Protocol for Success in Managing, Even Curing, Feline Diabetes

Protocol for Success in Managing,

Even Curing, Feline Diabetes

______________________________________________________________________

Published by permission of Dr. Hodgkins on FelineDiabetes.com^TM

This protocol consists of three indispensable parts: Proper diet for the obligatory carnivore diabetic, proper drug/hormone therapy (that is, the right insulin), and proper use of that drug therapy and that diet to restore the patient to normal pancreatic function.

First, some background on the evolution of the cat for context. Today’s domestic cat evolved from one or more small wild cat species in Africa and southern Europe. The environment in which these progenitor cats developed was vegetation sparse and small-animal-prey rich, causing this top-predator mammal to become dependant on meat, and meat’s primary energy nutrients, protein and fat, for sustenance. Over time, some of the pathways for carbohydrate metabolism that were developing to a high degree in herbivorous and omnivorous species in more carbohydrate-rich environments were discarded by the primitive cat. In fact, eventually this species so drastically rearranged its processes for dietary energy extraction that its metabolic systems began to use protein for energy at a constant, almost invariable rate, without the switches for up- and down- regulation of that protein “burn” (gluconeogenesis from amino acids) that is active in omnivores and herbivores. That is, the cat will use dietary protein for routine energy production at a high level EVEN in situations where dietary protein is very limited. Because of these evolutionary “choices” made long ago, the cat rapidly begins to consume its structural proteins for energy during starvation or protein deprivation of any other kind (e.g., protein-restricted diets). In short, the cat is a “carbohydrate cripple” with a huge protein dependency!

Given the forgoing, it is not at all surprising that we now find many of our feline patients fat, sluggish, and eventually, diabetic. For all of our good intentions in bringing the cat into our homes as a pampered pet, we have done the species a tremendous disservice in providing its members a diet far more appropriate for a cow in a feedlot than an obligatory carnivore. Because of the food technology of dry food production, dry cat foods are loaded with carbohydrate from cereal. This carbohydrate is required to allow the extrusion process to take place; dry pet foods are essentially breakfast cereal for pets with a little added meat meal for palatability. Further, because this cereal undergoes processing at high heat and pressure during extrusion, it becomes pre-digested and enters the pet's bloodstream essentially as sugar. Nothing in the cat's evolutionary development could possibly prepare it for a steady diet of this sugar laden "junk food". Note: not all cereals are created equal, of course. Some have much higher glycemic indices than others, meaning they cause a greater rise in blood glucose when consumed and digested. Perhaps the most offensive of all cereals used in pet foods is corn, (from which corn syrup is derived, giving a good idea of how much sugar corn actually contains). Because it is plentiful and cheap in this country, corn is one of the favorite dry pet food cereals used by the industry. Sadly, even the most expensive, so-called premium dry pet foods contain high amounts of this ingredient.

An additional consideration is the cat’s unique system of satiety signals from food. Logically, because the cat evolved in an environment rich in protein and fat, but deficient in carbohydrate, consumption of fat and protein evolved as the signal to the cat that it could cease intake. Consumption of carbohydrate, however, has a minimal effect on intake in the cat even as energy requirements are met and exceeded with this nutrient. Thus, not only is the cat relatively incapable of handling repetitive substantial carbohydrate loads of the kind represented by dry cat food, it is also unable to respond appropriately to that consumption with appetite satisfaction. The end result is cats that overeat, constantly flood their systems with glucose overloads, spiking repeated surges of insulin from their limited carnivore’s pancreatic reserve, and become obese. For a large number of cats, their metabolic systems eventually become overwhelmed by this unphysiologic chain of events and its unremitting stress on the pancreas, resulting in diabetes.

I. Diet

Because improper diet is the cause of type II diabetes mellitus in the cat, diet must be the foundation of the management of this disease. Although the veterinary profession has been conditioned to believe that high fiber dry diets are capable of assisting in the management of feline diabetes, the reality is that this disease has historically been extremely difficult to deal with BECAUSE of this mistaken belief. The practice of using dry form, high fiber diets for our diabetic patients is utterly in error. In fact, high fiber dry foods have two massive flaws. The first is the high amount of carbohydrate in them (no, they are not immune from the requirement of extruded foods for high cereal content) which promotes high blood glucose notwithstanding the fiber contained in them. These diets are usually "low fat" as well as high fiber and because of thus, much of the usual fat in the formula has been replaced with even more digestible carbohydrate than is present in regular formulas (in the highly mistaken belief that it is dietary fat that makes cats fat).

The second serious flaw is the high fiber itself. As an obligatory carnivore, the cat's GI tract is short compared with that of the dog or humans. During evolution, the cat's gastrointestinal tract adapted to the intake of calorie-dense, vegetation-poor foods by reducing its length and ability to undertake prolonged digestion of fibrous foods. High fiber foods ignore this fact, providing an unnatural burden on the feline GI tract that results in excessive system bulk and reduced nutrient absorption.

Therefore, to manage feline type II diabetes, the patient MUST be provided a diet that is high in protein, moderate-to-high in fat and ultra low in carbohydrate, especially carbohydrate from extruded cereals and those with high glycemic indices, like corn.

No feline diabetic should eat any type or brand of dry food. This includes Purina DM dry (a high carbohydrate, corn-containing formula with no relationship whatsoever to the canned version of this food) and Hills m/d dry (not only does this food contain corn carbohydrate, it also has increased fiber). Allowable foods include canned DM, Fancy Feast, and a number of other brands. For a comprehensive list of canned cat foods and their nutrient levels, see the following listing of most major canned foods: FelineDiabetes.com: Canned Cat Food Nutritional Content . Look for foods with low % of calories from carbohydrate.

Not only will a low carbohydrate canned food reduce the wide blood glucose swings seen in feline diabetics, it will also reduce the pathologic overeating seen in cats consuming dry foods that provide little or no sense of satiety.

II. Proper insulin

Protamine zinc insulin is, by far, the most effective form of insulin available for use in the diabetic cat today. Beef and pork insulin molecules (beef is closer than pork) are more closely analogous to endogenous feline insulin and give the greatest response to the lowest dosages in the vast majority of feline diabetics. It can be dosed at 12 hour intervals and, because canned cat food is supportive of low blood glucose from diet, PZI allows good control of the diabetic cat, far superior to that from NPH or Humulin insulins.

III. Blood glucose control strategy

It is conventional wisdom within the veterinary profession that hypoglycemia in the feline diabetic is to be feared more than any other eventuality. Thus, veterinarians inadvertently strive to perpetuate their patients' diabetes, not realizing that deliberately maintaining a patient's blood glucose in the hyperphysiological range insures that the cat will never recover from its disease. While hypoglycemic seizures are to be avoided, no question, it is not necessary to keep a patient's blood glucose above 200mg/dl, or even above 150, to accomplish this. Through its evolved physiology, the cat LIKES to operate at blood glucose levels below 100! In fact, if we could test our healthy patients without the "white coat effect" elevating their blood glucose levels in our clinics, we would realize that most cats are perfectly happy with BG levels around 60!). In nature, most of the cats' blood glucose is glucose produced by its liver from amino acids on an as needed basis. Large surges from dietary carbohydrate intake, well tolerated by omnivores and herbivores, are essentially unknown to the cat in the wild setting and clearly unwelcome as well.

A well known feline specialist at one of the large US veterinary teaching hospitals once observed to an audience that it was very easy to cause a transient diabetic state in the cat by infusing IV glucose solution. This is, in fact, quite true, and highly relevant to the logic of managing the chronic diabetic. Elevated blood glucose is either toxic or suppressive (or both) of the feline endocrine pancreas, a fact no doubt related to the almost vestigial nature of this function in a species that evolved with little need to process and store dietary carbohydrate.

Therefore, the objective of managing the feline diabetic is to assist the cat's endocrine pancreas to resume some or all of its prior function. This is virtually always possible in the cat that has been diabetic for a short period of time. As a matter of fact, brand new diabetics often respond to a change of diet alone, and never need insulin because the pancreas has not really gone "dormant" from chronic hyperglycemia at that point. Immediate relief from dietary glucose overload can allow immediate reactivation of the cat's own pancreatic capabilities. This cat, however, like its more chronic colleagues, will NEVER be able to consume high carbohydrate (dry) foods again for its entire life and its owners must understand this. Such a cat will become diabetic very quickly once again if its pancreas is stressed again by high sugar foods (or exogenous glucocorticoids, which are extremely diabetogenic in the cat!).

In the more chronic diabetic, diet alone will often not provide immediate cure. Those cats that have been diabetic a long time, especially those that have been "managed" with dry foods and insulin types other than PZI, the road to cure will be longer. This is only logical. The intoxication/suppression of the endocrine pancreas in these cats has been prolonged and severe, and in some cases there may be no residual function left at all. However, you will not be able to predict with certainty merely from the duration of the cat's disease process whether or not a particular cat can been cured. We have seen cats with relatively long histories respond well, in time (several months), to proper regulatory efforts. Even those that never come completely off insulin due to the chronicity of their disease and its improper management are much healthier and more clinically normal on a low carb diet and PZI insulin at the right dose than they have been previously.

For those cats that do not become euglycemic with diet alone, the objective of PZI insulin therapy is to bring the cat into a normal range of blood glucose (80-130) and keep it there! I cannot emphasize this enough. Because continual hyperglycemia perpetuates the pancreatic suppression/toxicity that has caused the diabetes in the first place, cure can only happen if the highly effective PZI tool is used to titrate the diabetic cat into the normal range for glucose in this species. In fact, the 80-130 range is a bit high for the cat at rest without excitement. Most cats operate when relaxed between 50-80! As long as you make increases in your insulin dose to achieve these lower BG numbers gradually, you will not cause seizures in your patients. In dozens of cats that I have put through this protocol, I have never caused a single one to seizure, despite taking many below 100 mg/dl. You must give up the fear you have been taught about taking a diabetic cat into the normal BG range, or your patients will always be diabetic. They will be healthier diabetics on step one and step two alone, but without step three, and maintenance of step three for several weeks or months until the patient demonstrates the ability to take over production of insulin endogenously, the pancreas will never be released from its suppressed/intoxicated state and will not being to function again. On the other hand, with step three added, 75-80% of your reasonably healthy male diabetics will resume normal endocrine pancreatic function and resume normal lives without drug support.

TA note about female type II feline diabetics: type II diabetes is harder to induce in the female, whether the induction agent is diet, or exogenous glucocorticoids or both. This is why 80% or more of our diabetic patients are male, but the exact pathophysiological explanation for this is unknown. It is a fact that female diabetics do not respond to this protocol by achieving cure as routinely as do males. Certainly the difference in susceptibility to diabetes and the resistance to proper treatment for diabetes must be related to the same physiologic difference between males and females, but until we know what that is, the prognosis for cure is poorer for females than males. I have cured females, however, and even when they do not cure, they are much healthier overall when they are managed with this protocol than otherwise.