This study extends previous work on stress and wound healing by demonstrating that trait PA buffered the effects of stress on skin barrier recovery. Specifically, individuals with greater trait PA showed faster skin barrier recovery within 1 hr after skin disruption, and that faster recovery was maintained up to 2 hr after disruption. Trait PA was not significantly related to skin barrier recovery in individuals who did not undergo the psychological stressor. Thus, these data support the stress-buffering model of the effects of trait PA on health (Pressman & Cohen, 2005
). The effects of trait PA on skin barrier recovery were independent of the effects of trait NA, which is worth noting because considerable evidence suggests that NA is related to poor health outcomes (Kiecolt-Glaser et al., 2002
). We included NA in our analyses to ensure that the effects of PA on skin barrier recovery were not driven by the effects of NA. The magnitude of the effect of PA on skin barrier recovery was similar to the effect size of psychological stress on skin barrier recovery reported in previous studies (r
= .36, derived from Altemus et al., 2001
, and Robles, 2007
). Notably, we found effects for trait PA on biological responses to stress, whereas most studies of PA and biological responses to stress have focused on inducing positive mood states.
To impact skin barrier recovery, psychological factors would have to affect key biological processes involved in skin barrier recovery (lipid synthesis and inflammation; Elias, 2005
) through mechanisms that communicate psychosocial “messages” to the skin. Several candidate messenger systems that could explain links between trait PA and skin barrier recovery are systemic glucocorticoids, neuropeptide release from afferent nerves in the peripheral nervous system, and activation of immune and inflammatory processes in the skin (Garg et al., 2001
). Although studies in rodent models clearly show that elevated glucocorticoids can delay skin barrier recovery (Choi et al., 2005
), we and others previously showed that salivary cortisol levels during stress were not related to skin barrier recovery (Altemus et al., 2001
; Robles, 2007
). Thus, beyond glucocorticoid levels, psychosocial factors may influence neuropeptide and neurotransmitter release in the skin (e.g., substance P, norepinephrine, acetylcholine; Arck, Slominski, Theoharides, Peters, & Paus, 2006
), but no empirical studies to date have studied psychological factors in humans and skin levels of neuropeptides and neurotransmitters. Finally, psychological factors such as trait PA may influence immune processes in the skin. While no studies have explicitly studied trait PA and immune mechanisms involved in wound healing, several studies suggest that state PA can influence skin response to allergens. A reduction in allergic response was found when pleasantness and relaxation were induced by hypnosis (Laidlaw, Booth, & Large, 1996
) and when humor was induced by a movie (Kimata, 2001
). Moreover, greater self-reported vigor was related to smaller allergy responses (Laidlaw, Booth, & Large, 1994
). Thus, the precise biological mechanisms through which trait PA acts on the epidermis are not known, but several candidates are possible for future exploration.
One notable finding in this study is that skin barrier recovery was highest level at 1 – 1.5 hr after disruption, and decreased slightly at 2 hr after disruption. Few studies have reported the hour-to-hour kinetics of skin barrier recovery. Thus, the extent to which our U-shaped results are similar to other work is unknown. Potential explanations for the increase, followed by a decrease in recovery must be consistent with several observations in our data. The explanations and mechanisms must covary with performing a mental task (No Stress and Stress groups showed a U-shaped curve), and be specific to processes related to skin barrier recovery and not basal TEWL, as basal TEWL did not significantly change across the session, and the kinetics of basal TEWL did not differ across groups. One possibility is sweating, which can increase TEWL and thereby decrease skin barrier recovery (Rogiers & EEMCO Group, 2001
). Individuals low in trait PA may have been sweating more during the TSST, which may explain why their TEWL was higher in the 1 – 1.5 hr after tape-stripping. However, increased sweating would not be consistent with our basal TEWL findings or with lower skin barrier recovery 2 hr after tape-stripping (up to 1.5 hr after the TSST). A more plausible explanation is increased skin surface temperature, potentially caused by increased blood flow to the skin. Experimentally raising skin surface temperature for 1 hr after tape-stripping results in faster recovery, which persists up to 6 h after skin disruption (Denda, Sokabe, Fukumi-Tominaga, & Tominaga, 2007
). Moreover, increased skin blood flow after removing occlusion corresponds with decreased TEWL and faster recovery after disruption (Rodrigues, Pinto, Magro, Fernandes, & Alves, 2004
). However, increased skin surface temperature should be related to elevated basal TEWL, which is not consistent with our results. Future work should consider measuring these potential mechanisms, including local skin blood flow and skin conductance.
The limitations of this study provide areas of improvement for future work. We used a single self-report measure of trait affect, which may be less reliable compared to multiple measures of daily affect over several weeks (Cohen et al., 2003
). In addition, our trait affect measure was not administered to the entire sample (n
= 85, compared to n
= 60 in this study). Moreover, our findings may reflect a limited range of PA and NA, and future work should obtain a wider range of individual differences in trait affect through larger and more representative samples. For example, this study does not generalize to older, less educated, or less healthy individuals. Future work should also incorporate additional facets of positive emotions, such as those developed in the expanded version of the PANAS (PANAS-X; Watson & Clark, 1999
). Although we experimentally manipulated stress, we did not manipulate levels of PA; thus, the conclusions regarding the relationship between PA and skin barrier recovery should be considered correlational and not causal. Finally, future work should measure the skin barrier recovery process as it unfolds over several days, rather than hours.
What are the implications of these findings for the larger literature on PA and health? Moreover, how might the effects of trait PA on the healing of a relatively minor wound translate to long-term effects of trait PA on health? The skin serves as the first line of defense against foreign pathogens (Elias, 2005
). Thus, delays in skin barrier recovery in a particular area of the skin represent a “leak” in the body’s defenses, increasing the probability of foreign pathogens penetrating the skin and spreading to inner tissues. Therefore, a faster healing skin barrier during stressful periods, perhaps observed in individuals with greater trait PA, may reduce the probability of certain pathogens migrating from the skin surface to the interior. Beyond risk of infection, which would be relevant to most individuals (though more pronounced in older adults), trait PA may play a role in disease progression in individuals who have certain skin diseases that may be exacerbated by stress, such as psoriasis or atopic dermatitis, though this is an empirical question that should be addressed with future research. More broadly, relationships between trait PA and skin barrier recovery may reflect a larger link between PA and biological mechanisms that influence health and disease in other organ systems, such as the cardiovascular system. Establishing that trait PA can literally “get under the skin” is an important first step in determining the many ways in which trait PA benefits health.