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Cancer, Nutrition, and Eating Behavior: Introduction and Overview
Beth E. Meyerowitz
Thomas G. Burish
Vanderbilt University
Sandra M. Levy
University of Pittsburgh School of Medicine
Cancer causes 20% of all deaths in this country, making the disease the second leading cause of death. The American Cancer Society (1983) estimated that in 1983 855,000 new cases of cancer were identified in the United States. Over half of the people who develop cancer are expected to die within five years from the time of their diagnosis. Moreover, even those people who eventually recover from cancer face major life disruptions as a result of the disease and its treatments. In short, millions of Americans are affected by cancer, its treatment, and its aftermath.
Nutritional status plays a major role in the morbidity and mortality associated with cancer. A leading cause of death in cancer patients is cachexia, a syndrome characterized by malnutrition and progressive physical wasting (Lindsey, Piper, & Stotts, 1982). Not only does malnutrition lead directly to death, but it can also jeopardize indirectly the well-being of patients by causing reductions in the doses of potentially life-saving therapy that patients can tolerate. Malnutrition can also compromise host stamina in other ways; for example, by affecting immunological function, rendering the individual susceptible to infections. In addition, nutrition may play a role in the onset of cancer. A growing number of foods have been identified as contributing to the development of cancer. Thus, cancer can be both a cause and an effect of poor nutrition.
The role of nutrition in the prevention and treatment of cancer has begun only recently to receive empirical and theoretical attention. In 1982 the National Cancer Advisory Board Ad Hoc Subcommittee on Nutrition and Cancer (NCAB, 1982) concluded that insufficent emphasis had been placed on research in diet, nutrition, and cancer. Their report stated that "Research in nutrition and cancer is at an evolutionary stage in its development. It needs to bring new sciences and scientists into the field and persuade them to apply their technologies to cancer research. It has to conceive and implement multidisciplinary research approaches. . . ." (p. 13, emphasis in original).
In this volume we provide such a multidisciplinary approach to one determinant of nutritional status-eating behavior. Individuals' abilities to eat and the foods that they choose to consume contribute to health status both before and after the diagnosis of cancer. Understanding, measuring, and modifying eating behavior have been goals of psychological research for decades. In this book, basic biobehavioral research on the role of learning in determining eating behavior is reviewed and its implications for understanding the relation between nutrition and cancer are explored. Before providing an overview of the volume, we briefly discuss factors that affect the nutritional status of cancer patients and the role of nutrition in cancer etiology.
NUTRITIONAL STATUS OF CANCER PATIENTS
Malnutrition is the most common secondary diagnosis in cancer patients (Harvey, Bothe, & Blackburn, 1979). More than one-half of all cancer patients experience cancer cachexia or physical wasting and the nutritional deficits associated with it (Lindsey, Piper, & Stotts, 1982). Cachexia may be the most prevalent immediate cause of death among cancer patients (Theologides, 1977), and improved nutrition may be associated with decreased mortality rates (Harvey etal., 1979).
Nutritional status among cancer patients is influenced by the tumor itself and by various treatments and their side effects (e.g., Chencharick & Mossman, 1983; Donaldson & Lenon, 1979). In general, cachexia is the result of a negative energy balance in which food intake is not adequate to meet the metabolic needs of the host. This condition can be caused by increased energy utilization, decreased food intake, or both (Theologides, 1979). In the case of many cancer patients, both mechanisms play critical roles.
Cancer-caused increases in energy requirements and changes in carbohydrate, protein, and lipid metabolism are well documented. However, these changes do not account entirely for weight loss. As Bernstein (1982) has pointed out, under most circumstances organisms compensate for increased or inefficient energy expenditure by increasing their food intake. Cancer patients rarely increase food intake and, in fact, are more likely to reduce the amount of food they eat.
Although the specific causes of diminished food intake in tumor-bearing organisms are not completely understood, a number of explanations have been offered. Occasionally, observed dismptions in eating behavior can be attributed to obstructions or other mechanical problems in the head and neck region or in the gastrointestinal tract (Lindsey, Piper, & Stotts, 1982). Most disruption in eating, however, probably results from problems that are more closely tied to psychobiologic mechanisms. Changes in chemoreceptors that lead to alterations in taste and smell, and accumulation of food in the intestinal tract that causes a feeling of fullness have been identified as possible determinants of reduced food intake (DeWys, 1979).
Eating behavior is also affected by the side effects of cancer treatments. For example, radiation to the head and neck area can alter taste acuity, produce mouth sores, and make swallowing difficult; and treatment with chemotherapy can produce a variety of gastrointestinal problems including diarrhea, nausea, and vomiting. In addition, the emotional distress, depression, and fatigue that many patients experience when diagnosed or treated for cancer may also lead to anorexia or loss of desire to eat (Neumann, Jelliffe, Zerfas, & Jelliffe, 1982). Finally, changes in eating patterns can result from learned taste aversions (Bernstein, 1982), a process whereby gastric illness can lead to the avoidance of foods that were ingested prior to the illness. These and other possible determinants of decreased food intake in cancer patients are a major focus of this volume.
Although cancer and its treatment often result in decreased food intake, increased nutritional ingestion may not automatically improve the patient's resistance to the cancer or increase his or her ability to withstand more aggressive anticancer treatments. On the contrary, improved nutrition may feed the tumor more than the host, and thus may increase the proliferation rate of the cancer cells (see Levine, this volume).
NUTRITION AND CANCER ETIOLOGY
Nutritional status is not only influenced by cancer and its treatments, it can also contribute to cancer's development. In a recent report on diet, nutrition, and cancer by the National Research Council (described in Maugh, 1982), it was estimated that approximately one-third of the cancers in this country could be prevented through dietary modification. The rate may be even higher for cancers specific to women such as breast or endometrial cancers (Marks, 1977). Epidemiologic research and laboratory experimentation with animals have led to the identification of a number of foods that appear to be associated with an increased or decreased risk for specific cancers. For example, dietary fat, smoked and saltcured foods, mold contaminated foods (such as nuts and cheese), and burned foods have been linked to cancer (Ames, 1983; Maugh, 1982). Natural mutagens and carcinogens have also been identified in a variety of commonly ingested vegetables and herbs (Ames, 1983). In contrast, other vegetables, specifically those in the Cruciferae family (such as broccoli and cabbage), as well as foods containing β-carotene, selenium, and Vitamins C or E appear to have anticarcinogenic properties (Ames, 1983). Clearly, clinical trials that test directly the causal relationship between these foods and the incidence of cancer in humans are critically important. These studies can also demonstrate the feasibility of enlisting compliance from large numbers of people in changing dietary habits.
ORGANIZATION OF THIS VOLUME
This volume is divided into three sections that explore the role of nutrition and eating behavior in cancer: (1) basic processes in taste aversions and eating behavior; (2) taste aversions and eating behavior in cancer; and (3) interventions for improving the nutritional status of cancer patients and for modifying the diet of populations at high risk for developing cancer.
In the first section, basic biobehavioral research into selective processes underlying eating behavior is reviewed. Robertson and Garcia review the animal research on learned taste aversions. They explain why, for example, animals that ingest certain foods or beverages and then receive X-ray radiation will subsequently develop an aversion to those foods or beverages. The authors then discuss how this basic learning process may occur in cancer patients who receive radiation or chemotherapy. Their chapter highlights the role that learning can play in altering the eating behavior of organisms who are exposed to aversive radiation or chemical substances, and thus how psychological or behavioral factors can interact with biological processes to disrupt eating patterns. In the next chapter, Grunberg argues that learned taste aversions provide only a partial explanation for the altered eating behavior patterns shown by cancer patients. He suggests that many eating problems result from altered taste preferences. Specifically, he presents data from research with both animals and humans which demonstrate that nicotine can alter taste preferences in noncancer-bearing organisms. The author then discusses how cancer may also produce changes in taste preferences and how these changes may lead to decreased caloric intake and weight loss. Grunberg concludes by suggesting methods for overcoming the negative effects of altered taste preferences and for reversing the weight loss that such alterations may cause.
While the first section focuses primarily on basic biobehavioral processes underlying eating disorders in cancer-free animal and human populations, the focus of the second section is on nutritional and eating problems specifically associated with cancer. Research is reviewed that applies the basic mechanisms described in the first section to cancer patients. Bernstein and Treneer, for example, demonstrate that tumor growth per se can result in learned aversions to food. The authors speculate about the physiological basis for this phenomenon, suggesting that certain amino acid deficiencies caused by some tumors can lead to the development of learned food aversions and can result in substantial weight loss. On the basis of their hypotheses, the authors suggest straightforward dietary supplementation procedures that they believe can be effective in preventing and alleviating weight loss among cancer patients. In the next chapter, Smith, Blumsack, and Bilek discuss the role of radiation therapy in the development of taste aversions. They describe a series of studies in which the traditional research paradigm for studying radiation as a cause of learned taste aversions in rats was modified to approximate the experience of cancer radiotherapy patients. These studies demonstrate that under radiotherapy-like conditions, rats learn long-lasting aversions to both unfamiliar and familiar tastes. When conditioned aversions are studied in patients receiving radiation therapy, conditioning also appears to have some effect on eating behavior. The authors discuss possible mechanisms underlying changes in eating behavior and offer recommendations for the prevention of learned taste aversions in radiotherapy patients. In the next chapter, Bernstein and Webster demonstrate that anorexia and altered food preferences can be learned effects of gastrointestinally toxic cancer chemotherapy. They present clinical data from adult and child chemotherapy patients and laboratory data from animals that document the occurrence of learned taste aversions to unfamiliar and familiar foods. Research that explores possible intervention strategies for preventing the development of aversions is also described. In the final chapter of this section, Redd, Burish, and Andrykowski explain how conditioning can cause some chemotherapy patients to experience nausea and vomiting even before their chemotherapy medication is administered, and other patients to display postchemotherapy nausea and vomiting that are more severe than their disease state and treatment protocol would typically induce. These conditioned side effects are experienced by over 25% of cancer chemotherapy patients and can severely compromise the eating behavior and nutritional status of these patients. Included in the chapter is a review of the literature on prevalence rates, underlying mechanisms, and individual differences in the development of conditioned nausea and vomiting.
The third section of the volume focuses on intervention strategies for optimizing the nutritional status of people with cancer or for altering dietary intake of individuals at high risk for developing the disease. DeWys begins the section with an overview of cachexia in cancer patients. He points out that 30% to 90% of cancer patients, depending on tumor type, experience weight loss. Moreover, weight loss is a major prognostic factor, associated with shorter survival and inadequate response to treatment. Clearly, the high incidence and serious consequences of weight loss make effective preventive strategies critically important. DeWys' description of the extent and nature of the problem and of its pathophysiology provide a useful context for understanding intervention strategies. In the next chapter, Bright-See and Levy discuss methodological issues that require consideration when measuring eating behavior and designing interventions to change such behavior. They describe strategies that are appropriate with healthy individuals and with patients with early stage cancers, including strategies for large scale dietary intervention trials with high risk populations. They also discuss techniques for measuring the intake of various foods and food components that are thought to be either carcinogenic or anticarcinogenic. The chapter ends with a brief discussion of issues that are relevant to teaching clinical and research skills in the area of nutrition and cancer.
Following the introduction and perspective provided by DeWys and by BrightSee and Levy, there are three chapters which present specific intervention strategies for influencing nutritional status in relation to cancer. First, Boyd, Cousins, Bayliss, Fish, Fishnell, and Bruce describe an ongoing dietary modification program for cancer prevention. They outline procedures by which they were able to design and implement a program that was successful in markedly reducing the level of dietary fat consumed by women at high risk for breast cancer. Epidemiologic and animal research suggest that this reduction will minimize risk for breast cancer, an hypothesis that Boyd and his colleagues will test. In the next chapter Levine describes a strategy for circumventing the need to change eating behavior in chemotherapy patients. He reviews the literature and presents two studies that test the effects of total parenteral nutrition (TPN), a treatment that provides necessary nutrients to patients intravenously. These studies suggest that although TPN leads to weight gain, it does not appear to ...