Treatment of disease

There is a dearth of well-described controlled randomised prospective clinical trials of the effect of diet on naturally-occurring diseases of dogs and cats. Within veterinary medicine there has been a proliferation of diets for the nutritional management of various disease states⁽Reference Plumb¹²⁾. Such diets include those for the treatment of chronic kidney disease, diabetes mellitus, osteoarthritis, chronic heart failure, hepatic encephalopathy, cancer, intestinal disease and dietary allergies, as well as for the dissolution and prevention of uroliths, weight control, the moderation of cognitive dysfunction and the prevention of formation of dental calculus. Reports of studies that have been performed in support of these diets, however, have often left much to be desired. The composition of the diet is often described incompletely because pet food companies consider the composition of their diets to be proprietary and editors are often reluctant to include more than the analysis of the major nutrients. This situation makes any trial that uses a commercial diet difficult to interpret or to apply in a wider setting. Furthermore, many studies change more than one nutrient so that it is difficult to ascertain which nutrient or combination of nutrients is responsible for the effect observed. The amount of diet consumed and the conditions in which animals are maintained are also often not described, and many investigators measure changes in metabolism rather than more substantive measures of benefit such as a clinical response or survival. As a result, there is much controversy as to the usefulness of using diet to treat dogs and cats with disease. The authors of the National Research Council recommendations⁽¹⁾, it should be noted, have confined their recommendations to normal animals and the maintenance of health, rather than the treatment of disease.

The dietary treatment of chronic kidney disease in dogs and cats has received considerable attention because the prevalence in cats and dogs is high. Diets designed for the treatment of chronic renal failure typically contain less protein and P than most diets designed for maintenance of normal animals. They also often contain increased amounts of fish oil and moderate amounts of Na and are designed to moderate acidosis. P restriction has been shown to slow the progression of disease and adding fish oil has been shown to slow the development of pathological changes in the kidney in the nephrectomised dog model⁽Reference Brown, Crowell and Barsanti^13, Reference Brown, Brown and Crowell¹⁴⁾, but the value of protein restriction in slowing progression of disease remains uncertain⁽Reference Finco, Brown and Crowell¹⁵⁾. Nevertheless, prospective controlled clinical trials have shown that survival is prolonged more than twofold in animals with chronic kidney disease when animals are fed commercial ‘kidney’ diets with less protein and P compared with when cats are fed normal maintenance diets. Thus, median survival time (d) is increased from 188 to 594 in thirty-eight dogs (randomised)⁽Reference Jacob, Polzin and Osborne¹⁶⁾ and from 264 to 633 in fifty cats (not randomised)⁽Reference Elliott, Rawlings and Barber¹⁷⁾. Such numbers are compelling despite the failings in the description of experimental detail discussed earlier. As some cats with renal failure will not eat readily, simply providing a renal diet and water via a feeding tube may be sufficient to prolong the cat's life and reduce an owner's perception of the need for transplantation.

Malignant tumors are relatively common in some breeds of dogs and in cats but there has been only one prospective trial examining the effect of diet on survival. Adding fish oil to the diet in high concentrations and a modest increase in dietary arginine increases median survival from 270 d to 350 d in dogs with stage III lymphoma receiving regular chemotherapy (doxorubicin)⁽Reference Ogilvie, Fettman and Mallinckrodt¹⁸⁾; there is a correlation between survival and DHA concentrations in the blood. This increase is only modest, but a retrospective study has reported that in dogs with mammary carcinomas fed lower-fat diets containing <39% metabolisable energy (ME) as fat median survival is increased from 6 months to 3 years when dietary protein is increased from <23% ME to >27% ME⁽Reference Shofer, Sonnenschein and Goldschmidt¹⁹⁾.

Cardiac infarction is rare in dogs and cats but cardiac failure occurs secondary to cardiomyopathy or chronic valvular disease. A retrospective study of 180 dogs with heart failure has found that dogs that gain weight during the course of their disease and dogs that consume more n-3 fats survive longer than those that do not⁽Reference Slupe, Freeman and Rush²⁰⁾. A prospective randomised controlled study of Boxer dogs with arrhythmogenic right ventricular cardiomyopathy has reported a decrease by more than half in the median frequency of abnormal heart beats (ventricular premature contractions) in dogs fed fish oil but not in dogs fed flax or sunflower oil⁽Reference Smith, Freeman and Rush²¹⁾.

The dietary management of cats with diabetes has received some attention. A prospective randomised controlled trial involving sixteen cats with diabetes maintained on insulin has found that including 120 g insoluble fibre/kg DM reduces postprandial blood glucose, although body weight is not changed by either high- or low-fibre diets⁽Reference Nelson, Scott-Moncrieff and Feldman²²⁾. Another trial has found that significantly more cats (68% v. 41%) revert to a non-insulin-dependent state when fed a canned diet containing almost no carbohydrate or fibre than when fed a moderate-carbohydrate higher-fibre canned food⁽Reference Bennett, Greco and Peterson²³⁾.

Prevention of disease

Dogs and cats in developed societies are mostly fed complete and balanced foods made by commercial manufacturers to conform to the current understanding of the essential nutrient requirements of these species. Nutritional deficiencies are therefore uncommon in normal animals, except when human food in unbalanced proportions provides the preponderance of energy⁽Reference Freeman and Michel²⁴⁾. The debate among companion animal nutritionists, therefore, currently revolves around whether increased or decreased amounts of some nutrients may be beneficial.

Urolithiasis is common in dogs and cats and can result in life-threatening obstruction of the urinary tract. For many years cat foods have been mostly designed to produce acid urine to reduce the risk of struvite urolithiasis. This approach has been very successful but the number of oxalate uroliths submitted to analytical laboratories has increased as the number of struvite uroliths has decreased⁽Reference Osborne, Lulich and Polzin²⁵⁾. To compensate for this development some diets are being produced that contain higher concentrations of Na (>2 g/4184 kJ (1000 kcal)) to promote diuresis and thus lower the concentration of urine solutes. The long-term benefit of this approach has yet to be adequately evaluated in clinical patients.

Improvements in learning and retention of learned behaviour have been reported in old beagles supplemented with a cocktail of antioxidants (/kg; 1050 mg dl-α-tocopheryl acetate, 260 mg l-carnitine, 128 mg dl-α-lipoic acid, 80 mg Stay-C (Argent Laboratories, Redmond, WA, USA; mono-, di- and triphosphate esters of l-ascorbic acid providing 150 g ascorbic acid/kg dry weight) and 10 g each of spinach flakes, tomato pomace, grape pomace, carrot granules and citrus pulp)⁽Reference Cotman, Head and Muggenburg^26, Reference Milgram, Zicker and Head²⁷⁾ or α-lipoic acid combined with l-carnatine⁽Reference Milgram, Araujo and Hagen²⁸⁾. This improvement has been shown to be enhanced in animals receiving behavioural enrichment⁽Reference Milgram, Head and Zicker²⁹⁾. The prevalence of cognitive dysfunction in pet dogs is, however, uncertain and increased concentrations of antioxidants are not always beneficial. In racing greyhounds, for example, high doses (1 g daily) of vitamin C appears to reduce performance⁽Reference Marshall, Scott and Hill³⁰⁾.

Obesity is the commonest nutritional disease of companion animals. In various countries the prevalence has been reported as being from 19% to 52% in domestic cats⁽Reference Robertson^31–Reference Anderson³⁴⁾ and from 22% to 44% in dogs⁽Reference Robertson^31, Reference Robertson^35–Reference Wolfsheimer³⁷⁾. Orthopedic, endocrine, cardiac, respiratory, neoplastic, urinary, reproductive and dermatological disease and reduced resistance to infection have been associated with obesity in dogs and cats⁽Reference German³⁸⁾. A prospective randomised controlled trial has shown that food restriction prolongs survival in Labrador retrievers kept in kennels with runs⁽Reference Kealy, Lawler and Ballam³⁹⁾. Overweight dogs (median body condition score 6·9 on a nine-point scale) have been found to require medication for osteoarthritis 3 years earlier, and median survival is 2 years shorter than that for lean dogs (median body condition score 4·6) fed 75% of the amount of food fed to their paired littermates. It has also been reported that racing greyhounds run 0·7 km/h faster when they are fed 85% free-choice food and weigh 6% less⁽Reference Hill, Lewis and Randell⁴⁰⁾. Labrador retrievers are prone to osteoarthritis and racing greyhounds have a normal body condition that is lower than that of other breeds (3·5 on a nine-point scale), so it remains to be determined whether similar effects would be obtained with other breeds.

There are also important metabolic differences between dogs and cats and human subjects that must be taken into account before dogs and cats should be considered as potential models of metabolic syndrome in human subjects. Both obese dogs and obese cats can develop insulin resistance⁽Reference Hoenig⁴¹⁾. Overweight cats also commonly develop non-insulin-dependent diabetes mellitus but dogs usually develop insulin-dependent diabetes mellitus⁽Reference Hoenig⁴²⁾. Only a very small increase in blood pressure has been documented as dogs gain weight, although the amount of change is affected by the type of fat in the diet⁽Reference Bodey and Michell^43, Reference Truett, Borne and Monteiro⁴⁴⁾. Lipoprotein concentrations also change slightly in association with insulin resistance in dogs fed energy-dense diets⁽Reference Briand, Bailhache and Andre^45, Reference Bailhache, Nguyen and Krempf⁴⁶⁾, but such changes may not have the same consequences as in human subjects because most of the lipoprotein in fasted dogs and cats is HDL and the prevalence of atherosclerosis and cardiac infarction in dogs and cats is very low⁽Reference Watson and Barrie⁴⁷⁾.

Dogs derive twice as much energy from fat oxidation at rest and during exercise and starvation as human subjects⁽Reference McLelland, Zwingelstein and Taylor^48, Reference de Bruijne, Altszuler and Hampshire⁴⁹⁾. The distance beagle dogs could run before exhaustion has been reported to increase from 24 km to 48 km when the fat in their diet is increased from 30% ME to ≥50% ME⁽Reference Downey, Kronfeld and Banta⁵⁰⁾. Dogs undertaking endurance exercise use glycogen more slowly as fat intake increases⁽Reference Reynolds, Fuhrer and Dunlap⁵¹⁾. In contrast, in human athletes carbohydrate loading increases stamina by increasing glycogen in muscle without affecting the rate of glycogen use⁽Reference Bergstrom, Hermansen and Hultman⁵²⁾. However, fat oxidation does not increase with exercise in untrained dogs because increased lactic acid concentrations limit fat utilisation⁽Reference Paul and Holmes^53, Reference Issekutz, Miller and Paul⁵⁴⁾. Untrained dogs may represent a better model for study than trained dogs.

When studying companion animals it is also essential to take account of differences in energy consumption. The National Research Council recommendations for adult maintenance are based on studies involving adult laboratory dogs consuming a mean of 544 kJ (130 kcal)/kg body weight (BW)^0·75 daily and average lean adult laboratory cats consuming a mean of 418 kJ (100 kcal)/kg BW^0·67 daily⁽¹⁾. Nevertheless, many pet and laboratory animals are overweight, their activity and the conditions in which they are kept can be quite varied and there is great variation in the energy requirements among different breeds and among individual animals. As a result, many pet adult dogs require much less energy for maintenance than 544 kJ (130 kcal)/kg BW^0·75 daily and some working dogs require much more. Similarly, pet cats often require much more or less than the mean of 418 kJ (100 kcal)/kg BW^0·67 daily. Even in dogs that are undertaking no exercise and consuming no food in a thermoneutral environment ME requirements have been measured to vary from 201 to 477 kJ (48 to 114 kcal)/kg BW^0·75 daily, whereas average ME requirements in fed dogs may vary from 352 kJ (84 kcal)/kg BW^0·75 daily in resting dogs to as much as 4393 kJ (1050 kcal)/kg BW^0·75 daily in dogs racing long distances while pulling a sled⁽¹⁾. Thus, the amount of food consumed needs to be individualised for each pet or participant in a study if each dog or cat is to maintain body weight. Unfortunately, many reports do not describe the amount or energy density of food, which makes comparison among studies difficult. Only if food and ME intake, the ME and nutrient density of the food and any change in BW, body conditioning score and extent of muscle wasting are reported can a better understanding of the relationship between energy and nutrient requirements in sick and healthy animals be achieved.