Leptin Secretion Linked to Severity of Disease in Bulimia Nervosa

Leptin is a hormone, produced by adipose tissue, which is thought to affect some of the many factors that influence satiety and to regulate body weight by adjusting feeding behavior and energy use. Factors other than size of fat cells and fat content influence the production of leptin, and thus the macro- and micronutrients in the diet have an important effect upon leptin production.

Work by a group at the University of Naples may help explain why lower leptin levels have been reported in some patients with bulimia nervosa (BN), but not in others. This group has tied decreased leptin secretion to more chronic disease and greater binge eating/vomiting behavior among a subgroup of patients with chronic BN (Psychosomatic Med 2002; 64:874).

Palmiero Monteleone, MD, and colleagues measured plasma leptin levels and other hormone levels among a group of 127 women, including 33 patients with anorexia nervosa (AN), 56 women with BN, and 38 healthy controls. All the women were evaluated with the Eating Disorders Inventory, the BITE (Bulimic Investigation Test Edinburgh), and the Hamilton Depression Rating Scale, and had morning blood samples taken.

Decreased leptin levels reported

Compared with the healthy controls, underweight AN and normal-weight BN patients had decreased plasma levels of leptin, prolactin, and 17-beta estradiol. Cortisol levels were increased among AN patients but not BN patients. Among the bulimic patients, plasma leptin levels were inversely correlated with the duration of the disease and the frequency of binge eating/vomiting. In addition, 29 bulimic women had anorexic-like plasma leptin concentrations; the other 27 women had circulating leptin levels similar to that of the normal controls.

Thus, a subgroup of BN patients apparently secreted lower-than-normal levels of leptin despite having normal body weight. Therefore, something other than current body weight was involved in reducing leptin production in these patients. One contributing factor, according to the authors, might be a history of substantial weight loss—sustained weight loss has been shown to lead to a persistent reduction in circulating leptin in humans (Horm Metab Res 1996;28:698). Other researchers, such as Jimerson et al. (J Clin Endocrinol Metab 2000;85:4511) have also identified a relationship between decreased leptin levels and increased frequency of binge eating.

Can nutrition affect leptin levels?

The Italian scientists believe that the association between leptin levels and binge eating/vomiting frequency and the correlation between leptin and the duration of the illness, reflect changes in the subjects’ nutrition and/or eating patterns and that this then affects leptin synthesis. They point out that in spite of the large number of calories bulimics ingest during a binge, these patients vomit a relatively large amount of calories and then engage in calorie restriction. A caloric intake below the normal requirements, even with no loss of fat mass, may have an impact on leptin synthesis. In addition, although BN is not characterized by lack of nutrition and cachexia, as in AN, incorrect selection of foods may lead to the lack of certain macro- and micronutrients in the diet that may then affect the production of leptin. Finally, experimental binge eating dramatically flattens the leptin diurnal rhythm even when the total calories are appropriate for weight.