Longevity Futures: Reverse Aging
Leslie J. Farer
In the past, halting the aging process was the goal of longevity enthusiasts. Now, research shows that it is possible to not just stop, but to reverse some of the infirmities associated with growing older and rejuvenate age-damaged tissues. Ensuring the integrity of telomeres, small segments of repeating DNA at the ends of our chromosomes that decay with time, has the potential to greatly extend youthful vitality and vibrant health. A novel concentrated plant extract known as TA-65 acts at the genetic level to maintain the structure of DNA, restore cellular function, and possibly keep you years younger than your chronological age.
What are Telomeres?
Telomeres are strips of DNA located at the ends of chromosomes. They are composed of a few hundred or more repeats of the nucleotide sequence TTAGGG (1,2) (where T= thymine; A = adenine; G= guanine). They act as protective ‘caps’ preventing loss of DNA, and also guard against fusing, fraying and unraveling of chromosomes, (1,3,4) which can expose and damage the genetic material and cause mutations.
Since investigators in the 1930’s coined the term telomere (from the Greek telos for ‘end’ and meros for ‘part’), a massive amount of research has been undertaken to explore the structure and function of these important chromosomal caps. More than 8,000 scientific papers have been written and the 2009 Nobel Prize in physiology and medicine was awarded to three scientists for their work involving telomeres.
Hayflick’s Fifty Year-Old Observation
Back in the 1960’s, geneticist Leonard Hayflick observed dividing human cells and made an important discovery that had a substantial impact on the future of anti-aging research. But before we examine his finding, let’s look very briefly at cell division, or mitosis ─ a fundamental, genetically-controlled process that enables a cell to duplicate itself, including chromosomes (through the process of DNA replication), to form two identical ‘daughter’ cells. Cell division allows an organism to develop and differentiate into an adult from multiple progressive stages beginning with the initial union of reproductive cells (the germ cells, egg and sperm), and after growth and birth, to construct and repair tissues.
Hayflick reported that human cells cultured under perfect conditions in his lab divided only a finite number of times in a progressive course leading to replicative senescence, (5) when they stop dividing altogether and become dysfunctional (the term senescence is roughly equivalent to ‘aged.’). Once cells have reached their proliferation maximum, or so-called Hayflick limit, they stop functioning properly or die through the process of apoptosis. (1,6,7)
Why do cells stop dividing when they reach their Hayflick limits? Is there a cellular mechanism that monitors and counts each cell division up until the final one? And does Hayflick’s observation have any relevance to aging?
In the early 1970’s, Russian scientist Alexey Olovnikov began to answer some of these questions ─ he made the connection between a DNA replication problem involving telomeres and the limitation on cell division reported by Hayflick.