Bob Church's Adrenal Articles

[Editor's note: The following series of posts were the result of a survey
taken by Bob Church.  These posts appeared in the FML over the span of a
few weeks, which made things a bit hard to follow.  So, by popular demand,
all are assembled together here.  I've also included one or two responses
which appeared in the FML at the same time that I happened to notice.  BIG]
-------------------------------------------------------------------------

Date:    Sun, 1 Feb 1998 03:50:08 -0600
From:    Bob Church 
Subject: BOb C: Adrendal Stuff

Ok.  folks, I'm running a bit behind on finishing the adrenal post, mainly
becuase 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.

Thats 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, thats 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 whould be as good as "96% of all
Americans who die in accidents are wearing clothing, therefor 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.

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Date:    Tue, 10 Feb 1998 05:13:22 -0600
From:    Bob Church 
Subject: Bob C: Adrenal Post, Part Uno.

Ok, folks, here are the offical 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 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 embarrased 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 vigourous scientific
examination and still result in positive results.  Homopathic 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 superfical 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
droped 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 aggresion, 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 theis
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 discriptions 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 livespan.  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 manifistation (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 healthly 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, rigourous 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 proceedure 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

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Date:    Thu, 12 Feb 1998 17:16:38 -0600
From:    Bob Church 
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 hobbs 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 susceptable
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 supect 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 phenonmenon 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

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Date:    Mon, 16 Feb 1998 00:38:27 -0600
From:    Bob Church 
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 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 etal 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
inflamatory 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 eated 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 
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 encouragment, 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 potiential 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 supression, or even blow their coats.  I
commonly heard shelter operators say, "this little ferret is sufferring 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 belive, 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, diarrhrea, 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 confinment 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, whats 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
definate negative impact on the ferret in regards to adreanal 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 attemping 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 
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 hemorroids 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 rigourous controlled testing, which for those
of you who are squimish 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
esentially 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 constaint 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 spenta 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 occurrs with the
constant infux 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
persoanlly 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
proceedure, known demographics, and careful analysis of the results, we
really don't have anything other than rumor and enuendo.  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 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 sureal waiting period until you see stuff.  That isn't me
back-pedalling 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 
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 orginally 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 infinate
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 thrity 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 possiblity of occurence.  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 unpredictible.  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 intital 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 differen--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.  Im 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 credability in the ferret issue.  Still, dogs and cats are
not typically neutered at the same relative stage of growth as many ferrets,
expecially 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 distinquish
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 treaments 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 petter 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 reall 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 
Subject: Bob C: Round One: Adrenal Reposts

Q: "I have had great success with [homeopathic] remidies 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
compliling 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 explaination 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?
Infinate 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
differntly 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:    Mon, 2 Mar 1998 11:32:38 -0500
From:    Alicia K Drakiotes 
Subject: Adrenal disease -- more thorughts

Hello again Bob-- you wrote:
>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, expecially those neutered at about a month of age.  This is
>because the growth curves of the various species are different, so one
>being neutere d at 6 weeks might be the physiological equal to another
>species being neutered at 3 weeks.  I know of no research into this issue.

I do admire your extensive undertaking-- if you have delved at all into the
study of endocrinology-- the manifestation of adrenal disease in the ferret
should not be so surprising.

I realize their is no study on endicrinology OF the ferret-- but truly it
does not differ so drastically from us humans-- if it did the ferrets woudl
not be used so extensively in human research.

It is demonstrated in printed matter, and publications that the pituitary
gland looks first within the network of systems to the gonad group-- that is
the mammory's and the testis.  These are the very same components which are
removed during the early alter-- then once the messages are not being sent
from this region the pituitary goes shopping for input- and in a round about
way the adrenals are next in line to fill in the missing messages.  NOw I do
admit this explanation has been somewhat tailored so our readers can relate
to the post ..

 ...the adrenals then manage their own messages and pick up the slack
for the missing gonads.  Overwork is easy to interpret.  Combine that
the overwork from very early onset with any one of the conditions
aforementioned--

POOR NUTRITION: which could be lack of nutrition- either due to improper
diet, neglect etc.; or nutrition which is composed of caustic ingredients (
those which cause difficulty to the systems) such as artificial colors,
preservatives, etc.; or incorrect ingredients.  Nutrition today is not what
it was many years ago-- even grains to feed poultry and cattle - for food
basis - are chemically treated these days-- and many other variables in
developing the feed could fall under the nutrition aspect-

STRESS: could be from early onset with removing the kit prematurely from the
mother-- ; or it might be from the stress and trauma of shipping, pet store
holding and transfer, or from being in an unsettling environment, improper
training, a violent household... it could even be the result of prolonged
illness...

ENVIRONMENTAL: this could be anything from photoperiods to allergens etc.
We would need a week to discuss environmental causes-- especially if the
immune system were to be compromised from the beginning due to early alter...
the case is we need to study and one quick answer will not say it all.

The underlying fact is the system (the early alter- case specific) is taxed
from the beginning.  Any additional attack from any of the stated factors--
and perhaps more not stated will surely make the system crash earlier.

While many folks are finding some band aids to the adrenal disease-- that is
all that it is -- a short term remedy to buy some quality time-- we are not
"fixing" anything.  In comparing the ferrets to dogs and cats we miss the
boat-- the animals (cats and dogs) have a longer lifeline to begin with...
then you compare the ferrets higher metabolic rate---- and do not forget (
you didn't-- it is in the copied text) that comparatively the ferret is
altered at / before 6 weeks of age-- where cats and dogs are usually 12
weeks-- perhaps 10 weeks-- when their bodies do benefit from developing more
completely.

I have conferred with a few vets who have stated that they do see some
bladder and cushings in dogs they know were altered earlier than in previous
years-- and while a few more cases do not make a grand case-- it should be a
consideration.

Truly we need a study-- but in the end I will not be surprised to see that
the disease is related to endocrinology-- with many varying conditions which
provoke it- of course in this case hormonal supplements might make up for
the loss of hormonal messages-- but there would be no way to regulate these
in a growing and developing ferret body-- at least not easily.  What all
this discussion has shown us is that there is a definite need for study.
There are no easy answers-- in fact there to date are no answers at all....

The need is here for those who want to invest their time, talents and gifts,
in the end we might see healthier, happier ferrets, and perhaps a longer
lifeline for them as a result.

Good discussion-- where does it lead to now?

Alicia

------------------------------

Date:    Tue, 3 Mar 1998 05:37:56 -0600
From:    Bob Church 
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 independantly verifiable, reproducable
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
noticable as between them and the late neutered guys, who are truely
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 betwen 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

------------------------------

Date:    Wed, 4 Mar 1998 18:16:22 -0600
From:    Bob Church 
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 foriegn 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

------------------------------

Date:    Thu, 5 Mar 1998 08:35:50 -0600
From:    Bob Church 
Subject: Bob C: Last Adrenal Questions (for now)

This is the last I've recieved 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 potiential 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 advertizing.  Large incomes = large
ad budgets = slick ads.  Advertizers 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 disapointing 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 expoited 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 tatooed 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 expoiting 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 truely
(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 noticable.  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 strengh 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

------------------------------

Date:    Fri, 6 Mar 1998 04:16:19 -0600
From:    Bob Church 
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, rivialing 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 fooods for ferrets have also
become quite popular.  Create a graph in your mind.  One line the is incease
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 definately 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, temperment 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 nonMF 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
definately 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 foriegn 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.

BOb C and 19 Furbutts pulling for Jet.

------------------------------

Date:    Fri, 6 Mar 1998 15:21:32 EST
From:    Miska BC 
Subject: Adrenal Article

I'm not sure if anything has been posted about this, since I'm weeks
(months?) behind in my fml reading, other than what people send me.  My
vet, Charles Weiss, completed an adrenal study of 96 ferrets - 94 with
adrenal tumors.  The article was published in the Journal of the American
Animal Hospital Association, December 997, Vol.  33.  If anyone would like
a copy, just send me a private e-mail with your name and address.
Unfortunately, the cost of doing color copying is prohibitive, but there
are only 3 small pictures and the text tells the story anyway.

When I asked Dr. Weiss what stood out the most in the study, he discussed
two items.  The first is male agression, or "return to sexual behavior." In
100% of the males who exhibited a return to male sexual behavior, the
diagnosis was cancer - adrenocortical carcinoma, rather than benign tumors.
Since there were only 7 subjects who fit this profile, he said further
research would be needed to see if the trend held, but it would make sense
to get males who are exhibiting this behavior, to the vet rather than
waiting.

The second had to do with the use of prednisone after adrenal surgery.  In
dogs and cats post-op glucocorticoids are administered for unilateral and
bilateral adrenalectomies.  The drug appears to be unnecessary for ferrets.
95.6% did not require steroid replacement following surgery.  The 4% that
did showed mild lethargy and anorexia but did not develop life-threatening
symptoms.  It is suggested that glucocoricoid replacement is only
administered if these symptoms are present for more than four days post-op.

This is particularly valuable for ferrets who also have concurrent insulinoma
surgery (26.6% in his study) since ferrets recuperating from insulinoma
surgery are more prone to developing pancreatitis if they receive
glucocorticoids.

A second study involving bilateral adrenal ferrets is about 18 months
underway.  Removing the larger tumor and about 50-60% of the right one seems
to be resulting in no recurrance so far.

Last, Dr. Weiss has just completed a large insulinoma surgery.  His journal
article is making it's way through the slow journal process, and hopefully
will be published within 4 to 6 months.  Better results are being obtained
with partial pancreatectomies - removal of the tumor(s) and about 1/3 to 1/2
of the pancreas, rather than just the tumors or "popping" the tumors, which
can seed rapidly.  This surgery is more difficult when the tumor(s) is/are
on the side closer to the intestinal tract.

Veterinarians who want to discuss the partial pancreatectomy technique or
the adrenal study are welcome to call Dr. Weiss at (301) 299-4142.  While he
will make every attempt to call back owners who call him, at times it can be
extremely difficult with his surgeries, medical appointments and family -
including a toddler.  So I know you will be respectful of his time and
invitation.  His e-mail address is CLT@aol.com and he tries to check it once
or twice a week.

BTW, I keep hearing about vets who are fasting ferrets pre-op from midnight
the night before surgery.  Three hours is plenty, and if your vet doesn't
believe it, they may want to call him or another skilled ferret vet, or read
Hillyer's vet book, Ferrets, Rabbits, and Rodents.  Please excuse my rushed,
non-medical words.  I keep meaning to polish this post up, but if I wait
until I have the time to do that, I'll never post.  I'm not a vet, vet tech
or medical anything, just an owner struggling to learn as much as I can.

Beth

------------------------------