Front Page Congress Site WSAVA Author Index Search Go to First Presentation Go to Previous Presentation Go to Next Presentation Go to Last Presentation World Congress 2001 CVMA WSAVA
 
Back to Previous Page Print This Page Save This Page Bookmark This Page Go to the Top of the Page

Feline Nutrition Update

Vincent Biourge France

Our knowledge of the nutritional needs of cats has expanded greatly over the last 30 years thanks to the work of many dedicated researchers and particularly the team of Prof. Q. R. Rogers and Prof. J. G. Morris, at the University of California, Davis. It is now recognized that cats require specialized diets formulated for their specific nutritional needs. Those specific needs are the result of their long history as flesh eaters that lead into modifications of enzyme activities and thus, nutrient metabolic pathways.

Protein

Cats have a high protein requirement. This requirement is not explained by a higher amino acid requirement for protein synthesis but rather by their limited ability to control the activity of amino acid catabolic enzymes. Whatever the protein content of their diet, the activities of those enzymes in cats will correspond to the activities in dogs or humans receiving a high protein diet. This adaptation is beneficial to cats. It allows them to transform the protein that is plentiful in their natural food into glucose, an essential nutrient that is present only at low concentration in their prey.

Fasting in obese cats has been associated with liver lipid accumulation that becomes pathological over a five to six week period and mimics Idiopathic Feline Hepatic Lipidosis. Protein supplementation during the fast slows down this accumulation.

Amino acids

Cats require the same nine essential amino acids that are needed in the diet of all mammals. However, cats also require arginine and taurine. Although cats fed a diet deficient in arginine will develop severe hyperammonemia and may die as a result, protein sources commonly used in the formulation of cat food will easily fulfill all the arginine requirements. Lipid accumulation observed in cats suffering from hepatic lipidosis does not appear linked to arginine deficiency or orotic acid accumulation as has been described in rats.

Taurine is essential in the diet of cats and its deficiency results in a wide range of clinical signs including fetal abnormalities, delayed growth and development, central retinal degeneration and dilated cardiomyopathy. While the ability of cats to synthesize taurine from methionine and cystine is very limited, they are obligate users of taurine to conjugate with bile acids. Formation of bile salts results in a continual loss of taurine, as a proportion of the taurine is not recovered in the enterohepatic re-circulation. In order to provide sufficient taurine in cat foods to maintain plasma and blood levels in the optimal range, studies at Davis found that dry extruded cat foods required about 1 g/kg diet, but canned foods required up to 2.5 g/kg. Indeed, canned diets have been shown to promote a gut flora with a higher rate of taurine degradation than that supported on expanded diets. One may question why cats would have evolved with limited synthesis of a key nutrient such as taurine. The answer is that cats do not need to synthesize any taurine if they consume a diet only of animal tissue and that the synthesis of taurine represents a loss of potential energy to cats as excess taurine is excreted in the urine.

Lipids

Cats have the ability to digest and utilize high levels of fat in their diets. High fat, low carbohydrate diets commonly improve the condition of feline patients suffering chronic diarrhea and most “premium” diets are formulated accordingly.

One gram of fat provides 2.25 times more calories (9 kcal/g) than 1 g of protein or carbohydrate (4 kcal/g). Fat is thus a concentrated source of energy and diets that are high in fat, although well tolerated by the animal, may promote obesity if not strictly rationed. Cats being fed high fat (± 20%) premium and super-premium diets are two to three times more likely to become overweight. On the other hand, cats being fed a diet containing around 10 % fat are 50 % less likely to be overweight. A recent study at the Veterinary School of Nantes confirmed those observations; neutered cats fed a 20 % fat dry food, gained more weight and accumulated significantly more body fat than control cats fed an otherwise similar 10 % fat diet.

Most cat owners tend to feed their animals free choice. A common belief is that cats are better than dogs at maintaining their body condition. The latest epidemiological studies no longer support this idea. If cats are offered a highly palatable, high fat, diet-free choice, they tend to overeat, especially if they are neutered. Although the prevalence of neutered cats presented to veterinarians ranges from 75 to 95 % depending on the country, a survey of 500 practitioners showed that while most of them were aware of the weight-gain predisposition of sterilized cats, only 10 % of them advised owners to reduce the fat content of diets fed to their neutered pet.

Essential fatty acids

All mammals require a diet that contains at least one essential fatty acid that they cannot synthesize de novo: linoleic acid from the omega-6 family. The essentiality of alpha-linolenic acid (omega-3 family) remains controversial in dogs and cats. While cats can elongate these fatty acids, their ability to desaturate them, particularly to produce arachidonate from linoleate is limited. Therefore, cats also need arachidonic acid in their diet. Diets deficient in arachidonic acid will induce in cats poor reproductive performances and insufficient platelet aggregation. The only practical dietary source of arachidonate has been animal fats and tissues particularly fatty acids from membranes. This is one of the reasons why people should be discouraged from offering exclusively vegetarian diets to cats.

There has been considerable recent interest in whether there is an optimal ratio of n-3 to n-6 fatty acids in the diet of normal cats. Eicosanoids derived from the n-6 fatty acids tend to be pro-inflammatory, whereas those derived from the n-3 fatty acids less so, or anti-inflammatory. In inflammatory conditions, it has been suggested that n-3 to n-6 fatty acid ratio should be increased but there has not been a clear definition of what is an optimal ratio for all physiological functions. Fish oil, richer in long-chains n-3 fatty acids would be a better source than vegetable oil such as linseed oil.

Carbohydrates

Although a diet of animal tissues contains very little carbohydrates, the cat is quite capable of digesting and assimilating sugars and starches present in foods. Thus while the cat appears to have evolved as a strict carnivorous, there is no nutritional basis for precluding a portion of the energy in the diet being supplied from carbohydrates, provided needs for all other nutrients are met. However, limited amylase activity in the pancreas and the small intestine of cats compared to dogs, may explain why some sensitive cats will not always tolerate high starch diets and why those individuals do better on higher fat diets.

Dietary fibers

Although not usually found in the natural diet of cats, dietary fibers are commonly present in commercial foods, mainly in expanded diets but also in some canned food. Dietary fibers have been shown in many species to have an important role on intestinal transit time, to balance the microflora and for the nutrition and health of the colon. Dietary fibers also play an important role on fecal volume and appearance. Fecal moisture is very much linked to fiber source; therefore, source of soluble fibers (beet pulp, soy fiber, oat bran, psyllium) might be of benefits in the prevention and treatment of constipation. Higher levels of fibers are recommended to reduce the energy content of the diet but will promote bulky feces. Insufficient fiber content will result in poorly formed and odorous feces.

Minerals and urinary calculi

Diet formulation, amount and balance of mineral elements in the food have marked effect on the formation of urinary calculi. The two most common calculi that occur in cats are struvite and calcium oxalate calculi. Before the 90’s, struvite (MgNH4PO4·6H20) uroliths were the most common causes of lower urinary tract diseases in cats. An alkaline urinary pH and high dietary magnesium are generally considered the most important factors in their formation. Urine pH is much more important, however, and struvite crystals formation is not possible at pH below 6.5. The ability of a diet to induce acidic urine depends on the ingredients used and the addition of acidifiers such as methionine, ammonium chloride and phosphoric acid. Animal proteins, corn gluten and digests promote acidic urine while most vegetable proteins and some mineral salts such as calcium carbonate promote alkaline urine. Urine acidification is not without potential toxicity. Excessive acid load can overwhelm the ability of the kidney to excrete protons and induce uncompensated metabolic acidosis. Chronic acidosis in cats increases urinary potassium losses, and could potentially slow growth, increase urine calcium excretion and promote bone demineralization. Acidifiers have toxicity on their own. Acidifying diets that have been tested are thus the safest way to prevent and manage struvite-related LUTD. Today, many commercial cat foods are formulated to induce acidic urine even if they are not marketed as acidifying diets. Acidifying diets are not recommended for kittens since they may interfere with bone formation. Acidifying diets might also not be ideal in older cats (> 10 years) since these animals are at higher risk for calcium oxalate uroliths and renal disease. Healthy kidneys are essential for proton excretion.

 In the last 15 years, the proportion of uroliths analyzed at the University of Minnesota Urolith Center and composed of struvite has steadily decreased whereas the percentage of calcium oxalate has increased. Although it has not been proven, this observation is attributed to the widespread use of acidifying diets that, aside from unmasking other causes of LUTD, could theoretically promote calcium oxalate crystals formation in sensitive animals. The pathophysiology of calcium oxalate crystal formation in cats is not understood and deserves further studies. Factors known in human beings and laboratory animals to stimulate their formation include: urine pH below 7.0, increased urinary calcium, oxalate and urate excretions, decreased urinary magnesium and citrate concentrations, and abnormalities or absence in proteins known to inhibit crystal formation. Calcium oxalate develops in older cats than those that develop struvite. No diet will promote the dissolution of calcium oxalate uroliths but based on the current knowledge and in order to minimize the risk of crystal formation, diets for mature and older cats should be formulated to induce higher urinary pH.

 The current recommendation is to avoid high dietary NaCl in feline acidifying diets to minimize urinary Ca excretion and therefore urinary Ca oxalate (CaOx) saturation. Recent studies in our laboratory, comparing commercial diets or diets differing only by their NaCl content, concluded that higher dietary NaCl intake increases urine output, which is beneficial against all forms of urolithiasis, and was not associated with increased CaOx saturation. This observation suggests that moderate increase of dietary NaCl might be of benefits in acidifying diets.

Vitamins

Vitamin A

It has long been appreciated that cats are unable to use the ß-carotene from plants as a source of vitamin A. Cats lack the enzymes required to cleave the carotene molecule to retinal. A continual diet of liver has been reported to produce skeletal changes such as exostoses of the spine in cats in countries such as Australia and Argentina where livers are from cattle grazing on pasture before slaughter. Liver is commonly used to produce digests or as an ingredient in cat foods explaining the high levels of vitamin A that are observed in some commercial foods. Studies designed to evaluate if high levels of vitamin A could be associated with health problems in queens showed that cats were quite resistant to vitamin A toxicity.

Vitamin D

For most animals, vitamin D is a conditional nutrient in the diet in that it is only when that animal does not receive exposure to sunlight that it becomes an essential nutrient. Dr J.G. Morris recently demonstrated the inability of kittens to synthesize vitamin D when exposed to sunlight or UV light. The explanation is that the 7-dihydrocholesterol (the precursor for vitamin D synthesis) is in very low concentration in cat skin. In the wild state cats, obtain sufficient vitamin D from prey. Although we know now that vitamin D is an essential nutriment in cats, the dietary levels already recommended in commercial foods will fulfill all their requirements.

Conclusions

As cats evolved eating a strict carnivorous (meat) diet, many of the enzymes required for the synthesis of nutrients present in meat (but not in omnivorous diets) became redundant. The activities of these enzymes have declined, as maintenance of redundant enzymes is an unnecessary energy cost for cats. Examples of such enzymes include those involved in the synthesis of arginine, EFA, and vitamin A. For other nutrients, the activities of enzymes remain elevated (high protein requirement) and result in substrates not being available for synthesis (vitamin D), or produce a change in the flux along a pathway away from nutrient synthesis (niacin, taurine). These enzymatic modifications presumably served cats well until very recent times when cats could no longer meet their nutritional needs from predation but had to rely on the consumption of foods that do not always contain the nutritional profile of prey.

Formulation of commercial cat food must take those peculiarities into account in order to fulfill the dietary requirements of cats, promote health and minimize the risks of deficiencies. As some diseases such as obesity, hepatic lipidosis, or lower urinary tract diseases have been associated to the diet in cats, formulation should be adapted to the most up-to date information in order to minimize their occurrence. Pet owners should also be correctly advised on how to feed these diets (e.g., free-choice or limited intake) for their particular animal (e.g., younger vs. older cats).

REFERENCES are AVAILABLE ON REQUEST


Back to Previous Page Print This Page Save This Page Bookmark This Page Go to the Top of the Page

Alternative Medicine
Anesthesia
Animal Welfare
Behaviour
Cardiology
Clinical Pathology
Dental Congress 1:1
Dental Congress 1:2
Dental Congress 1:3
Dental Congress 2:1
Dental Congress 2:2
Dental Congress 2:3
Dermatology
Emergency & Critical Care
Feline Endocrine & Infectious Dz
Feline Gastroenterology
 
Hepatobiliary Disease in the Cat
 
Feline GI Pearls
 
Feline Esophageal Disease
 
Cats with Chronic Diarrhea
 
Is Helicobacter A Problem In Cats?
 
Feline Constipation, Obstipation, and Megacolon
 
You are hereFeline Nutrition Update
 
Feline Pancreatitis
Feline Urology/Nephrology
Gastroenterology
Imaging
Infectious & Zoonotic Diseases
Management
Medicine
Neurology
Nutrition
Oncology
Ophthalmology
Pharmacology
Respiratory Medicine
Surgery & Sports Medicine
Surgery
Oral Presentations
Poster Presentations