Despite the considerable efforts made by scientists and doctors to determine a single, unified theory of aging, there is still no strong consensus within the longevity community as to its actual root cause. The various aging theories that have been developed over the past century have largely failed to explain aging on their own, but they have shed some good light on the aging process, and our understanding of it, so it’s worth taking a brief look at two of the most notable theories:
If you have ever heard of antioxidants, then you are already familiar with one of the oldest and most popular theories of aging—the free radical theory. (Free radicals are single atoms with unpaired electrons, usually oxygen atoms.) Developed in the 1950s, this theory came from Denham Harman, a former Shell Oil biochemist who had seen how free radicals caused unwelcome chemical changes in some compounds. Harman wondered if the same kind of damage could occur in human cells: Perhaps wrinkly skin, declining memory, and failing organs were the biological equivalent of rusty iron.
It was an electrifying idea, to be sure. So much so, in fact, that to this day, much is made of the damage that free radicals cause and the benefits that antioxidants offer. Unfortunately, laboratory tests have failed to consistently demonstrate that antioxidants do anything to stop aging.
The discovery of another component of aging—telomeres—won Australian scientist Elizabeth Blackburn a Nobel Prize in 2009. See, whenever a cell divides, the famous DNA double helix unzips itself into two single strands, each of which is replicated to complete two full new sets. This unzipping and recomposing business takes place inside of you about 2 trillion times every day. But to err is human, even on a cellular level. Mutations happen. Too many mutations result in loss of function, disease, and death.
That’s where telomeres come in. The most sensitive and damage-prone part of a DNA strand is its end, much like a shoelace. Because the loose, flappy ends of your shoelaces are much more likely to get frayed, shoemakers protect them with those protective plastic caps. Telomeres, sequences of proteins that live on either end of your DNA strands, serve just like those protective caps on your shoelaces: They replicate differently and are therefore not prone to the same kind of damage as the rest of a DNA strand. However, every time DNA replicates, these telomeres get “worn down” just a little bit. When telomeres become too short, they signal to the cell that “it’s time to die.” When scientists observed that mice with longer telomeres lived longer and had less DNA damage than shorter-telomered mice, they theorized that stimulating the production of telomerase—the enzyme that lengthens telomeres—might be the secret to slowing or reversing aging.
Of course, nothing is simple when it comes to the multiplex process of aging: Excess telomerase is also linked with cancer. It has even yet to be proved if telomere length is a cause of aging or merely a byproduct of it. Like other theories of the root cause of aging, telomere theory is a definite “maybe.”
And so it goes. There are many more theories of aging—some are quite brilliant and add considerably to our understanding of why and how we age, but none succeed in fully explaining the causes and mechanisms of aging.
