For the afficionados, there's an excellent paper titled "The neurobiological basis of narcolepsy" published in Nature Reviews Neuroscience which examines the relationship between orexin and sleep as it relates to narcolepsy patients: https://pmc.ncbi.nlm.nih.gov/articles/PMC6492289/
In narcolepsy type 1 (NT1), patients have severely diminished orexin levels. This appears to cause them to inappropriately enter REM sleep.
OP notes that the mutation lowering the sleep requirement causes an increase in orexin. I wonder whether the increased orexin could be inhibiting REM and perhaps facilitating a more restful architecture of sleep. Alternatively, perhaps elevated orexin levels during the day cause wakefulness such that you just don't need as much sleep, regardless of how efficient the sleep is.
It would be interesting to compare sleep tracking data of people with and without this mutation to see if there are significant differences in time spent in different sleep stages.
Why is it not a survival advantage? Probably because we didn't work 18 hour days, the extra wakeness would just be used for rest.
Night shifts that anyone can do are still needed if you need tribal watchers, and normal 8hr sleeping people can wake upnand fight when needed.
In terms of the gene, I am suprised how rare it is (90 families?) given I have met someone who needs only 4hr sleep.
Another point is less sleep doesn't mean you can do 2 more hours work a day. That is another vector: how much work per day (physical, mental) can be done.
How about — instead of making sleep more "efficient" — we engineer our lives to provide decent amount of sleep and not stress over having more and more of the waking hours to do stuff.
After all, we live in the age of abundance.
(Though I admit I might not be the best person to ask for this as I am on the lower end of how much sleep I need)
How about engineering the society/civilization(?)/world so that "all can" work hard (8hrs), rest hard (8hrs), live hard (8hrs) and die hard when the eventuality arrives?
In narcolepsy type 1 (NT1), patients have severely diminished orexin levels. This appears to cause them to inappropriately enter REM sleep.
OP notes that the mutation lowering the sleep requirement causes an increase in orexin. I wonder whether the increased orexin could be inhibiting REM and perhaps facilitating a more restful architecture of sleep. Alternatively, perhaps elevated orexin levels during the day cause wakefulness such that you just don't need as much sleep, regardless of how efficient the sleep is.
It would be interesting to compare sleep tracking data of people with and without this mutation to see if there are significant differences in time spent in different sleep stages.
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