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maxititer
02-10-2009, 01:46 AM
Mr. Naltexone - definite male

This is very valuable drug for those who running long bulking cycles and it was neglected for long time. In fact natrexone may become a revolutionary drug or may remains in private domain. In any way it is up to you to decide and I'm posting here natrexone related abstracts for your consideration.



Naltrexone administration modulates the neuroendocrine control of luteinizing hormone secretion in hypothalamic amenorrhoea
Alessandro D. Genazzani1, Mario Gastaldi, Felice Petraglia, Cesare Battaglia, Nicola Surico2, Annibale Volpe and Andrea R. Genazzani3

Department of Physiopathology of Human Reproduction, University of Modena Italy 2Department of Obstetrics and Gynecology, University of Novara Italy 3Department of Obstetrics and Gynecology, University of Pisa Italy

Correspondence: 1 To whom correspondence should be addressed at: Department of Obstetrics and Gynecology, University of Modena, Via del Pozzo 71, 41100 Modena, Italy

Because endogenous opioids have been considered to be deeply involved as a causal factor of hypothalamic amenorrhoea, this study was designed to evaluate the efficacy of the administration of naltrexone, an antagonist of opioid receptors, on luteinizing hormone (LH) secretion in patients with hypothalamic amenorrhoea. A total of 30 patients with hypothalamic amenorrhoea were studied. Patients were divided into two groups: group A, hypogonadotrophic (n = 15), and group B, normogonadotrophic (n = 15). All patients were administered naltrexone at a dose of 50 mg/day per os for 6 months. A third group of 10 amenorrhoeic patients was treated with placebo per os with the same schedule. All patients were evaluated for LH spontaneous pulsatile release in baseline conditions and after 3 and 6 months of treatment. Plasma gonadal steroid concentrations increased significantly in all patients after 3 months of naltrexone therapy, but only hypogonadotrophic patients showed a sharp increase in both LH plasma concentrations and LH pulse amplitude within the first 3 months of treatment which remained unchanged until the sixth month of treatment. Plasma follicle stimulating hormone concentrations did not change significantly in any patient. Menstrual bleeding occurred within 90 days of the beginning of treatment in 24 out of the 30 patients. Patients treated with placebo did not show a significant change in gonadotrophin and gonadal steroid plasma concentrations. The results of our study support the efficacy of naltrexone administration on neuroendocrine pathways controlling LH secretion in patients with hypothalamic amenorrhoea.So, it is good for bridges too, b/c it can increase "Plasma gonadal steroid concentrations"


Neuroendocrine Abnormalities in Hypothalamic Amenorrhea: Spectrum, Stability, and Response to Neurotransmitter Modulation1
Rebecca B. Perkins, Janet E. Hall and Kathryn A. Martin

Reproductive Endocrine Unit, Reproductive Endocrine Sciences Center and National Center for Infertility Research, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114

Address correspondence and requests for reprints to: Kathryn A. Martin, Reproductive Endocrine Unit, Massachusetts General Hospital, Bartlett Hall Extension 5, 55 Fruit Street, Boston, Massachusetts 02114.


To characterize the neuroendocrine patterns of abnormal GnRH secretion in hypothalamic amenorrhea (HA), 49 women with primary and secondary HA underwent frequent sampling of LH in a total of 72 baseline studies over 12–24 h. A subset of women participated in more than one study to address 1) the variability of LH pulse patterns over time; and 2) the impact of modulating opioid, dopaminergic, and adrenergic tone on LH secretory patterns.

The frequency and amplitude of LH secretion was compared with that seen in the early follicular phase (EFP) of normally cycling women. The spectrum of abnormalities of LH pulses was 8% apulsatile, 27% low frequency/low amplitude, 8% low amplitude/normal frequency, 43% low frequency/normal amplitude, 14% normal frequency/normal amplitude. Of patients studied overnight, 45% demonstrated a pubertal pattern of augmented LH secretion during sleep. Of patients studied repeatedly, 75% demonstrated at least 2 different patterns of LH secretion, and 33% reverted at least once to a normal pattern of secretion. An increase in LH pulse frequency was seen in 12 of 15 subjects in response to naloxone (opioid receptor antagonist). Clonidine (alpha-2 adrenergic agonist) was associated with a decrease in mean LH in 3 of 3 subjects. An increase in LH pulse frequency was seen in 4 of 8 subjects in response to metoclopramide (dopamine receptor antagonist), but the response was not statistically significant. Baseline abnormalities in LH secretion did not appear to influence response to neurotransmitter modulation. Conclusions: 1) HA represents a spectrum of disordered GnRH secretion that can vary over time; 2) LH pulse patterns at baseline do not appear to influence the ability to respond to neurotransmitter modulation; 3) Opioid and adrenergic tone appear to influence the hypothalamic GnRH pulse generator in some individuals with HAno comments


The frequency of gonadotropin-releasing hormone stimulation determines the number of pituitary gonadotropin-releasing hormone receptors.

Katt JA, Duncan JA, Herbon L, Barkan A, Marshall JC

Gonadotropin-releasing hormone [?] (GnRH) induces both synthesis and release of pituitary gonadotropins, but rapid or slow frequencies of stimulation result in reduced LH and FSH secretion. We determined the effects of frequency of GnRH stimulation on pituitary GnRH receptors (GnRH-R). Castrate male rats received testosterone implants (cast + T) to inhibit endogenous GnRH secretion. GnRH pulses were injected by a pump into a carotid cannula and animals received GnRH (25 ng/pulse) at various frequencies for 48 h. In control animals (saline pulses) GnRH-R was 307 +/- 21 fmol/mg protein (+/- SE) in cast + T and 598 +/- 28 in castrates. Maximum GnRH-R was produced by 30-min pulses and was similar to that seen in castrate controls. Faster or slower frequencies resulted in a smaller GnRH-R response and GnRH given every 240 min did not increase GnRH-R over saline controls. Equalization of the total GnRH dose/48 h (6.6 ng/pulse every 7.5 min or 200 ng/pulse every 240 min) did not increase receptors to the maximum concentrations seen after 30-min (25 ng) pulses. Serum LH responses after 48 h of injections were only present after 30-min pulses, and peak FSH values were also seen after this frequency. Serum LH was undetectable in most rats after other GnRH frequencies, even though GnRH-R was increased. These data show that GnRH pulse frequency is an important factor in the regulation of GnRH-R. A reduction of GnRH-R is part of the mechanism of down-regulation of LH secretion by fast or slow GnRH frequencies, but altered frequency also exerts effects on secretory mechanisms at a site distal to the GnRH receptor.Important poin here is that the number of gonadotropin-releasing hormone receptors in pituitary and as well response on stimulation depend on frequency of gonadotropin-releasing hormone secretion.
If no secretion for long time, like during long cycle, number of gonadotropin-releasing hormone receptors in pituitary will be near zero. We can stimulate testes by HCG, but how we can restore number of gonadotropin-releasing hormone receptors in pituitary.

In short, just take some naltrexone during long cycle and it is better.

Morphine exerts testosterone-like effects in the hypothalamus of the castrated male rat.
Cicero TJ, Meyer ER, Gabriel SM, Bell RD, Wilcox CE.

Previous research has indicated that endogenous opioids participate in the regulation of activity in the hypothalamic-pituitary-luteinizing hormone (LH) axis and mediate the negative feedback control exerted by testosterone. If this assumption is correct, then two predictions can be made. First, the effects of testosterone should be competitively inhibited by narcotic antagonists; and, second, opiates should mimic the acute and chronic effects of testosterone in the castrated male rat. The results of the present investigations support both of these predictions. We found that naloxone competitively antagonized the depressive effects of testosterone on serum LH in the castrated rat and, conversely, that testosterone competitively antagonized the LH-releasing properties of naloxone. In addition, morphine and testosterone both depressed serum LH levels in a dose-dependent fashion in the acutely castrated animal. Moreover, morphine was just as effective as testosterone in reversing the castration-induced fall in hypothalamic-LH-releasing hormone (LH-RH), which occurs in the chronically castrated male rat. On the other hand, morphine failed to reverse the long-term changes in pituitary LH content and increase in serum LH, which is consistent with prior observations that morphine affects only the hypothalamic aspect of the hypothalamic-pituitary-LH axis in the male rat. These results, thus, support the concept that an as yet unidentified opioid-containing neuronal system regulates activity in the hypothalamic-pituitary-LH axis and mediates the effects of testosterone on this axis.

PMID: 7427731 [PubMed - indexed for MEDLINE]hello morphine, bye bye testosterone


Endogenous opioids participate in the regulation of the hypothalamus- pituitary-luteinizing hormone axis and testosterone's negative feedback control of luteinizing hormone

TJ Cicero, BA Schainker and ER Meyer

Two narcotic antagonists, naloxone and naltrexone, significantly elevated serum LH levels in male rats within minutes after their sc injection. The peak increase in serum LH occurred 20 min after the injection. Naloxone increased LH levels up to a dose of 1 mg/kg, after which no further increases were found. A dose of 0.35 mg/kg produced a half-maximal response. The exogenous opioid morphine blocked the increase in LH produced by naloxone in a dose-dependent fashion, suggesting that the specific receptor-blocking effects of the antagonist could account for its enhancement of serum LH levels. The locus of action of naloxone within the hypothalamic-pituitary-LH axis appeared to be at the level of the hypothalamus since the drug had no effect on LHRH-stimulated release of LH by the anterior pituitary and did not block dihydrotestosterone's suppression of pituitary LH release in vitro. Naloxone also prevented testosterone's negative feedback inhibition of serum LH in the castrated male rat. The results of these studies suggest that endogenous opioids exist in brain tissue which normally inhibit activity in the hypothalamic-pituitary-LH axis and participate in the androgen-dependent feedback control of LH elaboration by this axis.That is some thing what is definitely wrong in human body design.
Happy man with a lot of endorphins cannot have good amount of testosterone, that is wrong design, comrade God.


Role of endogenous opiates in the expression of negative feedback actions of androgen and estrogen on pulsatile properties of luteinizing hormone secretion in man.
J D Veldhuis, A D Rogol, E Samojlik, and N H Ertel
This article has been cited by other articles in PMC.
Abstract
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)One more prove of concept of wrong design and that been a happy man and testosterone man is not the same.


Naltrexone-Induced Augmentation of Sexual Response in Men


To ascertain the role of endogenous opioids in sexual response, naltrexone, an opiate receptor antagonist, was administered to men, and its effect on selected self-report measures of sexual response to masturbation was recorded.
Methods

The data are based on results from 20 healthy, sexually active (alone or with a partner) men, aged 20–29 years, who ingested naltrexone (25 mg/day × 3) or placebo in a randomized, double-blind crossover design. There was at least a 14-day interval between drug and placebo treatment. Between 18 and 22 h after the most recent dose of drug or placebo, subjects viewed sexually explicit videos in privacy for 2 h. They were instructed to masturbate and have as many orgasms as desired. The following three different self-report measures of their responses were recorded: number of orgasms; intensity of sexual arousal, and orgasmic intensity.
Results

Under the naltrexone condition, the volunteers experienced a significantly greater mean number of orgasms (3.4 ± 0.2 SEM) than under the placebo condition (2.6 ± 0.3). The total number of orgasms was 67 under the naltrexone condition and 51 under the placebo condition. At the first orgasm, the measure of intensity of arousal was significantly greater in the naltrexone (3.9 ± 0.2) than placebo (3.4 ± 0.2) condition, and the measure of orgasmic intensity was significantly greater in the naltrexone (3.7 ± 0.2) than in the placebo (3.0 ± 0.3) condition.
Conclusions

The present study provides evidence that endogenous opioids modulate orgasmic response and the perceived intensity of sexual arousal and orgasm in men. The findings suggest that naltrexone could be clinically useful in cases of inhibited sexual desire and erectile dysfunction.Wow, that is statistically significant orgasmic drug
The total number of orgasms was 67 under the naltrexone condition and 51 under the placebo condition.


sexually active (alone or with a partner) men - sorry for that


Influence of nandrolondecanoate on the pituitary-gonadal axis in males.
Bijlsma JW, Duursma SA, Thijssen JH, Huber O.

Different anabolic steroids can exercise different effects on the pituitary-gonadal axis in males. During a pilot study regarding the possible beneficial effect of the anabolic steroid nandrolondecanoate (ND) on bone metabolism in patients with rheumatoid arthritis additional endocrinological parameters were studies. A significant decrease was found in the serum levels of testosterone, androstenedione and FSH and the ratio of testosterone/oestradiol. There was a significant increase in the serum levels of oestrone. The levels of oestradiol, SHBG, LH and cortisol remained unchanged. An inhibitory effect of ND on testicular testosterone secretion is assumed. The decrease in androstenedione levels is explained by the diminished testosterone secretion. The rise in oestrone levels is explained by peripheral aromatizing of ND to oestrogens. The presented findings are in accordance with the hypothesis that sex steroids can act directly on the pituitary resulting in selective FSH and LH secretion. The possible role of the ratio testosterone/oestradiol in controlling gonadotrophin output is discussed.some bad message for deca lovers.


Effect of antagonists of dopamine and opiates on the basal and GnRH-induced secretion of luteinizing hormone, follicle stimulating hormone and prolactin during lactational amenorrhoea in breastfeeding women
C.C.K. Tay1, A.F. Glasier2,3 and A.S. McNeilly2,4

1Department of Obstetrics and Gynaecology, University of Edinburgh Centre for Reproductive Biology 37 Chalmers Street, Edinburgh EH3 9EW, UK 2Medical Research Council Reproductive Biology Unit, University of Edinburgh Centre for Reproductive Biology 37 Chalmers Street, Edinburgh EH3 9EW, UK

Correspondence: 4To whom correspondence should be addressed

The role of dopamine and opiates in the suckling-induced suppression of gonadotrophin secretion and prolactin release was investigated during lactational amenorrhoea in fully breastfeeding women at 12 weeks post-partum. A total of 26 women, 20 using non-steroidal methods of contraception and six using the progestogen-only pill, Noriday (POP), breastfed their babies on demand at a frequency of 3.6 ±; 0.2 suckling episodes during the 8 h study period while blood samples were collected at 10-min intervals. Five hours after the start of sampling six women were given the dopamine antagonist metoclopramide (10 mg, i.m.) while four women received saline. In a second experiment, six women using nonsteroidal contraception and three women on the POP received an i.v. infusion of the opiate antagonist naloxone (1.6 mg/h) for 2 h, while four women using non-steroidal contraception and three women on the POP were infused with saline. Two hours after the i.m. injection or start of infusion all women were given an i.v. injection of 10 µ;g gonadotrophin releasing hormone (GnRH) and samples were collected for a further 1 h. All samples were assayed for luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin. Plasma concentrations of oestradiol were <;60 pmol/l in all women and they remained amenorrhoeic for at least 10 weeks after the study. Pulsatile release of LH was only observed over the 5 h pre-treatment period in 10 of the 20 non-steroid taking women (1–;3 pulses/5 h), and in one of the six women (1 pulse/5 h) on POP. Treatment with metoclopramide caused a substantial (29-fold) increase in prolactin over baseline, 7.4 times the maximum released in response to suckling. There was no effect of metoclopramide on the pattern of release of LH or FSH or the response to GnRH. Infusion of naloxone in women using either non-steroidal contraceptives or progestogen-only pill did not affect prolactin release. Naloxone infusion did not affect LH or FSH in women using nonsteroidal contraceptives, but caused a small but significant (P <; 0.05) increase in both LH and FSH in women taking the progestogen-only pill. There was a significantly greater release of LH and FSH after GnRH in all women after naloxone infusion. These results in breastfeeding women during lactational amenorrhoea confirmed that suckling suppresses the pulsatile release of LH but not through a dopaminergic pathway, showed that prolactin remains under dopaminergic control during human lactation, but suckling does not appear to affect prolactin secretion via an opiate pathway and indicated only a minor, if any, role for opiates in the sucklinginduced suppression of GnRH/gonadotrophin secretion but a potential, previously unreported, effect of opiates in reducing pituitary responsiveness to GnRH.
and that was the last abstract … h-u-h

drab4
02-10-2009, 11:20 AM
Yeah this is an interesting drug, I started looking into it a few years ago with regards helping reduce cravings for alcohol. It seems that it can have an effect on the gonadotropins and may also be of interest to anyone experiencing sexual dysfunction post cycle. I've not personally used it but certainly one to watch

Do you use it yourself Maxititer?

maxititer
02-10-2009, 12:02 PM
yes, I'm on naltrexone for about one and half year. Naltrexone is definitely worth to consider be used as immunomodulator, few times I have been close to become a sick and it did not happen because I used naltrexon, at the same time all my household were battling with high temperature, running noses etc.


It help me well to keep the bolls in shape too, even during the cycle with deca. Two guys, whom I know, have done testing before and after 16 weeks bulking cycle with orals and test E about 1.5 g per week and after the cycle androgen profile come out to be the same as before cycle, no suppression and no need in PCT.

Arbel
02-10-2009, 12:31 PM
Thanks for the great read ,i'll be runing some long cycles soon,this is worth looking into.

JamesWebb
02-10-2009, 06:42 PM
good read thanks bro

PA Viking
02-28-2009, 10:18 PM
So what is an effective dose of this stuff to take while on cycle to prevent shutdown?

maxititer
02-28-2009, 10:45 PM
depend on what kind of cycle are going to run, average is 6-12 mg per week.

PA Viking
02-28-2009, 11:03 PM
I would just be bulking. Test, T-bol, and eq maybe

maxititer
02-28-2009, 11:18 PM
T-bol - is turinadol?

if so then it is very week steroid, not sure if it is good for bulking.

PA Viking
02-28-2009, 11:23 PM
Yes t-bol is turinabol. I heard it was like d-bol but without all the extra water retention, but I have no idea how bad d-bol is for water retention since I haven't had the privilege of trying it yet. I just don't want to get that puffy face look and be stuck with it over the summer. (That's when I was planning to do my cycle)

maxititer
03-01-2009, 12:57 AM
turinabol has low androgenic acivity index 0.10=0.15 and low myotrophic activity index 0.50. but been 17 alfa alkylated it will put some load on your liver. Think twice if there any benefit in using it.

Klaus Urine
06-08-2009, 01:14 AM
yes, I'm on naltrexone for about one and half year. Naltrexone is definitely worth to consider be used as immunomodulator, few times I have been close to become a sick and it did not happen because I used naltrexon, at the same time all my household were battling with high temperature, running noses etc.


It help me well to keep the bolls in shape too, even during the cycle with deca. Two guys, whom I know, have done testing before and after 16 weeks bulking cycle with orals and test E about 1.5 g per week and after the cycle androgen profile come out to be the same as before cycle, no suppression and no need in PCT.
Injections or pills?

maxititer
06-08-2009, 03:07 AM
natrexone coming as a strip of 10 tablets 50 mg each, one strip will last for long time.

5 mg 3x week is maximum of what any one may need on 1-3 g per week cycle, in most cases 5 mg once in a week will do the same. Effect of single dose quite lasting.

Natrexone works well aslo with drugs like 19-nors like deca, tren, methyltrienolone

JWolfe
06-08-2009, 06:32 PM
so you only need to take the pill 1 time per week?

thepump
06-08-2009, 06:40 PM
Thanks for bringing that out of the dark. It's a good read.

Dr Pangloss
06-08-2009, 06:52 PM
my bp is fine now and i'm still taking naltrexone at 1 mg eod. It works well.

This is, imo, Maxi's best find right here. it blocks both estrogenic and progestin feedback onto the hypothalamus and keeps you making lh and thereby testosterone.

I buy the 50 mg pills and them dilute them in 50 ml of distilled water. i use a syringe to take 1 ml by mouth eod.

the pills are cheep.

for older men, i think this would be a grea way to keep natural test levels up...

Klaus Urine
06-08-2009, 06:56 PM
Contraindications? Side effects?

Dr Pangloss
06-08-2009, 07:30 PM
dont take it with opioid pain killers. can cause nausea at high doses. initially it causes vivid dreaming and may mildly affect sleep.

in a very small population it causes increased bp (1%).

imo, people should be taking this while on, during pct, and perhaps even while off to make sure natural test levels are optimal.

Klaus Urine
06-08-2009, 07:45 PM
dont take it with opioid pain killers. can cause nausea at high doses. initially it causes vivid dreaming and may mildly affect sleep.

in a very small population it causes increased bp (1%).

imo, people should be taking this while on, during pct, and perhaps even while off to make sure natural test levels are optimal.Thanks for the info, man. Sounds fucking awesome.

Dr Pangloss
06-08-2009, 08:10 PM
the beauty of it is that its not controlled and its a very good way to keep your test levels up.

Klaus Urine
06-09-2009, 04:45 AM
What's the half life, and how do you determine dosage?

Dr Pangloss
06-09-2009, 05:55 AM
What's the half life, and how do you determine dosage?


naltrexone is converted to beta-naltrexol in the body. both of these molecules are mu and kappa antagonists. naltrexone has a hl of 4 hrs and naltrexol 13.

The doses that maxi and i are talking about fall into the range of low to very low dose naltrexone treatment.

i forgot to mention it also enhances the immune system and sense of well being after a few weeks.

vld to ld protocols range from .2 mg to 5 mg ed from what i've seen.

the traditional dose is 50 mg for alcoholsim. Oh, another effect: low dose trials have also found a decrease in alcohol consumption.


i started at 2 mg ed and dropped to 1 mg eod. i thought i might be getting a blood pressure effect.

maxititer
06-09-2009, 11:31 AM
sense of well being after a few weeks

thanks, now I understand from where it is. My sense of well being really been a bullet prove for last few months.

there is a lot of resources on low dose naltrexone on net

hilly
06-09-2009, 11:44 AM
max if i am just cruising on 250mng test per week would 5mg per week of naltrexone be enough then say bump it upto 10mg during blasts?

maxititer
06-09-2009, 12:34 PM
max if i am just cruising on 250mng test per week would 5mg per week of naltrexone be enough then say bump it upto 10mg during blasts?

amount of naltrexone taken does not directly correlated with amount of gear, but with number of expressed receptors in hypothalamus which can be blocked with naltrexone. once receptors are blocked, amount steroids in blood really did not play an important role, because GnRH still secreting.

There is some genetic variations, but imo in most cases 5 mg will do the same job as 10 mg.

Fluid Karma
06-09-2009, 02:36 PM
the beauty of it is that its not controlled and its a very good way to keep your test levels up.

You don't need a prescrip to buy?

Klaus Urine
06-09-2009, 03:13 PM
Does the efficacy of this stuff indicate that exogenous testosterone shuts down LH production by interacting with opioid receptors?

Dr Pangloss
06-09-2009, 05:05 PM
You don't need a prescrip to buy?


yes, but if you order from an overseas pharmacy, there is zero chance of a seizure.

hilly
06-09-2009, 05:06 PM
good stuff max i will run 5mg then

Dr Pangloss
06-09-2009, 05:11 PM
Does the efficacy of this stuff indicate that exogenous testosterone shuts down LH production by interacting with opioid receptors?


it works like thiis (this is simplified): estrogen and progesting cause modulation of a set of hypothalamic neurons that connect to GnRH releasing neurons that are also in the hypothalamus. this estrogen/progesterone modulated set of neuons produces endorphin/enkaphalin which is secreted onto the GnRH secreting neurons.

Estrogen/progesterones cause increased production and secretion of endorphin/enkephalin onto GnRH neurons.

the inicreased endorphin/enkephalin secretion shuts down GnRH secretion from the GnRH secreting neurons.

no GnRH means no LH.

No LH means no Test.

Dr Pangloss
06-09-2009, 05:17 PM
sorry. also, naltrexone blocks endorphin/enkephalin signalling by blocking the receptors that they would bind to and activate. Namely mu and kappa opioid receptors on the GnRH secreting neurons.

Fluid Karma
06-09-2009, 05:25 PM
yes, but if you order from an overseas pharmacy, there is zero chance of a seizure.

Thanks:)

Klaus Urine
06-09-2009, 06:08 PM
it works like thiis (this is simplified): estrogen and progesting cause modulation of a set of hypothalamic neurons that connect to GnRH releasing neurons that are also in the hypothalamus. this estrogen/progesterone modulated set of neuons produces endorphin/enkaphalin which is secreted onto the GnRH secreting neurons.

Estrogen/progesterones cause increased production and secretion of endorphin/enkephalin onto GnRH neurons.

the inicreased endorphin/enkephalin secretion shuts down GnRH secretion from the GnRH secreting neurons.

no GnRH means no LH.

No LH means no Test.


sorry. also, naltrexone blocks endorphin/enkephalin signalling by blocking the receptors that they would bind to and activate. Namely mu and kappa opioid receptors on the GnRH secreting neurons.That's quite a cascade.

Dr Pangloss
06-09-2009, 06:14 PM
What is really interesting is there are not a lot of other bodybuilders talking about using naltrexone to keep test levels up, or for pct, but the science is sound.

i actually did the background when he brought it up. Not that he hadn't; but honestly i didnt understand everything he said, so i did my own research, and he's right.


Props to maxi for recognizing it.

maxititer
06-09-2009, 10:31 PM
another thing is that naltrexone can prevent also pituitary atrophy not only testicular.

GnRH plays important role in keeping pituitary cells proliferating and renewing it self. In absence of GnRH pituitary will shrink. That is far more dangerous and more difficult to reverse. I have seen quite few bodybuilders in mid 30s with low TSH, low thyroid function, low GH secretion, so that is practically happening.

in this regard cjc 1295 is another valuable drug which can stimulate pituitary and keep it in shape. Plus cjc1295 can rise basal IGF1 like nothing else.

Tatyana
06-11-2009, 05:55 AM
The only thing that hasn't been mentioned is ACTH and CRF and cortisol.

If Naltrexone is going to have an impact on all the other hypothalmic-pituitary axis, then it can be assume the same is going to be true for ACTH.

It does sound like a fantastic drug.

Dr Pangloss
06-11-2009, 05:57 AM
The only thing that hasn't been mentioned is ACTH and CRF and cortisol.

If Naltrexone is going to have an impact on all the other hypothalmic-pituitary axis, then it can be assume the same is going to be true for ACTH.

It does sound like a fantastic drug.

there is some evidence that it raises morning cort levels. i'll check.

Tatyana
06-11-2009, 06:00 AM
there is some evidence that it raises morning cort levels. i'll check.

That really isn't that big an issue, it would probably get you moving a wee bit quicker in the morning.

Dr Pangloss
06-11-2009, 06:24 AM
yeah i'll check though. there are lots of long-term trials of this. low dose and very low dose.

maxititer
06-11-2009, 09:20 AM
with those amounts of steroids which are used routinely nowadays, elevated cortisol rather a good thing, as corticotropins play an important anti inflammatory role.

I know one guy he bench 200 kg and his cortisol always high.

maxititer
06-11-2009, 09:29 AM
googled this article (http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowPDF&ArtikelNr=126715&Ausgabe=234603&ProduktNr=223855&filename=126715.pdf)

naloxone - fast acting naltrexone analog (if I'm not mistaking something)
in fact suppresing basal ACTH and cortisol in plasma.


Corticotropic Axis and Adrenal Feedback

In Man the Mu-Opiate Agonist Loperamide Specifically Inhibits ACTH Secretion Induced by the Cholecystokinin-Like Peptide Ceruletide
C.J. Auernhammera,b, R.L. Riepla, J. Schopohla, P. Lehnerta, O.A. Müllerc, G.K. Stallab

aDepartment of Medicine, University of Munich;
bClinical Institute, Max Planck Institute of Psychiatry, Munich, and
cDepartment of Medicine, Red Cross Hospital, Munich, FRG

Address of Corresponding Author

Neuroendocrinology 1994;60:16-22 (DOI: 10.1159/000126715)

Key Words
Ceruletide
Loperamide
Naloxone
Adrenocorticotropin
Hypothalamus
Anterior pituitary
Vagus nerve
Opiates-agonists
Antagonists
Corticotropin
Cholecystokinin
Cholecystokinin-analogues
Clinical neuroendocrinology

Abstract

Ceruletide, a cholecystokinin-8-like peptide, was recently reported to stimulate ACTH secretion in man. The aim of this study was to investigate the effect of the µ-opiate agonist, loperamide, and the opiate antagonist, naloxone, on ceruletide-induced ACTH secretion in man. In 6 normal subjects, basal ACTH and cortisol plasma levels were significantly suppressed 3 h after loperamide administration (16 mg, orally) from 5 ± 0 to 2 ± 0 pmol/l and from 356 ± 44 to 154 ± 16 nmol/l. After stimulation with 8 ng ceruletide/kg body weight/min over a period of 5 min, the maximum ACTH levels (at 7.5 min) were significantly reduced by loperamide from 26 ± 7 to 6 ± 1 pmol/l and the maximum cortisol levels (at 30 min) were significantly reduced from 676 ± 47 to 392 ± 58 nmol/l. Furthermore, the ACTH peak ( = 7.5 min) was significantly blunted by loperamide from 21 ± 7 to 5 ± 1 pmol/l and the integrated area under the curve from 0 to 120 min (AUC) of ACTH was significantly reduced from 40 ± 11 to 14 ± 4 pmol × 120 min/1. The cortisol peak ( = 30 min) and the AUC of cortisol were not significantly diminished. The suppressive effect of loperamide on basal and ceruletide-induced ACTH and cortisol secretion was completely reversed by the administration of 0.8 mg naloxone, 20 min before and during infusion of ceruletide. The administration of naloxone itself had no significant effect on ACTH or cortisol levels. In conclusion, ACTH is released by peripherally administered ceruletide within a short period. The µ-opiate agonist, loperamide, is able to suppress basal and ceruletide-induced ACTH release in man by a naloxone-reversible mechanism. The ceru-letide-stimulated HP A axis in man is influenced by the opioidergic system.

Copyright © 1994 S. Karger AG, Basel

Dr Pangloss
06-11-2009, 05:24 PM
Long-term use of naltrexone elevates Test levels significantly. in fact if brought low test abstinent alcoholics to a mean in the high-normal range, which indicates it elevates them above normal.

but it also results in a significant increase in morning cort values. I must say the cort values were not that much above control. perhaps 20 percent.

pm cort levels appeared not different than normal.

Dr Pangloss
06-11-2009, 05:27 PM
based on the elevated cort levels, i would never suggest taking naltrexone alone for pct. better to use an ai or anti-e also.

All the low dose studies report summaries leading me to believe that somehow, via elevated endorphin or cort or test levels or some or all of those, naltrexone improves the physiological response to stressors.

more on that later.

Klaus Urine
06-11-2009, 05:58 PM
based on the elevated cort levels, i would never suggest taking naltrexone alone for pct. better to use an ai or anti-e also.Wouldn't the higher endogenous testosterone compensate for the elevated cortisol?

Dr Pangloss
06-11-2009, 06:10 PM
Wouldn't the higher endogenous testosterone compensate for the elevated cortisol?


sure. it should counteract the catabolic effect of cort, but i just think its worthwhile to take extra precautions to cut feedback, since one is coming off much higher than normal doses of testosterone.

trial and error may prove me wrong here.

I has worked great for me on and off, but i'm not coming completely off since im over 40. if i were coming completely off, i would be more cautious.

mrmeotz
06-12-2009, 08:32 AM
do i recall right?

if u take i.e. 5mg 3x per week, there is little chance of shutting down ur natural testosterone production? so pct and cycling ur aas COULD be a thing of the past?
you could stay on for long time,without damaging ur natural test production and u would stay in homoeostasis (http://www.dict.cc/englisch-deutsch/homoeostasis.html)?

but if the naltrexone blocks the receptors for the shutdown, how can the body convert the exogenous testosteron and use it for bodybuilding purposes?

im very interested in this drug...sounds to good to be true..

greets

Tatyana
06-12-2009, 12:12 PM
do i recall right?

if u take i.e. 5mg 3x per week, there is little chance of shutting down ur natural testosterone production? so pct and cycling ur aas COULD be a thing of the past?
you could stay on for long time,without damaging ur natural test production and u would stay in homoeostasis (http://www.dict.cc/englisch-deutsch/homoeostasis.html)?

but if the naltrexone blocks the receptors for the shutdown, how can the body convert the exogenous testosteron and use it for bodybuilding purposes?

im very interested in this drug...sounds to good to be true..

greets

It doesn't block testosterone receptors or any of the other enzymes, like 5-alpha reductase, so you would still convert exogeneous testosterone to dihydrotestosterone and oestrogen.

Judge
06-12-2009, 06:33 PM
..shit they sell it only with prescription here in Greece!

Dr Pangloss
06-12-2009, 06:50 PM
..shit they sell it only with prescription here in Greece!


well, it''s not likely 'controlled.' that's weird though. when i was in greece, i could get a lot of stuff in the pharmacy i couldnt get in the us.

Judge
06-13-2009, 03:34 AM
well, it''s not likely 'controlled.' that's weird though. when i was in greece, i could get a lot of stuff in the pharmacy i couldnt get in the us.
this is true, most of the useful stuff that is controlled in the U.S here in Greece is easily accesible but still this naltrexone is hard to get without a psychiatrist's prescription!

Klaus Urine
06-13-2009, 04:25 AM
Yep, it's a prescription medicine here, too.

apex23
06-13-2009, 04:26 PM
Fuck I would love to know where to shop for this!!!!

Chris the Swede
06-14-2009, 04:03 AM
Hmm, suddenly I´m cruising online pharmacies. Sounds very interesting!

hilly
06-14-2009, 05:37 AM
i have links to online pharmacies both uk based and other that sell this drug. not sure on the rules about posting here so if a mod can jump in and let me know i will post up if allowed.

apex23
06-14-2009, 12:06 PM
i have links to online pharmacies both uk based and other that sell this drug. not sure on the rules about posting here so if a mod can jump in and let me know i will post up if allowed.
'

If you know if they are legit...PM me please.

apex23
06-14-2009, 03:53 PM
Hmm, suddenly I´m cruising online pharmacies. Sounds very interesting!


Make sure it is a legit site bc there are a lot of scammers out there.

musclempire
06-19-2009, 07:00 PM
Anyone find some legit naltexone..PM please if so..thanx

apex23
06-19-2009, 08:58 PM
That is what I am talking about,,,,hit me up!!!

apex23
06-19-2009, 09:52 PM
yes, but if you order from an overseas pharmacy, there is zero chance of a seizure.


Problem is most overseas pharmacies suck and you will get screwed out of your money and product.

Pretzel Logic
08-09-2009, 11:13 AM
it works like thiis (this is simplified): estrogen and progesting cause modulation of a set of hypothalamic neurons that connect to GnRH releasing neurons that are also in the hypothalamus. this estrogen/progesterone modulated set of neuons produces endorphin/enkaphalin which is secreted onto the GnRH secreting neurons.

Estrogen/progesterones cause increased production and secretion of endorphin/enkephalin onto GnRH neurons.

the inicreased endorphin/enkephalin secretion shuts down GnRH secretion from the GnRH secreting neurons.

no GnRH means no LH.

No LH means no Test.

If this is the mechanism of action, wouldn't it only prevent shutdown caused by elevated estrogen and progestin, which are not the only reasons you get shutdown while taking AAS?

Chris the Swede
10-13-2009, 05:03 AM
I have a question about Naltrexone. If the half-life is short how come it is sufficient to take it eod or even once or twice a week?

Torturemaster
10-19-2009, 05:27 PM
Since it blocks the feedback of HPTA, can you use that as a testosterone booster? Has someone mesure how effective it would be at low dose?

Torturemaster
11-09-2009, 04:45 AM
Bump

Torturemaster
12-25-2009, 07:52 AM
Hi guys,
I decided to make a 25 day run of LDN and here is what happened:
started at 14 nmol/l feeling all the simptoms of low test
took 1 mg every night except 2, or three times when I took 2mg;
had high BP and headaches only during the first week, started noticing possitive rezults after that;
stamina, libido and mood went up; 2mg felt much better than 1mg in terms of night and morning wood and apetite (had my first night spontanious ejaculation in probably 7-8 years);
ended up short (20 days), because the preparation was 25mg/25mg and I took couple of 2mg doses. I should note that week 3 was better than week 2;
desided to draw blood to see where I am. Waited 2 days for it to clear from ths system and went for BW
24 nmol/l - 70% INCREASE IN 20 DAYS
Libido joint pain, stamina, streght, mood - all is improved.
I highly recomend this drug to anyone who has problems with test. Worked wonders for me!