Social Safety Theory: A Biologically Based Evolutionary Perspective on Life Stress, Health, and Behavior

Abstract

Social Safety Theory hypothesizes that developing and maintaining friendly social bonds is a fundamental organizing principle of human behavior and that threats to social safety are a critical feature of psychological stressors that increase risk for disease. Central to this formulation is the fact that the human brain and immune system are principally designed to keep the body biologically safe, which they do by continually monitoring and responding to social, physical, and microbial threats in the environment. Because situations involving social conflict, isolation, devaluation, rejection, and exclusion historically increased risk for physical injury and infection, anticipatory neural-immune reactivity to social threat was likely highly conserved. This neurocognitive and immunologic ability for humans to symbolically represent and respond to potentially dangerous social situations is ultimately critical for survival. When sustained, however, this multilevel biological threat response can increase individuals' risk for viral infections and several inflammation-related disease conditions that dominate present-day morbidity and mortality.

Keywords: affiliation; belonging; disease; evolution; health; inflammation.

Figures

Figure 1

Social Safety Theory is grounded in the understanding that the primary purpose of the human brain and immune system is to keep the body biologically and physically safe. To accomplish this challenging task, humans developed a fundamental drive to create and maintain friendly social bonds and to mount anticipatory biobehavioral responses to social, physical, and microbial threats that increased risk for physical injury and infection over the course of evolution. (a) Accordingly, the brain continually monitors the (❶) social environment, interprets social signals and behaviors, and judges the extent to which its surroundings are socially safe versus threatening. These appraisals are subserved by the (❷) amygdala network, mentalizing network, empathy network, and mirror neuron system (i.e., the social brain). When a potential social threat is perceived, the brain activates a multilevel response that is mediated by several social signal transduction pathways—namely, the (❸) SNS, (❹) HPA axis, (❺) vagus nerve, and (❻) meningeal lymphatic vessels. These pathways enable the brain to communicate with the peripheral immune system and vice versa. Whereas the main end products of the SNS (i.e., epinephrine and norepinephrine) suppress transcription of antiviral type I interferon genes (e.g., IFNA, IFNB) and upregulate transcription of proinflammatory immune response genes (e.g., IL1B, IL6, TNF), the main end product of the HPA axis (i.e., cortisol) generally reduces both antiviral and inflammatory gene expression but also can lead to increased inflammatory gene expression under certain physiologic circumstances (e.g., glucocorticoid insensitivity/resistance). The vagus nerve in turn plays a putative role in suppressing inflammatory activity, whereas meningeal lymphatic vessels enable immune mediators originating in the CNS to traffic to the periphery, where they can exert systemic effects. (b) This multilevel “Biobehavioral Response to Social Threat” is critical for promoting well-being and survival. However, it can also increase risk for negative health and behavioral outcomes when it is sustained by internal physiologic or external social recursion. Several factors can also moderate these effects, including birth cohort, childhood microbial environment, sleep, genetics, air pollution, diet, and self-harm behavior. A person’s developmentally derived social safety schemas play a particularly important role in this multilevel process as they shape how social-environmental circumstances are appraised. Social safety schemas thus influence neurocognitive dynamics that initiate the full range of downstream biological interactions that ultimately structure disease risk and human behavior. Abbreviations: ACTH, adrenocorticotropin hormone; ADRB2, β2-adrenergic receptor; CNS, central nervous system; CRH, corticotropin-releasing hormone; CSF, cerebrospinal fluid; DAMPs, damage-associated molecular patterns; HPA, hypothalamic– pituitary–adrenal; PRR, pattern recognition receptor; SNS, sympathetic nervous system. Adapted with permission from Slavich & Cole (2013), SAGE Publishing; Slavich & Irwin (2014), American Psychological Association; and Slavich & Sacher (2019), Springer Nature.

Figure 2:

Individuals are embedded in a variety of social safety circles that determine their moment-to-moment and lifelong experiences of social safety and threat. These social networks directly affect human health and behavior by influencing the extent to which people are exposed to objective forms of social safety (e.g., strong family cohesion, welcoming neighbors, inclusive public policy) and social threat (e.g., family conflict, hostile neighbors, divisive public policy). In addition, these networks indirectly affect health and behavior by exposing individuals to construals, messages, and meanings that shape their social safety schemas, which in turn influence their perceptions of the surrounding environment as being socially safe versus threatening. Strategies for promoting social safety can target any of these circles to promote social safety and reduce social threat as a means of improving human health and behavior.