This is a long read – but it starts the process of going into detail about telomeres and the theory of longevity so it’s an important read! I’ve broken it into 2 parts to keep it manageable, but make sure you don’t miss any of the info in this article!
Ever since the dawn of man
The desire for eternal life has been a compelling dream. From Methuselah to Ponce de Leon to Dorian Gray, stories of what might happen if man could live for extended periods have permeated every culture and every consciousness.
But it has only been in the last 50 years that the sobering reality of death has bumped up against a real hope for a longer disease and pain free life. It all began ironically enough with a question. A young scientist at the Wister Institute in Philadelphia named Lenhard Hayflick wanted to know whether human cells were really immortal as was then the accepted dogma.
Hayflick found that normal human cells can only divide a certain number of times and accordingly have a finite life span that under ideal conditions could allow a person to live for approximately 120 years. The number of times a cell can divide became known as the Hayflick limit.
It took more than 20 years before the actual mechanism of the Hayflick limit began to be understood and another 20 before it was completely explained.
The Biological Time Clock
While over simplified, the nature of cellular aging and thus the aging of the human organism can be summed up by the “biological time clock theory.” There is a natural biological time clock in every single cell in the body. This “time clock” resides in a simple end cap sequence of repetitive DNA known as the telomere.
The telomere functions to keep our DNA in its optimum double helix form. It also acts as a primer sequence that allows proper replication of the DNA when the cell divides.
Unfortunately with each and every replication of our DNA, part of the telomere sequence is chopped off. It is in this “chopping off” that the key to aging has been found.
For a better perspective
Let’s look at conception, birth and finally death from a cellular standpoint.
When we are conceived the union of sperm and egg has some 15,000 base pairs in its telomeres. After many replications a newborn human is formed and born with approximately 10,000 base pairs in each telomere sequence.
Thus in the uterine development of a human, when cells are dividing furiously to make a newborn baby, 5000 base pairs of telomere length are lost. In a sense we start to die the minute we are conceived!
During the continuum of human life
The trillions of cells that make up a person continue to divide, grow and replicate. With each cell division a few base pairs of DNA are lost until when the critical limit of approximately 5000 base pairs is reached, the cell is no longer able to divide. Then one of two things happens; either it enters a phase called senescence which is like retirement where the cell doesn’t work much anymore but is still alive or the cell commits suicide (apoptosis) and dies.
Whether senescent or dead, such cells are obviously no longer able to function in the ways they did when they were “young”. If one extrapolates this process to billions of cells within each organ system, we can see why organ function declines with age and eventually people wear out.
Even if we never contracted a disease of any kind, we would eventually wear out because of this mechanism. The oldest man has lived to 113 years and the oldest woman Jeanne Calment actually approached the theoretical Hayflick limit by reaching an age of 122 years before passing away in 1997.
But such people were clearly anomalies
Unfortunately most of us will die before reaching the age of 85. Why you ask?
The answer to this question may lie in a combination of Telomere Biology and the insight of Shakespeare! In Hamlet when the bard wrote the phrase, “The slings and arrows of outrageous fortune,” he may have unknowingly been describing the mechanism that will eventually kill most of us.
Stress; environmental exposure to toxins including UV radiation; excesses of drink, tobacco, drugs, and food; lack of sleep; and of course physical trauma all accelerate the cellular replication process, accelerating telomere loss.
The body tries to maintain a normal compliment of functioning cells and our behavior or sometimes simply the slings and arrows of our environment and our misfortunes forces our cells to replicate faster and in larger quantities than would be “normal.” That accelerates the march toward reaching our finite Hayflick limit which under perfect conditions equals about 120 years.
Each cell replication accelerates telomere shortening and each replication brings us one step closer to death.
Our current average lifespan
Of around 80 years (in America) is caused by the interplay between telomere length, “average” genetics, and environmental factors.
While the direct correlation of telomere length and disease process in humans is generally not understood, there is now overwhelming evidence that people with diseases associated with aging have shorter telomeres than healthy people. And the other theories of aging can’t account for this fact.
The free radical theory of aging
Postulates that cumulative free radical damage to cells causes aging and eventually death. Clearly if an organism had unlimited ability to replicate and replace damaged cells with healthy ones, free radicals would cease to be an issue.
Also intriguing is the fact that human cancer cells, even though immortal, have very short telomeres, which allows the DNA orientation to change and gene expression to change thereby unmasking oncogenes and encouraging mutations.
More research is needed in the area of telomeres and disease but the emerging evidence points to the benefits of maintaining a telomere length that is above the critical level of 5000 base pairs at which point cells go into a state of “crisis”.
All of this begs the question: what would happen if we could stop telomeres from shortening or maybe even lengthen them in spite of advancing chronological age?
For the sake of keeping this email under “epic novel” length I’m going to be covering that in my next chapter of my Telomere guide – so stay tuned!