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Discussion Starter · #1 ·
Clonidine. It is prescribed as an anti-hypertensive drug PO or transdermally. Apparently it stimulates the release of HGH, but is not currently banned by USADA for cycling (maybe for archery or those types of sports, like beta-blockers are).

Effect of oral clonidine, insulin-induced hypoglycemia and exercise on plasma GHRH levels in short-stature children.


Human growth hormone release is affected by a variety of pharmacological and physiological stimuli. We have studied the effect of oral clonidine, insulin hypoglycemia, and exercise on plasma human growth hormone - somatropin - and GHRH levels in 31 healthy short-stature children. Thirteen underwent an oral clonidine test (0.15 mg/m2), 12 an iv. insulin test (0.1 U/kg), and 6 performed exercise (running for 10 min in a defined route). GHRH-1-44 was extracted from plasma on silica columns and determined by RIA. Although all three stimuli induced a marked increase in plasma human growth hormone - somatropin - levels, only clonidine induced a significant increase in plasma GHRH levels. Maximal increment in GHRH during clonidine was 6.82 +/- 1.05 pmol/l (mean +/- SEM) as compared with 0.51 +/- 0.28 and 0.53 +/- 0.62 during hypoglycemia and exercise (p less than 0.0005 and p less than 0.005), respectively. An additional 24 subjects received TRH 0.2 mg/kg iv: 8 TRH alone, 8 TRH and insulin, and 8 TRH and clonidine. Only insulin potentiated the TRH-induced TSH response with a peak of 22.0 +/- 3.2 vs 16.0 +/- 0.8 and 15.3 +/- 1.5 mU/l (p less than 0.025) for TRH alone and TRH and clonidine, respectively. It is suggested that clonidine stimulates human growth hormone - somatropin - secretion mainly through an enhancement of GHRH release, whereas stress stimuli such as hypoglycemia and exercise achieve human growth hormone - somatropin - release by a different mechanism, possibly inhibition of somatostatin.

Comparison of the effect of insulin hypoglycemia and clonidine on secretion of growth hormone, cortisol and beta-endorphin in children and adolescents.


Plasma beta-endorphin, human growth hormone (human growth hormone - somatropin - ) and cortisol were measured concomitantly during insulin hypoglycemia (0.1 u/kg i.v.) or clonidine administration (0.075 mg/m2 orally) in children with idiopathic short stature. Whereas hypoglycemia raised plasma beta-endorphin levels, clonidine slightly decreased beta-endorphin in six subjects and had no effect in four. Cortisol levels increased following hypoglycemia and decreased markedly after clonidine. human growth hormone - somatropin - increased to greater than 20 ng/ml in all but one subject. The findings are interpreted as further evidence that the human growth hormone - somatropin - stimulation of clonidine is not stress-mediated.

Plasma growth hormone response to oral clonidine as compared to insulin hypoglycemia in obese children and adolescents.


The response of plasma growth hormone (human growth hormone - somatropin - ) to a single oral dose of clonidine (0.15 mg/m2) was compared with that obtained with insulin hypoglycemia (ITT) induced by administration of double the usual dose (0.2 U/kg i.v.) in 13 obese subjects aged 5-17 years (7 males, 6 females) with a subscar skinfold greater than 20 mm and a weight greater than 2 SD of the median. Six healthy subjects (3 males, 3 females), aged 8-14 years who served as controls received the usual dose of 0.1 U/kg i.v. in the ITT. Clonidine induced an increase of more than 10 ng/ml in the plasma human growth hormone - somatropin - levels in 10 (4 males, 6 females) of the 13 obese subjects and in all of the healthy controls, with peak levels ranging from 14.3 to 31.0 ng/ml (m +/- SD 21.0 +/- 5.2 ng/ml); the ITT elicited a similar rise in only 6 of the 13 subjects and 3 of the healthy controls, with peak levels ranging from 9.8 to 20.0 ng/ml (m +/- SD 14.4 +/- 4.5 ng/ml). Clonidine decreased plasma insulin levels in all the obese female subjects (by a mean of 65%) whereas in the obese males the insulin pattern was variable. There was no change in blood glucose levels following the administration of clonidine; during the ITT all subjects showed a decrease to less than 50 mg/dl. Blood pressure decreased by a mean of 20 mmHg during the clonidine test. This study demonstrates that clonidine is a more effective human growth hormone - somatropin - stimulus than insulin induced hypoglycemia in normal and in obese children and that the lower human growth hormone - somatropin - secretion of the obese is confirmed by the clonidine test.

Basal plasma human growth hormone - somatropin - and cortisol levels and the effect of clonidine administration in female migrainous patients.


Clonidine, a central alpha-adrenergic agent and prophylactic antimigraine drug is known to stimulate human growth hormone (human growth hormone - somatropin - ) release and to suppress cortisol secretion. A possible association between basal hormonal levels and response to either acute clonidine test or chronic treatment in female migrainous patients was investigated. 15 females, aged 18-43 years, suffering from migraine, underwent an acute clonidine test by administration of a single oral dose of 0.15 mg. High basal human growth hormone - somatropin - levels (greater than or equal to 9 ng/ml) were observed in 6 patients, while the other 9 patients demonstrated normal low basal human growth hormone - somatropin - levels. Acute clonidine administration induced a marked rise of human growth hormone - somatropin - in 8 of the 9 patients with low basal human growth hormone - somatropin - . In 4 of the 8 responders human growth hormone - somatropin - levels exceeded 20 ng/ml and 3 subjects reached the acromegalic range (greater than 90 ng/ml). The mean response in this group was higher than in a reference group consisting of children and adolescents. It is suggested that the basal hycretion and the hyperresponsiveness of human growth hormone - somatropin - to clonidine provocation test in some migrainous patients results from a hynsitivity of the central alpha-adrenergic receptors. 12 of the 15 females were treated for 10 weeks with clonidine at gradually increased doses of 0.05 mg/day up to a maximal dose of 0.15 mg/day. A marked suppressive effect on cortisol secretion was observed in the migrainous patients after acute and chronic administration of clonidine. No correlation was observed between human growth hormone - somatropin - and cortisol response to acute or chronic clonidine administration and the prophylactic effect of clonidine on migraine.
I'm not advocating use of this drug, just thought it was worth bringing up. I'm contemplating a letter to USADA... thoughts? There are other studies that show correlation to HGH release so I'm curious as to why this isn't even on the "monitored" list. Any ideas?
 

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I would think the decrease in blood pressure would negate any benefits of HGH.
There are also the CNS effects. When I've been on it in the past I always had a rather profound brain fog, and all the drugs in that class are generally taken right before bed because they can knock your a$$ out. Not exactly performance enhancing side effects.
 

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Discussion Starter · #5 ·
The CNS effects are negated by the fact that it is, how you said, usually taken before bed (although some take it two to three times a day). I'd imagine that during the training season where the need to get up at 5am and start training is not required, it could be a slight edge to take some clonidine before bed (in addition to skeletal muscular stress they already encounter from training). Since the half-life is so variable (12+ hours, although dose-dependent and chronic vs acute usage), there may be no benefit if it is still exerting an effect on catecholamine levels.

I'm not arguing for using it (by any means) but I think that there is some merit to the fact that it could be performance enhancing in some aspects (but then again, maybe not). Just found it interesting.
 
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