Back to Menu

There are three components of increasing longevity. First is preventing premature deaths (defined as dying before the expected life expectancy of the individuals birth cohort) due primarily to heart disease, cancer, infections, smoking-related illness, trauma. All in all, we are not doing badly in this regard. Second is doing something about potentially preventable chronic diseases occurring after a specified age (for example, 60 or 65 or 70 years), particularly heart disease, cancer, stroke, and smoking-related diseases. Potentially, that could increase life expectancy by 10 to 20 years. Finally, there is the possibility of modifying the aging process itself, literally preventing aging. That could increase life expectancy to an extraordinary extent.

On April 30, 2004, under the auspices of my medical school, a marvelous conference was held in New Jersey on the scientific advances that create the possibility of extraordinary longevity (average life expectancy of 110 to 120 years or longer) and on the potential individual and societal consequences (good and bad). The major technologies discussed were: caloric restriction and caloric restriction-mimicking drugs; genetic manipulation; stem cells; nanotechnology; and telomeres (and telomerase). As of this moment, one year later, that conference needs updating because of new, important scientific progress that has appeared since the conference. That shows how fast the field is moving.

The best studied and most predictable way to extend life spans in fruit flies, earthworms, and rodents is by reducing calories (but keeping nutritional status normal). This has resulted in a determined effort to find drugs that mimic caloric restriction (but allow unrestricted diets). The most interesting of the agents is resveratrol, a flavonoid found in red wine and grape skins. At the time of the conference, resveratrol had been shown to extend the life of yeast cells. Now, the same group of investigators from Harvard Medical School have shown modest increases in life spans in both fruit flies and earthworms given resveratrol. Of even greater interest, they have shown that caloric restriction and resveratrol act by the same mechanisms, stimulation of a gene called SIR2 that starts a cascade of events. They have also shown that this sequence of events occurs not only in fruit flies and earthworms, but also in the cells of rodents on a calorically-restricted diet. If human cells are exposed to blood of those calorically-restricted rats, the human cells show the same gene activation.

These are stunning studies. We are now getting very close to understanding how to modify the aging process; and we have the first inklings of specific drugs that might be used to achieve this effect. So far, the completed studies are in a variety of species up to rodents. Primate (monkey) studies with caloric restriction are well underway. Sometime in the next ten years, preliminary studies could be started in humans.

The field is moving incredibly quickly. That is why we had better start looking very carefully at the potential individual and societal consequences of extending average life spans at birth to 110 to 120 years or beyond (see essay on potential societal consequences).

The conference, which will soon be published, should serve as a wake-up call for policy makers. Waiting until the demographic changes are upon us is a recipe for catastrophe.

Supported by