Excerpt from "The Aging Factor in Health and Disease"

In 1825, an English actuary named Benjamin Gompertz observed that death rates in humans rise exponentially after sexual maturity, and he proposed a simple formula to define the relationship between the force of mortality and age within a population. This is often used to characterize the age-related changes in mortality of a genetically heterogeneous population, whether human or animal. The Gompert z curve implies no finite maximum age for a species, strain or population, but does predict decreasing probabilities of survival with increasing age. The crucial question now is: Can the slope of the Gompertz curve be altered by biological interventions, i.e., can basic research on aging provide interventions to improve quality of life by decelerating the rate of senescence.
A different, but simpler way to present survival data is to plot the fraction of individuals remaining in a population as a function of the age of the population, i.e., a survival curve. From such a plot it is possible to: 1) detect early deaths which presumably are not due to the usual senescence - related changes; 2) determine the median age of death of the individuals within the population; and 3) estimate the maximum life span of the species, i.e., an age at which the chance of survival of any individual is negligibly low. The past century has been characterized by large decreases in early deaths caused by infectious diseases, and a dramatic i n c rease in the average life expectancy of humans due to improvements in sanitation, health care, housing, nutrition, the development of vaccines, and the discovery of antibiotics (see F i g u re 1). Substantial future pro g ress will depend upon obtaining a much better understanding of what aging is, particularly the adverse components, and how to intervene to either prevent, reverse or retard these adverse age-related changes.
As a result of the striking increase in the life expectancy of Americans in the 20th century, the United States of America is now anticipating a doubling of Americans aged 65 or older, from 35 million in 2000 to at least 69 million in 2020. This doubling in the number of individuals aged 65 or more could bring with it large increases in d i s a b i l i t y, loss of function, and the cost of health c a re for this segment of the population. Thus, it is imperative that the biomedical community make substantial advances in reducing the major causes of disability in the elderly population. This can only occur with appropriate levels of investment in aging re s e a rch. Edward Schneider estimates that the United States currently spends only 0.3% as much on aging re s e a rch as it does on health care services for older people ( S c h n e i d e r, 1999). Money spent on re s e a rch to better understand the mechanisms of aging and the causes of age-related disease may lead to i n t e rventions to both postpone the need for a g i n g - related health care, and partially pay for itself in reduced health care costs. Whether these practical benefits will start to accrue in years or in decades will depend on the vigor of the investment.

Aging vs. Age-related Pathology:
The Role of Age-Related Changes

A continuing debate has been whether a pattern of aging free of disease can be dissected away from the overlapping development of age-related diseases such as cancer, cardiovascular disease, osteoporosis, osteoarthritis, diabetes, and a large variety of neurodegenerative diseases, including Alzheimer disease. The most substantial attempt (more..) (Full Version in PDF)