In addition to metacognition, people with anorexia also have difficulty with social cognition including interpreting others emotions, and demonstrating empathy. Abnormal interoceptive awareness and interoceptive sensitivity shown through all of these examples have been observed so frequently in anorexia that they have become key characteristics of the illness. Comorbidity
Other psychological issues may factor into anorexia nervosa. Some people have a previous disorder which may increase their vulnerability to developing an eating disorder and some develop them afterwards. The presence of psychiatric comorbidity has been shown to affect the severity and type of anorexia nervosa symptoms in both adolescents and adults.Obsessive-compulsive disorder (OCD) and obsessive-compulsive personality disorder (OCPD) are highly comorbid with AN. OCD is linked with more severe symptomatology and worse prognosis. The causality between personality disorders and eating disorders has yet to be fully established. Other comorbid conditions include depression, alcoholism, borderline and other personality disorders, anxiety disorders, attention deficit hyperactivity disorder, and body dysmorphic disorder (BDD). Depression and anxiety are the most common comorbidities, and depression is associated with a worse outcome. Autism spectrum disorders occur more commonly among people with eating disorders than in the general population. Zucker et al. (2007) proposed that conditions on the autism spectrum make up the cognitive endophenotype underlying anorexia nervosa and appealed for increased interdisciplinary collaboration. Causes
There is evidence for biological, psychological, developmental, and sociocultural risk factors, but the exact cause of eating disorders is unknown. Genetic
Anorexia nervosa is highly heritable. Twin studies have shown a heritability rate of 28–58%.
A review of functional neuroimaging studies reported reduced activations in "bottom up" limbic region and increased activations in "top down" cortical regions which may play a role in restrictive eating.Compared to controls, people who have recovered from anorexia show reduced activation in the reward system in response to food, and reduced correlation between self reported liking of a sugary drink and activity in the striatum and anterior cingulate cortex. Increased binding potential of 11C radiolabelled raclopride in the striatum, interpreted as reflecting decreased endogenous dopamine due to competitive displacement, has also been observed.Structural neuroimaging studies have found global reductions in both gray matter and white matter, as well as increased cerebrospinal fluid volumes. Regional decreases in the left hypothalamus, left inferior parietal lobe, right lentiform nucleus and right caudate have also been reported in acutely ill patients. However, these alterations seem to be associated with acute malnutrition and largely reversible with weight restoration, at least in nonchronic cases in younger people. In contrast, some studies have reported increased orbitofrontal cortex volume in currently ill and  in recovered patients, although findings are inconsistent. Reduced white matter integrity in the fornix has also been reported. Diagnosis
A diagnostic assessment includes the persons current circumstances, biographical history, current symptoms, and family history. The assessment also includes a mental state examination, which is an assessment of the persons current mood and thought content, focusing on views on weight and patterns of eating.