Nutrition: Cancer and Patient Care

Dr Anthony Zambelli BSc(Hons) BVSc DiplSenMgmt MMedVet(Med),                                                                               Email: info@inandavets.com Tel: 031 762 1816                                                                                                                Inanda Veterinary Hospital & Specialist Referrals

Key Points

• Malignancy creates profound metabolic changes in patients, which can persist into remission

• Treatments and dietary manipulation can blunt or exaggerate these metabolic alterations

• A cancer treatment plan that does not address dietary issues is incomplete and harms patient welfare and outcomes

• It appears that a high protein, high fat, low carbohydrate, moderate insoluble fibre diet high in ω3 fatty acids is ideal for cancer patients

Introduction

The management of a veterinary cancer patient may include one or more of: surgery (sometimes quite aggressive), chemotherapy, radiation therapy, immunotherapy as well as control of concurrent illnesses (comorbidities) that influence overall health e.g. obesity, osteoarthritis, organ dysfunction (e.g. kidney or cardiac disease). The veterinarian embarking on even the most basic oncotherapy should include a nutritional needs assessment as part of the minimum database, and manage the patient’s needs on an ongoing basis.

This recognises the profound and fundamental influences a malignancy has on metabolism and thus the response to treatment. A basic understanding of cancer nutritional metabolic pathology is adequate but necessary to manage this class of patient.

Cancer and metabolism in a nutshell

Various cancers have been demonstrated to affect the patient’s metabolism in manifold ways. It is safe to say that all malignancies can be underfed or misfed, and any the minority are properly fed. Although cancer patients have a tolerance range for dietary intake of various nutrients e.g. lactate1, this homeostatic reservoir is narrower than for healthy patients.

Essentially, malignancy causes alterations in the major nutritional axes as follows:

PROTEINS – patients have skeletal muscle loss due to increased activity of proteolytic (catabolic) pathways and processes, even though liver protein synthesis increases. This causes protein metabolism to be shifted toward the tumour(s), and not replacing the muscle loss (sarcopenia). The altered liver metabolism is typical of the “acute phase protein response” seen in many inflammatory diseases.

Clinical consequence – if protein intake does not match requirements, poor wound healing and immunity and altered GIT function result.

FATS/LIPIDS – the cachexia seen with malignancy is also due to reduce fat synthesis with concurrent lipolysis, driven by various cytokines and chemicals. Insulin resistance caused by various cytokines and tumour-derived factors may be an important driver of this altered lipid state.2 In addition, the finding that some tumour cells have only a limited ability to utilise fats for gluconeogenesis (the generation of glucose from non-carbohydrate sources) leads some to believe a higher fat diet is physiologically appropriate to cancer patients. In fact, dogs allowed to self-select foods according to the satisfaction of energy intake, will tend to select a diet that is 30% protein, 63% fat and only 7% carbohydrate.3 In addition, the type of fat eaten seems to be important, with diets higher than 5% in ω3 fatty acids advised by veterinary nutritionists.4

Clinical consequence – patients with inadequate lipid intake may experience alterations in energy status, increased usage of muscle amino acids to drive gluconeogenesis (further sarcopaenia), altered lipid-soluble vitamin homeostasis (Vit A, D, E and K) and greater susceptibility to oxidative damage of other organs.

CARBOHYDRATES – at the centre of many arguments about cancer metabolism are carbohydrates (CHO). In this respect we are not discussing fibre, which is discussed below. Carbohydrate is an energy source used by all cells, but less effectively in cancer, due to insulin resistance at the cell membrane. This is aggravated by a relative or absolute hyperlactataemia which may be worsened by administration of Ringer’s Lactated intravenous solutions1, 5 Malignancy sufferers express embryonic versions of certain enzymes and have defective Cori-cycles which promote the formation of lactate, and furthermore rob the patient of energy in the form of expenditure required to correct this very abnormality.

Tumour tissue consumes glucose anaerobically, leaving a net gain of only 2 moles of ATP, versus normal metabolism using the Krebs Cycle, which generate 38 moles of ATP from the same amount of glucose.1, 5-8

οοClinical consequence – hyperlactataemia and metabolic acidosis. This affects the function of almost every body system, enzyme and membrane by altering the ionisation and movement of electrolytes, the pKi of enzymes (as proteins their binding to substrate is specific to a pH and temperature band) and broader processes such as vascular tone and muscle and nerve impulse conduction. Hyperlactataemia can suppress appetite, further worsening cachexia.

BCS is graded 1 to 5, with 2.5 – 3.0 being considered “normal”, 1 cachexic and 5 grossly obese.

MCS is graded from 0 to 3, with 3 = no wasting, 2 = mild, 1 = moderate, and 0 = severe.

The nutritional needs assessment                                                                                                                                      Why is a nutritional assessment necessary?

It appears that the majority of patients presenting to vets with cancer are in an abnormal body (BCS) or muscle condition score (MCS).9

It is important to grade BOTH BCS and MCS to have a fuller appreciation of the patient’s needs. Do this at each visit, along with the weigh-in and TPR.

For example, a patient may have BCS 4.5 and MCS 1, if it had a functional adrenocorticotrophic tumour – fat but with little muscle. Some practical considerations for such a patient might include:

• Poor wound healing.

• Increased infection rate.

• Increased friability of the skin.

• Fewer sites for safe or comfortable intramuscular injection.

• Poor muscle strength resulting in slower return to mobility after anaesthesia, and increased risk of tendon or ligament rupture.

• Osteopenia and joint pain from excessive weight without matching supportive strength.

• Easy spread of infection along muscle planes e.g. injection site reactions.

What would be appropriate here, in this patient?

This is the line of reasoning the vet would need to pursue, which requires an understanding of metabolic physiology, diet characteristics and so forth.

Another relevant example might be a rostral mandibulectomy for a fibrosarcoma.

• The patient would require a temporary oesophagostomy tube and then transition onto solid food after 2 weeks.

• The non-nutritive characteristics of the diet are therefore important. Can it be tube fed? What is its water content? What is the patient’s water requirement?

• Water intake (in the form of liquidised food) reduces the caloric and nutrient density of the diet. Is this taken into account?

• What is the patient’s stomach capacity?

• An adult cat can tolerate 300ml of stomach fluid given over 10+ minutes.

• A dog of 15kg can tolerate 450ml; a dog of 55kg+ up to 3L over the same period.

Never feed a sick animal >5% of its body weight at a time if it has not eaten properly in over 3 days; transition it back with small, frequent meals. For dogs undergoing chemotherapy, the prophylactic use of antiemetics (maropitant, ondansetron, metaclopramide) before therapy, and feeding on the morning of chemotherapy, helps offset catabolism from repeated and extended periods of hyporexia some drugs cause.

Diet Selection                                                                                                                                                                            In general, aim for a diet with:

• A high quality protein at 35 – 45% DMB (dog) or 40 – 50% (cat) which is readily available and diverse in amino acid profile

• Low readily-soluble carbohydrates (<25%), but dietary fibre of 2.5%+

• Fats 25 – 40%, with ω3 fatty acids >5%

Adjust this according to comorbidities e.g. chronic kidney disease, joint disease. Avoid excessive antioxidant supplementation directly before or during radiation therapy, as this reduces the efficacy of treatment. Some suitable diets of various manufacturers have been graphically represented as examples of diets you can use in SA. This list is not all-inclusive. (Fig 1)

NEVER use raw meats or unwashed vegetables in patients with cancer as they have less tolerance to the myriad of potential parasites and infections carried in unprocessed food, which also has NO improvements in digestibility or nutrient profile over premium ingredient, quality-assured commercial diets. Client compliance with recipes provided for home cooked diets is also abysmally poor; it cannot be recommended at all.10-16

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