If I'm reading this correctly, the only "food" involved is cannibalism, although they didn't end up doing so with the mice due to supply issues. It doesn't explain why eating another organism's "accumulated damage" reduces the eater's own lifespan but says they expected it to have even more effect than it did.
Clearly, eating works differently than I thought it did, because I'm at a complete loss.
Not really a specialist or anything, but I surmised that aging creates what you could call "bad chemicals" in your body.
> unavoidable byproducts of enzyme function, for example, or of protein-to-protein interactions, errors in DNA transcription or translation.
One would surmise that aging adds "bad chemicals" to your body at some set rate. If you ALSO eat old things, that are already full of these "bad chemicals", your body will acquire these bad chemicals faster (because of the extra source).
In short, this research shows that there is some byproduct of the aging process that can be transferred from one organism to another and cause aging in the second organism.
How is that your take? It seems that would completely contradict it. If it's just accumulation of errors how would that be impacted at all by what you eat? Especially the age of what you eat!
A first guess would be that these diets are passing over aggregate compounds and compatible metabolic waste: misfolded proteins, lipfuscin, oxidized lipids, and so forth, and enough of those escape the stomach to be incorporated into tissues to do harm.
That said, 10% for mice is well within the "try it again in a different lab, get a different result" margin of error for this sort of study.
Older organisms have added time to ingest toxins like heavy metals (especially prevalent in carnivorous fish like tuna). I suspect this plays some role here.
Of the three experimental groups in the article, it sounds like two, the yeast and fruit flies, were all lab grown grown. Where would the toxins have come from.
In the third, the Deer meat fed to mice was 25 years old and clearly had fewer controls, despite this room for toxins, the mice had the smallest effect of any of three groups.
Possibly, but they weren't really testing to learn about the effects of old vs new foods in general. It's more a test of whether "metabolic junk" is significant to aging, so they used food sources that would have more or less of those factors present. The relevant compounds are different and not precisely known for the different organisms, thus the cannibalistic diets.
>The effect of consuming an old versus a young diet, he says, was “statistically significant, but it wasn’t huge. Honestly, I thought it would have a much larger effect on lifespan, but it was on the order of about 10 percent.”
There is an effect that works in the opposite direction that might explain why the effect was smaller than expected:
Younger organisms (presumably) have a higher percentage of inflammatory amino acids than older organisms and restriction of some of these is known to extend life. Methionine restriction has been established I think.
In the other direction, Ray Peat claims that a higher percentage of older organisms is collagen. The consumption of collagen (bone broth for example) is possibly life extending.
Maybe they should have had another set that had their usual diet for comparison just to ensure that they are not making their observations on cannibalism. As one can take the study to mean if cannibals chose young for their dietory needs they would survive 10% longer except in the case of mice however.
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[ 3.8 ms ] story [ 62.4 ms ] threadClearly, eating works differently than I thought it did, because I'm at a complete loss.
> unavoidable byproducts of enzyme function, for example, or of protein-to-protein interactions, errors in DNA transcription or translation.
One would surmise that aging adds "bad chemicals" to your body at some set rate. If you ALSO eat old things, that are already full of these "bad chemicals", your body will acquire these bad chemicals faster (because of the extra source).
In short, this research shows that there is some byproduct of the aging process that can be transferred from one organism to another and cause aging in the second organism.
For example, does feeding a mouse young plant parts result in a longer lifespan than using seeds that have taken many months to ripen?
That said, 10% for mice is well within the "try it again in a different lab, get a different result" margin of error for this sort of study.
In the third, the Deer meat fed to mice was 25 years old and clearly had fewer controls, despite this room for toxins, the mice had the smallest effect of any of three groups.
1) Advanced Glycation End-productions (AGE) from normal metabolism
2) Trace levels of heavy metals, dioxins, etc. from the growth media
3) Reactive oxygen species (ROS) generation increasing with age-related damage
4) BPA, phthalates, or other potentially nasty things leaching from the plastic growth containers
5) Lipofuscin
6) Misc age-related inflammatory cytokines
7) ????
There is an effect that works in the opposite direction that might explain why the effect was smaller than expected:
Younger organisms (presumably) have a higher percentage of inflammatory amino acids than older organisms and restriction of some of these is known to extend life. Methionine restriction has been established I think.
In the other direction, Ray Peat claims that a higher percentage of older organisms is collagen. The consumption of collagen (bone broth for example) is possibly life extending.