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How estrogen effects muscle growth.

I’m wondering if all the evidence of combined therapy and being able to drop total SERM dosage crosses over to our needs. So they found the combination works better and allows the patient to lower their tamoxifen dose...great that’s less sides. But does it work for our purposes or is this combo only effective for fighting cancer not stopping breast gland growth?
Breast tissue is composed of epithelial and stromal cells (fibroglandular tissue) and fat (in men and women). Mammographic density (MD) is the relative amount of fibroglandular tissue to fat, and is often reported as percentage mammographic density (PMD) that is a proportion of the dense tissue area over the total breast area,. The authors of the cited Clinical Trial results themselves cite a study where 18 mo tamoxifen reduced PMD by 4.4% versus placebo, and here the results were identical (-4.4% versus placebo). The green tea extract formulation was: daily 4 decaffeinated GTE capsules containing 1,315 mg total catechins, including 843 mg epigallocatechin-3-gallate (EGCG) for 12 months.

It is most plausible that the mechanism is mediated by endogenous estrogen levels, as these circulating hormones would be higher in the younger (50-55) versus older postmenopausal women.

In breast tissues, raloxifene acts as an estrogen receptor antagonist to attenuate the estrogen-dependent proliferative effects of epithelial cell expansion.

In gynecomastia, the concern is the growth of the fibroglandular tissue and is caused by an increase in the estrogen to androgen ratio.

From all this, it can be tempting suppose that green tea extracts may combat AAS-induced gyno (I am guilty of this sort of supposition with antiglucocorticoid activity of particular AAS and aggression). The question then becomes - since if these extracts work for gyno, then they do so by modulating estrogen - why it is thought that green tea extracts would be superior versus proven SERMs (ie, ralox) with proven favorable effects on bone mineral density, serum lipids, and collagen?
 
Breast tissue is composed of epithelial and stromal cells (fibroglandular tissue) and fat (in men and women). Mammographic density (MD) is the relative amount of fibroglandular tissue to fat, and is often reported as percentage mammographic density (PMD) that is a proportion of the dense tissue area over the total breast area,. The authors of the cited Clinical Trial results themselves cite a study where 18 mo tamoxifen reduced PMD by 4.4% versus placebo, and here the results were identical (-4.4% versus placebo). The green tea extract formulation was: daily 4 decaffeinated GTE capsules containing 1,315 mg total catechins, including 843 mg epigallocatechin-3-gallate (EGCG) for 12 months.

It is most plausible that the mechanism is mediated by endogenous estrogen levels, as these circulating hormones would be higher in the younger (50-55) versus older postmenopausal women.

In breast tissues, raloxifene acts as an estrogen receptor antagonist to attenuate the estrogen-dependent proliferative effects of epithelial cell expansion.

In gynecomastia, the concern is the growth of the fibroglandular tissue and is caused by an increase in the estrogen to androgen ratio.

From all this, it can be tempting suppose that green tea extracts may combat AAS-induced gyno (I am guilty of this sort of supposition with antiglucocorticoid activity of particular AAS and aggression). The question then becomes - since if these extracts work for gyno, then they do so by modulating estrogen - why it is thought that green tea extracts would be superior versus proven SERMs (ie, ralox) with proven favorable effects on bone mineral density, serum lipids, and collagen?
I don’t think anybody has claimed they are superior! I think the claim is their combination allows a smaller total SERM dose to be used. Some studies were supposing it was an intestinal transferase that was responsible for breaking down the raloxifene and that the green tea was inhibiting that but that seems incorrect now.

It’s a mystery to me why green tea extract (GTE ) + raloxifene is better at cancer killing in breast tissue than just ralox.
 
"combined implant treatments synergistically increased average muscle protein accretion by 25% (TBA + E2 > E2 [alone]; P < .lo1 and 60% (TBA + E2 > TBA [alone]; P < ,011 compared with TBA and E2 treatments (Table 4)."

Hayden, J. M., Bergen, W. G., & Merkel, R. A. (1992). Skeletal muscle protein metabolism and serum growth hormone, insulin, and cortisol concentrations in growing steers implanted with estradiol-17β, trenbolone acetate, or estradiol-17β plus trenbolone acetate2. Journal of Animal Science, 70(7), 2109–2119. doi:10.2527/1992.7072109x

"Carcass characteristics
No linear (P ≥ 0.14) or quadratic (P ≥ 0.40) effects were observed for dressing percentage, rib fat, yield grade, or USDA marbling scores. However, a quadratic increase (P = 0.01) in HCW was noted. HCW was increased by 4.6% and 5.5% for CH and PL, respectively, compared with NI. A linear increase (P = 0.01) in REA was observed. Ribeye area was increased by 4.1% and 7.7% for CH and PL treatments, respectively, compared with NI steers."

Smerchek DT, Smith ZK. Effects of increasing doses of trenbolone acetate and estradiol on finishing phase growth performance, carcass trait responses, and serum metabolites in beef steers following implantation. Transl Anim Sci. 2020;4(3):txaa158. Published 2020 Aug 26. doi:10.1093/tas/txaa158
? none of these things have anything to do with my post
 
Don't make jokes. We are probably talking about bodybuilding and not about lowering estradiol in old women

if someone uses 1250-2500mg of testosterone per week (which is really the norm in super heavy categories whether you want to believe it or not) then they must use IA and not green tea lol to keep estrogen in check (unless it's a genetic anomaly and hardly aromatizes - they are that kind of people)
 
Don't make jokes. We are probably talking about bodybuilding and not about lowering estradiol in old women

if someone uses 1250-2500mg of testosterone per week (which is really the norm in super heavy categories whether you want to believe it or not) then they must use IA and not green tea lol to keep estrogen in check (unless it's a genetic anomaly and hardly aromatizes - they are that kind of people)
Luki serious question that follows up on your last point. How OFTEN do you come across guys who HYPER respond to aromasin/arimidex/etc? We hear on the forum about people that crash their estrogen with very small AI dosages but do you see them ever as clients?
 
Also @luki7788 if somebody is trying to get a baseline for a new test dosage...say they bumped up from TRT to blast/cycle...how often should they test e2 while dialing in estrogen control with AI? Is 4 weeks minimum they need to wait for new e2 level to stabilize from cycle?

Also you mentioned how e2 is always rising or falling because of many different factors...does this mean you are testing e2 frequently? Like 1x month?
 
Luki serious question that follows up on your last point. How OFTEN do you come across guys who HYPER respond to aromasin/arimidex/etc? We hear on the forum about people that crash their estrogen with very small AI dosages but do you see them ever as clients?
very, very rarely, to be honest. Usually if someone is taking 1-1.2g of testosterone, they need 1mg of adex or 25mg of aromasin daily to maintain estradiol between 40-50
If someone takes 1.5 g of the test and more, it is usually already letro to keep it normal.

It is very rare that someone does not need to use IA at all or very small doses - although there are sometimes people who do not really aromatize
 
Also @luki7788 if somebody is trying to get a baseline for a new test dosage...say they bumped up from TRT to blast/cycle...how often should they test e2 while dialing in estrogen control with AI? Is 4 weeks minimum they need to wait for new e2 level to stabilize from cycle?

Also you mentioned how e2 is always rising or falling because of many different factors...does this mean you are testing e2 frequently? Like 1x month?
I do blood tests every 2-4 weeks
 
Don't make jokes. We are probably talking about bodybuilding and not about lowering estradiol in old women

if someone uses 1250-2500mg of testosterone per week (which is really the norm in super heavy categories whether you want to believe it or not) then they must use IA and not green tea lol to keep estrogen in check (unless it's a genetic anomaly and hardly aromatizes - they are that kind of people)
If going for mass in offseason for one year . Given training / nutrition / rest are all on point will going from 750 test a week to 2000mg of test a week for the whole year give you more muscle faster than if you only went from 750mg a week to 1000mg a week?
 
If going for mass in offseason for one year . Given training / nutrition / rest are all on point will going from 750 test a week to 2000mg of test a week for the whole year give you more muscle faster than if you only went from 750mg a week to 1000mg a week?
Pretty sure the answer here is yes
 
If going for mass in offseason for one year . Given training / nutrition / rest are all on point will going from 750 test a week to 2000mg of test a week for the whole year give you more muscle faster than if you only went from 750mg a week to 1000mg a week?
More will always yield better results, it’s just that there is a drop off after a certain point in terms of additional beneift. The difference between 500 Mg and 1500 Mg is big! But the difference between 4 and 5 grams is not so impactful
 
If going for mass in offseason for one year . Given training / nutrition / rest are all on point will going from 750 test a week to 2000mg of test a week for the whole year give you more muscle faster than if you only went from 750mg a week to 1000mg a week?
Of course, yes, and no matter what, more milligrams means bigger gains - this is even confirmed by research studies.
But if you are using 750mg total and you want to increase it gradually to 2000mg, adding the test alone will not be the best solution, I would rather add a little more testosterone and something highly anabolic, e.g.
1000mg test + 500-700mg nandrolone
1000mg test + 800-1000mg primo
1000-1200mg test + 300-400mg tren

each of these combinations will definitely give better results than 2g of the test alone
 
Of course, yes, and no matter what, more milligrams means bigger gains - this is even confirmed by research studies.
But if you are using 750mg total and you want to increase it gradually to 2000mg, adding the test alone will not be the best solution, I would rather add a little more testosterone and something highly anabolic, e.g.
1000mg test + 500-700mg nandrolone
1000mg test + 800-1000mg primo
1000-1200mg test + 300-400mg tren

each of these combinations will definitely give better results than 2g of the test alone
:love::love::love::love::love::love: best gains i am having atm.
 
tren will always be your best bet if you only look at the profit side
Yes... Indeed.... Healthy side isn't the best... It is what it is... I do my cardio, take supper, try to limit damage.
 
If i overdo with AI or DHT compounds i get flat as a pancake, unable to get a pump and my strength goes to shit.
I tried nolva for gyno and it made me feels even worse than AI. No pump, no energies, no vascularity, joint pain...
 
I know that I've never used an AI on cycle. I've done only 3 cycles in my life but never needed an AI before for the "issues" I've presently experienced on cycle.... At 500mg a week of sustanon I just recently introduced Arimidex .5mg eod and it's been about a week. Holy Smokes, the difference is absolutely unreal!...I was getting a fat foot and swelling in my left leg periodically, then I noticed my left nipple a little puffy. That's why I decided to finally utilize it after several weeks of these "on and off episodes". I'm just now going on my 9th week of cycle. I've gained about 25pounds.....in the last week I've lost 3-4lbs of water I'm certain as I can now see the muscles fibers threw my shoulders and vascularity is up.... I've got a clearer head, and haven't had a headache. Like I said these things never effected me in my precious cycles....I'm 40 now so I'm sure the age has something to do it....

I can't speak on if an AI effects growth or not, because of my own lack of experiences using it; I've always been able to handle it and let it run high and have always had very apparent growth. Not incorporating it until absolutely necessary I would say is optimal as a no-brainer.

I don't expect it at all to crash my gains, actually feeling much better I'd assume it would allow me to be able to push harder. Wishing now I would had used it much sooner but tried seeing if it would work itself out or subside.

Is there any tips or advise you more experienced guys with AI use can offer, I'd appreciate it.
 
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Who here experimented with taking pure estrogens for growth?
From a post on another forum from waay back:

Also just because I found it funny, here's DDuchaine getting snippy with Kneller and PA over how to use any of the cattle pellets :/
;D
-

"So fancy-schmansy. Just take the damn pellets, grind them find with a mortal and pestle, get some vet injectable oil vitamins (Jeffers Vet
Supply 800-533-3377) and dump the powder into the oil by popping the top off and inject the mixture. Make sure that you shake the suspension well.

Bruce is one of those armchair experts that needlessly worry aboutpotential sterile, infection, blah-blah-blah. Tony Fitton and I both did
the same thing 12 years ago with Ralgro (Zeranol) and nobody got sick. Look it this way: many current steroid users have injected even less sterile counterfeits into their bodies with no ill effect.

*Zeranol - https://en.wikipedia.org/wiki/Zeranol .

--------------

Pat Arnold on Ralgro -

There is no great mystery about Ralgro (amongst animal scientists at least). It is an anabolic estrogen, a class of compounds (which also includes DES, and steroidal estrogens as well) assumed to manifest their anabolic actions primarily thru stimulation of GH output. Large amounts of estrogenic compounds are markedly anabolic, but due to obvious undesirable side effects are not suitable for human anabolic enhancement.

Small amounts of estrogens are good potentiators of the growth promoting actions of androgens, but the unacceptable risks of inducing negative reactions like gynecomastia make thier usage in this regard not an accepted practice.

For animals a good growth promoting stack might be androgen/progestogen/estrogen (10:10:1 ratio) maybe testosterone propionate/hydroxyprogesterone caproate/estradiol benzoate.

It would work great on humans too, but you would probably be setting yourself up for some nasty side effects (though I am sure their are few that would still find the risk/benefit acceptable)

PA
 
I've written about ER-β agonists before, see https://www.professionalmuscle.com/...terone-potential-mechanisms-of-action.168468/

Estradiol activates ER-α and -β, but with a host of negative effects on physique/hypertrophy/health (gynecomastia, water retention, psychological effects, worsened glucose metabolism/G6PD, prostate, etc.)

Most of the benefits attributed to ingesting E2 are far better accomplished by the use of an aromatizing androgen (i.e., TEST). In fact, the positive effects on glucose metabolism/G6PD Llewyln (years ago, surely) attributed to E2 can really only be attributed to aromatizing androgens, as the opposite effects have been demonstrated in C2C12 skeletal muscle cells. But consistently demonstrated in humans on TEST.

Recent work has honed in on the function of this (good for us) receptor, as well as on the work of economical processes for mass-production of 20-HE (ecdysterone).

Here are some notes I have kept on ER-β:

ER-β: Whereas ER-α regulates blood lipids, ER-β is thought to mediate remodeling in muscle tissue.
Broadly, activation/agonism of the receptor causes increased protein synthesis, promotion of IGF-1 synthesis (paracrine), increased insulin sensitivity, and improved utilisation of glucose and lipids, while reducing protein degradation.
++ muscle cell sigaling: mTOR/p70S6K (ribosomal protein/translation ⇒ protein synthesis), FOXO inhibition ⇒
+ fat cell: inhibition of PPAR𝛾 (which promotes lipid uptake and adipogenesis) ⇒ lipolysis and apoptosis of adipose cells and a decrease in visceral fat, adipocyte size, and overall decrease in serum lipid concentration
....

To be clear: I just don't like ingesting E2. Its benefits can come from aromatization. The only benefit that ingested E2 arguably brings to the table versus an aromatizing androgen is its effects on cIGF-I, which rhGH takes care of far more cleanly.

I strongly recommend people take a look at this recent article on the myriad anabolic as well as cardioprotective and other benefits of this phytoecdysteroid:
20-Hydroxyecdysone, from Plant Extracts to Clinical Use: Therapeutic Potential for the Treatment of Neuromuscular, Cardio-Metabolic and Respiratory Diseases
 

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