Quote:
Originally Posted by Right Hook
Some will debate its suppressive to whatever degree (likely not to bad though). This is why Primordial has gone away from recommending Dermacrine for PCT purpose (contains "topical" DHEA). Either way it seems hit or miss with guys. I have seen some blood tests showing larger increases in E2 comparable to Test increases.
Wiki has a pretty good DHEA diagram as well as Primiordial's site.
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DHEA is suppressive at a elevated dose. That is not a debate here. BUT elevated dosage is the key suggestion here.
You can utilize low doses of testosterone in your PCT so you do not feel like shit, and still recover nicely (And no I am not advising that). Low dosing DHEA during PCT will just turn over test, and help you feel better along the way. The estrogen should be controlled while in PCT as for the increases in such. Not to mention the LDL help along the way.
Dehydroepiandrosterone reduces serum low density lipoprotein levels and body fat but does not alter insulin sensitivity in normal men.
Nestler JE,
Barlascini CO,
Clore JN,
Blackard WG.
Division of Endocrinology and Metabolism, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298.
To assess the effects of dehydroepiandrosterone (DHEA) on body fat mass, serum lipid levels, and tissue sensitivity to insulin, five normal men were given placebo and five normal men were given oral DHEA [1600 mg/day (554.7 mmol/day)] for 28 days in a randomized, double blind study. In the DHEA group serum DHEA-S levels rose 2.5- to 3.5-fold, and mean (+/- SEM) serum androstenedione rose from 4.3 +/- 0.6 to 8.6 +/- 1.2 nmol/L (P less than 0.004, by paired t test), but serum total testosterone, free testosterone, sex hormone-binding globulin, estradiol, and estrone levels did not change. In the DHEA group the mean percent body fat decreased by 31%, with no change in weight. This suggests that the reduction in fat mass was coupled with an increase in muscle mass. DHEA administration also resulted in a fall in mean serum total cholesterol concentration (4.82 +/- 0.21 vs. 4.48 +/- 0.29 nmol/L; P less than 0.05), which was due almost entirely to a fall of 7.5% in mean serum low density lipoprotein cholesterol (3.21 +/- 0.11 vs. 2.97 +/- 0.14 nmol/L; P less than 0.01). No changes in anthropometric parameters or serum lipid levels occurred in the placebo group. Tissue sensitivity to insulin, assessed by the hyperinsulinemic-euglycemic clamp technique, did not change in either the placebo or DHEA groups. These results suggest that in normal men DHEA administration reduces body fat, increases muscle mass, and reduces serum low density lipoprotein cholesterol levels. Tissue sensitivity to insulin was unaffected by short term DHEA administration.
1: J Steroid Biochem Mol Biol. 2006 Apr;99(1):50-8. Epub 2006 Mar 9. Links
Dehydroepiandrosterone and its metabolites: differential effects on androgen receptor trafficking and transcriptional activity.
Mo Q,
Lu SF,
Simon NG.
Department of Biological Sciences, Lehigh University, Bethlehem, PA 18015, United States.
Dehydroepiandrosterone (
DHEA) is a multi-functional steroid that has been implicated in a broad range of biological effects in humans and rodents. Recent studies demonstrated that
DHEA acts genomically through the androgen receptor (AR) in addition to its well-known effects on cell surface receptors. However, the relative contribution of
DHEA and its major metabolites, including DHEA-Sulfate (DHEA-S), 7alpha-OH-DHEA, 7beta-OH-DHEA, 7-oxo-DHEA, androstenedione (Adione), and androstenediol (Adiol), in the production of genomic effects remains controversial, in part because the metabolism of
DHEA varies in different cells and tissues. In the current study, the ability of
DHEA and its metabolites to promote AR intracellular trafficking and regulate AR-mediated reporter gene expression, which are characteristic effects of androgens, was determined. Intracellular trafficking of AR-GFP protein was assessed in COS-7 cells while AR transcriptional activity was tested in CV-1 cells transiently co-transfected with AR expression plasmid and an MMTV-ARE-CAT reporter. The results demonstrated that
DHEA, the 3beta-HSD metabolite Adione, and the 17beta-HSD metabolite Adiol, were androgenic. Each promoted AR-GFP intracellular trafficking, the formation of nuclear clusters, and AR-dependent transcriptional activity in a dose-dependent manner. In contrast, DHEA-S, 7alpha-OH-DHEA, 7beta-OH-DHEA, and 7-oxo-DHEA were ineffective and exhibited minimal androgenic activity, even at relatively high concentrations (10(-6) M). These results provide the first systematic comparison of the (i) androgenic activity of
DHEA and its sulfated and hydroxylated metabolites, (ii) relative androgenicity of
DHEA itself vs. the established androgens Adione and Adiol, and (iii) ability of
DHEA and its major metabolites to promote AR-GFP intracellular trafficking. In addition to partitioning
DHEA and its metabolites into compounds with (
DHEA, Adione, Adiol) and without (DHEA-S, 7alpha-OH-DHEA, 7beta-OH-DHEA, and 7-oxo-DHEA) androgenic activity, the findings improve our understanding of the intracellular processes mediating the genomic effects of
DHEA through AR.
PMID: 16524719 [PubMed - indexed for MEDLINE]
Adams