There is no clear separation between inbreeding and linebreeding. Both terms are used to describe having the same ancestor on both the top and bottom of a pedigree (on both the sire and dam side), typically within the last few generations.
in·breed·ing [in-bree-ding]
noun Biology
the mating of closely related individuals, as cousins, sire-daughter, brother-sister, or self-fertilized plants, which tends to increase the number of individuals that are homozygous for a trait and therefore increases the appearance of recessive traits.line·breed·ing [lahyn-bree-ding]
noun Genetics
a form of inbreeding directed toward keeping the offspring closely related to a superior ancestor.
Linebreeding is a form of inbreeding and its goal is the same, to increase the appearance of recessive traits that are manifest within a desired ancestor by increasing homozygosity in the offspring. Linebreeding is only effective because it increases homozygosity, that is the mechanism through which it works to “fix” traits. Homozygosity is directly causative to recessive allele expression. Homozygosity “fixes” recessive traits without distinction to their merits. “Good” and “bad” alleles are doubled up just the same and at random.
Just as linebreeding is only as effective as its ability to fix desired recessive traits by making them homozygous, linebreeding is only as dangerous as its ability to fix undesired recessive diseases by making them homozygous and the limiting of diversity in the MHC. Therefore, linebreeding will always have benefits and risks that are in proportion to the closeness of the breeding and the resulting level of homozygosity. If you breed closer to fix more traits you also increase the risk of expressing recessive disease. This is not to say that the benefits are equal to the risk, a close breeding might be done to “fix” some superficial physical traits that have no utility save fashion and have no impact on performance or health, but in doing so the chance of expressing recessive deleterious disease traits is also greatly increased.
Moral people would not weigh fixing of superficial traits as an equal benefit to offset the expression of a horrible disease. But again and again we observe in the world of purebred dogs people who take the risk for purely cosmetic reasons and their dogs who suffer heavily for it.
While parts of the genome are not specifically more dangerous when they are homozygous, it is certain that the Major Histocompatibility Complex (MHC), which codes for immune response, is greatly disadvantaged by being in a homozygous state: impairing immune function and increasing autoimmune disease result. Deleterious mutations are also a random and constant occurrence in all life, and all recessive disease alleles can hide within lines and populations for many generations before they are doubled up by inbreeding. This “genetic load” is an unknown quantity as we do not have tests for every disease gene, nor have we even identified them all (or most). We have only identified a small fraction of disease causing alleles. There are hundreds of millions of dogs in the world, and almost 100 million in the US alone, and each of those dogs have new mutations that are unique to them and many more mutations that were new to their parents and grandparents. There are potentially hundreds of millions of unidentified mutation alleles and yet we have DNA tests for fewer than 200 diseases and many breeds have no breed-specific DNA tests at all.
For all we do know, we are still in a profound state of ignorance. And while helpful, testing is no panacea to compensate for continued over-use of linebreeding, inbreeding, and closed stud books.
With both inbreeding and linebreeding: the greater the benefit, the greater the homozygosity, and the greater the risk. And it is a risk that we can not hope to mitigate fully with any sort of disease testing. Nor can it be mitigated with pedigree research or “knowing your lines.” You might be able to dodge one or two known issues that other breeders have been open about, but we must admit that we don’t know anything about 99% of our dogs’ genetics. We can know a few things about their size and color, a few things about the disease history of some of their ancestors, but at most this accounts for a few dozen genes. Dogs have tens of thousands of genes.
How “close” a breeding is can be measured using the Coefficient of Inbreeding, abbreviated COI. Depending on how many ancestors are in common and how far back they are and how inbred they were themselves, different ancestry patterns can create the same level of homozygosity for a trait in the offspring. For example, a half-sibling mating has the same COI and the same level of increased homozygosity as an Uncle-Neice/Aunt-Nephew breeding. Both have a COI of 12.5%. Brother-Sister breeding and Parent-Child breeding are different but both have a COI of 25%. A COI of 25% means that on average 25% of the offspring’s alleles are going to be in a homozygous state (like-pairs) based only on the pedigree information we’ve used in the calculation. This is referred to as “identical by decent.”
Whereas COI only accounts for homozygosity created by recent generations, all dog breeds have a “background” level of homozygosity which is the result of breed formation and a history of discarding genetic diversity by choice and by consequence of a limited number of founders, popular sires, only breeding a few dogs each generation, quickly purging disease carriers out of the gene pool, and the prior fixation of traits like color or hair length. This existing level of homozygosity makes further linebreeding even more problematic as far as disease expression. This homozygosity is referred to as “identical by state.”
When linebreeding more alleles double up than the ones we wish to fix. In fact many times more. There are more recessive genes that cause disease than we have tests for. We can not test for every disease. And we have no idea about new mutations. When we double up huge swaths of alleles for the sake of aesthetics or performance we create collateral damage. And this is how recessive disease becomes prevalent in lines and breeds and why dogs have rates of disease expression that are epidemic compared with other species.
As the genetic load of more than a century of closed stud books and breeding behaviors that increase homozygosity and decrease what genetic diversity remains takes its toll, more and more breeds are now finding themselves plagued by epidemic levels of inbred disease. Linebreeding as the go-to strategy to win ribbons and “improve” breeds is doing the opposite of improvement. Not only do we need to open stud books and make routine introduction of new blood a part of the culture of dog breeding, we also need to promote effective breeding strategies that still result in fixing desirable traits without compromising the immune systems and without inflicting such high levels of disease on our dogs. One such strategy is called “Assortative Mating” where breeding stock is chosen because of its likeness in the traits we desire without being closely related. Breed two fast dogs together instead of two fast siblings. Breed a dog with the desired ear-set to another dog with the desired ear-set, but not father to daughter. And if that fast dog or perfectly eared dog is from another breed, by all means include it in your breeding program.
We can have predictability without sacrificing health. Do the work to find appropriate stock outside of your own kennel instead of promoting recessive disease expression though incest.
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The problem in dogs is this quest of individual excellence at the expense of sound population genetics. When we have the same values applied to dog breeding that we would give a football game, that is the very moment we stop breeding animals and start breeding to satisfy one’s own ego.
This is the big problem with dogs. No one wants to say it, but the entire values system of breeding dogs for competition is what is destroying them.
This wouldn’t be so bad if dogs were all bred like lurchers or the way retrievers used to be bred, but within closed registries or registries that allow in only a little bit of new blood at a time, it’s a disaster that just gets worse every time.
The notion that you can just breed out all the diseases in an inbred population of dogs is lunacy of the worst order. If there were a genetic test for everything and you could breed it all out, every one of those disorders that gets expressed is likely very close on the chromosome to something your probably don’t want to breeding out at all.
Dog breeders who claim to be able to do this actually think they know more than the best geneticists in the world. If they only understood this, they would be much more willing to question the system we currently have.
But that requires critical thought, and it will make the mandarins angry.
So best not to think about it and continue on chopping away at gene pools and blaming it all on vaccines or dog food.
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Christopher, you write of ‘Assortative Mating” and suggest using dogs that are not closely related. So what is your definition of ‘closely related’ in that context? In breeds with only a few founders all the dogs will be related so even assortative mating would involve related dogs.
Is it inevitable that a numerically small breed can only go downhill healthwise or does the content of the genomes of the original founding dogs play a part, so different breeds would vary?
Well in some sense we can say that almost all breeding within a breed is “inbreeding” or over time eventually will be because we do not have an infinite number of founders and eventually we will have the same founders on the top of the pedigree as the bottom. But this is better treated as an issue of “Founder Effects” than inbreeding because the similar relationships are more distant.
And distance helps us. Not only are we less likely to double up on a great proportion of alleles with distance, we also have all that distance to select AWAY from the bad things that do crop up. The only way to know if we’ve dodged the bullet, so to speak, is to see what we’ve produced and how they lived and died. And that takes time and a lot of record keeping. While it’s not always done, or done well, at least time will out some (if not all) of the problems and we can breed away from them.
The closer the breeding, the less time we have to discover the new issues and breed away from them.
As far as small number of founder breeds go, that’s a bit different and worthy of its own post but I’ll try and be succinct here. A small number of founders is almost always a death sentence for a breed. Biologists speak of minimum viable populations and those numbers are at minimum in the 500-1000 range and often MUCH higher. Small breeds simply do not have enough genetic diversity going in to be sustainable for long.
Adding to that the fact that most small breeds STAY small. This is a problem because the only way to even attempt to survive a small number of founders is to preserve as much diversity as possible (unless you do the smart thing and bring in other breeds! But few want to do that, sadly). This requires LOTS of puppies. You basically need to have every single stud bred to every single bitch and then all those puppies need to pass along their genetics as well.
If you only have one child, you’ve only passed along 50% of your genes. If you only have 2, you’re about 75%. Three gets you to 87.5% on average. AND those children need to have lots of children too just to keep your genes in the gene pool.
And that never happens with small founders. I’ve never seen a small breed where they round-robin bred the founders with each other and kept a lot of children breeding. So much of the founder population is just LOST after the first two or three generations.
An interesting paper you might want to look at is Katariina Maki’s work on the Lancashire Heeler and Nova Scotia Duck Tolling Retriever. She covers this issue.
http://www.instituteofcaninebiology.org/7/post/2012/04/population-genetics-suggests-dire-straits-for-tollers-and-heelers.html
While you are absolutely correct that the composition of the founders will lead to different results, it’s very hard to overcome the genetics of small populations. Many many more species have simply gone extinct rather than survive bottlenecks and small founder populations and those that have survived often had protected status within their ranges. Like living on an island with no predators or being an apex predator, etc.
And sadly, many of those that have survived are one bad virus away from going extinct, still. Like Cheetahs.
There are dog breeds that physically would go extinct tomorrow if man stopped helping them whelp, like bulldogs. There are also breeds that would genetically be dead ends save for modern medicine and a ton of effort to sustain them in their genetic decrepitude.
http://www.border-wars.com/2012/01/those-inbred-lab-mice.html
If you’re bringing in a dog for heterozyosity (hybrid vigor) the only way you’re going to get problems from genes not in your population already is if you later INBREED on this dog again. Duh. Problem with inbreeding, not outcrossing. AND, I’ll note, that if the genes are recessive and new to the breed, they are EASY to remove by drift alone, let alone selection.
The notion that new blood is somehow contagious and is going to spread like wildfire through a breed is just INANE, although that doesn’t stop people from making that claim.
Much of this is good science & a reasonably easy way to follow genetics but a few areas need some additional clarification. You can line breed to fix good traits as in health, etc as well as bad traits. Recessive traits are not necessarily bad though many of them are (some might argue most). Line breeding can fix dominant traits as well as recessives- you just may not have an easy way to tell if you have homozygous dominants or heterozygous dominants.
Also, outbreeding may bring in new & “bad” recessives.
Breeding dogs is fraught with hazards & not for the faint of heart 🙂
You can’t “fix” health. Health is not a positive quality, it is the LACK of disease. And inbreeding on “health” is truly a losing proposition because you not only destroy hybrid vigor, you cripple the immune system.
You can also “fix” good traits by SELECTION instead of close breeding. You can breed fast to fast, tall to tall, long haired to long haired. Assortative mating.
Recessive traits are NOT necessarily bad. But they are often caused by breaking some normal extant process in the body.
http://www.border-wars.com/2011/03/recessive-means-broken.html
And yes, you CAN fix dominant traits as well, but normally you don’t NEED to “fix” dominant traits because they appear even in heterozygous form and thus they are rather easy to track through your lines and puppies and they don’t NEED to be homozygous. Sometimes, they are actually lethal in homozygous form and thus CAN’T be fixed.
http://www.border-wars.com/2011/07/something-is-rotten-in-harlequin-danes.html
and
http://www.border-wars.com/2011/03/the-unfortunate-case-of-the-wild-australian-shepherd.html
And yes, you can “introduce” bad recessives by outcrossing. But they will only be expressed if you INBREED on them after they are introduced. So this is clearly a problem with INBREEDING and LINEBREEDING, not with out-crossing. If you outcross wisely, you keep the heterozygosity and don’t then inbreed on it again. So you don’t actually RAISE disease expression even if you are introducing different and potentially problematic recessives.
The winning strategy is to NOT express those in the first place. Thus you keep them rare and hidden.
And just because breeding is hazardous doesn’t mean we can’t be RISK AVERSE and still effective.
Current popular breeding methods are RISK SEEKING. This is not a wise strategy, despite the cultural popularity. Russian Roulette went out of fashion for much the same reason.
Pardon dumb questions, but I’m confused. As I understand it, you can’t have heterozygosity without recessive genes. In theory, a population with no ‘broken’ recessive genes would be entirely homozygous, no? Wouldn’t a count of recessive alleles be more useful than a measure of hetero-/homo- zygosity? Isn’t diversity bad if it is imparted by proliferation of recessives?
Or is there a bigger picture in which relatively rare benign or advantageous mutations creep into populations over millennia, creating evolutionarily advantageous diversity? Eg, genes that favor light colors over black may help a population move into niches like diurnal hunter in open grassland or snow.
Not really. We all have a ton of recessive, some of which are really bad for us. But they are almost never expressed because don’t have close breedings The problem with dogs is that when you have close breedings, you increase the likelihood of bad recessives being expressed. This is the value of sexual reproduction.
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Maybe a good way to look at it would be to study how hemophilia ran its course in the Russian royal family — that’s a pretty good disease for showing the vagaries of how genes work on an individual, and what can happen when inbreeding is carried too far (it isn’t all readily apparent on the outside, and it doesn’t express itself in a clear cut fashion). The Hapsburg chin is a good example of a cut and dry situation — but often these things don’t make it so readily apparent or easy to track.
Recessive genes aren’t all bad or all good — they have their purposes for nature. But excessive inbreeding/linebreeding essentially increases the odds that a particularly nasty gene expression can get the opportunity to rear its head — to the obvious detriment of an individual.
Get enough individuals suffering from the problem or enough breeding pairs within a population carrying the ability for producing more and more of those individuals, and you have not only a health crises, but the likelihood that a population crash will soon happen due to decreased fertility or just no fertility at all due to premature morbidity taking place.
Just one virus, or nosebleed, away from extinction.
I’d posit that some of the insulin resistance issues we see in some domesticated animals, and people, may have started out as a very smart evolutionary option that has (for now) outlived their usefulness — the “easy keeper” may have been a winning genetic proposition when times were tough, but for modern, developed societies it isn’t.
Another interesting thing to look at may be the Silicon Valley effect that some people are noticing in the children of computer programmers.
Great article. I am the editor for a national breed club newsletter and I would like to contact you privately regarding permission to reprint your article (with full credit to you) in our newsletter. Please email me if you would be willing to discuss that. Erika
I have no problem with the concept that inbreeding increases the probability of doubling up, and hence expression, of recessives. The question is, is homozygosity a good measure of the risk?
Presumably, some fraction of homozygosity is caused by doubling of dominant alleles and some fraction by doubling of recessive alleles. I don’t hear anyone saying the problem is doubling up of dominants.
Elsewhere, Christopher states that recessive means broken, with the caveat that “Recessive traits are NOT necessarily bad. But they are often caused by breaking some normal extant process in the body.” Link to:
http://www.border-wars.com/2011/03/recessive-means-broken.html
If the danger is only, or heavily weighted to, doubling up of recessives, I can’t see how an index, such as homozygosity, that counts the doubling up of dominant alleles equally to the doubling up or recessive alleles, is a good measure of the problem.
To turn the question around, focus on the MHC. If we have an arbitrary gene, A, will, on average, AA be equally deleterious as aa? Is Aa always preferable to AA, or is it pretty much a toss up?
Corillary (sp?) question: Do populations that suffer ill health due to a heavy genetic burden have more total recessive alleles than relatively healthy populations?
Yes. Homozygosity is absolutely a good measure of the risk. ALL measuring risk is either pre-event which entirely relies on probability or post-event which relies on observation of the outcome. With disease in dogs, we can observe the genetics after by DNA study and “observing” which alleles are present. Pre-event you could add specificity to your risk analysis if you have DNA tested the parents, but probability comes into play there as well. Even if it tells you that there’s a ~100% or ~0% chance of passing along a trait to a child (for example if both parents are clear or both are affected).
Um, the focus is on recessives but dominants double up just the same. And um, depending on the expression of the dominants, you absolutely can get problems. And yes, I’ve actually talked a lot about this.
First, the reason we discuss recessives more is because they are NOT EXPRESSED in carrier (heterozygous) status. Thus they can hide, thus they are only a problem when homozygous, thus they are hard to select away from without DNA testing or test-mating or careful tracking of offspring and backward looking analysis to ferret out carriers, etc. For GOOD recessives, you NEED to increase homozygosity to make them express. Some people do this by breeding like-to-like or by testing and breeding carriers or homozygous parents, etc. OTHER people do it more blind by inbreeding. Thus the BREEDING BEHAVIOR of BREEDERS changes between recessive traits and dominant ones.
With dominants, they express in a single form. There’s no way to harmlessly carry them if they are deleterious. They are apparent wherever they exist and they are much easier to select for or against. There’s NO NEED to double up on them unless you want to GUARANTEE that they will be passed on to the offspring. And given that if the allele is dominant AND deleterious it can horribly cripple your population, most breeding schemes axe those out of the population rather quickly.
Now, consider the semi-dominants that I have written SO MUCH about. Merle, Bobtail, Harlequin, Hairless, etc. Those ACT like both dominant traits and recessive diseases. In a single copy you get trait expression but no disease. Doubled up you get an often-lethal disease. ALL the same things I’m saying about recessive allele thus disease expression applies to these semi-dominants. People trying to “fix” the merle color or harlequin color are killing their puppies.
“With dominants, they express in a single form. There’s no way to harmlessly carry them if they are deleterious. They are apparent wherever they exist and they are much easier to select for or against.”
Don’t forget incomplete penetrance.
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Anything with incomplete penetrance is a major challenge and typically requires the sort of data only a research team and large large samples of dogs being tested to even hope to identify and ascertain a gene for. I don’t know that there’s any easy wisdom to pass along here, save that heterozygosity is still more beneficial in those cases because you’ll have something to turn to and increase the chance of clear puppies every litter. It’s just frustrating. Doubling up on dominants with incomplete penetrance is still more likely to cause disease, and even if we don’t know the actual gene or have a test we’re better off outcrossing.
And it can fool you into thinking that you’re dealing with a recessive.
Jess Ruffner recently posted..Afghan Hounds in ‘The Egyptian,’ 1954
I think you’re having a bit of a math fail here. If I say: 50% of both boys and girls will get the flu this year… does it make any sense to say “well since that 50% includes boys it’s totally distorting the true risk of flu to the girls!” Nope.
Well, so does saying “doubling up of dominant alleles is obscuring the risk caused by doubling up of recessive alleles.” Pre-breeding your COI is an estimate of the chance that ANY SINGLE allele (and also the proportion of ALL alleles… but it’s BOTH, not just one or the other) that are going to be placed in a homozygous state from decent.
I conclude I’m going to have to do some basic study in genetics to make sense of this all. I learned some very simple genetics to understand PRA and coat color in Labradors. And I’ve read a few articles on diversity and population health. Then I go back and do my homework as best as can be done with google and come to realize that the ‘dominant’ vs ‘recessive’ paradigm is a gross simplification . . . many alleles are monomorphic, but polymorphic loci are more likely to take many (3+, sometimes a dozen or more) forms as to be dimorphic. Dominance will have a heirarchy among the many morphs, but in many cases the heirarchy isn’t known. Then there’s the question of ‘junk’ DNA that may not be junk after all. My head spins….and I realize I need much broader understanding to say whether homozygosity is a good measure . . . not to mention the question of what sampling procedure is used to determine homozygosity.
I’ve done a fair amount of mathematical modelling; also criticism of mathematical models. If the core conceptualization of a model isn’t accurate, the ice is thin. At this point I don’t understand the core conceptualization well enough to evaluate the value of ‘homozygosity’ as an index.
Still, happy to buy the argument that , if for no reason other than the precautionary principle, inbreeding should be avoided.
btw. it would be interested to know how much of the ‘Fido needs special food’ due to allergies or ‘sensitive’ digestion is due to loss of MHC diversity…though I think science is a long way from being able to answer such questions.
p.s. In the broader picture there’s a lot to reconcile re., genetic exchange. Many plants self-pollinate, and some animals are parthenogenic. Fungi may have dozens of ‘mating-types’, roughly equivalent to sexes. It’s easy to conceptualize alleles as binary. Computer-science loves binaries. But when it comes to alleles, multi and mono are more common than di-morphic. Homozygous when there are two possible states is different to homozygous when there are 43 possible states . . . or only one possible state. And one’s measure of homozygosity must be sensitive to where one chooses to sample the genome.
Understand a very simple– yet very complex– fact.
It makes sense in a type of logic to inbreed and select out traits you don’t want, including disease.
However, it’s not that simple at all. Each diseased gene is not an island unto itself, and many are not caused by one gene but by many.
If you start breeding this way, you may find that you’ve actually removed something important just by breeding out the disease. Or you may have doubled up on something you didn’t know was there, which is what I suspected happened with golden retrievers when they began to breed out the dyplastic hips. Hip dysplasia is much less of a common problem in the breed, but now, it’s cancer.
The best way to manage these kinds of diseases are:
1. Keep very genetically diverse strains. Understand the reason for sexual reproduction. Clones aren’t as able to survive as those with 2N.
2. Stop breeding dogs exaggerations that are so removed from the wolf or wild dog phenotype.
No. 1 deals with genetic diseases.
No. 2 deals with health problems that come about whenever you breed a freak dog.
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Should probably add, keep records and make them transparent. If I want to breed pedigree dogs who are not prone to cancer, it would be very helpful to have several generations of data on what ancestors died of. Diversity alone isn’t going to fix everything.
Should probably add, keep records and make them transparent. If I want to breed pedigree dogs who are not prone to cancer, it would be very helpful to have several generations of data on what ancestors died of. Diversity alone isn’t going to fix everything. Say you have a dominant gene with incomplete penetrance that acts with some other gene to increase the probability of cancer developing. You’re not going to catch that, or fix it, by out-crossing.
Great article but possibly many will not understand what science has discovered as fact.
Major histocompatibility complex (MHC) class II genes are important genetic risk factors for development of immune-mediated diseases in mammals. Recently, the dog (Canis lupus familiaris) has emerged as a useful model organism to identify critical MHC class II genotypes that contribute to development of these diseases.
“Dr. Pedersen has collaborated on a number of studies that have documented genetic diversity within indigenous (village) dog populations across the Middle East, main-land SE Asia, and Island SE Asia and Pacific. It was shown that village dogs in these regions have been randomly interbreeding for 3,000 to over 12,000 years before present and have retained the genetic diversity of the earliest dogs. In contrast, this genetic diversity has been largely packaged into smaller pieces over the last several hundred years within the various modern breeds. The question is whether all of the genetic diversity found in indigenous dogs still exists among the totality of modern breeds, or if a considerable amount has been lost with the extensive inbreeding that has gone into breed development. This research has been reported in the following scientific publications:”
Source:
http://www.vgl.ucdavis.edu/pedersen/canine.php
Christopher,
I have been reading quite a few posts in your blog which I appreciated, many thoughtful, some controversial, some hilarious and many I agreed in essence. I do myself have a prematurely retired border collie (we sold our sheep farm) but kept the dog and an interest for the breed. I would say she was an honest working dog and now she is a very good pet. That is what farmers look for, an honest working dog. Some dairy guys will use their BC to fetch the cows if the dog is calm. But that is beside the point.
I was about to link your very funny piece about BC smugness because many of my acquaintances are farmers who still use working dogs and I thought they would have a chuckle. But I can’t honestly refer to your writings, and here is why. Now, I would not consider myself an expert on dogs but probably an enlighten amateur. You gotta learn something about them if you hope finding a decent one for farm work. Which is why I ask, in the name of anything that is decent and rational, is your website linked to Craven Desires, one of the most noxious cesspools of the internet, only one notch under animal crush videos sites?
I am absolutely in favor of more dangerous dog laws, but the focus on type is uninformed and irresponsible. And the hate coming of that blog is well…While you seem opinionated, and in my book, that is a good thing, you do not come across as a spawn from the dog fancy equivalent of the Westboro Baptist Church. So I fail to understand your stance in endorsing that blog. It’s the second time I stumbled upon the blog of a working dog guy that I respect the opinion (the other one being terrierman, Patrick Burns) whose talking points have been lifted and used out of context by the Dogbites Klan. That is sad. Considering that most working dogs over 25 pounds have drives and seize which can make them a liability in the wrong hands, those who have such breeds should feel really lucky they had not become a fad and think of the pit breeds as a cautionary tale. Most importantly, we should not condone fanatics’ pro-BSL. We should promote a generic, sensible approach to canine aggression. Or eventually the people who preach that we should only keep stuffed dogs will go down the list and we will be left with poms and show golden retrievers. One of these days you should take a look at the list of banned dog breeds worldwide. One of them is the blue heeler. Now I admit the worst dog I ever had was an Australian Cattle Dog which had to be put down after attacking repeatedly our livestock and nipping people. I was fortunate that it was my responsibility and my decision to euthanize the dog for behavioral issues, not pressure from my neighbor’s paranoid hysteria. But recently I helped a farmer whose neighbors were having a shit fit over his meramma guarding his sheep (lots of coyote predation in his neck of the wood). I also have a friend who keeps a pitbull, as he keeps bulls for his breeding program and use it for his own safety. Dogos which are very useful for feral hogs control are now on many lists of banned dogs. Maybe your answer would be to keep those dogs only in the countryside as working dogs. But then what do you do with all the pups which do not meet working dog grade but would be great pets for an active family? Anyhow, my apology for being off topic. I am just thoroughly disappointed that I will have to flush a potentially interesting resource because I will not help spreading breed dog hysteria. The fact that you linked your web to that crowd well known for their disinformation also cast a doubt on yourself. I personally only recommend what I trust and I will assume you do to. I am not expecting this will be published but at least I am hoping you will ponder on it.
I used to publish a blog roll of blogs I personally read and recommend, but when Google Reader died so did my ability to post a conglomerate feed of all of those blogs’ recent posts. I have yet to find a good solution so I have not yet brought that back to my blog sidebar.
All of the blogs listed on my “INCOMING!” list are blogs that link back to Border-Wars. Plain and simple. And Craven Desires and all the others link back here based solely on the authors of those blogs’ choice. I don’t trade links, but when I see traffic coming in from other blogs, I link back.
And I’m pretty sure that there are things on every single one of those blogs that link to me and which I have created a list back, that I fundamentally disagree with. I’m fine with this. I publish my own content in my posts and I stand by that content and will defend that content and even correct it if you make a good argument on why I’m wrong. I don’t police those links for some litmus test of agreement or friendship other than the simple fact that those blogs link in to mine.
I do not support BSL in any form, but I also do not support the horrible arguments that come out of the pit bull apologist community and the blame they place on everyone else, on breeders, on people who buy from breeders, on people who get dogs at all, on people who make the decision to relinquish their dogs to a shelter. That community is vile and venomous and they need to be confronted for the collateral damage they do with their zealotry.
If you have a SPECIFIC problem with something on Craven Desires, I’d be happy to offer my views on it, but I don’t play the guilt by association game. I rise and fall on my own merits, I have not hitched my wagon to anyone else. If you’re curious as to my own views on pit bull culture, here’s a link, I’ll be happy to entertain your thoughts on any of those posts:
http://www.border-wars.com/category/dogs/pit-bulls
Thank you kindly for your thoughtful reply Christopher. My apology for my faulty assumptions. As I said, I was quite surprised about the connection because I agree with so much of the content of your blog. And the witty delivery definitely makes it all an enjoyable read.
In essence, I agree with your position. I do think while some of the pitbull advocates are honest and well-meaning, they do a disservice to the dogs in the long run. IMO, a healthy, properly raised pitbull is not for the average owner, much less one which does need extensive rehabilitation from being neglected and/or abused. I would say the same thing of an Airedale or a BC by the way. Many folks overestimate their skills and resources in dealing with them and just sneak the dog back at the shelter when they realize its just not working for them. Methink pitbull advocates should aim a diminishing the market, not creating one for unethical breeders who can always dump their surplus in shelters and rescues. No way there are that many home which can be deemed adequate for that many pitbulls. A pitbull is bad fit for most homes, and quite a few who say otherwise are lying and pushing emotional arguments without the best interest of all parties concerned, foremost uninformed but well-meaning families. They do not acknowledge the risks of placing them. Again, a very interesting blog and a lot of what you say about genetics remind me of Jeffrey Bragg thoughts on the Seppala husky.
Chris how many DNA markers will good breeders have to add to the list? Some breeds have none at this time while others can spend $1,000 on DNA markers.
http://www.akcchf.org/canine-health/your-dogs-health/major-histocompatibility.html
When the price of DNA work drops a bit more, why not do the whole damn thing. Or at least do a large set, as in 23andme.com. It’s idiotic that we’re being nickled and dimed on individual tests when a single lab could do a comprehensive job from one sample of DNA. Is there a way around all the damn copyright problems?
Btw. The article you cite is interesting. Note the AKC-funded source goes on about MHC problems without mentioning the problem of homozygosity in the MHC weakening immune system function, or inbreeding as a likely cause. He who pays the piper calls the tunes?
You’re echoing the comments I made on this post:
http://www.border-wars.com/2013/05/health-testing-in-dogs-is-limited.html
And in this article I wrote:
http://www.mydogdna.com/blog/new-mydogdna-genome-wide-testing-program-major-step-forward-making-comprehensive-health
Yup. I tend to echo arguments that I buy as correct. I don’t always remember the source. Sometimes they owe to multiple sources. Sometimes I figure stuff out in my own little brain.
Not all echos. Years before I started reading your column, I arrived at the point of being pissed off at being nickled and dimed into doing multiple genetic tests separately when they could efficiently be combined. I suspect anyone who is used to thrashing data sets would arrive at this conclusion based on the same evidence.
From a pragmatic and utilitarian point of view, which is the perspective in agriculture, maintaining purebred is very useful to produce stable crosses. The hybrids from these crosses can prove remarkably homogeneous and fitting to the production goals of the farmers. Chickens are probably one of the best example. I would tend to believe that as a hobby pursued seriously, poultry breeding is one of cheapest, best and fastest way to learn a lot about the art of breeding. For one, a serious poultry hobby breeder can build ethically a decent population of breeder stock to select from and cull. If he is not happy about the results of a breeding, well…mmm…it ends up in the pot instead of being passed to somebody who does not know any better.
I can see advantages in fixing some traits with line breeding, but then farmers use a tool which would be questionable for dogs, culling. They don’t live for long with the results of a poor breeding match. It seems to have been an effective strategy for the establishment of a breed when breeders had a big genetic pool to draw from. If the goal is to produce reliably from a small population of companion animals with a fighting chance of a long and healthy life, line breeding does not seem sensible as a common practice. In any case, and maybe its an unfair generalization, but “peasants” and so called “primitives” have contributed to development of many landraces for centuries producing healthy and useful animals, only to see the same animals ruined by the arguably more sophisticated and knowledgeable fanciers over a relatively short period of time.
An interesting article, which might be a further help in determining just what the original founder population for all dogs was:
http://news.discovery.com/animals/pets/dogs-not-as-close-kin-to-wolves-as-thought-140116.htm
Couple that in with the fact that dogs and modern wolves can freely breed and produce viable, fertile young — plus the ability of both to breed with other close relatives, coyotes and golden jackals, albeit for now not a long term successful strategy (for now — we don’t know if in the not immediate future it could be), and I think we see how it has been so easy to get away with linebreeding in dogs, but everything has a balance point. This particular branch of the canid family has had most of its evolutionary success in being very pliable — the worst thing probably for such an animal would be to take that pliability away from it. At this point I don’t think we’re quite there, and may never be, but in order to stay genetically flexible over specialization and extreme culling of gene pools will over time take that ability away.
In which case the peasants and the sophisticates alike were not completely helpful…but we really can’t harsh on them as they just didn’t know…we are at a point of knowing better. And to a certain extent culling of individuals does make sense (we wouldn’t have been able to domesticate the suckers if we did not engage in it after all). So, linebreeding and hard culling does make sense from a domestication standpoint, and that’s part of the balancing act/issue with keeping domesticated animals.
What’s our main fault (a worse one really) is that we have the knowledge at hand (or are beginning to get that knowledge) to know better, and yet still continue with the breeding practices of our great grandparents as though they were some sort of rules set in stone.
http://stephenbodio.blogspot.com/2013/09/more-on-closed-registries.html
Of interest.
I kinda like his ideas.
I tend to look at dogs in general as a sort of closed registry to begin with — a much bigger registry, that if we availed ourselves of it would not have such problems with inbreeding, Of course, some crosses make more sense than others — then again, would have never thought of crossing a Pug with a Beagle, and some of them I’ve met have been quite charming pets.
I think, thanks to the original qualities that made up dogs’ DNA, that we still have time to dig out of this mess that inbreeding has put dogs into — what worries me is that the will isn’t there, and in fact, it’s being marketed against by society (you’re a VBP if you even cross different types within a breed, let alone if you produce a crossbred!). I mean, there are some that want to legislate so people can’t…so, there’s a huge problem!
Most of the Champion Herding Dogs were line bred. It didn’t hurt them. All Border Collies have Wartime Cap in them because he was the only proven herding dog in Scotland anyone could breed to. One example is Templetons; Roy was bred to his mothers sister and produced Bathgates Vic, the Scottish driving champion. The only problem that occcured was in some cases infertility that resulted in smaller litters.
Cattle are line bred all the time. The only case of a problem that i know of is with Herfords. After a while the Domino line dwarfed.
There really isn’t line breeding now. It’s characterisitc breeding. Breeding for characteristics that you like.
These comments compliments of that guy in Texas you need to call Chris. I asked a few questions and he knew the answers. 🙂
The issue with Wartime Cap 3036 isn’t so much that he was heavily linebred on, it’s that he was one of the few sires to survive the war thus he became a de-facto popular sire and there was a large breed-wide bottleneck!
I’ve covered this issue in:
http://www.border-wars.com/2013/07/the-border-collie-bottleneck.html
This bottleneck and continued breeding behavior with over-emphasis on a few sires has lead to massive loss in genetic diversity in the Border Collie breed:
http://www.border-wars.com/2011/04/only-8-border-collies.html
And the incestuous over-use of basically one of two families for most of the trial dogs is not healthy at all.
http://www.border-wars.com/2011/01/sire-lines.html
An you assertion that there was no disease spread because of this is provably false. The entire expression of CEA in the breed can be traced back right to Wartime Cap and Wiston Cap.
http://www.border-wars.com/2010/10/through-anomalous-eyes.html
It’s also disingenuous to say that “well this one high achieving dog was line bred thus it’s all ok!” That doesn’t look at the entire picture of what limiting diversity does because you aren’t looking at any of the collateral damage. For example, let’s say we have a population of 100 babies but they are very inbred and 80 of them die of horrible diseases. Well, of the 20 remaining we might have 1 that gets an A+ in Preschool Coloring With Crayons. Are we going to claim that inbreeding is fine because this one inbred kid got a good grade?
See it ignores that so many other kids suffered and it’s only one metric about the life and health of that kid. It doesn’t look at things like litter size, average longevity, the incidence of disease across the entire population going up or down. It just says that one dog got a trophy for performance on the field at a young age. Doesn’t tell us about that dog’s health, or how long he lived, or if he was a healthy sire or had trouble passing on his genes.
I’ve covered a HIGHLY successful show dog family that was inbred and highly diseased and people make the same claim… but this dog sired so many Champions! It’s all OK. Well, tell me, read these posts and tell me if you think this is ok just because trophies were given out.
http://www.border-wars.com/2011/06/whos-your-double-merle-daddy.html
http://www.border-wars.com/2012/02/westminster-rewards-cruelty.html
http://www.border-wars.com/2011/06/double-merle-breeders-dont-want-you-to-see-this.html
As for Herfords, come cattlemen inbred up the wazoo in various lines but that ultimately failed! And they fixed the problem rather openly by outcrossing. Especially to Angus, which are superior and almost all herds of Hereford had Angus brought in and were hybridized. AND the great thing about cattle is that you don’t have any close stud books, they were free to keep their herds registered and when the move to outcrossed Angus came they could sell the mixes still on the books and when they had a certain percentage of Angus (something like 40%) they could sell their beef as “purebred Angus.”
So cattle have a much more sustainable model than the fixed stud book we have in Border Collies. And cattle have plenty of issues when they are highly inbred. They are also a food animal that only has to live to 2 years, we don’t ask for much longevity from them. But just because you’re ignorant of issues in cattle doesn’t mean they don’t exist.
And I fully support characteristic breeding, also called assortative mating. It’s much healthier without sacrificing genetic diversity on all the traits you want to keep diverse and heterozygous.
Open registry is a common practice for many breeds of livestock. Heck, even the American Quarter Horse Association has an open registry.
One interesting development which happened in Canada in the 60s-70s for cattle is the differentiation between fullblood and purebred (not sure how that works for other countries). A cow can be registered as purebred if 6/7 of her genetics is from the breed, the bull, 15/16 . Fullblood means that all the animals can be traced back on both sides to the original herdbook. It seems like a very good compromise. This is an example (from the Limousin) of how the calculations are done. http://www.limousin.com/Registration/USAImports/tabid/117/Default.aspx You end up with an animal true to type with a mechanism which keeps the breed healthy.
I’m going to quibble and correct you a bit: the American Quarter Horse Registry isn’t an open registry persay. Not as it is generally defined in the horse world.
The AQHA has a quasi-open registry: the horses eligible for the main studbook have to be from parents registered as Quarter Horses (at one time horses could get into the registry based on characteristics considered breed traits, but that was some time ago that this was widespread). Lately they have allowed horses back in that did not pass the high white exception (it used to be that the Quarter Horses could not have excessive, by their standards, white markings…most of these horses went into the Paint registry, they are now allowed back; I’m pretty sure this had to do with politics more than anything).
There is an appendix registry for only TB crosses (no other breeds allowed) — those horses cannot be placed into the full studbook unless they meet certain criterion, but they are allowed to be bred. There was a push to allow appendix registry of European warmblood breeds to Quarter Horses and possibly Iberian (Lusitano or Andalusian), but I don’t think it went anywhere — those horses usually go to another breed registry (which is a problem in the horse world…there are a million and one “breeds” out there; you can register anything in something, although most of it is pretty bogus and a waste of money and paperwork).
This is the way most horse studbooks work — about the most open are the warmblood breeds, but even they operate under this general idea and have the extra policy of inspecting, testing, and licensing breeding stock (which isn’t a fail safe method really either…it comes down to the judges that day and their opinion, which try as one might isn’t often the most objective) or registered for breeding on merit (which is only an option for the wealthy the way it is set up).
But you can’t just breed X to Y and expect to have a registered foal (and, not every registry is held in the same regard).
Thanks for the clarifications :).
“They are also a food animal that only has to live to 2 years, we don’t ask for much longevity from them. But just because you’re ignorant of issues in cattle doesn’t mean they don’t exist.”
Health and longevity are important for the cow in a cow/calf operation. Its a major determinant of profitability.
Coming into fertility early and remaining fertile for several years is important to cow/calf operations . . . longevity is not.
And if natural selection favors survival beyond the reproductive years, it only does so because the elders presence increases the probability of survival of the younger generation. At best a minor factor in most wild populations.
It follows that the ‘wild form’ may carry genes for late onset cancers, epilepsy, blindness, or other maladies.
Some of the old age problems we wonder about may have been latent all along. We only see them because more dogs are living longer lives.
I’m going to agree with Lia…to a point.
Good producing cows who have long productive lives and pass on desirable traits to their offspring are very valued in the cow industry — which is one of the catch-22s of farm production animals: they have to try and select for traits such as fast, easy, and above average finish weight — as most of the animals end up going to slaughter — but at the same time balance out production traits such as good frame, overall health, fertility and longevity of productive life (which truly, isn’t quite the same as with non-ag production animals, but is there nonetheless).
A lot of time those two forces compete with one another; hence the reason why those studbooks are allowed to stay as open as they are 😉
And this is just within production lines; show lines are a bit different (if related) ballgame!
I don’t know much about cow calf operations. I presume that cows, like bitches, have a point in their lifespan where they reach peak fertility, and that they are taken out of production (and slaughtered) some years thereafter.
Bitches seem generally to peak by six years and they are often taken out of ‘production’ around that time, often earlier, sometimes later. Most of us hope our girls will live to a ripe old age that something like double their age at retirement. Those post-retirement years are statistically bad for cancer, epilepsy, arthritis, and many late-onset maladies.
I find it hard to believe that cow/calf operations care for their cows when they are past their breeding years and can no longer justify the cost of the feed needed to keep them alive — much less pay vet bills on non-productive stock. Is there any motivation (or effort) to reduce incidence of late onset diseases in cattle?
You’re right Jennifer. Its about the number of years the animal is productive rather than absolute longevity. As for your question about motivation or effort about dealing with late onset diseases with cattle, I would tend to say no, not much of that going on. If anything, even less incentives now than ever because with the possibility of collecting and implanting embryos, keeping your valuable breeding cows for as long as possible is not as critical since we have other ways to preserve her genetics. Cows can be bred all their life. As long as they live, they have the potential to calve. Average lifespan is 15 years under current production practice, but they could live as long as 25-30 years. Culling criterias vary. Vet care on a farm is a compromise between economic and welfare criteria. That might explain why the small animal vet fees always scandalized me compare to the large animal ones.
That being said, I have rarely been on a farm where there was not a very special animal lavished with extra care and kept until it kicked the bucket or had to be put down for compassionate reasons. Farmers are people too 😉 . The most colorful case was a Highland oxen in a Holstein herd.
The difference is that cows (and horses) have a different fertility cycle than dogs (or cats). Probably has something to do with only having, usually, one offspring and a long gestation period. They can remain remarkably productive throughout their lifespans.
Conversely, a cow past its reproductive prime isn’t worth much as a slaughtered carcass — they aren’t exactly prime meat.
The dairy cows are a bit of a different story, but again — the reproductive peak and quality of the carcass is the same. It just makes little economic sense to have breeding stock turning over quickly with the cows (and horses). Pigs are another matter entirely, as are poultry; they peak out quite quickly and have a better carcass value, so within commercial lines you don’t see the emphasis on longevity and conversely I have seen more problems with linebreeding in those two animals — they also have a much different reproductive cycle, and this is also I believe a contributing factor….although closed studbooks isn’t (they’ll breed whatever it takes to get the desired market, or markets, characteristics — right now I’ve noticed a trend to develop pigs who provide a more desirable carcass for the Asian market, which demands different from N. America).
As for keeping livestock for sentimental reasons doesn’t really happen — except on small holdings that are usually breeding for show stock…or just a small holding; that sort of operation is really an anomaly at this point, but true enough — many of the old, small holders could get quite attached to certain animals.
Jennifer
There are no fast rule with farmers. The Highland ox was kept on a fairly large dairy operation run very professionally. I cant say that I have seen the same on chicken farms so far. From my experience working professionally with farmers for nearly 20 years, it happens more frequently than people would think. My bias coming maybe from working with many dairy farmers.
I was born and raised on a small family holding — and have had experience with all manner of operations.
While individual farmers may keep their “pet” (and this goes for chickens too), most large commercial farms are no longer owned by individual farmers (though they may rent/hire themselves out to them or sell to them) — and they do not have pet cows and the like (unless of course the CEO/owner of the farm keeps one at home, but that is hardly the same as the situation of the traditional small holder).
In a desperate attempt to get this back to dogs — this is probably the reason why Border Collies are becoming a vestige of an older time!
This is the trend, while there are some individual holders left that is becoming a rarity. It is what it is.
Sorry for going off topic . . .well, it it does relate to inbreeding
Looks like all the cold weather may give a lifeline to the Isle Royale wolves . . . or may be dealing the populaiton a final blow.
http://abc10up.com/ice-bridge-isle-royale-impacts-wolf-population/
Yes, the whole “ice bridge will save them” logic didn’t really work out. The wolf went the other way, off the island, and promptly died.
http://www.telegraph.co.uk/health/petshealth/10762988/Pedigree-dogs-as-healthy-as-mongrels-say-vets.html
‘Dr O’Neill, who was a practising vet for 20 years, said: “My hypotheses was that crossbreeds would have a lower prevalence of common disorders than purebreds. But the overwhelming evidence for that has not been proved. ‘
Er…aren’t you missing the point? Isn’t it genetic health and breeding for exaggeration that we are seriously concerned with here? What are the ‘common disorders’ anyway? And didn’t a study recently prove that mutts were genetically healthier but more prone to ACL tears than purebred dogs. Possibly due to spay/neuter or lack of supplements etc.
I haven’t read the actual paper yet but something stinks…
Nick1 Thank you for sharing. I especially like the closing:
emima” Harrison, who produced the original documentary, said: “That this study showed only a small crossbreed advantage overall doesn’t mean breeders of pedigree dogs are off the hook. There is still an unacceptably high level of defect, deformity and disease in individual breeds – the direct result of a Kennel Club culture that rewards inbreeding and selection for often ridiculous show-ring aesthetics. It remains a largely preventible scandal that pedigree dog breeders have barely begun to address.””
Yes Kathy, at least Jemima got to contribute. She’s going to review the paper on her blog too.