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The Programmed Cellular Death Approach to Anti-Aging Treatment
Modern anti-aging treatments are based on a common foundation of knowledge that I will quickly review. Biochemistry and molecular biology tell us that there are many types of chemical reactions in the human body. We know that it is the genetic information programmed into our cellular DNA that dictates what reactions occur. Genetic information, expressed in regulatory ways, instructs the body’s proteins and enzymes, and controls how the enzymes carry out the biochemical reactions of the cell.
This information, contained in our biological DNA, consists of many thousands of long, often repeating, sequences of base pairs made from four basic nucleotides. Mapping the human genome has shown that there are over three billion bases in our DNA. They are estimated to have about 20,000 protein-encoding genes. All bodily functions are controlled by the expression of genes in our genome. The mechanisms that control the aging process are believed to be programmed into our DNA but only a fraction of the biochemical reactions related to the aging process have been looked at in any detail. Cellular aging is a very complex process and many of its low-level functional details have yet to be discovered.
The theory of aging has aligned itself with two lines of thought: programmed cell death theory and cellular damage theory. The programmed death rate depends on the root causes of aging. The cellular damage process looks at the visible signs of aging; ie symptoms of aging. Both theories are equivalent and often overlap. Both theories are evolving rapidly as anti-aging research reveals more details. As works in progress these theories may take years to complete. This broad classification also applies to the types of anti-aging treatments currently available.
The programmed death theory of aging suggests that biological aging is a process orchestrated by a series of lifelong processes. They express themselves through a lot of expression. Gene expression also controls body processes such as our body’s maintenance (hormones, homeostatic signaling etc.) and repair processes. With increasing age the efficiency of all types of processes decreases. Programmed cell death researchers want to understand which processes are directly related to aging, and how to influence or improve them. Many ideas are being pursued but one major area of focus is on reducing or stopping telomere shortening. This is considered to be the main cause of aging.
Apart from germ cells that produce ova and spermatozoa, most human dividing cell types can divide only about 50 to 80 times (also called the Hayflick limit or biological death clock). This is a direct result of all cell types having long telomere chains fixed at the end of their chromosomes. This is true for all animal (Eukaryotic) cells. Telomeres play an important role in cell division. In very young adults the telomere chains are about 8,000 base pairs long. Each time a cell divides its telomere chain loses about 50 to 100 base pairs. Eventually this shortening process disrupts the telomere chain pattern and becomes sterile. Cell division is then no longer possible.
Telomerase, the enzyme that builds long, fixed telomere chains, is normally only active in undifferentiated embryonic cells. Through the process of differentiation these cells eventually become the specialized cells from which all our organs and tissues are made. After a cell has matured, telomerase activity stops. Normal elderly people have little or no detectable telomerase activity. Why? The limited length telomere chain maintains chromosomal integrity. This preserves the species more than the individual.
During the first months of development the embryo’s cells organize into about 100 highly specialized cell lines. Each cell line (and the tissues they produce) has a different Hayflick limit. Some cell lines are more vulnerable to the effects of aging than others. In the heart and other parts of the brain, cell loss is not complete. With advancing age such tissues begin to fail. In other cells damaged cells die off and are replaced by new cells with shorter telomere chains. Cell division itself only causes about 20 telomere base pairs to be lost. The rest of the telomere shortening is believed to be due to free radical damage.
This limitation on cell division is why efficient cell regeneration cannot go on forever. When we are 20 to 35 years old our cells can completely renew themselves. A study found that by age 20 the average length of telomere chains in white blood cells is about 7,500 base pairs. In humans, skeletal muscle telomere chain lengths remain more or less constant from the early twenties to the mid-seventies. By age 80 the average telomere length decreases to about 6,000 base pairs. Different studies have different estimates of how telomere length varies with age but the conclusion is that between the ages of 20 and 80 the length of the telomere chain decreases by 1000 to 1500 base pairs. Then, as telomere lengths shorten even more, severe signs of aging begin to appear.
There are genetic variations in human telomerase. Tall Ashkenazi Jews are said to have an active form of telomerase and longer than normal telomere chains. Many other genetic differences (for example: efficiency of DNA repair, antioxidant enzymes, and rates of free radical production) influence how quickly one ages. Statistics suggest that having short telomeres increases your chance of dying. People whose telomeres are 10% shorter than average, and people whose telomeres are 10% longer than average at different rates. Those with shorter telomeres die at a rate that is 1.4 greater than those with longer telomeres.
Many improvements in telomerase-based anti-aging treatments have been documented. I have only chance to mention some of them.
– Telomerase has been successfully used to extend the lifespan of certain mice by up to 24%.
– In humans, gene therapy using telomerase has been used to treat myocardial infarction and many other conditions.
– The related telomerase, mTERT, treatment has modified many different cell lines.
In one particular example, researchers using a synthetic telomerase that encodes a telomere-shortening protein, have extended the telomere lengths of human skin and muscle cells by up to 1000 base pairs. This is a 10%+ extension of length. telomere chain. The treated cells then showed significantly fewer markers than the untreated cells. After these treatments these cells behave normally, losing part of their telomere chain after each division.
The effects of using such techniques successfully in humans are amazing. If telomere length is the main cause of normal aging, then, using the previously mentioned telomere length numbers, it may be possible to double the healthy period during which telomere chain lengths are constant; ie from about 23 to 74 years to a wider range of 23 to 120 or more years. Of course this is very hopeful because we know that cells grown in vitro are able to divide a greater number of times than cells in the human body but it is reasonable to expect some progress (not 50 years but say 25 years).
We know that treatments based on telomerase are not the last answer to anti-aging but there is no doubt that they can, by being Hayflick’s limit, cause or even immortalize the life of many cell types. It remains to be seen whether this can be done safely in humans.
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