Jack Bowden

This study identifies genetic variants causal for multiple long-term conditions, revealing shared biological pathways and potential drug targets while highlighting adverse effects of interventions.

This study identifies C1R as a molecular link between coronary artery disease and dementia through proteogenomic analysis of circulating proteins and genetic causal-inference.

This study uses MR-Clust to identify three MDD genetic clusters with opposing effects on T2D and cardiometabolic risk, linking them to distinct biological pathways and depression subtypes.

This study integrates primary care and genetic data to identify multimorbidity patterns and shared genetics across 72 chronic conditions, revealing both concordant and discordant relationships.

The paper introduces two new methods to estimate genetically driven effect heterogeneity and causal effects in Mendelian Randomization using the TWIST framework and applies them to study smoking during pregnancy on offspring birth weight.

This paper uses Mendelian randomization to estimate the causal effect of smoking during pregnancy on placental weight, finding that continued smoking increases placental weight.

This paper combines pharmacogenetic variants and polygenic scores for patient characteristics to improve prediction of clinical outcomes in Calcium Channel Blocker treatment.

The paper reviews current methods for Mendelian randomization and proposes a regression calibration approach to correct for bias in causal effect estimates using GWAS summary data.

This paper uses Mendelian randomization to investigate the causal relationship between maternal serum urate and offspring birthweight, finding a weaker causal effect compared to observational studies.

This paper develops a Bayesian model averaging approach for Mendelian randomization to address horizontal pleiotropy, demonstrating its application to study cholesterol's causal role in age-related macular degeneration.

This study finds that CYP2C19 loss-of-function variants are associated with increased risk of ischemic stroke and MI in patients on long-term clopidogrel therapy in primary care.

The paper introduces the TWIST framework for causal inference in pharmacogenetics, showing how to combine different estimation strategies to improve robustness and efficiency in estimating genetically moderated treatment effects.

Summary-data conditional F-statistics detect conditionally weak instruments in multivariable Mendelian randomisation, and Q-statistic minimisation gives weak-instrument and balanced-pleiotropy robust estimates plus an exact pleiotropy test.

This paper introduces GRAPPLE, a framework for causal inference using heterogeneous genetic instruments, and applies it to study the causal effects of blood lipids, BMI, and systolic blood pressure on 25 diseases.

This paper evaluates the performance of two-sample Mendelian randomization methods in one-sample MR analyses, finding that most methods perform well except MR-Egger, which shows bias due to confounding.

This study identifies 42 genetic loci associated with excessive daytime sleepiness and links them to phenotypic subgroups and related traits.

This paper evaluates the causal effect of fibrinogen on coronary heart disease using Mendelian randomization, finding a small effect with multi-variant methods but not with single variant approaches.

The paper identifies 57 genomic regions associated with insomnia symptoms, linking them to phototransduction, ubiquitination, and potential causal relationships with coronary heart disease and depression.

This study identifies 351 new genetic loci associated with chronotype using data from 697,828 individuals and links them to circadian biology and disease.

This study identifies new genetic loci associated with sleep disturbance traits and finds shared genetic links with neuropsychiatric and metabolic traits.