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Chunk #16 — Discussion

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Shared genetic risk between eating disorder- and substance-use-related phenotypes: Evidence from genome-wide association studies.
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Finally, the significant negative rgs between three smoking phenotypes—smoking initiation, current smoking, and cigarettes per day—and AN without binge-eating are intriguing, suggesting that increased genetic liability to AN without binge-eating is associated with decreased genetic liability to multiple smoking behaviors. Phenotypic studies are inconsistent about the association between the restricting subtype of AN and smoking. Some studies suggest that individuals with restricting AN have a higher prevalence of various smoking phenotypes than controls (Krug et al., 2008), whereas other studies indicate no significant difference between the two groups (Anzengruber et al., 2006). A recent meta-analysis did not find differences in the odds of lifetime smoking between individuals with AN and healthy controls (Solmi et al., 2016), yet the authors did not assess differences by AN subtype. Individuals with AN may smoke as a way to control or lose weight (White, 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,