Assessment, Gastroenterology, Breast, Esophageal Head and Neck, Gynecologic, Lung, Prostate, and Palliative Care
The prevalence of malnutrition in people with cancer has been estimated to be up to 85%, particularly in cancers that affect the gastrointestinal (GI) tract. According to the National Cancer Institute (NCI), 20%–40% of people with cancer die from malnutrition, cachexia, or complications attributed to these conditions. Therefore, any unintended weight loss should be evaluated during cancer treatment. It has been reported that as little as a 5% weight loss can reduce tolerance to chemotherapy, increase side effects, and decrease quality of life. Weight loss can also interfere with patients’ ability to complete or stay on track with their prescribed cancer therapy.
Cancer and cancer treatments can impact patients’ ability to ingest, digest, absorb, and metabolize nutrients, making the management of nutritional status challenging in this population. For this reason, most evidence-based guidelines for oncology nutrition recommend that all patients being treated for cancer be screened for malnutrition and rescreened throughout treatment. Some of the main goals of nutrition therapy for those at risk are as follows:
• Prevent or treat nutrition deficiencies and problems, including preventing muscle and bone loss
• Decrease or manage symptoms that impact nutrition
• Maintain the immune system to help fight infection
• Aid recovery and healing from surgery, chemotherapy, and/or radiation therapy
• Maintain or improve the patient’s strength, energy, and quality of life
Also, for patients who are well nourished, good nutrition and physical activity behaviors are important during and after treatment. All patients, especially those with excess body weight, should be counseled on eating and activity behaviors to help them achieve and maintain a healthier body weight, since obesity has been associated with poorer outcomes during treatment, as well as an increase in risk of recurrence in some cancers.
This chapter will outline approaches to nutrition screening, assessment, interventions, and monitoring in the oncology population. The chapter begins with a review of screening tools that have been validated for use in this population. After that, a review of many of the most common cancers will include a brief overview of the cancer, risk factors, and common treatments, including some nutrition interventions. Finally, the appendices in this chapter can serve as a reference to help the provider anticipate side effects of common treatments as well as offer suggestions for nutritional management of those symptoms.
NUTRITION SCREENING AND ASSESSMENT
Nutrition screening in the oncology population is used for the early identification of patients who are malnourished or at nutritional risk. A nutrition screen can be completed by any qualified health care professional, including those other than the registered dietitian (RD). The screening process enables a timely referral for nutrition assessment and intervention. Owing to the duration of cancer treatments, adjustments in regimens and modalities, and changes in an individual’s tolerance to treatment over time, it is imperative that patients are screened at initial presentation and regularly rescreened at each clinic visit thereafter. There should be a process in place whereby a positive screening alerts the RD for referral. Once a patient is referred, nutrition interventions and education require continuous modification to meet the patients’ dynamic needs.
A screening tool provides a valid, standardized, and efficient method to identify nutrition impact symptoms and clinical signs of malnutrition (see Chapter 1). Based on The Academy of Nutrition and Dietetics Evidence Analysis Library (EAL), there are four nutrition screening tools that have proven to be valid and reliable in the inpatient setting, two of which are appropriate in the outpatient setting (Table 6.1).
The purpose of the oncology nutrition assessment is to perform a comprehensive evaluation of the patient’s nutritional status, nutrition impact symptoms, and nutritional requirements. Furthermore, the assessment is utilized by the RD to form individualized interventions, monitoring, and continued evaluation as appropriate. As stated by the EAL Oncology Work Group, “An adult oncology nutrition assessment should characterize and document the presence of (or expected potential for) altered nutrition status and nutrition impact symptoms that may result in a measurable adverse effect on body composition, function, quality of life (QOL) or clinical outcome, and may include indicators of malnutrition.”2
The SGA and PG–SGA nutrition assessment tools have been validated by the EAL for use among adult oncology patients in acute care and ambulatory settings.3 Both tools include assessment of intake, weight, GI symptoms, and functional status. However, the SGA incorporates a physical examination, while the PG–SGA covers a more comprehensive review of nutrition impact symptoms.
Malnutrition is extremely prevalent in the oncology population, with incidence rates estimated to be between 40% and 80%.4,5 Malnutrition is defined as “a state of nutrition in which a deficiency, excess or imbalance of energy, protein, and other nutrients causes adverse effects on body form, function and clinical outcome.”6 Complications of malnutrition include increased therapy-related toxicity, poor performance status, lower quality of life, reduced survival, increased number of hospitalizations and length of stay, and increased health care costs.7–10
Patient generated–subjective global assessment (PG–SGA)
Weight, nutrition impact symptoms, intake, and functional status
Malnutrition screening tool (MST)
Weight and appetite
Malnutrition screening tool for cancer patients (MSTC)
Intake, weight, ECOG, and BMI
Malnutrition universal screening tool (MUST)
BMI, weight, acute illness, and intake
Percentage of lean body weight
Source: Onc: Nutrition screening tools. 2012. Academy of Nutrition and Dietetics Evidence Analysis Library. http://www.andeal.org/topic.cfm?cat=5452&conclusion_statement_id=251796&highlight=oncology%20assessment&home=1. Updated 2012. Accessed March 2015.
The oncology nutrition assessment is a multifactorial approach that should be completed at every clinic visit for patients who are at risk for malnutrition or are already malnourished. Evaluation of nutrition impact symptoms that the patient is already experiencing, or is at risk for developing, is critical in helping to maintain or improve their nutritional status. Nutrition impact symptoms are defined as side effects from treatment or the cancer itself that impair intake, digestion, or absorption. Examples commonly seen in the oncology setting include nausea, vomiting, diarrhea, constipation, dysphagia, odynophagia, anorexia, mucositis, early satiety, and alterations in taste and smell.
The careful monitoring of weight status and implementation of nutritional interventions to support a healthy body weight is a key component of the nutrition assessment. Cancer-induced weight loss and more recently, lean body mass, have both been used as primary outcomes in clinical trials. Patients with significant weight loss and/or sarcopenia have been associated with greater treatment toxicity and shorter survival. Significant weight loss is defined as 1%–2% in one week, 5% in 1 month, 7.5% in 3 months, and 10% in 6 months. Computerized tomography (CT) images, bioelectrical impedance analysis (BIA), dual-energy x-ray absorptiometry (DXA), and anthropometry are used to assess changes in lean body mass.
In addition to using a validated assessment tool, the oncology nutrition assessment should encompass each component of the nutrition care process, including an in-depth diet history, medication list review, anthropometric measurements, biochemical data, nutrition-focused physical exam, and psychosocial factors.
The GI tract refers to the route from the mouth to the anus that is responsible for digestion, absorption, and elimination. The GI tract is also host to a plethora of microorganisms that are responsible for 70% of the body’s immune function, making it the largest immune tissue in the body. The GI tract is a very complex and dynamic system that is impacted by what we eat and by exposure to toxins. Chronic inflammation is linked to breakdown in this complex immune system, which triggers the formation of cancerous growth. GI cancers include organs in the upper and lower GI tract, namely, the esophagus, stomach, pancreas, liver, gallbladder, colon/rectum, and anus. GI cancers can cause alterations in anatomy and function that can affect nutritional status, quality of life, and treatment outcomes. Aberrations commonly experienced with GI cancers that make nutritional management challenging will be covered. Cancers of the head and neck and esophagus are discussed in their own section.
Cancers of the GI tract are collectively the most lethal cancers worldwide. Lifetime risk of developing a cancer in the GI tract ranges from 0.2% to 5%, depending on location and tumor type, with anal cancer being the least common and colorectal being the most common. Survival rates depend on stage at diagnosis and tumor type, with advanced stages having much less favorable prognosis.11
Common risk factors for GI cancers include tobacco use; alcohol consumption; history of infection, such as Helicobacter pylori, chronic hepatitis, Epstein–Barr virus, and human papilloma virus; and genetics and chronic inflammation.11 Diet plays a key role in the development of several GI cancers. For example, high saturated fat and low fiber intake has been linked to colorectal cancers, and intake of smoked, salted, cured, and pickled foods are known risk factors for stomach cancer.11,12 Furthermore, it is estimated that 15%–50% of GI cancers are preventable by diet, activity, and weight management.13
Energy (kcal/kg/day Actual Weight)
Protein (g/kg/day Actual Weight)
Stomach, pancreas, gallbladder, colon, rectum, anus
30–35: repletion, weight gain
25–30: inactive, nonstressed
1.5–2.5: cancer cachexia
1.0–1.5: inflammatory bowel disease
1.5–2.0: short bowel syndrome
25–40: based on dry weight
1.0–1.5: all except those with encephalopathy
35–40: stable cirrhosis
25–35: without encephalopathy
0.6–0.8: acute encephalopathy
35: acute encephalopathy
30–40: stable, malnourished
Source: Adapted from Huhmann M. Oncology Nutrition for Clinical Practice. 3rd ed. Chicago, IL: Oncology Nutrition Dietetic Practice Group of the Academy of Nutrition and Dietetics; 2013:14.
Recognizing symptoms that are considered “red flags” for GI cancers is important for early detection. These include
• Unexplained weight loss
• Abdominal pain that lasts longer than 4 weeks
• Unexplained loss of appetite
• Change in bowel habits
• Nausea and vomiting lasting for more than a week
• Symptoms related to anemia (fatigue, shortness of breath, and weakness)
• New onset back pain
Early detection of GI cancers is difficult due to latent signs and symptoms and lack of routine screening tests. It is very important to recognize these warning signs so that timely referral to a gastroenterologist can be made.
Nutrition assessment should include a determination of energy and protein needs. Although predictive equations have been proposed for the outpatient and home care population, specific recommendations related to the type of cancer may lead to more accurate provision of nutrients (see Table 6.2).
The presence of cancer in the GI tract predisposes one to malnutrition. Patients who are malnourished preoperatively are significantly more likely to have longer length of hospital stay and postoperative morbidity and mortality.14–17 Nutrition screening is essential for identifying patients at increased risk for perioperative morbidity, and early intervention is critical to improving outcomes.
Optimization of nutritional status preoperatively is imperative. In patients who are at severe nutritional risk, nutrition support should be implemented for 10–14 days preoperatively, and surgery should be postponed until this is achieved. Severe nutritional risk is defined as one of the following:18
• Weight loss of 10%–15% within 6 months
• Body mass index (BMI) <18.5 kg/m2
• Subjective Global Assessment Grade C
• Serum albumin <3.0 g/dL (with no evidence of hepatic or renal dysfunction)
In oncology patients unable to consume above 60% of estimated intake for more than 10 days or in whom inadequate intake is anticipated for more than 7 days perioperatively, regardless of nutritional status, it is recommended that nutrition support via the enteral route (oral or tube feeding) be implemented without delay.18 Preoperative parenteral nutrition (PN) for 7–15 days has been shown to reduce postoperative morbidity and should be considered in severely malnourished patients in whom oral or enteral nutrition (EN) is contraindicated or insufficient.17–19
Postoperatively, the traditional practice of holding oral or enteral feeds until return of bowel sounds is without evidence yet pervasive as a standard of care.20 Early feeding should be initiated to promote bowel hypertrophy and anastomotic healing.21 Feeding proximal to an anastomosis may prevent disruption or leak.22 If feeding is started within 24 hours, dysmotility can be attenuated, even in the absence of peristalsis.23 In patients undergoing gastrectomy, rectal pelvic surgery, pancreaticoduodenectomy, and colon resection, a normal diet should be offered on postoperative day one without restrictions, and patients should be advised caution in increasing intake according to tolerance. Early feeding reduces the risk of infection and length of hospital stay.24–27
Immunonutrition or pharmaconutrition refers to immune-modulating formulas containing sup-raphysiological doses of arginine, with or without glutamine, omega-3 fatty acids, and nucleotides, which are recommended for their effect on reducing postoperative infectious complications and hospital length of stay.28 Results from a systematic review and meta-analysis of randomized controlled trials evaluating the effect of pharmaconutrition on postoperative clinical outcomes compared with standard nutritional provision highlight the importance of timing in the provision of immunonutrition.28 Preoperative provision, as defined by 5–7 days prior to surgery, shows no advantage on outcomes over standard nutrition. However, perioperative and postoperative administration are associated with significantly reduced infectious complications and length of stay. Additionally, perioperative administration was associated with significant reduction in anastomic dehiscence and postoperative administration was associated with reduction in noninfectious complications. Perioperative nutrition was defined as 5–7 days before surgery plus postoperative day (POD) commencement via jejunal tube on POD 1–2 until POD7 or until oral intake was established. Postoperative nutrition was defined as pharmaconutrition commencement via jejunal tube on POD 1–2 until POD7 or until oral intake was established.28
Altered GI function is a common etiology for malnutrition diagnosis in the oncology population.
Partial or total gastrectomy and pancreaticoduodenectomy may disrupt gastric motility, resulting in delayed emptying or rapid transit of stomach contents into the small intestine, known as dumping syndrome. Removal or manipulation of the pyloric valve during surgery predisposes one to dumping syndrome. Early symptoms manifest as cramping, bloating, nausea, and diarrhea within 10–15 minutes of eating due to the influx of fluid into the small intestine in response to a concentrated sugar load. Hypotension, weakness, and faintness may follow. Late symptoms of dumping syndrome occur 2–3 hours after eating when the sugar from the intestines is absorbed and the body’s response to hyperglycemia is accelerated. Elevated insulin levels cause hypoglycemia. Symptoms include high heart rate, dizziness, shakiness, sweating, fainting, and confusion.29
To prevent or manage the occurrence of postoperative dumping syndrome, follow these guidelines for 6–8 weeks:
• Eat slowly and chew foods thoroughly to liquefy the bolus since the digestive capability of the stomach is decreased or naught.
• Eat 6–8 small meals per day.
• Consume fluids 45 minutes before eating or 1 hour after eating, not with meals.
• Avoid raw fruits and vegetables and other fibrous foods, including whole grains, nuts, seeds, peas, and beans.
• Limit fruit to 1/2 cup cooked or canned at a time.
• Limit or avoid milk or milk products if unable to tolerate.
• Consume protein foods with each meal and snack.
• Avoid high-sugar foods such as fruit juice, sugar-sweetened beverages, honey, jam, jelly, molasses, ice cream, pudding, pastries, pies, cake, fruit ice, sherbet, and gelatin.
• Avoid foods that contain sugar, honey, corn syrup, fructose, lactose, dextrose, maltose, sorbitol, xylitol, or mannitol in the first three ingredients.
Delayed Gastric Emptying
The presence of gastric and pancreatic tumors, duodenal ulcers, subtotal gastrectomy, Whipple procedure, and narcotic use are common etiologies for gastroparesis in the oncology setting. Symptoms include protracted nausea and vomiting, decreased appetite, bloating, fullness, early satiety, and alteration in glucose control. Oral diet manipulation includes small frequent meals, use of liquid calories, and avoidance of high-fiber and high-fat foods. Prokinetic and antiemetic agents should accompany diet modification. In cases of severe gastroparesis or when symptom management is unsuccessful, jejunal feeding should be considered to prevent malnutrition. When delayed emptying occurs as a result of gastrectomy, supplementation with vitamin B12, vitamin D, calcium, and a multivitamin with minerals should be considered.29
Removing segments of the small intestine can alter digestion and absorption. Symptoms may include nausea, abdominal cramping, and diarrhea. Functional adaptation can occur; however, significant loss of small bowel may require PN support to maintain fluid and electrolyte balance. Diet guidelines for the first 4–6 weeks after small bowel surgery include the following:
• Eat small, frequent meals.
• Chew foods thoroughly.
• Consume protein with each meal or snack.
• Avoid high-fiber foods; limit total fiber to <20 g per day.
After 4–6 weeks, add new foods back to the diet one at a time and assess for tolerance prior to continuing transition to regular diet.30 If short bowel syndrome (SBS) is severe, more extensive nutrition support may be required.
Diversion of fecal transit may be required temporarily or permanently for management of bowel obstruction or removal of GI malignancy. A colostomy is performed when it is necessary to bypass or remove the distal colon, rectum, or anus. Removal of the colon typically requires minimal diet modification (except for ascending colostomy, covered below). Sufficient fiber and fluid can prevent constipation. In cases of loose stool, thickening foods may be beneficial. Similarly, reducing gaseous and odorous foods may be advised.31
Removal or bypass of the entire colon and rectum requires an ileostomy. High fluid output can cause dehydration and electrolyte imbalance for patients with ileostomies and ascending colostomies. Also, risk of stoma blockage exists because the ileal lumen is <1 inch in diameter. Large amounts of insoluble fibers should be avoided. Follow the below guidelines for nutritional management status post ileostomy placement31,32:
• Eat small frequent meals.
• Chew foods well to prevent foods from causing a blockage or obstruction as stool exits the ileostomy.
• Stay hydrated. Do not attempt to control diarrhea by restricting fluids. Monitor ostomy output and consume 1 L fluid in addition to output volume.
• Avoid fiber. Avoid stringy vegetables, foods with skins, and dried fruits. Limit foods to those with 2 g or less of fiber per serving.
• Choose low-fat foods. Avoid meats with casings.
• Avoid simple sugars (sweetened beverages and sugary foods).
After 6–8 weeks, add new foods back to the diet one at a time and assess for tolerance prior to continuing transition to regular diet.
Fat maldigestion can occur following GI surgeries and in the presence of GI malignancies. Following gastrectomy, accelerated transit of food into the small intestine can prevent adequate mixing of food contents with bile salts and digestive enzymes. Additionally, large food particles entering the small intestine may impair adequate degradation by enzymes. Alternatively, pancreatic exocrine insufficiency (PEI) may accompany a diagnosis of pancreatic cancer or bile duct blockage, or may occur during nonsurgical treatment and/or following whipple surgery. PEI can be ruled in by measuring pancreatic elastase. In cases of PEI, pancreatic enzyme replacement and fat-soluble vitamin supplementation may be warranted.29
Short Bowel Syndrome
Surgical resection of the small bowel leaving <200 cm is termed short bowel syndrome. Initially, PN and or EN will be necessary to achieve adequate nutritional provision, but over approximately 2 years, the remaining gut adapts, whereby the surface area and absorptive capacity of the small bowel increases. Loss of the terminal ileum and the ileal break mechanism results in gastric hyper-secretion and accelerated transit. Without the terminal ileum, the site for bile salt reabsorption, bile salts enter the colon and cause choleric diarrhea. Cholestyramine can be helpful if <100 cm of distal ileum is resected, and the colon is intact, but should be avoided if 100 cm of terminal ileum is resected. Antimotility agents such as loperamide, diphenoxylate, and opiates can be used to slow transit and should be administered 30 minutes before meals.29
Patients with SBS are at risk for deficiency of fat-soluble vitamins, vitamin B12, and magnesium. Supplementation with a liquid or chewable vitamin/mineral supplement should be considered. Bowel adaptation occurs with macronutrient exposure. Whole food and/or use of a polymeric formula maximizes intestinal stimulation. Semielemental EN formulas can be considered if needed, but elemental formulas should be avoided because they are hypertonic. PN may be required to maintain electrolyte and fluid balance. Oral diet guidelines for patients with SBS include the following29:
• Macronutrient composition of 20%–30% carbohydrate, 20%–30% protein, and 50%–60% fat for patients with jejunostomies/ileostomies.
• Macronutrient composition of 50%–60% carbohydrate, 20%–30% protein, and 20%–30% fat for patients with intact colon.
• Avoid concentrated sweets/fluids.
• Chew foods well.
• Limit fluids with meals and drink isotonic beverages.
Mechanical obstruction of the small bowel can occur from adhesions from previous abdominal GI surgeries or from the presence of gastrointestinal tumors. Colonic pseudo-obstruction can develop from narcotic use and lead to significant constipation. Symptoms of obstruction include nausea, vomiting, abdominal pain, abdominal distention, and inability to pass flatus or stool.33 Nutritional management for partial small bowel obstruction includes liquid oral nutrition drink supplements and foods that are moist and soft. For partial colonic obstruction, a very low-fiber diet and stool softeners are recommended. Complete bowel obstruction warrants nil per Os (NPO) to limit bowel distension. In the presence of weight loss and/or malnutrition, or anticipation of prolonged NPO, PN should be initiated. In some patients with chronic obstruction, PN is required long term. For patients in whom surgical intervention is appropriate, refer to “Surgical Management” section above.
Small Intestinal Bacterial Overgrowth
Small intestinal bacterial overgrowth (SIBO) is a condition in which mostly anaerobic bacteria colonize the small intestine in larger than normal quantities, causing symptoms of gas, bloating, abdominal distention, diarrhea, and weight loss. SIBO should be suspected in GI cancer patients with gastroparesis, impaired peristalsis, removal of the ileocecal valve, PEI, stricture/obstruction/adhesion of the GI tract, gastrocolic fistula, surgical bind loops, intestinal pseudo-obstruction, and/or hypochlorhydria/achlorhydria.29,34 SIBO is diagnosed by an ileal aspirate and culture; however, the practice of empirically treating patients for SIBO without diagnostic confirmation is not uncommon.29 Treatment includes antibiotic therapy and dietary manipulation. Since carbohydrates are fermented by bacteria and fermentation in the small bowel can contribute to symptoms, the diet should be modified to reduced carbohydrate and fiber. Fat should be substituted for carbohydrates to supply adequate calories and reduce the production of gas and bloating.34 Nutrients of concern requiring monitoring include calcium, magnesium, iron, vitamin B12, and fat-soluble vitamins.
A fistula is an abnormal passageway or connection between two organs or structures. Enteric fistulas are connections of the small intestine/bowel with other abdominal organs or with the chest or skin. They are named by the originating segment of bowel (gastro-, duodeno-, entero-, jejuno-, ileo-, colo-, recto-) and the point of termination (-cutaneous, -enteric, -colonic, -rectal, -vesical, -vaginal, -aortic). Etiologies include distal obstruction, radiation, and infection and can occur from the presence of tumors and from injury during surgery.35 Malnutrition preoperatively increases the risk of fistula development. Fistulas requiring nutritional management include those that have a high output of fluid and nutrients (a high-output fistula drains more than 500 mL/day) or increased output stimulated by PO intake that prevents the fistula from closing. In either case, NPO may be indicated and PN will be necessary. Patients with high-output fistulas who are not on PN may require extra vitamin/mineral supplementation.29 When output is <500 mL/day, enteral feeding may be possible; feeding proximal to the fistula enhances absorptive area. Fiber-free formulas or diets should be used when the fistula is distal and fiber containing products or diets can be used when the fistula is proximal to the site of feeding entry.29
GI cancers pose nutritional challenges that require a knowledgeable dietitian and team of providers. The functions of digestion and absorption may be altered or severely compromised; in many cases, multimodal treatment requires medical therapy and dietary modification or nutrition support to prevent or reverse malnutrition. Nutrition support or supplemental nutrition individualized by a dietitian is necessary for optimal management of GI cancer patients.
Breast cancer remains the most commonly diagnosed cancer in women, and the second leading cause of cancer death in women in the United States. Between 2007 and 2011, breast cancer occurrence rates remained stable for Caucasian women, and increased by 0.3% per year in African American women.36 Death rates from breast cancer decreased by 34% from 1990 to 2010 related to advances in early diagnosis and treatment.37 For all women, 5 year survival is 99% for women with local disease (stages 0 and I, some stage II), 84% for regional disease (stage II and some stage III), and 24% for advanced disease (stage IIIc and stage IV).38
Subtypes of breast cancer are determined by the presence of biological markers or receptors present on tumor cells. Pathologists classify a breast tumor as estrogen receptor (ER) positive or negative, progesterone receptor (PR) positive or negative, as well as human epidermal growth factor 2 (HER2neu) positive or negative through the examination of tissue biopsied or excised.
Tumors identified as ER positive and/or PR positive are generally less aggressive and also less responsive to chemotherapy. Typically, these tumors respond to hormonal therapies. HER2 positive tumors are often more aggressive than HER2 negative tumors. Women diagnosed with triple negative tumors (no ER, PR, or HER2 receptors on the tumor cell) unfortunately have a poorer short-term prognosis, in part related to the lack of specific therapies toward this tumor type.39 Triple negative cancers are in general more responsive to chemotherapy.
Lifestyle Risk Factors
Lifestyle factors that increase the risk of breast cancer include weight gain after age 18, being overweight or obese (related to postmenopausal breast cancer) and alcohol. Physical activity has been shown to reduce risk.40
Obesity has also been strongly correlated with the risk of postmenopausal breast cancer.41 In addition, overweight and obesity status at diagnosis increases the risk of recurrence and adversely impacts breast cancer and all-cause mortality. Data have shown this obesity effect regardless of stage, treatment, and menopausal status.42 Further, weight gain through breast cancer treatment is correlated with poor prognosis.
Unfortunately, a breast cancer event increases a woman’s risk of weight gain. Recent studies have shown an average weight gain of 5–14 pounds.43 In the HEAL study of breast cancer survivors, 68% of women gained weight, and 74% gained body fat and maintained that gain at 3 years from diagnosis.44
Weight gain after diagnosis is most related to chemotherapy, compared to radiation and hormonal therapy. Menopausal status and decreased activity levels appear to be the most impactful variables contributing to weight change after breast cancer.45
Research has suggested that it may be beneficial for women to focus on healthy weight loss during treatment, which is much different from other cancer types.46 Clinicians are encouraged to guide women toward appropriate dietary and physical activity goals.
The benefits of adequate physical activity for health cannot be understated. The Nurse’s Health Study documented in a cohort of 2987 women diagnosed with breast cancer stages I–III who achieved 3–5 hours of walking per week (>3 metabolic equivalent task-hours per week, MET-h/week) reduced their risk of dying from breast cancer by half. The Collaborative Women’s Longevity Study (CWLS) followed 4400 American women ages 20–79 beginning at breast cancer diagnosis for 6 years and noted that women with >2.9 MET-h/week had a reduced risk of breast cancer and all-cause mortality. Results showed that increased physical activity consistently provided a survival benefit regardless of age, stage of breast cancer, and BMI.47
The World Cancer Research Foundation and the American Institute for Cancer Research (WCRF/AICR) have published comprehensive reports on the evidence linking diet and lifestyle to cancer. Their general cancer recommendations are to follow a plant-based diet rich in vegetables, fruits, whole grains, beans, and limited in red and processed meats, as well as high calorie, high sugar foods and alcohol.
While no specific nutrients or foods (other than alcohol) are consistently linked to breast cancer risk, two large-scale trials reviewed diet changes and risk of breast cancer recurrence. Specifically, the Women’s Healthy Eating and Living (WHEL) trial implemented a low-fat (goal 15%–20% dietary fat) and increased fruit and vegetable regimen (three fruit and five vegetable servings daily). Women in the intervention group were successful in increasing produce intake to goal and reducing dietary fat from 28% to 21% on average (did not meet target). No significant benefit of this intervention was found in relation to breast cancer recurrence after 7 years.48
The Women’s Intervention Nutrition Study (WINS) focused specifically on reducing fat intake to 15%–20% of diet to decrease risk of breast cancer recurrence. Women were able to meet the goal of 20% dietary fat or less. This trial of nearly 2500 women, begun in 1987, did find a significant reduction in recurrent breast cancer.49 However, a large percentage of women also experienced weight loss. Therefore, it is not possible to determine if diet change or weight loss or the combination most impacted the risk reduction noted in this study.
The AICR found convincing and dose–response evidence that alcohol intake is a risk factor for cancer. One standard drink per day increased breast cancer risk by 10%.40 There are several specific mechanisms by which alcohol causes cell damage. First, alcohol influences estrogen breakdown and effects, and persons who heavily consume alcohol may have nutrient-poor diets. The detoxification of alcohol produces carcinogens and free radicals, and alcohol enhances the absorption of free radicals into cells. Finally, increased folate intake may partially reduce the risk of alcohol damage.
Omega-3 Fatty Acids
In vitro and animal studies elucidated several mechanisms by which eicosapentanoic acid and docosahexanoic acid may inhibit breast cancer.50 Research in humans has been inconsistent but promising; more large-scale studies are needed. One report from the WHEL study noted that food intake of 73 mg EPA daily provided a 25% reduced risk of breast cancer recurrence.51 It is appropriate to recommend two to three servings of oily fish per week. It is important to note that flax seed oil primarily contains alpha-linolenic acid (ALA), and only 5%–10% of ALA is converted to EPA and DHA by the liver, therefore limiting effective vegan options to increase intake of EPA/DHA.
Soy foods contain phytoestrogens from isoflavone components. In the past, there was concern about phytoestrogen intake promoting ER+ breast tumor growth. Soy foods are recommended for children and adolescents to reduce breast cancer risk.52 Further studies have shown no detriment to the intake of soy food up to three servings daily for breast cancer survivors, and potential benefit on the effectiveness of tamoxifen.53
It is prudent to recommend whole food sources of soy such as tofu, soy milk, soy nuts, tempeh, or miso as one serving provides 30 mg isoflavones. The isoflavone content of processed soy protein powders or soy isoflavone supplements may exceed the daily recommended limit of 100 mg. Soy foods that do not contain soy protein, such as soybean oils or soy sauce, do not contain isoflavones. Other foods such as legumes, nuts, and some fruits do contain minute amounts of isoflavones. However, the quantity is measured in micrograms (mcg), making it difficult to approach the daily limit of 100 mg.
Vegetables from the Brassica family have been investigated for their content of glucosinolates, including indole-3-carbinol. This phytochemical participates in liver detoxification and is involved in the breakdown of estrogen. In vitro studies have shown antiapoptotic and antiangiogenetic effects.54 Large-scale studies have not been carried out to review the effects of increased consumption of cruciferous vegetables on breast cancer risk. However, increasing consumption is obviously part of a plant-based diet.
Lignans are present in nearly all plant foods, but flax seeds are the most significant source. These compounds have been investigated for anticancer effects, and benefit has been seen in vitro and in rodent studies. Human data have been mixed, with one study of over 1200 women showing lower risk of aggressive breast tumors, and another of nearly 335,000 women not showing any relationship between dietary lignans and breast cancer risk over 11.5 years.55,56
While all tea is a source of antioxidants, green tea is specifically noted for its catechin content, specifically epigallocatechin-3-gallate (EGCG). It is known that tea catechins have antioxidant, anti-angiogenic, anti-inflammatory, and antiproliferative actions in the body. As yet, data relating green tea to breast cancer are limited to in vitro and epidemiological evidence only. Some observational studies have linked a higher intake of green tea to a reduced risk of breast cancer while others have shown no effect.57
Energy and Protein Requirements
Typical energy requirements are between 25 and 30 kcal/kg actual weight and protein requirements vary 1–1.5 g/kg for normal women.58
The cardiotoxicity of breast cancer therapies is well established, and is a concern in patients who now survive decades after completing treatment. Patnaik et al. found that in older breast cancer survivors, cardiovascular disease actually surpassed breast cancer recurrence as cause of mortality.59
Bone health is an important focus for this population due to the adverse effects on bone related to chemotherapy and aromatase inhibitor therapies.60 Women should consume adequate calcium and vitamin D from food or supplements as indicated by the Dietary Reference Intakes (DRI). Although a 25-hydroxyvitamin D (25(OH)D) level of >20 ng/mL is appropriate for bone health, some researchers have suggested that the most beneficial level of 25(OH)D for breast cancer risk is between 40 and 60 ng/dL.61,62 This topic remains controversial, but it is valuable to assess serum vitamin D status in this population.
Dietary Reference Intakes for Bone Health
Source: Institute of Medicine (US) Committee to Review Dietary Reference Intakes for Vitamin D and Calcium; In: Ross AC et al. eds. Dietary Reference Intakes for Calcium and Vitamin D. Washington (DC): National Academies Press (US); 2011.
a International units.
Vitamin D has been investigated in the last few decades for anticancer benefits. While research is ongoing, potential mechanisms include induction of cell differentiation and apoptosis, inhibition of abnormal cell proliferation, and tumor angiogenesis. A recent meta-analysis found serum vitamin D levels at diagnosis to be strongly predictive of survival.64
The most common surgical interventions are lumpectomy, mastectomy, and breast reconstruction. While there are no nutrition-related side effects, it is recommended to ensure that the daily protein needs of 1–1.2 g/kg are met.
Chemotherapy was traditionally given in the breast cancer population as an adjuvant treatment, that is, after a surgical procedure to remove the tumor. However, it is increasingly employed as a neoadjuvant therapy to assess the tumor’s response to the treatment, reduce the quantity of tissue resected, and target any cells outside the immediate breast region.
Side effects of chemotherapy vary based on type of drug, dose, and single- versus multiple-agent therapy; frequency of treatment; and individual differences. See Appendices 6.1 and 6.2 for specific interventions related to each drug or symptom.
Common therapeutic drugs used for breast cancer:
• Capecitabine (Xeloda)
• Carboplatin (Paraplatin)
• Cyclophosphamide (Cytoxan)
• Docetaxel (Taxotere)
• Doxorubicin (Adriamycin)
• Epirubicin (Ellence)
• Fluorouracil (5-FU)
• Gemcitabine (Gemzar)
• Ixabepilone (Ixempra)
• Methotrexate (MTX)
• Paclitaxel (Taxol)
• Paclitaxel albumin-stabilized nanoparticle formulation (Abraxane)
• Vinorelbine (Navelbine)
Common multiple-agent chemotherapy regimen acronyms used in breast cancer:
• TAC (Taxotere/Adriamycin/Cytoxan)
• A/C, then T (Adriamycin/Cytoxan, usually followed by Taxol)
• THP (Taxotere/Herceptin/Perjeta)
• TCHP (Taxotere/Cytoxan/Herceptin/Perjeta)65
Common Side Effects of Common Endocrine Therapies
Nutrition-Related Side Effect
Take with a glass of water
Mild nausea, abdominal pain
Take with food
Nausea, weight gain
May elevate cholesterol levels
Nausea, vomiting, diarrhea, constipation
Common Side Effects of Biologic Agents
Nutrition-Related Side Effect
Nausea, diarrhea, mucositis
Nausea, vomiting, diarrhea
Take 1 hour before, or 1 hour after eating; no grapefruit juice
Take with water, with or without food;monitor serum lipids
Common Radiation Treatment Areas in Breast Cancer
Area of Body
Nutrition-Related Side Effect
Protein intake 1–1.2 g/kg daily
Intraoperative radiation therapy (IORT)
Potential nausea/vomiting, hyperglycemia
Monitor blood glucose levels
NUTRITION INTERVENTION SUMMARY
Dietitians are most frequently called upon in this population to manage nutrition impact symptoms during chemotherapy, provide counseling and support to guide food choices. In the survivorship phase, dietitians remain indispensable to help patients implement a plant-based, heart-healthy diet and work toward weight loss, if indicated. Finally, dietitians can encourage weight-bearing exercise and assure adequate calcium and vitamin D intake to reduce the risk of osteoporosis.
ESOPHAGEAL, HEAD AND NECK