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Genetics of attention deficit hyperactivity disorder
Open accessAbstract
Decades of research show that genes play an vital role in the etiology of attention deficit hyperactivity disorder (ADHD) and its comorbidity with other disorders. Family, twin, and adoption studies show that ADHD runs in families. ADHD’s high heritability of 74% motivated the search for ADHD susceptibility genes. Genetic linkage studies show that the effects of DNA risk variants on ADHD must, individually, be very small. Genome-wide association studies (GWAS) have implicated several genetic loci at the genome-wide level of statistical significance. These studies also show that about a third of ADHD’s heritability is due to a polygenic component comprising many common variants each having small effects. From studies of copy number variants we have also learned that the rare insertions or deletions account for part of ADHD’s heritability. These findings have implicated new biological pathways that may eventually have implications for treatment development.
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“A review of 37 twin studies from the United States, Europe, Scandinavia, and Australia found that genes and their interaction with the environment must play a substantial role in causing ADHD”
From The World Federation of ADHD International Consensus Statement: 208 Evidence-based conclusions about the disorder (2021) · cites this paper as Faraone and Larsson, 2018
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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“Family, twin, and DNA studies show that genetic and environmental influences are partially shared between ADHD and many other psychiatric disorders (e.g. schizophrenia, depression, bipolar disorder, autism spectrum disorder, conduct disorder, eating disorders, and substance use disorders) and with somatic disorders (e.g. migraine and obesity)”
From The World Federation of ADHD International Consensus Statement: 208 Evidence-based conclusions about the disorder (2021) · cites this paper as Faraone and Larsson, 2018
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 influences exert differential effects depending on genotype, such that individuals with specific genetic profiles (e.g., variants in dopaminergic or serotonergic genes such as 5-HTTLPR) are more susceptible to the neurobehavioral impact of early adversity and psychosocial stress”
From ADHD in Adulthood: Clinical Presentation, Comorbidities, and Treatment Perspectives (2025) · cites this paper as [57]
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.
In the citing paper
“gene-environment interactions (G×E) determine the likelihood, severity, and developmental timing of symptom expression”
From ADHD in Adulthood: Clinical Presentation, Comorbidities, and Treatment Perspectives (2025) · cites this paper as [57]
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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“The etiology of ADHD is most accurately conceptualized not as the consequence of a single etiological source but as a multifactorial neurodevelopmental condition arising from the interaction between genetic predisposition and environmental influences (G×E).”
From ADHD in Adulthood: Clinical Presentation, Comorbidities, and Treatment Perspectives (2025) · cites this paper as [57]
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“The etiology of adult ADHD is complex and multifactorial, involving interactions among genetic, neurobiological, and environmental factors.”
From ADHD in Adulthood: Clinical Presentation, Comorbidities, and Treatment Perspectives (2025) · cites this paper as [57]
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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“Recent advances in genetics have enabled the identification of numerous genetic polymorphisms associated with ADHD, including variants in genes encoding DA transporters (DAT1), DA receptor D4 (DRD4), as well as genes related to NA and serotonin metabolism [57].”
From ADHD in Adulthood: Clinical Presentation, Comorbidities, and Treatment Perspectives (2025) · cites this paper as [57]
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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“However, many of these studies are limited to pediatric populations, and evidence concerning adults remains fragmented.”
From ADHD in Adulthood: Clinical Presentation, Comorbidities, and Treatment Perspectives (2025) · cites this paper as [57]
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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“Genetics has a great weight in ADHD, with a heritability ranging from 60% to 90% according to several studies carried out in twins [54, 56].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [56]
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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“Genome-wide association studies (GWAS) have indicated genes playing a role in ADHD that could be linked to neuronal plasticity mechanisms (neuronal migration, cell adhesion and neuron proliferation) [61] or to deficiencies in the synthesis or release of neurotransmitters (NTs), mainly DA, but also serotonin and NE [56, 62].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [56]
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“In rare cases, however, ADHD-like symptoms can be caused by extreme deprivation early in life (Kennedy et al., 2016), a single genetic abnormality (Faraone and Larsson, 2018), or traumatic brain injury early in life (Stojanovski et al., 2019).”
From The World Federation of ADHD International Consensus Statement: 208 Evidence-based conclusions about the disorder (2021) · cites this paper as Faraone and Larsson, 2018
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In the citing paper
“Very large studies of families suggest that ADHD shares genetic or familial causes with autoimmune diseases (Li et al., 2019), hypospadias (Butwicka et al., 2015), and intellectual disability (Faraone and Larsson, 2018).”
From The World Federation of ADHD International Consensus Statement: 208 Evidence-based conclusions about the disorder (2021) · cites this paper as Faraone and Larsson, 2018
The cited source says what the claim attributes to it.
In the citing paper
“ADHD can also be the result of rare single gene defects (Faraone and Larsson, 2018) or abnormalities of the chromosomes (Cederlof et al., 2014).”
From The World Federation of ADHD International Consensus Statement: 208 Evidence-based conclusions about the disorder (2021) · cites this paper as Faraone and Larsson, 2018
The cited source says what the claim attributes to it.
In the citing paper
“Evidence from twin studies consistently demonstrates a robust genetic contribution to ADHD, with heritability estimates of approximately 74%”
From ADHD in Adulthood: Clinical Presentation, Comorbidities, and Treatment Perspectives (2025) · cites this paper as [57]
In the citing paper
“Neurodevelopmental conditions are highly heritable31,32 but have multifactorial origins alongside biology–environment interplay33–35.”
From Sex and gender in neurodevelopmental conditions (2023) · cites this paper as [32]
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Metadata
- Authors
- Faraone, S. V., & Larsson, H.
- Affiliations
- SUNY Upstate Medical University (US)
- Örebro University (SE)
- Corresponding author
- Faraone, Stephen V.
- Venue
- Molecular Psychiatry
- Published
- 2018-06-11
- Volume
- 24
- Issue
- 4
- Pages
- 562-575
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC6477889
- OpenAlex
- W2808011097
- Semantic Scholar
- ad9e986f545bd6c311bb93268c15d5dba58452a3
- Cited by
- 1,338
- References
- 327
- Citations by year
- 2026: 234 · 2025: 201 · 2024: 158 · 2023: 160 · 2022: 151 · 2021: 145 · 2020: 105 · 2019: 68 · 2018: 7
- FWCI
- 12.55
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Molecular Psychiatry (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Eli Lilly and Company
- European Commission (HORIZON2020, 667302, 602805)
- Vetenskapsrådet (20132–280, (2014-3831))
- Universitetet i Bergen
- H. Lundbeck A/S
- National Institute of Mental Health (U01MH085518, U01MH109536, R01MH101519)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- attention deficit hyperactivity disorder, ADHD genetics, heritability, polygenic risk, copy number variation, genetic susceptibility loci, twin and family studies, ADHD comorbidity, biological pathways
- MeSH terms
- Attention Deficit Disorder with Hyperactivity, Humans, Genetic Linkage, Genetic Predisposition to Disease, Multifactorial Inheritance, Genome-Wide Association Study, DNA Copy Number Variations
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