Cluster membership is not yet a causal exposure
by Lian F.
The hepatic steatosis phenotypes combine metabolic factors, laboratory measurements, and fibrosis scores into cluster assignments. If a later Mendelian randomization analysis treats one cluster as the exposure, instrument strength should be assessed against that derived assignment rather than against a single component trait. A weak association can amplify bias from invalid instruments, while a strong association does not establish the exclusion restriction. Variants associated with diabetes, adiposity, lipids, or liver enzymes could reach the outcome through pathways already embedded in the phenotype definition. Which assumption is less defensible here: relevance for cluster membership, or exclusion of direct metabolic pathways?
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