|Yes, I know this is not a Toller...|
Three and a bit weeks ago, I blogged about German breeder, Alexander Dauber, who had decided to outcross his Nova Scotia Tolling Retriever to an Australian Shepherd - the first step of a project aimed at introducing a shot of genetic diversity into the Toller. Boy, from the response, you'd have thought I'd advocated murder ("You did... he's murdering the breed!), not just one man's effort to do what he thinks is right which no one else is remotely obliged to be involved with if they don't want to be.
It has become the blog's third most read post of all time. It attracted 74 comments that I published and another 10 or so that I thought were too awful to make public - although I'll share one of them now; this anonymous one from someone clearly very irate that I hadn't published Toller researcher Dr Danika Bannasch's reponse (which I had asked for and which she provided shortly after I'd published the post).
You promised to put Dr. Bannasch's responses on as soon as you got them. You've had them for weeks. Meantime, your anti-purebred shill "researcher" Maki has had multiple chances to comment, which have all been published. Put Dr. Bannasch's information up as you promised - or were you lying and now need time to "spin" things your way?Nice. And, of course, there's the small point that health test results for German dogs are not normally listed on the (American) OFA database.
The rogue breeder has no proven info on health other than what he claims on his website. The dogs are not on OFA nor are they in Tollerdata, which responsible breeders use to post real results, and not just "my vet says" bs put out by people who can't be bothered to follow any rules.
Many people feel if haplotypes were the reason for him using an Aussie male (when Goldens were approved), then what possible excuse is there for not doing it ahead of time? ...except that he's no more than the usual Doodle breeder, sadly given blessing by someone whose never bred in their life.
I have, in fact, written to Dr Bannasch to apologise and explain the reason for the delay - which is that I have been waiting for a response from Dr Maria Wilbe, another Toller-owning scientist. I explained that I felt that the two responses would be better incorporated into a new post rather than editing into the original, as most people do not go back to review posts they have already read. I also felt they were too important to just post as a Comment where they might not be found.
Anyway, I received the response from Maria Wilbe two days ago and it transpires that a whole bevy of impressive names have signed up to it too, so I am finally in a position to return to the Tollers as promised.
First, if you haven't already read the original post, please do (you can find it here) before reading on.
To quickly recap for those who need a quick reminder, essentially, the fuss centres on two issues. The first is whether Toller diversity is compromised sufficiently to warrant an outcross; and the second is over the usefulness of DLA haplotyping testing as a means to reduce the incidence of immune-mediated disease in the breed.
On the first, there is clearly a bit of a science stand-off (as documented in the first post), muddied at times by a sometimes near-hysterical response from some Toller breeders to the very idea of sullying their breed with foreign blood. Some won't even consider seeking out and using the unregistered Tollers that can still be found in Canada, one breeder dismissing them as just "Toller-like mutts".
Regarding DLA haplotype testing, this is a DNA test which looks at a key section of the immune system. In 2009, Swedish scientist Maria Wilbe and her co-authors found an association between one particular DLA haplotype* and immune-mediated rheumatic disease (IMRD). This is one of two troublesome immune-mediated conditions found in Tollers (and which together are often called Toller Disease). The team found an elevated risk of developing the condition in dogs with one copy of this haplotype - and a higher risk in dogs that had two copies of it. (Abstract here.)
(*haplotype = a group of genes inherited as one)
So, given that a test is now available that allows you to ensure that there would be no doubling up of the IMRD-risk haplotype in any puppies bred, surely it would make sense for breeders to avail themselves of the test? Well, no - not according to the scientists who have signed the statement below. In fact, they absolutely insist that breeders should not make breeding decisions on the basis of any such test until all the genetic risk factors (and it is true that there are others) are known.
This statement and Dr Bannasch's are in full below (as well as Dr Bannasch's answers to three supplemental questions I asked).
As you'll see, Dr Bannasch views outcrossing as an absolute a last resort and argues that Tollers are only as inbred as any other pure breed. (Not a huge comfort, surely?) I was also disappointed that she feels it impossible to collect reliable information re the incidence of immune-mediated disorders in the breed given that it is perfectly feasible to recruit a birth cohort of Tollers and follow them through their lives. (This has been done in other breeds.) And I was surprised that Dr Bannasch cited laboratory mice as an example of a healthy inbred population when, in fact, over 90 per cent of these inbred lines die out in the process of creating them, many do indeed suffer from specific genetic problems and all have to be kept in a protected environment - unable to withstand the environmental, bacterial and viral onslaught they would be exposed to in the real world. Not something we'd want for our dogs.
As for the joint statement issued by the various researchers involved in DLA testing, I do understand the scientists' caution, but I believe that if some early adopters want to expore DLA testing then they should be free to do so, as long as they are fully aware that it is only one small part of the story and things might not work out as planned. I would hope too, that, what they discover along the way is passed on to the scientists to help their research - and the breed.
Why wouldn't you want to avoid doubling up on a haplotype if its been found that two copies of it increases the risk of IMRD, even if other genetic risk factors are involved? After all, cutting down on butter is only one way of reducing cholesterol, but it is better than doing nothing at all.
I can also see some sense in, generally, using DLA testing to try to ensure as diverse an immune system as possible in a breed as we know that is, in general, a good thing (notwithstanding that some individual haplotypes might be associated with a specific disease). In fact , this is the whole basis of the commerial DLA haplotype testing offered by Professor Hannes Lohi at Genoscoper whose name appears on the statement below advising against DLA testing as a means of reducing the risk of immune-mediated disease in Tollers.
DLA testing also affords an opportunity to increase the number of dogs carrying very rare haplotypes. Although 11 in total have been found so far in the breed, only five have been found with any great frequency and the rest are vanishingly rare. This table is in Finnish but you'll get the idea..and see how common the IMRD risk haplotype is. (NB again, it is only a risk factor and one of several. There are Tollers who have one and two copies of this haplotype who have never gone on to develop IMRD and, equally, those that don't have any copies of it who have.)
|Click to enlarge|
So there we go. As clear as mud, I expect. But it's a complex subject.
DR BANNASCH'S RESPONSE
I would be the first person to support purposeful cross breeding and in the event that we discover through our research that it is the ONLY way to correct an inherited problem in the breed I will be the first one leading the effort.
The most important point that you and others are missing is that the Maki report does not compare the NSDTR to other purebred breeds. This could be done for all breeds and may uncover that certain breeds are in more critical shape than others. The NSDTR breeders are fortunate that since the breed was more recently admitted to registration status we have computer access to complete pedigrees since that time. That is what gives the apparently very high inbreeding coefficients. If this same analysis could be done in other breeds the numbers would likely be similar. It is not correct to compare the numbers to wild animal populations and make conclusions about the dire straits that this breed is in. You assume that tollers are much worse off than other breeds and I believe based on our unpublished data (see below) they are about average among purebreds.
My laboratory has been working on identifying the genes that causes tollers to develop Addison's disease. As part of this work we have genotype data from the NSDTR as well as other breeds and can compare the genotype based inbreeding coefficient. These numbers are based on data for about 30,000 markers in 10 unrelated animals.
Dachshund- 0.1242, Lab 0.1635, Beagle 0.2043, NSDTR 0.2064, German Shepherd 0.3150 and greyhound 0.3238
We also performed Y haplotype analysis of 33 tollers and obtained diversity values of 0.76 +/- 0.04 based on identifying 5 different haplotypes in the NSDTR. You can see numbers from other breeds in the following paper for comparison:
Y chromosome haplotype analysis in purebred dogs (pdf) Danika L. Bannasch,1 Michael J. Bannasch,2* Jeanne R. Ryun,1* Thomas R. Famula,3 Niels C. Pedersen
Inbreeding and genetic diversity in dogs: Results from DNA analysis (Claire M. Wade)
You also state that 11 DLA haplotypes is "low" for a breed but actually although most of the scientific manuscripts on the subject do not have the haplotypes published in this way, 11 is above average for a purebred dog breed. Please see partial reference list below.
This paper found 11 haplotypes in the GSD:
MHC class II risk haplotype associated with Canine chronic superficial keratitis in German Shepherd dogs. Päivi Jokinena, Elina M. Rusanenc, Lorna J. Kennedy and Hannes Lohi.
This paper found 6 haplotypes in Pugs:
Necrotizing meningoencephalitis of Pug Dogs associates with dog leukocyte antigen class II and resembles acute variant forms of multiple sclerosis. K. A. Greer et al.
This paper found 9 haplotypes in Weimaraners:
Expanded dog leukocyte antigen (DLA) single nucleotide polymorphism (SNP) genotyping reveals spurious class II associations. N. Safraa, N.C. Pedersena, Z. Wolfa, E.G. Johnsona, H.W. Liua, A.M. Hughes, A. Young and D.L. Bannasch
This paper found 6 haploytpes in over 500 Dobermans:
Association of hypothyroid disease in Doberman Pinscher dogs with a rare major histocompatibility complex DLA class II haplotype. (pdf) L. J. Kennedy1, H. J. Huson, J. Leonard, J. M. Angles, L. E. Fox, J. W. Wojciechowski, C. Yuncker & G. M. Happ
JH supplemental questions:
JH: what is your estimate of the incidence of immune-mediated disorders in the breed?
DB: Unfortunately this number is extremely difficult to get or even estimate. When polls are taken more people with diseased dogs are likely to respond. The ideal sampling would be to follow a cohort of dogs and report their incidence of disease. Obviously this is impossible.
JH: an Ne of 18 is extremely low - Calboli et al found only one breed lower of the 10 they looked at. Why do you not consider this a problem? (Ne is "effective populaton size" - a measure of genetic diversity).
DB:Again if you look closely they followed out nine generations not to the beginning of the closed stud book. It is like comparing oranges to steak.
JH: how is saying that other breeds are worse an argument for not taking action in the Toller?
DB: I don't know if you are familiar with inbred mice. There are 100s of laboratory strains that are completely inbred- ie homozygous at every locus. They breed prolifically and are healthy. They are not living in the wild but neither are domestic dogs. Purebred dogs are definitely inbred and have small effective population sizes. The majority of them are healthy, look and act like each other (within a breed) which is what people want. It may be that there are some breeds that are in danger- I have not seen any scientific evidence for that. The "action" that I have read about in the Toller was not based on a scientifically documented need. In addition the "action" that I read included testing parents of the outcross to ensure that they did not have or carry all the diseases that NSDTR have been documented to get. The problem with that is we do not have tests for those diseases... Outcrossing without a clear scientific plan does not make sense to me.
STATEMENT FROM MARIA WILBE ET AL
To whom it may concern
A statement concerning the genetic basis for the immune-mediated rheumatic disease and steroid-responsive meningitis arteritis disease complex in Nova Scotia duck tolling retriever dogs
It has come to our attention that our recent publications concerning the genetic risk factors for the immune-mediated rheumatic disease (IMRD) and steroid-responsive meningitis arteritis (SRMA) disease complex in Nova Scotia duck tolling retriever dogs or “Tollers”, has left some uncertainty concerning the genetic basis for the disease complex. We would therefore like to explain our views and to clarify this subject and its implications for breeding. The disease is complex and has many genetic risk factors and therefore we cannot provide recommendations for breeders exclusively on the basis of genetic testing for dog leukocyte antigen (DLA) class II genotype.Edit September 20: added links to Dr Bannasch's references
1. The inheritance of the IMRD and SRMA disease complex All our data and all data we are aware of concerning the inheritance of IMRD and SRMA disease complex indicate complex inheritance. This means that there are several genetic factors involved that will influence the disease phenotype. Furthermore, environmental factors will also influence disease status. This means that any given Toller dog has inherited a particular combination of genetic risk factors and that the development of and severity of disease will depend on which combination of the genetic risk factors it has inherited, but also the overall genetic background and the environmental factors that the dog will experience during its lifetime. Importantly, like in other complex diseases, as a consequence of unique environmental exposure the disease aetiology for the disease complex will differ in different Tollers even though they have inherited the same set of genetic risk factors.
It should be noted that our genome-wide association (GWA) study presented in our Nature Genetics paper from 2010 (Wilbe et al. Nature Genetics 42:250-254) was based primarily on a case- control population of Tollers from Sweden and Finland and validated using Tollers from the US. In these Tollers, significant association was obtained for all five regions. Importantly, some were stronger than others and only two was shared between IMRD and SRMA. The frequency of the actual genetic risk factors may differ in different Toller populations present in different countries. However, they are likely to be similar given the population structure in Tollers and how the breed was created. All of the current Tollers, world-wide, are derived from a small group of dogs that survived two devastating outbreaks in the early 20th century of canine distemper virus epidemics. This resulted in what geneticists call “genetic bottle-necks” and a strong founder effect for the genetic risk factors causing IMRD and SRMA.
The results from the GWA study identified five regions containing many strong candidate genes involved in T-cell activation (Wilbe et al. Nature Genetics 42:250-254). In our Immunogenetics paper from 2009 (Wilbe et al. Immunogenetics 61:557-564) we showed that dog leukocyte antigen (DLA) is another genetic risk factor for development of IMRD. The studies provided conclusive evidence that there are multiple genetic risk factors underlying the IMRD and SRMA disease complex. Importantly, we showed that some of these risk factors were specific for IMRD and that some were common between IMRD and SRMA. The actual mutations causing the disease have not yet been conclusively determined. Intensive research efforts in our laboratory are in progress to identify and validate such mutations. When the mutations have been identified and correlated genetically to disease development genetic tests for all the mutations can be developed.
2. The role of dog leukocyte antigens (DLA) class II in Immune-mediated rheumatic disease The results presented in our Immunogenetics paper from 2009 (Wilbe et al. Immunogenetics 61:557- 564) identified one DLA class II type as a genetic risk factor for the immune-mediated rheumatic disease (IMRD) but not for steroid-responsive meningitis arteritis (SRMA). If a dog has inherited the risk DLA class II type from both parents it likely has an increased risk of developing IMRD. Importantly, the DLA class II type is not the only genetic risk factor, which means that some dogs without this risk factor can still develop IMRD and the opposite is also true. Some individuals with the DLA class II risk type do not develop disease. Our data clearly showed that homozygosity for the risk DLA type is increased among IMRD-affected Tollers. The results from this study were based on a case-control population, which means that we used all our cases and compared to the same number of healthy dogs. Therefore, neither the frequencies of diseased dogs nor the frequencies of haplotypes do reflect the total frequency in the Toller population. A total of five DLA class II haplotypes was identified and this is similar to most other dog breeds. Furthermore, Hughes et al. (Tissue Antigens 75(6):684-90, 2010) identified two additional haplotypes which gives the Tollers a total of seven known DLA haplotypes. Typically, one or a few DLA types are increased in frequency in any given dog breed. However, we cannot accomplish reduced incidence of IMRD only based on a breeding practice based on DLA genotyping. Inadvertent increase in the frequency of any of the other five known genetic risk factors may be a consequence. We anticipate that when we have DNA tests for all genetic risk factors and knowledge of how they interact we may be able to give potential breeding recommendations how to reduce incidence of the disease.
3. DNA tests and Recommendations for breeding Commercially available DNA tests for DLA have been offered to Toller breeders since 2010. This DNA test can be used to identify carriers of the DLA risk type in heterozygous or homozygous form. Any DNA laboratory skilled in the art of DNA testing can perform this test and there is no patent protecting its use. Importantly, we have not yet established diagnostic DNA tests for the other five genetic risk factors. The establishment of such tests will require some further research. However, at present testing for DLA only is of limited use. We cannot provide recommendations for breeders exclusively on the basis of genetic testing for dog leukocyte antigen (DLA) class II genotype. We strongly discourage breeders to perform their dog breeding only on the basis of DLA genotyping. This may lead to increased risk of inheriting unwanted combination of other major genetic risk factors for the disease complex. Attempts to reduce the incidence of the IMRD and SRMA disease complex can and should only be based on genotype data on all the genetic risk factors, thereby avoiding the most disadvantageous combinations of genetic risk factors. Therefore, there is no current way for breeders to perform DNA testing to reduce or eliminate this disease.
Göran Andersson1, Dannika Bannasch2, Helene Hansson-Hamlin3, Kerstin Lindblad-Toh4,5, Hannes Lohi6, Claire Wade7 and Maria Wilbe1 1Department of Animal Breeding and Genetics, Swedish University of Agricultural Sciences (SLU), Biomedical centre, Box 597, SE-751 24 Uppsala, Sweden.
2Department of Population Health and Reproduction, School of Veterinary Medicine, University of California Davis, Davis, CA 3Department of Clinical Sciences, SLU, Box 7054, SE-750 07 Uppsala, Sweden 4Department of Medical Biochemistry and Microbiology, Uppsala University, Box 597, SE-751 24 Uppsala, Sweden.
5Broad Institute of Harvard and MIT, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA. 6Department of Veterinary Biosciences, University of Helsinki, Box 63, 00014 Helsinki, Finland. 7Faculty of Veterinary Science, University of Sydney, NSW 2006, Australia
September 12, 2011
"That is what gives the apparently very high inbreeding coefficients. If this same analysis could be done in other breeds the numbers would likely be similar."ReplyDelete
Actually, calculating the COI in Staffordshire Bull Terriers is quite easy due to the online pedigree databases we have.
(27.000 + pedigrees online)
and this one, that does not show the inbred percentage:
The inbred percentage of my own two dogs is 4.064% and 9.9837% and they are considered to be "line bred" seeing a dog of above 15% is quite rare in Staffordshire Bull Terriers.
The most inbred dog I know of is 27.6789% and is out of a brother to sister mating which is now banned.
Shame on you, Dr Bannasch, letting your hobby interfere with scientific thinking. I'm simply speechless that someone who calls herself a scientist can ignore - or as in the case of lab mice, distort - scientific facts in such a manner.ReplyDelete
"The ideal sampling would be to follow a cohort of dogs and report their incidence of disease. Obviously this is impossible."ReplyDelete
Am I being dense in not understanding why this is impossible?
I would submit to Dr Bannasch that the goal in purebred dogs and dogs in general should not be compared to other animals with perhaps the exception of the domestic cat. We ask far more of dogs, over a longer period of time than we do any other domestic animal. No one cares if you have a particularly stupid neurotic steer with a COI of 65% or a rabbit that is suffering from an impaired immune system that would manifest into cancer at an earlier age.ReplyDelete
I raised show rabbits for years. Some I admit were very inbred but to me the stakes in that realm is different than an animal who needs to have a long life and die of old age related issues. In rabbits, it's ok to literally eat your mistakes at any point in the process and never allow an animal to needlessly suffer either from poor health or poor conf. With dogs we have no such luxury because dogs are special in western society.
The bottom line is that someone sought to be the change they wanted to see in the world and they did it with the dogs in mind. I will be eager to see a few years down the line how this German project progresses.
"The inbred percentage of my own two dogs is 4.064% and 9.9837% and they are considered to be "line bred" seeing a dog of above 15% is quite rare in Staffordshire Bull Terriers.
The most inbred dog I know of is 27.6789% and is out of a brother to sister mating which is now banned."
Excellent example---I believe that Staffies have a huge effective population.
I'm the owner/operator of TollerData, the world-wide database of Tollers. While I certainly applaud the AmStaff community for their database of 27,400 dogs, Tollerdata already slightly exceeds that number.ReplyDelete
What is more important to this conversation is that we can trace every dog in TollerData back to the breed foundations. In many dogs, there only 9 or 10 generations before the pedigree completely terminates. What's interesting is that this is true of Canadian, US, and the European dogs. In short, though we don't necessarily have the entire gene pool, TollerData may represent the most complete look at the Toller in existance. From this, of course we have a higher COI than some other breeds. Where we have complete records and all are included in the COI computations, other breeds have holes in the pedigree records and those holes produce a lower COI.
Further, rather than just a pedigree database, we've made a real effort to make TollerData a repository of health and genetic information so that breeders world-wide can make informed decisions. Thus, while all Tollers can't have their hips graded and recorded by OFA, they can be graded according to the specific national grading scheme and then recorded in TollerData.
While I applaud legitimate efforts to improve the quality or programs of the breed and breed clubs, the effort by Mr. Dauber merely produces a cute puppy of no real value to the art or science of breeding better dogs.
Eric Johnson said...ReplyDelete
"Where we have complete records and all are included in the COI computations, other breeds have holes in the pedigree records and those holes produce a lower COI."
This is frank excuse making. I have a wonderfully researched analysis of Afghan hound pedigrees, comprising dogs born from 1998 to 2008, that goes back a complete twenty-four generations. Most of the pedigrees go back somewhat farther than that. The average COI is about 20%. Tollers obviously do not have a lockdown on long, complete pedigrees.
Due to the research of dedicated breeders, I can trace the pedigrees of my Salukis back to the original imports, some of which are fairly recent as such things go, and can, depending on the breeding, lower the COI. Not always, though, which is why your remark is especially specious, because you can run that COI up pretty high very quickly depending on how you breed. I own a Saluki bitch (not of my breeding) that goes back to a Saudi import from 1970 (which means that part of the pedigree stops there), and six more imports in the fifties (more blanks.) Her COI is (to me) a staggering 37.6% for her entire pedigree.
One of my Azawakh has two dogs from Africa four generations back and her COI is 15%. Her pedigree goes back ten generations, and quite a lot of that is blank because Azawakh have only been in the West since the early seventies.
Don't talk garbage.
"While I applaud legitimate efforts to improve the quality or programs of the breed and breed clubs, the effort by Mr. Dauber merely produces a cute puppy of no real value to the art or science of breeding better dogs."
Bushwah. You want a lesson in really selective breeding? Breeding for 'real' traits, not just cosmetics? Do a cross-breeding with the goal of back-crossing. That is, is is not, how all recent dog 'breeds' were created, through the 'art or science of breeding better dogs.'
Jess, Toller breeders, by and large, breed for the TOTAL dog. That's why so many of the top show dogs since we went into AKC have performance titles as well. We pride ourselves on it, there is much pressure on breeders and owners to ensure we prove our stock.ReplyDelete
As I posted after the mutt pictures, of the five AKC Best in Show Tollers, ALL have performance titles, four of the five, field titles, the one that doesn't have a field title is hunted over each season.
You're the one who is spewing garbage. Keep to your own breed. Leave ours alone.
@ Eric Johnson:ReplyDelete
Its not an Amstaff pedigree database.
They are Staffordshire Bull Terriers.
You can trace most dogs all the way back to 1936 to the founding dogs of the breed.
So please don't say the pedigrees have holes in them as they don't.
So your comment: "From this, of course we have a higher COI than some other breeds." does not stand.
Thank you Danika for the infomation, we're lucky to have people like you and claire in our breed.ReplyDelete
I wish the blog owner would post the links to the papers you cited, but, they would prove your point so I suppose its moot and I will have to look them up on my own. As it is, this comment will probably not get through, as all are being screened and anything proving her wrong is not allowed on.
What I would like to see is real discussion allowed up where breeders and non breeders can discuss this fully and un edited. But, like I stated before, the point is moot because if shes proven wrong when she attacks a breed, she stops getting paid.
Anonymous of 18.36 and some others posting here - you are beyond belief. What a credit to pedigree breeding you lot are!ReplyDelete
So, Jemima - being, I believe, a journalist running a chronicle on dog affairs - tells us about an outcrossing experiment which she finds interesting and wants to inform her readers of. Well, what do journalists usually do?
But, no - this is an attack, and if she gives over attacking the breed, she stops getting paid. Ehh - by whom? The HSUS, who perhaps bear this poor breed a particular hatred?
Are you for real?
Patrick Burns comes up with arguments against this outcross and what he says is worth reading. Is that kind of effort quite beyond you? If so, please reconsider before coming up with the antipurebred, AR, etc, etc howl of hogwash over and over again, and not merely because it is so tiresome. It discredits dog breeding. Do you ever stop to think about how you look to the rest of the world?
Gun dogs and hunting dogs are not my strong side, and I could agree with PBurns - why not choose to outcross with a lab variety? But then again, in a few generatuions of back-crossing to Tollers, will not the offspring of these puppies look like Tollers, work like Tollers, and so... ehh, actually be Tollers? Like somebody said: isn´t that how most existing breeds were once created?
So what are you so up in arms about?
The most inbred dog I know of is 27.6789% and is out of a brother to sister mating which is now banned."ReplyDelete
KC banned yes.. does not mean it does not happen..
Glad to see the post made it through, now how about those toller breeders that are complaining that their posts were rejected?ReplyDelete
Probably HSUS, wouldn't put it past them. Hey, weren't they recently given a D because less than 1% of their donations goes to helping dogs? But right, the auditors must be lying!
What we're so "Up in arms" about is the fact that they are taking one of the more healthy breeds out there, and crossing it with a breed that will increase the health problems, not decrease.
But arguing is also moot, just like the people who defended PETA for years.(weren't there reports of them burning down houses of breeders in an extremist plot?) People will defend her because, of course, if you see it on TV and read it online, it MUST be true, right? This is an attention grabber, Dauber is doing this for attention, and so is the owner of this blog. When facts start get put up there, people will respond more positivly. Until then, its people who don't know what they're doing, who have not been breeding for that long, and have no genetics expirence trying to attack a group of people who have apparently been too honest. Its people like this that make real breeder's jobs harder because now other breeders won't want to admit whats in in their line. Thanks, SO much.
Anon@18.36 - I moderate posts to guard against legal issues but as I have said many times before, I publish almmost everything unless it is just pointlessly abusive - although, actually, I publish most of those too.ReplyDelete
It can sometimes take a while for Comments to appear if I'm busy. I missed one this morning, for instance, which I have only just published. Please note too that Blogger won't accept very long Comments and it's rather easy to miss the notification telling you that your Comment is too long. You may, then, have to split a long Comment into two.
I am not into censorship and the whole point of the blog is debate. There has been lots of great Toller info posted in the past few days which helps inform everyone (such as, for instance, the breeder who said that a group of Toller breeders were exploring using unregistered Tollers). Retrieverman, meanwhile, has posted some useful history - and there's been an interesting exchange re Toller working ability. I've learned something and I hope others have too.
I see that some Toller forums are claiming I am censoring posts. I am not - other than for the reasons clearly stated.
If you - or anyone - feels I have not published a Comment that makes a useful point, please email me: firstname.lastname@example.org.
Anonymous (19 September 2011 05:06) whined...ReplyDelete
"Jess, Toller breeders, by and large, breed for the TOTAL dog. That's why so many of the top show dogs since we went into AKC have performance titles as well. We pride ourselves on it, there is much pressure on breeders and owners to ensure we prove our stock."
Blah blah blah. "Ourrrrrr dogs have titles at both enddddddssssssss. That makes it A-OKAY for us to LIE THROUGH OUR TEETH about why the average COI is so hiiiiiiiiiigh."
You know what? If you'd said something like, "Yeah, we know the COI is high, but we're really working to lower the average as much as we can. The breeders of the past made some breeding decisions that didn't take the overall genetic health of the breed as a whole into consideration. They didn't have the knowledge we do today, and we're trying to fix any damage that was done." You'd have the high ground. But you didn't. You made excuses, and LIED about why the COI is so high.
I could give a rat's ass whether your dog is the freaking Pope. YOU DO NOT DO YOUR CAUSE ANY FAVORS WHEN YOU LIE. Especially when it's such an easy lie to expose. You know why? Because now people are going to wonder just what else you are lying about.
Have fun with that.
"Jess, Toller breeders, by and large, breed for the TOTAL dog. That's why so many of the top show dogs since we went into AKC have performance titles as well. We pride ourselves on it, there is much pressure on breeders and owners to ensure we prove our stock."ReplyDelete
"As I posted after the mutt pictures, of the five AKC Best in Show Tollers, ALL have performance titles, four of the five, field titles, the one that doesn't have a field title is hunted over each season."
Both of these are red herrings. Those has nothing to do with the dog. They are merely values humans have imposed onto them.
Yes, working the dog does ensure the traits are still there, however it is not without consequences. An artificial genetic bottleneck is still created. See, genes don't really care if they will run into a dead-end as long they are passed on despite being compromised by other factors.
Secondly, performances don't really means anything with the onset of technology. An American performance-bred dog is going to have a different selection pressure than one derived from Danish stock. Why? The politics behind the usage shock collar alone. One is preferred on one side of the pond; the other is banned. Right from the get-go, there are going to be different qualities valued by their trainers.
So quit imposing your own cultural values onto the dogs and start thinking scientifically.
Anon 18:36 said, 'I wish the blog owner would post the links to the papers you cited, but, they would prove your point so I suppose its moot and I will have to look them up on my own.'ReplyDelete
Nasty comments reveal so much about their authors.
Firstly, yes, copying and pasting a title into Google search is SO much effort!
Secondly, Jemima can't post the links to these papers. There's this thing called copyright. Such papers are published in academic journals that are not open-access. You either have to work in an academic institution that subscribes to such journals or pay to get the articles yourself.
Actually, I could post links to the abstracts - but as you say, in most cases not the full text. If I can spare a few minutes, will add them - just horrendously busy at mo.ReplyDelete
And, as you say, not that hard to copy and paste into Google..
I think we all know the real reason that Toller breeders (and just about all breeders) can't make a statement such as Jess suggests is that yes, though many of them are much more conscious of and knowledgeable about the connection between genetics and health than their predecessors, because they are trapped by the outdated science required by 'purity', they want to fix the problem through variations on more of the same bad practices.ReplyDelete
As Dr Bannasch points out, if you take a pedigree back to the founders, the COI of any 'purbred' dog will be high. You can fool yourself that you are lowering the COI as long as you don't go too far back. That does not change any facts.
I agree with Dr Wilbe et al that making breeding decisions solely on the basis of one genetic test is not the answer to the problem. Of course such tests are valuable for the information they provide and I'm not saying that the tests shouldn't be done and taken seriously, but to see them as a solution in themselves is a bit like thinking that if you take vitamin pills and continue to eat nothing but junk, all will be well. It isn't going to work because it is not that simple.
I do find Dr Bannasch's position that the introduction of new genetic material to solve a genetic problem should be a last resort somewhat disturbing. How bad does it have to get before such action would be acceptable? Would such a position be acceptable if we were talking about humans?
"I do find Dr Bannasch's position that the introduction of new genetic material to solve a genetic problem should be a last resort somewhat disturbing."
I'm so glad someone else thought that too. As we've seen time and again, you can get back to a desired conformation in a few generations if you plan well, so what's the problem?
All this 'purity' nonsense is really creepy.
I apologize for mis-identifying your breed...truly I am.
The point is that we have a far more complete entry of dogs in TollerData than do many of the other breed databases simply because of the relative "newness" of the breed. We can trace our records to the original dogs truly named Lassie and Rufus and Bobo and those dogs lived in the 1960's!
One of the things that doesn't seem to be recognized here is the wide diversity that has always been in the breed. I won't attempt a complete history lesson. The short version is that in 1936, Col Cyrill Coldwell began his quest to have Tollers recognized by the CKC. This was completed in 1945. However, the interest in the breed was not there and between 1945 and 1960, no Tollers were even registered. There was some breeding going on but the offspring were not registered.
Enter the Nickerson's, Avery and Erna. Avery had a nearly life-long passion for the breed and he and Erna developed almost from scratch their line of Tollers under the Harbourlights (initially Green Meadows) kennel name. They were assisted by Eldon Pace from Schubendorf kennel.
At about the same time, Hettie Bidewell began to register her dogs, first under the Bidewell kennel name and then later as Chin-Peek. She'd been breeding for perhaps 10 years but had not registered them. In 1962, she was contacted by Eldon Pace and Avery Nickerson seeking help registering a litter.
The point of all of this is to create a historical perspective. Col Colwell began with unregistered dogs from the backyards of NS. There wasn't the care in breeding then that there is now. A farmer would take two dogs that he thought would get him to where he wanted to go and simply breed them. Then the breed appeared to die out but after 15 years, began it's resurgence. Both Ms. Bidewell and the Nickersons kept other breeds and there is supposition that before they began registering dogs that some cross-breeding either was done or just happened.
Thus, while the breed had an earlier beginning, the records largely can be traced to the early 60's. However, for the years before that, all manner of breeds were used to eventually produce the Toller of today. If you look at a 10th generation pedigree of a Toller, you'll often find 1 or more of the first dogs of the resurgence, dogs whose parents could indeed by anything. This would be unlike some of the other breeds.
Now, let's look at a couple of genetic issues, PRA and CEA. When PRA was discovered in the breed, there was no genetic test. Within the past 10 years, PRA has been established to be a simple recessive and the genetic test proven. Under normal circumstances, the population of Tollers should have been 25% clear, 50% carriers, and 25% affected dogs. This hasn't proven true. The huge population in the US and Canada that has been tested has produced far fewer affected dogs (8% or so). This is because the Toller breeder in the US and Canada went after the PRA problem with hammer and tongs to the point of eliminating, before there was a test, many dogs that could have been PRA carriers and affected. However, the Toller breeder of today has no interest in eliminating PRA from the breed. Instead they use the genetic test to make informed decisions on breeding partners. The recessive gene will always be in the breed but we hope to not produce PRA affected dogs. (Interestingly, the Toller community in Europe was late in adopting the PRA test because the registering agencies were very slow in recognizing the validity of the test. Now, in the name of genetics, a European breeder cross-breeds a dog that is perhaps only 8-9 generations "a Toller" to a breed that may in fact be one of the progenitors of the breed?)
In December of 2006, a routine CERF examination discovered Collie Eye Anomoly in a Toller. Less than 6 months later, the genetic test for CEA was announced and already hundreds of dogs had been tested. Again, it's a simple recessive so again, breeders are managing the problem without resorting to draconian measures. This makes two points. First, the disease is called Collie Eye Anomoly for a reason and its prescence in the breed is a bit of proof of genetic diversity. Second, the speed at which the test was found, validated, and put into service shows the committment of the Toller community. The breeder whose dog was discovered with the problem didn't hide it and neither did the Toller community exhibit kennel blindness on a grand scale.
Given the reasonably short time that the Toller has been bred under the controls of a registration process and the diversity that was already within the breed "founders", the Toller community simply sees no reason why we need to contribute a Toller-Doodle to the population of dogs. If Mr Dauber wishes to breed his dog to another breed, I have no interest in stopping him. However, I would expect him to not claim that his puppies are Tollers.
then why are you on this blog if you think the pure bred dog is "creepy"? .. get yourself a nice mutt ( like the ones pictured here)ReplyDelete
Anyone who doesn't find the concept of purebred 'creepy' simply doesn't know their history. Do a Google search on dogs/eugenics/Leon Whitney.
"then why are you on this blog if you think the pure bred dog is "creepy"? .. get yourself a nice mutt ( like the ones pictured here)"ReplyDelete
Because (unlike you, it would seem), I understand the difference between a pedigree dog and the creepy need of some breeders to close a registry for a misconceived notion of keeping the registry 'pure'. And like many others on here, I understand and share the concern that breeders with creepy notions of the value of purity in genetic material based on arbitrary delineations created by a bunch of Victorians are causing untold suffering to dogs.
Besides, owning a mutt (which I do, proudly) does not preclude having an opinion on the topics explored in this blog. As I've said before, it's not just breeders who have the right to an opinion on dog breeding. You could have bred dogs for thirty years, and still be utterly clueless of the damage you are causing.
Thank you for the considered response and thehistorical info, Eric.ReplyDelete
Do all the dogs go back to just those three dogs in the 60s? If so, could you explain why you think today's dogs may be benefitting from those original dogs'presumed diversity given 50 years of breeding within a small gene pool since then? Has there been any ingress of new blood at all in that time? Perhaps from unreg'd dogs?
Of course many breeds are founded on very few effective founders, so the Toller is not unique in that sense. But I do think it makes keeping a breed healthy long-term an uphill battle, however vigilant breeders are.
"Within the past 10 years, PRA has been established to be a simple recessive and the genetic test proven. Under normal circumstances, the population of Tollers should have been 25% clear, 50% carriers, and 25% affected dogs. This hasn't proven true."
Don't quite understand your stats. This would be entirely dependent on the carrier rate within the breed, surely?
"First, the disease is called Collie Eye Anomoly for a reason and its prescence in the breed is a bit of proof of genetic diversity."
Well not really proof of genetic diversity today - although granted a bit of proof that there's a collie breed in the mix somewhere. So perhaps the Aussie is not that illogical a choice to go for as an outcross?
"If Mr Dauber wishes to breed his dog to another breed, I have no interest in stopping him. However, I would expect him to not claim that his puppies are Tollers."
Well he's certainly not claiming that his first-gen cross are Tollers. Would there be any point in a backcross project that you would consider them Tollers? Three gens? Five Gens? Ten gens? Twenty gens?
Lying? Toller breeders are not the liars here. Jemima is a liar (she said she would post Dr. Bannasch's reply "as soon as" she got it. It was weeks. She put on the Can-Gen list that she was doing a film, and that it would NOT be sensationalistic - but it most certainly was). The people who don't know Tollers are probably less liars than just stupid like you Jess.ReplyDelete
No point in discussing because we can't fix stupid.
As has been put on the Toller list, we shall ignore the many troglodytes on the blog and go onto our business of breeding the best dogs we can with direction from several great researchers.
And Jess, if I were your Mother, I'd send you to bed without dinner. Does she know about that mouth of yours? I'm quite sure she'd be horrified.
All the registered dogs go back to dogs like those three. I simply picked out those three names. We also have a LassieA and Quinnie and Sassie and Flash and Dilly and Buffy ..... etc. The point is that the dogs at the root of the pedigrees all had an unnamed sire and dam and they are at only the 9th or 10th generation. Who knows what was at the 11th. As for your question of unregistered dogs....that would be telling stories out of a school that was before my time.ReplyDelete
The typical distribution of a single recessive condition would be 25%, 50%, and 25%. The early breeders would find a dog with PRA and then use reverse pedigree analysis to remove dogs from the gene pool, both affected dogs and suspected carriers. The result is that carrier and clear dogs are in the over-whelming majority today. Whereas, random distribution would say 25% are affected, we are showing 8%. The PRA researchers were amazed at this number because there is simply no way it could occur naturally. The Toller breeders were determined, even without a genetic test, that they could defeat this and very nearly did. Now that we have a test, our emphasis is elsewhere. Whereas PRA was a horrible condition, now it hardly exists. However, the Toller breeder has learned to not eliminate the gene but rather to simply breed around it.
I guess what I'm saying is that the outcrosses have already been done. This is supported by both the science and by the history of the breed. There's really no reason for them now other than to stir up controversy.
Thank you Eric. Am still confused re your PRA stats. Your randome distribution figure assumes that every Toller is a carrier - when presumably this is/was far from the case? No real matter if, as you say the PRA affected rate is dropping thanks to careful breeding and a DNA test, although I do think that 8 per cent affected is still fairly high - clearly some carrier/carrier matings are still being done?ReplyDelete
A bit of research also reveals that the founder dogs you mention were not as genetically diverse as you wrote before:
"The first registered litter of Tollers appears in the 1959 CKC Stud Book. The parents of this litter were full siblings - Chin-Peek Golden Kim x Chin-Peek Trixie Girl. Over approximately a five year period Hettie Bidewell (Chin-Peek), Eldon Pace (Schubendorf) and Avery Nickerson (Green Meadows, which later became Harbourlights) had nine individual Tollers, whose parents were unregistered, approved for registration with the CKC. All of today's registered Tollers can trace their pedigree back to these dogs, often within five or six generations. Six of the nine individually registered Tollers were full siblings, offspring of Bidewell's Flip and Bidewell's Lady who were Hettie Bidewell's first Tollers.
"In the late 1960's, after a decade of working to build up her breeding stock, Hettie Bidewell and the registered Toller population suffered a huge setback when many of her dogs were destroyed in a kennel fire. She painstakingly contacted puppy buyers in order to find dogs she had sold that were not neutered or spayed and also imported Pat of Schubendorf from Nova Scotia so that she could start over.
"It's interesting to note that the nine original dogs produced a total of 81 registered puppies and more than one-third of those puppies, 30 in total, were actually bred. However, Chin Peek Trixie Girl produced two registered dogs but neither of these produced any registered puppies. Essentially, this means that Toller breeders today are dealing with four individual lines, no matter what they're currently breeding. Chin-Peek Golden Lucky Kim represents the most diverse of early pedigrees by encompassing all four original lines."
Anyone who doesn't find the concept of purebred 'creepy' simply doesn't know their history. ..
I know my history.. and I appreciate the pedigreed dogs and their breeders. are you trying to say that pedigreed dog shoud be eliminated like the belief of the HSUS/RSPCA and their minions?
The result is that carrier and clear dogs are in the over-whelming majority today. Whereas, random distribution would say 25% are affected, we are showing 8%.ReplyDelete
I do think that 8 per cent affected is still fairly high - clearly some carrier/carrier matings are still being done?
what part of 92% don't you understand?
So, Anon @ 20:48, you think that it's OK that one in 12 Tollers have PRA when you have a DNA test that should enable you to avoid producing any affecteds?ReplyDelete
Anon 20:45 said,ReplyDelete
‘I know my history.’
If you know your history and aren’t disturbed by it, I’ll let your statement speak for itself.
‘are you trying to say that pedigreed dog shoud be eliminated like the belief of the HSUS/RSPCA and their minions?’
Oh, that tiresome leap in logic again.
No, I’m not.
Why does criticizing the notion of absolute purity, and calling it what it is, always result in the accusation that this automatically means that the critic wants the destruction of recognizable breeds? Can’t those of you in the Purity Brigade come up with something better than an illogical leap to attack your critics and defend your position of purity above all?
I too value the different breeds and want them preserved. I currently have Belgian shepherds myself, for heaven’s sake, and if you want to know about how passionately I feel about their preservation, take a look at my comments in the ‘M is for…?’ blog. I just live in the 21st century, not the 19th, and reject pseudoscience based on morally repugnant social theory of another era.
And yes, I too value the dogs and those breeders who breed for function and health. I do not value breeders who are destroying the health and welfare of sentient beings through playing God while adhering to detrimental practices that are long past their use-by date.
If you think that anyone who does not insist on absolute purity at all costs is out to eliminate breeds, why don’t you add the Government of Canada to your Official List of Enemies of the Purebred Dog:
Animal Pedigree Act (R.S.C., 1985, c. 8 (4th Supp.))
30. (2) No association may, by its by-laws, determine that an animal is a purebred of a distinct breed if the animal has less than SEVEN-EIGHTHS of its inheritance from the foundation stock of the animal’s breed or from animals previously registered as purebreds by the association (my capitals).
Thank you for this link which explains:ReplyDelete
"CERF reports the combined frequency of PRA and PRA-suspicious status in Tollers as 7% of 693 dogs with CERF exam records between 1991-1999. This is a high disease frequency, and might suggest that a large proportion of dogs at risk for PRA are selected for CERF exams. If the CERF frequency is valid, it indicates a high rate of carriers in the Toller population, possibly as high as 40%. This will become clearer as larger numbers of Tollers are OptiGen tested."
So in dogs up to 1999, 7% PRA affected - which is considered a "high disease frequency" by Optigen - and a suggested carrier rate of up to 40 per cent. Eric, are you know saying that the rate is 8 per cent - in which case it hasn't improved?
As Eric points out above, Optigen has also offered a DNA test for CEA/CH in Tollers since 2006. I realise this condition can be very mild. How common is it in Tollers?
Eric Johnson said...ReplyDelete
"The early breeders would find a dog with PRA and then use reverse pedigree analysis to remove dogs from the gene pool, both affected dogs and suspected carriers. The result is that carrier and clear dogs are in the over-whelming majority today."
What Eric does not say is that this would eliminate large numbers of dogs from the breeding population. A single affected puppy in a litter would slate both parents and all the puppies for removal from the gene pool. This creates an artificial bottleneck, and would possibly negate any 'diversity' that comes from the 'unknown' ancestors, much like popular sire syndrome does.
I must not have expressed myself clearly. In the beginning, there was no test for PRA. The breeders did reverse pedigree analysis and removed from the gene pool lots of dogs, probably many that were neither affected nor carriers of the condition. When the test that was developed, the first dogs that were submitted for testing produced an affected rate of only 7%. Now, look at the mode of inheritance and frequency of PRA.ReplyDelete
A dog is defined as clear or normal if it has no PRA genes. A dog is defined as a carrier if it has one PRA gene and one clear or normal gene. Both the carrier and the clear dogs will be unaffected and will test negative for PRA in an eye exam. A dog is defined as affected if they carry two copies of the PRA gene. The outcomes of the different crosses of these dogs are as follows:
Clear X Clear = 100% PRA Clear puppies
Clear X Carrier = on average, 50% PRA Clear, 50% PRA Carriers
Clear X Affected = 100% PRA Carriers
Carrier X Carrier = on average, 25% PRA Clear, 50% PRA Carriers, 25% PRA Affected
Carrier X Affected = on average, 50% PRA Affected, 50% PRA Carriers
Affected X Affected = 100% PRA Affected
The first three crosses or breeding strategies will not produce disease and can be implemented without producing an affected dog. The latter three crosses do produce disease and are not recommended.
The breeders, without benefit of a genetic test, were producing puppies that were essentially clear or carriers, not affected. This is way better than random selection. The 7% of the dogs produced were from before the test was available. The rate is continuing to decline but the rate still includes those early, pre-test, breedings.
Now, let's look at the statistics on PRA from the OFA site. For PRA in Tollers, they show an n value of 693 dogs as of Dec 2010. Of this, there are only 0.5% dogs affected and 77.9% dogs with a "normal" ("clear") rating. What we've seen is that since the test was created and the offspring of successive breedings tested, the "affected" share has plummented.
However, the breeder attitude towards PRA has changed and changed drammatically. Whereas the breeder used to aim for only clear to clear breedings, now any breeding involving one clear dog is accepted because none of the dogs will be worse than a carrier. This attitude was recommended by Dr. Aquirre (developer of the test) with the thought that breeding only clear dogs to eliminate the disease could bring about the rise of some disease for which we don't have a test. This happened with both the Malmute and the Portie.
You argue that there are too few dogs in the ancestry of today's Toller. Granted, there are only a few dogs that are named as the orgins of the breed. (As it happens, on TollerData we have a number of unregistered dogs shown as sires and dams that you would not know about from the studbook.) However, simply put, how does this breeding help? There will always be Dakota and Tessa as the F0 generation. Suppose that this cross takes off and there are hundreds of dogs by the time of the F10. Still, every one of those dogs will genetically go back to Dakota and Tessa. How is that better? In fact, asked another way, how is that not worse than the current situation?
Now, let's look briefly at genetic disease and it's incidence using Dr Padgett's book. At the back of the book is an appendix called "Genetic Disease Predisposition by Breed". When we look at the physiological systems (eyes, immune, hearing, etc) involved in both the Australian Shepherd and the Toller, we find that the Aussie has 13 systems with issues whereas the Toller has but 6. Drilling down into one of these, the Toller has one disease related to Immune issues but the Aussie has the 5. System after system we see the same thing. In short, the Aussie is a train wreck compared to the Toller. Why do you expect the Toller community to support a breeding that potentially goes backward, not forward?
I did a little digging into the "Lab mice are inbred and totally healthy" argument presented by Bannasch, and found that the leading supplier of lab mice is rather candid about how messed up they really are:ReplyDelete
Those Inbred Lab Mice
I don't think anyone wants dogs like that nor does anyone have the resources to breed dogs in that manner which actually tries to minimize those already horrible outcomes (massive breeding programs with huge failure rates).
Thanks for this, Christopher - useful.ReplyDelete
I think some thought needs to go in to how to construct a strong, scientific argument. Your argument should have nothing to do with the person behind the comment, it should clearly and concisely take what they have said and give a counter debate using evidence as a basis. Getting nasty doesn't help your point and only belittles your own argument.ReplyDelete