Dog Health, health testing, hip dysplasia, Intervertebral disc disease (IVDD), Responsible Breeding

Degenerative myelopathy – my unpopular view (refreshed for 2015)

I first wrote this post six years ago, when the DM test had very recently come out and I was beginning to see people using it as one of their questions as they made breeding decisions.

Now, six years later, it’s usually the FIRST question. Instead of “Is he finished” or even “Is he health tested?” I hear “What’s his DM status?” Dogs who are DM A/A (what we call “at risk” or homozygous for the mutated allele) are presented in a half-whisper, an apology built in to the telling. In other words, exactly what I worried about six years ago has started to happen; the large proportion of our breed that is homozygous for the allele is being deliberately bred away from.


I’ve been accused of being unfeeling or some such great evil because, six years ago, I pointed out that degenerative myelopathy is an old-age disease that is painless. How dare you! was the cry. Painless! The owners feel such pain!

And I agree, I AM unfeeling, when it comes to this kind of thing. Not because I don’t adore dogs, but because I don’t think you can answer scientific questions by making yourself cry. I am so incapacitated when one of my dogs dies that I die myself inside. But when it comes to how I breed those dogs, I try to not change anything until I am not just emotionally but rationally convinced.

The argument as currently presented is that we MUST get rid of DM because even though it is painless to the dog, it’s painful to the owner, and all involved, and we’ve GOT to get rid of it. I’m also seeing a boatload of bad science, not from the researchers but very definitely from breeders and armchair commenters. Everybody’s 
saying “The breed incidence has always been very low, but we assume
 that’s because people weren’t necropsying,” or “We’ve always thought 
that very few of breed X had DM, but now we assume that many of the 
deaths we have seen are the result of undiagnosed DM.” Assume
 schmassume, people. It’s bad science. It’s because the incidence of
 at-risk dogs is so shockingly high that everybody is now scrambling to 
attribute deaths to DM. Statistics do NOT work that way. You never take 
a result and apply it to the population; you take the population and 
develop a result. What we KNOW is a picture of an extremely low 
proportion of clinical DM compared to the at-risk (“positive”) dogs. If,
 over the next two decades, good controlled studies show that proportion 
to be higher, we can say something. We should not be assuming or
 conjecturing now.

Here’s the thing.

Every dog is going to die. And every time a dog dies, it is intensely emotionally painful. Whether the dog is young, old, or in between, it rips your heart out.

And yet, every dog dies.

If any form of death is a failure on our part as owners or breeders, then we are ALL failures and we are ALL failing EVERY time.

So the question is not whether we can keep dogs from dying. The question is whether we can give dogs as long and happy and functional and pain-free a life as they can possibly have. That means breeding FOR maximum freedom from disease and maximum lifespan, not just AWAY FROM certain diseases. And there is a huge, huge difference between those two concepts.

So how do we start to frame this conversation? Well, there are a few ground rules we have to follow, HAVE TO, when we talk about degenerative myelopathy.

1) The DM mutation is an extremely ancient, extremely widespread one, which likely arose before wolves even became dogs. It is not a new disease and the incidence has not increased lately. 

Many of my readers have been “in dogs” for their entire lives and have decades of experience. When you first got into dogs, DM was just as common as it is now. That’s just scientific fact, based on the widespread nature of the mutated gene. Was it a disease that you saw frequently? Obsessed about? Wondered how to prevent and wished for a test for? I suspect, unless you were in GSDs or MAYBE in Pems, you had never even heard of it until the test came out. Don’t let the visibility of a disease fool you about its incidence.

DM gets a lot of press because it’s “dogs in carts.” Unlike cancer or autoimmune or heart or the scores of other disorders that are likely killing your breed with far more regularity, dogs in carts live for years. They get Facebook followers. They get press conferences. And, even though in the years since they went into the cart dogs of their breed have died by the thousands from OTHER diseases, when the dog in a cart dies, the outcry of “Why did this happen? Why didn’t a breeder do something different?” is deafening.

2) ANY dog can get DM. No matter what their gene test result. 

Welcome to the brave new world. When the gene test first came out, we told ourselves “No more at risk, no more DM.” FALSE. Clear and carrier dogs have been confirmed with DM on necropsy.

Any dog can get DM. Being homozygous for the gene makes it more likely that a dog will get clinical DM, but you are NOT allowed to tell your puppy buyers or your breeding friends that a clear or carrier means they’re “safe.” If you ARE doing so, you must stop now.

3) There is no such thing as a DM diagnosis without a necropsy. DM is a disease that looks like other diseases, and many other diseases can look like DM. DM is a VERY SPECIFIC disorder that is characterized by aggregates containing SOD1 antigen. It is NOT “back problems” or “going down in the back” or limping or progressive paralysis. It is not the only nerve disorder and it is not the only thing that makes dogs lose rear function. Dogs can “go down” because of disc disease, a whole bunch of muscle diseases, other nervous disorders, vestibular issues, a huge range of injuries, and even the simple muscle atrophy of old age. Any one of these can mimic DM.

So no matter how much it “looks like” or “acts like” DM, until the nerves are examined under a microscope there’s no true diagnosis. Dogs with DM can have normal myelograms, normal bloodwork, and very subtle symptoms. And, conversely, dogs WITHOUT DM can have abnormal myelograms, abnormal movement, very dramatic symptoms. And (KEY): All these other things can happen to a dog with a positive DM gene result. Even if a dog has a gene-positive result, it cannot be diagnosed with DM without a necropsy.

4) THERE IS NO SUCH THING AS A DM DIAGNOSIS WITHOUT A NECROPSY. It’s so important, I’ll say it again. So you can’t say “We now know that dogs we thought died of injuries had DM” or “We believe there’s a much higher incidence than we had thought” or anything of the kind. If the dog did not have an autopsy, it cannot go in the disease statistics.  Oh, and did I mention that

5) DM remains a disease that is extremely rare compared to its gene result. 

Let’s look at numbers. Most of our good numbers for degenerative myelopathy in corgis are in Pems, because only one Cardigan has been diagnosed with DM on necropsy. So we have to extrapolate from our cousin breed.

* Pembrokes have a 50-60% A/A (homozygous, or “at risk”) rate for DM, and a 90% rate of being either at risk or carrier. That means that virtually all Pems that you see around you, that you’ve known throughout your entire life in dogs, have been at risk or carriers for DM.
* Pembrokes, when euthanized for DM, die at an average of 13 years.
* PWCCA reports an average estimated Pem lifespan of 13 years. This would seem to correspond well with what we see in Cardigans, where 13-14 is our normal end of life for a healthy dog.
* Pembrokes do not get clinical DM at a rate that even approaches their gene-positive rate. There are very few good incidence studies out there (one of the big problems in analyzing this disease) but the highest rate of DM Berghaus found was 2%, in GSDs.

This is a VERY OLD 
disease, so if 50%-60% are testing at-risk now, it’s likely been close to 
that for decades. Are even close to that number dying of DM? Are even 6% 
dying of DM? If the rate is closer to 3%, which seems more reasonable, 
then around ninety percent of at-risk Pems will never get this disease. But, meanwhile, those dogs will have been selected out of the gene pool as though they are radioactive.

6) The DM test is merely the first of many, many similar tests that are coming out. These tests will not show that an animal WILL get the disease, merely if the animal is somewhat MORE LIKELY to get the disease. The recent test for PLL (primary lens luxation) in terriers seems to be the same. Absolutely enormous at risk and carrier population compared to a low clinical population. So now we have two. There are going to be scores and scores and scores more.

In fact, I am ABSOLUTELY CERTAIN that within a few decades – within the lifetime of our younger breeders – the time when you can say “He passed all his health testing” will be a distant memory. Dogs will he forty or fifty or a hundred DNA results, susceptibilities to dozens of diseases.

Here are the big things we’re doing wrong. 

1) We talk as though we know what this disease is and reassure each other that a clear or carrier will never get a disease. 

Again, this is not true. We have no idea why some dogs get the disease and some do not. We have no idea how to either prevent or encourage its expression. Clear and carrier dogs have been confirmed with the disease. You must tell your puppy buyers and your peers that any dog can get DM – clinical, verified-on-necropsy DM. The gene affects the frequency or likelihood.

2) We make stupid breeding decisions when we make them out of fear.

We are immediately ready, because we hate the idea of dogs dying, to RADICALLY change the entire genetic makeup of multiple breeds in order to eliminate a gene. When we know JACK ALL about to what extent the gene will actually affect the dog.  I am pretty dang sure that if we screw around with our existing gene pool this much, cut out this many dogs, we’ll discover that dying at 13 was not so bad after all. We’ll uncover something, or many somethings, that kill them far earlier and far more painfully.

We ALL KNOW how this works. Everybody promises that we’ll still use
carriers, but it becomes “Oh, he’s a great dog, fabulous 
temperament…but you know he’s a DM carrier, right?” Or “I’d love to
 use XX dog, but… he’s a DM carrier.” Or, even more deadly to the 
breed, “I know he’s not perfect, but he doesn’t carry DM.”

DM is the disaster of the month, and humans have very short 
memories. THERE WILL BE A NEXT MONTH. There will be a next year, and a 
next decade, and (should the Lord tarry) 50 years from now when we’re
all gone, purebred dogs will have a vial taken at eight weeks old and 
there will be a printout of seventy or eighty acronyms, most of which we
 haven’t even conceived of yet. Right now, it seems like the worst thing 
in the world is this disease. I strongly suspect that we aren’t
even at the tip of the iceberg. Radically changing our breeding habits 
to accommodate this disease, which we have almost no accurate hold on 
yet, will open us up to concentrating many more diseases that have the 
potential to be far more damaging.

3) We forget that there is no such thing as removing a big portion of our gene pool without other, unintended, consequences.

If I had to choose between a disorder that kills at 13 and a
host of other issues, I’m going for the old-age disease every time.

We need to take a lesson from the Basenji breeders, and we need to look 
at it very hard. They created the Fanconi epidemic by breeding rigidly 
away from another disorder. The difference is that they can go (and are
 going) back to Africa to get new foundation stock and hopefully solve 
the problem. We don’t have a pocket of fresh Cardigan genetics somewhere 
in Wales. We’re stuck with what we’ve got. So deliberately narrowing the 
gene pool should be done only with GREAT fear and trembling. Oh, and a super key statement from one of the UK Chessie breeders–a 
very influential dog in the UK was imported because he was PRA-negative. 
Turns out he was bringing DM. This is why you don’t freak out and dump gene
pools–or start entirely new ones–when you have a disease discovered.

4) We act as though good breeding is defined not by what you DO breed, but by what you DON’T. 

I sometimes feel like, in contrast to the bad breeders and puppy mills 
who will look for any opportunity to breed, we make the opposite
 mistake. We’ll jump all over the slightest excuse to NOT breed an 
individual dog. And then, in an example of massive irony, we end up
reducing the gene pool so much that we are stuck with a set of genetic 
diseases that exactly fulfills the “Don’t buy a purebred; they’re all 
riddled with health problems” propaganda.

We MUST reduce disease, or at 
least maintain the healthy breed we have. But we MUST do it cautiously 
and with ALL the information we need to make a good, wise, considered

If I can distill my soapbox, which I know is not popular, into one 
paragraph, it would be this.

Please do not EVER think that I am not in favor of testing, or in favor 
of shaping a population to lessen the incidence of a disease. 
Maintaining, if not bettering, a breed is our sacred duty; nothing can 
be more important. I just think that with DM we are nowhere near that 
point yet. This is NOT like PRA, this is not like thyroid, this is not 
like heart, this is not even like hip dysplasia. We need a lot of years 
of testing and observation to confirm that we have a handle on this gene and its action before we take the extremely 
risky step of narrowing our gene pool.

Here’s what I am personally doing, knowing all the above facts:

1) We are testing every single one of our dogs, and then we are waiting. We are NOT using the test results to guide our breeding. We need to see if the generations being tested actually end up 
dying from the disease, and in what proportion, whether diet affects it, 
whether exercise, whether family X gets it when the dogs are 14 but family Y 
gets it when the dogs are 5, and so on. Please note that I don’t mean we
never change our breeding habits, just that we don’t change them YET. We 
just simply don’t know how to do it right.



Knowing this is an unpopular opinion, I just wanted to mention the 
statistical data for a minute.

To give you the sources of the statistics I know:

Clear and carrier dogs showing the aggregates that provide a diagnosis of DM:

Current DM statistics:

The under 2% affected is Roy Berghaus’s study of dogs coming into vet 
universities. Two percent incidence in GSDs, 1.51 in Cardis, .83 in 
Chessies, etc. He analyzed records of a total of 432,467 dogs; 664
 Cardis, 19,000 GSDs, 1500 Chessies, and the list goes on. I think you
 could argue that those numbers are actually high, because dogs with DM
 are more likely to end up at vet universities than at local vet offices.
 If better incidence statistics exist (and by better I mean newer,
 involving a larger group of dogs, and more controlled), I would love to
 be corrected.

The median euthanasia age in Pems was from Coates, March, Oglesbee, 
Ruaux, et al., in J Vet Intern Med in late 2007. Again, if better
 studies exist, tell me so I won’t go spreading misinformation.

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  • Reply cardigancorgis March 27, 2009 at 12:30 am

    I still can’t find an actual published paper with these stats, but I did find a brief article where the date is referenced:

    In the article, Berghaus is quoted as saying:

    “One thing to keep in mind is that dogs presenting to veterinary teaching hospitals are not necessarily representative of the general population of dogs, and the prevalence of DM in the general population is probably different.”

    Different–he doesn’t say higher or lower. Just different.

    While you argue that the rates he quotes are probably high because dogs with DM are MORE likely to end up at vet universities, I would actually argue the opposite.

    There are 28 veterinary teaching universities in the United States that are members of the AAVMC:

    If a dog owner doesn’t live in a state with a veterinary teaching university or if they live more than a few hours away from such an institution, how likely are they to take their dog to such a location as opposed to driving 5 or 10 miles to their local veterinarian? DM is not such a unusual or uncommon problem that a local vet can’t provide some preliminary diagnostic tools and ideas for treatment.

    Doesn’t it also seem odd that Cardigan Corgis were included in the data set and Pembrokes apparently weren’t?

  • Reply cardigancorgis March 26, 2009 at 10:54 pm

    Can you give me the title of the Berghaus study with the breed incident rates? I searched PubMed and found 19 papers published by Berghaus but couldn’t find this specific one. If it’s not published in a journal, can you direct me to a website or other location? I am really into gathering as much info. about DM as I can right now. Thanks.

  • Reply rufflyspeaking March 26, 2009 at 11:19 pm

    I had the text of the study more fully, but all my data from that era is now gone (house fire). Here’s a PDF snapshot:

  • Reply rufflyspeaking March 27, 2009 at 12:44 am

    Unfortunately, you’re now deep into the supposition of rates land. Remember the cardinal rule: It’s not DM until the dog has been necropsied. So unless you have an incredibly savvy local vet who happens to know an extraordinary amount about neurological issues on necropsy, what your vet is giving you is a best guess and not a diagnosis.

    Berghaus comes the closest to an actual study, and I tend to think is more reliable because teaching hospitals are, as a rule, employers of more highly trained/specialized vets and more rigorous in terms of testing and diagnosis.

    One of the reasons more data about incidence is so DESPERATELY needed is that we really don’t know much about the actual penetration or incidence of DM. We have a lot of dogs that we think may have DM or we’re assuming have DM or we’re assuming DON’T have DM. But the insisting on necropsy results is for a very good reason–DM is a very specific disease that shares symptoms with a whole bunch of other things, both diseases and injuries.

    It’s possible that part of our behavior change when it comes to thinking about DM is that we’ll begin to ask that all dogs with a suspected DM diagnosis be escalated to a teaching hospital or all dogs with a suspected diagnosis be necropsied.

  • Reply Cait March 27, 2009 at 4:05 am

    THANK you for this article – I love your thoughtful pieces on genetics and population issues, because they always make me think.

    One TINY thing I think I would mention though is that PRA in Cardis is not the only type of PRA. In some breeds (Springers and Eskies), they’re having an issue with the DNA test for the specific type of PRA they have not being 100%, and in those cases it’s an old age thing. If the dog dies with early stages of PRA at 15 (especially in springers!) and no other health problems, that’s still a darn good set of genetics for a breed that is losing ground on the age-of-death statistics.

  • Reply cardigancorgis March 28, 2009 at 11:30 pm

    Well see–we are finally beginning to agree about some things: like the idea that there may not be any ACTUAL studies out there about DM rates (things that ‘come close to actual studies’ are just so darn hard to get published in those pesky peer-reviewed scientific journals).

  • Reply rufflyspeaking March 28, 2009 at 11:42 pm

    The lack of real data is EXACTLY why I think it is a really, really bad idea to start changing our gene pool because of this. I don’t understand why we have a situation where the scientific community says:

    So we have this gene that appears in DM dogs. It also appears in lots and lots and lots of normal dogs. We have no idea how much it decreases life span, though we think it’s very little, and we have no idea what triggers the dog to actually develop DM or even what role this gene has in the development of DM.

    And breeders go:

    AAAAAAAAAAAAAAAAAAAAAAAAHHHHHHHHHHHHHHHH! OMG! OH NOES! Must stop breeding dogs with the gene! Must stop!

    It makes no sense to me. We are so far from knowing how to wisely address this situation that it’s not an exaggeration to say several decades will go by before we really know the implications of this gene discovery. We are in no place to screw with our gene pool.

  • Reply cardigancorgis March 29, 2009 at 12:48 am

    I absolutely agree there is a lack of real (scientifically published in a peer-reviewed journal) data in regards to rates of DM in various breeds of dogs.

    We do have real data showing that a very specific mutation in the SOD1 gene consistantly shows up in dogs that have been strictly diganosed with DM. And, if you look at the Awano et al. paper (figure 5) you will see that approximately 35% of the ‘normal’ dogs (those not showing symptoms of DM) who test positive for the DM SOD1 mutation are ages 6 and under–thus we wouldn’t necessarily expect them to show signs of the disease yet.

    And yes, there are several A/A dogs older than 6 (up to age 15) in the study that weren’t yet exhibiting signs (hence the idea of other genetic or environmental factor playing a role in disease development).

    Are there still more questions to be answered about DM? Sure. But the authors of the Awano et al. paper did a good enough job presenting their collective evidence that a group of their peers–researchers who work in the same fields as they do–felt the information they were presenting was not only valid but also compelling enough to publish in a journal (PNAS) considered to be among the most prestigious around (see for more information about the journal and it’s editorial board).

  • Reply rufflyspeaking March 29, 2009 at 12:59 am

    The Awano paper was accepted because it did what it said it was going to do–it suggested that canine degenerative myelopathy is a valid model for human ALS because it shares a genetic region and has some similarities in physical expression.

    That paper was not about the implications for dog breeding and offered no normative recommendations for dog breeding. The only remark about breeding is that it’s going to take a long time to eradicate in dogs, and can’t be done without affecting a huge proportion of the breeds involved, so there are a lot of years left to use DM dogs as ALS models.

    It said a very narrow thing (as all good studies do): The gene is strongly conserved in dogs with DM (true) and DM is similar to ALS and therefore dogs with DM are theoretically better experimental models and subjects for ALS than rodents with the rodent version of ALS (true). I have no problem with the conclusions of the study, but I have no illusions that the study meant to say anything about how dog breeders should deal with the DM gene.

  • Reply rufflyspeaking March 29, 2009 at 1:17 am

    Also, in terms of the ages of the normal dogs, there’s no reason we should conclude anything from the fact that 35% of them were under the age of six. Average dog lifespan is about twelve or thirteen, so if there was anywhere close to a normal spread of dog ages in the study, around half would be under six.

    It’s a little like the Pit Bull dog bite statistics–the proportion of serious dog bites attributed to Pits is disproportionate only if you think that every breed in the US has the same number of individual dogs. When you realize that Pit-type dogs are by far the most numerous breeds in the country, representing about a quarter or a third of the entire purebred dog population (they are far more common than Labs, far more common than coonhounds, which would be the #2 and #3 if you look at AKC/UKC statistics), then the fact that a third of all bites are attributed to Pit-type dogs makes sense.

    The study was NOT about age of onset of DM. It never even pretended to say anything about that, and we should not ask it to. It was NOT about how many gene-positive dogs eventually develop DM. It was ONLY about whether that particular gene is conserved in clinically ill dogs, and whether therefore DM dogs represent a valid model for human ALS research.

  • Reply Chaiah October 20, 2011 at 10:20 pm

    First of all, DM is NOT an “old age disease that is painless.” Our first DM victim was 6 years old when initially diagnosed. She was a GSD. I would love for you brilliant individuals who think this is a painless old age disease to have been here to explain to my middle aged dog why she could no longer go for walks (not even a block) because, initially, her hips would start to hurt her and her toes would drag. She would whimper in pain. Though the part of her body that was paralyzed didn’t hurt, the rest of it did. The 5+ years she had with us after she was diagnosed (a veterinarian from the University of Pennsylvania diagnosed based upon all of her symptoms and then an necropsy afterward only confirmed it) were ones for which our family was very grateful. I got my puppy almost 5 years ago and Lacy, our GSD with DM, taught her so much. The morning it was time for us to take Lacy in to say goodbye – she fell backwards down the stairs. Painless, you say? That wasn’t painless to her – or to us. January 8, 2008 will always have me looking up at the sky and wishing beyond hope that we could have taken that DM away from her and allowed her to live the life she should have been able to live… It looks like my “puppy” who will be 5 years old on Jan 20th is showing signs of DM. She is a Shepherd breed. Those of you who think this is painless and an old age disease need a good swift slap in the head. It is a genetic problem.

    If any of you care about your dogs and the health of whatever breed you have, you WILL be very careful about how you breed your dogs and test them for DM. Period. The heartbreak that results from not doing it is devastating.

    PS – Lacy was a puppy mill breeder whom we rescued. G-d knows how many pups she may have produced who carried DM on to their progeny.

    • Reply rufflyspeaking October 21, 2011 at 7:30 am

      Hi – and as a Bostonian, thanks for saying you’re too far away from it! I feel that way whenever I get more than a couple hours distance.

      I appreciate your experience and I feel for your dogs. It’s always awful to lose any dog. However, my statements are based on studies, not my own feelings. DM is *by definition* a painless disease. The page you linked to mentions that specifically. And GSDs are the only breed that seems to have some sort of early-onset DM; the average age of onset for other breeds is well up over ten. In fact, one of the reasons that such an incredibly common disease (genetically, it’s SUPER SUPER common in ALL breeds tested so far) has been seen to be a problem in so few breeds is that most dogs die of old age before the DM becomes clinical. It’s the long-lived dogs that we notice it in.

      My point in the article was not that DM is something I ignore. My point is that as breeders we must make choices based on a huge number of different possible dooms. DM is incredibly common; in order to avoid it I have to make other compromises. If I breed a dog who is out at elbows because he’s DM-free, the owners of his puppies are likely to have their dogs unable to move comfortably long before the owners of a DM dog. If I breed to a dog who has thyroid issues because he’s DM-free, the owners of his puppies are going to have major vet bills years before the owners of a DM dog. If it were as simple as just not breeding to a DM carrier, the decision would be brainless. OF COURSE I’d never breed to one. But it’s a system of compromises, and avoiding all DM carriers is going to dramatically skew our breed (or any breed) toward one small subset of dogs. Without knowing what that subset of dogs also brings to the table (very possibly something much, much worse), we can’t wisely make the decision. Until we know more – about what switches a DM-positive dog to a DM-clinical dog being the primary consideration for me – I am not going to throw every other part of the dog under the bus for the sake of a DM-free genetic test.

  • Reply Gina Downin July 26, 2015 at 12:14 pm

    Thanks so much for sharing your thoughts on this topic in such a smart, articulate, well-reasoned manner. I own and breed Chesapeakes. And, as you know, we struggle with these issues as well. I’ll be sharing this article with others in our breed community. Thanks again!

  • Reply Kathy July 26, 2015 at 3:45 pm

    Is it not a breeders ethical responsibility to manage disease? If we do not make some consideration to a mutation identified to be associated with identified DM victims in our breeding programs where is our love of our individual breeds? Is the simple cost of this marker to much to ask? Should the test price be reduced since we actually are participating in scientific research not only for our dogs but for the human race?
    When I ran into DM type symptoms it was most definitely misdiagnosed. However, did not change the outcome. The bloodlines that I carried in my breeding group all died in the same fashion ages 8-13 years old. The frustrations only remind me of proper identification of PRA in my breed which took decades. Looks like this crippler of varies breeds is heading for this same long term identification. My experiences this is not a painless disease until paralysis is complete.

  • Reply Kathy July 26, 2015 at 4:04 pm

    I should mention that over 17 years ago when we were dealing with symptoms that were misdiagnosed in all seven Collies they were all OFA excellent with the exception of one which was good. Dog Breeders have been doing OFA’s for decades and finally the question on seems to have a partial answer: Why do two OFA excellent dogs produce hip dysplasia?

    Let us understand when we are dealing with a disease such as DM for which “family history” of that disease is a risk factor that are apparently polygenic diseases subject to multifactorial inheritance, rather than true genetic diseases. . However, family history is obviously a very strong risk factor from my experiences with any monogenic disease

  • Reply Kathy July 26, 2015 at 6:40 pm

    I wish to express that I agree with Nancy Willoughby this mutation is likely to be found in other autoimmune diseases this is not a simple recessive disease. Seemingly most diseases are not including Cancer. I note many canines tested affected by this mutation die of cancer before DM can get them. Late on set diseases are dangerous to any breeding program and breed. Are we not as Breeders responsible to manage such diseases?
    It seems it is equally important …early or late on set of any disease that can be spread quickly especially when inbreeding remains popular protocol among especially show breeders.

  • Reply Sandy July 29, 2015 at 6:31 pm

    I suppose if I had a corgi, I could just carry it where it needs to go once it is paralyzed. Having to try that with a breed weighing 100lbs & up is not fun. Then having to look into her eyes while she died, simply because she could no longer walk and I wasn’t strong enough to carry her. Shame on any breeder who breeds so irresponsibly!

    • Reply Joanna Kimball July 29, 2015 at 7:20 pm

      Sandy, this attitude is exactly what I am trying to answer in the post. Please read it carefully. OF COURSE, if the choice is between DM and a healthy breed, anybody is stupid to NOT choose to eliminate it! What I have been saying over and over is that by breeding away from a third or a half of our already very small gene pools, we are quite possibly introducing something that doesn’t kill slowly at 13. It kills quickly and painfully at four.

  • Reply Susan Sullivan August 5, 2015 at 4:29 am

    Genetic testing should be done not to eliminate animals from the gene pool, but to allow the breeding of at risk and carriers without producing more at risk progeny. Breeding at risk and carriers to clears allows breeders to include all of the population. Unfortunately, breeders tend to use genetic testing as a selling point and in doing so toss the proverbial baby out with the bath water.

  • Reply Beth October 1, 2015 at 12:39 am

    Ah, just seeing this now, a little late. I read the original post years ago. I have been beating this same drum about Pems for as long as the test is out. Only about 10% of Pems are “clear” and breeding every at-risk or carrier into that 10% of clears, and then breeding the next generation of carriers back to that same 10%, would be a genetic disaster. Disaster with a capital “D”. The smart scientists studying this are looking at modifier genes now. My guess is modifier genes probably change age of onset. If age of onset is, say, 10 you will probably see the disease. But if age of onset is programmed to be 20, then you will never see it. Once we have more info on modifier genes, MAYBE we can make smarter breeding decisions.

    One of my dogs, my sweet and lovely girl who trusts everyone completely and greets each day with unmitigated joy, is down behind and in a cart. We THINK it is likely DM because her litter brother has probably DM. But she also has spondylosis. And she also apparently has one fairly crappy hip. Either of which could also put her down behind. Two vets aren’t sure. One leans toward DM, one leads toward spondylosis.

    She is in a cart. And guess what? If even the VETS can’t tell if it’s DM or the spondylosis or maybe something else (she has neurological problems as well— maybe a brain tumor?), well then breeding away from DM into that 10% of the gene pool that is clear will not eliminate Corgis in carts.

    And what if the 10% clear also have higher rates of cancer? Or lower average life spans? Or higher risks of IVDD? I’d rather have a dog who lives til 12 in a cart than one who dies at 9 of cancer.

    When she first started going down, it was hard. It was very hard. I was depressed. As soon as we got a handle on things (her worn nails, her worn toes, her staggering) and had a system, she got worse and the system didn’t work.

    And then one day I looked at her. I looked at HER, not her bad feet or her wobbly back end. And she smiled and smiled and I thought “What the heck am I doing?” and I stopped being depressed about it.

    She is in a cart. She is happy. She stops traffic and she loves it. She grins and grins and has learned that Rules Don’t Apply anymore and she gets away with murder.

    DM (or spondylosis, or wonky hips, or maybe that tumor) ARE hard on the owner. But guess what? I had a cat who died at 17 from cancer. From a big, ugly, visible lump of cancer growing out of her haunch and every day for a month I looked at her and knew she was dying and cried and cried. And she got sicker and she got miserable and she refused to eat, and I tried too long to keep her alive and it was horrible.

    So yes, my girl is in a cart. And she smiles and gets extra cuddles and attention and she loves life. One day she will lose enough function that we say “Here is where we stop” and we will cry our hearts out and send her on her way, knowing she had a beautiful life and was well-loved. And that’s what I want people to know about DM. It’s awful. Every death is awful. But it’s not the end of the world. There are worse ways to lose a dog.

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