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Review
. 1997 Oct 2;337(14):986-94.
doi: 10.1056/NEJM199710023371407.

Seminars in medicine of the Beth Israel Deaconess Medical Center. Caloric intake and aging

R Weindruch  1 , R S Sohal
Affiliations
Review

Seminars in medicine of the Beth Israel Deaconess Medical Center. Caloric intake and aging

R Weindruch et al. N Engl J Med. .
No abstract available

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Figures

Figure 1
Figure 1. Effect of Caloric Restriction, Initiated at 1 Month or 12 Months of Age, on Body Weight and Life Span in Mice
Panels A and B show data from female C3B10F1 mice subjected to restricted caloric intake (40, 50, or 85 kcal per week) starting at one month of age. The maximal life span (inset, Panel B) is the mean survival for the longest-lived decile of each group. Panels C and D show data from male B10C3F1 mice subjected to restricted caloric intake (90 kcal per week) as compared with control mice (160 kcal per week), starting at 12 months of age. Caloric restriction at both ages extended both average and maximal life span. Each symbol in the survival curves (Panels B and D) represents one mouse. The bars in Panels A and C represent standard deviations. (Data in panels A and B are from Weindruch et al.; data in panels C and D are from Weindruch and Walford.11)
Figure 2
Figure 2. Effect of Caloric Restriction on Body Composition and Organ Weights in Rats
Data are from studies of 24-month-old male Sprague–Dawley rats either fed a control diet (80 percent of the average ad libitum intake) or subjected to caloric restriction (approximately 50 percent of the ad libitum intake) starting at 1 month of age. The numbers in parentheses are percentages of control values. The reduction in the weights of organs with caloric restriction varies widely. (Data kindly provided by Dr. Kevin Keenan, Merck, West Point, Pa.)
Figure 3
Figure 3. Cumulative Oxidative Damage during Aging
Reactive oxygen metabolites (ROMs) such as superoxide anion ( ·O2−), hydrogen peroxide (H2O2), and nitric oxide (NO·), are generated at several intracellular sites and either are inactivated by antioxidative defenses or give rise to a constellation of secondary ROMs. Interactions with ROMs may cause oxidative modifications in macromolecules, some of which may be repaired. The age-related accumulation of unrepaired, irreversible oxidative damage may be a causal factor in aging and certain diseases. ROMs have also been linked to differentiation and signal transduction. An X indicates the interdiction by nonenzymatic antioxidant defense mechanisms (e.g., glutathione [GSH], vitamin E, vitamin C, and urate). SOD denotes superoxide dismutase.
Figure 4
Figure 4. Effects of Age and Caloric Restriction on Rates of Mitochondrial Oxygen Consumption, Mitochondrial Superoxide Anion and Hydrogen Peroxide Production, and Concentrations of Protein Carbonyls in the Brain in Mice
Data are for male C57BL/6NNia mice either fed ad libitum or subjected to a 40 percent reduction in caloric intake from four months of age. ·O2− denotes superoxide anion, O2 oxygen, and H2O2 hydrogen peroxide. The bars represent standard errors. Data were adapted from Sohal et al.
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References

    1. Bray GA. Obesity. In: Zicgler EE, Filer LJJ, editors. Present knowledge in nutrition. Washington, D.C: ILSI Press; 1996. pp. 19–32.1.1.
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    1. Weindruch R, Walford RL. The retardation of aging and disease by dietary restriction. Springfield, Ill: Charles C Thomas; 1988.
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