The modern anti-aging treatment is built on a common knowledge base that I will quickly examine. Biochemistry and molecular biology tell us that there are many types of chemical reactions in the human body. We know that it is the programmed genetic information in our cellular DNA that defines the reactions that occur. Regulated genetic information constructs proteins and enzymes in the body and controls how enzymes perform biochemical reactions in the cell.
This information, contained in the DNA of our genome, consists of several thousand long base pair sequences, often repetitive, consisting of four basic nucleotides. The mapping of the human genome has shown that there were more than 3 billion base pairs in our DNA. It is estimated that they contain about 20,000 genes encoding proteins. All body functions are controlled by the expression of genes in our genome. Mechanisms controlling the aging process are thought to be programmed into our DNA, but only a fraction of the biochemical reactions related to the aging process have been examined in detail. Cell aging is a very complex process and many of its low operating details have yet to be discovered.
The anti-aging theory is consolidated according to two axes of thought: the theory of programmed cell death and the theory of cellular damage. The theory of programmed death focuses on the root causes of aging. Cell damage theory examines the visible aspects of aging; that is, the symptoms of aging. Both theories are correct and often overlap. Both theories are developing rapidly as the anti-aging research reveals more details. As work progresses, these theories can take years. This broad characterization also applies to the types of anti-aging treatments currently available.
The theory of programmed death of aging suggests that biological aging is a programmed process controlled by many mechanisms of regulation of life. They manifest themselves by the expression of genes. Gene expression also controls bodily processes such as the maintenance of our body (hormones, homeostatic signaling, etc.) and the mechanisms of repair. With age, the effectiveness of all these regulations decreases. Researchers in programmed cell death want to understand what regulatory mechanisms are directly related to aging and how to affect or improve them. Many ideas are under study, but one of the main areas of action is slowing down or stopping telomere shortening. This is considered a major cause of aging.
With the exception of germ cells producing ova and spermatozoa, most types of dividing human cells can only divide 50 to 80 times (also called Hayflick limit or biological death clock). This is a direct consequence of all types of cells having fixed length telomere chains at the ends of their chromosomes. This is true for all animal cells (eukaryotes). Telomeres play a vital role in cell division. In very young adults, telomere chains have about 8,000 base pairs. Whenever a cell divides, its telomere chain loses approximately 50 to 100 base pairs. Finally, this shortening process distorts the shape of the telomere chain and becomes dysfunctional. 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 from which all our organs and tissues are made. After a cell is specialized, the activity of telomerase ceases. Normal adult human tissue has low or no detectable telomerase activity. Why? A limited length telomere chain maintains chromosomal integrity. This preserves the species more than the individual.
During the first months of development, embryonic cells organize about one hundred distinct specialized cell lines. Each cell line (and the organs it constitutes) has a different Hayflick limit. Some cell lines are more vulnerable to the effects of aging than others. In the heart and in some parts of the brain, cell loss is not restored. With age, these tissues begin to degrade. In other tissues, the damaged cells die and are replaced by new cells with shorter telomere chains. Cell division itself only loses about 20 base pairs of telomeres. The rest of telomere shortening is thought to be due to free radical damage.
This limitation of cell division is the reason why effective cell repair can not last indefinitely. When we are 20 or 35 years old, our cells can renew themselves almost perfectly. One study found that at age 20, the average length of telomere chains in white blood cells was approximately 7,500 base pairs. In humans, the length of skeletal muscle telomere chains remained more or less constant from the early twenties to the mid-1970s. At age 80, the average telomere length decreases to about 6,000 base pairs. Different studies offer different estimates of age-dependent telomere length variation, but it is generally accepted that between the ages of 20 and 80, the length of the telomere chain decreases from 1000 to 1. 500 base pairs. Subsequently, as telomeres become even shorter, signs of severe aging begin to appear.
There are genetic variations in human telomerase. Long-lived Ashkenazi Jews would have a more active telomerase form and longer telomere chains than normal. Many other genetic differences (eg, efficiency of DNA repair, antioxidant enzymes, and free radical production rates) affect the speed with which one ages. Statistics suggest that having shorter telomeres increases your chances of dying. People with telomeres that are 10% shorter than average and those with telomeres that are 10% longer than average die at different rates. The shortest telomeres die at a rate 1.4 times greater than those of the longest telomeres.
Many advances in telomerase-based anti-aging treatments have been documented. I only have room to mention a few.
– Telomerase has been used successfully to prolong the life of some mice up to 24%.
– In humans, gene therapy using telomerase has been used to treat myocardial infarction and several other conditions.
Telomerase-mediated mTERT treatment has rejuvenated many cell lines.
In a particularly important example, researchers using synthetic telomerase encoded in a telomere extended protein extended telomere chain lengths of cultured human skin and muscle cells up to 1000 base pairs. It is an extension of more than 10% of the length of the telomere chain. The treated cells then showed signs of being much younger than the untreated cells. After the treatments, these cells behaved normally, losing part of their telomere chain after each division.
The consequences of the successful application of such techniques in humans are staggering. If telomere length is one of the main causes of normal aging, then, using the telomere length numbers mentioned previously, it might be possible to double the healthy period during which telomere chain lengths are constant. ; that is, between 23 and 74 years old and over 23 to 120 years old. Of course, this is too optimistic because it is known that cells in vitro culture are able to divide a larger number of times than cells of the human body, but it is reasonable to expect some improvement (not 50 years but 25 years old).
We know that telomerase-based treatments are not the definitive answer to the fight against aging, but there is no doubt that they can, by increasing the Hayflick limit, extend or even immortalize the lifespan of many types of cells. It remains to be seen if this can be done safely in humans.