Psychological Medicine

Original Articles

Genetic and environmental contributions to retrospectively reported DSM-IV childhood attention deficit hyperactivity disorder

B. C. Habersticka1a2 c1, D. Timberlakea1a3, C. J. Hopfera2, J. M. Lessema1, M. A. Ehringera1 and J. K Hewitta1

a1 Institute for Behavioral Genetics, University of Colorado, Boulder, CO, USA

a2 Department of Psychiatry, University of Colorado Health Science Center, Denver, CO, USA

a3 College of Health Sciences, University of California, Irvine, CA, USA


Background A variety of methodologies and techniques converge on the notion that adults and children with attention deficit hyperactivity disorder (ADHD) have similar deficits, but there is limited knowledge about whether adult retrospective reports reflect similar genetic and environmental influences implicated in childhood ADHD.

Method DSM-IV ADHD symptoms were collected retrospectively from 3896 young adults participating in the National Longitudinal Study of Adolescent Health. Responses from this genetically informative sample of same- and opposite-sex twins and siblings were used to determine the magnitude of genetic and environmental influences. Possible gender differences in these effects were also examined. The degree of familial specificity of the genetic and environmental influences on the Inattentive and Hyperactive-Impulsive symptom dimensions was also determined.

Results Additive genetic effects contributed moderately to DSM-IV Inattentive, Hyperactive-Impulsive and Combined ADHD subtypes (heritability estimates of 0.30–0.38). Individual-specific influences accounted for the remaining proportion of the variance. Both genetic and individual-specific environmental effects contributed to the covariation of Inattentive and Hyperactive-Impulsive symptomologies.

Conclusions Results from our genetic analyses agree with previous findings based on self-assessment of current and retrospectively reported ADHD symptoms in adolescents and adults. Large individual-specific environmental influences as identified here suggest that current questionnaires used for retrospective diagnoses may not provide the most accurate reconstruction of the etiological influences on childhood ADHD in general population samples.

(Received August 29 2006)

(Revised July 10 2007)

(Accepted July 17 2007)

(Online publication September 25 2007)


c1 Address for correspondence: Dr B. C. Haberstick, Institute of Behavioral Genetics, University of Colorado, Campus Box 0447, Boulder, CO 80309-0447, USA. (Email: