The drop in libido is very real, but I might not be comparing it to baseline here. Previously I have been taking tons of stuff that boosts libido, but for this log I wanted to use bulbine as my only herbal. Before this I was taking a gram of lj100, tribulus, pink magic, t-911, sustain alpha - all stuff that boosts libido.
Also it could be the anti-estrogen effect. I am not sure how or why estrogen affects libido, but I think I am responding really well in this aspect. Someone suggested I try some dermacrine along with the bulbine. I think my estrogen has tended to be on the higher end of the spectrum and dermacrine exacerbates that issue. I started getting puffy on dermacrine, so I am going to try that out after running phytoserms-347 for a whole month without anything else. Next month I am going to start adding to the bulbine and see what stacks well with it.
You would think that Dermacrine (transdermal only) being as powerful of a test booster that it is would raise estrogen levels. But That is not the case at all my friend.
First off lets take a look at a few studies
Physiological changes in dehydroepiandrosterone are not reflected by serum levels of active androgens and estrogens but of their metabolites: intracrinology.
Labrie F, Belanger A, Cusan L, Candas B.
Medical Research Council Group in Molecular Endocrinology, Centre Hospitalier de l'Universite Laval Research Center, Le Centre Hospitalier Universitaire de Quebec, Canada.
This study analyzes in detail the serum concentration of the active androgens and estrogens, as well as a series of free and conjugated forms of their precursors and metabolites, after daily application for 2 weeks of 10 mL 20% dehydroepiandrosterone (DHEA) solution on the skin to avoid first passage through the liver. In men, DHEA administration caused 175%, 90%, 200% and 120% increases in the circulating levels of DHEA and its sulfate (DHEA-S), DHEA-fatty acid esters, and androst-5-ene-3 beta,17 beta-diol, respectively, with a return to basal values 7 days after cessation of the 14-day treatment. Serum androstenedione increased by approximately 80%, whereas serum testosterone and dihydrotestosterone (DHT) remained unchanged. In parallel with the changes in serum DHEA, the concentrations of the conjugated metabolites of DHT, namely androsterone glucuronide, androstane-3 alpha,17 beta-diol-G, and androstane-3 beta,17 beta-diol-G increased by about 75%, 50%, and 75%, respectively, whereas androsterone-sulfate increased 115%. No consistent change was observed in serum estrone (E1) or estradiol (E2) in men receiving DHEA, whereas serum E1-sulfate and E2-sulfate were slightly and inconsistently increased by about 20%, and serum cortisol and aldosterone concentrations were unaffected by DHEA administration. Almost superimposable results were obtained in women for most steroids except testosterone, which was about 50% increased during DHEA treatment. This increase corresponded to about 0.8 nM testosterone, an effect undetectable in men because they already have much higher (approximately 15 nM) basal testosterone levels. In women, the serum levels of the conjugated metabolites of DHT, namely androsterone glucuronide, androstane-3 alpha,17 beta-diol-G, androstane-3 beta,17 beta-diol-G, and androsterone-sulfate were increased by 125%, 140%, 120% and 150%, respectively. The present study demonstrates that the serum concentrations of testosterone, DHT, E1, and E2 are poor indicators of total androgenic and estrogenic activity. However, the esterified metabolites of DHT appear as reliable markers of the total androgen pool, because they directly reflect the intracrine formation of androgens in the tissues possessing the steroidogenic enzymes required to transform the inactive precursors DHEA and DHEA-S into DHT. As well demonstrated in women, who synthesize almost all their androgens from DHEA and DHEA-S, supplementation with physiological amounts of exogeneous DHEA permits the biosynthesis of androgens limited to the appropriate target tissues without leakage of significant amounts of active androgens into the circulation. This local or intracrine biosynthesis and action of androgens eliminates the inappropriate exposure of other tissues to androgens and thus minimizes the risks of undesirable masculinizing or other androgen-related side effects of DHEA.
PMID: 9253308 [PubMed - indexed for MEDLINE]
This study proves that Transdermal DHEA causes a marked increase to both test ( but more so androgens overall) . Also that in woman Transdermal DHEA will send there tesosterone levels sky high.
At the same time it should be dually noted that the study was done on the 2 week mark. Through my studies,self administration/testing, and speaking with others. The 2 week mark is the point at which Transdermal DHEA reaches "Peak levels of circulating DHEA" It is beyond this point that the body then begins to utilize these high circulating dhea levels and and moves into a Peak conversion state.
Now From My own experience through studding the subject as well as doing my own testing I have found that the product Dermacrine when administered Topically on the skin not only raises DHEA levels and tesosterone levels, but it also lowers estrogen rather then raises it.
Here you can see My before Dermacrine and after (trandermal) dermacrine results. The paperwork states I was using oral dhea but that was a mistake on my part in filling out the paperwork. But this was done well using Transdermal Dermacrine only and was done for the sole reason of finding out what effects it would have on me. Now you can see that at the 2 week mark my DHEA levels were about triple and my tesosterone levels were double. Then Interestingly you will notice my estrogen levels were decreased .I feel this proves Transdermal Chrysin and Resveratrol do a good enough job of preventing any conversion to estrogen.
From what I have read, seen, heard from others, and experienced My self is that the Transdermal dermacrine works awesome for raising test levels and does not significantly raise estrogen levels. More often then not it lowers estrogen levels