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Naltrexone

AWARE72

AWARE72

MuscleHead
Oct 17, 2010
323
18
#1
I been doing some reading on Naltrexone and its use on cycle to stimulate the pituitary gland similar to the use of HCG for the testes. The one thing I've read is that it does not help if you use a progestin-based such a tren. Has anyone used this before? Do you think that it would be worth while to run say after a progestin based like tren? maybe into PCT
 
HawaiianPride.

HawaiianPride.

Senior Member
Oct 21, 2010
152
51
#2
I don't know an excessive amount about this but I might be able to assist...

My buddy previously took this antagonist for his opdiate addiction. He wasn't on any anabolics at the time but he did note that his libido shot way up. This may be a sure indication that it does mimic HCG in a way, via linking the hypothalamus to stimulate the secretion of pituitary hormones. So IMO it would signal the pituitary glands to secrete LH/FSH and the Testes. And we all know the hypothalamus contains neurons that react strongly to all AAS.

In regards to the theory of conflicting Tren's abilities, I would certainly disagree since it acts virtually the same way HCG would. It should even maintain GnRH when on 19-Nor's. What would be even better is if you added a GnRH agonist causing constant stimulation of the pituitary.

Also, from what I've read, you'll get better effects running it the entirety of the cycle, even in PCT. Unless you are already utilizing HCG of course.

Keep in mind, it'll definitely shift your liver values around. Not sure if you are prescribed this or not but if you are, take heed to that. If not, take this into consideration and monitor your liver if you plan on supplementing this in the future.

I wish I had more information and studies on this but I'll definitely look into it tonight and keep you posted.
 
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AWARE72

AWARE72

MuscleHead
Oct 17, 2010
323
18
#3
This is an article I read about it use.

Health and fitness articles: Opioid-Modulation for preventing AAS induced HPTA supression

Essentially, a u-opioid antagonist such as naloxone takes the brakes off of GnRH release and allows pulses of GnRH to occur as if no steroid hormones are present. (17) Naloxone, and related u-opioid antagonists have consistently proven to block the suppressive effects of testosterone, DHT, and estrogen administration in both animals and humans. (18-25) It also appears that these drugs have the ability to increase pituitary sensitivity to GnRH. (26,27)

Remember, progestin based anabolics such as trenbolone and nandrolone are "double suppressive" because they desensitize the pituitary directly by PR activation. It also appears that no opioid receptor antagonist or aromatase inhibitor can prevent suppression via the PR. Therefore, trenbolone or nandrolone are going to cause unavoidable inhibition of HTPA function by causing suppression via the ER, AR and PR. (40,41) If one hopes for a prompt and full recovery post cycle, perhaps progestin based anabolics are better avoided, or at least limited in duration of use.

As it was pointed out earlier in this article, estrogen has a markedly stronger effect on suppression of LH release compared to androgens since estrogen suppresses the hypothalamus and pituitary. Usage of an AI such as anastrozole, letrozole, or exemestane (Aromasin) can reduce estrogen and greatly reduce suppression on GnRH, LH and FSH release by preventing excessive ER activation in the hypothalamus and desensitization of the pituitary GnRH receptors. (35,37,38) Anastrozole has ~50% maximal total estrogen suppression at 1mg/day. Exemestane has ~50% maximal total estrogen suppression at 25mg/day. While letrozole has ~60% at 1mg/day. These are averages based on compiled data from several studies. Similar estrogen suppression can also been seen from only twice a week administration of these AI's. (43-47)
I'm currenlty using HCG at 250iu twice a week and was thinking about maybe adding Naltrexone 50mg twice a week for 4-6 weeks towards end of cycle into PCT.

So any more information that someone has or experiences would be great to hear about...Just doing some reshearch...Thanks!
 
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HawaiianPride.

HawaiianPride.

Senior Member
Oct 21, 2010
152
51
#4
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.
 
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AWARE72

AWARE72

MuscleHead
Oct 17, 2010
323
18
#5
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.

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...

Testosterone does not act directly on the pituitary (the AR),only the ER does. Testosterone requires aromotasation to inhibit piuitary LH/FSH.
I hope it wasn't too much time spent. I think I have your comments qoute here? I am running AI (Aromasin) to keep estro in check. What about the PR being inhibited by a progestin based anabolics such as trenbolone and nandrolone? If I understand this correctly a progestin will act direclty on the pituitary. So this is where I was thinking that the use of Naltrexone would help simulate the pituitary after, let say the use of Tren
 
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