Nutrition plays major (but not always fully understood) roles in many aspects of cancer development and treatment.[1] Malnutrition is a common problem in cancer patients that has been recognized as an important component of adverse outcomes, including increased morbidity and mortality and decreased quality of life. Weight loss has been identified as an indicator of poor prognosis in cancer patients.[2] It has been shown that at the time of diagnosis, 80% of patients with upper gastrointestinal cancer and 60% of patients with lung cancer have already experienced a significant weight loss,[3] generally defined as at least a 10% loss of body weight in 6 months' time.[4] Good nutrition practices can help cancer patients maintain weight and the body's nutrition stores, offering relief from nutrition impact symptoms and improving quality of life.[5] Poor nutrition practices, which can lead to undernutrition, can contribute to the incidence and severity of treatment side effects and increase the risk of infection, thereby reducing chances for survival.[6] Nutrition impact symptoms are those symptoms that impede oral intake. They include, but are not limited to, anorexia, nausea, vomiting, diarrhea, constipation, stomatitis, mucositis, dysphagia, alterations in taste and smell, and pain.[7] Early recognition and detection of risk for malnutrition through nutrition screening followed by comprehensive assessments is increasingly recognized as imperative in the development of standards of quality of care in oncology practices.[2] Undesirable weight gain may be an effect of chemotherapy treatment for early-stage cancers, possibly resulting from decreases in resting metabolism.[8] Consequently, the eating practices of individuals diagnosed with cancer should be assessed throughout the continuum of care to reflect the changing goals of nutritional therapy.

Nutritional status is often jeopardized by the natural progression of neoplastic disease. (Refer to the Tumor-Induced Effects on Nutritional Status ¹ section.) Alterations in nutritional status begin at diagnosis, when psychosocial issues may also adversely affect dietary intake, and proceed through treatment and recovery. Protein-calorie malnutrition (PCM) is the most common secondary diagnosis in individuals diagnosed with cancer, stemming from the inadequate intake of carbohydrate, protein, and fat to meet metabolic requirements and/or the reduced absorption of macronutrients. PCM in cancer results from multiple factors most often associated with anorexia, cachexia, and the early satiety sensation frequently experienced by individuals with cancer. These factors range from altered tastes to a physical inability to ingest or digest food, leading to reduced nutrient intake. Cancer-induced abnormalities in the metabolism of the major nutrients also increase the incidence of PCM. Such abnormalities may include glucose intolerance and insulin resistance, increased lipolysis, and increased whole-body protein turnover. If left untreated, PCM can lead to progressive wasting, weakness, and debilitation as protein synthesis is reduced and lean body mass is lost, possibly leading to death.[9]

Anorexia, the loss of appetite or desire to eat, is typically present in 15% to 25% of all cancer patients at diagnosis and may also occur as a side effect of treatments. Anorexia is an almost universal side effect in individuals with widely metastatic disease [10,11] because of physiologic alterations in metabolism during carcinogenesis. (Refer to the Tumor-induced Effects on Nutritional Status ¹ section.) Anorexia can be exacerbated by chemotherapy and radiation therapy side effects such as taste and smell changes, nausea, and vomiting. Surgical procedures, including esophagectomy and gastrectomy, may produce early satiety, a premature feeling of fullness.[4] Depression, loss of personal interests or hope, and anxious thoughts may be enough to bring about anorexia and result in PCM.[3] Evidence-based recommendations have been published describing various approaches to the problems of cancer-related fatigue, anorexia, depression, and dyspnea.[12] Other systemic or local effects of cancer or its treatment that may affect nutritional status include hypermetabolism, sepsis, malabsorption, and obstructions.[9]

Anorexia can hasten the course of cachexia,[3] a progressive wasting syndrome evidenced by weakness and a marked and progressive loss of body weight, fat, and muscle. Cachexia is estimated to be the immediate cause of death in 20% to 40% of cancer patients; it can develop in individuals who appear to be eating adequate calories and protein but are malabsorbing nutrients because of the disease. Particularly at risk are patients with diseases of the gastrointestinal tract.

The etiology of cancer cachexia is not entirely understood. Cachexia can manifest in individuals with metastatic cancer as well as in individuals with localized disease. Cachexia does not appear to be the result of tumor size, type, or extent. Several theories suggest that cachexia is caused by a complex mix of variables, including tumor-produced factors and metabolic abnormalities.[11] The basal metabolic rate in cachectic individuals is not adaptive, that is, it may be increased, decreased, or normal.[13] Some individuals do respond to nutrition therapy, but most will not see a complete reversal of the syndrome, even with aggressive therapy.[6] Thus, the most prudent and advantageous approach to cachexia is the prevention of its initiation through nutrition monitoring and nutrition intervention.[14]

Reference citations in some PDQ Supportive and Palliative Care information summaries may include links to external Web sites that are operated by individuals or organizations for the purpose of marketing or advocating the use of specific treatments or products. These reference citations are included for informational purposes only. Their inclusion should not be viewed as an endorsement of the content of the Web sites or of any treatment or product by the PDQ Supportive and Palliative Care Editorial Board or the National Cancer Institute (NCI).

References

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