Familial factors inflate the estimated effects of genetic liability to ADHD on behavioural outcomes

D. C. P. Crick; N. M. Davies; S. Medland; D. Evans

doi:10.64898/2026.10.27.26366008

AI summary · DOI: 10.64898/2026.10.27.26366008 · medRxiv: Psychiatry and Clinical Psychology

Familial factors inflate the estimated effects of genetic liability to ADHD on behavioural outcomes

D. C. P. Crick, N. M. Davies, S. Medland, D. Evans

Original paper Published on 27 Oct. 2026 medRxiv preprint License: CC BY 4.0 Also in: fr

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The essentials

Within-family Mendelian randomization attenuated many population-based estimates linking ADHD genetic liability to adverse outcomes, suggesting familial confounding, particularly for depressive symptoms and age at first child.

Question

Do associations between genetic liability to ADHD and adverse health, behavioural and social outcomes reflect an individual’s own liability or familial and social confounding?

Method

The authors compared population-based and sibling-based two-sample Mendelian randomization across 16 outcomes, using 21–22 ADHD-associated variants from a European GWAS of 38,691 cases and 186,843 controls. Within-family outcome data covered 18 European cohorts and up to 164,220 siblings. Primary inverse-variance weighted analyses were supplemented with pleiotropy-robust estimators, instrument-shrinkage analyses and comparisons between designs; effects were expressed in outcome standard deviations per doubling of genetically predicted ADHD odds.

Findings

Result Population-based associations with depressive symptoms and age at first child attenuated toward zero within families, with nominal between-design differences of p=0.048 and p=0.034, respectively.
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In family-based analyses, these estimates were attenuated for most outcomes and exhibited a trend of differing from the population-based estimates, e.g. for depressive symptoms (p=0·048) and age at first child (p=0·034), cigarettes smoked per day (p=0·051), cognitive performance (p=0·054) and educational attainment (0.064).
Result The educational-attainment estimate attenuated within families to −0.033 standard deviations per doubling of genetically predicted ADHD odds, with a 95% confidence interval of −0.061 to −0.005.
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The effect on educational attainment also attenuated (beta:-0.033,95%CI:-0.061,-0.005).
Result For BMI, waist-to-hip ratio, glycated haemoglobin and CRP, within-family analyses provided little evidence of effects but did not establish differences from population-based estimates.
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The population-based and family-based estimates were statistically consistent for these outcomes, with their confidence intervals overlapping despite differences in point estimates.
Result Sensitivity analyses applying shrinkage to population-derived SNP–ADHD associations left the findings largely unchanged.
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Results were largely unchanged, suggesting that our findings are robust to even substantial inconsistency in the SNP-exposure associations (eFigure 2).
Authors’ interpretation The authors interpret some population-based associations as reflecting familial and social context rather than direct effects of an individual’s ADHD liability.
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Instead, these estimates may reflect the family and social context in which ADHD occurs, most plausibly through confounding of the population-based estimates by population stratification, assortative mating, and/or dynastic effects[26, 29].

Limitations

Both designs used population-derived SNP–exposure associations that could retain familial confounding, although shrinkage analyses suggested robustness.
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The SNP–exposure associations were derived from a population-based GWAS and could be influenced by familial factors; however, estimates were essentially unchanged across a wide range of shrinkage parameters, suggesting that inflation of the SNP–ADHD association is unlikely to affect our conclusions.
Within-family estimates were less precise, limiting the ability to distinguish null effects from population-based estimates for several outcomes.
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Family-based Mendelian randomization is inherently less precise than population-based analysis, because it uses only within-family variation and genotyped relatives remain scarce[26, 27]; this likely explains why we could not detect heterogeneity for some outcomes.
The estimates include pathways through ADHD treatment and cannot identify treatment effects separately.
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Our estimates, including the family-based estimates, therefore reflect the total effect of genetic liability to ADHD, including any pathways acting through treatment, and cannot isolate the effect of treatment itself.

Why it matters

The authors argue that familial data are needed to distinguish direct effects of ADHD liability from familial confounding. Attributing all associated harms to individual ADHD may overstate what individual treatment can modify, but implications for interventions require further testing.

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AI-generated keywords: ADHD Mendelian randomization genetic liability within-family analysis familial confounding

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Comprehensive Summary
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Original abstract

This medRxiv preprint examines whether adverse outcomes associated with attention-deficit hyperactivity disorder (ADHD) reflect an individual’s own genetic liability or the family and social environments in which ADHD occurs. Previous population-based Mendelian randomization studies have suggested that ADHD liability causes poorer behavioural, social and health outcomes. However, these estimates can be distorted by population ancestry differences, assortative mating and “genetic nurture,” whereby parental genetic characteristics influence children through the environments parents provide. The researchers compared conventional population-based Mendelian randomization with within-family analyses that use genetic differences between siblings. Genetic instruments for ADHD came from a European-ancestry genome-wide association study involving 38,691 people with ADHD and 186,843 controls. After harmonization, 21–22 genetic variants were available for each outcome. Within-family outcome data included up to 164,220 siblings from 18 European cohorts. The study examined 16 outcomes, including smoking, alcohol consumption, depressive symptoms, education, cognitive performance and biological health measures. The primary analysis used inverse-variance weighting, supplemented by alternative estimators, tests for pleiotropy and sensitivity analyses. Effects were reported in outcome standard deviations per doubling of genetically predicted odds of ADHD, with false-discovery-rate correction across outcomes. Population-based analyses reproduced several previously reported associations. A doubling of genetically predicted ADHD odds was associated with increases of 0.059 standard deviations in depressive symptoms, 0.094 in cigarettes smoked daily and 0.065 in alcohol-consumption frequency. It was also associated with decreases of 0.065 standard deviations in educational attainment, 0.075 in cognitive performance and 0.045 in age at first childbirth. Most corresponding within-family estimates were substantially smaller and compatible with no effect. Estimates were 0.002 for depressive symptoms (95% confidence interval: −0.052 to 0.055), 0.021 for cigarettes smoked daily (−0.047 to 0.088) and 0.003 for age at first childbirth (−0.040 to 0.047). Educational attainment retained a smaller negative estimate of −0.033 (−0.061 to −0.005). Differences between the two designs were nominally significant for depressive symptoms and age at first childbirth, with p-values of 0.048 and 0.034, respectively. Differences for smoking, cognition and education narrowly missed the conventional 0.05 threshold. Population-based analyses also suggested increases in body mass index, waist-to-hip ratio, glycated haemoglobin and C-reactive protein. Within-family estimates provided little evidence of effects on these measures. However, their confidence intervals remained compatible with the population-based estimates, so attenuation alone could not establish that familial factors explained these associations. Sensitivity analyses generally supported the main findings, including analyses using more closely matched samples and rescaling potentially inflated genetic associations with ADHD. The authors conclude that familial and social factors probably inflate some estimated consequences of ADHD genetic liability, particularly those involving depressive symptoms and earlier childbirth. This suggests that treating individuals alone may not address every associated disadvantage. However, the study neither estimates treatment effectiveness nor demonstrates that ADHD treatment is unnecessary. Important limitations include the lower precision of within-family analyses, restriction to European-ancestry samples and reliance on population-based genetic associations for ADHD in both designs. The approach also cannot identify which familial mechanisms explain the attenuation. For most outcomes, the uncertainty remains compatible with both no direct effect and the population-based estimate. Larger, more diverse family-based studies are therefore needed. This preprint should be interpreted alongside other evidence, rather than as definitive proof that causal effects are absent.

ADHD, Genetics and Family Life: Untangling the Roots of Adverse Outcomes

People with attention-deficit hyperactivity disorder (ADHD) often face challenges beyond its core symptoms, including difficulties with education, depression and smoking. But how much of that pattern reflects an individual’s genetic liability to ADHD, and how much reflects the family and social circumstances surrounding them? A new study suggests these influences may be harder to separate than earlier genetic research implied.

The medRxiv preprint “Familial factors inflate the estimated effects of genetic liability to ADHD on behavioural outcomes,” by D. C. P. Crick, N. M. Davies, S. Medland and D. Evans, compares two approaches to investigating this question. Its central finding is that several estimated consequences of ADHD genetic liability become smaller when researchers compare siblings rather than unrelated people.

Why Genetic Associations Can Be Misleading

The researchers used Mendelian randomization, a method that uses genetic variants associated with a characteristic—in this case, liability to ADHD—to investigate its possible effects on other outcomes. Because genetic variants are inherited before most life experiences occur, the approach can help address some problems that complicate conventional observational research.

However, it does not automatically establish causation. Population-based analyses can be distorted by ancestry differences, patterns in who partners with whom, and “genetic nurture.” Genetic nurture occurs when parents’ genetic characteristics influence their children through the environments parents provide, rather than solely through the variants children inherit.

For example, an association between ADHD-related variants and an educational outcome could partly reflect family circumstances linked to parental characteristics. A conventional genetic analysis might attribute too much of that association to the individual’s own ADHD liability.

What Comparing Siblings Adds

Siblings share many aspects of their family background but inherit different combinations of genetic variants. Comparing genetic differences within families therefore helps reduce several sources of bias that can affect comparisons between unrelated people. It does not eliminate every uncertainty, but it offers an important check on population-based findings.

The ADHD genetic instruments came from a European-ancestry genome-wide association study involving 38,691 people with ADHD and 186,843 controls. After harmonization, 21–22 variants were available for each outcome. The within-family outcome data included up to 164,220 siblings from 18 European cohorts.

The researchers examined 16 outcomes, covering behaviour, social circumstances and biological health. Their main analysis used inverse-variance weighting, supported by alternative methods, checks for genetic variants acting through other pathways, and sensitivity analyses. They also applied false-discovery-rate correction across outcomes.

Several Associations Became Smaller Within Families

The population-based analyses reproduced several previously reported associations. Effects were expressed as changes in outcome standard deviations per doubling of genetically predicted odds of ADHD. This scale describes genetic liability; it is not a comparison of receiving versus not receiving an ADHD diagnosis.

Depressive symptoms increased by 0.059 standard deviations in the population analysis, compared with 0.002 within families.
Cigarettes smoked daily increased by 0.094 standard deviations in the population analysis, compared with 0.021 within families.
Age at first childbirth decreased by 0.045 standard deviations in the population analysis, compared with a near-zero within-family estimate of 0.003.
Educational attainment decreased by 0.065 standard deviations in the population analysis, with a smaller negative within-family estimate of −0.033.

The within-family confidence intervals for depressive symptoms, smoking and age at first childbirth included zero. Education retained a negative estimate, with a 95% confidence interval from −0.061 to −0.005. Population analyses also linked ADHD liability to more frequent alcohol consumption and lower cognitive performance; most corresponding within-family estimates were smaller and compatible with no effect.

Smaller Estimates Do Not Settle Every Question

The differences between designs were nominally significant for depressive symptoms and age at first childbirth, with p-values of 0.048 and 0.034. Differences for smoking, cognition and education narrowly missed the conventional 0.05 threshold. These results suggest familial influences may inflate some estimates, but they do not establish that every population association is explained by family background.

Population analyses also suggested increases in body mass index, waist-to-hip ratio, glycated haemoglobin and C-reactive protein. Within-family analyses provided little evidence of effects on these measures. Crucially, however, their confidence intervals remained compatible with the population estimates. Smaller point estimates alone cannot show that familial factors explain these associations.

What This Means for ADHD Support

The findings encourage a broader view of ADHD-associated disadvantage. Supporting individuals may be important, while family and social environments may also warrant attention. However, this study did not test treatment effectiveness. It does not show that ADHD treatment is unnecessary, nor that changing family circumstances would necessarily prevent particular outcomes.

Important limitations remain. Within-family estimates were less precise, all samples were of European ancestry, and both designs relied on population-based genetic associations for ADHD. The approach also cannot identify which familial mechanisms explain the attenuation. Sensitivity analyses generally supported the main findings, but did not remove these uncertainties.

The takeaway is not that ADHD has no consequences. Rather, some genetic estimates may combine individual liability with broader familial influences. Larger, more diverse family-based studies are needed, and this preprint should be considered alongside other evidence—not treated as definitive proof that causal effects are absent.

BackgroundPeople with ADHD have worse health, behavioural and social outcomes, widely interpreted as evidence that ADHD causes these harms, justifying early identification and treatment. But ADHD clusters in families, and conventional studies cannot separate the effect of a persons own ADHD from the family environment in which it arises. We used a family-based genetic design to distinguish the two. MethodsWe used up to 22 genome-wide significant variants associated with ADHD (38,691 cases, 186,843 controls) to estimate effects of genetic liability to ADHD on 16 health and behavioural outcomes. We compared population-based estimates with family-based estimates from within-sibship analyses of up to 164,220 siblings. We tested for heterogeneity between the designs, and applied sensitivity analyses. We involved individuals with lived experience of ADHD in interpreting the findings and shaping how the clinical/public-health implications were described. FindingsPopulation-based analyses implied that greater genetic liability to ADHD increased smoking, alcohol use and depressive symptoms, and reduced educational attainment, age at first child and cognitive performance. In family-based analyses, these effects attenuated. For example, the effect on number of depressive symptoms fell from 0{middle dot}059 SD (95% CI 0{middle dot}039, 0{middle dot}080) to 0{middle dot}002 SD (-0{middle dot}052, 0{middle dot}055), and age at first child increased from -0{middle dot}045 SD (-0{middle dot}058, -0{middle dot}033) to 0{middle dot}003 SD (-0{middle dot}040, 0{middle dot}047), with significant differences between designs (p=0{middle dot}048 and p=0{middle dot}034). Findings were consistent across sensitivity analyses. InterpretationMuch of the excess health and behavioural burden attributed to ADHD may reflect the family and environmental context in which ADHD occurs, rather than an individuals own ADHD. Interventions targeting the individual might not reduce these outcomes as much as expected. Distinguishing such effects requires family-based designs. FundingMedical Research Council, UK Research and Innovation, Research Council of Norway, US National Institute of Mental Health, and Australian National Health and Medical Research Council. Research in contextO_ST_ABSEvidence before this studyC_ST_ABSAttention-deficit hyperactivity disorder (ADHD), and higher genetic liability to ADHD, are associated with a wide range of adverse health, behavioural, and social outcomes. A 2024 umbrella review of the impacts of ADHD summarised consistent associations with addiction, mental and physical illness, lower educational attainment, and social difficulties. Earlier reviews of Mendelian randomization studies of ADHD reached similar conclusions, reporting apparent causal effects on smoking, depression, body-mass index, and educational attainment. A broad two-sample Mendelian randomization analysis of ADHD across more than 100 traits corroborated these findings. Almost all of this genetic evidence, however, comes from samples of unrelated individuals, in which estimates can be confounded by population stratification, assortative mating, and dynastic effects. We searched PubMed and Google Scholar from database inception to 20/07/26 using terms related to ADHD, Mendelian randomization, and within-family designs (Supplementary note), without language restrictions. We identified eight relevant studies, however only three used a within-family or trio Mendelian randomization design. None used a large within-family Mendelian randomization design to investigate the effects of genetic liability to ADHD on health or behavioural outcomes while separating individuals liability from familial influences. Added value of this studyTo our knowledge, this is the largest within-family Mendelian randomization study of genetic liability to ADHD, comparing conventional population-based estimates with family-based estimates across 16 outcomes in up to 164,220 siblings. Population-based estimates reproduced previously reported associations, but most attenuated in family-based analyses. For depressive symptoms and age at first child, the two designs significantly differed, indicating that the population-based estimates were inflated by familial factors. Implications of all the available evidenceMuch of the excess health, behavioural, and social burden attributed to ADHD may reflect the family and environmental context in which ADHD arises, rather than an individuals own liability. If so, interventions directed solely at the individual may not reduce these outcomes as much as observational and population-based estimates imply. These findings should be interpreted alongside the broader evidence rather than as a basis for immediate changes in practice, and they underscore the need for larger family-based genetic studies.

Created on 02 Nov. 2026

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Weekly letter Presented in "Brain and behaviour this week" of 2 November 2026. Brain and behaviour this week: What wiring explains—and what context changes

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Familial factors inflate the estimated effects of genetic liability to ADHD on behavioural outcomes

The essentials

Question

Method

Findings

Limitations

Why it matters

Read further

Definitions

ADHD, Genetics and Family Life: Untangling the Roots of Adverse Outcomes

Why Genetic Associations Can Be Misleading

What Comparing Siblings Adds

Several Associations Became Smaller Within Families

Smaller Estimates Do Not Settle Every Question

What This Means for ADHD Support

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