Mayor has written a fascinating review of the role of telomeres in ageing in the BMJ of 17th January 2009.
Chromosome in the body carries a marker that counts down from the day of birth to death, rather like a cellular sand clock. These biological timers are telomeres-repeat sequences of DNA that, together with associated proteins, cap the ends of chromosomes and protect them from degradation.
Telomeres shorten with each cell division. This shortening is accelerated in diseases associated with ageing-particularly cardiovascular disease and cancers-and in the presence of risk factors for these diseases such as obesity and high blood pressure. Shorter telomeres have also been found in women under chronic, severe stress More than 30 years ago, Olovnikov proposed that this shortening could provide a mechanism for a biological clock that determines cell behaviour. (Olovnikov’s clock )-The measurements of telomere length could be used to detect early disease, allowing preventive measures to be put in place, and eventually that methods will be found to slow or even reverse the shortening.
Telomeres are made up of a large number of tandem repeats of the sequence TTAGGG. DNA polymerase cannot fully replicate the 3′ end of linear DNA, so telomeres shorten progressively with each repeated cell division. Laboratory studies have shown that the telomere length of replicating cells is inversely correlated with age.
Telomere length is essentially a measure of biological age. This may partly explain why women live longer than men in most societies, as a: they generally have longer telorneres. .
Telomeres isolated from leucocytes from blood samples collected during major epidemiological and clinical trials are proving a rich hunting ground for information on telomeres and disease risk.
The average telomere length is shorter in people who have had a myocardial infarction before the age of 50 years than in controls matched for age and sex. Telomeres are also shorter in patients with severe triple vessel coronary artery disease than in people with angiographically normal coronary arteries.
But telomere length is not simply a consequence of the disease, but a risk factor.
The presumed biological mechanisms underlying telomere shortening are our old friends, oxidative stress and inflammation.
Physical activity reduces telomere length shortening, one study showed that 16 minutes of physical activity a week resulted in 200 nucleotide extra shortening in the telomere than in individuals active for three hours a week. These active individuals had telomere lengths equivalent to people 10 years younger.
So telomerase is the enzyme to watch and its control and the effect of nutrition and exercise. . Or is this cause or effect?
Mayor 2009 Unravelling the secrets of ageing BMJ vol 338 136-38

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