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]