A study presented at the just-finished American Society of Human Genetics 2018 Annual Meeting in San Diego reported a way to estimate whether an individual can expect to live longer or shorter than average.
An international research group studied the effect of genetic variations on lifespan across the human genome, which could improve our understanding of the diseases and cellular pathways involved in aging.
In the largest ever genome-wide association study of lifespan, the researchers paired genetic data from more than 500,000 participants in the United Kingdom Biobank and other cohorts with data on the lifespan of each participant's parents.
They didn' t study the effects of one or more selected genes on lifespan, but looked across the whole genome to answer the question in a more open-ended way.
The paper's first author Paul Timmers from the University of Edinburgh said that because the effect of any given gene is so small, the large sample size was necessary to identify genes relevant to lifespan with enough statistical power.
They confirmed six previously identified associations between genes and aging, such as the APOE gene, and they also discovered 21 new genomic regions that influence lifespan.
Using their results to develop a polygenic risk score for lifespan, they developed a single, personalized genomic score that estimates a person's genetic likelihood of a longer life.
"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 five years longer than the least protected 10 percent," said Timmers.
Also, they wanted to know whether genetic variants were affecting the aging process directly or affecting risk of individual diseases that could lead to death.
They found that among common variants, those found in at least one in 200 people that are associated with Alzheimer's disease, heart disease, and smoking-related conditions were linked to overall lifespan.
However, they did not find lifespan associations for other cancers, suggesting that susceptibility to death caused by other cancers is due to rarer genetic variants or the environment.
"We suspect that the variants we found, such as for smoking and Alzheimer's disease, pertain uniquely to the modern period of human history," said Timmers.
"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," Timmers explained.
