TY - JOUR
T1 - Immune response to stress induction as a predictor of cognitive-behavioral therapy outcomes in adolescent mood disorders
T2 - A pilot study
AU - Pearlstein, Jennifer G.
AU - Staudenmaier, Paige J.
AU - West, Amy E.
AU - Geraghty, Shauna
AU - Cosgrove, Victoria E.
N1 - Publisher Copyright:
© 2019
PY - 2020/1
Y1 - 2020/1
N2 - Cognitive-behavioral therapy (CBT) alleviates symptoms of depression in youth with bipolar disorder (BD) and major depressive disorder (MDD). Empirical research has linked inflammatory markers to depressive symptoms and acute psychosocial stress; however, a gap remains as to whether immune response to stress may serve as a putative mechanism of treatment. This preliminary pilot study determined the modest feasibility of assessing psychobiological response to stress as a predictor of CBT outcomes for youth with mood disorders. We evaluated whether participation in a 10-session group-CBT intervention for mood disorders altered inflammatory response to a laboratory psychosocial stress induction and if this alteration in immune stress responsivity was related to a decrease in depressive symptoms. Thirty-four youth (age M = 15.03, SD = 1.91) diagnosed with BD or MDD participated in a 10-session CBT group and pre- and post-group assessments; twenty-eight participants who completed the group had usable cytokine data. Pre- and post-group assessments included stress induction with the Trier Social Stress Test (TSST) during which inflammatory cytokines were measured at baseline (time 0) and after the TSST at 30, 60, and 90 min. Results suggest it is modestly feasible to measure immune response to stress alongside CBT treatment for adolescent mood disorders. Our findings were mixed; across seven cytokines, hierarchical linear models indicated two cytokines, IL6 and IL12, were sensitive to acute laboratory stress. We also found significant correlations between life stress, inflammation, and depression both pre- and post- CBT group. Inflammation pre-group, as measured by IL12 and IL1 β predicted depressive symptoms following treatment. Although we did not find significant within-subject reductions in inflammation, chronic stress predicted changes in IL β, signaling the central role of chronic stress. This study offers preliminary evidence that immune responsivity to stress induction could serve as a mechanism of treatment for mood disorders in youth, indicating a potential marker for more personalized model of healthcare.
AB - Cognitive-behavioral therapy (CBT) alleviates symptoms of depression in youth with bipolar disorder (BD) and major depressive disorder (MDD). Empirical research has linked inflammatory markers to depressive symptoms and acute psychosocial stress; however, a gap remains as to whether immune response to stress may serve as a putative mechanism of treatment. This preliminary pilot study determined the modest feasibility of assessing psychobiological response to stress as a predictor of CBT outcomes for youth with mood disorders. We evaluated whether participation in a 10-session group-CBT intervention for mood disorders altered inflammatory response to a laboratory psychosocial stress induction and if this alteration in immune stress responsivity was related to a decrease in depressive symptoms. Thirty-four youth (age M = 15.03, SD = 1.91) diagnosed with BD or MDD participated in a 10-session CBT group and pre- and post-group assessments; twenty-eight participants who completed the group had usable cytokine data. Pre- and post-group assessments included stress induction with the Trier Social Stress Test (TSST) during which inflammatory cytokines were measured at baseline (time 0) and after the TSST at 30, 60, and 90 min. Results suggest it is modestly feasible to measure immune response to stress alongside CBT treatment for adolescent mood disorders. Our findings were mixed; across seven cytokines, hierarchical linear models indicated two cytokines, IL6 and IL12, were sensitive to acute laboratory stress. We also found significant correlations between life stress, inflammation, and depression both pre- and post- CBT group. Inflammation pre-group, as measured by IL12 and IL1 β predicted depressive symptoms following treatment. Although we did not find significant within-subject reductions in inflammation, chronic stress predicted changes in IL β, signaling the central role of chronic stress. This study offers preliminary evidence that immune responsivity to stress induction could serve as a mechanism of treatment for mood disorders in youth, indicating a potential marker for more personalized model of healthcare.
KW - CBT
KW - Immune system
KW - Mood disorders
KW - TSST
KW - Youth
UR - http://www.scopus.com/inward/record.url?scp=85073335749&partnerID=8YFLogxK
U2 - 10.1016/j.jpsychires.2019.10.012
DO - 10.1016/j.jpsychires.2019.10.012
M3 - Article
C2 - 31634750
AN - SCOPUS:85073335749
SN - 0022-3956
VL - 120
SP - 56
EP - 63
JO - Journal of Psychiatric Research
JF - Journal of Psychiatric Research
ER -