Interpersonal life stress, inflammation, and depression in adolescence: Testing Social Signal Transduction Theory of Depression
Background Depression rates increase markedly for girls across the adolescent transition, but the social‐environmental and biological processes underlying this phenomenon remain unclear. To address this issue, we tested a key hypothesis from Social Signal Transduction Theory of Depression, which pos...
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Published in | Depression and anxiety Vol. 37; no. 2; pp. 179 - 193 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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Hindawi Limited
01.02.2020
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Abstract | Background
Depression rates increase markedly for girls across the adolescent transition, but the social‐environmental and biological processes underlying this phenomenon remain unclear. To address this issue, we tested a key hypothesis from Social Signal Transduction Theory of Depression, which posits that individuals who mount stronger inflammatory responses to social stress should exhibit greater increases in depressive symptoms following interpersonal life stress exposure than those who mount weaker inflammatory responses to such stress.
Method
Participants were 116 adolescent girls (Mage = 14.71) at risk for psychopathology, defined as having a history of mental health concerns (e.g., psychiatric treatment, significant symptoms) over the past 2 years. At baseline, we characterized their inflammatory reactivity to social stress by quantifying their salivary proinflammatory cytokine responses to a laboratory‐based social stressor. Then, 9 months later, we assessed the interpersonal and noninterpersonal stressful life events that they experienced over the prior 9 months using an interview‐based measure of life stress.
Results
As hypothesized, greater interpersonal life stress exposure was associated with significant increases in depression over time, but only for girls exhibiting stronger salivary tumor necrosis factor‐α and interleukin‐1β reactivity to social stress. In contrast, noninterpersonal stress exposure was unrelated to changes in depression longitudinally, both alone and when combined with youths' cytokine reactivity scores.
Discussion
These results are consistent with Social Signal Transduction Theory of Depression and suggest that heightened inflammatory reactivity to social stress may increase adolescents' risk for depression. Consequently, it may be possible to reduce depression risk by modifying inflammatory responses to social stress. |
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AbstractList | BackgroundDepression rates increase markedly for girls across the adolescent transition, but the social‐environmental and biological processes underlying this phenomenon remain unclear. To address this issue, we tested a key hypothesis from Social Signal Transduction Theory of Depression, which posits that individuals who mount stronger inflammatory responses to social stress should exhibit greater increases in depressive symptoms following interpersonal life stress exposure than those who mount weaker inflammatory responses to such stress.MethodParticipants were 116 adolescent girls (Mage = 14.71) at risk for psychopathology, defined as having a history of mental health concerns (e.g., psychiatric treatment, significant symptoms) over the past 2 years. At baseline, we characterized their inflammatory reactivity to social stress by quantifying their salivary proinflammatory cytokine responses to a laboratory‐based social stressor. Then, 9 months later, we assessed the interpersonal and noninterpersonal stressful life events that they experienced over the prior 9 months using an interview‐based measure of life stress.ResultsAs hypothesized, greater interpersonal life stress exposure was associated with significant increases in depression over time, but only for girls exhibiting stronger salivary tumor necrosis factor‐α and interleukin‐1β reactivity to social stress. In contrast, noninterpersonal stress exposure was unrelated to changes in depression longitudinally, both alone and when combined with youths' cytokine reactivity scores.DiscussionThese results are consistent with Social Signal Transduction Theory of Depression and suggest that heightened inflammatory reactivity to social stress may increase adolescents' risk for depression. Consequently, it may be possible to reduce depression risk by modifying inflammatory responses to social stress. Background Depression rates increase markedly for girls across the adolescent transition, but the social‐environmental and biological processes underlying this phenomenon remain unclear. To address this issue, we tested a key hypothesis from Social Signal Transduction Theory of Depression, which posits that individuals who mount stronger inflammatory responses to social stress should exhibit greater increases in depressive symptoms following interpersonal life stress exposure than those who mount weaker inflammatory responses to such stress. Method Participants were 116 adolescent girls (Mage = 14.71) at risk for psychopathology, defined as having a history of mental health concerns (e.g., psychiatric treatment, significant symptoms) over the past 2 years. At baseline, we characterized their inflammatory reactivity to social stress by quantifying their salivary proinflammatory cytokine responses to a laboratory‐based social stressor. Then, 9 months later, we assessed the interpersonal and noninterpersonal stressful life events that they experienced over the prior 9 months using an interview‐based measure of life stress. Results As hypothesized, greater interpersonal life stress exposure was associated with significant increases in depression over time, but only for girls exhibiting stronger salivary tumor necrosis factor‐α and interleukin‐1β reactivity to social stress. In contrast, noninterpersonal stress exposure was unrelated to changes in depression longitudinally, both alone and when combined with youths' cytokine reactivity scores. Discussion These results are consistent with Social Signal Transduction Theory of Depression and suggest that heightened inflammatory reactivity to social stress may increase adolescents' risk for depression. Consequently, it may be possible to reduce depression risk by modifying inflammatory responses to social stress. Depression rates increase markedly for girls across the adolescent transition, but the social-environmental and biological processes underlying this phenomenon remain unclear. To address this issue, we tested a key hypothesis from Social Signal Transduction Theory of Depression, which posits that individuals who mount stronger inflammatory responses to social stress should exhibit greater increases in depressive symptoms following interpersonal life stress exposure than those who mount weaker inflammatory responses to such stress. Participants were 116 adolescent girls (M = 14.71) at risk for psychopathology, defined as having a history of mental health concerns (e.g., psychiatric treatment, significant symptoms) over the past 2 years. At baseline, we characterized their inflammatory reactivity to social stress by quantifying their salivary proinflammatory cytokine responses to a laboratory-based social stressor. Then, 9 months later, we assessed the interpersonal and noninterpersonal stressful life events that they experienced over the prior 9 months using an interview-based measure of life stress. As hypothesized, greater interpersonal life stress exposure was associated with significant increases in depression over time, but only for girls exhibiting stronger salivary tumor necrosis factor-α and interleukin-1β reactivity to social stress. In contrast, noninterpersonal stress exposure was unrelated to changes in depression longitudinally, both alone and when combined with youths' cytokine reactivity scores. These results are consistent with Social Signal Transduction Theory of Depression and suggest that heightened inflammatory reactivity to social stress may increase adolescents' risk for depression. Consequently, it may be possible to reduce depression risk by modifying inflammatory responses to social stress. |
Author | Hastings, Paul D. Nock, Matthew K. Prinstein, Mitchell J. Helms, Sarah W. Rudolph, Karen D. Giletta, Matteo Slavich, George M. |
AuthorAffiliation | 6 Department of Psychology, Harvard University, Cambridge, MA, USA 2 Department of Developmental Psychology, Tilburg University, Tilburg, The Netherlands 4 Center for Mind & Brain and Department of Psychology, University of California, Davis, CA, USA 5 Department of Psychology, University of Illinois, Urbana-Champaign, Champaign, IL, USA 3 Department of Psychology and Neuroscience, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA 1 Cousins Center for Psychoneuroimmunology and Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA, USA |
AuthorAffiliation_xml | – name: 6 Department of Psychology, Harvard University, Cambridge, MA, USA – name: 1 Cousins Center for Psychoneuroimmunology and Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA, USA – name: 2 Department of Developmental Psychology, Tilburg University, Tilburg, The Netherlands – name: 5 Department of Psychology, University of Illinois, Urbana-Champaign, Champaign, IL, USA – name: 3 Department of Psychology and Neuroscience, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA – name: 4 Center for Mind & Brain and Department of Psychology, University of California, Davis, CA, USA |
Author_xml | – sequence: 1 givenname: George M. orcidid: 0000-0001-5710-3818 surname: Slavich fullname: Slavich, George M. email: gslavich@mednet.ucla.edu organization: University of California – sequence: 2 givenname: Matteo surname: Giletta fullname: Giletta, Matteo organization: Tilburg University – sequence: 3 givenname: Sarah W. surname: Helms fullname: Helms, Sarah W. organization: University of North Carolina at Chapel Hill – sequence: 4 givenname: Paul D. surname: Hastings fullname: Hastings, Paul D. organization: University of California – sequence: 5 givenname: Karen D. surname: Rudolph fullname: Rudolph, Karen D. organization: University of Illinois at Urbana‐Champaign – sequence: 6 givenname: Matthew K. surname: Nock fullname: Nock, Matthew K. organization: Harvard University – sequence: 7 givenname: Mitchell J. surname: Prinstein fullname: Prinstein, Mitchell J. organization: University of North Carolina at Chapel Hill |
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Depression rates increase markedly for girls across the adolescent transition, but the social‐environmental and biological processes underlying this... Depression rates increase markedly for girls across the adolescent transition, but the social-environmental and biological processes underlying this phenomenon... BackgroundDepression rates increase markedly for girls across the adolescent transition, but the social‐environmental and biological processes underlying this... |
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SubjectTerms | Adolescent Child Child & adolescent psychiatry Cytokines Depression - complications Depression - immunology Depression - psychology development disease Female Girls Humans Inflammation Inflammation - complications Inflammation - immunology Inflammation - psychology Interleukin-1beta - analysis Interleukin-1beta - immunology Interpersonal Relations Interviews as Topic major depressive disorder Male Mental depression Models, Psychological Psychopathology risk Saliva - immunology Signal transduction Social interactions social stress Stress Stress, Psychological - complications Stress, Psychological - immunology Stress, Psychological - psychology Teenagers Tumor Necrosis Factor-alpha - analysis Tumor Necrosis Factor-alpha - immunology vulnerability |
Title | Interpersonal life stress, inflammation, and depression in adolescence: Testing Social Signal Transduction Theory of Depression |
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