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How nutrient restriction affects mitochondria and promotes cellular "toughness".

A common notion of how CR works is through making our cellular power plants, the mitochondria, "burn more cleanly". This generally gets translated into "generate fewer ROSs (free radicals) when converting food into useable energy". Many people believe it is ROSs that drive the aging process.

But there is substantial evidence to suggest this isn't the *whole* story. In this post from February 2, 2004, CRON4healthyfuture outlines some of the evidence that the stress of CR may "rough up" our mitochondria, toughening up the good ones and killing off bad ones. In the end, this may have the same result -- surviving mitochondria will be cleaner burners. But the picture is likely a lot more complicated than some had previously thought.

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In my previous speculation A Theory of Aging, I advanced the notion
that mitochondria, the "blast furnaces" of the cell, actually run
into "rough straits" under CR. I want to just present a couple of
studies that demonstrate how nutrient restriction can specifically
trigger these kind of changes that would have been considered
"detrimental" under previous perspectives on aging.

1) PMID: 12954482 shows that CR makes mitochondria swell and call for
"apoptosis" more. These do not sound like "protected" mitochondria,
but rather more like "expendable" mitochondria whose very dysfunction
could be just the ticket for wiping out cancer cells who will be
doing some goofy things metabolically that will make them
hypersensitive to malfunctioning mitochondria.

2) PMID: 12868592 shows that a 60-70 hour fast causes a bunch of
"giant mitochondria" to form in gastric cells. These mitochondria
result as the normal mitochondria actually start to fuse in some sort
of "we are really in trouble" phase of activity. Doesn't sound like
CR is the mitochondria's friend to me.

3) PMID: 14592935 shows that carbonyl content in mitochondria
increases during what they term "short-term" CR. They did it for 2
months. Carbonyl content is supposed to be measure of "man on the
street" oxidative stress, and yet it went up on CR. This makes
interpretation of changes in H2O2 production under CR considerably
more difficult.

4) PMID: 12969875 shows that electron transport itself is impaired in
CR organisms.

5) If PMID: 14660625 and PMID: 14739295 are to be believed, than such
mitochondrial dysfunction may be just what is needed to make normal
cells "tough" and cancer cells "dead".

Just a thought.