Journal
PSYCHOLOGICAL MEDICINE
Volume 38, Issue 7, Pages 1057-1066Publisher
CAMBRIDGE UNIV PRESS
DOI: 10.1017/S0033291707001584
Keywords
Add Health; adult attention deficit hyperactivity disorder (ADHD); genetics; retrospective
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Funding
- NIAAA NIH HHS [AA 015336, AA 07464] Funding Source: Medline
- NICHD NIH HHS [HD 31921] Funding Source: Medline
- NIDA NIH HHS [DA 15522] Funding Source: Medline
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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.
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