Alright, after much research last night I've gathered a bit of info.
First off, it's GnRH agonist's, not antagonists. Not sure what I did up there but it was late and I was tired.
"Originally Posted by Michael Scally MD View Post
I comment on a separate thread about rhLH. On the thread, I believe I include the following study between hCG and rhLH (Cailleux-Bounacer et al.). One of the primary differences is the half-life, which makes use of rhLH unwieldy and problematic. Interestingly, the abstract following (Handelsman et al.), concludes, "Effective rhLH doping, which relies on a sustained increases in endogenous T, would require much higher and more frequent daily rhLH doses." Add the cost to this and hCG is the hands down choice.
Cailleux-Bounacer A, Reznik Y, Cauliez B, Menard JF, Duparc C, Kuhn JM. Evaluation of endocrine testing of Leydig cell function using extractive and recombinant human chorionic gonadotropin and different doses of recombinant human LH in normal men. Eur J Endocrinol 2008;159(2):171-8. Evaluation of endocrine testing of Leydig cell function using extractive and recombinant human chorionic gonadotropin and different doses of recombinant human LH in normal men -- Cailleux-Bounacer et al. 159 (2): 171 -- European Journal of Endocrinol
BACKGROUND: The functional testing of endocrine testis uses extractive human chorionic gonadotropin (ehCG). Recombinant human hCG (rhCG), avoiding any contamination, should replace ehCG. Moreover, a functional evaluation with recombinant human LH (rhLH) would be closer to physiology than a pharmacological testing with hCG.
METHODS: The study was conducted in normal men. We first evaluated the dose-effect of ehCG on plasma testosterone and estradiol levels, before and after injection of either hCG or vehicle. Secondly, the responses to the optimal dose of ehCG were compared with those of rhCG. Thirdly, we investigated the dose-effect of rhLH, on steroid hormone secretion. LH, testosterone, and estradiol plasma levels were measured after the injection of either rhLH or placebo.
RESULTS: ehCG induced dose-dependent increases in plasma estradiol and testosterone levels. They respectively peaked at 24 and 72 h after the injection. The most potent dose of ehCG (5000 IU) induced results similar to those observed with 250 microg (6500 IU) rhCG. By comparison with placebo, rhLH induced a significant and dose-dependent increase in plasma testosterone levels 4 h after the injection. Peak response of testosterone to rhLH and rhCG was significantly correlated. rhLH did not induce significant change in plasma estradiol level.
CONCLUSIONS: In normal men, a single i.v. injection of 150 IU rhLH induces a 25% rise in plasma testosterone levels by comparison with placebo. At the moment, the dynamic evaluation using hCG remains the gold standard test to explore the Leydig cell function. The use of 250 microg rhCG avoiding any contamination should be recommended.
Handelsman DJ, Goebel C, Idan A, Jimenez M, Trout G, Kazlauskas R. Effects of recombinant human LH and hCG on serum and urine LH and androgens in men. Clin Endocrinol (Oxf) 2009;71(3):417-28.
CONTEXT: The administration of gonadotrophins is prohibited in sport but the effect in men of recently available recombinant hCG and LH on serum and urine concentrations of gonadotrophins and androgens has not been systematically evaluated in the antidoping context.
OBJECTIVE: To determine the time-course of recombinant LH (rhLH) and hCG (rhCG) on blood and urine hormone profiles in men to develop effective tests to detect rhLH and rhCG doping.
DESIGN: Two randomized controlled studies with a 2 x 2 factorial design.
SETTING: Academic research centre.
PARTICIPANTS: Healthy male volunteers aged 18-45 years.
INTERVENTIONS: In the rhLH study, men were randomized into (i) either of two single doses of rhLH (75 IU or 225 IU), and (ii) suppression of endogenous LH and testosterone by nandrolone or no suppression. In the rhCG study, men were randomized into (i) either of two single doses of rhCG (250 or 750 microg), and (ii) suppression of endogenous LH and testosterone by nandrolone decanoate (ND) or no suppression. ND suppression comprised a single dose of 200 mg ND 3 days prior to, and in the rhCG study an additional dose 1 day after gonadotrophin injection.
MAIN OUTCOME MEASURES: Serum and urine hCG, LH, T, T : LH ratio, urine epitestosterone (E) and urine T : E ratio. RESULTS: Neither rhLH dose produced a significant increase in serum or urine LH or T or in the T : E or T : LH ratios regardless of ND-induced suppression of endogenous LH and T. Nor did an even higher dose (750 IU) in three healthy men with unsuppressed gonadal axis. These findings were confirmed with two different commercial LH immunoassays together with adjustment for any influence of urine sediment and dilution. Both rhCG doses produced a steep, dose-proportional increase in serum and urine hCG with increases in serum and urine T and suppression of serum and urine LH, regardless of hCG dose. Serum but not urine T was lowered by ND suppression. The T : LH ratio showed a progressive increase unrelated to rhCG dose or ND suppression, whereas both rhCG and ND suppression minimally increased T : E ratio.
CONCLUSIONS: Both rhCG doses produce a striking increase in serum hCG and T with suppression of serum LH but, at single doses up to 750 IU, rhLH has no influence on serum or urine LH or T. Effective rhLH doping, which relies on a sustained increases in endogenous T, would require much higher and more frequent daily rhLH doses. Use of LH immunoassays optimized for serum to detect rhLH doping by urine LH measurement requires more standardization and validation and, at present, is unreliable. The T : LH ratio is, however, a useful screening test for hCG doping although its utility requires further evaluation."
The fact is the hypothalamus recovers fairly quickly post cycle. I have never had an issue with endogenous LH or FSH post cycle (secondary hypogonadism), only keeping the testes active. The testes are the weak link in the long chain of endogenous androgen release. So address them directly with HCG or HMG.
Don't think Nalt doesn't serve any benefits, but I think it may be better used during PCT now. Another study...
Originally Posted by Michael Scally MD View Post
This is one of the dumbest and foolish posts/articles I have ever read. It does not surprise me though, hucksters like the author are constantly trying to boost their bona fides on this type of garbage. There is absolutely no scientific basis for this except in his imagination. As a note, a few years back I reviewed a supplement the author was trying to develop. I told him in no uncertain terms, the supplement would not work and was potentially harmful. As is typical for many of these so-called ideas/supplements, they only wanted to "persuade" the buying public.
I have many more important projects on my table. However, I will point out over the weekend some of lunacy in this article. I challenge the author to refute my points. Some of the problems are his willingness to misquote and misrepresent authority; use nonhuman studies, and make assumptions without evidence.
First, T and E2 do not act only centrally (hypothalamus). but act at the level of the pituitary.
Second, this model assumes that the only so-called intermediary is the endorphin receptor, which is far from the evidence.
Third, this model takes into account no literature other than that he picks and chooses to try and arrive at a predetermined conclusion, badly. What about the current best evidence for HPTA regulation(i.e., the role of kisspeptin). Of course , this works against his predetermined conclusion!
***Fourth, it is apparent that this author does not know the meaning of "nongenomic." If he did, he would recognize the errors of his ways. The conclusion is that he did this purposefully or does not know the meaning. Either way, this demonstrates the article to be pure unadulterated BS.
Fifth, . . . at a later time.
***In the classical model of steroid action, the effector mechanism involves the binding of steroids either to receptors present in the nucleus or in the cytosol, followed by translocation of the receptor-ligand complex to the nucleus, with subsequent modulation of transcription and protein synthesis.
It has become increasingly clear that rapid actions of steroids, occurring within a few minutes after the addition of the agent, exist that are incompatible with the classical model of action. To address the diversity of mechanisms for rapid steroid signaling described over the past years, a classification of rapid steroid effects has been proposed to promote the discussion and understanding of nongenomic steroid action. In other words, the steroid acts directly upon the cell without the presence of a receptor."
Testosterone does not act directly on the pituitary (the AR), only the ER does. Testosterone requires aromotasation to inhibit piuitary LH/FSH.