In this installment of Inbred Mistakes, I take on a highly educated and well respected man of letters who is also an experienced breeder: Dr. Bruce M Cattanach BSc PhD DSc FRS. You might know him as the breeder who introduced Corgi into the UK Boxer breed to achieve a short tail without the need to dock. His resume speaks for itself:
B.Sc (Hons) in Agriculture, 1955; Ph.D in Mutagenesis and Mammalian Genetics, 1959; D.Sc in Mutagenesis and Mammalian Genetics, 1972; Elected Fellow of the Royal Society, 1985. Scientist Medical Research Council Mutagenesis Unit, Edinburgh,1959-62 and 1964-66; National Institute of Health Post-doctoral Fellow, Oak Ridge , Tennessee, 1962-64; Senior Scientist City of Hope Medical Center, Duarte, California, 1966-69; Senior Scientist Medical Research Council Radiobiology Unit, Harwell, Oxford, 1969-85; Head of Genetics Division, 1985-97; Director of the newly created Mammalian Genetics Unit 1997-2000. Author of over 250 published papers. Specialist subjects; chemical and radiation mutagenesis in mice, analysis of mutations, control of X-chromosome inactivation, sex determination, genomic imprinting.
It’s obvious that Dr. Cattanach knows what he’s talking about with genetics, which is why I was disappointed to come across the following sentence in an otherwise excellent article about inbreeding:
It seems fixed into the minds of human geneticists that every one of us harbours about 7 deleterious recessive genes. Hence the scientific basis for the taboos on inbreeding in humans. But the concept is now applied to dogs and claimed as a reason why inbreeding should be avoided. But were deleterious recessives to be so common in dogs, every one of us who breeds dogs would be finding abnormal pups in most litters, and this is patently not the case. Explanations offered for this have included the reductions in dog population numbers during World Wars, the small size of founding populations, and maybe even the tough association canines have had with man over historical times. All may have done much to weed out deleterious genes that were originally present!
I think that’s a loaded statement and an appeal to ignorance. It assumes that breeders have the ability to diagnose genetic disease in their litters and that such diseases act on puppies. It ignores the deleterious recessives that result in abortions at midgestation and stillbirths at term. Plus all those puppies that just “fail to thrive.” It also appears to confuse “common” with “ubiquitous;” since common is an imprecise term, I’ll point out that diseases that are billed as “epidemic” in humans are well below the rates of “rare” diseases in dogs. There are breeds where deleterious recessive disease is rampant and some times pervasive: cardiomyopathy in Dobermans, molera in the Chihuahua, hyperuricemia in the Dalmatian, etc.
While cancer is probably more complex than a single recessive allele, Mastocytomas (skin cancer) usually present in middle aged or older dogs. Mammary Tumors usually present with the highest frequency between 6-10 years of age and rarely prior to 2 years of age. Lymphomas usually appear in dogs over 5. Oropharyngeal Cancers set in between 7 and 11 years. Osteosarcomas present between 2 and 8 with 7 years being the average. In the show world, these dogs could be retired for a decade and have 4 generations of offspring before the breeder just might get wind of the disease.
Many diseases are also idiopathic or variable in expression. There’s also a strong bias to under report disease, even ones where there’s a DNA test for and no real bias against. How many diseased puppies do you just not hear about? I don’t think it’s stretch to say that there are far more diseases that have neither names nor DNA tests than there are named conditions or easily testable diseases.
If the question is “how many deleterious recessive diseases are there in dogs” and “how prevalent are they” then the answer will come with objective and comprehensive genome analysis and greater awareness of causal factors in disease. It will not come with a subjective “well we’d see more of it if it were really that common” statement that has really no grounding in either statistical relevance or observational fact.
We see in almost all species that the tolerance for inbreeding is actually quite low, with failures to sustain progeny after 30% COIs and up. I contend that if the danger zone between complete infertility and disease load is so low, so too is the observed line between apparent disease and fetus failure that most often goes undocumented. It should not sound radical to assert that the observed ratio of diseased dogs to healthy dogs completely neglects the dogs that fail before birth from being counted. Even if we had complete data, we’d still only be looking at the subset of deleterious recessive diseases that are not serious enough to cause fetus failure but serious enough to cause disease progression in a diagnosable fashion.
I also think the larger point Dr. Cattanach is seemingly trying to make, that dogs carry less of a disease load than humans, is false. Isn’t it the observation that dogs are both more inbred, suffer from higher levels of recessive disease, and have many analogous diseases to humans that makes them so attractive for scientists who are focused on curing human disease?
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I remember hearing on Pedigree Dogs Exposed that dogs have fewer of these diseases than people do. However, dogs are much, much more likely to be affected by these diseases.
But that isn’t what he’s saying here: He’s saying they are less likely to experience these diseases.
And that’s incorrect.
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On the first interpretation, I wonder if that’s a matter of fact or a matter of ignorance. Do we not have as many named and documented diseases in dogs because there are fewer of them or because we simply haven’t done an equivalent amount of research combined with the limitations having a non-speaking patient that can’t cooperate as fully in diagnosis?
Even then, the issue is sort of moot. It doesn’t really matter what the number of diseases is, but the total degree of expression across all diseases.
I think it’s simple ignorance. We just don’t know all the genetic diseases dogs can have.
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Dog owners, particularly those with expensive purebreds, are likely to pursue aggressive treatment from specialists for any symptoms their pets present and necropsies when they die from mysterious causes. It would take a pretty sneaky genetic disease to sneak by. Plus with the demand of human medical science to find animal models a fairly aggressive push has been made to discover and study dogs with human diseases. Probably the mouse, rat, and fruit fly genomes are better understood but both the number of dog diseases already found and the amount of scrutiny dogs are under make it hard for me to believe that they are hiding much more.
That’s a laugh, Lindy. We should shut down medical research because all the diseases have been found. We know everything. Close the patent office! (an urban myth). Not only do we know more than we don’t know, we know everything!
PLEASE! Don’t substitute arrogance for ignorance. We don’t know more than we do know. We are only beginning to document the extent of deleterious mutations. There are any number of harmful disorders that have neither a name nor a diagnosis.
“Aggressive Treatment” is not a cure. Chemotherapy and radiation don’t prevent cancer, they don’t even point to the cause. They are brutal and barbaric treatments that sometimes work, for some period of time. They don’t heal the gene pool any more than your eye glasses prevent your children from going blind.
You can start bragging to me about sneaky diseases when you can tell me what genes cause epilepsy and hip dysplasia.
You can pretend that we have the answers on disease when we don’t have any more “new” diseases like TNS that turn out to be very old, and many times more widespread than previously “known.”
When I started looking into Border Collie health seriously, no one mentioned TNS. No one talked about it. It didn’t have a name. There wasn’t an epidemic. There wasn’t a common “failure to thrive” syndrome. No one was demanding research. It wasn’t on the RADAR at all.
But BAM, a popular show breeder has a few litters that were inbred and had most of the puppies sick or dead at only weeks old, and suddenly it’s an epidemic!! Suddenly there’s a new killer out there. Suddenly it’s everywhere and it gets a name and some research, and then people come forward and admit that they lost a litter to what must have been Parvo, but it was never confirmed. “Failure to thrive” now has a disease name to go along with many of the cases. Then we get a DNA test. Then we see that the simple recessive gene that causes it was in several popular show dogs. Then we find that it was in non-show stock half way around the world too.
TNS is a perfect example of how we don’t know everything, plenty of diseases don’t have names or easy diagnoses, we don’t have tests for them and we don’t know how widespread they are.
Admitting our ignorance is the first step in combating it.
You’re welcome to live in dream world. The evidence doesn’t support it.
“You can start bragging to me about sneaky diseases when you can tell me what genes cause epilepsy and hip dysplasia.”
Oh, boy, I’d love to have the answer to epilepsy. Azawakh have it, and it does horrible things like skip generations, not show up at all in pups from an affected parent, and generally make a confusing nuisance of itself. Most affected dogs are very, very mild, but still. Considering teh very small gene pool and the fact that seizures came down from two of the founders, it’s unlikely to be eliminated, but I want to know.
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My own personal and completely unfounded theory about hip dysplasia is that it is a polygenetic consequence of domestication and that’s why it is so hard to breed away from. The connection between domestication and physical traits is poorly understood, but we do know that they are linked in some way. For example, foxes that have been selected for non-aggressive behaviors (domesticated) have tails that curve over their backs and white spotting.
Domestication can be thought of as the suppression of adult behaviors and the inability of the animal’s brain to mature.You can consider dysplasia as an inability of the joint to mature, thus, dysplasia could be one of those physical traits that has been affected by domestication. About the only way you can fight dysplasia is to breed dogs by using pedigrees “horizontally”. You are better off breeding a dog less than perfect hips, but with a lot of brothers, sisters, aunts and uncles that are HD clear than you are breeding a dog with perfect hips but with sideways relatives that have a lot of HD.
Terry,
That’s a better theory than this gem, by Denise Wall:
http://www.stilhope.com/writings/hips.html
She contends that HD is beneficial to working border collies and that getting rid of it just might ruin the breed’s ability to work.
I hope that she’s horribly wrong.
That’s an interesting theory. Dogs, on average, have much shorter limbs than wild dogs in proportion to their body size.
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One of the most interesting things to do is to compare dog tracks to coyote tracks. Dog tracks will be more bunched together and one on each side. Coyotes will have each track in a straight line.
retrieverman recently posted..Working terriers on the Isle of Skye
Most of my dogs single track.
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‘Converging toward the center line’ as their movement speeds up is expected of many breeds, I believe?
Sighthounds gait even better than the wild type!
retrieverman recently posted..Working terriers on the Isle of Skye
Look how fluid the gait is:
retrieverman recently posted..Working terriers on the Isle of Skye