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Comment by spudlyo | Hacker News Reader

Fasting seems like a solution because in the fasted state your body doesn't need to produce insulin. Your body needs insulin to push fat into cells. Your pancreas gets a break, and perhaps sensitivity improves when you go on an extended insulin-free holiday.

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I'm no biologist but it's my understanding that insulin causes cells take up glucose, not fats. And I don't see anyone suggesting insulin or the pancreas is involved in any of this. So what does the pancreas have to do with Alzheimers?

> I don't see anyone suggesting

Have you looked?

"Although many factors affect fat cells, the hormone insulin exerts dominant anabolic control. Insulin decreases the circulating concentration of all major metabolic fuels by stimulating glucose uptake into tissues, suppressing release of fatty acids from adipose tissue, inhibiting production of ketones in the liver, and promoting fat and glycogen deposition." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6082688/

Or this one: https://www.nih.gov/news-events/news-releases/nih-study-show...

There are many many other studies and articles, as the insulin-fat storage connection is very well documented

It depends what cells we're talking about. Thanks to insulin, glucose can be stored in the liver and muscle tissues as glycogen. In folks with poor insulin sensitivity these cells do not respond as effectively to insulin, and their uptake and storage is reduced, leaving more glucose in the bloodstream. In the obese, it's also likely the liver and muscle tissue glycogen stores are near max capacity. In this case insulin facilitates the uptake of glucose into adipose (fat) tissue through a process known as lipogenesis. When I wrote "insulin pushes fat into cells" that's what I meant.

The insulin protein promotes glucose (not fats) uptake into the muscles (~75%), liver (~15%), and other tissue (~10%) to aggressively lower blood sugar levels back to a total circulating amount of ~5g.

In the obese, glucose is preferentially directed to adipose tissue for storage as fat. This is due to both insulin resistance, and to the limited storage capacity in muscles and the liver for glucose in the form of glycogen. I was writing colloquially and intentionally left out details like lipogenesis, which in retrospect probably wasn't a great idea.

Except there's literally a result out this week linking fasting (specifically 16+ hour intermittent fasting) with a 91% increase in cardiovascular disease deaths, which if it holds up would utterly swamp any incremental improvements to alzheimers risk.

No free lunch in personal health decisions, alas. Really the only good advice is stick to well-established science, be healthy in general, avoid internet advice, and don't sweat the small stuff.

The results unfortunately are too vague to support that interpretation.

There was no causal linkage because they couldn't determine why people were fasting: suppressed appetite due to illness, suppressed appetite due to being a smoker (which is very common), skipping meals due to poverty.

It also found that while cardiovascular deaths increased by 91% overall deaths were completely unchanged...which is a bit difficult to reconcile.

> The results unfortunately are too vague to support that interpretation.

I think you completely missed the point. Sure, it's a new result and being an outlier needs to be treated with care (which I believe I said). It's still a more rigorous finding of health effect than anything in the grandparent's comment about how you should fast to avoid Alzheimer's. Ergo advice like that is bad.

Thank You

It seems counterintuitive, and opposite of what is promoted.

I'll have to check it out more.

But from AHA, this is enough of a dramatic result to at least follow up on.

8-hour time-restricted eating linked to a 91% higher risk of cardiovascular death

https://newsroom.heart.org/news/8-hour-time-restricted-eatin...

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