Telomeres at the end of chromosomes shorten with age Gene variants that might show how fast people's bodies are actually ageing have been pinpointed by scientists. Researchers from the University of Leicester and Kings College London say the finding could help spot people at higher risk of age-related illnesses. People carrying the variant had differences in the "biological clock" within all their cells. The British Heart Foundation said the findings could offer a clue to ways of preventing heart disease. While doctors know that as people age they are more at risk from diseases such as Alzheimer's, Parkinson's and heart disease, some people fall prey to these at an earlier age than expected. Telomeres One theory suggests that biological timers called "telomeres", part of the chromosomes in every cell that carry genetic code, may be a factor in this. What our study suggests is that some people are genetically programmed to age at a faster rate

Professor Tim Spector, King's College London From birth, every time a cell divides, the telomeres get shorter and there is some evidence that people with shorter telomeres, either because they diminish more quickly or because they were born with shorter versions, may be at higher risk from age-related illness. The researchers say in the journal, Nature Genetics, that they looked at more than 500,000 genetic variations across the entire human genome to see which variants cropped up more frequently in people known to have shorter telomeres. They eventually located a number of variants located near a gene called TERC which, in people carrying them, seemed to be equivalent to an extra three or four years of "biological ageing". Bad lifestyles Professor Tim Spector, from King's College London, said: "What our study suggests is that some people are genetically programmed to age at a faster rate. "Alternatively, genetically susceptible people may age even faster when exposed to proven 'bad' environments for telomeres such as smoking, obesity or lack of exercise - and end up several years biologically older or succumbing to more age-related diseases." Professor Jeremy Pearson, associate medical director at the British Heart Foundation, which part-funded the study, said it was not yet clear whether telomeres did contribute to an increased risk of disease. He said: "Understanding how our cells age is an important step in our quest for better ways to prevent and treat heart disease. "Perhaps in the future one of the ways we try to reduce the risk of, or treat, heart disease would be to use an 'anti-ageing' approach for our arteries."



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