Epidemiology of stress and asthma: from constricting communities and fragile families to epigenetics

Abstract

Several epidemiologic frameworks, exemplified through extant research examples, provide insight into the role of stress in the expression of asthma and other allergic disorders. Biologic, psychological, and social processes interact throughout the life course to influence disease expression. Studies exploiting a child development framework focus on critical periods of exposure, including the in utero environment, to examine the influence of stress on disease onset. Early stress effects that alter the normal course of morphogenesis and maturation that affect both structure and function of key organ systems (eg, immune, respiratory) may persist into adult life underscoring the importance of a life course perspective. Other evidence suggests that maternal stress influences programming of integrated physiologic systems in their offspring (eg, neuroendocrine, autonomic, immune function) starting in pregnancy; consequently stress effects may be transgenerational. A multilevel approach that includes an ecological perspective may help to explain heterogeneities in asthma expression across socioeconomic and geographic boundaries that to date remain largely unexplained. Evolving studies incorporating psychological, behavioral, and physiologic correlates of stress more specifically inform underlying mechanisms operating in these critical periods of development. The role of genetics, gene by environment interactions, and epigenetic mechanisms of gene expression have been sparsely examined in epidemiologic studies on stress and asthma although overlapping evidence provides proof of concept for such studies in the future.

Figure 1

Conceptual model for stress-induced perinatal programming of asthma, atopy, and lung function

Figure 2

Characterizing stress across the life course: an ecological approach