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Genetic moderation of interpersonal psychotherapy efficacy for low-income mothers with major depressive disorder: Implications for differential susceptibility

  • Dante Cicchetti (a1) (a2), Sheree L. Toth (a2) and Elizabeth D. Handley (a2)

Abstract

Genetic moderation of interpersonal psychotherapy (IPT) efficacy for economically disadvantaged women with major depressive disorder was examined. Specifically, we investigated whether genotypic variation in corticotropin releasing hormone receptor 1 (CRHR1) and the linked polymorphic region of the serotonin transporter gene (5-HTTLPR) moderated effects of IPT on depressive symptoms over time. We also tested genotype moderation of IPT mechanisms on social adjustment and perceived stress. Non-treatment-seeking urban women at or below the poverty level with infants were recruited from the community (N = 126; M age = 25.33 years, SD = 4.99; 54.0% African American, 22.2% Caucasian, and 23.8% Hispanic/biracial) and randomized to individual IPT or Enhanced Community Standard groups. The results revealed that changes in depressive symptoms over time depended on both intervention group and genotypes (5-HTTLPR and CRHR1). Moreover, multiple-group path analysis indicated that IPT improved depressive symptoms, increased social adjustment, and decreased perceived stress at posttreatment among women with the 0 copies of the CRHR1 TAT haplotype only. Finally, improved social adjustment at postintervention significantly mediated the effect of IPT on reduced depressive symptoms at 8 months postintervention for women with 0 copies of the TAT haplotype only. Post hoc analyses of 5-HTTLPR were indicative of differential susceptibility, albeit among African American women only.

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Corresponding author

Address correspondence and reprint requests to: Dante Cicchetti, Institute of Child Development, University of Minnesota, 51 East River Road, Mineapolis, MN 55455; E-mail: cicchett@umn.edu.

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Genetic moderation of interpersonal psychotherapy efficacy for low-income mothers with major depressive disorder: Implications for differential susceptibility

  • Dante Cicchetti (a1) (a2), Sheree L. Toth (a2) and Elizabeth D. Handley (a2)

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