TRANSLATED WITH A MACHINE
https://landgestuetcelle.de/de/aktuelles/wege-zum-angemessenen-umgang-mit-wffs-und-anderen-genetischen-eigenschaften.html
Als Ausgangspunkt für die Untersuchung von WFFS als Ursache für frühe und größtenteils vorgeburtliche (embryonale) Fohlenverluste dienten die Deckdaten einiger Verbände, die PressemitteilungWFFS.vit20190327.docx 2 / 2 eine Pilotstudie angeregt hatten. Aus den letzten 10 Jahren standen damit rund 80.000 Bedeckungen von Stuten mit 882 WFFS getesteten Hengsten für die Analysen zur Verfügung. Für WFFS-Anlageträger ließ sich eine Verringerung der Abfohlraten (bzw. des Anteils überlebensfähiger Fohlen) um etwa 3 % gegenüber WFFS-freien Hengsten statistisch absichern. Um die eigenen Ergebnisse einordnen zu können, wurde ein mathematisches Modell der Populationsgenetik, das Hardy-Weinberg-Gesetz, angewendet.
The data of the mares covered from some associations (verbands) were used as a starting point for the investigation of WFFS as cause for early and largely prenatal (embryonic) foal losses that a pilot study had stimulated. From the last 10 years, some 80,000 coverings of mares with 882 WFFS positive tested stallions were for the analyses at the disposal. For WFFS carrier stallions a decrease of foaling rates (or the proportion of viable foal) to approximately 3% over WFFS-free stallions was statistically proven. A mathematical model of population genetics, the Hardy-Weinberg law, was used to arrange the results.
What is interesting to me when I read that is that the authors point our their belief that the recent spike in breakdowns at Santa Anita is due to WFFS. But nowhere do they explain why–if this problem is rampant in the TB population and there are TBs racing all over the country every week–only Santa Anita seems to be affected.
I tried to comment and the post was “unapproved”. Never had that happen before. Don’t know why.
Tried to comment twice and have 2 “unapproved” posts. I don’t know why. 
So I guess you won’t be hearing my thoughts.
Did you read the article linked in this one that was published on April 3rd? This author seems to be making a number of claims without any actual clinical proof.
What was not known before and has been discovered by Winand in research since 2011, is that it only takes one copy to be present for the horse to exhibit signs of what seems to be a recessive defect, however WFFS appears to be an unusual dominant mutation. The weak foal phenotype mimics a recessive but there are for the most part sub clinical abnormalities in horses with one mutant gene copy.
The above quote is an excellent example. Are there any published articles in scientific journals yet? I didn’t believe Dr Winand’s research has yet been released, and I wasn’t aware that any others had either - so I am uncertain how someone can reliably make these claims?
Significantly, breeding horses with this genetic defect is a death sentence. When combined with bisphosphonates, the horses’ whose bones are exposed to stress are ready to implode at any time.
“I think you have to see what the injuries have in common and what the injuries tell you [to examine],” said Dr. Larry Bramlage, renowned veterinary orthopedic surgeon. “We now have that information to make those determinations.”
“Implode” is an interesting word choice and not tremendously scientific. I have reservations about this author and his claims, based on the agenda he seems intent on pushing (WFFS is to blame for the Santa Anita breakdowns). He doesn’t address several critical issues in either article that would help validate his perspective.
(The article I am referencing that he links to in the link Elles posted above is here.)
:mad: I just got slapped with an unapproved, too.
ETA: And now my second. For anyone trying to comment, I don’t think COTH likes the link to this website. My second time quoted Elles’ post and then I used the quotes function. Maybe avoid those for a while?
Short summary previewing my comments whenever they deign to show up -
This author has an agenda and fails to address several critical issues in both articles. Please click the link in the article that Elles links to above (it will take people to an article dated 4/3). He uses phrases like “Implode” in a scientific context which is not a verifiable metric of any sort and I find it difficult to read either article without extreme skepticism based on his own bias (he clearly wants to blame the Santa Anita breakdowns on WFFS). There is no released scientific research on WFFS yet to corroborate his assertions and he seems to be cherry picking a number of quotes from different topic-specific authorities (Dr Winand among them) that I am uncertain the original context of their commentary, so I am uncertain if he is just cobbling them together in a way to create something that seems to support his argument. I would love to see the original context of many of these as it seems like it would be highly educational.
Okay based on my post above: This link contains a link to another article published a few days earlier, titled “Mutant Gene Causes Bleeding and Breakdowns”. Please read this. It is by the same author as the one linked above.
There are several major red flags for me.
He makes claims without any clinical evidence backing it up. Dr Winand’s research has yet to be made public and to my knowledge, no one else has published anything either. I believe the second article (which is the one Elles published) is an attempt to “corroborate” his claims but there is still no clinical proof to support his claims.
He uses fantastical language like
Significantly, breeding horses with this genetic defect is a death sentence. When combined with bisphosphonates, the horses’ whose bones are exposed to stress are ready to implode at any time.
If there is a scientific argument to be made, it should be made scientifically - not using words like “implode” or “death sentence”.
This author is clearly very invested in blaming WFFS for the Santa Anita breakdowns, and is not addressing a myriad of absolutely critical questions related to his claims that would make his argument far more compelling (if WFFS is to blame for this, why is there such an irregular number of breakdowns happening at Santa Anita and why is it only happening now? Addressing this would be a fantastic place for him to really lend authority to his assertions).
Does anyone have any updated information on when research is going to be released on WFFS? And is anyone other than Dr Winand looking at this yet?
He blames the Santa Anita breakdowns on WFFS?!? That’s hilarious! Clearly has no idea how the disease works or what problems is causes.
@Laurierace yes he does, and how! The article itself reads like a checklist of how to write a hyperbolic article meant to hook people into believing it without any substantive critical evidence to support it. Cherry picked quotes, exaggerated language, selective misrepresentative use of facts and all…
“Mutant gene causes horse bleeding and breakdown” is the title and it just goes downhill (??) from there. When the article leads off with this paragraph (“Everyone at Santa Anita Park looked for a silver bullet, that one thing that caused the recent cluster of catastrophic breakdowns at the Arcadia track. Officials of The Stronach Group, owners of Santa Anita, said it is multifactorial, but they are wrong. The single uniting factor is Warmblood Fragile Foal Syndrome (WFFS), a genetic mutation first discovered in Warmblood horses.”) without actually coming out to state that all horses who broke down were tested and found to be WFFS carriers? My academic skepticism is piqued.
Honestly that would be great news if they did find something that linked all those horses together as maybe that would lead to figuring out how to prevent future breakdowns. I don’t think a horse affected with WFFS has lived more than a day or two at most. I don’t believe they have found injuries or even a common unsoundness between carriers. If it is true that they were all carriers that would be something to think about I guess but I don’t believe they were even tested for it at all let alone all tested positive.
And bleeding being selected for?! Why would anyone do that?!
In sporthorses WFFS is not a cause for breakdowns so why would it be for Thoroughbreds? There is no proof that carriers are different from non carriers.
Bleeders are not being selected, they just aren’t being culled because they all bleed to some extent. If you culled any horse that bled on a scope exam ever there wouldn’t be any horses left to breed.
If you read the story, you will see that bleeding wasn’t considered disqualifying for a sire in the early days of the sport. For instance, Barlett’s Childers was also known as “Bleeding Childers”; story states that Herod bled after one of his races. Story also mentions that in the old days the only way bleeding could be diagnosed was if a horse bled through the nose; now, with scopes, bleeding is found in virtually 100% of American horses. (One should also mention that Pocahontas, one of the true foundation mares in TB history, was a roarer, as was her dam, but that didn’t stop breeders from using her and her offspring --she was the dam of, for instance, Stockwell, who is sire line for almost the entire Whalebone/Eclipse family who, as do all modern TBs, also descend from Bloody Childers. The Australian study on genetic strength/weakness of ancient ancestors found that multiple instances of Stockwell in a modern pedigree was a minus for strength and longevity.)
Nena Winand is the person on whom the article relies on for its science, and she is the one who believes that a heterozygous horse may have a proclivity for bleeding. She is quoted as talking about the many different possible phenotypes that “bad genes” can produce in other heterozygous situations and thinks that is quite possible with this gene in horses. She is also the person who first identified the WFFS gene and developed the test with Cornell; and Cornell makes money off the test.
From TB Heritage:
Bartlett’s Childers
SIRE: DARLEY ARABIAN. Darley Arabian Sire Line
DAM: Betty Leedes by Old Careless - Cream Cheeks by Leedes Arabian - Mare by Spanker (to Family 6) or Wyvill Roan Mare.
Bay 1716. Bred by Leonard Childers; owned by John Bartlett and stood at Masham, Yorkshire. Brother to the better-known Flying Childers, Bartlett’s Childers (a.k.a. Bleeding Childers) never raced, but it was he who continued this line of the Darley Arabian forward, primarily through son Squirt, who leads in sire-line descent to Eclipse. Squirt sired Tim, Syphon (sire of the classic winning Yellow Filly, Sweet Briar and Sweet William), and Marske (sire of Eclipse, Shark (exported to the U.S.), Stripling, Hephastion). Bartlett’s Childers also got the racing colts Fig and Merry Andrew; the important mares Coughing Polly (Family 19, dam of Grey Starling, Phaeton); the good race mare and producer Jenny-come-tye-me; Amorett (Family 15, a.k.a. the Little Hartley Mare (dam of Blank, Slugg (a.k.a. Old England), Tortoise and granddam of the Gower Stallion)); a mare in Family 3, dam of Squirrel (1741), Camilla (1746), Miss Belsea (1753) and Twackum (1745)); a mare in Family 18, dam of Volunteer; Flora (Family 22, dam of Weasel, Hotspur, etc.), and the dams of other good racehorses and producers.
Vineyridge, I believe Cornell sold the rights to the test to Labkolin. I am uncertain if Cornell (and Winand) make money off of the test at this point although if she does she should be disclosing this information as it is clearly a conflict of interest and transparency at this juncture is crucial.
Ultimately, the racing articles make claims that they aren’t substantiating with evidence. Dr Winand is making comments (quoted in the article published second but that Elles posted first) that again, aren’t being substantiated with her research findings. I am troubled by this as I find the lack of transparency concerning. If Dr Winand is going to share her research prior to the peer review/publication process (as she evidently is, based on the author of these articles suggesting they had access to it) then I would have hoped she would be forthcoming to everyone. (What is her hypotheses? What is the research methodology? Sample sizes?)
at this point the authors of these articles are essentially saying “we have proof. It exists. But we know it and you can’t so you’ll have to take our word for it” which isn’t a process I’m comfortable with. Transparency in this entire process is crucial, not fear mongering or making claims that they aren’t willing to actually back up with evidence…
becsuse they didnt say, even once, that every horse who broke down had been tested and found a carrier of WFFS. to claim that we can blame WFFS for the breakdowns without even the most basic corroborating evidence is grossly irresponsible. (They are presenting their speculation as “fact” … if they wanted to formulate a hypothesis and write articles calling for the need to test horses to prove or disprove it I think that would be fantastic for raising awareness - but to promote a pet theory as fact without zero evidence is not just bad science, but also dead wrong…)
This is one thing that would be super easy to prove or disprove since the JC has DNA samples on every horse in their database going back many years, I don’t remember how many exactly. Obviously it would cost money to run those tests but it could be done.
It’s my understanding that Labkolin performs WFFS testing under license granted by the patent owners i.e., Cornell and/or Dr. Winand. According to the latter, the testing reported in the Eurodressage article was done by an unlicensed lab and misquotes her in multiple instances, including in regard to Bay Ronald’s role, if any, in spreading the WFFS mutation.
The hypothesis that WFFS carriers may be more prone to breakdown is quite plausible but unproven. Horses with one normal allele and one WFFS allele are not metabolically identical to horses with two normal alleles.
Per personal communication rec’d. from Dr. W., peer-reviewed research on carrier fitness will at some point be published. She is speaking out before then in the best interest of the horses. I’m surprised that she has not dissociated herself with the headlines at HRI that jump to grossly premature conclusions. Common sense alone should tell us that WFFS carriers probably aren’t the reason for a sudden increase in fatal breakdowns at a single track.
@jadebe Good information to know about the labs, thank you for clarifying this. Do you know if this means that Dr Winand profits from this (and if so, would it be on a by-test basis)? While I don’t think it’s inherently biased if she does, this is information I believe should be public if this is the situation.
Do you mind my asking where you got information about the metabolic differences between carriers and non carriers? This isn’t something I had heard previously. Is this more information that, like which is alluded to in the HSI articles, Dr Winand says she has been researching but isn’t publicly sharing findings on yet?
I find the HSI articles troubling for the way they present their theory as fact. It’s not responsible reporting and in the comments, there are people who clearly are taking this slant and running with it without having any evidence. it is an unfortunate situation.
One would assume that a showjumper jumping 1.60 m courses would certainly be prone to breakdown if this would be true.
