A Long Tail Cut Short

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.


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.


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.


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

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.

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About Christopher

Christopher Landauer is a fifth generation Colorado native and second generation Border Collie enthusiast. Border Collies have been the Landauer family dogs since the 1960s and Christopher got his first one as a toddler. He began his own modest breeding program with the purchase of Dublin and Celeste in 2006 and currently shares his home with their children Mercury and Gemma as well. His interest in genetics began in AP Chemistry and AP Biology and was honed at Stanford University.