The science of aging is among the most dynamic and provocative in modern biology. Over the past two decades we have seen a virtual explosion in research investigating the molecular and behavioral systems that control the aging process. But the more researchers uncover about the science of aging, the more questions emerge.
Dietary restriction has long been considered the most potent regulator of aging. Restricting food intake by any means induces a series of metabolic changes in organisms from yeast to primates that serve to extend life. Studies are currently underway to investigate the ability of dietary restriction to extend life in humans.
Several biological changes are known to occur upon the onset of dietary restriction including a decline in reproductive ability, increased stress resistance and a slowdown of some metabolic processes.
Insulin signaling was among the first molecular pathways to be identified in the regulation of aging, and offered a direct tie between diet and the aging process. In 1998 UCSF scientist Cynthia Kenyon showed that removing an insulin receptor gene (daf-2) in worms could double their lifespan. Her lab later showed that removing another insulin signaling gene (daf-16) could extend life even longer. I spoke to Kenyon about the relationship between diet and aging for this article.
Blocking insulin signaling in these worms did not just prevent the worms from dying and allow them to age longer. Instead the aging process actually slows so that older worms continue to behave like young worms. Also, as these experiments were repeated in different animals, it was shown that lowering insulin signaling also helps protect animals from stress and diseases such as cancer and heart disease.
Insulin is released as a direct response to glucose in the blood. This means that any time you eat a meal with carbohydrates, you are increasing your insulin signaling and likely accelerating aging. But this does not mean that you will live forever if you stop eating carbohydrates.
Interestingly, protein metabolism also contributes to accelerated aging, but through a different mechanism. Even more intriguing is that restricting protein increases lifespan to a greater extent than restricting sugar.
So is it simply calories that promote aging?
Probably not. For one thing, the effect of a calorie from protein is greater than a calorie from carbohydrate, making it unlikely that a calorie is the basic unit of impact. Second, there is evidence that calories are not required to accelerate aging.
Recent studies have shown that the mere act of smelling food can reduce lifespan. The mechanism for this effect is still unknown, but seems to be tied to respiration.
According to Kenyon it is clear that “sensory perception influences lifespan,” at least in worms and flies.
Thus it is likely that aging is controlled by the interaction of several pathways, including metabolism, respiration and stress. Importantly, however, lifespan seems to be dependent on a handful of specific pathways rather than global changes in cellular function or breakdown. The idea that aging is an inevitable function of time must be put aside given the evidence that it is controlled at a genetic and environmental level.
This makes sense when you think about it. Different organisms exhibit vastly different lifespans and rates of aging that are too great to be explained by some kind of universal cellular breakdown. A more parsimonious hypothesis is that organisms differ in specific genetic factors that, combined with environmental influences, regulate lifespan.
So how should we mortal humans react to these findings?
The genes linking diet and aging are highly conserved through evolution, indicating that there is a great chance human aging is sensitive to diet. Indeed, insulin-related genes have been found to be important in long-lived human populations. This suggests that the pathways discovered in worms and other organisms have similar functions in humans.
What is not clear is how much influence diet has on lifespan and to what extent we are able to manipulate it. It is already known that abnormal insulin activity in humans is linked to higher disease rates, especially “diseases of civilization” such as heart disease, hypertension, type 2 diabetes and cancer. And these diseases are clearly associated with diets rich in processed foods, especially refined carbohydrates.
The effect of protein consumption on lifespan in humans has yet to be investigated. Envisioning an experiment that would test the influence of smelling food on human aging is difficult to even imagine.
Although direct evidence is not available, there is good reason to suspect that a diet with low glycemic load may extend human lifespan. In November 2009, Kenyon’s lab reported that adding glucose to a worm’s normal diet shortens lifespan, but has no effect on the long-lived worms that lack insulin signaling genes daf-2 and daf-16. This discovery prompted Kenyon herself to adopt a low-carbohydrate diet.
Despite this there is still not sufficient evidence to recommend a calorie restricted diet for humans to extend life, largely because optimal nutrition levels for a given individual are unknown. However, most people would benefit vastly by eliminating processed foods and refined carbohydrates from their diets as much as possible.
Focusing on fresh, whole foods, enjoying an occasional glass of wine, avoiding smoking and getting regular exercise can add 14 years to the life of an average person. Maintain a healthy weight as well and your outlook gets even better.
Would you change your diet to be healthier and live longer?