Clustering of Depression and Inflammation in Adolescents Previously Exposed to Childhood Adversity

There is mounting interest in the hypothesis that inflammation contributes to the pathogenesis of depression and underlies depressed patients' vulnerability to comorbid medical conditions. However, research on depression and inflammation has yielded conflicting findings, fostering speculation t...

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Published inBiological psychiatry (1969) Vol. 72; no. 1; pp. 34 - 40
Main Authors Miller, Gregory E., Cole, Steve W.
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.07.2012
Elsevier
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Abstract There is mounting interest in the hypothesis that inflammation contributes to the pathogenesis of depression and underlies depressed patients' vulnerability to comorbid medical conditions. However, research on depression and inflammation has yielded conflicting findings, fostering speculation that these conditions associate only in certain subgroups, such as patients exposed to childhood adversity. We studied 147 female adolescents. All were in good health at baseline but at high risk for depression because of family history or cognitive vulnerability. Subjects were assessed every 6 months for 2.5 years, undergoing diagnostic interviews and venipuncture for measurement of two inflammatory biomarkers, C-reactive protein (CRP) and interleukin-6 (IL-6). Childhood adversity was indexed by parental separation, low socioeconomic status, and familial psychopathology. Multilevel models indicated that childhood adversity promotes clustering of depression and inflammation. Among subjects exposed to high childhood adversity, the transition to depression was accompanied by increases in both CRP and IL-6. Higher CRP remained evident 6 months later, even after depressive symptoms had abated. These lingering effects were bidirectional, such that among subjects with childhood adversity, high IL-6 forecasted depression 6 months later, even after concurrent inflammation was considered. This coupling of depression and inflammation was not apparent in subjects without childhood adversity. These findings suggest that childhood adversity promotes the formation of a neuroimmune pipeline in which inflammatory signaling between the brain and periphery is amplified. Once established, this pipeline leads to a coupling of depression and inflammation, which may contribute to later affective difficulties and biomedical complications.
AbstractList There is mounting interest in the hypothesis that inflammation contributes to the pathogenesis of depression and underlies depressed patients' vulnerability to comorbid medical conditions. However, research on depression and inflammation has yielded conflicting findings, fostering speculation that these conditions associate only in certain subgroups, such as patients exposed to childhood adversity.BACKGROUNDThere is mounting interest in the hypothesis that inflammation contributes to the pathogenesis of depression and underlies depressed patients' vulnerability to comorbid medical conditions. However, research on depression and inflammation has yielded conflicting findings, fostering speculation that these conditions associate only in certain subgroups, such as patients exposed to childhood adversity.We studied 147 female adolescents. All were in good health at baseline but at high risk for depression because of family history or cognitive vulnerability. Subjects were assessed every 6 months for 2.5 years, undergoing diagnostic interviews and venipuncture for measurement of two inflammatory biomarkers, C-reactive protein (CRP) and interleukin-6 (IL-6). Childhood adversity was indexed by parental separation, low socioeconomic status, and familial psychopathology.METHODSWe studied 147 female adolescents. All were in good health at baseline but at high risk for depression because of family history or cognitive vulnerability. Subjects were assessed every 6 months for 2.5 years, undergoing diagnostic interviews and venipuncture for measurement of two inflammatory biomarkers, C-reactive protein (CRP) and interleukin-6 (IL-6). Childhood adversity was indexed by parental separation, low socioeconomic status, and familial psychopathology.Multilevel models indicated that childhood adversity promotes clustering of depression and inflammation. Among subjects exposed to high childhood adversity, the transition to depression was accompanied by increases in both CRP and IL-6. Higher CRP remained evident 6 months later, even after depressive symptoms had abated. These lingering effects were bidirectional, such that among subjects with childhood adversity, high IL-6 forecasted depression 6 months later, even after concurrent inflammation was considered. This coupling of depression and inflammation was not apparent in subjects without childhood adversity.RESULTSMultilevel models indicated that childhood adversity promotes clustering of depression and inflammation. Among subjects exposed to high childhood adversity, the transition to depression was accompanied by increases in both CRP and IL-6. Higher CRP remained evident 6 months later, even after depressive symptoms had abated. These lingering effects were bidirectional, such that among subjects with childhood adversity, high IL-6 forecasted depression 6 months later, even after concurrent inflammation was considered. This coupling of depression and inflammation was not apparent in subjects without childhood adversity.These findings suggest that childhood adversity promotes the formation of a neuroimmune pipeline in which inflammatory signaling between the brain and periphery is amplified. Once established, this pipeline leads to a coupling of depression and inflammation, which may contribute to later affective difficulties and biomedical complications.CONCLUSIONSThese findings suggest that childhood adversity promotes the formation of a neuroimmune pipeline in which inflammatory signaling between the brain and periphery is amplified. Once established, this pipeline leads to a coupling of depression and inflammation, which may contribute to later affective difficulties and biomedical complications.
There is mounting interest in the hypothesis that inflammation contributes to the pathogenesis of depression and underlies depressed patients' vulnerability to comorbid medical conditions. However, research on depression and inflammation has yielded conflicting findings, fostering speculation that these conditions associate only in certain subgroups, such as patients exposed to childhood adversity. We studied 147 female adolescents. All were in good health at baseline but at high risk for depression because of family history or cognitive vulnerability. Subjects were assessed every 6 months for 2.5 years, undergoing diagnostic interviews and venipuncture for measurement of two inflammatory biomarkers, C-reactive protein (CRP) and interleukin-6 (IL-6). Childhood adversity was indexed by parental separation, low socioeconomic status, and familial psychopathology. Multilevel models indicated that childhood adversity promotes clustering of depression and inflammation. Among subjects exposed to high childhood adversity, the transition to depression was accompanied by increases in both CRP and IL-6. Higher CRP remained evident 6 months later, even after depressive symptoms had abated. These lingering effects were bidirectional, such that among subjects with childhood adversity, high IL-6 forecasted depression 6 months later, even after concurrent inflammation was considered. This coupling of depression and inflammation was not apparent in subjects without childhood adversity. These findings suggest that childhood adversity promotes the formation of a neuroimmune pipeline in which inflammatory signaling between the brain and periphery is amplified. Once established, this pipeline leads to a coupling of depression and inflammation, which may contribute to later affective difficulties and biomedical complications.
BackgroundThere is mounting interest in the hypothesis that inflammation contributes to the pathogenesis of depression and underlies depressed patients' vulnerability to comorbid medical conditions. However, research on depression and inflammation has yielded conflicting findings, fostering speculation that these conditions associate only in certain subgroups, such as patients exposed to childhood adversity. MethodsWe studied 147 female adolescents. All were in good health at baseline but at high risk for depression because of family history or cognitive vulnerability. Subjects were assessed every 6 months for 2.5 years, undergoing diagnostic interviews and venipuncture for measurement of two inflammatory biomarkers, C-reactive protein (CRP) and interleukin-6 (IL-6). Childhood adversity was indexed by parental separation, low socioeconomic status, and familial psychopathology. ResultsMultilevel models indicated that childhood adversity promotes clustering of depression and inflammation. Among subjects exposed to high childhood adversity, the transition to depression was accompanied by increases in both CRP and IL-6. Higher CRP remained evident 6 months later, even after depressive symptoms had abated. These lingering effects were bidirectional, such that among subjects with childhood adversity, high IL-6 forecasted depression 6 months later, even after concurrent inflammation was considered. This coupling of depression and inflammation was not apparent in subjects without childhood adversity. ConclusionsThese findings suggest that childhood adversity promotes the formation of a neuroimmune pipeline in which inflammatory signaling between the brain and periphery is amplified. Once established, this pipeline leads to a coupling of depression and inflammation, which may contribute to later affective difficulties and biomedical complications.
Author Cole, Steve W.
Miller, Gregory E.
AuthorAffiliation 2 Department of Medicine, UCLA School of Medicine; UCLA AIDS Institute; UCLA Molecular Biology Institute; Jonsson Comprehensive Cancer Center; Norman Cousins Center at UCLA
1 Department of Psychology, University of British Columbia
AuthorAffiliation_xml – name: 2 Department of Medicine, UCLA School of Medicine; UCLA AIDS Institute; UCLA Molecular Biology Institute; Jonsson Comprehensive Cancer Center; Norman Cousins Center at UCLA
– name: 1 Department of Psychology, University of British Columbia
Author_xml – sequence: 1
  givenname: Gregory E.
  surname: Miller
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– sequence: 2
  givenname: Steve W.
  surname: Cole
  fullname: Cole, Steve W.
  organization: Department of Medicine, University of California—Los Angeles (UCLA) School of Medicine, Los Angeles, California
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Issue 1
Keywords Adolescence
cytokines
depression
childhood adversity
inflammation
socioeconomic status
Human
Mood disorder
Socioeconomic status
Cytokine
Depression
Infantile experience
Inflammation
Sociodemographic factor
Adolescent
Early traumatism
Language English
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CC BY 4.0
Copyright © 2012 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.
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Snippet There is mounting interest in the hypothesis that inflammation contributes to the pathogenesis of depression and underlies depressed patients' vulnerability to...
BackgroundThere is mounting interest in the hypothesis that inflammation contributes to the pathogenesis of depression and underlies depressed patients'...
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StartPage 34
SubjectTerms Adolescence
Adolescent
Adult
Adult and adolescent clinical studies
Biological and medical sciences
Biomarkers - blood
C-Reactive Protein
Canada - epidemiology
childhood adversity
Cluster Analysis
cytokines
Depression
Depressive Disorder - blood
Depressive Disorder - epidemiology
Female
Follow-Up Studies
Humans
inflammation
Inflammation - blood
Inflammation - epidemiology
Interleukin-6 - blood
Interview, Psychological - methods
Life Change Events
Medical sciences
Mood disorders
Psychiatric Status Rating Scales - statistics & numerical data
Psychiatric/Mental Health
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Risk Factors
socioeconomic status
Young Adult
Title Clustering of Depression and Inflammation in Adolescents Previously Exposed to Childhood Adversity
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https://dx.doi.org/10.1016/j.biopsych.2012.02.034
https://www.ncbi.nlm.nih.gov/pubmed/22494534
https://www.proquest.com/docview/1020050896
https://pubmed.ncbi.nlm.nih.gov/PMC3493164
Volume 72
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