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WFFS

It also seemed like more dressage stallions were coming up positive (ok a nonscientific observation) yet these seem like what are jumping lines pinpointed as the source.

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Similar to TBs, I haven’t ever read or heard of Arab breeders discussing problems that seem WFFS like. We have our own genetic issues for sure. Based on that shared experience, I can’t imagine that if something else had been kicking around that people wouldn’t have discussed it. So did all the Arab carriers get culled inadvertently? Very interesting but seems like a lot more work needs to be done.

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I don’t know if I buy it. By virtue of being “thoroughbreds”, which at its core really means “of recorded parentage”, TBs have more named ancestors. How can we know from pedigree analysis if the allele was introduced by an unnamed non-TB ancestor?

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I continue to have reservations about linking WFFS to unproven things that implicate it being anything other than a true recessive gene that has no impact on a horse’s wellbeing - suggesting that it influences elasticity, for example, is an indication that it would not be a true recessive gene (which we have no indication of to date). I wish Dr Winand had clarified what she meant when she stated that the trait had been “selected for” in recent generations. Is this a case of a popular stallion being a carrier and selecting for the popular stallion also meant selecting for the gene? (I am thinking specifically of Donnerhall in this case, although Balou du Rouet is an example for the jumpers out there - popular WFFS carrier stallions who came of age in an era where international breeding really became an option.)

Does anyone have any idea what the numbers of tested thoroughbreds looks like? We have seen some numbers floating around for warmbloods so at least we know how to contextualize the information we get in that regard (and if it is a statistically significant sample size). It sounds like the Jockey Club is not interested in promoting education and testing, and I don’t know of many thoroughbreds who have been tested. Is it possible that the low incidence of TBs found to be carriers has to do with a low number of tested individuals, total? (Essentially, the sample size is too small to actually make any conclusions about?)

As far as the jumper/dressage thing, @omare, I don’t really think that holds much water. We see the G jumping line represented (Graf Grannus, a Grannus son, is a known carrier), Balou du Rouet of course is a big one, and a bunch of C-line horses as well, for some of the big jumping line representation.

All things considered, I think the articles all get around to the same point but every notification could be more clear: while the two Ronalds may be the introductory point for the gene to the warmblood populations, the mutation itself is much likely centuries older.

No one has posted Westfalen’s statement, so I’ve pasted the (terribly translated) version below.

WFFS origin identified, genetic analysis reveals inheritance trends Ways to Appropriately Use WFFS and Other “Genetic Properties”

Initial evaluations of the WFFS topic have led to a result. The corresponding data of the horse breeding associations Westfalen, Oldenburg and Trakehner were analyzed by the service data center vit.

The pedigree analysis of around 2,000 WFFS tested horses in the data center provided the crucial clue: The 1905-born English Thoroughbred Dark Ronald xx and his sire Bay Ronald xx (1893) were among the 15,000 horses that appeared in the pedigrees which occurred as ancestors of all known gene carriers. So the mutation may have occurred in these stallions or even earlier. Since these stallions were very formative father animals, they were expected to be also in the pedigree of almost all free horses, but on average over significantly less lines than with the gene promoters. The entry of the mutation into the horses populations then took place over the sons of dark Ronald xx, mainly herold xx (1917) and son-in-law xx (1911).

In addition, the use of stallions with the WFFS facility was examined for early and mostly prenatal (embryonic) foal losses. The cover data from the last 10 years was used for this, about 80.000 mating of mares with 882 WFFS tested stallions. For WFFS carriers, a reduction in foaling rates (or proportion of survivable foals) of about 3% was statistically secured against WFFS-free stallions. These results are consistent with the statistical expectations of genetic models and confirm that WFFS is predominantly hidden.

When mutations are negative, they seldom stay in a permanent population. Conversely, the fact that WFFS has been present for a long time and is widespread justifies the hypothesis that carriers may have a selective advantage. This assumption was checked on the breeding values ​​of the stallions for the equestrian sport performance. Although no significant results were found, there was a slight tendency v. a. in the dressage and the rideability: The breeding values ​​of the carriers were on average about 2 - 4 points higher.

The most important thing about the handling of wffs remains the testing of the stallions and broodmares to avoid crossbreeding from two gene carriers. Because only from such crossbreeding, characteristic carriers can emerge (embryonic losses, non-viable and non-viable foals). The task of horse breeding is now to find the appropriate treatment with wffs. With a WFFS-free population, it would be possible to increase the foaling rates by about 3% according to current knowledge. However, this would be in no relation to the loss of genetic diversity, which would be linked to the breeding exclusion of all currently known gene carriers. Because the same effect is achieved by the consistent consideration of the WFFS status in mating decisions

Original is here.

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German Breeders have selected for Bay Ronald since the early 1900s. German Warmblood breeders have selected for Bay Ronald stallions in their import choices as well as their home bred TB stallions. Bay Ronald lines have been used all over the globe for TB race breeding for at least a century and probably more. Think of Gainsborough and his impact on the breed; think of Teddy. Hell, think of Bay Ronald’s parents–Black Duchess and Hampton. Both of them are extremely prominent through other descendants. Blandford is from the Black Duchess mare line; Hampton is everywhere, including Man O’War. Far more TBs are bred worldwide every year than WBs and that has been the case for many, many years. Those lines are in virtually every TB ever bred in modern times. We’re talking Hyperion and Mahmoud and Nasrullah and Phalaris and Blandford and all their sons and daughters if we also use Black Duchess and Hampton. Among all those hundreds of thousands of thoroughbreds over more than a century, surely it would have been identified before now.

Research into covers and live foal certificates would be extremely useful. Carrier mares from all those hundreds of thousands of horses must have met carrier stallions from all those hundreds of thousands of horses not infrequently, if 50% of offspring are carriers, and failure to produce a live foal from a cover will be included in all those decades of JC records of coverings and live births.

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Yes, that is exactly why I said really?! in the posting of this topic Vineyridge.

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I get that, but the reason I am scratching my head is that if it is the case, and that if WFFS is as prevalent in TBs as it is in WBs (which it should be, if Bay Ronald was indeed a carrier) is why is it not already recognized or being tested in TB populations? JC requires live cover and most stallions have “stand-and-nurse” guarantees. If there was a disproportionate amount of pregnancies lost, you know this would be recorded. The JC would definitely investigate that - reproductive health is at the forefront of the JC’s concerns IMHO.

As Vineyridge said, Bay Ronald himself was just as influential in TBs as it was in WBs. I’d argue even more so, because of how influential and heavily linebred Bay Ronald’s descendents are, including Teddy, Hyperion, and Gainsborough; three stallions that are very frequently linebred to (even inadvertently) because it’s almost impossible to find a TB that doesn’t have one of those three stallions in their pedigree.

The JC is not an organization I would say has “Ostrich Syndrome”. Some of the the most exhaustive studies about horses from nutrition to reproduction to musculoskeletal growth/conditioning/rehab has come from the JC. I would argue that without the JC there would be so much depth and understanding about the horse not present today, especially in terms of medicinal and musculoskeletal studies. They are far from the type to hide or refuse studies for fear of scandals. My two cents, in why the JC has not acted yet, is that they have not seen sufficient evidence to do so.

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I understand what you are saying about the US Jockey Club. My position is that they do not test or even offer testing for ANY issues unlike some other registries. Their entire focus is on racing, not the breed per se. I was very disappointed that they even refused to acknowledge the possibility. I have spoken with several friends that are TB racehorse breeders and they think I’m nuts.

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I wrote this:

UC Davis has found the allele that if homozygous results in Warmblood Fragile Foal Syndrome. The Trakehner Verband and the Westfalen Verband in Germany have asserted that it crossed into the Warmblood population through Bay Ronald/Dark Ronald and Furiosio, both pure Thoroughbreds and claimed carriers, and Bay Ronald, at least, is present in vast numbers in the American Thoroughbred population. UC Davis found the allele in a pure, registered, TB mare recently. It has also published a carrier rate of 4% in the past. I’ve read that the Jockey Club has denied the existence of the allele in the Thoroughbred.

Given the information above, shouldn’t research be done to determine if it is, in fact, present and in what numbers. WFFS is said to primarily result in spontaneous abortion when two carriers are bred together. I would think that Grayson Foundation would be interested in a genetic cause for spontaneous abortion in thoroughbreds. its frequency and preventability.
and got this answer from the Grayson Foundation.

Here is the scientific response we received.

It was agreed that, even though the mutant allele was detected in Thoroughbreds (TBs), testing TBs for Warmblood Fragile Foal Syndrome (WFFS) is not recommended at this time as a clinical affected case has never been reported in this breed. These carriers may be from TBs that were bred to WBs. The carrier frequencies that were reported were based on samples submitted for WFFS testing and not from the general population.

As it has been postulated that affected foals could be lost due to early embryonic loss or abortion, there is a strong need to provide more supportive evidence for this. Similar to GBED, samples from aborted fetuses could be tested for the mutation to further support or refute this claim.

We cannot predict long-term consequences for TBs with this mutation without more information. We need to have aborted fetuses/cases of early embryonic loss genotyped to see if this is a true cause for concern in the TB.

They don’t say who pays to have aborted fetuses genotyped.

I am speechless but not surprised at their reply. I just spoke with them as well and they told me that someone has to apply for a grant for a project and they vote on whether the project meets their criteria for research funding and they vote on whether or not to fund it. They said that they do not do research themselves. So if no one is submitting a proposal for researching WFFS in tb’s they aren’t looking for it themselves.

From WFFS Facebook page:
'… Kendal and the 2 Ronnies have something in common in their pedigrees and that is this Hampton, sire of Bay Ronald and Kendal have Whalebone - Herod etc in common.
It remains to be seen whether Hampton via Orange Peel etc. and other connections such as Birdcatcher/Whalebone and others will also turn up in the pedigrees of carriers in other breeds, e.g. Selle Francais etc.
In the end, it is just an exercise in curiosity and trying to find out where it comes from - but all these thorougbred stallions such as Dark Ranold and his decendents had traits that were valuable for warmblood breeding. Such stallions were Der Loewe, Lugano L, Cottage Son, Ladykiller, Furioso and many wonderful mares.
Similarly there were wonderful Holsteiner stallions derived from these lines also that carry these stallions and others such as Kendal, e.g. Cor de la Bryere, Alme Z and others.

Kendal appears in the pedigree in for exemple the following stallions:
TB: Black Sky, Cottage Son, Der Löwe, Furioso, Poet, Blue Peter, Ladykiller, Persian Gulf, Ultimate, Laudanum, Burgermeister, Pasteur, Coronach, Pluchino, Grey Sovereign, Stern.
Trakehner: Hyperion, Termit, Heristal, Flaneur.
HAN: Eisenherz, Spartan, Donnerwetter, Grannus, Gotthard, Woermann, Werther, Pik König.
HOLST: Sandro.
WESTF: Rosenkavalier, Rubinstein. SF: Double Espoir, Quastor.
IRE: Cruising.
SWB: Gaspari.
NLD: Amor, Irco Marco.
ZANG: Alme, Ramiro. …’

I wonder if positive xx stallions would have lower live foal to bred mare rates? I know the answer is likely too many factors involved.

http://www.jockeyclub.com/default.asp?section=Resources&area=19&report=LF&reportyear=2017&letter=A

http://www.jockeyclub.com/default.asp?section=Resources&area=19&report=LF&reportyear=2017

A TB son of Kendal, Galtee More, was sent to Germany in the 1880s and is found in almost every German bred TB.

Kendal himself was sent to Argentina for stud duty later in life.

Every TB on this planet has Herod and Whalebone numerous times. Anyone suggesting that Herod and Whalebone mean anything particular in thoroughbred breeding is grasping at straws.

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https://sporthorse-data.com/articles/2016/11/19/bay-ronald-part-one

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I have to admit I am also a bit skeptical unless as someone suggested it has been bred out of the xx line. That genetics of the stallion(s) named are everywhere. The cost of a high-end stakes winning/producing /closely related mare aborting in xx land has no comparison to the cost of it happening in warm-blood land, Weanlings and yearlings regularly go for 6 figures. And the scale of the breeding is huge. I guess we will see!

I looked up a Knabstrupper pedigree and it turns out that this one had Bay Ronald at least right times:
https://www.allbreedpedigree.com/marster+lynghoj

Re: Skepticism from the Jockey Club

There are around 100,000 thoroughbreds born worldwide each year. I don’t know how many foals warmblood registries produce worldwide, but I can’t imagine it even comes close. Thoroughbreds are a multi-billion dollar industry.

Northern Dancer is the most prevalent modern stallion across the globe. He has 2(?) crosses to Bay Ronald. Just that fact alone makes it safe to assume that basically every thoroughbred on the planet has Bay Ronald lines.

No one, to my knowledge, has come forward with a thoroughbred foal displaying symptoms of WFFS. That’s what it took for WB registries to get on board with acknowledging the allele.

There is no evidence that incidences of pregnancy loss are directly related to this.

So I understand why they would toe the line and separate themselves from this frenzy until they have more evidence of its impact.

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I was made aware of this thread because @Elles posted a link to it in the Racing Forum and asked for a response from TB breeders. This is a repost of what I said there:

I’ve read all the above links with interest because this is the first time I’ve heard of WFFS. In the COTH thread noted above, the Jockey Club is excoriated by some for not looking for instances of the syndrome in the TB breed. I would imagine that’s because it’s not currently perceived to be a problem.

I live in central KY where the vast majority of U.S. TB foals are born each year. We also have access to some of the best equine medical care in the country. Breeders here regularly share info with each other regarding odd or unexplained reproductive issues (like MRLS in 2002-2003). The two major vet clinics also get the word out if they are seeing something unusual happening–so breeders can take a proactive approach to their vet care.

The fact that no one hear is talking about FFS makes me think that’s it not being seen. Or if it is, the occurrences are isolated enough not to sound an alarm among TB breeders.

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The US Jockey Club has DNA on every registered TB for at least fifteen years. If they could find an interested researcher, seems to me that a genome scan could be run on the sires and dams and foals for one year. Given the large number of registered foals per year, one year ought to give a good indication of how prevalent the allele is in the TB. 5% of 25,000 is still a high number.–1250. Scanning the sires and dams would also give an indication of how high the presence is in breeding stock. It’s just a matter of funding the genome scans. And since we know which chromosome the allele is on and the gene in question, a full genome scan wouldn’t be necessary.

Isn’t UC-Davis already the Jcckey Club repository for DNA?

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