As it turns out, there are good reasons to believe we can or will be able to control our aging, at least to some extent and within the limits imposed by our genetic endowment.
Previous research done with a variety of lower animals has shown that their lifespans can be lengthened by caloric restriction — that is, by significantly limiting their food intake for periods of time. And this may well prove to be true for humans. However, because it would be unethical to conduct such experiments in humans, it will be more difficult to clearly demonstrate this effect in us.
But recent research has given us some additional clues as to why we age and thus opened up other possibilities for slowing the aging process. Some of these studies have focused on a tiny organelle that lives within almost all living cells of higher organisms. This organelle, called a mitochondrium, is thought to have been acquired early on in the evolution of life on Earth as a result of primitive cells ingesting a bacterium that could use oxygen to generate useful energy.
This bacterium, instead of being fully digested and destroyed by the primitive cell, set up residence there and became a mutualistic symbiont with its own genetic material. In turn, it provided its host with the ability (in an oxygen-rich atmosphere) to efficiently obtain energy from its stored calories. Thus was born an ancestor of all living plants and animals that rely on oxygen for life. An interesting aspect of these tiny organelles (of which there are many in each of our cells and which are inherited only from our mothers) is that they can digest themselves (a process called autophagy) when they become defective either from injury or disease. They are then replaced through the synthesis of new mitochondria (by a process akin to cell division). In much the same way, whole cells can and do replace themselves in various tissues of our bodies.
This process of autophagy followed by replacement is necessary (for both mitochondria and the cells in which they reside) in order for us to maintain optimum functioning. Indeed, research has shown that the accumulation of old and poorly functioning mitochondria has detrimental effects on the health of mice and that giving these mice a drug that enabled them to clear their bodies of aging mitochondria improved their health. Surprisingly, regular exercise has also been shown recently to act in the same way, promoting the self-digestion of old and decrepit mitochondria and their replacement with new ones, with a resultant increase in longevity.
What we know presently about slowing the aging process can be summed up as follows: both exercise and a more restricted food intake helps organisms maintain their ability to digest dysfunctional mitochondria and replace them with newly formed healthy organelles, while exposure to toxins, excessive food intake, chronic inflammation, or a lack of exercise, damages this process and accelerates aging. Will acting on this knowledge prove too difficult for many of us?
Questions and suggestions from readers are welcomed and will be responded to in future editions of this column. Contact me at firstname.lastname@example.org.