Can We Delay Aging?

by Brad Gibson, Ph.D.

The Damsel of the Holy Grail
by Dante Gabriel Rosetti

�No, we cannot �prevent aging�� but what if we could delay it?

Unfortunately, the deterioration that comes with aging is part of a fundamental aspect of the universe, so it cannot be eliminated. Recent research suggests, however, that the rate of deterioration is indeed malleable, at least in many different animal models. So why not in people?� � Dr. Felipe Sierra

Dr. Felipe Sierra's post Can We Delay Aging? on the Next Avenue site is a reasonable and thoughtful response to what is actually a very difficult question. While, some researchers in the aging field have gone so far as to talk about extending one�s life to 200 years or more, or even becoming immortal, Dr. Sierra sidesteps these assertions and instead tackles the more practical, and the less politically charged issue, of targeting an increase in ��healthspan,� or what is known in the field as �compression of morbidity.�

�Traditionally, research on aging has focused on longevity, but we all recognize that longevity without health is a hollow goal. As the field has matured, we are paying more attention to healthspan � the proportion of lifespan spent in reasonably good health.

Many of the interventions identified in animals lead to improved healthspan. Not only do the animals die later, they die with fewer diseases and debilitating conditions than their control counterparts. This suggests that, at least in mice and other species, it might be possible to attain the Holy Grail of aging research: compression of morbidity.�

This �compression of morbidity� hypothesis, first proposed by James Fries at Stanford Medical School back in 1980, states that the �Extension of adult vigor into a fixed life span compresses the period of senescence near the end of life� (J. F. Fries, The New England Journal of Medicine July 17, 1980). From the NIH and governments budget perspective, this is a laudable goal, as it would potentially lead to less healthcare expenditures in the later years of one�s life, which currently consume over 50% of all medical costs. It would also have the obvious advantages of reducing chronic illness and diseases associated with aging, such as cancer, Alzheimer�s disease, and diabetes.

But can it be achieved? Evidence in model organisms from worms to flies to mice suggest that many of the underlying molecular pathways that appear to have an effect on the lifespan of an organism also tends to improve other phenotypic traits, such as movement, and cognitive and behavioral functions. This is important, as many of the early studies just examined lifespan extension in these model organisms without a close examination of whether there was also an increase in the health or robustness of the organisms. Clearly, the last thing we want to experience for ourselves is an increase of 10-20 years of our lifespan if it was to be lived in a chronic state of debilitation. And while we all know that improved exercise and diet can have significant effect on our health or robustness, the question of whether this will lead simply to an increase in our lifespan but not a compression of morbidity or an increase in our healthspan. 

The jury is still out with respect to unequivocal evidence of the compression of morbidity hypothesis, but several published studies suggest that it may be achievable. Indeed, the term �geroscience� that Dr. Sierra invoked in his essay as a new field of research devoted to answering this question was first coined by scientists at my own institute, the Buck Institute for Research on Aging. It was the title of a successful NIH proposal, �Geroscience� to the NIH to �support interdisciplinary approaches to solving significant and complex biomedical problems, particularly those that have been resistant to traditional approaches.� The essential notion of geroscience was that processes that drive aging and the diseases of aging overlap. And if we are to make any real progress in understanding aging, scientists need to study age-related diseases in the context of aging in a truly interdisciplinary manner. 

This may seem like an obvious statement, but most basic science research into diseases that occur late in life were not, and are still not, conducted with aging as a major variable in the overall experimental design. For example, the vast majority of studies of neurodegenerative diseases, such as Alzheimer�s or Parkinson�s diseases, where mouse models were used, the age of the mice were typically 6 months old, or about late-adolescence in human terms. But this is changing, and there is now an emerging consensus in the scientific community that we need to study these diseases in aging models to gain the insight we will need to find cures. So where are we in this process? Dr. Sierra concludes by saying:

�When will people benefit from this?

It is definitely too early to say, which is why I have refrained from even mentioning the interventions that work in animals. So, despite the thriving industry of �anti-aging� treatments, nothing that we know of today has been shown to prevent or delay the aging process in people. Thus, the current generation may not benefit from this groundbreaking research. But maybe our children and grandchildren will.�

Indeed, there are no anti-aging treatments available today that have proven effects on delaying aging despite some interesting studies in animal models. And I mostly agree with him that progress will be slow and we are unlikely to benefit from this basic research in our own lives. So in the meantime we are left with what we know can affect our general health: diet, exercise, reducing stress, etc. So instead of waiting for the miracle cure or fountain of youth�when and if it ever comes�there are plenty of non-pharmacological ways to improve your health, whether or not that they will delay the rate of your aging.

Subscribe to Yoga for Healthy Aging by Email � Follow Yoga for Healthy Aging on Facebook � Join this site with Google Friend Connect