In Sickness and in Health: The Co-Regulation of Inflammation and Social Behavior

Abstract

Although it has commonly been assumed that the immune system and the processes that govern social behavior are separate, non-communicating entities, research over the past several decades suggests otherwise. Considerable evidence now shows that inflammatory processes and social behavior are actually powerful regulators of one another. This review first summarizes evidence that inflammatory processes regulate social behavior, leading to characteristic changes that may help an individual navigate the social environment during times of sickness. Specifically, this review shows that inflammation: (1) increases threatrelated neural sensitivity to negative social experiences (eg, rejection, negative social feedback), presumably to enhance sensitivity to threats to well-being or safety in order to avoid them and (2) enhances reward-related neural sensitivity to positive social experiences (eg, viewing close others and receiving positive social feedback), presumably to increase approach-related motivation towards others who might provide support and care during sickness. Next, this review summarizes evidence showing that social behavior also regulates aspects of inflammatory activity, preparing the body for situations in which wounding and infection may be more likely (social isolation). Here, we review research showing: (1) that exposure to social stressors increases proinflammatory activity, (2) that individuals who are more socially isolated (ie, lonely) show increased proinflammatory activity, and (3) that individuals who are more socially isolated show increased proinflammatory activity in response to an inflammatory challenge or social stressor. The implications of the co-regulation of inflammation and social behavior are discussed.

Psychosocial issues for adolescent and young adult cancer patients in a global context: A forward‐looking approach

“…Similar studies of circulating white blood cells have also documented systematic increases in expression of inflammatory genes and decreases in expression of antiviral (type I interferon) genes in people confronting a diverse array of adverse life circumstances including poverty, post‐traumatic stress, chronic loneliness, low social status, and immanent bereavement . Additional research has shown that activation of inflammatory genes in somatic tissues can signal back to the brain to stimulate negative emotional states, reduce social motivation, and impair problem‐solving skills . Together, these lines of research indicate a bidirectional feedback loop between psychosocial conditions and molecular processes involved in cancer progression and treatment.…”

“…29,30 Additional research has shown that activation of inflammatory genes in somatic tissues can signal back to the brain to stimulate negative emotional states, reduce social motivation, and impair problem-solving skills. 31,32 Together, these lines of research indicate a bidirectional feedback loop between psychosocial conditions and molecular processes involved in cancer progression and treatment. More broadly, this research provides a molecular framework for mapping the biological pathways through which the social determinants of health at the macrolevel ultimately impact disease pathogenesis at the microlevel.…”

Opioids and Social Connection

“…Social factors are also emerging as key contributors to the entire trajectory of disease, from identifying those at risk (e.g., Slavich & Irwin, 2014), to estimating the progression of disease (e.g., Lutgendorf & Sood, 2011), to predicting recovery (e.g., Heilig et al, 2016). Opioids should be considered among other healthrelated pathways in the body (e.g., inflammation; Eisenberger, Moieni, Inagaki, Muscatell, & Irwin, 2017) to better understand how social interactions affect health outcomes. OPIOIDS AND SOCIAL CONNECTION 11 As one example of the translational implications of the current results, opioid medications are often prescribed to aid recovery in addicted populations.…”

Stress and the psyche–brain–immune network in psychiatric diseases based on psychoneuroendocrineimmunology: a concise review

“…This reaction affects social cognition and behavior by enhancing the sensitivity to (thus the saliency of) threatening social experiences, while promoting a behavioral approach toward supportive figures (for a recent review see Ref. ). Stress and inflammation are thus inextricably linked and can influence each other.…”