Nathan said:
I do believe it did. I tried nolva and l-dex for a few weeks nd while it didn't seem to get worse, it didn't go away. I started bromo few days ago and it seems to be clearing up again. Fucking hell. I'm glad I catch this shit in reasonable time. I was not expecting that. I stopped the gh as well. I'm not sure but it may also have fuckedup my immune system. Is that possible?
The Hgh induced gynaecomastia is primarily from increased IGF-1 levels. If you persisted with the nolvadex therapy@20mgs/day your gyno would eventually disappear due to it's robust IGF-1 decreasing abilities.
I dont know about synthetic HGH causing prolactin increases.I doubt it very much. However dopamine agonists such as bromo and dostinex which are D2 agonists increase endogenous HGH,as well as lowering prolactin.Also selegeline and L-Dopa have been demonstrated to increase HGH as well as the libido drug Apo-morphine.
HGH is not immunosupressive, as it is prescribed for AIDS and other wasting diseases where the immune system is very sensitive.
Carpal tunnel syndrome and gynaecomastia during growth hormone treatment of elderly men with low circulating IGF-I concentrations.
Cohn L, Feller AG, Draper MW, Rudman IW, Rudman D.
Department of Medicine, Medical College of Wisconsin, Milwaukee.
OBJECTIVE--We studied the relationship between plasma level of insulin-like growth hormone I (IGF-I), changes in lean body mass and in adipose mass, and adverse side-effects during human growth hormone (hGH) treatment of elderly men who had low IGF-I levels. DESIGN--The first six months was a period of baseline observation. The subjects were then randomized into two groups so that during months 7-18, men in group I received hGH, and men in group II served as untreated controls. SUBJECTS--Eighty-three overtly healthy elderly men, who were selected because their plasma IGF-I level was less than 0.35 units/ml. The men were randomly assigned in a ratio of three to one into group I (n = 62) or into group II (n = 21). MEASUREMENTS--Plasma IGF-I level was measured monthly. Lean body mass and adipose mass were measured every six months. RESULTS--Fifteen men left the study during the baseline period because of personal reasons or intercurrent medical events. In those who received drug (group I), there were a number of adverse reactions which could have been related to the hGH therapy: carpal tunnel syndrome 10, gynaecomastia 4, and hyperglycaemia 3. In total there were 27 dropouts from group I and two dropouts from group II after the six-month point, for a variety of medical and non-medical reasons, the majority probably not related to hGH therapy. During the hGH treatment of group I, plasma IGF-I increased from the range 0.10-0.35 units/ml into the range 0.5-2.2 units/ml. Among the 18 men who completed 12 months of hGH treatment without experiencing one of the three above-noted presumed hGH side-effects, mean and peak plasma IGF-I during treatment were significantly lower than among the 13 men who experienced carpal tunnel syndrome or gynaecomastia (one subject had both) while on hGH. With one exception, neither carpal tunnel syndrome nor gynaecomastia occurred in any individual with a mean IGF-I level less than 1.0 units/ml during hGH treatment. Twelve months of hGH treatment (group I) caused an increase in lean body mass to 106% of the initial baseline (month one of the protocol), and a reduction in adipose mass to 84% of the baseline. Meanwhile, the lean body mass of the untreated men in group II declined to 97% of the initial baseline. The body composition responses after 12 months of treatment in group I were larger in the men whose mean intra-treatment IGF-I level was 0.5-1.0 units/ml, than in the men whose mean intra-treatment IGF-I level was 1.0-1.5 units/ml. CONCLUSIONS--These observations show that when elderly men with low circulating IGF-I concentrations are treated continuously with hGH,
elevation of plasma IGF-I above 1.0 units/ml is associated with a substantial frequency of carpal tunnel syndrome or gynaecomastia. It may be that the effects of the hormone in expanding lean body mass and reducing adipose mass can be achieved, and the side-effects avoided, by
maintaining the mean IGF-I level in the range 0.5-1.0 units/ml.
: J Clin Endocrinol Metab. 1975 Aug;41(2):408-11. Related Articles, Links
Suppression by thyrotropin-releasing hormone (TRH) of human growth hormone release induced by L-dopa.
Maeda K, Kato Y, Chihara K, Ogo S, Iwasaki Y.
Oral administration of L-dopa (600 mg) significantly raised plasma human growth hormone (hGH) in 6 of 7 normal subjects examined. This L-dopa induced hGH release was significantly suppressed by the intravenous infusion of 1 mg of thyrotropin-releasing hormone (TRH). TRH administration alone had no significant effect on plasma hGH. In contrast, plasma human prolactin (hPRL) consistently increased following TRH infusion. L-dopa significantly lowered basal plasma hPRL levels and also significantly blunted TRH-induced hPRL release. These results suggest that TRH plays an inhibitory role in the regulation of hGH secretion in normal subjects, whereas it stimulates hPRL release.
Dopamine function in obsessive-compulsive disorder: growth hormone response to apomorphine stimulation.
Brambilla F, Bellodi L, Perna G, Arancio C, Bertani A.
Psychoneuroendocrine Center, Istituto Scientifico H. San Raffaele, Milan, Italy.
Indirect observations suggest that the dopaminergic system may be involved in the pathophysiology of obsessive-compulsive disorder (OCD). The dopaminergic function of 15 patients with OCD and 15 age/sex-matched controls was evaluated by measuring the growth hormone (GH) responses to stimulation with the dopaminergic agonist apomorphine (APO), which increases growth hormone-releasing hormone (GHRH), GH, and somatomedine C (SMD-C) secretions. Therefore, we measured basal plasma GH and SMD-C concentrations and GH responses to GHRH stimulation to exclude that a downstream pathology of the somatotropic axis could obscure the significance of the results of the APO test. The response of prolactin (PRL) to APO inhibition were also measured. Basal plasma levels of GH, SMD-C, and PRL, GH responses to GHRH stimulation, and PRL responses to APO inhibition did not differ in the two groups of subjects. GH responses to APO stimulation were blunted in obsessive-compulsive (OC) patients. The emetic response to the same stimulation was stronger in patients than in controls. These responses suggest that in our OC patients there is a dysregulation of the dopaminergic system, which is possibly expressed in different ways in the various areas of the central nervous system.
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