We went on to examine the genomic distribution of liability by partitioning the heritability by chromosome. We found that the additive heritability estimated by chromosome for either OCD or TS was not significantly different from the cumulative univariate heritability calculated by using all data together. This served as an additional quality control check and confirmed the absence of residual LD between chromosomes, which can arise in a sample with cryptic relatedness or population substructure [51]. We examined the relationship between chromosome length and proportion of heritability detected, which also provides insight into the distribution of risk alleles throughout the genome and helps to characterize the polygenic contribution to risk. We found evidence, in both TS and OCD, of a highly polygenic architecture, as demonstrated by the significant correlation between chromosomal length and heritability. In addition, the observation that individual chromosomes in both phenotypes contributed to heritability disproportionately suggest these chromosomes may harbor loci with larger effect sizes on a polygenic background of small effect susceptibility variants distributed equally throughout the genome.
