Obtaining the Benefits
of Caloric Deprivation

Without Going Hungry

or the last 60 years, longevity researchers have been investigating caloric restriction (CR) as a means of extending lifespan. They have tested it in mammals (typically mice and rats) and have repeatedly found it to increase maximum lifespan while retarding the onset of age-associated changes, both normal and pathological.1

It is important to stress that, while most researchers have initiated CR early in the life of the animal (at the human equivalent of 3-6 years of age), a few studies have found that CR can extend maximum lifespan in mice even when begun later, at middle age (at the human equivalent of 36-48 years of age).2 Although the mechanisms by which CR retards aging and disease processes in rodents are not clear, there is some evidence that oxidative damage may represent a primary aging process that is attenuated by CR. This is known as the oxidative stress hypothesis of aging.3 Now that studies are underway in primates, will their response to CR be similar to that of rodents? So far there seems to be justification for believing that the findings in lower species can be extended to humans, so the benefits of CR may be ours for the taking.

Also encouraging is that the mechanisms by which CR works may turn out to be "soft-gene-based," meaning that the genes that determine when the aging clock ticks may be manipulable (in the sense of having their action inhibited) by certain molecules4 and that the production of these molecules is rate-limited by the deficiency of certain nutrients.5 When these nutrients are abundantly supplied, then the benefits of CR may be obtained, and maximum lifespan may be increased without going hungry.

References

  1. Weindruch R. The retardation of aging by caloric restriction: studies in rodents and primates. Toxicol Pathol 1996 Nov-Dec;24(6):742-5.
  2. Pugh TD, Oberley TD, Weindruch R Dietary intervention at middle age: caloric restriction but not dehydroepiandrosterone sulfate increases lifespan and lifetime cancer incidence in mice. Cancer Res 1999 Apr 1;59(7):1642-8.
  3. Sohal RS,Weindruch, R. Oxidative stress, caloric restriction, and aging. Science 273:59-63,1996.
  4. Imai S, Armstrong CM, Kaeberlein M, Guarente L. Transcriptional silencing and longevity protein Sir2 is an NAD-dependent histone deacetylase. Nature 2000 Feb 17;403(6771):795-800.
  5. Micheli V, Simmonds HA, Sestini S, Ricci C. Importance of nicotinamide as an NAD precursor in the human erythrocyte. Arch Biochem Biophys 1990 Nov 15;283(1):40-5.

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