common in individuals with hypothyroidism, and that subclinical hypothyroidism could play a role in a subset of persons diagnosed with major depression; thus cross-contamination of GWAS samples could lead to a biased positive correlation. However, the second observation is that there is an increased incidence of major depression and depressive symptomatology in persons with autoimmune thyroiditis receiving hormone replacement therapy (Dayan & Panicker 2013; Giynas Ayhan et al. 2014). It is worth noting that GWAS data for allergy, asthma, hypothyroidism, childhood ear infection, and Parkinson’s disease were obtained through 23andMe, Inc.. These data are based on self-report, and thus could be more susceptible to bias stemming from misdiagnosis or misreporting, though previous work supports their validity (Tung et al. 2011). None the less, the samples sizes are an order of magnitude larger than many other datasets, resulting in smaller standardized errors and better power for the detection of weak genetic correlations. It is yet unclear whether small magnitude genetic correlations like these might be clinically meaningful. The LDSC correlations observed presently were relatively weak magnitude (rgs ≈ 0.12 to 0.30) and of modest modest statistical significance (1×10−5 ≤ uncorrected p ≤ 5×10−3), when compared to the strongest genetic correlations observed
