Genetic factors Sample Clauses

Genetic factors. Twin and family studies provide support for the role of genetic factors in ED (Xxxxxx & Xxxxx, 2011). ED are highly familial and heritability ranges between 50-83% (BED (Xxxxxxx et al., 2008) AN (Bulik, Slof-Op't Xxxxx, xxx Xxxxx, & Xxxxxxxx, 2007) BN (Bulik & Xxxxx, 2004). Serotonergic, dopaminergic, opioid, appetite regulation and genes influencing food intake and weight regulation systems have all been under investigation, although conclusions cannot be drawn owing to small sample sizes and lack of replication (Trace, Xxxxx, Xxxxx-Xxxxx, & Xxxxx, 2013). A third of the genetic risk for ED is shared with depression (Wade, Bulik, Neale, & Kendler, 2000), anxiety (Keel, Klump, Miller, McGue, & Xxxxxx, 2005) and addictive disorders (Baker, Mazzeo, & Kendler, 2007). To date, two genome- wide association studies (GWASs) have been conducted in ED. The results of the first GWAS detected that common single-nucleotide polymorphism (SNP), such as those within the OPRD1, and copy number variants (CNV) confer risk for AN (Wang et al., 2011). The findings from the second GWAS analysis of six ED related phenotypes noted an association of eight genetic variants (Xxxxxxx et al., 2012). Thus far, no GWAS has found genome-wide significant results in ED. Genetic factors appear to play a key role in the aetiology of ED although the highly variable ED phenotype poses a challenge for the study of candidate genes (Xxxxxxx & Treasure, 2004).
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