X-Message-Number: 25863
Date: Tue, 22 Mar 2005 20:25:14 -0800 (PST)
From: Doug Skrecky <>
Subject: caloric modulation

[Although caloric restriction may appeal to a few, caloric modulation
might win many more converts. More calories from fruits & vegetables,
and fewer from saturated fat appears to additively affect human mortality
beneficially.]

Gerontology. 2005 Mar-Apr;51(2):73-82
The unfortunate influence of the weather on the rate of ageing:
why human caloric restriction or its emulation may only extend
life expectancy by 2-3 years.
de Grey AD.
Department of Genetics, University of Cambridge, Cambridge, UK.
    Much research interest, and recently even commercial interest,
has been predicated on the assumption that reasonably
closely-related species--humans and mice, for example--should, in
principle, respond to ageing-retarding interventions with an
increase in maximum lifespan roughly proportional to their control
lifespan (that without the intervention). Here, it is argued that
the best-studied life-extending manipulations of mice are examples
of a category that is highly unlikely to follow this rule, and
more likely to exhibit only a similar absolute increase in maximum
lifespan from one species to the next, independent of the species'
control lifespan. That category--reduction in dietary calories or
in the organism's ability to metabolize or sense them--is widely
recognized to extend lifespan as an evolutionary adaptation to
transient starvation in the wild, a situation which alters the
organism's optimal partitioning of resources between maintenance
and reproduction. What has been generally overlooked is that the
extent of the evolutionary pressure to maintain adaptability to a
given duration of starvation varies with the frequency of that
duration, something which is--certainly for terrestrial animals and
less directly for others--determined principally by the weather.
The pattern of starvation that the weather imposes is suggested
here to be of a sort that will tend to cause all terrestrial
animals, even those as far apart phylogenetically as nematodes and
mice, to possess the ability to live a similar maximum absolute
(rather than proportional) amount longer when food is short than
when it is plentiful. This generalization is strikingly in line
with available data, leading (given the increasing implausibility
of further extending human mean but not maximum lifespan in the
industrialized world) to the biomedically and commercially sobering
conclusion that interventions which manipulate caloric intake or
its sensing are unlikely ever to confer more than 2 or 3 years'
increase in human mean or maximum lifespan at the most.

J Nutr. 2005 Mar;135(3):556-61
The Combination of High Fruit and Vegetable and Low Saturated Fat
Intakes Is More Protective against Mortality in Aging Men than
Is Either Alone: The Baltimore Longitudinal Study of Aging.
    Saturated fat (SF) intake contributes to the risk of coronary
heart disease (CHD) mortality. Recently, the protective effects of
fruit and vegetable (FV) intake on both CHD and all-cause
mortality were documented. However, individuals consuming more FV
may be displacing higher-fat foods. Therefore, we investigated the
individual and combined effects of FV and SF consumption on total
and CHD mortality among 501 initially healthy men in the Baltimore
Longitudinal Study of Aging (BLSA). Over a mean 18 y of follow-up,
7-d diet records were taken at 1-7 visits. Cause of death was
ascertained from death certificates, hospital records, and autopsy
data. After adjustment for age, total energy intake, BMI, smoking,
alcohol use, dietary supplements, and physical activity score, FV
and SF intakes were individually associated with lower all-cause
and CHD mortality (P < 0.05). When both FV and SF were included in
the same model, associations of each were attenuated with CHD
mortality, and no longer significant for all-cause mortality. Men
consuming the combination of >/=5 servings of FV/d and </=12% energy
from SF were 31% less likely to die of any cause (P < 0.05), and 76%
less likely to die from CHD (P < 0.001), relative to those consuming
<5 FV and >12% SF. Men consuming either low SF or high FV, but not
both, did not have a significantly lower risk of total mortality;
but did have 64-67% lower risk of CHD mortality (P < 0.05) relative
to those doing neither. These results confirm the protective effects
of low SF and high FV intake against CHD mortality. In addition,
they extend these findings by demonstrating that the combination of
both behaviors is more protective than either alone, suggesting that
their beneficial effects are mediated by different mechanisms.

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