Nutrition Support and Cancer

Cancer does not discriminate on the basis of stage of life, gender, or ethnicity. Recent data suggest about 50% of cancer patients are at risk of malnutrition (Biggs, 2012; Brinkama et al., 2012). Malnutrition is one of many factors that can delay recovery from cancer therapy and can contribute to complications(Zimmermann et al., 2012), and it is more complicated in pediatric populations (Bauer et al., 2011). Children are more susceptible to growth impairment and are at risk for numerous adult-onset negative consequences (Gurney et al., 2006; Meacham et al., 2009). Weight loss, BMI, biomarkers of immune compromise, and indicators of protein-energy malnutrition strongly suggest nearly all those with advanced cancer present subclinical malnutrition status (Prevost and Grach, 2012).

Nutrition support can improve quality of life while improving nutritional status and effectiveness of therapeutic interventions. For example, omega-3 fatty acids, vitamin D, some spices, and perhaps some strains of probiotics may improve outcomes during chemotherapy and may modulate the risk of developing some forms of cancer (Laviano et al., 2013; Meyer et al., 2013; Sung et al., 2012; Kumar et al., 2013). However, doses, intake frequency, pharmacokinetics, and other variables associated with these dietary interventions remain poorly defined.

As investigators delve deeper into the nutrient and cell function relationships in an attempt to understand the factors that affect initiation, promotion, and progression of abnormally proliferating cells and the dysfunction of normal apoptosis, it appears that numerous signaling pathways that affect these processes impact nutrient uptake and utilization and cellular energetics (Vander Heiden, 2011; Levine & Puzio-Kuter, 2010). Altered cellular energetics, particularly during cancer cell proliferation, indicate that these cells rely on aerobic glycolysis for energy and a high demand for glucose, instead of classical mitochondrial phosphorylation for normal cells (Lunt & Vander Heiden, 2011). This observation, in turn, may offer metabolic targets for nutrition support and therapeutic intervention.

The complexities within the metabolism and cancer intersection are noted in 2005 collaborative research announcements by the National Cancer Institute. Primary TREC (Transdisciplinary Research on Energetics and Cancer) efforts focus on understanding the dynamics of cancer associated with obesity, low levels of physical activity, and poor diet. With respect to cancer risk and adiposity, factors affecting cellular energetics, such as insulin resistance and inflammation, and appropriate biomarkers (e.g., inflammatory cytokines, indicators of gene expression and gene polymorphisms, endogenous sex hormones) are further targets of breast cancer research.

Many animal studies suggest proinflammatory cytokines cross the blood brain barrier and suppress appetite. There are many ensuing issues associated with cancer-related anorexia (loss of desire to eat) and tumor-associated cachexia (progressive wasting) (Fearon et at., 2012; Tisdale, 2009). Notably, the continuous loss of skeletal muscle mass presented by cancer patients is not necessarily reversed even by aggressive nutrition support. Most approaches include providing adequate calories to reduce the risk of weight loss, yet this avenue may not be sufficient (Miller & Bozeman, 2012). A recent analysis of nutrition support indicates inconsistency in dietary interventions to improve outcomes, including treatment tolerance in patients with cancer cachexia (Bauer et al., 2006; Tisdale, 2009; Paccagnella et al., 2011).

As with any cancer patient, malnutrition is not acceptable, and nutrition intervention is critical. Yet considerable evidence suggests nutritional strategies among pediatric populations with cancer may not be effective (Bauer et al., 2011). Animal models suggest nutrition support in cachectic children may increase tumor burden and accelerate proliferation of cancer cells, yet these dysfunctions have not been detected in the pediatric population (Nitenberg and Raynard, 2000). Even medications that stimulate appetite and promote weight gain may result in unintended negative consequences in tumor cells and skeletal muscle (Evans, 2010; Gullett et al., 2010). When it comes to frontiers in nutrition support and cancer, our understanding of altered metabolism and cellular energetics represent the next steps to improved patient survival and quality of life (Patterson et al., 2012).

References cited in this article are available from the authors.

Peter Pressman, M.D.,
Contributing Editor
Medicine & Public Health Advisor, Daedalus Humanitarian Inc.
[email protected]

Heather Rodriguez,
R.D., Contributing Editor 
Clinical Dietitian, Peterson Regional Medical Center, Kerrville, Texas
[email protected]