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I am not aware of any research to date that directly links T to hair loss. Yes, by administration of T there will be conversion to DHT which is, as we all know, strongly associated to hairloss. The problem is that even Dutasteride only inhibits something like 60% of scalp DHT, leaving 40% untouched. Theoretically, a topical regimen could drive this percentage down further, but there are not many success stories out there of topical finasteride/dutasteride (there are, but they are not better than oral finasteride/dutasteride. Also the distinction between purely local action and systemic overspill cannot be made here). Driving scalp DHT down to zero would, according to all the research I did to date, be a cure for androgenic hair loss. Administration of T causes hairloss because there is always overspill to DHT, and even a minute amount of DHT can decimate hair. That does not mean that T itself causes hairloss!Now as far as Yar’s experiment, I personally would not do that. Not unless he was using an androgen that is weaker than testosterone, like a SARM or AAS since they are less androgenic than the androgens you produce endogenously, and could prevent T and DHT from binding to AR. There is a thread on this particular topic and some have had hair gains from taking such compounds orally. I can’t imagine using testosterone and expecting hair to grow though.
To fortify these claims, I did some research on why T would not generally be associated with hairloss. Of course, we are dealing with a far more complex issue that just "this compound binds the AR, so it will induce hairloss". It all depends on the genes that are subsequently transcribed. This article states:
Also from this study:Downstream of AR there are many AR coregulators such as coactivators, integrators or corepressors. One of the AR coactivators, Hic-5/ARA55 (57), is highly expressed in DP cells from androgen-sensitive sites such as Androgenetic Alopecia and beard, suggesting that Hic-5/ARA55 can enhance androgen sensitivity in DP (58). On the other hand, another in situ labelling study showed that expression of another AR coactivator, ARA70, was weaker in the DP of balding recipient areas than in those from the donor areas (59), thus indicating that selective AR coactivators may be involved in the pathogenesis of Androgenetic Alopecia.
In short, T and DHT have different downstream effects and cannot be treated on equal footing. The fact that they are androgens does not say much, only that they latch onto the same receptor. Fun fact: E2 can also bind the AR. Does it induce heavy epigenetic transcription upon binding? Hell no!Moreover, the finding that DHT increases inducible nitric oxide (NO) synthase (iNOS) from occipital DP cells suggests that iNOS and NO are downstream effectors of AR in DP cells (67) (Table S2). Other reported findings are that beard DP cells produce more stem cell factor (SCF) than non-balding scalp DP cells (68) and conversely that balding DP cells produce less SCF than non-balding scalp DP cells (69). However, testosterone did not alter the amount of SCF from balding DP cells.
I would love to have someone point me at research that directly shows that T shortens anagen, because I have been looking for it for a long time. It should be research completely lacking the expression and/or use of 5AR enzymes to exclude overspill effects from DHT.