Degenerative Myelopathy:
Degenerative Myelopathy (DM) is a progressive neurological disorder that affects the spinal cord of dogs. Dogs that have inherited two defective copies will experience a breakdown of the cells responsible for sending and receiving signals from the brain, resulting in neurological symptoms.The disease often begins with an unsteady gait, and the dog may wobble when they attempt to walk. As the disease progresses, the dog's hind legs will weaken and eventually the dog will be unable to walk at all. Degenerative Myelopathy moves up the body, so if the disease is allowed to progress, the dog will eventually be unable to hold his bladder and will lose normal function in its front legs. Fortunately, there is no direct pain associated with Degenerative Myelopathy. The onset of Degenerative Myelopathy generally occurs later in life starting at an average age of about 10 years. However, some dogs may begin experiencing symptoms much earlier. A high percentage of dogs that have inherited two copies of the mutation will not experience symptoms at all. Thus, this disease is not completely penetrant, meaning that while a dog with the mutation can develop Degenerative Myelopathy, the disease does not affect every dog that has the genotype.
Requires both parents to have or carry the gene for DM. DM is a recessive disorder and a dog must have two copies of this mutation for the disease to manifest. This means that a dog can have one copy of the mutation and not experience any signs or symptoms of DM; this dog would be known as a carrier. The carrier can then pass on either the normal gene or the mutated gene to any offspring. If two carriers are bred, a dog could potentially receive the mutated gene from each parent and be affected by DM.
Symptoms include: Hind leg weakness and eventual inability to walk. As disease progresses dog will lack bladder control and will lose normal function in front limbs.
**Disease itself is NOT painful, and is onset around 10 years of age +
**Disease CANNOT be diagnosed without a necropsy - therefore only after the death of the dog. There are many things that mimic DM that are not DM.
**Disease mutates, so clearance by parentage is not accurate after second generation.
Requires both parents to have or carry the gene for DM. DM is a recessive disorder and a dog must have two copies of this mutation for the disease to manifest. This means that a dog can have one copy of the mutation and not experience any signs or symptoms of DM; this dog would be known as a carrier. The carrier can then pass on either the normal gene or the mutated gene to any offspring. If two carriers are bred, a dog could potentially receive the mutated gene from each parent and be affected by DM.
Symptoms include: Hind leg weakness and eventual inability to walk. As disease progresses dog will lack bladder control and will lose normal function in front limbs.
**Disease itself is NOT painful, and is onset around 10 years of age +
**Disease CANNOT be diagnosed without a necropsy - therefore only after the death of the dog. There are many things that mimic DM that are not DM.
**Disease mutates, so clearance by parentage is not accurate after second generation.
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Here's an article on DM in Corgis that everyone should read, because it's spot on. A breeder's job is to eradicate health issues in foundation stock and future foundation stock by breeding progressively for the better. But, sometimes lack of real information can be detrimental. Here's a good article about DM. You can read it in the original form via the title below (linked). |
Degenerative Myelopathy: An Unpopular View
rufflyspeaking.wordpress.com/2009/03/26/degenerative-myelopathy-my-unpopular-view/
I’ve been accused of being unfeeling or some such great evil because I pointed out that degenerative myelopathy is an old-age disease that is painless. 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. So even though I am so incapacitated when one of my dogs dies that I die myself inside, when it comes to asking whether we should stop breeding dogs I try to not change anything until I am not just emotionally but rationally convinced.
The argument is that it’s painful to the owner, and all involved, and we’ve GOT to get rid of it.
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.
There are a few ground rules we have to follow, HAVE TO, when we talk about degenerative myelopathy.
1) There is no such thing as a DM diagnosis without an autopsy.
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 the result of an autoimmune response. 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 without an autopsy.
2) THERE IS NO SUCH THING AS A DM DIAGNOSIS WITHOUT AN AUTOPSY.
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
3) THERE IS NO SUCH THING AS A DM DIAGNOSIS WITHOUT AN AUTOPSY.
Let’s look at numbers. Most of our good numbers for degenerative myelopathy in corgis are in Pems, because they are much more numerous as a breed and are more frequently affected by the disease. In other words, they have a much bigger problem with DM than Cardis do. Chessies are also very helpful.
* Pembrokes have a 60% gene-positive rate 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 that Berghaus found was 2%, in GSDs.
* Like it or not, the statement “The disease is painless” really is true. If a dog has to die of something at age 13, this is not the worst one.
We honestly know ALMOST NOTHING about the connection between this gene and this disease. But 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 the gene. When we know JACK ALL about the gene. So yes, I strongly object to the idea of making breeding decisions yet. Because 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.
These are several posts I put on ShowCardi-L last year. I’ll come back and editorialize later tonight.
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.”
I just attended an absolutely wonderful lecture by Francis Collins, head of the Human Genome Project. He’s arguably the world’s top expert on genetic issues. He said point-blank that relying on genes to determine the course of a life is bankrupt and insane. If there’s one thing we have learned, it’s that environment is everything.
It seems to me that the only proper response both to DM and to IVDD, and realistically to any brand-new genetic test, is to test like crazy (and I do intend to test my girls) and then do absolutely nothing for 15 years. 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 vaccination affects it (if vaccination can strongly influence autoimmune hypothyroiditis, no reason it can’t cause this autoimmune disease too), whether family X gets it when the dogs are 14 but family Y gets it when the dogs are 5, and so on. The Pem studies show that median age of euthanization for DM in that breed is 13 years. And as much as I hate the idea of any genetic disease, good grief, they’ve gotta die from something! 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. Knowing this is an unpopular opinion, I just wanted to mention the statistical data for a minute.
We are IN NO WAY ready to make any statements about DM in the breed based on the OFA results for Cardigans thus far. With so few turned in, we’re in a margin of error that is probably 20% or higher–in other words, the number at risk could actually be as low as approaching 0% or as high as 30% or more.
OFA-type results already break one of the major rules of statistical surveys–that you don’t wait for the results to come to you; you go get them. Volunteered information and responsive surveys (where it’s the people involved that send you the information, rather than you using a random number generator and polling a truly random segment of the population) are always skewed because the people who care enough to send back a survey or click on your link or send in a blood test are rarely totally uninvolved. They all have an axe to grind, whether positive or negative, so their input is far less than optimal when it comes to saying something trustworthy about statistics.
Even if we ignore that, if we look at the numbers as though they’re a genuine sample, we have an incredibly tiny number of submissions right now.
It’s like spooning up alphabet soup–if you have a bowl that holds 8 oz and a big soup spoon, each spoonful will look like the soup as a whole.
But if you have a bowl the size of a coffee table and a teaspoon, some of the spoonfuls will be all broth, some all letters, some broth and celery, etc. You have to take many, many more spoonfuls before you know what the soup really looks like.
If we assume a population of 10,000 Cardigans in the US (of all ages, registered or not, etc.) we won’t be looking at an even close to accurate survey (plus or minus about 4 percent) until we’re up to several hundred, probably over 500, submissions. To give you the sources of the statistics I know:
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.
OK, personal opinion (though hopefully not one without thought) on:
The Chessies are beating us all hollow in terms of submitting dogs. They’re up to 131 dogs [edited 2009: 421 dogs] tested. And of that number, 60% are either carriers or at risk. For a breed with, according to Berghaus, a LESS THAN ONE PERCENT clinical rate. Twelve percent [edited 2009: 14%] are genetically at risk.
They need to get up to several hundred submissions before making a statistical statement would be wise, but–just building air castles right now, so don’t take this with too much weight, but it’s VERY interesting–IF this proportion holds true and IF Berghaus’s retrospective was correct, 93% of at-risk dogs will not die from DM. [Edited 2009: This rate seems to be holding true] Ninety-three percent.
Or let’s look at Pems, with a 60% at-risk rate. This is a VERY OLD disease, so if 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 ninety-five percent of at-risk Pems will never get this disease.
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 has DM. This is why you don’t freak out and dump gene pools–or start entirely new ones–when you have a disease discovered. DM and IVDD are 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 set of diseases. 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. 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.
I’m also seeing a boatload of bad science, not from the researchers but from the statements about the disease incidence for DM. 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. And, holy hannah, we should not be removing dogs from the gene pool yet.
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.
Rant off.
Adding today: Nancy Willoughby brings up a very important point, that a gene like this could be one that influences a broad range of autoimmune
disorders. Which begs the question “What is an autoimmune disease?” These are not simple equations. Autoimmune diseases, whether this one (DM) or looking at the entire spectrum, are extremely complex and we really don’t know how much genetics influences them–or, I should say, we know it does but we have no idea to what extent. I am most familiar with autoimmune hypothyroidism, which (at least in the Dane study) was heavily influenced by vaccination because (it was conjectured) the dogs were becoming sensitized to the adjuvant of the vaccines in a way that encouraged them to attack their own thyroids.
So do you then say “Well, it was a genetic weakness, dogs shouldn’t do that,” or do you say “The dog was fine until it was vaccinated; it’s the vaccine’s fault.” (I’m not anti-vaccine, by the way.) Even if it DOES turn out to be a generalized measure of a certain predilection toward autoimmune disorders, we still would be looking at environment, injury, and assaults on the immune system as heavy, even primary, causes.
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 this gene is the correct one and that we have a handle on its action before we take the extremely risky step of narrowing our gene pool.
I’ve been accused of being unfeeling or some such great evil because I pointed out that degenerative myelopathy is an old-age disease that is painless. 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. So even though I am so incapacitated when one of my dogs dies that I die myself inside, when it comes to asking whether we should stop breeding dogs I try to not change anything until I am not just emotionally but rationally convinced.
The argument is that it’s painful to the owner, and all involved, and we’ve GOT to get rid of it.
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.
There are a few ground rules we have to follow, HAVE TO, when we talk about degenerative myelopathy.
1) There is no such thing as a DM diagnosis without an autopsy.
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 the result of an autoimmune response. 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 without an autopsy.
2) THERE IS NO SUCH THING AS A DM DIAGNOSIS WITHOUT AN AUTOPSY.
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
3) THERE IS NO SUCH THING AS A DM DIAGNOSIS WITHOUT AN AUTOPSY.
Let’s look at numbers. Most of our good numbers for degenerative myelopathy in corgis are in Pems, because they are much more numerous as a breed and are more frequently affected by the disease. In other words, they have a much bigger problem with DM than Cardis do. Chessies are also very helpful.
* Pembrokes have a 60% gene-positive rate 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 that Berghaus found was 2%, in GSDs.
* Like it or not, the statement “The disease is painless” really is true. If a dog has to die of something at age 13, this is not the worst one.
We honestly know ALMOST NOTHING about the connection between this gene and this disease. But 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 the gene. When we know JACK ALL about the gene. So yes, I strongly object to the idea of making breeding decisions yet. Because 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.
These are several posts I put on ShowCardi-L last year. I’ll come back and editorialize later tonight.
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.”
I just attended an absolutely wonderful lecture by Francis Collins, head of the Human Genome Project. He’s arguably the world’s top expert on genetic issues. He said point-blank that relying on genes to determine the course of a life is bankrupt and insane. If there’s one thing we have learned, it’s that environment is everything.
It seems to me that the only proper response both to DM and to IVDD, and realistically to any brand-new genetic test, is to test like crazy (and I do intend to test my girls) and then do absolutely nothing for 15 years. 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 vaccination affects it (if vaccination can strongly influence autoimmune hypothyroiditis, no reason it can’t cause this autoimmune disease too), whether family X gets it when the dogs are 14 but family Y gets it when the dogs are 5, and so on. The Pem studies show that median age of euthanization for DM in that breed is 13 years. And as much as I hate the idea of any genetic disease, good grief, they’ve gotta die from something! 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. Knowing this is an unpopular opinion, I just wanted to mention the statistical data for a minute.
We are IN NO WAY ready to make any statements about DM in the breed based on the OFA results for Cardigans thus far. With so few turned in, we’re in a margin of error that is probably 20% or higher–in other words, the number at risk could actually be as low as approaching 0% or as high as 30% or more.
OFA-type results already break one of the major rules of statistical surveys–that you don’t wait for the results to come to you; you go get them. Volunteered information and responsive surveys (where it’s the people involved that send you the information, rather than you using a random number generator and polling a truly random segment of the population) are always skewed because the people who care enough to send back a survey or click on your link or send in a blood test are rarely totally uninvolved. They all have an axe to grind, whether positive or negative, so their input is far less than optimal when it comes to saying something trustworthy about statistics.
Even if we ignore that, if we look at the numbers as though they’re a genuine sample, we have an incredibly tiny number of submissions right now.
It’s like spooning up alphabet soup–if you have a bowl that holds 8 oz and a big soup spoon, each spoonful will look like the soup as a whole.
But if you have a bowl the size of a coffee table and a teaspoon, some of the spoonfuls will be all broth, some all letters, some broth and celery, etc. You have to take many, many more spoonfuls before you know what the soup really looks like.
If we assume a population of 10,000 Cardigans in the US (of all ages, registered or not, etc.) we won’t be looking at an even close to accurate survey (plus or minus about 4 percent) until we’re up to several hundred, probably over 500, submissions. To give you the sources of the statistics I know:
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.
OK, personal opinion (though hopefully not one without thought) on:
The Chessies are beating us all hollow in terms of submitting dogs. They’re up to 131 dogs [edited 2009: 421 dogs] tested. And of that number, 60% are either carriers or at risk. For a breed with, according to Berghaus, a LESS THAN ONE PERCENT clinical rate. Twelve percent [edited 2009: 14%] are genetically at risk.
They need to get up to several hundred submissions before making a statistical statement would be wise, but–just building air castles right now, so don’t take this with too much weight, but it’s VERY interesting–IF this proportion holds true and IF Berghaus’s retrospective was correct, 93% of at-risk dogs will not die from DM. [Edited 2009: This rate seems to be holding true] Ninety-three percent.
Or let’s look at Pems, with a 60% at-risk rate. This is a VERY OLD disease, so if 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 ninety-five percent of at-risk Pems will never get this disease.
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 has DM. This is why you don’t freak out and dump gene pools–or start entirely new ones–when you have a disease discovered. DM and IVDD are 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 set of diseases. 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. 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.
I’m also seeing a boatload of bad science, not from the researchers but from the statements about the disease incidence for DM. 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. And, holy hannah, we should not be removing dogs from the gene pool yet.
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.
Rant off.
Adding today: Nancy Willoughby brings up a very important point, that a gene like this could be one that influences a broad range of autoimmune
disorders. Which begs the question “What is an autoimmune disease?” These are not simple equations. Autoimmune diseases, whether this one (DM) or looking at the entire spectrum, are extremely complex and we really don’t know how much genetics influences them–or, I should say, we know it does but we have no idea to what extent. I am most familiar with autoimmune hypothyroidism, which (at least in the Dane study) was heavily influenced by vaccination because (it was conjectured) the dogs were becoming sensitized to the adjuvant of the vaccines in a way that encouraged them to attack their own thyroids.
So do you then say “Well, it was a genetic weakness, dogs shouldn’t do that,” or do you say “The dog was fine until it was vaccinated; it’s the vaccine’s fault.” (I’m not anti-vaccine, by the way.) Even if it DOES turn out to be a generalized measure of a certain predilection toward autoimmune disorders, we still would be looking at environment, injury, and assaults on the immune system as heavy, even primary, causes.
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 this gene is the correct one and that we have a handle on its action before we take the extremely risky step of narrowing our gene pool.
