Causal Effect Of Educational Attainment Research Articles

Understanding the educational inequalities in suicide attempts and their mediators: a Mendelian randomisation study

BackgroundEducational inequalities in suicide have become increasingly prominent over the past decade. Elucidating modifiable risk factors that serve as intermediaries in the impact of low educational attainment on suicide has...

Causal effects of educational attainment on temporomandibular disorders and the mediating pathways: A Mendelian randomization study.

As one of the most important indicators of socioeconomic status, educational attainment (EA) exhibits a strong association with temporomandibular disorders (TMDs). Despite this link, there is a lack of evidence regarding the causal role of EA in either facilitating or preventing TMDs. This study aimed to investigate the causal effect of education on TMDs and explore potential mediating pathways. Utilizing summary statistics from genome-wide association studies on years of schooling (N = 766 345) and TMDs (N = 211 023), we conducted Mendelian randomization (MR) to assess the overall effect of education. Additionally, a two-step MR approach was employed to evaluate 30 potential mediators and calculate the mediation proportions in the association. Comprehensive sensitivity analyses were used to verify the robustness, heterogeneity, and pleiotropy. Univariable MR analyses revealed a causal effect of lower EA on an increased risk of TMDs (OR: 0.53, 95% CI: 0.43-0.66, p < .001). Five out of 30 modifiable factors were identified as causal mediators in the associations of EA with TMDs, including feeling nervous (mediation proportion: 11.6%), feeling tense (10.2%), depression (9.6%), feeling worry (7.6%) and daily smoking (8.9%). Meanwhile, no pleiotropy was detected in the analyses (p > .05). Our findings supported that higher EA has a protective effect on the onset of TMDs, with partial mediation by psychological disorders and daily smoking. Interventions on these factors thus have the potential of substantially reducing the burden of TMDs attributed to low education.

Cognitive performance's critical role in the progression from educational attainment to moderate to vigorous physical activity: insights from a Mendelian randomization study.

In individuals with high educational levels, moderate to vigorous physical activity (MVPA) is often elevated, yet the causal direction and the role of cognitive performance in this association remain ambiguous. Herein, Mendel randomization (MR) was employed to measure the causal relationship between education, cognitive performance, and moderate to vigorous physical activity. The purpose of this study was to analyze the causal effects of educational attainment on moderate-to-vigorous physical activity (MVPA) levels and to explore potential mediating factors. Two-sample univariate MR analysis was conducted to assess the overall effect of education on moderate to severe physical activity. Besides, a two-step MR analysis was carried out to evaluate the mediating effect of cognitive performance on the impact of education on moderate to severe physical activity. Individuals included were exclusively of European ancestry, with data gathered from extensive genome-wide association studies (GWAS) on education (n = 470,941), cognitive performance (n = 257,841), and moderate-to-vigorous physical activity (MVPA) (n = 377,234). Educational attainment was measured by college graduation status. Cognitive performance encompasses not only psycho-motor speed, memory, and abstract reasoning abilities but also knowledge and skills acquired in professional domains. MVPA is defined as any physical activity that produces a metabolic equivalent (MET) of ≥3.0. The positive two-sample MR analysis showed that education level had a significant protective effect on MVPA deficiency (β = -0.276, 95% CI = -0.354 to -0.199, p = 2.866 × 10-12). However, the reverse two-sample MR analysis showed that MVPA had no significant causal relationship with education level (p = 0.165). Subsequently, the two-step MR analysis indicated that the potential causal protective effect of education on the risk of MVPA deficiency was mostly mediated by cognitive performance (mediating effect β = -0.235, 95% CI = -0.434 to -0.036, and the intermediary ratio was 85.061%). Cognitive performance holds considerable significance in the relationship between education level and MVPA. Consequently, the intervention of cognitive performance may greatly improve the risk of physical inactivity caused by education, thereby promoting individual health.

Causal effect of educational attainment on psoriasis risk mediated by obesity-related traits: Mendelian randomization study.

Causal effect of educational attainment on psoriasis risk mediated by obesity-related traits: Mendelian randomization study.

The causal effect of educational attainment on stress urinary incontinence: a two-sample mendelian randomization study

BackgroundStress urinary incontinence (SUI) is characterized by involuntary urine leakage in response to increased abdominal pressure, such as coughing, laughing, or sneezing. It significantly affects women’s quality of life and imposes a substantial disease burden. While pregnancy and childbirth have been previously identified as risk factors for SUI, educational attainment may also play a role. Therefore, this paper investigates the causal relationship between educational attainment and SUI using two-sample Mendelian randomization (TSMR) analysis, years of schooling (YOS), and college or university degree (CUD) as proxies.MethodsSummary statistics of YOS, CUD, and SUI were obtained from genome-wide association studies (GWAS), and TSMR analysis was applied to explore potential causal relationships between them. Causal effects were mainly estimated using the standard inverse variance weighting (IVW) method, and complementary and sensitivity analyses were also performed using multiple methods.ResultsThe results indicate that both YOS (OR = 0.994, 95% CI: 0.992–0.996; P = 7.764E-10) and CUD (OR = 0.987, 95% CI: 0.983–0.991; P = 1.217E-09) may have a negative causal effect on SUI.ConclusionsImproving educational attainment may go some way towards reducing the risk of SUI. Therefore, it is important to increase efforts to improve the imbalance in educational development and safeguard women’s health.

Women’s educational attainment, marriage, and fertility: Evidence from the 1944 G.I. Bill

In contemporary settings, greater earnings among women are typically associated with reduced marriage rates and lower fertility. One way that women’s earnings may increase is via changes in educational attainment. To study whether educational attainment affects marriage and fertility choices in a historical setting, I rely on the variation in educational attainment among female WWII veterans created by the 1944 G.I. Bill. Using data from the long-form 1980 census, I first show that WWII veteran status is associated with reduced rates of marriage, increased age at first marriage, and lower fertility, which suggests that G.I. Bill-related education could have had an important effect for veteran women. I then use age at the time of the G.I. Bill announcement as an instrument to establish a causal effect of educational attainment on marriage and fertility outcomes among female veterans. My instrumental variable estimates suggest that each year of G.I. Bill-induced educational attainment is associated with an 8 percentage point decrease in the probability of ever getting married, a 4.7 year increase in age at first marriage, and a 0.67 reduction in the number of children. Using age at the time of the G.I. Bill announcement as an instrument is valid because the benefits could not have been easily anticipated, women had to be 21 to enlist, and the generosity of one’s G.I. Bill benefits depended on the number of years of WWII service.

Modifiable risk factors that mediate the effect of educational attainment on the risk of stroke: a network Mendelian randomization study

BackgroundStroke is a common cerebrovascular disease with great danger to public health. Educational inequality is a universal issue that influences populations’ stroke risk. This study aimed to investigate the causal relationship between education and stroke risk and the contributions of effects mediated by four modifiable factors.Materials and methodsPublic large-scale genome-wide association study (GWAS) summary data associated with educational attainment, hypertensive diseases, body mass index (BMI), smoking behavior, time spent on watching the television (TV), and stroke were obtained from European ancestry. The data were used to investigate the causal relationship among educational attainment, hypertensive disease, BMI, smoking, watching TV, and stroke risk. Inverse variance weighted (IVW) method was used as a primary algorithm for estimating causal direction and effect size in univariable and multivariable Mendelian randomization (MR) analyses.ResultsHigher educational attainment was a causal protective factor, while hypertensive diseases, higher BMI, smoking, and longer time spent on watching the TV were all causal risk factors for the risk of stroke. Hypertensive disease, BMI, smoking, and watching TV were all mediators for linking the causal relationship between educational attainment and stroke risk. Hypertensive disease, BMI, smoking, and watching TV explained 47.35%, 24.74%, 15.72%, and 2.29% of the variance in educational attainment’s effect on stroke risk, respectively. The explained proportion reached 69.32% after integrating the four factors.ConclusionsThese findings support the causal effect of educational attainment on the risk of stroke, with a substantial proportion mediated by modifiable risk factors. Interventions on these modifiable factors would lead to substantial reductions in stroke cases attributable to educational inequality.

Educational attainment, structural brain reserve and Alzheimer's disease: a Mendelian randomization analysis.

Higher educational attainment is observationally associated with lower risk of Alzheimer's disease. However, the biological mechanisms underpinning this association remain unclear. The protective effect of education on Alzheimer's disease may be mediated via increased brain reserve. We used two-sample Mendelian randomization to explore putative causal relationships between educational attainment, structural brain reserve as proxied by MRI phenotypes and Alzheimer's disease. Summary statistics were obtained from genome-wide association studies of educational attainment (n = 1 131 881), late-onset Alzheimer's disease (35 274 cases, 59 163 controls) and 15 measures of grey or white matter macro- or micro-structure derived from structural or diffusion MRI (nmax = 33 211). We conducted univariable Mendelian randomization analyses to investigate bidirectional associations between (i) educational attainment and Alzheimer's disease; (ii) educational attainment and imaging-derived phenotypes; and (iii) imaging-derived phenotypes and Alzheimer's disease. Multivariable Mendelian randomization was used to assess whether brain structure phenotypes mediated the effect of education on Alzheimer's disease risk. Genetically proxied educational attainment was inversely associated with Alzheimer's disease (odds ratio per standard deviation increase in genetically predicted years of schooling = 0.70, 95% confidence interval 0.60, 0.80). There were positive associations between genetically predicted educational attainment and four cortical metrics (standard deviation units change in imaging phenotype per one standard deviation increase in genetically predicted years of schooling): surface area 0.30 (95% confidence interval 0.20, 0.40); volume 0.29 (95% confidence interval 0.20, 0.37); intrinsic curvature 0.18 (95% confidence interval 0.11, 0.25); local gyrification index 0.21 (95% confidence interval 0.11, 0.31)]; and inverse associations with cortical intracellular volume fraction [-0.09 (95% confidence interval -0.15, -0.03)] and white matter hyperintensities volume [-0.14 (95% confidence interval -0.23, -0.05)]. Genetically proxied levels of surface area, cortical volume and intrinsic curvature were positively associated with educational attainment [standard deviation units change in years of schooling per one standard deviation increase in respective genetically predicted imaging phenotype: 0.13 (95% confidence interval 0.10, 0.16); 0.15 (95% confidence interval 0.11, 0.19) and 0.12 (95% confidence interval 0.04, 0.19)]. We found no evidence of associations between genetically predicted imaging-derived phenotypes and Alzheimer's disease. The inverse association of genetically predicted educational attainment with Alzheimer's disease did not attenuate after adjusting for imaging-derived phenotypes in multivariable analyses. Our results provide support for a protective causal effect of educational attainment on Alzheimer's disease risk, as well as potential bidirectional causal relationships between education and brain macro- and micro-structure. However, we did not find evidence that these structural markers affect risk of Alzheimer's disease. The protective effect of education on Alzheimer's disease may be mediated via other measures of brain reserve not included in the present study, or by alternative mechanisms.

Cognitive performance protects against Alzheimer's disease independently of educational attainment and intelligence.

Mendelian-randomization (MR) studies using large-scale genome-wide association studies (GWAS) have identified causal association between educational attainment and Alzheimer's disease (AD). However, the underlying mechanisms are still required to be explored. Here, we conduct univariable and multivariable MR analyses using large-scale educational attainment, cognitive performance, intelligence and AD GWAS datasets. In stage 1, we found significant causal effects of educational attainment on cognitive performance (beta = 0.907, 95% confidence interval (CI): 0.884-0.930, P < 1.145E-299), and vice versa (beta = 0.571, 95% CI: 0.557-0.585, P < 1.145E-299). In stage 2, we found that both increase in educational attainment (odds ratio (OR) = 0.72, 95% CI: 0.66-0.78, P = 1.39E-14) and cognitive performance (OR = 0.69, 95% CI: 0.64-0.75, P = 1.78E-20) could reduce the risk of AD. In stage 3, we found that educational attainment may protect against AD dependently of cognitive performance (OR = 1.07, 95% CI: 0.90-1.28, P = 4.48E-01), and cognitive performance may protect against AD independently of educational attainment (OR = 0.69, 95% CI: 0.53-0.89, P = 5.00E-03). In stage 4, we found significant causal effects of cognitive performance on intelligence (beta = 0.907, 95% CI: 0.877-0.938, P < 1.145E-299), and vice versa (beta = 0.957, 95% CI: 0.937-0.978, P < 1.145E-299). In stage 5, we identified that cognitive performance may protect against AD independently of intelligence (OR = 0.74, 95% CI: 0.61-0.90, P = 2.00E-03), and intelligence may protect against AD dependently of cognitive performance (OR = 1.17, 95% CI: 0.40-3.43, P = 4.48E-01). Collectively, our univariable and multivariable MR analyses highlight the protective role of cognitive performance in AD independently of educational attainment and intelligence. In addition to the intelligence, we extend the mechanisms underlying the associations of educational attainment with AD.

PSweight: An R Package for Propensity Score Weighting Analysis

Propensity score weighting is an important tool for comparative effectiveness research. Besides the inverse probability of treatment weights (IPW), recent development has introduced a general class of balancing weights, corresponding to alternative target populations and estimands. In particular, the overlap weights (OW) lead to optimal covariate balance and estimation efficiency, and a target population of scientific and policy interest. We develop the R package [PSweight](https://CRAN.R-project.org/package=PSweight) to provide a comprehensive design and analysis platform for causal inference based on propensity score weighting. PSweight supports (i) a variety of balancing weights, (ii) binary and multiple treatments, (iii) simple and augmented weighting estimators, (iv) nuisance-adjusted sandwich variances, and (v) ratio estimands. PSweight also provides diagnostic tables and graphs for covariate balance assessment. We demonstrate the functionality of the package using a data example from the National Child Development Survey (NCDS), where we evaluate the causal effect of educational attainment on income.

Education and Atrial Fibrillation: Mendelian Randomization Study.

Low social-economic status is associated with atrial fibrillation (AF), but the extent of any causative effect is unclear. In the present study, we evaluated the causal role of educational attainment (EA) on AF using Mendelian randomization (MR) analysis. Results from traditional single-variable MR indicated a modest causal effect of EA on AF. Sensitivity analyses using different MR methods yielded consistent results. Multi-variable MR and mediation analysis revealed that the protective effect of higher EA on AF was partially mediated by reducing cardiometabolic risk factors and smoking behavior. Our findings suggest that extending education, for example increasing school-leaving age, could lower the global burden of AF.

Socio-economic position as a moderator of cardiometabolic outcomes in patients receiving psychotropic treatment associated with weight gain: results from a prospective 12-month inception cohort study and a large population-based cohort

Weight gain and metabolic complications are major adverse effects of many psychotropic drugs. We aimed to understand how socio-economic status (SES), defined as the Swiss socio-economic position (SSEP), is associated with cardiometabolic parameters after initiation of psychotropic medications known to induce weight gain. Cardiometabolic parameters were collected in two Swiss cohorts following the prescription of psychotropic medications. The SSEP integrated neighborhood-based income, education, occupation, and housing condition. The results were then validated in an independent replication sample (UKBiobank), using educational attainment (EA) as a proxy for SES. Adult patients with a low SSEP had a higher risk of developing metabolic syndrome over one year versus patients with a high SSEP (Hazard ratio (95% CI) = 3.1 (1.5–6.5), n = 366). During the first 6 months of follow-up, a significant negative association between SSEP and body mass index (BMI), weight change, and waist circumference change was observed (25 ≤ age < 65, n = 526), which was particularly important in adults receiving medications with the highest risk of weight gain, with a BMI difference of 0.86 kg/m2 between patients with low versus high SSEP (95% CI: 0.03–1.70, n = 99). Eventually, a causal effect of EA on BMI was revealed using Mendelian randomization in the UKBiobank, which was notably strong in high-risk medication users (beta: −0.47 SD EA per 1 SD BMI; 95% CI: −0.46 to −0.27, n = 11,314). An additional aspect of personalized medicine was highlighted, suggesting the patients’ SES represents a significant risk factor. Particular attention should be paid to patients with low SES when initiating high cardiometabolic risk psychotropic medications.

Educational attainment protects against epilepsy independent of cognitive function: A Mendelian randomization study

Observational studies have suggested that increased levels of education and cognition are associated with a reduced risk of epilepsy. However, such associations are easily influenced by confounding or reverse causality. Hence, we conducted a two-sample univariable and multivariable Mendelian randomization (MR) to estimate the total and independent causal effects of educational attainment and cognition on epilepsy risk. We performed MR estimates on International League Against Epilepsy (ILAE) Consortium genome-wide association study (GWAS) data (15212 epilepsy cases and 29677 controls). We then validated the results in FinnGen (3424 epilepsy cases and 110963 controls) and applied meta-analysis to all the results. In the meta-analysis of the ILAE and FinnGen results, genetically determined increased educational attainment was associated with a reduced risk of epilepsy (odds ratio [OR] 0.84, 95% confidence interval [CI] 0.80-0.88; P<.001). Similarly, genetically determined increased cognitive function was associated with a reduced risk of epilepsy (OR 0.94, 95% CI 0.88-1.00, P=.043). When educational attainment and cognitive function were included in the same multivariable MR, only educational attainment was still associated with a reduced risk of epilepsy (OR 0.88, 95% CI 0.81-0.95, P=.002). This MR study provides evidence to support that increased educational attainment can reduce the risk of developing epilepsy independent of cognitive function.

Two-Sample Mendelian Randomization Estimates of the Effects of Educational Attainment on Osteoporosis

Background: Osteoporosis is a complex disorder, with multiple biopsychosocial contributors. As a principal influencing factor of socioeconomic status, education is commonly regarded associated with osteoporosis. However, the associations between education and osteoporosis are inconsistent in different researches, and we aim to investigate it under two-sample Mendelian randomization analysis framework. Methods: A series of quality control steps were taken in our analysis to select eligible instrumental SNPs which were strongly associated with exposure. To make the results more robust and reliable, we utilized several robust analytical methods (inverse-variance weighting, weighted median, MR-Egger regression and MR.RAPS) that based on different assumptions of two-sample Mendelian randomization analysis. MR-Egger intercept test, Cochran’s Q test and “leave-one-out” sensitivity analysis were performed to remove outliers and evaluate the horizontal pleiotropy, heterogeneities and stability of these genetic variants on outcomes. Outlier variants identified by MR-PRESSO outlier test were removed to reduce heterogeneity and the effect of horizontal pleiotropy. Two-sample Mendelian randomization approach was also employed to determine the mechanism by which education affects osteoporosis. Results: Our two-sample Mendelian randomization analyses suggested a causal effect of longer educational attainment on lower risk of osteoporosis and higher heel-BMD, FN-BMD and LS-BMD, but lack of evidence on lower risk of osteoporostic fracture or higher FA-BMD. Our MR analyses also determined the probability of serum lipid level, smoking, magnesium supplements, selenium supplements and physical activity working as mediators in the causal effect of educational attainment on osteoporosis. Interpretation: Our results can be helpful for education policy making to increase BMD, or reminding clinicians of taking integrated biopsychosocial measures and efforts to prevent or intervene with bone loss when patients are high risk population of osteoporosis. Funding Statement: Not applicable Declaration of Interests: The authors declare that they have no competing interests. Ethics Approval Statement: Our analysis used published study or publicly available GWAS summary data. No original data was collected for this manuscript, and thus, no ethical committee approval was required. Each study included was approved by their institutional ethics review committees, all participants provided written informed consent.

Educational attainment protects against type 2 diabetes independently of cognitive performance: a Mendelian randomization study.

Observational studies have reported a negative association between educational attainment and type 2 diabetes (T2D), but the causality remains largely unknown. The aim of this study is to investigate the potential causal effect of educational attainment on T2D and whether such an effect is independent of cognitive performance. We conducted two-sample Mendelian randomization (MR) analysis using genetic variants strongly associated with educational attainment and cognitive performance to estimate the causal associations with T2D, among 61,714 T2D cases and 593,952 controls. We also performed multivariable MR to explore the independent effects of educational attainment and cognitive performance on T2D risk. In univariable MR, we found evidence that genetically predicted higher educational attainment [odds ratio (OR) 0.53 per 1-standard deviation (SD) increase; 95% confidence interval (CI) 0.47-0.60] and cognitive performance (OR 0.79 per 1-SD increase; 95%CI 0.69-0.91) were related to decreased risk of T2D. Our further multivariable MR results suggested that more years of education led to a reduced likelihood of T2D independently of cognitive performance (OR 0.52; 95%CI 0.42-0.64). However, the protective effect of cognitive performance on T2D was attenuated once educational attainment was controlled for (OR 1.08; 95%CI 0.88-1.32). We provided evidence to suggest that educational attainment protects against T2D independently of cognitive performance, but does not support a negative causal association between cognitive performance and T2D independently of educational attainment. Education might represent a potential target for intervention to battle type 2 diabetes risk.

Education, intelligence and Alzheimer's disease: evidence from a multivariable two-sample Mendelian randomization study.

ObjectivesTo 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 AD risk.Participants17 008 AD cases and 37 154 controls from the International Genomics of Alzheimer’s Project (IGAP) consortium.Main outcome measureOdds ratio (OR) of AD per standardized deviation increase in years of schooling (SD = 3.6 years) and intelligence (SD = 15 points on intelligence test).ResultsThere 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).ConclusionsThere 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.

2070-P: Role of Education Attainment in Obesity: A Two-Sample Mendelian Randomization Study

Lower educational attainment has been associated with an increased risk of obesity; however, the causality of educational attainment in relation to adiposity, body composition, and fat distribution remains to be established. We used two-sample Mendelian randomization (MR) analyses of summary statistics with participants number ranged from 330,762 to 1,131,881 to test the causal effects of educational attainment in body fatness phenotypes [e.g., BMI, body fat mass, and waist-to-hip ratio (WHR)]. A total of 1,196 available single nucleotide polymorphisms associated with educational attainment were included in the current analysis. Eight complementary MR methods were used to test the robustness of our results. The genetically-instrumented higher educational attainment was consistently associated with a lower BMI [β -0.42, 95% confidence interval (CI) -0.45 to -0.39], body fat percentage (-0.31, -0.33 to -0.28), body fat mass (-0.36, -0.39 to -0.33), and waist circumference (-0.31, -0.33 to -0.28). The causal relationships of higher educational attainment with lower body weight, fat-free mass, and hip circumference were less consistent. There was no causal relation between educational attainment and WHR (Figure 1). In conclusion, our findings indicate low educational attainment may causally increase BMI, body fat and waist circumference. Disclosure T. Zhou: None. D. Sun: None. X. Li: None. Y. Heianza: None. L. Qi: None. Funding National Heart, Lung, and Blood Institute (HL0791981, HL034594, HL126024); National Institute of Diabetes and Digestive and Kidney Diseases (DK115679, DK091718, DK100383, DK078616); Boston Obesity Nutrition Research Center (DK46300); United States-Israel Binational Science Foundation (20110360); American Heart Association (0730094N to L.Q.)

Instrumental variable approaches to identifying the causal effect of educational attainment on dementia risk

PurposeEducation is an established correlate of cognitive status in older adulthood, but whether expanding educational opportunities would improve cognitive functioning remains unclear given limitations of prior studies for causal inference. Therefore, we conducted instrumental variable (IV) analyses of the association between education and dementia risk, using for the first time in this area, genetic variants as instruments as well as state-level school policies. MethodsIV analyses in the Health and Retirement Study cohort (1998–2010) used two sets of instruments: (1) a genetic risk score constructed from three single-nucleotide polymorphisms (SNPs; n = 7981); and (2) compulsory schooling laws (CSLs) and state school characteristics (term length, student teacher ratios, and expenditures; n = 10,955). ResultsUsing the genetic risk score as an IV, there was a 1.1% reduction in dementia risk per year of schooling (95% confidence interval, −2.4 to 0.02). Leveraging compulsory schooling laws and state school characteristics as IVs, there was a substantially larger protective effect (−9.5%; 95% confidence interval, −14.8 to −4.2). Analyses evaluating the plausibility of the IV assumptions indicated estimates derived from analyses relying on CSLs provide the best estimates of the causal effect of education. ConclusionsIV analyses suggest education is protective against risk of dementia in older adulthood.

The Effect of Education on Criminal Convictions and Incarceration: Causal Evidence from Micro-data

This article studies the causal effect of educational attainment on conviction and incarceration using Sweden’s compulsory schooling reform as an instrument for years of schooling and a 70% sample from Sweden’s Multigenerational Register matched with more than 30 years of administrative crime records. We find a significant negative effect of schooling on male convictions and incarceration; one additional year of schooling decreases the likelihood of conviction by 6.7% and incarceration by 15.5%. Though OLS estimates for females are of a similar magnitude to those for males, we find no evidence of a significant causal effect for women.

The Causal Effect of Educational Attainment on Completed Fertility for a Cohort of Danish Women—Does Feedback Play a Role?

This study focuses on the causal effect of educational attainment on completed fertility for a cohort of Danish women born in 1963. The relationship between education and completed fertility (here defined as the number of children at age 41) is the result of a dynamic interplay between the two processes; in particular, educational attainment at a given time might be influenced by previous fertility. This notion is referred to as feedback from the fertility process to the education process. In this study population, feedback turns out to be present, and marginal structural models are used to construct a hypothetical population in which the feedback mechanisms are lifted out of the data. This gives rise to the conclusion that educational differences in completed fertility are to some degree attributable to feedback mechanisms and that they become smaller or are even reversed when this is taken into account. The study is based on data from individual-level, administrative registers.