Abstract
Cancer cachexia is a complex metabolic syndrome characterized by involuntary skeletal muscle loss and is associated with poor clinical outcome, decreased survival and negatively influences cancer therapy. No curative treatments are available for cancer cachexia, but nutritional intervention is recommended as a cornerstone of multimodal therapy. Optimal nutritional care is pivotal in the treatment of cancer cachexia, and the effects of nutrients may extend beyond provision of adequate energy uptake, targeting different mechanisms or metabolic pathways that are affected or deregulated by cachexia. The evidence to support this notion derived from nutritional intervention studies in experimental models of cancer cachexia is systematically discussed in this review. Moreover, experimental variables and readout parameters to determine skeletal muscle wasting and cachexia are methodologically evaluated to allow critical comparison of similar studies. Single- and multinutrient intervention studies including qualitative modulation of dietary protein, dietary fat, and supplementation with specific nutrients, such as carnitine and creatine, were reviewed for their efficacy to counteract muscle mass loss and its underlying mechanisms in experimental cancer cachexia. Numerous studies showed favorable effects on impaired protein turnover and related metabolic abnormalities of nutritional supplementation in parallel with a beneficial impact on cancer-induced muscle wasting. The combination of high quality nutrients in a multitargeted, multinutrient approach appears specifically promising, preferentially as a multimodal intervention, although more studies investigating the optimal quantity and combination of nutrients are needed. During the review process, a wide variation in timing, duration, dosing, and route of supplementation, as well as a wide variation in animal models were observed. Better standardization in dietary design, and the development of experimental models that better recapitulate the etiology of human cachexia, will further facilitate successful translation of experimentally-based multinutrient, multimodal interventions into clinical practice.
Highlights
Cancer cachexia is a debilitating syndrome characterized by involuntary weight loss that affects adipose tissue and leads to wasting and weakness of skeletal muscle
Experimental animal models are used extensively to study mechanisms underlying cancer cachexia and evaluate potential treatments. In this narrative review, based on a systematic evaluation of the current literature (Supplementary Table 1), we provide an overview of preclinical studies focused on nutritional interventions in cancer cachexia, and discuss the gaps and highlight opportunities in current experimental models
Diet supplementation with fish oil, which is rich in n3 long chain polyunsaturated fatty acids (lcPUFAs) eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), has been investigated to preserve skeletal muscle mass in various experimental animal models of cancer cachexia
Summary
Cancer cachexia is a debilitating syndrome characterized by involuntary weight loss that affects adipose tissue and leads to wasting and weakness of skeletal muscle. Diet supplementation with fish oil, which is rich in n3 lcPUFAs EPA and DHA, has been investigated to preserve skeletal muscle mass in various experimental animal models of cancer cachexia Most of these studies show that fish oil is an effective nutritional intervention to induce body weight gain, reduce tumor growth rate and reverse food intake. Van Norren et al examined the effect of dietary supplementation with a specific combination of high protein (100% casein), leucine and fish oil (EPA and DHA in a ratio of 2.2:1) on body composition in mice bearing the C26 tumor [138]. The effect of a more humanized diet on weight loss, muscle function and physical activity was studied, referred to as Specific Nutritional Composition, containing high protein (68% casein and 32% whey), leucine, fish oil (EPA and DHA in a ratio of 2.2:1), and the oligosaccharides GOS and FOS.
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