There is accumulating evidence that the risk of age-associated diseases including heart disease and some types of cancers are more closely related to biological rather than chronological age.
For the first time researchers have identified definitive variants associated with biological aging in humans. Scientists at University of Leicester and King's College London, working with University of Groningen in the Netherlands, analyzed more than 500,000 genetic variations across the entire human genome to identify the variants which are located near a gene called TERC. They say the discovery has important implications for the understanding of cancer and age associated diseases.
The study, published in Nature Genetics, distinguishes between chronological aging, how old a person is in years, and biological aging whereby the cells of some people are older or young than suggested by their actual age.
British Heart Foundation Professor of Cardiology at the University of Leicester Professor Nilesh Samani, of the Department of Cardiovascular Sciences, who co-led the project explained that there are two forms of aging – chronological aging, how old you are in years, and biological aging whereby the cells of some individuals are older (or younger) than suggested by their actual age.
“There is accumulating evidence that the risk of age-associated diseases including heart disease and some types of cancers are more closely related to biological rather than chronological age,” says Samani.
The researchers studied telomeres, structures that are part of a person’s chromosomes. Individuals are born with telomeres of certain length and in many cells telomeres shorten as the cells divide and age. Telomere length is therefore considered a marker of biological aging. They found that those individuals carrying a particular genetic variant had shorter telomeres, or, in other words, appeared biologically older.
“Given the association of shorter telomeres with age-associated diseases, the finding raises the question whether individuals carrying the variant are at greater risk of developing such diseases,” says Tim Spector, a professor at King's College London and co-leader of the project. “The variants identified lies near a gene called TERC, which is already known to play an important role in maintaining telomere length. What our study suggests is that some people are genetically programmed to age at a faster rate.”
Spector says the effect was considerable in people who had the variant, equivalent to between 3-4 years of biological aging as measured by telomere length loss. Alternatively genetically susceptible people may age even faster when exposed to environments proven to be bad for telomeres, such as smoking, obesity, or lack of exercise – and end up several years biologically older and succumbing to more age-related diseases.