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Journalism of Courage
Biomedical researcher Leonard Hayflick, who discovered that normal somatic cells can divide (and thus reproduce) only a certain number of times, died on August 1 at the age of 98. Hayflick’s discovery fundamentally changed the understanding of aging — especially the thesis that cells are capable of being immortal, and aging is simply a factor of externalities such as disease, diet, and solar radiation.
In the early 1960s, Hayflick, at the time a researcher at the University of Pennsylvania, discovered that cell division in somatic (non-reproductive) cells stopped after roughly 40-60 times. This cessation in cell division is what Hayflick posited causes aging — as senescent cells (those that have stopped dividing) accumulate, one’s body begins to age and decline.
This means that there is an in-built cellular clock in the human body (and that of other organisms) which determines how long one can live. This “ultimate Hayflick limit”, as scientists have termed it, is around 125 years for humans, beyond which no amount of diet, exercise, or even genetic tweaking against diseases can extend the human lifespan.
Since the discovery was made, Hayflick and other scientists have documented the Hayflick limits of cells from animals with varied life spans, from Galapagos turtles to laboratory mice. The cells of the former species, which can live for a couple of centuries, divide approximately 110 times before senescing, whereas cells of the latter become senescent within 15 divisions.
Correlation or causation?
Hayflick’s discovery got further weight after researchers in the 1970s discovered telomeres. As cells divide, they create copies of DNA strands. Telomeres are repetitive DNA sequences at the very end of these strands, meant to protect the chromosome. Crucially, with each cell division, these telomeres get slightly shorter. Eventually, the telomere loss reaches a critical point at which cell division ends.
That said, while shortening telomeres is related to aging, the exact relationship between telomere length and lifespan remains unclear. Lab mice, for instance, have telomeres that are five times longer than humans, but their lives are 40 times shorter.
This is what has led to some researchers arguing that telomere loss and the Hayflick limit are not limits on aging, but rather symptoms of aging. Theoretically, it might be possible to thwart telomere loss or replace telomeres, as the differential rates of telomere loss among different species indicates.
The discovery in the 1980s of a protein called telomerase, capable of producing new telomeres, has strongly suggested this possibility. Telomerase is present in all cells, but it is seemingly “turned on” in only cancer cells. This is why, as Hayflick himself said, cancer cells are not subject to his limit.
Although scientists have been able to synthesise telomerase, and some in vitro studies have indicated that they may slow down telomere loss in normal human cells, any practical application for this seems some distance away.
