We also observed significant negative genetic correlations between anorexia nervosa and insulin and glucose related traits—e.g., exceeding those of BMI for both insulin resistance (HOMA-IR) (rg =−0.50, SE=0.11, p=1.3×10−5) and fasting insulin (rg =−0.41, SE=0.09, p=5.2×10−6); as well as a similar correlation with fasting glucose (rg =−0.26, SE=0.07, p=3.0×10−4). Although BMI corrected HOMA-IR GWAS statistics were not available genome-wide, additional analyses with the available BMI corrected GWAS results for related phenotypes suggest that this metabolic signal is at least partly independent of BMI with leptin levels (rg = −0.24, SE=0.11, p=0.03). Regarding cholesterol and lipid measures, a distinction between different lipid fractions emerges when comparing high density lipoprotein (HDL), low density lipoprotein (LDL), and very low density lipoprotein (VLDL) phenotypes. Genetic correlations between anorexia nervosa and HDL phenotypes were positive: e.g., total cholesterol in large HDL particles (rg =0.39, SE=0.12, p=1.6×10−3); free cholesterol in large HDL particles (rg =0.37, SE=0.12, p=2.2×10−3); and phospholipids in large HDL particles (rg =0.30, SE=0.11, p=6.7×10−3). In contrast, VLDL cholesterol phenotypes were negatively correlated with AN, albeit with nominal significance (i.e., uncorrected p<.05): e.g., total
