Families with a history of long life have been found to have a mutation that appears to temper body inflammation.
A European Society of Human Genetics study, reported this week by Science Daily, said the mutation was potentially delaying disease and extending years of healthy living.
The study report said that some people remained free of major diseases well into old age, while others developed serious health problems much earlier.
“Understanding why this happens is becoming increasingly important as populations grow older around the world,” the report said.
“Although life expectancy has risen dramatically over the past 200 years, the number of years people spend in good health has not increased at the same pace.
“Researchers have long known that exceptional longevity often runs in families and is linked to a later onset of chronic illnesses. However, the genetic factors that help protect these families remain poorly understood.”
The new research, presented at the annual conference of the European Society of Human Genetics in Gothenburg, has painted a clearer picture of the biological mechanisms that support a longer healthspan (disease-free years).
Researcher Pasquale Putter, from Leiden University Medical Center in The Netherlands, said middle-aged individuals with long-lived parents developed cardiometabolic diseases an average of 13 years later than their partners whose parents had shorter lifespans.
“This made it clear that their longer healthspan was passed down to subsequent generations,” he said.
“We hope that taking this family approach will help us to untangle some of the environmental factors from those that are truly genetic, particularly those where rare mutations are involved.”
The researchers analysed the genomes of 212 groups of long-lived offspring with the same two parents.
They identified four regions of the genome that appeared likely to contain genes linked to longevity.
One of those variants was found in the CGAS gene, which has previously been linked to aging.
CGAS helps trigger inflammation when DNA is detected where it does not belong inside a cell. This can happen during viral infections or when cells are damaged.
“It is likely that members of these families had only one active copy of the CGAS gene, rather than two,” Mr Putter said.
“This will have reduced the inflammatory response in their bodies, while still being sufficient to clear infections and repair damage, thereby contributing to the protective mechanisms that enable extended healthspan and survival.”
The researchers believe this reduced inflammatory response may help protect against some of the damaging effects associated with aging while preserving the body’s ability to defend itself.
The full report is here.
