sharing more of the environment (siblings are born in the same family, during a similar period of time, and grow up in the same household). Furthermore, maternal and paternal half-siblings (both sharing 25% of genes but paternal half-siblings sharing less environment, as >90% of Swedish children continue living with their mothers after a divorce)34 had very similar risks of AD. Consistent with a potential genetic mechanism, a recent study using publicly available genome-wide association (GWAS) data to explore the genetic correlations between a range of psychiatric and medical phenotypes with immunological and/or inflammatory disorders35 revealed significant positive genetic correlations (uncorrected for multiple testing ±standard error) between OCD and celiac disease (rg=0.39±0.18) and ulcerative colitis (rg=0.29±0.09), and negative correlations with type 1 diabetes mellitus (rg=-0.28±0.10).35 It should be noted that current published GWAS for OCD36, 37 and TD,38 as well as some AD, are underpowered to detect genome-wide significant associations and much larger studies are needed. For example, it remains unclear whether OCD or TD/CTD are associated with variation in the major histocompatibility complex region on chromosome 6, which has a major influence on risk for many AD.
