3 minutes a day in a centrifuge was part of the failed biosensor "super dog" program.

Dog culture is lazy and unoriginal, and profoundly stagnant. The desire for easy answers, simplistic how-tos and formulas for success is rampant. Just do this one simple thing! 

Breeders eschew complexity, uncertainty, and experimentation. They fear change and embrace unproven tradition on face value.  We do it this way because we’ve always done it this way.

Reason gives way to mimicry, and that is the true mark of conformation: not in the dogs keeping to a written standard but in breeders kowtowing to the unwritten rites and rituals to fit in.

One cherished ritual that can be found proudly advertised on numerous breeder websites (usually after the “Our Boys” and “Our Girls” links) as a sign of their reputable status and deep commitment to superior dogs is the adoption of the “Bio-Sensor” program as the one true path™ to dog raising.

In only 15-25 seconds a day for only 14 days in a dog’s life you will realize “life long lasting effects:” “improve performance,” “respond maximally,” “attain sexual maturity sooner,” “resist cancer and infectious disease,” “withstand terminal starvation,” achieve “psychological superiority,” “stronger heart beats,” “stronger adrenal glands,” and “improved cardio vascular performance!”

That’s less than 6 total minutes of work to make a super dog!  AMAZING!

The brains over at the sci-ence blog have come up with a handy chart to recognize quackery, the relevant parts of which I’ve reproduced here.  Their instructions:

“If you come upon a treatment or product that seems too good to be true, consult this handy guide to finding pseudoscience, scams, and quack medicine. Remember, it only takes one match to be considered suspect! Be safe, and be skeptical!”

This widely tauted “Bio Sensor” a.k.a “Super Dog” a.k.a “Early Neurological Stimulation” program has many warning signs of quack science.

Let’s start with who is peddling this pseudoscience:  Dr. Carmen a.k.a Carmelo Battaglia, Board of Directors of the American Kennel Club.

Dr. Carmen L. Battaglia, of Roswell, Georgia, owns and breeds German Shepherd Dogs and is Delegate and Past President of the German Shepherd Dog Club of America. Carmen has chaired the Committee for the Future and Business/Planning Committee and as a former AKC Director, served as Board liaison for the Health, Parent Club, HEC and By-Laws Delegates committees. He has published articles on breeding and legislation as well as several award-winning books. He also serves as an AKC expert witness in dog legislation cases and has written county dog legislation which resulted in the model that is used in several states. Carmen possesses a Doctorate from Florida State University and has been Assistant Dean at Emory University and Regional Administrator at the US Department of Education. He is also the President of Atlanta Student Aid (financial aid consulting Firm) as well as the past president/owner of three post secondary schools which were located in two states.

You’ll remember Dr. Battaglia from his resurrection of Lloyd Brackett and his infamous “Brackett’s Formula.”  Dr. Battaglia gives lectures on cruise ships to up-and-coming brown-nosers in the AKC hierarchy who want to buy the secret knowledge and pay the right gate keepers to fast track show success.  He’s the closest thing the AKC community has to a celebrity doctor.

But don’t get too comfortable with the idea that he’s a medical doctor, he isn’t.  He’s a Ph.D. doctor, which he readily advertises at the end of his publications:

Carmen L Battaglia holds a Ph.D. and Masters Degree from Florida State University. As an AKC judge, researcher and writer, he has been a leader in promotion of breeding better dogs and has written many articles and several books.

Dr. Battaglia is also a popular TV and radio talk show speaker. His seminars on breeding dogs, selecting sires and choosing puppies have been well received by the breed clubs all over the country. Those interested in learning more about his seminars should contact him directly.

Visit his website at http://www.breedingbetterdogs.com

What he doesn’t advertise anywhere that I’ve found despite an extensive search is what subjects his degrees are in.  So I contacted the Curriculum Publications Coordinator at Florida State University and found out the unpublished truth:  B.A. Psychology 1958, M.S. Social Welfare 1960, PhD Joint Doctoral Program in Criminology Corrections and Sociology 1968.

So by way of education, Dr. Battaglia is more equipped to run a prison than a breeding program.  His dissertation was titled “Deviant behavior of parolees and the decision-making process of parole supervisors.”

The next indicator that “Bio-Sensor” is quack science is because it’s being SOLD as a how-to guide to success without having been vetted in any way by scientists in peer reviewed publications resulting from studies done according to the scientific method.

Dr. Battaglia sells his program along with breeding and puppy selection advice as part of his self-help for dog breeding commercial venture.  You can buy books, videos, DVDs, and subscribe to his newsletter and attend his lectures.

In accordance with yet another quackery red flag, Dr. Battaglia is pitching program that offers medical benefits but he (nor anyone else) has no peer-reviewed journal articles on his protocol. And it’s not for lack of trying.  If you visit his website you will find a link to request his so far unpublished journal article.  When you do so, you will be e-mailed a copy of an extended version of his Bio-Sensor article spruced up to look like an actual experiment with “Methods and Materials” and everything.

It appears from the file that Dr. Battaglia has attempted to get this article published since at least 2007, but he will warn you that the article is still under intense review and thus you can not share it.

This wouldn’t be the first time that the “Bio Sensor” program has been used to sell a self-help program, however, as Dr. Battaglia collaborated with Stanley Coren–king of marketing shoddy dog science to pet owners in book form–who included the information in his book Why Does My Dog Act That Way?

Battaglia and Coren’s considerable influence on the dog fancy combined with Battaglia offering the super simplified how-to instructions for achiving super dog success for free on his website as a teaser for his suite of videos, books, and lectures the “Early Neurological Stimulation” program has saturated the hobby pet breeder culture.  Breeder testimonials and reprints of the method are everywhere.

Diligently following Dr. Battaglia’s advice, there are breeders out there inbreeding their lines and producing singleton puppies who none-the-less credit Brackett’s Formula and the amazing Bio-Sensor program for giving them a super puppy abounding with exceptional qualities.

Apparently I’m part of a silent minority who have even questioned this program’s merits and the academic bona fides of the man who peddles it from coast to coast, as I’ve found no online criticism of the methods and not even one other soul who questioned what Dr. Battaglia’s field of study was until I sent out feelers over a year ago.

But it’s clear to me that Bio-Sensor is being marketed just like quack science is marketed, by people who have a vested financial interest in selling easy answers and quick fixes to gullible pet breeders who spend fortunes trying to rectify their ignorance with short cuts and feel-good nonsense.

In a quadrumvirate of quackery, Battaglia also uses his “Breeding Better Dogs” website to sell Japanese (think Eastern medicine) magic magnetic shoe inserts and magic magnetic dog beds that are “combined with magnetic technology, another ancient principle” and “enhance the body’s energy flow to allow healing and proper metabolism.”  This is a man perfectly willing to market quack science as a miracle product for profit.

So far I’ve shown that Bio-Sensor looks like a duck, and in a future post I’ll show you how it quacks like a duck as well.

Dr. Bruce Cattanach turned to the dark side, using the NBT gene when manual tail docking was outlawed.

In Without a Tail to Sit On I laid out the current body of evidence regarding deleterious health effects of the Bobtail gene and in the Like a Bobtail Without an Anus post, I called out Dr. Bruce Cattanach for failing to update his published views on Bobtail (NBT) complications and efficacy.

I contacted Dr. Cattanach for comment and this is our conversation wherein Dr. Cattanach can find no specific errors in my arguments and argues only that I didn’t paint a balanced enough picture of his efforts.  When presented with new findings and documented DNA studies, Dr. Cattanach has chosen to take his ball and go home, mad that I’d dare question the efficacy of using Bobtail.  He failed to answer very simple and direct questions such as “Do you still claim that there are no ill effects from NBT?” and “Do you still claim that litter sizes are not reduced by NBT?”

He is totally unwilling to reconsider his position or even admit that there is new documented DNA evidence. He still claims that no DNA tests have been done to confirm live birth homozygous NBT puppies.  He also incorrectly claims that there is only one form of bobtail, this is also false.

While his continued denial is unfortunate, I feel totally vindicated in all my criticism of Dr. Cattanach and his publications.  He has talked all around the issue but has failed to provide a single fact that would contradict even one statement I have made.

Here is our correspondence for you to decide for yourself.  My post is on the left, his on the right.  While I’ve broken it up for comprehension, you can chose to read down each column if you’d like to reconstruct our e-mails in an undivided manner, no material was left out.  This is best read here on the blog webpage versus in an e-mail or feed reader given the easy color coding I’ve used.

Dr. Cattanach,

I’m disappointed that you have come out against the Australian Shepherd x Nova Scotia Duck Tolling Retriever cross that was discussed on Jemima Harrison’s Pedigree Dogs Exposed blog.  I think that someone of your clout coming out so hard against this cross is detrimental and I’ve made my case in a series of posts on my blog.  I’m not just disappointed because I disagree with your conclusion, I don’t find merit in your arguments against the cross.

http://www.astraean.com/borderwars/2011/11/like-a-bobtail-without-an-anus.html

I also think that research done since (and often with the help of) the work you did on Bobtail has now made it clear that all of your assumptions regarding the health implications of the Corgi Bobtail gene are wrong.  Litter sizes are reduced, homozygous bobtail puppies are born and they are grotesque, and we have mounting reasons to believe that even a single copy of bobtail is not benign. My analysis is documented in full in the following post.

http://www.astraean.com/borderwars/2011/11/without-a-tail-to-sit-on.html

I invite you to rebut my points and comment.

Christopher Landauer
BorderWars Blog
Colorado, United States

Dear Christopher,

I think you are misreading or misinterpreting my writings. Not very nice. But since you appear well-motivated I will try to present things to you in a different light. I would normally do this right away, immediately, but I am in the midst of a huge chore connected with a search for the gene for Boxer cardiomyopathy – with a Friday deadline. Since this has priorities way above petty bobtails I cannot reply to your message at this minute but I will write at the weekend or very shortly thereafter.

Bruce

Dr. Cattanach,

Thank you for your reply during this busy season. I appreciate you finding the time to consider and respond to my questions. Can I share our continued discussions on my blog?

I managed to get my essential cardiomyopathy work done yesterday and today is going to be a very broken day so I thought I would use the time on you and start work again tomorrow.

My general view of what you have written is that while most points are not incorrect they are not in balance. There is no quantitation of risk…

I’m very specific about the documented risks. I have in no way overstated the case and I have avoided making gross speculations as to the incidence of disease, and thus risk.

I actually quoted several risk statements lifted directly from the linked papers.

“short-tailed x short-tailed crosses revealed a 29% reduction in litter size”
“Avg. # pups in NBT X NBT litters = 5.83
Avg. # pups in Full-tail X NBT litters = 7.55
Avg. # pups in Full-tail X Full-tail litters = 7.22″
“Norwegian Corgi data indicated a shortage of bob-tail pups (66%) relative to the 75% expected from bob-tail x bob-tail matings, suggesting that the homozygotes are lost before birth.”
“This clearly means a failure rate of 34% versus 25%.”

Etc. etc. etc.

… and there is no recognition that there is a progression of evidence collection – what is known today may be modified tomorrow.

I attempted to make this idea clear with phrases like:

“New research and understanding…”

“in the light of more evidence”

“Unlike our state of uninformed ignorance when Dr. Cattanach first made his proclamation of a harmless NBT gene and worry-free NBTxNBT breeding, time and more rigorous examination (including a DNA test for NBT which was developed with assistance from Dr. Cattanach) has begun to document that Dr. Cattanach’s bases for concluding that there was no ethical considerations no longer hold true and never did.”

“Given that Dr. Cattanch’s assertions are now documented false,”

“In a previous post I spoke about new research making Dr. Bruce Cattanach’s old understanding of the Bobtail Gene obsolete and reopening the debate about the ethics of this gene which he had previously (more than 15 years ago) declared problem free.”

I’m not sure what else I can do to establish that this is an evolving issue with more information over time, specifically 15+ years. I’m not criticizing your position 15 years ago, I’m criticizing you for not changing your position in light of more evidence which I believe makes a compelling case to justify a radical change in view and a recognition that the blanket dismissals of downside risk you made before are now inappropriate and factually incorrect.

If you have reviewed this information, I do not find evidence of this on your webpage.

I have had to reappraise my thinking as evidence has accumulated, and while at times I have been very worried about certain findings nothing has turned up that has really changed things – one can easily and ethically live with the bobtail.

Really? Nothing has changed?

Do you still stand by this statement 100%:

I have to conclude that while the evidence of lethality is disappointing, it is not an ethical problem. Without any detectable ill-effects, the only undesirable feature of the bob-tail condition is that it will not breed true. There will always be a 25% expectation of long tailed pups appearing. That we now know why this occurs simply means that, in a sense, we now know too much.

So! If there are no ill effects, if litter sizes are not reduced, if the only unwanted feature is the persistent appearance of some long tailed pups in litters, is this acceptable in the event of a docking ban?

Do you still claim that there are no ill effects?

Do you still claim that litter sizes are not reduced?

Do you also agree that it would be wise to inform breeders that there’s a real difference between prior probability and posterior probability and that they should actually expect to realize up to a 33% chance of tailed puppies appearing (surviving)?

I should start  with a word of yours that I do object to – assumption.  I do not assume anything.  I place a educated interpretation on findings.

The interpretations may change as the findings change.  And by educated, I mean a lifetime in mouse genetics, handling, analysing lab mouse mutants of all kinds, investigating inheritances and learning about the biological events that occur during development.

So do I.  There is a very high burden of proof if you want to claim no ill effects and litter sizes not being reduced.  The actual findings where I have seen published data and methods suggest that those two assertions have ample evidence against them being true.

 I would hope that everything I have said or concluded is based on established fact.

Again, the burden of proof is high for you to continue to stand by those statements. I realize that one does not prove a negative, as well as “the absence of proof is not the proof of absence” so we are dealing with a diagnosis by exclusion in some cases.  I am advocating for the third path here, that there is insufficient investigation to date and thus inadequate data to conclude one way or another on the actual health risks of this gene.  It could very well be that another midline defect causing gene is mostly or even solely responsible for imperforate anus and that the vast majority of documented disorders in single NBT dogs can be traced to another gene (achondroplasia, etc.). But until I see a study designed to test and exclude these possibilities I don’t think it’s prudent to table the discussion.

I have worked with many mouse tail mutations, some nasty, some benign.  The question has always been, where in the range of effects seen does the canine bobtail does fit.  The was, as always, a progression in the acquisition of knowledge.

When I started some 20 years ago it followed a little task I had conducted in Pembroke Corgis to clarify the mode of inheritance.  The breeders were convinced that there were homozygotes, these having the short stumpy tails and others with the somewhat longer tails were the heterozygotes.  I did find that the inheritance was that of a dominant, and this is what interested me later when thinking about the bobtail project;  it meant that I should be able to introduce the bobtail gene easily into a recipient breed very easily and then see how hard it would be to regain recipient type.  The first Boxer x Corgi cross established the dominant inheritance. (PROGRESS).

Didn’t Burns and Fraser (1966) and Pullig (1953) already establish inheritance patterns being dominant in several breeds and recessive and semi-dominant in others before the Boxer x Corgi cross?  I thought Corgi bobtail inheritance was a known issue long before 1992.

 Somewhere about this time I was introduced to the Corgi breed archivist in Norway.  He produced a substantial body of data which indicated a total absence of abnormal pups from BT x BT matings (with heavy cross-questing from me) and the further finding was that such breeding did not appear to reduce litter size.  (PROGRESS).  So were homozygotes born and indistinguishable from heterozygotes, or what happened to them?

And this data and methodology is as of yet unpublished? What value is it if it can not be reviewed.  If we took an breed acrhivist’s word on health, we’d have to agree with Dr. Claire Wade that Tollers are not inbred.  Method and published data are everything and I don’t think it’s wise to rely on untrained and undisciplined observers.  Nor do I have any trust in dog breeders to be honest and forthright about stillborn, malformed, and failure to thrive puppies.  There’s always some reason why such occurrences get attributed to “normal” and “natural” and thus not noteworthy or even worthy of documentation.

I’m not sure how a breed archivist could speak with any authority on a total absence of abnormal pups. In fact that finding alone is totally suspicious.  How could it be that there wasn’t so much as one reported umbilical hernia or cleft palate.

It’s a horrible assumption, and yes I’m using that word again, to put faith in something which has not only not been published but which is at face value preposterous.

If we are to rely on breeder’s words, why did you not include the 1991 calculations of Swedish Vallhund breeder Beng-Arne Bergman of Boerasens kennels who observed a ~25% litter size decrease in NBT x NBT matings.  The Vastgotaspets magazine carried the story and it was possibly in SKKs Hundsport as well.  Bergman reaffirmed Burns & Fraser’s theory.

About this time I got together with Astrid Indrobo at the Norwegian vet school in Oslo and found that a detailed search on bobtail Corgis had failed to find any trace of spinal or other defects (PROGRESS).  This is published work; you will have seen this in her 2007 paper.

The INDREBØ paper is the one I acquired the images of from, so of course I’ve read it. I also read that they studied 19 adult dogs. Were these randomly selected adults or were they volunteered dogs?  I don’t see 19 dogs as a good sized N, and if I were designing a study, I’d track entire litters and do x-rays in-utero and of puppies in addition to adults.

To avoid selection bias, a much larger N and an improved method should be conducted before I’d put much weight in concluding that the absence of evidence suggests strongly that there are no associated defects.

I’ve said before with respect to the merle gene:
Until I see a study which compares breeds using a sound method (like looking at whole litters, not just tested adults), I don’t think there’s much value in assuming that some breeds are magically protected from the effects of double merle.

Even with these limitations for bobtail, the Indrebo study found this:

Short-tailed dogs
No congenital spinal defects were diagnosed in any of the examined shorttailed dogs. Consequently, none of their long-tailed siblings were summoned for examination. The examinations revealed degenerative changes in two dogs. A 10-year-old dog had ventral spondylosis between C2 and C3, with a narrow intervertebral space, and small osteophytes were seen in several places in the lumbar column. Another dog, two years old, had a narrow intervertebral space between C2 and C3 and ventral osteophytes bridging these two vertebrae.

Is that worth writing off? Two dogs out of 19 with documented degenerative changes.

 The Boxer backcrosses provided the perfect material for finding the gene responsible and this I managed to do by getting some colleagues with molecular biology experience to do the work.  The T-box gene as it is called and the specific mutation responsible  was identified  and note this was done in my crosses, not in Corgis, as Hyotonin incorrectly states in her paper.  I was disappointed in the finding as I knew T mutations in the mouse could cause homozygous abnormality – but where did the canine bobtail fit within the wide range of effects/no effects seen in the mouse?  (PROGRESS)

You do know that there are documented abnormalities in mice for HETEROzygous Tbox mutations, no? e.g. cardiac outflow tract anomlaies consistent with DiGeorge syndrome as reported by Jerome and Papaioannou in 2001?

Here I got in touch with Indrebo again to investigate. The reason for this was that bobtail Boxers or crosses were rare, while bobtail Corgis in Norway were almost the norm. The breed archivist provided the material, about 20 bobtails were screened for the gene by the vet school molecular biologist and none were found to be homozygotes. It was concluded that the homozygote does not survive to term. The total work was published (Haworth). It had a flaw that I was very angry about but nevertheless it established that homozygotes are not normally recoverable. (PROGRESS)

At this point I nearly quit. It was clear that the bobtail would never breed true. What was the purpose to having only a proportion of dogs with short tails? Some argued that this was OK; it allowed choice and it would allow Boxers with the original image to be shown. So?? But by this time the bobtail story was big news in terms of the ease with which two very discordant breeds could crossed and type very quickly re-established. It became teaching material at vet schools and a lever for breed crossing as was surely going to be necessary in the future. Do I stop and therefore probably convince recalcitrant dog breeders that breed crossing cannot work without losing breed type.

I should say that I looked around for other ‘better’ short tails that might have a recessive inheritance and breed true, and I had even worked out a scheme by which a recessive could be used. But then I knew I would be branded as a mongrel breeder and all progress towards making breed crossing for whatever purpose acceptable. I chose to keep going.

I personally X-ray screened about 15 heterozygotes with my own vet.  Nothing was found wrong with the spines that cannot regularly be found in ‘normal’ dogs/Boxers (mine).  So, we have agreement with the Norwegian Corgi data (PROGRESS)  Please forget rumours.

I’m not sure what rumors you’re referring to.

Then Catherine Andre and Marjo Hyotonin independently got in touch with me, both having screened some short tail breeds and finding that the bobtail gene was present in most. It was tricky being in the middle but I got them together and this resulted in the paper you have seen. And since then further breeds with the gene have surfaced. I had also looked for such bobtails in other breeds; and the numbers continue to increase. There was a fair consistency in the findings in these very different breeds.

Some had a reduced litter size in BT x BT matings as reported in Vallhunds, some did not, like Corgis.

Do you really think that if a proper study was done with Corgis that we would not find reduced litter sizes?

Not one breed could tell of a single occurrence of an abnormal pup, and given the type of people I was talking to, I believed them.

Again, this is preposterous on its face. There was not so much as a single puppy worthy of investigating? I just don’t believe blanket denials.  This is as silly as interviewing an entire convention of Alcoholics Anonymous and finding zero relapses.  Relapse is an expected result and so are sub-optimal puppies.

But then I have also done a few BT x BT matings myself with 20 t0 30 pups.  Not many perhaps but all were OK – bar one.  This did not indeed have an anus, but then I found the same occurring the non-bobtail line I had used.  Panic over, or reduced. (PROGRESS)

Was this documented on your website? I was prepared to chastise a Vallhund breeder who is publishing essays on your work claiming that it documents double bobtails, but I failed to find evidence that you ever performed an NBT x NBT mating.

I would not be so quick to write off a 3-5% rate of imperforate anus. The fact that this also occurs in another normal line is no conciliation.

This observation fits with the findings of the Finnish breed club for Swedish Vallhunds which suggests ~5% abnormal puppies born from NBTxNBT.  The club did not document similar abnormal puppies in Long Tail x LT breedings.

One of these abnormal NBTxNBT puppies has been sent to researchers and tested and found to be homozygous.  Given the sensitive and emotional nature of breeding abnormal puppies, how many were just trash canned and undocumented in any way?

If you read the Australian Shepherd study I referenced they use your writings to go out of their way to discount negative findings and leave them out of their results and they still find problems.  I don’t consider soft-pedaling negative outcomes a responsible stance.

Frankly, I see that you are very easy to dismiss damaging data and very easy to accept any excuse or assumed cause that allows you to do so.  If you want me to table imperforate anus as a possible side effect of NBT, show me data that excludes a conclusion of correlation.

If this midline defect exists in your lines, as another comment as arrived on the blog to indicate, were they tested for NBT and are you looking for a possible genetic cause for imperforate anus? I’m going to keep imperforate anus in the possible NBT side effect column until it fits better in another column.

Then I recognised that all these bobtail breeds were working/droving/farm dogs (except two which had working dogs in their ancestry). What does this mean? The breeds were so different, from OESs to Corgis, Mountain dogs to Vallhunds, and therefore of very different evolutionary ancestry such the mutation (and there is only the one responsible) must have occurred many centuries ago and spread to different breeds doing different but superficially similar jobs, all well before today’s breeds were thought of? I can’t really understand the selection pressure needed but I have some theories. (PROGRESS in understanding)

Then I hear this year of the bobtail in Rotties (DNA verified), another drovers dog. And then only this morning I hear about a group of Dobes (being DNA tested) and here there is an extra twist to the tale (excuse me). Boxers have a range of bobtail expression. Chunky solid heavy-boned European types most often have the short stubby tail. But lighter bones racier American types tend to have much longer tails often with kinks. Dobes have, to my eyes, thin whippy tails. Within a litter with the one bobtail Dobe I have seen (short stubby tail), were 4 others with slightly short tails, and these had clear traces of kinks. Almost certainly these would be genetically bobtail. I have asked the owner to DNA test them to confirm this, and test breed them if she can. And of course all these breeds were traditionally docked, and one can be sure that a kinked tail would not be noted particularly; it would simply be docked. So the bobtail in different guises are common enough in various breeds. It is all beginning to fall in to place. (PROGRESS INDEED). Incidentally, I have urged the owners to think carefully about promoting bobtails in this breed. Most commonly the tails is not even of the type wanted. But the bobtail can now be seen to be the hallmark of the true working farm/drovers dog.

However we have the two abnormal Corgis  that were claimed to be homozygotes.  The finding was made in a purely descriptive paper, there was no molecular data presented (just a statement), there was no further investigation within the breed or any breed.

Please refresh my memory which Corgi claim is just descriptive because the Indrebo paper claims to have done the DNA analysis to establish homozygous NBT.

 The finding stands alone.  If correct, there may be further cases, but with what frequency?  This is the point.  Were it 25% as one might expect, this would be horrendous and no one would want to breed such dogs.  But very clearly, it can be nowhere near 25%; there would be an uproar.

Well, we now have plenty of documentation of 25% reductions in litter sizes and there’s little uproar.  I’ve read Puppy Intensive Care manuals and videos and my interpretation from the people who put those out that abnormalities are much more common and severe than I had anticipated. Luckily I have a healthy breed and have yet to deal with any abnormal puppies or failures to thrive.  But I don’t think the general temperature around the dog world is healthy large litters with few issues.

So what about 5%.  I doubt this too (only the one breeding).

If we water the potential homozygous and even heterozgous dogs down, 5% doesn’t sound horrible, but what if we find that about 20% of NBTxNBT potential puppies die in utero and 5% are born with problems.  That does add in different ways to our failure rate, no?

We are talking about posterior (observed) probabilities of 33% tailed dogs (undesirable) and 5% abnormal dogs (undesirable).  38% failure rate is not something to ignore.

So maybe 1% or 0.1%?  And here you are getting into the range of deaths occurring spontaneously for all sorts of reasons.  Some of these may be due to lethal genes which have no effect in the heterozygote and these would be so easily missed.  I actually found one in mice a few weeks ago.  It was in an inbred strain that is well-monitored but nobody had detected anything amiss – until I found the deaths in routine ‘opening’ done for a different purpose.

So you agree that until we can put a solid number based upon comprehensive and well designed science on the true incidence of disorder here, it’s foolish to over-sell the idea that such disorder does not exist, period.

Few prenatal deaths occur late enough to see abnormal embryos.  Most die around the time of implantation and all that is left when one looks later are the implantation sites,  which are smaller than a match-stick head.

I’ve never seen a comprehensive and objective look at this phenomenon with data.  And I’m not suggesting that it’s not out there just that I have not come across it.

Normal matings have measurable incident of these, up to 5 or even 10%.  Losses like this affect nothing but, as I have said bobtail losses may replace the natural deaths.

I don’t know if it’s safe to assert that nothing is different if you start adding lethal semi-dominants.  In the Aussie study, a whole NBTxNBT litter was both smaller than average and lost in totum for being premature.  The compiler decided to leave that data out.  I think that’s questionable.  If you keep leaving out negative outcomes, you preclude any findings of correlated disorder through cherry picking.

This is old news for me.  Of course there are neonatal deaths with some mutants where the newborn cannot cope independently outside the uterus, but these are a very different group.  You can have one or the other depending upon when the gene has its effect, but it is truly rare to find early deaths AND neonatal deaths.

Again, I have not seen any work on this published.  I would like to have some means of quantifying the incidence of these issues but I don’t see any breed clubs rushing to fund studies or any having been published in the past.  If you know of any, I’d be interested in reading them.

It is for the this reason that I also question the two surviving bobtails.  They do not fit the standard biological picture. I really can’t get too worried about a very rare event, or at least not enough to suggest eliminating the bobtail from all the 20 to 30 breeds.  What level of damage would this cause?

Eliminating bobtail is certainly a radical position. You don’t see me making that suggestion, but I’m not going to deny the possibility that breeders might want to breed away from it.  Just because it’s historical and exists in multiple breeds is not sufficient justification for me to ignore it.  If we are going to accept these iffy genes like merle, we are going to have to do so with an open mind and aware of the choice we are making.  If there is a balance argument here, we have to be honest and place the negative elements on the scale, we can’t simply refuse to make that calculation because it might make us look bad.

The means to breed out disease or not is really in the details of how it is done.

 As well as this, unless something different is found, I suggest the risk of abnormal bobtails is far less than the cancer risk in gray horses, or the deafness and blindness in merle breeding (up to 25%),  or the dermoid sinus in RRs (not much lower I expect), or the deafness in Dalmatians (maybe 10% bilaterally and  a much higher incidence unilaterally, with somewhat lower incidences of deafness in other such white breeds, or the toothlessness of naked breeds(50%).  If these breeds are to be ‘hit’ then maybe bobtail breeds should too, but I don’t think this would make much sense.  It is unfortunate that so many of the fancy features we have introduced into and maintained in dogs have some level of deleterious effect.  I think a lot could and should be done about many of these.

I’m not sure that comparative health gets us anywhere. I don’t believe that anyone wants a dog that is marginally more healthy than the neighbor, I think the goal should be measured in absolute health. We want healthy dogs. If there is value to be had in comparative disorder/disease load then we’ll need a lot more comprehensive studies than we have now and I don’t see anyone rushing to fund those.

As for me, I write about all of those issues.  Bobtail is of interest because I’m working my way though the lethal semi-dominant genes, which are a curiosity.  I’ve written about merle, bobtail, harlequin, and will eventually work through hairless (Xolo, C.Crested) and possibly the new “panda” color in GSDs.  If I find any more lethal semi-dominants in dogs, I’ll write about them as well.

I have not dealt with breed crossing issues or Tollers but I think I have written enough here to show you my own excitement and enthusiasm for animal breeding, and my  constant quest to investigate and research unusual situations.  But I am first and foremost a geneticist with a log association with dogs and their breeding.  But I do not have the more basic dog breeder attitudes and I do not get involved in ringside gossip, innuendo and all that I am afraid is becoming more and more the norm in dog showing today.

Well then we at least share much of the same motivation, although I cannot claim to have as deep an education in genetics as you do, nor have I been breeding as long.  But I am an accomplished student of science winning numerous awards in the sciences throughout my education, including Engineering at Stanford, and I have tutored Chemistry and Biology at AP and college level, so I don’t have too much trouble deciphering the published material in these areas.  This is less an appeal to any of my arguments being correct as it is an explanation of why I am motivated to raise the level of discourse in the dog world regarding genetics issues.  There is just SO MUCH junk science being spewed on the internet and in conformation publications that an autodidact like me can spot as horribly wrong.

I have an entire series of posts dealing with inbreeding mistakes alone. http://www.astraean.com/borderwars/category/health-genetics/inbred-mistakes

I can’t bear to check what I have written but I hope it answers some of your questions. The rest later.

I appreciate the dialogue. Thank you.

Christopher Landauer
BorderWars blog

My correspondence with you stopped when I was hit with a load of work in connection with Boxer cardiomyopathy and junior kidney disease.  Actual work on both, I think you would agree, are far more important than discussions about bobtails.  And this work is still in progress and will no doubt keep me busy, step by step, until  the processes towards finding the genes responsible either succeed or fail.  So, I’m sorry but I cannot take time away from this to deal with your ongoing questions about bobtails.

I would only say that you are have selected one set of data and are ignoring the big picture; and your are over-interpreting.  And the last line is absolutely reasonable.  66% of pups born from BT x BT matings being bobtails (2 out of 3) is spot on.  Think again.

No doubt you think you are doing canine health a service with your arguments.  I don’t think you are helping anything and are simply confusing people and causing trouble for bobtail lines of dogs (all farm animal working dogs) that have been favoured by one means or another over many centuries and well before breeds were even thought of.

I do not want to play any part in your blog or anybody else’s.  I have tried, quite hard I think, to present you with the rationale development of understanding in bobtail genetics which no one in the field of genetics or even veterinary medicine would disagree.  But that’s it.  Think again.  You have spun off track.

Bruce Cattanach
bcattanach@steynmere.freeserve.co.uk

It seems to me that Dr. Cattanach is more concerned with his own legacy than with the true health of NBT breeds.  He’s very concerned with documenting the progress made and how he advanced knowledge of the genetics (sometimes taking credit for things that he was not the first to discover), which is really a matter that I am not contesting.  What he is clearly unable to do is re-evaluate the ethics of NBT and even the basic nature of NBT given more detailed studies that have been published since he began his work.

He has provided every excuse, mainly that he is busy with more important matters in Boxer health, but this doesn’t really hold water.  These studies have been out for years and years now and his failure to appreciate them is troubling and his outright lies about their rigor (claiming that there have been no DNA tests to confirm homozygous NBT live births when there have, instead claiming that the paper was merely descriptive) is rather unforgivable.

Cattanach is eternally skeptical of real published results but infinitely forgiving of his own use of bobtail.  He is now resorting to a string of logical fallacies to justify his whitewash of NBT: appeal to tradition, appeal to history, appeal to common practice, appeal to novelty, and even appeal to authority.

Dr. Cattanach has the history and the education to make better choices, but it is clear to me that he has walked down this path too far to be an objective judge of NBT and a fair critic of his own work.  He’s too wrapped up in telling the story of how bobtail knowledge evolved and blinded to the actual state of knowledge today.  He is clinging too adamantly on to the past, to a time when you could claim that NBT was problem free in good faith.  Those days are over and it’s time to get real.

Again, I call for the retirement of Dr. Cattanch as the go-to authority on the ethics and consequences of NBT in dogs.  His ethics and his understanding is out of date. He’s gone to the dark side.

Claire, a disabled harlequin Great Dane on the first day of her new life after being rescued from a torture breeder where she suffered for 4 years. She is doing much better now.

Oh Claire,

I’m sorry for all the suffering you’ve experienced in your life.  It’s one thing for me to write about qualzucht, torture breeding, and to think and debate about it in the abstract.  But when theory hits reality, when real dogs with real names and real stories come forth, it’s nearly impossible to remain objective and dispassionate given the true suffering you qualzucht dogs go through.

You have been tortured.  You were genetically tortured by the breeder who created you when they deliberately bred two Harlequin Great Danes together, doubling up on at least two lethal genes (harlequin and merle) and possibly doubling down on other genes known to contribute to deafness and blindness.  It’s likely that more than half the puppies that shared your mother’s womb died before birth from these defects, but you survived.

You were further tortured by this breeder when they neglected to provide any real care for you, letting you suffer from a slew of debilitating conditions.  They allowed parasitic demodectic mange mites to run rampant and cover the majority of your body, they allowed parasitic yeast to invade most of your orifices, and they allowed parasitic worms to invade your heart.  Your hearing, vision, and immune system were trashed by your parasitic breeder leaving you defenseless against further exploitation.

You were tortured again when this breeder used you to produce Great Dane Puppies to sell in the open market and then dumped you in a shelter as soon as the puppies were sold.

Parasites are organisms that invade other life forms and leech sustenance at the expense of their host.  Mange, yeast, and heartworms are all lower life form parasites that prey on higher life forms.  The person who bred you is just a low life who has habitually tortured and exploited you and gave you nothing in return.

Man is the highest life form known to exist, yet the person who tortured you in so many ways is the lowest of the low.

I’m sorry Claire.  I’m sorry we did this to you by not speaking out stronger against horrible breeding practices and condemning parasite breeders.   I’m sorry that we rewarded your parasite breeder by buying your puppies.  I’m sorry that those breeders who consider themselves elite and the highest of the high do the exact same things that have caused you so much pain by breeding harlequin to harlequin, merle to merle.  They are parasites too.

But there are better people out there Claire and I’m glad you’ve finally found some at the Foster to Furever community, the people at Big Dog Rescue, and April Albin who has been fostering you during your recovery.  The last four years of abuse and starvation must have been hell, Claire, but you’ve been given a new life now.

So happy one month rebirthday, Claire, you’re already a new dog and on your way to a better life.

Claire, one month into her recovery. The mange can be treated but her compromised immune system is forever. Food can cure the starvation she suffered. But the deafness and blindness that were caused by her breeder are permanent and not treatable.

Doctors Wade and Cattanach don't want you to buy this puppy. They'd rather have you buy one without an anus or a functioning immune system.

In a previous post I spoke about new research making Dr. Bruce Cattanach’s old understanding of the Bobtail Gene obsolete and reopening the debate about the ethics of this gene which he had previously (more than 15 years ago) declared problem free. But Dr. Cattanach decided to weigh in on the current debate over the Toller x Aussie outcross and his position is disappointing and uninformed.

Bruce Cattanach said…

I am somewhat amazed at the positive responses to this cross. I have had 20 years of vitriol against my Corgi x Boxer cross for every reason imaginable, but I kept it going as I felt that to give up – and so failing – I would damage the leverage it gave to the concept of breed crossing for health reasons. So the seemingly easy acceptance of the Toller cross is perplexing even if done for a different reason.

I really don’t know what to make of this statement, as it sort of reads like sour grapes. It’s unfortunate that Dr. Cattanach has gotten “vitriol” against his work, but he’s clearly learned enough to handle just criticisms. My analysis against his outcross comes after decades of new evidence and his unwillingness to acknowledge new findings. I don’t consider it vitriol.

It’s strange that Dr. Cattanach is seemingly jealous about the positive vibes the dog world has for the Toller cross litter. If I had to estimate why one has been received with more praise I can think of two immediate causes. One, Dr. Cattanach’s work paved the way and quelled many fears, so this new cross is benefiting from Cattanach’s work. It’s a pity he’s not more supportive. Two, this cross was done for much more noble reasons. As I’ve already documented, Dr. Cattanach inserted a problematic gene into a breed to avoid a docking ban. While it’s an interesting effort for the political reasons and documenting how easily breed type could be restored, the motives are decidedly shallow and superficial.

Does Dr. Cattanach really expect the world to beat a path to his door when he built a WORSE mouse trap?

However I had great difficulty achieving what I did with just the one gene to be transferred. It really needed more than one individual to succeed fully. I am therefore quite sceptical about this Toller effort to increase the diversity across the whole genome.

Dr. Cattanach has really moved the goal posts to an unjust distance in coming out against this one cross. He is holding this one cross to the standard of “increase the diversity across the whole genome.”

That’s unfair. No one claimed that doing one outcross could accomplish this goal! How about we evaluate a single outcross in a rational manner and judge its power to effect change commensurate with what we should expect from a single breeding. A single outcross can not save an entire breed, but it can certainly bring in much needed diversity and vitality to a single breeding program, a whole kennel and all the dogs that are bred to that line for several generations.

Any breeder who is disappointed with the options within their breed can accomplish this style of outcrossing themselves. And many more breeders will need to do this before we can claim that Tollers as a breed are refreshed.  The LUA Dalmatian project was only one out-cross and the entire breed is not yet free from uric acid problems, nor will it be for many generations to come. But you have to start somewhere and if we want fundamental change in our breeds, we’re going to have to accept that breeders will out-cross for a slew of reasons and that this isn’t that scary of a prospect.  It might just mean that we have to go back to objectively evaluating the dogs we see right before us instead of being overly obsessed with their hidden and mostly irrelevant pedigrees.  If we limit “allowable” out-crosses to combat single recessive diseases that are 100% saturated in our breed pool then we will never see the day when our breeds are getting healthier rather than the current reality where they are getting worse.

I think this needs to be done at a scale only possible at KC level with several crosses perhaps involving several breeds, and then there would be the yet trickier part of keeping the diversity while somehow getting back to breed type. That numbers of people might independently attempt this is frightening; it could result in no more than a mongrel mix-up.

I agree with Cattanach, this does “need to be done at a KC level” and of course I’m in support of using “several breeds” with “several crosses.” This is all true, but it’s not a just criticism of what this one breeder has begun to do. It really should be reserved as a criticism for the Toller breed club and for double-speak geneticists like Claire Wade who put their name on papers which advocate genetic diversity and proactive health measures but then declare zero reason to out-cross in their own breeds and attack those who do.

What good does Dr. Cattanach do by bashing this beginning step? He didn’t bring his out-cross program to the world after just one breeding, the dogs weren’t even retroactively registered with the KC until he had back-crossed several generations. So if there is some amount of “sausage making” with out-crossing, where the intermediate results aren’t indicative of the final product, isn’t it a bit rash to just criticize this nascent effort?

Is this out-cross so detrimental that it needs to be cut off at the knees by someone with Cattanach’s clout? I think he does great harm to anyone who would choose to out-cross for any reason by being so negative.

Jemima said…
Bruce’s position and enthusiasm managed to get the project sanctioned by the Kennel Club and the acceptance of it has paved an important way. Of course, the KC’s endorsement of the project was because of the impending threat of the docking ban; which the anti-dockers would argue is not the most worthy of motives.

His stance here even brings into question my previous view that his out-cross program was a good example of how one can work within the registry/breed club to accomplish something like this. In retrospect, Jemima makes a good point, that it’s perhaps much easier to get a conformation club to go along with an out-cross for conformation reasons when they are being threatened with a BIG BAD BAN on docking tails from those EVIL AR folks. Perhaps Dr. Cattanach’s efforts aren’t that informative to the rest of us who would support an outcross that you can’t see in the breed ring, one that is done for health reasons, for vitality, for genetic diversity, for longevity, for temperament, instead of one that allows you to keep some little irrelevant but highly valued feature like an earset or a particular length of tail.

If Dr. Cattanach paved a trail for future breeders, no one has yet to walk down that path in the 20 years since his out-cross and we’ll soon celebrate the 40th anniversary of the commencement of the LUA Dalmatian out-cross.  The first and last men to walk on the moon completed their missions in the years and days before the LUA Dalmatian cross and man has not set foot on the moon since; nor has man endeavored to out-cross a breed for health reasons.  One requires billions of dollars and the greatest minds the world has to offer in an attempt to overcome nearly insurmountable odds.  The other requires two dogs and a little patch of grass.  Why must we create political obstacles which make an out-cross more rare than a man walking on the moon?

If superficial out-crosses are the first step, how are we ever going to get to the next phase if the heroes of Step One decide to handicap future efforts like Cattanach is doing here? There hasn’t been another example of an out-cross in the KC since Cattanach did it, so the theory that he greased the wheels for those that followed hasn’t produced any results.  If we want results, we should try a new strategy, 20 years between out-crosses is long enough.

I am sceptical for another reason too. It almost seems that the Toller cross was done to resolve the high level of inbreeding but if there is no consequent problem of the inbreeding, to my view, the need for the cross does not exist. Is the breed impaired by the inbreeding? Frequencies of certain defects have been presented but I have seen nothing on the distribution across the breed (is the whole breed at risk?) and any indication of the inheritances. Everything seems based on a ‘belief’ that there will be problems even if there are none as yet. If there are indeed problems now or clearly looming, yes, go ahead or at least experiment and see what difficulties there are. But let this be done in an organised controlled way and on a scale commensurate with that needed.

Did Bruce just criticize someone about the NEED to out-cross? Really? Perhaps he can review my Toller articles and comment. Recall that Cattanach argued from ignorance before, claiming that there were no side effects from the bobtail gene, that litter sizes were not reduced, homozygous puppies and their problems never lived long enough to be born, etc. None of his assumptions were true and the bobtail gene is decidedly less wonderful the more we find out about it.

We already know that Tollers don’t live long, they have high rates of auto immune disease due to an MHC allele that is pervasive in the breed and few other alleles to turn to, as well as growing evidence of numerous other problems. We also know that the gene pool is severely limited due to a very very small founding population in the KC dogs.  Is that not reason enough?  How small of a founding population can we justify?  Only two dogs perhaps?  Is that where we’re going to draw the line.

Cattanach was wrong about the dangers of Bobtail and if he thinks there’s no justification to outcross Tollers, he’s wrong again.  Here’s a small list of conditions known to run in Tollers: Hemolytic Anemia, Addison’s Disease, Hypothyroidism, Pemphigus, Immune-Mediated Polyarthritis, Systemic Lupus Erythematosus, Congenital Deafness, Epilepsy, Pulmonary Stenosis, Steroid responsive Meningitis-arteritis, Cleft Lip and Cleft Palate, Mega-esophagus, Collie Eye Anomaly, Skeletal Dysplasia & Chondrodysplasia, and Herniated discs. More Tollers will suffer one or more of these conditions than will toll ducks even once in their lives, more will die young than will win Conformation Championships, and many more Tollers will be bred to dogs that are as close as siblings than will ever hoped to be out-crossed.

What more does Cattanach need to see?

Finally, there was a question on unneeded puppies in my breed cross. This was no problem when one presented the objective. Potential owners were told what the cross was all about. There was annual get-together where everybody met together with their dogs of different generations to observe progress It was a tea-and-cakes gathering in the garden and all were made to feel part of a research study that all could, and did, boast of participation. I still have contacts with many of the owners although the early dogs are long since dead.

Bruce Cattanach
www.steynmere.com
25 August 2011 22:56

Is Cattanach suggesting here that because the breeder of this Toller x Aussie litter isn’t a research scientist who can cloak his project in a veil of academia that these puppies aren’t going to find good homes? The sales value of “pedigree” and “purity” are as low now as it has ever been and the public’s awareness of hybrid vigor and appetite for designer dogs and other mixes is as high as ever. Given the choice between a show bred Aussie or a pedigreed Toller, I think any rational human would look at these hybrid puppies and agree that it’s a better product.

I see a resistance in Cattanach to come to terms with the health concerns in the bobtail gene in the same way Claire Wade doesn’t want to consider an outcross for MHC or any other reason. They both downplay the health concerns and I’d say both have a biased reason to do so: they are both highly invested in their dogs as they are. Wade doesn’t want to give up “purity” and Cattanach doesn’t want to reconsider the bobtail gene. Both are highly educated biologists who should know better.

Neither one thinks that you should buy what the Toller x Aussie breeder is selling, but do you buy what Wade and Cattanach are selling? I don’t.  Like a bobtail without an anus, I think they’re both full of it.

Dr. Cattanach claims puppies like this don't exist. It's a homozygous NBT bobtail corgi without a tail, no anal opening, structural defects, and an opening to the spine. Defective puppies like this are the direct result of breeding bobtail x bobtail and are sometimes carried to term and born alive.

I am somewhat amazed at the positive responses to this [Toller x Aussie] cross. I have had 20 years of vitriol against my Corgi x Boxer cross for every reason imaginable, but I kept it going as I felt that to give up – and so failing – I would damage the leverage it gave to the concept of breed crossing for health reasons. So the seemingly easy acceptance of the Toller cross is perplexing even if done for a different reason.

- Dr. Cattanach

Those of us in the dog world who support the free and open application of outcross breedings within a registry system have previously looked to the work of Dr. Bruce Cattanach’s natural bobtail boxer program with interest.  Along with the LUA Dalmatian project, it served as a go-to example of a practical out cross with good documentation that could quell the fears of the Pure-Blood-Brigade™ regarding instant and permanent breed ruination should someone anywhere breed two dogs that weren’t pedigreed in the same breed.  It still stands as an excellent example of how quickly you can restore breed type even with an extreme outcross.

But as the movement matures I think it’s advisable to retire Dr. Cattanach as a spokesman for the moral implications and justifications for outcross breeding. It must be noted that despite claiming that he persevered criticism of his program to one day help others who would outcross for health reasons, his Steynmere Boxer x Corgi program is exactly the opposite of this ideal.  He purposely inserted a gene which causes dysfunction into a breed which did not have this gene and he did so for the explicit purpose of evading a ban on manual tail docking.  This is a net-increase in disease, infertility, and disorder in the breed and I don’t think this action squares ethically.

No tail, no rectal opening, open hernia leading to spinal canal.

Compare a surgical procedure with very few complications or side effects that can be carried out with skill and efficiency and which leaves no permanent genetic mark on the breed vs. a semi-lethal gene which is implicated in a plethora of complications and negative side effects which can’t so easily be removed and which is far from precise in presentation.  The gene doesn’t even solve the issue 25-33% of the time and it will never breed true.  If tail docking is thought to be overly cruel simply for the momentary pain it causes, how can the basket of crap that comes along with the bobtail gene be considered more humane?

The greater theme of the outcross for health movement is to combat and repair the damage done by questionable breeding practices done in the name of conformation.  Isn’t inflicting the bobtail disfigurement gene on a breed so that they can still be made to fit a conformation ideal (and for no other reasonable purpose) the exact sort of breeding scheme the outcross movement is against? The Cattanach boxer-corgi cross was not done for health, it was done to promote disease.  It was not done to add or preserve diversity, it was actually done to preserve a conformation ethic and subvert an animal cruelty law.  This is not an outcross done for noble reasons, it was done to replace surgical scissors with a genetic hammer for the shallowest of reasons: historical aesthetics. New research and understanding of the T-box mutation also casts doubt on Cattanach’s assertion that there’s “nothing to worry about” with a single copy of the bobtail gene, that all homozygotes are harmlessly lost before birth, and that litter sizes are not affected.

ETHICAL CONSIDERATIONS

Whatever the correct interpretation of the discordant evidence, the molecular data establish that the homozygous Corgi bob-tail is a lethal condition. The term, lethal, has an ominous ring to it. It suggests something totally undesirable. Yet, having pondered the issue at length I have to conclude that while the evidence of lethality is disappointing, it is not an ethical problem. Without any detectable ill-effects, the only undesirable feature of the bob-tail condition is that it will not breed true. There will always be a 25% expectation of long tailed pups appearing. That we now know why this occurs simply means that, in a sense, we now know too much.

So! If there are no ill effects, if litter sizes are not reduced, if the only unwanted feature is the persistent appearance of some long tailed pups in litters, is this acceptable in the event of a docking ban? I suggest that it is now up to individuals to decide on this, and as I am now content that there is nothing nasty about the gene, I see no ethical reason for continuing to keep total control over these bob-tail Boxers. The situation is no different from that for all other breeds having this bob-tailed gene.

- Dr. Cattanach

The arguments Cattanach makes for bobtail don’t hold true in the light of more evidence: Litter sizes are reduced, there’s actually up to a 33% expectation of long tailed pups making this scheme considerably less effective, and ill effects from a single bobtail gene can not be ruled out in good faith.

For the Swedish Vallhunds [who have the same mutation as Corgis and Bobtil Boxers], analysis of the litter sizes from short-tailed x short-tailed crosses revealed a 29% reduction in litter size, further supporting recessive embryonic lethality of the mutation.

Hytonen, et al. Ancestral T-Box Mutation Is Present in Many, but Not All, Short-Tailed Dog Breeds, Journal of Heredity 2009.

Another survey study of bobtail Australian Shepherds which share the same gene also documented a reduction in litter size in NBT x NBT matings:

Avg. # pups in NBT X NBT litters = 5.83
Avg. # pups in Full-tail X NBT litters = 7.55
Avg. # pups in Full-tail X Full-tail litters = 7.22

This documented reduction in litter size is consistent with homozygous NBT puppies being killed and not being harmlessly replaced as Cattanch suggested: “The hypothesis for the bob-tails is therefore simply that homozygous bob-tail loss replaces natural loss. Their loss in effect enhances the chances of other embryos surviving.”  There is no documented evidence that loading up a uterus with fetuses that will mostly die at some point before birth is in any way beneficial to the dam or the other puppies.  Frankly, this idea is ridiculous and opens the door to lesser minds and breeders with questionable ethics using Dr. Cattanach’s words to justify doubling up on any sort of lethal genes for aesthetic purposes while claiming that they’re helping the surviving puppies and that small litter sizes are good.

Cattanach also downplays the failure rate of NBT to achieve bobtail dogs:  “There will always be a 25% expectation of long tailed pups appearing.”  This is only correct if every homozygous NBT is born and thrives, but we know this isn’t the case.  If all homozygous pups are nonviable, then we have a resulting ration of 2/3 bobtail and 1/3 normal tail because the original homozygous NBT population doesn’t appear and thus can’t be counted.  A breeder who doesn’t realize this change in expected ratios would expect only 1 in 4 puppies to be long tailed, but nature will actually produce up to 1 in 3 undesirable long tails.  This is not an insignificant difference and makes the NBT gene solution a less attractive option.

The Australian Shepherd study confirms the ~33% failure rate:

% Full-tailed pups in this study = 66.25%
% NBT pups in this study = 33.75%

Cattanach is aware of the Norwegian study which shows the same effect:

Norwegian Corgi data indicated a shortage of bob-tail pups (66%) relative to the 75% expected from bob-tail x bob-tail matings, suggesting that the homozygotes are lost before birth.

This clearly means a failure rate of 34% versus 25%.

The final claim Dr. Cattanach makes is that a single copy of the bobtail gene is “Without any detectable ill-effects.”  While no study to my knowledge has intended to look specifically at lumbar disease within breeds comparing no copies to one copy of the bobtail gene, there is too much lumbar disease in T-box breeds to rule this out in good faith without further investigation.

The Australian Shepherd study documented that NBT puppies were 7 times more likely to have kinked tails than normal puppies (5.76% versus 0.8%), and that 1.6% of the NBT puppies were born with imperforate anuses and all three died before 8 weeks.  No non-NBT puppies had imperforate anuses.  Of the 6 NBT x NBT litters in the study, one litter of 5 puppies was born premature and nonviable.  No other litters were premature.

The survival rate of NBT x NBT litters was also lower (the study did not publish individual dog data):

8 week survival rate NBT x NBT: 77.14%
8 week survival rate NBT x full:  97.99%
8 week survival rate full x full: 94.58%

Pembroke Welsh Corgis, the breed Cattanach turned to for his outcross are noted for their “High” risk profile for Intervertebral Disc Disease, which is consistent with the malformations of the spine that have been documented both in dogs and in the many other species which have a T-box mutation.

A discussion this week on a Swedish Vallhund group also suggests that the bobtail gene causes problems in housebreaking single copy NBT puppies:

Barahwolfe Kennel
Rose Madsen believed that sometimes the bobtailed or no-tailed examples of the breed could be hardest to toilet train taking longer than the dogs with tails.

November 12 at 12:29am

Lucy Smith They [bobtails] toilet differently too.

November 12 at 12:31am

A survey of the other breeds with the same T-box mutation shows a consistent pattern: even a single copy of the bobtail mutation might have adverse health effects in regards to musculature, bone structure, and vasculature of the lumbar region.  Possibly related conditions include: degenerative myelopathy (disease of the spinal nerves leading to muscle weakness and lack of coordination and paralysis), cervical spondylosis,  narrow intervertebral space, vertebral osteophytes, hemivertebrae, incontinence and delays in housebreaking, Legg–Calvé–Perthes syndrome (necrosis of the hip joint due to underdevelopment in the lumbar region, also consistent with the abdominal wasting seen with T-box mutations.), etc.

The last assertion Dr. Cattanach makes is that the homozygous NBT puppy is never born and absorbed harmlessly very early in the pregnancy.  Not only is there zero evidence (due to a lack of scientific inquiry) of when homozygous puppies become nonviable and die nor their direct effects on the health of the dam and womb mates, there have been documented homozygous bobtail puppies now that there is a DNA test and a few rigorous inquiries looking for them.

A homozygous NBT puppy born alive but without a tail or an anal opening.

Here is an x-ray of a Pembroke Welsh Corgi puppy (distinct from the one pictured above) that was tested homozygous for bobtail and was born alive.  The puppy presented without a tail and atresia ani.  You can see air in its lungs and the build up of gas in the intestines.  A stillborn normal tailed puppy from the same litter was x-rayed above and to the right of the double NBT puppy for comparison and you can see not only how much smaller the NBT puppy is but also the deformity of the spine and the significant rear wasting in muscle mass.  The puppy was euthanized.

Unlike our state of uninformed ignorance when Dr. Cattanach first made his proclamation of a harmless NBT gene and worry-free NBTxNBT breeding, time and more rigorous examination (including a DNA test for NBT which was developed with assistance from Dr. Cattanach) has begun to document that Dr. Cattanach’s bases for concluding that there was no ethical considerations no longer hold true and never did.  Homozygous NBT puppies ARE born alive and they are a mess.  Litter sizes are smaller and not in an insignificant way.  NBT as a substitute for tail docking is largely ineffective with up to a third of puppies having long tails and some percent more of heterozygous NBTs having shorter but not stubby tails.  And even a single copy of NBT is not cleared as harmless, certainly not less than a manual tail docking procedure.

Given that Dr. Cattanch’s assertions are now documented false, his conclusion is invalidated and the ethics of breeding NBT to NBT is not so cut and dry.  Should Dr. Cattanch choose not to revise his position, invoking his name in the movement to open stud books and demystify the routine practice of outcrossing is a poor strategy and unjustly opens the movement to criticism that should be reserved for those who stubbornly seek to avoid outcrossing–namely that the opponent’s advocated breeding scheme increases disease and disorder within the breed for little to no apparent gain solely to attempt to conform to an historical aesthetic.

This is the sort of breeding scheme we should seek to avoid, not one we should hold up as an example.

Snowy, the double merle breeder sheltie, blind - deaf - mute - club footed. Everything you want out of a brood bitch.

The blog got a nice shout out in the comments of a recent post at Pharyngula: “Written by a border collie owner who is interested in and actually understands a fair amount of genetics” (love when people appreciate the blog) but the rest of the comment is an interesting introduction to a video of a double merle sheltie with hearing and vision problems and possibly a seizure disorder.

Anj says: 5 November 2011 at 7:56 pm

Cats doing something truly insane?

Might be a seizure disorder. “Fly biting” (snapping at apparently nothing) or any momentary action that seems completely unconnected to any environmental stimulus may well be seizures.

I am interested in genetic disorders of dogs and cats mostly because I wonder why we breed dysfunction into animals we supposedly love and care for. Sorry to say, some of those pet quirks that people think are unique or funny are may be signs of congenital disorders.

..

The dog in the video does appear to snap at invisible flies in the air and has a general loss of coordination and tongue control.  So too, as Anj predicted, these twitches are seen as cute by the owner.  The comments on the video make it clear that the owner isn’t reveling in this dysfunction as much as sharing their experience with a dog they rescued.

I think it’s cruel to breed double merles, they can become deaf and blind. Is it forth of the white colour?
Sxcs00 3 years ago 3

I agree, It is a horrible practice. We got Snowy from a rescue, but before we got her she was used as a breeding dog, even with all her issues.
keenergc 3 years ago

your dogs are beautiful. i too have a sheltie (sable & white) whom i love to death. how did snowy become both deaf and mute? ive never seen a white sheltie before, let alone one who is deaf and mute
yorktown99 4 years ago

She is a double merle, a genetic defect that can happen from bad breeding – when merles are bred together. The deafness is common with that. as for being mute, she was born with excess cartiledge around her trachea that won’t allow her voice box to work. She also has a club foot and limited vision, but she is a happy little thing despite all!
keenergc 4 years ago 2

Unbelievably, “Snowy” wasn’t just a placement of an unfortunate pup, she was a breeder who was dumped after.  That suggests to me the worst kind of breeder, who would intentionally create a double merle dog just to create merle puppies.  How jaded and monstrous must you be to look at this dog as a cash cow?  How callous to you have to be to think, “this is good for the breed, for the dogs, for their new families!” ?

Blind and abandoned double merle Lily and her seeing eye guide dog Maddison.

There are very few homes equipped to adopt one Great Dane, let alone two. Add in advanced age and congenital blindness, and it’s not surprising that the former owners just couldn’t handle the onus any more and ditched blind Lily and her seeing-eye-dog Maddison at the shelter.

When illness forced vets to remove Great Dane Lily’s eyes, the prospects of a fulfilling life didn’t look good. But then no one had reckoned on her pal Maddison stepping in to turn guide dog. The pair have been inseparable for years but now find themselves looking for a new home because their owner could no longer cope. The catch for anyone interested is that the Great Danes come as a package. They have been waiting at the Dogs Trust re-homing centre in Shrewsbury since July.

Lily, six, was barely a puppy when she was struck down by a condition that caused her eyelashes to grown into her eyeballs, damaging them beyond repair. It was after this traumatic event that her relationship with seven-year-old Maddison developed as she took her under her wing. The best buddies lived together until their owners decided they couldn’t look after them any more. Miss Campbell said: ‘With her lack of sight, Lily’s other senses have heightened so although we don’t split them up often she can tell if Maddison is nearby.

“They curl up together to go to sleep and they are very vocal with each other. We haven’t analysed their different barks but if Lily wants to go forward and Maddison is in her way, the bark will have a different pitch. They are very close to one another and enjoy each other’s company.”

This is the burden created by breeders who mate merle to merle, merle to harlequin, and harlequin to harlequin.  They afflict their puppies and the big hearted owners who adopt them with a lifetime concern.  Dealing with a blind puppy might pull at the heart strings enough, but compassion fatigue and mounting veterinary bills can quickly make the prospect of caring for two middle aged or geriatric dogs more burden than bliss.

Before you start judging the owners, realize that up 80% of parents with special needs children divorce due to the stress.  It takes extraordinary people to care for a special needs child or pet, but it only takes one uninformed or callous breeder to create them and flood the local community’s ability to cope.

How come "improvement" in dog breeds always seems to mean taking physical features to the extreme while minimizing health and longevity?

If the highest and best goal of eugenics is to improve the genetic composition of a breed, what–if anything–can we say has been improved in the pedigree dog in the last 100 years?

What breed lives longer today than a century ago?  Where do we find evidence of larger litter sizes and increased vitality? Has any insurance company lowered their rates for coverage of any breed because the breeding community has successfully created a healthier animal?  What breed has fewer total health problems in number and incidence today versus the past?

What breed is more capable?  What breed does its job better now than in the past?  What new job can dogs do well now that they couldn’t do before?  Has anyone founded a breed that meets a new working or sporting need driven by demand?

Do our dogs even look better on the most shallow of aesthetic measures?  Are consumers flocking to buy more dogs with excessive hair, excessive skin, or insufficient length of limb or depth of face?  Do the dogs that win in the show ring really win in the open market?  Are people more nostalgic for the dog of their childhood that no longer exists due to changing show fads or are they more impressed with the improved models and wonder how they ever got along with the less improved versions?

If there are tens of thousands of breeders creating millions of dogs every year in this country, where are the results?

100 years ago the human life expectancy was 50 years and in those five short decades you were likely to have lived without anything electronic or digital, no drip coffee or band-aids, no animation motion pictures, no quartz clocks, no disposable diapers or electric guitars, no internet, no TV, no bras.

We’ve lifted and separated humans in the last century, have we elevated and distinguished our dog breeds?

Many dogs are alarmed when the Sheepdog card is drawn. They mistakenly think they have to work for a living. Don't worry dogs, these days job cards are more metaphorical than literal.

Read the following blurb, determine who the critic writer/journalist/filmmaker in question is, and make an educated guess on when the article describing this critic’s efforts was written.

An institution founded to defend the integrity of canine pedigrees has become, a critic contends, unreasonable in its measure of “excellence” and complicit in rewarding close breeding for suspect qualities resulting in breeds that are now unable to perform their historical functions and which suffer from debilitating diseases.

Don’t bother using google, the blurb has been anonymized so you won’t find the article searching for the quote.  Multiple guesses are allowed as long as you pair a critic with a year.

Bonus points if you can name which country and institution is being discussed.

For example:

The blurb describes Christopher Landauer’s article “Border Collie War: AKC vs. ABCA” published 9/10/2007 which critcises both the American Kennel Club and the American Border Collie Association in the USA.

Of course that’s not the right answer, and there are perhaps numerous critics that this could apply to, let’s see how many you can name and I’ll bring you a follow-up article featuring at least one of them I don’t think too many of you know about.

A sample of dog breeds with sine-qua-non disorders.

A sine qua non disorder is one that is both universal and definitional within a breed.  To remove the genes that cause the trait, disorder, dysfunction, or disease would fundamentally alter essence of the breed.

Any rational and humane breeder would want to remove disease from their breed if given the chance.  No Border Collie is benefited by epilepsy or collie eye anomaly, and if we could wave a wand and rid them from the breed, it wouldn’t take much thought to do so.

Alas, there are dog breeds where dysfunction and disease are part of the breed standard or inextricably linked with traits that are required in the dogs.  No matter how many DNA tests become available, such diseases will not be removed from the breed because the breeders want them there, require them there, and even cull puppies that are unaffected!

Such disorders are sine qua non to the identity of the breed.  If they didn’t exist, the breed would not exist, certainly not as we know them.  Unlike CEA or HD or epilepsy, removing a sine qua non disease requires breed standards to be rewritten, not genetic tests.  The major obstacle is not genetic, it’s political.

A sample of such diseases and the breeds they are inextricably linked to:

Chondrodystrophy
Abnormal cartilage growth causing short legs:
Basset Hound, Beagle, Cavalier King Charles Spaniels, Cocker Spaniels, Dachshund, Lhasa Apso, Pekingese, Pomeranian, Scottish Terrier

Dermoid Sinus
A neural tube defect inextricable from the “ridge:”
Rhodesian Ridgeback, Thai Ridgeback

Micromelic Achondroplasia
Abnormal cartilage growth causing short legs and trunk:
Bulldog, Corgi, some Jack Russell Terriers, Pekingese, miniature Poodle, Shar Pei, Shih Tzu, Skye Terrier, Swedish Vallhund

Polydactyly
Extra digits on the foot:
Beauceron, Briard, Great Pyrenees,  Norwegian Lundehund

Pituitary (Ateliotic) Dwarfism
Boston Terrier, Chihuahua, Miniature Dachshund, Italian Greyhound, Maltese, Minature Pinscher, Minature Spaniel, Pekingese, Pomeranian, Pug, Shih Tzu, Toy Poodle, Yorkshire Terrier

Congenital Alopecia
Inherited baldness:
American Hairless Terrier,  Chinese Crested Dog, Inca Orchid Hairless Dog, Mexican Hairless Dog, Peruvian Inca Orchid

Color Mutant Alopecia
Hair loss and breakage seen in “Blue” and “Fawn” coat colored dogs: 
Blue Lacys

Brachycephalic Achondroplasia
Boston Terrier, Boxer, Brussels Griffon, Bulldog, Cavalier King Charles Spaniel, Japanese Chin, Pekingese, Pug, Shih Tzu, Yorkshire Terrier

Periodic Fever Syndrome
Fever, swelling, and Amyloidosis inextricable from the skin folds:
Shar Pei

Congenital Anurousity
Lacking a tail; associated defects of the spine and anus.
(Non-C189G mutation) Boston Terrier, English Bulldog, Miniature Schnauzer;

(C189G mutation) Australian Shepherd, Australian Stumpy Tail Cattle Dog, Braque du Bourbonnais, Brittany Spaniel, Croatian Sheepdog, Mudi, Polish Lowland Sheepdog, Pyrenean Shepherd, Braque Francais, Schipperke, Spanish Water Dog, Pembroke Welsh Corgi

Obviously the severity of these disorders ranges from very minor and unlikely to cause inconvenience in the case of a Beauceron’s extra dewclaws to chronic and potentially lethal conditions like Shar Pei Fever.

Such conditions provoke Qualzucht considerations as there’s precious little other than aesthetic fads to weigh against the potential suffering of the animal.  You’ll notice that many of the disorders here mirror those that are enumerated in Qualzucht laws.

For individual analysis of some of these conditions, refer to the “sine qua non disease” category under “health and genetics.”

Beyond the physical, we might also include inbred mental disorders that are definitional of breeds.  Ojeriza in the Fila Brasiliero maps to the human mental disorder Xenophobia.  Border Collie eye would be considered an Obsessive Compulsive Disorder if a human displayed the same traits.

If you can think of another disorder that is quintessential to a breed’s definition that I have neglected to include, please leave a comment and I’ll be sure to update the list.