The key to understanding the interrelationship between diet physiology and the evolutionary history of the ferret lies in its digestive anatomy. Species tend to be either carnivores (flesh eaters) or herbivores (plant eaters). Some carnivores eat so little plant material that they are called "dedicated," "primary," or "obligate" carnivores. These animals have structural changes in the teeth, stomach, intestines, and even in the amount and types of secretions necessary for digestion which makes digestion of plant material difficult if not impossible. The ferret is such an animal; highly adapted to a flesh diet, it has almost NO ability to digest plant materials other than simple sugars. The teeth chew poorly (designed to cut), the stomach is simple, small and empties fast, the intestines are short and have a high transit speed, there is no caecum and the digestive glands are designed to secrete the hormones, digestive enzymes, bile acids and pancreatic enzymes and hormones for a flesh-based diet. One of the more striking changes in ferret diseases is a recent increase the the number and severity of insulinomas. In a review of the last 130+ years of published literature on ferrets and ferreting, insulinomas--or even their symptoms--are so infrequently mentioned that they appear primarily a modern phenomenon. Arguments that the symptoms were overlooked, misinterpreted or ignored are obtuse to anyone who has gone through the material and seen the dedication spent describing the ferret's medical needs and diseases. Looking at modern veterinary literature as a chronological ruler for the incidence and severity of insulinomas, it would appear that they first start becoming a serious problem in the early to mid 1980s, they seem to usually occur in older ferrets (3+ years) and they are most common in North America. These data are a red flag for either an environmental disease, or a genetically-predisposed disease requiring an environmental trigger ( a classic disease of ageing). Since the problem is on the rise, it suggests a correlation to some other factor which is also increasing in popularity. Since the disease appears to be primarily a North American phenomenon, it is probably the result of some environmental factor which also tends to be found in the region. I do not think the disease is strictly environmental because it does not always effect all members of a household and there is some anecdotal evidence it runs in families, especially among sibling groups. This is highly suggestive of a genetic predisposition for insulinomas, triggered by an external environmental factor, not unlike a similar linkage found among some Pacific Islanders and Native Americas for diabetes. IF insulinomas have some sort of environmental trigger, THEN the identification of that trigger might be found in the differences between areas of low and high disease rates, such as between North America and Europe. If the trigger is indeed environmental, then there should be correlation of factors between time (the chronological comparison) and space (the geographic comparison). There does seem to be such a correlation. Like with changes in caging, diet has also significantly changed in North America since the 1970s, with a shift from prepared wet foods, natural meats and animal carcasses to various processed dry foods, primarily extruded and expanded kibbles. To be honest, there are other changes as well (which will be discussed later), but the shift in diet is paramount because of ties between pancreatic disorders and diet in other species, as well as because the kibbled diet is so different from the evolutionary diet of the ferret. There are other possibilities, such as viral or bacterial infections, genetic disease, or some other environmental factor, but since diet is most probable, it should be considered first. It requires 50-60% of starchy plant carbohydrates to be included in the mixture to make kibble. Kibbles are, in essence, a biscuit or cake, dried to a percentage of moisture lower than found in bone to retard spoilage. Carbohydrates are long chains of sugars strung together; when digested, they result in a mass of complex sugars that are further broken into simple sugars. These sugars are dumped into the blood stream, increasing blood sugar and pancreatic response. The digestion of fats, however, results in fatty acids when are then metabolized or stored via the liver. Only when they are broken down as sugar do they enter the blood stream, requiring pancreatic response. I cannot prove the hypothesis that the constant exposure to unnatural levels of carbohydrates are the trigger for pancreatic problems at the moment, but it is supported by the improvement seen when switching ferrets from a kibbled to a high protein, meat based diet (commonly supported in the veterinary literature). These suggestions may not prevent or cure pancreatic disease, but they certainly can impact quality of life. 1. Resist the temptation to consider kibbled foods as the "proper" food. Wet foods, pelleted foods and balanced meat combinations are all good alternatives having less carbohydrates in the diet. A good alternative is to use kibbles as a supplement to these foods. 2. Recognize that sometimes the best diets are marred by the fact that they result in a smellier litter box. It is unethical to shorten a ferret's life (or even decrease its quality) simply because your nose is offended. Get over it; and change the box more often. 3. If you have no choice but to feed kibble, then eliminate carbohydrate rich snacks. Its just gas on the fire. 4. Talk to your vet about meat-based diets for your ferret. Some ferrets have medical problems which would preclude a dietary shift, and your vet probably has valuable suggestions, especially for older ferrets. 5. Read some of the published literature on natural diets for cats and dogs. The same principles apply to the ferret, only more so because the ferret is so highly evolved as an obligate carnivore. Bob C and 16 Mo' Fleshmeisters [Posted in FML issue 2976]