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The Programmed Cellular Death Approach to Anti-Aging Treatment
Modern antiaging treatment is built on a common foundation of knowledge that I will quickly review. Biochemistry and molecular biology show us that there are many types of chemical reactions that occur in the human body. We know that it is the genetic information programmed into our cellular DNA that determines what reactions occur. Genetic information, expressed in regulated ways, builds the body’s proteins and enzymes and controls how the enzymes carry out the cell’s biochemical reactions.
This information, contained in the DNA of our genome, consists of thousands of long, often repeating, sequences of base pairs that are built from four basic nucleotides. Mapping the human genome has shown that there are over 3 billion base pairs in our DNA. It is estimated that they contain about 20,000 protein-coding genes. All body 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 associated with the aging process have been seen in any detail. Cellular aging is a very complex process, and many of the details of its low-level functioning have yet to be discovered.
The anti-aging theory is consolidated into two lines of thought: the programmed cell death theory and the cellular damage theory. The programmed death theory focuses on the root causes of aging. The cellular damage theory looks at the visible aspects of aging; i.e. the symptoms of aging. Both theories are correct and often overlap. Both theories are rapidly evolving as anti-aging research uncovers more details. While works in progress, these theories may take years to complete. This broad characterization also applies to the types of antiaging treatments currently available.
The programmed death theory of aging suggests that biological aging is a programmed process controlled by many mechanisms regulating lifespan. They manifest through gene expression. Gene expression also controls body processes such as our body’s maintenance (hormones, homeostatic signaling, etc.) and repair mechanisms. With increasing age, the efficiency of all such adjustments declines. Programmed cell death researchers want to understand which regulatory mechanisms are directly related to aging and how to influence or improve them. Many ideas are being pursued, but a major area of focus is slowing or stopping telomere shortening. This is considered to be the main cause of aging.
With the exception of germ cells that produce eggs and sperm, most types of dividing human cells can divide only about 50 to 80 times (also called the Hayflick limit or the biological death clock). This is a direct consequence of all cell types having fixed-length telomere chains at the ends of their chromosomes. This is true for all animal (eukaryotic) cells. Telomeres play a vital role in cell division. In very young adults, telomere chains are about 8,000 base pairs long. Each time a cell divides its telomere chain, it loses about 50 to 100 base pairs. Eventually, this shortening process distorts the shape of the telomere chain and it becomes non-functional. Cell division is then no longer possible.
Telomerase, the enzyme that builds fixed-length telomere chains, is normally active only in young, undifferentiated embryonic cells. Through the process of differentiation, these cells eventually form the specialized cells that make up all of our organs and tissues. Once the cell is specialized, telomerase activity stops. Normal adult human tissues have little or no detectable telomerase activity. Why? A length-limited telomere chain maintains chromosomal integrity. This preserves the species more than the individual.
During the first months of development, embryonic cells are organized into about 100 separate specialized cell lines. Each cell line (and the organs they comprise) has a different Hayflick limit. Some cell lines are more sensitive to the effects of aging than others. In the heart and parts of the brain, the loss of cells is not replenished. With age, such tissues begin to fail. In other tissues, damaged cells die and are replaced by new cells that have shorter telomere chains. Cell division itself only causes the loss of about 20 base pairs of telomeres. The rest of the telomere shortening is believed to be due to free radical damage.
This limit on cell division is why efficient cell repair cannot continue indefinitely. When we are 20 to 35 years old our cells can be renewed almost perfectly. One 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 length remains 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 changes with age, but the consensus is that between the ages of 20 and 80 the length of the telomere chain decreases by 1,000 to 1,500 base pairs. Then, as the length of the telomeres shortens even more, the signs of severe aging begin to appear.
There are genetic variations in human telomerase. Long-lived Ashkenazi Jews are said to have a more active form of telomerase and longer than normal telomere chains. Many other genetic differences (eg: efficiency of DNA repair, antioxidant enzymes, and rate of free radical production) affect the rate of aging. Statistics suggest that having shorter telomeres increases the chance of dying. People whose telomeres are 10% shorter than average and people whose telomeres are 10% longer than average die at different rates. Those with shorter telomeres die at a rate that is 1.4 times greater than those with longer telomeres.
Many advances in telomerase-based antiaging treatments have been documented. I have room to mention only a few of them.
– Telomerase has been used successfully to extend the life of some mice by up to 24%.
– In humans, gene therapy using telomerase has been used to treat myocardial infarction and several other conditions.
– The telomerase-related treatment, mTERT, has successfully regenerated many different cell lines.
In one particularly important example, researchers using synthetic telomerase that is encoded in a telomere-extending protein have extended the length of the telomere chain of cultured human skin and muscle cells by up to 1,000 base pairs. This is a 10%+ extension of telomere chain length. The treated cells then showed signs of being much younger than untreated cells. After the treatments these cells behaved normally, losing part of their telomere chain after each division.
The implications of successfully applying such techniques to humans are staggering. If telomere length is the primary cause of normal aging, then, using the telomere length numbers mentioned earlier, it may be possible to double the healthy period of time during which telomere chain lengths are constant; ie from the range of 23 to 74 years to an extended range of 23 to 120 or more years. Of course this is very optimistic because it is known that cells cultured in vitro are able to divide a greater number of times than cells in the human body but it is reasonable to expect an improvement (not 50 years but let’s say 25 years).
We know that telomerase-based treatments are not the ultimate anti-aging answer, but there is no doubt that they, by increasing the Hayflick limit, can extend or even perpetuate the lifespan of many cell types. Whether this can be done safely in humans remains to be seen.
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