As you should know, UPenn tests hips according to how far out of the socket they will move when the dog is in different positions. This result, called the “distraction index,” is expressed as a percentage of the hip itself. If the hip moves 30% of its own diameter, the DI is 0.3. If it moves 60%, the DI is 0.6. And so on.
DI correlates to the chances of the dog developing osteoarthritis of the hip joint later in life. The lower the DI, the lower the chance of developing osteoarthritis.
UPenn has determined that a DI lower than .3 is associated with virtually zero arthritis.
OK, that’s the backstory.
What this study did was quite simple: It compared OFA ratings and DI scores on about 400 dogs.
It found that a huge number of dogs who had Good and Fair ratings had DI scores over 0.3.
– This is NOT new news. Every study that’s ever been done to compare OFA and PennHIP scores shows that they don’t correlate very well, because they’re looking at COMPLETELY DIFFERENT things.
– You are seeing the outworkings of a longstanding feud between the two camps – expect to see some kind of answering research from OFA.
– The headline of the study makes it sound like OFA is some kind of crashing disaster, and all OFA results are invalidated or something. That’s actually not what the study showed. It set an extraordinarily high cutoff – 0.3 – and considered a “failure to predict” anything that OFA passed that turned out to have a DI higher than that number.
– Numbers above 0.3, in real life, don’t automatically get arthritis. IN THE FOUR BREEDS STUDIED (and this is critical), which are Labs and Goldens and Shepherds and Rotties, the risk of arthritis is around zero for 0.3 and rise to close to 100% for a DI of 1.0 (obviously, since that indicates a hip that comes completely out of its own socket). A dog with a DI of, say, .33 is listed as a “failure to predict” in this study, but UPenn’s own numbers would give it only a very, very small chance of developing arthritis (and, critically, in all of those four breeds a .33 would be a “do breed this dog” result).
– This study looked at UPenn’s four target breeds. The extent to which this study applies to you as a breeder honestly depends on how closely your breed resembles one of these four. UPenn does not have (repeat: DOES NOT HAVE) any published data reliably linking distraction index scores and arthritis risk for any other breeds. The extent to which, say, a bulldog’s DI influences arthritis is not known.
– Once you get out of the sighthounds and the very leggy dogs, you’re not going to find very many scores smaller than 0.3 regardless of breed. This actual study showed an average DI across all breeds of .435 +/- .14. In other words, not only did the average dog fail this “predictive” score, the sizeable majority of the entire study failed.
– According to this study, every single Cardigan on earth would “fail,” because our mean DI is higher than 0.6. We’re in absolutely hideous shape, according to UPenn.
– This study wasn’t really designed for breeders, except to imply that nobody should use OFA and everybody should use PennHIP. If the 0.3 cut-off was used to actually drop dogs from breeding programs, we’d be wiping out a good hundred breeds and decimating most of the rest.
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.
This is RIDICULOUS.
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, becauseonly 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 decision.
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: http://onlinelibrary.wiley.com/doi/10.1111/jvim.12317/full
Current DM statistics: http://www.offa.org/dnateststats.html
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.