I was browsing through some of the comments on the ridiculous Say No to Mutt Breeders FB page, and while it’s easy to just laugh (or inwardly cringe) over how wrong some of them are, this thread caught my eye. I wanted to write a serious explanation about why the second commenter’s reasoning is incorrect because it’s a very common argument against crossbreeding that I hear all the time, but it has no foundation in science.
This will get very long since it involves explaining some of the basic principles of population genetics and how they apply to dog breeding and dog breed health. This post assumes you’re familiar with basic genetics terms and concepts. If you’re not, I’d highly recommend reading this basic introduction to genetics and this glossary of basic genetics terms which both use dog breeding examples. I’ll also link to additional articles and research studies throughout this piece for those who want to read more on the concepts addressed.
Without further ado, here is the long answer to this common question:
Is crossing two breeds more or less likely to produce health problems than breeding two purebreds?
First off, I need to clarify that it is not true that by crossing two breeds, you will always produce healthy progeny that are free from the genetic diseases of their purebred parents. Mixes and crosses can and do inherit genetic disorders, which is why it’s important to health test your dogs and be familiar with their genetic background whether you’re breeding mixes or purebreds. However, the idea that crossing two breeds will inevitably increasetheir risk for health problems moreso than breeding two purebreds would is false. In fact, crossing two breeds will always reduce the probability of the offspring having poor health due to genetic factors when compared to the probability of this occurring when breeding only the purebred parents with other purebreds. There is a well-documented scientific reason for this, a genetic principle called heterosis.
Heterosis is the scientific name for what is more commonly known among animal breeders as “hybrid vigor.” In short, it describes the trend of increased reproductive fitness in animals that are the result of interbreeding between two different subpopulations, whereby on average the offspring have overall better reproductive fitness than either parent. Reproductive fitness describes the overall health and vitality of an animal which helps to contribute to its ability to survive and produce offspring. For example, animals that suffer from inherited diseases have a lower reproductive fitness than those who don’t.
A common claim among dog breeders is that “hybrid vigor” is a myth and doesn’t apply to dogs, despite the fact that this effect has been studied and observed for over 100 years in a diverse myriad of species, including dogs(these studies will be discussed later on). In order for this to be true, it would mean that dogs would need to have a system of genetics and inheritance which is different from that of every other mammal, but there is simply no evidence for this. The entire dog genome has been sequenced and hundreds of genetic studies have been conducted on dogs, all of which affirm that canine genetics are nothing unique in the animal kingdom.
In order to fully understand what heterosis is and how it works, one must understand the inverse of this phenomenon which causes the opposite effect, one which is prolific in pedigree dogs: inbreeding.
Inbreeding is defined as the mating between two animals that are more closely related than average. Though most people think of extreme examples like breeding father to daughter or sibling to sibling as inbreeding, in fact virtually all breeding of pedigreed dogs is technically inbreeding. This is due to the way that purebred dogs are registered and bred.
In most kennel clubs and registries, in order for a dog to be considered purebred, it must be the offspring of parents who are also registered as purebred. In turn, those dogs must meet that same requirement of having registered parents, and then those dogs also must also be offspring of registered parents etc. This continues down the generations until you get to the very first dogs that were ever registered for the breed, who are thefounders of that breed’s studbook. Most breeds have only a handful of founders, and some have as few as three. Generally, all dogs of a pedigree breed must descend from that same group of founders in order to be considered purebred. Furthermore, most kennel clubs are closed registries, meaning dogs that are not offspring of registered dogs are not eligible to be registered at all. In effect, no new genes can be introduced in a closed system. Consequently, this model of breeding leads to accumulating gene loss through the generations, and the longer a breed remains in a closed registry, the lower their genetic diversity inevitably becomes.
This type of system necessitates all dogs within a breed to ultimately descend from the same small group of ancestors, meaning they are all related to each other by varying degrees. Since they are related to each other, breeding them is always inbreeding, though the degree of inbreeding varies with the number of common ancestors two dogs share and how recently in their pedigree these common ancestors appear. Using breeding techniques like popular sires can rapidly increase the level of inbreeding found in a breed, as it widely distributes the genes of single dog throughout many bloodlines so many pedigrees will have this dog as a common ancestor, sometimes to the degree that it’s difficult or impossible to breed two purebred dogs without having one of these popular sires in common.
Though it typically has a very negative connotation, inbreeding has benefits in addition to risks. On the plus side, inbreeding can be used to “fix” traits in dogs which makes breeding them more predictable. This is the reason that you can be sure that by crossing two German Shepherds, you’ll get more German Shepherds but never run the risk of a Poodle or Corgi popping up in a litter. However, the genetic basis for this increase in predictability is the same reason inbreeding has negative effects, so it’s a double-edged sword. The scientific name for this underlying genetic principle behind both the pros and cons of inbreeding is homozygosity.
Homozygosity describes the state of a gene which has two of the same alleles, and is the opposite of heterozygosity which is the state of a gene having two different alleles. In simple Mendelian terms, if a dog is heterozygous for a gene, the dominant allele will be the one that is expressed (generally speaking, though there are some exceptions in which expression is more complex and may be a mixture of two alleles), while recessive traits can only be expressed if a gene is homozygous for the allele responsible for that trait. It’s possible to determine an animal’s overall level of homozygosity, and even the level of homozygosity of an entire population by measuring the overall number of homozygous genes. If this level is high, then the genetic diversity of those animals is low as a direct result due of this lack of variation. The higher the level of homozygosity in a population, the more predictable the genotypes of any breeding within that population will be due to the lack of genetic variability, which is why inbreeding leads to an increase in predictability of offspring.
This is a fairly abstract concept that may be difficult to grasp, so here’s a simple, concrete example from real dog breeding. In dogs, there are two alleles for the gene that produces either black or chocolate/liver coat: B which is dominant and produces a black coat, and b which is recessive and produces a chocolate coat. In Labradors, both black and chocolate are acceptable colors and therefore both alleles are found within the population. If you cross two Labs whose genotypes at that locus are Bb and Bb respectively (heterozygous), each puppy in the resulting litter has a 75% chance of being black (either BB or Bb) and a 25% chance of being chocolate (bb). Though you can predict the probability of getting either a black or chocolate dog through this mating, you cannot predict for certain the actual outcome of it as it’s all up to chance how the genes randomly assort during meiosis. It’s statistically possible, though unlikely, to produce a litter of 12 puppies through this mating which are all black. The fact that the parents are heterozygous at this locus means that inheritance is ultimately left up to chance.
However, there are some breeds where chocolate is the only acceptable color, so the allele for black has been bred out of the population. An example would be the Chesapeake Bay Retriever. In this breed, you can cross any two random dogs, whose genotypes must be bb since they’re chocolate, and the resulting puppies will have a 100% chance of being chocolate. The fact that that locus is homozygous for chocolate in every Chessie means that the coat color of all Chessies is extremely predictable, barring a rare spontaneous mutation which happened to affect coat color. This is an example of a trait that has become “fixed” within a population, meaning every animal carries the same alleles for that trait with little or no variation within the population. Not all traits are inherited so simply as this example, but the principle is still the same when extrapolated to many genes rather than just a single one: homozygosity leads to much better predictability than heterozygosity when breeding any two animals.
Since a dog’s physical appearance is controlled by a relatively small number of genes, it’s not difficult to achieve a fairly consistent, predictable breed type by breeding for homozygosity for those traits. The problem with this is the fact that by breeding a dog which has these desirable traits, it’s impossible to select for only those desirable genes. When you breed a dog, you’re passing on all of those dog’s genes to their offspring; conversely, when you choose to eliminate a dog as a breeding candidate, you eliminate all of that dog’s genes as well. It’s an all or nothing process. Therefore, when linebreeding (a form of inbreeding involving the mating of close relatives) is used to fix certain desirable traits within a population, many other genes may also become fixed unintentionally as well. And when a popular sire fathers dozens of litters, all of his genes become widely distributed throughout the population as a result. While a dog may have many highly desirable traits, he will also inevitably carry some deleterious genes which will be passed on when he is bred.
A good tool for better understanding the full impact of how selecting for homozygosity in desirable genes will also lead to homozygosity all other genes, including deleterious ones, is a calculation called the coefficient of inbreeding (COI). As the level of inbreeding in an animal or population increases, so does the COI. For example, if two cousins who share the same grandparents (who are unrelated to each other) are bred, the COI of their offspring will be 6.25%. If two dogs with no common ancestors are bred and then one of their offspring is bred back to a parent, the COI of the offspring will be 25%.
Since COI is calculated according to the total number of common ancestors an animal has, it can accumulate through the generations and can even reach levels which are unachievable through any single, isolated instance of inbreeding. For instance, the Nova Scotia Duck Tolling Retriever has an average COI of 25% for the entire breed, the same COI that would result from a father-daughter mating. Obviously, not every Toller is actually the product of a father-daughter mating. On the surface their pedigrees may not appear very inbred, but on a genetic level their level of homozygosity is indistinguishable from father-daughter offspring. Since inbreeding trends tend to be high around the time of a breed’s founding, it’s vitally important to get as complete a pedigree as possible in order to calculate an accurate COI. Shallow and incomplete pedigrees can easily obscure a dog’s true level of inbreeding.
While most breeders are aware of COI and how it relates to measuring levels of inbreeding, fewer understand what the actual percentage derived by this equation really means. When a COI is calculated, the resulting percentage is the probability that an animal will be homozygous for any of its genes due to common descent (the calculation cannot predict those genes which will be homozygous but not as a result of common ancestry, so the actual homozygosity may be higher). Therefore a dog with a COI of 25% has a 25% chance of being homozygous at any locus. The dog may be homozygous for a gene which produces the desired coat type for their breed, but they have an equally good chance of being homozygous for a gene which causes congenital heart disease.
While inbreeding is the most salient factor responsible for high levels of homozygosity in purebred dogs, there is another, more easily overlooked factor which is just as important: the founder effect. As previously mentioned, all pedigreed dogs trace their lineage back to the founders of their breed. In practice, this means thatall the possible genetic variation found within a breed is that which was present in the breed’s founders. Compared to the total number of dogs in the world at the time of a breed’s founding, the number of founders per breed represent only a minuscule fraction. This is why the founder effect is considered a type of genetic bottlenecking, which dramatically reduces the genetic diversity within a population by limiting the number of breeding individuals that will pass their genes on to their descendants.
While genetic bottlenecks greatly reduce genetic diversity, and thereby increase homozygosity, in and of themselves, there are additional factors that make this effect even more pronounced within dog breeds. Firstly, the founders of a breed may all be related, resulting in a higher degree of homozygosity between them. For example, the Norwegian Lundehund has 5 founders, but all 5 founders shared a grandmother and 3 shared a mother. Right off the bat, the bar is set for a high COI and small gene pool for the entire Lundehund breed.
Secondly, due to selective breeding performed after the founding of a breed, some of the genetic variation that was present in the founders will be inevitably lost from the population. Additionally, the genetic contributions made by each founder are often very unequal which further minimizes genetic diversity. An example of this is the Nova Scotia Duck Tolling Retriever. Though the breed had 22 actual founders, through selective breeding, enough genetic diversity has been lost that the effective number of founders has been reduced to 9.8. Furthermore, 50% of genes in all Tollers were contributed by a mere 2 founders, boosting the breed’s overall level of homozygosity far beyond that which would occur if every founder had made an equal genetic contribution to the modern breed. According to a recent study, about 90% of the Toller’s initial genetic diversity has been lost. Similar findings have been made in a variety of purebred dog breeds.
Once a population reaches a significantly high level of homozygosity, additional factors of population genetics come into play which can create a snowball effect for rising homozygosity levels, increasing the population’s risk for inheriting recessive disorders, and sometimes even causing a disease to become a fixed trait. These effects are based in the way which homozygosity affects the effective population size (Ne) of a breed.
While a breed may contain many registered dogs (the actual population size), this does not accurately predict the breed’s effective population size. For one thing, effective population size takes into account only those individuals which will actually genetically contribute to the next generation, so only those dogs which will be bred can count toward the breed’s effective population size. Additionally, effective population size does not measure all these animals as equal individuals but only the approximate genetic variation present in the population sufficient enough to account for genetically distinct individuals.
Therefore, if a breed has a large number of animals which will be used for breeding but these animals have a high average level of homozygosity, the Ne will be significantly lower than the real number of breeding animals. A breed which has a small but genetically diverse breeding population will have a higher Ne, possibly even higher than an inbred breed with hundreds or thousands more individuals in their breeding population. Quite a few dog breeds have the unfortunate combination of a small breeding population that is also highly homozygous, which can lead to a tiny Ne. The smaller the Ne of a breed, the faster inbreeding trends will accelerate, leading to a rapidly shrinking gene pool.
Having a small Ne has several negative consequences besides accelerating inbreeding. Firstly, it makes a population especially vulnerable to a phenomenon called genetic drift. Genetic drift is an evolutionary force which causes shifts in allele frequencies within a population. These shifts can be caused by numerous factors including genetic bottlenecks, selective pressure, and random chance due to the nature of Mendelian genetics. Genetic drift is unavoidable and can cause various effects by altering allele frequencies (how common a certain allele is within a population), including the permanent loss of alleles from a population. This can also cause certain genes which are not typically associated with each other to become invariably inherited together through an effect called linkage disequilibrium.
Linkage disequilibrium can also be created via selective breeding. For example, there may be a successful show dog that carries a desirable trait for an unusual coat pattern; however, he also invisibly carries a rare recessive gene which causes congenital heart disease. If that dog is then widely bred in order to distribute the desired coat pattern into his breed, the disease-causing gene will also become widely distributed throughout the population. The dog’s descendants also have this desirable coat pattern, and are bred to distribute the first dog’s genes even more widely throughout the population. This pattern of disseminating the first dog’s genes continues through several more generations.
Eventually, once the first dog’s genes become prevalent enough throughout the population, some of his descendants will be mated with each other and produce offspring with congenital heart disease. If the majority of dogs with the first dog’s unusual coat pattern descend from that first dog, there is a high likelihood that all dogs with that coat pattern will also carry the gene causing heart disease. Though there is no true biological reason for the gene causing the coat pattern to be associated with the gene causing heart disease, since all dogs carrying the coat pattern are descended from a dog which also carried the mutation causing heart disease, there is “suddenly” an association between the two genes. The two genes are considered to be in linkage disequilibrium. Unless a genetic test is developed which identifies the gene responsible for causing heart disease which allows breeders to prevent mating dogs which both carry the gene, there will always be a high risk of a dog with the coat pattern developing heart disease or producing offspring with heart disease. However, evenwith a genetic test, it would be difficult or impossible to “breed out” congenital heart disease from the affected lines without also eliminating the trait of the desirable coat pattern, due to linkage disequilibrium.
This is one of several major causes of inherited diseases in purebred dogs, and in some cases a disease can become fixed for an entire breed. This is what has happened in Dalmatians with kidney disease. A particularly good example of this effect is the Basenji. As a breed prone to progressive retinal atropy (PRA), when a genetic test was developed for PRA, Basenji breeders made incredible efforts to completely breed out the disease by eliminating all carriers of the PRA gene, even those which were unaffected, from their breeding programs. Unfortunately, what breeders didn’t realize is that the only lines of Basenji which didn’t carry the gene for PRA happened to commonly carry a gene which caused a devastating kidney disease called Fanconi syndrome. Therefore, when breeders stopped using dogs that carried the gene for PRA and exclusively bred those which were tested clear for that disease, the entire breed suddenly became fixed for the genes causing Fanconi syndrome. The breed was at risk for extinction due to how widely spread and severe the disease became, but was saved by crossbreeding with Basenji-like dogs imported from the breed’s native Africa which did not carry the disease-causing genes. Though there was no underlying biological reason for all PRA-clear Basenjis to carry the genes for Fanconi Syndrome, via linkage disequilibrium the two traits became associated and nearly caused the extinction of Western pedigree Basenjis.
While selective breeding can inadvertently create linkage disequilibrium between desirable traits and genetic diseases, as previously mentioned, genetic drift also plays a large part in the process. While proper management of breeding techniques, such as avoiding linebreeding and using popular sires while striving to maintain genetic diversity, can potentially reduce the risk of this happening due to selective breeding, it is impossible to stop the effects that genetic drift has upon a population, which can be potentially disastrous.
A population with a large Ne is only minorly affected by genetic drift. Since there is a good amount of allelic diversity distributed fairly evenly throughout the population, even if many of that population’s individuals fail to reproduce due to a dramatic random event like a natural disaster, the overall genetic diversity and allele frequencies of the population will not be so greatly affected.
The opposite is true for populations with a small Ne. In such a population, a rare allele may only be present in a very small handful of individuals, so if the population undergoes even a relatively minor culling, there is a good chance that those rare alleles will be permanently lost from the population. Consequently, these populations are inherently at greater risk for loss of genetic diversity, which may be sudden and dramatic or a more subtle process which takes place over a long period of time.
As more and more alleles are lost, the homozygosity of the population increases, which then reduces the Ne. The smaller the Ne, the more vulnerable that population becomes to the effects of genetic drift, which in turn causes even more loss of genetic diversity. If the Ne becomes small enough and the level of homozygosity high enough, this creates a negative feedback loop of accumulating gene loss that spirals down until the population becomes extinct. This downward spiral is called the extinction vortex, and once a population enters this vortex, it’s very difficult to break the cycle.
Besides genetic drift, there is another factor which creates this deadly cycle which is also illustrated in the graph above: inbreeding depression. Inbreeding depression is the negative impact which a high level of homozygosity has upon reproductive fitness. As previously discussed, though inbreeding is a major cause of homozygosity, it’s not the only factor involved, so the name “inbreeding depression” is somewhat misleading as it refers to negative effects caused by homozygosity in general, not just those due to inbreeding.
The factors which contribute to inbreeding depression are classified into two distinct groups: dominance andoverdominance.
Dominance is the name given to all detrimental effects on health caused by recessive mutations. Since recessive alleles are invisible in a heterozygous state and cause little or no harmful effects unless they are doubled up in a homozygous state, they are easily unintentionally spread throughout a population by selective breeding.
There is no such thing as a truly 100% genetically healthy dog, even though he may be phenotypically very healthy. All organisms, including dogs, carry some deleterious genes regardless of how healthy or genetically diverse they may be. Houseflies carry on average ~1.6 recessive lethal mutations per individual; in humans, this number is ~0.29. Estimates for the average number of deleterious non-lethal genes carried per individual are much higher, being about 4-6 in humans. Additionally, new harmful genes can appear at any time through spontaneous mutation, even within a closed population.
Though a small handful of these harmful genes can now be identified via genetic health testing, it is inadvisable to prevent all dogs carrying these genes from breeding altogether due to the risk of creating a situation similar to what occurred with Basenjis and Fanconi Syndrome. The cost of lowered genetic diversity is not worth the benefit of eliminating a single harmful mutation from the population. Therefore, it’s unrealistic to believe that these harmful recessive mutations can truly be bred out of any breed without causing additional health problems as a result. Once a deleterious gene has reached a high enough prevalence in the population to become a noticeable problem resulting in the development of a genetic test, it is probably too widely distributed to fully eliminate without causing a dangerously precipitous reduction to the breed’s gene pool.
Additionally, many health problems common in dogs such as hip dyslpasia, epilepsy, and increased risk of cancer are polygenic (controlled by the interaction of numerous genes) and these deleterious mutations have an additive effect (numerous genes interacting with each other to increase the severity of an inherited disorder). Due to their complex means of inheritance and expression which remain poorly understood, conventional health testing is ineffective at preventing these types of diseases. Though phenotypic tests are available for some of these conditions such as hip dysplasia, these tests have proven to have little or no predictive value useful for preventing the disease in a dog’s offspring.
As previously mentioned, every animal carries several harmful genes, so recessive, disease-causing mutations are neither rare nor unique and every animal must be considered a potential carrier for genetic disease. However, it’s apparent from real life examples that individual animals in a population can carry several deleterious mutations while the overall population remains quite healthy and has a relatively low risk for developing congenital disease. On the other hand, some populations, like purebred dog breeds, have a much higher than average risk for congenital diseases.
The underlying reason for this ties back into the overall homozygosity of the population. In a population that is highly heterozygous with a large degree of genetic diversity, the statistical probability of two animals carrying the same recessive allele mating and producing affected offspring is low. However, in a highly homozygous population where many of the animals carry the same genes with little variation, the chances of producing diseased offspring is significantly higher. This is why wild animal populations generally tend towards higher levels of heterozygosity under ideal conditions. The same is true for feral, free-ranging street dogs, which genetic analysis has shown to be quite heterozygous in contrast with purebred dog populations.
The bottom line is that it’s impossible to keep all recessive, disease-causing mutations out of any population. Therefore, the only way to prevent epidemics of genetic disease is through effective management of the population’s genes so as to maximize genetic diversity and thereby lower the risks of inherited illness.
The second factor which contributes to inbreeding depression is overdominance. Unlike dominance, overdominance is caused not by the effects of deleterious mutations but by the effects of two alleles which function well independently but actually provide greater benefit to the animal when they’re present together in a heterozygous state. Another name for this effect is heterozygote advantage, since heterozygotes for the gene will have greater reproductive fitness than homozygotes for either of the two alleles involved.
A real life dog breeding example of heterozygote advantage is found in Whippets. Some Whippets carry a mutated version of the myostatin gene, which affects muscling. Dogs which are heterozygous for this allele are significantly faster than dogs which are homozygous for the unmutated allele. However, dogs which are homozygous for the mutated gene are overmuscled, producing “bully Whippets” with massive muscles that are so large that they’re actually detrimental to the dog’s speed and racing ability.
One vital biological function which is greatly affected by overdominance is the immune system. In dogs as in other vertebrates, the immune system is responsible for defending the body from foreign invaders like viruses and infections. If an immune system is weak, it will be unable to fight off infectious diseases effectively. Furthermore, a dysfunctional immune system may fail to successfully distinguish between foreign cells and those belonging to an animal’s own body, causing the immune system to attack the body it’s supposed to protect.
Those genes which are responsible for encoding the function of the immune system belong to special set of genes called the major histocompatibility complex (MHC), and in dogs these groups of genes are commonly referred to as dog leukocyte antigen (DLA) haplotypes. A haplotype is a collection of individual genes which are commonly inherited together, which is true of MHC genes as they are rarely inherited individually. Though the mechanisms responsible for building a healthy immune system are currently poorly understood, one known fact is that genetic diversity is vital to a high-functioning immune system.
Unlike typical deleterious traits, autoimmune diseases are rarely connected with a single problematic haplotype. When associations are found, it’s inadvisable to attempt to breed out that haplotype since the interaction between DLA haplotypes is complex and certain DLA haplotypes have been found to have both deleteriousand beneficial genes. Since genetic diversity is key to a healthy immune system, breeds with only a few, unevenly distributed DLA haplotypes rather than many, evenly distributed DLA haplotypes are especially prone to immune-mediated diseases. Several examples of this include Norwegian Lundehunds, Nova Scotia Duck Tolling Retrievers, and Italian Greyhounds. Once immune problems develop in a breed, they are extremely difficult to eliminate.
Dominance and overdominance have a synergistic effect on reproductive fitness and together produce the effect known as inbreeding depression. In populations with high levels of homozygosity, dominance lowers reproductive fitness by introducing genetic diseases and other harmful effects through the homozygous state of deleterious genes while overdominance lowers reproductive fitness by limiting an animal’s fitness potential through a lack of heterozygosity for specific alleles. Together, they highlight the importance of maintaining a high level of genetic diversity in a population to ensure maximum health and performance as well as long-term survival.
It’s all well and good to discuss the underlying factors which cause inbreeding depression, but what kind of measurable effects does inbreeding depression cause in dogs specifically? Here are several graphs from studies on inbreeding depression in dogs which demonstrate some of its effects:
In this study, inbreeding in Standard Poodles was associated with shorter lifespan and higher risk of dying from bloat.
In this study, inbreeding in Bernese Mountain Dogs was associated with decreased longevity.
In this study, inbreeding was associated with smaller litter sizes and shorter lifespan in several breeds.
This study also found that inbreeding was associated with smaller litter sizes in several breeds.
Overall, high levels of homozygosity leading to inbreeding depression causes numerous harmful effects including:
reduced fertility both in litter size and sperm viability, developmental disruption, lower birth rate, higher infant mortality, shorter life span, increased expression of inherited disorders, reduction of immune system function and cancer.
With all this in mind, you may be wondering how to remedy inbreeding depression to avoid these nasty consequences and prevent a breed from entering the extinction vortex. Since inbreeding depression is caused by a high level of homozygosity, the answer lies in increasing genetic diversity.
However, since breeds within a closed registry system get all of their genes from the breed founders, no new genes can be introduced which leads to an inevitable loss of genetic diversity over time. While mutations can potentially introduce new genes into a closed population, the mutation rate is far too slow to keep up with the intense selective pressure exerted by dog breeders in order to restore this much needed genetic diversity. In some breeds, their subpopulations are genetically isolated enough that outcrossing between them can provide a modest boost to the breed’s average heterozygosity. Unfortunately, the most effective solution, and in breeds with dangerously small gene pools the only solution, is also taboo among many purebred breeders: crossbreeding.
This is where this detailed analysis of the wide-reaching effects of homozygosity ties back into our original topic of heterosis. Every factor previously discussed which leads to inbreeding depression in dogs also leads to hybrid vigor in crossbreeds. Since homozygosity and heterozygosity have a direct, inverse relationship with each other, inbreeding depression cannot cause detrimental effects without heterosis causing beneficial effects; one cannot be true without the other. Where homozygosity leads to lower reproductive fitness, heterozygosity leads to the opposite. With greater genetic diversity, a population is overall less prone to inherited disease and less vulnerable to being driven into the extinction vortex whether by selection or random chance, all while having greater reproductive success, longer lifespans, and healthier immune systems.
Since crossbreeding involves interbreeding between genetically isolated populations, it will always introduce greater genetic diversity into the offspring of the cross than was present in the parents individually. Some crosses will introduce more diversity than others depending on how extensively and recently the two dogs shared common ancestors, but nevertheless, all crosses will produce more genetically diverse offspring. This is true for all outcrossing of genetically distinct populations, whether the cross involves totally separate breeds, geographically separated subpopulations of purebreds, or distinct, genetically isolated bloodlines within a breed.
What of the initial commenter’s concern about crossbreeding leading to dogs that inherit double the defects of their parents? Well, the same rules of population genetics apply to purebreds and crosses alike. Recessive and additive disease-causing genes are only a concern when a population becomes saturated with these genes. If the two breeds involved in a cross are not both already saturated with these genes, then the chance of an F1 cross being affected is very low especially when compared with the chance of purebred offspring being affected by that same deleterious gene which has become common in its breed. Health issues “doubling up” is only a concern when the offspring of an F1 cross are interbred with a breed or population where the genes responsible for the disease are already common, whether through inbreeding or poorly planned backcrossing. If a disease is polygenic and/or additive such as hip dysplasia, the offspring may indeed inherit some level of the disease if bred from an affected parent. However, on average these offspring will be less affected by the disease than the purebred offspring of the affected parent. If a disease is caused by a dominant mutation, then the parent will be affected and should not be bred, regardless of whether the mating would involve crossbreeding or purebreeding.
Many people misunderstand hybrid vigor to mean that crosses or mixes will always be healthy and totally free from congenital defects. However, it’s important to remember that as with everything else in genetics, it’s a matter of probability. It’s statistically inevitable that some crosses and mixes will suffer from health problems due to genetic factors. However, anecdotes of mixed breeds with poor health do not negate the fact that on average, mixes and F1 crosses especially have a lower risk of inherited disorders than purebred dogs.
As always, breeding from diseased stock is overall more likely to produce diseased offspring, regardless of whether the offspring are crosses or purebred. Crossbreeding breeding stock with poor health does not automatically create offspring with perfect health. Even so, contrary to the original comment’s assumption, there is certainly not a greater propensity toward genetic disorders that is inherent in crossbreeding compared to traditional purebred breeding.
The bottom line is that highly homozygous animals have a higher probability of suffering from the negative effects of inbreeding depression than animals with a greater degree of heterozygosity. Purebreds, crosses, and mixes alike are all affected equally by this principle. Ultimately, maintaining genetic diversity for maximum health should be one of every dog breeder’s most important goals. Even the best health screening ultimately cannot emulate the major benefits of genetic diversity on canine health, and any breed or population whose diversity is allowed to be continually lost is at risk for future extinction.
To learn more on this topic, I highly recommend taking the Institute of Canine Biology’s course on Basic Population Genetics for Dog Breeders.