New paper includes mechanism for CR benefit w/r mitochondria

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Russ
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New paper includes mechanism for CR benefit w/r mitochondria

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Interesting tweet from the ever provocative Jack Kruse links this intriguing new 2014 paper…

Mitochondria hyperfusion and elevated autophagic activity are key mechanisms for cellular bioenergetic preservation in centenarians
http://www.impactaging.com/papers/v6/n4 ... 00654.html

…with final Discussion pgph…
Finally, it is to note that DFs from LLI are able to respond to metabolic impairment due to starvation much better than those from Young and, mainly, Old subjects. This is in line with the hypothesis that cells derived from centenarians could be endowed with an exceptional capacity to engulf and digest in huge vacuoles their siblings, likely a strategy of food supply [52]. It has also been suggested that cells from LLI could be characterized, at least to some extent, by a phenotype similar to that induced by the so called caloric restriction, a sort of mild starvation, which is the most efficient method to extend life span in animal models and humans [53,54]. In agreement with this view, we observed that mitochondria of LLI maintain their energetic capacity by increasing their mass and forming large networks, as it occurs under starvation conditions in cells from young subjects, suggesting that also from a bioenergetic point of view cells from LLI behave as if they were naturally calorie restricted. This hypothesis needs further investigations to be validated.
Note 'DF' = Dermal Fibroblasts - the cells studied, and LLI = Long Lived Individuals (centenarians).

In short they looked at the mitochondria form in young old and LLI's and found that the LLI's had noticeably aggregated (hyperprofused) mitochondria and propose that this is an energy efficiency thing naturally occurring in some LLI old people but phenomenologically similar to conditions observed in calorie restricted people.

Now it would be interesting to know if similar can be induced by periodic/episodic variability?
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Re: New paper includes mechanism for CR benefit w/r mitochondria

Post by circular »

Very cool!
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Re: New paper includes mechanism for CR benefit w/r mitochondria

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To a certain extent, the body's response to being in ketosis seems to be similar to the response to CR. I wonder if you can extrapolate?
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Re: New paper includes mechanism for CR benefit w/r mitochondria

Post by Russ »

George, great question!
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Re: New paper includes mechanism for CR benefit w/r mitochondria

Post by Hepoberman »

Caloric restriction or Metformin!? It seems to me Metformin might benefit us with a similar Complex I reducing effect. (I still wonder about increased phosphorylation of tau proteins though)

I am visualizing lean, mean mitochondria, ftw. This is probably what underlies some of the benefits of fasting.

I assume a person with low body fat will have leaner meaner mitochondria too (more hypertrophic?). Could this underpin the rate we age? It fits well with the micro-nutrient triage theory of aging too.

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Re: New paper includes mechanism for CR benefit w/r mitochondria

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From the OP's quoted paragraph...
This is in line with the hypothesis that cells derived from centenarians could be endowed with an exceptional capacity to engulf and digest in huge vacuoles their siblings, likely a strategy of food supply.
So, in order to live to 100, my cells need to have a cannibalistc bent?

They mention autophagy in the article, which in the usual meaning is a process by which cells consume their own components during times of food deprivation.

But here, they're using it to mean that when a cell gets hungry and can't get food through the usual channels, it grabs a neighbor cell, wrestles it into submission, and eats it, thereby forestalling starvation and, as part of the deal, it acquires additional mitochondrial cells that it can integrate into its internals.

Nature. Red in tooth, claw, and mitochondria... :shock:
It's weird how I'm constantly surprised by the passage of time when it's literally the most predictable thing in the universe. -- xkcd
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Re: New paper includes mechanism for CR benefit w/r mitochondria

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I personally would choose CR, IF and/or ketosis over Gucophage because it can reduce stomach acid, absorption of B12 and increase serum homocysteine.
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Re: New paper includes mechanism for CR benefit w/r mitochondria

Post by Welcomeaboard »

So George you would not want cr, if and ketosis then if you had low stomach acid as you would not want to decrease that or if you were high homocysteine as you would not want to increase that either, thereby proving cr is not a n=1 solution for everyone and could lead to poorer health outcomes in people is what I am reading from that post.
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Re: New paper includes mechanism for CR benefit w/r mitochondria

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WA,

To be clear I'd choose CR, IF and/or ketosis over Metformin (Gucophage) as Metformin can reduce stomach acid, reduce absorption of B12 and increase serum homocysteine (which I view as bad outcomes). In addition I look at CR, IF and ketosis as natural and normal body states (some may not agree) vs. a drug. If I were a diabetic, my relative value equation might be different, and I might consider Metformin, but I'm not.
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