Can increasing years of schooling reduce type 2 diabetes (T2D)?: Evidence from a Mendelian randomization of T2D and 10 of its risk factors

© 2020, The Author(s). A focus in recent decades has involved examining the potential causal impact of educational attainment (schooling years) on a variety of disease and life-expectancy outcomes. Numerous studies have broadly revealed a link suggesting that as years of formal schooling increase so too does health and wellbeing; however, it is unclear whether the associations are causal. Here we use Mendelian randomization, an instrumental variables technique, with a two-sample design, to probe whether more years of schooling are causally linked to type 2 diabetes (T2D) and 10 of its attendant risk factors. The results revealed a protective effect of more schooling years against T2D (odds ratio = 0.39; 95% confidence interval: 0.26, 0.58; P = 3.89 × 10–06), which in turn might be partly mediated by more years of schooling being protective against the following: having a father with T2D, being overweight, having higher blood pressure and higher levels of circulating triglycerides, and having lower levels of HDL cholesterol. More schooling years had no effect on risk for gestational diabetes or polycystic ovarian syndrome and was associated with a decreased likelihood of moderate physical activity. These findings imply that strategies to retain adults in higher education may help reduce the risk for a major source of metabolic morbidity and mortality

A Mendelian randomization study of telomere length and blood-cell traits

© 2020, The Author(s). Whether telomere attrition reducing proliferative reserve in blood-cell progenitors is causal has important public-health implications. Mendelian randomization (MR) is an analytic technique using germline genetic variants as instrumental variables. If certain assumptions are met, estimates from MR should be free from most environmental sources of confounding and reverse causation. Here, two-sample MR is performed to test whether longer telomeres cause changes to hematological traits. Summary statistics for genetic variants strongly associated with telomere length were extracted from a genome-wide association (GWA) study for telomere length in individuals of European ancestry (n = 9190) and from GWA studies of blood-cell traits, also in those of European ancestry (n ~ 173,000 participants). A standard deviation increase in genetically influenced telomere length increased red blood cell and white blood cell counts, decreased mean corpuscular hemoglobinand mean cell volume, and had no observable impact on mean corpuscular hemoglobin concentration, red cell distribution width, hematocrit, or hemoglobin. Sensitivity tests for pleiotropic distortion were mostly inconsistent with glaring violations to the MR assumptions. Similar to germline mutations in telomere biology genes leading to bone-marrow failure, these data provide evidence that genetically influenced common variation in telomere length impacts hematologic traits in the population

Using multiple Mendelian randomization approaches and genetic correlations to understand obesity, urate, and gout

Observational studies suggest relationships between obesity, urate, and gout but are possibly confounded. We assessed whether genetically determined obesity, higher urate (and related traits), and gout were causal using multiple Mendelian randomization (MR) approaches and linkage disequilibrium score regression for genetic correlations (rg). For data, we used genome-wide association study summary statistics available through MR-Base. We observed that obesity increased urate (beta = 0.127; 95% CI = 0.098, 0.157; P-value = 1.2E−17; rg = 0.25 [P-value = 0.001]) and triglycerides (beta = 0.082; 95% CI = 0.065, 0.099; P-value = 1.2E−21; rg = 0.23 [P-value = 8.8E−12]) and decreased high-density lipoprotein cholesterol (HDL) (beta = − 0.083; 95% CI = − 0.101, − 0.065; P-value = 2.5E−19; rg = − 0.28; [P-value = 5.2E−24]). Higher triglycerides increased urate (beta = 0.198; 95% CI = 0.146, 0.251; P-value = 8.9E−14; rg = 0.29 [P-value = 0.001]) and higher HDL decreased urate (beta = − 0.109; 95% CI = − 0.148, − 0.071; P-value = 2.7E− 08; rg = − 0.21 [P-value = 9.8E−05]). Higher urate (OR = 1.030; 95% CI = 1.028, 1.032; P-value = 1.1E−130; rg = 0.89 [P-value = 1.7E−55]) and obesity caused gout (OR = 1.003; 95% CI = 1.001, 1.004; P-value = 1.3E−04; rg = 0.23 [P-value = 2.7E−05]). Obesity on gout with urate as a mediator revealed all the effect of obesity on gout occurred through urate. Obesity on low-density lipoprotein cholesterol (LDL) was null (beta = −0.011; 95% CI = −0.030, 0.008; P-value = 2.6E−01; rg = 0.03 [P-value = 0.369]). A multivariable MR of obesity, HDL, and triglycerides on urate showed obesity influenced urate when accounting for HDL and triglycerides. Obesity’s impact on urate was exacerbated by it decreasing HDL

Exploring the Genomic Architectures of Health, Physical Traits and Antisocial Behavioral Outcomes: A Brief Report

© Copyright © 2020 Tielbeek and Boutwell. A widely replicated finding across the behavioral sciences is that antisocial behaviors correlate with an array of health problems. Less clear, however, is the precise nature of this association. There is reason to suspect that a direct causal link exists between incarceration—a consequence of some antisocial behaviors—and certain negative health outcomes, for instance. However, it might be the case that broader phenotypes like antisocial behavior may correlate with certain health and physiological traits at a genomic level. We explore this possibility from a theoretical vantage point, while also presenting some preliminary data from existing secondary sources. Tentatively, no significant genetic correlations emerged across a host of health, physiological, and wellbeing outcomes after correction for multiple testing. However, more work is needed exploring this topic. We propose that future studies should make use of larger, more diverse samples and examine the genetic overlap between homogeneous clusters of antisocial behavioral subtypes and disease traits or symptoms

Handgun carrying among youth in the United States

Despite a wealth of research finding that adolescents who carry handguns are involved in risky behaviors, there has been little exploration into the heterogeneity of this behavior. Using a pooled sample of 12- to 17-year-olds from the National Study on Drug Use and Health who report past-year handgun carrying (N = 7,872), this study identified four subgroups of handgun carriers: low risk (n = 3,831; 47.93%), alcohol and marijuana users (n = 1,591; 20.16%), fighters (n = 1,430; 19.40%), and severe externalizers (n = 1,020, 12.51%). These subgroups differed on demographic, behavioral, and psychosocial characteristics. Findings are discussed in light of prevention and focused deterrence

Shared genomic architectures of COVID-19 and antisocial behavior

Little is known about the genetics of norm violation and aggression in relation to coronavirus disease 2019 (COVID-19). To investigate this, we used summary statistics from genome-wide association studies and linkage disequilibrium score regression to calculate a matrix of genetic correlations (rgs) for antisocial behavior (ASB), COVID-19, and various health and behavioral traits. After false-discovery rate correction, ASB was genetically correlated with COVID-19 (rg = 0.51; P = 1.54E-02) and 19 other traits. ASB and COVID-19 were both positively genetically correlated with having a noisy workplace, doing heavy manual labor, chronic obstructive pulmonary disease, and genitourinary diseases. ASB and COVID-19 were both inversely genetically correlated with average income, education years, healthspan, verbal reasoning, lifespan, cheese intake, and being breastfed as a baby. But keep in mind that rgs are not necessarily causal. And, if causal, their prevailing directions of effect (which causes which) are indiscernible from rgs alone. Moreover, the SNP-heritability (hg2) estimates for two measures of COVID-19 were very small, restricting the overlap of genetic variance in absolute terms between ASB and COVID-19. Nonetheless, our findings suggest that those with antisocial tendencies possibly have a higher risk of exposure to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) than those without antisocial tendencies. This may have been especially true early in the pandemic before vaccines against SARS-CoV-2 were available and before the emergence of the highly transmissible Omicron variant

Enlisting in the Military: The Influential Role of Genetic Factors

Given that enlistment in the U.S. military is completely voluntary, there has been a great deal of interest in identifying the various factors that might explain why some people join the military, whereas others do not. The current study expanded on this line of literature by estimating the extent to which genetic and environmental factors explained variance in the liability for lifetime participation in the military. Analysis of twin pairs drawn from the National Longitudinal Study of Adolescent to Adult Health (Add Health) revealed that 82% of the variance was the result of genetic factors, 18% of the variance was the result of nonshared environmental factors, and none of the variance was accounted for by shared environmental factors. In light of a number of limitations, replication studies are needed to determine the robustness of these findings and whether they are generalizable to other samples and populations

A Quantitative Genetic Analysis of the Associations Among Language Skills, Peer Interactions, and Behavioral Problems in Childhood: Results From a Sample of Twins

A body of empirical research has revealed that there are associations among language skills, peer interactions, and behavioral problems in childhood. At the same time, however, there has been comparatively less research devoted to exploring the mutual unfolding of these factors over the first few years of life. The current study is designed to partially address this gap in the literature by examining how language skills, negative peer interactions, and behavioral problems are interrelated in a sample of twins drawn from the Early Childhood Longitudinal Study–Birth Cohort (ECLS-B). Employing a quantitative genetic framework, the results of the current study revealed that variance in language skills, negative peer interactions, and externalizing behavioral problems were all due to a combination of genetic and environmental factors. Bivariate Cholesky models indicated that most of the covariance among language skills, negative peer interactions, and externalizing behavioral problems was due to common genetic factors. Additional analyses using a modified DeFries–Fulker approach nested within a path model revealed a bidirectional association between negative peer interactions and externalizing behavioral problems, wherein there appeared to be feedback loops between the two. Implications of the results are discussed and avenues for future research are offered

Exploring the genetic correlations of antisocial behaviour and life history traits.

UNLABELLED: Prior evolutionary theory provided reason to suspect that measures of development and reproduction would be correlated with antisocial behaviours in human and non-human species. Behavioural genetics has revealed that most quantitative traits are heritable, suggesting that these phenotypic correlations may share genetic aetiologies. We use genome-wide association study data to estimate the genetic correlations between various measures of reproductive development (N = 52 776-318 863) and antisocial behaviour (N = 31 968). Our genetic correlation analyses demonstrate that alleles associated with higher reproductive output (number of children ever born, r g = 0.50, P = 0.0065) were positively correlated with alleles associated with antisocial behaviour, whereas alleles associated with more delayed reproductive onset (age at first birth, r g = -0.64, P = 0.0008) were negatively associated with alleles linked to antisocial behaviour. Ultimately, these findings coalesce with evolutionary theories suggesting that increased antisocial behaviours may partly represent a faster life history approach, which may be significantly calibrated by genes. DECLARATION OF INTEREST: None

The longitudinal association between resting heart rate and psychopathic traits from a normative personality perspective

A large body of research has accumulated investigating the possibility of an association between resting heart rate and psychopathic traits, with meta-analysis suggesting a modest, negative association. Some recent research suggests that prior findings of an association between heart rate and psychopathy may be influenced by inclusion of antisocial behavior in the assessment of psychopathic traits. The current study explores this possibility in a longitudinal sample of British males by comparing resting heart rate at age 18 to psychopathy assessed from a Five Factor Model perspective and from the Psychopathy Checklist: Screening Version (PCL:SV) at age 48. Our psychopathic personality scale, created using the Big Five Inventory (BFI), was significantly correlated with the PCL:SV and was most related to the antisocial factor. In correlation analyses, resting heart rate at age 18 was not significantly related to BFI psychopathy, but was positively related to BFI Openness and Conscientiousness, and these associations held up after controlling for childhood SES, BMI at 18, and whether the participant smoked during the age 18 assessment. Additional analyses controlling for smoking status were conducted to address the biasing effect of smoking on heart rate during the age 18 assessment and a significant, albeit weak, negative association between resting heart rate and BFI psychopathy emerged. Future research should replicate these results using other normative personality approaches to assess psychopathic traits.We are very grateful to the Home Office, the Department of Health, the Department of Education, the Rayne Foundation, the Barrow Cadbury Trust, and the Smith-Richardson Foundation for funding the Cambridge Study in Delinquent Development