The retina of a Briard with an inherited blindness disease that was later cured with gene therapy.

Back in 2001, scientists first treated inherited blindness in dogs using gene therapy. In that instance it was Congenital Stationary Night Blindness which manifests in Briards and is analogous to Leber congenital amaurosis in humans, both defects in the RPE65 gene.

Dogs blinded by an inherited retinal degenerative disease had their vision restored after treatment with genes from healthy dogs, marking the first successful gene therapy for blindness in a large animal. The treatment offers hope for humans with a similar condition.
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“We have shown that gene therapy can restore vision in dogs with one of the most clinically severe retinal degenerations,” says Acland, a research veterinarian at Cornell’s James A. Baker Institute for Animal Health.
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The RPE cell layer in the eyes of humans, dogs and other mammals supports the retina by providing nourishment and removing waste products while supplying vitamin A to the photoreceptors. Puppies and human infants with defective RPE65 genes produce a mutant form of the RPE65 protein, resulting in early vision loss, degeneration of the retinas and near-total blindness later in life.

The canine form of this retinal degenerative disease has been found only in the briard dog breed. In the gene therapy experiments, researchers used RPE65 genes that were cloned from dogs without the disease, together with a viral vector (recombinant adeno-associated virus, or AAV) to carry the normal dogs’ DNA. They injected the combination into the subretinal space of the eyes of 3-month-old briard-beagle mix dogs that were known to have the defective RPE65 gene and had been blind since birth. Within six weeks, the treated eyes were producing the correct form of RPE65 protein. By three months, a series of tests (electroretinography, pupillometry and obstacle-avoidance tests in a dimly lit room) demonstrated that vision was restored to the treated eyes.

In 2010, the same team successfully returned function to the cones of previously blind dogs affected by a form of blindness called Achromatopsia.

Now, scientists have again used gene therapy to prevent and reverse another form of blindness in dogs and humans called X-linked Retinitis Pigmentosa associated with a mutation in the RPGR gene.

The disease in humans and dogs is caused by defects in the RPGR gene and results in early, severe and progressive vision loss. It is one of the most common inherited forms of retinal degeneration in man.

“Every single abnormal feature that defines the disease in the dogs was corrected following treatment,” said lead author William Beltran, assistant professor of ophthalmology at Penn’s School of Veterinary Medicine.

“We were thrilled,” said senior author Gustavo Aguirre, professor of medical genetics and ophthalmology at Penn Vet. “The treated cells were completely normal, and this effect resulted from introducing the normal version of the human gene into the diseased photoreceptor cells.”

This is exciting for dog owners because there are numerous breeds that have epidemic levels of eye disease and the proliferation of these advancements could lead to routine treatments that would treat or cure the disease in individuals.

There’s still a barrier to a permanent cure for breeds that would extend to the offspring of treated individuals.  Treated dogs only receive the working DNA in the somatic cells at the location of the viral vector.  Somatic cells are all the cells in the body besides those directly involved in producing offspring.  If there’s a mutation in a somatic “body” cell, it will not be passed on to future generations.

The cells that produce the sperm and egg are called germline cells and they are not necessarily amenable to the same gene therapy techniques that work on individual somatic cells.  You can effectively cure the blindness by providing a working copy of the genes within the eye, but other cells in the body will not have the new gene and the germline cells will not produce sperm or eggs that benefit from the disease-free allele either.

This effect is called the Weismann barrier, which is the theory that genetic information moves only in one direction, from germline cells to somatic cells.  This is why when you get an x-ray the tech is more concerned with lead shielding your private parts than the rest of your body because germline mutations have serious consequences for your offspring and germline cells are theoretically immortal (they can replicate for the entire life of the organism) whereas somatic cells only divide 30-50 times.

If the Weismann barrier can be broken, it’s theoretically possible for the treatment of eye cells to result in genetic change in somatic cells and thus in the offspring.

There’s also the potential to apply gene therapy techniques to germline cells (such as the sperm or egg) directly and this would enable genetic engineering that would last over generations.  Scientists have already created lasting changes in organisms that do not differentiate somatic-germline cells (like plants: thus we have GMOs), but I’m not aware of any ongoing progress on germline gene therapy and there are currently institutional barriers against work in that area given the potential ethical implications of genetic engineering.  Scientists have successfully inserted synthetic chromosomes into mice that were heritable but the current focus in treatment of human offspring disease is to perform IVF and genetically profile the blastocysts before implantation.

So this is good news for dogs, and possibly the beginning of an amazing new world of animal husbandry when genetic engineering will allow for some truly incredible health advancements and possibly some radical experimentation.

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.

The breed is believed to be the creation of one man, Heinrich Essig, who was a dog dealer and traveling salesman; his claimed formula was Landseer Newfoundland x Saint Bernard, followed by more Saint Bernards and a Pyrenean Mountain Dog with the goal being a large white dog that was fashionable at the time.  After Essig’s death in 1889 his nephew had the inspiration to promote the breed as a lion-like mascot for the town of Leonberg and established the final conformation of the dogs as having a lion-like rough coat with reddish-brown coloration, a black mask and black sable accents.  Like most breeds, the origin mythology is poorly documented and stud books were not kept in earnest on the breed for several decades after its establishment.

As a German breed, the Leonberger was severely affected by both World Wars: only 5 known breeding dogs survived the first war and only 8 pedigreed dogs emerged from the second.  Two severe bottlenecks like this are not conducive to preserve genetic diversity within a closed population.

That is why I was surprised to find that the 5 Leonbergers which were DNA tested as part of a study analyzing the genetic composition of Alaskan Sled Dogs showed that they had excess heterozyosity compared to Hardy-Weinberg equilibrium. Of 141 breeds tested over 96 genetic marker sites, there were only 9 purebred breeds found to be surplus heterozygous and most of those are only marginally so.

Note, this is not a measure of gross diversity in the breed, it’s a measure of which way the breed is being pushed genetically, either toward more conformity and homozygosity or toward more diversity and heterozygosity.

Genetic rescue requires a push toward heterozygosity before reaching a new equilibrium with the new alleles.

Inbred or Outcrossed? Bars that extend to the left indicate excess heterozygosity compared to the Hardy-Weinberg equilibrium (red line), suggesting active selection for allele diversity (i.e. outcrossing). The Leonberger is one of the most heterozygous breeds tested.

Here is the actual data represented in the chart.  The purposely out-crossed hybrid sled dogs were found to be 20% more diverse than equilibrium and the Leonberger was second only to the Puli with over 10% excess heterozyosity.

I’ve only found one documented outcross on the Leonberger books: In 1954 a Leonberger stud Arko von Leonberg with a COI of 20% was bred to a Newfoundland dam Grisette von Bruckberg and one female from that litter, Alma von Rossbach, would cement herself into the Leonberger gene pool.

More recently European kennel clubs have registered Leonbergers with full breeding rights certificates “titre initial” (as opposed to a 3 generation provisional appendix registration “registre initial”) which are given after a number of criteria are met; typically an evaluation against the breed standard or significant show success, health testing, and perhaps even temperament evaluations.  These dogs are believed to be pure-blooded Leonbergers instead of hybrid dogs which would normally take 3 generations to be admitted into the gene pool with full breeding rights and purebred status in registries that allow new blood.  Sometimes they come with full pedigree and while the kennel club would void the known pedigree and perhaps calculate the COI of offspring as 0%, it’s not clear that either the registre initial or titre initial schemes are a source of new Leonberger blood.

Another possible source of Leonberger diversity lies in the history of Germany and the East after the wars.  The Leonberger isn’t just a dog of the West and so it existed on both sides of the Iron Curtain.  It is unknown and undocumented what sorts of possible crosses came into the breed during the Cold War before the reunification of Germany and the resumption of normal trade across Europe.

The last and least verifiable source of unexpected diversity would be intentional and unintentional pedigree fraud or error.  It’s possible that some breeders when faced with a line that was not producing what they wanted or suffering from inbred disease or infertility decided to outcross, or an accidental litter proved sufficiently virtuous to register and the breeder either could not or did not choose to disclose this.

There’s also the possibility that I simply haven’t accounted for some factors which would have preserved heterozygosity in Leonbergers and that the bottlenecks did not have the expected effects on the gene pool.  Certainly more questions than answers, but what an intriguing mystery it is.

This is not an apple, it's a pipe.

It is the nature of Evolution and the human mind to repurpose what exists into what could be: to innovate, experiment, and sometimes to improve. The fate of such change is almost always failure–99.9 % of all species to ever have lived are extinct and 95% of new businesses fail within 5 years–but occasionally unplanned, unimagined, and even unwanted uses and abilities surpass the ability, potential, or popularity of the original.

This isn’t a simple re-purposing, such as using an apple or corncob to create a pipe; such uses don’t surpass the original nor are they particularly exemplary in their new form.  Though I couldn’t resist bringing surrealist painter René Magritte into this thought stream by combining two of his images which both ask about the fundamental nature of reality, representation, symbolism and existential identity.

In branding, especially in branding dogs, I think the community is way too hung up on the past–and often an artificial past–in how we define and value our dogs. We turn them into symbols and representations and we place the story over the existential truth.

Conformation shows are very much about the painting of the pipe versus the pipe itself. The goal of a painting is to exhibit the skill of the artist, not to make a superior pipe. The painting just has to LOOK like a wonderful pipe. Then, as artists are want to do, trends and abuses turn into movements and in some epochs the art is realist, even romantic, other times it’s impressionistic and then downright absurd.

Conformation is all about the change, never about performance.

The trialists are also absorbed in the past, but in a different way; they are fundamentally against the evolution and repurposing of dogs. They find value in the antique nature of the breed and revel in stasis and reenactment. While a performance standard does speak to an existential truth (and this is why we don’t see the grotesque distortions we find from conformation artists), it doesn’t prevent the performance task from becoming obsolete or surpassed in popularity.

Trials are all about performance, never about change.

So what happens when we don’t constrain either of those variables and take a measure of what is produced in an existential, realist, and measured manner?

The Internet is for social networking and porn.

The Internet was funded by the Department of Defense for use by the military.  National defense and elite scholarship were the original use and designing factors governing its design.  Now, the military and elite institutions are taking more and more of their networks offline and spend fortunes putting up barriers to those that are still connected to the Internet.

In reality, the Internet is primarily for social networking and pornography, not national defense or scholarship.  An impartial observer who was not indoctrinated in what the Internet is supposed to be or what it was in the past would hardly notice the national defense and scholarship aspects and would declare it to be a massive undertaking which people use to convince others that they are having lots of sex followed closely by actually viewing images and videos of strangers pretending to have lots of sex.

Last year, social networking surpassed pornography as the most popular use of the internet and more social networking activity takes place over the Internet than any other outlet.  Likewise, pornography is the second most common use of the Internet and more people get their pornography over the Internet than any other source.

These are unintended and arguably unwanted developments in the use of the Internet, but the reflexive superiority of the task and the platform  are undeniable.  It’s not for education or defense, it’s for social wish fulfillment and fantasy.

Love and other drugs: Viagra and Ecstasy are far more popular for carnal pursuits than for their original medical uses.

While we’re on the subject of unexpected innovation for purposes of initiating or aiding sexual activity, here are three examples of other tools (all pharmaceuticals in this case) which have surpassed their initial use in pursuit of that goal.  Viagra was developed specifically to treat hypertension and angina, with zero thought or design given to a secondary use as an erection inducer.  It wasn’t until the drug made it to human trials that it was found to be useless for angina but effective for increasing blood flow to the penis.  That is now its primary use and it is the primary drug prescribed for that condition.

Methylenedioxymethamphetamine was first synthesized a century ago as an intermediary product in part of a Merck plot to plagiarize a successful Bayer drug used to treat hemorrhages.  Its psychotropic effects wouldn’t be appreciated for another six decades after it had been investigated as an appetite suppressant and decongestant like Ephedrine, and later as an analog to Mescaline in a study done by the US Army.  MDMA found its way to the streets by the 1970s and soon into the basket of drugs offered to patients by psychotherapists. Ecstasy was classified as a Schedule I controlled substance by the mid 1980s, but that didn’t prevent its rise to prominence as a recreational drug second only to Marijuana in popularity, passing Cocaine and Heroin as drug-of-choice for first illicit drug experience.

Latisse is a far more popular cosmetic than it was a medical treatment.

Bimatoprost (“Lumigan”) was a rather unremarkable member of a family of drugs (prostaglandins) used to treat glaucoma until it was discovered that a side effect of the drug was the darkening and thickening of the eyelashes.  Rebranded as “Latisse” the drug is now FDA approved for cosmetic use and is being sold as a beauty product.  Its value as a cosmetic has already far surpassed its use as a medicinal drug.  It is the only drug approved for cosmetic eyelash enhancement, so it currently dominates a much larger market than its previous incarnation as one of many treatments for hypertension in the eye.

This is not a phone. It's a clock with some extra features.

Perhaps the most obvious approachable and active nursery for useage drift is the cell phone.  It’s hardly a phone any more, as by any measure what used to be subordinate bonus features are now vastly more popular than the once sole raison d’être of the phone: to make voice calls.  Teens send 6 times as many text messages as phone calls and even the least likely to text adults still use that feature more than dialing calls.  The most popular use of the device is actually to tell the time though, and the ubiquity of cell phones has made the wrist watch an increasingly obsolete tool.  Applications and Games have recently surpassed Internet browsing and e-mail as the largest share of data bandwidth and now people spend more time listening to music on their phone than making phone calls.

We might call it a phone, but that’s hardly its main use anymore.  While there are still single purpose phones in the world, their use is dropping like a stone and the number of cellphone only households has surpassed the number of landline only households and the recession has caused many dual-phone households to ditch their landline to save money.  The landline will likely live on, but only at a fraction of its previous popularity and in instances where the downside of cell phones (reliability, battery driven) make them impractical.

A dog is what you make of it and more people are making sport dogs than working dogs.

All of these tools were manipulated by man into filling a niche use.  So too is the dog a man-adapted tool that has been continually manipulated to fill existing and new human niches.

So what IS a Border Collie then? By far its most popular use is as a pet. Not only does this use easily make up more than 90% of Border Collies, they are quite successful and good pets–easily a Top 10 breed and perhaps as high as Top 5.  This has probably been the case for over a century going right back to the very founding days of the breed as a trial dog. It’s an undeniable truth that despite having the goal of creating winning trial dogs, the majority of puppies in a litter never stepped on a trial field.  This is true for all competitive endeavors, it’s just that all the hype and branding comes from the minority use.

Among the fraction of Border Collies that are trained and compete, there are many times more Border Collies who play Frisbee, Flyball, Agility, and Obedience than have ever entered a sheep or cattle trial; and their ability in all these venues is exemplary.  There isn’t another breed that can hold a candle to the Border Collie at dog sports, they are so dominant that they have been given a Border Collies Only division to compete in.  Participation and growth in dog sports is robust and although some performance events started as a side show to conformation shows, they are now independently sustainable and there are numerous organizations that organize dog sport events that have no connection to and compete directly with the AKC.

This isn’t a “paradigm shift” in the formal sense, as the sport dog in no way precludes the use of the “working” dog despite surpassing it in popularity.  I’ve been accused of putting dog sport Border Collies forth as “the new paradigm” but I make no such claim. Not only is ‘paradigm’ so over-used as to be meaningless, the original definition required a true revolution in understanding such that the use or way of thinking before the shift was eclipsed and supplanted (think “the earth is flat” to “the earth is round;” when you accept the latter, the former is meaningless).

Sport dogs and working dogs can co-exist and the value of the breed stock is not mutually exclusive.  Creating pet and sport Border Collies is not a revolution, it’s a concurrent evolution.  The reality is such though, that the market and demands of the sport world are larger and more intricate than the working breeders can provide.  Thus, breeders can and will continue to breed to a sport and pet standard despite the moral cries from the sheeple that they should not do so.

This is not speculative advocacy on my part, projecting what I wish the reality were, it is a simple observation of the extant truth.

We know that ancient man was picking his teeth with small sticks at the exact same time he began to domesticate the wolf.

The modern toothpick began as a utilitarian tool used by the native Brazilians to clean their teeth. The idea to mass produce these twigs–which had theretofore been whittled by hand–came to a marketing genius named Charles Foster who witnessed their utility and decided he could “sell ice to the Eskimos” by bringing machined and standardized toothpicks to the Brazilians and the world. Today, Brazil exports more toothpicks than any other nation.

While there’s no evidence that chimps cultivated wolves as animal companions, the bond between humans and canids does extend back to our very origins. It is likely that after proto-man held that scrap of meat in the fire with a proto-toothpick, he threw the scraps to his proto-dog. And like the toothpick, dogs were crudely hewn objects of utility before they were standardized by the whims of fashion.

Though readily promoted by manufacturers, usage drift is more often created by consumers of a product. People are natural inventors, and they are constantly finding new uses for common objects of all kinds. The best ideas propagate quickly through the culture and then become embraced by manufacturers as their own. Before there were Q-tips, young mothers wrapped a bit of cotton around the point of a toothpick and used it to clean out baby’s ears and nose. This practice came to be recommended by ladies’ magazines and advice columnists, and led to the invention of the Q-tip itself.

At first, the hard wooden stick terminating in soft cotton swabs suggested the toothpick connection, but today’s Q-tip disguises its origins with a white paper body that blends almost seamlessly into the swab ends. The latest supply of Q-tips bought for our bathroom goes even further in removing the product from its ancestry and infancy. Except perhaps for the ironic admonition to “Keep out of reach of children,” there is no hint on the package that these were once made exclusively for babies. On this “vanity pack,” Q-tips are described as “the ultimate beauty tool.”

Thus, products that result from usage drift over time can ultimately assume an identity that gives little hint of their true origins and once-primary use. The mass-produced wooden toothpick that Charles Forster introduced to Boston in the 1860s has given rise to countless fads, uses, and spinoff products, all of which ultimately owe their existence to his marketing genius, whether we realize it or not.

- Henry Petroski, Stick Figure, Slate 10/31/3007

The process where a technology evolves from the early adopters into the majority often involves friction between the elite early adopters who covet their history with the technology and the exclusivity they have enjoyed. This is evident in the Border Collie world where those who use the dogs strictly for “work” claim to be the inheritors of the storied old ways and the comparatively new adopters who don’t herd or who see herding as a sport rather than a religion are blasphemous corrupters.

I see the broadening appeal of the Border Collie as another example of usage drift. Just like the toothpick, the Border Collie is a technology that has been shaped by growing popularity and changes in fashion. And just like the Border Collie, there is no “ideal” toothpick, despite the brand name that suggests otherwise.

Despite being a rather simple piece of technology, the toothpick comes in many forms and serves several uses. The tapered tooth pick, single pointed or double, barrel shaped for easy dispensing, or the broad flat Jordan for easy manipulation. Smooth, rough, or wax coated; dyed, painted or lacquered; mint flavored. Wooden, bone, plastic, metal, or bamboo; wrapped in paper, cellophane, or naked. Adorned with dental floss or even frilly plastic pompoms.

We use them to clean our teeth, to sample hors d’oeuvres politely, to adorn our drinks with olives or umbrellas, to test the moisture in the middle of cooking cakes, and to construct bridges for science experiements.

Just as there is no singular, ideal use for a toothpick, I don’t believe there is a singular perfect use for the Border Collie. Not even herding and especially not sheep trials. If society has progressed just fine calling the many varieties of small sticks, singularly and collectively the same name, I don’t see any reason to rename the Border Collie. Nor do I see a compelling reason to limit the diversity of the breed by forcing a genetic split by closing the registries or limiting participation to a select group based upon politics.

reprint

Hot Nun knows a species when she sees one. Obey the Sister.

After the smashing success of my Multiple Orcasms post which still brings considerable daily traffic to the blog from furries looking for orca and vore themed pornography, I couldn’t resist tiptoeing around cheeky references to bestiality once again; but this time the human interest in animal sex is strictly like-on-like and the link to pornography is in the tricky means of defining concepts that are both familiar and yet abstract.

Trying to define what is necessary and sufficient to designate a “species” is rather like the problem the US Supreme Court ran into when trying to define pornography.  In the decision for Jacobellis v. Ohio, Justice Stewart coined a now famous phrase when trying to draw a line between protected speech and unprotected obscenity:

In saying this, I imply no criticism of the Court, which in those cases was faced with the task of trying to define what may be indefinable… I shall not today attempt further to define the kinds of material I understand to be embraced within [hardcore pornography]; and perhaps I could never succeed in intelligibly doing so. But I know it when I see it, and the motion picture involved in this case is not that.

Many definitions, while concrete, are rather relative and not absolute. Darwin failed to define species in his Origin of Species:

Nor shall I here discuss the various definitions which have been given of the term species. No one definition has as yet satisfied all naturalists; yet every naturalist knows vaguely what he means when he speaks of a species.

He goes on to say just how blurred that line can be:

I was much struck how entirely vague and arbitrary is the distinction between species and varieties.

The “species debate” is a problem that existed before Darwin and which continues today.  The current tone of the debate has been most significantly influenced by evolutionary biologist Ernst Mayr whose definition of a species graces most modern textbooks:

species are groups of actually or potentially interbreeding natural populations, which are reproductively isolated from other such groups

I had a laugh when I read Ernst Mayr’s essay “What is a Species, and What is Not?” published in Philosophy of Science in 1996:

The term ‘species’ refers to a concrete phenomenon of nature and this fact severely constrains the number and kinds of possible definitions. The word ‘species’ is, like the words ‘planet’ or ‘moon,’ a technical term for a concrete phenomenon. One cannot propose a new definition of a planet as “a satellite of a sun that has its own satellite,” because this would exclude Venus, and some other planets without moons. A definition of any class of objects must be applicable to any member of this class and exclude reference to attributes not characteristic of this class.

It doesn’t help Mayr’s point that the International Astronomical Union had no formal definition for ‘planet’ at the time of his essay or for a complete decade after it. When they did finally vote on one in 2006, the former planet Pluto got downgraded to a dwarf planet leaving every science textbook published in the preceding 80 years obsolete and violating Mayr’s apparent rule that one can not propose a new definition that would exclude an existing member of a class. Pluto was declared a planet upon its discovery in 1930 and now it’s not even the largest “plutiod”–that honor falls to Eris, which was discovered in 2005 and found to be larger than Pluto which prompted Astronomers to actually look at the definition of what makes something a planet versus something else.

If you take a moment to look around the blogosphere this week, you’ll realize that the uncertainty of this issue is present just beneath the surface of numerous topics of conversation:

Retrieverman asks if the Island Fox is a valid species which must be understood within the context of the greater Canid complex several species of which would violate the basic Mayr definition of a species, but his post on the Polar Bear is also framed by the species debate as genetic analysis shows that Polar Bears can be considered a variety of Brown Bear and the two can and do form fertile hybrids.

The Dog Zombie looks at Canid DNA to question the recipe of different flavors of “Canid Soup.”

Jess at Desert Wind Hounds picks up on the food metaphor at Dog Zombie and asks what the recipe is for a “purebred” and how one goes about creating one.  This is ultimately just a more zoomed in analysis of the species debate: how much distance in time, space, genetics and niche constitutes a different breed, a different type, a different landrace, or a different species?

Stephen Bodio asks the same question with a simple image comparison of two dogs.

Razib Khan shows that the species debate is applicable to humans, and the notion that Neanderthals or Denisovians were somehow not human falls when you realize that their genes are still in us (Border Wars is written by a 2.7% certified Neanderthal):

In my post below I argue that it’s most useful to reconceptualize “human” as an ecological niche, rather than a descent group. All the confusion as to whether Neandertals, or any other group of divergent hominins, were, or weren’t, “humans like us,” exists in the context of the idea that “humans like us” are a very specific and sui generis  cladewith special traits. I think “we” need to get a little off our high horse here.

You’ll notice that the notion of “niche” becomes more and more important as we realize just how blurry the lines between interfertile species really is.  Niche is what separates Polar Bears from Brown Bears and it’s also what separates Dogs from Wolves:

The co-evolution between social canids and primates is I think not a random chance event. To some extent I think “man’s best friend” was a necessary outcome of evolutionary forces. Barring the total extermination of one lineage or the other, some sort of cooperative relationship is I suspect something that will naturally reoccur. Dogs are not simply a specific derived lineage of wolves, they’re an ecological niche created by the existence of hominins with social complexity.

Dave at Prick-Eared has a post which documents another canid rapidly invading the very niche that once brought man and wolf together to co-evolve.

There are no hard and fast answers here, no absolute definitions, no minimum standards or list of traits that are both necessary and sufficient to differentiate one “thing” from another “thing” in a meaningful way.  This is the place where the objectivity of science meets the subjectivity of philosophy and those questions like “what is a dog” start to look a lot like “what is an ideal Afghan Hound.”

There are some questions that are worth answering “I don’t know and I probably never will, but that won’t stop the investigation.”

Inbred lab mice are so healthy you only have to keep them in a sterile bubble and wear biohazard getup just to watch them.

The Pure Blood Brigade™ (licensed for use from Jess Ruffner) will sometimes invoke laboratory mice as the go-to example of a perfectly healthy inbred population. Here’s a quote from NSDTR-apologist and accomplice to Dr. Claire Wade, Dr. Danika Bannasch:

I don’t know if you are familiar with inbred mice.  There are 100s of laboratory strains that are completely inbred- ie homozygous at every locus.  They breed prolifically and are healthy.  They are not living in the wild but neither are domestic dogs.

To verify the health of laboratory mice I went to Jackson Laboratory–the “most important supplier of lab animals to science“–and viewed their “Breeding Strategies for Maintaining Colonies of Laboratory Mice.”  The manual claims that the breeding strategies that are used to create inbred lab mice are:

“safe, reliable, economical, efficient, and ensure that the mouse strains produced are genetically well-defined.”

Notice that they don’t claim that the mouse strains produce healthy mice that live long and have good temperaments, they are just genetically well-defined (highly homozygous).  Here are snippets which hint at the deep underlying dysfunction that is found in inbred lab mice:

• Reproductive life span. Typically, laboratory mice can breed for about seven to eight months, producing four or more litters (Table 1). However, some strains produce only one or two litters, usually because strain-specific characteristics or mutant phenotype affect their fertility. AKR/J mice (000648) develop leukemia, and breeders must generally be replaced when they are about six months old. C3H/HeJ mice may stop breeding early because they have a high frequency of ovarian cysts and tumors. NOD/ShiLtJ (001976) females may develop diabetes when they are 12 weeks old, but their reproductive lives can be extended with foot pad injections of Freund’s Adjuvant.

• Fertility. Fertility of inbred strains varies. For example, whereas nearly all breeding pairs of C3HeB/FeJ (000658) mice are fertile, less than half of C57L/J (000668) breeder pairs are fertile.

Wild mice breed for up to 24 months. Laboratory mice can breed for only 7-8 months.

Wild mice can have 5-10 litters per year, so 10-20 litters over their two year reproductive lifespan. These lab mice have 1-6 litters, the most popular strains average 3-4 litters.

Average wild mouse litter size is 10-12 pups. The mean litter size of the top 12 most popular lab strains are: 5.4, 5.2, 4.5, 5.0, 5.6, 4.0, 4.7, 7.3, 7.7, 5.8, 6.4, 4.9; so about 5 pups.

• Birth defects in the pups. C57BL/6J (000664) mice tend to have more pups with hydrocephaly than do other strains. A/J (000646) mice tend to have relatively more pups with cleft palates, the incidence of which can be influenced by the uterine environment.

• Hybrid vigor. Hybrid mice tend to have more, larger, and healthier litters than inbred strains.

• Strain-specific behaviors. The aggressive behaviors of some strains and the poor mothering instincts of others affect breeding performance and pup survival. For example, SJL/J (000686) males are aggressive and attack their mates and offspring; NZB/BlNJ (000684) females are poor mothers.

Here we have pretty much the death knell for using lab mice as an excuse to inbreed dogs.  Aggressive behaviors and poor mothering are deal breakers for almost any decent dog breeder.  Birth defects in many breeds are at epidemic levels, and yet many breeders are so jaded they consider it normal. We should not consider it normal and those of us in healthy breeds should steel our spines against becoming such moral sellouts.

Oh, and hybrid vigor is real. We can reverse this.

Don't let outcross breeders tell you otherwise, small litter sizes are actually a bonus! Who needs those extra offspring, they are just a hassle.

• Mutations and transgene effects. Some mutations are embryonic lethal; some cause infertility or reduced fertility; some affect mammary gland function. For example the Tg(SOD1*G93A)1Gur transgene (also found in several strains) induces neurodegeneration. The severity of such effects depends on strain background.

If you’ve been reading this blog for any amount of time you should be well aware of the embryonic lethal mutations that are prevalent in certain breeds of dog.  Many of these have been identified because they associate with a marked phenotype change of interest such as merle or bobtail. How many more exist that do not have a visible phenotype?

• Feed. Some strains of mice have bad teeth, no teeth, or other phenotypes that affect their ability to eat grain pellets. These mice need special foods, such as ground or dampened grain.

Does this remind you of the poor dentition we see in several toy breeds and especially hairless dogs?

Females of some strains are poor mothers (e.g., NZB/BlNJ, 000684) or cannot nurse, and a few mutations, such as toxic milk (Atp7btx) and lethal milk (Slc30a4lm), render the mother’s milk harmful to her pups.

I wonder if those toxic and lethal milk mothers were intentionally bred to have harmful milk or if those are just known side effects of strains used for other kids of research.

Some strains are so screwed up they are only viable by transplanting the ovaries of the inbred mice into healthier females:

Some strains are best maintained by ovarian transplantation. Homozygous B6C3Fe a/a-Csf1op/J (000231) females fail to lactate, and homozygotes of both genders are extremely fragile. Therefore, we transplant ovaries from a homozygous (op/op) female into a recipient female of a histocompatible strain. To quickly expand the colony, the donor ovaries may be quartered and each quarter ovary transplanted into a ovariectomized recipient female. We also maintain B6.V-Lepob/J mice (000632) by ovarian transplantation because, though the females produce functional gametes, they cannot sustain a productive pregnancy. Additionally, we maintain colonies of B6CBA-Tg(HDexon1)62Gpb/1J (002810), B6CBA-Tg(HDexon1)62Gpb/2J (004601), and B6CBA-Tg(HDexon1)62Gpb/3J,(006494) by ovarian transplantation to extend the breeding lifespans of the females. Although these females produce viable oocytes for a long time, they develop a progressive neurological disease that renders them physically incapable of mating or sustaining a pregnancy.

Fantastically healthy, no?

Don't worry, not all inbred lab mice are satanic albino demons, some are really cute! And that makes everything ok.

But all is not lost, the manual provides some advice on how to maintain an outbred colony to turn to if your inbred strain crashes and burns.

Maintaining Outbred Stocks

The genomic diversity of individual outbred mice contrasts directly with the genetic identity among individual mice of an inbred strain. To maintain genetic diversity in an outbred colony, matings between related individuals should be avoided; however, some inbreeding may be inevitable over time in any relatively small, closed outbred colony.

Therefore, the following should be considered when establishing an outbred colony:

• Use numerous, genetically diverse founder mice

• Use a defined breeding scheme that is designed to minimize inbreeding: Several different outbred breeding program have been described (see Berry & Linder, 2007)

• While random breeding — using a random number table or computer program to select breeders — can be used, random breeding will result in occasional matings between closely related individuals

• Keep the colony at a minimum size of approximately 25 breeder males per generation

So if you’re interested in breeding dogs that burn out young, are riddled with disease, have nasty temperament issues, have trouble conceiving, develop horrible diseases young, etc., then believe that you too can develop an inbred strain and it’ll all turn out just dandy, just like those inbred lab mice.  Just be sure to buy yourself a nice dog bubble and some bio-hazard gear to wear around your dog while you keep it in a perfectly sterile environment after burying a truck load of its siblings and ancestors who died in the process of making your inbred little mess.

The wolves of Isle Royale Michigan

Sweeping comparisons between wild animals and domesticated pets are dangerous given the unique and often mutually exclusive conditions in which those two groups often find themselves.  Wild animals must hunt for their food, compete for resources, suffer predation, lack medical intervention, self-select their mates, and exist in numbers based upon a complex interaction between their own merits and the conditions in their environment. Pet dogs are fed from a bowl daily, compete only for our affection and attention, are largely free of predation, have ready access to modern veterinary techniques and treatments, have their mates chosen for them–sometimes from dogs long dead or on other continents, and exist in numbers based upon human concerns and rarely on their own merits or the environmental carrying capacity.  Their selection is very much unnatural. But there are very few scientific studies of domesticated pets versus numerous investigations into wild populations, so dog lovers would be remiss in not learning lessons from our pets’ wild cousins.  One particularly interesting ongoing scientific inquiry is the study of the wolf and moose populations on Isle Royale Michigan.

Wolves colonized Isle Royale, a wilderness island in Lake Superior, North America, in 1949 or 1950. The population is isolated from mainland wolves by a channel of frigid water, 24 km wide. In many, but not all years, this channel freezes for several days or weeks. Although an occasional ice bridge makes immigration possible, the analysis of mitochondrial DNA and the Y chromosome suggests that the population was originally founded by only one female and two males.

This makes Isle Royale analogous to a small dog breed based on a few founders or even a single kennel that rarely brings in any new blood.  Nova Scotia Duck Tolling Retrievers, Leonbergers, Cavalier King Charles Spaniels, Vallhunds, and many other breeds were founded by only a few sires and dams and have had very little influx of blood since and there are quite a few old time breeders who would only occasionally bring in a sire from outside their own moderately sized kennels. As with the above breeds, the mostly-closed gene pool on Isle Royale became steadily inbred over time.

By the late 1990s, the population’s estimated inbreeding coefficient had risen to 81%. Fifty-eight per cent of Isle Royale wolves showed congenital bone deformities compared with only 1 per cent in two outbred wolf populations. Some of these deformities could reduce individual fitness, particularly components of fitness associated with predation and reproduction.

So the first lesson to be learned from the Isle Royale Wolves is that isolation leads to inbreeding and inbreeding is detrimental.  In dogs, closed registries and kennel blindness are a form of isolation and in both cases we see rising inbreeding followed by increased expression of otherwise rare diseases.

Some of the most studied wolf packs in the world are in serious jeopardy. Researchers report that the occurrence of debilitating bone deformities in wolves marooned on Isle Royale, an isolated island in Lake Superior north of Michigan, has risen sharply over the past five decades due to inbreeding.

Diseased wolf vertebra due to inbreeding of Isle Royale wolves.

A genetic defect now common in the Isle’s wolves causes bones in the spine, the vertebrae, to grow gnarled and crooked. Also found in domestic dogs – close wolf relatives – the bone malformations  can pinch nerves in the spinal cord, causing pain that makes it tough to walk and can lead to paralysis of the back legs and tail in severe cases, according to research published in February’s issue of Biological Conservation. Back in the 1960s, about a quarter of Isle Royale’s wolves appeared to have the anatomical abnormality, but now the percentage of afflicted wolves has risen to nearly 60 percent of the population. “In normal, healthy wolf populations without inbreeding, you are only supposed to see this kind of defect in about one out of a hundred animals,” says paper coauthor John Vucetich, an assistant professor of wildlife biology at Michigan Technological University (MTU) in Houghton. The deformity, discovered during autopsies of recovered, dead wolves, has grown so rampant, Vucetich says, “we haven’t found a normal wolf in the past decade.”

- Scientific American

The second lesson to learn from the Isle Royale Wolves is that hybrid vigor is real and powerful and that inbreeding depression is real and powerful.

We used molecular techniques to document the consequences of a male wolf (Canis lupus) that immigrated, on its own, across Lake Superior ice to the small, inbred wolf population in Isle Royale National Park. The immigrant’s fitness so exceeded that of native wolves that within 2.5 generations, he was related to every individual in the population and his ancestry constituted 56 per cent of the population, resulting in a selective sweep of the total genome. In other words, all the male ancestry (50% of the total ancestry) descended from this immigrant, plus 6 per cent owing to the success of some of his inbred offspring. The immigration event occurred in an environment where space was limiting (i.e. packs occupied all available territories) and during a time when environmental conditions had deteriorated (i.e. wolves’ prey declined).

This event is an excellent example of what one outcross might do for a small breed and especially a single kennel. The immigrant wolf’s offspring were true hybrids, a mix of the formerly isolated pool and fresh blood; versus having an outside pack supplant the locals in toto, as one might expect in a contiguous geography that was not isolated like the Isle.

We have here an analogous situation that fits existing human patterns of behavior regarding dog breeds and strains that have virtual barriers instead of physical ones.

The astounding aspect of this immigrant on Isle Royale is just how potent his genetics were to effect change on the island.  None of the existing males could even compete with him and he became the sole sire.  His initial success is likely caused by the inbreeding depression in the inbred Isle wolves.

The high fitness of this immigrant wolf was also associated with distinctive behaviour and physical appearance. First, he was physically larger than most Isle Royale wolves. As alpha male of the Middle Pack, his high fitness was also reflected by his dominance over other ISRO packs. Specifically, he exhibited strong territorial behaviour that completely displaced West Pack, driving that pack to extinction by 1999.

This immigrant wasn’t necessarily a super-wolf, he was in all probability a young male that was driven out of his birth pack’s territory for being non-competitive with that pack’s alpha male. His success on Isle Royale shows just how compromised the inbred population had become.

The inbred Wolves of Isle Royale, genetically refreshed by the genes of a new sire.

It’s an open question if and how much the influx of new genes has changed the bone deformities which had come to define Isle wolves.  Surprisingly, before the results of the bone study were published, Isle Royale was used as an example of a wild population that was thriving and unharmed by inbreeding and isolation.  This is why I’m cautious of anyone who argues from ignorance regarding their ability to inbreed and avoid disease.  This is the third lesson: don’t assume that inbreeding can exist in high levels without detriment and don’t cite wild populations if no one has ever done a detailed health study to document the true health of the population.

The new results offer the first evidence of the wolves’ closed population leading to a decline in natural fitness. This is important, Vucetich says, because for years some policy makers and conservationists have pointed to the apparent health of the Isle Royale wolf packs as an indication that small animal populations can maintain proper genetic diversity. “Isle Royale is not this robust place that some people thought it was,” says Vucetich.

Now, not all the lessons are positive ones.  Given the isolation of the island, the complete genetic sweep of the immigrant male, and the small population size the rates of inbreeding swiftly ticked back up.  The smaller the population size and the greater degree of inbreeding done following new blood, the shorter time you’re going to reap the benefits of that new genetic material.  Outcrossing can forgive a myriad of sins, but it needs to be used in measure to the problem.  On Isle Royale, this new wolf didn’t simply add to the sires on the island, he supplanted them and then bred with his children, creating more inbreeding instead of extending the benefits of outcrossing.

This isn’t an advisable strategy for refreshing a dog breed, essentially going from one popular sire to another.  Diversity in breeding males should be maintained over each generation and proceeding to breed father to daughter–and similar–after a single outcross will swiftly return the gene pool to inbred status. The other issue that researchers have is that to complete a “genetic rescue” one must be able to document the benefit on a population level, an this is often done with the most crude methods, namely demography (head counting).  An increase in population size was not observed here, although there was a precipitous drop in the wolves’ main food source, Moose, during this time and the wolf numbers did not suffer either.

Genetic rescue, in which the introduction of one or more unrelated individuals into an inbred population results in the reduction of detrimental genetic effects and an increase in one or more vital rates, is a potentially important management tool for mitigating adverse effects of inbreeding. … The immigration event occurred in an environment where space was limiting (i.e. packs occupied all available territories) and during a time when environmental conditions had deteriorated (i.e. wolves’ prey declined). These conditions probably explain why the immigration event did not obviously improve the population’s demography (e.g. increased population numbers or growth rate). Our results show that the beneficial effects of gene flow may be substantial and quickly manifest, short-lived under some circumstances, and how the demographic benefits of genetic rescue might be masked by environmental conditions.

This is not a problem with outcrossing at all, rather it’s a problem of the limitations of the crude science of demography. Head counting might speak to quantity, but it is wholly lacking in useful information about quality.

Demography is likewise a poor tool to employ when analyzing domesticated dog health.  The numbers of dogs within breeds has little to do with their vitality and much more to do with fashion and the whims of a handful of breeders.  No one would claim that a Pug is popular due to competitive natural gifts of robust health and fitness, rather they are much like the inbred wolves on Isle Royale, they are artificially supported by beneficial conditions, easy access to food, and a blunting of natural pressures against their survival; in the wolves’ case it’s the benefits of living on an island, in the case of the Pug it’s being coddled by owners and breeders willing to spend a pretty penny on their upkeep.

In open and competitive environments, population numbers can serve to estimate vitality when better data has not been taken, but it seems that on Isle Royale, the wolves have a sheltered niche as the apex predators with ample food supply.  The Moose can’t migrate away and there is little in the way of competition for the wolves.  In such conditions, even sickly inbred wolves can reach a carrying capacity at about the same numbers as more robust wolves can.  It’s possible that more wolves could have thrived had the main food source not plummeted, or it could be that even at the lowest levels the moose populations were not small enough to be a significant factor in the head count of the wolves.

Without a marked improvement in population size on the island and without documentation of the rates of disease and bone deformities improving with the influx of the immigrant wolf, the technical definition of a “genetic rescue” has not been met with the current state of knowledge about the Isle Royale wolves.

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.

Dublin is hinting that he wants a dog bed for Christmas.

I had my laundry neatly folded in an IKEA bag waiting to get put in a drawer and Dublin decided that he really liked the bold yet sleek Scandinavian design and made an ad hoc dog bed for himself. Border Collies sure are clever; he actually used his nose to push up the lip once he got in to provide more support.

I guess I’ll have to get him a legit dog bed of his own for Christmas, but sadly it doesn’t look like IKEA makes dog beds and I don’t think anyone who does will sell me one for the 59 cents that the IKEA tote bag cost.