Estrogenex for AI?

ongos

Bluelighter
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Aug 9, 2011
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Estrogenex is a nutritional supplement, available without a prescription, designed to normalize all hormone levels, yielding a wide spectrum of health and anti-aging benefits. Estrogenex is a multi-pathway formulation that minimizes or eliminates the undesirable effects associated with an estrogen dominant environment.

Hi Tech Pharmaceuticals put this out. Has anyone tried it? I don't think I like those cancer medication type AIs which are toxic.
 
Estrogenex is a nutritional supplement, available without a prescription, designed to normalize all hormone levels, yielding a wide spectrum of health and anti-aging benefits. Estrogenex is a multi-pathway formulation that minimizes or eliminates the undesirable effects associated with an estrogen dominant environment.

Hi Tech Pharmaceuticals put this out. Has anyone tried it? I don't think I like those cancer medication type AIs which are toxic.

Proprietary Blend – Chrysin, Green Tea Extract, Beta- Sitosterol, Muira Puama Root Extract, Quercitin, Soy ISO Flavones, Coumestrol Flavones, Dihydroxybergamottin Fruit and Naringen Fruit. This compound also contains Microcrystalline cellulose, Starch, Stearic Acid, Magnesium Stearate, Sodium Starch Glycolate, Triacetin, Silica, FD&C Red #3, and FD&C Yellow #6.

At high concentrations, chrysin is reported to be an aromatase inhibitor in vitro. However, studies performed in vivo show that orally administered chrysin does not have clinical activity as an aromatase inhibitor

No evidence for the in vivo activity of aromatase-inhibiting flavonoids.
Saarinen N1, Joshi SC, Ahotupa M, Li X, Ammälä J, Mäkelä S, Santti R.
Author information
Abstract
Measurements of the aromatase-inhibiting and antioxidative capacities of flavonoids in vitro showed that slight changes in flavonoid structure may result in marked changes in biological activity. Several flavonoids such as 7-hydroxyflavone and chrysin (5,7-dihydroxyflavone) were shown to inhibit the formation of 3H-17beta-estradiol from 3H-androstenedione (IC(50)<1.0 microM) in human choriocarcinoma JEG-3 cells and in human embryonic kidney cells HEK 293 transfected with human aromatase gene (Arom+HEK 293). Flavone and quercetin (3,3',4',5,7-pentahydroxyflavone) showed no inhibition (IC(50)>100 microM). None of the requirements for optimal antioxidative capacity (2,3-double bond with 4'-hydroxy group, 3-hydroxyl group, 5,7-dihydroxy structure and the orthodihydroxy structure in the B-ring) is relevant for the maximum inhibition of aromatase by flavonoids. After oral administration to immature rats at a dose of 50 mg/kg body weight, which considerably exceeds amounts found in daily human diets, neither aromatase-inhibiting nonestrogenic flavonoids, such as chrysin, nor estrogenic flavonoids, such as naringenin and apigenin, induced uterine growth or reduced estrogen- or androgen-induced uterine growth. The inability of flavonoids to inhibit aromatase and, consequently, uterine growth in short-term tests may be due to their relatively poor absorption and/or bioavailability.

http://www.ncbi.nlm.nih.gov/pubmed/11595503

β-sitosterol is being studied for its potential to reduce benign prostatic hyperplasia (BPH) and blood cholesterol levels. β-Sitosterol is also not recommended for individuals with sitosterolemia, a rare inherited fat storage disease. Because people with this condition have too much β-sitosterol and related fats in their system, taking β-sitosterol will only worsen this condition.

High levels of β-sitosterol concentrations in blood have been correlated with increased severity of heart disease in men having previously suffered from heart attacks

Dietary supplements for benign prostatic hyperplasia: an overview of systematic reviews.
Kim TH1, Lim HJ, Kim MS, Lee MS.
Author information
Abstract
Benign prostatic hyperplasia (BPH) is a common chronic condition in older men. The aim of this overview of systematic reviews (SRs) is to summarise the current evidence on the efficacy and adverse effects of dietary supplements for treating BPH with lower urinary tract symptoms. We searched 5 electronic databases and relevant overviews without limitations on language or publication status. Six SRs of 195 articles were included in this overview. Serenoa repens was reviewed in 3 studies and no specific effect on BPH symptoms and urinary flow measures was observed. However, β-sitosterol, Pygeum africannum and Cernilton were reviewed in one study each, and significant improvement was observed for all three. All the included compounds have mild and infrequent adverse effects. SRs on β-sitosterol, Pygeum africannum and Cernilton have not been updated since 2000, thus an update of reviews on these compounds will be necessary in the future.

http://www.ncbi.nlm.nih.gov/pubmed/22883375


Muira Puama Root Extract: The root and bark are used for a variety of ailments by indigenous peoples in the Rio Negro area of South America, but the effectiveness of Muira Puama preparations are unproven. However, in a 1990 study conducted by Jacques Waynsberg at the Institute of Sexology in Paris, 62% of men who took muira puama extract noted an increase in sex drive and 51% of participants reported an increased ability to produce an erection..?

Quercetin has not been confirmed scientifically as a specific therapeutic for any condition nor approved by any regulatory agency. The European Food Safety Authority evaluated possible health claims associated with consumption of quercetin, finding that no cause-and-effect relationship has been established for any physiological effect

Soy-Isoflavones may affect human and animal health, although research is preliminary. Isoflavones such as genistein and daidzein, may affect the growth of estrogen-receptor positive and negative breast cancer cells in vitro. However, a 2010 meta-analysis of fifteen placebo-controlled studies said that "neither soy foods nor isoflavone supplements alter measures of bioavailable testosterone concentrations in men." Furthermore, isoflavone supplementation had no effect on sperm concentration, count or motility, and showed no changes in testicular or ejaculate volume, in one study. Studies using chemically pure isoflavones or plant materials with known concentrations of these compounds have indicated both positive and negative effects of isoflavones on disease progression and fertility.

Studies on mice indicate that isoflavones may cause thymic and immune system abnormalities and reduction in immune system activity

Clinical studies show no effects of soy protein or isoflavones on reproductive hormones in men: results of a meta-analysis.
Hamilton-Reeves JM1, Vazquez G, Duval SJ, Phipps WR, Kurzer MS, Messina MJ.
Author information
Abstract
OBJECTIVE:
To determine whether isoflavones exert estrogen-like effects in men by lowering bioavailable T through evaluation of the effects of soy protein or isoflavone intake on T, sex hormone-binding globulin (SHBG), free T, and free androgen index (FAI) in men.
DESIGN:
PubMed and CAB Abstracts databases were searched through July 1, 2008, with use of controlled vocabulary specific to the databases, such as soy, isoflavones, genistein, phytoestrogens, red clover, androgen, testosterone, and SHBG. Peer-reviewed studies published in English were selected if [1] adult men consumed soy foods, isolated soy protein, or isoflavone extracts (from soy or red clover) and [2] circulating T, SHBG, free T, or calculated FAI was assessed. Data were extracted by two independent reviewers. Isoflavone exposure was abstracted directly from studies.
MAIN OUTCOME MEASURE(S):
Fifteen placebo-controlled treatment groups with baseline and ending measures were analyzed. In addition, 32 reports involving 36 treatment groups were assessed in simpler models to ascertain the results.
RESULT(S):
No significant effects of soy protein or isoflavone intake on T, SHBG, free T, or FAI were detected regardless of statistical model.
CONCLUSION(S):
The results of this meta-analysis suggest that neither soy foods nor isoflavone supplements alter measures of bioavailable T concentrations in men.

http://www.ncbi.nlm.nih.gov/pubmed/19524224
 
what do you guys think of proviron as an AI? Or even Masteron?
 
what do you guys think of proviron as an AI? Or even Masteron?

From Big Cat:

I've read this stupidity in so many threads on here, and literally every other board, book and article. But apparently no one in the whole AAS game understand the difference between androgen mediated repression of estrogenic actions and actual anti-estrogenic actions.

SERMS, are partial agonists and partial antagonists at the ER. Where they are antagonistic (like all of them are in the breast), they can be considered anti-estriogens. Aromatase inhibitors are anti-estrogens.

Dihydrotestosterone and ONLY dihydrotestosterone, as an androgen, has very mild anti-aromatase activity and could be considered a very mild anti-estrogen. THIS DOES NOT, NEVER DID, AND NEVER WILL MEAN THAT EVERY 5-ALPHA-REDUCED HORMONE (or DHT derivative as some like to call it) HAS ANTI-AROMATASE ACTION.

Androgens of all sorts, including actual testosterone, have been used in the clinical treatment of breast cancer, because androgen receptor binding in the breast, outweighing estrogen receptor activation, will counteract the estrogen-induced proliferation of breast cells. This is not an anti-estrogenic action, this is merely a function of androgens in the breast to counteract breast growth. This applies to :

- Mesterolone. Basically 1-methyl DHT, but the A-ring modification would interefere with aromatase binding. Meaning if DHT is a weak anti-aromatase drug, then the activity mesterolone might still have would require in excess of 500mg per day to have any direct anti-aromatase effect worth having. If you are using Proviron specifically as an anti-estrogen, you are wasting your money. It's effect in this regard is no different than any other potent androgen.

-Drostanolone, the 2-methyl group isn't just an A-ring modification that prevents or limits aromatase binding, it structurally protects the 3-keto group from being reduced, which is a requirement for aromatase function. Drostanolone is absolutely NOT an aromatase blocker. This is just some label given to it by people who saw it was predominantly used in treatment for breast cancer (which it was quite good at, because despite its weak nature, it is a very pure androgen, with little or no interaction outside of the AR) and the fact that it was structurally related to DHT.

So please, do not confuse these things. known AI's like letrozole, anastrozole and exemestane are anti-estrogens. SERMs are conditional anti-estrogens. DHT, as a very, very mild AI, could potentially be termed modestly anti-estrogenic. Pretty much all other androgens we use ARE NOT ANTI-ESTROGENIC. Their effect in counteracting estrogen is purely based on their activity at the AR, and the effect is always going to be greater for more potent androgens.

If there is no evidence of anti-estrogenic action, please don't go around saying it's anti-estrogenic. Any increase in A:E ratio by the addition of a non-aromatizing, non-estrogenic androgen will in fact have some apparent estrogen countering effect, simply because you are increasing the ratio of androgens to estrogens.
 
i'm not on doing an oppressive cycle. 200mg of test and 200mg of masteron weekly. Do I need a "real" AI or I can get away with just masteron or even proviron?
 
i'm not on doing an oppressive cycle. 200mg of test and 200mg of masteron weekly. Do I need a "real" AI or I can get away with just masteron or even proviron?

The post above explains things clearly... Do you not bother to read..?
 
I'm curious about the same thing as ongos. Since you are a moderator and carry the power to kill threads, would you mind pointing out exactly where your previous post explains whether or not a real AI is needed for a low dose test / mast cycle or if the androgenic properties of masteron or proviron would be enough to counter problematic estrogenic side effects?
 
Very nice. So where exactly does he explain, or even write about, whether or not you need an AI for a low dose cycle with a low dose high androgenic? Please point out the exact sentence that even mentions this, because I have read the text several times and fail to find it.
 
TipmanTim_Spoon.jpg
 
Who am I kidding, no one's tried my cycle so who would really know. I think bitch tits only come around when you're dosing too high to begin with.
 
i'm not on doing an oppressive cycle. 200mg of test and 200mg of masteron weekly. Do I need a "real" AI or I can get away with just masteron or even proviron?

Masteron doesn't aromatize, therefore the only compound that could potentially convert to estrogen is the 200mg Testosterone, unsure of your ester, if enanth' or cyp' inject twice a week, if prop' EOD, to reduce the plasma spike, and thus any metabolization via CYP19A1 (aromatase) to estrogen...
You don't need an AI on 200mg/week.. :)
 
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test acetate 50mg EOD 4x a week = 200mg weekly.

Masteron doesn't aromatize, therefore the only compound that could potentially convert to estrogen is the 200mg Testosterone, unsure of your ester, if enanth' or cyp' inject twice a week, if prop' EOD, to reduce the plasma spike, and thus any metabolization via CYP19A1 (aromatase) to estrogen...
You don't need an AI on 200mg/week.. :)
 
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unsure of your ester, if enanth' or cyp' inject twice a week, if prop' EOD, to reduce the plasma spike, and thus any metabolization via CYP19A1 (aromatase) to estrogen... :)
whoa! is that really a thing? Stabler test levels reduce aromatase? How? Less active aromatase, less aromatase produced? Could you tell me what you will about this, I'd never heard it before! Is e3d of cypionate stable enough to be considered for low aromatase metabolism? For understanding relative aromatase activity, would you say this variance between stable/erratic blood levels is significant enough to be affecting AI needs during cycle? Like, if people were taking equal amounts testosterone base weekly, but one was doing daily cypio shots, and the other was doing weekly enanthate shots - and all other things equal - the enanthate guy would need more letro/adex/whatever on cycle? Thanks for any elucidation, this is exciting I'd never heard it before!
 
whoa! is that really a thing? Stabler test levels reduce aromatase? How? Less active aromatase, less aromatase produced? Could you tell me what you will about this, I'd never heard it before! Is e3d of cypionate stable enough to be considered for low aromatase metabolism? For understanding relative aromatase activity, would you say this variance between stable/erratic blood levels is significant enough to be affecting AI needs during cycle? Like, if people were taking equal amounts testosterone base weekly, but one was doing daily cypio shots, and the other was doing weekly enanthate shots - and all other things equal - the enanthate guy would need more letro/adex/whatever on cycle? Thanks for any elucidation, this is exciting I'd never heard it before!

I wouldn't state stabler blood levels reduce the aromatase enzyme, but I believe stable blood levels that don't create a high plasma spike, leave the body less susceptible to high aromatase activity, therefore less aromatization to estrogen, the same seems to go for DHT conversion also... It has been hypothesised for a number of years on other boards I use that more frequent injections of longer esters create more stable bloods, and hence less metabolization...
A medical colleague and myself did some research into esters a number of years ago, I believe we posted up results which concluded the same..!!
 
test acetate 50mg EOD 4x a week = 200mg weekly.

EOD = 3.5 X/week... = 175mg/week... Acetate should be pinned ED..... EOD would be 3.5 times a week, as there are only 7 days in a week not 8...
 
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OK I will consider Test ace ED. That's 350mg weekly then if dosing 50mg ED. What is the 175mg weekly you're talking about? if doing 25mg daily?

My intent was 50 mg EOD, which is 200mg weekly.

I would use the same amount of Masteron (drostanolone propionate). Could Masteron be used by itself without test or not recommended?

Here's how I may run my cycle:

Monday - Test 50mg
Tuesday - Mast 50mg

Repeat.

How would you run Masteron propionate?
 
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OK I will consider Test ace ED. That's 350mg weekly then if dosing 50mg ED. What is the 175mg weekly you're talking about? if doing 25mg daily?

My intent was 50 mg EOD, which is 200mg weekly.

I would use the same amount of Masteron (drostanolone propionate). Could Masteron be used by itself without test or not recommended?

Here's how I may run my cycle:

Monday - Test 50mg
Tuesday - Mast 50mg

Repeat.

How would you run Masteron propionate?

You can run any prop ester at eod as its life is long enough. Me personally I'd do minimum 50/day to keep dry and get its effects visible.
 
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