Feeding the indoor cat for health and longevity

As obligate carnivores, feline physiology explains why the diets of indoor cats need to model those of their wilder relatives. 

As obligate carnivores, cats require animal protein. Domestic and wild felines have minimal ability to convert plant material into nutrients, relying instead on animal tissue in their diets to provide taurine and other essential amino acids, arachidonic acid, and preformed vitamin A. Feeding the indoor cat for optimal health necessitates a food that comes as close to the wild or feral feline diet as possible — ones that’s high in moisture and animal proteins, and low in carbohydrates. Recent research from UC Davis School of Veterinary Medicine supports these requirements. An examination of wild or feral cat diets showed a combination of rodent and small bird carcasses. The dietary analysis revealed 67% water content, 62% crude protein, 11% crude fat, 14.8% ash and 2% carbohydrate (nitrogen-free extract), with an average prey energy content of 3,929 kcal/kg DM. Interestingly, the diets of these wild cats exceeded the recommended allowances for fat, crude protein and essential amino acids set forth in the National Research Council’s (NRC) 2006 publication, Nutrient Requirements of Dogs and Cats.1,2

Water, dehydration and cystitis

Cats are less sensitive to the sensation of dehydration than dogs are, and have a very weak thirst drive; therefore, they have a tendency to consume smaller volumes of water. However, the wild cat’s normal eating behavior may also play a role in water consumption. These felines tend to hunt and consume from six to ten small rodents and birds throughout the course of a day, nourishing their bodies periodically with small amounts of moisture from their prey.

Cats are capable of producing very concentrated urine to conserve water. However, concentrated urine can be linked to inflammation of the bladder wall and a concentration of minerals leading to cystitis, crystal formation and subsequent urinary stone formation. When cats are dehydrated, it takes longer for them to restore their water balance by drinking alone, further evidence that supports their physiological need for dietary sources of moisture. If we want to nourish the indoor cat adequately, we need to give him foods high in moisture.

Dietary protein and amino acid needs

Cats have a higher dietary protein requirement, and a particular need for dietary sources of amino acids. Required taurine comes from the tissues of the prey they consume. In the wild cat diet study, for instance, the combination of rodents and small birds had a taurine concentration of 0.92 +/- 0.33 g/16 g N, which is above the NRC recommendation.1,2 Taurine is an essential amino acid; cats cannot produce it from dietary sources of cysteine and methionine. Necessary for heart, eye and immune function, it is highly concentrated in meats and organs, particularly the heart, as well as seafood. There is little to no taurine in plant material, milk or eggs, so it must be obtained from meat proteins.

Cats are also vulnerable to a deficiency of arginine, an essential amino acid. The combination of rodents and small birds in the wild cat diet study had an arginine concentration of 5.63 +/- 0.46 g/16 g N, also above the NRC recommendation.1,2 Even one meal without arginine leads to severe hyperammonemia. Catabolism of the high quantities of meat protein in carnivore diets leads to a large production of nitrogen, which needs to be converted and excreted as urea via the urea cycle. Arginine is necessary for this urea cycle conversion to occur. Without arginine, free urea and ammonia rapidly build up in the blood, leading to severe tremors, weakness, vomiting, ataxia and eventually coma and death. Fortunately, most to all meat-based diets have adequate levels of arginine.

Unique vitamin and mineral needs

Cats are unable to convert the amino acid tryptophan to the B vitamin, niacin; as such they require more dietary niacin than other animals. They are also unable to convert beta-carotene, found particularly in orange-colored fruits or vegetables, into the active form of vitamin A, retinol. The enzyme necessary to convert beta-carotene into retinol is underactive in the feline. Additionally, cats have a limited ability to convert 7-dehydrocholesterol in the skin to vitamin D, also necessitating a dietary animal source of this vitamin.

Unique glucose balance and carbohydrate metabolism

There are two ways to get glucose into a kitty’s body: one is via a dietary source of carbohydrates or sugars, and the other is through a conversion process called gluconeogenesis. The latter occurs when the amino acids from dietary proteins are converted into glucose. There is little ability to conserve amino acids in the body, so they need to be used throughout the day, either as a component of protein synthesis or converted to glucose. Healthy cats tend to have consistent blood glucose concentrations, as carnivores maintain a constant state of gluconeogenesis throughout the day, with a slight increase in blood glucose levels immediately after eating.

What happens if a cat is subjected to high dietary carbohydrates?

Remember, the combination of rodents and small birds in the study mentioned above had a carbohydrate concentration of only 2%.1 Kibble is notoriously high in carbohydrates because it is necessary to form and hold the kibble together during the extrusion process. Commercially available dry kibble diets for cats have up to 60% carbohydrates (mean 41%). The carbohydrate is broken down into glucose via pancreatic enzymes. The glucose is then absorbed and transported via the portal vein to the liver. Within the liver, the glucose is phosphorylated into the active metabolizable glucose-6-phosphate. The phosphorylation process requires two enzymes: glucokinase, which becomes active in high blood glucose levels, and hexokinase, which becomes active in low blood glucose levels.

Cats have minimal activity rates of glucokinase and high activity rates of hexokinase. Glucokinase in the cat also cannot be upregulated or increased during times of high blood glucose. Compared to dogs and humans, cats have a reduced capacity to metabolize large amounts of glucose, resulting in higher blood glucose concentrations after a carbohydrate load. Cats also have an extended postprandial period of eight to 15 hours compared to two to three hours for humans and three to six hours for dogs. Feline physiology favors glucose formation via gluconeogenesis, not glucose spikes produced by dietary carbohydrates.

When cats eat high-carbohydrate dry kibble diets

The cat’s liver does not have the enzymes to convert high blood glucose into the active metabolic form of glucose (glucose-6-phosphate). Consequently, after a cat eats kibble, his blood glucose remains high — much higher than an omnivore’s blood sugar, and for a longer period of time. Carnivores cannot rapidly respond to these spikes in blood sugars and are subject to longstanding hyperglycemia.Obesity from high glucose levels has reached epidemic levels in our cats, a reflection of the trend in people. Chronic high blood glucose associated with obesity leads to a cascade of physiologic events. High blood glucose signals the release of insulin from the pancreas. With time, the pancreas will eventually lose the “blood glucose battle”, which leads to an insensitivity of insulin receptors in the tissue. The buildup of hyper-produced and released insulin leads to hyperinsulinemia, which leads to abnormal fat deposition, obesity and constant unrelenting hunger. The vicious cycle continues, as the addiction to carbohydrates grows. The obese “carbaholic” cat is created by a chronic species-inappropriate diet consisting of high dietary carbohydrates.

As any pet parent of an obese “carbaholic” kitty knows, it is difficult to convert these cats to a species-appropriate, high-meat protein, low-carbohydrate diet. They refuse to eat. The pancreas is in overdrive producing insulin, and the tissue that is insulin-resistant is screaming for energy. So the cat is hungry, doesn’t feel well, and frankly, is unwilling to buckle to any dietary change.

To keep our indoor cats happy and healthy their entire lives, we must honor their physiology. Their nutritional needs are unique and their welfare requires a commonsense approach. Recommending a high-moisture, high-meat protein diet low in carbohydrates for your feline patients is imperative to their lifelong health.

References

1 Kremen NA, Calvert CC, Larsen JA, Baldwin RA, Hahn TP, Fascetti AJ. “Body composition and amino acid concentrations of select birds and mammals consumed by cats in northern and central California”. J Anim Sci. 2013;91(3):1270–1276.

2 National Research Council. Nutrient Requirements of Dogs and Cats — Animal Nutrition Series. Washington, DC: The National Academies Press, 2006.

American Diabetes Association. “Diagnosis and classification of diabetes mellitus”. Diabetes Care. 2014;37(Suppl 1): S81–S90.

Appleton DJ, Rand JS, Sunvold GD. “Insulin sensitivity decreases with obesity, and lean cats with low insulin sensitivity are at greatest risk of glucose intolerance with weight gain”. J Feline Med Surg. 2001;3(4):211–228.

Bradshaw JWS. “The evolutionary basis for the feeding behavior of domestic dogs (canis familiaris) and cats (felis catus)”. J Nutr 136:1927S-1931S, 2006.

Case LP, Daristotle L, Hayek MG, Raasch MF, Canine and Feline Nutrition Third Edition, Mosby, 2011.

Crenshaw KL, Peterson ME. “Pretreatment clinical and laboratory evaluation of cats with diabetes mellitus: 104 cases (1992–1994)”. J Am Vet Med Assoc. 1996;209(5):943–949.

Elliott KF, Rand J, Fleeman LM, et al. “A diet lower in digestible carbohydrate results in lower postprandial glucose concentrations compared with a traditional canine diabetes diet and an adult maintenance diet in healthy dogs”. Res Vet Sci. 2012;93(1):288–295.

Goossens MM, Nelson RW, Feldman EC, Griffey SM. “Response to insulin treatment and survival in 104 cats with diabetes mellitus (1985–1995)”. J Vet Intern Med. 1998;12(1):1–6.

Gottlieb S, Rand J. “Managing feline diabetes: current perspectives”. Vet Med (Auckl) 2018; 9: 33-42.

Hewson-Hughes AK, Gilham MS, Upton S, Colyer A, Butterwick R, Miller AT. “Post-prandial glucose and insulin profiles following glucose-loaded meal in cats and dogs”. Br J Nutr. 2011;106(Suppl 1): S101–S104.

Morris JG, Rogers QR. “Ammonia intoxication in the near adult cat as a result of a dietary deficiency of arginine”. Science 199(4327):431-432, 1978.

Yu S, Rogers QR, Morris JG. “Absence of salt (NaCl) preference of appetite in sodium-replete or depleted kittens”. Appetite 29: 1-10, 1997.

Zini E, Hafner M, Kook P, Lutz TA, Ohlerth S, Reusch CE. “Longitudinal evaluation of serum pancreatic enzymes and ultrasonographic findings in diabetic cats without clinically relevant pancreatitis at diagnosis”. J Vet Intern Med. 2015;29(2):589–596.

IVCVX Bottom Banner

LEAVE A REPLY

Please enter your comment!
Please enter your name here