Study subverts the prevailing hypothesis that long telomeres delay ageing. Rather, they would be linked to a higher risk of getting cancer.
Imagine them as caps responsible for protecting the ends of chromosomes: they are telomeres, small repeated segments of DNA that close the final part of the double helix, preventing it from weakening and damaging itself.
The role of telomeres in determining the life span of each cell has been debated for some time. Now a study published in the prestigious scientific journal New England Journal of Medicine it seems to subvert the few certainties we thought we had about these structures.
Molecular clock. Telomeres are often referred to as a kind of molecular clock that determines how long a cell will live – and by extension how long humans, who are made of cells, will live. In fact, every time a cell duplicates, its telomeres shorten, and when studying cells in the laboratory, telomere length is predictive of the life span of that cell: short telomeres, short life.
Furthermore, young people have been observed to have longer telomeres than the elderly, and short telomeres are known to be associated with premature aging and a number of diseases.
long is better? “Short telomeres were thought to be bad – people with premature aging syndromes have them like this – so, by analogy, long telomeres were thought to be good, and longer even better,” he explains. New York Times Mary Armanios, an oncologist at the Johns Hopkins University School of Medicine who signed the research. But as often happens in science things are not so simple.
Cancer risk. Even if it remains established that short telomeres lead to health problems, long telomeres bring others of a different nature.
According to the new study, they would cause a predisposition to cancer and a condition called clonal hematopoiesis of indeterminate potential (CHIP), a biological process of blood aging relatively frequent in the elderly, associated with an increased risk of blood cancer and death from cardiovascular events.
In the right middle. Armanios’ work that lasted 20 years started from the observation that the length of telomeres seems to have to remain in a certain range, not too short nor too long, as if there was a “price to pay” for telomeres at either end of the spectrum.
Observational studies, which did not demonstrate a cause and effect relationship, suggested that those with shorter than average telomeres are at increased risk of immune or degenerative diseases, as well as pulmonary fibrosis (a respiratory disease), and that those with longer telomeres have a increased risk of getting cancer.
Cells free to mutate. The scientist worked on the latter hypothesis by studying 17 people from 5 different families with a genetic mutation, POT1, which leads to longer than normal telomeres and also an increased risk of cancer (which, however, was not previously thought to be due to the length of telomeres ).
These people, ranging from 7 to 83 years of age, not only suffered from various forms of benign or malignant tumors but also, in some cases, from clonal hematopoiesis. The team was able to show that it is precisely extra-long telomeres that cause both cancer and blood disease. In people affected by the POT1 mutation, telomeres do not shorten with each cell division, and remaining long they are unable to put a stop to the life of the cells, which continue to duplicate and therefore have more time to accumulate potentially dangerous mutations.
Nothing given. It therefore appears evident that long telomeres are not the secret of eternal youth (nor of good health). And that the promises of certain companies on the possibility of curbing aging by lengthening telomeres not only make no sense, but could be dangerous.