Trait positive affect buffers the effects of acute stress on skin barrier recovery

The experience of positive affect (PA) is related to a variety of health benefits such as increased longevity, decreased morbidity, and less experience of pain (reviewed in Pressman & Cohen, 2005). Several prospective studies show that PA predicts decreased morbidity, such as lower incidence of stroke in older adults (Ostir, Markides, Peek, & Goodwin, 2001), and lower incidence of developing symptoms of the common cold after inoculation with cold virus (Cohen, Doyle, Turner, Alper, & Skoner, 2003). iThese studies importantly demonstrated that the effects of PA are independent of disease processes, as participants were healthy at baseline, and that dispositional or trait PA showed effects on morbidity independent of the effects of negative affect. Moreover, prospective effects of trait PA were observed in a range of health outcomes (e.g., pregnancy outcomes, injury, stroke, and hospital readmission). The specific mechanisms through which trait PA influences health operate through two general frameworks proposed by Pressman and Cohen (2005). One proposed framework is a direct effects model, in which trait PA impacts behaviors and biological systems relevant for health in general, irrespective of its effects on responses to stress. For example, individuals with high trait PA may be more likely to engage in health-promoting behaviors or have lower tonic levels of catecholamines or glucocorticoid hormones. By contrast, in a stress-buffering model, dispositional levels of PA may “buffer” against the harmful biological and health consequences of exposure to stressors. Individuals with high trait PA may be able to cope more effectively with stressful events and consequently, may not experience the negative health consequences of psychological stress. This stress-buffering hypothesis is consistent with Fredrickson’s “Broaden and Build” theory of positive emotions (Fredrickson, 1998), in which positive emotions result in the building of social, intellectual, and physical resources by broadening action tendencies and generating psychological resources (Salovey, Rothman, Detweiler, & Steward, 2000). Thus, social and psychological resources available to individuals high in trait PA may be drawn upon when challenged with stressful events. Regardless of whether PA influences health through direct effects or by buffering stress, there is some evidence for specific biological mechanisms that may tie PA to health, including neuroendocrine and immune function (Cohen et al., 2003; Marsland, Cohen, Rabin, & Manuck, 2006; Steptoe, Wardle, & Marmot, 2005). An additional biological mechanism that may explain links between trait PA and health is processes involved in skin repair and wound healing, which are clinically relevant and can be measured in a brief period of time in healthy individuals. The skin is the largest organ of the body. The outermost layer of the skin, the stratum corneum, has a number of protective “barrier” functions, including defending against microbes; keeping the skin cohesive and intact despite physical damage; protecting the interior against chemical absorption, ultraviolet rays, and extreme temperature; and preventing water loss (Elias, 2005). If the skin barrier is compromised by wounding, all the previously described functions are impaired, which further impair recovery from skin damage, protection against future damage, and susceptibility to infectious illness. Much like inflammatory processes, which have multiple effects on the organism and are of considerable interest to health psychologists (Kiecolt-Glaser, McGuire, Robles, & Glaser, 2002), problems with skin repair and wound healing extend to other important biological activities that protect and preserve our health. More generally, wound healing provides a model system for understanding the impact of psychological factors on health within a short period of time. Exposure to acute and chronic stress is related to delayed healing of full-thickness wounds (e.g., punch biopsy) that penetrate both the epidermis and underlying dermis (reviewed in Christian, Graham, Padgett, Glaser, & Kiecolt-Glaser, 2006). Psychological stress may also disrupt the skin’s ability to recover its function as a barrier against moisture loss and pathogens after more minor disruption, such as damage to the stratum corneum. Across several studies, skin barrier recovery was reduced by 10%–15% following a brief laboratory stressor (Altemus, Rao, Dhabhar, Ding, & Granstein, 2001; Robles, 2007). Approximately 30% recovery was achieved at 3 h after skin disruption during medical school examinations, compared to 45% recovery during the end of winter and spring vacation (Garg et al., 2001). These studies suggest that skin barrier recovery may be a useful model for examining the impact of psychosocial factors such as psychological stress on health and suggest a pathway through which trait PA may impact health. However, few studies published to date have explored the role of individual difference characteristics, such as trait PA, on wound healing in response to stress. This study tested whether individual differences in trait PA are related to skin barrier recovery, and whether the role of trait PA in wound healing is consistent with the direct effects model or the stress-buffering model. In this study, we assessed trait levels of PA and negative affect (NA) in participants, who were then randomly assigned to go through a brief psychological stressor or no stressor. The direct effects model predicts that individuals with greater trait PA will show faster skin barrier recovery, regardless of the presence of psychological stress, while the stress-buffering model predicts that greater trait PA will be related to faster skin barrier recovery in individuals undergoing a stressor. Based on previous work on the effects of PA on reducing the negative psychological and biological impact of psychological stress (Steptoe et al., 2005; Tugade & Fredrickson, 2004) and the effects of psychological stress on skin barrier recovery (Altemus et al., 2001; Garg et al., 2001), we predicted that greater trait PA would be related to faster skin barrier recovery following exposure to a laboratory stressor, consistent with the stress-buffering model.