Is Aging a Treatable Condition?
Imagine living to age 200 and beyond without the typical aches and pains that accompany advanced age. Impossible, you say. Well, consider this. If you were alive at the time our country was founded, you could expect to live to the ripe old age of 40. Today, the average life expectancy exceeds 75. Plus, with some of the recent advances made in the field of age-extension, many of us will live past the century mark.
At one time disease was considered a natural process. There was nothing you could do about it. Tuberculosis, smallpox, dysentery, the plague and other deadly diseases were just part of the human condition. It wasn't until we discovered that diseases were caused by viruses, bacteria, or the environment that it became possible to cure them.
We are now at the same point with regard to aging. Science is now learning that aging is a condition that is amenable to intervention and treatment.
Why We Age
Recent scientific research has found three major biological processes that to a great extent contribute to the aging process. They are: the creation of oxygen free radicals in the cells that use oxygen for energy, the reduction in the release of a substance produced by the pituitary gland called "human growth hormone", and a biological clock or counter in each cell, called a "telomere", that controls cell division.
The balance of this report will explain these biological processes and point out some of the recent advances in the study of aging and disease that may prove to extend our life spans far beyond what we have ever imagined.
Oxygen Free Radicals
According to Grace Wong, Ph.D., a scientist in the department of molecular oncology at Genentech, the original developers of synthetic growth hormone, a great deal of aging is due to the breakdown of proteins in the cell, as well as the DNA and RNA that provide the blueprint for making protein. A major cause of this cellular breakdown, says Dr. Wong, is the creation of oxygen free-radicals in cells that use oxygen to produce energy.
When oxygen is broken down in the cell, it can result unavoidably in the production of these short-lived, destructive particles. These oxygen free radicals activate destructive enzymes called proteases which damage and degrade the proteins in the cell. When enough proteins are damaged, the cell dies, followed by a fragmentation of the DNA.
Human Growth Hormone
Human growth hormone, a substance released by our pituitary gland, also acts directly on the proteases by activating a cellular defense force called protease inhibitors. This means that even though oxygen free-radicals are still present in the cell, the protease inhibitors prevent them from doing their deadly work.
While the pituitary continues to produces ample amounts of human growth homone, as we get older release of this miraculous substance is diminished. The pituitary of a 60 year old may release less than one-fourth of the growth homone as that of a 20 year old.
This decline in growth hormone with age may be a major factor in the loss of proteins that occurs in later life. According to Dr. Wong "As you age you are releasing less growth hormone, your immune response is decreasing, and at the same time the amount of oxygen free radicals are increasing." Without growth hormone in the cell to induce protease inhibitors, the proteases activated by the oxygen free-radicals are free to destroy the cell's proteins.
The Telomere -- Our Biological Clock
When you put cells into a test tube and grow them, they divide for only a finite period of time. This is known as a Hayflick limit, named for the scientist who discovered it, Leonard Hayflick, Ph.D. Once a cell stops dividing, it ages and dies. Studies have shown that age is related to our cells' division potential. Older people's cells stop dividing out much sooner than the cells of younger people.
The latest scientific evidence indicates that there is a "clock" or "counter" in each cell that is governed by a piece of DNA which is located at the end of each chromosome in the nucleus of a cell known as the telomere. After each cell division, the telomere becomes shorter. Once the telomere shrinks to a certain level, the cell can no longer divide. Its metabolism slows down, it ages, and dies.
Research also shows that the counter that controls the wasting away of the telomere can be "turned on" and "turned off". The control button appears to be an enzyme called telomerase which can rejuvenate the telomere and allow the cell to divide endlessly. Most cells of the body contain telomerase but it is in the "off" position so that the cell is mortal and eventually dies. But some cells are immortal because their telomerase is switched on. For instance, the hemopoietic cells, the progenitors of blood cells, are immortal. Unfortunately for us, so is cancer. Cancer cells do not age because they produce telomerase, which keeps the telomere intact.
In the not too distant future, we will have therapies that will block telomerase in cancer cells, so that they stop dividing and die off, and relengthen the telomere in aging cells, so that they become young again.
Turning Our Biological Clock Back On
To actually reverse the aging process to the point that we can expect to live to age of 150 to 200, or more, we will need a substance that will restore telomere length and turn old cells into young ones. While this is not yet available, many scientists believe it will be in less than a decade. Until then, antioxidant supplementaion and growth hormone therapy can do the next best thing -- help keep our cells in as healthy a state as possible.
A cell's ability to function depends on its genetic material, the DNA, in the nucleus of the cell which codes for all the proteins, hormones, and enzymes that make the cell run. DNA is under constant attack from oxygen free-radicals, ultraviolet light and other damaging factors. Although our DNA has the ability to repair itself, it falls down on the job as we age. Up till now, one of the few ways we could limit the damage to our DNA was to take antioxidant supplements to bolster our own defenses.
The latest European research shows that growth hormone therapy can go further and do what antioxidants cannot. Growth hormones act like carriers to bring the cell the raw materials needed for renovation and repair. Growth hormone initiates the transport of amino acids, the building blocks of protein, and nucleic acids into the cytoplasm of the cell, the area outside the nucleus. Growth hormone doesn't just minimize the damage to the DNA and cellular structures, it helps heal the cell and the DNA.
There is abundant evidence that growth hormone therapy decreases your chances of dying prematurely from disease, which is another way of saying that it increases your chances of celebrating your 100th birthday.
Extending Your Maximum Life Span
Many gerontologists contend that we have not yet reached the limits of our maximum life span. With advancing technology such as the ability to engineer the genes at will, we will push back the frontier of aging even further. Within five to fifteen years, we will have agents that will repair damage to cells, stimulate the telomere to regrow itself, and manipulate the DNA. At that point, we will have true age reversal.
But the train is leaving the station, and anyone past the age of thirty-five will have to climb on board now. If you don't limit cellular damage and treat the DNA now, in the next five to ten years when telomere stimulants and other DNA modifiers are available, you will have so much extra damage to your chromosomes and DNA that you won't be able to benefit.
The best prescription now is to limit the damage to the DNA with antioxidants, vitamins, and minerals, and to treat the DNA with a growth hormone enhancement program that includes a more nutritional diet, exercise, and growth hormone releasers. This is the bridging formula that will get you to the future.
There are advancements being made in medical technology that will extend the maximum life span to 150 to 200 years or more! If that's not a good incentive to remain healthy and alive, I'd like to know what is.
Author: Robert M. Gallo