Does the body have a feedback loop for DHT similar to the one for testosterone?
In other words, if the body senses high(er) levels of DHT (thanks to an exogenous source, like the DHT-derived AAS) will it affect test production or the amount of 5-alpha reductase? Can the body even control the amount of 5-alpha reductase? Could this rise in exogenous DHT levels affect the levels of estradiol, since the body breaks testosterone down into estradiol and DHT? [/quote]
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This is sort of a difficult question to answer because of the way it’s phrased, and some of the assumptions made in the initial query. Here’s some information you might find useful, however:
Testosterone is manufactured in the Leydigs cells in the testes, at about 2.5-11mgs/day for the average male, and is largely influenced by another hormone: LH (Leutenizing Hormone). LH promotes the secretion of testosterone by being released in pulses which trigger pulses of testosterone. Both LH as well as testosterone are secreted in pulses between eight and fourteen times, daily. Testosterone secretion typically precedes an LH pulse by approximately one hour.
Testosterone is, of course, controlled via a negative feedback loop. As such, a higher level of testosterone in your body causes a decrease in LH, which in turn causes less testosterone to be released. Testosterone converts to Dihydrotestosterone (DHT) in your body via the 5alpha-Reductase enzyme (5a-R). DHT is very odd from a biological point of view (or from mine, anyway)?more in a second. Testosterone also converts to estrogen via the aromatase enzyme.
DHT is considered quite androgenic compared to testosterone but is not highly anabolic because it is not very active in skeletal muscle (it is enzymatically deactivated by 3-alpha hydroxysysteroid dehydrogenase). However, in most of the body, its androgenic effects are felt quite profoundly: in the brain (the CNS), skin and genitals DHT is the most active androgen because 5-AR is concentrated heavily in practically every androgen-dependent area of the body, barring skeletal muscle. Remember however that 5a-R is not DHT; we need to add testosterone to 5a-R to make DHT.
Now, let?s talk about DHT and 5-alpha-reductase, in terms of LH and testosterone. In some studies (predictably), Dihydrotestosterone has been shown to inhibit LH and FSH secretion and serum testosterone concentrations. In addition, and very importantly for this discussion, the actual conversion process of testosterone being metabolized into DHT via this 5a-R enzyme may act in some way to inhibit Leutenizing Hormone Release (and ergo would inhibit your HPTA and natural testosterone production). Yeah, the actual conversion process is inhibitory, as (apparently) is the actual end product (DHT) to some degree (it’s part of the hormonal cascade and negative feedback loop that controls testosterone production). DHT actually has been shown in cell cultures to be as inhibitory to the LH response on LHRH as Testosterone itself.
We know that anavar is inhibitory to testosterone production (anavar is 2-oxygenated and 17a-alkylated DHT)even in moderate to low doses…while Proviron (which is DHT with the addition of a 1-methyl group) has not been shown to be inhibitory to testosterone production even at pretty high doses.
DHT is actually anti-estrogenic, so the answer to that last question is yes- taking DHT derived drugs will likely have a negative effect on estrogen levels in the body (i.e. they will be lowered).