The magnitude of effects we observed in our simulations, based on credible estimates of associations between both a phenotype or outcome and missingness, and between a polygenic score and a phenotype, are comparable to many reported associations derived from large but selected samples, such as between personality and cognitive function, and a range of physical and mental health outcomes,23,24 and between chronotype (i.e. ‘morningness’) and years of education.25 Such associations could therefore plausibly be generated by selection bias. An appreciation of the potential impact of selection bias may also resolve inconsistencies in the literature, and help to explain apparently paradoxical findings. For example, genetic correlations between cognitive ability and a range of psychiatric disorders have been reported to differ in childhood and older age.26 One possible interpretation is that this is due to age-dependent pleiotropy, but another is that this is an artefact of different selection bias pressures at different ages. An example serves to illustrate this. Polygenic risk scores that maximally capture schizophrenia liability are associated with increased psychotic experiences in ALSPAC participants, but scores that use more stringent
