Dog population (cont.)

The two comments illustrate EXACTLY what I am talking about. And I don’t mean to pick on their authors–what they said is perfectly accurate about the situation as it is now. And that’s the problem.

1. But then, you’re always going to have those people who would never be able to acquire a dog from a responsible breeder…what of them? Well, I guess in this perfect dog Utopia, they simply wouldn’t be able to GET a dog, right? And boy, wouldn’t that be ideal…

2. I don’t think you’re ever going to get rid of BYBs. Standards may be encouraged to rise a bit for most of them (as in, more that do breed-specific health testing) but since the majority of people are not anywhere NEAR as picky about ‘breed standards’ as the minority of quality show breeders, they are often happy with a dog that is less-than a quality example of a breed, as long as it ‘mostly’ looks like whatever breed it’s supposed to be. I see people with ‘Chihuahuas’ that are not only HUGE but their entire structure is only vaguely Chihuahua-like. Their owner doesn’t even notice — they’re perfectly happy with their wierdo-Chi, and to -them- it is exactly what they wanted. BYBs cater entirely to people like that, and they’re the majority.

I have to admit that someone like me, who only wants a pet dog yet is obsessed about their breed’s standard and history, and is VERY picky about a breeder’s lines looking ‘just so’ in accordance to the standard before I’d consider buying a dog from them, is simply not the norm among dog folks.

 

This is the problem. We tell people that they should only do things a certain way. But either we’re lying, because we don’t really mean it, or we’re completely resigned to the fact that they’re not going to do it.

Either result is wrong. We shouldn’t lie to people, and we shouldn’t give lip service and have no commitment. 

With some rather stunning exceptions, PEOPLE ARE NOT STUPID. They are not intractible, they are not out to kick puppies and make bad decisions. What they are is UNAWARE.

Think about it: How many purchases to you make that are over a thousand dollars in one place? Not many. A car, a house, maybe some of your appliances, your engagement ring… probably not more than one or two items a year. When you are getting ready to make that purchase, what do you do? You research. Some do it on the Web, but most just ask around. “Hey, nice fridge. How’s it working for you?” “Wow, that is one gorgeous rider mower. You get a good deal on that?” 

Now let’s look at a dog purchase. For whatever (good or bad) reason, you’ve decided you want to buy a purebred puppy rather than rescue one. Who are the people you are asking? Think about your family or your friends or your work colleagues – do you know even a single one with a beautifully bred dog? I doubt it. So you don’t have a high-quality Chihuahua to look at, and nobody’s extolling the virtues of their show-bred Spinone and telling you that it’s totally worth paying the extra little bit because you get these fifteen advantages.

And why don’t they have a beautifully bred dog? Because there’s a perception that they’re unnecesary. Why? Because no one has seen the difference between a well-bred dog and a poorly bred one. Why? Because there are so few well-bred dogs out there. Why? Because there’s an assumption that they’re super expensive and difficult to find. Why? Because there are only a few hundred thousand good breeders out there, they’re mostly invisible and not involved in their communities, and the average “career” of a show breeder is five years. Why? Well, I don’t know all the reasons for that, but the fact that show breeders seem to put ten times as much effort into telling everyone what a bad breeder Diana is because she doesn’t X, or because she does Y, than they do into either attracting or supporting new show breeders, may have a little to do with it. 

The fact that ANYBODY thinks that there are people who “would never be able to” get a dog from a good breeder shows how truly horrendous the situation is. Why on earth would you not be able to get a dog from a good breeder? The answer is you CAN, but the fact that the assumption exists should make us duck our heads in shame.

If anyone is reading this who is not a breeder, do you know that most of us are middle income, even decidedly on the low end of that? Did you know that we routinely give dogs to each other not just because we know that they’d be well taken care of by a friend but because we know our friend can’t afford our normal puppy price? Did you know that you can tell the handler side of a show site from the breeder side because the handlers all have RVs and big new vans and the breeders have a raggedy line of ten-year-old Astros? I promise you, if you can pay your bills every month you CAN get a dog from a good breeder, even if your house isn’t huge and fabulous (whatever it is, it’ll probably be better than ours!) or you don’t have thousands of dollars sitting in a bank account. You can start with a retired dog, you can start by fostering and then come to a breeder once you’re known in the rescue community, you can save up half the price and add $50 a month to the account while you wait for your breeder to breed and raise the litter. It’s completely doable and NOBODY is going to look at you and say “No designer purse, no dog for you!”

It’s obvious that we’ve created a gulf between the “normal” owner and the show breeder. And it will only get worse. If we are perceived as a source that is not appropriate for the normal/average/middle income owner, they will keep on going to the breeders who tack up a sign at the end of their driveway; they’ll keep going to the friend of a friend who has chi-weenie puppies. If we cannot clearly and convincingly show the difference between the well-bred and the poorly bred dog, they have no reason to come to us. If we look like an exclusive clique, they will go elsewhere. 

This is not a problem that can be solved by expecting irresponsible breeders to raise their standards. They don’t care and they never will. This is a problem that must be solved by removing the market for poorly bred dogs. This is a BUYER problem, not a seller problem. Everybody should think of poorly bred dogs as a waste of their money and a questionable ethical proposition. As it is today, they think of SHOW-bred dogs as a waste of their money and quite possibly unethical!

And, tragically, they don’t want to do what we do. They don’t want to become exhibitors and breeders themselves, but they do want to make a little money back on the cute little Chessie-Poo they just bought, and the cycle will be perpetuated.

There is no question that the “sports” associated with the animals and with the outdoors are declining. Shooting, hunting, archery, agriculture, fishing, they’re all falling off in membership. The response of most has been to work aggressively to recruit as many as they can – the rifleman associations get kids involved in target shooting, the bird-dog folk are encouraged to grab every niece and nephew and get them out in the field. Meanwhile, aside from the tireless and un-thanked trainers who keep steadily cranking out junior handlers, we show breeders put every ounce of effort we can muster up into discouraging people from breeding.

Why are we DOING this? Why have we bought the lie that infrequent breeding is better than frequent breeding, and the best kind of breeding is no breeding at all? Why do we immediately throw away the applications of any puppy person interested in eventually getting a litter from a bitch we breed? Why do we call EACH OTHER puppy mills when we know perfectly well that the person we’re hanging that placard on has happy dogs who are well cared for?

Think about the fundamental issue that was revealed by the very existence of Pedigree Dogs Exposed and its ripple-effect programs in the US and elsewhere. Dog owners and dog lovers were [US] and dog breeders were [THEM]. And a very creepy, snobby, odd “them,” too. The fact that people watching were so instantly willing to see dog breeders as hostile to the very notion of dogdom, that breeders were arrayed against those who love their dogs, highlights how dire this divide has become. It was literally like going to an Army base and going on for 90 minutes about how much Lieutenants hate the soldiers in their platoon. It should have been exactly that laughable, with everyone saying “What a ridiculous notion; of course that’s not true.” 

We SHOULD be able to offer ample evidence that there is a difference between well-bred purebreds and the “counterfeits” that are poorly bred dogs. We SHOULD give the impression that every puppy buyer is foolish not to buy from a good breeder because they’re getting ripped off if they go anywhere else. We SHOULD be the very first thought that any family has when they’ve decided to buy a purebred puppy. And we should be friendly, supportive, active recruiters of new exhibitors and breeders.

Is there a problem with our dog population?

We tell people to only buy from a reputable breeder or adopt from rescue. Let’s see what happens if they take our advice.

There are 72 million dogs in the US.

If we assume an average lifespan of 10 years per dog (which is pretty accurate according to Nathan Winograd), that means 

7.2 million dogs are replaced each year; there are 7.2 million “holes” that people are looking to fill with a dog.

AKC registrations have been falling precipitously; it registered something like 800,000 this last year.

UKC registers 250,000 per year.

Of the AKC-registered dogs in the US, a VERY generous number for those that are well-bred would be 25%, or about 200,000 dogs.

Let’s be very generous with the UKC and say that half are reputably bred. Another 125,000 dogs.

We’ll throw in another 10,000 dogs from the single-breed registries and hunting dog registries.

So the total number of what we’d call reputably bred puppies born each year is under 500,000.

To fill 7.2 million homes.

There are 4 million dogs in rescue in the US.

Let’s see what happens over a decade of people only buying from reputable breeders or adopting from rescue.

We’ll assume that the surrender rate remains the same (which it wouldn’t, but that lets me make these figures as conservative as possible).

Year 1: 7.2 million homes, filled by 500,000 puppies and 4 million dogs from rescue. Almost three million homes don’t get a dog.

Year 2: 10 million homes, filled by 500,000 puppies and 4 million dogs from rescue. 5.5 million don’t get a dog.

Year 3: 12.5 million homes, filled by 500,000 puppies and 4 million dogs from rescue. 8 million don’t get a dog.

Year 4: 15 million homes, filled by 500,000 puppies and 4 million dogs from rescue.  10.5 million don’t get a dog

Year 4: 18 million homes, filled by 500,000 puppies and 4 million from rescue. 13.5 million don’t get a dog.

Year 5: 20 million homes, filled by 500,000 puppies and 4 million from rescue. 15.5 million don’t get a dog.

Year 6: 23 million homes, filled by 500,000 puppies and 4 million from rescue. 18.5 million don’t get a dog. 

As of year 11, there are no more dogs surrendered to rescue (because all the non-reputably-bred dogs have died). At this point around 26 or 27 million homes who want a dog will be empty, with 7 million empty homes added per year, and the supply will be 500,000 puppies per year. 

Within a few years after that, there will be 5 million dogs in the US, replaced at the rate of 500,000 per year. That’s a decrease in ownership of 93%.

It’s obvious that there is indeed a population problem –  a critical shortage of dogs from good breeders.

Do you see my problem? 

We tell people that every puppy should be a reputably bred puppy, but we don’t make even seven percent of the number of puppies they’d like to own.

And that number is shrinking by the day, as registrations fall, number of dogs shown is reduced, and number of breeders shrink.

The breeders who do exist are told that a sign of a good breeder is having very few litters – people brag that they’ve only had five or six litters in 20 years in a breed. If a breeder has more than a couple litters a year, her peers whisper that she’s a “puppy mill.”

The vast majority of people have never met, touched, or interacted with a well-bred dog in their entire lives. 

But we keep saying that the fewer litters are born, the better. And we’re referring to our OWN dogs, the beautifully bred ones. 

Anyone have any solutions for me?

Dwarfed dogs: Ethical considerations for breeders

If I were giving this wrap-up as an oral presentation, I’d first ask for a show of hands from everybody who believed that deliberately producing puppies with a vastly increased probability of a painful genetic disorder that results in an early death is always wrong and the sign of a bad breeder. 

Then I’d ask if more hands would go up if that painful and often deadly genetic disorder could easily be prevented. 

Or maybe I’d ask it this way: Is it our responsibility to do absolutely everything we possibly can to reduce genetic disease?

If there were hands up from breeders involved in Corgi, Basset, Sussex, Dachshund, Skye, you fill in the rest of the list… those breeders have a lot of thinking to do.

When we breed dwarfed dogs, we are producing puppies that have a one hundred percent chance of getting spinal arthritis, and they’ll do so at an extremely premature age when compared to other breeds.

When we breed dwarfed dogs, we are producing puppies that have a risk of intensely painful disc disease and spinal cord injury that is, easily, an order of magnitude greater than the risk faced by non-dwarfed breeds. Dachshunds are up to 20% of all individuals experiencing catastrophic disc failure in the prime of their lives.

When we breed dwarfed dogs, we are selecting for traits that lead to a vastly higher rate of painful arthritis in the limbs, a vastly higher rate of painful growth plate injuries, a vastly higher rate of ligament damage that can render the dog unable to do his or her job. 

You think degenerative myelopathy is the bogey man? Disc disease is MUCH more common, incredibly painful, strikes in the prime of life, and is very likely to recur even if the owner can spend the four thousand dollars to get the sharp fragments of blown-out disc picked out of the dog’s rapidly swelling and dying spinal cord AND the dog is lucky enough to recover after surgery. 

The solution to ALL these issues is very simple, cheap, and easy to implement: Stop breeding dwarfed dogs. We can either end with this generation or we can begin to interbreed with Border Collies or something so we can push the breed up to normal leg length; either would be appropriate. Each breed club could decide which approach to take, with the goal of ending the production of defective dogs.

But we can’t possibly do that! I hear people saying. The price is too high! My dogs are perfectly healthy! The height has a vital function! These dogs were bred for a reason!

Well, then, PUT YOUR HANDS DOWN. Because you DON’T actually think that genetic health is the top priority. You DON’T think that deliberately producing at-risk dogs is wrong. 

If you breed dwarfed dogs — and I could have made this series about giant dogs, or brachycephalic dogs, or any number of the mutations we cultivate as part of breed type, but dwarfed dogs are very close to my heart right now and so, as usual, I’m trying to preach to myself — YOU MUST LOOK THIS IN THE FACE.

There are no scenarios under which the deliberate breeding of dwarfed dogs is without cost. It is a genetic malformation and it makes a whole bunch of the dog defective in function. 

What I strongly suspect that dwarfed-dog breeders ACTUALLY mean is that health is the top priority AFTER the maintenance or improvement of the breed itself. So do giant-breed breeders, and Boxer breeders (cancers) and Flatcoat breeders (even worse cancers) and so on. 

That approach is valid. But you need to admit to yourself that you are doing it, and you need to be consistent about implementing it. Don’t say that So and So who is breeding Snarfblat carriers is such a terrible person if you’re pumping out dogs who have a pretty decent chance of catastrophic spinal injury. Take out the log in your own eye before you look for the fleck in someone else’s, as a very wise book says. 

So how CAN we remain ethical breeders, responsible for each puppy’s entire life, under these circumstances? How can we fulfil our commitment to puppy owners?

I think that answer, too, is simple. We remain responsible for each puppy’s entire life. And we don’t throw puppy buyers under the bus.

Prospective owners MUST be told about the unique skeletal system that they are buying. They MUST walk away from your living room with enough information that they are making a decision with their eyes wide open. I think it’s entirely appropriate to also tell them that despite these limitations their dog will most likely live a very long, healthy, and happy life. But they should never think that nothing can happen. If they know the problems that are characteristic of dwarfism, they will be much more motivated to work to prevent the issues (a careful diet to prevent hip problems, supplementation for disc health, careful conditioning to exercise, avoiding the falls and concussive events that hurt growth plates, etc.) and much more prepared to respond to the issues when and if they occur. You want a puppy buyer who knows enough about disc disease that she suspects it quickly and gets the dog to the vet in time to prevent nerve death. You want a dog owner who knows enough about achondroplasia that they are not blindsided by diagnoses, so that they can become their dog’s best advocate when decisions about care, treatment, pain relief, euthanasia decisions, and eventual necropsy are demanded of them.

Carolyn asked if breeders were willing to chip all their dogs and take them back when something happens. To that I say OH MY HECK YES. In fact, that should be standard and expected of all breeders, now that chips are so much cheaper than they were even a few years ago. I used to have to ask the puppy buyers to do it and to add me as a secondary contact, back when chips were $75-$100 each, so having it come down to a tenth that much is absolutely wonderful. I am THRILLED that Kate is chipping all of Bronte’s puppies and will remain on the record as a contact forever. I look forward to being able to do the same.

And as for taking them back when catastrophe hits, I think that is one of the MOST IMPORTANT jobs a breeder can do. Owners often feel completely powerless to face the diagnosis, prognosis, and decision making that come with an end-of-life disease. I have told puppy owners that if they get to that point and just can’t handle it, the dog can come back to me. I’ll hold their hand and the dog’s paw and, either together or with the owner separated from the process if they desire, we’ll get through those last weeks or months. I think this is something that all breeders of all breeds should be willing to do, and when you’re producing puppies with specific weaknesses you should expect to do it at one point or another. Cradle to grave is the only right way to do it. 

I know I keep harping on this phrase, but OWN YOUR DECISIONS. Be willing to look very difficult facts in the face. Be willing to admit that you’re breeding dogs with some serious potential problems, and you’re doing so deliberately even though there are alternatives that will not cause the same problems. Be willing to lay out the honest facts in front of puppy buyers.

I don’t care if you do one health test or twelve. I don’t care if you produce one litter every three years or ten litters a year. Being an ethical breeder is about being willing to pick up a trembling old fat and incontinent dog that you sold twelve years ago, and keep him on your bed on a heating pad and feed him gruel for six weeks until you and the vet decide that it’s time for him to go to heaven. It’s about crying like a fool when he goes, and burying him next to his mother, and crying more when you think about her.  Being there for your dogs and your owners is the key.

Dwarfed dogs: What exactly is going on in there? Part 3: Other concerns

Because of the way in which achondroplasia/chondrodystrophy affects cartilage and other connective tissue throughout the dog, in addition to the issues that the dog WILL experience (vastly decreased growth, twisted bone, and spinal disc calcification), there are some problems that are a lot more common in dwarfed dogs.

Growth plate injuries (angular limb deformities): When the growth plate on one of the leg bones is injured (the cells are crushed by a blow or a very bad twist), even if there’s no fracture of the bone the growth plate can just shut down. The bone will end its growth cycle abruptly. However, the other leg bones will continue to grow. The most common place that this happens is in the radius/ulna (the lower bones of the front legs). The ulna stops growing while the radius continues, or the radius stops growing but the ulna continues. The bone that stopped growing keeps the growing one from pushing the leg down evenly. When the other bone continues to grow it buckles and bends outward, because the injured bone binds it to a certain length. This causes a major bow and twist to the entire leg.

Angular limb deformities (which we call “knuckling over” though it’s really not that) are much more common in dwarfed breeds than in other breeds. I’ve not seen a study that describes exactly why, but common sense would indicate that it’s a combination of thin, fragile growth plates that are already dysfunctional and the fact that the dwarfed breeds tend to be solid dogs who land heavily on front legs and are therefore are more likely to crush the growth plate cells. I can’t think of a single dwarfed dog that is not heavy-bodied; the early breeders didn’t shorten the legs of whippets. They shortened the legs of heavy hounds, shepherd-type herding dogs, the big terriers, etc., because the whole point of the short legs was to make dogs who could do the same sorts of jobs as the big dogs, but at a much slower speed or in a smaller area, or to accomodate handlers on foot rather than on horses.

So even as puppies, dwarfed dogs are heavy and sturdy of body. All it takes is for a six-week-old puppy to get her foot caught in the bars of the ex-pen and twist really hard getting it out, or one bad jump of a three-month-old off the porch steps (when the same jump a thousand times has done no damage), and the growth plate will give up the ghost. 

Unfortunately, angular limb deformities are not just unsightly; they’re quite painful for most dogs.

Joint issues: Achondroplasia in dogs is poorly understood. So there’s not a lot out there about exactly how each joint is affected by the dwarfism. But we do know certain things. Where bones come together, dwarfed dogs have shorter, wider, shallower joints than longer-legged dogs do. A perfect example of this is in the hips. The dwarfed hip has almost no neck on the femoral head. The femoral head is flattened and tends to form a “cap” rather than a smooth egg shape. And the acetabulum (the socket, which is part of the pelvis), in order to remain functioal with the femoral head, is also wider, shallower, and flattened. If I used the above three sentences to describe a longer-legged dog, I’m practically giving you the textbook definition of hip dysplasia. In a dwarfed dog, the hips are “bad.” The shoulder joint and the elbow joints are “bad.” Of course, that’s if you define “good” as “looks like a sighthound,” which is not what we have, but there’s no question that if a dwarfed hip was submitted as a longer-legged breed the diagnosis would be poor. If a dwarfed elbow was submitted for examination under a longer-legged breed’s name, that elbow would be seen as deformed. 

Ligament laxity: There’s definitely SOMETHING going on with achondroplastic ligaments. Humans with achondroplasia are known to have very lax ligaments compared to normal. Dog achondroplasia is NOT the human disorder, but I think the ligament issues may be analogous. You can see this most clearly in the front legs (again) in the wrists. Dog wrists are like marbles packed in a strong rubber tube–there are a bunch of round bones that don’t sit in balls and sockets but are held next to each other by strong ligaments. In most dogs, the marbles stay in a nice compact formation and can flex slightly and return to their former shape. In achondroplastic dogs, the strong rubber tube, it seems, is not so strong. It holds the marbles straight when the leg is just hanging there, but lets the marbles slump over to the side when weight is put on them. The “hush puppy” Basset hound front legs, where the feet end up going completely east-west when the dog stands up, represent the worst of this. 

Our boy Bramble (who is half dachshund and half achondroplastic Jack Russell Terrier) has one leg that is a perfect example of ligament failure. If you pick him up by the chest so his front legs dangle, the sections from the wrists to the toes are straight up and down. The toes point to the floor without much deviation. Put him down, and one wrist buckles rather dramatically. His wrist deviates inward toward his chest while his toes deviate outward and end up twisted to the outside of his body. The problem is not with his skeleton–the bones hang together normally. The problem is with his ligaments, which don’t keep the bones together when weight is put on the limb.

Watch Cardigans when they trot toward you. When they pick up the leg (taking weight off the wrist), the “crook” (which is the way we describe the wrist deviation) almost disappears. As the dog puts the leg down, the wrist deviation becomes much more apparent. 

Arthritis in the small bones: Lack of proper cartilage = the cartilage deteriorates and bone begins to rub against bone. The bones respond by growing spurs or bumpy bits. Bony changes in a joint are called arthritis; arthritis is painful because, well, bone isn’t supposed to grind against bone. Achondroplastic dogs get spinal arthritis very early, as we saw in the post about vertebral disc disease. They also tend to get arthritis in the bones of their wrists and feet. Several of my friends who are or were groomers absolutely refuse to accept Basset Hounds because in their experience Bassets ALWAYS bite when their nails are done. Picking up and squeezing the foot to get access to the nails is so painful to the dog that he sees no choice but to bite. I think their universally bad experiences are due to the fact that there are so many poorly bred Bassets with really terrible fronts, but the fact that dwarfed dogs get more arthritis is inescapable. 

Next up: What does all this mean to us as breeders?

Dwarfed dogs: What exactly is going on in there? Part 2: Not the legs

Yesterday I wrote about how the growth plates in Cardigan legs are dysfunctional and don’t grow a normal length of bone. Today I want to look at the second reason we care about cartilage as breeders:

Because the bad cartilage isn’t just in the legs.

Dogs with chondrodystrophy or achondroplasia have bad cartilage EVERYWHERE. It has abnormal cell distribution and formation all over the place, from the front of the dog to the back. 

Dogs function perfectly well with bizarre cartilage, as long as no growth plates are actually injured and the cartilage doesn’t fail and cause arthritis, just about everywhere. The major exception is in one of the other places where the body has very, very important connective tissue: the spine.

As almost everyone knows, between the individual bones of the dog’s spine there are “discs” of squishy stuff. What does that have to do with cartilage? That the squishy stuff, which is basically like those (awesome!) 80’s bubble gum flavors with a soft outside and liquid inside, is a bit like very young baby cartilage. It’s not actually cartilage yet; it’s a fibrous sack with liquid in the center. That nucleus of liquid is what makes the spine such an amazing shock absorber; the bones can compress without touching each other and can be stretched apart without injury.

As dogs age, and this means ALL dogs, not just ours, that young baby cartilage (fibers and liquid) begins to age and dry out and turn into real cartilage. Most dogs are experiencing some lack of flexibility in the discs by the time they’re ten or so. Real cartilage is not as soft and bouncy as the disc used to be, so the spine becomes less able to flex. The now-cartilagenous discs begin to degenerate as the dog gets older and older, and so the bones (the individual vertebrae) grow little bony spines to try to stabilize the disc material. This is spinal arthritis or spondylosis.

Spinal arthritis is VERY normal in elderly dogs of all breeds. In most of them it just makes them say “Oh my achin’ back” in the same way that we do (or will eventually) as we age.

In an unlucky few the bony spines grow into the spinal cord or begin to squeeze some of the big trunk nerves that come off the spinal cord. This can lead to progressive weakening, instability, and paralysis (which, by the way, can mimic DM and is one of the many reasons you NEVER definitively diagnose DM without a necropsy).

In a few breeds, there is a tendency toward a severe form of spondylosis that occurs early in life and in the neck vertebrae. This causes progressive weakness and a “wobbly” gait as the spinal nerves are squished, so owners and breeders call it Wobblers. Wobblers is unfortunately more common than any of us would like to see it in Dobermans and Danes, and as of yet nobody knows what makes it happen. Bony growths are usually associated with injury, so we’ve all wondered whether these were dogs who had their necks traumatized at some point (Dobies and Danes have very long necks for their bodies), or if there is some familial relationship, but you don’t see it reliably passed along and predicting it is impossible.

Thankfully, most breeds don’t see any disc problems or bony changes in the vertebrae until they are advanced in age.

But… and you know there has to be a but… there is one class of breeds that has major disc damage at a very early age. And yes, you guessed it. We’re part of it.

Remember how the growth plates of the long leg bones in achondroplastic dogs age much more quickly than they do in longer-legged dogs? The same thing happens in the discs between the spinal bones.

In achondroplastic dogs, the liquid center of the discs doesn’t stay liquid. By the time the dog is six months old (yes, SIX MONTHS) the liquid center is being replaced by cartilage. This isn’t quite the same thing as what happens with longer-legged dogs; the liquid doesn’t gradually dry out like happens as those dogs age. In dwarfed dogs the liquid is actively replaced by cartilage. By twelve months the replacement is dramatic. By the time the dog is three years old, each disc has only a fraction of the liquid that should be in its center, and the center has actually begun to calcify (become like bone). The fibrous outer layer of the disc now has to absorb all the strain on each vertebra, and it is beginning to degenerate too. 

Eventually, in a lot of dogs, the fibrous outer layer of the disc gives way, letting the inner material get out. The fibers are thinnest right below the spinal cord, so when the outer layer ruptures it usually does it there. This allows the inner material (which is by this point bony cartilage) to squirt out. It either squirts out upward, squishing the big bundle of nerves that is the spinal cord, or it squirts out up and to the side, squishing one or more of the big nerves that come down off the spine.

That’s why you can have a dog go down with a complete rear-end paralysis, or it can seem to go down worse on one side or the other. 

The final strike against achondroplastic discs is that when the discs rupture, it’s usually catastrophic. In other breeds when elderly dogs get disc problems it’s often that the fibrous outer layer tears slightly, allowing only a small bulge of inner disc into the spine. In dwarfed dogs the fibrous layer fails completely, allowing a great deal of actual disc material to the nerve bundles. 

What happens next (as though enough hasn’t already happened!) is that the disc material that’s exploded out of the ruined fibrous layer can directly harm or cut the nerves of the spine. If it doesn’t harm the nerves, it often cuts off the blood and oxygen supply to the nerves by blocking or tearing blood vessels. Even if it avoids those two disasters, the disc rupture is interpreted by the body as a major wound and the body rushes all sorts of vasoconstrictors (signals that tell blood vessels to stop letting blood through) to the area, causing damage to the nerves’ blood supply.  And even of NONE of those things happen, within hours the body will try to respond to the damage by causng a huge amount of swelling in the area. Again, spinal cord death all too often results. 

If the dog has a very small rip in the disc with only a bulge of inner tissue, it can recover with rest and meds. Unfortunately, that kind of tear is not very common in dwarfed breeds. If there is a catastrophically ruptured disc but there’s no swelling around the disc and the spinal cord is normal, there’s a decent chance that surgery (to the tune of about four grand) can restore function. The surgeon carefully removes the disc material and the nerves can recover. However, a different disc will often herniate later, especially if multiple discs are showing calcification. If the ruptured disc has already caused swelling of the spinal cord, even with surgery the dog has the odds against him or her ever recovering the ability to walk.

Disc rupture occurs in dwarfed breeds most often in their middle years, from age 3 to age 8 or so. It is intensely and horribly painful, at least until the spinal cord dies. It’s a true emergency, and in our breed non-surgical methods are rarely effective.

Dwarfed dogs: What exactly is going on in there?

Watching Bronte’s puppies has been nothing but pure joy for me. OK, well, pure joy plus obsessively bugging Kate for weight progress (what can I say; I’m a former Dane breeder who was trained by a NICU nurse–weights are what I wake up at night thinking about). But most of it has been just fabulous.

One of the things that I found EXTREMELY interesting is that the puppies were born with (proportionally) long legs, as long as the legs I saw on any Dane born in my kitchen. But, very quickly, as bodies filled out and lenghthened, as weights soared (sigh of relief on my part) the legs got bigger and thicker but, length-wise, stayed pretty much where they were when they were born. It’s very easy for me to see that by the time the puppies are eight weeks old, they’ll be nearly twice as long as they are high whereas my Danes were about as tall as they were long. 

So what is going on here? Why do Cardigans, along with so many other breeds, end up with such short legs?

The answer lies in a word we throw around a lot but often don’t understand–achondroplasia, or chondrodystrophy. Those are the words that are used to describe what happens in dwarfed dogs, but they’re rather distressingly poorly understood by most. 

Both words–achondroplasia and chondrodystrophy–basically mean “crappy cartilage” or “failure of cartilage.” In humans with dwarfism, achondroplasia is a much more exact word that labels a particular type of dwarfism associated with a particular gene. In dogs, the word is a descriptor rather than a diagnosis–we have no idea what gene or genes make dogs short-legged, and aside from the fact that we’re sure they have deformed cartilage with a bunch of bone problems there’s not a lot of information out there. 

So why is our unique conformation associated with cartilage? For two reasons. The first is that cartilage is where bone growth occurs.

If you want a complex description of what happens, look here. I’m going to try to make it a little easier to understand. 

Look at your arm from your shoulder to your elbow. That’s the humerus bone. It’s the same bone as goes from the center of your Cardi’s body (the “shoulder” joint actually points toward her nose) to her elbow. If you feel your own humerus (if you’re like me you have a healthy fat covering over the bone, but try) it’s pretty long and skinny and straight, with swellings at the shoulder end and the elbow end. If you felt a Lab or Great Dane humerus, it would feel the same way–long and thin, with swellings at both ends. If you feel the same bone in your Cardigan, hers will be mostly lumpy end and other lumpy end, with a tiny section in the middle. Your Cardi’s humerus will also be MUCH shorter than your Lab’s–the long-legged dogs have elbows roughly at the level of the bottom of their chests, while Cardigans’ humerus ends several inches above the bottom of the chest.

The difference between these two lies in how the growth plate works. 

In a normal dog, when it is a puppy, those lumpy ends of the bone have a layer of slippery cartilage that allows the joint to move freely, and then right above that slippery layer is a VERY active layer called the growth plate.

The growth plate has a bunch of round cells in it. As those cells get a little older, they begin dividing rapidly, almost frantically. The result is a whole ton of round cells. Meanwhile, behind this whole ton of round cells, the new baby cells are being born. Then that whole ton of cells move from being round to being veerrrrry long and stretched-out, with lots of little arms that reach out upward and downward. Then the cells die, but they leave their skeletons (veeerrry long and stretched) behind. Then more cells come and build calcium all around those stretched-out arms, making the skeleton of the former cell extremely strong, but still lace-like, with lots of tiny holes. Eventually little blood vessels come and grow all through the holes and laces, and then you have mature bone.

So, basically, the way bone grows is that it pushes from either end, building the long skinny bit in the middle. Eventually hormonal signals that say “I have a grown-up pee-pee, and I like girls!” or “I have a strange feeling that I might like boys” come along, and those hormones gradually shut down the growth plates and the growth of those bones is finished. 

What’s different in dwarfed breeds is that the growth plate is a big pile of FAIL. Instead of having a big thick layer of a ton of those round cells dividing like crazy, it has a thin layer of many fewer round cells. Instead of a steady march of cells from round to long and thin, some cells fail entirely and some go really tall. The lengthening cells turn to mature bone LONG before they are supposed to.

The result is that the bone does not form a long thin straight column; it forms a thick, twisted, short column. And then it shuts down entirely. 

In the next post, we’ll look at what ELSE can go wrong with our cartilage failure, and why this is important to us as breeders.

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 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 conection 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.

Choosing and using a grain-free kibble

Because of living in the Tiny Apartment of Happiness (we love it, but 1000 sq ft with six people and two dogs is tight), for the first time in ten years we’re not feeding a raw diet to our dogs. I tried, because I believe in it so much, but the kitchen is very small (the floor space is maybe 6×4) and every other square inch of the place (aside from the bathrooms) is carpeted. Neither dog particularly likes Bravo, because they like the experience of chewing bone. They were dragging the Bravo around or trying to bury it in the carpet, giving me heart attacks and making me spend hours scrubbing up after them.

So for the months we’re here, we’ll be using a grain-free kibble. As a result, I’ve spent more hours than I’d care to count researching ingredients and the different brands that are available in our area. The choice I made may not be the choice you’ll make, but since there are so many misconceptions about grain-free kibbles I thought it would be worthwhile to look at them in depth.

Misconceptions about grain-free foods:

1) They are made of meat. Sorry; no. As far as I am aware, any conventionally made kibble that goes through a normal extrusion/cooking process has to be bound together as a dough.

Conventional kibble uses a mixture of different grain flours, meeting a nutritional profile as cheaply as they possibly can. They usually rely on either inexpensive feed grains (ground corn–which, by the way, includes the dried cob; it’s not just the corn kernels) or the bits and portions left after another industry uses the whole grain. That’s where brewer’s rice, feeding oatmeal, and anything called “fines” or “gluten” or “meal” come from.

Grain-free kibbles need to make a dough too, so instead of using grains they’ll use vegetable matter that when ground is like flour, and can hold things together the way flour does.

The most common thing used is potato. When potato is dried and powdered, you can mix it with other stuff and cook it and the result will make a decent kibble. Other companies use pea flour (dried field peas–the kind that you make split pea soup with, not sweet peas–makes a flour when ground). A few use tapioca, which is powdered manioc root.

Whatever they use, the result is a kibble that is NOT all meat. You’re still feeding kibble; it’s not the same thing as a raw diet. It’s not even a substitute for a raw diet–I would say that in many cases it’s the best kind of kibble you can feed, but it’s still a kibble.

2) They’re all basically the same.

WOW is this not true. They vary wildly in terms of ingredients, protein, fat, vegetable sources, etc. It’s a brand-new industry and there’s virtually no standardization yet. You need to read and compare ingredients carefully, and stay on top of new introductions. One good place to begin is at the Dog Food Project, but even as good as they are they don’t have an encyclopedic list. So expect to do quite a bit of research and be very cautious about reading ingredients and analysis data.

3) The more meat is in the ingredients, the more is in the kibble.

I spent a ridiculous amount of time looking at ingredient lists before I came to this conclusion, and I’m still not a million percent sure, but I think that the old rule of “look at the first four ingredients” is wrong when it comes to grain-free kibbles.

The reason I think the ingredient list can be misleading is that in several of the kibbles it doesn’t at ALL match with what the protein percentage would be if the kibble really did have that much meat.

Dried cooked meat is between 60 and 80 percent protein. So any time you have a protein percentage below that, you know other things are in the mix. Bone is one of them, which is fine because we want some bone, but bone doesn’t change it all that much. What really brings the protein percentage down is vegetable matter.

Take Taste of the Wild High Prairie as an example. The entire ingredient list (removing the vitamins) is bison, venison, lamb meal, chicken meal, egg product, sweet potatoes, peas, potatoes, canola oil, roasted bison, roasted venison, natural flavor, tomato pomace, ocean fish meal.

The protein percentage of this kibble is 32%. That’s HALF what you’d expect if it was pure meat, and about as much as lots of puppy kibbles. One that has an identical protein percent is one of the Royal Canin puppy foods, the ingredients of which are chicken meal, brown rice, chicken fat, rice, corn gluten meal, dried beet pulp, chicken, natural chicken flavor, powdered cellulose, dried egg powder.

Look at these two–reading the ingredients, there’s no question which one you’d point to as having more meat. So why do the protein percentages not bear out a difference?

My guess – and I am not sure exactly how to confirm or deny this – is that potato is so light that you can have a huge amount of it and it still stays in a low position in the ingredient list (which is in the order of decreasing weight). The company also splits the potato ingredients by using sweet potatoes and “potatoes” (white potatoes). So between the sweet potatoes (very light) the pea (I would guess a dried pea flour) and the potato, there’s a lot of vegetable matter in this kibble. When you consider that the first meat ingredients are listed in their whole (uncooked, undried) forms, which means they were weighed before being cooked and dried, you can see how the meat ingredients got bumped to the top of the list and the vegetables to the end.

This kind of manipulation of ingredient lists is VERY VERY common, especially with foods that are marketed based on your perception of them being mostly meat, and that’s why you have to question whether the analysis of the food reflects the picture that is implied by the ingredient list.

Now look at the ingredient list of Orijen’s Adult grain-free food: Deboned chicken, chicken meal, turkey meal, russet potato, lake whitefish, chicken fat, sweet potato, whole eggs, turkey, salmon meal, salmon and anchovy oils, salmon.

At first glance, you would prefer the Taste of the Wild. It has “sexy” ingredients like venison and bison; it just seems more exclusive. And it has more meat ingredients before you get to the potato.

But the analysis of Orijen’s food tells a different story. It’s 42%, much higher than Taste of the Wild’s. And the company states that the kibble is 70% meat products.

To make a long story short, look closely at the analysis to tell you how much meat is actually in a grain-free kibble. Higher protein typically means more meat.

4) You should follow the AAFCO recommended ages and feeding amounts on the bag.

In my opinion, grain-free kibbles are much easier to wreck a dog with than conventional kibbles.

Conventional kibbles are crap, sure, but they will at least minimally nourish your dog and there’s a lot of fudge factor in how much or how little you can feed.

Grain-free kibbles, at least the good ones, are more like racing fuel. You have to very carefully control how much you feed, because they’re so high-calorie that dogs can get overweight VERY quickly. And in my opinion, even if the AAFCO says that the food is for all life stages, I would never feed a puppy a grain-free kibble.

When you feed a raw diet, you’re actually feeding only a small amount of food plus a ton of moisture. But because the portion size is big, the dog feels satisfied, tired, and full. That makes it a great diet to feed to puppies–they get relatively few calories for a big payoff of chewing and a full stomach.

Grain-free foods, on the other hand, have all that moisture taken away and are very nutritionally dense. You’ll feed a fraction of what you’re used to feeding in conventional kibble. That can be really tough for a dog to adjust to–they’re used to walking away from the food bowl feeling full. So many owners will feed too much, because the dog acts starving all the time. And a starving puppy is that much harder to resist.

An adult that eats too much will just get fat–which can be difficult to reverse but as long as you get on top of it quickly no long-term damage is done.

A puppy that gets too many calories doesn’t get fat–it grows too quickly. It will grow its bones faster than its muscles and tendons can match, and fast growth/heavy calorie load is STRONGLY associated with joint disorders later in life. Yes, this includes hip dysplasia–puppies kept lean and slow-growing become adults with an EIGHTY PERCENT reduction in hip dysplasia when compared to adults who were puppies that ate as much as they wanted.

I would also say that for the average adult dog, the recommended feeding amounts for the grain-free foods are too high. Right now we’re going through a bag of Solid Gold Barking at the Moon, which recommends 1.5 to 1.75 cups a day for a dog Clue’s size. She is actually getting HALF A CUP a day. The amount she gets looks comically small. But she maintains her weight on that amount; she’s even put on some bulk. We’re very close to being able to lift exercise restrictions for her, so at some point she’ll be able to run a couple miles a day and I’ll have to bump her food up a little, but there is no way she’s going to ever get 1.75 cups.

A friend of mine who was feeding her elderly GSD (intact dog) a grain-free kibble found that she had to feed no more than three-quarters of a cup a day. If she went up from there he gained too much weight.

So I would strongly advise, especially in a breed like the Cardigan where most of them have low metabolic needs and gain weight quickly, that you start off with a very small amount and only increase it if the dog starts getting too thin. And, I might add, get to know what normal weight is–way too many corgis of both types are fat, even though their owners or breeders think they’re normal because corgis tend to stay rather tubular. They go from a thin tube to a thick tube and owners think it’s OK because they don’t have a belly or a fat rear like a Lab gets. Not so.

So what did we end up using? I actually plan to rotate a couple of brands. Right now we’re about half-way through a bag of Solid Gold Barking at the Moon. It has a high protein percentage, indicating that it’s got a lot of meat, but at least some of its protein is coming from potato. I like Solid Gold as a brand because my Danes tended to do very well on it (when they went into homes that didn’t feed raw), and to be honest I had a choice between this and a brand I really didn’t like (you may guess from my picking on it above that it was Taste of the Wild, which is a Diamond food and I think is rather deceptive in its descriptions).

I didn’t realize that a 15-lb bag was going to last us eight weeks, even feeding it to two dogs. It may even go longer. If I had, I would have gotten a 4-lb bag instead!

I think it’s doing a decent job with the dogs–it’s not raw, and I immediately notice the difference in skin and coat and muscle, but they look better than conventional-kibble-fed dogs–but I’m not thrilled about one of the protein sources being potato.

So when we’re coming to the end of the bag (or, if I start to see something I don’t like in the dogs, even sooner) we’re probably going to switch to Orijen, since I found a source for it that is not terribly far away. Orijen is by far the most forthcoming about actual proportions and ingredients, which I find refreshing and want to support.

If we want to further switch, I’ve been wanting to try the fresh meat mixes, like Volhard’s NDF or Sojos grain-free. Those are an entirely different method, and I would like to have some personal experience with them so I know whether to recommend them to friends and puppy buyers.

Until then, you can listen closely and hear the rustle of big foil-plastic bags in my kitchen for the first time in a decade. I wince a little bit each time, but so far the dogs are OK and that’s all that matters.

The dog word I HATE: Aggression

Yeah, I get a little… um, aggressive about “aggression.” I think this word has done more to hurt our understanding of dog behavior than just about any other.

The word is perfectly normal, and accurate. It describes any action that a dog does that intentionally hurts.

The huge problem is that this word, which should be a descriptor without any values or bias attached, hasn’t stayed a scientific term.

Katz’s The New Work of Dogs is an absolute MUST READ to understand this background, but to summarize, the average dog owner no longer has any experience in watching dogs behaving normally, furthermore doesn’t WANT the dog to behave normally, and so everyone is hiring people to help them understand dog behavior, and those people are reading behavioral studies and scientific descriptions of how dogs interact.

Researching is GOOD. Reading is GOOD. The whole “machine” that unfortunately begins going at this point is sad because so few people “get” dogs anymore, and even sadder because the typical owner, family, municipality, and even many trainers don’t have any desire to have the dog behave in a normal doggy way. They try to use the research to get dogs to behave like Disney characters or like children or like punching bags, instead of trying to use what we know about dogs to make the dogs happy and meet their needs.

The behaviorists and scientists have introduced certain words that they are used to using in their research, and that they find helpful in labeling behaviors. One of those is “aggression.” It’s a useful word. Unfortunately, this word has become VERY misused and it’s gotten to the point that I now cringe every time I hear it.

Because this word has done two terrible things: It has demonized or criminalized NORMAL dog behavior, and it has become a way to switch the blame for undesired behaviors from the human or the circumstance to the dog.

Dog  behavior follows along lines that are MUCH more rational and measured than human behavior. The “worst” dog shows more restraint in his or actions than most humans could ever dream of. As I addressed in an earlier post, when a dog is in a situation that he finds unpleasant, or feels pressure or stress (and here I mean those words in the behaviorist way, as a change in the environment that requires a response–pressure or stress can be positive, even welcomed, like the introduction of a bitch in heat or the return of a beloved human; it’s not a negative word), or feels that the society he lives in has become disorganized, he has a huge repertoire of behaviors that he uses to diffuse or change or influence the situation. Typically his behavior of last resort is using his mouth.

Again, as I said earlier, the mouth is the dog’s megaphone. When a dog has run through every other way she knows of righting what she feels to be wrong, and nobody is listening to her, she will use her mouth.

This is very analogous to walking into a room and seeing your teenage son or daughter in a chair watching TV when you are carrying a heavy load of their laundry. You immediately recognize that Something Is Not Right (hey, if you’re home, and idle, why didn’t you get your laundry yourself?). You will typically run through the following series of behaviors, escalating from one step to the next when the earlier step gets no response:

1) Pause (allowing a cessation of movement to get the attention of your kid–humans always look at change, so either moving when you were still or stopping when you were moving is a potent behavioral cue)

2) Perhaps deliberately make a “random” noise, like sighing or “accidentally” knocking the laundry basket against a chair

3) Speaking, usually their name

4) Speaking louder, emphasizing their name

5) Approaching closely, speaking even more loudly

6) Putting your hand on their shoulder or head

7) Slightly shaking their body with your hand

All of these are normal behaviors; none of them indicate that you have criminal intent or in fact anything but your child’s best interests in mind. However, somewhere between “4″ and “6″ you moved into aggressive behavior. You spoke loudly enough to create an unpleasant sensation in your child’s experience, with the goal of making him or her want to get the unpleasant sensation to stop (by responding to you or by showing that they are paying attention).

Any time you behave in a way that is intended to create an unpleasant sensation in another creature, it’s behavioral “aggression.”

Imagine you’re the mom or dad who has just done this–are you an “aggressive” person? Does your behavior need to be modified? Is what you did an indication that you are likely to go shoot someone?

No, of course not.

But behavior EXACTLY that rational, exactly that measured, exactly that common-sense, exactly that restrained, causes dogs to be put to death every single day in this country, and causes countless more to be labeled bad, dangerous, or undesirable.

Now imagine that you are the parent of this same teenage son or daughter and this kind of situation repeats itself ten or twelve times a day (my oldest daughter just turned twelve; ask me how experienced I am at coming into a room and finding her physically present and mentally absent–and I know that in three or four years it’s going to be ten times worse). Before long, you will skip everything up to step 5. You know that steps one through four haven’t gotten her attention the last fifty times you tried them, so you now skip them altogether. Every time you come into a room and need to get her attention, you speak her name loudly or walk over and touch her.

Again, this is completely normal and expected. We’d even criticize a parent who didn’t collapse the steps. “That kid is totally blowing her off, and all she ever whispers is ‘Oh, honey, could you please…?’ He’s going to grow up into a holy terror if she doesn’t start to expect better behavior of him!”

Dogs are exactly the same. If the early steps don’t work, never work, they will begin by speaking very firmly. And for a dog this means using their mouth. They’ve been very effectively taught, usually by a human who doesn’t see or respond to any of the early steps that the dog had tried a hundred times before escalating to using their mouths, that talking softly doesn’t work with these dummies. You have to yell or nobody hears you. So they use a bite immediately.

See what I’m NOT saying about these dogs? I’m not saying they’re “aggressive.” I’m not hanging other adjectives off, like “dominance aggression” or “fear aggression” or “leash aggression.” That’s not because those phenomena don’t exist. It’s because they have been hideously misused to make the behavior the dog’s fault. The dog IS aggressive; that dog IS dominant; her dog IS fear-aggressive. These become labels that we apply to dogs as though the behaviors they display are uncalled for, irrational, evil, bad.

And once we label them, the dog just IS–”I can’t fix this; he is fear-aggressive.” Like “he’s brown.” Or “he’s schizophrenic.”

We tell ourselves–and trainers tell us, and vets tell us–hundreds of lies about aggression. We use language like “He just snapped” or “He could turn at any time” or “You did what you could; he was too aggressive for you.”

All of them demonize any behavior involving a dog’s mouth, and all of them blame the dog and not the human.

If I could, I would wipe out this word from every trainer’s mouth, every owner’s brain. No more! From now on, you have to describe the dog’s behavior using REAL emotions, REAL words.

Instead of “She’s fear-aggressive” I want to hear “She’s afraid.”

AHA! See what happened there? You stopped looking at that poor terrified dog and blaming her for her frantic and panicked behavior. She’s AFRAID, you moron! Stop scaring her!

Instead of “He’s leash-aggressive” I want to hear “He believes that when on leash he’s supposed to skip the greeting steps and go right to mouth.”

OK, that’s a genuine description of something the dog has been taught by humans. Now un-teach it. IMMEDIATELY read everything you can get your hands on about increasing drive in working dogs and then smack yourself on the forehead when you realize that you’ve been extremely effectively training him to use his mouth on other dogs.

Instead of “she’s food-aggressive,” say “She thinks she must guard her food or it will be taken away.”

Well, who taught her that? Who gave her that message? It didn’t fall from the sky, people! Somebody screwed up, and now they have to fix THEIR OWN behavior; she’s just doing she thinks she has no choice but to do.

Instead of “He’s dominance-aggressive”–which is the worst of all–you need to say one of a hundred things: “She believes that her status is at risk because of his behavior.” “He does not like it when other dogs behave chaotically” (see the huge reversal on that one? Suddenly he’s the one making the right choice and the other dogs are at fault–which is the case a HUGE percentage of the time). “She doesn’t know proper calming behaviors, so she’s unable to defuse status-related conflicts.” (And who didn’t socialize her enough, so she doesn’t know how to talk “dog” well enough? Yeah, you there. Not her.)

We need to reverse the two huge lies that labeling have told us.

1) WE MUST ACCEPT BLAME ON THIS. Ninety-nine-point-eight percent of bad dog behavior is HUMAN fault. If your dog is behaving in a way that is lowering his quality of life, you need to look in the mirror long and hard. VERY VERY few dogs are genuinely mentally ill. Almost all of them have been TAUGHT, yes, by YOU, to do what they are doing.

If you want proof of this, talk to any breeder who has been around long enough to get “bad” dogs returned to her. Ask her how the owners described the dog and what she actually got back. Every single breeder has these stories. On the phone, as described, the dog is out of control, aggressive; she’s usually done damage to several animals and often bitten the owner as well. They have been told to euthanize the dog, but as per your contract they are returning her.

You gird your loins and get ready for a dog who is completely nuts. You set up the crates, divide the fenced yard, work out a schedule for who can be in or out and when. You get the behaviorist on the phone, you set up the vet. You get mentally prepared for euthanasia; you don’t sleep the night before.

In comes the dog–or you go get her, or you meet half-way. However it happens, finally the dog bounds in to your house, and usually does something like try to jump up on your dining room table. You look her in the eye and say, very calmly, with a big growly edge in your voice, “GET. OFF. RIGHT. NOW.”

And — I have had this happen twice, and I pray with every litter that it won’t happen a third time, but it’s just incredibly striking — something behind the dog’s eyes shifts. Something in their brain goes from panicchaosdisorderfear (for the “soft” ones) or gottacontroleveryoneortheworldwillend (for the harder ones) to Oh thank God someone else is in charge; I can relax.

Sometimes, what the previous owner has taught the dog is so well learned that she must be placed very, very carefully–though I still have NEVER had a dog, either my returns or my rescues, behave “as advertised.” Many times, it seems that the knots unwind almost instantly. This dog who was a “nightmare” is a sweet, goofy, relaxed and mellow dog who is a joy in your home and becomes a joy in their next home.

(As an aside, the person who returned the dog, even if they cried when they handed the dog over and talked about the mistakes they had made, always changes the story within a week or two. It always becomes “I did everything right and I ended up with nightmare aggression.” “That dog had everything, and he turned on me.” “There was no reason for it; it’s bad breeding/bad breeder.” Breeders are often tempted to respond by e-mailing a picture of the dog with its tongue lolling out as it blissfully rolls around with her other dogs in the back yard, or running through a field with its next owner, but we all shut up and nod and accept the blame. Because the most important thing is to always get the dog back. We’re willing to accept any kind of criticism or hear any crap if it means that the dog ends up safe and happy.)

Why do dogs do this huge turnaround, why so suddenly? Why can they so often be placed again and thrive? BECAUSE THERE WAS NEVER ANYTHING WRONG WITH THEM.

Which brings me to the next truth we must accept:

2) THESE BEHAVIORS ARE NOT ABNORMAL.

ANY dog who is afraid enough, and her early signals have been ignored, will use her mouth.

ANY dog who has no security about food will use his mouth.

ANY dog who knows that the sacred duty of healthy dogs is to maintain a calm pack will use his mouth to control chaos.

ANY dog who is frustrated by unpredictable behavior will use his mouth to try to stop the behavior.

ANY dog who is wound tight by lack of exercise, lack of stimulation, lack of interaction will be more likely to skip the initial steps and go right to the mouth.

Saying that no dog should ever bite is like saying that no human should ever yell. If you have a calm, mature, well-trained group of humans who have great people skills and a steady supply of good food and an in-ground pool, they will probably go years without ever having to yell. If you have a chaotic, immature, uneducated group of humans who all speak a different language and who are rude, you put them in a 10×10 room and you throw two tuna sandwiches in there once a day, you’ll hear nothing BUT yelling. The difference, of course, is that if we look at a group of humans yelling we say “Something is wrong. We need to help them understand each other. We need to give them tools. We need to communicate to them that the others mean them no harm. They’re obviously stressed because they’re hungry and they can’t move around.” The humans themselves are assumed to be basically decent people with the cards stacked against them in an impossible situation.

But if we have a bunch of dogs who fight constantly, who try to bite other dogs constantly, who bite humans, our first response is to say “Those are bad dogs. They need to be put down.” The first assumption is that the dogs are at fault, not that they’re good dogs and would not be biting if they were being understood, if their needs were being met.

Behaviors are responses to needs, desires, fears, dread, hope, etc. A creature who behaves a certain way because he IS a certain thing is called a robot. Living creatures respond to their environments.

So stop using labels; stop filing behaviors as though they define the dog. First, learn what normal, unstressed dogs do and how normal, unstressed dogs behave. Learn enough about your breed to know what additional behaviors are completely normal for your breed. You’ll probably realize that about half the stuff you were freaking out about is completely normal. For example, if your dog is defending his food bowl from other dogs and he’s a Corgi, he’s probably stressed and you need to change or teach something. If your dog is defending his food bowl from other dogs and he’s a Malamute, welcome to normal life. Don’t feed him in a room with other dogs. Bam, problem solved. If your dog is “attacking” other dogs on a regular basis in daycare or in playgroup, but none of these “attacks” leave a mark, it’s very possible that your dog is actually the best-behaved one there and is doing her job of trying to keep the pack functioning well. She doesn’t need to re-learn anything or be punished; she needs to be congratulated, then moved to a playgroup where the human in charge knows enough to keep things calm and happy.

Once you know enough to separate normal, unstressed behavior from behavior that is a sign of stress or frustration, use words that reflect behavior the way it really is. Try to begin with “She’s afraid of…” or “She wants…” or “She needs…” or “He has learned that X leads to Y.” If in doubt, blame yourself, not the dog. “By keeping the leash tight and pulling back, I have taught her that she should try to bite other dogs.”

Dogs ARE individuals. Some dogs come to conclusions faster; some dogs are more tolerant, some are more instinctively physical and some are less so. I am not saying that some dogs are not extremely difficult, or that some breeds are not more challenging than others, or anything of the kind. I am not a Pollyanna about dogs. I am also not saying that every dog is the right fit for every family or every individual; all you have to do is work harder at it. Sometimes it’s just impossible to work any harder than you already are. Sometimes rehoming is the best possible thing that can happen for everyone. And very often an easier dog of a different breed can tolerate that owner’s particular brand of crazy and will thrive. What I am saying, and trying to say clearly and frankly, is that the overwhelming majority of dogs are sane; there are almost no genuinely “bad” dogs. There are millions and millions of stressed, frustrated, misunderstood, disfunctionally trained dogs whose owners have – often with the encouragement of trainers – labeled “bad.” And that needs to stop.

Believe me that I don’t do everything right with my dogs. I make hundreds of mistakes every day. Every post I write I’m preaching to myself, trust me. I am nowhere near a finished product, and neither are my dogs. But it really is true that by realizing that the vast majority of the time dogs behave in ways that are completely rational, I have improved our life with our dogs by a huge amount. My dogs are not perfect but they’re pretty dang happy, and our pack is very functional. Because it works so well we’re able to be “contagious” to other dogs, and make them more functional too, which has led to some real miracles as we’ve done rescue. And, if you haven’t already realized this by reading this blog, we’re very happy with our dogs.

Really, really, the last thing I want to write on OFA testing.

I have SO MUCH more to write about and think about and wrestle with than this topic. I hate the fact that it becomes The Thing instead of only a thing, most correctly a small thing. It’s like yelling “A! A! A! A!” and leaving off the rest of the alphabet. So I will continue to respond to comments or questions about hip testing but I don’t intend to write many more posts about it. I have PLENTY that is controversial to talk about without ever mentioning hips again, trust me.

So here’s my last thing, what I’ve tried to make a distillation of the questions I am asking.

Let me suggest what may be a helpful analogy:

I am a pharmaceutical company bringing a blood pressure drug to market. This drug, as all drugs do, has side effects.

I must answer the questions “Does this drug lower blood pressure?” and “Do its benefits outweigh its risks?”

Both of those are medical and statistical questions. The drug must be proven to be significantly better than a placebo AND it must be proven that its benefits produce greater health in the population of people taking it than its risks hurt that population.

The answer to both must be yes. A drug can work but have such significant side effects that it is rejected, and a drug can be very safe but not actually work.

The answers to those questions are NOT any of the following:

“I know someone with high blood pressure.”
“I know a doctor who was sued because one of his patients has high blood pressure.”
“I think we need to care more about high blood pressure.”
“If we don’t control blood pressure, we’re going to lose our jobs.”

And, because anecdotal evidence must always bow to studies, the answer is also not any variation on the following:

“I know someone who took this drug and he was fine.” or “I really respect Dr. Smith and he prescribes this drug.”

Any or all of those may be true statements, but they have nothing to do with whether this drug should be approved.

Let’s apply that to what I am hoping is the question here: Does following OFA’s recommendations
lower the proportion of painful hip changes in our breed?

THAT’S the only question that is relevant. Because following it DOES have side effects–we cull certain dogs and we favor the genetics of other dogs. Those are powerful and potentially dangerous decisions, so we shouldn’t be making them if we get no benefit.

And we most definitely should not be making the use of this “drug” a condition for being called a reputable breeder.

So we need to stop responding to that question with “I know a dog with hip dysplasia” or “I think we need to care more about hip dysplasia” or “I got a dog from breeder X and she had hip dysplasia” or “we’re all going to get sued if we don’t eliminate hip dysplasia.” And we need to reject, as a justification, “I really respect breeder Y and she has always OFAd.”

The OFA self-reports a decrease in failing scores over the last 30 years. However, a careful reading of the statistics shows that the vast majority of the “improvement” was before 1990. Since 1990, which is at least six generations and in some breeds more like ten, most breeds have shown only a tiny improvement. That strongly indicates to me that between 1970-whatever and 1990 was when breeders were figuring out which hips would fail, and learning not to submit them. I could be wrong, but it’s pretty striking how the “improvement” abruptly slowed to a tiny trickle.

Since 1990 there’s been a small improvement in most of the breeds. However, that result is not “controlled.”

If I look in my kitchen and the floor is dirty, and then ten hours later the floor is clean, I can’t give my husband credit if I know that both my daughters, my mom, my best friend, and the US hockey team was also in my house in those ten hours.

Since 1990, we’ve used OFA. We’ve ALSO changed the way we feed, vaccinate, exercise, supplement, and so on. We’ve also gotten even better at not submitting films we believe will fail.

That’s why the only number you can trust is one derived from an experiment where it is absolutely known that there’s only one factor in play, only one person on the house with access to the mop.

Some Cardigans are dysplastic.
Some Cardigans have painful hip arthritis (note that this is not the same as the statement above).
We are pretty constantly in danger of being legislated out of breeding.
We have responsibilities to our eventual puppy buyers.

None of those statements are being debated here, and unfortunately none of are relevant. The ONLY thing that is in question is “Does following the OFA’s recommendations decrease the proportional amount of painful hip arthritis in our breed?”

The best study I can find, the only one that is controlled, says that the influence of OFA’s recommendations is not statistically greater than zero, even in long-legged breeds it was designed to fit. If it were a drug, it would be rejected as being no more effective than a placebo. And it has demonstrable side effects.

So you tell me. Why are we pushing this “drug” as a sign of “good breeding”?