I have a question about epistane, I read it doesn’t aromatize to estrogen, but in male, I know estrogen are produced by aromatizatio of testosterone, as epistane supress natural testosterone and doesn’t aromatize, how the body produce estrogen in this cas ? (i know a small amount are produced by testicles)
Given appropriate dosing over time, it wouldn’t. Check out the dosing in 1988 study.
Commonly known as ‘epistane’, this compound is the 17-alpha-alkylated version of the known AAS epitiostanol (Fig. 1), an androgen developed in Japan for the treatment of breast cancer (Konishi et al., 1988). Regarded as a steroidal antiestrogen as well as an androgen (Konishi et al., 1988), epitiostanol inhibits the hypothalamic-pituitary-gonadal (HPG) axis (Kurachi et al., 1975) and thus has the potential to cause ASIH (Rahnema et al., 2014). As a 17-alpha-alykylated androgen, there is a potential for hepatotoxicity (Kazlauskas, 2010). Methylepithiostanol has been chemically detected in nutritional supplements and it is suspected that methlyepithiostanol may degrade into the controlled AAS desoxymethyltestosterone (Madol) while in some product containers (Okano et al., 2009). We identified over 30 currently sold products listing methylepitiostanol (2α,3α-epithio-17α-methyl-5α-androstan-17β-ol) as an ingredient on their product label.
The answer to your question, is why most people recommend using testosterone with almost every cycle. To feel good, and get better results, most need estrogen. There are a few compounds that do produce estrogen, or something similar enough (like methylated estrogen) that they can be run solo though.
DHT derivatives, I wouldn’t run solo. You can probably get away with dbol, nandralone (if high enough to get enough E2, and that’s individual if you’ll feel good), and trestalone (Ment).
I understand, so why people speak about clomid for pct when you take compounds that don’t aromatize. If i have a good understanding of the studies and your comment, with these compounds, estrogen levels will be very low, so hypothalamus detect a low estrogen level, and to balance this low level, it will stimulate the testosterone production, so why is a need for product like clomid in this case ?
And a second question, i tought first, non aromatizing coumpound are good because they don’t aromatize, so we don’t have a risk to have too much estrogen, but why people prefer to use this type of coumpound instead of other coupounds like testosterone with a serm to balance the estrogen ?
Ideally, yes. But in practice, no, this doesn’t always happen. This is why PCT exists in the first place. Sometimes, people rebound from a cycle without any PCT, quickly, with no issue. Sometimes, people do a solid pct protocol and still never recover. There is a very broad range of outcomes with this stuff.
So, I have the benefit of having used epistane in isolation, prior to using any other steroid, AND I got blood work done 2-3 weeks after I came off of it. So, at least anecdotally, I can tell you what happened. I can’t say for sure what would have happened if I had waited more than 3 weeks, as I went on TRT at that point in my life, but I can tell you the short term effect on testosterone and estrogen.
In short, both testosterone and estrogen, 3 weeks after my epistane-only cycle, both read at a negligible level. Below the threshold that the tests could read. I think that’s a pretty big deal. You should consider epistane, particularly run on its own, to be extremely suppressive in a very short period of time. I ran it for 5 weeks at the ‘standard’ 40mg dose that was recommended at the time. I think epistane is an excellent steroid, but I would never run it by itself again.
Thanks for the fantastic personal experience and data point @flipcollar. Very suppressive.
Below may be a good link and paper for you to review @Remi1.
Conclusions: 1) T and E2 have independent effects on LH. 2) Inhibition of LH by T requires aromatization for its pituitary, but not hypothalamic effects. 3) E2 negative feedback on LH occurs at the hypothalamus.
This human investigative model employing sex steroid ablation and selective physiological sex steroid add-back in healthy and GnRH-deficient men provides novel insights into the study of LH regulation in men. These data suggest a model of sex steroid feedback whereby 1) T and E2 have independent effects on LH secretion, 2) inhibition of LH by T requires aromatization for its pituitary but not its hypothalamic effects, and 3) E2 has dual sites of feedback, but its predominant effect is at the hypothalamus.
You need to understand the suppressive effects of the epistane itself and not just its indirect supressive effect of limiting E2 production. Check out the AR / ER effects of epistane itself in references above.
Really cool to have such a sweet data point from @flipcollar. Think about what he shared above vs result from coming off 40 mg/day of oxandrolone mono and then testing at 3 weeks post.