Why has this been such a tough nut to crack? If we knew that, we would probably be making better progress, but we do know much more about it than we did 50 years ago. Here are some statements commonly seen in discussions about hip dysplasia. Five (5) of these statements are FALSE. Do you know which ones?

a) Hip dysplasia is a "large breed" disease.
b) Genetic factors are more important than environment in the development of hip dysplasia.
c) Environmental factors are more important than genetics in the development of hip dysplasia.
d) Dogs that develop hip dysplasia had normal hip anatomy at birth.
e) Vitamin C supplements prevent hip dysplasia.
f) Calcium supplements prevent hip dysplasia.
g) Obesity increases the risk of hip dysplasia.
h) If hip dysplasia is caught early enough it can be reversed.
i) Zinc supplements reduce the risk of hip dysplasia.
j) Too much exercise can cause hip dysplasia.
k) Not enough exercise can cause hip dysplasia.
l) Two dogs with severely dysplastic hips can produce puppies with normal hips.
m) Two dogs with excellent hips can produce dysplastic puppies.

(You can take this pool in ICBs Breeding for the Future Facebook group.)

Now try this one: which of these breeds has the highest incidence of hip dysplasia and which has the lowest?

Borzoi
Bloodhound
Bullmastiff
Chesapeake Bay Retriever
Doberman Pinscher
Dogue de Bordeaux
Irish Wolfhound
Kerry Blue Terrier
Komondor
Newfoundland
Norfolk Terrier
Pug
Schipperke
Shih Tzu
Siberian Husky
​

Scientists have discovered something that dramatically reduces the risk of hip dysplasia in dogs, as shown in this graph: at both 1 year and 13 years old, dogs in the group that received the treatment were much less likely to develop hip dysplasia. Do you know about this treatment? Are your dogs benefiting from it?

How can you learn what you need to know about hip dysplasia? Can you rely on what you read on websites?There is lots of misinformation out there about this problem. Check out this great example of really bad information -

Hip Dysplasia Facts, Fallacies, and Fairy Tales

​Are you really doing everything you can to reduce the risk of hip dysplasia in the dogs you breed? Are you relying on facts or fiction to manage the risk of hip dysplasia?

ICB's course Understanding Hip and Elbow Dysplasia focuses on what we know and what we don't, what is fact and what is fiction, what works and what doesn't in reducing the risk of dysplasia.

​The next online course STARTS 5 September and is open to students anywhere in the world. You can get more information and register HERE.

Also, students who finish the course will be eligible to participate in ICB's Citizen Science Project, which you can read about HERE.

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*** Understanding Hip and Elbow Dysplasia ***
Starts 5 September 2016

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By Carol Beuchat PhD

Just published today in Canine Genetics and Epidemiology is a study of the population statistics and genetic diversity of all 215 breeds registered by the Kennel Club, using data from the pedigree database from 1980-2014. The paper is a welcome addition to the literature, updating and eclipsing the earlier (and epic at the time) study by Calboli et al in 2008.

If you've been wondering if you should take a course in population genetics, this paper will convince you. (Check out the courses that ICB offers here.) The health of the dogs we breed depends fundamentally on the quality of the gene pool, and assessments of the genetic health of the gene pool are necessarily based on population-wide analyses. So there is much here about effective population size (Ne), which is determined by the rate of change in the average level of inbreeding in the population.

At the core of the paper are data for inbreeding over the years since 1980. Unfortunately, the data for individual breeds are not in the paper, or even in the supplementary documents available from the publisher (where they would be available in perpetuity), but instead are available as individual pdf documents on the Kennel Club website. If the address to that web page should ever change (and surely it will), the link published in the manuscript will be useless. So, download your favorite breed now, just to be safe.

Below are some examples of breeds in which inbreeding doesn't stabilize after 2000, but increases continuously over the period of the study. Perhaps these are breeds that didn't benefit from a surge in imports after 2000 (wish we could see the data for imports), but there is no evidence that breeders have been adjusting breeding strategies to reduce the level of inbreeding. If that was happening, it would be evident in the distance between the observed and expected inbreeding lines in these graphs. The expected level of inbreeding assumes that breeding is random; the higher observed level indicates that the animals being bred together that are more closely related than the population average. This also indicates the potential magnitude of the reduction in inbreeding that could be achieved by a change in breeding strategy.

As I noted above, the effective population size (Ne) is determined by the rate of inbreeding in the population. The rule of thumb used by conservation biologists as the minimum Ne necessary to maintain a sustainably breeding population has risen over the last few years from 50 unrelated, randomly breeding animals to 100, and even more recently 500, as biologists reassess the realities of both in situ and captive animal management (you can read about the latest argument over revision here). That aside, it is useful to look at some of the data on Ne from the present study.

Below I have graphed the data for Ne (from the Supplementary documents) for those breeds in which there were more than 50 registrations per year; that is, the more populous breeds. I have superimposed lines at Ne = 50 (red), Ne = 100 (yellow), and Ne = 500 (green), to correspond with the various rules of thumb under debate.

If we wanted to conservatively go with the minimum Ne of 500, only 2 breeds would make the grade, and only about half of the breeds with registrations higher than 50/year would make the Ne = 100 cutoff. There are a good number of breeds for which Ne is <50 on this graph, and I haven't looked at it yet but I would wager that the majority of breeds with fewer than 50 registrations per year will be below the red line as well. (If there were 50 dogs in the population, half male and half female, and all animals bred, the Ne would be 50. Breeds with fewer than 50 registrations per year would be cutting it mighty close.) 

There is much more that could have been done with the data available to the authors than they presented in the paper and supplements. Just for fun, I have pulled the data for Labrador Retrievers from the paper and supplements and (quickly) put together some graphs that might be useful for breeders. (Similar analyses can be done for the other breeds on request.)

For instance, below is a graph of the fraction of puppies produced each year by top-ranking sires. You can see that about 30% of the pups born yearly were produced by only the top 5% of sires.

The impact of top-ranked popular sires is even more obvious in this figure of the maximum number of pups produced by a single sire in a year compared to the population average. Note that the y axis is logged, otherwise the data for the averages would all be to low to see.

(You can see more of the analyses of the Labrador data here.)

I would have to say that, after a few hours of fiddling with the available data, the paper's summary is rosier than the actual picture. The statement that levels of inbreeding are looking much better since 2000 is quite misleading - it could simply be an artifact of the importation of unrelated dogs, and there are plenty of breeds in which the rate of inbreeding has stayed on the same trajectory for decades and could very well continue. The number of breeds with effective population sizes well into the danger zone should be a heads up for breeders, especially in those breeds that could increase Ne with the simple strategy of breeding a larger fraction of available dogs and balancing the ratio of males to females (as I discuss here).

The caveat here is that these data are for an artificial population - the dogs registered with The Kennel Club. Before 2000, it was effectively a closed population, and since then has the addition of imports with only 3 generations of pedigree information, which makes them appear in analyses like this to be new, unrelated founders. At least The Kennel Club should be congratulated for including geneticists on their staff who have access to the pedigree data and the expertise necessary for these analyses. What a pity that the AKC does not do the same.

You can read The Kennel Club's press release about the study here.

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*** Understanding Hip and Elbow Dysplasia ***
Starts 1 October 2015

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...the science of animal breeding 

There are clearly differences among breeds in growth rates. This is a graph of the growth curves of 12 breeds of dogs that cover the range in adult body size from Papillon to Mastiff. The large breeds are substantially heavier than the smaller ones by 2 or 3 weeks after birth, and the trajectory of their growth is exponential for about the first 8 months. While the small breeds reach adult body mass by 6-8 months, the larger breeds don't attain adult body weight before 1 year and the largest among them continue to put on weight for up to 18 months.

So, growth rate is linked to adult body size, and dogs that grow faster will weigh more, so it's hard to experimentally separate the effects of food consumption and weight.

But we can look at the effect of size without the confounding effect of food consumption if we look at newborn puppies. A study of Newfoundlands, Labradors, Leonbergers, and Irish Wolfhounds followed dogs from birth until up to 9 years (Vanden Berg-Foels et al 2006). They found that the weight of puppies at birth was affected by litter size: smaller litters had puppies that weighed more at birth. Furthermore, these larger pups had a higher risk of abnormalities or lesions of the hip cartilage by 8 months. This is despite the fact that the pups that were smaller at birth had exponential "catch-up" growth, so that by 12 days there were no longer differences in weight due to litter size.

This experiment suggests that it is the weight of the puppy very early in life, and not growth rate, that is the significant factor in the development of HD.

As the authors of this study point out, heavier puppies could challenge the capacity of the immature connective tissues and skeleton for support. If this allows some laxity of the head of the femur, the contact area over which force is distributed would be reduced, putting greater stress on the areas of contact. As the weight of the animal continues to increase with growth, a less than perfect fit of the head of the femur in the hip socket could produce a viscous cycle of damage and greater laxity that could eventually manifest as dysplastic hips.

They conclude that "These results support the hypothesis that increased body weight during the critical early postnatal period was sufficient to alter the course of hip development and result in measurable degenerative changes at adulthood."

So we're left with these thoughts:

• Puppies from larger litters weigh less at birth
• Puppies that weigh less at birth grow faster and catch up with the larger pups
• Puppies from smaller litters weigh more at birth, don't grow as fast as pups from larger litters, and are more likely to show degenerative changes in the hip joint when they get older

The bottom line:

• The risk of hip dysplasia is related to how much a puppy weighs when it is born.​

Sometimes, the traditional ways of doing things really are better. 

In the stark landscape of Mongolia, nomadic herders have migrated with their livestock to follow the forage for thousands of years.

During the Soviet occupation of Mongolia, most of their livestock guarding dogs were shot or released. Without the dogs, herdsmen resorted to shooting the predators - the wolves and the endangered snow leopard.

ICB is proud to be assisting The Mongolian Bankhar Dog Project in a breeding program to bring back the dogs that have protected the livestock for thousands of years, the Mongolian Bankar. 

To gear up for this year's breeding season, The Bankhar Dog Project has launched a crowdfunding campaign on IndieGoGo. 

You can read more about this great project on the Bankhar Dog Project website and follow them on Facebook.

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By Carol Beuchat PhD

No disorder causes more pain and suffering in dogs than hip and elbow dysplasia. The Orthopedic Foundation for Animals was founded in 1966 specifically to address the growing problem of these two disorders, and although there has been some reduction in incidence in some breeds thanks to the efforts of breeders, after 50 years of research and selective breeding, hip and elbow dysplasia still remain at the top of the list of issues affecting the welfare of dogs.

This is a huge problem for breeders. Dogs with good hips can produce puppies with bad hips, and vice versa. Should dogs with less than stellar hip scores be removed from the breeding pool? What if the breed already has dangerously low genetic diversity and myriad serious health problems - is it worth taking a risk breeding a dog if it is matched with a dog with excellent scores? Should you breed a dog with one good hip and one bad one? What if a dog had bad hips but the rest of the litter had great scores?

These are tough questions, and the conundrum is evident here in this table of data produced by OFA (Keller 2012). You can see that pairing two dogs with excellent hips will still produce some offspring (3.6%) that are rated dysplastic based on x-rays. And breeding two dogs with less-than-perfect hips (e.g., mild with mild) can produce some dysplastic dogs, but also still a majority (about 70%) with acceptable hip scores. Note that this might be an overly rosy assessment because of incomplete, biased data; if bad scores are not submitted, the fraction of dysplastic offspring will be an underestimate.

To breed or not to breed? It's a really tough question.

The economic consequence of hip dysplasia

Of course, there is a cost to these problems. OFA provides the data for the number of dogs in their database by breed for the years 2006-2010, so these would be animals that submitted x-rays for evaluation. I assumed very conservatively that a hip x-ray costs $250, and multiplied that by the number of scans submitted per year over this period, separated by breed.

The numbers are staggering. To avoid using fractional numbers on the y-axis of this graph, I have logged that axis and run the scale from 10 to 2,000, and the unit is $1,000 per year. This means that 2,000 on the graph is $2 Million, 1,000 is $1 Million, and so on. X-rays for Labrador Retrievers alone over this 5 year period averaged $1.58 Million/yr. This is just for the dogs that submitted x-rays to OFA, which is certainly not every Labrador in the world that had its hips x-rayed (e.g., very poor results might not be submitted, and evaluations in other countries would not be in the OFA database). That number for Labradors - $1.5 Million, is only a fraction of the actual cost for the entire breed.

(You can download a larger version of this graph here.)

I tallied up the cost for the breeds at the top of the OFA list in terms of number of x-rays submitted (again using $250 as the cost of an x-ray), and the total expenditure comes to $7.518 Million/year. If I add to this the rest of the breeds that I didn't include on this graph, the total comes to $8.16 Million/year.

Take a moment to let that number sink in.

So, in the US alone, we're spending >$8 Million per year just for hip x-rays. Most dogs with dysplastic hips will have also vet visits, pain meds, and some even surgery. The total cost over the life of a dysplastic dog could be thousands of dollars.

The scary thing here is that there is no end in sight. This is costing us many millions per year, and we have to expect that this will continue for the foreseeable future. On top of that, we can't put a number on the suffering of the dogs, not to mention the heartache of a family that can usually do little to alleviate the pain. We can continue to get the x-rays done, and OFA and other health organizations can continue to collect the data, but are we headed towards a solution? I don't think so.

So, what can we do? Some very, very smart people have been thinking about this for decades. But sometimes fresh eyes coming from another perspective can see things that have been missed by others, and this can make all the difference. I'm not an orthopedist; I'm not even a veterinarian. But I am a biologist with broad expertise in vertebrate biology and a similarly broad approach to solving problems in science. Let me tell you what I saw when I started thinking about the problem.

The evidence from phenotype

A few years ago, I was puttering around on the OFA website for some reason and happened to look at the statistics for hip dysplasia. The data are ranked, so the breeds with the highest frequency of dysplastic hips are at the top of the list. Hip dysplasia is a notoriously "large breed" problem, but what caught my eye was that the top 2 breeds on the list were the Bulldog and the Pug. Neither of those would have been on my list of "large breeds". Similarly, at the bottom of the list was another surprise. Among those breeds with the lowest incidence of dysplasia were the Borzoi and Greyhound; in terms of height, I would consider them large.

The message suggested by the data was clear. Hip dysplasia is not a "large breed" problem. Rather, hip dysplasia is most prevalent among breeds that are heavy for their size, whether they be large or small, and conversely dysplasia is rare in breeds of moderate to light build.

This observation alone - that it's not large dogs but heavy dogs that are at higher risk of dysplasia - reframes the question. We should be looking for answers not by comparing large breeds with small, but by comparing heavy breeds with light ones.

The phenotype and genotype of hip dysplasia

We know that both hip and elbow dysplasia are heritable; that is, genetics can account for some of the variation in the quality of these joints from animal to animal. But efforts to identify the genes responsible have been frustrating, because both problems are certainly polygenic, with dozens or even hundreds of genes involved, and there is no indication that we will ultimately identify a set of "risk genes" that we can simply select against in the relevant breeds.

Of course whether a breed has a light or heavy build is genetic, and within a breed there can be variation among individuals in what we call "substance". So I wondered - could the variation in build among and within breeds account for at least some of the variation in the incidence of hip dysplasia? Have we been looking for "hip dysplasia genes" when the responsible genes have nothing to do with hips, but instead determine the "robustness" of the dog? Could this be a biomechanical problem of weight relative to the size of the dog?

Of course, this feeding experiment is a manipulation of the "environment" of the dogs. What it shows us is that although genetics might play a role in the development of bad hips, the effects of non-genetic factors - food consumption, in this case - can be very significant. They noted that the restricted dogs were 25% smaller and lighter than the control dogs, which supports but doesn't confirm the idea that robustness is a causal factor in the development of hip dysplasia. The observed effects could have been the result of growth rate, or consumption of some nutrient (the restricted dogs would have consumed less), or some other factor we haven't considered.

So we can expect the environment might have a significant effect on the quality of the hips, but what about genetics? Several studies have looked at this and found the heritability of hip dysplasia to range usually from about 0.15-0.4; that is, 15-40% of the variation in hip scores among dogs is accounted for by genetics. Genetics definitely matters, but are the genes breed-specific? Are they related to some aspect of hip development? Are they related to body "robustness"? Or maybe none of these?

Unfortunately, we don't have the data to answer this question, and it's not likely that someone will do another 13 year experiment like the one Purina did. But I don't think this necessarily leaves breeders twisting helplessly in the wind. We can be certain that food consumption matters. There is also some evidence of other factors such as type of exercise, stair-climbing, growth rate, and other things could be important, and some of these are things breeders can do something about if they are aware of the existing data and what it means.

Let's do some Citizen Science!

I think breeders can play a role in figuring out the most effective ways to reduce the incidence of hip dysplasia. After all, every breeding you do is a genetics experiment, and if you collect the right data we might be able to address some questions that would be nearly impossible to do any other way because of the time and expense that would be involved.

So here's my idea. I would like to do a Citizen Science project. I want to round up a group of breeders that have data for litters they have bred in the past for which the hips were evaluated. At the very least, we would want the pedigree information, but if there are data for growth (did you periodically weigh the puppies?), adult body weight, height, etc., we will collect that too. Let's gather together all of the data we can come up with (and you can provide not just your own data but perhaps also more from other breeders), do some analyses, and see what we can learn. Then I want at least some of these people who plan to have a litter in the near future to collect some specific data on those dogs as well. If we don't get enough participants and data for a particular breed, we won't be able to do much. But I think if we get the data collection started, we can build on it over however long it takes, and eventually (and I think it won't take long) we might learn some interesting things. The alternative, of course, is that nobody does anything, so even if this is far-fectched we don't have much to lose.

One thing that I think will be necessary as a part of this is to get breeders up to date on what is known about hip dysplasia. They will need to understand heritability in order to make appropriate breeding decisions. They need to understand the hip and femur anatomy in order to make sense of the role of biomechanics. They need to be familiar with the studies that have looked at various potential risk factors, as well as the cross-breeding experiments that have been done.

To this end, I've designed a new ICB course, Understanding hip and elbow dysplasia. Of course, anybody can take the course, but those that want to be a part of the Citizen Science experiment need to take it so all of us will be up on the information we will need to understand in order to design and interpret our data. What we learn from the project will depend on how much participation we have, but at the very least the participants will learn a lot and it might also be the beginning of a more systematic way of gathering information that is presently unavailable in any form. 

So if you're interested in participating in a Grand Experiment in Citizen Science, please join us. I just set up the course registration page, and I'll form a private Facebook group where we can gather and discuss how to proceed. The course will have a separate group so communication will be easier, but I hope to see lots of you in both.

You can get to the Hip and elbow dysplasia course info page HERE.

By Carol Beuchat PhD

Epilepsy is one of the most debilitating and frightening disorders suffered by dogs, and finding up to date information is not always easy for breeders and owners. 

Introduction

1. International Veterinary Epilepsy Task Force consensus report on epilepsy definition, classification and terminology in companion animals

2. International Veterinary Epilepsy Task Force Consensus Proposal: Diagnostic approach to epilepsy in dogs

3. International Veterinary Epilepsy Task Force current understanding of idiopathic epilepsy of genetic or suspected genetic origin in purebred dogs

4. International Veterinary Epilepsy Task Force consensus proposal: Medical treatment of canine epilepsy in Europe

5. International Veterinary Epilepsy Task Force Consensus Proposal: Outcome of therapeutic interventions in canine and feline epilepsy

6. International Veterinary Epilepsy Task Force recommendations for a veterinary epilepsy-specific
MRI protocol

7. International Veterinary Epilepsy Task Force recommendations for systematic sampling and processing of brains from epileptic dogs and cats