scholarly journals Mendelian randomisation analysis of the effect of educational attainment and cognitive ability on smoking behaviour

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Eleanor Sanderson ◽  
George Davey Smith ◽  
Jack Bowden ◽  
Marcus R. Munafò
Keyword(s):  
Educational Attainment ◽  
Cognitive Ability ◽  
Smoking Behaviour ◽  
Mendelian Randomisation

scholarly journals Mendelian randomisation analysis of the effect of educational attainment and cognitive ability on smoking behaviour

2018 ◽  
Author(s):  
Eleanor Sanderson ◽  
George Davey Smith ◽  
Jack Bowden ◽  
Marcus R. Munafò
Keyword(s):  
Educational Attainment ◽  
Health Outcomes ◽  
Cognitive Ability ◽  
Smoking Behaviour ◽  
Mendelian Randomisation ◽  
Individual Data ◽  
General Cognitive Ability ◽  
Uk Biobank ◽  
The Uk ◽  
Summary Data

AbstractRecent analyses have shown educational attainment to be associated with a number of health outcomes. This association may, in part, be due to an effect of educational attainment on smoking behaviour. In this study we apply a multivariable Mendelian randomisation design to determine whether the effect of educational attainment on smoking behaviour could be due to educational attainment or general cognitive ability. We use individual data from the UK Biobank study (N = 120,050) and summary data from large GWAS studies of educational attainment, cognitive ability and smoking behaviour. Our results show that more years of education are associated with a reduced likelihood of smoking which is not due to an effect of general cognitive ability on smoking behaviour. Given the considerable physical harms associated with smoking, the effect of educational attainment on smoking is likely to contribute to the health inequalities associated with differences in educational attainment.

scholarly journals Modifiable traits, healthy behaviours, and leucocyte telomere length

2021 ◽  
Author(s):  
Vasiliki Bountziouka ◽  
Crispin Musicha ◽  
Elias Allara ◽  
Stephen Kaptoge ◽  
Qingning Wang ◽  
...  
Keyword(s):  
Life Expectancy ◽  
Educational Attainment ◽  
Telomere Length ◽  
Lower Risk ◽  
Smoking Behaviour ◽  
Mendelian Randomisation ◽  
Age Related ◽  
Clinical Consequences ◽  
Artery Disease ◽  
Sufficient Magnitude

Background: Telomere length is associated with risk of several age-related diseases and cancers. The extent to which telomere length may be modifiable through lifestyle and behaviour and whether this has any clinical consequences is unknown. Methods: In up to 422,797 participants in UK Biobank, we investigated associations of leucocyte telomere length (LTL) with 117 potentially modifiable traits, as well as two indices of healthy behaviours incorporating smoking, physical activity, diet, maintenance of a healthy body weight and alcohol intake. Associations were interpreted as age-related change in LTL by dividing the trait beta coefficients with the age-coefficient. We used Mendelian Randomisation (MR) to test causality of the observed associations of educational attainment and smoking behaviour with LTL. We investigated whether the associations of LTL with 22 diseases were modified by the number of healthy behaviours and the extent to which the associations of more healthy behaviours with greater life expectancy and lower risk of coronary artery disease (CAD) may be mediated through LTL. Results: 71 traits showed significant associations with LTL but most were modest, equivalent to <1 year of age-related change in LTL. In multivariable analyses of 17 traits with stronger associations (equivalent to ≥2 years of age-related change in LTL), five traits (oily fish intake, educational attainment, general health status, walking pace and current smoking) remained significant. MR analysis suggested that educational attainment and smoking behaviour causally affect LTL. Both indices of healthy behaviour were positively and linearly associated with LTL, with those with the healthiest behaviour having longer LTL equivalent to approx. 3.5 years of age-related change in LTL when compared with those with the least heathy behaviours (P<0.001). However, healthy behaviours only explained <0.2% of the total variation in LTL and did not significantly modify the association of LTL with risk of any of the diseases studied. Neither the association of more healthy behaviours on greater life expectancy or lower risk of CAD were substantially mediated through LTL. Conclusions: Several potentially modifiable traits and healthy behaviours have a quantifiable association with LTL, at least some of which are likely to be causal. However, these effects are not of a sufficient magnitude to substantially alter the association between LTL and various diseases or life expectancy.

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 Measuring social origin, cognitive ability and educational attainment in the Longitudinal Study of Young People in England (LSYPE)

2020 ◽  
Author(s):  
Mollie Bourne ◽  
Bastian Andreas Betthäuser ◽  
Erzsebet Bukodi
Keyword(s):  
Longitudinal Study ◽  
Young People ◽  
Educational Attainment ◽  
Cognitive Ability ◽  
Parental Education ◽  
Descriptive Statistics ◽  
Social Origin ◽  
Education Class ◽  
Key Variables ◽  
Class Status

This data note presents and discussed descriptive statistics of the key variables on individuals’ social origin, cognitive ability and educational attainment that have been constructed based on the information contained in the Longitudinal Study of Young People in England (LSYPE). The main sets of variables presented are (1) measures of respondents’ cognitive ability in childhood, (2) parental education, class, status and income, and (3) respondents’ highest qualification and measures indicating whether respondents have crossed different educational qualification thresholds.

scholarly journals Pleiotropic Meta-Analysis of Cognition, Education, and Schizophrenia Differentiates Roles of Early Neurodevelopmental and Adult Synaptic Pathways

2019 ◽  
Author(s):  
Max Lam ◽  
W. David Hill ◽  
Joey W. Trampush ◽  
Jin Yu ◽  
Emma Knowles ◽  
...  
Keyword(s):  
Educational Attainment ◽  
Cognitive Ability ◽  
Genetic Correlation ◽  
Allelic Variation ◽  
Meta Analysis ◽  
Genetic Correlations ◽  
Biological Mechanisms ◽  
Genetic Level ◽  
Higher Educational Attainment ◽  
Synaptic Pruning

AbstractLiability to schizophrenia is inversely correlated with general cognitive ability at both the phenotypic and genetic level. Paradoxically, a modest but consistent positive genetic correlation has been reported between schizophrenia and educational attainment, despite the strong positive genetic correlation between cognitive ability and educational attainment. Here we leverage published GWAS in cognitive ability, education, and schizophrenia to parse biological mechanisms underlying these results. Association analysis based on subsets (ASSET), a pleiotropic meta-analytic technique, allowed jointly associated loci to be identified and characterized. Specifically, we identified subsets of variants associated in the expected (“Concordant”) direction across all three phenotypes (i.e., greater risk for schizophrenia, lower cognitive ability, and lower educational attainment); these were contrasted with variants demonstrating the counterintuitive (“Discordant”) relationship between education and schizophrenia (i.e., greater risk for schizophrenia and higher educational attainment). ASSET analysis revealed 235 independent loci associated with cognitive ability, education and/or schizophrenia at p<5×10−8. Pleiotropic analysis successfully identified more than 100 loci that were not significant in the input GWASs, and many of these have been validated by larger, more recent single-phenotype GWAS. Leveraging the joint genetic correlations of cognitive ability, education, and schizophrenia, we were able to dissociate two distinct biological mechanisms: early neurodevelopmental pathways that characterize concordant allelic variation, and adulthood synaptic pruning pathways that were linked to the paradoxical positive genetic association between education and schizophrenia. Further, genetic correlation analyses revealed that these mechanisms contribute not only to the etiopathogenesis of schizophrenia, but also to the broader biological dimensions that are implicated in both general health outcomes and psychiatric illness.

scholarly journals Role of obesity in smoking behaviour: Mendelian randomisation study in UK Biobank

BMJ ◽  
2018 ◽  
pp. k1767 ◽  
Author(s):  
Robert Carreras-Torres ◽  
Mattias Johansson ◽  
Philip C Haycock ◽  
Caroline L Relton ◽  
George Davey Smith ◽  
...  
Keyword(s):  
Smoking Behaviour ◽  
Mendelian Randomisation ◽  
Uk Biobank

scholarly journals Evidence for causal effects of lifetime smoking on risk for depression and schizophrenia: a Mendelian randomisation study

2019 ◽  
Vol 50 (14) ◽  
pp. 2435-2443 ◽  
Author(s):  
Robyn E. Wootton ◽  
Rebecca C. Richmond ◽  
Bobby G. Stuijfzand ◽  
Rebecca B. Lawn ◽  
Hannah M. Sallis ◽  
...  
Keyword(s):  
Causal Effect ◽  
Association Studies ◽  
Smoking Initiation ◽  
Smoking Behaviour ◽  
Positive Control ◽  
Mendelian Randomisation ◽  
Genome Wide Association Studies ◽  
Weak Evidence ◽  
Smoking Duration ◽  
The Uk

AbstractBackgroundSmoking prevalence is higher amongst individuals with schizophrenia and depression compared with the general population. Mendelian randomisation (MR) can examine whether this association is causal using genetic variants identified in genome-wide association studies (GWAS).MethodsWe conducted two-sample MR to explore the bi-directional effects of smoking on schizophrenia and depression. For smoking behaviour, we used (1) smoking initiation GWAS from the GSCAN consortium and (2) we conducted our own GWAS of lifetime smoking behaviour (which captures smoking duration, heaviness and cessation) in a sample of 462690 individuals from the UK Biobank. We validated this instrument using positive control outcomes (e.g. lung cancer). For schizophrenia and depression we used GWAS from the PGC consortium.ResultsThere was strong evidence to suggest smoking is a risk factor for both schizophrenia (odds ratio (OR) 2.27, 95% confidence interval (CI) 1.67–3.08, p < 0.001) and depression (OR 1.99, 95% CI 1.71–2.32, p < 0.001). Results were consistent across both lifetime smoking and smoking initiation. We found some evidence that genetic liability to depression increases smoking (β = 0.091, 95% CI 0.027–0.155, p = 0.005) but evidence was mixed for schizophrenia (β = 0.022, 95% CI 0.005–0.038, p = 0.009) with very weak evidence for an effect on smoking initiation.ConclusionsThese findings suggest that the association between smoking, schizophrenia and depression is due, at least in part, to a causal effect of smoking, providing further evidence for the detrimental consequences of smoking on mental health.

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