What really cause the differences between pre-industrial and industrial societies' sleep?

This seems to be the forum for interesting takes on sleep, so here are some of my thoughts and questions.

In 2015, Yetish Et al. published “Natural sleep and its seasonal variations in three pre-industrial societies” finding that the three pre-industrial societies that they collected data on only slept, on average 5.7 to 7.1 hours each night, which is similar to the the amount of sleep found in industrial populations.

Some differences they found in the pre-industrial groups compared to what’s typically seen in industrial populations: there were very low rates of insomnia, very low rates of awake periods in the night, low rates of napping, sleep lengths were almost an hour longer in the “winter” than in the summer, and the sleep offset seemed to be entrained by ambient temperature nadir.

The authors suggest that environmental temperature control may be causing things like insomnia or other sleep disturbances in industrial societies, and they end the discussion section with this paragraph: “Our findings indicate that sleep in industrial societies has not been reduced below a level that is normal for most of our species’ evolutionary history. Recreating aspects of the environments we observed in preindustrial societies might have beneficial effects on sleep and insomnia in industrial populations.”

I wonder though, with insomnia being incredibly comorbid with and often clearly caused by sleep apnea (which is surprisingly common even in skinny, young people), could the main difference between the pre-industrial and industrial societies’ sleep be sleep apnea?

Sleep apnea often begins in or before childhood. Theories claim it often starts with poor orofacial development due to premature birth, tongue tie, or bottle feeding in place of breastfeeding. It’s also believed that mouth breathing in childhood due to allergies or enlarged adenoids and tonsils can lead to adenoid facies and subsequent deficiencies in the sleep breathing. There are surely many other factors coming into play. One is clearly fat which can make the airway smaller.

How much insomnia in industrial societies is actually caused by sleep apnea and how much of this difference between pre-industrial and industrial societies is better explained by sleep apnea than light and temperature?

A quote from a good book: “The use of PSG is not indicated for routine evaluation of a transient or chronic insomnia disorder, which places primacy on the subjective complaint for diagnosis. It is indicated to rule out the presence of a sleep-related breathing disorder (e.g., OSA) or a periodic limb movement disorder, or when the initial insomnia treatment fails. However, emerging evidence suggests that sleep-related breathing disorders in particular may be underrecognized causes of insomnia complaints, even among individuals who deny cardinal sleep-related breathing disorder symptoms on initial presentation.” (page 791 of Meir Kryger et al.'s “Principles and Practice of Sleep Medicine”)

From everything I’ve read, sleep apnea is incredibly underdiagnosed, in both the young and old, and even when it is diagnosed is often poorly treated both because poor application of treatment by providers and poor compliance by patients (though my person theory is that the poor compliance is often due to the poor application by providers and patients subsequently not finding full relief from sleep apnea symptoms).

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Excellent post. OSA is vastly underdiagnosed, and it might make sense for everybody health-conscious or driven towards self-enhancement to do a PSG once a year, or at least sometimes wear a continuous SPO2 monitor. It is a pity that Oura did not manage to integrate SPO2 yet - a product like Oura pointing out that people might have apnea problems could significantly increase diagnosis rates in the (health-conscious) population.l

I agree that OSA is vastly underdiagnosed (and would add that after diagnosis it is incredibly undertreated or poorly treated). But I think that for a lot of people a yearly PSG would be way to much, at least an in-clinic PSG would be.

I think an ECG headband during sleep, something like the Dreem, coupled with a nasal pressure transducer would be sufficient as long as the data were read intelligently. We really need AI-scored PSG’s!

Also, SPO2 monitoring is a step in the right direction, but non-hypoxic sleep apnea won’t be picked up, and this is the type that is more common in the young and non-obese, the theory being that their blood does not desaturate as easily as the old and obese and that the nerves in their airway are more intact such that they will be aroused sooner in a apneic/hyponeic event than others making them still less likely to have meaningful oxygen desaturation even though they still have the sleep fragmentation (which seems to cause a bulk of the symptoms of sleep apnea).