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Veterinarian Technician May 2013 (Vol 34, No 5)

Nutrition Know-How: Cachexia in Chronically Ill Patients

by Ann Wortinger, BIS, LVT, VTS (ECC, SAIM, Nutrition)

    Cachexia is a multifactorial syndrome characterized by progressive weight loss that is often accompanied by anorexia.1 Unlike weight loss seen with starvation or anorexia, cachexia is distinguished by a loss of adipose tissue with accompanying loss of lean body mass, primarily muscle. Nonmuscle protein, such as in the organs, is preserved in cachexia, but not in starvation. In dogs with illness or injury, amino acids from lean body mass are the primary source of energy instead of glucose from carbohydrate during normal digestion.2 Significant loss of mineral content in the bones can also contribute to the overall weakness in many cachexic patients.1

    The beginning phase of cachexia can be very subtle, even in obese animals, and many clients may perceive the associated changes as simply “growing old.”3 When evaluating a patient for cachexia, it is important to remember than cachexia is a process—the loss of lean body mass—and not an end-stage syndrome.4 A similar syndrome known as sarcopenia is also common in dogs and cats; however, sarcopenia is the loss of lean body mass associated with aging in the absence of disease.4

    The loss of lean body mass has a deleterious effect on strength, immune function, and survival.3 This loss can first be noticed over the epaxial, gluteal, scapular, and temporal muscles2 and is easily detected during a routine physical examination (TABLE 1). There does not appear to be a cause-and-effect relationship between anorexia and cachexia: cachexia-associated weight loss often exceeds weight loss expected from only a decrease in caloric intake.1 Cachexia is a profound state of general illness, malnutrition, and disability that can affect animals with cancers, cardiac disease, renal disease, and other significant illnesses and injuries.5 Loss of 25% to 50% of lean body mass compromises the immune system and affects muscle strength, with death resulting from infection, pulmonary failure, or both.5


    The primary cause of cachexia is alterations in the body’s metabolism of carbohydrate, fat, and protein.6 These metabolic alterations can lead to anorexia, fatigue, weight loss, impaired immune function, and malnutrition.6 Cachexia is often due to various cancers, and the associated tumors can induce many of these changes in the patient’s body. Most cancer cells use anaerobic glycolysis at a higher rate than normal tissue to generate adenosine triphosphate for energy.1 In general, cancer cells cannot obtain a significant amount of energy from aerobic glycolysis or fat oxidation.6 Anaerobic glycolysis results in a gain of energy for tumor cells and a net loss of energy for the patient as well as the generation of a large amount of lactic acid that the patient must convert to glucose.6


    The presence of cachexia increases patient morbidity and can adversely affect a patient’s quality of life.4 Early identification of cachexia and subsequent intervention can be important for improving the success of treatment and the quality of life of patients and owners.

    The Phases of Cachexia

    The three phases of cachexia identified in humans are presumed to be the same in dogs and cats (TABLE 2). In the first phase, the patient does not exhibit clinical signs, but biochemical changes include an increase in the lactate level due to glycolysis; an increase in the insulin level, causing peripheral insulin resistance; and alterations in the amino acid and lipid profiles.6

    In the second phase of cachexia, clinical signs can include anorexia, weight loss, and depression. Many owners attribute these early signs to their pet “getting old” and do not recognize the clinical significance.

    The final phase is characterized by marked loss of body fat and protein stores, severe debilitation, weakness, and biochemical evidence of negative nitrogen balance.6 If untreated, cachexia can cause death.

    Biochemical Changes

    The biochemical changes caused by cancer or another disease lead to inefficient energy use by the patient and enhanced energy use by the tumor or the disease process.6 The prevalence of glucose intolerance and insulin insensitivity (resistance) requires limitation of the amount of carbohydrate and careful selection of the type of carbohydrate used in foods for affected animals. With the patient and the tumor having obligatory protein requirements, a negative nitrogen balance is often seen in cachexia patients. If this imbalance is not corrected, it leads to increased loss of skeletal muscle, hypoalbuminemia, compromised immunity, impaired gastrointestinal function, and delayed wound healing, as is seen in any condition that impairs protein use by the body. In cancer, several tumor-derived factors and cytokines that influence this increased protein breakdown have been identified, including proteolysis induction factor, tumor necrosis factor α, and interleukin-1β.6

    Loss of lean body muscle accounts for most of the weight loss in animals and humans with cancer cachexia and other chronic diseases, such as kidney disease and congestive heart failure. Although reduced food intake is a significant contributor to this loss, decreased nutrient absorption and increased metabolic alterations also trigger loss of muscle rather than fat.4 One of the metabolic alterations is a decrease in leptin production, which is inversely related to the intensity of the inflammatory response created by the body: as the leptin level decreases, inflammatory mediators increase, causing increased production of inflammatory cytokines.1 Leptin—a protein with hormone-like activities—is produced by adipocytes (fat cells); it causes a decrease in appetite and an increase in energy expenditure. These cytokines contribute to anorexia, increase energy requirements, and increase catabolism of lean body mass.3 The most common inflammatory cytokines active in this process include proteolysis induction factor, tumor necrosis factor α, and interleukin-1β.6

    Tumors obtain energy primarily through anaerobic metabolism of glucose, resulting in excess production of lactate in the body.6 The lactate must then be recycled at an additional energy cost to the animal, resulting in a net energy loss. This is not the only energy-wasting process in a cachexic animal. Additional energy losses can be due to cytokine-induced increases in glucose recycling, protein degradation, and overall energy expenditure.6 Because cachexia develops in phases and biochemical alterations typically precede clinical signs, animals in the preclinical phase would be expected to have normal energy requirements. Animals in phase 2 (active untreated cachexia) would be expected to have an elevated energy expenditure, while animals in the final phase may be hypometabolic.6

    Dietary Management

    While the wasting process associated with cachexia cannot be reversed through nutritional supplementation alone, manipulation of patients’ nutrient intake can be beneficial in managing some of the effects of cachexia on the body.1 Adequate nutrition can be key to managing cachexia by providing calories, protein, and fat and modulating cytokine production.3 It may not be intuitive that nutrition modulates cytokine production. Inflammatory cytokines, specifically tumor necrosis factor, interleukin-1β, and interleukin-6, can contribute to anorexia, increase energy metabolism, and increase the loss of lean body mass. Modulating these cytokines can decrease the energy burden on the body and direct energy use toward production of lean body mass. Specific dietary recommendations should consider the phase of cachexia as well as the patient’s energy needs, current and past nutritional status, and ability or willingness to eat.6 Because these patients do not tend to eat well, dietary recommendations should consider routes of nutrition that do not require voluntary consumption of food.

    Studies using animal models have shown that supplementation using the omega-3 fatty acids EPA and DHA can help to prevent cachexia and metastatic disease processes.6 Omega-3 fatty acids produce less potent inflammatory mediators than do omega-6 fatty acids. When the body uses omega-3 fatty acids to produce cytokines, the inflammatory response is decreased in proportion to the level of omega-3 fatty acids in the diet. Preferentially increasing the amount of omega-3 fatty acids in the diet and, therefore, their availability in the body can help to increase the production of less inflammatory cytokines. Dr. Freeman3 recommends 40 mg/kg of EPA and 25 mg/kg of DHA per day. Based on the common formulation of most fish oil capsules, a patient would need ~1 g (1 capsule) per 10 lb of body weight per day.3 Many recovery diets already incorporate this concentration, so additional supplementation is not recommended.

    The caloric distribution in the food should emphasize calories from fat and protein rather than carbohydrate since we know that glucose is the preferred fuel of tumor cells, but fatty acids and amino acids are not.6 The goal is to feed the patient and starve the tumor cells. In an ideal food, 50% to 60% of calories would be from fat, 30% to 50% from protein, and the remaining percentage from carbohydrate6 (TABLE 3).

    A diet’s protein level should be at the upper limit recommended by AAFCO (Association of American Feed Control Officials), and the protein should be high quality to facilitate digestibility and use by the body. A protein level of 30% to 50% dry matter is recommended, with dogs at the lower end and cats at the higher end.6 In relation to energy intake, the minimum recommended protein intake is 5.14 g/100 kcal, with 6 to 7 g/100 kcal preferred.3

    Because tumor cells preferentially use glucose for energy, selecting a carbohydrate with a low glycemic index can provide a slower release of carbohydrate-generated glucose into the bloodstream than would a carbohydrate with a high glycemic index. The glycemic index is used to measure how quickly a carbohydrate source is converted into glucose during digestion. Rice has one of the highest glycemic indexes; barley, sorghum, and corn have much lower glycemic indexes.6 Moderately soluble fibers can also be used to slow the entry of glucose into the bloodstream, with the added benefit of providing additional short-chain fatty acids specifically for enterocytes. Certain short-chain fatty acids, specifically butyric acid (butyrate), are produced by intestinal bacteria from moderately soluble fibers and used preferentially by enterocytes and colonocytes for energy.

    Feeding Methods

    Enteral feeding is always preferred if the patient has a functional gastrointestinal tract. Oral feeding of a canned or dry pet food should be the first choice for cachexia patients.6 When a patient is unwilling or unable to consume the desired amount of food orally, various feeding tubes can be used. The patient must be able to consume at least 85% of its resting energy requirement for oral feeding to be used. If this amount cannot be voluntarily consumed, alternative ways of supplying nutrition must be considered. Tube selection should be based on the patient’s condition, the desired period of use, and the owner’s willingness to feed at home. The only tubes that are appropriate for at-home use are esophagostomy and gastrostomy tubes. Tube selection is based on the patient’s ability to undergo anesthesia, the doctor’s skill level, the availability of special equipment (an endoscope) and nursing care, and the overall cost to the client.

    Diet selection should also be based on the route selected for feeding. The energy density of a diet fed through a feeding tube can directly affect the success of feeding: a food that has a low energy density may contribute to vomiting or osmotic diarrhea due to a high feeding volume or poor digestibility.6 Feeding multiple, small meals frequently is easier on the patient, although this may not be easier on the client. Small meals decrease the incidence of nausea related to feeding, increase the transit time of food through the stomach, and help ensure that the nutrition is usable by the animal.6

    Home-cooked diets can be used in the short term to tempt a patient to eat; long-term use of these diets must be approved by a nutritionist. Homemade diets are frequently unbalanced and therefore detrimental to animals. Calculating the energy density and amounts of nutrients and micronutrients in homemade diets is difficult, if not impossible, for the average clinician, technician, or client. A board-certified veterinary nutritionist can help clients formulate a diet that is acceptable to their pets and provides the best possible nutrition. Several excellent therapeutic diets meet the recommended diet profile for cachexia patients and can be fed orally or by tube.


    While cachexia can be a fairly obvious sign of biochemical imbalances within the body, the condition has often been present for a while by the time physical changes are seen. We need to know how to feed our patients during treatment for cancer or other diseases. By recognizing the physiologic changes caused by disease and cancer, we can recommend diets that can help patients rather than a tumor or a disease process, resulting in more positive patient outcomes and a better quality of life for patients and clients.

    Ann Wortinger is the Nutrition Know-How section editor for Veterinary Technician.

    1. Tisdale M. Mechanisms of cancer cachexia. Physiol Rev 2009;89(2):381-410.

    2. Freeman LM, Rush JE. Cardiovascular diseases: nutritional modulation. In: Pibot P, Biourge V, Elliott D, eds. Encyclopedia of Canine Clinical Nutrition. Aimargues, France: Royal Canin; 2006:321-336.

    3. Freeman LM, Rush JE. Nutritional management of cardiovascular diseases. In: Fascetti AJ, Delaney SJ, eds. Applied Veterinary Clinical Nutrition. Ames, IA: Wiley-Blackwell; 2012:304-307.

    4. Freeman LM. Cachexia and sarcopenia: emerging syndromes of importance in dogs and cats. J Vet Intern Med 2012:26:3-17.

    5. Saker K, Remillard RL. Critical care nutrition and enteral-assisted feeding. In: Hand MS, Thatcher CD, Remillard RL, et al, eds. Small Animal Clinical Nutrition. 5th ed. Topeka, KS: Mark Morris Institute; 2010:441-442.

    6. Case L, Daristotle L, Hayek M, Raasch M. Nutritional care of cancer patients. Canine and Feline Nutrition. 3rd ed. Maryland Heights, MO: Mosby Elsevier; 2011:479-486.

    References »

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