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Practitioner Review: What have we learnt about the causes of ADHD?
Anita Thapar, Miriam Cooper, Olga Eyre and 1 more
Journal of Child Psychology and Psychiatry · 2012 · Review
doi:10.1111/j.1469-7610.2012.02611.x
Abstract
Background: Attention deficit hyperactivity disorder (ADHD) and its possible causes still attract controversy. Genes, pre and perinatal risks, psychosocial factors and environmental toxins have all been considered as potential risk factors. Method: This review (focussing on literature published since 1997, selected from a search of PubMed) critically considers putative risk factors with a focus on genetics and selected environmental risks, examines their relationships with ADHD and discusses the likelihood that these risks are causal as well as some of the main implications. Results: No single risk factor explains ADHD. Both inherited and noninherited factors contribute and their effects are interdependent. ADHD is familial and heritable. Research into the inherited and molecular genetic contributions to ADHD suggest an important overlap with other neurodevelopmental problems, notably, autism spectrum disorders. Having a biological relative with ADHD, large, rare copy number variants, some small effect size candidate gene variants, extreme early adversity, pre and postnatal exposure to lead and low birth weight/prematurity have been most consistently found as risk factors, but none are yet known to be definitely causal. There is a large literature documenting associations between ADHD and a wide variety of putative environmental risks that can, at present, only be regarded as correlates. Findings from research designs that go beyond simply testing for association are beginning to contest the robustness of some environmental exposures previously thought to be ADHD risk factors. Conclusions: The genetic risks implicated in ADHD generally tend to have small effect sizes or be rare and often increase risk of many other types of psychopathology. Thus, they cannot be used for prediction, genetic testing or diagnostic purposes beyond what is predicted by a family history. There is a need to consider the possibility of parents and siblings being similarly affected and how this might impact on engagement with families, influence interventions and require integration with adult services. Genetic contributions to disorder do not necessarily mean that medications are the treatment of choice. We also consider how findings might influence the conceptualisation of ADHD, public health policy implications and why it is unhelpful and incorrect to dichotomise genetic/biological and environmental explanations. It is essential that practitioners can interpret genetic and aetiological research findings and impart informed explanations to families.
Shown for reading. Its publisher allows quoting it, not republishing it.
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Taylor E, Chadwick O, Heptinstall E, Danckaerts M. Hyperactivity and conduct problems as risk factors for adolescent development. Journal of the American Academy of Child and Adolescent Psychiatry. 1996;35:1213-1226.
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Taylor E, Sonuga-Barke EJ, Rutter M, Bishop DV, Pine D, Scott S, Stevenson J, Taylor E, Thapar A. Disorders of attention and activity. Rutter’s textbook of child psychiatry. 2008;521-542.
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Thapar A, Collishaw S, Pine DS, Thapar AK. Depression in adolescence. Lancet. 2012;379:1056-1067.
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Thapar A, Harrington R, McGuffin P. Examining the comorbidity of ADHD-related behaviours and conduct problems using a twin study design. British Journal of Psychiatry. 2001;179:224-229.
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Thapar A, Holmes J, Poulton K, Harrington R. Genetic basis of attention deficit and hyperactivity. British Journal of Psychiatry. 1999;174:105-111.
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Thapar A, Langley K, Fowler T, Rice F, Turic D, Whittinger N, O’Donovan M. Catechol O-methyltransferase gene variant and birth weight predict early-onset antisocial behavior in children with attention-deficit/hyperactivity disorder. Archives of General Psychiatry. 2005;62:1275-1278.
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Thapar A, Rice F. Twin studies in pediatric depression. Child and Adolescent Psychiatric Clinics of North America. 2006;15:869-881.
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Thapar A, Rutter M. Do prenatal risk factors cause psychiatric disorder? Be wary of causal claims. The British Journal of Psychiatry. 2009;195:100-101.
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Thompson MJ, Laver-Bradbury C, Ayres M, Le Poidevin E, Mead S, Dodds C, Sonuga-Barke EJ. A small-scale randomized controlled trial of the revised new forest parenting programme for preschoolers with attention deficit hyperactivity disorder. European Child and Adolescent Psychiatry. 2009;18:605-616.
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Tully EC, Iacono WG, McGue M. An adoption study of parental depression as an environmental liability for adolescent depression and childhood disruptive disorders. American Journal of Psychiatry. 2008;165:1148-1154.
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Weaver IC, Diorio J, Seckl JR, Szyf M, Meaney MJ. Early environmental regulation of hippocampal glucocorticoid receptor gene expression: Characterization of intracellular mediators and potential genomic target sites. Annals of the New York Academy of Sciences. 2004;1024:182-212.
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Willcutt EG, Nigg J, Pennington BF, Solanto MV, Rohde LA, Tannock R, Lahey BB. Validity of DSM-IV attention deficit/hyperactivity disorder symptom dimensions and subtypes. Journal of Abnormal Psychology. 2012.
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Willcutt EG, Pennington BF, DeFries JC. Twin study of the etiology of comorbidity between reading disability and attention-deficit/hyperactivity disorder. American Journal of Medical Genetics. 2000;96:293-301.
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Williams NM, Franke B, Mick E, Anney R, Freitag C, Gill M, Faraone SV. Genome-wide analysis of copy number variants in attention deficit hyperactivity disorder: confirms the role of rare variants and duplications at 15q13.3. American Journal of Psychiatry. 2012;169:195-204.
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Williams NM, Zaharieva I, Martin A, Langley K, Mantripragada K, Fossdal R, Thapar A. Rare chromosomal deletions and duplications in attention-deficit hyperactivity disorder: A genome-wide analysis. Lancet. 2010;376:1401-1408.
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Yang B, Chan RC, Jing J, Li T, Sham P, Chen RY. A meta-analysis of association studies between the 10-repeat allele of a VNTR polymorphism in the 3′-UTR of dopamine transporter gene and attention deficit hyperactivity disorder. American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics. 2007;144B:541-550.
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