Cited by 701Attention Deficit Hyperactivity DisorderAutism Spectrum Disorder ResearchChild and Adolescent Psychosocial and Emotional Development

Practitioner Review: What have we learnt about the causes of ADHD?

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Thapar, Anita, Cooper, Miriam, Eyre, Olga, Langley, Kate·2013·Journal of Child Psychology and Psychiatry

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.

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Crossref · 10.1111/j.1469-7610.2012.02611.x

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  • Most comorbid conditions 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.

    “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]

    In “The overlap of ADHD with other developmental and psychiatric disorders” (page not provided), the review says some comorbid problems can present later and might arise as a consequence of ADHD, with an exception for early-onset conduct problems. It does not say that most comorbid conditions usually appear later; the claim overstates that part. (LLM, conf=0.86)

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  • 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.

    “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]

    The ‘Family adversity and early care-giving’ section reports associations of low income, family adversity, maltreatment and family conflict with child mental health problems, including ADHD. It does not report the full list of specific factors in the claim, such as paternal violence, maternal psychiatric disability and parental disapproval. It also cautions that, except for rare extreme early deprivation, psychosocial adversity has not clearly been shown to cause ADHD. (LLM, conf=0.86)

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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.

    “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]

    The “Pre and perinatal risks” section associates maternal smoking and stress with offspring ADHD and reports a less consistent association for prenatal alcohol exposure. It does not identify reduced maternal thyroid capacity, poor maternal wellness, maternal age, post-maturity, long working hours, foetal stress, or antepartum haemorrhage as ADHD risks; it discusses prematurity, not post-maturity. The review also cautions that causation has not been established. (LLM, conf=0.88)

    Experimental — accuracy not yet measured
  • Environmental factors such as chemical contaminants (pesticides and harmful agricultural chemicals) may promote the neural structure impairments involved in ADHD.

    “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]

    The Environmental toxins section says organic pollutants may damage neural systems implicated in ADHD. The Pesticides section reports associations between pesticide exposure and ADHD-related outcomes, but does not show that pesticides cause structural neural impairments; it also notes inconsistent findings. No page numbers are available in our copy. (LLM, conf=0.84)

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  • The probability of developing ADHD is around 2-8 times more likely in close relatives of patients with ADHD than relatives of unaffected individuals.

    “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].”

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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
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
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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