Bi-Directional Links Between Social Stress and Inflammation
In addition to my interest in health disparities, I have a complementary line of research that investigates the relationship between stress and health more generally. This area of my work focuses on understanding the bi-directional links between social stress and inflammation. I am particularly interested in inflammation as a biomarker of stress and mechanism linking the social world and health because of its established role in the onset and course of many physical and mental health conditions (e.g., some cancers, cardiovascular disease, diabetes, major depression). Interestingly, while stress can lead to increases in inflammation, recent research suggests that inflammation can also feed back to the brain to influence mood and social behavior. As such, inflammation represents a key physiological process linking the brain and body, and may represent a “final common pathway” linking stress and a number of chronic diseases.
From Brain to Body: Neurocognitive Processes Linking Stress and Inflammation.
One of my most novel findings in this area of research shows that acute stress is linked to changes in the genes that are being expressed in immune cells. Specifically, after going through a stressor involving negative social evaluation, participants showed increased expression of genes involved in inflammation (Muscatell et al., in prep). Interestingly, individuals differed in the degree of gene expression they showed in response to the stressor. In particular, those who showed greater activity in a key threat-related region (i.e., pregenual anterior cingulate cortex) also showed greater changes in inflammatory gene expression. This is the only known study to link neural responses to stress and changes in gene expression, and adds to a growing body of research in “human social genomics” suggesting that exposure to adverse life experiences leads immune cells to over-express genes involved in inflammation, which may lead to disease.
From Body to Brain: Inflammation Causes Increases in Neural Sensitivity to Stress.
On the flip side, I have also investigated how increasing levels of inflammation can influence perceptions of the social world and neural responses to social stress. These studies utilize methods from psychopharmacology to experimentally-induce an inflammatory response by exposing participants to an antigen that causes a safe, time-limited increase in inflammation. Thus, I create a temporary physiological state akin to what individuals suffering from an acute infection are experiencing, and examine how it affects perceptions of the social world and neural reactivity to social threat. This allows me to circumvent the issue of reverse causation that plagues the majority of studies investigating stress and illness, as I have randomly assigned participants to experience a physiological condition often seen in chronic disease, and measured the corresponding changes in stress reactivity.
Results from this study have proved informative, and in some cases, surprising. For example, I found that individuals exposed to an inflammatory challenge showed greater threat-related neural activity in response to receiving negative social feedback (Muscatell et al., under review). This makes good sense: While in a vulnerable physiological state akin to sickness, one needs to be especially attuned to potential threats in the environment. More surprisingly, I also found that elevated inflammation was associated with greater reward-related neural activity in response to receiving positive feedback (Muscatell et al., under review). In other words, when levels of inflammation are heightened, the brain is also more sensitive to friendly, supportive information, thus suggesting a possible mechanism underlying the effects of social support and connection on disease outcomes. Together, these findings help shed light on the neural and psychological changes that take place when levels of inflammation are elevated, such as in chronic disease states or among individuals with low SES.