Some people who fill their lives with fitness and healthy habits die younger than peers who live a much less healthy life.
This turns out that your life expectancy is at least partially determined by your DNA, regardless of your lifestyle choices.
A new international study suggests that some people have died very young, even after leading a healthy lifestyle, indicating that life expectancy is dependent on their genes.
UCLA geneticist Steve Horvath led a team of 65 scientists in seven countries to record age-related changes to human DNA, calculate biological age and estimate a person’s lifespan.
A higher biological age, regardless of chronological age, consistently predicted an earlier death.
“Our research reveals valuable clues into what causes human aging, marking a first step toward developing targeted methods to slow the process,” said principal investigator Horvath, a professor of human genetics and biostatistics at UCLA’s David Geffen School of Medicine and Fielding School of Public Health.
Drawing on 13 sets of data, including the landmark Framingham Heart Study and Women’s Health Initiative, a consortium of 25 institutions analyzed the DNA in blood samples collected from more than 13,000 people in the United States and Europe.
Applying a variety of molecular methods, including an epigenetic clock developed by Horvath in 2013, the scientists measured the aging rates of each individual.
“We were stunned to see that the epigenetic clock was able to predict the lifespans of Caucasians, Hispanics and African-Americans,” said first author Brian Chen.
“We discovered that 5 percent of the population ages at a faster biological rate, resulting in a shorter life expectancy,” Horvath said, adding, “Accelerated aging increases these adults’ risk of death by 50 percent at any age.”
The preliminary finding may explain why some individuals die young, even when they follow a nutritious diet, exercise regularly, drink in moderation and don’t smoke.
“While a healthful lifestyle may help extend life expectancy, our innate aging process prevents us from cheating death forever,” Horvath emphasised. “Yet risk factors like smoking, diabetes and high blood pressure still predict mortality more strongly than one’s epigenetic aging rate.”
The precise role of epigenetic changes in aging and death, however, remains unknown, said coauthor Dr. Themistocles Assimes, an assistant professor of cardiovascular medicine at Stanford University School of Medicine.
Larger studies focused only on cases with well-documented causes of death will help scientists tease out the relationship between epigenetic age and specific diseases, he added.
“We must find interventions that prolong healthy living by five to 20 years. We don’t have time, however, to follow a person for decades to test whether a new drug works.” said Horvath. “The epigenetic clock would allow scientists to quickly evaluate the effect of anti-aging therapies in only three years.”
The group’s findings, however, don’t bode well for everyone.
The University of California has applied for a provisional patent on the epigenetic clock.
The findings are published in today’s edition of the journal Aging.
(With agency input)