Structural Brain Volumetry Changes in Eating Disorders.

Eating disorders (EDs) are complex psychiatric conditions characterized by persistent disturbances in eating behaviors, body weight regulation, and self-perception, often accompanied by severe physical health consequences and high mortality rates (1). They typically emerge during adolescence or early adulthood but may develop at any age, with a multifactorial etiology involving genetic, neurobiological, psychological, and sociocultural influences (2).

The main diagnostic categories include anorexia nervosa (AN)-marked by significantly low body weight, intense fear of weight gain, and body image distortion; bulimia nervosa (BN)-characterized by recurrent binge eating followed by compensatory behaviors such as vomiting, fasting, or excessive exercise; and binge-eating disorder (BED)-involving recurrent episodes of excessive food intake without compensatory behaviors (3). Other specified feeding or eating disorders (OSFED) encompass clinically significant presentations not meeting full criteria for the above disorders.

In Egypt, eating disorders represent an under-recognized public health concern. Recent epidemiological studies have found that approximately 13.3% of Egyptian youth meet criteria for an ED, with BN being the most prevalent (8.4%) and BED affecting 1.4% (4). The apparent absence of AN cases in some surveys may reflect cultural perceptions of thinness, under-diagnosis, and stigma rather than true absence (5). Risk factors identified in Egyptian samples include high body mass index (BMI), exposure to Westernized beauty ideals, depression, and a history of psychological trauma (6).

Structural neuroimaging, particularly MRI, has revealed consistent alterations in ED patients. AN is often associated with global and regional gray matter reductions-particularly in the parietal, frontal, and temporal cortices-along with decreased subcortical and cerebellar volumes (7). BN has been linked to structural changes in frontal and striatal regions, potentially reflecting alterations in impulse control and reward processing (8). Some volumetric changes may partially reverse with nutritional rehabilitation, suggesting neuroplasticity (9).

Psychiatric comorbidities are highly prevalent in EDs, affecting more than 70% of patients (10). Anxiety disorders, mood disorders, obsessive-compulsive disorder (OCD), post-traumatic stress disorder (PTSD), and substance use disorders are common, often worsening symptom severity and complicating treatment (10, 11). OCD traits are especially frequent in AN, while BN shows strong associations with depression and anxiety.