The wolves of Isle Royale Michigan
Sweeping comparisons between wild animals and domesticated pets are dangerous given the unique and often mutually exclusive conditions in which those two groups often find themselves. Wild animals must hunt for their food, compete for resources, suffer predation, lack medical intervention, self-select their mates, and exist in numbers based upon a complex interaction between their own merits and the conditions in their environment. Pet dogs are fed from a bowl daily, compete only for our affection and attention, are largely free of predation, have ready access to modern veterinary techniques and treatments, have their mates chosen for them–sometimes from dogs long dead or on other continents, and exist in numbers based upon human concerns and rarely on their own merits or the environmental carrying capacity. Their selection is very much unnatural. But there are very few scientific studies of domesticated pets versus numerous investigations into wild populations, so dog lovers would be remiss in not learning lessons from our pets’ wild cousins. One particularly interesting ongoing scientific inquiry is the study of the wolf and moose populations on Isle Royale Michigan.
Wolves colonized Isle Royale, a wilderness island in Lake Superior, North America, in 1949 or 1950. The population is isolated from mainland wolves by a channel of frigid water, 24 km wide. In many, but not all years, this channel freezes for several days or weeks. Although an occasional ice bridge makes immigration possible, the analysis of mitochondrial DNA and the Y chromosome suggests that the population was originally founded by only one female and two males.
This makes Isle Royale analogous to a small dog breed based on a few founders or even a single kennel that rarely brings in any new blood. Nova Scotia Duck Tolling Retrievers, Leonbergers, Cavalier King Charles Spaniels, Vallhunds, and many other breeds were founded by only a few sires and dams and have had very little influx of blood since and there are quite a few old time breeders who would only occasionally bring in a sire from outside their own moderately sized kennels. As with the above breeds, the mostly-closed gene pool on Isle Royale became steadily inbred over time.
By the late 1990s, the population’s estimated inbreeding coefficient had risen to 81%. Fifty-eight per cent of Isle Royale wolves showed congenital bone deformities compared with only 1 per cent in two outbred wolf populations. Some of these deformities could reduce individual fitness, particularly components of fitness associated with predation and reproduction.
So the first lesson to be learned from the Isle Royale Wolves is that isolation leads to inbreeding and inbreeding is detrimental. In dogs, closed registries and kennel blindness are a form of isolation and in both cases we see rising inbreeding followed by increased expression of otherwise rare diseases.
Some of the most studied wolf packs in the world are in serious jeopardy. Researchers report that the occurrence of debilitating bone deformities in wolves marooned on Isle Royale, an isolated island in Lake Superior north of Michigan, has risen sharply over the past five decades due to inbreeding.
Diseased wolf vertebra due to inbreeding of Isle Royale wolves.
A genetic defect now common in the Isle’s wolves causes bones in the spine, the vertebrae, to grow gnarled and crooked. Also found in domestic dogs – close wolf relatives – the bone malformations can pinch nerves in the spinal cord, causing pain that makes it tough to walk and can lead to paralysis of the back legs and tail in severe cases, according to research published in February’s issue of Biological Conservation. Back in the 1960s, about a quarter of Isle Royale’s wolves appeared to have the anatomical abnormality, but now the percentage of afflicted wolves has risen to nearly 60 percent of the population. “In normal, healthy wolf populations without inbreeding, you are only supposed to see this kind of defect in about one out of a hundred animals,” says paper coauthor John Vucetich, an assistant professor of wildlife biology at Michigan Technological University (MTU) in Houghton. The deformity, discovered during autopsies of recovered, dead wolves, has grown so rampant, Vucetich says, “we haven’t found a normal wolf in the past decade.”
The second lesson to learn from the Isle Royale Wolves is that hybrid vigor is real and powerful and that inbreeding depression is real and powerful.
We used molecular techniques to document the consequences of a male wolf (Canis lupus) that immigrated, on its own, across Lake Superior ice to the small, inbred wolf population in Isle Royale National Park. The immigrant’s fitness so exceeded that of native wolves that within 2.5 generations, he was related to every individual in the population and his ancestry constituted 56 per cent of the population, resulting in a selective sweep of the total genome. In other words, all the male ancestry (50% of the total ancestry) descended from this immigrant, plus 6 per cent owing to the success of some of his inbred offspring. The immigration event occurred in an environment where space was limiting (i.e. packs occupied all available territories) and during a time when environmental conditions had deteriorated (i.e. wolves’ prey declined).
This event is an excellent example of what one outcross might do for a small breed and especially a single kennel. The immigrant wolf’s offspring were true hybrids, a mix of the formerly isolated pool and fresh blood; versus having an outside pack supplant the locals in toto, as one might expect in a contiguous geography that was not isolated like the Isle.
We have here an analogous situation that fits existing human patterns of behavior regarding dog breeds and strains that have virtual barriers instead of physical ones.
The astounding aspect of this immigrant on Isle Royale is just how potent his genetics were to effect change on the island. None of the existing males could even compete with him and he became the sole sire. His initial success is likely caused by the inbreeding depression in the inbred Isle wolves.
The high fitness of this immigrant wolf was also associated with distinctive behaviour and physical appearance. First, he was physically larger than most Isle Royale wolves. As alpha male of the Middle Pack, his high fitness was also reflected by his dominance over other ISRO packs. Specifically, he exhibited strong territorial behaviour that completely displaced West Pack, driving that pack to extinction by 1999.
This immigrant wasn’t necessarily a super-wolf, he was in all probability a young male that was driven out of his birth pack’s territory for being non-competitive with that pack’s alpha male. His success on Isle Royale shows just how compromised the inbred population had become.
The inbred Wolves of Isle Royale, genetically refreshed by the genes of a new sire.
It’s an open question if and how much the influx of new genes has changed the bone deformities which had come to define Isle wolves. Surprisingly, before the results of the bone study were published, Isle Royale was used as an example of a wild population that was thriving and unharmed by inbreeding and isolation. This is why I’m cautious of anyone who argues from ignorance regarding their ability to inbreed and avoid disease. This is the third lesson: don’t assume that inbreeding can exist in high levels without detriment and don’t cite wild populations if no one has ever done a detailed health study to document the true health of the population.
The new results offer the first evidence of the wolves’ closed population leading to a decline in natural fitness. This is important, Vucetich says, because for years some policy makers and conservationists have pointed to the apparent health of the Isle Royale wolf packs as an indication that small animal populations can maintain proper genetic diversity. “Isle Royale is not this robust place that some people thought it was,” says Vucetich.
Now, not all the lessons are positive ones. Given the isolation of the island, the complete genetic sweep of the immigrant male, and the small population size the rates of inbreeding swiftly ticked back up. The smaller the population size and the greater degree of inbreeding done following new blood, the shorter time you’re going to reap the benefits of that new genetic material. Outcrossing can forgive a myriad of sins, but it needs to be used in measure to the problem. On Isle Royale, this new wolf didn’t simply add to the sires on the island, he supplanted them and then bred with his children, creating more inbreeding instead of extending the benefits of outcrossing.
This isn’t an advisable strategy for refreshing a dog breed, essentially going from one popular sire to another. Diversity in breeding males should be maintained over each generation and proceeding to breed father to daughter–and similar–after a single outcross will swiftly return the gene pool to inbred status. The other issue that researchers have is that to complete a “genetic rescue” one must be able to document the benefit on a population level, an this is often done with the most crude methods, namely demography (head counting). An increase in population size was not observed here, although there was a precipitous drop in the wolves’ main food source, Moose, during this time and the wolf numbers did not suffer either.
Genetic rescue, in which the introduction of one or more unrelated individuals into an inbred population results in the reduction of detrimental genetic effects and an increase in one or more vital rates, is a potentially important management tool for mitigating adverse effects of inbreeding. … The immigration event occurred in an environment where space was limiting (i.e. packs occupied all available territories) and during a time when environmental conditions had deteriorated (i.e. wolves’ prey declined). These conditions probably explain why the immigration event did not obviously improve the population’s demography (e.g. increased population numbers or growth rate). Our results show that the beneficial effects of gene flow may be substantial and quickly manifest, short-lived under some circumstances, and how the demographic benefits of genetic rescue might be masked by environmental conditions.
This is not a problem with outcrossing at all, rather it’s a problem of the limitations of the crude science of demography. Head counting might speak to quantity, but it is wholly lacking in useful information about quality.
Demography is likewise a poor tool to employ when analyzing domesticated dog health. The numbers of dogs within breeds has little to do with their vitality and much more to do with fashion and the whims of a handful of breeders. No one would claim that a Pug is popular due to competitive natural gifts of robust health and fitness, rather they are much like the inbred wolves on Isle Royale, they are artificially supported by beneficial conditions, easy access to food, and a blunting of natural pressures against their survival; in the wolves’ case it’s the benefits of living on an island, in the case of the Pug it’s being coddled by owners and breeders willing to spend a pretty penny on their upkeep.
In open and competitive environments, population numbers can serve to estimate vitality when better data has not been taken, but it seems that on Isle Royale, the wolves have a sheltered niche as the apex predators with ample food supply. The Moose can’t migrate away and there is little in the way of competition for the wolves. In such conditions, even sickly inbred wolves can reach a carrying capacity at about the same numbers as more robust wolves can. It’s possible that more wolves could have thrived had the main food source not plummeted, or it could be that even at the lowest levels the moose populations were not small enough to be a significant factor in the head count of the wolves.
Without a marked improvement in population size on the island and without documentation of the rates of disease and bone deformities improving with the influx of the immigrant wolf, the technical definition of a “genetic rescue” has not been met with the current state of knowledge about the Isle Royale wolves.
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Anton
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What a nice Christmas present!
Retrieverman recently posted..Rudolph the fang-toothed deer
The outcross is the big grey one.
The other wolves on Isle Royale are a very strange color.
Retrieverman recently posted..Christmas present from BorderWars
And yet there is the island fox (Urocyon littoralis)of the California channel islands. For that matter, there’s the Galápagos Islands and Hawaii. Obviously, given “enough” time a small population can evolve into a functional and sound species. The problem with the Isle Royal wolves is that there hasn’t been enough time & selection pressure. I think Dingos are estimated to have come from “one” pregnant bitch. Again, a LOT more time has occured to allow problems to be eliminated. And it’s probably true that many “start up” species failed (as perhaps the Isle Royal wolves will). Isle royal could be “fixed” by bringing in one or two outside wolves (male & female, unrelated) every 10 or so years. For dogs, part of the problem is that the deformities many object to are DESIRED by others — the English bulldog didn’t become what it is by simple genetic isolation, nor did the Neo Mastiff. They got that way because some people WANT them that way. No one desires cancer, PRA or epilepsy, but some of the other issues? the physical changes are a major controversy not because they can’t be altered, but because some WANT the dogs the way they are. While we can “ban” serious issues, at what point does one say, “this modification is ok”? When all dogs look like wolves? Or are hanging (hound) ears ok? how about coat length? It’s not as simple as one may think once one’s past the worst examples.
I enjoy your comments in this blog. I hope there is an interesting discussion on how much distortion is OK in a breed.I personally prefer, and always have, sticking to the basic wolfie looking types of dogs, without much type change except a little in the ears- if it isn’t too exaggerated.
But people love to pick the different one out of the litter, and always have, probably from the moment those collapsed ears or spots, showed up.
The original Sharpeis were far less exaggerated, but breeding for extremes of type is encouraged, not discouraged, in the present atmosphere. The Old Fashioned bull dogs were far less extreme, but still recognizable today. Were they genetically unfit?
Perhaps just a wave of judges choosing the least extreme types could reverse this trend in a very few years. But it would have to happen in an atmosphere that supports avoiding extreme types.
Kate Williams recently posted..Big Chihuahua
You will not see this because the human brain is not wired for it. Judging dogs is very like a game of One of These Things Is Not Like the Others. The human brain is programed to look for patterns and differences. The eye will naturally go to the dog that stands out, it takes a conscious effort to avoid the effect. The development of extreme or overtyped animals is a natural consequence of show ring, because objective judging is not possible when you’re dealing with human brains.
Jess recently posted..The Big Day is Only a Few Hours Away Now
This does explain why breeds are changing so much even though the standards rarely do. If the show ring worked as it’s marketed to, you would not see extreme changes in morphology without extreme changes in the breed standard.
What changes we DO see in standards often _follow_ the change in the dogs. Again, rewriting what is perfect to match what we have actually created instead of doing the hard work of changing what we have into something better.
‘Better’ in regards to phenotype is subjective. I happen to like very rustic looking dogs; many people do not.
‘Better’ should be in regards to health and function. Since function depends only partly upon the gross phenotype, it is entirely plausible that making a better dog (better function, better health) would result in a dog that looks the same as the previous unimproved model.
Breed ‘development’ (standardization) seems to be the initial downfall, both in terms of breeding philosophy, if you want to call it that (reasons for breeding, perhaps?) and in terms of loss of diversity, both in type and in genes. Breeding to ‘improve’ the breed seems to go hand in hand with *change.* Maybe because improved function must be *demostrated.*
Jess recently posted..The Big Day is Only a Few Hours Away Now
The subjectivity of ephemera isn’t what I’m getting at, although it is much of what “improvement” has come to define.
My point is that it’s easier to say “this dog is improved, just look at it!” than to actually make a substantial improvement. This is how breeders walked themselves down a long path of self deception and now claim that the kangaroo-GSDs are BETTER, more sound, can do more than they could 50 years ago.
The flat pug face is declared an improvement. The wrinkled Shar Pei is improved.
There never seems to be a moderating factor, so none of these things has an end to the vector. Old Shar Peis are slightly more wrinkly than some other breeds, so wrinkles must be important! More wrinkles are better! They are always better, never worse. There is never going too far.
The pug’s nose can not be too short. The Afghan’s hair can not be too long. The roach back can not droop too low.
Whereas nature has diminishing returns, the fancy has none.
My point is that the fancy doesn’t actually make better dogs in any respect, they don’t create faster greyhounds, but they do declare that what they have created LOOKS faster, and thus must be. No need to verify. So they declare that this is now better and that is sufficient.
This works for aesthetics as well as practical traits. I mean really, do we think that Pekes look better now? Do GSDs? Bassets? Neapolitans?
It reminds me of my Banana post. Are we in any position to know that the product we’re being sold is actually inferior than what we used to have? Memory is very short.
How right you are. The Leonbergers are already changing and looking more like a Newf. I’ve seen this in just the past 3 years. You put a classic Leo, the kind the standard calls for, and one with a boxier head in the ring, I guarantee the one with the shorter muzzle will win. Plus they are getting smaller with a shorter coat. Definitely not what they are supposed to be.
I disagree a bit because the most average human faces are considered the most beautiful. I can’t defend what dog show judges do, because I am totally against them even as I have an opinion on what they could do to avoid extremes.
The same thing has not happened with horses because they are not purebred. I personally advocate other than purebred approaches to dog breeding. I tolerate a much wider range of types than a breed would show because there actually is a landrace chihuahua type very common along the border from LA to El Paso. It is bred and maintained in backyards and the pups go to neighbors. This style of breeding has kept the original chihuahua types going strong for the last 150 years of documented history, and it can be inferred, they were around much earlier as many of them look like xolos with hair. In spite of all kinds of out-crosses, the type persists.
Kate Williams recently posted..Xolo Teeth
Don’t you see a difference in the faces that scientists measure to be the most beautiful based upon surveys, popular opinion and the faces (and bodies) of runway models? Gaunt, androgynous, bony and strung-out are high fashion, yet you’d probably keep your distance from them in person. There’s a big gap between what we are TOLD is beautiful and what we actually find beautiful. Sure, some people buy what they are selling, but rarely would they arrive at those conclusions without being persuaded to.
Judges can only reward what they see in the ring, and given the horrible feedback system in the AKC at least, it’s not like there is enough communication between the judges and the exhibitors. How often do you see a Judge reject every dog in the ring and not award a single ribbon? I imagine if you did see this, that judge would not be hired any more. Conformation is about peer pressure, not selective pressure. Big wig breeders pressure the newbies into using their dogs and they pressure judges to reward them with ribbons. Noobs who get in with the old guard pressure those who do not (protect that investment!), etc.
I so agree with you, but, the Chinese Crested Breeders and Xolo breeders are working with judges to educate them as to the the best types, and it is working according to the various lists I follow. Some judges are judging the way the breed club wants them to and people mention their names. Then, I imagine, at the next time the judge will have more entries. That is how judging works.
Also the biggest corporate breeders are heavily influencing both the AKC and the judges, providing the vast majority of registrations in the first case, and making sure their dogs win, in the second. It would be in good keeping with the new corporate policy to start breeding less extreme animals, unless the people who buy them want dogs to only last 4-6 years, as in the case of many over-bred extreme dogs now.
Kate Williams recently posted..Xolo Teeth
The island foxes aren’t a good analogy to domestic dogs or wolves.
http://desertwindhounds.blogspot.com/2010/12/closed-registries-dogs-in-handbasket-to.html
If natural selection exists and the animals can somehow remain productive through the inbreeding depression, they can survive.
Most rodents have evolved some level of inbreeding tolerance.
Dogs and wolves don’t have much because in their natural state, the offspring of both sexes leave their natal packs.
Also, no one is saying that dogs must look like wolves, but when they have severe pain or health conditions that are the result of their bizarre conformation, that is a major welfare issue. A drop-eared dog that has a heightened tendency to get ear infections is not as severe an issue as a bulldog that cannot mate or whelp without assistance and then cannot cool itself or breathe efficiently.
Retrieverman recently posted..Christmas present from BorderWars
Yes, it’s important to note that the protective elements of islands allow species to change based on mere survival to breeding age, not THRIVING.
One must thrive in the face of competition. One can merely survive when coddled by external factors.
My guess is that cheetahs and island foxes had severe problems in the earliest generations of their bottleneck. Nature culled out as many of these problems, because nature– even in places where there are no other predators in the case of the island foxes– doesn’t tolerate disabilities.
Of course, it’s not been explained to me why we consider island foxes a separate species. They have a different mtDNA sequence from California gray foxes on the mainland, but it’s never been compared to other gray fox populations.
There are no nuclear DNA studies either.
My guess is that if we did those kinds of studies, they wouldn’t be any more unique than dogs are from wolves.
And thus, not an endangered species.
They would be like Mexican wolves, an endangered subspecies.
Retrieverman recently posted..Christmas present from BorderWars
The Island foxes are considered different species due to each Island having a specific morphology. IIRC, vertebrae count, but don’t quote me on that.
Jess recently posted..The Big Day is Only a Few Hours Away Now
Those traits, when we look at how they vary among other species of the dog family, are actually pretty superficial. The fewer vertebrae in the island foxes is that their tails are shorter in proportion to their body size.
From what I’ve seen, it might be easier to declare the Mexican wolf its own species than it is to adhere to the species status of the island fox.
However, there are political reasons why this species exists.
It’s not entirely bogus as organism like the red wolf (a type of Eastern coyote) is.
Retrieverman recently posted..Christmas present from BorderWars
There are fewer vertebrae in the back of an Arab horse, but it is not a different species, even though it looks so different. The horse genome is freely shared among all horses, yet types persist.
My point is that it is the entire fox genome that counts. Species can come and go (or different varieties, if not actually species)because of genetic bottlenecks and every other mechanism, but it is ultimately the genome that survives, taking different forms as circumstances dictate.
Kate Williams recently posted..Xolo Teeth
Gray foxes range from the US/Canadian border to Venezuela, and they vary a lot in appearance. There are many different subspecies, and because this species is really old, they likely vary a lot in terms of their genetics.
We have to see where island foxes fit with the whole population. And we need nuclear DNA studies of all the gray fox populations to make that comparison. Thus far, I’ve not seen anything like that.
And there are political reasons why any study like this would probably not be performed or accepted by officialdom.
My guess is the island fox is nothing more than an insular subspecies of the gray fox.
Retrieverman recently posted..Christmas present from BorderWars
No. This is where ‘survival of the fittest’ becomes a misnomer. It is more like ‘survival of the lucky.’ The Isle Royale wolves were unlucky in that one (or more) of the found population carried deleterious genes. It has nothing to do with ‘time’ and everything to do with the genetic health of the founding population, much like we see in dog breeds (CKCS comes to mind.) And it’s probably true that *most* isolated populations die out.
The Island foxes are an entirely different case than the Isle Royale wolves but I don’t have time to get into why right now.
Jess recently posted..The Big Day is Only a Few Hours Away Now
RE: Channel Island Foxes:
There is good evidence for the fox being introduced to the Channel Islands between 5000-6400 years ago by Native Americans. Not only that, but there is evidence that they moved foxes from island to island. There was, of course, a small founding population, but there is also no reason to believe that there was only ONE introduction of foxes to the islands, and no reason to believe that there was no *natural* movement of foxes from the mainland as well. The founding population was larger, certainly, than the three animals that made up the original Isle Royale wolf founders.
The San Nicolas Island foxes underwent an extreme bottleneck in the seventies due to distemper, down to less than ten animals. Their subsequent survival and resurgence comes down to balancing selection AND a long history of already being selected for inbreeding tolerance.
Jess recently posted..The Big Day is Only a Few Hours Away Now
The last thing I read on them was that they made it to the northern Channel Islands 16,000 to 10,000 years ago (when the sea levels were lower) and then were introduced to the other islands by Native Americans over several thousands years.
The big thing that declares them to be a unique species is they have a very different mtDNA sequence from mainland California gray foxes.
I have a little problem with being so sure in that declaration. The Urocyon foxes are quite prone to distemper. It’s not just the island foxes that get bad distemper outbreaks. The mainland grays get it, too. It would have not been unusual for the ancestral California population of gray fox to have been wiped out in distemper outbreak in the past 10,000 to 16,000 years years. My guess is the whole mitochondrial lineage has been replaced in this species several times across both North and South America in different regions.
We need a nuclear DNA study on these foxes to find out exactly what they are, but one thing is clear, they likely split from the mainland gray fox after domestic dogs started splitting from wolves.
And the morphological differences between them and the mainland gray are trifling compared to the differences between dogs and wolves and those that exist between different wolf subspecies.
I am very skeptical that this is actually a valid species.
Retrieverman recently posted..Falsifying hybrid origin
Origins and antiquity of the island fox (Urocyon littoralis) on California’s Channel Islands (2009)
The island fox (Urocyon littoralis) is one of few reportedly endemic terrestrial mammals on California’s Channel Islands. Questions remain about how and when foxes first colonized the islands, with researchers speculating on a natural, human-assisted, or combined dispersal during the late Pleistocene and/or Holocene. A natural dispersal of foxes to the northern Channel Islands has been supported by reports of a few fox bones from late Pleistocene paleontological localities. Direct AMS 14C dating of these “fossil” fox bones produced dates ranging from ∼6400 to 200 cal yr BP, however, postdating human colonization of the islands by several millennia. Although one of these specimens is the earliest securely dated fox from the islands, these new data support the hypothesis that Native Americans introduced foxes to all the Channel Islands in the early to middle Holocene. However, a natural dispersal for the original island colonization cannot be ruled out until further paleontological, archaeological, and genetic studies (especially aDNA [ancient DNA]) are conducted.
Jess recently posted..The Big Day is Only a Few Hours Away Now
Wow.
Not a real species at all.
It’s like the Channel Islands dingo.
Retrieverman recently posted..Falsifying hybrid origin
Yes, islands are fascinating incubators for major evolutionary change often at a pace faster than on larger landmasses. This is due to many of the same reasons we have at play here, mainly very unique and focused selective pressures: the protection of boundary waters prevents migration in or out; smaller scale forces morphological change; absence of predators and access to sufficient food buffer otherwise deleterious mutations; etc.
The lessons I highlight in this post deal more with the unintentional consequences of our breeding choices, not the intentional ones. No one WANTS inbred disease, but we still breed in a manner that brings deleterious recessives to the surface.
Regarding the active and intentional crippling of our breeds, I’d refer you to my posts on “Sine Qua Non” disease. I make much the same observation that you do: some disorder/dysfunction/disease/exaggeration is wanted and selected for.
I personally think that it’s worth separating those issues out from the unintentional disease issues as the solutions to combat that problem are different. Limiting the impact of CEA in Collies, for example, will take a very different course of action than moderating their extreme head shape, oblique eyes, excessive coat, etc. This isn’t to say that the action will be radically different, a few outcrosses to moderate dogs with moderate coats, less extreme heads, etc. and without CEA would work against all the genetic issues at once. BUT, there is a political desire to eliminate CEA, there is much less will to change the Collie into a less extreme and fancy animal, and so far the breeders have shown that they are more concerned with fancy than with healthy.
A new point I’d like to make is that perhaps some of the extreme exaggeration fetish is driven by biology and not by any initial desire. For example, do you really think that Neo people decided 40 years ago that they wanted an elephant-scrotum faced dog? Or perhaps they started on a slow path to more “furnishings” and every generation was just a little more and a little more wrinkly. The second generation of two moderately wrinkled dogs was slightly more wrinkled and ‘slightly more’ WON out of fashion or out of being the only thing in the ring. The problem snowballed over generations, with no one willing to breed in moderate dogs to reverse the trend, probably because it was 4-5 generations back the last time any moderate dog won anything.
Isn’t it possible that these breeders decided “this is good, this is better, this is near-perfection!” only after it was ALL THEY HAD? What’s easier, to achieve perfection or to redefine it to something you’ve already accomplished?
“Isn’t it possible that these breeders decided “this is good, this is better, this is near-perfection!” only after it was ALL THEY HAD? What’s easier, to achieve perfection or to redefine it to something you’ve already accomplished?”
I have thoughts on this that I cannot seem to organize into coherency. Something along the lines of ‘people see what they want to see.’
Jess recently posted..The Big Day is Only a Few Hours Away Now
Here’s another thought.
Multi-objective optimization is a real headache, compared to merely striving toward this or that individual extreme. And overall success across diverse categories is far more challenging to recognize, quantify, or foster.
The human preference for comparing apples to apples, and even then, only Red Delicious apples to other Red Delicious apples, is hard to escape. We’re just a lot more comfortable operating within narrow enough constraints that we can make decisions without a ton of calculus. Plus, the narrower the field of contestants, the better the opportunity to demonstrate how very discerning we are, right?
I mean, anyone can tell the difference between a dog that can walk or breathe and one that can’t. But what about between two equally handicapped dogs? That takes a trained eye, doesn’t it? And yet, ever so much simpler to rest one’s final judgement on coat color than on, say, overall health, appearance, and function.
Ruth Crisler recently posted..Worthy Causes
Chris intentional or unintentional issues to address solutions for CEA, micropthalmic eyes, blind and deafness by modifications in breeding programs of collie fancy is warranted. The extreme head shape of show dog fanciers which can create a shallow structural orbit for the eye should be part of not just an artist, but breeders should be good constructional engineers to produce not only elegance, but proper structure for health. KATHY
This is right up your alley! Thanks for writing about it.
And, I like the blue and yellow sidebars or boxes;they really make it easy to parse.
Merry Christmas!
Kate Williams recently posted..Wolves in Mind
Even if one discounts the island fox, there remains the dingo, Hawaii and the Galapagos. Clearly a “bottleneck” can be survived. I think Jess is right, it often is, “survival of the lucky” – the animal “stranded” on the island or otherwise isolated happen to have reasonably healthy genes and manage to evolve into a new species (or subspecies). In the case of the Isle Royale wolves, it may be that the island just isn’t large enough to have a population size capable of diversity and without a competitor, the wolves there simply don’t “need” to be that fit. Again, IMO, that could be addressed with judicious introductions of new wolves from time to time – which of course flies in the face of the “non interference” views of many conservationists.
Christopher said: “but when they have severe pain or health conditions that are the result of their bizarre conformation, that is a major welfare issue” – yes, but there are those that assert that Merle is a major welfare issue, that even double dewclaws are, the ridge in “ridgebacks”, hairlessness, even drop ears (one hears about hematomas, ear infections, etc. – and some of this is quite valid. SOME, however, is questionable. If “K” provides a better immune system, should we insist that all dogs be K dominant black? How about dilute blues? (or worse, double dilute “Isabella” Dobes) – there ARE skin and immune issues with dilutes, even though one does see the occasional “color morph” in wild animals. It is easy to condemn extremes and yes, conformation does pick the one that “stands out” and thus promotes that (I suppose one could start pushing “the one closest to the 1930s dogs” and push for the one that stands out in that respect).
Actually I DO think the “elephant scrotum face” was desired. The more wrinkled, the more the dog won. The more the dog won, the more the next breeder selected for more wrinkle – same for the Shar Pei and the same for the hock / banana back of the GSD. It wasn’t that this was “all they have”—it was that this was what won. And this, in turn, pushes the breeding “ in a manner that brings deleterious recessives to the surface” – because each generation selects for those who are “top winners” with those “desirable traits” and thus pushes those recessives which, as with the dominant NBT, are often considered “just a minor inconvenience to achieving the goal”. Those that have “issues” are simply discarded or, as with cancer, bred before the problem comes up. It’s this that will make eliminating some of those “breed specific” problems so hard – no one wants to have a “generic” dog for that F1 or even F2 generation, even if the F3s look just fine for the show ring. Add to the “purity” quasi religion of registries, and one has a major uphill battle.
I don’t intend to discount any of the examples per se, but I do think that what we see in the island wolves and what we see elsewhere are anywhere from many decades to millenia apart in progress. No one is suggesting that the Isle Royale wolves are well on their way to SPECIATION.
The more we know about canids, the more fuzzy we have to make our line between dog and wolf and coyote, so treating the Isle Royale wolves as anything other than a sub-population is premature. I don’t know if there’s a lesson to be learned about speciation from them. The lessons I see are more along the lines of kennel level and perhaps breed level (and of course, breeds have little true meaning except superficially in the species of canis lupus familiaris).
I think all these are open for debate, certainly. If we are going to say that we allow Merle, let us say so while admitting that it comes along with X% of problems. Let us be honest about it. Same with all of these possible deleterious alleles. These are not black and white issues, they must be weighed. And that evaluation might have things weighed differently, say health versus aesthetics. Some people might put a higher factor on aesthetics. We certainly see this with things like the ridge. It serves no other positive purpose except aesthetics, and there is some degree of risk to health.
As a libertarian, I don’t typically think “there should be a law” when there is some issue I’d like to see resolved differently. Laws rarely have the nuance to effect the right sort of change and they come with huge institutional problems. For example, at what level do we think Hairlessness should be banned at if we decided that the problems outweigh the benefits? Municipal laws in each city? Breed club laws? AKC registration restrictions? Something like the DACH countries EU-wide laws? What if ear cropping bans don’t do much damage in England, but they are unduly burdensome in Turkey? Like there there are no wolves in the UK so dogs do not get in fights with them, but livestock guardian dogs in Turkey start getting killed by being pinned down with ear holds by wolves. This is a totally made up example, but there are examples where laws are passed in an area where legislators have no reason to think they’d be burdensome, but it turns out they are on another group that falls under the jurisdiction.
My goal is to expose these issues because I think very few people are being honest about them. You can’t make good decisions based on bad information. If breeders want to continue with these issues, let them do so honestly and circumspectly. It’s too often that people decide on a path and then want to make it a less nuanced decision. Just look at what Dr. Cattanach is trying to do with bobtail. He doesn’t want to be fully honest because that would make breeders have to THINK and weigh options. It’s so much easier in his mind to just tell them it’s all ok because he himself has decided so. Don’t worry about the details, please, they will just confuse you and you are unable to make decisions for yourself!
I’d rather live in complicated reality than idealized fiction.
I agree that “species” isn’t quite the same as “breed” but it’s the only human/non human comparison available. I also think that folk tend to forget that in domestication, NO ONE was really looking for a healthier, more fit animal. They were looking for a sheep with more wool (or whiter wool), a bigger, stronger (or faster) horse — but not an animal less subject to cancer, better able to survive in the wild, etc. Selection criteria were things like “gives more milk as a cow”, “can find the scent better when trailing”.
I once read a statistic that showed that the average working cow dog has a working life of about 6 years — so if your dog is slow enough to be kicked at 7, are you really selecting any that live past 10? It’s quite true that breed “purity” has distilled disorders to be more prevelant in one breed vice another, but it’s not true that none of these disorders existed in landraces. Merle came before Australian Shepherds. Was there ever any “rule” about not breeding Merle-merle BEFORE registrations? In many Aussie histories, a point is made that “if it wasn’t merle, it wasn’t an Aussie”. It was the breed club that figured out the problem with Merle/Merle and recommends against it. ASCA also investigated the NBT issue and also opted to recommend against breeding for NBT. While I don’t have a breed that is cropped or docked, I can think of worse things than cropping or docking, both of which are pretty similar in “pain” to what people do to themselves for the sake of “conformation”. I don’t put dogs above people.
I think an honest breed club should refuse registration of Merle/merle breedings — but note that the Doberman club tried that with albino Dobes and it was AKC, not the breed club that rejected that idea. All AKC would do was to annotate the pedigrees to show if the dog was albino. When a club DOES recognize an issue, the least the registry could do is to support them.
Peggy Richter
This goes to an interesting point that I think is worth making. Outcrossing and even the creation/fostering/return to a landrace model does not purge disease genes, that’s not the point. The smarter road to increased health is not swift disease allele elimination, it’s promoting heterozygosity and breeding for type by breeding away, not close. We do not need to give up on “predictability” for the few traits we really want homozygous and which are known to be benign.
It would also help if we let go of some of those deterministic desires too, but that’s not strictly necessary. We _can_ increase the intentional and decrease the unintentional. We don’t need to ban Merle or Bobtail, we just need to be smarter about it. We don’t need to exterminate those nasty little recessives either, we can keep them from expressing (at best, greatly decrease their expression at worst) and we can let them drift away into oblivion on their own, not taking huge chunks of good diversity with them on their way out.
Kate said: The same thing has not happened with horses because they are not purebred — uh, Quarter horse & “IMPRESSIVE” anyone? Halter horses? Tennessee walking horse and “high step” anyone? http://en.wikipedia.org/wiki/Tennessee_Walking_Horse#Showing. The difference is that the “pet” horse is usually a generic, and this is the “horse” most people see. It is NOT that there aren’t plenty of “show” exaggerated animals (minature horses?). You see it in show sheep and cattle, for that matter. The difference is that in sheep, cattle and even horses, a performance requirement tends to override the conformation exaggerations to some degree. You certainly see such morphs in chickens, pigeons and even fish. Cats seem to be more resistant to morphing, but you see the conformation issues in some of them too. It’s just “human nature” to want the “biggest”, “wierdest”, etc. Retrieverman had a post that showed that some arguements about ‘destroying the dogs” started almost simultaneously with the creation of “conformation breeds”. The trick is to find a way to encourage breeders to select for sounder animals — by either educating judges or changing the way competition “chooses”, but you will always see a push for someone to have “something different” — no matter WHAT animal is involved and regardless of if it is/isn’t registered. Peggy Richter.
I think that the idea of “decrease in overall fitness” will always continue to be a tough sell in genetics research in companion animal breeds. In most genetics research, very few researchers will take a chance on this sort of unknown. It is much easier to speak in terms of narrow recognizable phenotypic changes in grant proposals and academic papers, so this is what gets funding and this is what will allow researchers to be prolific enough to survive and thrive with the “publish or perish” attitude.
There are a handful of labs that study genetic diversity, to be sure. But IMO there is a difficult-to-navigate gap between this work which is mostly seen as “background” stuff that other researchers use solely for citation purposes (often without fully understanding it) and work that examines health and disease genetics (focusing on discrete phenotypes such as PKD and CEA). A major problem seems to be that many of the established canine and feline geneticists come from human genetics academic pedigrees, where the latter makes a whole lot more sense. And old habits tend to die hard, particularly in a society that seems to be more willing to compare dogs and cats to humans than to wildlife or livestock species, where such “genetic fitness” studies are more accepted. Even if it’s ostensibly for a compilation of individual traits – it’s undoubtedly better than saying ‘well, we just won’t breed these dogs that have PRA’ without looking at other genetic factors.
I don’t really know where to go with this kind of thing. In my own academic career to now, I have unsuccessfully been trying to figure out how to build a bridge for this gap, but it sometimes seems quite insurmountable.
I think that pet research can suffer from the same pitfalls as human research, e.g. preventative measures never get the same funding or focus as treatment methods for disease because there’s a lot more money an interest in treatments. Prevention typically requires action at a pre-clinical stage, long before a Doctor or a Veterinarian sees a patient, even as early as during breeding decisions (many generations back even).
People pay $$ to save them after they’ve screwed the pooch, they don’t generally value being lectured before disaster happens (but after it’s well on its way).
The guy who turned himself blue like a smurf didn’t stop after ingesting just a little Colloidal Silver, perhaps he didn’t even notice that he was turning blue until long after a rational person who wasn’t self-blinded to it would have. And clearly somewhere along the line he decided that it was worth paying the price of being blue for the rather flimsy “benefits.”
Genetic disease in dogs is similar. These people take risks without real benefit, over and over, until it is custom. This is how it is done! We’ve always done it this way! By the time their dogs are riddled with disease, they don’t realize that it has been a road they walked down steadily over time, it must be something new and drastic (and thus easy to get rid of just as easily as it sprang on the gene pool). No need to re-examine anything. Those early breeders got away with inbreeding just like Mr. Smurf got away with poisoning himself with silver. A bit more over time and never anything to combat what was already done.
And one day, blue was the new normal, and don’t tell me otherwise.
It may be much more insidious than that. For example, in Belgians, epilepsy is estimated to occur in 17-22% of the dogs. The clubs have sponsored several studies. The upshot has been a report that it is a single recessive “of large effect” with a modifier, one that states it is “polygenetic” (unknown number, possibly recessives of varying penetrance) and one that indicates it could be a dominant gene with “repressor genes” in play. With this kind of “information”, it’s pretty impossible for a Belgian breeder to make a useful decision. From personal research, I feel that while epilepsy undoubtedly existed in the dogs at the “normal rate”, the increase came from Willy de la Garde Noire LOF 100 (T) w: 14-Mar-1948, who is generally considered one of the major “revitializers” of the Tervuren color. Now this dog was bred, used and died long before the vast majority of current Belgian breeders ever got involved in the dogs.
I have yet to find a Belgian of any flavor that doesn’t have Willy as an ancestor at least once. And of course, once may be all one needs.
Were there breeders who were indifferent to epilepsy? Indeed there were, and some of them did a lot of breeding of some very major influence in subsequent generations. But even those who made efforts (and some did so as early as the 60s) to avoid the problem have had little success. The problem is far too widespread and breeders have no tools to detect carriers or even to detect the affected dogs prior to actual seizures. It might be possible to use outcrosses to breeds like the Picardy shepherd, Bouviers or other related herding breeds, but without knowing the mode of inheritance, one is stuck with F1s – the F2s are just as likely to have the problem gene(s) as the purebred, since one is backcrossing to Belgians.
I know friends who have ACDs – do they eliminate PRA carriers? http://www.optigen.com/opt9_test_prcd_pra.html or do they eliminate parents that produce deaf puppies? Or do they breed carriers to non carriers, look for dogs that have good hips, herding ability, and baer test to keep hearing offspring? No matter what choice they make, there are going to be some pups that “don’t measure up” in all respects, even if conformation plays no part in it. It’s just not as easy as one might wish to select among multiple factors for the “right” dogs to breed.
Obviously, one would like those who have rough & smooth collies to start selecting more for dogs that look like the movie “lassie” http://www.lassie.net/wopmd.htm who has far more moderate eyes and head than most conformation dogs. But the “lassie” type IS available to people. Do we educate or force people to select for a “lassie” (or farm collie) type? Or do we figure out a way to reward those conformation folk for selecting more moderate heads in collies?
Do we force pug or peke conformation people to change or reward those that do?
And how do we address the “don’t know how to get out of the situation”?
IMO Epilepsy is a disease that will have to be tolerated, it can not be excised like a simple recessive with a test (not that I think those should be swiftly bred out either). But variable penetrance and late-onset is a horrible combination to solve problems. It’s why, say, Alzheimer’s has very few selective pressures against it vs. infertility or childhood disease.
But it is eminently possible to do just what you said. Decrease incidence of the disease without even having a test. Outcross.
F2s are NOT actually as likely to have the problem genes. They are of course more than F1s, but they are not the same as purebreds.
The solution to decreasing epilepsy is just like my general proscription for all breeds: open the stud books, outcross, and continually recreate your breed using an appendix registry.
Decreasing incidence of all disease versus permanently removing any one disease is what I think is the best way forward. But this is a paradigm shift that I don’t think the current people in dogs will ever embrace, because it flies in the face of tradition.
I think what I’m getting at, as far as wanting to research this topic, is that I would really like to get some solid research out there that can more definitively PROVE that outcrossing and increasing the effective population sizes of breeds will improve health. Perhaps that’s way too ambitious, I don’t know – you’re right, it’s a paradigm shift, but various aspects of society have had these before. They just take time and evidence.
Thinking through the problem logically (full disclosure: I hold a Masters degree with thesis work in domestic feline genetics and am currently a veterinary student) it would require some way to quantify “health” which is really the first hurdle to jump over – as you can see, these dogs can be really messed up and have multiple nasty conditions. I don’t know, there are lots of steps to go through. My general overarching idea is that breeds could have their own unique “health chips” to look at common markers both for health and for analysis of inbreeding coefficients and other parameters, and run some comparisons. Then perhaps breeding could be a more informed decision and if breeders chose to ignore/discount different points that represent “health,” they can perhaps be held a little more accountable? Or at the very least the phenotypic changes can be matched better with genotypic?
Probably not making much sense, but it’s something I think about a lot.
Do you not already see enough evidence of inbreeding and closed breeds leading to severely increased incidence of otherwise rare diseases?
This isn’t theory, it’s fact. We know how genetics works, there is really nothing left to prove here at all. There’s no magic way for outcrossing to not work, or for more inbreeding and extensive DNA testing to work.
Do you agree that the reason we see breed specific incidence of disease that far outpace other breeds or mixed breed populations is due to the genetic loss and increased homozygosity caused by inbreeding and closed gene pools?
So can you agree that inbreeding causes increased disease incidence because otherwise rare deleterious alleles are more likely to be doubled up?
If A causes B, then stopping A stops B.
I’m going to throw this challenge back at you. Find me some studies or examples of otherwise rare diseases that have shown up in inbred populations. Then tell me how outcrossing back to healthy populations would not decrease the expression?
You can start with looking at Tay-Sachs, and filling in the blanks here:
Children that are the product of first cousin sex have this much increased risk of….
Stillbirth: ? %
Deaths before first birthday: ? %
Congenital malformations: ? %
Deaths following 1 year until adult: ? %
Then tell me what’s going on with the Mormons in Colorado City, AZ. This is just a start, report back.
You don’t have to sell me on the idea – I’m sold. But that approach looks at this through again narrow phenotypic traits where people can just say “well yeah maybe we’ve got PKD in our breed, but we can just get a test and make it go away” and then miss the entire point of overall decrease in health and in the process make the gene pool even smaller!
Increased incidence of rare diseases and inbreeding depression are kind of two sides of the same coin, but not the same exact thing, if you understand what I’m trying to say…
An acquaintance of mine had a strain of dogs with a very high COI, over 40%. These dogs produced large litters and were apparently robustly healthy. His bitches simply stopped producing litters when bred with his males. These dogs did go through inbreeding depression and seemed to recover. This is what makes ‘health’ and ‘inbreeding depression’ so hard to quantify. I really don’t see how you can do a study on this, simply because each group of dogs is going to respond differently, depending on what genes they have. Some breeds are very tolerant of inbreeding because they were lucky enough to not have a large genetic load to start with. (Explaining this will get you nowhere, btw.)
Jess recently posted..Tazis, Tazis, Everywhere
also I prefer the plight of the Amish as I was born and raised in western PA.
The problem is that you would need information from the time the breed entered the closed registry system to track changes. You can’t go back in time, and the records we have are not complete. A proper study would involve following lots and lots of dogs for generations; it would take decades.
It’s too late for such a study now. The damage has already been done, it’s continuing to be done. What would be the point?
Let them drive their dogs into the ground.
Jess recently posted..Tazis, Tazis, Everywhere
Regarding reducing incidence rate of epilepsy: the natural rate of epilepsy is already well-documented across all breeds.
In one of the problem breeds, they are trying to reduce the rate down to that.
Epilepsy in Finnish Spitz
From Puppy to Hunting Dog
Finnish Spitz – Epi-Figure
I once had an epileptic dog – her seizures began after a brutal attack and shake though, so probably not from an hereditary cause. This comment made me curious about the epilepsy rate in dogs. Clare Rusbridge has it at 1%. “It is generally regarded that epilepsy has a 1% incidence in the dog population i.e. higher than this suggests a breed tendency” – http://www.veterinary-neurologist.co.uk/seizures_epilepsy.htm
Kary
IMO Epilepsy is a disease that will have to be tolerated, it can not be excised like a simple recessive with a test (not that I think those should be swiftly bred out either). But variable penetrance and late-onset is a horrible combination to solve problems. It’s why, say, Alzheimer’s has very few selective pressures against it vs. infertility or childhood disease.
But it is eminently possible to do just what you said. Decrease incidence of the disease without even having a test. Outcross.
F2s are NOT actually as likely to have the problem genes. They are of course more than F1s, but they are not the same as purebreds.
The solution to decreasing epilepsy is just like my general proscription for all breeds: open the stud books, outcross, and continually recreate your breed using an appendix registry.
Decreasing incidence of all disease versus permanently removing any one disease is what I think is the best way forward. But this is a paradigm shift that I don’t think the current people in dogs will ever embrace, because it flies in the face of tradition.
—Obviously, one would like those who have rough & smooth collies to start selecting more for dogs that look like the movie “lassie”—
That’s still breeding for an arbitrary “look” instead of taking the whole dog into consideration. And simply breeding for “Lassie face” is not the way to go – that’s the thought process behind the Cavalier, and look how healthy and sound they are.
Thistle has big, soulful eyes and is PRA blind.
http://adopt.dogtime.com/animals/2468734
Going to a show and looking at the dogs isn’t really the best way to gauge the direction of the breed. What percentage of all collies are show-ring champions? Not many. To see the real state of the breed, look at the pets. There are a fair number of “old-fahioned” pets out there. Cena, Kaleb, Cloe, and Beeline for example.
http://tristatecollierescue.net/collies.htm
The farm collie is a dog defined by its ability, not its looks. It may be an english shepherd, a collie, or a crossbreed.
Breeding for several things at once isn’t as easy as simply breeding based on conformation, but it’s the best way to proceed. Temperament, genetic soundness, efficient movement, biddability – it’s all important.
Collie breeders are fortunate – we now have DNA tests available for PRA and CEA. The difficult part is getting people to use these tools, show and pet breeders included. And clear eyes are far from the only thing that defines a good breeder. Stirling Collies – the kennel that produced the two MM blind/deaf puppies – uses mostly CEA noncarrier dogs.
christopher said: F2s are NOT actually as likely to have the problem genes. They are of course more than F1s, but they are not the same as purebreds.
== i don’t see how. if dominant (A) with a repressor gene (r), breeding Arr to another breed aR, doesn’t improve. AR would be a likely result for a reasonable % of pups.(it might however indicate the dominant theory is correct) If recessive, one has F1 Aa but is the Belgian you are using for F2 Aa or aa? You have the same odds as using another Belgian because the incidence of carriers is so high when you have 17-22% incidence. My view is that the answer is to do a test breeding (or several) of two affected Belgians and to determine the genes (or at least eliminate one of the three options as the results will differ if dominant vice recessive vice poly genetic). But that’s an effort that will likely result in many offspring who are affected and so far not enough members of the clubs are desperate enough to go there, and you’d certainly need a vet school research group to assist. The alternative of outcrossing (to malinois in Europe and to duch shepherds by KNPV) has merely spread it to malinois lines (and hints it’s crossed into the Dutchies). The best gambit suggested has pretty much been to use the oldest healthy stud of a line that one likes and to prefer dogs that don’t have any siblings or offspring that seize, but this is hardly an ideal solution.
I find my ACD friends are pretty reasonable in how they are going about reducing PRA in the breed, but I admit, most of the folk I know in the herding breeds are performance (with some also doing conformation) rather than conformation only folk. Peggy Richter
And this might be a bit nitpicky but the offspring of F1 & one of the parent populations are NOT an F2 generation. They are a backcross generation of some kind.
Peggy, you’ve come up with a very complicated and convoluted example but let me start simply.
Breeding high incidence to low incidence will improve the high incidence stock. Even if you have some other disease in the low incidence stock that is high there, it is probably low in the main stock and when you cross back, you are again going high to low.
I’m not sure about your Dominant with repressor example, perhaps you have an example of one of those in real life? Until I can read more about what you’re referring to, I can’t process your example.
Are we talking about one single hypothetical breeding or are we going to talk about merging two populations over several breedings? I could run those numbers with H-W assumptions, but I still think they’d all favor my position.
Taking a wild guess at what you’re getting at with a Dominant deleterious gene with some magic repressor which makes it benign… well of course if you split the antidote from the poison you’re going to see bad outcomes, but I don’t think that even in that case this is really a problem.
I’d need to know how this supposed Dominant works when homozygous and if in your source population if they are magically all homozygous for the repressor. This repressor sort of throws a wrench in the works, but really I’d need to read how this really works.
Dave mentioned the Finnish Spitz epilepsy — yes. I note two things in the study “Test matings with three epileptic dams to an epileptic sire” – I mentioned in a previous post that this is my view of where Belgian folk need to go to get a grip on epilepsy in Belgians. The other recommendation in the study: It is unwise to breed from an epileptic dog or to repeat a mating that has produced epileptic pups.” is already something most Belgian folk are doing. The issue is avoiding dogs that have epileptic siblings, aunts/uncles, nieces/nephews. That has pretty much proved unworkable as too many dogs are thus removed from the gene pool. Yes, the F2 I mentioned is a “back cross” but even F1 x F1 — if one doesn’t even know if the genes involved are one, several, recessive/dominant, your F1s can be as much carriers as the original Belgian parent. aR x Ar? not an improvement if the Belgians being used are already Arr or AaRr (ie, not affected). (by the way, the NBT study also used backcrosses, as did the Dalmatian effort). Unless you do a LOT of F1 breeding, creating as it were a new “breed” (bulldog/mastiff = bull mastiff), you have to backcross at some point. And most breeders no longer have the funds, facility or even the interest in having so many dogs as to do such a project on their own. Coordination with others becomes essential.
I’m not a fan of inbreeding. I personally would like to see “appendix registries” similar to those used in other livestock applied to dog registries. It would allow for controlled reduction of COI and introduction of new genes without making it so easy as to suffer at whatever whims there might be. However, most of the studies comparing health of mixes (random bred dogs) to purebreds are rather flawed. The study usually picks the purebred that has a problem in an area and then compares. But how many mixes of “rottweiler size and conformation” have better hips than OFA line Rottweilers? Certainly racing greyhounds (purebred) have better hips than the general population, including mixes. I expect most Belgians have better skulls and dentition than the average “chi mix” out of the shelters. And then there is the issue of function — if you are selecting for a dog that can herd well, you really do need to select within a relatively restricted gene pool. I know about the “herding greyhound” etc — but in 20+ years of American Herding breed Assn being “open to any dog”, there have been 2 mixes that achieved the highest levels. One was a retriever something. The other was very likely mostly Schnauzer/Bouvier. You can manage with a Queensland/ACD, BC/Aussie, etc, but you aren’t going to have significant success with a Bulldog/Staff/Dane, or a Shih-Tzu/cocker cross. A great trainer MIGHT manage, but that’s the exception, not the rule — it would be like a grade horse managing to win in horse races. It happens, but not so often anyone would abandon the purebred lines they use.
I would love to see more veternary schools working WITH breeders and maybe even setting up competitions (best collie with a “lassie face” and no CEA) rather than the current situation in the US, where “every” breeder is lumped in as a “bad purebred breeder”. – I don’t have a degree in any of the biology/medical fields. However I consider myself a pretty well self-educated layman. I spent about 31 years as a technical writer of contracts in the research/development area of military aviation/ energy, so I do know science when I see it. I’m also familiar with “reports” or “studies” like that of the NBT boxer that tend to, shall we say, omit inconvenient facts?
Peggy Richter
Point is, the inheritance of epilepsy in Finnish Spitzes is yet to be understood. The breeders knew if they cull known carriers, they would lose genetic diversity. The fact they haven’t understood how epilepsy is inherited doesn’t deter them from taking actions.
So they are perfectly aware culling leads to genetic loss; but they also couldn’t turn a blind eye. So they actually derived quite an ingenious way to dilute the frequency of the disease through mathematics.
Dave wrote regarding the Finnish Spitz that the breeders have come up with a way to “dilute the frequency” via mathematics. That’s not how I read what they’ve done:
http://www.finnishspitzhealth.org/fshealth.html “the Finnish Spitz Club in Finland developed an epilepsy pedigree with a probability indicator of which lines were most likely to carry the defective gene and attempted to eliminate the breeding of these dogs. As a result, the gene pool in Finland was dramatically reduced four years ago.” — so yes, they’ve reduced epilepsy. But they’ve ALSO reduced the gene pool and probably lost OTHER diversity. The mathematical “probability” calculator could probably be used for a number of breeds. Is it open access information?
Peggy Richter
Of course, it is just commonsense that some potential breeding dogs will be lost in the process.
You either throw out the baby with the bathwater by removing every single suspect; or you can target what is assumed to be the worst of the carriers, and still keep the other carriers that are of moderate or mild risks.
I’m not trying to be difficult here. I just know that several Belgian breeders have been trying for decades to avoid or reduce epilepsy in the dogs using the techniques referenced for the Finnish Spitz. There is an epilepsy database for Belgians. There is a pedigree search engine (although I haven’t seen the mathematical formula used for the Finn spitz, I do know several Belgian folk who have tried applying probability formulas of their own). Using dogs that have “not had epileptic sibs, offspring and avoiding using epileptic dogs has pretty much been the goal of all. And it hasn’t worked. Using a test breeding (which the Finn spitz folk did) would, I think, at least give us a grip on the method of inheritance but a lot of folk are disturbed by the ethical issue of deliberately breeding several litters of epileptic dogs. Outcrossing to another breed HAS been considered by some and a method to do it figured out, at least on a small scale. BUT, which breed to use? (Altdeucher, Picardy, Dutch Shepherd, bouvier, other?) AND my concern is that if one is going to take that leap, is that it would be EFFECTIVE. I am not one of those resisting the idea. I am one of those SUPPORTING the idea — as I’m well aware of the instances of crossing such as the LUA Dalmation (my idea of a success story except for the long time it took to get registration acceptance). I’m equally familiar with the KNPV dogs which are a quasi-open registry of mostly Belgian/Dutch dogs. The problem with both the Finn spitz and the Belgians is that as breeds, their numbers are relatively small. That would make it easy to “diffuse” new blood in, but it does, IMO, make it hard to eliminate a problem if one does not know the mode of inheritance FIRST. I also think that if one does elimination breeding (the Malamute folk have done it with dwarfism, the ACD folk are progressing with PRA) it really really helps to have a university assisting, it really really helps to have some kind of carrier or affected test. OFA is an “affected” test and it does indeed help reduce hip issues. Pushed in noses, etc — most skeletal issues seem to be under the control of very straightforward genes and “correction” accomplished pretty fast if desired — you also can SEE if you got it right or not. The other problems? without a test of any kind other than “dog got cancer at 8” (and cancer does have some tests) — it’s a LOT harder. And progress much slower. Belgian breeders have been funding one study or another on epilepsy for more than 20 years. From my perspective, we are at exactly the same place as in 1980s — don’t breed an epileptic dog, try to breed dogs that don’t have sibs, aunts/uncles nephews/nieces that seize wherever you can. And to tell if a dog is/isn’t epileptic? — use the oldest sound dog where there is a choice between studs. I’d like a bit more progress than that.
Peggy Richter.
True and true. This is why I say that the goal should be for disease dilution versus elimination outright. Even simple recessives with full penetrance and a perfect and cheap DNA test can be excluded too quickly, especially given the other breeding patterns most breeders use. Some hot show stud that has passed 3 or 4 tests might be wrongly thought to be “problem free” and will be over-bred compared to more diverse studs that have a carrier status or aren’t as shiny in the show ring.
There are plenty of big diseases that have proven much less tractable to cure/diagnose/test-for despite “major advances” in science. I’ve made this complaint several times… we have a handful of DNA tests, but really are there tests for the worst stuff? IMO, the library of tests available does not overlap the important diseases enough yet.
There are also some really minor diseases that are very rare, but because there is a test, OMFG if you don’t drop the money to get tested you’re eeeevil. This slow trickle of tests, one at a time, will not be good for dogs if breeders over-react to the small and rare diseases and use a few tests to pretend that they know anything about the other big and more prevalent diseases.
dominant with a repressor gene: simple example: K dominant black and ee red. You’ll note how long it took to find the K gene and to determine it was NOT part of the A gene group. http://homepage.usask.ca/~schmutz/brindle.html (it says brindle, but K includes brindle). There’s a theory that epilepsy in Belgians could be like K dominant with “repressors” like b, d and e. If only one could look at the dogs and tell!!!
Peggy Richter.
My impression is that K being affected by e/e is epistatic, not repressive. K is not inactive, it’s not being altered by e/e, just it’s expression via the inability to form black pigment in the hair. My understanding of ‘repressors’ is that they work on a molecular level to affect expression, the repressor is actually bound to the gene it’s affecting. K and e/e are not like that.
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Coat color examples may or may not be directly applicable. One caveat is that coat color issues often revolve around what you can SEE versus what is going on chemically. You can apparently get very white Goldens that are still e/e and yet I don’t recall reading any associated sensory defects associated with that. But other visual whites are knock-out situations with faulty genes that do associate with deafness or blindness or whatnot. Chocolate might be recessive to black, but the chemical pigments we see in chocolate are there in black, along with more when a dog is black.
If brindle were a disease, would it still harm you if it was covered with dominant black? Is that a prepressor or is it simply hiding the phenotype?
“If brindle were a disease, would it still harm you if it was covered with dominant black? Is that a prepressor or is it simply hiding the phenotype?”
Yes, it would still harm you, because the black is simply hiding it, it’s not chemically changing the *expression* of brindle *on* the brindle gene.
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Actually, I think coat color examples are pretty good. One, it’s an example that is reasonably clear regarding a “dominant with recessive modifiers” and two, yep, you can have the same genes and variant colors (has happened even with identicals) AND you can get similar cases with entirely different genes /chemistry (dominant black K and recessive black aa being perfect examples of this). So too one can get “epilepsy” from the “breed specific problem” and your “ordinary” epilepsy from trauma, toxins, and even the odd “genetic oops” that is entirely seperate from the norm. So the outward appearance “has seizures” does in fact mimic the complexity of coat color to some extent. What I find very annoying is all the research done on coat color so that now we have many of the genes involved clearly defined, and yet we are still searching for the “DNA” test for say, HD as opposed to sticking with the OFA “identify the affected animal” method. It’s harder to develop a test for HD – it may not show up until the dog is 2 years, it probably is polygenetic, not all dogs with HD are lame and not all lame dogs have HD. But it certainly affects more dog’s lives than if they are red golden, black and tan or brindle in color. Peggy Richter
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