The Cause Of Aging
The Cause of Aging
The root cause of aging is very straightforward: we age because our cells age.
In 1961, Leonard Hayflick, a researcher at the Wistar Institute in Philadelphia, discovered that there was a limit to the number of times a human cell could divide.1 After about 70 divisions, a cell derived from embryonic tissue enters a stage where its ability to divide slows and eventually stops. This stage is called cellular senescence. Hayflick also observed that the number of times a cell could divide was governed by the age of the cells: cells from a twenty-year-old could divide more times than cells from a fifty-year-old, which in turn would divide more times than cells from a ninety-year-old.
Hayflick discovered that, in essence, there is a clock ticking inside every dividing cell of our body. Our aging process isn’t simply a consequence of accumulated damage: there is a specific property of our cells that limits how long we can live. The cause of aging
The nature of this property was proposed independently in the early 1970s by both Soviet and American scientists. When a cell divides, the genetic material inside that cell needs to be copied. This process is called DNA replication. These scientists suggested that the limitation on cell division is rooted in the very nature of DNA replication. The enzymes that replicate a strand of DNA are unable to continue replicating all the way to the end, which causes the loss of some DNA.
A Good Analogy About The Cause of Aging
As an analogy, think of a DNA as a long row of bricks, and of DNA replication as a bricklayer walking backwards on top of a brick wall laying a new layer on top of that row. When the end of the wall is reached, the bricklayer finds himself standing on top of the brick he’s supposed to replicate. Since he can’t put down a brick where his feet are, he steps back and falls off the wall – leaving the very end of the wall bare. As a result, the new copy of the wall is shorter.
1 Hayflick L. (1965). The limited in vitro lifetime of human diploid cell strains. Exp. Cell Res. 37 (3): 614–636.
2 Olovnikov AM. Principle of marginotomy in template synthesis of polynucleotides. Doklady Akademii nauk SSSR . 1971; 201(6):1496-9. Watson, J. D. Origin of concatemeric T7 DNA. Nat New Biol. 1972; 239(94):197-201.
The Cause of Aging is Shortened Telomeres
If we lost portions of the information encoded in our DNA every time it replicated, human life would be impossible. Our cells couldn’t even divide enough times to allow us to be born. Fortunately, we are born with long, repetitive sequences of DNA at the end of each of our chromosomes, which later shorten during the normal DNA replication process.
These repetitive sequences are called “telomeres.”
Telomeres, like all DNA, are made up of units called nucleotides, arranged like beads on a string. The nucleotides in human telomeres are arranged in the repeating sequence TTAGGG (two thymine nucleotides, one adenine nucleotide, and three guanine nucleotides). This sequence is repeated hundreds of times in tandem in every telomere.
Each time our cells divide and our chromosomes replicate, our telomeres become shorter. When we are first conceived, the telomeres in our single-cell embryos are approximately 15,000 nucleotides long. Our cells divide rapidly in the womb, and by the time we are born, our telomeres have decreased in length to approximately 10,000 nucleotides. They shorten age throughout our lifetime, and when they reach an average of about 5,000 nucleotides, our cells cannot divide any further, and we die of old age.
Leonard Hayflick had discovered that there was a clock ticking in every dividing cell of our body; telomere shortening explains what makes that clock tick.
Dr. Bill Andrews does espouse some views that support evolution. And despite my misgivings (because I believe in a short history of earth and Biblical Creation) about this he has done some stellar scientific research that may be one of the most important breakthroughs in anti-aging research and development. Awesome Stuff!
– Greg Eddolls