**5. Epidemiology**

Estimating the prevalence of anorexia nervosa is problematic because it is a rare problem. The course of illness is variable, and sufferers are usually reluctant to report their situation or take part in studies [33]. Lifetime prevalence of DSM-5 diagnosis of AN in the West varies between 1 and 4% [27], but it has also been recently increasing in the non-Western world such as in Asia and the Middle East [34]. The problem is that most cases do not meet the full diagnostic criteria; resulting subthreshold EDs are more common in at-risk populations like high school and college samples [35]. Anorexia nervosa diagnosis is the most sexually based psychiatric problem, and the stereotypical patient is usually considered to be a young, white female from a higher socioeconomic class. This stereotype is not true all the time. However, the vast majority of the cases are women and the current malefemale ratio is standing at 1:10 [5]. Nevertheless, recent studies show that between 3 and 20% of AN cases are male [36, 37]. Underdiagnoses of AN in men are a result of several factors that include sociocultural expectations towards women and the difference in symptom presentation in men. The mean age of onset is 17 in AN and the risk decreases with age [38]. However, onset of the disorder can be after age 40 or even later in some cases [39]. AN has been found to be less common among Black than White Americans [40], possibly due to underrepresentation in specialist eating disorder services and under detection in primary care [41]. Other than that, there is no systematic association between ethnicity/race or socioeconomic status and eating disorder occurrence [42]. Being in a sexual minority is a risk factor for EDs which is general for both women and men [43, 44]. In conclusion, it is noted that anorexia can affect people of all ages, genders, races, ethnic origins, socioeconomic status, and sexual orientations [45].

**71**

*Anorexia Nervosa*

**6. Etiology**

anorexia.

**6.1 Genetic explanations**

likelihood of repetition of these studies.

order to explain the roles of genes in the AN etiology.

**6.2 Neurobiological explanations**

*DOI: http://dx.doi.org/10.5772/intechopen.91278*

Several theories have been proposed to understand the etiology of AN. Although

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

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

Neurobiological studies of AN focus on the brain areas, biological origins of symptoms, and neurochemical differences between people diagnosed with AN and healthy controls. Severe weight loss in anorexia causes a decrease in gray matter in several areas of the brain [56]. Moreover, a review of neuroimaging studies (PET, MRI, and fMRI) noted dysfunction in certain brain areas such as the amygdala, basal ganglia structures, and hippocampus [57]. On the other hand, research indicates dysfunctions in dopaminergic and serotonergic (5-HT) systems that are responsible for food, motivation, the reward system, executive function, emotion regulation, and impulse control [58]. Thus, food as a natural reward becomes a

these theories will be presented individually, it is recognized that a multidimensional approach is helpful to understand the causes of AN, even though such a comprehensive model has not yet been developed. Biological, psychological, and social factors interact with each other in the etiology. Prominent models include the genetic and neurobiological model, the psychodynamic model, the sociocultural model, and the cognitive behavioral model. Significant life events, personality, and a family system approach are also productive in understanding the causes of
