scholarly journals Exploring the causal effects of genetic liability to ADHD and Autism on Alzheimer’s disease

2020 ◽  
Author(s):  
Panagiota Pagoni ◽  
Christina Dardani ◽  
Beate Leppert ◽  
Roxanna Korologou-Linden ◽  
George Davey Smith ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Educational Attainment ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Autism Spectrum ◽  
Causal Effects ◽  
Direct Effects ◽  
Limited Evidence ◽  
Genetic Liability

ABSTRACTBackgroundThere are very few studies investigating possible links between Attention Deficit Hyperactivity Disorder (ADHD), Autism Spectrum Disorder (ASD) and Alzheimer’s disease and these have been limited by small sample sizes, diagnostic and recall bias. However, neurocognitive deficits affecting educational attainment in individuals with ADHD could be risk factors for Alzheimer’s later in life while hyper plasticity of the brain in ASD and strong positive genetic correlations of ASD with IQ and educational attainment could be protective against Alzheimer’s.MethodsWe estimated the bidirectional total causal effects of genetic liability to ADHD and ASD on Alzheimer’s disease through two-sample Mendelian randomization. We investigated their direct effects, independent of educational attainment and IQ, through Multivariable Mendelian randomization.ResultsThere was limited evidence to suggest that genetic liability to ADHD (OR=1.00, 95% CI: 0.98 to 1.02, p=0.39) or ASD (OR=0.99, 95% CI: 0.97 to 1.01, p=0.70) was associated with risk of Alzheimer’s disease. Similar causal effect estimates were identified when the direct effects, independent of educational attainment (ADHD: OR=1.00, 95% CI: 0.99 to 1.01, p=0.07; ASD: OR=0.99, 95% CI: 0.98 to 1.00, p=0.28) and IQ (ADHD: OR=1.00, 95% CI: 0.99 to 1.02. p=0.29; ASD: OR=0.99, 95% CI: 0.98 to 1.01, p=0.99), were assessed. Finally, genetic liability to Alzheimer’s disease was not found to have a causal effect on risk of ADHD or ASD (ADHD: OR=1.12, 95% CI: 0.86 to 1.44, p=0.37; ASD: OR=1.19, 95% CI: 0.94 to 1.51, p=0.14).ConclusionsIn the first study to date investigating the causal associations between genetic liability to ADHD, ASD and Alzheimer’s, within an MR framework, we found limited evidence to suggest a causal effect. It is important to encourage future research using ADHD and ASD specific subtype data, as well as longitudinal data in order to further elucidate any associations between these conditions.

scholarly journals Education, intelligence and Alzheimer’s disease: Evidence from a multivariable two-sample Mendelian randomization study

2018 ◽  
Author(s):  
Emma L Anderson ◽  
Laura D Howe ◽  
Kaitlin H Wade ◽  
Yoav Ben-Shlomo ◽  
W. David Hill ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Educational Attainment ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Univariate Analysis ◽  
Causal Effects ◽  
Training Interventions ◽  
Bidirectional Relationship ◽  
Years Of Schooling

AbstractObjectivesTo examine whether educational attainment and intelligence have causal effects on risk of Alzheimer’s disease (AD), independently of each other.DesignTwo-sample univariable and multivariable Mendelian Randomization (MR) to estimate the causal effects of education on intelligence and vice versa, and the total and independent causal effects of both education and intelligence on risk of AD.Participants17,008 AD cases and 37,154 controls from the International Genomics of Alzheimer’s Project (IGAP) consortiumMain outcome measureOdds ratio of AD per standardised deviation increase in years of schooling and intelligenceResultsThere was strong evidence of a causal, bidirectional relationship between intelligence and educational attainment, with the magnitude of effect being similar in both directions. Similar overall effects were observed for both educational attainment and intelligence on AD risk in the univariable MR analysis; with each SD increase in years of schooling and intelligence, odds of AD were, on average, 37% (95% CI: 23% to 49%) and 35% (95% CI: 25% to 43%) lower, respectively. There was little evidence from the multivariable MR analysis that educational attainment affected AD risk once intelligence was taken into account, but intelligence affected AD risk independently of educational attainment to a similar magnitude observed in the univariate analysis.ConclusionsThere is robust evidence for an independent, causal effect of intelligence in lowering AD risk, potentially supporting a role for cognitive training interventions to improve aspects of intelligence. However, given the observed causal effect of educational attainment on intelligence, there may also be support for policies aimed at increasing length of schooling to lower incidence of AD.

scholarly journals Education, intelligence and Alzheimer’s disease: evidence from a multivariable two-sample Mendelian randomization study

2020 ◽  
Vol 49 (4) ◽  
pp. 1163-1172 ◽  
Author(s):  
Emma L Anderson ◽  
Laura D Howe ◽  
Kaitlin H Wade ◽  
Yoav Ben-Shlomo ◽  
W David Hill ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Educational Attainment ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Univariate Analysis ◽  
Causal Effects ◽  
Bidirectional Relationship ◽  
Robust Evidence ◽  
Years Of Schooling

Abstract Objectives To examine whether educational attainment and intelligence have causal effects on risk of Alzheimer’s disease (AD), independently of each other. Design Two-sample univariable and multivariable Mendelian randomization (MR) to estimate the causal effects of education on intelligence and vice versa, and the total and independent causal effects of both education and intelligence on AD risk. Participants 17 008 AD cases and 37 154 controls from the International Genomics of Alzheimer’s Project (IGAP) consortium. Main outcome measure Odds ratio (OR) of AD per standardized deviation increase in years of schooling (SD = 3.6 years) and intelligence (SD = 15 points on intelligence test). Results There was strong evidence of a causal, bidirectional relationship between intelligence and educational attainment, with the magnitude of effect being similar in both directions [OR for intelligence on education = 0.51 SD units, 95% confidence interval (CI): 0.49, 0.54; OR for education on intelligence = 0.57 SD units, 95% CI: 0.48, 0.66]. Similar overall effects were observed for both educational attainment and intelligence on AD risk in the univariable MR analysis; with each SD increase in years of schooling and intelligence, odds of AD were, on average, 37% (95% CI: 23–49%) and 35% (95% CI: 25–43%) lower, respectively. There was little evidence from the multivariable MR analysis that educational attainment affected AD risk once intelligence was taken into account (OR = 1.15, 95% CI: 0.68–1.93), but intelligence affected AD risk independently of educational attainment to a similar magnitude observed in the univariate analysis (OR = 0.69, 95% CI: 0.44–0.88). Conclusions There is robust evidence for an independent, causal effect of intelligence in lowering AD risk. The causal effect of educational attainment on AD risk is likely to be mediated by intelligence.

scholarly journals Is genetic liability to ADHD and ASD causally linked to educational attainment?

2020 ◽  
Author(s):  
Christina Dardani ◽  
Beate Leppert ◽  
Lucy Riglin ◽  
Dheeraj Rai ◽  
Laura D Howe ◽  
...  
Keyword(s):  
Educational Attainment ◽  
Causal Effect ◽  
Educational Interventions ◽  
Autism Spectrum ◽  
Causal Effects ◽  
Sensitivity Analyses ◽  
Reverse Direction ◽  
Genetic Liability ◽  
Higher Educational ◽  
Higher Educational Attainment

ABSTRACTBackgroundIndividuals with Attention Deficit Hyperactivity Disorder (ADHD) or Autism Spectrum Disorder (ASD) are at risk of poor educational outcomes. Parental educational attainment has also been associated with risk of ADHD/ASD in the offspring. Despite evidence that ADHD and ASD show genetic links to educational attainment, less is known on the causal nature of the associations and the possible role of IQ.MethodsWe assessed the total causal effects of genetic liability to ADHD/ASD on educational attainment using two-sample Mendelian randomization (MR). We assessed the possible contribution of IQ to the identified causal effects by estimating the “direct” effects of ADHD/ASD on educational attainment, independent of IQ, using Multivariable MR (MVMR). Reverse direction analyses were performed. The latest GWAS meta-analyses of ADHD, ASD, educational attainment and IQ were used. Causal effect estimates were generated using inverse variance weighted models (IVW). Sensitivity analyses were performed to assess the robustness of the estimates and the presence of pleiotropy.ResultsGenetic liability to ADHD had a total (MRIVW:-3.3 months per doubling of liability to ADHD; 95%CI: -4.8 to -1.9; pval= 5*10−6) and direct negative causal effect on educational attainment (MVMRIVW:-1.6 months per doubling of liability to ADHD; 95%CI: -2.5 to -0.6; pval= 4*10−4). There was little evidence of a total causal effect of genetic liability to ASD on educational attainment (MRIVW: 4 days, per doubling of liability to ASD; 95%CI: -4.9 months to 5.6 months; pval= 0.9) but some evidence of a direct effect not via IQ (MVMRIVW:29 days per doubling the genetic liability to ASD; 95%CI: 2 to 48; pval= 0.03). Reverse direction analyses suggested that genetic liability to higher educational attainment was associated with lower risk of ADHD (MRIVWOR: 0.3 per standard deviation (SD) increase; 95%CI: 0.26 to 0.36; pval= 6*10−51), even after IQ was entered in the models (MVMRIVWOR: 0.33 per SD increase; 95%CI: 0.26 to 0.43; pval= 6*10−17). On the contrary, there was evidence consistent with a positive causal effect of genetic liability to higher educational attainment on risk of ASD (MRIVWOR: 1.51 per SD increase; 95%CI: 1.29 to 1.77; pval= 4*10−7), which was found to be largely explained by IQ (MVMRIVWOR per SD increase: 1.24; 95%CI: 0.96 to 1.60; pval= 0.09).ConclusionsOur findings suggest that despite the genetic and phenotypic overlap between ADHD and ASD, they present highly differentiated causal associations with educational attainment. This highlights the necessity for specialized educational interventions for children with ADHD and ASD. Further research is needed in order to decipher whether the identified causal effects reflect parentally transmitted effects, diagnostic masking, or selection bias.

scholarly journals Causal Association Between Heart Failure and Alzheimer’s Disease: A Two-Sample Bidirectional Mendelian Randomization Study

2022 ◽  
Vol 12 ◽  
Author(s):  
Chenglin Duan ◽  
Jingjing Shi ◽  
Guozhen Yuan ◽  
Xintian Shou ◽  
Ting Chen ◽  
...  
Keyword(s):  
Heart Failure ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sensitivity Analysis ◽  
Causal Relationship ◽  
Observational Studies ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Causal Relationships ◽  
Simple Mode

Background: Traditional observational studies have demonstrated an association between heart failure and Alzheimer’s disease. The strengths of observational studies lie in their speed of implementation, cost, and applicability to rare diseases. However, observational studies have several limitations, such as uncontrollable confounders. Therefore, we employed Mendelian randomization of genetic variants to evaluate the causal relationships existing between AD and HF, which can avoid these limitations.Materials and Methods: A two-sample bidirectional MR analysis was employed. All datasets were results from the UK’s Medical Research Council Integrative Epidemiology Unit genome-wide association study database, and we conducted a series of control steps to select the most suitable single-nucleotide polymorphisms for MR analysis, for which five primary methods are offered. We reversed the functions of exposure and outcomes to explore the causal direction of HF and AD. Sensitivity analysis was used to conduct several tests to avoid heterogeneity and pleiotropic bias in the MR results.Results: Our MR studies did not support a meaningful causal relationship between AD on HF (MR-Egger, p = 0.634 > 0.05; weighted median (WM), p = 0.337 > 0.05; inverse variance weighted (IVW), p = 0.471 > 0.05; simple mode, p = 0.454 > 0.05; weighted mode, p = 0.401 > 0.05). At the same time, we did not find a significant causal relationship between HF and AD with four of the methods (MR-Egger, p = 0.195 > 0.05; IVW, p = 0.0879 > 0.05; simple mode, p = 0.170 > 0.05; weighted mode, p = 0.110 > 0.05), but the WM method indicated a significant effect of HF on AD (p = 0.025 < 0.05). Because the statistical powers of IVW and MR-Egger are more than that of WM, we think that there is no causal effect of HF on AD. Sensitivity analysis and horizontal pleiotropy were not detected in the MR analysis.Conclusion: Our results did not provide significant evidence indicating any causal relationships between HF and AD in the European population. Therefore, more large-scale datasets or datasets related to similar factors are expected for further MR analysis.

scholarly journals Causal effect of Insulin Resistance on Small Vessel Stroke and Alzheimer's Disease: A Mendelian Randomization Analysis

2021 ◽  
Author(s):  
Mengyuan Zhou ◽  
Hao Li ◽  
Yongjun Wang ◽  
Yuesong Pan ◽  
Yilong Wang
Keyword(s):  
Alzheimer’S Disease ◽  
Insulin Resistance ◽  
Alzheimer's Disease ◽  
Gold Standard ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Small Vessel ◽  
European Ancestry ◽  
Fasting Insulin ◽  
Inverse Variance

Abstract Background The causal effect of insulin resistance on small vessel stroke and Alzheimer Disease was controversial in previous studies. Methods We selected 12 single-nucleotide polymorphisms (SNPs) associated with body mass index (BMI)-adjusted fasting insulin levels and 5 SNPs associated with gold standard measures of insulin resistance as instrumental variables in Mendelian randomization (MR) analyses. Summary statistical data of SNP-small vessel stroke and of SNP-AD associations were derived from the Multi-ancestry Genome-Wide Association Study of Stroke Consortium and Psychiatric Genomics Consortium-Alzheimer’s Disease Workgroup data of individuals of European ancestry. Two-sample MR estimates were conducted with inverse-variance-weighted, robust inverse-variance-weighted, simple median, weighted median, weighted mode-based estimator, and MR pleiotropy residual sum and outlier methods. Results Genetically predicted higher insulin resistance had a higher odds ratio (OR) of small vessel stroke (OR 1.23; 95% confidence interval [CI] 1.05–1.44; P = 0.01 using BMI-adjusted fasting insulin; OR 1.25; 95% CI 1.07–1.46; P = 0.006 using gold standard measure of insulin resistance) and AD (OR 1.13; 95% CI 1.04–1.23; P = 0.004 using BMI-adjusted fasting insulin; OR 1.02; 95% CI 1.00-1.03; P = 0.03 using gold standard measures of insulin resistance) using the inverse-variance-weighted method. No evidence of pleiotropy was found using MR-Egger regression. Conclusion Our findings provide genetic support for a causal effect of insulin resistance on small vessel stroke and AD. Further investigation on the involved mechanisms is needed.

scholarly journals Multigenomics Reveals the Causal Effect of Herpes Simplex Virus in Alzheimer’s Disease: A Two-Sample Mendelian Randomization Study

2022 ◽  
Vol 12 ◽  
Author(s):  
Yuwei Zhang ◽  
Jiaojiao Qu ◽  
Li Luo ◽  
Zhongshun Xu ◽  
Xiao Zou
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Herpes Simplex Virus ◽  
Herpes Simplex ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Sensitivity Analyses ◽  
Analysis Model ◽  
Simplex Virus ◽  
Hsv 1

In recent years, the herpes virus infectious hypothesis for Alzheimer’s disease (AD) has gained support from an increasing number of researchers. Herpes simplex virus (HSV) is a potential risk factor associated with AD. This study assessed whether HSV has a causal relationship with AD using a two-sample Mendelian randomization analysis model. Six single-nucleotide polymorphisms (SNPs) associated with HSV-1 and thirteen SNPs associated with HSV-2 were used as instrumental variables in the MR analysis. We estimated MR values of relevance between exposure and the risk of AD using inverse-variance weighted (IVW) method, MR-Egger regression (Egger), and weighted median estimator (WME). To make the conclusion more robust and reliable, sensitivity analyses and RadialMR were performed to evaluate the pleiotropy and heterogeneity. We found that anti-HSV-1 IgG measurements were not associated with risk of AD (OR, 0.96; 95% CI, 0.79–1.18; p = 0.736), and the same was true for HSV-2 (OR, 1.03; 95% CI, 0.94–1.12; p = 0.533). The findings indicated that any HSV infection does not appear to be a genetically valid target of intervention in AD.

Social Isolation, Social Interaction, and Alzheimer’s Disease: A Mendelian Randomization Study

2021 ◽  
Vol 80 (2) ◽  
pp. 665-672
Author(s):  
Ling-Xiao Shen ◽  
Yu-Xiang Yang ◽  
Kevin Kuo ◽  
Hong-Qi Li ◽  
Shi-Dong Chen ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Social Interaction ◽  
Social Isolation ◽  
Social Engagement ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Sensitivity Analyses ◽  
Epidemiological Methods ◽  
Sports Club

Background: Social isolation and social interaction have been suggested to be associated with Alzheimer’s disease. However, the causality cannot be unambiguously assessed as traditional epidemiological methods are easily subject to unmeasured confounders and potential bias. Objective: To examine bidirectional relationships between social isolation, social interaction, and Alzheimer’s disease using Mendelian randomization method for assessing potential causal inference. Methods: This bidirectional two-sample Mendelian randomization study used independent genetic variants associated with social isolation and social interaction (n = 302,567–487,647), and Alzheimer’s disease (n = 455,258). MR analyses were performed using the inverse-variance-weighted (IVW) as the main MR analytical method to estimate the causal effect. For sensitivity analyses, we applied weighted median, MR Egger to further assess the credibility of the causal effect. Results: Of the five types of social engagement examined in our study, only one showed evidence of an association with the risk of Alzheimer’s disease. Attendance at a gym or sports club (IVW OR per SD change: 0.670; 95% CI: 0.463–0.970; p = 0.034) was inversely associated with the risk of Alzheimer’s disease. We also found that AD may reduce the attendance at religious group (IVW OR per SD change: 1.017; 95% CI: 1.005–1.030; p = 0.004). Conclusion: This study suggests that regular attendance at a gym or sports club is causally associated with reduced risk of Alzheimer’s disease. Further studies are warranted to elucidate potential mechanisms.

scholarly journals Is disrupted sleep a risk factor for Alzheimer’s disease? Evidence from a two-sample Mendelian randomization analysis

2020 ◽  
Author(s):  
Emma L Anderson ◽  
Rebecca C Richmond ◽  
Samuel E Jones ◽  
Gibran Hemani ◽  
Kaitlin H Wade ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Risk Factor ◽  
Daytime Sleepiness ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Association Studies ◽  
Self Report ◽  
Genome Wide Association Studies ◽  
Tentative Evidence

Abstract Background It is established that Alzheimer’s disease (AD) patients experience sleep disruption. However, it remains unknown whether disruption in the quantity, quality or timing of sleep is a risk factor for the onset of AD. Methods We used the largest published genome-wide association studies of self-reported and accelerometer-measured sleep traits (chronotype, duration, fragmentation, insomnia, daytime napping and daytime sleepiness), and AD. Mendelian randomization (MR) was used to estimate the causal effect of self-reported and accelerometer-measured sleep parameters on AD risk. Results Overall, there was little evidence to support a causal effect of sleep traits on AD risk. There was some suggestive evidence that self-reported daytime napping was associated with lower AD risk [odds ratio (OR): 0.70, 95% confidence interval (CI): 0.50–0.99). Some other sleep traits (accelerometer-measured ‘eveningness’ and sleep duration, and self-reported daytime sleepiness) had ORs of a similar magnitude to daytime napping, but were less precisely estimated. Conclusions Overall, we found very limited evidence to support a causal effect of sleep traits on AD risk. Our findings provide tentative evidence that daytime napping may reduce AD risk. Given that this is the first MR study of multiple self-report and objective sleep traits on AD risk, findings should be replicated using independent samples when such data become available.

scholarly journals The causal effect of educational attainment on Alzheimer’s disease: A two-sample Mendelian randomization study

2017 ◽  
Author(s):  
Emma L Anderson ◽  
Kaitlin H Wade ◽  
Gibran Hemani ◽  
Jack Bowden ◽  
Roxanna Korologou-Linden ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Educational Attainment ◽  
Genome Wide Association Study ◽  
Causal Effect ◽  
Sensitivity Analyses ◽  
Nucleotide Polymorphisms ◽  
Inverse Variance ◽  
Higher Educational Attainment ◽  
Years Of Schooling

ABSTRACTBackgroundObservational evidence suggests that higher educational attainment is protective for Alzheimer’s disease (AD). It is unclear whether this association is causal or confounded by demographic and socioeconomic characteristics. We examined the causal effect of educational attainment on AD in a two-sample MR framework.MethodsWe extracted all available effect estimates of the 74 single nucleotide polymorphisms (SNPs) associated with years of schooling from the largest genome-wide association study (GWAS) of educational attainment (N=293,723) and the GWAS of AD conducted by the International Genomics of Alzheimer’s Project (n=17,008 AD cases and 37,154 controls). SNP-exposure and SNP-outcome coefficients were combined using an inverse variance weighted approach, providing an estimate of the causal effect of each SD increase in years of schooling on AD. We also performed appropriate sensitivity analyses examining the robustness of causal effect estimates to the various assumptions and conducted simulation analyses to examine potential survival bias of MR analyses.FindingsWith each SD increase in years of schooling (3.51 years), the odds of AD were, on average, reduced by approximately one third (odds ratio= 0.63, 95% confidence interval [CI]: 0.48 to 0.83, p<0.001). Causal effect estimates were consistent when using causal methods with varying MR assumptions or different sets of SNPs for educational attainment, lending confidence to the magnitude and direction of effect in our main findings. There was also no evidence of survival bias in our study.InterpretationOur findings support a causal role of educational attainment on AD, whereby an additional ∼3.5 years of schooling reduces the odds of AD by approximately one third.

scholarly journals Genetic liability to rheumatoid arthritis on autism and autistic traits: polygenic risk score and Mendelian randomization analyses

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
Amanda Ly ◽  
Beate Leppert ◽  
Dheeraj Rai ◽  
Hannah Jones ◽  
Christina Dardani ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Autistic Traits ◽  
Causal Effects ◽  
Risk Scores ◽  
Polygenic Risk Score ◽  
Genetic Liability ◽  
Polygenic Risk ◽  
Genome Wide

AbstractHigher prevalence of autism in offspring born to mothers with rheumatoid arthritis has been reported in observational studies. We investigated (a) the associations between maternal and offspring’s own genetic liability for rheumatoid arthritis and autism-related outcomes in the offspring using polygenic risk scores (PRS) and (b) whether the effects were causal using Mendelian randomization (MR). Using the latest genome-wide association (GWAS) summary data on rheumatoid arthritis and individual-level data from the Avon Longitudinal Study of Parents and Children, United Kingdom, we constructed PRSs for maternal and offspring genetic liability for rheumatoid arthritis (single-nucleotide polymorphism [SNP] p-value threshold 0.05). We investigated associations with autism, and autistic traits: social and communication difficulties, coherence, repetitive behaviours and sociability. We used modified Poisson regression with robust standard errors. In two-sample MR analyses, we used 40 genome-wide significant SNPs for rheumatoid arthritis and investigated the causal effects on risk for autism, in 18,381 cases and 27,969 controls of the Psychiatric Genetics Consortium and iPSYCH. Sample size ranged from 4992 to 7849 in PRS analyses. We found little evidence of associations between rheumatoid arthritis PRSs and autism-related phenotypes in the offspring (maternal PRS on autism: RR 0.89, 95%CI 0.73–1.07, p = 0.21; offspring’s own PRS on autism: RR 1.11, 95%CI 0.88–1.39, p = 0.39). MR results provided little evidence for a causal effect (IVW OR 1.01, 95%CI 0.98–1.04, p = 0.56). There was little evidence for associations between genetic liability for rheumatoid arthritis on autism-related outcomes in offspring. Lifetime risk for rheumatoid arthritis has no causal effects on autism.

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