Modern anti-aging treatment is built on a standard base of data that I’ll quickly review. Biochemistry and molecular biology tell us there are a lot of forms of chemical reactions occurring within the human body. We all know that it’s the genetic information programmed inside our cellular DNA that defines what reactions occur. Genetic information, expressed in regulated ways, builds the body’s proteins and enzymes, and controls how enzymes perform the cell’s biochemical reactions.
This information, contained within the DNA of our genome, consists of many hundreds of long, often repetitive, sequences of base pairs which are built up from 4 basic nucleotides. Human genome mapping has shown there are over 3 billion base pairs in our DNA. It’s estimated they contain some 20,000 protein-coding genes. All body functions are controlled by the expression of the genes in our genome. The mechanisms controlling 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 checked out in any detail. Cellular aging is a really complex process and lots of of its low level operating details have yet to be discovered.
Anti-aging theory has consolidated itself along two lines of thought: the programmed cellular death theory and the cellular damages theory. The programmed death theory focuses on the basis causes of aging. The cellular damages theory looks on the visible facets of aging; i.e. the symptoms of aging. Each theories are correct and sometimes overlap. Each theories are developing rapidly as anti-aging research uncovers more details. As works in progress these theories may take years to finish. This broad characterization also applies to the currently available forms of anti-aging treatments.
The programmed death theory of aging suggests that biological aging is a programmed process controlled by many life span regulatory mechanisms. They manifest themselves through gene expression. Gene expression also controls body processes resembling our body maintenance (hormones, homeostatic signaling etc.) and repair mechanisms. With increasing age the efficiency of all such regulation declines. Programmed cellular death researchers want to grasp which regulatory mechanisms are directly related to aging, and affect or improve them. Many ideas are being pursued but one key area of focus is on slowing or stopping telomere shortening. This is taken into account to be a significant explanation for aging.
Aside from the germ cells that produce ova and spermatozoa, most dividing human cell types can only divide about 50 to 80 times (also called the Hayflick limit or biological death clock). It is a direct consequence of all cell types having fixed length telomere chains on the ends of their chromosomes. That is true for all animal (Eukaryotic) cells. Telomeres play an important role in cell division. In very young adults telomere chains are about 8,000 base pairs long. Every time a cell divides its telomere chain loses about 50 to 100 base pairs. Eventually this shortening process distorts the telomere chain’s shape and it becomes dysfunctional. Cell division is then not possible.
Telomerase, the enzyme that builds the fixed length telomere chains, is often only energetic in young undifferentiated embryonic cells. Through the technique of differentiation these cells eventually form the specialized cells from which of all our organs and tissues are made from. After a cell is specialized telomerase activity stops. Normal adult human tissues have little or no detectable telomerase activity. Why? A limited length telomere chain maintains chromosomal integrity. This preserves the species greater than the person.
Through the first months of development embryonic cells organize into about 100 distinct specialized cell lines. Each cell line (and the organs they make up) has a special Hayflick limit. Some cell lines are more vulnerable to the results of aging than others. In the center and parts of the brain cell loss shouldn’t be replenished. With advancing age such tissues begin to fail. In other tissues damaged cells die off and are replaced by recent cells which have shorter telomere chains. Cell division itself only causes about 20 telomere base pairs to be lost. The remaining of the telomere shortening is believed to be as a result of free radical damage.
This limit on cell division is the explanation why efficient cell repair cannot go on indefinitely. After we are 20 to 35 years of age our cells can renew themselves almost perfectly. One study found that on the age 20 the common length of telomere chains in white blood cells is about 7,500 base pairs. In humans, skeletal muscle telomere chain lengths remain kind of constant from the early twenties to mid seventies. By the age of 80 the common telomere length decreases to about 6,000 base pairs. Different studies have different estimates of how telomere length varies with age however the consensus is that between the age of 20 and 80 the length of the telomere chain decreases by 1000 to 1500 base pairs. Afterwards, as telomere lengths shorten much more, signs of severe aging begin to look.
There are genetic variations in human telomerase. Long lived Ashkenazi Jews are said to have a more energetic type of telomerase and longer than normal telomere chains. Many other genetic differences (ex.: efficiency of DNA repair, antioxidant enzymes, and rates of free radical production) affect how quickly one ages. Statistics suggest that having shorter telomeres increases your probability of dying. People whose telomeres are 10% shorter than average, and folks whose telomeres are 10% longer than average die at different rates. Those with the shorter telomeres die at a rate that’s 1.4 greater than those with the longer telomeres.
Many advances in telomerase based anti-aging treatments have been documented. I only have room to say a couple of of them.
– Telomerase has been used successfully to elongate the lifetime of certain mice by as much as 24%.
– In humans, gene therapy using telomerase has been used to treat myocardial infarction and several other other conditions.
– Telomerase related, mTERT, treatment has successfully rejuvenated many various cell lines.
In a single particularly essential example researchers using synthetic telomerase that encoded to a telomere-extending protein, have prolonged the telomere chain lengths of cultured human skin and muscle cells by as much as 1000 base pairs. It is a 10%+ extension of telomere chain length. The treated cells then showed signs of being much younger than the untreated cells. After the treatments these cells behaved normally, losing an element of their telomere chain after each division.
The implications of successfully applying such techniques in humans are staggering. If telomere length is a primary explanation for normal aging, then, using the telomere length numbers previously mentioned, it may be possible to double the healthy time period during which telomere chain lengths are constant; i.e. from the range of 23 to 74 years to an prolonged range of 23 to 120 or more years. After all this is simply too optimistic since it is thought that in vitro cultured cells are capable of divide a bigger variety of times than cells within the human body nevertheless it is affordable to expect some improvement (not 50 years but say 25 years).
We all know that telomerase based treatments should not the ultimate answer to anti-aging but there isn’t any doubt that they will, by increasing the Hayflick limit, extend and even immortalize the lifespan of many cell types. It stays to be seen if this could be done safely done in humans.
