scholarly journals Causal effect of children’s secondary education on parental health outcomes: findings from a natural experiment in Botswana

BMJ Open ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. e043247
Author(s):  
Jan Ole Ludwig ◽  
Neil M Davies ◽  
Jacob Bor ◽  
Jan-Walter De Neve
Keyword(s):  
Educational Attainment ◽  
Natural Experiment ◽  
Policy Reform ◽  
Causal Effect ◽  
Sensitivity Analyses ◽  
Secondary Outcome ◽  
Secondary Schooling ◽  
Mothers And Fathers ◽  
Random Samples ◽  
Exposed Child

ObjectivesA growing literature highlights the intergenerational transmission of human capital from parents to children. However, far less is known about ‘upward transmission’ from children to parents. In this study, we use a 1996 Botswana education policy reform as a natural experiment to identify the causal effect of children’s secondary schooling on their parents’ health.SettingBotswana’s decennial census (2001 and 2011). Data were obtained through the Integrated Public Use Microdata Series and are 10% random samples of the complete population in each of these census years.ParticipantsSurvey respondents who were citizens born in Botswana, at least 18 years old at the time of the census and born in or after 1975 (n=89 721).Primary and secondary outcome measuresParental survival and disability at the time of the census, separately for mothers and fathers.ResultsThe 1996 reform caused a large increase in grade 10 enrolment, inducing an additional 0.4 years of schooling for the first cohorts affected (95% CI 0.3 to 0.5, p<0.001). The reform, however, had no effect on parental survival and disability by the time exposed child cohorts reach age 30. Results were robust to a wide array of sensitivity analyses.ConclusionsThis study found little evidence that parents’ survival and disability were affected by their offspring’s educational attainment in Botswana. Parents’ health may not be necessarily affected by increasing their offspring’s educational attainment.

Causal Returns to Education

2006 ◽  
Vol 226 (1) ◽  
Author(s):  
Anton L. Flossmann ◽  
Winfried Pohlmeier
Keyword(s):  
Educational Attainment ◽  
Educational Policy ◽  
Empirical Evidence ◽  
Returns To Education ◽  
Causal Effect ◽  
Causal Effects ◽  
Continuous Treatment ◽  
Treatment Variable ◽  
Secondary Schooling ◽  
Upper Secondary

SummaryThis paper surveys the empirical evidence on causal effects of education on earnings for Germany and compares alternative studies in the light of their underlying identifying assumptions. We work out the different assumptions taken by various studies, which lead to rather different interpretations of the estimated causal effect. In particular, we are interested in the question to what extend causal return estimates are informative regarding educational policy advice. Despite the substantial methodological differences, we have to conclude that the empirical findings for Germany are quite robust and do not deviate substantially from each other. This also holds for the few studies which rely on ignorability conditions, regardless of whether they use educational attainment as a continuous treatment variable or as a discrete treatment indicator. Own estimates based on the matching approach indicate that the selection into upper secondary schooling is suboptimal

scholarly journals Does smoking cause lower educational attainment and general cognitive ability? Triangulation of causal evidence using multiple study designs

2020 ◽  
pp. 1-9
Author(s):  
Suzanne H. Gage ◽  
Hannah M. Sallis ◽  
Glenda Lassi ◽  
Robyn E. Wootton ◽  
Claire Mokrysz ◽  
...  
Keyword(s):  
Educational Attainment ◽  
Cognitive Ability ◽  
Fluid Intelligence ◽  
Causal Effect ◽  
Smoking Initiation ◽  
Sensitivity Analyses ◽  
Mendelian Randomisation ◽  
General Cognitive Ability ◽  
Inverse Variance ◽  
Lower Educational Attainment

Abstract Background Observational studies have found associations between smoking and both poorer cognitive ability and lower educational attainment; however, evaluating causality is challenging. We used two complementary methods to explore this. Methods We conducted observational analyses of up to 12 004 participants in a cohort study (Study One) and Mendelian randomisation (MR) analyses using summary and cohort data (Study Two). Outcome measures were cognitive ability at age 15 and educational attainment at age 16 (Study One), and educational attainment and fluid intelligence (Study Two). Results Study One: heaviness of smoking at age 15 was associated with lower cognitive ability at age 15 and lower educational attainment at age 16. Adjustment for potential confounders partially attenuated findings (e.g. fully adjusted cognitive ability β −0.736, 95% CI −1.238 to −0.233, p = 0.004; fully adjusted educational attainment β −1.254, 95% CI −1.597 to −0.911, p < 0.001). Study Two: MR indicated that both smoking initiation and lifetime smoking predict lower educational attainment (e.g. smoking initiation to educational attainment inverse-variance weighted MR β −0.197, 95% CI −0.223 to −0.171, p = 1.78 × 10−49). Educational attainment results were robust to sensitivity analyses, while analyses of general cognitive ability were less so. Conclusion We find some evidence of a causal effect of smoking on lower educational attainment, but not cognitive ability. Triangulation of evidence across observational and MR methods is a strength, but the genetic variants associated with smoking initiation may be pleiotropic, suggesting caution in interpreting these results. The nature of this pleiotropy warrants further study.

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 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 Does Smoking Cause Lower Educational Attainment and General Cognitive Ability? Triangulation of causal evidence using multiple study designs

2019 ◽  
Author(s):  
Suzanne H. Gage ◽  
Hannah Sallis ◽  
Glenda Lassi ◽  
Robyn Wootton ◽  
Claire Mokrysz ◽  
...  
Keyword(s):  
Cohort Study ◽  
Educational Attainment ◽  
Cognitive Ability ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Smoking Initiation ◽  
Sensitivity Analyses ◽  
Genome Wide Association Studies ◽  
Summary Statistics ◽  
Lower Educational Attainment

AbstractObjectivesObservational epidemiological studies have found associations between smoking and both poorer cognitive ability and lower educational attainment; however, evaluating causality is more challenging. We used two complementary methods to attempt to ascertain whether smoking causes poorer cognitive ability and lower educational attainment.DesignA cohort study (Study One) and a two-sample Mendelian randomization study using publicly-available summary statistics (Study Two).SettingThe Avon Longitudinal Study of Parents and Children (ALSPAC), a birth-cohort study based in Bristol, United Kingdom, and general population samples from published genome-wide association studies (GWAS).ParticipantsUp to 12,004 young people in ALSPAC (complete case analysis N = 2,107) (Study One and Study Two), and summary statistics from three previously published GWAS (not individual-level data) (Study Two).Main outcome measuresCognitive ability at age 15 (assessed via the Wechsler Abbreviated Scale of Intelligence) and educational attainment at age 16 (assessed via school records) (Study One), and educational attainment (measured as years in education) and fluid intelligence from previously published GWAS (Study Two).ResultsIn Study One, heaviness of smoking at age 15 was associated with lower cognitive ability at age 15 and lower educational attainment at age 16. Adjustment for potential confounders and earlier cognitive ability or educational attainment attenuated findings although evidence of an association remained (e.g., fully adjusted cognitive ability beta - 0.736, 95% CI −1.238 to −0.233, P = 0.004; fully adjusted educational attainment beta −1.254, 95% CI −1.597 to −0.911, P < 0.001). Comparable results were found in sensitivity analyses of multiply imputed data. In Study Two, two-sample Mendelian randomization indicated that both smoking initiation and lifetime smoking lower educational attainment and cognitive ability (e.g., smoking initiation to educational attainment inverse-variance weighted MR beta −0.197, 95% CI −0.223, −0.171, P = 1.78 × 10−49). Educational attainment results were robust to various sensitivity analyses, while cognition analyses were less so.ConclusionsOur results provide evidence consistent with a causal effect of smoking on lower educational attainment, although were less consistent for cognitive ability. The triangulation of evidence from observational and Mendelian randomisation methods is an important strength for causal inference.Summary boxesWhat is already known on this topicAssociations are seen between smoking and both educational attainment and cognition. These is some evidence that educational attainment might causally influence smoking, but causality in the opposite direction has not been assessed.What this study addsUsing multiple methodologies, we found evidence consistent with a causal effect of smoking on lower educational attainment. An exploration of potential mechanisms could inform the development of interventions to mitigate this risk.

Educational Attainment Has a Causal Effect on Economic, But Not Social Ideology: Evidence from Discordant Twins

2021 ◽  
pp. 003232172110087
Author(s):  
Stig Hebbelstrup Rye Rasmussen ◽  
Aaron Weinschenk ◽  
Asbjørn Sonne Nørgaard ◽  
Jacob von Bornemann Hjelmborg ◽  
Robert Klemmensen
Keyword(s):  
Educational Attainment ◽  
Causal Effect ◽  
Local Context ◽  
Parental Socialization ◽  
Twin Design ◽  
Social Ideology ◽  
Economic Ideology ◽  
Discordant Twins ◽  
The Relationship ◽  
Political Variables

In this article, we examine the nature of the relationship between educational attainment and ideology. Some scholars have argued that the effect of education on political variables like ideology is inflated due to unaccounted-for family factors, such as genetic predispositions and parental socialization. Using the discordant twin design and data from a large sample of Danish twins, we find that after accounting for confounders rooted in the family, education has a (quasi)-causal effect on economic ideology, but not social ideology. We also examine whether the relationship between education and economic ideology is moderated by levels of economic hardship in the local context where individuals reside. We find that the (quasi)-causal effect of education on economic ideology increases in economically challenged areas.

scholarly journals Mindfulness-based and acceptance-based programmes in the treatment of obsessive–compulsive disorder: a study protocol for a systematic review and meta-analysis

BMJ Open ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. e050329
Author(s):  
Johannes Julian Bürkle ◽  
Johannes Caspar Fendel ◽  
Stefan Schmidt
Keyword(s):  
Systematic Review ◽  
Depressive Symptoms ◽  
Obsessive Compulsive Disorder ◽  
Meta Analysis ◽  
Sensitivity Analyses ◽  
Secondary Outcome ◽  
Controlled Trials ◽  
Obsessive Compulsive ◽  
Compulsive Disorder

IntroductionCognitive–behavioural therapy (CBT) with exposure and response prevention is the recommended standard for the treatment of obsessive–compulsive disorder (OCD). However, a high proportion of patients refuse this treatment, do not respond or relapse shortly after treatment. Growing evidence suggests that mindfulness-based and acceptance-based programmes (MABPs) are an effective option for the treatment of OCD. This systematic review and meta-analysis will examine the effectiveness of MABPs in treating OCD. We also aimed to explore potential moderators of the programmes’ effectiveness.Methods and analysisWe will systematically search MEDLINE, Embase, PsycINFO, PSYINDEX, Web of Science, CINAHL and Cochrane Register of Controlled Trials (no language restrictions) for studies that evaluate the effect of MABPs on patients with OCD. We will conduct backward and forward citation searches of included studies and relevant reviews and contact corresponding authors. The primary outcome will be pre-post intervention change in symptom severity. A secondary outcome will be change in depressive symptoms. Two reviewers will independently screen the records, extract the data and rate the methodological quality of the studies. We will include both controlled and uncontrolled trials. Randomised controlled trials will be meta-analysed, separately assessing between-group effects. A second meta-analysis will assess the within-group effect of all eligible studies. We will explore moderators and sources of heterogeneity such as the specific programme, study design, changes in depressive symptoms, hours of guided treatment, control condition and prior therapy (eg, CBT) using metaregression and subgroup analyses. We will perform sensitivity analyses using follow-up data. A narrative synthesis will also be pursued. We will use the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system to assess the quality of the evidence.Ethics and disseminationEthical approval is not required. Results will be published in peer-reviewed journals and presented at international conferences.

scholarly journals Bias in two-sample Mendelian randomization when using heritable covariable-adjusted summary associations

2021 ◽  
Author(s):  
Fernando Pires Hartwig ◽  
Kate Tilling ◽  
George Davey Smith ◽  
Deborah A Lawlor ◽  
Maria Carolina Borges
Keyword(s):  
Waist Circumference ◽  
Genetic Variants ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Association Studies ◽  
Real Data ◽  
Sensitivity Analyses ◽  
Effect Estimate ◽  
Genome Wide Association Studies ◽  
Residual Confounding

Abstract Background Two-sample Mendelian randomization (MR) allows the use of freely accessible summary association results from genome-wide association studies (GWAS) to estimate causal effects of modifiable exposures on outcomes. Some GWAS adjust for heritable covariables in an attempt to estimate direct effects of genetic variants on the trait of interest. One, both or neither of the exposure GWAS and outcome GWAS may have been adjusted for covariables. Methods We performed a simulation study comprising different scenarios that could motivate covariable adjustment in a GWAS and analysed real data to assess the influence of using covariable-adjusted summary association results in two-sample MR. Results In the absence of residual confounding between exposure and covariable, between exposure and outcome, and between covariable and outcome, using covariable-adjusted summary associations for two-sample MR eliminated bias due to horizontal pleiotropy. However, covariable adjustment led to bias in the presence of residual confounding (especially between the covariable and the outcome), even in the absence of horizontal pleiotropy (when the genetic variants would be valid instruments without covariable adjustment). In an analysis using real data from the Genetic Investigation of ANthropometric Traits (GIANT) consortium and UK Biobank, the causal effect estimate of waist circumference on blood pressure changed direction upon adjustment of waist circumference for body mass index. Conclusions Our findings indicate that using covariable-adjusted summary associations in MR should generally be avoided. When that is not possible, careful consideration of the causal relationships underlying the data (including potentially unmeasured confounders) is required to direct sensitivity analyses and interpret results with appropriate caution.

The Causal Effect of Polls on Turnout Intention: A Local Randomization Regression Discontinuity Approach

2021 ◽  
pp. 1-7
Author(s):  
Pablo Brugarolas ◽  
Luis Miller
Keyword(s):  
Political Science ◽  
Natural Experiment ◽  
Regression Discontinuity ◽  
Time Window ◽  
Causal Effect

Abstract This letter reports the results of a study that combined a unique natural experiment and a local randomization regression discontinuity approach to estimate the effect of polls on turnout intention. We found that the release of a poll increases turnout intention by 5%. This effect is robust to a number of falsification tests of predetermined covariates, placebo outcomes, and changes in the time window selected to estimate the effect. The letter discusses the advantages of the local randomization approach over the standard continuity-based design to study important cases in political science where the running variable is discrete; a method that may expand the range of empirical topics that can be analyzed using regression discontinuity methods.

scholarly journals Using genetic variants to evaluate the causal effect of serum vitamin D concentration on COVID-19 susceptibility, severity and hospitalization traits: a Mendelian randomization study

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Zhiyong Cui ◽  
Yun Tian
Keyword(s):  
Vitamin D ◽  
Fixed Effects ◽  
Mendelian Randomization ◽  
Causal Effect ◽  
Serum Vitamin ◽  
Vitamin D Supplementation ◽  
Sensitivity Analyses ◽  
Global Test ◽  
Serum Vitamin D

Abstract Background The coronavirus disease 2019 (COVID-19) pandemic has struck globally and is exerting a devastating toll on humans. The pandemic has led to calls for widespread vitamin D supplementation in public. However, evidence supporting the role of vitamin D in the COVID-19 pandemic remains controversial. Methods We performed a two-sample Mendelian randomization (MR) analysis to analyze the causal effect of the 25-hydroxyvitamin D [25(OH)D] concentration on COVID-19 susceptibility, severity and hospitalization traits by using summary-level GWAS data. The causal associations were estimated with inverse variance weighted (IVW) with fixed effects (IVW-fixed) and random effects (IVW-random), MR-Egger, weighted edian and MR Robust Adjusted Profile Score (MR.RAPS) methods. We further applied the MR Steiger filtering method, MR Pleiotropy RESidual Sum and Outlier (MR-PRESSO) global test and PhenoScanner tool to check and remove single nucleotide polymorphisms (SNPs) that were horizontally pleiotropic. Results We found no evidence to support the causal associations between the serum 25(OH)D concentration and the risk of COVID-19 susceptibility [IVW-fixed: odds ratio (OR) = 0.9049, 95% confidence interval (CI) 0.8197–0.9988, p = 0.0473], severity (IVW-fixed: OR = 1.0298, 95% CI 0.7699–1.3775, p = 0.8432) and hospitalized traits (IVW-fixed: OR = 1.0713, 95% CI 0.8819–1.3013, p = 0.4878) using outlier removed sets at a Bonferroni-corrected p threshold of 0.0167. Sensitivity analyses did not reveal any sign of horizontal pleiotropy. Conclusions Our MR analysis provided precise evidence that genetically lowered serum 25(OH)D concentrations were not causally associated with COVID-19 susceptibility, severity or hospitalized traits. Our study did not provide evidence assessing the role of vitamin D supplementation during the COVID-19 pandemic. High-quality randomized controlled trials are necessary to explore and define the role of vitamin D supplementation in the prevention and treatment of COVID-19.

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