Researchers have found a way to predict a person's lifespan by studying the genetic variations in the human genome that are responsible for the inevitable process of aging.
We are all interested in living longer, healthier lives.
New research delves deeper into our genetic fate. A new study presented at the American Society of Human Genetics 2018 Annual Meeting, held in San Diego, CA, suggests that our genetic variations can predict who will live longer.
Paul Timmers, a graduate student at the University of Edinburgh in the United Kingdom, is the first author of the paper, and he presented the study at the conference.
21 new genetic locations may predict lifespan
Timmers and team wanted to discover the genetic factors that "decide" who gets to live longer. So, they matched genetic data on over half a million people with information on the lifespan of each of these individuals' parents.
The large sample allowed the researchers to gain statistical insights into the effects of individual genes. Overall, the researchers confirmed six genetic associations with aging that scientists had already established, such as the link between the APOE gene and the risk of developing Alzheimer's.
Also, the team uncovered 21 novel genetic locations that have a bearing on a person's lifespan. Using this new information, Timmers and colleagues devised a so-called polygenic score that predicted a person's survival.
The score accurately predicted lifespan "into deciles of expectation of life with a difference of more than 5 years from top to bottom decile." The study's first author explains what these findings mean, saying:
"Using a person's genetic information alone, we can identify the 10 percent of people with the most protective genes, who will live an average of 5 years longer than the least protected 10 percent."
Gene variants linked to disease, lifespan
They estimate that at least 1 in 200 people have such genetic variants, also called single nucleotide polymorphisms (SNPs).
Intriguingly, the study did not find any lifespan predictions for other cancers. This suggests that the risk of dying from other forms of cancer may be down to different, rarer SNPs, or to the environment.
The study's first author comments on these findings, saying, "This was an interesting result [...] We suspect that the variants we found, such as for smoking and Alzheimer's disease, pertain uniquely to the modern period of human history."
"For example," Timmers adds, "a genetic propensity to smoke wasn't harmful before we discovered tobacco, but it is now. Since natural selection has not yet had many generations to act on these variants, the variants are still fairly common."
Finally, the new study also revealed the brain's fundamental role in determining a person's survival. The cells and protein pathways most strongly influenced by the lifespan-predicting SNPs were fetal brain cells and cells found in the prefrontal cortex.
In the future, Timmers and colleagues plan to study precisely how these genetic variants influence a person's lifespan. Ultimately, the researchers are hopeful that one day, they could slow down the aging process.