[size=+2]ANTI-CATABOLICS[/size]
7-oxo DHEA (3-acetoxyandrostat-5-ene-7,17-dione) / 7-ketoDHEA
DHEA finds conversion into some 150 metabolites (that we are currently aware of), each with unique actions within the body. One of the reasons my aforementioned comments about the mother-compound DHEA on how I think it is a prohormone that should in fact be banned are worrisome is due to the likely subsequent banning of potentially-useful metabolites. In the early get-go, 7-oxo, TM’d as 7-keto products seem to hold the most promise supported by the literature. I like its seemingly absent conversion to estrogen or testosterone and its anti-catabolic properties (which are purported to control and/or reduce body fat.
The rationale supplied for use of this compound in the post-cycle era, however, through cortisol suppression, I have never understood effectively as stated in Part II and in various posts. Exogenous androgen introduction tends to universally suppress the adrenal gland via feedback inhibition of ACTH. Recall that ACTH subsequently imparts action on production of various adrenal hormones, in this case cortisol being one. For how this effect is seen here, I offer the following “simplified” model:
Step 1: “On” cycle = exogenous androgen introduction, not only leading to subsequent endogenous shutdown of the Leydig cell production of testosterone through feedback inhibition of the pituitary’s production of LH, but also a negative feedback that mimics adrenal cortical (zona reticularis) overproduction of androgenic outflow offering negative feedback tie-in to ACTH pathways.
Step 2: “Off” cycle (PCT) = cessation of exogenous androgen introduction in a still suppressed ACTH (albeit partial) environment (hypOadrenalism) and subsequent low-level cortisol production, amongst other adrenal byproducts.
Step 3: ACTH regeneration BEFORE LH regeneration (due to partial vs. complete negative feedback mechanisms). The question we set out to answer was when this becomes clinically significant. The answer appears to be more complex than the time I would like to offer here, however, I will summarize a few key points:
(1) Half-life of the exogenous compound seems to play a role on ACTH regeneration (which may seem “common sensical”, but how many automatically have assumed immediate catabolism?).
(2) Many factors (dietary as well as other) seem to impart a role on anti-catabolic nature of post-cycle time frame (again, perhaps another “common-sensical” point, but how often is it seen that people go from a hypERcaloric state while “on” cycle into a state of immediate hypOcalorism?).
(3) Another in-house study has given us some answers into regeneration-time frames. Oveall, the 3-week mark post-cycle appears preliminarily to be a time of universal cortisol up-regulation. The first two weeks are assumed to remain in suppression almost independent of the type of agent used. Use of substances such as 7-oxo / 7-keto compounds seems better left out of post-cycle planning for that immediate 2-week time frame.
[author’s note: complete in-house study results will too appear in upcoming book release!]
