Speaking on ‘Chromosome ends and human health and disease’ at the 2009 Cell Press-TNQ India Distinguished Lectureship Series, Dr Blackburn, who discovered this fascinating property of telomeres, likened them to the tips of shoelaces--the dictionary calls them aglets. “Telomeres are the aglets of our genome,” Blackburn said. Just as laces fray when the tips fall off, our genetic blueprint gets all mussed up when telomeres shorten, which is what happens when we age and succumb to disease.

Fortunately, as Blackburn found while studying single-celled pond dwellers, these quintessential ends are replenished by an enzyme called telomerase. Blackburn discovered that cells with a good deal of telomerase kept dividing whereas the DNA in telomerase-deactivated cells progressively shortened with each division.

In humans, telomerase works differently in case of healthy cells and cancerous ones. In normal cells it protects the telomeres, but in cancer cells that have suffered some genetic and non-genetic alteration, it promotes endless division. In such ‘rogue’ cells, telomerase was found to be highly activated. Blackburn’s research has raised interesting questions on the manipulative ability of science in curing diseases like cancer and stretching human lifespans.

While the issue of genetic manipulation is an unfailing eyebrow-raiser, Blackburn is one of those scientists who believe that scientific evidence, not dogma, should govern policy. Blackburn stepped down from George Bush’s Council on Bioethics in February 2004 owing to restrictions on stem cell research.

Ageing, which brings with it increased susceptibility to diseases, is governed by our lifestyle as well as by genetic factors, Blackburn said. Establishing a conclusive correlation between the length of telomeres and these two factors is tricky. A credible association is all that science has been able to produce. But that’s enough to get excited about.

Variations in telomere maintenance are common enough among humans, but sometimes the differences are stark. Blackburn cited a survey of people aged 60 and above, which showed that those with shorter blood cell telomeres had much higher mortality rates.

Coming to the second factor, lifestyle, and how it might affect telomeres and vice versa, Blackburn cited recent research on high-stress groups like ‘caregiving’ mothers to show that telomerase activity was 50 per cent lower and telomeres were shorter among such people.

“Low telomerase alone, even without telomere shortage, is associated with major risk factors for cardiovascular diseases,” she said, adding that in a study of elderly men, loss of telomere length statistically predicted death by cardiovascular disease.

Yet another study of adult twins found that a twin who exercised typically had longer telomeres than his twin who did not exercise.

Even as major diseases that characterise ageing are being linked to shorter telomeres, the causality between the two has not been established till date.