Pathways to aging: the mitochondrion at the intersection of biological and psychosocial sciences

Abstract

Compelling evidence suggests that both biological and psychosocial factors impact the process of aging. However, our understanding of the dynamic interplay among biological and psychosocial factors across the life course is still fragmentary. For example, it needs to be established how the interaction of individual factors (e.g., genetic and epigenetic endowment and personality), behavioral factors (e.g., physical activity, diet, and stress management), and psychosocial experiences (e.g., social support, well-being, socioeconomic status, and marriage) in perinatal, childhood, and adulthood influence health across the aging continuum. This paper aims to outline potential intersection points serving as an interface between biological and psychosocial factors, with an emphasis on the mitochondrion. Mitochondria are cellular organelles which play a critical role in cellular senescence. Both chronic exposure to psychosocial stress and genetic-based mitochondrial dysfunction have strikingly similar biological consequences; both predispose individuals to adverse age-related health disorders and early mortality. Exploring the interactive nature of the factors resulting in pathways to normal healthy aging, as well as those leading to morbidity and early mortality, will continue to enhance our ability to translate research into effective practices that can be implemented throughout the life course to optimise the aging process.

Figure 1

Mitochondria influence pathways to aging by operating at the intersection of biological and psychosocial factors. Biological and psychosocial factors dynamically/bidirectionally interact to influence mitochondrial content and function in the body's tissues. The same factors can exert opposite effects on mitochondrial function, depending on the duration of exposure. For instance, acute stressors tend to upregulate mitochondrial biogenesis and function, whereas chronic stressors tend to downregulate mitochondrial biogenesis and function (top center graph). Mitochondrial-level factors influence mitochondrial function and may determine mitochondrial responsivity to upstream biological and psychosocial influences. In response to multiple individual and environmental factors, mitochondria produce outputs influencing cellular function, gene expression, and cellular senescence. As a result, pathways to aging are ultimately determined by the integrated and synergistic influence of multiple biological and psychosocial factors.