(The standard rodent chow used by gerontologists does not have
whole natural foods in it like berries or seeds. Instead cooked
cornstarch is used, which has an unusually high glycemic index.
The use of this high GI carbohydrate is partly responsible for
the high rates of glucose tolerance which occur in lab animals
that are cared for by gerontologists.
Another important factor is to be the relative lack of insulin
sensitising substances, which are readily available in natural
diets, but which are largely stripped out of the "purified"
diets used by uninformed gerontologists. These scientists as a
group well illustrate the dangers of over-specialization, any
scientist involved in diabetes research would tell gerontologists
that a phytochemical stripped high glycemic index diet is a
recipe for adult onset diabetes, and lowering caloric intake of
such a poor diet can lower risk, via a reduction in glycemic load.
The so called called anti-aging calorically restricted diet
appears to be merely an artifact of using a poor diet that
induces glucose intolerance when fed ad-libitum.
One rat strain that was fed insulin sensitising chromium
picolinate had their average lifespan restored to what appears
to be "normal" values. This is well in excess of that yielded by
caloric restriction of a purified diet. Chromium picolinate
has no effect on healthy non-diabetic humans.
Caloric intake as measured by height has no effect on
longevity in humans, and weight loss diets do not reduce
mortality rates in this species. Obesity also has no effect
on mortality, provided physically fit obese humans are
compared with physically fit lean humans. In physically unfit
humans, lean people have a higher mortality than obese.
These basic facts have been available for quite some time,
but have been largely ignored by over-specialized gerontologists.
It is unfortunate, but the primary roadblock to continuing advances
in gerontology appear to be the incompetence of the gerontologists
---------- Forwarded message ----------
Longitudinal determination of
skin collagen glycation and glycoxidation rates predicts
early death in C57BL/6NNIA mice.
FASEB Journal. 14(1):145-56, 2000 Jan.
In 1988, the National Institute on Aging launched a 10-year program aimed at
identification of biomarkers of aging. Previous results from our laboratory
showed that pentosidine, an advanced glycation product, formed in
skin collagen at a rate inversely related to maximum life
span across several mammalian species. As part of the Biomarkers Program, we
investigated the hypothesis that longitudinal
determination of glycation and glycoxidation rates in
skin collagen could predict longevities in ad libitum-fed
(AL) and caloric restricted (CR) mice. C57BL/6NNia male mice were biopsied at
age 20 months and at natural death. Glycation (furosine method) was assessed
by gas chromatography/mass spectrometry (GC/MS) and the glycoxidation
products carboxymethyllysine (CML) and pentosidine were determined by GC/MS
and HPLC, respectively. CR vs. AL significantly (P<0.0001) increased both
mean (34 vs. 27 months) and maximum (47 vs. 31 months) life spans.
Skin collagen levels of furosine (pmol/&mgr;mol lysine) were
approximately 2.5-fold greater than CML levels and 100-fold greater than
pentosidine. Individual accumulation rates modeled as linear equations were
significantly (P<0.001) inhibited by CR vs. AL for all parameters and in all
cases varied inversely with longevity (P<0.1 to <0.0001). The incidence of
three tissue pathologies (lymphoma, dermatitis, and seminal vesiculitis) was
found to be attenuated by CR and the latter pathology correlated
significantly with longevities (r=0.54, P=0. 002). The finding that markers
of skin collagen glycation and glycoxidation rates can
predict early deaths in AL and CR C57BL/6NNia mice strongly suggests that an
age-related deterioration in glucose tolerance is a life span-determining
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