Melatonin secretion is actually a response to various light input on retinal receptors and a complex cascade of events thereafter that follow:
Step 1) Light –> eye –> (+) Hypothalamic suprachiamatic nucleus / (+) Hypothalamic paraventricular nucleus –> hindbrain –> spinal cord –> superior cervical ganglion –> divergent outflow tracts [go to Step 2a OR 2b]
Step 2a) Superior Cervical ganglion –> Norepinephrine –> Beta-adrenergic receptor [go to Step 3a]
Step 2b) Superior Cervical ganglion –> Norepinephrine –> Alpha-adrenergic receptor [go to Step 3b]
Step 3a) (beta-adrenergic sequelae) ATP –> cAMP-dependent phosphorylation via AA-NAT promotor binding –> 5-HT N-Acetyl Transferase - 5-HT NAT [move on to Melatonin-processing cascade]
Step 3b) (alpha-adrenergic sequelae) C-kinase input into beta-adrenergic cAMP phosphorylation crossover [Return to Step 3a]
1. Tryptophan –> 5-HTP
2. 5-HTP –> 5-HT
3. 5-HT –> N-Acetylserotonin (via 5-HT NAT from Step 3a)
4. N-Acetylserotonin –> Melatonin (via hydroxyindole-O-methyltransferase - HOMT)
The model is consistent with the suggestions offered in PCT: ACV III regarding hypOadrenalism in the “immediate” post-cycle realm contributing to a DECREASE in catabolic balance in roughly the first 2.5 weeks of post-cycle era, inclusive of not only cortisol, BUT also catecholamine (i.e. - NE) output. This is where the difference arises in PoCI - outisde of its intimate connection with serum gonadotropin-effects, you also have changes in enzymatic processing unique to PCT.
So Dana, melatonin supplementation would be the simple answer, right? NOT SO FAST! You really don’t think I spent all that time on the melatonin processing cascade to talk about simple melatonin supplementation, did you? Now, remember with our crossover pathway, melatonin has crossover feedback to follow suit and a subsequent DECREASE in serum gonadotropin [FSH + LH] via GNRH outflow during the sleep hours as shown in most current research. Decreased Melatonin is actually a good thing in PCT as the body’s own mechanism for restoring balance [though beyond our scope here it may be a GH deficiency you have then to worry about if sleep deprivation results - quite complex, huh? Though the hormonal chaos always gets oversimplified! ALL HOMRONES DO NOT ACT IN A VACUUM, THERE ARE ALWAYS ATTEMPTS AT HOMEOSTATIC BALANCE! Disrupt it, and its like tipping a scale where but another hormonal pathway will suffer]. In people experiencing PoCI, the likelihood of reaching serum gonadotropin suppression is nearly 100%.
What’s more...Melatonin 1 [MT1, not to be confused with M1T] receptor subtypes are also present in the pars tuberalis to increase prolactin output possibly potentiating post-cycle galactorrhea (nipple discharge).
[author’s note: melatonin conveys photoperiodic info influencing the pattern of something called mPer expression in the pars tuberalis for the control of seasonal variations of that MT1 receptor - which is way beyond the scope of this article, but explains even furthermore why simple supplementation here is NOT warranted in everyone].
These effects seem to dissipate, however, with long-term supplementation BUT it is likely NOT a good plan in the post cycle era to be trying melatonin or secretagogues (i.e. - 5-HTP, et al.] for the first time.
So, what you’re telling me is that should insomnia crop up in the post-cycle era, I am left to suffer, right? Nah, there are some potential alternatives which offer sedative effects that could override this melatonin system.