Thanks for pointing that out. That was a misstatement on my part. Where I said "body" I should have said "brain", which was what I was thinking. And "only" maybe should have "primarily" or "required for" or something. I don't remember the exact phrasing that was used. The overarching context was avoiding Alzheimer's and similar neurodegenerative brain diseases. Occasional "little" gaffs like that explain my interest in the topic.frugaldoc wrote: ↑Mon May 12, 2025 4:42 amI am curious as to where you picked up this factoid. It does not correspond to any cellular biology I learned although I will grant that my knowledge may be a bit out of date. With DNA dividing throughout the day, being able to repair DNA damage only two hours per day seems quite risky. I feel that an organism that could repair over a greater span of time would have a selection advantage. Unless the results of this damage only manifested themselves after the reproductive years.

The original statement was made in reference to the brain itself, and in context was referring to the neural system components there, and within that was possibly specific to mitochondrial repair/biogenesis, but it wasn't stated as such. That was the specific topic of the talk: mitochondrial health in neurons, specifically in the brain. The sleep aspect was thrown in the context of "other things that are important to maintain healthy neurons in the brain as we age".
Unfortunately, I consume information through podcasts in sipping from a fire hydrant fashion and in a quick perusal of my recent playlist I didn't locate the statement. My recollection is that the interviewee was a cellular biologist who specializes in mitochondrial health through nutrition intervention. If I eventually find it I'll drop a link in the thread. Just to demonstrate I'm not disseminating random posterior retrieval information, I included part of AI response to the query "Which phase of sleep facilitates DNA repair?" at the bottom of the post.
Sleep itself is a risky behavior, and it's been identified in every animal that's been studied in that regard. So from an evolutionary perspective it would make sense that it provides unique critical benefits, and that it would be as efficient as possible. I don't think science has a great handle on why it's so necessary, but it seems like there's quite a lot of multitasking going on, on both sides of the BBB. The link to DNA repair was established relatively recently, within the last 5-10 years or so, I believe.
I don't know much about DNA upkeep outside the BBB, except that mitochondrial repair/upkeep requires periods of low insulin sufficient for the body to switch over to fat burning mode, and that is when they repair themselves or if too damaged get discarded and (hopefully) replaced by new healthy ones. Much of that happens during sleep simply because it's probably the longest stretch of time where the body is not processing incoming calories and gets into a semi-fasted state (especially in Western lifestyle high carbohydrate grazing), but I don't think is sleep specific. I get the impression that apoptosis processes are more active in a fasted state. But I don't know when or how DNA repair happens in general human cells. Seems like it would happen during inactive times, but different parts of the body are inactive at different times and some are never inactive (heart and lungs, e.g.) so to your point, I would guess that in general it's a continuous process. Maybe neurons are somewhat different because they are so long lived compared to other cells.
AI response to "Which phase of sleep facilitates DNA repair?"
While not a specific sleep phase, studies suggest that deep sleep, specifically slow-wave sleep, is associated with increased DNA repair in neurons. PARP-1, a protein involved in DNA damage repair, promotes sleep, and this sleep in turn facilitates the repair process.
Here's a more detailed explanation:
Slow-wave sleep and DNA repair:
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During deep sleep, particularly slow-wave sleep, there's a general decrease in neuronal activity, reducing stress on the chromosomal structure. This decreased activity also leads to synchronized bursts of neuronal firing, which increase intracellular calcium levels and activate DNA repair mechanisms like PARP-1.