From: Al Villalobos (al.villalobos@qm.com)
Date: Wed Apr 05 2000 - 15:03:24 MDT
Aha! Here is some more recent work by Parr.
Please! does anyone have access to back issues of Gerontology? The full
text of the papers
I posted would be very enlightening, I'm sure.
Insulin exposure and unifying aging.
Gerontology 1999 May-Jun;45(3):121-35 (ISSN: 0304-324X)
Parr T [Find other articles with this
Author]
USC Department of Medicine, University of Southern California, Los
Angeles, Calif., USA.
72237.570@compuserve.com.
BACKGROUND: Absence of a widely agreed upon central paradigm for mammalian
aging. OBJECTIVE: Detailed elaboration of a proposed mammalian aging
paradigm. METHODS: Elaboration of a new theoretical model. RESULTS: Hormonal
imbalance-growth factor exposure theory (HI-GFE theory) can account for two
major aging phenomena: (1) decline in mammalian 'reserve capacity' and
consequent rise of diseases of maintenance, and (2) rise then peaking of
most age-associated proliferative diseases. Reserve capacity decline via
gradual decline in mitochondrial maximal energy production
(state 3) accounts for the gradual redirection of declined maximal energy
production toward survival functions like ion pumping to the relative
detriment of RNA and protein synthesis as seen in lesser synthetic rates and
slower turnover with consequent gradual cellular impairment. Developmental
program triggered, and over-ample nutritionally driven, growth factor
exposure in
youth to middle age encourages promotional events that lead to proliferative
diseases that rise coincident to rapidly declining reserve capacity and
cumulative increased mutational status of age. CONCLUSIONS: Declining
mitochondrial state 3 aging energy production status is easily and safely
reversible with probable consequences of greatly postponing the decline in
overall
'reserve capacity' which may also improve insulin: growth hormone balance
and result in lower overall growth factor exposure and consequent longer
healthy life of a potentially greater magnitude increase in life spans than
that seen in calorie-restricted
animals.
Also...
In a message dated 4/5/00 12:52:32 PM Pacific Daylight Time,
cyn386@flash.net
writes: "I am pretty sure that the reason for this, is that sugar, not fat
is
the dietary culprit."
Exactly! see how that ties in with Parr's work on Insulin exposure? For me,
I try to keep my overal carb consumption to complex carbs low on the
glycemic index and around 30-50% total carbs. I also try to keep to a bare
minimum bread, rice, pasta and potatos. I know that implies a generous 30%
fat, but about 90% of my fat intake is from Olive oil, nuts and chicken.
Regards,
Al Villalobos
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