Naltrexone discussion.

[HawaiianPride.]

I'm fairly new to this antagonist and know somewhat about it's correlation and benefits to bodybuilding so I just want to clear the air and see what you guys have to say. (especially you swifto you smart bastard)

Questions first...

1. Has anybody used Nalt before? While on cycle or not, doesn't matter.

2. If so, how were your liver enzymes and did it improve your libido?

3. Did it's effects remind of you HCG ? (in terms of stimulation and curing atrophy)

4. Did you run Nalt with any 19nors? If so, did it have negatively conflict with the AAS in any way?

Now the point of my thread..

I have read that it has the ability to improve an individuals libido. Maybe this may be some type of indication that it does mimic HCG in a way, via linking the hypothalamus to stimulate the secretion of pituitary hormones. If this is the case, then the pituitary glands would in turn, secrete both the luetinizing (spelling?) and follicle stimulating hormones. And since we do know the hypothalamus contains specific neurons that react strongly to AAS, Nalt might be a huge benefit, right? (assuming what I am saying is half correct, lol)

Furthermore, I've read that "stacking" certain GNRH antagonists would enhance the overall objective noted above since it constantly stimulates the pituitary. However, this is where I'm a bit confused. Since certain GnRH antagonists decreases pituitary secretion of the luteinizing hormone and follicle stimulating hormone, and Nalt plays a role in discharging these, what is the point of stacking GnRH antagonists? Is it for the sole purpose of constant overall stimulation?

Hope I didn't confuse anyone, but I'll look more into it tonight. In the meantime if you guys have any input, I'd surely appreciate it.

[Swifto]

GnRH agonist's, not antagonists. So it should increase endogenous LH and FSH.

Unfortunately, I've seen this ripped apart by both Dr. Crisler (Swale) and Dr. Scally, which doesnt do it any favours.

If this does work it still doesnt take account estrogen's inhibitive effect DIRECTLY at the pituitary, nor does it take into account estrogen's DIRECT inhibitory effect on leydig cell function (see where I'm going...).

[Swifto]

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.

HCG is still king, even against newer more advanced compounds being developed.

[Swifto]

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.

There are studies on animals's that state the testes become MORE sensitive without stimulation, that doesnt translate to human's (males) though. Other wise PCT and recovery would be simple and easy after years of HPTA shutdown.

The testes are the weak link in the long chain of endogenous androgen release. So address them directly with HCG or HMG.

I'm not saying Naltrexone has no place, but I think it may be better used during PCT now.

[Swifto]

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. Point 1.

[HawaiianPride.]

That's exactly what I was looking for Swifto. Questions have been answered, and this thread has been bookmarked.

[Swifto]

That's exactly what I was looking for Swifto. Questions have been answered, and this thread has been bookmarked.

Glad I was of some help.

[baseline_9]

Swifto

Can you make some recomendations with regards to this compound and PCT

How would you recomend using it durring PCT....


Example PCT

Week 1. 100mg clomid or 80mg Tore + 40mg nolva
Weeks 2-6 50mg clomid or 40mg Tore + 20mg nolva

Asuming HCG has been run on cycle at 250 IU 3x a week and 'ramped' for the final week, where would the Nalt fit into ur PCT

[brad1986]

I dont see how an opiate blocker relates to aas. It just doesnt sit right with me.

[Lemonada8]

Role of endogenous opiates in the expression of negative feedback actions of androgen and estrogen on pulsatile properties of luteinizing hormone secretion in man.

We have tested the participation of endogenous opiate pathways in the negative feedback actions of gonadal steroids on pulsatile properties of luteinizing (LH) hormone release in normal men. To this end, sex steroid hormones were infused intravenously at dosages that under steady state conditions selectively suppressed either the frequency or the amplitude of the pulsatile LH signal. The properties of pulsatile LH secretion were assessed quantitatively by computerized analysis of LH series derived from serial blood sampling over 12 h of observation. When the pure (nonaromatizable) androgen, 5-alpha-dihydrotestosterone, was infused continuously for 108 h at the blood production rate of testosterone , we were able to achieve selective inhibition of LH pulse frequency akin to that observed in experimental animals after low-dosage androgen replacement. Under these conditions, serum concentrations of testosterone and estradiol-17 beta did not change significantly, but serum 5 alpha-dihydrotestosterone concentrations increased approximately two- to threefold, with a corresponding increase in levels of its major metabolite, 5 alpha-androstan-3 alpha, 17 beta-diol. In separate experiments, the infusion of estradiol-17 beta at its blood production rate over a 4.5-d interval selectively suppressed LH pulse amplitude without influencing LH pulse frequency. Estrogen infusion increased serum estradiol-17 beta levels approximately twofold without significantly altering blood androgen concentrations. We then used these schedules of selective androgen or estrogen infusion to investigate the participation of endogenous opiates in the individual inhibitory feedback actions of pure androgen or estrogen on pulsatile LH release by administering a potent and specific opiate-receptor antagonist, naltrexone, during the infusions. Our observations indicate that, despite the continuous infusion of a dosage of 5 alpha-dihydrotestosterone that significantly suppresses LH pulse frequency, co-administration of an opiate-receptor antagonist effectively reinstates LH pulse frequency to control levels. Moreover, during the infusion of a suppressive dose of estradiol-17 beta, opiate receptor blockade significantly augments LH pulse frequency and increases LH peak amplitude to control levels. Thus, the present studies in normal men demonstrate for the first time that the selective inhibitory action of a pure androgen on LH pulse frequency is effectively antagonized by opiate-receptor blockade. This pivotal observation indicates that opiatergic and androgen-dependent mechanisms specifically and coordinately control the hypothalamic pulse generator for gonadotropin-releasing hormone (GnRH)

[SC_ROYALS]

Shit, i got a 10ml vial of this stuff right now, my buddy is a heroin addict and he gets me free pins, alcohol pads from the needle xchange, lmao.... I gave him a ride last week and he left this shit in my car, I guess dopefiends use this shit in case they OD, seems kinda hard to use if your layin on the ground foaming at the mouth no? Lmao.... I am goin to do further research on this topic, now that i think about it ive seen this stuff advertised on a few "source" websites ive visited. I know I got an unlimited free supply. As the needle exchange gives away free pins, 3cc, and insulin ****, i havent had 2 pay for my pins in years, lol. Thanks to my buddy, if he ever goes and gets cleaned up I might be shit out of luck, lol... cant be mad about that though.... If any of you have any more NEW info, study results, personal results plz enlighten me as im pretty interested in this whole philosophy.