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Peptides, 11, 995 1001 La Via, MC, Gray, N & Kaye, WH (2000) Case reports of olanzapine treatment of anorexia nervosa Int J Eat Disord, 27 (3), 363 366 Laessle, RG, Fischer, M, Fichter, MM, Pirke, KM & Krieg, JC (1992) Cortisol levels and vigilance in eating disorder patients Psychoneuroendocrinology, 17 (5), 475 484 Laorden, ML, Castells, MT, Martinez, MD, Martinez, PJ & Milanes, MV (2000) Activation of c-fos expression in hypothalamic nuclei by mu- and kappa-receptor agonists: Correlation with catecholaminergic activity in the hypothalamic paraventricular nucleus Endocrinology, 141 (4), 1366 1376 Lee, GH, Proenca, R, Montez, JM, Carroll, KM, Darvishzadeh, JG, Lee, JI & Friedman, JM (1996) Abnormal splicing of the leptin receptor in diabetic mice.

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Swartz, L. (1985) Anorexia nervosa as a culture-bound syndrome. J. Soc. Sci. Med., 20 (7), 725 730. Szmukler, G. (1983) Weight and food pre-occupation in a population of English school girls. In B.G. Bergman (Ed.), Understanding Anorexia Nervosa and Bulimia (pp. 21 27). 4th Ross Conference on Medical Research. Ohio: Ross Laboratories. Taylor, D. (1985) The sick child predicament. Aust. N.Z.J. Psychiat., 19, 130 137. Troop, N., Treasure, J. & Schmidt, U. (1993) From specialist care to self directed treatment. Br. Med. J., 307 (6904), 577 578.

Nature, 379 (6566), 632 635 LeGoff, DB, Leichner, P & Spigelman, MN (1988) Salivary response to olfactory food stimuli in anorexics and bulimics Appetite, 11 (1), 15 25 Legradi, G & Lechan, RM (1999) Agouti-related protein containing nerve terminals innervate thyrotropin-releasing hormone neurons in the hypothalamic paraventricular nucleus Endocrinology, 140 (8), 3643 3652 Leibowitz, SF & Alexander, JT (1998) Hypothalamic serotonin in control of eating behavior, meal size, and body weight Biol Psychiat, 44 (9), 851 864 Leonard, T, Perpina, C, Bond, A & Tresaure, J (1998) Assessment of test meal induced autonomic arousal in anorexic, bulimic and control females Eur Eat Disord Rev, 6, 188 200 Li, BH, Xu, B, Rowland, NE & Kalra, SP (1994) c-fos expression in the rat brain following central administration of neuropeptide Y and effects of food consumption Brain.

Understanding the basic science underpinning appetite and weight homeostasis is vital if we are to pose useful hypotheses and interpret ndings appropriately in the study of eating disorders. Peripheral signals of energy homeostasis, such as leptin and insulin, modulate appetite and energy expenditure via complex orexigenic and anorexigenic neuroendocrine pathways of the hypothalamus. Here, information from higher centres, such as those governing motivation and reward, can be integrated before an appropriate response is elicited. Anorexia nervosa is characterised by severe energy de cit that may re ect impairment of appetite. Studies implicate impaired hypothalamic function, rather than peripheral energysignalling de cits. Neuroendocrine stress response and serotonergic systems may be particularly relevant. Bulimia nervosa is characterised by periods of over-eating coupled with efforts to compensate in order to achieve lower weight. Reduced leptin signalling may enhance activity in orexigenic pathways such that there is a tendency to gain weight. Overweight in the context of low self-esteem and emotional dysregulation may increase the risk of engagement in weight reduction behaviours. Once established, these behaviours appear to maintain the disorder via effects upon mood, satiety and appetite. Binge eating disorder is characterised by a tendency towards over-eating and excessive weight gain, in the absence of food restriction. Little is known about the biology of appetite in this group as yet. The reward value of food is high and it is likely that there is an imbalance between central orexigenic and anorexigenic pathways of the hypothalamus, favouring positive energy balance. It is hoped that a better understanding of the abnormalities of appetite and weight regulation contributing to the aetiology of eating disorders will lead to improved treatment.

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