Extending life: scientific prospects and political obstacles.
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.
Miller
Richard A
RA
University of Michigan, USA. millerr@umich.edu
D000368:Aged; D000375:Aging / Q000235:genetics / Q000473:pathology; D000818:Animals; D001683:Biological Clocks; D035843:Biomedical Research; D001824:Body Constitution; D002423:Cause of Death; D018752:Diet, Fat-Restricted; D005853:Geriatrics; D013006:Growth Hormone / Q000172:deficiency; D006801:Humans; D008017:Life Expectancy; D008136:Longevity / Q000235:genetics; D011057:Politics; D011287:Prejudice; D011634:Public Health; D012109:Research Support as Topic; D014481:United States / Q000453:epidemiology
D013006:Growth Hormone