Taking Chrysin to lower estrogen

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    Taking Chrysin to lower estrogen


    I was wondering if anyone has used Chrysin to help lower estrogen levels. I picked up some Chrysin 750 and am starting to use with my test booster - bulbine product. I read elsewhere it does help , just wanting others opinions.

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    There's much better things out there to lower estrogen than Chrysin.

    Quote Originally Posted by Schwaugher View Post
    Chrysin:

    Is It An Effective Aromatase Inhibitor?
    Ward Dean, MD

    A question that Ive been asked on a number of occasions is: Why doesnt VRP carry Chrysin?

    Chrysin is a flavonoid that has been purported especially in the bodybuilding world to be an effective inhibitor of an enzyme known as aromatase. Aromatase is the enzyme that causes the conversion of testosterone into estradiol and androstenedione into estrone. This would have a definite theoretical advantage to bodybuilders especially those who are taking high doses of potent anabolic steroids.

    However, if true, it would have significant advantages for many outside the bodybuilding community, as well.

    Aromatase levels are known to rise with age.1 This increase often causes a relative imbalance of estrogen and testosterone in men as they grow older. In addition to having a decreased output of testosterone with age , the age-related increase of aromatase causes older men to convert what testosterone they do produce into estrogen. This is not a desirable phenomenon for aging men, and explains part of the interest in finding an effective inhibitor of aromatase.


    Thus, its not just an interest in maintaining strength, energy, muscle mass and libido in older men that generates the interest in aromatase inhibition. In addition, bodybuilders, postmenopausal women with estrogen-receptor positive breast cancer, men suffering from Benign Prostatic Hypertrophy (BPH), and older men undergoing testosterone replacement therapy can all benefit from decreased conversion of androstenedione and testosterone to estrogen.

    The idea that chrysin might be an effective natural aromatase inhibitor originated by a combination of science and unsubstantiated hype.

    Chrysin, Flavonoids and Aromatase Inhibition

    Flavones, or flavonoids, are a large group of compounds found throughout the plant kingdom and in many foods. Theyve been used as drugs and food supplements and are reported to have antioxidant, antibacterial, anti-inflammatory and antiviral properties. 2,3

    The flavonoid that has created the greatest publicity is chrysin (5,7-dihydroxyflavone). There are a number of in vitro studies which support chrysins aromatase inhibitory activity. In 1984, researchers found that chrysin had significant aromatase-inhibitory activity when tested with placental microsomes.4,5 A flurry of studies followed.6-11

    Campbell and Kurzer, in their 1993 study with preadipocytes (a fancy term for young fat cells), found that chrysins anti-estrogen activity was reduced 10-fold (compared with the placental microsome model) presumably, because the chrysin could not effectively enter the cells. Thus, these researchers discovered the the cell membraine was the first barrier to the ability of chrysin to work in an animal system.7 Other in vitro studies with chrysin indicate that intestinal absorption is also poor.12

    However, we are unable to determine from the above studies whether these same effects take place in vivo (inside us) or what the proper dosages would be to get an inhibitory effect on aromatase. If we could extrapolate from the in vitro studies, it appears that wed need several grams of chrysin to have any effect at all (if it worked). However, it is not always possible to make direct in vitro (laboratory Petri dish) to in vivo (in the body) applications.

    The obvious question regarding chrysins effectiveness is: Can chrysin reduce estrogen in animals and humans? A group of researchers administered chrysin to mice both orally and via injection to see if chrysin effectively reduced serum estrogen levels. They had 10 mice in four groups: one receiving nothing, one took chrysin orally at 5 mg/kg, one received an intraperitoneal injection with the vehicle solution only, and one received chrysin at 5 mg/kg in the vehicle solution via an intraperitoneal injection. After 30 days, blood samples were drawn. Serum estrogen levels were determined by radioimmunoassay. The scientists found that estrogen levels were unchanged in any of the groups.13

    Another discouraging finding from this study was that chrysin-treated rats were considerably fatter than the controls. This may be due to chrysins known ability to disrupt thyroid function by blocking the conversion of T4 to T3 (a key step in thyroid hormone metabolism). This is due to chrysins inhibition of the enzyme deiodinase.14

    Further evidence of chrysins lack of effectiveness in inhibiting aromatase is found in an article in JAMA several years ago.15 Researchers tested an androstenedione product, fortified with chrysin, to determine if chrysin would prevent estradiol levels from increasing. It didnt.

    Another study to evaluate the aromatase-inhibiting ability of chrysin was conducted by scientists at the Institute of Biomedicine in Turku, Finland.16 The scientists administered chrysin to rats at a dose of 50 mg/kg body weight, which is considerably more than is found in human diets or dietary supplements (thats about 3.5 grams, human equivalent). The scientists found that chrysin had no ability to inhibit aromatase in these intact animals, hypothesizing that the lack of in vivo efficacy was due to poor aborption or bioavailablity.

    It appears clear that chrysin may be an effective aromatase inhibitor for cells in a Petri dish but not in humans. While there are several very effective (and very expensive) aromatase inhibiting drugs (i.e., Arimidex (anastrozole), Femara (letrozole), and Aromasin (exemestane), for the time being, it appears that there are no effective aromatase-inhibiting natural substances of which I am aware.

    What To Do About Excess Estrogen Naturally?
    Estrogen (estradiol) is metabolized by the body via one of two pathways. One pathway 16 alpha-hydroxylation is known as the tumor enhancer metabolic pathway. This is the predominant pathway in patients with breast and endometrial cancer, and in those at increased risk for such cancers. 16 alpha-hydroxylation activity precedes clinical evidence of cancer, and is a significant risk factor for estrogen-dependent tumors.17 16-alpha hydroxylation is nearly five times higher in patients with breast cancer than patients who dont have cancer.18

    The other pathway is called the tumor suppressor pathway. This process transforms estrogen into 2-hydroxyestrone (20HEI), an antiestrogen. When estrogen takes the 2-hydroxylation pathway, the incidence of cancer decreases. Healthy individuals not at risk for breast or endometrial cancer bypass the 16-alpha route and metabolize estrogen through the 2-hydroxyestrone pathway.

    Scientists found that Indole-3-Carbinol (I3C) causes the body to metabolize estrogen via the 2-hydroxylation pathway. By funneling estrogen into this tumor suppressor pathway, I3C stimulates the rate at which the body expels estrogen, essentially vacuuming away the estrogen. These scientists found that 400 mg of I3C given daily resulted in a 50 percent increase of 2-hydroxylation.19,20 I3C (Indole-3-Carbinol) appears to be an effective weapon against breast, cervical and skin cancer, respiratory papillomas and other estrogen-related conditions. An alternative to I3C, with similar effects, is the I3C metabolite, diindolylmethane (BioDIM).

    Conclusion
    Unfortunately, there does not appear to be any effective natural inhibitor of aromatase. Those who require the specific benefits of aromatase inhibition (for now, at least) must rely on the safe but expensive prescription aromatase inhibitors. Nevertheless, some of the benefits of aromatase inhibition may be gained by enhancing the metabolism and excretion of estrogen by using I3C or BioDIM.

    References
    1. Cohen, P.G. Aromatase, adiposity, aging and disease. The hypogonadal-metabolic-atherogenic-disease and aging connection. Medical Hypotheses, 2001, 56(6): 702-708.

    2. Formica, J.V. and Regelson, W. Review of the biology of Quercetin and related bioflavonoids. Food Chem Toxicol, 1995. 33(12): 1061-1080.

    3. Kuhnau, J. The flavonoids. A class of semi-essential food components: their role in human nutrition. World Rev Nutr Diet, 1976. 24: 117-191.

    4. Kellis, JT and Vickery, LE: Inhibition of Human Estrogen Synthetase (Aromatase) by Flavones. Science, 1984, 225: 1032-34.

    5. Kellis, J.T., Jr., Nesnow, S. and Vickery, L.E. Inhibition of aromatase cytochrome P-450 (estrogen synthetase) by derivatives of alpha-naphthoflavone. Biochem Pharmacol, 1986, 35(17): 2887-2891.

    6. Ibrahim, A.R. and Abul-Hajj, Y.J. Aromatase inhibition by flavonoids. J Steroid Biochem Mol Biol, 1990. 37(2): 257-260.

    7. Campbell, DR and Kurzer, MS: Flavonoid Inhibition of Aromatase Enzyme Activity in Human Preadipocytes. J Steroid Biochemistry and Molecular Biology, 1993, 46: 381-388.

    8. Wang, C. Lignans and flavonoids inhibit aromatase enzyme in human preadipocytes. J Steroid Biochem Mol Biol, 1994, 50(3-4): 205-12.

    9. Pelissero, C. Effects of flavonoids on aromatase activity, an in vitro study. J Steroid Biochem Mol Biol, 1996, 57(3-4): 215-223.

    10. Le Bail, J.C. Aromatase and 17 beta-hydroxysteroid dehydrogenase inhibition by flavonoids, Cancer Letters, 1998, 133: 101-106.

    11. Jeong, H.J. Inhibition of aromatase activity by flavonoids. Arch Pharm Res, 1999, 22(3): 309-312.

    12. Walle, U.K., A. Galijatovic, and T. Walle, Transport of the flavonoid chrysin and its conjugated metabolites by the human intestinal cell line Caco-2. Biochem Pharmacol, 1999, 58(3): 431-438.

    13. Shibayama, J. The Oral Bioavailability and In Vivo Activity of Chrysin in Exercising and Non-Exercising Mice. Submitted for publication.

    14. Koehrle, J. Iodothyronine deiodinase is inhibited by plant flavonoids, Prog Clin Biol Res 1986, 213: 359-371

    15. King, D.S. Effect of oral androstenedione on serum testosterone and adaptations to resistance training in young men: a randomized controlled trial [see comments]. JAMA, 1999, 281(21): 2020-2028.

    16. Saarinen, N., Joshi, S.C., Ahotupa, M., Li, X., et al. No evidence for the invivo activity of armatase-inhibiting flavonoids. J Steroid Biochem Mol Biol, 2001, 78 (3): 231-9.

    17. Fishman J., Schneider J., Hershcope RJ., Bradlow HL. Increased estrogen 16-alpha-hydroxylase activity in women with breast and endometrial cancer. J Steroid Biochem. 1984; 20(4B): 1077-1081.

    18. Osborne MP, Bradlow HL, Wong GY, Telang NT. Upregulation of estradiol C16 alpha-hydroxylation in human breast tissue: a potential biomarker of breast cancer risk. J National Cancer Inst. 1993; 85(23): 1917-1920.

    19. Michnoviez JJ, Bradlow HL. Induction of estradiol metabolism by dietary indole-3-carbinol in humans. J Natl Cancer Inst, 1990; 82(11): 947-949.

    20. Michnoviez JJ, Bradlow HL. Altered estrogen metabolism and excretion in humans following consumption of indole-3-carbinol. Nutr Cancer, 1991;16 (1): 59-66.

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