Alternative HPTA recovery methods.

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expreses his opinions that tradional HPTA recovery methods using clomid, HCG, Nolvodex, etc are "antiquated" because they do "not take into account prolactin, which hinders HPTA recovery."

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Oh my god.

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Unfortunately, Fonz hasn't yet gone into any details about doses, duration of therapy, etc

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Really? Hmmm.....figures.

Posted by: JGUNS

Oh my god.

Really? Hmmm.....figures.

Guns, sorry if I inadvertently implied that Fonz was being an asshole or anything. I meant that he just hasn't yet gotten around to the details yet. I honestly do think that he's trying to be helpful and I just want more opinions. Looking forward to yours. And Nandi's et al.

Androgel for recovery? heh, androgel surpresses test just as much as injectible test does...

He keeps repeating that using HCG and clomid is antiquated because it "does not take into consideration prolactin." He also posted an abstract in which the subject had a prolactinoma in which test and Arimidex were used in treatment. I am not sure how relevant that is to our discussion. Give me some time, I need to get my response together.

Quote:Androgel for recovery?

This is why I don't waste my time at Elite anymore.

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Androgel for recovery

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Actually Nandi this doesn't seem too far off base. Androgel doesn't raise test levels off the chart like inj Test enth anate and it appears to leave the system quickly. Those aspects of it maybe worth looking into.

However it is still an exogenous Testosteroneso it should suppress natural production to some extent.

I was always puzzled by some of the guys at ELite who agreed that being juiced for extended periods of time was bad but then included anabolics in their recovery or bridging cycles? Personally I am half tempted to never use any anabolics of any sort again. I can't be on for long periods of time and it feels so good to be juiced. It sucks to cycle off. In case anybody is wondering I am a tested athlete so I can't run stuff for long time periods.

FHG

This "theory" on HPTA recovery is utter nonsense:

"Serum LH. Testosterone treatment was associated with a significant suppression of serum LH on day 28, compared with baseline (Table 5, from 6.6 to 3.3 U/L, P = 0.016 in healthy hypogonadal men, and from 12.8 to 2.9 U/L, P = 0.069 in men with ESRD). The degree of suppression was greater in men with ESRD, compared with healthy hypogonadal men (mean suppression, 91 � 3% in men on hemodialysis vs. 57 � 12% in healthy hypogonadal men, P = 0.035)." (1)

(1) J Clin Endocrinol Metab 2001 Jun;86(6):2437-45

Pharmacokinetics of a transdermal testosterone system in men with end stage renal disease receiving maintenance hemodialysis and healthy hypogonadal men.

Singh AB, Norris K, Modi N, Sinha-Hikim I, Shen R, Davidson T, Bhasin S.

Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, California

In another trial of dihydrotestosterone gel, which should have less of an effect on LH because it does not aromatize, LH levels were depressed significantly (see fig 1)

http://jcem.endojournals.org/cgi/content/full/86/9/4078

Posted by: Nandi12

This "theory" on HPTA recovery is utter nonsense:

"Serum LH. Testosterone treatment was associated with a significant suppression of serum LH on day 28, compared with baseline (Table 5, from 6.6 to 3.3 U/L, P = 0.016 in healthy hypogonadal men, and from 12.8 to 2.9 U/L, P = 0.069 in men with ESRD). The degree of suppression was greater in men with ESRD, compared with healthy hypogonadal men (mean suppression, 91 � 3% in men on hemodialysis vs. 57 � 12% in healthy hypogonadal men, P = 0.035)." (1)

(1) J Clin Endocrinol Metab 2001 Jun;86(6):2437-45

Pharmacokinetics of a transdermal testosterone system in men with end stage renal disease receiving maintenance hemodialysis and healthy hypogonadal men.

Singh AB, Norris K, Modi N, Sinha-Hikim I, Shen R, Davidson T, Bhasin S.

Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, California

Yeah makes sense. It never seemed logical to use one AAS to recover from another. And what is Elite's obsession with ALA?

Those charts on Andrgel in that previous post were very very interesting though. Makes one think it could work. Obviously it won't though. I'm sure Fonz saw something similar and that prompted him to think it could be useful for recovery.

You're the shit Nandi. I am making you my official drug researcher. Being an elite cyclist I need one-it says so in my handbook on page 55 "Have a drug consultant".

FHG

BMJ posted this at AF. Any responses. AND NO BIG WORDS j/k

The Journal of Clinical Endocrinology & Metabolism Vol. 87, No. 10 4447-4451
Copyright � 2002 by The Endocrine Society

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CLINICAL CASE SEMINAR

"The Novel Use of Very High Doses of Cabergoline and a Combination of Testosterone and an Aromatase Inhibitor in the Treatment of a Giant Prolactinoma"

Mary P. Gillam, Stewart Middler, Daniel J. Freed and Mark E. Molitch

Division of Endocrinology, Metabolism, and Molecular Medicine (M.P.G., M.E.M.), Northwestern University, The Feinberg Medical School, Chicago, Illinois 60611; and Cedars-Sinai Medical Center (S.M.), University of California at Los Angeles School of Medicine, Los Angeles, California 90048

Abstract

Most prolactinomas respond rapidly to low doses of dopamine agonists. Occasionally, stepwise increases in doses of these agents are needed to achieve gradual prolactin (PRL) reductions. Approximately 50% of treated men remain hypogonadal, yet testosterone replacement may stimulate hyperprolactinemia.

A 34-yr-old male with a pituitary macroadenoma was found to have a PRL level of 10,362 �g/liter and testosterone level of 3.5 nmol/liter. Eleven months of dopamine agonist therapy at standard doses lowered PRL levels to 299 �g/liter. Subsequent stepwise increases in cabergoline (3 mg daily) further lowered PRL levels to 71 �g/liter, but hypogonadism persisted. Initiation of testosterone replacement resulted in a rise and discontinuation in a fall of PRL levels. Aromatization of exogenous testosterone to estradiol and subsequent estrogen-stimulated PRL release was suspected. Concomitant use of cabergoline with the aromatase inhibitor Anastrozole after resuming testosterone replacement resulted in the maintenance of testosterone levels and restoration of normal sexual function, without increasing PRL. Ultimately, further reduction in PRL on this therapy permitted endogenous testosterone production. Thus, novel pharmacological maneuvers may permit successful medical treatment of some patients with invasive macroprolactinomas.

BMJ

And could someone please explain to me how any form of exogenous test, even in the form of androgel, won't suppress your natural test production. It doesn't make sense to me, yet the above article seems somewhat convincing to a non-scientist guy like me.

HPTA recovery is so critical to what we do, I wish some kind of consensus could be reached.

This has less to do with prolactin and more to do with dopamine regulation. Dopamine has been shown to have a positive effect on many brain functions including mood, cognitive functions, strength, drive, coordination etc. When dopamine becomes depleted due to physical or psychological stress, testosterone response and therapies will not be as effective. Restoration of dopamine levels will enhance therapy whether it is natural or by replacement.

Medical science has also proven dopamine has a positive impact on growth hormone secretion. Growth hormone secretion is regarded as the key factor for the regeneration of cells and tissue. Increased dopamine production enhances the body's ability to repair or replace damage and wounded cells.

In this case, it would appear that a dopamine agonist could have a positive effect on restoration of HPTA.

Study of the effects of neurotransmitters on the hypothalamus-pituitary-testis function in vitro cell suspension system. Vermes I, Varszegi M, Toth EK, Telegdy G Arch Androl 1979;3(2):127-33.

The effects of different neurotransmitters were tested in vitro on a hypothalamic tissue, collagenase-digested isolated anterior pituitary and Leydig cell suspension system by measuring the testosterone production of the Leydig cells. Neurotransmitters were used in concentrations of 0.25, 1.0, 2.5, 5.0, and 10.0 micrograms/ml incubation medium. Dopamine in doses of 1.0, 2.5, and 5.0 micrograms/ml increased the hypothalamic tissue-induced pituitary-testis activation, while it had no direct effect on pituitary and Leydig cells. Noradrenaline in the concentration range 2.5--10.0 micrograms/ml decreased the luteinizing-hormone-releasing-hormone (LHRH) sensitivity of the pituitary cells. 5.0 and 10.0 micrograms/ml 5-hydroxytryptamine decreased the testosterone production and the hCG sensitivity of the isolated Leydig cells. Carbamylcholine and pilocarpine had no action on the in vitro system at the different levels studied.

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 still wouldn't resign clomid and HCG to "antiquated" status. Clomid (or nolva), by blocking estrogen receptors in the hypothalamus, may serve to stimulate GnRH production, which is a key component to HPTA. HCG as we know, essentially sends a signal to the testes to begin test production by mimicking LH. Doctors have used a combination of HCG and Clomid with pretty good success, and there are indications that this is more effective than clomid alone. These tactics don't always work in everyone either. There are other methods as well. Beta agonists like clen or ephedrine may help. Let's not forgot either that prolactin inhibits test production in the long term, but in the short term it can be stimulatory!

Bromocriptine might be a good choice not because it is a prolactin inhibitor, but because it is a dopamine agonist. Another choice is pergolide, deprenyl, etc.

One more thing: Using androgel is a ridiculous idea.

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And could someone please explain to me how any form of exogenous test, even in the form of androgel, won't suppress your natural test production. It doesn't make sense to me, yet the above article seems somewhat convincing to a non-scientist guy like me.

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It only seems to make sense until you understand the difference between hypogonadism induced by prolactin, and post-cycle hypogonadism. They are two completely different things.

A prolactinoma is a benign pituitary tumor that secretes large amounts of prolactin. Prolactin suppresses testosterone production. How exactly does this happen? The preponderance of the evidence is that prolactin interferes somehow with either GnRH (Gonadotropin Releasing Hormone) production in the hypothalamus or the signal it sends to the pituitary gland to produce LH. LH is reduced in people with hyperprolactinemia for this reason. When bromocriptine or some other dopaminergic agonist which blocks prolactin secretion is given to these people, usually testosterone and LH rise together. See abstract below. This case was an exception worthy of writing up and publishing.

Post cycle, the situation is completely different. The hypothalamus produces adequate GnRH but the pituitary is not resposive to it. Administering androgens, especially ones that aromatize would only make matters worse, desensitizing the pituitary even more. Clomid and Nolvadex sensitize the pituitary to GnRH. That is one reason why they are used post cycle. The other is to block the negative feedback of rising estrogen levels on the pituitary.

The flaw in the "theory" from Elite comes from trying to extrapolate the results of a single anomalous case of hyperprolactinemia to a completely different condition, post cycle AAS recovery.

Clin Endocrinol (Oxf) 1984 Sep;21(3):257-63

Altered pulsatile secretion of luteinizing hormone in hypogonadal men with hyperprolactinaemia.

Winters SJ, Troen P.

To explore the mechanism for the hypogonadism associated with prolactin hypersecretion in men we examined luteinizing hormone (LH) secretory profiles in four hyperprolactinaemic men before and during treatment with bromocriptine. Pretreatment serum prolactin levels were increased 4-100 fold and serum testosterone levels were low in three men and low-normal in the fourth subject. Mean LH levels were low-normal and the frequency of spontaneous LH secretory episodes was less than normal in three of four men. Bromocriptine reduced serum prolactin levels to normal; subsequently, serum testosterone levels increased and libido and potency improved markedly in each man. The rise in serum testosterone levels was associated with an increase in mean LH concentrations and in LH pulse frequency. Mean follicle-stimulating hormone levels also increased during bromocriptine treatment. Insofar as each LH pulse is believed to reflect a discharge of gonadotrophin releasing hormone from the anterior hypothalamus, our data suggest that a major abnormality in hyperprolactinaemic men with hypogonadism is a disorder of the neuroregulatory mechanism for pulsatile gonadotrophin-releasing hormone secretion

Nandi, amazing...

Exactly what I wanted to hear in words that I could actually understand. Thank you.

Nevertheless, it would appear that a dopamine agonist like bromocriptine could help to restore HPTA.