Between family, the Ferret Project, work, and medical issues, it seems
as if I have to get an appointment just to sneeze, much less read all
my emails, various ferret lists, and my professional correspondence
(including journals still needing review). In truth, I hadn't read an
FML for about a month. You will understand then why my interest was
peaked to see a "please read" email copied and posted a dozen times in
order to get my attention. It did. I opened it to discover scores of
copied posts from the FML regarding, a) my remarks made in Portland in
2007, b) a lot of stuff about the raw v. kibble diet, and c) a plea to
say something.
Holy cow! I can be off the FML for weeks and *still* get stuck in the
middle of a controversy! I was at a loss for words, but you know me;
I found some. I sent the stuff, with my response post, to a good
friend for an "outsider evaluation" to tell me if my response was
over-reactive. I was told it was and that it was clear from posters
on both sides of the controversy that I was seen as an authority. I
was advised to delete my initial response and write another. There is
nothing better than a third party to evaluate a post to determine if
it is reactionary or simply a strong debate. More people should do it.
The 2007 Portland symposium was an interesting one. While driving out,
I contracted severe food poisoning that rather violently reared its
ugly head Saturday morning. It didn't care that I had a presentation
later that day. However, friends and vets helped me with the worst of
the symptoms and the IFC kindly moved presentations around to give me
a better chance of talking without the embarrassment of vomiting in
public -- or worse, and believe me there was much worse. Sunday was no
better, and by Monday I was in a local hospital where I spent most of
the week in treatment. During that time, I was on IV morphine, the
result being my memory is a bit spotty. Nonetheless, I still have my
notes and original powerpoints and surprisingly I can recall the
presentations I was able to attend or give.
Not that it matters; my opinions -- and remarks -- haven't changed
very much since then. However, I do think my remarks -- as presented
recently on the FML -- are taken a bit out of context in that they
report a conclusion without offering the explanation for why it was
made. In this case, the explanation is as important as the conclusion.
Please, allow me to clarify for the benefit of all.
I try to be extremely unbiased and honest about my research.
Consequently, I tend to err on the side of the angels when drawing
conclusions. If I am not sure why a ferret is doing something, I will
say my opinion is suppositional and lacks evidence. If there is not a
direct link between two phenomena, then I do not report it as such. For
example, there *is* a direct link between insulinoma and carbohydrate
consumption, as well as between neutering and adrenal disease, but
there is *not* a direct link between kibble consumption and tartar
formation.
One reason is because ferret saliva lacks some of the enzymes found
in human saliva that are responsible for initiating the breakdown of
carbohydrates. This is why ferrets don't get caries; their saliva is
mostly a lubricant for bolting food particles rather than a
pre-digestive agent for starches. While ferrets can still form the
bacterial mats necessary for the initial formation of plaque, which
progresses to tartar, it is at a much-reduced rate because the saliva
is not converting starches into oral sugars.
Buildup of tartar in ferrets is mostly due to a lack of mechanical
abrasion, such as achieved when teeth are plunged through fur, skin,
fat, muscle, bone, and all the intermediate connective tissues when
killing and eating prey. This is generally true for all carnivores,
especially for hypercarnivores such as ferrets. When a carnivore
consumes whole prey, the food itself acts as a toothbrush to cleanse
the teeth from the crown facets to below the gum line. Kibble does not
perform the same function, not in ferrets, and not in cats or dogs
(all three species have roughly a 90-95% periodontal disease rate). In
ferrets, the reason is because the teeth are extremely thin with a
chisel-like point. There is not a kibble made that can brush down the
sides of the teeth, much less under the gum line, to cleanse them in a
manner similar to when eating a whole carcass. The kibble breaks on the
tooth's cutting facets and is simply swallowed. There is no mechanical
cleansing.
There is a second factor that complicates matters. Whole prey is juicy,
not sticky, so little remains in the ferret's mouth to initiate the
formation of plaque and tartar. Ferrets and polecats that consume whole
prey have extremely minor rates of tartar buildup. You can't say the
same for ferrets eating kibble. It doesn't clean teeth and because
tiny particles of kibble get trapped in the mouth and turn to sludge,
it becomes a contributing factor in tartar formation. The same thing
happens when a ferret eats a soft or liquid diet. It is astounding to
see the exaggerated rates of tartar buildup in ferrets on soft foods;
they are the absolute worst tartar buildup and periodontal disease
rates I've found. Kibble does the same thing, albeit at a much slower
rate.
So, kibble is not *directly* responsible for periodontal disease. It is
a contributing factor in ferrets that are not given veterinary dental
cleanings or tooth brushings. Understand how kibble can be a
contributing factor and not a direct cause? Because the direct link for
periodontal disease is the lack of mechanical cleansing of the teeth,
not the food. Excepting whole prey, all the food really does is change
the rate of the disease, not initiate it.
So, if someone says I said kibble is not responsible for dental disease
(excluding dental attrition), they are reporting a truth. Still, unless
the entire story is told, it leaves the reader with the impression my
opinion is that kibble is a non-factor in dental disease, which it is
decidedly not. It is not a cause of periodontal disease, but it
certainly exacerbates the problem.
I have to point out my dental data is empirical and forms a continuum
in the shape of a normal distribution, or "bell curve." There are
several implications inherent in these types of continuums, the first
being that tartar buildup starts at nothing and continues without
interruption to 100 percent. This makes division points arbitrary; I
simply use standard deviations to form categories that artificially
define specific points on a continuum, but they are not real divisions.
Second, because it is a bell curve, the majority of ferrets score
somewhere near the middle of the curve, with fewer ferrets seen towards
the two extremes. In other words, most ferrets show an average amount
of tartar, while less show below average or above average, and very
few show rare or excessive amounts. My bell curve is a bit skewed
towards the periodontal disease side, but it is a normal distribution
nonetheless.
Another implication is you can predict in generalities (or
populations), but not in specifics (or individuals). While the vast
majority of ferrets and polecats that eat a whole prey diet have little
tartar, some do. Likewise, some ferrets consuming an all-liquid diet
might not show any tartar. You can accurately predict at the population
level, but not so accurately with individuals.
Lastly, there *are* other factors involved. A person might claim their
ferrets eat nothing but kibble and lack tartar, but a close inspection
of husbandry might reveal the ferrets eat cheweasels, foamy fries,
n-bones, chicken wings, might have regular dental care, or
ferret-show-related tooth scraping. Some ferrets are fabric or toy
chewers. Some ferrets might be stressed or ill. Without an evaluation
of all possible factors, any given example is nothing more than an
anecdotal observation. These stories could certainly be true, but they
are not considered empirical evidence. I have counted at least a dozen
such factors that complicate prediction of tartar. This doesn't mean
there is a problem with the overall conclusions; it simply means it is
hard to predict which ferrets will have periodontal disease and how
much. Like with the diseases of smoking, predicting periodontal disease
rates is best at the population level.
end of part 1
[2-part post combined. BIG]
Part 2
Some of you might ask why I am so confident of my findings if there
are so many factors involved. The reason is because I have refused to
publish early, insisting on waiting until I have reached statistical
redundancy. That means I have counted samples until percentages no
longer change; they have reached redundancy. Further counting is
redundant. When you reach redundancy you have empirical evidence your
sample -- regardless of size -- matches the greater population. It
*includes all* possible variations, except perhaps those that are
extremely rare, but they have no real impact on the numbers anyway.
Pointing out exceptions to a redundant sample has no value; such
exceptions are already included in the sample. Redundant samples
accurately reflect the population from which they were derived.
With a redundant sample of ferrets with dental disease, I can construct
a bell curve that will show numbers of ferrets affected by periodontal
disease, as well as how many will have rare amounts, moderate amounts,
average amounts, more-than-normal amounts, and excessive amounts of the
problem. Those numbers will be accurate, even if I cannot accurately
predict how an individual ferret might be impacted.
By now you probably realize the various factors involved in periodontal
disease are best characterized as "risks" or "probabilities." If you
feed a liquid diet and don't brush the ferret's teeth, they have a high
risk for periodontal disease. The risk is above average for a ferret
eating kibble with no other dental care. For a ferret eating a whole
carcass diet, the risk is low. So, to put it in better perspective,
even though the lifetime risk of being hit by lightning has been
calculated as 1/80,000, people still get hit and killed. Even if risks
are low or high, there are always exceptions. Those exceptions *do not*
falsify the risks. Showing a handful of ferrets having a horrible diet
but escaping periodontal disease does *not* prove such a connection
does not exist, especially when the sample in question has been tested
to redundancy.
Perhaps this is the time to point out my research is already published
in the vet literature, and I've lectured on it to vet students, as well
as presented the information to the NAVC (North American Veterinary
Conference). An independent study of ferret dental problems by a group
of dental vets has confirmed my results, with the exception of fracture
rates. Other vets are starting to publish similar findings as well.
Which brings up the raw v. kibble diet. I have a major paper on the
subject that is currently being written and reviewed. It will be
difficult to post in the FML because of the inability to publish
illustrations, requiring the use of language to get a point across.
This makes the posts long and involved. I am considered using my
Facebook Notes to publish the posts so I can include illustrations. In
the past, Bill has temporarily posted pictures for people to download,
but in the long run, the posts and the illustrations are orphaned from
one another. I'll probably post them in both locales.
The need for illustrations is important because trying to explain
how kibble damages teeth without showing photos of the injuries is
extremely difficult, and perhaps unbelievable. The pictures are
valuable in showing the direct effects of eating kibble. The same is
true when discussing diet. A single illustration can be worth many
paragraphs of descriptive language. I hope to start posting on diet
before the end of the year. Until then, I'll just make a few comments
about this whole 'mess' (pun intended...mess? Place to eat? Mess hall?).
I never feed live animals to my ferrets. I buy mice, rats, chicks,
and other types of foods that have been killed and frozen. This is a
personal choice. I can find no nutritional advantages to feeding live
animals to ferrets. I simply cannot do it. I can feed a dead animal to
a ferret.
Feeding raw is not the same as feeding whole carcass. A whole carcass
includes everything; skin, fur, bone, muscle; you name it. Raw could
be just a chicken wing. Feeding a raw diet might or might not be
nutritionally complete depending on the exact food and proportions
offered. Carnivores evolved consuming whole carcasses and they can
be considered nutritionally complete. A whole carcass diet meets or
exceeds all AAFCO (Association of American Feed Control Officials)
requirements for all life stages, so it is minimally as good as *any*
commercial diet that meets AAFCO requirements.
Most of the other points can wait for the dietary posts; this mini-tome
is already too long. However, there is one final point I wish to make.
I simply do not understand why people are not allowed to explain their
viewpoints without it degenerating into personal attacks. It is simply
beyond my understanding. I think it would be a safe bet if I said I
have probably visited more ferret people and seen more ways to keep
ferrets than anyone else on the planet. I've taken care to document
those differences -- and similarities -- in order to try to figure out
the best way to keep our little pets. I think I finally have a good
handle on it. If my past actions are an indication of what I will do in
the future, it is likely I will educate, explain, and allow people to
take what they will from the advice offered. My name-calling will be,
well, nonexistent. Well, except for the CF&G, but then they deserve it.
Although I am quick to defend others or my work, I don't typically
defend myself. Nor do I typically attack others without some extreme
degree of outrage or provocation. That is not to say I don't
occasionally vent; but Bill and I have a long history of him telling me
a post is personal, and of me willingly pulling it from publication. It
doesn't happen very often and usually because of long-term frustration.
The truth is, the overlying principle to my philosophy is not so much
of a grand sense of ethics, but more of a decidedly strong dislike of
censorship. Censorship can be a good thing when used to save lives, but
generally speaking, it is *not* a good thing for any other purpose.
When it comes to discussions of ferret husbandry, it is *not* good
because it not only prevents the free discussion of ideas, but it also
quiets other voices that might be able to give insight. One of those
silenced voices might hold the answer we all need, but they have been
intimidated -- censored -- by the outrageous voices of a few "idea
bullies" who want no other viewpoint but their own been known or
discussed.
I don't buy into the idea that censorship will help to save ferret
lives. I would expect substantial and repeatable evidence offered for
me to accept it. In an open forum, where people can express their
viewpoints without fear of personal attack, a free discussion is
illuminating, not dangerous. Problems caused by "idea-bullying" are
reflected in natural history; the more variation in a species, the
better it can respond to change. Those species with little variation
tend to fail to respond to change and go extinct. The more ideas we
have, the better we can respond to problems in our ferrets. You don't
have to accept other viewpoints and you can certainly debate them, but
you can do both without ever resorting to a personal attack. Ever.
There are a lot of ways to enforce censorship, including interrupting
people, throwing out numerous references to prove a position,
name-calling, shutting down a discussion, or even off-list personal
emails. They are *all* designed to silence the voice of the person by
making it difficult for them to express their ideas, so they are all
forms of censorship. I've been all over the world and have met
thousands of ferret people; I've yet to met one that didn't know
something I yearned to learn. Like pure cream, good ideas "float" to
the top of open and fair discussions. You can only have those types
of talks when censorship is prohibited. Just my 2-cents.
Bob C
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[Posted in FML 6896]
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