Hayflick limit: Why immortality remains out of humans’ reach

Subject: Science

Section: Health

Context:

Biomedical researcher Leonard Hayflick, known for his discovery of the Hayflick limit, passed away on August 1 at the age of 98.

The Hayflick Limit:

Hayflick’s work fundamentally altered the understanding of aging by demonstrating that normal somatic cells can only divide a finite number of times.
Discovered in the early 1960s at the University of Pennsylvania, the Hayflick limit refers to the maximum number of times somatic cells can divide—approximately 40-60 times—before they stop dividing.
This cessation of cell division, leading to the accumulation of senescent cells, contributes to aging and bodily decline.
The “ultimate Hayflick limit” for humans is estimated to be around 125 years, beyond which lifespan cannot be extended by diet, exercise, or genetic modifications.

Telomeres and Aging:

Telomeres are repetitive DNA sequences at the ends of chromosomes, protecting them during cell division. Telomeres shorten with each division, eventually leading to cell senescence.
Although telomere shortening is associated with aging, the precise link between telomere length and lifespan remains unclear. For example, lab mice have longer telomeres than humans but live much shorter lives.

Research on Telomeres and Telomerase:

Some researchers argue that telomere loss and the Hayflick limit might be symptoms of aging rather than direct causes. It may be possible to counteract telomere loss or replace telomeres.
The discovery of telomerase in the 1980s, a protein capable of generating new telomeres, suggests potential avenues for extending cell lifespan. However, telomerase is typically active only in cancer cells, leading to ongoing research into its practical applications.
While in vitro studies have shown promise in slowing telomere loss, practical applications for extending human cell lifespan are still developing.

Source: IE