Plasma concentrations of tumor necrosis factor-alpha (TNF-alpha) and soluble TNF receptors in patients with anorexia nervosa.

Tumor necrosis factor-alpha (TNF-alpha) is a cytokine with numerous immunological and metabolic activities. To study the role of TNF-alpha on the pathophysiology of anorexia nervosa and its complications, plasma concentrations of TNF-alpha, 2 soluble TNF receptors (sTNF-RI and sTNF-RII), and leptin were measured in 20 female patients with anorexia nervosa (AN) and 20 age-matched normal women (N). Plasma TNF-alpha concentrations in AN were significantly higher than those in N (4.1 +/- 0.6 pg/mL vs. 1.6 +/- 0.1 pg/mL; P < 0.01). Although no significant difference was observed in plasma sTNF-RI concentrations between the two groups, plasma sTNF-RII concentrations in AN were significantly higher than those in N (2094.0 +/- 138.5 pg/mL vs. 1569.5 +/- 84.0 pg/mL; P < 0.01). Plasma concentrations of TNF-alpha and sTNF-RII after treatment of 8 anorectic patients were not different from those before treatment, although body fat mass and plasma leptin concentrations significantly increased after treatment. Plasma TNF-alpha concentrations were not related to body fat mass in anorectic patients. These results suggest that the adipose tissue may not be the immediate source of TNF-alpha in anorectic patients and that TNF-alpha may contribute to the pathophysiology of immunological and metabolic abnormalities in anorexia nervosa.

Leptin in women with eating disorders.

The aim of the present study was to determine the factors controlling leptin secretion and to clarify the role of leptin in eating disorders. The subjects were 152 eating-disordered women with different fat mass, eating behavior, and endocrine abnormalities and 24 age-matched control subjects. The body fat mass, eating behavior score, and plasma leptin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), triiodothyronine (T3), free thyroxine (T4), insulin, and cortisol levels were evaluated for each subject. In patients with eating disorder, logarithmic values for leptin were significantly correlated with the body fat mass (r = .828, P < .001), eating behavior score (r = .777, P < .001), and LH (r = .465, P < .001), FSH (r = .440, P < .001), T3 (r = .572, P < .001), insulin (r = .410, P < .001), and cortisol (r = -.389, P < .001) levels. After adjusting for fat mass, the partial correlations of log leptin with LH, FSH, insulin, and cortisol were not statistically significant, but log leptin remained correlated with T3 (r = .390, P < .01). Stepwise regression analysis showed that the body fat mass and eating behavior score were significant determinants of leptin levels. These results suggest that eating behavior, as well as the body fat mass, is the control factor for leptin secretion in eating disorders.

[The dialectic of the obsessionality and the dissociativity: toward a psychopathology of binge-eating].

Binge-eating is one of the most paradoxical phenomena in the symptomatology of anorexia nervosa and bulimia nervosa. The patients seem to be struggling to control their eating behaviors as strictly as possible, and at the same time, they repeat chaotic patterns of binge-eating. The author investigated the descriptive psychopathology of binge-eating in this paper. The author recognized the impulsive nature of binge-eating at first, and compared it with the clinical features of so-called impulse control disorders, such as kleptomania, trichotillomania, and so on. According to the literature review, most impulse control disorders tended to show high coincidence with eating disorders. The mode of the coincidence and the alternation of the symptoms suggested the common psychopathologies between eating disorders and impulse control disorders. The author then inquired into their common psychopathologies, and revealed characteristic features which could be formulated as dissociative. The study of the concept of dissociation proved that this formulation was not only valid, but also useful in understanding eating disorders clinically and theoretically. Binge-eating could be regarded as a manifestation of dissociative pathology. The author inquired further into the psychopathologies of eating disorders and impulse control disorders, and revealed obsessional features in these disorders. Though some investigators regarded the symptoms of eating disorders as compulsive behaviors and considered that eating disorders were variants of obsessive-compulsive disorder, the author pointed out some descriptive differences between them. Nevertheless, the obsessionality formed an important basis of the psychopathology of binge-eating. Finally, the author discussed the relationship between the obsessionality and the dissociativity in eating disorders. These two features were reciprocal factors in mental activity, and were forming dialectical dynamism in general psychological functioning. In anorexia nervosa and bulimia nervosa, the opposition between two factors was morbidly rigid and their sublation could not occur. Though the obsessional and the dissociative features of binge-eating were opposite phenomena, it was important to comprehend them as an incorporated psychopathology. The conceptualization of the dialectic of the obsessionality and the dissociativity could also be useful in understanding other psychopathological phenomena such as addiction and splitting.

Role of leptin in women with eating disorders.

OBJECTIVE: This study investigated the role of leptin on eating behavior and reproductive function in eating disorders. METHOD: The subjects included 80 eating-disordered women, having different fat mass, eating behavior, and endocrine abnormalities, and 26 control women. Plasma leptin, insulin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), cortisol, insulin growth factor-1 (IGF-1), free T4 levels, percent body fat, eating behavior score, and menstrual status score were evaluated for each subject. RESULTS: In eating-disordered patients, log of leptin levels were significantly correlated with body fat mass, eating behavior score, menstrual status score, and insulin, LH, and FSH levels. Stepwise regression analysis showed that fat mass and eating behavior score were significant determinants of leptin levels. Furthermore, in patients undergoing recovery, leptin levels were determined by fat mass and/or eating behavior. DISCUSSION: These results suggest that leptin may play some role in counteracting the abnormal eating behavior, reproductive function, and fat mass in these disorders.

Plasma concentrations of tumor necrosis factor-alpha (TNF-alpha) and soluble TNF receptors in patients with bulimia nervosa.

BACKGROUND: Tumor necrosis factor-alpha (TNF-alpha) is a cytokine with numerous immunological and metabolic activities. In addition, TNF-alpha can stimulate a variety of physiological, neuroendocrine and behavioural responses of the central nervous system. In experimental animals, TNF-alpha induces changes in physiological and behavioural parameters which have also been observed in eating disorders. The biological activities of TNF-alpha are mediated by two structurally related, but functionally distinct receptors, TNF-RI and TNF-RII. Since injection of TNF-alpha results in increased shedding of TNF-alpha receptors, it is likely that TNF-alpha release is reflected by soluble TNF-receptors (sTNF-Rs) levels. AIMS: We studied plasma concentrations of TNF-alpha and two sTNF-Rs (sTNF-RI and sTNF-RII) in female patients with bulimia nervosa. DESIGN AND PATIENTS: Twenty female patients with bulimia nervosa (BN) and 20 age-matched normal women (N) were studied. MEASUREMENTS: Plasma TNF-alpha concentrations were measured by enzyme immunoassay kit and plasma concentrations of sTNF-RI and sTNF-RII were measured by enzyme-linked immunosorbent assay. RESULTS: Plasma TNF-alpha concentrations in BN were significantly higher than those in N (4.7+/- 0.5 ng/l vs. 1.6+/-0.1 ng/l; P<0.01). Although no significant difference was observed in plasma sTNF-RI concentrations between the two groups, plasma sTNF-RII concentrations in BN were significantly higher than those in N (2080.0+/-107.5 ng/l vs. 1569.5 +/-84.0 ng/l; P<0.01). Plasma TNF-alpha concentrations were significantly related to plasma sTNF-RI concentrations (r = 0.511, P<0.05) and to plasma sTNF-RII concentrations (r = 0.532, P<0.05) in bulimic patients. However, plasma TNF-alpha concentrations were not related to body fat mass or to bulimic behaviours in these patients. CONCLUSIONS: Our present findings suggest that the adipose tissue may not be the immediate source of TNF-alpha in bulimic patients but the increase in plasma TNF-alpha in these patients may be derived from the central nervous system sources. The elevated sTNF-RII may reflect different shedding kinetics compared with sTNF-RI in bulimic patients.