Stress, aging, and resilience: Can accrued wear and tear be slowed?

Abstract The impact of stress on age-related physiological capacities (i.e., resilience) is influenced not only by endowed genetic substrate, but also by individual differences, including the frequency of exposure to stress, the nature and intensity of psychological and physiological reactions to stress, and the efficacy of restorative processes that replenish physiological reserves and fortify against future stress (Cacioppo, Hawkley, &: Berntson, 2003). This paper outlines a conceptualization of stress that acknowledges human susceptibility and resistance to the stresses of life and considers the net impact of human frailties and strengths on physiological resilience and health during the aging process. Aging is inevitable. Indeed, one could say it is written into our genes. Cellular biological age is reflected in the gradual shortening of telomeres, the protective caps at the ends of chromosomes that normally prevent cell senescence (Frenck, Blackburn, & Shannon, 1998). Although the relationship between cellular and organismic age is not well understood (Chan & Blackburn, 2003), chronological age is inversely correlated with telomere length in adults across all age groups (Brouilette, Singh, Thompson, Goodall, & Samani, 2003; Cawthon, Smith, O'Brien, Sivatchenko, & Kerber, 2003; Epel et al., 2004). Moreover, stress appears to contribute to cellular aging. For instance, among 20- to 50-year-old mothers who had been caring for a chronically ill child, telomere length in peripheral blood mononuclear cells was inversely related to the duration of caregiving (Epel et al.), even after controlling for mother's age. This finding lends credence to the notion that stress is bad for the organism, and that it contributes to the wear-and-tear on the organism that marks the aging process. The thesis here is that aging is not simply equivalent to accrued exposure to stress, however. In the study referred to above, telomere length did not differ between the group of caregiving mothers and the group of control mothers not subjected to this chronic stress. However, telomere length was inversely related to perceived stress in both groups (Epel et al., 2004). Using established age-related means of telomere length, and controlling for chronological age and body mass index, the authors estimated that the lymphocytes of those in the highest perceived stress quartile were 9-17 years older than those in the lowest stress quartile (Epel et al.). Importantly, however, telomere length is insufficient to index cellular age. Telomere length is regulated by the telomere-protective and lengthening actions of telomerase, a cellular enzyme (Chan & Blackburn, 2003) whose activity decreases under conditions of repeated exposure to antigenic stimuli and with the approach of cellular senescence (Weng et al., 1997). Notably, then, caregiving and control mothers whose perceived stress scores were in the highest quartile not only had shorter telomeres, but also had significantly lower telomerase activity than those in the lowest stress quartile (Epel etal, 2004). These data suggest that, across the spectrum of stressful experiences, the impact of stress on age-related physiological capacities (i.e., resilience) is influenced not only by individual differences in exposure to stress, but also by individual differences in responses to and recovery from stressful experiences. In addition, we maintain that stress effects are influenced by the efficacy of restorative (e.g., anabolic) processes that serve to replenish physiological reserves. Our goal in this paper is to outline a conceptualization of stress that acknowledges not only human susceptibility but also human resistance to the stresses of life, and to consider the net impact of these frailties and strengths on physiological resilience and health during the aging process. Stress is Neither Good Nor Bad The central dogma of stress research has long been that stress is "bad. …