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How estrogen effects muscle growth.

Interesting read and some first hand anecdotal evidence to share: I have never previously used AAS, but I have been a TRT guy for years. I decided to cross over to the dark side and I ran Primo for 10 weeks. About 6 weeks in I had my bloodwork done to see what impact, if any Primo had. First, my Estrogen CRASHED. It was previously in the mid 30's and after 6 weeks of primo it was undetectable (chart said < 5). My HDL CRASHED. It went from 60 to 28. My IGF-1 lowered pretty significantly...from approx 210 to 170. My joints, particularly my shoulders and elbows began aching. My gains were modest (at best). Probably 2 lbs of muscle. It now makes sense that the reason for the achy joints and perhaps lack of significant gains were attributed to having no Esto in my system.
 
True. They want mass/bulk weight.

Good find! In terms of research, Tren+E2 pellets (rather than Tren alone) in cattle yields far greater quantity and quality of meat (due mostly to elevated IGF-I), for what it's worth.
Tren and Estradiol use in cattle is purely for mass to feed ratio, it's all about reducing the cost of the fattening up period before slaughter, the can get the same results from increased feed but it's more expensive (due to the cost of feed), they also don't care about quality, only that mass to feed ratio...
 
Does Ralox also block the hgh/igf1 action of estrogen?
It lessens it significantly. There have been pilot studies investigating its potential therapeutic use in acromegaly.

Attanasio, R., Barausse, M., & Cozzi, R. (2003). Raloxifene lowers IGF-I levels in acromegalic women. European Journal of Endocrinology, 148(4), 443–448. doi:10.1530/eje.0.1480443
 
Tren and Estradiol use in cattle is purely for mass to feed ratio, it's all about reducing the cost of the fattening up period before slaughter, the can get the same results from increased feed but it's more expensive (due to the cost of feed), they also don't care about quality, only that mass to feed ratio...
"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
 
It lessens it significantly. There have been pilot studies investigating its potential therapeutic use in acromegaly.

Attanasio, R., Barausse, M., & Cozzi, R. (2003). Raloxifene lowers IGF-I levels in acromegalic women. European Journal of Endocrinology, 148(4), 443–448. doi:10.1530/eje.0.1480443
Thanks for sharing that!

So to avoid gyno would it be better to use low dose aromasin/arimidex or a low dose of a serm when the goal is to gain mass and keeping estrogen higher?

What is the lesser evil here lol
 
Thanks for sharing that!

So to avoid gyno would it be better to use low dose aromasin/arimidex or a low dose of a serm when the goal is to gain mass and keeping estrogen higher?

What is the lesser evil here lol
I am not a scientist but I write everything from my experience. If you want to avoid gyno, just keep estrogen in the normal range, I don't know where the theory comes from and people believe that too high estrogen levels are better than normal. Use as much IA as you need to keep your estrogen in the normal range - that's logical
 
i was pinnin my hrt dose 12.5mg a day, my test was 946, free 167 but my e2 was only 15....
i was feeling pretty low for those weeks, i went from wackin off 2-3 times a day to not even wanting to at all.
i wanted the e2 to be around 25-30. i dont KNOW if 15 is too low for me but i did decide to pin twice a week 50mg each, to see if i'll aromatize
more. at this point im not wanting to do a cycle, just real trt. last time i overused ai my e2 was 8.
its the good and bad with everyday pinning. great test levels, lower e2. but not THAT low
 
I am not a scientist but I write everything from my experience. If you want to avoid gyno, just keep estrogen in the normal range, I don't know where the theory comes from and people believe that too high estrogen levels are better than normal. Use as much IA as you need to keep your estrogen in the normal range - that's logical
Would you say you are a high aromatiser @luki7788?
 
Interesting read and some first hand anecdotal evidence to share: I have never previously used AAS, but I have been a TRT guy for years. I decided to cross over to the dark side and I ran Primo for 10 weeks. About 6 weeks in I had my bloodwork done to see what impact, if any Primo had. First, my Estrogen CRASHED. It was previously in the mid 30's and after 6 weeks of primo it was undetectable (chart said < 5). My HDL CRASHED. It went from 60 to 28. My IGF-1 lowered pretty significantly...from approx 210 to 170. My joints, particularly my shoulders and elbows began aching. My gains were modest (at best). Probably 2 lbs of muscle. It now makes sense that the reason for the achy joints and perhaps lack of significant gains were attributed to having no Esto in my system.
All of those side effects seem estrogen related even HDL
 
Thanks for sharing that!

So to avoid gyno would it be better to use low dose aromasin/arimidex or a low dose of a serm when the goal is to gain mass and keeping estrogen higher?

What is the lesser evil here lol
I think Ralox should be used until Asin becomes necessary, sparingly, to get your absolute E2 levels back into the normal reference range if/when your E2 does become clinically elevated. Ralox should be the SERM (mostly due to its effects on collagen and joint pain so training can be frequent and heavy versus similar SERMs) of choice and Asin should be the AI of choice (due to its improved side-effect profile in most versus similar AIs)-- and the goal should be to “dial in” high normal E2.
____________________________________________________

I’ll explain for anyone interested in my reasoning: I think the guiding principle should be to manage E2 levels (i.e., within the Normal reference range) due to the strong negative impacts of elevated E2 on:

- gynecomastia
- water retention
-- sexual function, and
--- the degree of HPG axis suppression (which is relevant if you’re not BnCing).

The countervailing interests of E2:
+ increased serum IGF-I levels [probably due to a higher GH peak amplitude]
+ some evidence [very mechanistic- in rats and cancer cell lines- for example the citation from the OP which was ‘x’d-out is to a 3-page rat study from 1980- but still interesting to some of us] of improved glucose metabolism and perhaps most interestingly-
+ increased serum concentrations of the adjunct AAS [e.g., Tren+E2 increases serum concentrations of Tren far more than Tren alone]

are better dealt with by increased AAS dosage and the use of and increased dosage of rhGH (and arguably slin as well), when the sole interest is growth.
 
I think Ralox should be used until Asin becomes necessary, sparingly, to get your absolute E2 levels back into the normal reference range if/when your E2 does become clinically elevated. Ralox should be the SERM (mostly due to its effects on collagen and joint pain so training can be frequent and heavy versus similar SERMs) of choice and Asin should be the AI of choice (due to its improved side-effect profile in most versus similar AIs)-- and the goal should be to “dial in” high normal E2.
____________________________________________________

I’ll explain for anyone interested in my reasoning: I think the guiding principle should be to manage E2 levels (i.e., within the Normal reference range) due to the strong negative impacts of elevated E2 on:

- gynecomastia
- water retention
-- sexual function, and
--- the degree of HPG axis suppression (which is relevant if you’re not BnCing).

The countervailing interests of E2:
+ increased serum IGF-I levels [probably due to a higher GH peak amplitude]
+ some evidence [very mechanistic- in rats and cancer cell lines- for example the citation from the OP which was ‘x’d-out is to a 3-page rat study from 1980- but still interesting to some of us] of improved glucose metabolism and perhaps most interestingly-
+ increased serum concentrations of the adjunct AAS [e.g., Tren+E2 increases serum concentrations of Tren far more than Tren alone]

are better dealt with by increased AAS dosage and the use of and increased dosage of rhGH (and arguably slin as well), when the sole interest is growth.
AAS + GH + slin is a recipe for gyno without proper e2 control. Definitely agree with you there.

Anybody care to take a look at the literature on green tea extract and SERM use especially regards dropping dosage of SERM (thus ameliorating some of the SERM sides). I’ve been trying to figure out if it would pertain to our needs because the research is all about green tea+SERMs+breast cancer.
 
AAS + GH + slin is a recipe for gyno without proper e2 control. Definitely agree with you there.

Anybody care to take a look at the literature on green tea extract and SERM use especially regards dropping dosage of SERM (thus ameliorating some of the SERM sides). I’ve been trying to figure out if it would pertain to our needs because the research is all about green tea+SERMs+breast cancer.
Interesting. So there's this: https://pubmed.ncbi.nlm.nih.gov/28904061/ which is promising, some significant reduction (in younger postmenopausal women only, though) of mammographic density, perhaps comparable to tamoxifen. I definitely, definitely wouldn't use this as sufficient evidence for prevention of gynecomastia from AAS, though. You can certainly experiment with it, but don't neglect to have a SERM on hand based on this.
 
Interesting. So there's this: https://pubmed.ncbi.nlm.nih.gov/28904061/ which is promising, some significant reduction (in younger postmenopausal women only, though) of mammographic density, perhaps comparable to tamoxifen. I definitely, definitely wouldn't use this as sufficient evidence for prevention of gynecomastia from AAS, though. You can certainly experiment with it, but don't neglect to have a SERM on hand based on this.
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?
 
I think Ralox should be used until Asin becomes necessary, sparingly, to get your absolute E2 levels back into the normal reference range if/when your E2 does become clinically elevated. Ralox should be the SERM (mostly due to its effects on collagen and joint pain so training can be frequent and heavy versus similar SERMs) of choice and Asin should be the AI of choice (due to its improved side-effect profile in most versus similar AIs)-- and the goal should be to “dial in” high normal E2.
____________________________________________________

I’ll explain for anyone interested in my reasoning: I think the guiding principle should be to manage E2 levels (i.e., within the Normal reference range) due to the strong negative impacts of elevated E2 on:

- gynecomastia
- water retention
-- sexual function, and
--- the degree of HPG axis suppression (which is relevant if you’re not BnCing).

The countervailing interests of E2:
+ increased serum IGF-I levels [probably due to a higher GH peak amplitude]
+ some evidence [very mechanistic- in rats and cancer cell lines- for example the citation from the OP which was ‘x’d-out is to a 3-page rat study from 1980- but still interesting to some of us] of improved glucose metabolism and perhaps most interestingly-
+ increased serum concentrations of the adjunct AAS [e.g., Tren+E2 increases serum concentrations of Tren far more than Tren alone]

are better dealt with by increased AAS dosage and the use of and increased dosage of rhGH (and arguably slin as well), when the sole interest is growth.
Wow thanks for the detailed answer! Really appreciate it
 

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