Eating disorders (EDs) in adolescents, including anorexia nervosa, bulimia nervosa, and binge-eating disorder, are frequently accompanied by executive dysfunction, a set of higher-order cognitive processes governing self-regulation, planning, and decision-making. While impulsivity and poor inhibitory control predominate in bulimia nervosa and binge-eating disorder, anorexia nervosa is often characterized by cognitive rigidity and overcontrol. These contrasting neuropsychological patterns may represent distinct manifestations of executive dysfunction. Emerging evidence suggests that lipid metabolism, particularly serum cholesterol levels, may influence executive functioning, although findings in ED populations remain inconsistent. Given that cholesterol and other lipids are critical for neuronal membrane integrity, neurotransmission, and brain network function, disruptions in lipid homeostasis could contribute to specific executive functions in ED subtypes. This perspective highlights the need for targeted research linking lipid profiles to executive dysfunction within ED populations, moving beyond transdiagnostic generalizations. Understanding these relationships could inform tailored interventions that address both metabolic and neurocognitive dimensions, potentially improving long-term clinical and cognitive outcomes for adolescents with EDs.
Cholesterol and executive dysfunction in adolescents with eating disorders
Luca A.
2026-01-01
Abstract
Eating disorders (EDs) in adolescents, including anorexia nervosa, bulimia nervosa, and binge-eating disorder, are frequently accompanied by executive dysfunction, a set of higher-order cognitive processes governing self-regulation, planning, and decision-making. While impulsivity and poor inhibitory control predominate in bulimia nervosa and binge-eating disorder, anorexia nervosa is often characterized by cognitive rigidity and overcontrol. These contrasting neuropsychological patterns may represent distinct manifestations of executive dysfunction. Emerging evidence suggests that lipid metabolism, particularly serum cholesterol levels, may influence executive functioning, although findings in ED populations remain inconsistent. Given that cholesterol and other lipids are critical for neuronal membrane integrity, neurotransmission, and brain network function, disruptions in lipid homeostasis could contribute to specific executive functions in ED subtypes. This perspective highlights the need for targeted research linking lipid profiles to executive dysfunction within ED populations, moving beyond transdiagnostic generalizations. Understanding these relationships could inform tailored interventions that address both metabolic and neurocognitive dimensions, potentially improving long-term clinical and cognitive outcomes for adolescents with EDs.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.


