Neural pathways link social support to attenuated neuroendocrine stress responses.
It is well established that a lack of social support constitutes a major risk factor for morbidity and mortality, comparable to risk factors such as smoking, obesity, and high blood pressure. Although it has been hypothesized that social support may benefit health by reducing physiological reactivity to stressors, the mechanisms underlying this process remain unclear. Moreover, to date, no studies have investigated the neurocognitive mechanisms that translate experiences of social support into the health outcomes that follow. To investigate these processes, thirty participants completed three tasks in which daily social support, neurocognitive reactivity to a social stressor, and neuroendocrine responses to a social stressor were assessed. Individuals who interacted regularly with supportive individuals across a 10-day period showed diminished cortisol reactivity to a social stressor. Moreover, greater social support and diminished cortisol responses were associated with diminished activity in the dorsal anterior cingulate cortex (dACC) and Brodmann's area (BA) 8, regions previously associated with the distress of social separation. Lastly, individual differences in dACC and BA 8 reactivity mediated the relationship between high daily social support and low cortisol reactivity, such that supported individuals showed reduced neurocognitive reactivity to social stressors, which in turn was associated with reduced neuroendocrine stress responses. This study is the first to investigate the neural underpinnings of the social support-health relationship and provides evidence that social support may ultimately benefit health by diminishing neural and physiological reactivity to social stressors.
Eisenberger
Naomi I
NI
Cousins Center for Psychoneuroimmunology, University of California, Los Angeles, CA 90095-7076, USA. neisenbe@ucla.edu
Taylor
Shelley E
SE
Gable
Shelly L
SL
Hilmert
Clayton J
CJ
Lieberman
Matthew D
MD
D000293:Adolescent; D000328:Adult; D002540:Cerebral Cortex / Q000502:physiology; D004644:Emotions / Q000502:physiology; D005260:Female; D006801:Humans; D006854:Hydrocortisone / Q000378:metabolism; D007031:Hypothalamus / Q000503:physiopathology; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging; D008297:Male; D009434:Neural Pathways / Q000503:physiopathology*; D009490:Neurosecretory Systems / Q000503:physiopathology*; D017397:Prefrontal Cortex / Q000502:physiology; D012463:Saliva / Q000737:chemistry / Q000378:metabolism; D012934:Social Isolation; D012944:Social Support; D013315:Stress, Psychological / Q000503:physiopathology*
D006854:Hydrocortisone