isolated form which limits their practical usage. This poor bioavailability measured at less than 1% seems to be due to both extensive metabolism (sulphation and glucuronidation accounting for about 99% of orally ingested chrysin) and subpar intestinal transportation, as although chrysin is transported across the intestines an oral dose of 400mg results in less than 1% free chrysin (unconjugated) in the urine but only 1-7% of the total chrysin dose even when conjugates are included; most is left unabsorbed.
Chrysin can be absorbed, but it is poorly absorbed. Beyond that, chrysin is also very readily conjugated by the liver and other organs containing the P450 system into its metabolites (chrysin glucuronide and chrysin sulphate) which may not be bioactive. Less than 1% of chrysin is absorbed
One study found Chrysin to induce UGT1A1 expression in intestinal cells (Caco-2), which increases glucuronidation rates. When tested in vivo, the side-effects of a pro-drug associated with insufficient glucuronidation were reduced, contributing some validity to the results seen in vitro.
To add insult to injury, chrysin upregulates the enzyme that mediates its own conjugation
The Cmax values from an oral dose of 400mg Chrysin was 3-16ng/mL while the AUC was 5-193 ng/mL/h. The Cmax was reached (Tmax) about 1 hour after ingestion, fell rapidly at 6 hours, and returned to baseline 48 hours after ingestion. The half-life for the first 12 hours was 4.6 hours.
Chrysin (free form) can be detected in the plasma in the 3-16ng/mL range
After oral ingestion of 400mg Chrysin, plasma levels of Chrysin sulphate appear to be 30-fold higher than plasma levels of bioactive Chrysin. Glucuronide conjugates appear to be present in plasma at undetectable levels, and together conjugates consist of 99% of total oral chrysin. In rats, glucuronide conjugates are 10-fold higher but this is likely due to species differences.
The majority of serum chrysin is conjugated, with the predominant conjugate being chrysin sulphate
When tested in vivo and vitro, there does not appear to be any evidence of oxidative metabolism of Chrysin. Oxidative metabolism is known as Phase I of drug metabolism, and structurally modifies drugs for better conjugation in Phase II, but chrysin seems to directly and readily get conjugated by Phase II.
There is no apparent Phase I oxidative metabolism of chrysin
Chrysin is fairly potent in inhibiting aromatase in vitro with a Ki of 2.6+/-0.1µM and an IC50 of 4.2μM, comparable efficacy to apigenin and hesperidin as hydroxylated flavonoids seem to be among the flavonoid structures with most efficacy in inhibiting this enzyme (more than methoxylated).
This aromatase inhibiting property likely does not apply to humans following oral ingestion of chrysin due to its poor absorption, as the 4.2μM IC50 value (also reported to be 1.1µg/mL) is about 69 times greater than the 16ng/mL concentration reported from ingestion of 400mg chrysin.
In vitro, chrysin appears to be quite a potent aromatase inhibitor similar to other lightly hydroxylated flavonoids. This likely does not apply to standard chrysin supplementation due to very poor absorption
Chrysin appears to be able to inhibit a protein known as DAX-1, which is a negative regulator of the StAR protein (rate limit in testosterone synthesis) resulting in an upregulation of StAR and testosterone synthesis (also can be seen as a 'sensitization' of the testes to stimulated testosterone production); the suppression of COX2 from chrysin may also play a role, as COX2 is known to be a negative regulator of StAR. This effect was only seen at concentrations of 5µM or higher, which is over 70-fold higher than the detectable serum concentrations from 400mg oral chrysin ingestion.
Similar to D-Aspartic Acid, Chrysin's molecular target appears to be the StAR protein. However, rather than directly stimulating this protein's actions chrysin reduces the influence of negative regulators and causes an indirect increase in StAR activity
In rats, an increase in testosterone of approximately 30% has been noted with oral intake of 50mg/kg bodyweight for 60 days, which is a human estimated dose of 8mg/kg bodyweight.
There are a variety of studies investigating testosterone production of which include chrysin, but are too highly confounded with other active agents (such as Dehydroepiandrosterone) to attribute benefits to the chrysin being used at 300-625mg. One study with of propolis and eucalyptus honey (1,280mg and 20g, respectively) conferring 69.12mg flavonoids and 20mg chrysin failed to significantly influence testosterone levels in otherwise healthy men.
Although there was once rat study showing that supplementation of chrysin could increase testosterone, this does not appear to occur in humans based on the limited testing available
Chrysin appears to be an modifier of P-glycoprotein efflux pumps and reduce their activity; this can act synergistically with compounds that are subject to P-gp efflux, such as the anti-cancer drug epirubicin. It shows potential at alleviating multi-drug resistance and exhibits anti-proliferative properties in isolation and in conjunction with other compounds.
- Dhawan K, Kumar S, Sharma A. Beneficial effects of chrysin and benzoflavone on virility in 2-year-old male rats. J Med Food. (2002)
- Ko WC, et al. Inhibitory effects of flavonoids on phosphodiesterase isozymes from guinea pig and their structure-activity relationships. Biochem Pharmacol. (2004)
- Saarinen N, et al. No evidence for the in vivo activity of aromatase-inhibiting flavonoids. J Steroid Biochem Mol Biol. (2001)
- Walle T, et al. Disposition and metabolism of the flavonoid chrysin in normal volunteers. Br J Clin Pharmacol. (2001)
- Galijatovic A, et al. Extensive metabolism of the flavonoid chrysin by human Caco-2 and Hep G2 cells. Xenobiotica. (1999)
- Walle UK, Galijatovic A, Walle T. Transport of the flavonoid chrysin and its conjugated metabolites by the human intestinal cell line Caco-2. Biochem Pharmacol. (1999)
- Tobin PJ, et al. A pilot study on the safety of combining chrysin, a non-absorbable inducer of UGT1A1, and irinotecan (CPT-11) to treat metastatic colorectal cancer. Cancer Chemother Pharmacol. (2006)
- Kao YC, et al. Molecular basis of the inhibition of human aromatase (estrogen synthetase) by flavone and isoflavone phytoestrogens: A site-directed mutagenesis study. Environ Health Perspect. (1998)
- Aromatase inhibition by bioavailable methylated flavones.
- Sanderson JT, et al. Induction and inhibition of aromatase (CYP19) activity by natural and synthetic flavonoid compounds in H295R human adrenocortical carcinoma cells. Toxicol Sci. (2004)
- Jeong HJ, et al. Inhibition of aromatase activity by flavonoids. Arch Pharm Res. (1999)
- Preoperative Oral Passiflora Incarnata Reduces Anxiety in Ambulatory Surgery Patients: A Double-Blind, Placebo-Controlled Study.
- Role of chrysin in the sedative effects of Passiflora incarnata L.
- Stocco DM. StAR protein and the regulation of steroid hormone biosynthesis. Annu Rev Physiol. (2001)
- Jana K, et al. Chrysin, a natural flavonoid enhances steroidogenesis and steroidogenic acute regulatory protein gene expression in mouse Leydig cells. J Endocrinol. (2008)
- Wang X, et al. Cyclooxygenase-2 regulation of the age-related decline in testosterone biosynthesis. Endocrinology. (2005)
- Ciftci O, et al. Beneficial effects of chrysin on the reproductive system of adult male rats. Andrologia. (2012)
- Kohut ML, et al. Ingestion of a dietary supplement containing dehydroepiandrosterone (DHEA) and androstenedione has minimal effect on immune function in middle-aged men. J Am Coll Nutr. (2003)
- Brown GA, et al. Effects of androstenedione-herbal supplementation on serum sex hormone concentrations in 30- to 59-year-old men. Int J Vitam Nutr Res. (2001)
- Brown GA, et al. Endocrine and lipid responses to chronic androstenediol-herbal supplementation in 30 to 58 year old men. J Am Coll Nutr. (2001)
- Brown GA, et al. Effects of anabolic precursors on serum testosterone concentrations and adaptations to resistance training in young men. Int J Sport Nutr Exerc Metab. (2000)
- Gambelunghe C, et al. Effects of chrysin on urinary testosterone levels in human males. J Med Food. (2003)
- Gyémánt N, et al. In vitro search for synergy between flavonoids and epirubicin on multidrug-resistant cancer cells. In Vivo. (2005)
- Sawicka D, et al. The anticancer activity of propolis. Folia Histochem Cytobiol. (2012)