What you need to know
Telomeres are structures at the end of our chromosomes that shorten every time a human cell divides. This problem is because of a telomerase enzyme deficiency syndrome, or TEDS that affects every one of us. If it weren’t for lack of this enzyme our telomeres stay long and healthy. The length of an individual's telomeres is closely associated with their biological age and research suggests that control of telomere length has the potential to treat many diseases associated with aging. Only in the last thirty years science has made real progress in understanding the fundamental question of why we age and what can be done about it. These discoveries have not been widely publicized-‐yet -‐ and so most people are unaware of how close we are to curing the disease of aging once and for all.
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. 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.
When a cell divides, the genetic material inside that cell needs to be copied. This process is called 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.
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. Our DNA is unable to perfectly copy itself; when a strand is replicated, the new strand is shorter than the old strand.
We call this anomaly TEDS. Telomerase Enzyme Deficiency Syndrome. Simply put, it there was Telomerase Enzyme present in these cells, (like there is in reproduction cells that don’t age) there would be no shortening of the Telomeres and no aging of the cell when division occurs.
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 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.