A Better Environment, Not Slower Aging, Increases Life Expectancy
Since the mid-1800s, the maximum human life expectancy has increased by about three months per year. Many people would like to see lifespans continue to increase, and scientists have been asking how easily it can be achieved.
A recent report by University of Minnesota College of Biological Sciences Professor Craig Packer, PhD, along with colleagues from many other institutions, presents evidence that nature has placed constraints on how much the underlying rate of aging can be slowed. This implies that the recent increase in life expectancy had nothing to do with slower aging.
"Essentially all of the extension in lifespan over the past century has resulted from improved nutrition and public health,” Packer said. “Any further increase by slowing the aging process will have to overcome powerful evolutionary constraints.”
The report is published in the journal Nature Communications.
New Data for an Age-Old Question
Major factors influencing life expectancy are infant and juvenile mortality rates, age-independent mortality (such as from accidents) and senescent mortality. Among these, senescent mortality—mortality among older individuals—is highly sensitive to the speed of aging. I.e., slow down aging, and older (senescent) members of the species will die off more slowly, resulting in a longer life expectancy.
The researchers asked if the rate of aging has been, in fact, the most important factor in determining life expectancies in related species, and if not, which ones have, whether among related species or in one species—humans—over time.
To answer this question, the researchers examined large data sets from six genera of nonhuman primates that together comprised 13 species, including chimpanzees, gorillas, baboons, and capuchin monkeys. Since humans are the only species in our genus—Homo—the team also examined nine data sets on populations that had not benefited from modern advances in medicine, public health, and standards of living. They took account of five parameters that reflected the age-dependent mortality rates for infants, juveniles, and older individuals, as well as for age-independent mortality rates.
Within each genus, they simulated the effects of variation in the parameters to see which, when varied, would yield the differences actually seen between the species in that genus (or between human populations). That is, which would reproduce the differences between real species in terms of life expectancy and also “lifespan equality.” Lifespan equality is high when most members of a species live long lives of comparable length, low when many members die in all age groups and few reach “a ripe old age.”
When the numbers had been crunched, variations in the pattern of early deaths best accounted for variation in life expectancy and lifespan equality actually seen within each primate genus. Age-independent mortality was also important, but “actuarial senescence” of adults and old individuals accounted for very little. In other words, the rate of aging had little effect.
Change-Resistant Aging Rates
The study supports the idea that historically, when life expectancies were low, mortality improvements for infants, and reductions in age-independent mortality, “were the central contributors to the decades-long trend toward longer human life expectancies and greater lifespan equality,” the researchers concluded.
Most improvements were in social, economic, and public health advances. Since the mid-20th century, declines in the baseline level of adult mortality— through improvements in workplace safety, smoking cessation, and treatment of adult-onset diseases—have likely played an important role in industrialized societies, the researchers added.
But while these improvements can increase lifespans by eliminating early deaths, people who live longer will still age at the rate nature has set.
Thus, “continued improvements in nutrition and public health are unlikely to translate into a substantial further reduction in the rate of aging,” Packer said. “It remains to be seen if future advances in medicine can address the underlying cellular processes that currently limit maximum human lifespans that have largely been determined by the long, slow process of evolution.”