By Jonny Lupsha, Wondrium Staff Writer
The “epigenetic clock” may gauge life expectancy and aging in dogs, according to an article in Science. By observing chemical changes in canine DNA, scientists can estimate dogs’ relative ages to ours—and maybe even how long they have left. Genes may be part of why we don’t live forever.
Geneticists at the University of California San Diego have developed a newer method of determining the human-equivalent age of man’s best friend, Science reported. According to the article, it’s “based on a relatively new concept in aging research: that chemical modifications to a person’s DNA over a lifetime create what is known as an epigenetic clock.” Based on this idea, scientists have built a promising model that adding methyl groups to certain parts of our DNA can determine our “biological age,” which it describes as “the toll that disease, poor lifestyle, and genetics take on our bodies.” The first step led to creating a more specific formula for determining canine lifespans than the old adage of “multiplying by seven,” but humans aren’t too far behind. So what else can our genes tell us about the future?
Proving the Correlation of Genes and Lifespans
Some of our traits are influenced by our genes, and we know that our genetic makeup comes from our parents. One of the most famous manifestations of genetics passed down from our parents is the idea of the “family resemblance.” The reason why doctors ask us if any illnesses “run in the family” is because that can influence your likelihood to get a specific disease. If they do, the odds are more likely that an inherited predisposition to that disease could shorten your lifespan. So what can twins tell us—not “fraternal twins,” who are two siblings born at the same time, but identical twins, who share so many genetic similarities that they’re built almost identically?
“In particular, if our genes really do influence our lifespan, then we would expect the lifespans of identical twins to be more similar than the life spans of fraternal twins,” said Dr. Thad Polk, an Arthur F. Thurnau Professor in the Department of Psychology and the Department of Electrical Engineering and Computer Science at the University of Michigan. “It turns out they are.”
“Dr. James Vaupel and some of his colleagues in Denmark and Minnesota analyzed the lifespans of 2,872 Danish twin pairs who were born between the years 1870 and 1900,” Dr. Polk said. “Sure enough, they found that the correlation between age at death was higher in the identical twins than it was in the fraternal twins. Based on their data, they estimated that about 25 percent of the variability in lifespan could be attributed to genetic factors.”
A Theory on Why We Die
Dr. Polk said that British biologist Sir Peter Medawar proposed a theory in 1952 about why we die at all. Calling it the “mutation accumulation theory of aging,” Sir Peter proposed that natural selection has less and less of an effect as we get older. Why would this occur?
“Two reasons: First, given that nature is dangerous and individual animals are getting killed off all the time, there simply won’t be that many old animals around,” Dr. Polk said. “So if a genetic variant exists that causes old animals to become frail and die, it won’t make much difference, because the animal isn’t likely to reach that age anyway.”
“The second reason is that genetic variants that have harmful effects late in life will have already been passed on to offspring,” Dr. Polk said. Sir Peter Medawar used to use Huntington’s disease as an example of this, which Dr. Polk illustrated. “The age of onset for Huntington’s disease is typically after age 35, and so many patients have already passed on the mutant gene to their offspring before they even knew that they have the disease.”
The mutation accumulation theory is no longer universally accepted, but it is the foundation for another popular theory that may provide answers in the future, called “antagonistic pleiotropy.”
According to Dr. Polk, pleiotropy describes how one gene can have different effects within a single organism. “George Williams at Michigan State University proposed that sometimes these effects could be antagonistic—one effect of the gene might be beneficial to the organism while another effect is harmful.” Finally, Williams said this may account for age-related genetic effects.
In a much simpler example, high testosterone levels in men fit Williams’s hypothesis. “Genetic variants that produce higher testosterone levels tend to increase fertility and reproductive success, but higher testosterone levels also increase the risk of developing prostate cancer later in life,” Dr. Polk said. “Nevertheless, from the viewpoint of natural selection, the benefit of improved reproductive success early in life outweighs the cost of increased cancer risk later in life, and so high testosterone levels continue to be selected for.”
While natural deaths are still sometimes muddied with riddles, the given proof of how genetics influence our lifespans lends credence to theories like antagonistic pleiotropy and the epigenetic clock. Studying methyl levels in DNA promises to yield insightful results in coming years.
Dr. Thad A. Polk contributed to this article. Dr. Polk is an Arthur F. Thurnau Professor in the Department of Psychology and the Department of Electrical Engineering and Computer Science at the University of Michigan. He received a B.A. in Mathematics from the University of Virginia and an interdisciplinary Ph.D. in Computer Science and Psychology from Carnegie Mellon University.