Alternative HPTA recovery methods.
Nevertheless, it would appear that a dopamine agonist like bromocriptine could help to restore HPTA
I really don't see how. While it's true that elevated prolactin levels suppress Testosterone production, and dopamine agonists reverse this by lowering prolactin, I have never seen any evidence that anabolic steroids acutely elevate prolactin, or that prolactin levels are elevated post-cycle. In fact, in the only study I have seen on the effects of chronic AAS use in humans, prolactin levels are depressed (see below).
Bromocriptine and other dopaminergic agonists may actually hinder recovery. I read your rat studies, but the situation seems different in vivo in humans and primates in general:
Fertil Steril 1991 Feb;55(2):355-7
Effects of chronic bromocriptine-induced hypoprolactinemia on plasma testosterone responses to human chorionic gonadotropin stimulation in normal men.
Oseko F, Nakano A, Morikawa K, Endo J, Taniguchi A, Usui T.
Department of Medicine, Shimane Medical University, Japan.
To study the role played by normal levels of plasma prolactin (PRL) in the secretion of testosterone (T) in the testes, we induced hypoprolactinemia with a daily dose of 5 mg bromocriptine administered orally in five normal men 20 to 35 years of age for 8 weeks. The basal PRL, T, luteinizing hormone, follicle-stimulating hormone, and maximum responses of plasma T to human chorionic gonadotropin (HCG) stimulation were measured every 2 weeks.Basal levels of plasma T were reduced in the 1st 2-week-long period of hypoprolactinemia. In the 4-week-long period of hypoprolactinemia, the maximal response of plasma T to hCG stimulation was significantly reduced. The findings suggest that normal levels of plasma PRL may play an important role in the secretion of T in the human testes in vivo.
Andrologia 1990 May-Jun;22(3):251-9
Effect of modulating endogenous prolactin secretion on testosterone production in the adult male bonnet monkey (Macaca radiata).
Rao AJ, Rani CS, Ravindranath N, Moudgal NR.
Department of Biochemistry, Indian Institute of Science, Bangalore.
Adult male bonnet monkeys maintained under regulated light: dark conditions exhibit a nycthemeral surge of testosterone. The present study attempts to determine the effect of administration of drugs that modulate prolactin levels like ergobromocriptine (EBC) and chlorpromazine (CPZ) on testosterone production.The injection of EBC, a known inhibitor of prolactin secretion, could abolish nocturnal testosterone surge irrespective of the drug being given at 8.00 or 17.00 h. Testosterone surge could likewise be inhibited by treating animals with CPZ, a potent stimulator of prolactin secretion. This suggests that alteration in endogenous prolactin level from the normal effects nycthemeral surges of testosterone. The in vivo responsiveness of the testes of monkeys injected either CPZ oder EBC to exogenous LH or LHRH stimulation was tested. While LH could completely override the CPZ induced inhibition in testosterone production it could only partially reverse the EBC effect.
Life Sci 2001 Mar 2;68(15):1769-74
Effect of androgenic anabolic steroids on sperm quality and serum hormone levels in adult male bodybuilders.
Torres-Calleja J, Gonzalez-Unzaga M, DeCelis-Carrillo R, Calzada-Sanchez L, Pedron N.
Unidad de Investigacion Medica en Biologia de la Reproduccion, Instituto Mexicano del Seguro Social, Mexico, DF.
The purpose of this study was to assess the influence of the administration of high doses of androgenic anabolic steroids (AAS) on endocrine and semen parameters. Thirty volunteering bodybuilders were studied (ages ranging between 26.6 +/- 4.1 years). A history of anabolic steroid administration was recorded for fifteen subjects, and results of semen analysis and endocrine parameters were compared with data from fifteen bodybuilders not using steroids. In those subjects using AAS, eight had sperm counts under the lower normal limit (20 x 10(6) sperm/ml), three had azoospermia, two polyzoospermia, and two had normal sperm counts. The percentage of morphologically normal sperm was significantly reduced, only 17.7% had normal spermatozoa. In the control group, only one subject had oligozoospermia.The hormonal parameters revealed reduced FSH (1.5 +/- 3.2 vs 5.0 +/- 1.6, p < 0.001) and PRL (5.1 +/- 4.9 vs 9.2 +/- 4.4, p < 0.01) levels. LH, T, E2 and DHEA levels did not vary. Last edited by Nandi on 10-12-2002 at 04:56 PM
Actually, bromocriptine seems to screw up rats as well...
Experientia 1984 Jan 15;40(1):88-9
Effects of bromocriptine on plasma testosterone and gonadotropin levels and testicular lipid fractions in adult rats.
Rao MR, Bartke A.
Bromocriptine treatment of adult male rats resulted in a decrease in testicular testosterone (T) content and a reduction in plasma T levels. This was accompanied by increase in testicular total lipids and cholesterol and depletion of testicular phospholipids.
It seems that normal levels of prolactin are necessary for maintaing adequate numbers of LH receptors in the testes.
I will certainly stop suggesting that anyone use bromocriptine for any purpose after reading all these studies. (Unless of course one happened to have a prolactinoma.) If you have any intention of using bromocriptine or an analog post cycle, you sure as hell should have a blood test done to see if in fact your prolactin levels are high (unlikely) otherwise the bromocriptine will have a negative impact on your recovery.
J Gynecol Obstet Biol Reprod (Paris) 1989;18(1):39-45
Peripheral effects of prolactin in reproductive function. I. Male reproductive function
Leroy-Martin B, Bouhdiba M, Peyrat JP, Saint Pol P.
Laboratoire d'Histologie, Faculte de Medecine, Lille.
Prolactin plays a peripheral role in male reproductive function just as it does in female function. Prolactin, through the medium of immunocytochemistry acts on testicular steroidogenesis through prolactin receptors which are sited on the Leydig cells. It alters the number of LH receptors and therefore the sensitivity of the testis to central stimulation and equally interferes with androgen synthesis. In the areas of physiological concentration the principal effect seems to be to stimulate secretion of testosterone by keeping up the number of LH receptors ; but when there is acute hyperprolactinaemia, testosterone secretion is lowered or perhaps not changed at all because of a "post-receptor effect", in spite of there being larger numbers of LH receptors. The direct effect of prolactin on spermatogenesis has not yet been worked out and the results that have been obtained are controversial. Prolactin exerts a direct stimulating effect on the growth of prostatic cells working synergistically with testosterone through specific prolactin receptors. It could play a role in certain cancers of the prostate.
??? Did you read my post Nandi? I didn't say much about prolactin. The only reason I brough up bromo is because it is a dopamine agonist, not because it is a prolactin inhibitor. It has nothing to do with Prolactin and everything to do with Dopamine's effect on HPTA. I will repost some of the highlight from my original post, but feel free to go back and read it.
Effects of drugs on brain neurotransmitter and pituitary-testicular function in male rats. Vermes I, Toth EK, Telegdy G Horm Res 1979;10(4):222-32.
The effects of different drugs influencing brain neurotransmitter contents have been tested on the pituitary-testicular function in male rats. L-dopa (200 mg/kg body weight, i.p.) increased the dopamine and noradrenaline contents of the hypothalamus, amygdala, striatum and mesencephalon, but it was ineffective as regards the 5-hydroxytryptamine contents of the same brain areas and increased the plasma testosterone level. Alpha-Methyl-p-tyrosine (250mg/kg b.w., i.p.) decreased the dopamine and noradrenaline contents of these brain areas, but it was ineffective to 5-hydroxytryptamine, and decreased the plasma testosterone level. Diethyldithiocarbamate (400 mg/kg b.w., i.p. twice a day) increased the dopamine levels in the hypothalamus, amygdala, striatum and mesencephalon, decreased the noradrenaline contents in the same brain regions but had no effect on the 5-hydroxytryptamine contents of these brain areas or on the testosterone level in the peripheral blood. p-Chlorophenylalanine (300mg/kg b.w., i.p.) decreased the 5-hydroxytryptamine contents of the different brain areas, while it had no effect on the dopamine and noradrenaline levels or on the plasma testosterone level. 5-Hydroxytryptophan (200mg/kg b.w., i.p.) increased the 5-hydroxytryptamine contents of all brain areas studied, but was without effect on the dopamine and noradrenaline contents or the plasma testosterone level. The data suggest that both dopamine and noradrenaline may be involved in the regulation of the pituitary-testicular function, and the ratio of the two transmitters might be more important that their actual levels in definite brain areas
Role of hypothalamic catecholamines in aging processes. Meites J Department of Physiology, Michigan State University, East Lansing. Acta Endocrinol (Copenh) 1991;125 Suppl 1:98-103
Defects that develop in the hypothalamic area of the brain are believed to initiate many declines in body functions in aging rats and mice. The decreases found in hypothalamic norepinephrine and dopamine are particularly important since they lead to reduced gonadotropic hormone secretin and cessation of estrous cycles in female rats and a decrease in testosterone secretion in male rats, lower GH and somatomedin (IGF-I) secretion and reduced protein synthesis, diminished thyroid hormone secretion and lower body metabolism, higher PRL secretion and development of numerous mammary and pituitary tumours, and reduced immune competence. The reduction in hypothalamic norepinephrine and dopamine activity is believed to be due to damage and loss of neurons owing to toxic products formed during metabolism of norepinephrine and dopamine; to the damaging effects to neurons produced by the chronic action of estrogen, PRL, and indirectly by adrenal glucocorticoids; and to changes in enzymes responsible for synthesis and metabolism of norepinephrine and dopamine. When old rats are given drugs that elevate norepinephrine and dopamine, most of the above and other decrements of aging are delayed or reversed, and length of lifespan may be prolonged. Decreases in hypothalamic norepinephrine and dopamine have also been reported in elderly human subjects, but it is unknown whether these are related to declines in body functions.
I wish my library had this journal. It's puzzling how LH and T decreased 2 to 6 hours after bromocriptine administration, then evidently returned to normal until 21 hours, then declined again.
Nippon Naibunpi Gakkai Zasshi 1985 Jun 20;61(6):701-9
The effects of bromocriptine on the pulsatile pattern and the circadian profile of gonadotropins and testosterone secretion in normal adult men
Aisaka K, Ogawa T, Mori H, Kigawa T.
To investigate the effects of bromocriptine on the secretion mechanism of pituitary gonadotropins and testosterone, 5 mg of bromocriptine was administered to five young adult men who were normal in their endocrinological states. Blood samplings were taken from two hours before until six hours after the administration every 15 min., and after that, blood samplings were continued until 21 hours every one hour by an intravenous indwelling catheter. Serum FSH, LH, prolactin and testosterone levels were determined by RIA, and the changes of the pulsatile patterns of FSH and LH, and the circadian profile of these hormones by the administration of bromocriptine were analysed. Serum prolactin levels decreased significantly (p less than 0.005) from two hours after the administration of bromocriptine and remained in a very low range until the end of the experiment. The basal levels of FSH showed a significant decrease from two to six hours after the administration (p less than 0.005). Also the basal levels of LH showed a significant decrease from two to six hours after the administration (p less than 0.005). However, the basal levels of serum FSH and LH did not show significant decreases after that until the end of the experiment. No significant change was observed in the amplitude or the frequency of the pulsatile patterns of FSH and LH until six hours after the administration of bromocriptine. The serum levels of testosterone were also significantly decreased from two to six hours after the administration (p less than 0.005), but they did not show a significant decrease after that until the end of the experiment
So what? Bromocriptine administration to normal men lowers testosterone. How is it going to help post-cycle HPTA recovery? Wasn't that your original premise?
My original premise is that Dopamine agonist's may play a role in restoration of HPTA. I only brought up bromo because it is a dopamine agonist, not because I had any sort of study indicating that Bromo would restore HPTA. I think that Fonz' assertion, however misplaced he is, may have some validity. Not because of prolactin's role in restoration, but because of the fact that Dopamine does seem to play a role in HPTA recovery.
Personally, I think the information I uncovered is interesting, and worth further evaluation.
Yes I read your studies and they are very interesting. So what? Bromocriptine administration to normal men lowers testosterone. How is it going to help post-cycle HPTA recovery
Take bromocriptine at your own risk.
Read more thoroughly before drawing conclusions.