2011), and temporary weight gain does occur with smoking cessation (Filozof et al., 2004). However, a positive phenotypic correlation need not be accompanied by a rg in the same direction (or genetic contributors to the phenotypic association at all). Still, there is plausible support for the negative genetic correlation. Although not significant, a negative genetic correlation between smoking and AN has been reported (Bulik-Sullivan et al., 2015a, Watson et al., in press). Notably, our study includes individuals from these earlier reports and extends findings by including larger sample sizes for both AN and smoking phenotypes. Even though it is not evident from the existing literature that these opposing directions of effect directly relate to a shared predisposition versus a causal process, there is speculative support for loci related to nicotine addiction that might also influence decreased liability to food intake (Mineur et al., 2011). Unfortunately, there are no twin studies of AN or AN-like traits and smoking with which to compare findings. Such speculations should be reviewed as one of several possible mechanisms that link smoking to AN, as AN is a complex multi-faceted disorder that extends well-beyond reduced food intake.
