Nothing seems more inevitable than aging and death—not even taxes. Every plant, animal and person you have ever seen will eventually die, including the person in the mirror. But some recent research suggests that aging as we know it may not be inevitable. Indeed, as our understanding of it grows, aging can be seen not as an immutable reality from which there is no escape, but as the product of biological processes that we may be able to control someday.
We already know that some animals do not seem to age. Many cold-water ocean fish, some amphibians and the American lobster never reach a fixed size; they continue to grow bigger, to be able to reproduce and to live until something kills them. What these creatures seem to be telling us is that something in their genes—and possibly in ours—controls the pace of aging, and that aging is not the fate of every living thing.
Throughout the history of life on earth, one of the most common difficulties that animals (and their cells) have faced has been a lack of food. About 70 years ago, scientists discovered that when animals are forced to live on 30 to 40 percent fewer calories than they would normally eat, something unusual happens: they become resistant to most age-related diseases—cancer, heart disease, diabetes, Alzheimer’s—and live 30 to 50 percent longer. Restricting calories slows aging.
But how? What are the underlying genes that preserve vitality and stave off disease? No one knows for sure why aging occurs, but one important reason is probably the accumulation of DNA damage—from radiation, mutation-causing chemicals or, particularly, oxidants. Inside every animal cell are many mitochondria—little "power packs" that use oxygen to generate energy. In doing their jobs, however, mitochondria produce chemical byproducts—oxidants —that damage DNA and other components inside cells. It may not seem fair, but it’s a fact of life. Fortunately, our cells are not defenseless against such assaults. They have genes that spring into action to defend against DNA damage, including genes that repair damaged mitochondria.
About 15 years ago, armed with powerful new molecular-research techniques, a few scientists began to investigate these genetic phenomena. At MIT, Dr. Leonard Guarente (along with one of the authors of this piece, David Sinclair) discovered that adding an extra copy of a gene called Sir2 caused yeast cells to live 30 percent longer. Today many researchers suspect that Sir2 or other sirtuin genes—which are present in all animals, including humans—are responsible for the health benefits of calorie restriction, perhaps by repairing our DNA. But if, in order to kick the sirtuins into action, we had to restrict our calorie intake by 30 to 40 percent, would it be of any practical use? Few of us would be capable of restricting our diets so severely that we were constantly hungry: whether or not it made life longer, it would surely make life feel longer.
