Robine and Michel (1) provide the reader with a useful overview (with key references) of the potential morbidity consequences of population aging. Although morbidity is the focus of the article, the implied life span implications of mortality lurk just below the surface of the morbidity arguments. The expansion and compression of morbidity hypotheses occupy the extreme poles of a debate over frailty and disability trends, while Manton's concept of increased prevalence counterbalanced by reduced severity occupies the middle ground. The authors' summary of evidence for these competing hypotheses clearly reveals the conflicting and contradictory evidence that has prevented the emergence of a single winning hypothesis.
The most interesting aspect of the article was the authors' attempt to reconcile the conflicting evidence into a unified theory by postulating population aging as a logical progression of stages couched in the language of epidemiological transitions. Human ingenuity (e.g., biomedical interventions and prevention, public health awareness and implementation) manufactures survival time for people who in earlier times would have died (2). One biological consequence of this manufactured time is that the postreproductive population should become progressively more heterogeneous (less selected) than was the case for this segment of the population in the past. A major demographic consequence of this enhanced survival is population aging; a rectangularization of the age pyramid that occurs as more people are ushered into the postreproductive period of the life span.
A complex milieu of forces are competing to shift the balance between the compression and expansion of morbidity as the population gets older. In the early stages of population aging, the expected good health of the relatively younger-old people in the emerging postreproductive population would favor the compression of morbidity hypothesis. As new cohorts join the postreproductive population and earlier cohorts grow older, there will be a tension between the aging and heterogeneity-driven expansion of morbidity and the biomedical/societal efforts to mitigate the morbidity consequences of aging (3).
It is very difficult to project how current changes in the health of younger populations may impact overall longevity. In the United States, for instance, the prevalence of childhood obesity is increasing in epidemic proportions, with presumably the long-term consequences of diabetes, hypertension, and heart disease, which would decrease longevity (4,5). On the other hand, uniformly fatal diseases of the past, such as HIV and childhood leukemia, are becoming curable or chronic diseases in settings where medications for management are available (6,7), with attendant increases in longevity.
The big unanswered question at this intermediate stage of population aging is whether human interventions have actually delayed the underlying etiology and progression of chronic diseases associated with growing older, or simply become more effective in managing the detrimental but nonfatal consequences of aging. The former has profound implications, while the latter is a strategy that is likely to reap diminishing returns. In the mature stages of population aging, the consequences (expressed as an expansion of morbidity) of bodies whose biological warranty periods are expiring can no longer be suppressed or even diminished (8). Despite the best efforts of modern health care, frailty and disability will emerge in accord with genetic makeup, environmental experiences, behavioral decisions, life style choices, and the fickle finger of luck. The ages at which this occurs is the focal point of debates on mortality that are as heated and vociferous as those on morbidity. Although the Robine and Michel paper (1) lacks the depth and breadth of details needed for a general theory of population aging, it does stimulate useful thinking about the needed ingredients for a population-based theory.