Social Support Can Buffer against Stress and Shape Brain Activity

Abstract

Social support from close relationship partners is an important resource for coping with stress, particularly during childhood. We discuss ethical challenges associated with studying stress and its social buffering in the laboratory, as well as emerging evidence regarding two potential neural substrates for the social buffering of stress: hypothalamic oxytocin activity and activation of areas in the prefrontal cortex associated with effective self-regulation. We also address the role of early-life social experiences in shaping brain development, as well as recommendations for practice and policy that would advance the ethical treatment of children and reduce social inequalities in early-life experiences and opportunities-e.g., investing in programs that prevent child maltreatment and facilitating access to high-quality child care for economically disadvantaged families. We also debate the ethical implications of using oxytocin nasal sprays to simulate the stress-reducing properties of social support and advise waiting for more evidence before recommending their use.

Keywords: HPA axis; cortisol; oxytocin; prefrontal cortex; social support; stress.

Figure 1

A developmental working model of the social buffering of the hypothalamic–pituitary–adrenal (HPA) axis in humans. Early-life social experiences are thought to shape the later effectiveness of social buffering of the HPA axis. Additionally, two sets of biological mechanisms are proposed to mediate the effect of social support on HPA reactivity to stressors: oxytocinergic functioning, including patterns of oxytocin release and receptor distribution; and PFC-based safety signaling/neural priming by stimuli associated with attachment figures. The role of other biological mediators (e.g., dopamine, serotonin, opioids, epinephrine, norepinephrine) has been suggested by some studies with nonhuman animals, but more research is needed to characterize their role in the social buffering of the HPA axis in humans. OT = oxytocin; vmPFC = ventromedial prefrontal cortex; Epi = epinephrine; NE = norepinephrine. Reprinted with permission from Hostinar, C. E., Sullivan, R. M., & Gunnar, M. R. (2014). Psychobiological mechanisms underlying the social buffering of the HPA axis: A review of animal models and human studies across development. Psychological Bulletin, 140(1), 256-282. Copyright 2014 by the American Psychological Association.