Energy Expenditure

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Increased REE in cancer is frequent but not universally found in cancer patients with progressive weight loss [12-14] (Fig. 4). Also, in studies of malnourished cancer patients, a large span from hypo-to hypermetabolism has been reported [15,16]. It would thus appear that cancer patients have a variable response to underfeeding, some being able to adapt appropriately to reduced REE for a period of time, while others show hypermetabolism or insufficient adaptation, accounting for low activity levels and anorexia. This would be in contrast to uncomplicated starvation, in which adaptation seems to occurs more effectively to reduced energy intake. Patients with cancer in some particular sites, such as lung and pancreas, may be more prone to develop hypermetabolism, although there are no clear-cut relationships to the type of tumor [17, 18]. Animal studies of cancer cachexia have suggested that there are changes in metabolic pattern over time, with initial hypermetabolism followed by hypometabolism preterminally [19]. Less is known about longitudinal changes in REE in cancer patients [17]. Jatoi et al. studied a small group of lung cancer patients and found decreased disease-free survival in eight hypometabolic compared to nine hypermetabolic patients [20]. In our

Fig. 4. REE in transectional analyses of weight-losing (WL) and weight-stable (WS) cancer patients compared to non-cancer patients with and without weight loss (p < 0.01 among all groups). (Data from [14])

own longitudinal observations, about half of the patients had elevated REE, defined as 110% or more of predicted REE [2]. Increased energy expenditure in cancer patients are significantly related to systemic inflammation, in which anaemia may attenuate the effectiveness of oxygen transportation and thereby increase the energy cost for circulatory homeostasis. However, anaemia may also correlate with increased energy consumption as a component of the acute-phase response, evident by an increased erythrocyte sedimentation rate or increased C-reactive protein levels [14]. In this context, it is noteworthy that pain does not seem to be a universal explanation to cancer cachexia in patients with solid gastrointestinal malignancy [21] (Fig. 5). Thus, it was possible to attenuate the increased REE in cancer patients by p-blockade to slow down hyperactive cardiovascular activity mediated in part by increased noradrenergic and adrenergic activity in combination with elevated production of gluco-corticoids [22, 23]. Thus, the classical hormone system is activated during increased metabolism and diminished food intake, together with cytokines; this response is usually attenuated by anti-inflammatory treatment [24]. Accordingly, it is well-recognised that cyclooxygenase inhibitors decrease inflammation in cancer patients and

Fig. 4. REE in transectional analyses of weight-losing (WL) and weight-stable (WS) cancer patients compared to non-cancer patients with and without weight loss (p < 0.01 among all groups). (Data from [14])

thereby improve energy balance by positive effects on both energy intake and production [24]. Another means to achieve this effect is to provide fish oils, which probably alter cell-membrane composition and thereby decrease production of powerful eicosanoids. Thus, it is conceptually possible to attenuate elevated REE in cancer patients on both the causative (cytokines, hormones, eicosanoids) and the effector (anaemia, hyperki-netic circulation, anorexia) sides. One simple way to improve energy balance would be to provide energy in excess of resting needs. This may, however, influence other components of total energy expenditure.

There have been few investigations of cancer cachexia and the other components of the total energy expenditure (TEE), i.e. TEF [25] and AEE [26]. Physical activity levels, as determined by questionnaires, was reported to predict chemotherapy toxicity in older lung cancer patients [27]. A study in 8 patients with advanced lung cancer found that TEE was not increased despite an increase in REE, indicating diminished activity [28]. A recent study made the same observation: TEE was assessed by doubly-labelled water in 24 patients with advanced pancreatic cancer. REE was increased but TEE was not changed, indicating decreased AEE [26]. During 8 weeks of

Fig. 5. REE in weight-losing cancer patients randomised to either P-blockade (propranolol), indo-methacin,morphine,or placebo compared to healthy individuals on P-blockade (propranolol), as described by Hyltander et al. (Data from [21])

treatment with a control nutritional supplement, TEE, REE, and AEE were unchanged, but in patients receiving a supplement enriched with EPA, physical activity was increased [26]. Thus, low physical activity levels may be an important feature of energy balance in cancer patients, which may, in turn, affect functional performance and quality of life.

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