chrysin, for anti- estrogen

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    chrysin, for anti- estrogen


    does anyone have solid evidence or personal encounters that this (chrysin) will actually help limit the estrogen and estrodial conversion in your body due to aromatazation?

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    I found this


    Chrysin:

    Is It An Effective Aromatase Inhibitor?
    Ward Dean, MD

    A question that Iïve 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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    nice post bro, thanks a bunch
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    Quote Originally Posted by lilman
    nice post bro, thanks a bunch
    No prob, just tryin to help a bro out.
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    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.

    This would seem to indicate that Indole-3-carbonal could be used as part of a PCT regime.....but it's not listed in many of the popular PCT regimes touted on the boards. Any thoughts as to why?
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    Prob because people usually run a serm and AI for PCT.

    For me, Im using 200mg of BioDim for pct, might up it to 300-400 when I taper nolva down. Stuff is expensive.
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    Quote Originally Posted by yeahright
    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.

    This would seem to indicate that Indole-3-carbonal could be used as part of a POCT regime.....but it's not listed in many of the popular PCT regimes touted on the boards. Any thoughts as to why?
    It is good stuff. But pricey, i think.
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    Quote Originally Posted by Robboe
    It is good stuff. But pricey, i think.
    Yeah, but it seems a superior way to deal with excess estrogen. SERMS just block the estrogen from acting on tissues....ATDs can causes too broad of systemic estrogen binding, the drugs that stop estrogen production seem pretty harsh. Here, we have a chemical which appears to tell the body to expel the excess estrogen through a "tumor suppressing" pathway. I'm not a biochemist but this seems much more elegant than currently used methods.
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    How effective it is though, is another question.

    have you done many pudmed runs on I3C?
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    Quote Originally Posted by Robboe
    How effective it is though, is another question.

    have you done many pudmed runs on I3C?
    Yes, unfortunately nobody is studying Ic3 for our purposes. There are studies of it as a chemopreventative agent and as an adjuct to chemotherapy (bottom line - mixed bag depending upon the type and location of the cancer). The study that was closest to addressing Ic3 usage fo rour purposes was this:

    Eur J Cancer Prev. 2002 Aug;11 Suppl 2:S86-93.
    Multiple molecular targets of indole-3-carbinol, a chemopreventive anti-estrogen in breast cancer.

    Ashok BT, Chen YG, Liu X, Garikapaty VP, Seplowitz R, Tschorn J, Roy K, Mittelman A, Tiwari RK.

    Department of Microbiology, Immunology and Medicine, New York Medical College, Valhalla, NY 10595, USA.

    The mechanism of action of the anti-estrogen indole-3-carbinol (I3C), present in cruciferous vegetables, is being examined in our laboratory with a view to promote the use of this naturally occurring chemopreventive as an alternative to synthetic anti-estrogens in human breast cancer. Our previous results clearly demonstrated that despite its low affinity for the estrogen receptor (ER), I3C abrogated estradiol-mediated cellular and biochemical effects in estradiol-responsive cells and tissues. In an earlier report, we identified ER phosphorylation as one of the targets of I3C, and in this communication we describe the consequence of inhibition of ER phosphorylation. Estradiol-induced DNA-binding proteins that bound to several DNA-responsive elements were inhibited by I3C and this effect was not at the level of DNA-protein physical interaction as inclusion of I3C in vitro in the reaction mix did not affect the binding. We analyzed the spectrum of genes induced by estradiol and modulated and/or intercepted by I3C. Our results conclude that although estradiol-mediated functions are affected by I3C, its biochemical targets are multiple and some of these may be modulated by the oligomeric products of I3C.

    PMID: 12570340 [PubMed - indexed for MEDLINE]
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    I3C, for anti- estrogen


    Here is another one. As I understand it, there are various types of estrogen....sme of which activate estrogen receptors more strongly than others. This article indicates that I3C causes the excretion of the "strong" estrogens leaving the "weaker"estrogens to take up the estrogen receptors where they cause less activity because they are "weaker."


    J Natl Cancer Inst. 1997 May 21;89(10):718-23.
    Changes in levels of urinary estrogen metabolites after oral indole-3-carbinol treatment in humans.

    Michnovicz JJ, Adlercreutz H, Bradlow HL.

    Rockefeller University Hospital and The Institute for Hormone Research, New York, NY 10016, USA.

    BACKGROUND: The oxidative metabolism of estrogens in humans is mediated primarily by cytochrome P450, many isoenzymes of which are inducible by dietary and pharmacologic agents. One major pathway, 2-hydroxylation, is induced by dietary indole-3-carbinol (I3C), which is present in cruciferous vegetables (e.g., cabbage and broccoli). PURPOSE: Because the pool of available estrogen substrates for all pathways is limited, we hypothesized that increased 2-hydroxylation of estrogens would lead to decreased activity in competing metabolic pathways. METHODS: Urine samples were collected from subjects before and after oral ingestion of I3C (6-7 mg/kg per day). In the first study, seven men received I3C for 1 week; in the second study, 10 women received I3C for 2 months. A profile of 13 estrogens was measured in each sample by gas chromatography-mass spectrometry. RESULTS: In both men and women, I3C significantly increased the urinary excretion of C-2 estrogens. The urinary concentrations of nearly all other estrogen metabolites, including levels of estradiol, estrone, estriol, and 16alpha-hydroxyestrone, were lower after I3C treatment. CONCLUSIONS: These findings support the hypothesis that I3C-induced estrogen 2-hydroxylation results in decreased concentrations of several metabolites known to activate the estrogen receptor. This effect may lower estrogenic stimulation in women. IMPLICATIONS: I3C may have chemopreventive activity against breast cancer in humans, although the long-term effects of higher catechol estrogen levels in women require further investigation.
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    I had a look into it before xmas, but i think the price put me off.

    The life extention folks love it apparently. They call it the natural SERM and alternative to tamoxifen.
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    Dr D had mentioned that Vitamin C has some natural AI properties. I took this to mean it was very weak otherwise we'd be hearing a lot more about it. I tried Ester C on a whim prior to my current cycle and I noted a increase in libido. I didn't really think much of it nor did I seriously attribute it to the Ester C.

    Well, my perception of it is changing now that I'm on a cycle of 4AD/19Nor/1 Test dermal. Last time I ran this stack I had puffy nipples and a lot of bloating. This resulted in the beginings of gyno which, forturnately, went away with aggressive Nolva and Ultra Hotter treatment during PCT.

    At 4-5 weeks into this cycle I am having very little nipple puffiness, no signs of gyno and less bloat than last cycle. The main difference is that I am taking 2-4 grams of Ester C per day along with the addition of 2 tablespoons of colloidal gold. I doubt that the CG is responsible for the AI-like effect.

    I am NOT saying that Ester C is a replacement for a proper AI, SERM or PCT protocol but I am encouraging people to give it a try during cycle and PCT just to see if I'm being crazy or not, lol. Can't hurt.

    Unfortunately, I have neither the time nor the money to get my E levels checked.
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    Quote Originally Posted by bioman
    Dr D had mentioned that Vitamin C has some natural AI properties. I took this to mean it was very weak otherwise we'd be hearing a lot more about it. I tried Ester C on a whim prior to my current cycle and I noted a increase in libido. I didn't really think much of it nor did I seriously attribute it to the Ester C.

    Well, my perception of it is changing now that I'm on a cycle of 4AD/19Nor/1 Test dermal. Last time I ran this stack I had puffy nipples and a lot of bloating. This resulted in the beginings of gyno which, forturnately, went away with aggressive Nolva and Ultra Hotter treatment during PCT.

    At 4-5 weeks into this cycle I am having very little nipple puffiness, no signs of gyno and less bloat than last cycle. The main difference is that I am taking 2-4 grams of Ester C per day along with the addition of 2 tablespoons of colloidal gold. I doubt that the CG is responsible for the AI-like effect.

    I am NOT saying that Ester C is a replacement for a proper AI, SERM or PCT protocol but I am encouraging people to give it a try during cycle and PCT just to see if I'm being crazy or not, lol. Can't hurt.

    Unfortunately, I have neither the time nor the money to get my E levels checked.
    Interesting.....yes I'm seeing these things as PART of a pct....certainly not a replacement for the tried and true but it would be delightful if we could compile a constellation of core and ancillary pct products that work together to be more effective.
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    Quote Originally Posted by Robboe
    I had a look into it before xmas, but i think the price put me off.

    The life extention folks love it apparently. They call it the natural SERM and alternative to tamoxifen.
    I bought a bottle from my local discount vitamin store (Solaray brand) for less than $10. It's 25 mg (30 capsules) per capusule so you'd need 8 capsules to get the 200 mg dose used in these studies but that's not too expensive in the big scheme of things....you'd think that some big supplement company could probably get it at a large discount. Drive the price down through economies of scale.
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    IIRC crysin has a POOR bioavailability
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    Quote Originally Posted by yeahright
    I bought a bottle from my local discount vitamin store (Solaray brand) for less than $10. It's 25 mg (90 capsules) per capusule so you'd need 8 capsules to get the 200 mg dose used in these studies but that's not too expensive in the big scheme of things....you'd think that some big supplement company could probably get it at a large discount. Drive the price down through economies of scale.
    I think NP has it at 200mgs per for 30 days for like 12 bucks
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    I ran across an article a long time ago that suggested that DIM, the chemical relative of IC3, binds to the Androgen Receptor and blocks Test and DHT in skeletal muscle. If I were looking at AI alternatives, that's the area I would research.
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    I researched it some time ago, tried it and found that it gave nipple itch, could just be me. I only talked to one person that liked it.
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    Quote Originally Posted by yeahright
    I bought a bottle from my local discount vitamin store (Solaray brand) for less than $10. It's 25 mg (30 capsules) per capusule so you'd need 8 capsules to get the 200 mg dose used in these studies but that's not too expensive in the big scheme of things....you'd think that some big supplement company could probably get it at a large discount. Drive the price down through economies of scale.
    I think you will need to run it longer than that, but let us know how it goes.
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    Quote Originally Posted by CDONDICI
    I think you will need to run it longer than that, but let us know how it goes.
    Yeah, the problem is separating out things. I'm ADDING the I3C to the PCT already underway (nolva, mATD) so to will be impossible to attribute anything specifically to the I3C....and since I'm already combating some nipple puffiness/itchiness, I'm not inclined to deviate away from the tried and true (add to it yes, substitute, not so much).

    However, on paper I3C appears to be an elegant addition.
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    Quote Originally Posted by yeahright
    Yeah, the problem is separating out things. I'm ADDING the I3C to the PCT already underway (nolva, mATD) so to will be impossible to attribute anything specifically to the I3C....and since I'm already combating some nipple puffiness/itchiness, I'm not inclined to deviate away from the tried and true (add to it yes, substitute, not so much).

    However, on paper I3C appears to be an elegant addition.
    O my fualt I thoughgt you were using it as standalone, but still let us know what the final results of you pct are and if you think it contributed anythign
  

  
 

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