Sorry the research was done on affected horses. So the statement is a pure guess. You are spreading a guess and make it sound probable…And you did a great job. Now everybody is mixing up different things…
I understand the financial implications may make it impossible to prevent the breeding of carriers, particularly if it’s already widespread, but I’m not sure ANY degree of athletic improvement makes it ethically defensible.
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I remember this topic being discussed 5 years ago on this board. When I did a search for the topic yesterday I found even earlier posts from 2009 buried in a rescue thread, about a foal who was euthed. In it, the poster was corresponding with Dr. Winand who was looking for data on the foal’s fatal HERDA-type problems. Fast forward to 2013, when it comes up again on a thread about an Arabian sporthorse sire that was known to be a CA carrier, again citing Dr. Winand who had now developed the genetic test for WFFS. At the time it was brought up, because I was completely unable to find anything other than commercial advertisements for the genetic test, I was quite convinced it was a money grab. I was very, very wrong, and there is peer-reviewed research now available.
Do a search for “winand” to see the threads. Make sure you go to the actual post, because the 2009 thread is 240 pages long.
Incredibly (in view of my past beliefs on the subject of heritable diseases) I find I am on the fence now as to whether WFFS carriers should be bred. Dr. Winand was of the opinion that this syndrome has been around for a long, long time. The extremely high morbidity of affected foals/fetuses was a smokescreen, so few affected offspring actually progress far enough to be foaled out.
And i agree with the posters that are viewing carriers with trepidation. It is too early to determine if carriers are completely unaffected. In order for a genetic mutation to spread in a large and diverse gene pool, it has to be selected for in some fashion. But it occurs to me that the fact that it is only found in 10% of the population after, say, 100 years, makes me think that carriers are not being selected for any specific trait. And I could be as wrong on that as I was about the notion that WFFS was a test in search of a disease.
As genetic knowledge improves, we may find many previously unknown afflictions. At what point do you stop culling? When there is nearly nothing left? What if gene therapy becomes feasible?
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You truly aren’t comprehending my posts are you? Let me pull out what I have stated, and I’ll bold the things that contradict what you seem to have decided I’ve said:
How does “might have” translate to “probable”? I’m not guessing at anything. I am re-stating what is is already being tossed around by those who are actually studying this stuff. The thought that HERDA carriers could ever have any competitive advantage never crossed my mind until several years ago when someone mentioned that was being studied. And nobody in that conversation ever took it as “probably”, but they did state they knew breeders who purposefully wanted HERDA carriers because they did believe there was a competitive advantage.
When you find that “one-third of the top hundred cutting horses (from 1985-2006) were confirmed HERDA carriers”, and “Twenty-seven percent of the lifetime earnings from progeny of these top 100 cutting sires are derived from 12 HERDA carriers” you can’t help but start to wonder.
See below. Again.
See? And all of it is “could”. Not “probably”, not “will”.
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I agree, I think (yes, an opinion lol) that WFFS does not bring any benefits to the horse. I actually DO suspect it is totally benign for a carrier. But the fact remains that we don’t know the history of enough carriers to have even a reasonable idea that it’s just fine.
But it occurs to me that the fact that it is only found in 10% of the population after, say, 100 years, makes me think that carriers are not being selected for any specific trait.
How reasonably accurate is that 6-11% guesstimate on its prevalence? I don’t know at what point someone makes that leap, especially since the test is only a few years old, and this thread started as the result of newly discovered carriers.
Do you remember why Winard suspected this has been around a long time?
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Oh, you are so right. I should say the SUSPICION that it occurs in only 6-11%. Because that is based on a small study in Europe.
I don’t remember why she thought that, or, being a non-scientist, I was unable to grasp the reason. I’ve torn the internet apart for the last few days trying to find that reference… and to make it worse I actually got the woman on the phone many years ago, and it could have been then.
I know that many warmblood breeders are witch-hunting for a bloodline right now. If Winands was right, I suspect they will be in for a shock. I’m testing my former stallion, and the two retired broodmares on the farm. They all have fairly obscure, old warmblood lines (No R, D, W or S) so if one of them comes up a carrier, the penetration is deep.
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I so very much wish people would stop being so offended and take things personally about things like this (well, and a lot more things :lol:) It’s a MUTATION. It happens. A LOT.
The majority we never know about because they amount to nothing. Occasionally one happens that is a BFD. And often, it takes a long time before someone connects some dots. So what. Learn as much as you can, and if people are REALLY about the betterment of a breed/registry, do the right thing.
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Perfect!! Thanks for clarifying… And what I read about this study, was that they tested and worked only with AFFECTED horses and tested their tendons. And their guesses were based on what breeders believe 
I mean thats not very scientific at all… I think if I would be a scientist I would not even dare to write something… Its amazing what breeders might believe or not… but its not scientific… Maybe they chose those stallions because they produced amazing offspring… would be the same outcome…
So basically we can forget about most what you wrote. Thanks again for clarifying… And you wanting to cull all carriers is your personal opinion not based on any study… I think it is important to make it clear because this is a very very sensitive topic which needs to be handled educated and sensible (I think I wrote this before…)
Dont worry, by now JB clarified that there is no proof whatsoever that breeding carriers will bring athletic improvement and he was also talking about HERDA, this thread is not about HERDA.
And I wish people would not throw in personal assumptions and make them sound like they are science… It can really confuse people
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Wrong. Did you read the paper? While you are correct that the paper looked at affected horses, here’s the relevant quote re: carriers (note that it says nothing about “what breeders believe”):
Accordingly, the homozygous HERDA phenotype is not restricted to integumentary tissues nor to dorsal regions of the skin. This constitutes a phenotype refinement that is relevant to the investigation of the broad role of CYPB in collagen metabolism and of the CYPB mutation in clinical HERDA. In the context of human patients who are heterozygous for PARKIN and PINK1 mutations and exhibit subtle manifestations of the associated homozygous Parkinson’s phenotype [32–34], the decreased TS of tendinoligamentous structures that we observed in HERDA homozygotes highlights the relevance of quantifying biomechanical properties of tissues from HERDA carriers for attributes that could convey an advantage in disciplines requiring extremes of flexibility and lateral movement.
This was published in a peer-reviewed journal. If reviewers had felt like the authors of the study were out of bounds by suggesting that carriers could be at an advantage, the statement wouldn’t be in the paper (and in my experience, reviewers are quite likely to throw a hissy fit over a sentence or two they view as unsupportable, even in an otherwise strong paper).
ETA: forgot the citation. Here it is: J.E. Bowser et al., “Tensile properties in collagen-rich tissues of Quarter Horses with heredity equine regional dermal asthenia (HERDA),” Equine Veterinary Journal 46.2
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And another paper (this one a “review” article of the extant literature). It seems very obvious from reading these papers that they are drawing direct parallels between HERDA & other known disorders, wherein carriers DO have symptoms (which may be good or bad). Why is this relevant to the discussion of WFFS? Well, it seems like horses effected with WFFS have symptoms similar to those seen in HERDA & other disorders:
Although HERDA occurs most frequently in popular cutting horse bloodlines with a carrier frequency of 28.3% (Tryon et al. 2009), horses shown for other disciplines, including reining and western pleasure also have also produced a significant number of affected individuals with a 9.2 and 12.8% carrier frequency, respectively (Tryon et al. 2009). The performance traits of selected HERDA carriers’ bloodlines are highly desirable, which increases the frequency of the causative mutation. Although cutting horses are most commonly affected, pleasure, reining, working cow and foundation bred horses are also affected. In cutting alone, 30% of the 10 leading lifetime sires (leading lifetime cutting horse sires, all ages, all divisions) are confirmed carriers (https://www.equistat.com/). As of 2012, these three popular N/Hrd sires have produced 5792 total registered offspring. By virtue of HERDAs autosomal recessive mode of inheritance, one half of these offspring (n=2896) would be predicted to be HERDA carriers if these sires were bred to normal (N/N) horses. With common breeding practices today of mating related horses within a discipline, the number of affected homozygotes will increase if care is not taken to avoid carrier‐to‐carrier matings.
The increased prevalence of the HERDA mutation in elite performance horses has raised the question as to whether the HERDA mutation or a closely linked gene confers a performance advantage. Alternatively, these horses are simply outstanding performers in the cutting discipline irrespective of the mutation.
And:
The prevalence and economic value of Quarter Horses which carry the genetic defect responsible for HERDA assures that this disease will be observed for many more generations. As has been demonstrated repeatedly with other heritable equine diseases, the popularity of these lineages promises that horses both heterozygous and homozygous for the trait will continue to be produced. The effect of the cyclophilin B genetic mutation on the heterozygote remains to be determined. Managed breeding strategies based upon DNA testing of horses or embryos is the only method currently available to minimise the production of affected horses.
(Rashmir‐Raven, A. M. and Spier, S. J. (2015), Hereditary equine regional dermal asthenia (HERDA) in Quarter Horses: A review of clinical signs, genetics and research. Equine Vet Education, 27: 604-611)
Ultimately, I think JB’s only point was that we don’t know what - if any - negative effects come from “just” being a carrier, and the prudent thing is to figure out what - if anything - being heterozygous for WFFS means, which means caution when breeding individuals who have tested as carriers. Is it like LWO, where only homozygotes have issues? Or is it like HYPP, where an N/H horse can also be symptomatic? And the academic research backs these questions up: the researchers don’t know either, though they’d clearly like to find out, & they’re not just blindly grasping in the dark based on “what breeders believe.” “Caution” doesn’t mean “witch hunt.”
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@Albion, thank you for posting these links. The first link compares studies performed with human patients which obviously indeed show changes.
But still it does not say that there are changes in horses as well. They assume it based on the results with human patients. And your other 2 links are again talking about breeding practices… And obviously QH breeders don’t care about producing affected horses which is horrible.
And again thats exactly why it is necessary to educate Warmblood breeders about it in a way that they understand that testing is nothing bad which will result in loosing their breeding stock but something good because they will avoid aborts and and dead foals… Sorry this is my opinion and nothing will change it. And with a smart approach it will be possible to eventually hopefully eliminate it. With the hammer method I think only confrontations will happen
And it may well be that I am overreacting but I have dealt in the past with these persons in breeders conventions who repeat monotonous their ideas without any sense except that they see an advantage for themselves. If their dog tested clear they of course call for culling carriers because they sense an advantage, if they know their dog is a carrier they cry out about preserving the genetic variety and the tight gene pool !! I do not trust breeders in general I believe in transparency and correct education for breeders and buyers which will result in decisions which make sense.
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and a very good read for this topic by the way… Omertà the breeders code of silence by Sierra Milton. And no, you don’t need to pay for the read. Google it and a lot of Canine boards (Bullmastiff) quote it. It sums it up perfectly!!!
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Please don’t “mansplain” the articles to me. I posted a few pertinent quotations myself. I am capable of reading (although not a scientist myself, my PhD is in another area) and interpolating what academic articles are saying. Did YOU read the full articles? I did.
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Now, my turn to mansplain, since your mansplaining was rather off target.
<- since you seem to think smiley faces make irritating/offensive statements better. They are NOT saying “obviously QH breeders don’t care about producing affected horses which is horrible.” They are saying that very desirable performance bloodlines carry these genes in a pretty high proportion (nearly 30% in cutting horses), meaning if you’re breeding desirable cutting horses, you have a pretty good chance of breeding a carrier, since nearly 1/3rd of the population (at large - not even consider which ones are actually breeding) carries those genes.
I don’t believe all carriers of every single genetic anomaly need to be culled (culling every carrier of LWO, for instance, would result in basically no more horses with the frame gene; good Arabian lines would go down the tubes if it were declared that CA carriers couldn’t be registered). I do think having a good understanding of what being a “carrier” means is a good idea, however. Obviously, Hilltop agrees with me, since they pulled the stallion from their lineup. This is not a rare line, 1 stallion “missing” for a year (or forever, at least where his semen is concerned) is not going to torpedo warmblood breeding. You, on the other hand, seem to think urging caution = completely tossing the baby out with the bathwater. Not so.
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I don’t want to mansplain, I just think its not useful to spread information which might be interpreted in different ways in a topic which is sensible and fresh.
And I think its not useful either to imply that everybody who does not want to cull every carrier (and I am not too sure whether you support culling carriers from breeding or not because you made 2 differing statements in your 3rd paragraph.) is a breeder who is careless and will ruin the breed.
And Hilltop published that they pull the Stallion from breeding this year!! They did not say that they geld him immediately because he is a carrier. I believe this is a new situation for them and they want to gather more information what they should do. And I think that is extremely correct what they are doing. They want to educate themselves!!! Who knows maybe they bring him back next year only for clear mares…
This may be a wasted effort but…
When you breed this stallion or other stallions (or studs from various animal species) then you have to rely on the fact that the mare is clean. Obviously, you can require proof of this for breeding as the stallion owner. It just becomes a trust/validation thing that owners will only breed clear horses. The 100% fail proof way is to not breed the horse that has the mutation/condition/genetic defect/whatever.
FWIW, Information will ALWAYS be interpreted in different ways. Even if it is a definite statement. This is humans.
I appreciate this breeder being transparent. It is better to come forward with it yourself as the breeder rather than other horse owners figuring it out down the road and it becomes more of a scandal. It sucks because you will lose money, breedings, and may have a very nice stallion in every other way. Breeding is not for the faint of heart, this happens. I have had horses gelded for a variety of reasons. Maybe I was a bit too “extreme” but there are far too many horses out there that are unwanted, have major defects, or were the result of a half assed program.
I think that this stallion could continue breeding IF there is a guaranteed way to make sure the mares are clean and this is monitored. Plus, as mentioned, more research about being a carrier and any other possible effects would be useful.
So, I commend them for coming forward and I am curious to see how they handle this from here.
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I know it was back a few pages but I do think the dog breeder analogy is way off base.
You breed your not carrier bitch to a carrier dog hoping to get an amazing not carrier offspring to carry on those lines that the dog has (missing the carrier status). Approximately 60 days after breeding the bitch will give you (hopefully) a litter of puppies. Since there are multiple offspring your chance of getting a N/N are higher. But even if the horrible thing happens and they are all carrier you can spay/neuter them all (so no risks of anyone else breeding those carrier babies that you produced, not even that horrible back yard breeder) and sell them as pets and try again, wait another 60 days and pop out another bunch. Repeat until you get your amazing N/N dog you want.
Horses give you one offspring a year. Spaying is not the norm in horses so if you get a carrier mare and sell it along because it is not what you were going for, there is one more carrier out there that some irresponsible person could be breeding to another carrier.
Have you forgotten that this is a discussion forum and even you are allowed to post your personal assumptions, which you have over and over again.
The way I read every post in this thread, including yours Manni, is that we need to figure out how this affects the carrier before final decisions are made on breeding.
The opinions split with the majority saying ‘while we wait it is the responsible thing to not breed any carriers’ and some saying ‘breed away, no science says it is an issue and how dare we damage any breeding programs while the science is looked into’.
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not sure whether i understand your post right… If you breed a carrier to a clear you have a 50% chance of a clear. So I don’t really understand why its necessary to breed several litters in dogs in order to get a clear. Also most breeders I know do not think its ethical to breed a bitch over and over again every 6 months… so thats not an option anyhow…
And with horses, you also have a 50% chance to get a clear and you also have a 50% chance to get a colt which is usually gelded in the first year, so no risk of breeding…
We are talking here not about backyard breeders but Breeders who register their foals with a registry. And if the situation developes as I hope it will, there will be a lot more testing done and I really hope that stallion owners will require clear test results from mare owners for their carrier stallions.
And BTW nobody can rescue the world… There will always be people who are not responsible and there is no way to stop them. And for sure it doesn’t make sense to scare of potentially responsible breeders right in the beginning. Thats all I am saying…
The smart thing is to get as many test results as possible to figure out as much information as possible and also in order to figure out how widely its spread in the population. And you need everybody to cooperate in order to get them to test…
curious did you read Omerta, the breeders code of Silence?? I really really recommend it…
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No, Manni, that is NOT what I said. Go back and read it again. What I said directly was “I don’t believe all carriers of every single genetic anomaly need to be culled” and “I do think having a good understanding of what being a ‘carrier’ means is a good idea, however” (those are not “2 differing statements,” unless you’re willfully making up false interpretations, which you seem to routinely do on this board). I provided 2 examples where culling carriers from the breeding population would be deleterious & rather pointless, because carriers don’t have issues (CA & LWO are different than HYPP, since N/H horses CAN and DO show negative, life-altering symptoms. HERDA - at least as far as the scientists are concerned - is possibly an attractive thing to select for, at least for heterozygous status, and they’re unsure on potential negative effects of being a carrier. Is WFFS the same? WE DON’T KNOW, and NEITHER DO THE SCIENTISTS RESEARCHING IT, which was my whole point).
YOU are the one who said that the studies said that “obviously QH breeders don’t care about producing affected horses which is horrible” based on your superficial readings of the studies (or, most likely, the short quotes I provided), which is NOT what the studies said. Instead of throwing a hissy fit about statements after willfully misreading posts & quotes, perhaps you should READ the studies and actually think long and hard about what they’re saying, rather than knee-jerk reactions. No one is suggesting sending this stallion to slaughter, chopping his balls off, or permanently culling every horse that tests positive for WFFS from the breeding population; rather, they are suggesting that “hey maybe we should learn more about what this means.” Which seems a fair statement to make, rather than shrieking that expressing concern over a horse carrying a copy of a gene that may have serious, devastating consequences for future offspring (again: WE DON’T KNOW. It could be CA, it could be HYPP) equals wanting to sterilize them all and send them to slaughter. Which, as far as I can tell, has been what you’ve been doing on this thread.
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