Social Rejection: Neurocognitive Pathways and Induction of Inflammatory Responses

Social Rejection Neurocognitive Pathways Induction Inflammatory Responses
Social Rejection – Inflammatory Responses

A study published in the Proceedings of the National Academy of Sciences of the USA (PNAS) indicates that a social stressor involving social-evaluative threat and rejection elicits significant increases in inflammatory activity, as indexed by both soluble receptor for tumor necrosis factor-alpha (sTNFalphaRII) and interleukin (IL)-6.

Humans are social animals by nature. We feel stronger mentally and physically when we believe we belong and are accepted as part of a family, friendship network, tribe or larger cultural group. Thus, loneliness is one of the largest predictors of ill health and early mortality. One specific cause of loneliness is ostracism (‘social rejection’) and is particularly hurtful psychologically and emotionally.

Social rejection occurs when an individual is deliberately excluded from a social relationship or social interaction. The topic includes interpersonal rejection, romantic rejection and familial estrangement. A person can be rejected by individuals or an entire group of people. Furthermore, rejection can be either active, by bullying, teasing, or ridiculing, or passive, by ignoring a person, or giving the “silent treatment”.

As researchers have dug deeper into the roots of rejection, they’ve found surprising evidence that the pain of being excluded is not so different from the pain of physical injury. Rejection also has serious implications for an individual’s psychological state and for society in general. Social rejection can influence emotion, cognition and even physical health.

Interestingly, Roy Baumeister, a social scientist, in a series of experiments conducted with colleagues found that following social rejection people become significantly more aggressive, prone to cheating and risk-taking, and unwilling to help others.

There are many kinds of stressors that increase our risk for disease, but stressors that threaten our social standing, such as targeted rejection, seem to be particularly harmful. Targeted rejection activates the molecular signaling pathways that regulate inflammation. Thus, participants had elevated levels of mRNA for both NF-κB and I-κB, following visits when a recent targeted rejection life event had occurred. Interestingly, the effect was more pronounced in those who perceived their social status to be higher.

Recent evidence indicates that psychological stress may affect the onset or progression of several common human diseases at least in part by up-regulating acute or chronic inflammatory processes.

Among various stressors, it appears that social stress is a particularly strong trigger of inflammation, but the neurocognitive pathways that underlie this effect remain unknown. In particular, no studies to date have investigated the neural regions associated with differences in inflammatory responding to acute social stress. The brain plays a critical role in appraising social stressors, as well as in modulating the immune system’s response to stressors that involve social or physical threat.

Differences in inflammatory responses to social stress may thus be explained, at least in part, by individual differences in activity in neural regions that process social threat-related information.

Prior research has shown that an acute episode of social rejection is linked to activation of specific brain regions such as the dorsal anterior cingulate cortex (dACC) and the anterior insula.

In the PNAS study, George Slavich and colleagues from the University of California, Los Angeles report that a social stressor involving social-evaluative threat and rejection elicits significant increases in inflammatory activity, as indexed by both sTNFαRII and IL-6.

To examine the neurocognitive pathways that might underlie this effect, the authors focused on brain regions previously implicated in processing rejection-related distress and negative affect. Anatomical ROI analyses revealed that greater activity in the dACC and bilateral anterior insula during social exclusion (vs. inclusion) was associated with greater sTNFαRII responses to the laboratory-based social stressor; greater activity in the right anterior insula was marginally related to increases in IL-6. These associations were consistent with whole-brain analyses, which confirmed that greater activity in the dACC and left anterior insula was associated with greater increases in sTNFαRII.

According to the authors this indicates that neural responses to social rejection are associated with potentiated inflammatory responses to an episode of acute social stress. This is consistent with previous studies showing that greater social rejection-induced dACC activity during an fMRI session is associated with greater self-reported distress during daily social interactions.

The authors discuss that brain regions involved in processing social rejection-related information are most likely associated with a variety of biological responses to social and physical threat. Thus, these brain regions may have important implications for health and/or the individual’s susceptibility to inflammatory diseases.

SOURCE:  Proc Natl Acad Sci USA 2010, 107:14817. Epub 2010 Aug 2
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