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corybroo

Fasting boosts intestinal stem cells

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Science Daily has an article about 24hr fast doubling regenerative capacity in intestinal step cells:  

https://www.sciencedaily.com/releases/2018/05/180503142852.htm

 

Intestinal stem cells are responsible for maintaining the lining of the intestine, which typically renews itself every five days. 

 

After mice fasted for 24 hours, the researchers removed intestinal stem cells and grew them in a culture dish, allowing them to determine whether the cells can give rise to "mini-intestines" known as organoids.

The researchers found that stem cells from the fasting mice doubled their regenerative capacity.

sequencing the messenger RNA of stem cells from the mice that fasted, revealed that fasting induces cells to switch from their usual metabolism, which burns carbohydrates such as sugars, to metabolizing fatty acids.

they could reproduce the beneficial effects of fasting by treating mice with a molecule that mimics the effects of PPARs.

The findings suggest that drug treatment could stimulate regeneration without requiring patients to fast

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Meh, nobody knows - it probably depends on the strain of mice, and it is entirely possible that you simply cannot extrapolate the effects AT ALL, because mice are different physiologically, have a different hormonal environment, different adaptations to food compared to humans, and in general, IMHO, should not be extrapolated from, except in very narrow and carefully considered parameters.

 

This is why when I see a study "in mice", I immediately lose interest. Good for the mice.

 

To give you just one example, there is already a huge difference between human beings in extremely basic ways, such as absorption of zinc (there's another thread on it here, so I happened to do some research). Here's one example:

 

https://academic.oup.com/jn/article/144/2/132/4637670

 

Key passage:

 

"A surprising finding from the present study is that 3 participants of the 15 absorbed little or no zinc from zinc oxide, suggesting that there is a portion of the population that is not able to dissolve zinc oxide in the gastric juice, probably because of a high intragastric pH making it poorly absorbable. Because the low absorption was measured in 3 individuals who absorbed zinc gluconate and zinc citrate normally and because all were apparently healthy at the time of supplement consumption, it is unlikely that this was a coincidence. Additional repeated measurements of their urine samples excluded an analytical error."

 

Do you see that? Healthy human beings, who CANNOT absorb certain forms of zinc, which the others can!

 

This is among a group of people - such fundamental differences in a very basic mineral during intestinal absorption. And now you want to compare the entire intestinal stem cell system in MICE and compare it to humans?? Forget it.

 

It's ridiculous. As I keep repeating - animal studies are at best an indication of potential avenues for more research, as pointers for starting studies in humans, not as CONCLUSIONS about human beings from animal studies. To make any conclusion from a mouse to a human, you must be extremely careful and in very narrow circumstances. Until something is shown in humans, mice studies have ZERO actionability for human beings.

 

Trumpeting conclusions from a mouse study is a waste of time (unless you have relatives who are mice - I know some of us have relatives who are real rats). 

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TomB, the resveratrol fiasco apparently confirms 100% what you say, although you say it in an extreme way (which may just be true).

 

Valter Longo extrapolated the minimum 5-days fast duration to rejuvenate teh system from a 48 hours fast duration in mice, if I remember well.

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This is why when I see a study "in mice", I immediately lose interest. Good for the mice.

...

Until something is shown in humans, mice studies have ZERO actionability for human beings.

 

 

I mostly agree with this.  There have been at least a dozen interventions found effective in mouse models of my disease, SBMA, but none have been translated into an approved therapy for humans.  But in part I blame the process which focuses almost exclusively on pharmaceuticals and the challenge of finding ones that don't have significant rates of severe side effects in large groups people.  By attempting to hit many targets of those interventions through non-pharmaceutical means I'm achieving good results despite being unable to quantify the effects of each factor.

Edited by Todd Allen

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