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[MR]

All:

CRBasics wrote:

> > reactive carbonyl species are listed [in (1)]
> > as one of the two primary biochemical aging mechanisms for all protein
> > life forms (with reactive oxygen species being the other primary aging
> > threat). We humans are 70% protein, and so must be sure to get sufficient
> > (balanced usable) protein to maintain health.

There actually should be no 'so' here. The 2 facts are in large part
unrelated.
> >
> > ---------
> > Question 1: Can anyone explain (in simple layman terms) how
> > non-oxidative degradation of protein occurs via interaction with
> > reactive carbonyl species?

The most familiar case would be by forming AGE crosslinks.

> > ---------
> > Question 2: Are reactive carbonyl species one of the two prima facia
> > mechanisms of aging (reactive oxygen species being the other),
> > in terms of biochemical aging (as appears to be the thesis of the
> > abstract below)?

No -- they're a CONTRIBUTOR to one of the SEVEN prima facia mechanisms
of aging:

http://sens.org/just7.htm
> >
> > ---------
> > Question 3: Is the evolutionary difference -- R-Selection versus
> > K-Selection -- significant enough for a solid rationale to expect
> > a biochemically-based significant difference in life-extension
> > benefit from CR for humans, as compared to mice?

Many people have argued that, yes -- see eg many of the skeptical papers
from a recent issue of _Biogerontology_:

http://www.springerlink.com/link.asp?id=p907gwpu5x36

In the (CR Society) Archives, Al P posted many of the abstracts & much of the guts of
many of these; go hunting if you want more.

I find these arguments cogent but not convincing, based in large part on
empirical data to hand in primates and humans trumping theoretical
arguments based on an hypothesis about the evolutionary origins of CR


> > [Biochemistry of lifespan extension]
> > Golubev AG. [Article in Russian]
> > Research Institute of Experimental Medicine, 12 Akademika
> > PMID: 14743602 [PubMed - indexed for MEDLINE]