Etiological role of aging in chronic diseases: from epidemiological evidence to the new geroscience

Abstract

Over the last decades epidemiological studies identified major risk factors for chronic diseases and these led to preventive interventions that reduced the burden of cardiovascular diseases and mortality and contributed to increased longevity in the population. In the epidemiological context, aging was considered as an important “confounder”, something to factor out so that the true relationship between risk factors and health outcomes would not be misinterpreted. This approach resulted in a lost opportunity. “Adjusting for age” ignores the contribution of age as the most powerful risk factor for most diseases and the critical nuance that chronological age is only a poor approximation of biological aging. With the aging of the population, the contribution of aging to chronic diseases can no longer be downplayed. Geriatricians and gerontologists have approached this problem through the conceptualization of frailty as a diagnosable clinical syndrome characterized by marked susceptibility to stress, underlying loss of resiliency and diminished functional reserve. As research on the biology of aging in animal models progresses, the hypothesis is emerging that the phenotypes of aging and frailty may both result from a core set of mechanisms. These same mechanisms may also contribute to disease and may be modifiable with appropriate interventions. In this chapter, we propose that chronic diseases in older age and frailty both originate, at least in part, from accelerated aging, and they may mutually precipitate or exacerbate one another. We suggest that this concept has enormous translational potential and that it is consistent with the new evidence emerging from the fields of Geroscience and Precision/personalized Medicine.