Extending life: scientific prospects and political obstacles

Abstract

Aging can be slowed in laboratory rodents by low-calorie diets, and changes in single genes can extend mouse life span by 40 percent or more. Therefore, despite its surface complexity and effects on multiple cells and intercellular systems, aging in mammals might also be retarded by both genetic and nongenetic means. If human aging could be slowed pharmacologically to the extent now possible in rodents, the effect on healthy life expectancy would exceed that of abolishing cancer, cardiovascular disease, and adult-onset diabetes. Why, then, is research on the biological control of aging and longevity poorly funded and shunned by both most scientists and those setting national research priorities? Economic disincentives, disease-specific lobby groups, scientific careerism, and ineffective nostrums, together with gerontologiphobia, must be overcome before such research can improve public health.

FIG. 1

Remaining life expectancy of a 50-year-old Caucasian woman in the United States in 1985, at then-current mortality risk schedule (top bar), or as projected under the assumption that adult mortality risks for specific diseases (cancer, cardiac disease, etc., as indicated) were reduced to zero from 1985 onward. The bottom bar shows projected life expectancy if human adult mortality risks could be reduced to the same extent that caloric restriction reduces them in mice. Data from Olshansky, Carnes, and Cassel 1990

FIG. 2

Number of deaths per 100,000 individuals at risk, by age decade, for the nine leading causes of death at age 75. Data from 1997 U.S. Vital Statistics.