The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
So that's what we're thinking is that the emotional parts are no longer-- are not able to be divorced because the norepinephrine system is not downscaled during REM sleep. And so that REM sleep serves to instead reinforce and in fact amplify the emotions because your emotional system is up, locus coeruleus is high, re-sewing in every night the emotionality of those memories and with the memory itself.
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So-- whereas their levels of norepinephrine might be similar to people without PTSD during the day and even during the first part of the night, during the wee hours of the morning. And when you measure norepinephrine levels from metabolites in the blood or the cerebrospinal fluid, you see that people with PTSD, it's during the wee hours of the morning when you have the most REM sleep that they have their norepinephrine levels differentiate most from those that don't have PTSD. And so that's evidence that the locus coeruleus is not shutting down during REM sleep like it should.
And I think the key to that again is the absence of norepinephrine. So even though the emotional system is in high gear, without norepinephrine, you can actually divorce those highly activated emotions from the cognitive parts of the memory that you have just written out in that N2 stage of sleep when the sleep spindles are going.
This almost starts to sound like a little bit of a built in while sleeping trauma therapy, because most trauma therapies involved trying to get people into states of counter to what most people think you actually want to get close to the trauma in terms of the narrative or try and suppress the emotional activity of it or-- I guess that's the motivation for ketamine-based therapies for trauma-- or I've also heard, and this is still perplexing to me, that other waking-based trauma therapies involve taking people the other way, making it very cathartic, take them to the peak of the emotional response but then allow that to finally cycle down into a more relaxed response.
but what was interesting in Marie Raskin studies when he started to treat patients with the pricin and Tamp down that noradrenaline one of the other things that returned back to normality was not just that the symptoms dissipated their REM sleep started to return with a greater amount and so I think it fits very well with this notion that whatever REM sleep that was going on may not necessarily have been electrical or neurochemically identical to normative REM sleep but when you assisted the system with a chemical to bring it back into normality REM sleep was gifted back to the brain and emotional resolution started to unfold
10 minutes of bright outdoor light within the first hour of waking anchors the circadian phase and improves sleep onset that night.
Morning sunlight exposure shifts the cortisol awakening response forward, improving daytime alertness.
Long-term morning sunlight reduces age-related macular degeneration risk.
Sleep regularity predicts all-cause mortality more strongly than sleep duration.
Tracking deep sleep on a wearable accurately reflects EEG-measured slow-wave sleep.
Caffeine has a half-life long enough that consumption after 2pm measurably degrades deep sleep in slow metabolizers.