Author Correction: Associations of mortality with own blood pressure using son's blood pressure as an instrumental variable.
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ABSTRACT:
SUBMITTER: Carslake D
PROVIDER: S-EPMC7930109 | biostudies-literature | 2021 Mar
REPOSITORIES: biostudies-literature
Publications
Author Correction: Associations of mortality with own blood pressure using son's blood pressure as an instrumental variable.
Carslake David D Fraser Abigail A May Margaret T MT Palmer Tom T Silventoinen Karri K Tynelius Per P Lawlor Debbie A DA Davey Smith George G
Scientific reports 20210303 1
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Project description:High systolic blood pressure (SBP) causes cardiovascular disease (CVD) and is associated with mortality from other causes, but conventional multivariably-adjusted results may be confounded. Here we used a son's SBP (>1 million Swedish men) as an instrumental variable for parental SBP and examined associations with parents' cause-specific mortality, avoiding reverse causation. The hazard ratio for CVD mortality per SD (10.80 mmHg) of SBP was 1.49 (95% CI: 1.43, 1.56); SBP was positively associated with coronary heart disease and stroke. SBP was also associated positively with all-cause, diabetes and kidney cancer mortality, and negatively with external causes. Negative associations with respiratory-related mortality were probably confounded by smoking. Hazard ratios for other causes were imprecise or null. Diastolic blood pressure gave similar results to SBP. CVD hazard ratios were intermediate between those from conventional multivariable studies and Mendelian randomization and stronger than those from clinical trials, approximately consistent with an effect of exposure duration on effect sizes. Plots of parental mortality against offspring SBP were approximately linear, supporting calls for lower SBP targets. Results suggest that conventional multivariable analyses of mortality and SBP are not substantially confounded by reverse causation and confirm positive effects of SBP on all-cause, CVD and diabetes mortality.
| S-EPMC6586810 | biostudies-literature
Project description:Height is associated with mortality from many diseases, but it remains unclear whether the association is causal or due to confounding by social factors, genetic pleiotropy,(1) or existing ill-health. The authors investigated whether the association of height with mortality is causal by using a son's height as an instrumental variable (IV) for parents' height among the parents of a cohort of 1,036,963 Swedish men born between 1951 and 1980 who had their height measured at military conscription, aged around 18, between 1969 and 2001. In a two-sample IV analysis adjusting for son's age at examination and secular trends in height, as well as parental age, and socioeconomic position, the hazard ratio (HR) for all-cause paternal mortality per standard deviation (SD, 6.49cm) of height was 0.96 (95% confidence interval (CI): 0.95, 0.96). The results of IV analyses of mortality from all causes, cardiovascular disease (CVD), respiratory disease, cancer, external causes and suicide were comparable to those obtained using son's height as a simple proxy for own height and to conventional analyses of own height in the present data and elsewhere, suggesting that such conventional analyses are not substantially confounded by existing ill-health.
| S-EPMC3685807 | biostudies-literature
Project description:Racial inequities in blood pressure levels have been extensively documented. Experiences of racial discrimination could explain some of this disparity, although findings from previous studies have been inconsistent. To address limitations of prior literature, including measurement error, we implemented instrumental variable analysis to assess the relationship between racial discrimination in institutional settings and blood pressure. Using data from 3,876 Black and White adults with an average age of 32 years from examination 4 (1992-1993) of the Coronary Artery Risk Development in Young Adults Study, our primary analysis examined the relationship between self-reported experiences of racial discrimination in institutional settings and blood pressure using reflectance meter measurement of skin color as an instrument. Findings suggested that an increase in experiences of racial discrimination was associated with higher systolic and diastolic blood pressure (β = 2.23 mm Hg (95% confidence interval: 1.85, 2.61) and β = 1.31 (95% confidence interval: 1.00, 1.62), respectively). Our instrumental variable estimates suggest that experiences of racial discrimination within institutional settings contribute to racial inequities in elevated blood pressure and cardiovascular disease outcomes in a relatively young cohort of adults and may yield clinically relevant differences in cardiovascular health over the life course.
| S-EPMC10691201 | biostudies-literature
Project description:A covariate-adjusted estimate of an exposure-outcome association may be biased if the exposure variable suffers measurement error. We propose an approach to correct for exposure measurement error in a covariate-adjusted estimate of the association between a continuous exposure variable and outcome of interest. Our proposed approach requires data for a reference population in which the exposure was a priori set to some known level (e.g., 0, and is therefore unexposed); however, our approach does not require an exposure validation study or replicate measures of exposure, which are typically needed when addressing bias due to exposure measurement error. A key condition for this method, which we refer to as "partial population exchangeability," requires that the association between a measured covariate and outcome in the reference population equals the association between that covariate and outcome in the target population in the absence of exposure. We illustrate the approach using simulations and an example.
| S-EPMC10144664 | biostudies-literature
Project description:This article was originally published under a CC BY-NC 4.0 license, but has now been made available under a CC BY 4.0 license. The PDF and HTML versions of the paper have been modified accordingly.
| S-EPMC6006216 | biostudies-literature
Project description:BackgroundThe developmental overnutrition hypothesis suggests that greater maternal obesity during pregnancy results in increased offspring adiposity in later life. If true, this would result in the obesity epidemic progressing across generations irrespective of environmental or genetic changes. It is therefore important to robustly test this hypothesis.Methods and findingsWe explored this hypothesis by comparing the associations of maternal and paternal pre-pregnancy body mass index (BMI) with offspring dual energy X-ray absorptiometry (DXA)-determined fat mass measured at 9 to 11 y (4,091 parent-offspring trios) and by using maternal FTO genotype, controlling for offspring FTO genotype, as an instrument for maternal adiposity. Both maternal and paternal BMI were positively associated with offspring fat mass, but the maternal association effect size was larger than that in the paternal association in all models: mean difference in offspring sex- and age-standardised fat mass z-score per 1 standard deviation BMI 0.24 (95% confidence interval [CI]: 0.22 to 0.26) for maternal BMI versus 0.13 (95% CI: 0.11, 0.15) for paternal BMI; p-value for difference in effect < 0.001. The stronger maternal association was robust to sensitivity analyses assuming levels of non-paternity up to 20%. When maternal FTO, controlling for offspring FTO, was used as an instrument for the effect of maternal adiposity, the mean difference in offspring fat mass z-score per 1 standard deviation maternal BMI was -0.08 (95% CI: -0.56 to 0.41), with no strong statistical evidence that this differed from the observational ordinary least squares analyses (p = 0.17).ConclusionsNeither our parental comparisons nor the use of FTO genotype as an instrumental variable, suggest that greater maternal BMI during offspring development has a marked effect on offspring fat mass at age 9-11 y. Developmental overnutrition related to greater maternal BMI is unlikely to have driven the recent obesity epidemic.
| S-EPMC2265763 | biostudies-literature
Project description: Not available
| S-EPMC9142497 | biostudies-literature
Project description:There is an extensive literature on the estimation and evaluation of optimal individualized treatment rules in settings where all confounders of the effect of treatment on outcome are observed. We study the development of individualized decision rules in settings where some of these confounders may not have been measured but a valid binary instrument is available for a binary treatment. We first consider individualized treatment rules, which will naturally be most interesting in settings where it is feasible to intervene directly on treatment. We then consider a setting where intervening on treatment is infeasible, but intervening to encourage treatment is feasible. In both of these settings, we also handle the case that the treatment is a limited resource so that optimal interventions focus the available resources on those individuals who will benefit most from treatment. Given a reference rule, we evaluate an optimal individualized rule by its average causal effect relative to a prespecified reference rule. We develop methods to estimate optimal individualized rules and construct asymptotically efficient plug-in estimators of the corresponding average causal effect relative to a prespecified reference rule.
| S-EPMC7959164 | biostudies-literature
Project description:This corrects the article DOI: 10.1038/ncomms11947.
| S-EPMC5869032 | biostudies-literature
Project description:ObjectiveHigh body mass index (BMI) is an important predictor of mortality but estimating underlying causality is hampered by confounding and pre-existing disease. Here, we use information from the offspring to approximate parental BMIs, with an aim to avoid biased estimation of mortality risk caused by reverse causality.MethodsThe analyses were based on information on 9674 offspring-mother and 9096 offspring-father pairs obtained from the 1958 British birth cohort. Parental BMI-mortality associations were analysed using conventional methods and using offspring BMI as a proxy, or instrument, for their parents' BMI.ResultsIn the conventional analysis, associations between parental BMI and all-cause mortality were U-shaped (Pcurvature < 0.001), while offspring BMI had linear associations with parental mortality (Ptrend < 0.001, Pcurvature > 0.46). Curvature was particularly pronounced for mortality from respiratory diseases and from lung cancer. Instrumental variable analyses suggested a positive association between BMI and mortality from all causes [mothers: HR per SD of BMI 1.43 (95% CI 1.21-1.69), fathers: HR 1.17 (1.00-1.36)] and from coronary heart disease [mothers: HR 1.65 (1.15-2.36), fathers: HR 1.51 (1.17-1.97)]. These were larger than HR from the equivalent conventional analyses, despite some attenuation by adjustment for social indicators and smoking.ConclusionsAnalyses using offspring BMI as a proxy for parental BMI suggest that the apparent adverse consequences of low BMI are considerably overestimated and adverse consequences of overweight are underestimated in conventional epidemiological studies.
| S-EPMC7612209 | biostudies-literature