Metabolic Consequences in Anorexia Nervosa

Abstract

In anorexia nervosa (AN), weight loss and malnutrition trigger a cascade of metabolic, hormonal, and behavioral consequences. A considerable decrease in energy expenditure (EE) is observed during fasting states of the disease, but refeeding and weight gain induce a marked increase in EE, including an increase in resting EE, in diet-induced thermogenesis (DIT), and in EE related to physical activity. There is also a dramatic fall in protein catabolism and in glucose disposal during the fasting stages of the disease. During renutrition, these profiles become normal a long time before normalization of body weight. Malnutrition and slimming diets induce alterations in muscle mass and function, leading to difficulties in refeeding, for example by slowing gastric emptying. As shown in rats, the restrictive diet together with access to physical activity, which is secondary to anorectic thought, is responsible for increasing the cognitive restrictive diet and for increasing mental and physical hyperactivity. Energy and nutrient deficiencies are the consequence of fear of becoming obese, but could also induce, in one-third of cases, binge eating and, thus, purging. Recent studies have provided no evidence that AN is caused by neural, hormonal or metabolic factors and/or damage. But these metabolic and cognitive changes, which are mainly the consequence of the starvation, could explain some symptoms or behavior observed in AN, i.e., those related to the compulsive needs to remain thin and to the fear of being fat.