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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Genetic factors and gene-environment interplay play a major causal role in ADHD.
“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
The 'Evidence for Heritability from family, adoption and twin studies' section reports a mean heritability of 74% across 37 twin studies, supporting a substantial genetic role. The 'Conclusions and Future Directions' section says gene–environment interactions are possible and may account for much of ADHD’s etiology, not that they must play a substantial role. The retrieved passages do not establish the stated geographic range of the 37 studies; page numbers were unavailable. (LLM, conf=0.86)
Experimental — accuracy not yet measuredADHD shares some genetic and environmental influences with many psychiatric and somatic disorders.
“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
The 'ADHD’s Clinical Features & Course' section (page not given) reports genetic overlap with several psychiatric disorders, and 'Common Variant ADHD as a Polygenic Disorder' (page not given) describes shared genetic risk with obesity. The cited text does not establish shared environmental influences across these disorders, and the searched passages do not substantiate the migraine or eating-disorder examples. (LLM, conf=0.87)
Experimental — accuracy not yet measuredEnvironmental influences exert differential effects on ADHD depending on genotype, such that individuals with specific genetic profiles (e.g., 5-HTTLPR variants) are more susceptible to the neurobehavioral impact of early adversity and psychosocial stress.
“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]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredGene-environment interactions determine the likelihood, severity, and developmental timing of ADHD symptom expression.
“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]
The Conclusions and Future Directions section says gene–environment interactions may account for much of ADHD’s etiology, supporting a possible role in likelihood but not the claim that they determine it. The Clinical Features & Course section discusses developmental differences in genetic risk, not gene–environment interactions; the copy does not establish that those interactions determine symptom severity or developmental timing. Page numbers are unavailable in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredADHD etiology is a multifactorial neurodevelopmental condition arising from interaction between genetic predisposition and environmental influences (G×E).
“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]
The Conclusions and Future Directions section says both genes and environmental factors contribute to ADHD’s etiology, supporting the multifactorial account. It says gene–environment interactions may account for much of that etiology, however, rather than establishing interaction as the mechanism the claim states definitively. Page numbers are unavailable in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measured
The etiology of adult ADHD is complex and multifactorial, involving interactions among genetic, neurobiological, and environmental factors.
“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]
The Conclusions and Future Directions section says that both genes and environmental factors contribute to ADHD and that gene–environment interactions may account for much of its etiology. The Abstract also implicates brain circuits, while the Clinical Features & Course section discusses genetic risk in adults. The paper does not specifically establish the proposed combination of genetic, neurobiological, and environmental factors for adult ADHD; pages were not provided. (LLM, conf=0.82)
Experimental — accuracy not yet measuredRecent 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), and genes related to NA and serotonin metabolism.
“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]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredMany genetic studies of ADHD are limited to pediatric populations, and evidence concerning adults remains fragmented.
“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]
The Genome-wide Significant Common Variants section describes an early GWAS sample of parents and children with ADHD, and the review discusses other childhood-focused genetic studies. But it does not establish that many genetic studies are limited to pediatric populations. The Developmental Effects section reports differing early estimates for adult heritability, then explains the discrepancy and describes evidence for stable heritability; it does not characterize adult evidence as fragmented. Page numbers were not available in our copy. (LLM, conf=0.70)
Experimental — accuracy not yet measuredGenetics has a great weight in ADHD, with a heritability ranging from 60% to 90% according to twin studies.
“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]
The ‘Evidence for Heritability’ section reports a 74% mean across 37 twin studies and estimates of 77–88% for studies using categorical ADHD measures, supporting a substantial genetic contribution. It does not give a 60–90% range; the ‘Developmental Effects’ section also reports lower estimates from adult self-report twin studies. No page numbers are available in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredGWAS have indicated genes playing a role in ADHD that could be linked to neuronal plasticity mechanisms or to deficiencies in synthesis or release of neurotransmitters, mainly DA, but also serotonin and NE.
“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]
In “Genome-wide Significant Common Variants” (page not provided), the paper says analyses of ADHD GWAS data implicated pathways regulating neurotransmitter release, neurite outgrowth and axon guidance; it also describes GWAS-linked genes affecting dopamine levels and neuronal wiring. It does not say GWAS established deficiencies in neurotransmitter synthesis or release, nor does it link the GWAS findings specifically to serotonin or norepinephrine. Neuronal proliferation appears in its discussion of candidate-gene studies, not as a GWAS finding. (LLM, conf=0.88)
Experimental — accuracy not yet measuredRarely, ADHD-like symptoms arise from severe early deprivation, a single gene abnormality, or early traumatic brain injury.
“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
ADHD has familial or genetic causes in common with autoimmune diseases, hypospadias, and intellectual disability.
“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
Rare single-gene defects or chromosomal abnormalities can cause ADHD.
“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
Twin studies demonstrate a robust genetic contribution to ADHD, with heritability estimates of approximately 74%.
“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]
Neurodevelopmental conditions are highly heritable but have multifactorial origins involving biology-environment interplay.
“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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ADHD in Adulthood: Clinical Presentation, Comorbidities, and Treatment Perspectives
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“Instead, gene-environment interactions (G × E) determine the likelihood, severity, and developmental timing of symptom expression [57].”
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Self-citation
- 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
- 328
- Citations by year
- 2026: 234 · 2025: 201 · 2024: 158 · 2023: 160 · 2022: 151 · 2021: 145 · 2020: 105 · 2019: 68 · 2018: 7 · 2017: 1 · 2016: 5 · 2015: 4 · 2014: 7 · 2013: 11 · 2012: 10
- 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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