.gif "IP Gear")
- Joined
- Apr 30, 2007
- Messages
- 61
This valuable drug for those who running long bulking cycles was neglected for long time. It may be indeed a revolutionary drug or may remains in private domain. In any way I'm posting this abstracts here for your consideration.
Also I have full articles for most of abstracts posted here so, PM me if you feel that you really need some of those articles.
So, it is good for bridges too, b/c it can increase "Plasma gonadal steroid concentrations"
no comments
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.
hello morphine, bye bye testosterone
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.
One more prove of concept of wrong design and that been a happy man and testosterone man is not the same.
Wow, that is statistically significant orgasmic drug
The total number of orgasms was 67 under the naltrexone condition and 51 under the placebo condition.
some bad message for deca lovers.
and here is last abstract … h-u-h
Also I have full articles for most of abstracts posted here so, PM me if you feel that you really need some of those articles.
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 HA
no 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.
- sorry for thatsexually active (alone or with a partner) men
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.
and here is last abstract … h-u-h
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.
