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Genetic and environmental influences on adult attention deficit hyperactivity disorder symptoms: a large Swedish population-based study of twins

Published online by Cambridge University Press:  16 August 2012

H. Larsson*
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden Karolinska Institutet Center of Neurodevelopmental Disorders, Stockholm, Sweden
P. Asherson
Affiliation:
MRC Social Genetic and Developmental Psychiatry, Institute of Psychiatry, King's CollegeLondon, UK
Z. Chang
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
T. Ljung
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
B. Friedrichs
Affiliation:
Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden
J.-O. Larsson
Affiliation:
Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden
P. Lichtenstein
Affiliation:
Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden
*
*Address for correspondence: Dr H. Larsson, Karolinska Institutet, Department of Medical Epidemiology and Biostatistics, PO Box 281, SE-171 77 Stockholm, Sweden. (Email: [email protected])

Abstract

Background

Attention deficit hyperactivity disorder (ADHD) frequently persists into adulthood. Family and twin studies delineate a disorder with strong genetic influences among children and adolescents based on parent- and teacher-reported data but little is known about the genetic and environmental contribution to DSM-IV ADHD symptoms in adulthood. We therefore aimed to investigate the impact of genetic and environmental influences on the inattentive and hyperactive–impulsive symptoms of ADHD in adults.

Method

Twin methods were applied to self-reported assessments of ADHD symptoms from a large population-based Swedish twin study that included data from 15 198 Swedish male and female twins aged 20 to 46 years.

Results

The broad heritability [i.e. A + D, where A is an additive genetic factor and D (dominance) a non-additive genetic factor] was 37% (A = 11%, D = 26%) for inattention and 38% (A = 18%, D = 20%) for hyperactivity–impulsivity. The results also indicate that 52% of the phenotypic correlation between inattention and hyperactivity–impulsivity (r = 0.43) was explained by genetic influences whereas the remaining part of the covariance was explained by non-shared environmental influences. These results were replicated across age strata.

Conclusions

Our findings of moderate broad heritability estimates are consistent with previous literature on self-rated ADHD symptoms in older children, adolescents and adults and retrospective reports of self-rated childhood ADHD by adults but differ from studies of younger children with informant ratings. Future research needs to clarify whether our data indicate a true decrease in the heritability of ADHD in adults compared to children, or whether this relates to the use of self-ratings in contrast to informant data.

Type
Original Articles
Copyright
Copyright © Cambridge University Press 2012

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