Throughout human evolution, individuals have developed a tendency to form connections with others in order to counter external threats and ensure their survival. These social connections provide individuals with social support, and the phenomenon in which social support buffers the effects of stress and promotes physical and mental well-being is referred to as the social buffering effect. In this study, we systematically reviewed relevant animal and human studies, exploring how individuals perceive or receive social support through social relationships to mitigate stress.

Most animal studies on social buffering are conducted in laboratories, mainly using rodents and non-human primates, with common stressors such as novel environments, restraint, and electric shocks. These studies often employ two main paradigms: (a) exposure-type, in which both the subject and a partner experience the stressor together, and (b) housing-type, in which the subject receives support from a partner after exposure to stress. Social buffering can be maternal, mate, or conspecific. Maternal buffering is most effective early in life, primarily by inhibiting the release of norepinephrine to the paraventricular nucleus of the hypothalamus, thereby suppressing the HPA axis. As the offspring mature, the social buffering effect of the mother diminishes, and partners and peers become important sources of buffering, which is mainly associated with the ventromedial prefrontal cortex (vmPFC) and the anterior cingulate cortex (ACC). Recent research suggests that the effects of social buffering can persist, with findings indicating that neural mechanisms in the hypothalamus and amygdala contribute to this prolonged effect. Social buffering has also been observed in various other social species, including fish, birds, pigs, and cattle, highlighting its broad applicability.

In human studies on social buffering, common stressors include pain (e.g., electric, heat, or cold) and social stress (e.g., the Trier Social Stress Test or social exclusion). Social support, whether provided by real or virtual figures, has been shown to reduce pain perception and alleviate fear responses. The sources of social buffering vary by life stage. In infancy and childhood, parents provide the main buffering effect. As individuals reach adolescence, peer relationships, including friendships, become more significant, though sometimes these relationships can increase stress due to peer pressure. In adulthood, social buffering in romantic relationships is studied, with support provided either actively (e.g., physical touch, visual or auditory support) or passively (e.g., partner presence or imagined support). Interestingly, social buffering extends beyond romantic relationships, with friends, siblings, and even strangers offering support. The type of social support and gender differences play a role in buffering. While strangers can provide social support, support from close relationships tends to be more effective. Moreover, women benefit more from same-gender stranger touch, while men respond better to opposite-gender touch. However, these gender differences diminish when support is passive or indirect.

Social buffering effects are primarily mediated by reducing the activity of stress systems like the autonomic nervous system (ANS) and HPA axis. The HPA axis involves the hypothalamus, pituitary, and adrenal glands, with cortisol (or corticosterone in rodents) being released in response to stress. Social buffering modulates this system by regulating neuropeptides (e.g., oxytocin, vasopressin) and activating or inhibiting brain regions related to stress (e.g., amygdala, prefrontal cortex, hippocampus), thus reducing stress responses. Oxytocin plays a key role by downregulating HPA activity and affecting regions related to fear and attachment. In contrast, vasopressin, which antagonizes oxytocin, may contribute to stress responses, though its precise role in social buffering is less clear. The prefrontal cortex is involved in regulating stress responses, with social support activating this region and reducing fear-related activity. The amygdala, crucial for processing threat and fear, is also influenced by social buffering, where oxytocin release inhibits its activation, reducing threat responses. Lastly, the hippocampus, involved in memory and stress recovery, helps regulate the HPA axis and is protected from stress effects through social support. These neurobiological mechanisms illustrate how social buffering operates to mitigate stress and maintain physiological balance. In summary, the social buffering effect relies on the coordinated interaction between neuropeptides and key brain regions such as the prefrontal cortex and the limbic system, with oxytocin (OT) playing a central role.

Future research should further explore the physiological mechanisms of social buffering, such as olfactory cues, and employ more dynamic, real-world experimental designs. Additionally, the impact of parasocial relationships with virtual or AI companions on stress relief needs further exploration, while cross-species buffering, particularly between humans and pets, could reveal shared neurobiological responses. Finally, the social buffering effect plays a role in the intervention and treatment of psychological disorders. It may be incorporated into systematic desensitization therapy, integrated into standard cognitive behavioral therapy protocols, or combined with physical interventions, such as non-invasive.