Several factors may contribute to the decreased intake of food in cancer patients. Anorexia, due to the disease itself or its treatment, is commonly recognised. Cancer patients may frequently suffer from symptoms affecting the gastrointestinal tract, for instance due to physical obstruction, constipation, or malabsorption. The effects or consequences of treatment by opiates, radiotherapy, or chemotherapy may all explain decreased food intake in the palliative care of cancer patients. However, reports on the degree of anorexia do not always indicate low intakes. Cohn et al. assessed energy and protein intake in relation to lean body mass in 22 oncology patients and found no difference from normal subjects, unless weight loss was present . Parkinson et al., in a study of the effects of oral protein and energy supplements in 30 cancer patients, reported a mean intake of 1515 Kcal/day, corresponding to 25 Kcal/kg/day . Simons et al. studied the effects of medroxyprog-esterone acetate in 54 patients with advanced nonhormone-sensitive cancer, and reported a higher mean intake, about 2200 Kcal/day, corresponding to 34 Kcal/kg/day . In contrast, in an analysis of energy balance in 100 lung cancer patients, decreased intake was found in weight-losing patients with acute-phase response [7, 8]. Levine and Morgan studied food selection in 10 hospitalised cancer patients with weight loss and anorexia . They found low energy intake (24 Kcal/kg/d), but the patients had maintained normal macronutrient composition despite cancer anorexia compared with hospitalised control subjects.
These results agree with our own observations of low intake in 297 patients with advanced cancer, mainly gastro-intestinal tumours . Mean dietary intake was below maintenance requirements (26 Kcal/kg/day) but the patients' macronutrient composition was normal (Fig. 3). Weight loss of more than 10% was present in 43% of our patients, and elevated REE (> 110% of predicted) occurred in 48% of the patients. Dietary intake did, however, not differ significantly between normo- and hypermetabolic patients. Thus, weight loss was apparently not accounted for by diminished dietary intake, since absolute energy intake was not different; in fact, intake per kg body weight was higher in weight-losing patients than in weight-stable patients, although it is always diffi
cult to normalise energy intake and expenditure in weight-losing subjects. Food preferences did not seem to be altered, since the proportion of dietary protein, carbohydrate, and fat was generally the same as in a general elderly population from the same geographic area (Fig. 3). Also, Fordy et al., in a study of 40 colorectal cancer patients with disseminated disease, did not find differences in diet composition between weight-stable and weight-losing patients . Thus, reduced dietary intake has been repeatedly but not consistently reported of in weight-losing cancer patients, though long-term dietary intake may be difficult to assess precisely. The magnitude of reduced intake at the beginning of weight loss is, however, not clear, but diminished food intake cannot alone explain weight loss in all cancer patients. Accordingly, our own investigations indicated that REE was a more powerful predictor of weight loss than energy intake, based on multiple linear regression analysis. Thus, other components of the energy balance equation must be taken into consideration; dietary induced thermogenesis, AEE, and the energy cost of integrated metabolic and physiological home-ostasis may all contribute to explain the variance in weight loss of cancer patients during disease progression, and thus the energy loss in substrate cycling .
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