Aging research can be a surprisingly challenging undertaking, since it requires challenging some common beliefs. For instance, many believed a genetic theory of aging to be unfeasible due to the fact that its symptoms typically emerge post-reproductively – making selection unlikely to have an impactful role at such late stages in life.
With advances in molecular techniques that enable specific genes to be overexpressed or deleted from cells directly, and genomic analysis techniques that enable studying large numbers of human genotypes simultaneously, this view has largely been disproved. Today it is understood that early changes associated with aging stem from progressive loss of the small pieces of “junk DNA” known as telomeres at each chromosome’s ends – gradually shrinking shorter with every cell division until ultimately too little remains for it not self-destruct or undergo apoptosis triggering it’s demise or self-destruction or self-destruction/apoptosis or self-destruction/apoptosis or self-destruction/apoptosis or self-destruction or death occurs.
Longevity scientists have also learned that certain genetic mutations can extend an organism’s lifespan, yet none has been found that can completely halt aging in any species. This discovery may suggest either that there may be an extraordinarily robust genetic program for aging or that none exists at all.