Khaberni - Your DNA may play a much larger role in determining your lifespan than researchers previously thought, according to "futura-sciences".
For many decades, it was believed that the genetic impact on human lifespan was minor, not exceeding 6%, but new data published in the Science journal confirms otherwise, as genes are responsible for almost half of the variance in our average lifespans.
Historically, the genetic impact was obscured due to high rates of accidental deaths and infectious diseases.
Researchers at the Weizmann Institute of Science have reported that genetic differences explain about half of the variance in human lifespan, which is more than double what many previous calculations had found.
This research was conducted by Ben Sheinhar, a Ph.D. student in Professor Uri Alon's lab in the Department of Molecular Cell Biology at the Weizmann Institute.
Why did previous studies underestimate genetic factors?
The team attributed this variance to a specific flaw in old data sets, namely the absence of records of causes of death.
In these historical records, deaths from accidents, infectious diseases, and environmental hazards overwhelmed the biological signal of aging itself.
This external mortality rate was ten times what it is today, leading to a mathematical "distortion" of results.
When one of a pair of identical twins dies of natural aging at ninety, and the other dies of cholera at thirty, the genetic signal disappears, according to the report.
Repeating this pattern across thousands of pairs, the inherited component of lifespan appears minimal.
Previous researchers had no way to separate these environmental shocks from biological degradation, leading to lower past estimates of heredity.
How did the team correct this?
To solve this problem, Sheinhar and his colleagues analyzed three major twin registries from Sweden and Denmark using a more accurate methodology.
Because identical twins share most of their DNA, while fraternal twins share about half, comparing their lifespans reveals the genetic contribution versus the environment.
More importantly, the researchers included data from twins who were raised apart, a step that separated the genetic effects from shared family environments more clearly than previous methods allowed.
To maximize accuracy, the team built a mathematical simulation of "virtual twins," allowing them to model how different patterns of external mortality rates, like cholera rates or historical accidents, affected apparent heredity.
By filtering out this environmental noise, the team uncovered the true signal: the inherited component of lifespan exceeds 50%.
These results are consistent with heritability estimates for other complex human traits and match previous lifespan studies conducted on lab animals.
What varies with cause of death
The study showed that the heritability of death from cancer remains constant at about 30%.
Conversely, cardiovascular diseases are highly heritable (50%) at younger ages, but this decreases to nearly zero by the age of a hundred.
This suggests that while some genetic risks persist, others, specifically those affecting the heart, are expected to occur during a human's lifespan.
What does this discovery mean?
Low heritability estimates have long led to a shift in research funding away from the genetics of aging.
By isolating the genetic signal from environmental influences, the Weizmann Institute team successfully changed the scientific foundations for the study of lifespan.
The existence of a 50% genetic factor does not negate the influence of diet, exercise, smoking, or the availability of healthcare; these variables still determine the remaining half of the lifespan equation.
However, identifying the specific genetic variables contributing to lifespan has become an easier task, as the biological signal is much stronger than indicated by previous models, providing a clear mathematical basis for future therapeutic interventions.
