Research in our laboratory integrates social psychological theory and methods with pharmacological, genetic, and neuroimaging methods, which we have 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 with a particular emphasis on the neural mediators between these domains. Each path (social to immune and immune to social) is described below and depicted in the social and affective immunology model shown in the adjacent figure. Read on to learn about the specific ways we are studying social psychoneuroimmunology.
Social and Affective Influences on the Brain and Immune System
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; American Psychologist). 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; Current Directions in Psychological Science). In the lab, these social factors are studied at multiple levels from the sociocultural to the individual. Currently in 2024, we are focusing on 3 funded projects:
• Influence of Social Media Use on Inflammation Physical Health (R01MH135501)
The past decade has witnessed a sharp increase in the depression rates of adolescents, particularly teenaged girls. One common hypothesis for this change is the rapid spread of social media use among adolescents. Because inflammation is a well-documented risk-factor for depressive symptomatology, we have begun a line of studies examining the relationship between time spent using social media and inflammation. In our cross-sectional studies (Lee, Jiang, Crocker & Way, 2022; Cyberpsychology; Lee, Jiang, Crocker, & Way, 2023; Journal of Medical Internet Research), we have found that greater social media use is associated with greater inflammation. Furthermore, our longitudinal studies (Lee, Jiang, Crocker, & Way, 2023; Brain, Behavior, and Immunity; Lee, Jiang, Crocker, & Way 2023; Journal of Medical Internet Research) have shown that social media use increases inflammation and, conversely, that inflammation can also increase social media use. We are currently testing a model in adolescents where different facets of social media use (e.g. passive use that leads to greater envy and social comparison) is a stressor that elicits affective changes as well as alterations in parasympathetic nervous system activity, leading to increases in inflammation. We are also testing how effective social media use is as a coping strategy for geospatially measured stressors (e.g. walking down a crime-ridden block) or ecological momentarily assessed stressors.
• Neighborhood Influences on the Brain, Health and Substance Use (R01DA042080)
Living in a neighborhood with high levels of crime, poverty, and vandalism can increase inflammation and other markers of health risk. However, the bulk of evidence for these effects is based on data acquired using one’s home address as a measure. In actuality, many adolescents do not spend a large proportion of their time in the vicinity of their home. Therefore, our team has adopted novel GPS-based methods to measure with greater precision exposure to geospatial risk factors (e.g. time spent on streets with violent crime) and protective factors (e.g. time spent in green space) in order to determine how they sculpt development of the adolescent brain and immune system.
In a project funded by the National Institutes of Drug Abuse, we are longitudinally measuring these geospatial influences in a large socioeconomically, racially, and geospatially diverse cohort of adolescents living within the Interstate 270 beltway surrounding the city of Columbus. The study consists of in-home interviews of the adolescent and a parent, one week of ecological momentary self-reported assessment of emotional and social experiences along with geospatial tracking, and then an MRI neuroimaging season at Ohio State with the collection of biosamples to measure markers of stress and immune function.
The goal is test the Neural Embedding Model of Environmental Stress Induced Substance Use (NEMESIS), which hypothesizes that during adolescence there is a window of vulnerability where the stress of EtV elicits a recalibration of the neural circuits underlying emotion reactivity and regulation as part of adapting to this more stressful environment. This is hypothesized to lead to an integrated set of psychological changes, including increased risk-taking, impulsivity, reward-seeking, and threat reactivity. These stress-induced changes, in turn, perpetuate the addiction cycle (initiation, escalation, and dependence). Therefore, the neuroimaging session focuses on identifying neural differences in threat and reward reactivity as well as executive function. We are also determining the degree to which the behavioral and neural changes resulting from adversity are mediated by inflammatory processes. It is hoped that by better understanding these processes we will be able to identify neighborhood, community, and interpersonal factors that can bolster adolescent’s resilience.
• Effects of Religious Involvement on Health (JTF 61803)
Over the last several decades, there has been an accumulation of evidence indicating that religious involvement can have beneficial effects on physical health (VanderWeele, 2017). However, this evidence has primarily relied on self-reported religious service attendance, which can be biased. In work funded by the Templeton Foundation, we are supplementing traditional self-reported measures of religious involvement with geospatial diaries and GPS-based measures of time spent at a religious institution to obtain a more comprehensive picture of religious involvement. We will be determining the relationship between these measures of religious involvement and longitudinal changes in cumulative exposure to the stress related hormone cortisol, as measured in head hair of both adolescents and adults. Secondary goals of the project are to determine if religious involvement buffers the effects of stressors and whether there are racial differences in these effects.
Effects of Anti-Inflammatory Drugs (e.g. Tylenol) 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 and their influence on affect and cognition.