The primary limitation of this work is the relatively small sample size compared to other GWAS of complex disease. Also, the Yale-Penn sample had exclusion criteria for major psychiatric comorbidities including schizophrenia and suicidal ideation, which could have led to the exclusion of people with severe, possibly highly ‘genetically-driven’ CD or OD. Third, we did not detect GWS associations with our TD phenotypes with the top genes identified through the corresponding binary trait analyses, or vice versa. While we hypothesize that we may be detecting biologically distinct pathways and/or achieved better power (given the sample sizes) by using survival models, an alternative hypothesis is that our models were more prone to error and false positives.
