Aging is determined by biological, not environmental, factors, a study suggests. No matter how hard you try, it might be difficult to slow down aging, a depressing new study suggests. Across a range of primate species, including humans, aging rates are mostly determined by biological factors, not environmental ones. What's more, the rate of aging is mostly consistent within a primate group. For each primate population, the researchers determined that the "rate of aging seems to be about the same within that group," said Shripad Tuljapurkar, a professor of biology and population studies at Stanford University who helped review the study but was not otherwise involved in it. "That's a pretty significant finding." Still, it may one day be possible for humans to slow down biological aging with medicine, he said. Humans live longer today than we ever have. Since 1950, world life expectancy has increased by nearly 30 years, from 45 to 72 today, with the oldest humans living for more than 115 years. Researchers who study aging have increasingly sought to determine how far this upward trend can go, coming to opposing conclusions about whether the human lifespan has a limit, according to a 2018 study published in the journal Science. Life-extension research has also become a booming industry, with companies such as Google-backed Calico investing billions of dollars in research to extend human life. But so far, all of that research has focused on mortality data from humans only. "In general, people have not been very successful at finding anything that they can say that applies across species," Tuljapurkar told Live Science. The new study, by contrast, looked at aging in multiple species. An international team of 40 researchers examined mortality data from 39 populations of seven genuses of primates, including several species of great apes and monkeys, two lemur species and humans. The animal data came from both wild-animal studies and zoos. Seven sources of human data came from the Human Mortality Database and other historical archives, spanning a wide range of time periods, from England between 1600 and 1725 to Ukraine in 1933. Two came from relatively recent studies of hunter-gatherer groups. All of the human data was meant to represent a "natural" environment not influenced by recent public health advancements. First, the researchers looked at two measures — life expectancy as well as lifespan equality, the "shape" of the death curve across a lifespan. They found that for each genus, there was a fixed ratio between the two measures, despite wide variation in the environments for different populations. The researchers then used a mathematical equation, called the Siler mortality function, to calculate how different factors influenced the risk of mortality over a primate's lifetime. Some parameters represented the risk of infant mortality, which starts out high and drops rapidly; another represented constant mortality risk regardless of age (like from fatal falls or accidents); and another represented mortality risk that increases with age, or the rate of aging. Almost all the parameters varied widely from population to population. In different populations, factors like different predators, diseases, and surroundings influence infant mortality and the risk of non-biological causes of death, like accidents. But the parameters that determined the rate of aging barely varied within each individual group of primates, including humans. And when the researchers tried changing each individual factor in their equation, they found that only one made a notable impact on the ratio they calculated between life expectancy and lifespan equality for each genus. "It turns out that the only parameter that seems to matter a lot is this rate of aging," Tuljapurkar said. Changing the "rate of aging" variable seemed to transform the mortality patterns of one type of primate into that of another, while changing other parameters had very little impact. In other words, the rate of aging was the main factor that determined the lifespan of primates in different genuses, and only changing that rate would substantially change their mortality patterns. Many mortality factors are largely determined by environmental risks — for instance, spontaneous events, such as fatal accidents, are mostly not related to age. But mortality risk related to age is thought to be biologically determined, and the new research supports that theory. The biological factors that govern aging are complex, and many researchers study biological aging at different scales, from chemical bonds that deteriorate as we age to increasing genetic mutations to cells failing to repair damage. But just because these processes govern aging does not necessarily mean that humans' rate of aging will always be fixed, Tuljapurkar said. Though he agrees with the majority of the study's findings, he pointed out a limitation: The study used humans who had not benefited from modern medicine. So the study couldn't say whether modern medicine might change humans' rate of aging. Humans are living longer than ever, and whether that's partly because of decreases in biological aging is still unknown. Tuljapurkar said it's possible modern medicine has already effectively changed the human rate of aging by developing treatments for diseases like heart disease and cancer. "We're getting better and more sophisticated at analyzing some of these causes of death at advanced stages," Tuljapurkar said. "I think that that means we are changing the rate of aging." Regardless, Tuljapurkar said the study, which he described as well done, could serve as a baseline for future studies on public health and disease interventions. Comparing data like this to, for instance, mortality data from after we developed effective treatments for certain cancers, such as prostate and breast cancer, could tell us if those interventions have slowed our rate of aging. "Those are the things that I think are interesting questions that are worth thinking about," he said. Source
