**6.1 Genetic explanations**

Genetic explanations focus on the biological mechanisms behind AN. Family, twin, and genetic studies found that AN runs in families [46]. A family history of AN puts people fourfold more at risk and relatives of women diagnosed with AN are 11 times more at risk of developing AN than controls [47, 48]. Moreover there is strong evidence that all types of EDs (AN, BN, and not otherwise specified EDs) track together in families without specificity [48]. Twin studies also show a genetic heredity for AN of between 28 and 74% but fail to identify specific genes [49]. In addition to these, anorexia interacts with other psychiatric problems. For example, people with a diagnosis of AN have a higher risk of developing OCD or vice versa [50]. Thus, genetic factors are considered responsible for 48–74% of the total variance in liability to AN [46]. Nevertheless, genetic factors cannot alone predict who will develop AN, as most of the cases do not have a familial history of EDs. Furthermore, methodological problems due to small sample size also reduce the likelihood of repetition of these studies.

It is evident that genes play an important role in the development of AN, although how these genetic predispositions interact with environmental factors has been a focus of research lately. Candidate gene and genome-wide studies are considered helpful in finding the answers. Research on candidate genes examined the serotonergic system (5-HT system), dopaminergic system, and opioidergic system that affect appetite, reward mechanism, mood, and weight; nevertheless, statistically significant results have not been presented so far [51]. Genome wide studies showed a relation between chromosomes 1, 11, and 12 and genes related to leptin regulation, lipid and glucose metabolism, serotonin receptor activities, and the immune system [52–55]. This genetic presentation is also consistent with the clinical presentation of anorexia. Further studies in these areas can be productive in order to explain the roles of genes in the AN etiology.
