Random Doggage: Moody Kali

Are Mixed Breed Dogs Healthier Than Purebreds?

If you have reached this link via the Bark magazine blog, you should understand that this article is in no way a defense of closed registries. Rather, it is a statement that higher rates of genetic disease are an almost unavoidable consequence of closed populations, and thus the debate between which is healthier, pure- or mixed breed dogs, is just plain stupid, and purebred dog breeders need to own up to that fact. If you’d like to know more about the genetic consequences of closed registries, please see my articles Closed Registries: Dogs in the Handbasket to Hell, Part I and Part II.



The proper question would be:

What are the risks of (genetic) disease associated with this breed, and how do they compare with other breeds and mixed breeds as populations?

Because this question is, well, loaded in regards to dogs, we will consider it first in humans.

Increased or decreased risk of certain genetic diseases is well documented in humans. A well-known example would be Tay-Sachs disease, a neurological disease caused by a simple recessive (the child must inherit two copies of the gene to be affected, one from each parent.) Anyone can be a carrier of Tay-Sachs, but it is most common in the Ashkenazi Jewish population, with about one out of every twenty-seven people carrying the gene.

Why would this gene be so common in one population of people? Founder effect. In this case, it would be due to a population bottleneck, or reduction of the population to relatively few individuals, from which a larger population grew. Founder effect also occurs when a small population breaks off from a larger one. Like the Hutterites, a branch of Anabaptists that can be traced to a group of less than 100 individuals that migrated to North America in the 1800s. Almost one out ten Hutterites is a carrier of Bowen-Conradi syndrome, a disease that causes failure to thrive and various deformities in infants. Bowen-Conradi syndrome is considered a rare disease…unless you are a member of the Hutterite community.

Other examples of founder effect on genetic disorders would be Huntington’s disease in San Luis, Venezuela, a plethora of heritable diseases in the Amish and Mennonite communities, and the Finnish Heritage Diseases, a group of disorders that are rare elsewhere but more common in Finns due to their small founder population.

Why do some of these genetic disorders remain at such high frequencies in some populations? Many communities are genetically isolated, either through location (like on an island or remote village,) or through culture (religion.) These communities typically produce children with other members of their community, and thus are reproducing with people related to them, which would increase homozygosity in the offspring. This also keeps gene frequencies high. Producing children with unrelated outsiders would result in a continuous influx of new gene variants, changing the frequency of deleterious genes. Small, closed (or mostly closed) populations are especially vulnerable to genetic drift, or changing gene frequencies (spread of deleterious genes.)

(Something not usually seen in humans but common in dogs is the popular sire effect, where one male dog may produce many, many offspring, and alter the genetic signature of a breed or a large portion thereof. If this sire is carrying a gene for a genetic disorder, it can spread through a population rather easily.)

Not all genetic disorders are inherited in a simple dominant or recessive manner. Some dominants have incomplete penetrance, some are linked to either sex. Another type of inheritance is complex or multifactorial. This type of disorder commonly runs in families but the way it is inherited is unclear, and there is often an environmental component.

Why might some populations have higher or lower frequencies of disease?

  • Larger number of diverse founders (lots of founders, founders not related to each other)
  • Lower rate of inbreeding (mates as distantly related as possible)
  • Occasional influx of unrelated individuals (outcrossing)
  • LUCK! (low genetic load in founders, drift in favor of non-carriers, disease kills individuals before they can reproduce)

Okay, now that we have established that in small, closed populations of humans it can be typical for there to be higher rates of certain genetic disorders, and that this can be caused by founder effects, and maintained by breeding within the population instead of outbreeding, let us revisit the original question regarding dogs:

What are the risks of (genetic) disease associated with this breed, and how does this risk compare with other breeds and mixed breeds as populations?

Can we look at individual populations of dogs (single breeds) and discern rates of disorders? Yes. Can we look at mixed breeds and see the rates of genetic disorders in that population as compared to other populations? Yes. Can we look at ‘dogs’ as a population (all dogs) and compare rates of genetic disorders? Yes.

Why then do we accept that we can do this in humans, and accept the results (some populations have higher or lower rates of disease and disorders than other populations) but we adamantly deny this kind of data when it comes to comparing dog populations?

Just stupid, I guess.

Let’s look at some dog studies, shall we?

Canine breeds at high risk of developing inflammatory bowel disease in the south-eastern UK.

The breeds at significantly higher risk of developing IBD compared with mixed-breed dogs consisted of weimaraner (odds ratio [OR]=3.6797, 95 per cent confidence interval [CI]=2.0167 to 6.7141, P<0.0001), rottweiler (OR=2.9697, 95 per cent CI=1.7569 to 5.0196, P<0.0001), German shepherddog (GSD) (OR=2.4101, 95 per cent CI=1.5826 to 3.36705, P<0.0001), border collie (OR=1.9936, 95 per cent CI=1.1655 to 3.4101, P=0.0118) and boxer (OR=1.6961, 95 per cent CI=1.0441 to 2.755, P=0.0328). This study demonstrates for the first time canine breeds in the south-eastern UK that are highly susceptible to developing IBD. Identification of such breeds may allow for a more focused investigation of genetic mutations associated with canine IBD.

This tells us that Weimaraners, Rotties, GSDs, and Border Collies are at higher risk of developing IBD than mixed breed dogs in the Southeastern UK. Does this mean that mixed breed dogs are healthier than purebred dogs? No. Does this mean that purebreds are healthier than mixed breed dogs? No. It means that “Weimaraners, Rotties, GSDs, and Border Collies are at higher risk of developing IBD than mixed breed dogs,” and the fact that these breeds are over-represented in regards to being affected by IBD indicates there may be a hereditary, genetic component to the disease.

A human being of Ashkenazi Jewish heritage has a higher risk of being a carrier of Tay-Sachs disease than an individual who is not of that heritage. A German Shepherd Dog has a higher risk of being affected by IBD than a dog of mixed breed heritage. Why do we accept the former but the latter makes us start hand-waving and shouting?

Just stupid, I guess.

Let’s play the game again.

Prevalence of and intrinsic risk factors for appendicular osteosarcoma in dogs: 179 cases (1996-2005).

RESULTS: Breed period prevalence of OSA was highest for Greyhounds (21/339 [6.2%]), followed by Rottweilers (51/969 [5.3%]) and Great Danes (13/297 [4.4%]); all 21 Greyhounds with OSA were identified as having retired from racing. Sex was not identified as a risk factor for OSA in these breeds, but in all 3 breeds, risk of OSA increased with age. Greyhounds were significantly older at the time of OSA diagnosis (mean, 9.9 years) than were Rottweilers (8.3 years) and Great Danes (7.8 years). Rottweilers and Great Danes were more likely to have OSA involving the forelimbs than the hind limbs. The most frequent lesion sites for all 3 breeds were the proximal end of the humerus and distal end of the radius. The proximal end of the femur was also a common site for the Greyhounds.

CONCLUSIONS AND CLINICAL RELEVANCE: Results of the present study suggested that Greyhounds, Rottweilers, and Great Danes had an increased risk of developing OSA, compared with mixed-breed dogs.

Great Danes have a greater risk of developing osteosarcoma, bone cancer, than mixed breed dogs. Also, Great Danes are more likely to develop osteosarcoma in their front legs than in their hind legs.

Does this mean that mixed breeds are healthier than Great Danes? NO. It means that if you own a Great Dane you should be aware that they have a breed disposition towards osteosarcoma and you should watch your dog for signs of limping or other discomfort, especially as it gets older. If you are a breeder you may wish to think twice about breeding from or to a dog which has a familial history of osteosarcoma.

Exactly why is ‘risk factor’ is so hard to understand?

Just stupid, I guess.

Let’s spin the wheel one more time.

Breed distribution of dogs with diabetes mellitus admitted to a tertiary care facility.

PROCEDURE: 165 breeds (including a mixed-breed category) were represented in the hospital population. Breed-specific expected numbers of dogswith DM were calculated by multiplying the proportion of all dogs admitted to the hospital that were determined to have DM during the study period by the breed-specific totals during the study period. Breeds or breed groups evaluated in the analysis (n = 20) were restricted to those that had a combined observed and expected count > 5 to document breeds at low and high risk for developing DM. Proportionate changes in the risk of developing DM by breed were calculated and presented using exact odds ratios, 95% confidence intervals, and P values. Mixed-breed dogs were chosen as the reference breed.

RESULTS: Samoyeds, Miniature Schnauzers, Miniature Poodles, Pugs, and Toy Poodles were at high risk for developing DM. Dog breeds found to be at low risk for developing DM were German Shepherd Dog, Golden Retriever, and American Pit Bull Terrier.

CONCLUSION AND CLINICAL RELEVANCE: The finding that certain dog breeds are at low or high risk for developing DM suggests that some genetic defects may predispose dogs to development of DM, whereas other genetic factors may protect dogs from development of DM.

‘Reference breed’ means that mixed breeds were chosen as a population representing the ‘normal or typical’ rates of diabetes mellitus in dogs. Since mixed breeds can be presumed to have diverse genetic profiles, this can tell us whether a higher than normal rate of disease may be hereditary in nature, and allow us to look for clues in the genome as to how DM may be inherited in specific high risk breeds. In this study, Samoyeds, Miniature Schnauzers, Miniature Poodles, Pugs, and Toy Poodles were at higher risk than mixed breed dogs for developing DM. But, German Shepherd Dogs, Golden Retrievers, and American Pit Bull Terriers were at lower risk than mixed breed dogs.

Once again: does this mean that mixed breed dogs are healthier than purebred dogs? No. It means that mixed breeds are typically at lower risk for DM than purebred dogs, and that some breeds have a higher risk profile, and some have a lower risk profile, than mixed breeds.

Just like in human populations. And, just like in human populations, heterogeneous, genetically diverse populations typically have lower rates of heritable disease than homogeneous populations. In other words, mixed breed dogs are genetically more diverse than purebreds, and thus two disease causing genes are less likely to occur in the same dog. With more complex inheritance, purebred dogs are more likely to have ‘runs of homozygosity’ (long stretches of identical DNA, due to founder effects) than mixed breed dogs, and therefore more likely to have higher risk of diseases caused by polygenetic or complex inheritance.

There are a plethora of studies showing risks factors in purebred dogs compared to mixed breeds. Often, but not always, purebreds have a higher risk factor. Being a ‘breed’ means predictability, both in appearance and behavior, and that means a more homogeneous genetic population. A higher risk for certain disorders is a natural consequence of founder effects and closed populations. It is not something to be ashamed of, and it is not something to deny. It is something to be aware of, to work towards changing, and to educate the public about.

This is not rocket science. It is not hard to understand. Studies and good health surveys can tell us what the risks are for our breeds. This helps us make breeding decisions and it helps us to educate puppy buyers. Being honest about those risks helps us to mitigate them. Surveys, studies, databases, tests and even outcrossing to another breed are simply tools to help us deal with genetic disorders in our dogs.

No population is free of disease. A higher frequency of some diseases is a tradeoff for the predictability of being ‘purebred.’ Changing the frequency of disease in a population is possible, and this is what breeders are attempting to do when they conduct surveys and studies and do health tests and look for disease genes and choose certain dogs for breeding while passing others over. It has nothing to do with which kind of dogs are ‘healthier’ and everything to do with trying to decrease disease frequency in our own dogs.

Turning the discussion of dog health into a pissing contest between purebreds and mixed breeds and their fan clubs is counterproductive. Delving deeper into purebred health, which is easier due to their genetic consistency, helps all dogs, and humans. Why, then, does any discussion about dog health, diversity, disease rates, and genetics seem to devolve into “are mixed breeds healthier than purebreds?”

Just stupid, I guess.

References and resources

Disorders in human populations

Patterns of Inheritance

Genetic drift and gene frequency in small populations

Let’s not forget the Habsburgs!

Studies showing risk in purebred relative to mixed breed dogs (lots more out there, knock yourself out)


  1. I love it when you put this kind of post into your blog. thanks you for educating us all.

    Yet you referred to “Mixed breed dogs” as though mutts were mixes of purebreds. Do you think they are just mix of AKC “breeds” or is it possible that there are mutts who have been mutts forever? Every single bad gene in a purebred was there from the mutt in the beginning of a line. They don’t often show up until there is a bottleneck or another narrowed gene pool.

    So true mutts have all the possible genetic diseases in their genome, but generally, they show up at a much smaller frequency than in a purebred dog which inherits a couple of them from several sides.

    True heterogeneity should tend to limit the chances where bad recessives have an opportunity to manifest?

    1. ‘Mixed breed’ typically refers to a dog of either unknown background, which could be a heinz 57 or true mutt, or crossbreeds or backcrosses with known background. I’ve never actually run across a study that defined ‘mixed breed’ as anything other than ‘mixed breed.’ Occasionally you see ‘mongrels’ used in the same way.

      “True heterogeneity should tend to limit the chances where bad recessives have an opportunity to manifest?”

      Yes. Inbreeding will always result in loss of variants. Loss of variants means you have a greater chance of deleterious recessives getting together and having some kind of party.

      As more and more people have their genomes sequenced, they are finding that humans have a lot more ‘bad’ recessives than was previously thought. Humans are, for the most part, an outbreeding species. If this is also true of dogs (more recessives than we thought) then we are only seeing the tip of the iceberg in regards to detection of bad recessives through recognizing disease, isolating the gene involved, and developing a DNA test for it. The grand experiment that is ‘registered dog breeding’ is still fairly young, most registries did not truly close until after WWII. So, the true effects of closed registries remain to be seen. We just have a few outliers with high rates of disease as a bit of a teaser right now.

  2. It’s hard to understand why people cannot simply look at the health pros and cons of any breed or mixed breed of dog and come to the logical conclusions rather than get on the band wagon promoting their favorite breed and ignore scientific evidence. While I am a strong advocate of crossbreeding as the simplest and fastest way to improve genetic diversity, I cringe at people crossing two different breeds of dog simply because the combination of the two parent breeds names will make a cute new name. Crossbreeding should be used to create genetically stronger, healthier dogs.
    Another factor to be considered in crossbreeding is that a genetic cause for a certain “disease” in one breed may be caused by an entirely different set of genes in another breed, thus even if the parents of a mixed breed dog each carry a gene for that disability, they (the genes) may be unlikely to pair up and cause the problem in the resulting offspring. When I cross dogs of different breeds I not only consider how well the mix of the two breeds will complement each other, but also how far apart the breeds are genetically. When I cross Irish wolfhound and Alaskan malamute I believe I am introducing relatively unrelated genes that have not been in the same animal for thousands of years. But if I were to cross my Irish wolfhounds with Scottish deerhounds I might well be recombining unwanted genes that were found in a common founding ancestor of both breeds.
    Though I personally have no interest in dog shows, I don’t believe it’s actually the show ring that is destroying registered breeds of dogs, but the closed pedigree system required by the breed clubs such as the AKC. When I breed show pigeons or chickens I can cross any breed I want into my birds and as long as the resulting offspring meet the “breed standard” they can win in a show. If this type of breeding program were practiced with dogs, new, badly needed genetic material could be introduced into any breed and the resulting puppies that meet the breed standard could still be shown, and any puppies that didn’t meet the standard could become family pets. If people are insistent on breeding dogs for show purposes this is the only sensible and sane way to go about it. We must do away with the closed registry system. At the same time breed clubs must also rewrite the standards of some breeds, especially for brachycephalic dogs, so they do no harm to individual animals.

    1. My friends with rabbits think that dog people are crazy, since evidently it’s the same way with rabbits (apparently purebred animals are considered purebred.)

      Of course with rabbits or chickens or pigeons, you can eat the rejects. I think dog culture is fairly screwed up if it’s considered ‘not responsible’ to produce dogs for the pet market, and breeding within an open system like you describe would produce a lot more ‘pet quality’ dogs.

    2. The closed studbook thing for dogs is very AKC and KC, the FCI offers the possibility of outcrossing within a breed through its Registre Initial in which dogs imported from non KC, non AKC and non FCI countries can be introduced into a breeding program. Such is the case for indigenous breeds imported from country of origin. I have done that with my dogs (North African Sloughis) and the descendance has had great success in the show ring and performance events, with zero or very low Coefficients of Inbreeding. Of course other breeds do not have indigenous populations to draw from.

      1. In the US the decision of whether to open the stud book is held by the breed club. Period. If I were able to import an Afghan from Pakistan or Afghanistan I would have to petition the AHCA to get it registered (fat chance.) And no, most breeds do not have indigenous populations to draw upon, and even those that do have to have three generations behind them before being given full registration and cannot compete in conformation events. IIRC, they cannot compete in performance events, either. For a breeder who considers conformation and/or performance events paramount, IE has a lot of their ego tied up in titles, breeding dogs that cannot compete has no purpose. Indeed, I have had that same conversation with more than a couple breeders, namely, “What do you do with the dogs until they can achieve full registration?” as if the entire purpose of the dog is competition.

        Worse than the closed registry affect is the affect that magical thinking has on some (possibly many) purebred dogs. Most breeders of breeds developed within the last 150 years understand that their dogs were ‘made’ by combining different types of dog, but now it is ‘something else’ and if we outcross in an attempt to fix health problems then it won’t be ‘something else’ any more. Ridiculous. The fear of ‘those unknown genes’ locks the breeder into thinking that high rates of disease are acceptable. The vast majority of breeds do not have COO populations and therefore other options must be considered.

        1. Regarding first generation outcrosses to country of origin non registered dogs, I never had to go through a breed club and never will, I am not AKC, I have since 1993 always registered my Sloughis with the FCI system through the Federacion Canofila de Puerto Rico, the FCI registry for dogs born in the US. First, second and third generation Registre Initial FCI dogs can compete at the national level usually for national titles in FCI countries. They cannot compete at the international level. For me in the US, my dogs can compete in ASFA, LGRA and NOTRA with their FCI registration. AKC recognizes FCI registrations but I do not know what they do with incomplete pedigrees for conformation titles as I do not care about AKC……

          1. That’s nice.

            Unfortunately, your deal with the Sloughis and FCI doesn’t even come close to reflecting how AKC works, and equally unfortunately, AKC is, in the publics eye (and technically the worlds eye, due to it’s reciprocity deal with FCI), ‘purebred dog culture’ in the US.

            This is, after all, the country where writing an article like this one will get you branded an anti-purebred anti-dog anti-breeding animal rights activist.

          2. This is why I like the fact that you wrote this article anyway, and why I don’t “do” AKC which after all has only about 50% of dog registries in the US. There are plenty of other venues to do things with dogs in the US….

    1. This only works with recessives when the disease is caused by the same version of the gene in both breeds. This is why we don’t have blanket ‘all breed’ DNA tests for the recessives that have been identified and have a test developed, because a given disease, like PRA, may be caused by different genes in different breeds. If you breed two breeds together that have different versions of the PRA gene, for example, you are not having to deal with those genes causing disease.

      I don’t do maths, but I think if you breed a dog from breed A where there is a carrier rate of 10% with a dog from breed B where the carrier rate is 2%, you are still going to have less risk of producing affecteds than breeding two dogs of breed A together.

      I believe known crosses should be included in breed health surveys. It could be valuable information about how some diseases are inherited, and whether crosses are actually at lower risks for diseases with unknown inheritance (cancer.)

      Part of the problem is that dog breeders have gotten their egos tangled up in this discussion and made it into a competition, which dog is healthier. All dogs have bad genes. It’s certainly not that a given purebred has MORE bad genes than your average mixed breed, it’s by breeding within a closed system you are concentrating those bad genes. It’s a tradeoff.

      1. Yes, PRA has a mode of inheritance which is different for every breed that has it, but I was thinking more about things like IBD or DM, not being sure what the Genetics of these are. Also genes are influenced in their expression by the background in which they are inbedded, so the mixed breed may have an advantage there too. There is no doubt that inbreeding concentrates genetic defects, this is why this method of breeding is used to develop strains of mice with specific genetic defects to study in scientific research. And yes there is no living being with no bad genes, DNA constantly mutates, it is not static.

        1. Yes, PRA has a mode of inheritance which is different for every breed that has it, but I was thinking more about things like IBD or DM, not being sure what the Genetics of these are.

          Degenerative myelopathy is a simple recessive in at least some breeds. It is interesting because not all dogs that have two copies of the gene are affected, or they may be a very mild case. There is a DNA test for it. I know there has been a study done in GSD regarding IBD, as they are notorious for it, with a genetic association made. But I also think that ‘finding the gene for’ a lot of these complex diseases like IBD or cancers or auto-immune diseases or allergies is a bit of a crap shoot and gives breeders the wrong impression of the development of a lot of diseases.

          Also genes are influenced in their expression by the background in which they are inbedded, so the mixed breed may have an advantage there too.

          Oh, yes! Thank you for saying that. It is unfortunate that it’s not possible for there to be experimental outcrossings done here in the US with the goal of eventually reintegrating the offspring into the registry without the permission of the breed club. Some clubs are more open than others but we have the wonderful example the hard road the LUA Dalmatians took to get recognized by their breed club. I find it somewhat illogical that when you have a breed like Flatcoats with a high rate of cancer, and no ‘cancer gene’ in sight, that an cross-breeding cannot be done with a high risk line just to see what happens. This seems better to me than just accepting a high rate of disease, while we ‘look for the gene.’

    1. I just wish people would not represent the issue as ‘mixed breeds vs purebreds.’ It really should be closed populations compared to open populations. If I took all the dogs I have here (Afghans, Salukis, Azawakh, and Italian Greyhounds) and turned them into a closed population, they would likely end up with a higher rate of some genetic disorder (or more than one) than if you sampled all the mixed breed dogs entering the local shelter for a couple years.

      1. Amusingly enough, even if I eliminated all but one representative per ‘family’ of related dogs here, I would have a larger founder population for my hypothetical closed population than some breeds. Whether my closed group would be ‘healthy’ or ‘unhealthy’ (for lack of better words) would depend on the genetic load of my founders.

        And here’s the thing, (and I think this definitely where the arrogance involved in dog breeding trips breeders up,) dogs are complicated enough, genetically, that unless you are breeding VAST numbers of dogs and doing a shitload of inbreeding to bring recessives to the fore, you have NO CLUE what the genetic load really is. Like any breeder, I select for appearance and behavior (performance.) The genes controlling these aspects of the dog are only a teensy part of the whole; IOW, what am I inadvertently selecting for by selecting for the things I can see/experience? Aaaaand, is that kind of selection any ‘better’ than random selection (unintentionally bred mixed breed dogs)?

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