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An appreciation of nutritional support as a critical component of the continuum of cancer care has only recently emerged, bolstered by recent studies showing that support is critical not only to the maintenance of lean body mass (LBM), weight, and performance status and their impact on quality of life (QoL), but also to tolerance and completion of treatment itself.1
Only a generation ago, nutritional interventions were largely neglected and were begun late, if ever, due to theoretical concerns that nutritional support would ‘feed the tumor.’ This regrettably left a starved host as the unspoken alternative. Not until 1980 was the detrimental impact of malnutrition first quantified through an evaluation of 12 Eastern Co-operative Oncology Group trials that documented the poor prognosis associated with an unplanned weight loss of as little as 5%.2
However, widespread efforts to improve nutritional support for patients were not immediately implemented since many felt weight loss was merely an unavoidable consequence of aggressive disease. Almost two decades later, Andreyev offered an alternative explanation, exposing the fact that those with weight loss actually received less treatment.3 These patients developed more toxicity, resulting in dose reduction and abbreviated treatment courses. They had significantly lower QoL and performance status, poor response to treatment, and reduced overall survival. Yet, for those whose weight could be stabilized, survival was significantly improved—an observation confirmed by more recent studies.4,5 Other research has shown that, while nutritional deterioration was related to disease status, reduced energy and protein intakes and weight loss were also independently associated with impaired QoL. An emerging area of research, QoL has always been a prime concern of cancer patients themselves.1,6,7
This article will focus on the role of the registered dietician (RD) on the oncology team, identifying and implementing therapeutic nutritional interventions that both effectively stabilize weight and maintain and rebuild LBM. Planning effective strategies entails triaging patients to determine the source of their weight loss, allowing the team to target the specific underlying factors. Ultimately, there must be differentiation between patients experiencing symptom-related weight loss and those with metabolic abnormalities that define cachexia.
Calories, Protein, and Lean Body Mass
Adequate calories to provide the energy needed for normal function is the body’s top priority, and protein will be burned as energy when calories are grossly inadequate—a common consequence of cancer and treatment-related symptoms such as anorexia, taste changes, and early satiety. These symptoms are present in up to 80% of patients with gastrointestinal (GI) tumors and 60% of lung cancer patients, but much less frequently with breast or hematological malignancies.8 Muscle/LBM is directly affected by protein intake in the diet, replenishing the amino acids lost during the fasting state between meals. Optimal intake that supports muscle function is estimated at 1.8g protein/kg/day; this is met by the average American diet, but protein is one of the most common deficits when intake is limited.9 Exercise also improves function, with the most benefit from early interventions to limit loss of LBM. The stressed state seen in advanced cancer results in far greater demand for amino acids released from muscle breakdown than occurs in fasting alone.10 When dietary protein is not spared or is inadequate in the diet, muscle catabolism provides the amino acids to maintain the protein mass of critical organs and tissues. It is also used to maintain normal plasma glucose concentration, which ensures energy is available to essential organs. In addition, muscle reserves support the production of other critically essential proteins—i.e. albumin—though typically at suboptimal levels for conservation of LBM. The consequences of protein deficits are quickly exhibited as fatigue, delayed healing, poor immune response, and declining ability to maintain normal activities due to loss of LBM. When 40% of these critical protein reserves are exhausted, mortality approaches 100%, typically due to pneumonia/infection.