Social supports and serotonin transporter gene moderate depression in maltreated children

  1. Joan Kaufman*,,,
  2. Bao-Zhu Yang*,,
  3. Heather Douglas-Palumberi*,
  4. Shadi Houshyar§,
  5. Deborah Lipschitz*,
  6. John H. Krystal*,, and
  7. Joel Gelernter*,
  1. *Department of Psychiatry, Yale University School of Medicine, New Haven, CT 06511; Clinical Neuroscience Division, National Center for Post-Traumatic Stress Disorder, Veterans Affairs Healthcare Center, West Haven, CT 06516; and §Department of Psychology, Yale University, New Haven, CT 06511
  1. Edited by Bruce S. McEwen, The Rockefeller University, New York, NY, and approved October 15, 2004 (received for review June 18, 2004)

Abstract

In this study, measures of the quality and availability of social supports were found to moderate risk for depression associated with a history of maltreatment and the presence of the short (s) allele of the serotonin transporter gene promoter polymorphism (5-HTTLPR). The present investigation (i) replicates research in adults showing that 5-HTTLPR variation moderates the development of depression after stress, (ii) extends the finding to children, and (iii) demonstrates the ability of social supports to further moderate risk for depression. Maltreated children with the s/s genotype and no positive supports had the highest depression ratings, scores that were twice as high as the non-maltreated comparison children with the same genotype. However, the presence of positive supports reduced risk associated with maltreatment and the s/s genotype, such that maltreated children with this profile had only minimal increases in their depression scores. These findings are consistent with emerging preclinical and clinical data suggesting that the negative sequelae associated with early stress are not inevitable. Risk for negative outcomes may be modified by both genetic and environmental factors, with the quality and availability of social supports among the most important environmental factors in promoting resiliency in maltreated children, even in the presence of a genotype expected to confer vulnerability for psychiatric disorder.

Footnotes

  • To whom correspondence should be addressed at: Department of Psychiatry, Yale University, Child and Adolescent Research and Education Program, University Towers, Suite 2H, 100 York Street, New Haven, CT 06511. E-mail: joan.kaufman{at}yale.edu.

  • Author contributions: J.K. and J.H.K. designed research; J.K., H.D.-P., S.H., and D.L. performed research; J.K. and B.-Z.Y. analyzed data; J.K. and J.G. wrote the paper; and B.-Z.Y. proposed data analytic strategy and derived ancestral proportion scores.

  • This paper was submitted directly (Track II) to the PNAS office.

  • Abbreviations: DCF, Department of Children and Families; CC, community control; l, long; s, short; GEE, generalized estimating equation.

  • Freely available online through the PNAS open access option.

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