Diabetes and Obesity: Preventable Epidemics

Now, contrast the formulation and production of dry cat foods with the formulation and production of canned or "wet foods." The starch requirement that extrusion places upon dry pet food production is absent in wet foods. Pâtés, even chunked, sliced, or grilled meats, go perfectly well into a sealed can that is then sterilized in a high-heat retort. Happily, high meat formulas are highly palatable for cats, who recognize such ingredients as appropriate foods for their nutritional needs, which they usually eat happily without additional palatability enhancers added.¹ Thus, canned foods have macronutrient profiles that are high protein, moderate fat and low carbohydrate, because this is the nutrient profile of meat-based food that will not be extruded and will not require palatability enhancers. This is quite different from the macronutrient profile of dry foods, which are slave to the food technology of extrusion and the resulting need for intense palatability enhancement with "sugar coatings" of fermented digest post production. The ingredients and macronutrients of the different forms of cat food are dictated by the requirements of food technology, not the science of feline nutrition. To this day, not one person at any of the major or minor pet food companies has ever questioned the wisdom of feeding diets that are 30-50% pre-digested carbohydrate to an obligatory carnivore, and our cats have paid the price for that negligence.

 

Many pet owners believe that commercial pet foods are safe and efficacious to feed to their pets because they have been "feeding trial tested" and shown to be complete and balanced by this method. The AAFCO statement on many pet foods bears testament to the fact that the contents of the can or bag have undergone some kind of feeding trial that guarantees that the food in the container is good for your pet. This statement is extremely misunderstood by most pet owners and misleads them into believing that only good can come of feeding the product on which this statement appears. To illustrate this problem, let's go back in recent history.

 

In approximately 1988, a young cardiology resident at the University of California at Davis by the name of Dr. Paul Pion noticed something rather interesting. One of his feline patients, a cat he was treating for congestive cardiomyopathy, had an extremely low serum taurine level. Taurine is an essential amino acid in the cat (meaning it cannot be synthesized in sufficient quantities by the cat to meet its ongoing needs and must be supplied in the diet), known to be required for proper eye and cardiac function in this and many other species. Dr. Pion's patient was fed an exclusive diet of a "high quality" premium commercial canned cat food, which should have supplied all of the taurine this cat required. After all, the food was "feeding trial tested" and shown to be complete and balanced for all life stages in these feeding trials. Surely this cat's heart disease was not due to consumption of a taurine-deficient diet?

 

Over the months following his initial observation, Dr. Pion supplemented his original patient's diet with taurine and began to investigate other clinical cases of feline congestive cardiomyopathy. To his amazement, Dr. Pion discovered that virtually all of the cases he studied had low taurine levels in their bloodstream, and many of them improved dramatically, even returned to normal, when supplemented with taurine in addition to their regular diets, which were always canned commercial pet foods. Most of these cats were fed diets that had been "feeding-trial-tested" and shown to be complete and balanced for the appropriate life stage by this method.² How could foods produced by the "best" pet food manufacturers and tested according to the most stringent AAFCO guidelines be the direct cause of such pathologic deficiency in pet cats?

 

The answer, although not immediately evident, became clear over the first few months of Dr. Pion's investigation. The taurine in the implicated diets, often tested in the laboratory as adequate for the health of cats, was somehow not available to those cats when consumed in those diets. The processing of the canned formulations in the retort somehow "inactivated" the taurine contained in the foods so that it tested as adequate using laboratory methods, but in the "ultimate laboratory," the cat itself, the dietary taurine was not properly recognized and utilized. If this were the case, however, why didn't the feeding trials of these foods disclose this terrible flaw? Why? Because the vaunted feeding trials of which the companies and AAFCO are so proud are of such limited duration, usually no longer than 6 months, that only severe inadequacies and acute toxicities would ever be disclosed through them.

 

Further, had cats on a six-month feeding trial of a taurine-deficient diet developed congestive cardiomyopathy during the test period, it is extremely unlikely, prior to the problem discovered by Dr. Pion, that anyone would have recognized the condition as diet-related. Much more likely, any cat that developed cardiomyopathy during the test would have been diagnosed as having a congenital/hereditary defect and removed from the test cohort. Most cats would not become sufficiently deficient to develop overt clinical signs during the feeding trial. Thus, deficient diets were produced, feeding-trial-tested, and marketed for many years, causing the deaths of many cats, before a fortuitous turn of events and the keen observations of a young veterinarian allowed the problem to be identified and corrected. The pet food companies and their "rigorous testing for safety and efficacy" allowed the development of a fatal disease in thousands of cats, and that problem had to be discovered and corrected through the efforts of an outsider who was not even a nutritionist. The "scientific teams" within the implicated companies themselves were stunned by the discovery.

 

The presently prevalent nutritional diseases of obesity and diabetes share stunning similarities with the taurine-deficiency disease of feline congestive cardiomyopathy.³ True enough, the disease associated with dietary taurine was a disease of nutrient deficiency, while diabetes and obesity in cats are diseases of nutrient excess. Both cardiomyopathy of taurine-deficiency and obesity/diabetes of carbohydrate excess are diseases of insidious onset that can be attributed by non-astute or biased observers to chance or heredity. All are diseases that existed, and in the case of diabetes/obesity, continue to exist, despite assurances from nutritionists at major pet food companies and AAFCO that the diets causing them were, or still are, complete and balanced and perfectly healthful for cats. Both taurine-deficiency-cardiomyopathy and carbohydrate-excess-obesity/diabetes were made possible by inadequate laboratory testing of pet foods endorsed widely by pet care professionals, along with the pet food industry's failure to consider the effects of ingredient processing on ingredient nutritional value. Further, these diseases, and perhaps others yet to be uncovered in the future, are the result of an unfathomable failure by those most knowledgeable about the peculiar metabolic machinery and nutritional needs of the cat to properly consider those factors. By and large, the pet food industry has treated the cat like a "small dog," because it was expedient and seemed so harmless for so long.⁴