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Cancer cachexia is debilitating and distressing. not only for the patient. but for the family and friends who feel helpless to stop their relative 'dissolving before their eves'. Eating is normally a pleasurable and sociable occasion. which contributes to a sense of well-being. The normal physiology of hunger. appetite and satiety continue to be conjectural. What is known is that the hypothalamus plays a major facilitatoryand inhibitorrole in hunger and satiety. Feedback from plasma glucose. free fatty acids. glycerol. amino acids. peripheral metabolic state and signals from the gastrointestinal tract ensure the fine tuning of calorie intake. distribution. disposal and storage (Bray & Campfield 1975). Mayer (1953. 1955. 1957) suggested that blood glucose may be the link between the supply of nutrients and the hypothalamus. A 'normal' hunger is a result of physiological changes in the state of the body's stores of energy and is inhibited by fullness. a sensation arising from the alimentary canal (Davidson et al.. 1979). The desire to eat can be seen as a continuum with appetite at one end and satiety at the other. with the change occurrng gradually as the meal progresses (Silverstone & Goodall. 1986). Cancer cachexia is viewed as a complex syndrome, the aetiology of which is still uncertain and is often only reversed when the malignancy is treated effectively (Theologides. 1977). It occurs in one-half to two-thirds of patients with cancer and has long been recognised as a frequent cause of death in the cancer patient (Warren. 1932). The symptoms of cancer cachexia are anorexia, early satiety. loss of body protein and fat. anaemia and marked asthenia. In addition, there is an increase in the basal metabolic rate and a corresponding increase in energy expenditure. whilst there is frequently a decreased energy' intake (Theologides. 1979). Metabolic factors play a role in many patients and may include, altered carbohydrate and protein metabolism (Holrovde & Reichard. 1981; Young et al.. 1979). selective use and redistribution of nutrients by tumour cells (Theologides, 1979). alterations of total lipid mobilisation resulting in elevated free fatty acids (Knox et al.. 1983) and abnormal synthesis of peptides which may disrupt normal enzyme activity (Theologides. 1972: Young. 1977). Cancer patients commonly demonstrate disturbances of glucose metabolism, Glicksman & Rawson (1956) described this as a diabetic glucose tolerance. This is characterised by reduced insulin sensitivity (Lundholm et al.. 1978). increased glucose tur-

A study to investigate the incidence of early satiety in patients with advanced cancer