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Practitioner Review: What have we learnt about the causes of ADHD?
Open accessAbstract
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.
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“Most of these conditions/disorders usually appear later in development and can manifest as a result of ADHD, but this is not always the case with early stage behavioural problems directly related to ADHD [58].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [58]
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“Regarding the influence of psychosocial adversity in ADHD disorder development, extreme parental discord, poor socioeconomic status, paternal violence, inconsistent parent–child relationships, maternal psychiatric disability, parental disapproval, family anxiety and foster placement have been reported as family random factors associated with behavioural disorders in childhood [58, 70].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [58]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“Reduced maternal thyroid capacity, poor maternal wellness, maternal age, post-maturity of the foetus, long working hours, maternal stress, foetal stress, prenatal exposure to alcohol and tobacco, and antepartum haemorrhage are prenatal factors that could influence ADHD development [54, 58, 65].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [58]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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“Environmental factors such as chemical contaminants (pesticides and harmful agricultural chemicals) may promote the neural structure impairments involved in ADHD [58].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [58]
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“Another factor that supports an ADHD genetic background is the probability of developing ADHD being around 2–8 times more likely in the close relatives of patients with ADHD than relatives of unaffected individuals [58].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [58]
In the citing paper
“early environmental factors are also implicated in the etiology of ADHD including many factors associated with increased inflammation such as maternal infection (Werenberg Dreier et al., 2016), maternal smoking (Becker et al., 2008; Biederman, 2005; Mick et al., 2002; Neuman et al., 2007; Silva et al., 2014; Thapar et al., 2013), maternal obesity and poor diet (Andersen et al., 2018; Buss et al.,”
From Neuroinflammation as a risk factor for attention deficit hyperactivity disorder (2019) · cites this paper as Thapar et al., 2013
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Cites
Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene
Caspi, A., Sugden, K., Moffitt, T. E., Taylor, A., Craig, I. W., Harrington, H., McClay, J., Mill, J., Martin, J., Braithwaite, A., et al. (2003) · Science · doi:10.1126/science.1083968 · Cited by 8,120
Autism as a strongly genetic disorder: evidence from a British twin study
Bailey, A., Le Couteur, A., Gottesman, I., Bolton, P., Simonoff, E., Yuzda, E., & Rutter, M. (1995) · Psychological Medicine · doi:10.1017/s0033291700028099 · Cited by 2,461
Cognitive and Behavioral Outcomes of School-Aged Children Who Were Born Preterm: A Meta-analysis
Bhutta, A. T., Cleves, M. A., Casey, P. H., Cradock, M. M., & Anand, K. J. S. (2002) · JAMA · doi:10.1001/jama.288.6.728 · Cited by 2,392
Thapar, A., Collishaw, S., Pine, D. S., & Thapar, A. K. (2012) · The Lancet · doi:10.1016/s0140-6736(11)60871-4 · Cited by 2,365
Self-citationMolecular genetics of attention-deficit/hyperactivity disorder
Faraone, S. V., Perlis, R. H., Doyle, A. E., Smoller, J. W., Goralnick, J. J., Holmgren, M. A., & Sklar, P. (2005) · Biological Psychiatry · doi:10.1016/j.biopsych.2004.11.024 · Cited by 2,357
Personal genomes: The case of the missing heritability
Maher, B. (2008) · Nature · doi:10.1038/456018a · Cited by 1,737
Kraemer, H. C., Stice, E., Kazdin, A., Offord, D., & Kupfer, D. (2001) · American Journal of Psychiatry · doi:10.1176/appi.ajp.158.6.848 · Cited by 1,712
Autism genome-wide copy number variation reveals ubiquitin and neuronal genes
Glessner, J. T., Wang, K., Cai, G., Korvatska, O., Kim, C. E., Wood, S., Zhang, H., Estes, A., Brune, C. W., Bradfield, J. P., et al. (2009) · Nature · doi:10.1038/nature07953 · Cited by 1,421
A copy number variation morbidity map of developmental delay
Cooper, G. M., Coe, B. P., Girirajan, S., Rosenfeld, J. A., Vu, T. H., Baker, C., Williams, C., Stalker, H., Hamid, R., Hannig, V., et al. (2011) · Nature Genetics · doi:10.1038/ng.909 · Cited by 1,351
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Research works printed but not linked: 4
- Food and Agriculture Organization of the United Nations and World Health Organization, 2010, Joint FAO/WHO expert committee on food additives, seventy‐third meeting, summary and conclusions
- NICE, 2008, CG72 attention deficit hyperactivity disorder (ADHD): NICE guideline
- Rutter M., 2007, Identifying the environmental causes of disease: How should we decide what to believe and when to take action?
- Taylor E., 2008, Rutter’s textbook of child psychiatry, 521
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Items 701–701 of 701
Kang, S., Fu, Z., Li, Q., Yang, L., & Cao, Q. (2026) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2026.1782999
Metadata
- Authors
- Thapar, A., Cooper, M., Eyre, O., & Langley, K.
- Affiliations
- Cardiff University (GB)
- Corresponding author
- Thapar, Anita
- Venue
- Journal of Child Psychology and Psychiatry
- Publisher
- Wiley
- Published
- 2012-09-11
- Volume
- 54
- Issue
- 1
- Pages
- 3-16
- ISSN
- 0021-9630 (ISSN-L)
- 1469-7610
- PMC
- PMC3572580
- OpenAlex
- W1791898768
- Cited by
- 701
- References
- 119
- Citations by year
- 2026: 21 · 2025: 43 · 2024: 42 · 2023: 39 · 2022: 59 · 2021: 72 · 2020: 55 · 2019: 56 · 2018: 54 · 2017: 69 · 2016: 67 · 2015: 51 · 2014: 52 · 2013: 18 · 2012: 1
- FWCI
- 5.27
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Child Psychology and Psychiatry (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust
- Cardiff University
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Social Sciences › Psychology › Clinical Psychology › Child and Adolescent Psychosocial and Emotional Development
- Keywords
- attention deficit hyperactivity disorder, genetic risk factors, heritability, copy number variation, candidate gene variants, environmental risk factors, lead exposure, low birth weight, preterm birth, autism spectrum disorder, family history (medicine), psychosocial adversity, neurodevelopmental disorders, public health policy
- MeSH terms
- Attention Deficit Disorder with Hyperactivity, Developmental Disabilities, Environment, Female, Humans, Pregnancy, Prenatal Exposure Delayed Effects, Psychosocial Deprivation, Risk Factors, Comorbidity, Genetic Predisposition to Disease, Gene-Environment Interaction
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