The entirety of human history can be seen as a description of the constant, and fruitless, attempt to avoid death. Like the knight Antonius Block who plays chess with the Angel of Death in Ingmar Bergman’s film “The Seventh Seal,” human beings try to evade death on treadmills, helped by religious rites, vitamins, trust funds, by having children, and by writing.
In the modern period, even if death still has the upper hand, some might say it’s no longer the checkmate to which we have been accustomed since the beginning of time. Since the mid-19th century the global life expectancy has been increasing at an average rate of three months per year.
Researchers invest their time trying to decipher mechanisms for slowing down the aging process; the yearning to maintain youthfulness has also given rise to a vast anti-aging industry, which currently turns over $200 billion a year, a figure expected to double by the decade’s end. In effect, spry golden agers climbing mountains are no longer a rare sight.
But has the human race really managed, however slightly, to change the biological rules of the game? We may live longer, but do we age slower?
To answer this question, a team of scientists examined 39 populations of monkeys and human beings. Their findings were published in Nature Communications.
The improvement in average human life expectancy is mostly an artifact created by the improved survival among children and young adults. There has been no delay or slowdown in the aging process.
The study was based on testing the ratio between “life expectancy” and “lifespan equality”: If most people die at more or less the same age, the lifespan equality index is high. Where the probability of dying is relatively the same at various ages, lifespan equality is low.
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In humans, the two measures are closely connected. In populations in which life expectancy is high so is lifespan equality: members of the group tend to die at a similar age. In populations with low life expectancy, lifespan equality is also low: people die at a wide variety of ages.
First the researchers wanted to study whether the tight positive linear relationship between life expectancy and lifespan equality is unique to the human race.For that purpose they conducted statistical analysis on populations of gorillas, chimpanzees and baboons. They found much the same there.
Then the researchers used mathematical models to examine variations of the rate of aging. They discovered that even small differences in this rate lead to a drastic difference in the relationship between life expectancy and lifespan equality.
In other words, if the aging process really were slowed, the connection between the two indices would not have remained close – as it is now.
Other mathematical models, which factored in changes in the percentage of premature mortality, led to results similar to those that were actually found in populations that were examined. The researchers concluded almost the entire variance between the populations could be explained by changes in the premature death statistics, but not by changes in the onset of aging or the rate of aging.
Can we live forever, theoretically?
Study co-leader Susan Alberts, an evolutionary anthropologist from Duke University in North Carolina, explains that science is divided on the extent to which human life can be prolonged. She said that whereas there are some who think that there is no limit, others disagree.
To prolong life significantly, the rate of aging has to slow, she explained. In principle, deaths can be prevented; but is it even possible to slow aging? Part of the answer to that depends on the extent to which evolution enables different patterns of mortality within a species (as opposed to the “invariant rate of ageing’ hypothesis, which posits that the rate of ageing is relatively fixed within species, the researchers explain).
So, Alberts explained, they looked at monkeys and human beings to check for “plasticity” in the rate of aging. They found that the entire difference in mortality among all the populations they examined – which included captive and wild animals, human societies with the most advanced medical care and others almost totally lacking health care – was due to premature deaths. The rate of aging remained unchanged in all.
They couldn’t possibly demonstrate that aging can’t be slowed. But they did demonstrate that such a slowdown is simply not the way in which maximum life expectancy in humans actually increased, by as said, 3 months a year since the Industrial Revolution began.
The findings provide the strongest support to date for the “invariant rate of aging” hypothesis; aging is generally fixed for each species; and it explains why life expectancy and lifespan equality are correlated in the various species.
Belting the kids
So why has life expectancy constantly increased, even where infant mortality improved decades ago? Still because more relatively younger people are surviving longer. Twenty years ago, for example, a lot more young women died of breast cancer. Also, today we are more protective of children. When she was a child nobody had heard of seat belts, Alberts says: now it’s against the law not to “belt” the kids.
What about the mounting incidence of perky seniors, apparently up to a later age than in the past? Among the aged Alberts explains, the “rate of aging” is defined as the percentage at which the chances of dying increase with the increase in age, and does not necessarily reflect physical or cognitive feelings. They didn’t examine the rate at which people lose the ability to run a mile, and that may have improved; but the rate at which mortality increases with age hasn’t changed.
In the last 100 years, human life expectancy experienced three leaps, explains Prof. Haim Cohen, head of the Sagol Healthy Longevity Center at Bar Ilan University: the first due to antibiotics, which caused the greatest leap. “Until the 1940s the cause of death for 70 percent of human beings was infection,” he says. “In 2010, 70 percent died of age-related illnesses. In other words, this leap is not related to the slowing of aging.”
A second leap in average life expectancy was achieved by better treatment for cardiac disease: again aging was not halted or slowed, but illnesses were cured. And the third leap was due to a reduction in infant mortality.
“These are the three main reasons for the prolonging of life expectancy. In that sense, the authors of the article are correct in asserting that the changes in life expectancy are not because we have solved problems related to aging,” Cohen says.
Studies on lower creatures such as flies or worms, which involved substantial change in their genome, did manage to influence aging and to prolong their lives as much as sixfold. Not mammals.
“When we analyze the figures for the attempts to prolong lives among mammals, by means of genetic or nutritional changes, the increase ranges from 8 to 30 percent, no more. That’s still not bad, but that’s it,” Cohen says. “Will we break the 30 percent barrier? We don’t know. For the time being it’s science fiction. Maybe life can’t be extended beyond 30 percent. Or maybe something is waiting for us around the corner.”