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Calorie Restriction: Does it work as well as mice as on humans?

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Here is an interesting extract from the following article:

http://www.harvardmagazine.com/on-line/090548.html

Demetrius's hypothesis (see " A New Theory on Longevity, " November-

December 2004, page 17) links evolutionary history to longevity,

arguing that organisms that mature late sexually, have fewer

offspring, and spread their reproductive activity over a longer

period will also be long-lived, because the metabolic stability of

their cells and cellular networks have evolved to accommodate this

life history. And because such animals already enjoy high levels of

metabolic stability, interventions like CR (and, presumably, related

genetic manipulations)—which he believes work by increasing the

stability of cellular networks—will not benefit them as much as it

will benefit species characterized by early sexual maturity, a

narrow reproductive span, and large litter size: traits that reflect

a survival strategy of the sort that one finds in mice, which

evolved to cope with feast-or-famine circumstances. " Darwinian

fitness in a mouse is characterized by flexibility, " he

explains, " the ability of a population to respond to unpredictable

resource conditions, " whereas " Darwinian fitness in humans derives

from being robust. The stability of cellular networks has evolved in

concert with population stability, " he says. And, in fact, human

cells have been shown to be more resistant to stress than the cells

of mice. His theory also explains why, in humans and other long-

lived species, the rate of death ceases to increase exponentially

after a certain age, which is not the case in mice. (Human mortality

decelerates after about age 85.)

If Demetrius is right, then interventions that increase longevity

will have large effects on the mean and maximum life span of mice.

In rhesus monkeys, which share many genes with humans, he expects

that results of a continuing caloric-restriction experiment will

show a 15 percent increase in mean life span and have no effect on

the maximum. In humans, he predicts the effect will be much less,

adding perhaps 5 percent to average life span, and none to the

maximum.

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