anabolicminds.com/forum/supplements/165199-dermacrine-pct-needed.html
anabolicminds.com/forum/supplements/229761-dermacrine-supressive.html
and to quote:
The major risk with Dermacrine is suppression of HPTA; forget about suppressing DHEA. Even Eric agrees that LH values have come down drastically once testosterone levels went above baseline. That's why he recommends using the sustain afterward as a "post cycle therapy" for the Dermacrine. Basically the product is too strong of a prohormone. The study that he presented me with shows the test subjects having their Testosterone levels above baseline within 5 days of application of only 50mg/day of DHEA gel; therefore, dropping LH drastically. How about using the Dermacrine for the recommended four weeks??? ... might as well rub the old AndroGel packs on.. lol
I guess there's a huge difference between taking a 25mg orally vs. rubbing the same amount on one's skin. My understanding now is that the anzymes on the skin will convert the DHEA to testosterone, estrogen, etc.. too efficiently. That's why I see similarity to rubbing androgel on which is basically full blown HRT.
At this point I'm thinking I should just select the safe route and do what Dr. John has suggested to me in the first place and just take my LEF 25-50mg/day of oral DHEA... This will provide a very slow build up and avoid the huge jump dermacrine promises coupled with an HPTA shutdown. I just can't afford monkeying around with my HPTA at this point... lol
Or; I may do 5 days of Dermacrine at half the recommended dose and leave it alone; then do blood work a month later.
I'm still undecided.. Any valid input appreciated...
Here's the study:
Effects of transdermal application of DHEA on the levels of steroids, gonadotropins and lipids in men.
In order to ascertain the kinetics of absorption and metabolism of transdermally administered dehydroepiandrosterone (DHEA), 10 men 29-72 years old (mean 52.4+/-14.5) received 50 mg DHEA/day in a gel applied onto the skin of the abdomen for 5 consecutive days. The objective was to establish the extent to which DHEA influences the levels of gonadotropins, sex hormone-binding globulin and lipids. It was found that DHEA is well absorbed and rapidly metabolized to its sulfate (DHEAS), androstenedione, and consequently to testosterone and estradiol. The DHEA levels that markedly increased after the first doses gradually declined already during the application, and this decline proceeded even after it was discontinued, reaching levels significantly lower than the original ones. On the other hand, the levels of DHEA metabolites (with the exception of DHEAS) rose during the application and reached values significantly higher than the basal ones within 5 weeks. This effect was accompanied by significantly decreased levels of LH. The serum levels of lipids, namely of cholesterol (both HDL and LDL cholesterol), triglycerides, apolipoproteins A-I and B and lipoprotein(a) after DHEA application were not changed significantly, and the atherogenic index (AI) remained unaltered. However, some correlations between hormones and lipids were found. Negative correlations concerned the following indices: DHEA/Lp(a); DHEAS/cholesterol; DHEA, DHEAS, testosterone/TG; testosterone/AI. On the other hand, LH, FSH/cholesterol, FSH, SHBG/LDL cholesterol, FSH/Apo B, Lp(a) correlated positively. It can be concluded that transdermal short-time application of DHEA results in a decrease of endogenous DHEA after finishing the treatment, with a parallel marked increase in the levels of sex hormones. Using this application protocol, exogenous DHEA neither altered the lipid spectrum, nor did it influence the atherogenic index.
PMID: 11252535 [PubMed - indexed for MEDLINE]