Michael Vaclav Holmes

This paper shows that polygenic risk scores for CAD can create false treatment response patterns due to collider bias, not actual biological effects.

The paper analyzes the impact of CYP2C19 genotype on SSRI side effects and discontinuation rates in a large sample of individuals.

This study examines the psychological impact of viewing depression polygenic risk scores (PRS) in a real-world setting, finding no significant difference in depression or anxiety symptoms between those who viewed their results and those who did not.

This study finds that higher polygenic risk scores for breast cancer are associated with longer survival in patients, suggesting a link between genetic predisposition and less aggressive tumors.

This study performs a multi-ancestry GWAS of Long COVID, identifying immune-related loci and genetic links to chronic fatigue syndrome, fibromyalgia, and depression.

The paper analyzes 3.6 million individuals to find minimal evidence of non-additive genetic interactions for height.

This study performs a multi-ancestry GWAS of diarrhea during acute SARS-CoV2 infection, identifying six novel loci and contrasting genetic roles of IBS subtypes in COVID-19 diarrhea.

This study conducts a trans-ancestral GWAS of sporadic and recurrent miscarriage, identifying novel genetic associations and providing causal evidence for smoking and caffeine consumption.

The paper uses the 23andMe database to study MAP3K15's metabolic role, finding LoF carriers have delayed T2D diagnosis and reduced cholesterol.

This paper uses a polygenic risk score to identify undiagnosed diabetes cases, finding that combining BMI and PRS captures most undiagnosed cases, including those with normal weight.

The paper estimates polygenic risk scores (PRS) for 12 diseases in a diverse cohort and finds higher disease incidence and earlier clinical manifestation in top PRS individuals.

This study uses GWAS and Mendelian randomization to show that lower sclerostin levels increase risk of hypertension, type 2 diabetes, myocardial infarction, and atherogenic lipid profiles.

The paper constructs an atlas linking 129 polygenic risk scores to 249 metabolites in 83,004 UK Biobank participants, finding associations with BMI and smoking liability on systemic inflammation.

This paper improves genetic scores for adiposity traits in East Asian populations by using trans-ancestry meta-analysis, increasing variance explained compared to European-derived scores.

This study uses Mendelian randomization to compare the effects of lipid-modifying drug targets on CAD risk and blood metabolome traits across 115,082 UK Biobank participants.

This study uses Mendelian randomisation to investigate the causal effects of obesity on female reproductive conditions, finding that central obesity and metabolic hormones mediate these associations.

This paper uses Mendelian randomization and colocalization to identify causal relationships between plasma proteins and disease phenotypes, finding 111 putatively causal effects.

The paper identifies HLA-B*55:01 as a genetic risk factor for penicillin allergy through genome-wide analysis of electronic health records and imputed HLA data.

The paper identifies pQTLs for cardiovascular proteins and uses them to evaluate drug targets and suggest new candidates for precision medicine.

This study uses Bayesian colocalization to identify genes potentially mediating polycystic ovary syndrome risk by linking genetic risk loci to intermediate phenotypes.

The paper examines the effects of CETP and HMGCR genetic inhibition on lipoprotein profiles and CHD risk, finding distinct impacts on cholesterol and triglyceride compositions.

The paper analyzes genetic variants at the PCSK9 locus to assess their phenotypic effects on lipid levels and disease outcomes, finding concordance with PCSK9 inhibitor trials for myocardial infarction but discordance for type 2 diabetes.

This study assesses the transferability of lipid loci across African, Asian, and European populations, finding high consistency but also population-specific variations.

This study finds that genetically or therapeutically lowering sclerostin increases cardiovascular risk, based on genetic variant analysis and clinical trial data.

A GWAS of erectile dysfunction identifies a new locus at 6q16.3, implicating hypothalamic neurobiology and diabetes in its etiology.

This paper conducts a GWAS on objectively-measured physical activity and sleep traits, identifying 10 loci with potential causal roles in cardiometabolic disease.

This paper meta-analyzes two RCTs to assess if ADCY9 genotype modifies CETP inhibitor response on cardiovascular risk, finding heterogeneity and a trend across genotypes.