Black sheep get the blues: A psychobiological model of social rejection and depression

Major life events involving social rejection are strongly associated with onset of depression. To account for this relation, we propose a psychobiological model in which rejection-related stressors elicit a distinct and integrated set of cognitive, emotional, and biological changes that may evoke de...

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Veröffentlicht in:	Neuroscience and biobehavioral reviews Jg. 35; H. 1; S. 39 - 45
Hauptverfasser:	Slavich, George M., O’Donovan, Aoife, Epel, Elissa S., Kemeny, Margaret E.
Format:	Journal Article
Sprache:	Englisch
Veröffentlicht:	Kidlington Elsevier Ltd 01.09.2010 Elsevier
Schlagworte:	5- HTTLPR Adult and adolescent clinical studies Aging Animals Behavioral psychophysiology Biological and medical sciences Cortisol Depression Depression - genetics Depression - physiopathology Depression - psychology Dorsal anterior cingulate cortex Fundamental and applied biological sciences. Psychology Glucocorticoid resistance Humans Immune cell aging Inflammation Life stress Medical sciences Mood disorders Psychology. Psychoanalysis. Psychiatry Psychology. Psychophysiology Psychopathology. Psychiatry Rejection, Psychology Social rejection Stress sensitization Stress, Psychological - physiopathology Stress, Psychological - psychology Glucocorticoid resistance Life stress Stress sensitization 5- HTTLPR Social rejection Dorsal anterior cingulate cortex Depression Cortisol Inflammation Immune cell aging Senescence Central nervous system Review Hydrocortisone Glucocorticoid Encephalon Cingulate cortex Sensitization Ungulata Mood disorder Corticosteroid 5-HTTLPR Steroid hormone Antiinflammatory agent Stress Vertebrata Mammalia Serotonin transporter Animal Adrenal hormone Sheep Models Artiodactyla
ISSN:	0149-7634, 1873-7528, 1873-7528
Online-Zugang:	Volltext
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Abstract	Major life events involving social rejection are strongly associated with onset of depression. To account for this relation, we propose a psychobiological model in which rejection-related stressors elicit a distinct and integrated set of cognitive, emotional, and biological changes that may evoke depression. In this model, social rejection events activate brain regions involved in processing negative affect and rejection-related distress (e.g., anterior insula, dorsal anterior cingulate cortex). They also elicit negative self-referential cognitions (e.g., “I’m undesirable,” “Other people don’t like me”) and related self-conscious emotions (e.g., shame, humiliation). Downstream biological consequences include upregulation of the hypothalamic–pituitary–adrenal axis, sympathetic–adrenal–medullary axis, and inflammatory response. Pro-inflammatory cytokines play an important role in this process because they induce a constellation of depressotypic behaviors called sickness behaviors. Although these changes can be short-lived, sustained inflammation may occur via glucocorticoid resistance, catecholamines, sympathetic innervation of immune organs, and immune cell aging. This response also may be moderated by several factors, including prior life stress, prior depression, and genes implicated in stress reactivity.
AbstractList	Major life events involving social rejection are strongly associated with onset of depression. To account for this relation, we propose a psychobiological model in which rejection-related stressors elicit a distinct and integrated set of cognitive, emotional, and biological changes that may evoke depression. In this model, social rejection events activate brain regions involved in processing negative affect and rejection-related distress (e.g., anterior insula, dorsal anterior cingulate cortex). They also elicit negative self-referential cognitions (e.g., "I'm undesirable," "Other people don't like me") and related self-conscious emotions (e.g., shame, humiliation). Downstream biological consequences include upregulation of the hypothalamic-pituitary-adrenal axis, sympathetic-adrenal-medullary axis, and inflammatory response. Pro-inflammatory cytokines play an important role in this process because they induce a constellation of depressotypic behaviors called sickness behaviors. Although these changes can be short-lived, sustained inflammation may occur via glucocorticoid resistance, catecholamines, sympathetic innervation of immune organs, and immune cell aging. This response also may be moderated by several factors, including prior life stress, prior depression, and genes implicated in stress reactivity. Major life events involving social rejection are strongly associated with onset of depression. To account for this relation, we propose a psychobiological model in which rejection-related stressors elicit a distinct and integrated set of cognitive, emotional, and biological changes that may evoke depression. In this model, social rejection events activate brain regions involved in processing negative affect and rejection-related distress (e.g., anterior insula, dorsal anterior cingulate cortex). They also elicit negative self-referential cognitions (e.g., "I'm undesirable," "Other people don't like me") and related self-conscious emotions (e.g., shame, humiliation). Downstream biological consequences include upregulation of the hypothalamic-pituitary-adrenal axis, sympathetic-adrenal-medullary axis, and inflammatory response. Pro-inflammatory cytokines play an important role in this process because they induce a constellation of depressotypic behaviors called sickness behaviors. Although these changes can be short-lived, sustained inflammation may occur via glucocorticoid resistance, catecholamines, sympathetic innervation of immune organs, and immune cell aging. This response also may be moderated by several factors, including prior life stress, prior depression, and genes implicated in stress reactivity.Major life events involving social rejection are strongly associated with onset of depression. To account for this relation, we propose a psychobiological model in which rejection-related stressors elicit a distinct and integrated set of cognitive, emotional, and biological changes that may evoke depression. In this model, social rejection events activate brain regions involved in processing negative affect and rejection-related distress (e.g., anterior insula, dorsal anterior cingulate cortex). They also elicit negative self-referential cognitions (e.g., "I'm undesirable," "Other people don't like me") and related self-conscious emotions (e.g., shame, humiliation). Downstream biological consequences include upregulation of the hypothalamic-pituitary-adrenal axis, sympathetic-adrenal-medullary axis, and inflammatory response. Pro-inflammatory cytokines play an important role in this process because they induce a constellation of depressotypic behaviors called sickness behaviors. Although these changes can be short-lived, sustained inflammation may occur via glucocorticoid resistance, catecholamines, sympathetic innervation of immune organs, and immune cell aging. This response also may be moderated by several factors, including prior life stress, prior depression, and genes implicated in stress reactivity. Major life events involving social rejection are strongly associated with onset of depression. To account for this relation, we propose a psychobiological model in which rejection-related stressors elicit a distinct and integrated set of cognitive, emotional, and biological changes that may evoke depression. In this model, social rejection events activate brain regions involved in processing negative affect and rejection-related distress (e.g., anterior insula, dorsal anterior cingulate cortex). They also elicit negative self-referential cognitions (e.g., “I’m undesirable,” “Other people don’t like me”) and related self-conscious emotions (e.g., shame, humiliation). Downstream biological consequences include upregulation of the hypothalamic–pituitary–adrenal axis, sympathetic–adrenal–medullary axis, and inflammatory response. Pro-inflammatory cytokines play an important role in this process because they induce a constellation of depressotypic behaviors called sickness behaviors. Although these changes can be short-lived, sustained inflammation may occur via glucocorticoid resistance, catecholamines, sympathetic innervation of immune organs, and immune cell aging. This response also may be moderated by several factors, including prior life stress, prior depression, and genes implicated in stress reactivity.
Author	O’Donovan, Aoife Slavich, George M. Kemeny, Margaret E. Epel, Elissa S.
Author_xml	– sequence: 1 givenname: George M. surname: Slavich fullname: Slavich, George M. email: george.slavich@ucsf.edu – sequence: 2 givenname: Aoife surname: O’Donovan fullname: O’Donovan, Aoife – sequence: 3 givenname: Elissa S. surname: Epel fullname: Epel, Elissa S. – sequence: 4 givenname: Margaret E. surname: Kemeny fullname: Kemeny, Margaret E.
BackLink	http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=23259448$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/20083138$$D View this record in MEDLINE/PubMed
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Keywords	Glucocorticoid resistance Life stress Stress sensitization 5- HTTLPR Social rejection Dorsal anterior cingulate cortex Depression Cortisol Inflammation Immune cell aging Senescence Central nervous system Review Hydrocortisone Glucocorticoid Encephalon Cingulate cortex Sensitization Ungulata Mood disorder Corticosteroid 5-HTTLPR Steroid hormone Antiinflammatory agent Stress Vertebrata Mammalia Serotonin transporter Animal Adrenal hormone Sheep Models Artiodactyla
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Snippet	Major life events involving social rejection are strongly associated with onset of depression. To account for this relation, we propose a psychobiological...
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SubjectTerms	5- HTTLPR Adult and adolescent clinical studies Aging Animals Behavioral psychophysiology Biological and medical sciences Cortisol Depression Depression - genetics Depression - physiopathology Depression - psychology Dorsal anterior cingulate cortex Fundamental and applied biological sciences. Psychology Glucocorticoid resistance Humans Immune cell aging Inflammation Life stress Medical sciences Mood disorders Psychology. Psychoanalysis. Psychiatry Psychology. Psychophysiology Psychopathology. Psychiatry Rejection, Psychology Social rejection Stress sensitization Stress, Psychological - physiopathology Stress, Psychological - psychology
Title	Black sheep get the blues: A psychobiological model of social rejection and depression
URI	https://dx.doi.org/10.1016/j.neubiorev.2010.01.003 https://www.ncbi.nlm.nih.gov/pubmed/20083138 https://www.proquest.com/docview/749005990 https://www.proquest.com/docview/817603298 https://pubmed.ncbi.nlm.nih.gov/PMC2926175
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