Bjørn Olav Åsvold

This study uses Mendelian randomization to identify risk factors for kidney function decline in CKD and the general population, finding causal effects of type-2 diabetes and high TSH.

This study uses whole-genome sequencing to identify genetic variants associated with mitral valve prolapse and arrhythmias in a Norwegian cohort, finding enriched variants in genes related to extracellular matrix and electrophysiological pathways.

This study uses Mendelian randomization to examine the lifecourse effects of childhood and adulthood adiposity on sleep health outcomes, finding that adult adiposity is a risk factor for insomnia while childhood adiposity may have protective effects when maintained in adulthood.

This study identifies genetic risk factors associated with severe psoriasis and shows that polygenic risk scores can predict severe disease outcomes better than traditional risk factors.

This study uses Mendelian randomization to assess how cardiometabolic drugs affect kidney function, finding specific drug targets influence eGFR and related biomarkers.

This study identifies 40 genetic loci associated with placental weight using GWAS in 179,025 children and parents, revealing shared and distinct genetic influences with fetal growth.

This study uses Mendelian randomization to examine the causal effects of childhood and adulthood adiposity on anxiety and depression, finding childhood adiposity may protect against mental health issues if obesity is absent in adulthood.

This study uses within-sibship Mendelian randomization to show taller height reduces coronary heart disease risk but increases cancer risk, likely due to causal effects rather than confounding factors.

This study identifies 424 new loci associated with kidney function using GWAS data from over 1.2 million individuals and prioritizes 34 genes for further functional investigation.

A coronary artery disease GWAS of 181,522 cases among 1,165,690 participants yields 241 associations (54 new); an eight-predictor consensus nominates 185 candidate causal genes, 94 with ≥3 predictors.

In 159,701 siblings from 17 cohorts, population GWAS overstate direct effects on height, education, smoking, cognition, depressive symptoms and age at first birth; clinical traits mostly agree across models.

This paper conducts a genome-wide association study (GWAS) of skin and soft tissue infections (SSTIs), identifies genetic loci, and shows that BMI and smoking increase SSTI risk.

This paper introduces within-family Mendelian randomization methods to reduce biases from family structure and shows they yield different results compared to population-based analyses.

The paper identifies loss-of-function variants affecting liver-related blood traits that reduce CVD risk without increasing metabolic disease risk, highlighting potential therapeutic targets.

This study uses Mendelian Randomization to show that higher BMI causally increases the risk of psoriasis and eczema, with a stronger effect on psoriasis.

This study uses Mendelian randomisation to show that higher cigarette consumption causally increases coffee intake, with weaker evidence for tea.