Thank you for your kindly reply!
I will ask them if they sell abroad!
Thank you!
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Another person trying out 17 alpha estradiol…
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I’ve just bought 17-alpha estradiol from Chinese reseller
Would you have any updates on your 17-alpha estradiol, lab tests to establish purity, etc.? While I’m wary of Chinese compounds, I’ve hit a dead end with every other potential source and am considering following your lead. Thanks!!
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Last month, I took 60mg of 17-alpha estradiol, 20 mins later I had serious stomach cramps, one week later I had a gastroscopy , then an acute gastritis was diagnosed.
I don’t know if the gastritis is induced by 17-alpha estradiol (or the impurities in the compound), but I discontinue this product just in case.
I think it’s not safe enough to use pure chemical compound from China.
I am looking for a more reliable and cheaper source of 17-alpha estradiol.
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Thank you for the update, Lee! That’s good to know.
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Haha, I understand…but I seem to have a sad shortage of friends who run chemistry and biology labs.
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It seems likely that this was something specific to the product you purchased from China… given that no side effects at all have been reported in the clinical studies cited at the top of this page, in any clinical studies of 17 alpha estradiol in the past.
Seems likely to have been impurities in the product…
In the future - It think it would also be perhaps better to start with a lower dose - something similar to the dosing level that women currently use for 17 beta estradiol in terms of the common hormone therapy that is widely practiced in women near/after menopause - which I think is 50mcg (50 micrograms) per day, and slowly increase over a few months…
There have been no longer term studies of 17 alpha estradiol at the higher levels, so thats entirely new territory as far as human trials go. I think its best to be conservative when starting a new molecule…
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More good news on 17-alpha estradiol:
Using 10-month-old APOE3 or APOE4 targeted replacement male mice maintained on normal chow with and without 14.4 ppm 17aE2 for 20 weeks, our initial results indicate genotype differences in the efficacy of 17αE2 across multiple outcomes.
APOE4 mice exhibited an aged phenotype compared to APOE3, with APOE4 mice having a higher frailty index; however, 17αE2 treatment reduced the frailty index most strongly in APOE4 mice. APOE4 mice were impaired across multiple metabolic measures including body weight, plasma leptin, and hepatic steatosis. 17αE2 significantly attenuated the APOE4 metabolic phenotype. These data confirm and extend prior findings that APOE4 is linked to progeroid effects both peripheral and neural outcomes associated with AD risk. Importantly, 17αE2 significantly improved a range of measures, but showed the strongest effects in the APOE4 genotype.
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Great.
Is there a full paper?
Apoe4 is the #1 risk (not causative) gene for AD.
Improvement in frailty is nice, but sadly where is the cognitive data for these mice? They would have only pursued this work in apoe4 mice for AD implications.
This is the problem with ITP…it’s purely a mouse and cancer model, but we humans die of multiple other causes.
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Its not a paper - it was a poster presented at last summer’s American Aging Association meeting - here is a photo I found online of the poster:
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And a related summary. To get more detail, someone could probably contact the USC authors… please post here if you do.
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Thank you, will followup. Estrogen (loss of) is highly implicated in AD risk for post menopausal apoe4 women.
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Perhaps we need to be making skin cream with rapamycin and 17-alpha estradiol?
A patent application that looks to be from Johnson and Johnson’s China office.
Patent Application: Use of 17-‘alpha’-estradiol for treatment of aged or sundamaged skin and./or skin atrophy
Abstract
The present invention relates to a method for treatment of mammalian skin conditions where stimulated connective tissue synthesis is beneficial, comprising treating skin in need of such treatment with a safe and effective amount of 17-alpha-estradiol.
Description: The 17-alpha-estradiol is in the application on aging or sun damage skin and/or the atrophoderma
skin responds to some estrogen that comprise 17-.Fibroblast in the estrogen chafe, the level of increase connective tissue matrix molecule.When whole body or local approach give estrogen, the synthetic increase of non-protein moleculars such as collagen, elastin laminin and hyaluronic acid.As a result, skin keeps or increase thickness and integrity.These skin appearances are better, and that can resist environment on function stress.When making Local treatment with 17-, the Local treatment of women’s skin of estrogen deficiency also shows the increase of the disappearance of wrinkle, water content and the improvement of skin elasticity.In addition, when injured, can to expect under the estrogenic situation that skin healing gets faster having, because fibroblast is in state of activation.
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Well, it sounds interesting. My reading of the patent information gives me the impression that research for this may have started in the late 1990s. If so, I wonder why it hasn’t come to fruition yet?
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50μg to 70mg is a massive range. How would you even go about measuring 50 μg from a powder?
A very accurate laboratory $cale.
In one of the papers they mix the powder in distilled water for the clinical study. Different levels of dilution of the solution with distilled water will result in different quantities of 17-alpha estradiol being consumed for a given quantity. Not too hard to figure out…
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More good safety news on 17-alpha estradiol:
17α-estradiol does not adversely affect sperm parameters or fertility in male mice: implications for reproduction-longevity trade-offs
Despite an abundance of data indicating that 17α-E2 attenuates several hallmarks of aging in male rodents, very little is known with regard to its effects on feminization and fertility. In these studies, we evaluated the effects of 17α-E2 on several markers of male reproductive health in two independent cohorts of mice. In alignment with our previous reports, chronic 17α-E2 treatment prevented gains in body mass, but did not adversely affect testes mass or seminiferous tubule morphology. We subsequently determined that chronic 17α-E2 treatment also did not alter plasma 17β-estradiol or estrone concentrations, while mildly increasing plasma testosterone levels.
We conclude that chronic treatment with 17α-E2 at the dose most commonly employed in aging research does not adversely affect reproductive fitness in male mice, which suggests 17α-E2 does not extend lifespan or curtail disease parameters through tradeoff effects with reproduction.
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More good news on 17 alpha-estradiol for males:
17α-estradiol, a lifespan-extending compound, attenuates liver fibrosis by modulating collagen turnover rates in male mice
Estrogen signaling is protective against chronic liver diseases…We sought to determine if 17α-estradiol (17α-E2), a naturally-occurring diastereomer of 17β-E2, could attenuate liver fibrosis.
Findings: We found that 17α-E2 significantly reduced collagen synthesis rates and increased collagen degradation rates, which was mirrored by declines in transforming growth factor β1 (TGF-β1) and lysyl oxidase-like 2 (LOXL2) protein content in liver. These improvements were associated with increased matrix metalloproteinase 2 (MMP2) activity and suppressed stearoyl-coenzyme A desaturase 1 (SCD1) protein levels, the latter of which has been linked to the resolution of liver fibrosis. We also found that 17α-E2 increased liver fetuin-A protein, a strong inhibitor of TGF-β1 signaling, and reduced pro-inflammatory macrophage activation and cytokines expression in the liver.
Interpretation: We conclude that 17α-E2 reduces fibrotic burden by suppressing HSC activation and enhancing collagen degradation mechanisms. Future studies will be needed to determine if 17α-E2 acts directly in hepatocytes, HSCs, and/or immune cells to elicit these benefits
Full Paper PDF Here:
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