In addition to the large sample size, our project had a number of strengths. We used an unscreened, epidemiological sample, meaning that the results were not conditional on inclusion/exclusion criteria, hence making the sample suitable for investigating all the endophenotypes. We adopted the same set of a priori analyses for all 17 endophenotypes and published the entire set of findings simultaneously. Our hope was to eliminate effects attributable to selective reporting of results, post hoc analysis leading to irreproducible findings, the need to report positive findings to justify publication, and piecemeal publication that would make it difficult to understand how the results varied from one endophenotype to another. Because our sample included twin families, we were able to determine the heritability of each endophenotype measure in the exact same sample used for molecular genetic analyses. We employed discovery based analyses to examine the association between each endophenotype and a) common variants (single nucleotide polymorphisms; SNPs) throughout the genome, b) autosomal genes, c) rare exonic variants, and d) rare and common variants throughout the genome. Our analyses took advantage of improved
