Is there a widely available blood test for this?
Yea a basic testosterone test that shows LH levels as well. You would need a before test.
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We need to define an ideal “pre-test” and “post-test” protocol and for 17 alpha estradiol, so we can more easily track possible side effects and benefits of this compound… because it hasn’t yet gone through clinical trials in healthy males. If people are using this, or planning to use this compound, please review all the literature here: 17-Alpha Estradiol - Another Top Anti-Aging Drug
And try to develop what we should/might do for pre-testing (blood tests, etc.) and post testing, and post that information here for discussion.
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Since 17-AE is a weak estrogen I think there is good reason to think it will act like a SERM in men(Selective Estrogen Receptor Modulator). A SERM stimulates the HPTA axis by docking in the estrogen receptor of the hypothalamus with low/no estrogenic activity and thus stimulates endogenous LH/FSH and testosterone production. If true then blood tests should indicate elevated testosterone and estrogen levels in men with functional HPTAs. Of course if you are on TRT this will not be the case as endogenous test production is muted.
I think this jives well with Dr. Ecsta’s claim of increased acne. I would expect symptoms of elevated androgens like acne and libido.
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This makes sense. When they autopsied the mice didn’t they find the ones on 17ae2 had greater muscular and bone density? I think Richard Miller mentioned that in a podcast
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What proportion of transcutol did you use with Ell-Cranell ? 1:1 ?
I just ordered 300 ml Pantostin from Germany apohealth.de for 45.30 Euro ($48.62 on my Bank of America credit card) and shipping is free to USA.
I plan to mix with 25% transcutol (like Boldi suggested) (500ml Diethylene Glycol monoethyl Ether available from Eastchem on Amazon.com for $76) and apply 1ml Pantostin (0.25mg 17alpha-Estradiol) per day on my forearm.
Update : Lotioncrafter.com has Ethoxydiglycol 1 lb for $30.25, including shipping + tax and includes a certificate of analysis (claims to be 99.5% pure, vs 99% for the Eastchem version on amazon.com)
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Please do some pre and post blood testing and let us know how your experiment goes.
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I plan to do LEF CBC ($35) + CRP ($42) + Basic Male Hormones ($75 Estradiol + Free/Total Testosterone + PSA) + DHT ($50), figuring that 17alpha-Estradiol’s effect as a DHT blocker (like Finesteride and Duasteride) may need to be monitored.
Anything else ?
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Maybe albumin, SHBG, LH, and FSH. You could consider IGF
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Great suggestions :
I will add LH+FSH ($55 from LEF) for the baseline tests (and 1 month and 3 month follow up) after getting the Pantostin from Germany.
I already plan to do IGF1 + sirolimus to monitor my Rapamycin dosing. I get SHBG twice a year, so will defer that till my next test in April since that is unlikely to change rapidly.
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17 alpha estradiol binds to ER alpha receptors and I’m concerned of activation of autoimmune- of personal risks I have lupus. I currently have 17 alpha estradiol on-hand, but very concerned of using it.
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Yes - that seems to be the case. You probably want to discuss these with a doctor who can help you work through all this science and figure out what is best for you given your situation…
Herein, we show that 17α-estradiol elicits similar genomic binding and transcriptional activation through estrogen receptor α (ERα) to that of 17β-estradiol. In addition, we show that the ablation of ERα completely attenuates the beneficial metabolic effects of 17α-E2 in male mice. Our findings suggest that 17α-E2 may act through the liver and hypothalamus to improve metabolic parameters in male mice. Lastly, we also determined that 17α-E2 improves metabolic parameters in male rats, thereby proving that the beneficial effects of 17α-E2 are not limited to mice. Collectively, these studies suggest ERα may be a drug target for mitigating chronic diseases in male mammals.
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My background is microbiology so I have an understanding of mechanisms of each anti-aging compound, but generally on a large scale 17 alpha estradiol may be risky for average people as well because of the unspecific autoimmune attacks that increase with aging. The problem with these compounds is we’re looking at crude measurements.
There’s a ton of evidence, but it shows that ER alpha binding affinity is the primary reason for female specific autoimmune risk.
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Can you please post more detail on what the risk specifically is, as you understand it. I’m not familiar with this literature at all. Help us understand this risk as you see it, and any pointers to the literature greatly appreciated. By binding to the estrogen receptor (ERα), it increases risk of auto immune disorders (in both males and females?)
I look at this, and while it seems relevant to Lupus patients, Estrogen Receptor Alpha Signaling Is Responsible for the Female Sex Bias in the Loss of Tolerance and Immune Cell Activation Induced by the Lupus Susceptibility Locus Sle1b - PMC
I’m not clear why its relevant to the broader population of males considering 17 alpha estradiol.
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Can you share where you got this test information? Is this a 23&Me thing?
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This study used 3 min sublingual in 50% ethanol and got good results;
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There’s a lot to this to generalize and provide data for, but understanding the fundamentals of rheumatology, unspecific autoimmune attacks increase with age, that’s why immunity should not be boosted in aging populations rather than modulated which we do not have therapies for.
Estrogen is known to be a primary cause of autoimmune disorders in males and females. ER alpha rather than beta is the greatest risk factor. Although receptor density is different, the risks are the same for both male and female, but greater in women.
The topic is not only lupus, fundamentally autoimmune conditions or unspecific age-related attacks. Based on this evidence on a large population scale, 17 alpha estradiol and healthspan indication, it does not meet the criteria. Even if someone doesn’t have a diagnosed autoimmune condition it will still increase the risk of age-related autoimmune attacks.
It is an interesting compound nonetheless and we can learn from it, I’m not confident its actionable for large populations especially when some of the risks are not easily measurable.
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Are you aware of any data that suggests that women taking Estradiol as HRT have increased risk of auto-immune disease (compared to women not taking Estradiol)? It seems that men taking the 17-Alpha estradiol version may be a comparable situation.
I’m just trying to get some better quantification data on the risks. If anyone can find numbers on the absolute risk, it would be intereting.
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Some resources for people who want to learn more about this possible risk:
Here: https://www.scientificamerican.com/article/why-nearly-80-percent-of-autoimmune-sufferers-are-female/
Here: https://www.medpagetoday.com/meetingcoverage/oar/74787
Here: Sex Hormones in Acquired Immunity and Autoimmune Disease - PMC
Increased risk [of Lupus] has been associated with higher lifetime levels of estrogen exposure. In a cohort of 238,308 adult women evaluated prospectively over 27 years, the 262 women diagnosed with SLE over the course of the study were analyzed for relative risk factors. Increased risk was associated with early menarche (aged less than 10 years; relative risk: 2.1; 95% CI: 1.4–3.2) and oral contraceptive use (relative risk: 1.5; 95% CI: 1.1–2.1).[69] Menstrual irregularity increased risk of SLE diagnosis in a Japanese case–control study.[70] Menstrual cycles of abnormal length (either long and short) increased risk as well.[71] Estradiol treatment of mouse lupus-prone strains produces disease onset, increases autoantibody production, and increases risk of mortality.[23]
Above Quote, from Here: https://www.medscape.com/viewarticle/775536_6
Here: https://www.tandfonline.com/doi/full/10.1586/eci.10.60
Here (PDF) Sex-based Differences in Auto-immune Diseases
Quote from the above PDF:
Generally, estrogens, in particular 17- β *estradiol (E2) and prolactin, act as enhancers at least of humoral immunity, and testosterone and progesterone as natural immunosuppressants [3]. Sex hormones have different effects depending not only on the concentration but also on the type of target cell and the receptor subtype expressed on a given cell type.
At periovulatory to pregnancy levels [8], E2 has mainly anti-inflammatory effects, by inhibiting production and signaling of pro-inflammatory cytokines, such as tumor necrosis factor (TNF), interleukin (IL)-1* β and IL-6, and natural killer (NK) cell activation, and by inducing expression of anti-inflammatory cytokines favoring a T helper 2 (Th2) phenotype [9], such as IL-4, IL-10 and transforming growth factor (TGF)-* β*, and by activating regulatory T cells (Treg) [10]. At lower concentrations, E2 stimulates TNF, interferon (IFN)-* γ*, IL-1* β *and NK cells, while it enhances antibody production by B cells both at high and low concentrations [9]. Prolactin increases antibody production, regulates the development of CD4+ T cells and triggers pro-inflammatory cytokine production [11].
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