Simple supplements changing my life, how to start with the basics (Nootropics).

I was not conflating anything. I was giving you some studies that were interesting.

http://wurtmanlab.mit.edu/static/pdf/1049.pdf

> for the most part patients have not been able to use the
lowest fully effective doses because the only doses that are commercially
available have been substantially higher. Such doses, which raise
plasma melatonin to levels many times greater than those of younger people, produce side-effects not observed at the lower, more physiologic sleep-promoting doses, for example hypothermia; 7,8 hyperprolactinemia;
and ‘morning grogginess’. **Moreover, the markedly-elevated melatonin
levels can also desensitize the brain receptors on which melatonin must
act to promote sleep, 1probably causing some users to become refractory
to the beneficial effects of exogenous melatonin or even to the melatonin
their own pineal glands secrete.**

Yes, that study was providing recommendations for elderly people to bring their melatonin back to normal youthful levels, but the mechanisms are relevant to anyone.

http://www.ncbi.nlm.nih.gov/pubmed/15522910

The decrease in MT2 melatonin receptor number induced by melatonin (300 pM for 1 h) was reversible and reached almost full recovery after 8 h; however, after treatment with 10 nM melatonin full recovery was not attained even after 24 h. This recovery process was partially protein synthesis dependent. Furthermore, exposure to physiological concentrations of melatonin (300 pM) for a time mimicking the nocturnal surge (8 h) desensitized functional responses mediated through melatonin activation of endogenous MT2 receptors, i.e., stimulation of protein kinase C (PKC) in immortalized SCN2.2 cells and phase shifts of circadian rhythms of neuronal firing in the rat SCN brain slice. We conclude that in vivo the nightly secretion of melatonin desensitizes endogenous MT2 melatonin receptors in the mammalian SCN thereby providing a temporally integrated profile of sensitivity of the mammalian biological clock to a melatonin signal.

So the desensitization happens in vivo too.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2581482/

We found that MEL inhibits the magnitude of LTP measured in the CA1 region of C57 and C3H mouse hippocampus. This effect was most dramatic when a high concentration of MEL was applied (100 μM)

So higher concentrations of melatonin lead to more inhibition of long-term potentiation.

In the present study, we demonstrate that MEL (≥1 nM) can alter synaptic plasticity through MT2-mediated regulation of the AC–PKA pathway. MEL is secreted during the night and may function to keep the levels of AC–PKA restrained during the rodent’s active phase. We speculate that the secretion of MEL globally constrains synaptic plasticity so that the formation of LTP will be restricted to specific synaptic connections. We propose that MEL is a signalling molecule that may importantly impose a temporal structure on the hippocampal circuits involved in learning and memory. Our results also suggest that understanding the role of G-protein-coupled receptors that are negatively coupled to signalling cascades may provide important insights into the physiological regulation of synaptic plasticity.

We know that taking higher doses of melatonin at night can lead to higher MEL serum levels the next day. Since exogenous supplementation is not selective to the region of the body/brain like endogenous release is, and melatonin can inhibit LTP, it is reasonable to assume that taking too high of a dose of exogenous melatonin can be deleterious to one's cognition during waking hours. This is why I suggest taking the lowest effective dose possible.

Also, please leave your condescending asides like "Nice try though." out of the discussion. This is not a contest to see who can prove the other person wrong. This is a place for us to work together to figure out the best method for the use of these substances, and to understand the mechanisms at play.