What
@Zarati is doing makes all the sense in the world, and his competence doesn't surprise me - he and I have chatted variously about cycle design; he's knowledgeable. His application of T gel/cream also is supported for everything that he has said; and is in many ways superior to i.m. for that use.
10 mg/d Dianabol is about as androgenic as TRT (true replacement). It is also highly resistant to SHBG.
It is, therefore, at least at a glance, a sound strategy for this use.
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I will just interject a few points of my own, that are things that I have come to believe are true but that are very much minority viewpoints; but I that I believe to be true, nonetheless.
Firstly, I believe that aromatization (Dbol satisfies this) &
5α-reduction are important biological functions of T (Dbol does
not satisfy this function, it is 5β-reducible) for all of T's biological functions, including - importantly - sexual function.
T's 5α-reductase product, 5α-DHT (DHT; dihydrotestosterone) acts in periperpheral (e.g., gonadal) and CNS tissues to support male sexual function.
Secondly, I believe that for Zarati's purposes, combination with Halotestin (Androxy; fluoxymesterone) would be ideal (e.g., 5 + 5 mg). Besides having even less SHBG binding affinity than Dbol, it is 5α-reducible, itself potently androgenic, and actually is, and certainly has been, used clinically for this purpose - supporting sexual function in male hypogonadism - typically starting at 10 mg/d and titrating based on symptoms.
Famously, J.F.K. was prescribed Halotestin; and his reputation for promiscuity is legendary.
Thirdly, Halo is not without its own tradeoffs (see, every decision has them). It is more expensive and less available, is virtually nonaromatizable (hence, its being combined with Dbol)
, and competitively inhibits 11β-HSD2, thereby leading to glucocorticoid-mediated MR activation & therefore has particular cardiovascular disease risks (shared by trenbolone, Anadrol, and others; Halo is sort of medium-strong in this inhibition).
Reasonable minds may differ on their calculus of whether to combine the two based on those tradeoffs. My views are in the minority. Most scientists believe that androgenicity is androgenicity is androgenicity; and that 5α-reduction is inherently bad (because prostate); to which I pose the question: if these things are true, why is MENT unable to consistently and reliably support sexual function while serving as a male contraceptive?