Foods/Supplements-Vitamins: Chrysin

Prompted by a new study [4].

Chrysin is a natural polyphenol - a flavone.

It is an aromatase inhbitor & can therefore reduce the conversion of testosterone to estradiol. Although Wikipedia [1] cites studies that found it to be ineffective, I can vouch for it, when taken with Bioperine (piperine). I used it successfully for several years before obtaining an Arimidex prescription. It kept my estradiol in the 12-20 pg/mL range.

[2] (2007 - China)

"Chrysin is a natural flavonoid and has been shown recently to have anticancer effects. However, the mechanisms that chrysin inhibits cancers are not well known. In this study, we investigated the effects of chrysin on expression of hypoxia-inducible factor-1alpha (HIF-1alpha) and vascular endothelial growth factor in human prostate cancer DU145 cells. Chrysin inhibited insulin-induced expression of HIF-1alpha by reducing its stability. Chrysin increases ubiquitination and degradation of HIF-1alpha by increasing its prolyl hydroxylation. In addition, chrysin interfered with interaction between HIF-1alpha and heat shock protein 90. Chrysin was also found to inhibit HIF-1alpha expression through AKT signaling. Inhibition of HIF-1alpha by chrysin resulted in abrogation of vascular endothelial growth factor expression. Finally, we showed that chrysin inhibited DU145 xenograft-induced angiogenesis in nude mice."

[3] (2016 - Korea)

"Docetaxel (DTX) is an effective commercial anticancer agent for chemotherapy in non-small cell lung cancer (NSCLC), breast cancer, gastric cancer, and prostate cancer, but its adverse effects including edema, neurotoxicity, and hair loss limit its application. To improve the chemotherapeutic efficacy of DTX and reduce adverse effects, combination therapy is one of the alternative methods. So chrysin, which has various biological activities including anticancer effects, was considered. In vitro, the combination of chrysin and DTX was investigated in A549 cells. Increased cytotoxicity, suppressed cellular proliferation, and induced apoptosis were observed with posttreatment of chrysin following DTX treatment. In vivo, chrysin enhanced the tumor growth delay of DTX and increased DTX-induced apoptosis in the A549-derived xenograft model. Furthermore, chrysin prevented DTX-induced edema in ICR mouse. These results indicated that chrysin strengthened the therapeutic efficacy of DTX and diminished the adverse effect of DTX ..."

[4] (2017 - Korea)

"Chrysin is a natural flavone found in numerous plant extracts, honey and propolis that has multiple biological activities including anti-cancer effects. Understanding of biological mechanisms mediated in response to chrysin in cancerous cells may provide novel insight into chemotherapeutic approaches with reduced side effects in cancers. In the present study, we investigated functional roles of chrysin in progression of prostate cancer cells using DU145 and PC-3 cell lines. The results showed that chrysin induced apoptosis of cells evidenced by DNA fragmentation and increasing the population of both DU145 and PC-3 cells in the sub-G1 phase of the cell cycle. In addition, chrysin reduced expression of proliferating cell nuclear antigen in the prostate cancer cell lines compared to untreated prostate cancer cells. Moreover, chrysin induced loss of mitochondria membrane potential (MMP), while increasing production of reactive oxygen species (ROS) and lipid peroxidation in a dose-dependent manner."






8 Replies

  • Any opinions on raloxifine, a SERM? Do you watch estrogen levels?

  • Martin,

    I am familiar with SERMs, but not with raloxifene, in terms of PCa.

    (For others reading, a SERM is a synthetic estrogen that might be an estrogen receptor agonist for bone, say, bute an ER antagonist in breast tissue.)

    Seems to have limited activity in PCa [1], although [2] is interesting.

    It does seem to improve osteoporosis in men on ADT - but why not use low-dose estradiol?




  • Interested in it only because of this....

  • Martin,

    A good find! He says much that I agree with. Too many experts ignore ER.


  • A study of raloxifene in conjunction with casodex, but this was in 2015, and dont see any follow up since then. So. ....

    The doctor is Erik P Castle.

  • Well, the first paper I cited was published last year:


  • about 60% of the way through the talk

  • Patrick--I used it for years, before Prostate Cancer. I stopped it in favor of a very much stronger 5-alpha reductase molecule---DIM--which we have communicated on. Try BioResponse .com--and ask them to sent their book on Dim--much has to do with reduction of estradiol, especially those on T therapy.


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