Protocol for Success in Managing,

Even Curing, FelineDiabetes




© 2004  Elizabeth Hodgkins DVM, Esq.


Published by permission of Dr. Hodgkins on FelineDiabetes.comTM



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


            First, some background on the evolution of the cat forcontext.  Today’s domestic cat evolved from one or more small wild catspecies in Africa and southern Europe.  The environment in which these progenitor cats developedwas vegetation sparse and small-animal-prey rich, causing this top-predatormammal to become dependant on meat, and meat’s primary energy nutrients,protein and fat, for sustenance.  Over time, some of the pathways forcarbohydrate metabolism that were developing to a high degree in herbivorousand omnivorous species in more carbohydrate-rich environments were discarded bythe primitive cat.  In fact, eventually this species so drasticallyrearranged its processes for dietary energy extraction that its metabolicsystems 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 inomnivores and herbivores. That is, the cat will use dietary protein for routineenergy production at a high level EVEN in situations where dietary protein isvery limited.  Because of theseevolutionary “choices” made long ago, the cat rapidly begins to consume itsstructural proteins for energy during starvation or protein deprivation of anyother kind (e.g., protein-restricted diets). In short, the cat is a “carbohydrate cripple” with a huge proteindependency!


Given the forgoing, it is not at all surprising thatwe now find many of our feline patients fat, sluggish,and eventually, diabetic. For all of our goodintentions in bringing the cat into our homes as apampered pet, we have done the species a tremendousdisservice in providing its members a diet far moreappropriate for a cow in a feedlot than an obligatorycarnivore. Because of the food technology of dry foodproduction, dry cat foods are loaded with carbohydratefrom cereal. This carbohydrate is required to allowthe extrusion process to take place; dry pet foods areessentially breakfast cereal for pets with a littleadded meat meal for palatability. Further, becausethis cereal undergoes processing at high heat andpressure during extrusion, it becomes pre-digested andenters the pet's bloodstream essentially as sugar. Nothing in the cat's evolutionary development couldpossibly prepare it for a steady diet of this sugarladen "junk food". Note: not all cereals are createdequal, of course. Some have much higher glycemicindices than others, meaning they cause a greater risein blood glucose when consumed and digested. Perhapsthe most offensive of all cereals used in pet foods iscorn, (from which corn syrup is derived, giving a goodidea 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 usedby the industry. Sadly, even the most expensive,so-called premium dry pet foods contain high amountsof this ingredient. 



Anadditional consideration is the cat’s unique system of satiety signals fromfood.  Logically, because the cat evolvedin 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 couldcease intake. Consumption of carbohydrate, however, has a minimal effect onintake in the cat even as energy requirements are met and exceeded with thisnutrient.  Thus, not only is the catrelatively incapable of handling repetitive substantial carbohydrate loads ofthe kind represented by dry cat food, it is also unable to respondappropriately to that consumption with appetite satisfaction.  The end result is cats that overeat,constantly flood their systems with glucose overloads, spiking repeated surgesof insulin from their limited carnivore’s pancreatic reserve, and becomeobese.  For a large number of cats, theirmetabolic systems eventually become overwhelmed by this unphysiologicchain of events and its unremitting stress on the pancreas, resulting indiabetes.


I. Diet

Because improper diet is the cause of type II diabetesmellitus in the cat, diet must be the foundation ofthe management of this disease. Although theveterinary profession has been conditioned to believethat high fiber dry diets are capable of assisting inthe management of feline diabetes, the reality is thatthis disease has historically been extremely difficultto deal with BECAUSE of this mistaken belief. Thepractice of using dry form, high fiber diets for ourdiabetic patients is utterly in error. In fact, highfiber dry foods have two massive flaws. The first isthe high amount of carbohydrate in them (no, they arenot immune from the requirement of extruded foods forhigh cereal content) which promotes high blood glucosenotwithstanding the fiber contained in them. Thesediets are usually "low fat" as well as high fiber andbecause of thus, much of the usual fat in the formulahas been replaced with even more digestiblecarbohydrate than is present in regular formulas (inthe highly mistaken belief that it is dietary fat thatmakes cats fat).


            The second serious flaw is the high fiber itself. Asan obligatory carnivore, the cat's GI tract is shortcompared with that of the dog or humans. Duringevolution, the cat's gastrointestinal tract adapted tothe intake of calorie-dense, vegetation-poor foods byreducing its length and ability to undertake prolongeddigestion of fibrous foods. High fiber foods ignorethis fact, providing an unnatural burden on the felineGI tract that results in excessive system bulk andreduced nutrient absorption.


Therefore, to manage feline type II diabetes, thepatient MUST be provided a diet that is high inprotein, moderate-to-high in fat and ultra low incarbohydrate, especially carbohydrate from extrudedcereals and those with high glycemic indices, likecorn.


No feline diabetic should eat any type or brand of dryfood. This includes Purina DM dry (a highcarbohydrate, corn-containing formula with norelationship whatsoever to the canned version of thisfood) and Hills m/d dry (not only does this foodcontain corn carbohydrate, it also has increasedfiber). Allowable foods include canned DM, FancyFeast, and a number of other brands. For acomprehensive list of canned cat foods and theirnutrient levels, see the following listing of mostmajor canned Canned Cat Food Nutritional Content . Look for foods with low % of calories fromcarbohydrate.


Not only will a low carbohydrate canned food reducethe wide blood glucose swings seen in felinediabetics, it will also reduce the pathologicovereating seen in cats consuming dry foods thatprovide little or no sense of satiety.


II. Proper insulin


Protamine zinc insulin is, by far, the most effectiveform of insulin available for use in the diabetic cattoday. Beef and pork insulin molecules (beef iscloser than pork) are more closely analogous toendogenous feline insulin and give the greatestresponse to the lowest dosages in the vast majority offeline diabetics. It can be dosed at 12 hourintervals and, because canned cat food is supportiveof low blood glucose from diet, PZI allows goodcontrol of the diabetic cat, far superior to that fromNPH or Humulin insulins.


III. Blood glucose control strategy


It is conventional wisdom within the veterinaryprofession that hypoglycemia in the feline diabetic isto be feared more than any other eventuality. Thus,veterinarians inadvertently strive to perpetuate theirpatients' diabetes, not realizing that deliberatelymaintaining a patient's blood glucose in thehyperphysiological range insures that the cat willnever recover from its disease. While hypoglycemicseizures are to be avoided, no question, it is notnecessary to keep a patient's blood glucose above200mg/dl, or even above 150, to accomplish this. Through its evolved physiology, the cat LIKES tooperate at blood glucose levels below 100! In fact, ifwe could test our healthy patients without the "whitecoat effect" elevating their blood glucose levels inour clinics, we would realize that most cats areperfectly happy with BG levels around 60!). Innature, most of the cats' blood glucose is glucoseproduced by its liver from amino acids on an as neededbasis. Large surges from dietary carbohydrate intake,well tolerated by omnivores and herbivores, areessentially unknown to the cat in the wild setting andclearly unwelcome as well.


A well known feline specialist at one of the large USveterinary teaching hospitals once observed to anaudience that it was very easy to cause a transientdiabetic state in the cat by infusing IV glucosesolution. This is, in fact, quite true, and highlyrelevant to the logic of managing the chronicdiabetic. Elevated blood glucose is either toxic orsuppressive (or both) of the feline endocrinepancreas, a fact no doubt related to the almostvestigial nature of this function in a species thatevolved with little need to process and store dietarycarbohydrate.


Therefore, the objective of managing the felinediabetic is to assist the cat's endocrine pancreas toresume some or all of its prior function. This isvirtually always possible in the cat that has beendiabetic for a short period of time. As a matter offact, brand new diabetics often respond to a change ofdiet alone, and never need insulin because thepancreas has not really gone "dormant" from chronichyperglycemia at that point. Immediate relief fromdietary glucose overload can allow immediatereactivation 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 mustunderstand this. Such a cat will become diabetic veryquickly once again if its pancreas is stressed againby high sugar foods (or exogenous glucocorticoids,which are extremely diabetogenic in the cat!).


In the more chronic diabetic, diet alone will oftennot provide immediate cure. Those cats that have beendiabetic a long time, especially those that have been"managed" with dry foods and insulin types other thanPZI, the road to cure will be longer. This is onlylogical. The intoxication/suppression of theendocrine pancreas in these cats has been prolongedand severe, and in some cases there may be no residualfunction left at all. However, you will not be able topredict with certainty merely from the duration of thecat's disease process whether or not a particular catcan been cured. We have seen cats with relatively longhistories respond well, in time (several months), toproper regulatory efforts. Even those that never comecompletely off insulin due to the chronicity of theirdisease and its improper management are much healthierand more clinically normal on a low carb diet and PZIinsulin at the right dose than they have beenpreviously.


For those cats that do not become euglycemic with dietalone, the objective of PZI insulin therapy is tobring the cat into a normal range of blood glucose(80-130) and keep it there! I cannot emphasize thisenough. Because continual hyperglycemia perpetuatesthe pancreatic suppression/toxicity that has causedthe diabetes in the first place, cure can only happenif the highly effective PZI tool is used to titratethe diabetic cat into the normal range for glucose inthis species. In fact, the 80-130 range is a bit highfor the cat at rest without excitement. Most catsoperate when relaxed between 50-80! As long as youmake increases in your insulin dose to achieve theselower BG numbers gradually, you will not causeseizures in your patients. In dozens of cats that Ihave put through this protocol, I have never caused asingle one to seizure, despite taking many below 100mg/dl. You must give up the fear you have been taughtabout taking a diabetic cat into the normal BG range,or your patients will always be diabetic. They will behealthier diabetics on step one and step two alone,but without step three, and maintenance of step threefor several weeks or months until the patientdemonstrates the ability to take over production ofinsulin endogenously, the pancreas will never bereleased from its suppressed/intoxicated state andwill not being to function again. On the other hand,with step three added, 75-80% of your reasonablyhealthy male diabetics will resume normal endocrinepancreatic function and resume normal lives withoutdrug support.


TA note about female type II feline diabetics: type IIdiabetes is harder to induce in the female, whetherthe induction agent is diet, or exogenousglucocorticoids or both. This is why 80% or more ofour diabetic patients are male, but the exactpathophysiological explanation for this is unknown. Itis a fact that female diabetics do not respond to thisprotocol by achieving cure as routinely as do males. Certainly the difference in susceptibility to diabetesand the resistance to proper treatment for diabetesmust be related to the same physiologic differencebetween males and females, but until we know what thatis, the prognosis for cure is poorer for females thanmales. I have cured females, however, and even whenthey do not cure, they are much healthier overall whenthey are managed with this protocol than otherwise.