Posted by Diane Peterson

 

What seems to be intrinsic for most humans is the innate desire to live for eternity. Rather it be in physical form or spiritual, the motivation appears tangible. Hence, this concept has been speckled throughout our history, in not only our lives on Earth, but the promise of everlasting life through religion as well.  The search for “the holy grail” of life has been on ongoing quest throughout the centuries. 

For quite some time, we have been aware through hypothesis and research, of two primary means in which to influence aging; velocity and gravity. Both are effective concepts in terms of influencing aging, but obviously impractical for us “archaic Earthlings”. For the sake of simplicity, I will not address these subjects here, and for those who wish to learn more about these hypotheses; I refer you to the quantum physics section of your local library. 

There are now more current, significant theories which are showing great potential in the field of slowing the aging process and we are now on the verge of what could prove to be the medicine of the future. 

These more recent premises regarding anti aging revolves around genetics and the slowing of cell division. There are generally two types of aging theories; cell damage and cell programming. The first suggests that there are influential factors outside of the cell which impart damage to the structure itself. The second implies a genetic time clock which predetermines our cell’s life span. The former influences the programmed state of the cell and thus, can create an influence on the life of the cell to shorten. 

In the 1960s, Dr. L. Hayfick discovered that human fibroblasts (cells) divided no more than fifty times before they expanded and died. Even if he froze the cell at 14 divisions, they “remembered” that they had 36 divisions left after they were thawed. This indicated that the cell indeed had a predisposed coarse time of life. This set number is now referred to as the “Hayflick limit”. 

Based on this, researchers in gerontology have concluded that there is a genetic clock, literally “counting down the seconds” in each of our cells. This is what dictates when “old age” is to set in. This time clock can be influenced by many factors, but the most noteworthy appears to be the end caps of D.N.A., known as telomeres. Telomeres appear as two fingers like strands, gracing the end of our D.N.A. These have now been recognized as the “clocks of cellular aging” Every time a cell replicates, the telomere shortens. The shorter it becomes, the greater it affects the genetic coding of the cell. This is what gives us cellular aging. 

The question then begs, does the cell divide first, which then results in the fragmenting of the telomere, or does the telomere shorten, creating premature cellular division? New evidence suggests that the latter occurs much more frequently, which leads us to the conclusion that there are exogenous or external factors which participate in aging. The most significant of these would be peroxides, or singlet oxygen, which can implement a major destructive sequence on telomeres, as well as proteins and membranes. 

Oxygen is required for mammalian life; we cannot exist without it. But it can also generate highly reactive conditions within our bodies which are considered destructive, if not utilized correctly. This destructive potential extends to our D.N.A., and can literally “distort” it, creating expressions of different genetic material. In other words - mutations. It most likely will even lead to the premature death of the cell itself. 

Mammals have safety mechanisms which tend to defend against, to a degree, factors which influence telomere shortening and the premature division of the cell. But these factors are far less equal in strength than the detrimental candidates which harm our genetic coding and thus, expedite our aging process at a rate far greater than what could be considered as “normal”. 

When we observe an elderly person, we use references which determine aging; i.e., grey hair, wrinkled skin, age spots, etc. What we are actually observing is cell death, and the characteristics which are displayed by its biological diminishment. What we determine as “old” is actually the cells which no longer possess their biological activity. We also recognize the damage to the cells in the form of the diseases generally associated with old age. It then makes sense to us if we could slow the divisional time rate of the cell, we then could extend life itself.

Science now indicates that by influencing the factors which buffer, or harbor the damaging components so deleterious to our cells, we can actually extend our currently recognized life potential, by as much as 1/3, and prevent at least half of the diseases known to inflict our species. 

Science has discovered two primary enzymes (proteins which speed biochemical reactions) identified to specifically protect telomeres. These may be the key to life extension. The “holy grail” could very well be condensed down to these biological catalysts. 

Enzymes are highly specific for the reaction they catalyze and require specific substrates to generate the reaction. Many of you have probably heard of a class of these substrates, commonly called vitamins. Other classes of substrates are various minerals and amino acids. The substrates which we are concerned with here are the specific amino acids which increase the activity of the two enzymes directed at protecting the telomeres and their host, D.N.A. These amino acids contain sulfur, and the compound generating from their donating sulfur is what activates these enzymes. The lower the concentrate of this compound in our systems, the lower the protective capabilities we have at protecting our D.N.A. 

Research has demonstrated that mammals that have low activities of these enzymes show a shorter duration in life span. The condition known as Hutchinsom-Gilford syndrome is one example. We all have probably seen this at some point in our lives; the 12 year old that looks as if they are 90, taking their life within 14 years. This is due to an accelerated shortening of the telomere structure, and these children have all shown to have a greatly diminished activity of these enzymes along with low serum levels of activated sulfur. 

By maintaining a diet high in carotenes, cruciferous vegetables and flavonoids we increase the cofactors which support the enzyme pool which guards our D.N.A. An active lifestyle, both mental and physical, is important as well. 

We have the anatomical capacity of reaching beyond our current life expectancy. Now it is just a manner of providing the environment which will allow that to occur.

 

- By Kevin Meehan