Immortality

Cellular Aging, or senescence, is the phenomenon where cells lose the ability to divide. In response to DNA damage (including shortened telomeres) cells either senesce or self-destruct (apoptosis) if the damage cannot be repaired. Organism senescence is the aging of whole organism. This process has been studied for eternity, yet recent advancements in genetics have truly paved the way for future breakthroughs, probably within our lifetimes.

Why do we Age?
Evolutionists attribute the aging process to a "defect" in evolution. This defect is attributed to the specificity of natural selection to disease and traits which present themselves early in an organism’s lifespan. Because extrinsic factors (accidents, trauma, prey) affect the normal lifespan of animals, the traits that cause aging and early death are expressed in a smaller percentage of the population and therefore have little affect on advancement of the species. An example of this is seen in mammals: when mammals of a similar size have different extrinsic dangers (i.e. mice- highly preyed upon, and bats- few predators) evolution has allowed for the species with fewer extrinsic dangers to remove senescent traits from the genetic pool. Mice have a lifespan of only a few years in the wild- mostly because of predatory factors- yet due to the lack of genetic evolution this lifespan in replicated in a controlled environment without predators and accidents. Bats, which can live 30 years, on the other hand have few predators, thus the aging population of bats represents more of the genetic pool and allows for natural selection to remove aging traits.
This defect in natural selection can also be seen in Humans through the example of Huntington’s disease - an autosomal dominant disease; this is passed to all offspring and usually causes severe dementia, depression and movement disorders in the late 30's and typically death by 45. Natural selection should have removed this genetic disease, however if you consider the average lifespan in recent history is stands to explain why Hunington's is still with us. Until very recently 45 was old by many standards in human society and few lived to such an age after falling victim to or disease, trauma, or other extrinsic factors. Thus Huntington victims often died after procreation, but before representation of their disease, thus preventing the gene pool from being affected and "tricking" natural selection. This is not to say that Huntington’s is in any way related to human aging, but simply and example of how traits that are presented late in life are not easily selected for in evolution, and thus the reason we have not yet evolved to be immortal.

The Biology of Aging:

Many theories currently exist to explain why cells have limited number replications before becoming “post-mitotic” (unable to divide). Interestingly, it appears not all creatures age. For example lobsters, sponges and corals have an unlimited number of cellular divisions. Thus if you didn’t eat him, that lobster might have lived forever. Without going through the process of DNA replication a brief description of the causes of cellular aging is presented:

Theory 1: Sir2 – a silencing gene which plays a role in controlling certain characteristics of the genome. This gene has been shown to decrease the expression of rDNA and telomeres in yeast DNA. rDNA over multiple replications often creates extraneous stands of rDNA which can then bind together and create what is called extrachromosomal rDNA circles (ERCs), which is nothing more than extra DNA without a genetic purpose. However, this DNA tends to stay with the mother cell after replication and competes with the cell for nucleic factors during future replication processes, therefore diminishing the cells ability to replicate. This has not been proven in humans but similar forms of extrachromosomal circular DNA has been identified. Interestingly, up regulation of Sir2 in cells leads to an extended cellular life expectancy and the organism life expectancy of worms and flies (thank god, what would we do without the flies).

Theory 2: Telomeres – a telomere is basically a region of extra DNA found at the end of the DNA strand which does not code for anything. In fact, typically it is a repetitive pattern of nucleic acids and is virtually nonsense DNA. Its purpose is simple: DNA replication is not perfect, it is a complicated process fraught with errors which require constant monitoring and correction by proteins. In addition the process is incapable of replicating the very end of the DNA strand, thus if important information were carried on that part of the strand it would be lost during replication. To prevent this a nonsense strand of meaningless nucleic acids is placed at the end of the DNA strand to prevent loss of essential information. Over time this strand or telomere is lost and the replication process begins losing vital information of the genome. Humans code for a protein called Telomerase – kind of a chemical fountain of youth. This protein, although repressed in most cells of the human body, acts to extend the telomere. In 1998 a professor at UCSF found a technique to activate this protein and in 2006 the Geron company indicated they have two drugs currently under trial to activate telomerase. The concern is that activating this protein may lead to an increased risk of cancers.

Theory 3: Chemical Damage – it has long been known and proven that a 30% caloric deficit extends the lifespan of most mammals including monkeys and mice. This observation is at the root of free radical damage and a complex system in which that big Mac kills you. Under aerobic conditions proteins, fats, and carbohydrates are ultimately converted to glucose which is the body’s main source of usable fuel and the form that energy travels in your blood to tissues for utilization. Most cells contain mitochondria which use glucose along with oxygen to create ATP, which is then utilized to make muscles contract, drive reactions, and so forth. A byproduct of this metabolism of glucose is the production of hydrogen peroxide, peroxide, and hydroxyl radicals – highly reactive species of oxygen that can degrade proteins and DNA. The body has natural defenses to destroy these oxidants – and many believe that the ingestion of antioxidants (which I’m sure you’ve heard about) can slow this process. In any case, it seems undeniable that the higher the metabolic rate the shorter the life expectancy.

Aging is a complicated process that we have learned a great deal about through recent advancements in genetics and evolutionary biology. I imagine our near future will soon explode with ethical and scientific debate regarding the issue. Until then, I think it's just interesting understanding what makes us die and why evolution hasn't been able to thwart death.