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The following is the complete
and very lengthy series of Ferret Mailing List posts on adrenal
disease. Written by Bob Church. The e-mail address shown is
very likely no longer valid.
Date: Sun, 1 Feb 1998 03:50:08 -0600
From: Bob Church <c620213@SHOWME.MISSOURI.EDU>
Subject: Bob C: Adrenal Stuff
Ok. folks, I'm running a bit behind on finishing
the adrenal post, mainly because the data conflicts so much with a
couple of papers that I've read. I hesitate to post something that
may be obviously biased, so I am setting on the stuff and pondering
it. I will post the result no later than next weekend, although, like
I said, the results were somewhat different than what I expected.
That's the problem with being a scientist; the
ethics of reporting values which are apparently biased without attempting
to explain or correct for the problem. I've just been considering
reasons for the difference, that's all. I will report the findings,
I'll probably just put a lot of disclaimers into the post.
One other problem is the post will be quite long,
so I'll probably have to post it directly to Bill (and I know his
middle name, naa naa naa) so he can post it as space permits. Its
way longer than 125 lines so be prepared for a long read (I can never
figure out the 125-lines thing anyway because I use a file size method
that doesn't translate in my brain. Sort of like I can use metrics
or miles, but I have a hard time translating them. Well, I *know*
a pound is .45359237th of a kilogram. Just stuck in my head, like
pv=nrt and stuff like that. Just don't ask my phone number...)
As for *why* the adrenal reports were so biased?
The FML is *not* composed of typical ferret owners, its that simple.
Rather I should say, the people who reported the adrenal stuff are
not typical ferret owners. A very large part was reported from ferret
shelters or people who adopted ferrets that had a history of illness,
neglect or malnutrition. That means the sample was not random. What
I'm trying to do is see if I can correct for the skew, but it's not
looking favorable. As for any correlations, well, if I can't correct
for the skew, then any correlations would be as good as "96% of all
Americans who die in accidents are wearing clothing, therefore clothing
causes accidents." The skew can hide the cause-effect relationship.
Everyone knows its nudity that causes accidents.
Bob C and 20 MO Accidental Biters.
------------------------------
Date: Tue, 10 Feb 1998 05:13:22 -0600
From: Bob Church <c620213@SHOWME.MISSOURI.EDU>
Subject: Bob C: Adrenal Post, Part Uno.
Ok, folks, here are the official results and commentary,
with a few extra tidbits thrown in regarding sampling and observer
biases. Up front, I do not trust much of the data gathered from FML
members--not because of the dishonesty of FML readership, but because
of how *good* we are (I'll explain later). The post quite long, so
I've broken it into several parts for bathroom reading over the next
few evenings. I'll say some things some of you will *NOT* want to
hear (which included me), but please hold off flames or other comments
until the entire series is posted. It will save us all a lot of space
and time because what offends you today may be answered tomorrow.
What you will be reading is a combination of FML
data, compiled with about 20 scientific journal/book sources. Because
of the need for brevity, those sources will not be individually cited,
but will be added as a bibliography at the end and you can look it
up yourselves. Disclaimer: this is *not* a scientific study, and as
such, I would never submit it for publication. Do not assume it carries
the weight of papers that have undergone rigorous juried review. Also,
the FML format limits the length of posts, cannot carry graphics,
and is read by people of various educational levels. To write a paper
to the level of a scientific journal would require about 8 FMLs dedicated
to nothing but the subject, with 5 or 6 graphic attachments to demonstrate
the statistics. It is not possible to do such work, and if it were
possible to get the space and add the graphics, without being condescending,
few readers would have the necessary background to follow the paper
properly. Don't be insulted by this; I can fix a car but don't speak
"Autoshop," mathematics gives me a headache, and I will never be as
smart as the average European because even though I can read in several
languages, I can't hardly speak English good. The language of physiology
is a difficult one to learn, and no one should be embarrassed because
they don't speak or understand it.
With that in mind, let me give the bad news first.
1) Treatment of Adrenal Disease. I'm sorry to say,
*no* treatment but one has *any* long term effect on the disease,
and that one is only really effective if when the adrenal disease
starts early in the life of the ferret. Surgery is the only effective
treatment. No chemical treatment, such as Lupron, Lysodren, or Prednisone,
has been shown to significantly extend the ferret's life after the
initial onset of the disease, nor have they been proven to do anything
more than mask or slow the progress of the disease. No environmental
treatment has withstood vigorous scientific examination and still
result in positive results. Homeopathic remedies have not shown *any*
ability to extend the ferret's life, nor do they show any more than
a moderate lessening of symptoms. In the significant majority of cases,
any type of treatment, other than surgery, only offers superficial
and limited results.
HOLD OFF COMMENTS UNTIL THE SERIES IS DONE, PLEASE!
I know these statements are going to cause some disagreement, but
I will offer explanations in the next posts that will answer many
of your questions. Please wait, and we can hash this out at the end.
Ok?
The average reported lifespan of ferrets that did
not have ANY treatment or surgical intervention was 1 year +/- 6 months.
The same times were reported for *ALL* chemical treatments, including
Lupron, Lysodren, or Prednisone. If the adrenal disease had an onset
when the ferret was under or about 3 years of age, surgery gave the
ferret 3 years +/- 6 months. However, if the adrenal disease had an
onset after 4-5 years of age, that survivorship dropped down to 1.5
+/- 6 months. In all cases, the average length of life was longer
if surgery was performed, however, the risk of sudden death was significantly
higher in ferrets older than 4-5 years.
Chemical treatments were reported to partially
or completely return the ferret to working order, with partial or
complete return of hair as well as an improvement in other symptoms.
This was reported about the same in all age classes of ferrets. The
interesting thing about the chemical treatments, or even of homeopathic
treatments, was the degree of observed improvement was always higher
than the degree of actual improvement. In other words, if a ferret
had an improvement in hair growth, it was seen as "the ferret getting
better," even though the course of the disease was the same as if
nothing was being done and the ferret died within a year or so. This
is best illustrated by a comment mailed to me, "The vet said the situation
was hopeless, that the ferret could not survive surgery, and it could
die as early as in six months....But placed on [homeopathic] medicine,
the ferret lived another 14 months!!" 14 months is within the "mortality
window" of untreated adrenal disease, so there is no evidence the
treatment worked at all. What was seen as the improvement was a return
of most of the hair and decrease in aggression, which may have occurred
anyway, but such those type of improvements in no way should be taken
as evidence that microscopic changes took place within the adrenal
gland that altered the disease. Maybe it did, but there is *no* factual
evidence.
I want to emphasize this. In an extensive search
through all ferret-related papers since 1985, not a single published
study could demonstrate marked improvement of the ferret by any means
other than surgery. That is not so say such studies don't exist, nor
am I saying such results are not possible. What I am saying is nothing
has been published, other than a few articles with poor sample sizes
(or other methodological problems).
Surgery resulted in remission of symptoms in most
cases, but in those cases where surgery was not going to work, it
was immediately seen as a "non-improvement." If the ferret was left
untreated, the disease would kill the ferret between 6 months to 1.5
years, with the average death being about a year into the disease,
so on average (worst-case), the ferret got an extra 6 months or more
because of surgery, and in the best case, years of extra life.
Personal comments: I am a great believer in "less
is better" when it comes to medical care. Personally, I would be dead
six times over if not for the surgeries I have placed myself through.
Before I took on this self-assignment, I was essentially anti-surgery
for the older ferrets, supporting surgery only for those cases with
an early onset. For ferrets under 4 years of age, I believe surgery
is the only option; do it as soon as possible after blood tests have
confirmed the disease. There are a number of risks involved in such
surgical procedures, but they only result in a small number of serious
complications; the sudden death rate seems to be under 5% from what
I can dig up, which is fantastic considering the difficulties of operating
on such a small species. From the descriptions of ferrets dying during
surgery, they seem to be of two types; either they were extremely
ill ferrets with massive tumor involvement, (which suggests a late
diagnosis or multiple-organ involvement), or the deaths seem to be
anesthetic-related, such as from anesthesia-induced shock (happens
even in people). In the former, sudden death should be expected because
of the ferret's condition. In the later, such events are unpredictable.
In either case, unless some other proof exists of malpractice, these
deaths should be considered part of the risks of surgery, and accepted
as such without blame being assigned to doctor or owner.
For ferrets older than 5 years, there does not
seem to be any significant difference between chemical treatment nor
non-treatment. Surgery can add about 6 months on average to the lifespan.
I question the poor results from late surgery but cannot find any
outside stats to contradict them. I suspect the surgical results would
be better if the adrenal disease was of a primary onset rather than
a secondary manifestation (like when the ferret has already had an
adrenal removed). I just don't have enough data to be able to say
that ferrets over 5 years of age who get adrenal disease for the first
time have better surgical results than those who have already had
adrenal surgery. I strongly suspect it is so, but cannot say for sure.
Because of that, I recommend that if your ferret is otherwise healthy
and this is their first onset of adrenal disease, do the surgery.
As for the second onset, discuss all options with your veterinarian
and make your decision to best suit the needs of your ferret. You
have to weigh the additional 6 months or so with the surgical risks,
knowing the end results will not be much different.
Now, this is all very clinical and non-emotive,
which is what is needed for this type of discussion. If I wanted to
push my belief system, I would be arguing *against* surgical procedures.
I have been (mostly) convinced by looking at all available data; I
have refused to comment on this (or share this) with anyone associated
with the problem so no one could question the ethics of the study.
In other words; I can into this thinking I could find better options
than surgery. I found I was wrong.
This is *not* to say existing chemical or homeopathic
remedies (or future ones) will not eventually replace surgical treatment
in many cases. What I have found is a lot of research is needed in
those areas. It is also not to say that, for some, such treatments
actually result in improvement of symptoms, or even reversal of the
disease, but statistically, they are less than 10%. That means, 90
ferrets will take the treatment and will *not* be any better for it,
while 10 ferrets will show a reversal or improvement of symptoms.
The problem is, are these reversals due to the medicines or because
of the animal having a spontaneous remission of the disease? Like
I said, rigorous examination of the facts needs to be done, which
means, boys and girls, ferrets will die in scientific research. There
will be a price to pay for medical advances against this disease.
But there *is* something we can all do to help.
The problem with any research is getting the samples.
I am studying the differences between wild and domesticated forms
of the ferret, which could not be done if caring individuals have
not donated (and still donate) their ferrets to the cause. I'm not
going to kill an animal for its skeleton, so this allows some people
to have the satisfaction of helping determine ferret origins, and
I get what I need as well. The same is true here. If you choose to
treat your ferret with chemical or homeopathic remedies, at the ferret's
death donate whatever is needed to a researcher who is willing to
compile the medical and histological data. Perhaps Dr. Williams can
make some suggestions here. Special handing of specimens *must* be
done, but your vet can do it for you. As far as *I* am concerned,
if you want to promote any procedure other than surgery, you have
an ethical responsibility to provide proof of your claims, which is
tied up in the carcass of your dead and beloved pet. Until these types
of studies are done, THERE WILL NEVER BE PROOF that chemical or homeopathic
remedies (including light treatment) have any substance in the treatment
of ferrets suffering adrenal disease. Like it or not the proof is
in the pudding, so put up or close the trap.
I have myself in enough hot water until the next
post, which will cover why some forms of treatment seem to help (when
they don't really). Following posts will discuss the treatment of
symptoms, the USA-World adrenal difference, some genetic-environmental
questions, the question of early neutering, and finally, a summary
about everything. They will come every-other day, mostly because they
are difficult to write and I have school to think about. As I said,
please hold off all questions and flames until the series is finished;
write your questions down, but hold off on sending them until I finish
this thing, ok?
Bob C (C as in Custer) and 20 MO Wild Frettchens
------------------------------
Date: Thu, 12 Feb 1998 17:16:38 -0600
From: Bob Church <c620213@SHOWME.MISSOURI.EDU>
Subject: Bob C: Adrenal Post Nummer Zwei
I mentioned there seemed to be at least two different
things going on in ferrets, resulting in adrenal disease. Mind you,
there may actually be more, but from the data collected and the stuff
in print, I think right now all you can safely say is more than one
factor lurks behind this disease. So what is the implication of "more
than one?"
Before we answer, let's address the question of
what can *cause* adrenal disease. One of the first steps to any scientific
investigation is to try and limit the study to the possibilities,
rather than the "but what ifs..." So, making the assumption that adrenal
disease is initiated by some sort of abnormal growth within or adjacent
to the adrenal gland, what basic things could cause it?
The list could include genetics, environmental
pollutants, diet, body condition, stress, chance, or even that the
disease is a species "weakness" (like how specific diseases tend to
be more common in certain animals than others). While some people
may be convinced that only one of these is the "real" reason, remember
I said the disease appeared to have at least two different manifestations.
Now do you see the implication? It suggests at least two factors may
be responsible. These two factors could be linked, or they could be
independent, but only scientific testing will ever prove the relationship--or
the reasons--one way or another.
I believe there is a genetic component involved;
those that kept track of their kits noticed adrenal disease sometimes
ran in family lines. The statistics are very poor for this because
few breeders care to follow the babies they pump out. This is a shame,
because it is quite conceivable that vigorous and healthy hobs and
jills may be spreading a recessive trait within the population. This
is what all the hoopla about blood lines is all about, as well as
the "Marshall Farms Hypothesis," (being that MF ferrets are predisposed
to adrenal disease). If you accept the idea that non-American ferrets
have a very low incidence of adrenal disease, its quite easy to point
the finger at the DNA and blame it, when in fact there may not be
any relationship at all and the reason could be because of some other
factor within the US and Canadian populations.
For a moment, lets assume it is genetics. Do MF
ferrets have a higher proportion of adrenal disease than other ferrets?
Not if the people who sent data are to be trusted. About half of the
ill ferrets did not come from MF at all. Assuming MF supplies about
half of the ferrets for the pet market, if they were more prone to
adrenal disease, there would have more cases reported in proportion.
The reported statistics suggests parity; in other words, it seems
as if all "brands" of ferrets are equally susceptible in contracting
the disease. (I don't know what the actual percentages regarding how
many MF ferrets are produced compared to other breeders, nor do I
suspect anyone does because few breeders report their kit placement.
If you disagree with my assumption that 50% of ferrets are MF, then
by all means provide a substantiated source). One thing that has struck
me is the apparent inability of people to look past what the numbers
*are*, and see what they *mean*. For example, suppose 100 ferrets
are MF and 100 from other sources. 20 ferrets get adrenal disease
and about half are MF. That is parity because all populations contract
the disease equally. But what if 150 ferrets are MF and only 50 from
other sources and out of 20 cases, 15 are MF and 5 are other? Well,
that's STILL parity, but it appears MF ferrets get the disease more
than others; after all, its 15 to 5 right? The result is many people
point out the majority of adrenal cases occur in MF ferrets, but they
never correct for the proportionality of breeder demographics. And
even if Path Valley, MF, and all the other major breeders opened their
books to our inspection, it would still be useless until you figured
out how many ferrets were coming from unnamed hobby breeders.
The underlying assumption behind the idea that
New World ferrets get adrenal disease in higher proportions than other
ferrets is that some sort of founder's effect or breeding bottleneck
has taken place. In other words, if true, then some breeders have
inbred their ferrets so much that a genetic mistake has become visible.
This looks good on paper, but I don't buy it for many reasons, especially
two major ones. First, look around you; you see albinos, sables, silvers,
dark eyed whites, and so forth. Body sizes are small to large, whippet,
standard and bulldog. The amount of variation within the USA ferret-line
suggests inbreeding is not a problem. Remember the old biological
axiom; the older the species, the more variation, the older the genera,
the more species, and so forth? Of course the exceptions are lines
that are dying out, but that is not a problem in our furry mustelids.
We have *LOTS* of variation. If inbreeding is a problem anywhere,
it would be minor and essentially isolated. Support for this contention
comes from there being absolutely *NO* significant difference in the
numbers of one type of coloration or of body type being predisposed
towards adrenal problems. Albinos had adrenal problems about as frequently
as sables. I only had 87 reports of coloration, so obviously the sample
is small and better investigation may find such a link....maybe.
I also think the idea is flawed simply because
the ferrets in the USA came from Great Britain and Europe, precisely
where the ferrets in New Zealand and Australia came from. Those populations
tend to follow the basic European lead in lack of adrenal disease.
Remember, we are assuming accounts of rare adrenal disease are factual,
and without contrary evidence such assumptions are valid. I also have
to say that in reading dozens of European ferreting books published
during the last 80 years, every medical ailment from blackheads to
distemper to swollen prostates to torn nails is discussed, but significantly,
no mention of a class of symptoms that could be interpreted as adrenal
disease is mentioned. These "ferrets and ferreting" books include
three from Germany, one from France and 17 from Britain. I've noticed
the same pattern in American ferret books; the mention of adrenal
disease only dates back slightly more than a score of years ago. Like
I said, interesting. Considering the slow acting nature of the disease,
if it was a common problem, it would have been mentioned in one of
these books.
The same is true in the veterinary literature.
I scoured every possible source, from data bases to biological abstracts
to the journal indices to books. Nothing in the laboratory papers,
nothing in the literature *UNTIL* about a score of years ago, and
those reports were almost exclusively American in origin. This lends
great support to foreign claims that the disease is largely an phenomenon
of the Americas. This is not a claim that should be ignored nor dismissed.
Remember this for later.
Back to the idea of founder populations in the
USA/Canada, Australia and New Zealand. Modern day populations in all
three countries had origins in initial founding colonies that date
to the turn of the century. In Australia and New Zealand, except for
a handful of exceptions, the present populations are essentially direct
descendants from those founding ferrets, and adrenal disease is rare.
In the USA, because of the ratting industry from the 1880s to the
1920s, the initial populations were supplanted several times from
fresh European stock. Now, understand, founder effects take place
because a breeding restriction took place which shifted *EXISTING*
gene frequencies, or introduced a new mutation into the breeding pool;
if it isn't in other populations, then it must have been "invented."
Now, this begs the following two questions. If the problem preexisted,
why hasn't it shown up as much in non-New World ferrets, especially
those with similar founding populations? And if it is a New World
specific mutation, why is only now showing up and not 40 years ago?
This is the trouble. Ever try to introduce a new
trait into a population? It takes time; considering the existing range
of variation in body types, coloration, color patterns, and sizes,
there is virtually no possibility that such a trait could have become
established in such a large population is such a short time; if everyone
looked about the same or the variation was limited, weeelll maybe.
Of course, this is assuming the trait is recessive, which it has to
be because more than 70% of you stated the trait does not effect all
siblings in a birthing, and if it were dominant, it would. (Of course,
the jill could have been bred to more than one male, but that is not
common in USA breeding practices, and induced ovulation makes it basically
a moot point). So, if adrenal problems are genetic, it must be something
brought in with the original founding ferrets that only affected USA
populations, or something that started within a few generations of
the founding of USA populations.
But Bob, didn't you say you thought adrenal disease
had a genetic component? Yes I did. The truth is, I'm beginning to
wonder if the disease doesn't parallel a similar situation in some
forms of human diabetes. In Native Americans, diabetes is quite common,
but in earlier populations it was never manifested. So a group of
people lived in the Americas for 12,000+ years, and diabetes was rare.
Europeans come over, teach the locals how to eat better food, and
the locals respond with obesity and diabetes. In this case, there
is an demonstrated underlying predisposition for the disease, but
without the proper environmental factors, the disease never comes
out.
Its the old "nature-nurture/genotype-phenotype"
debate. And it makes perfect sense. Why is human cancer so difficult
to control? Because, in many cancers you don't get cancer unless you
have the predisposition AND are exposed to an environmental stimuli.
That is why some smokers get lung cancer and others merely die from
emphazema or heart disease. Smoking is the environmental component,
but some studies have shown that a genetic component is present as
well. Remember the last post (and the top of this one) where I said
the adrenal problems seem to have more than a single causality? This
would go a long way in explaining why more than 60% of you said your
adrenal ferret was currently in or came from a shelter. This suggests
some sort of commonality that is causing this predisposition to manifest
itself. What if the environmental component (if indeed this is the
case) was something that was common in the USA/Canada, but rare in
Europe, Australia and New Zealand?
Could this help explain 1) why adrenal disease
is so common in the New World; 2) why, with the introduction of USA
practices, adrenal disease seems to have been lately increasing in
Britain; 3) why the disease appears to be common in animals exposed--in
mass--to similar environments, such as in shelters or mass groups
in pet stores; and 4) why the disease responds poorly to non-surgical
treatment (because even with the treatment, the ferret is *still*
exposed to the triggering factor)? Stay tuned for further details
when Bob pulls down his shorts and dares all to light their flamethrowers.
Bob C and 20 MO Socksharks
------------------------------
Date: Mon, 16 Feb 1998 00:38:27 -0600
From: Bob Church <c620213@SHOWME.MISSOURI.EDU>
Subject: Bob C: Adrenal Post Numero Trois
The last post left off with my telling you about
a bit of the history of adrenal disease. I want to be clear on this;
just because something is not mentioned in a reference or it is not
diagnosed by veterinarians, it doesn't mean it isn't there. For example,
sometime ago I was interested in canine distemper and was looking
through the old literature and found very little. However, when I
started looking for the sweats, I found a tremendous amount. Just
because I couldn't find old references to adrenal disease doesn't
mean some are not there. On the other hand, using old documents for
an information search is a tried and true part of archaeology; these
old records are called ethnologies, and an archaeological report without
some reference to one is hard to come by. I have done a similar thing
with ferrets to build an ethographic reference. I've read about every
ferret book published (the first dates to 1790), put the data concerning
disease, life span, weights, reproductive age, etc., into tables and
gandered at the results.
What I found is, the ferrets about a hundred years
ago are about the same as those today in terms of life spans (6-8
years), body weight, diseases, reproductive cycles, and litter size.
Knowing that the quality of diet is very important to the reproductive
status, I specifically looked to see if the ferrets were breeding
at a year old or older. A good, high-quality diet assures the first,
but any mustelid that is nutritionally stressed will delay reproduction
until the second year, either by not coming into heat/rut, or by absorption
of the embryos. Almost all accounts had ferrets breeding at one year
of age, with litters averaging 4-8 kits. You can't expect better today,
with all our vast knowledge and vet care. In every field I looked,
I found the descriptions from the past to fit exactly in with today's
data. (I do feel the average age at death was lower, indicating more
ferrets died earlier, but the ranges were the same) To me, this means
people treated the ferrets quite well and were concerned with diet
and health. Therefore, I feel the assumption that adrenal disease
was uncommon a hundred years ago is safe to make. If they didn't know
that was causing it, they would have at least mentioned the symptoms.
I am convinced that the proportional differences
in adrenal disease rates between the Old and New Worlds have more
to do with environmental factors than genetics. I'm not implying genetics
is not important, for I actually feel ferrets as a "group" are prone
to them. I just feel various environmental factors are also important,
and an understanding of what is different between the two groups is
in order.
Food: The USA/Canada primarily feed dry kibbled
foods; while such foods are being accepted in other countries, pullets,
carcass parts and raw meat products are still commonly given. Think
about this; as far as I can reconstruct, ferrets in the USA had a
low incidence of *reported* adrenal disease until the late 1970s.
Now, this might be coincident with better veterinarian diagnoses,
more treatment of ill ferrets, or the widespread introduction of dry
kibbled foods, which took place at about the same time. A possible
problems are a shift from foods having lots of fiber (fur) and roughage
to eating something that comes out like paste.
I *have* to get off track just a moment here. I
just read Fox et al 1997 paper on Helicobacter.
A superb paper and one that left me wondering out loud if some of
the problems we are recently having with recurrent bowel inflammatory
disease, ECE and the like might be tied to expecting our little fursharks
to push their intestinal toxins out the back using paste rather than
fur and fiber. It is only a recent discovery that human bowel cancers
are tied to fiber content. Kibbled foods are essentially a paste made
of finely ground foodstuffs; a vole has fur, bone bits, teeth, and
non-digested parts pushing the nasties through. Some recent research
has shown dogs and cats are generally healthier with fewer down days
when fed a more natural diet. Aside over.
Feeding: Here we generally feed ad libatium; that
is, we leave food in a dish and the dish with the ferrets at all times.
This is in part because someone once erroneously equated a high metabolic
rate and food requirements to mean they have to eat all the time.
This is not only untrue in healthy ferrets, but it would be impossible
to do in the wild. What do you think fat is for? Ferrets do just fine
if fed twice a day, and will adjust their eating habits accordingly.
There are some very nasty little papers that suggest animals eating
ad lib have fatter bodies and shorter lives that animals on a bidaily
diet, which has been a traditional practice in most other places ferrets
are kept.
Living Environment: In the USA/Canada, ferrets
are house pets and are rarely taken into the out-of-doors. Most other
places house ferrets outside and they are rarely taken indoors.
Photoperiodism: In the USA/Canada, indoor ferrets
are constantly exposed to unnatural light periods. I remain unconvinced
that full-spectrum light is any different than the ol' tungsten lamps,
since the latter has been used for decades to control photoperiodic
cycles in both birds and mammals, but I am concerned about the photoperiod
cycle in general in modern environments. This isn't a problem for
ferrets housed outside.
Trace Nutrients: No one can tell you exactly what
trace nutrients human beings need, and we have been spending billions
to find out. Very little time or effort has been spend on discovering
the essential trace nutrients for ferrets. Remember, ferrets were
domesticated from polecats, who evolved as primary carnivores eating
fresh meat on a frequent basis. In a cosmic blink of an eye, they
have shifted from eating carcasses to eaten dried up bits of preground
paste.
Exercise: Ever try to work out in closet? Need
I say more?
Inactivity: Inactivity is mostly due to boredom
rather than small cages. I've included boredom because all systems
of the ferret are affected, including the endocrine system. Bored
animals and people have been shown to have higher disease and death
rates. It might take awhile, but you can be bored to death. Continued
in the next post.
Bob C and 20 MO Furrbutts
------------------------------
Date: Wed, 18 Feb 1998 13:20:20 -0600
From: Bob Church <c620213@SHOWME.MISSOURI.EDU>
Subject: Bob C: Adrenal Post Numerus Quattuor
Before I get into this next part, I just wanted
to thank all those who have helped the flow of this discussion by
refraining from posting comments until the series is finished because
it allows me to concentrate on getting the stuff out rather than defending
statements. Trying to take an in-depth look at a complex disease with
little published data regarding causes is not only time consuming
and difficult, but to then to spread them out in an attempt to lessen
reading (and FML space) burdens makes it all the harder. Thanks for
(private) letters of encouragement, and more thanks to those possessing
the maturity and insightfulness to withhold comments until the series
is finished. Especially after today.
So far I have compared basic environmental differences
between ferret ownership in the USA/Canada vs. everyplace else. But
environmental differences are not just food, housing and lighting.
By using the word environment, I am referring to anything not of a
genetic nature. In other words, your genes allow the potential of
growing to six feet, but outside factors can make you shorter (or
taller). American ferrets can be exposed to unique environmental factors
that are not typically found in other parts of the world; at least
not in the same degree.
Paramount among these factors are two which I will
discuss; shelter conditions and neutering. I expect to raise some
eyebrows in both areas. When I discuss shelter conditions in the USA,
I am not discussing filth nor inadequate conditions, so *NO* comments
on that. During my travels, I have visited maybe 35 shelters, and
not one, even on a bad day, was unsafe for the ferret. In some shelters,
the amount of resources spent was outstanding, with ferrets being
given wonderful care.
I'm thinking of something else; specifically, stress.
Ferrets are domesticated polecats, and as such follow a predictable
mustelid pattern of behavior (albeit somewhat modified by the constraints
of domestication). That means ferrets are territorial and solitary
animals, and indeed they are, as feral conditions and lab experiments
have shown repeatedly. But most mustelids, including ferrets, will
establish a sort of dominance structure when forced to live together.
Eventually, they accept each other more as siblings than anything
else as the community establishes. With a few exceptions, this never
happens in shelters. Ferrets come and go, cages are stacked next to
and on top of each other, and the entire room is filled from floor
to ceiling with the odors of strangers. If the shelter is full, human
contact can be short. Its no wonder that shelter ferrets can be nippy,
many show signs of immune suppression, or even blow their coats. I
commonly heard shelter operators say, "this little ferret is suffering
from stress right now..."
Of all the replies, almost 70 percent said their
ferret was either adopted from a shelter or lived in shelter conditions
for part of their lives (In this category, place getting thrown in
a box and stored behind plexiglass in a pet store until sold). Only
three out of ten ferrets reported to have adrenal problems came from
private breeders. On the surface, this might be seen as evidence that
commercial ferret farms are breeding ferrets with compromised genetics,
but it could just as easily mean that there may be a common environmental
trigger. One other thing; when a privately bred ferret was adopted
from a shelter, they also had the same 70% chance of contracting adrenal
disease down the line.
Hard to believe, isn't it? I have three fairly
good papers describing stress-related problems in ranched mink, who
show such symptoms as hyper-aggression, hair loss, diarrhea, extreme
apathy, neurotic behaviors and self-mutilation. Another paper talks
about how mink will form a ranked social grouping when forced to live
together, just like ferrets, and once the dominance relationships
are set up, rarely fight, just like in ferrets. But when placed into
conditions where they are constantly exposed to unknown mink, even
the sight of another mink causes quantifiable stress. Now, the papers
are really concerned in reducing fur injury, and the mink become coats
long before adrenal disease would have a chance to become apparent.
The reason I am mentioning the studies is because 1) no such study
exists for ferrets, 2) mink and polecats are acceptable analogs for
ferrets, and 3) the confinement and close proximity of mink closely
parallel that found in ferret shelters.
BTW, the fur farmers found placing wood barriers
between cages to block visual views was effective in reducing stress,
even if the mink could easily smell each other. The only other effective
stress-reducing procedure was increasing the space between cages.
Could this be a factor in adrenal disease in our little furbutts?
I suspect it is at least a part of the problem, but I admit there
has been no specific study looking into the issue. More comments later.
The other issue is early neutering. This is a monster
can-o-worms. Let me define early neutering. Growth patterns vary from
species to species; in most, the onset of sexual maturity is prior
to the mammal reaching full growth. But not in most mustelids. The
ferret reaches 90-95% of its growth in the first six months. By the
end of the first year, its bones have stopped growing and are fusing
together. This is before or at the onset of the first possible reproductive
cycle. I define early neutering as neutering before the growth cycle
is complete. Late neutering is after the growth cycle is complete.
I assume a growth cycle is complete when the ferret has reached 90%
of a typical adult weight, because even though the skeleton has stopped
growing, the ferret can still put on weight, especially the males.
In an unneutered male ferret, this is muscle mass due to testosterone;
in unneutered females, its body fat.
Now here is an instance where statistics can fool
you. The survey reported early neuters had almost a 80% higher rate
of adrenal disease compared to late neuters. Sounds terrible, right?
The problem is, what's the percentage of early neuters compared to
late neuters? At least 80%? When I normalized the values, I found
early neuters and late neuters to have about the same rate of adrenal
disease. The stats have other problems as well; the FML is not a typical
slice of ferretdom--not even in the USA--and FMLers are far more likely
to adopt sickly ferrets than other people, which has a serious impact
on the numbers. For both reasons (and more, including a possible bacterial
or viral link) I cannot determine if early neutering has a definite
negative impact on the ferret in regards to adrenal disease. Size?
Absolutely! Adrenal disease? Just can't tell.
What is interesting about the survey is it showed
females were twice as likely to get adrenal disease as males. This
could suggest adrenal disease was sex- or hormone-linked. Breeder
females had the lowest incidence of adrenal disease, followed by breeder
males. I don't trust the numbers because the reported sample was much
too small, but it does suggest a hormone-link. Or does it? Are breeder
animals housed or handled differently than neutered ferrets? Do they
handle stress differently? See how the question becomes convoluted
and difficult to define?
We are almost at the end, just a post to tie things
together and a post to suggest courses of action. Then feel free to
pepper me with any questions you wish; but I'll say right now, I'll
only answer those questions asked politely and will ignore any rude
question or questioner. This isn't about who is right or wrong, nor
is it about me or you. Its about a serious disease attacking our ferrets
and a simple exercise attempting to define the questions, because
currently, there are no answers.
Bob C and 20 MO Sockoholics
------------------------------
Date: Wed, 25 Feb 1998 17:06:21 -0600
From: Bob Church <c620213@SHOWME.MISSOURI.EDU>
Subject: Bob C: Adrenal Post Numero Cinque
The statistics gathered from the FML are biased
at best and unusable at worst because there is no way I can demonstrate
the demographics of the FML is similar to ferret owners as a whole,
and between you and me, just the fact that every FML person has or
uses a computer daily is evidence of that. Even taking into account
several previous surveys, the demographics of the FML cannot be fairly
compared to any other group. This has important implications regarding
the ferret list in general, and one I need to discuss prior to the
adrenal summary, because it sheds light on what we see posted here.
I'm sure you have all heard the joke, "Those who
are against me are liars, and those who use statistics against me
are damn liars." You can use statistics to prove almost anything.
All you need to find are two things that statistically correlate to
each other and you can make a point. The problem is, a statistical
correlation does not mean there is a cause and effect correlation.
My favorite illustration of this is "Nearly 100% of people with severe
hemorrhoids use toilet tissue." Statistically this is probably correct.
The trouble is, no cause/effect relationship has been demonstrated.
Statistics show mathematical correlations, but only people can take
those correlations and look for cause/effect relationships. Scientifically,
this requires rigorous controlled testing, which for those of you
who are squeamish about such things, usually involves the use of ferrets
for medical research and their subsequent sacrifice.
The toilet tissue argument is what is happening
on the FML regarding adrenal disease. Read carefully; I am *NOT* saying
*ANYONE* is wrong or right--all I am saying is not a single person
has shown a cause-effect correlation. In addition, each and every
one of the supposed solutions are done without scientific rigor nor
with controls. By itself, this makes the data essentially useless.
Not totally, but pretty much so.
For example, and I am talking not just about homeopathic
treatments but any treatment, how do you know the change in the ferret
is due to a specific treatment and not because of additional handling?
Touch therapy is as old as the beginning of human culture and it works;
lots of studies have shown touch to increase immune responses and
there are a couple of documented cases where touch therapy has been
attributed to the remission of cancers in terminally ill people. So
what part of treating the ferret is the additional touching, and what
part the medicine? You don't have any controls, so you can never be
sure. You can believe what you want, even suggest it as a course of
action, but you have no proof.
Another problem with FML data is we are subject
to a constant bombardment of symptoms, treatments, theories, etc.
We are not the typical ferret owner. I know; I've met some and you
would be extremely surprised to discover how little the average ferret
owner actually knows about their carpet monkey. The longer you read
the FML, the more you learn about ferrets until you reach the point
that there are few medical surprises. This does two things; it makes
each of us think we know as much as people who have spent a decade
learning the physiology of animals, and it makes us feel hopeless
in the face of certain severe illnesses.
For example, I have been told canine distemper
is 100% fatal, and I believe it. Yet, I know of at least three ferrets
that has survived it, albeit with some sort of permanent disability.
A similar thing occurs with the constant influx of adrenal posts;
we hear it so much that they become paramount in our mind, making
the actual severity, demographics or survival rate shift from reality
to FMLity, which you cannot assume to be true or real. In other words,
because we hear of it so often, we start to grant it far more importance
than it actually deserves.
I think that false sense of danger taints our perceptions
of how we view adrenal disease. While I may know what percentage of
FML ferrets display adrenal disease (maybe 10%), MOST of them don't
die from it until they are past 6 years of age. That is within the
mortality window of the average ferret, even without adrenal disease.
Think about this; what do you think *you* will die from when you get
near that magical 77 year mark? Humans die of strokes, heart disease
and cancers (unless you smoke and its much worse). Our species seems
to have a weakness in those areas. The same might be true of ferrets;
the "large" number of adrenal problems we see might be an indication
that the ferret is actually in its declining years. Don't confuse
the early onset type of adrenal disease with the late onset. I personally
believe we are looking at two different disease processes here, but
more on that in the next--and last--post.
So what I seem to be saying is we can come up with
all sorts of reasons for the adrenal disease we seem to be seeing,
but without proper statistical procedure, known demographics, and
careful analysis of the results, we really don't have anything other
than rumor and innuendo. Yes, we *know* something is going on, but
the relevance and extent of that knowledge is uncertain. What is needed
is solid scientific research, the kind that resorts to experimentation
on live animals. We need this basic knowledge base in order to accurately
assess the true danger that exists to our ferrets.
Science is very much like law (except a scientific
dream team rarely gets millions of dollars) in that you must have
unbroken links between the suspect and the event. Since arguments
are similar to a series of links in a chain, break a single link and
the entire argument fails. For every one of the possible reasons I
could come up with that could cause adrenal disease, I could break
one or more links, each the intellectual equivalent of "If the glove
don't fit, you must acquit."
Does this mean that none of the possibilities I've
mentioned are possible? Of course not. I'm convinced more than ever
that adrenal disease is an environmentally-triggered genetically-predisposed
disease. Which is probably old news to those investigating the issue,
but, belief is not evidence, and solid evidence for any cause/effect
relationship simply does not exist in the literature.
Now, I have a final post after this one and then
I'll make myself available to answer questions on any research I've
done, the references will be made available, etc. Bear in mind this
sort of discussion is necessarily verbose, and with the size of the
FMLs lately, when a post goes over 125 lines I have to ship them to
Bill who puts them in ASAP. So there is this sort of surreal waiting
period until you see stuff. That isn't me back-pedaling or running
off finding evidence, but just that I see the question one night,
post the answer the next night and you see it the 3rd night (or later
depending on various factors). Patience. And keep emotions out of
it, ok? For much of this, I could easily do the equivalent of smashing
a basketball in your face if I wanted to, but that would detract from
the true purpose which is discussing the adrenal issues. It would
only force me to use statistical evidence, making me a damn liar instead
of just a liar.
Bob C and 20 MO Four-Legged Fursnakes
------------------------------
Date: Sat, 28 Feb 1998 04:55:47 -0600
From: Bob Church <c620213@SHOWME.MISSOURI.EDU>
Subject: Bob C: Adrenal Post Number Five
This is the last of the adrenal posts, to which
I am sure some of you will applaud. It has been hard for me as well,
well maybe not from a boredom aspect, but hard nonetheless; I had
to give the inter-library loan people a box of designer chocolates
so they wouldn't complain. The greatest difficulty has been the long-term
posting; I think it would have had a lot more impact if they had ran
in a week rather than two. That was unintentional and caused by MF
debates, the Ohio bite case, and other stuff which is also important.
But those issues filled the FML and placed these posts into the category
of "I'll drop them in when I find space." Perhaps I should have divided
them into more posts, or posted several parts in a row to get around
the FML guidelines, but the work seemed to divide itself into five
parts, and I was too busy to argue with it. This last post will also
be long but hopefully will be posted sooner than the others. With
the publication of this post, feel free to pepper me with objects
no larger than a soda can, or questions, whichever you prefer. I will
not answer rude comments. I will provide specific references to those
with a bonafide interest.
250 years ago, the Philosopher David Hume said
that you couldn't infer an infinite cause from a finite effect. I
have a photocopy of the paper in which that statement was originally
written, and I look at it whenever I work on any scientific paper.
While the original purpose behind the statement has little place on
the FML, the statement itself can sum up the problems of ferret adrenal
disease. What can cause it? I came up with more than a dozen really
good ideas, but am no closer today at deciding what causes it that
I was three months ago when I started to look into the issue. In fact,
I think I know *less* now than then. Perhaps the answer has been scotch-taped
to my computer terminal all along; you cannot infer an infinite cause
from a finite effect.
What research I've done suggests adrenal disease
in ferrets is a multi-factorial problem resulting from a genetic predisposition
and an environmental trigger. Because the genetic heritage of ferrets
is little understood--we don't have coat colors worked out yet--that
aspect of adrenal problems has no current resolution. In other words,
ferrets as a group may be predisposed to adrenal problems, or just
USA strains, or just specific breeder strains; no one knows. After
working on the genetics of the problem, I'm inclined to believe it
is a ferrets-as-a group predisposition. Better statistics and controlled
testing could resolve this problem in a few years, provided funding
and animals for research be provided. There are a few studies, but
they do not answer the question of which type of ferret gets the disease,
nor location.
Adrenal disease seems to be a geographically isolated
disease. Statistically, ferrets in outside of the USA and Canada (or
America as in "North") have significantly lower reported rates. Adrenal
disease also seems to be a modern disease; that is, after scouring
all available records for the last 200 years, I was only able to find
a single incidence of what *could* have been adrenal disease, and
in that case, my "diagnosis" was based on hair loss and thirst, and
could have been something else. Even as soon as thirty years ago,
adrenal disease was uncommon enough to not be mentioned in USA publications,
including vet-care papers. Some might argue the sudden onset is due
to early ferret deaths--they didn't live long enough for the disease
to exhibit itself, or that the ferrets were simply killed and no record
was made. I reject both arguments because I actually waded through
reams of illness reports and cures. The average lifespan of ferrets
reported 100 years ago is essentially the same as today, except the
average age of death was a little bit lower. Certainly, they lived
4-5 years, which in today's American population, would mean adrenal
disease would have been noted. Most authors made every attempt to
mention illnesses that only had the faintest possibility of occurrence.
In an 1860's version of a vet how-to book, the symptoms of Cushing's
Disease is mentioned in dogs, and while the aliments of ferrets took
up a dozen pages, nothing similar was even remotely mentioned. I don't
think you can assume the disease was there but ignored. These guys
LOVED to get their names attached to a disease, as if they invented
it. I don't think they saw it or it was extremely rare.
Since the ferrets in the USA, Canada, Australia,
and New Zealand all come from the same basic stock, and those same
ferrets show a tremendous amount of variation in body shape, patterns,
fur color, and other morphological traits, arguing the American ferrets
have some sort of inbred genetic problem is rather pointless. It may
be that the supposition is true, and it certainly would explain why
so many American ferrets get the disease. But then, it doesn't explain
why so many American ferrets do NOT get the disease nor why it is
so unpredictable. Like cancer, it seems to run in families, but you
cannot predict which ferret will or will not get adrenal disease.
Which is exactly why I think an environmental trigger is also necessary
for the disease to show itself.
I have chosen to assume the genetics are about
the same between American ferrets and all others. That is because
the initial ferret population in the Americas was so high that a founder's
effect or genetic drift becomes improbable. Not impossible, but not
very likely either. While I doubt if the America population a century
ago rivaled that in Great Britain, it had to equal or exceed those
populations in New Zealand and Australia, and guess what? Those ferrets
are weaned on environmental conditions similar to those in Britain,
and they have similar adrenal disease rates. Assuming the USA has
vets better able to diagnose or identify the disease is both nationalistically
arrogant and well as unsupported by facts. Did you ever think the
reason American vets know more about the disease is because it occurs
at rates unnaturally high here? Or that the reason some of reports
starting to surface elsewhere might be because American ferret environments
are becoming more common?
The trouble is, if this is true, (and at best it
is only a working hypothesis), what are the environmental triggers?
Either the genetics of the American ferrets and all others are different,
or they are about the same. You must assume they are the same UNTIL
you can prove otherwise. If they are the same, then some environmental
factor must be behind the outbreaks. Since there are a number of environmental
differences, ranging from photoperiods to diet to a virus to stress
to early neutering, and not a single study has looked into THESE issues,
then at this point in time the issue is too complex to resolve. Its
that simple. Infinite causes and a finite effect.
Still, much can be learned if we set aside our
prejudices and take a careful look into what is the same between the
Americas and Europe, and what is different, because therein lies the
answer to the environmental trigger, should one exist. Like links
in a chain, it may be possible break a link and prevent the disease
from occurring. Sort of like the identical twin smoking study done
some time ago. One twin smoked, the other did not. In those cases
where the twins had a genetic predisposition towards cancer, the smoker
got lung cancer. Smoking was the environmental trigger, and breaking
the link--smoking--reduced the chances of lung cancer significantly.
Don't buy the comparison? Do you remember what adrenal disease is?
A tumorous growth in the adrenal gland? So what is lung cancer? I'm
not implying they are the same disease--and in fact they are quite
different--but just like comparing a TR-3 to a VW bug, they might
be different, but much of the mechanisms is similar. They are inherently
comparable.
Of all the possible environmental triggers, the
most plausible are some sort of biological agent, like a virus or
bacteria, stress, early neutering, diet or some combination of these.
Photoperiodism might be a contributing case, but since other animals
that are as subject to photoperiodism as ferrets, or more, do not
exhibit problems, I discount its contribution. An unknown biological
agent is certainly a viable option, but little is known of their relative
effects in tumor growth. I'm afraid the major environmental differences
between American and all other ferrets must lie in diet, stress and
early neutering, or some combination.
Early neutering does not seem to be a problem with
other species, so it loses some of its credibility in the ferret issue.
Still, dogs and cats are not typically neutered at the same relative
stage of growth as many ferrets, especially those neutered at about
a month of age. This is because the growth curves of the various species
are different, so one being neutered at 6 weeks might be the physiological
equal to another species being neutered at 3 weeks. I know of no research
into this issue.
Diet can also be an important factor. Adrenal disease
really didn't start making headway in the Americas until after kibble
became a popular food. It is quite possible that the lack of a micronutrient
could be causing a physiological problem resulting in the disease.
Convinced kibble is a perfect food? I have three references, none
more than 5 years old, that suggest "any kibbled food is an approximation
of a natural diet and as such cannot supply the diet the [predator]
consumed during its evolution." I have had so many requests that I
address the diet issue that I will drop it for now in favor of a future
post. Still, as a trigger in adrenal disease? I have some doubts.
That leaves stress. Some human research suggests
there is "good" stress and there is "bad" stress. Good stress are
those events that either strengthen or condition your body towards
some event, such as a sporting event or asking someone out on a date.
Bad stress is of the type that is not quickly resolved, like school
or work stress, and is thought to be a factor in human heart disease.
While I was able to find lots of info regarding maternal-separation
stress in lots of different animals, little has been done with ferrets,
and nothing looking into the possible link between stress and adrenal
disease. Stress is a natural suspect, because it is so intimately
involved with the adrenal gland itself. It may well be that unresolved
stress might be the triggering mechanism, and early maternal separation,
close (unresolved) shelter contact with unknown or strange ferrets,
or lack of physical contact be factors as important or more than genetics
or early neutering.
Of course, it could be a combination of those (or
others) that is trigging adrenal disease. For example, maybe a MF
ferret was early separated, early neutered, then shipped to a pet
store having a completely new environment, all full of stress. Feed
a kibbled diet which could possible cause some physiological stress,
the combinations of all the different stresses trigger the growth
of a small tumor in the left adrenal. This is just a story, but it
is a testable idea.
Complicating the entire argument is the observation
that adrenal disease seems to be exhibited in two different manners;
one a late onset, and the other is an early onset with often a later
recurrence. I cannot distinguish this from being two different diseases,
one disease that exhibits differently, or just random happenstance.
I know of no study into this issue.
As for treatment, surgery is the only treatment
that has any long term benefit for the ferret. As already discussed
in the 1st post, drug or chemical treatments do not offer a significant
difference in life span compared to no treatment at all. They do provide
the ferret with perhaps a slightly higher quality of life during that
time, but no real increase in lifespan. It is better to be aggressive
and remove the tumor as soon as possible, because the disease gradually
weakens the ferret and increases the chances of complications. The
younger the ferret, the better the prognosis, although the younger
the ferret, the more likely a second adrenal tumor will crop up.
I don't see an easy resolution to this problem.
It requires money, intelligent and dedicated people looking into the
issues, and time. Genetic and environmental factors need to be ruled
out, ferret *will* die to resolve this, that you can be sure. Can
we help? Hell yes!
The best way each of us can help is with GOOD records
on each and every one of your carpet sharks. As much of the lineage
as possible, estimated birth date, diet (including manufacturer of
diet), shot record, weekly temperatures and weights, record of treats,
social interactions, etc. We can be like Tyco Brahe, who painstakingly
measured the distances (time) between stars, knowing there was no
real good purpose for the data. Yet, that same data, in the hands
of Kepler and Newton, rewrote our history. We can create the data
that some smart whipper-snapper down the road can take and solve the
problem. I suggest those people who currently are on the adrenal mailing
list, work with some quasi-national club to create a scientifically
correct adrenal data base, gather info from vets, breeders and owners,
and provide it to bonafide researchers. We already have the answers;
we just need it in an unbiased and correct form of data.
So that's it. I recommend you go back and read
the preceding four posts (or just skim them) before firing off a question
just to remind yourself of what had been said already. I have tried
very hard not to offend anyone position or platform. Not really, I've
tried hard to offend them all. I have my asbestos lonhjohns on, my
trusty data base in one hand, and Carbone, just starting his first
rut, in the other. I'm ready.
Bob C and the 20 MO Ferrets just relieved its all
over.
------------------------------
Date: Mon, 2 Mar 1998 03:09:31 -0600
From: Bob Church <c620213@SHOWME.MISSOURI.EDU>
Subject: Bob C: Round One: Adrenal Reposts
Q: "I have had great success with [homeopathic]
remedies in adrenal disease. Why did you ignore such a large body
of evidence?"
A: I didn't. I use homeopathic treatments quite
often; when I was on high doses of chemicals, I used several teas
and even aroma therapy to get past the nausea. But very little is
known about homeopathic treatments and how they work in humans; next
to nothing has been done on animals of any sort. That isn't to mean
they don't have value; they are useful if nothing more than as a touch
therapy, and I think I said that. What I said was there is no proof
of their ability to extend life or make any changes in the quality
of life in a sick ferret. If such proof exists, and is published in
a referred scientific journal, please let me know and I will pass
it on with my heartfelt apologies.
Q: "I am very interested in the role of diet in
ferrets. Can you tell me more?"
A: I've had so many requests to discuss this in
the last weeks that I'm compiling the references for a nice post on
the subject, and will defer until then.
Q: "OK, Bob. If you don't think it is genetics,
then kindly explain why only [MF] ferrets get adrenal disease. I think
they accidentally bred it into them."
A: I'm sorry if my explanation wasn't clear. My
little survey, as well as others, seem to indicate more actual numbers
of MF ferrets get adrenal disease, but when factored to the proportion
of MF ferrets, the normalized number drops. I don't know if my numbers
are accurate because I don't know how many MF ferrets are sold compared
to other breeder's ferrets, and I doubt if such information is possible
to obtain. My best guess is the rates are roughly equal. That would
make the assumption that MF ferrets have a special flaw rather difficult
to support. Besides, if such a "flaw" existed, and adrenal disease
was purely a matter of genetics, then the number of adrenal cases
could be predictable in large populations, and thus far they are not.
While I do believe genetics is a very important factor in the onset
of adrenal disease, it simply cannot be the part of what is going
on because of the unpredictable nature of the disease.
Now, assuming adrenal disease is only a genetic
problem, then it should follow some pattern of heritability, which
it does not except in the most broad sense. You can say something
like 5-10% of ferrets will get adrenal disease in their lifetime,
but you can't say who will get the disease. This "random" selection
is not actually random; those with the disease must have some sort
of shared characteristic(s) which promote the onset, like smoking
and lung cancer, and since it is beyond the genetic level, it must
be at the environmental level. Because there are so many possible
causes, until each one is ruled out, you cannot define a cause-effect
relationship. That is why it is so complex an issue, and also why
so few treatments seem to work. For example, assume diet is the trigger.
You have a ferret with diseased adrenal glands and you start what
promises to be a good therapy. However, during the "cure," the ferret
continues with the same diet that caused the disease. What are the
chances the cure will work? See the complexity now? Infinite causes
and finite effect.
Q: "Do you really think ferrets in Britain are
kept differently than in the USA?"
A: Borrow a copy of James McKay's video "Keeping
Ferrets." You will not only see some of the fluffiest, largest, most
well-behaved ferrets you have ever seen, but you will discover they
are housed, fed and treated quite differently make the typical ferret
in the Americas. Of course, his ferrets seem to be complete with anal
sacs and gonads, so some of what you are seeing is due to hormones.
However, nothing McKay has to say is any different than can be found
in W. Carnegie's books from the 1910-20s or Ernest's book from the
1890s. They are virtually the same, with a few differences due to
technology changes.
There are more questions which I will answer in
the next day's post.
Bob C and 20 MO Rasslin' Weasels
------------------------------
Date: Tue, 3 Mar 1998 05:37:56 -0600
From: Bob Church <c620213@SHOWME.MISSOURI.EDU>
Subject: Bob C: Adrenal Responses, Part Two.
I have a basket of them, so if I don't mention
yours. I'll get to it soon.
Q: "You really didn't get into deep detail on early
neutering. Can you expand it a bit?"
A: Its simply a matter of trying to keep the post
as short as possible, so lots of stuff I want to say is never mentioned.
Sometimes, the effort of minimizing leaves the wrong impression. Sorry.
What early neutering is proven to do:
1) Reduces the odor in males. 2) Make males more
effeminate. 3) Reduces muscle mass, especially in males. 4) Reduces
over-all growth by preventing the hormone-mediated growth spurt near
the end of the growth cycle. 5) Prevent unwanted baby ferrets. 6)
Prevent female estrogen-related anemia. 7) Reduces aggression. 8)
Reduces (to a degree) the territorial desire.
What early neutering has never been proven to do:
1) Cause adrenal disease.
I have a fairly good understanding of the endocrine
system, I know exactly were the to find the hypophysis (and have physically
dissected it out in a dozen or more vertebrates, including humans
[I've taught human anatomy labs]), and I have read my share of research
papers on hormone balance/counterbalance. I even have a copy of a
1966 MSc thesis that touches on the interaction of pituitary hormones,
anal sac secretions and, yes, the adrenal glands. The problem is twofold.
A) No one has published an in-depth study of these interactions in
ferrets, and B) No one has published a link (that is, an independently
verifiable, reproducible cause/effect correlation) between early neutering
and *any* serious disease. I stress "published" because such scientific
papers normally undergo a review process which weeds out those experiments
that are faulty or containing serious flaws.
That doesn't mean such links do or do not exist.
It only means nothing has been shown to link the one with the other.
If my goal was to remain impartial, or to allow all points to be equally
expressed in a fair and open manner, then I had no choice but to draw
the line between the proven and the unproven, and only mention the
possibilities as such. Since I have heard from both sides of the issue,
I suspect I might have met that goal.
Personally, I am a strong supporter of late neutering.
I won't neuter a male until he ruts, which is usually the first spring
after he is born, providing he has had good nutrition. Foster and
Chrys are late neuters, Moose and Bear were neutered between 6-8 months,
and Apollo, Simon, and Sam are early neuters. Carbone is almost a
year old and not yet neutered. I can see a gradient in muscle mass
and body size between these males, with the early-neutered guys far
more girlish than the middle or late neuters. The difference between
the early and middle neuters is not nearly so noticeable as between
them and the late neutered guys, who are truly impressive in their
size. Chrys is 4.3 lbs. (3 years old), Foster is 3.3 lbs (13 years
old) and Carbone is 5.7 lbs (1 year old). My next largest male is
Bear, who is 2.8 lbs (4 years old) and was neutered at 8 months. To
get larger than this, you would have to have unaltered hobbs.
But even though I support late neutering, I also
feel it is more important to neuter ferrets BEFORE they are sold,
especially those sold through pet stores. The reason is simple; we
already have enough ferrets in shelters, and I hate to consider the
day when animal shelters are killing as many ferrets as they kill
dogs or cats. That will continue to be my position until some link
between adrenal disease and early neutering is proven, no matter what
I personally may suspect.
Q: "Is there a link between adrenal disease and
coat color?"
A: Not that I could find. If such a link existed,
it could be evidence the trait was carried near on of the genes coding
for pattern or color. But I could find no link, not even a possibility,
between color, pattern or adrenal disease.
From a personal perspective, Buddy died of adrenal
disease at 10 years old; he was a dark silver mitt. Sandy has suffered
from adrenal disease for most of a year; she is thought to be 5 years
old and is an albino. Razz died of a stroke, but her necropsy showed
she had a massive abdominal cancer that had spread into some of her
bones, and which included the adrenal glands. She was a chocolate
sable, and died at 8 years of age. I don't see a pattern in my own
ferrets, I didn't see one in the published accounts of adrenal disease,
and I didn't from the FML survey.
More to come....
Bob C and 20 MO Furrbutts
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Date: Wed, 4 Mar 1998 18:16:22 -0600
From: Bob Church <c620213@SHOWME.MISSOURI.EDU>
Subject: Bob C: Adrenal Responses part 3
Q: "Do you think adrenal disease may be more closely
related to the type of process than results in breast cancer than
the possible reasons you listed?"
A: If you mean just another type of tumor or cancer?
Maybe so, but keep in mind that many (if not most) human cancers have
multiple causes, such as genetics and environmental triggers. Some
even have viral triggers. So I can accept the statement in the broad
sense, but reserve judgment in the narrow sense.
Q: "Do you know....of a type of experiment that
could prove one way or another if [MF] ferrets had more adrenal disease
than other ferrets?
A: Sure. Get 300 unneutered kits from MF and 300
from randomly selected private breeders. House each kit identically,
feed the same food, allow to socialize with people identically. Early
neuter 100 from both groups (4 weeks), middle neuter 100 from both
groups (6 months) and late neuter 100 from both groups (1 year). Raise
them in identical conditions until they all die; about 8-10 years.
Count up the number that had adrenal disease. You would then know
just about for sure, but first you need the 600 baby ferrets, the
space to care for them, the money to feed them, vets to care for them,
and the people to help you do the experiment. I'll run the experiment
if someone will get me the grant.
Q: "I wasn't lost because of your writing, but
the long time between posts hurt my understanding of what you were
talking about...."
A: Yeah, I've heard this from several people now.
In the case of the adrenal posts, they were long, but there was quite
a bit of stuff to cover. This type of post is rare, even for my particular
style of long-windedness. Also, you have to remember the MF debate
and the ferret biting incident took place at the same time--both important
issues-- which made Bill's job all the harder. I have no complaints,
and suggest you print out those particular posts for ease of bathroom
reading.
Q: "Have you read anything relating Post-traumatic
stress syndrome to adrenal disease?"
A: There is a lot of information on this in humans,
but I'm not sure of any study done in ferrets. I've read that, in
humans, those subjected to long term stress will have elevated stress
indicators for a long period of time, even after the stress is removed,
including elevated adrenal hormones. However, each species has an
unique evolutionary history resulting in a unique physiology, so just
because it occurs in one species is not necessarily proof it occurs
in other species. Some drugs which have no side effects in animals
are dangerous in humans.
However, there are more more similarities in physiology
than differences, and I would suspect there might be some sort of
relatedness between the two. Ferrets are energetic, have metabolisms
on afterburner, and have a strong sense territory toward strangers.
In essence, they are fairly easy to stress. While suspecting a correlation
isn't proof, if I were actively looking into the causes of the disease,
this would be one of the first places I would check.
Q: "How many references did you consult for this
adrenal posts and can you download them for me?"
A: I managed to beg, borrow, photocopy, or buy
a total of 18 MA/MSc/PhD Theses/Dissertations, 36 books, 6 edited
books, and 97 journal articles. In addition, I was able to consult
an additional 21 paper abstracts, where the original was in a foreign
language or unavailable. The cost to me was in excess of $330 for
the mailing costs, photocopies, and purchased books. Quite honestly,
if I were to do an experiment or two, I could easily turn this in
for a master's degree. Of course, it would even be *longer* and more
involved.
This represents a tremendous effort on my part
to collect, collate, and just type in the references, which I haven't
had time to do as of yet. So I will make specific references available,
but as for the sum total, they are in a pile beside my desk, which
makes them hard to download.
Also, in most cases, having the entire list of
references is unnecessary unless you want to do academic research
in this area. If that is the case, I have two objections. First, researching
a subject is part of the learning process which shapes your personal
work, and second, I plan on using the references for some work of
my own which means you'll just have to wait and cite me.
Still a few more,
Bob C and 20 MO Poopmeisters
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Date: Thu, 5 Mar 1998 08:35:50 -0600
From: Bob Church <c620213@SHOWME.MISSOURI.EDU>
Subject: Bob C: Last Adrenal Questions (for now)
This is the last I've received so far. Most of
the private questions were also mentioned in FML posts, a couple,
like the post-stress question, were asked by three or more people.
Many questions were adrenal-off topic, or just FML off-topic. But
this is basically it (for now).
Q: "Can I use your [adrenal] posts in [my local
ferret club newsletter]?"
A: Its against the law to mail dangerous things,
and people have fallen asleep on the seat and almost drowned after
reading them! I'm not sure I want to be called the Unabob.
Sure. Send me a copy if you have an extra.
Q: "If the adrenal issue is so complex...and the
ferret is the third most popular pet, why isn't someone researching
a cure?"
A: That's 3rd most popular carnivore. The problem
in the USA is ferrets have a minor economic potential when compared
to livestock, horses, dogs, cats and even fish. There are three ways
to easily confirm this. First, look at the book section of your local
book store. At my favorite store, there were 7 shelves on dogs, 4
shelves on cats, 3 on horses, 3 on fish, and 4 on everything else.
There were exactly 4 books on ferrets from 3 authors, two were first
printed more than 10 years ago (The other two were Modern Mary Shefferman's
book "The Ferret," and the rebundled 1996 "Ferrets Today" disguised
as a new 1997 book, which it ain't).
The second way to tell is to look at the back of
pet magazines and see who pays for the slick ads and what they are
advertising. Large incomes = large ad budgets = slick ads. Advertisers
put their money where they think the profits are. I suspect most of
the big players are still waiting to see if ferrets pan out to be
more than just a passing fancy.
The third way is to see how many graduate students
are doing their research on ferret issues. Quite literally, scores
of theses (rhymes with feces) are approved each year for livestock,
dozens for companion pets, and very few on ferrets themselves; that
is, not including those using ferrets as research models for other
species.
The reason for the disappointing lack of interest
in all three categories is nothing but economics. The bottom line
is there are not enough bucks being spent by the ferret community
to attract the players who typically pay for the research grants that
cure this type of stuff. This isn't new; pets weren't really exploited
for the big bucks until the last couple of decades. Now, if the disease
affected cattle or sheep, it would have been called the "Mad Adrenal"
disease and livestock would have been recalled from pet shops and
people would have stopped eating hamburger. If it affected dogs or
cats, then a serious yet sensitive professor would have been asked
to the Today Show to profess his or hers serious yet sensitive views.
But stinky attack-ferrets are owned by tattooed weirdo nuts who only
spend millions instead of billions on our one-tracked begonia diggers,
so there is absolutely no incentive to exploit the market "at the
present time." Need I say more? Of course!
There are some ways to cure this problem. 1) Start
a program to make ferrets MORE popular than dogs or cats, possibly
by exploiting the Bud commercials. 2) Convince ferret owners to buy
cartons of tacky products with anything even resembling a ferret rubber-stamped
on it. 3) Get a couple hundred internet people to boycott, badger,
or belittle the players to make more monies available. 4) Get all
the little clubs to get over their regional squabbles and ego flailing,
band together and form a truly (Inter) National Ferret Club with enough
members and money to carry a politically big stick. 5) Form your own
little club so you have your own opportunity for regional squabbles
and ego flailing. 6) Wait and hope for the best, while bitching about
how unfair things are. 7) Write incredibly long posts that incite
people to riot, while wearing a t-shirt reading "David Hume and Patrick
Henry for President!"
This is America, where the currency says "In God
We Trust" on one side and "but all others pay cash" on the other.
If you want the players to take notice, you have to be noticeable.
That means money or political power and usually both. Are we, as ferret
owners, capable of such feats? Well, we beat rabies hysteria, have
had most anti-ferret laws changed, and just recently saved the life
of a "child-attacking ferret." Those times we banded together and
chose to ignore our differences, we beat or changed the system. Then
we just drift away to resume regional squabbles and ego flailing.
Ever wonder why you never see a dozen different Audubon Societies,
or a half dozen different Sierra Clubs? Its simply because ten clubs
are never as large as one single, giant, powerful "hit bad guys out
of the park" club. One voice, pooled resources, political strength.
I have been asked why *I* haven't formed a club, and the reason is
simple; ferrets DO NOT NEED yet another personality-based club that
only divides and fragments our meager resources and unity. What they
need is all the existing clubs to become a single strong organization!
Its just too bad the clubs won't see the light (or take the hint)
and merge themselves into a single national club with enough membership
and strength to show the big players we will be still be around in
the twenty years it will take their research money to turn the big
profits so when they die they can have all kinds of stuff for their
children to fight over.
Whatever happens, you can etch this in brass and
take bets on it. 1) No serious money for ferret research will be made
available until big business catches a whiff of profit, 2) No serious
advances in ferret diseases such as adrenal disease will be made until
serious research funds are made available, and 3) No serious political
power will be welded by the ferret community until it speaks with
one voice instead of 20. Or 21.
Bob C and 20 MO Silly Snapping FurSnakes
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Date: Fri, 6 Mar 1998 04:16:19 -0600
From: Bob Church <c620213@SHOWME.MISSOURI.EDU>
Subject: Bob C: Ok, some more Adrenal Questions
Q: "Do you really think [kibbled foods] can cause
adrenal problems...and is there any type of evidence?"
A: Most of my comments will be held off for a future
post series on diet. But as for the adrenal-specific part, it is difficult
to say. I think without research, ANY discussion is error-prone, so
I am reluctant to say anything is certain. But here are some things
to consider; bear in mind not a single point has been proven to cause
any problem in ferrets.
Using pet ads, ferret books and articles as a window
to the past, there was virtually *no* mention of adrenal problems
until the mid-to-late 1980s. Those articles initially treated adrenal
problems as a rarity, but that started to change in the late 1990s-to-early
1990s. Now it may be one of the most common reason for surgery in
ferrets, rivaling abdominal blockages (and excluding neutering). NOW,
either all the ferrets in the Americas since the mid-1980s are cousins
and the traits is a genetic defect, or there must be an environmental
cause or trigger.
Using that same window of history, kibbled foods
for ferrets have also become quite popular. Create a graph in your
mind. One line the is increase in adrenal disease in the last 20 years.
The other line is the increase in the use of kibbled foods (for ferrets)
during the same period of time. I have made such a rough chart, and
I have to tell you, the lines parallel each other. They are correlated.
Add a third line for the popularity of ferrets in the Americas. That
line also rises, but it rises at a lower curve than the other two
lines. They are not correlated. Adrenal disease is rising at a faster
rate than ferrets are becoming pets.
Ok, the lines are correlated, but are they cause
and effect? That I don't know, and it is definitely an area where
research is needed. Maybe ALL kibbled diets are missing something
and those ferrets suffering adrenal disease are lacking a specific
trace nutrient. Maybe the meat used to make the kibble contains nutrients
that *IN EXCESS* causes adrenal disease, and the ferrets are suffering
from overnutrition of a specific nutrient. This has happened in people,
where hamburger containing excess thyroid hormones seriously--and
negatively--impacted growing children. Maybe the kidneys added to
the kibble still have some adrenal tissue added, and the hormones
are not being destroyed during manufacturing. I can't tell you what
is happening, but I do know what a fish smells like when it rots,
and this mess has a very strange odor.
Q: "Can't inbreeding at [MF] have caused adrenal
problems?"
A: So why do non-MF ferrets get adrenal disease?
I'll let you in on a secret. Ferrets in Britain are often quite inbred,
and father X daughter, mother X son crosses are far more common than
you might think. The practice is normally done to "set" a characteristic,
such as size, temperament or build. They have an adrenal disease rate
far lower than our own. Also, IF adrenal disease was the result of
a random mutation in American stock, and increased in the population
because of inbreeding, why is it so prevailant in both MF and non-MF
ferrets? If the trait was dominant, all the offspring of an host parent
would have adrenal disease, but they don't. And you would expect at
least 25% to have the disease if it were a recessive trait and both
parents carried only a single copy of the defective gene, but even
that is way too high of a figure. At the very worse, adrenal disease
effects 10% of the population (FMLality), and the figure is probably
less than 3% (Reality). And it would *never* show at all if it were
recessive and only a single parent had the gene. This is not strictly
a genetic problem, so inbreeding is probably not much of a factor.
The key to the problem has to be something in the environment, and
will probably be found in the lifeway differences between American
and other ferrets. Genetics might be behind the locked door, but the
key is hidden somewhere in the environment.
Q: "How has [the adrenal posts] changed your opinions?"
A: Before I really looked into the question, I
suspected MF breeding practices, photoperiods and diet or some combination.
Now I realize the problem is a bit more complicated than that. Perhaps
I was secretly hoping I could brilliantly discover some sort of commonality
that would let me pontificate a cure.
I literally have almost everything written on adrenal
disease in ferrets, and lots of stuff on comparable diseases in other
animals, yet I cannot definitely say one aspect is more important
than another. Its a black box where everything goes in and adrenal
disease comes out, and I'm just as much in the dark as the rest of
you.
But here is where I stick my butt out for all to
flame. IF I am right and the key in something in the American ferret
lifeway, adrenal disease will begin to increase all over the world
as our ferret lifeway practices are exported. IF I am right, then
adrenal disease will continue to increase out of proportion to the
number of ferrets being produced and yearly totals of adrenal treatments
will increase. IF I am wrong, then the status quo will be maintained,
those breeders importing foreign blood into their ferret lines will
reduce the incidence of adrenal disease in their lineage, and adrenal
disease outside of the Americas will remain rare.
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