Research in our laboratory integrates social psychological theory and methods with pharmacological, genetic, and neuroimaging methods, which is referred to as the social neurochemistry approach. The lab is now almost exclusively focused on the bidirectional relationships between the social realm and the immune system, as described below and depicted in the social and affective immunology model shown in the figure.

Social and Affective Influences on Health

Self-assessment of perceived social support is the most robust behavioral or psychosocial predictor of longevity. Nonresolving inflammation, which reflects persistent activation of a portion of the immune system, is one of the key pathways by which social relationships have these health effects (Uchino & Way, 2017). Markers of non-resolving inflammation such as C-Reactive Protein (CRP) are increased by chronic social stress and robustly predict multiple health endpoints like cancer and cardiovascular disease (Fagundes & Way, 2014).

Social & Affective Immunology Model.jpg

In the lab, these social factors are studied at multiple levels from the  sociocultural to the individual. For example, we are currently using GPS tracking to study adolescent's social environmental exposures (e.g. time spent on streets with high levels of violent crime) on both neural and immune activity. We also have ongoing studies looking at the effects of social media use on inflammation. In addition, we have also found that religious influences on health are dependent on cultural region (Wallace et al., 2018) and are using GPS data to improve measurement of religious behavior and its biological effects.

We are also focused on specific psychological pathways that influence inflammation. For example, we found that the relationship between social support and C-Reactive Protein (CRP) was moderated by self-esteem in a national sample of midlife adults (Lee & Way, 2018). People with a positive self-view appeared to be able to rely on others for support and are buffered from stress-related inflammation, while the same benefits did not seem to apply to those with a negative self-view. In other ongoing research, we have found that both negative as well as positive valence weighting bias (Fazio, et al., 2015) are positively related to longitudinal increases in CRP (Keaveney dissertation).

Effects of Inflammation on Socio-Emotional Processes

Heightened peripheral inflammation is associated with increased probability of future depression, substance abuse, and PTSD. Similarly, experimental studies that induce peripheral inflammation can induce depression-like states and sickness behaviors (e.g. social avoidance, fatigue). Therefore, we have been focused on the question: is inflammation a mediator of the behavioral sequelae of stressful events and if so, how?

Because a critical effect of peripheral inflammation is to increase prostaglandins in the brain, we have been studying the effects of drugs that inhibit prostaglandins on social behavior. In particular, we have found that acetaminophen (active ingredient in Tylenol) alters important social processes including trust behavior (Roberts et al., 2018; 2019), risk-taking behavior (Keaveney, Peters, & Way, 2020), empathy (Misschkowski et al., 2016), and aggression (Mischkowski et al; in prep).

A current focus is on determining if blunting of affect is a mechanism explaining these effects. Consistent with social sensitivity theory (Way & Gurbaxani, 2008), acetaminophen blunted evaluations of negative as well as positive emotional images (Durso et al., 2015). These effects appear to be selective for emotionality rather than extremity (Rocklage et al., under review). We are working on fashioning these results into a larger theory of prostaglandins, stress, and their influence on affect and cognition.