Telomeres are DNA sequences at the ends of chromosomes, like a protective sheath. Telomeres were compared with the small pieces of plastic that protect the ends of the shoe laces preventing their untangling. Chromosomes contain the genetic material. Untangling may damage chromosomes and thus alter their genetic material or merging with other chromosomes leading to a mutant DNA.

In 1961 the scientist Hayflick said that aging (senescence) is a stage marked by morphological and biochemical alteration phenomena causing the body cells to cease proliferating because they have reached the limit of replicative life. Replication (regeneration) of cells is a process by which a cell divides into one “new” which theoretically should be identical, and in particular should contain an identical copy of DNA. James Watson, the discoverer of DNA observed what he called “end replication problem”, i.e. the inability to correctly copy all of the DNA, leaving not copied identically a small sheath located at the end, the sheath which he called “telomere”. Russian scientist Olovnikov could find link between cellular senescence and terminal replication problem described by Hayflick. For Olovnikov “end replication problem” was due to progressive shortening of chromosome ends (telomeres) functioning as a “molecular clock” that sets the maximum number of cell divisions throughout life, thus directly controlling the process of aging and life span of an individual.

Division and cell replication is the natural process by which cells are regularly replaced with new ones. But as Hayflick observed, a cell can replicate only a limited number of times, defining the physiological age and lifespan of everyone. This limited number of divisions is dependent on telomere length. Based on the Hayflick limit theory and on the latest statistics, chronological age the man could reach is approximately 120-125 years. After each cell division telomeres shorten. Over time, telomeres shorten to the maximum when the cell receives the signal “stop” and no longer divides. It is the moment when the aging (senescence) of that cell starts and it lasts until de cell is exhausted and receives the signal to die (apoptosis). In cases where the telomere is too short but the cell continues to divide, the chromosome is “falling apart” to a non-functional, mutant cell that does not die, such as is the case with cancer cells.

As each individual is genetically different and also lives in a different psycho-physical environment, telomere shortening process varies from one individual to another, resulting in a lifetime variable from one individual to another.

A weakened immune system can also be a factor in accelerating telomere shortening leading to accelerated aging and a shorter lifespan. In fact, lymphocyte and granulocytes telomere shortening also lead to a weakened immune system, creating a vicious circle. Immune cells in the blood regenerate from stem cells. It is therefore necessary that the body produces sufficient stem cells. A stem cell deficiency leads to the aging of lymphocytes and granulocytes due to the shortening of their telomeres.

Below is the statistical evolution of telomeres length with chronological age of lymphocytes and granulocytes telomeres length: