Sports Medicine Research: In the Lab & In the Field: Social Interactions may Influence Inflammation (Sports Med Res)
Tuesday, January 31, 2012

Social Interactions may Influence Inflammation

Negative and competitive social interactions are related to heightened proinflammatory cytokine activity

Chiang J, Eisenberger NI, Seeman TE, Taylor SE. Proc Natl Acad Sci U S A. 2012. Epub Jan 23.

Research has consistently demonstrated that psychosocial factors can influence inflammation in the body (e.g., stressful events may increase inflammation). Unfortunately, it’s still unclear what kind of events may be related to inflammation; especially when we consider multiple exposures. Therefore, Chiang et al evaluated if daily social interactions among 122 healthy young adults to determine if these interactions relate to systematic concentrations of proinflammatory mediators (measured via oral collection) at rest and after acute stress. Social interactions were classified into 3 categories: negative (e.g., conflict with another person), competitive (e.g., competing for attention, academic competition, games) and positive (e.g., time with friends, support from partner) daily interactions. Participants completed nightly diaries for 8 days to report the number of negative and positive social interactions as well as the most negative, positive, and competitive interaction they had that day. The total number of social interactions over 8 days was then calculated for each classification. Then within 4 days of finishing their diary, the participants completed the Trier Social Stress Test, a lab-based social-stress task. Levels of 2 systemic inflammatory mediators were evaluated with oral mucosal transudate (collected oral fluids) before as well as 25 and 80 minutes after the Trier Social Stress Test. More negative social events, during the previous 8 days, was related to higher resting levels of one of the inflammatory mediators. There was also a trend that more competitive social interactions may be related to higher resting systemic inflammation. When the participants were stressed the number of negative social interactions was related to greater levels of systemic inflammatory mediators 25 minutes after the stressor. The authors also explored three subtypes of competitive stress: 1) competitive leisure time activity (e.g., sports), 2) academic/work-related competitive events, and 3) competing for someone’s attention. While the number of leisure competition events did not relate to resting systemic inflammation, more academic/work-related competition and competing for attention events were related to greater resting inflammation. The authors conclude that daily social interactions that are negative and competitive, particularly if not leisure competition, are associated with heightened systemic inflammation that could have implications for mental and physical health outcomes related to inflammation.

This study raises some interesting questions for sports medicine clinicians who are immersed in treating patients with acute and chronic inflammatory conditions as well as athletes (sometimes college and high-school aged) that are exposed to academic and social stress (especially if injured and not participating in team practices). While this study cannot be used to determine if the social interactions led to the inflammation (or vice versa) and it cannot address how these interactions influence healing it should prompt us to pause and think about how we can provide an optimal psychosocial environment to promote healing and the wellbeing of our patients (e.g., counseling, self-meditation, mind-body interventions like Tai Chi, stress relieving drills). Have you noticed that patients experiencing stressful times (e.g., negative or competitive social interactions) are progressing slower than patients with good social support and a positive outlook?

Written by: Jeffrey Driban
Reviewed by:  Stephen Thomas

Related Posts:

Chiang, J., Eisenberger, N., Seeman, T., & Taylor, S. (2012). Negative and competitive social interactions are related to heightened proinflammatory cytokine activity Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1120972109

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