There seems to be a bit of abstract discussion on the effects of melatonin.
We have to bear in mind, melatonin has a very short biological half-life, rated in minutes. Not to mention the epigenetic/environmental disrupting actions posed on melatonin secretion.
Your fruits and vegetables that have been exposed to a few different pesticides have recently been shown to have high a affinity for hMT2 receptors, thus blocking melatonins action (I recently posted this on my Facebook page). Another example of melatonin disrupting factors are stims that create excessive norepinephrine secretion. This will inhibit pineal melatonin secretion via regulator of G-protein signaling 2 (RGS2). Any adenosine-receptor antagonist will blunt melatonins secretion.
Psychological stress exhibits a detrimental role on inhibiting melatonin secretion.
...keep your stressors in life to a minimum, limit over-expression of norepinephrine transporter expression. As well, nighttime light exposure induces norepinephrine transporter expression.
Unless one takes melatonin several times per day, the short duration of the transit rise of IGF1-BP3 will be miniscule.
Incidentally, not everyone responds equally to melatonin. Some individuals it affects them paradoxically.
Moral of the story. I wouldn't count on supplemental melatonin as a adjuvant for pulsatile GH.
Yes, I do use melatonin nightly.
What I was most impressed with was the impressive effects seen in a recent study showing a muscle gain in the "pounds" range and fat loss in the same range as well. To my knowledge, this was the first study of its kind. As a result, researcher's started to speculate there may be other mechanisms through which melatonin produces these affects, as a 187% increase in GH levels, especially considering the duration of elevation, will not produce those kind of results.
However, it's biggest indirect benefit probably comes from its ability to improve sleep quality, which in itself will increase GH production, but more importantly, this leads to improved recovery and growth via an increased rate of cellular repair. In fact, the regulation of the entire hormonal system is dependent on sleep quality and duration, as less than optimal rest negatively effects just about every hormonal system in the body, which is detrimental to a bodybuilder's recovery and growth in a multitude of ways.
Furthermore, melatonin helps lower cortisol levels, which is a plus for just about every bodybuilder. From what I've seen, almost every bodybuilder has elevated cortisol levels, especially stimulant users.
Regarding melatonin's ability to increase IGFBP-3 levels, using prolonged a release melatonin supplement will help overcome some of the limitations you mentioned in terms of duration of elevation.
In my eyes, all this makes it a great, CHEAP stacker with any GH releasing agent. certainly, stuff like CJC-1295 DAC or potent dopamine elevating agents like Pramipexole will produce higher increases in GH. The problem with CJC-1295 DAC is it is somewhat costly...and prami causes a lot of side effects for a lot of people, especially at optimal dosages for GH release. However, when it comes to cheap, OTC supps, melatonin is great. It's wide range of positive effects on recovery and growth compliments GH releasers very well...for pennies a day.
Melatonin reduces cortisol response to ACTH in humans.
[Article in Spanish]
Campino C1, Valenzuela F, Arteaga E, Torres-Farfán C, Trucco C, Velasco A, Guzmán S, Serón-Ferré M.
Author information
Abstract
BACKGROUND: Melatonin receptors are widely distributed in human tissues but they have not been reported in human adrenal gland.
AIM: To assess if the human adrenal gland expresses melatonin receptors and if melatonin affects cortisol response to ACTH in dexamethasone suppressed volunteers.
MATERIAL AND METHODS: Adrenal glands were obtained from 4 patients undergoing unilateral nephrectomy-adrenalectomy for renal cancer. Expression of mRNA MT1 and MT2 melatonin receptors was measured by Reverse TranscriPtase Polymerase Chain Reaction (RT-PCR). The effect of melatonin on the response to intravenous (i.v.) ACTH was tested (randomized cross-over, double-blind, placebo-controlled trial) in eight young healthy males pretreated with dexamethasone (1 mg) at 23:00 h. On the next day, at 08:00 h, an i.v. line was inserted, at 08:30 h, and after a blood sample, subjects ingested 6 mg melatonin or placebo. At 09:00 h, 1-24 ACTH (Cortrosyn, 1 microg/1.73 m2 body surface area) was injected, drawing samples at 0, 15, 30, 45 and 60 minutes after. Melatonin, cortisol, cortisone, progesterone, aldosterone, DHEA-S, testosterone and prolactin were measured by immunoassay.
RESULTS: The four adrenal glands expressed only MT1 receptor mRNA. Melatonin ingestion reduced the cortisol response to ACTH from 14.6 +/- 1.45 microg/dl at 60 min in the placebo group to 10.8 +/- 1.2 microg/dl in the melatonin group (p < 0.01 mixed model test). It did not affect other steroid hormone levels and abolished the morning physiological decline of prolactin.
CONCLUSIONS: The expression of MT1 melatonin receptor in the human adrenal, and the melatonin reduction of ACTH-stimulated cortisol production suggest a direct melatonin action on the adrenal gland.
PMID: 19301769
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