Re: Is ageing a disease

The phenomenon of aging, or senescence, is very complicated and represents an area where there is much active research and speculation. The short answer to your question is no, aging is not a disease. It is a normal, complex process that paradoxically involves the accumulation of abnormalities at the cellular level. While the life expectancy of humans in developed countries has doubled since the mid-19th century (from about 40 years to nearly 80), this has largely been due to advances in the treatment or elimination of disease and a reduction in accidental deaths. And even though our expected lifespan has increased, the prevalence of age- associated conditions such as Alzheimer’s disease, cancer, cardiovascular disease, and osteoporosis has increased accordingly.

Questions of major interest to researchers studying aging include determining why aging occurs, what key mechanisms are involved, and elucidating the roles of genes and non-genetic factors such as nutrition and exercise. Other studies try to differentiate features of “normal” aging from elements associated with diseases of old age. At the genetic level, senescence is a polygenic trait-that is, many genes and genetically- controlled processes are involved. Most of these have roles in somatic maintenance, the process by which the integrity of the cell and its DNA is maintained. Aging is really a loss of this integrity, as DNA mutations accumulate and cellular functions are lost. Genes involved in aging normally function in pathways of DNA repair, tumor suppression, immune system function, production of stress proteins, and maintaining accurate DNA replication, protein synthesis, and gene regulation. Other genes which are important are involved in susceptibility or resistance to age- associated diseases. The exact roles of these genetic factors, and how they are modified or interact with other environmental factors is, as you can guess, extremely complex and is not known at the present time.

Studies of the growth of cancerous cells can, as you suggested, provide a means of understanding aging. Cancer cells are not immortal, though they certainly do not experience senescence in the same way, or in the same time frame, as normal cells. Cancer is not the opposite of aging, but many of the same mechanisms which protect the cell from the accumulation of damage that causes senescence also protect against the mutations that cause cancer.

The role of nutrition in aging is also unclear. Research has shown that undernutrition (especially early in life) can result in an increased susceptibility to age-related diseases. On the other hand, calorie restriction has been shown to increase lifespan. In the same vein, exercise, by increasing wear and tear on muscles and joints, can increase the chances of developing age-associated conditions. But exercise also can improve age-related changes in the mitochondria (the energy-generating system in cells) of aging muscle, presumably by increasing the turnover rate of mitochondria in the cell, thus eliminating those which have accumulated abnormalities.

Confused? There is a great deal of biomedical research devoted to this area, and it is clear that any understanding of human senescence will come from multidisciplinary efforts which include cellular, molecular, and genetic studies of the normal aging process as well as age-related diseases and conditions. There is considerable speculation about future human longevity. While it is clear that life expectancy has increased, this has been due to reductions in early mortality. And one study has calculated that even if all remaining mortality under age 50 was eliminated, life expectancy at birth in the United States would increase by only 3.5 years. While we may be able to improve the quality of life as we age, there is no escaping senescence, which is probably a good thing when you consider the social and environmental implications of a longer-lived or immortal populaton!

Some useful references:
Science Vol 278 (No 5337) Oct 17, 1997 has much of the issue devoted to aging research in different organisms
Lithgow, G. and Kirkwood, T. (1996) Mechanisms and evolution of aging. Science 273:80
Kirkwood, T. (1996) Human senescence. BioEssays 18:1009 Smith, D. (1995) Evolution of longevity in mammals. Mechanisms of Aging and Development 81:51.