As I pointed out last week, feline heart disease is more prevalent than previously thought. We continue this week on the role of nutrition in dealing with these conditions.
Dilated Cardiomyopathy (DCM)
With the nutritional changes made to commercial cat food following the 1987 research revelation that linked taurine deficiency with feline heart disease, the diagnosis of DCM has significantly decreased. However, one cat population is still at significant risk.
Cat metabolism requires large amounts of taurine, an amino acid-like molecule. Unfortunately, this species has limited ability to convert other amino acids or molecules into taurine. Animal muscle tissue is rich in taurine, so for this carnivorous species that is not problematic. It is a problem, however, for cats fed a vegetarian diet. Plants contain little taurine, so homemade vegetarian diets need generous supplementation.
But it is not just the homemade vegetarian diets that pose a risk. A 2004 study found that two commercial feline vegetarian diets contained only 18-24 percent of the daily recommended allowance for taurine.
Regular veterinary exams are important for all animals, but for cats on vegetarian diets it is especially important. Routine assessment of blood taurine levels should be part of that evaluation. DCM is preventable and treatable with diets containing adequate amounts of taurine.
Hypertrophic Cardiomyopathy (HCM)
Presently there are no recommended dietary recommendations for cats diagnosed with early, non-clinical HCM. Recommendations generally address the needs of the various stages and treatments of congestive heart failure that result from this genetic disorder.
Adequate protein is essential for HCM at all stages. These patients often lose muscle mass from the condition as well as from the poor appetite often associated with heart conditions and the drugs used to treat them. Thirty-eight percent of cats with heart disease have histories of anorexia. Highly palatable (i.e., better tasting) foods that are rich in protein can slow or reverse the wasting that occurs for these patients. Switching from dry to wet is often helpful, but in some cats the reverse is true. Higher dietary fat also increases palatability.
Omega-3 fatty acids
Congestive heart failure (CHF) is associated with increased levels of pro-inflammatory chemicals that actually increase muscle breakdown and directly cause anorexia. Eicosapentaenoic acid, or EPA, and docasahexaenoic acid, DHA, are omega-3s that are known to decrease inflammation and reverse muscle loss. Fish oil is rich in preformed EPA and DHA, so conversion from other omega-3s in not required. Canola and flaxseed oils do not contain preformed EPA and DHA and require conversion from shorter chain omega-3 fats. Cats lack the ability to effectively make that conversion, so fish oil supplementation is the preferred choice for cats with HCM.
Unlike humans, the role of antioxidants in feline heart disease in undefined. However, reactive oxygen molecules, or “free radicals,” are known to increase as CHF progresses. The tissue damage created by these molecules increases the detrimental inflammatory response that intensifies CHF. Antioxidants neutralize these molecules and reduce that inflammatory response. Vitamin C and E are the most commonly used in cats and dogs. Vitamin C should be avoided in cats with a history of urinary calcium oxalate crystals or stones. (See Vitamin C and Calcium Oxalate Stones)
Salt restriction is not necessary in the early stages of HCM. Only as congestive failure progresses is consideration given to restriction. Even then recommendations are only for moderate restriction. Severe restriction can cause metabolic shifts that actually are harmful and counterproductive to the cat’s health. The amount and stage to initiate salt reduction is still a topic of feline cardiac research.
Potassium and Magnesium
As with dogs, treatments for CHF (diuretics, blood pressure medications) may cause alterations in blood potassium and magnesium levels that can affect heart and nerve function. Restriction or supplementation may be necessary to avoid such complications. Routine monitoring of blood electrolytes are essential in these patients.
Although no association between vitamin deficiency and feline heart disease has been made, cats with HCM tend to have lower blood levels of B6, B12, and folic acid. B-vitamins are water soluble and eliminated in the urine. Cats on diuretics for their CHF experience greater B-vitamin urinary loss and have greater requirements than healthy animals. B-vitamin supplementation is suggested with these patients.
The other nutritional interventions discussed with heart disease in dogs have not been studied as extensively in cats, so results are primarily anecdotal and subjective. With greater recognition of the prevalence of feline heart disease, I anticipate more research in this area, which will lead to a greater array of nutritional strategies.
Dr. Ken Tudor