Moderately suggested:LIGHT and Melatonin: Timing is Everything
And for a good old time: LIGHT Timing for Circadian Entrainment
I’m not anti-melatonin supps. Actually, I think they can be helpful in some #contexts. For example, adjusting to jet lag after a long eastward flight (in combination with blue blockers, of course). Melatonin supps are less helpful after westward flights because lengthened daylight wakeful hours means more adenosine accumulation and thus greater sleep pressure when it finally gets dark. The supps might be helpful for some in this context, but not as helpful as after eastward flights.
Another theoretical example would be if you had to work late on the computer and didn’t think blue blockers were adequate. In both of these scenarios supplementation is acute. Long-term use may be warranted in other cases, like circadian phase-related sleep disorders or blindness. And in some elderly populations, for whatever reason, endogenous melatonin secretion drops off and sleep quality declines. No bueno.
More work is needed on the MTNR1B polymorphisms, but if some low-functioning variants are found and associated with reduced melatonin signaling at comparable levels of melatonin, I can see some potential value here, too.
Back to the main story:
Acute melatonin administration in humans impairs glucose tolerance in both the morning and evening (Rubio-Sastre et al., 2014)
Take-home message: we’re supposed to have darkness & melatonin, not big meals at night. Thus, early(ish) lighter dinners and blue blockers. Melatonin appears to have a peculiar pro-fattening interaction with insulin on adipocytes. Maybe that helped breakfast-skipping hunter-gatherers better survive famine (if they even existed)... because hey, you die faster from starvation than obesity.
Study design: . 10-hour fast, then five milligram melatonin supp or placebo, then oral glucose tolerance test. Repeated on non-consecutive days at 9 AM or 9 PM.
Compare the light gray lines below. In the morning (top left graph), they’ve been exposed to physiological levels of melatonin all night (to sensitize the system), but then melatonin is gone by the time of the procedure. During the evening condition (top right), there was no melatonin to sensitize the system: glucose peaks about 20 points higher and AUC is nearly 4X!
In both conditions melatonin supps exacerbated the glycemic response.
In the morning, we're supposed to have SUNLIGHT and FOOD not MELATONIN.
In the evening, there hasn’t been 8 hours of melatonin to sensitize the system, so even though more insulin is secreted, it’s not enough to maintain euglycemia.
Some in the field interpret this as melatonin suppressing insulin secretion – “even though insulin is higher, it’s not high enough.”
But that doesn’t change the conclusion: you don’t want digesting a big meal to overlap with melatonin onset. Even in the control group, the amount of insulin that maintained euglycemia in the morning wasn’t enough in the evening. Hyperinsulinemia, combined with the pro-lipogenic interaction of insulin with melatonin on adipocytes, the intrinsically reduced energy expenditure at night, and… Mother Nature might be trying to tell you something.
Some people can get away with it, sure, and they may not know it, but the deck is stacked against them. There’s an easier way, folks.
(from Lopez-Minguez et al., 2017)