The Neuroendocrinology of Social Isolation

Cacioppo, John T.; Cacioppo, Stephanie; Capitanio, John P.; Cole, Steven W.

doi:10.1146/annurev-psych-010814-015240

Cited by 649 publications

(533 citation statements)

References 127 publications

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“…Apart from being intrinsically rewarding and motivating, social interactions (or their absence) can also constitute an important stressor [71,72], which may be particularly true for individuals for whom positive reinforcement in social interactions is very important and/or for individuals who react strongly to signs of social rejection or inclusion [73,74]. Indeed, neuroimaging studies have found reduced brain activations in rewardrelated neurocircuitry during depressive episodes ( [75][76][77]; see tables 1 and 2), but social interaction-based rewards have not yet been systematically studied.…”

Section: (C) the Case Of Depressionmentioning

confidence: 99%

Towards a second-person neuropsychiatry

Schilbach

2016

Phil. Trans. R. Soc. B

192

163

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Psychiatric disorders can affect our ability to successfully and enjoyably interact with others. Conversely, having difficulties in social relations is known to increase the risk of developing a psychiatric disorder. In this article, the assumption that psychiatric disorders can be construed as disorders of social interaction is reviewed from a clinical point of view. Furthermore, it is argued that a psychiatrically motivated focus on the dynamics of social interaction may help to provide new perspectives for the field of social neuroscience. Such progress may be crucial to realize social neuroscience's translational potential and to advance the transdiagnostic investigation of the neurobiology of psychiatric disorders

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Section: (C) the Case Of Depressionmentioning

confidence: 99%

Towards a second-person neuropsychiatry

Schilbach

2016

Phil. Trans. R. Soc. B

192

163

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“…For social species, the perception of being socially isolated even when in the presence of others signals danger and evokes a dysphoric state termed loneliness in humans (Cacioppo et al, , 2015a. A variety of biological mechanisms have evolved that capitalize on aversive signals to motivate people to act in ways that are essential for reproduction and survival.…”

Section: Introductionmentioning

confidence: 99%

Genome-Wide Association Study of Loneliness Demonstrates a Role for Common Variation

Gao

Davis

Hart

et al. 2016

Neuropsychopharmacol

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Loneliness is a complex biological trait that has been associated with numerous negative health outcomes. The measurement and environmental determinants of loneliness are well understood, but its genetic basis is not. Previous studies have estimated the heritability of loneliness between 37 and 55% using twins and family-based approaches, and have explored the role of specific candidate genes. We used genotypic and phenotypic data from 10 760 individuals aged ⩾ 50 years that were collected by the Health and Retirement Study (HRS) to perform the first genome-wide association study of loneliness. No associations reached genome-wide significance (p45 × 10 − 8 ). Furthermore, none of the previously published associations between variants within candidate genes (BDNF, OXTR, RORA, GRM8, CHRNA4, IL-1A, CRHR1, MTHFR, DRD2, APOE) and loneliness were replicated (p40.05), despite our much larger sample size. We estimated the chip heritability of loneliness and examined coheritability between loneliness and several personality and psychiatric traits. Our estimates of chip heritability (14-27%) support a role for common genetic variation. We identified strong genetic correlations between loneliness, neuroticism, and a scale of 'depressive symptoms.' We also identified weaker evidence for coheritability with extraversion, schizophrenia, bipolar disorder, and major depressive disorder. We conclude that loneliness, as defined in this study, is a modestly heritable trait that has a highly polygenic genetic architecture. The coheritability between loneliness and neuroticism may reflect the role of negative affectivity that is common to both traits. Our results also reflect the value of studies that probe the common genetic basis of salutary social bonds and clinically defined psychiatric disorders.

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“…An important question concerns the biological mechanisms linking childhood trauma, defensive programming of stress response systems, and health risk in adulthood. Stress-related alterations in immune response gene expression programs have been hypothesized to be one of the pathways through which environmental adversity influences disease processes (Irwin and Cole, 2011;Cacioppo et al, 2015). A growing number of studies in adults experiencing a range of current chronic stressors or adversities have shown that immune response genes are highly sensitive to social-environmental conditions.…”

Section: Introductionmentioning

confidence: 99%

Altered Stress-Induced Regulation of Genes in Monocytes in Adults with a History of Childhood Adversity

Schwaiger

Grinberg

Moser

et al. 2016

Neuropsychopharmacol

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Exposure to serious or traumatic events early in life can lead to persistent alterations in physiological stress response systems, including enhanced cross talk between the neuroendocrine and immune system. These programming effects may be mechanistically involved in mediating the effects of adverse childhood experience on disease risk in adulthood. We investigated hormonal and genome-wide mRNA expression responses in monocytes to acute stress exposure, in a sample of healthy adults (n = 30) with a history of early childhood adversity, and a control group (n = 30) without trauma experience. The early adversity group showed altered hypothalamus-pituitaryadrenal axis responses to stress, evidenced by lower ACTH and cortisol responses. Analyses of gene expression patterns showed that stress-responsive transcripts were enriched for genes involved in cytokine activity, cytokine-cytokine receptor interaction, chemokine activity, and G-protein coupled receptor binding. Differences between groups in stress-induced regulation of gene transcription were observed for genes involved in steroid binding, hormone activity, and G-protein coupled receptor binding. Transcription factor binding motif analysis showed an increased activity of pro-inflammatory upstream signaling in the early adversity group. We also identified transcripts that were differentially correlated with stress-induced cortisol increases between the groups, enriched for genes involved in cytokine-cytokine receptor interaction and glutamate receptor signaling. We suggest that childhood adversity leads to persistent alterations in transcriptional control of stress-responsive pathways, which-when chronically or repeatedly activated-might predispose individuals to stress-related psychopathology.

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The Neuroendocrinology of Social Isolation

Cited by 649 publications

References 127 publications

Towards a second-person neuropsychiatry

Towards a second-person neuropsychiatry

Genome-Wide Association Study of Loneliness Demonstrates a Role for Common Variation

Altered Stress-Induced Regulation of Genes in Monocytes in Adults with a History of Childhood Adversity

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