Is there a list of the TB’s that tested as carriers or mention of their breeding anywhere? I am a member of the WFFS Face Book group that was listing the status of tested horses but I never saw any on there that were carriers that were TB. Although I haven’t checked the list in a long time. I am just curious because I personally think the gene is very rare in TB’s. And the small sample sizes could skew the percentages.
No one has comprised a list of just thoroughbreds, but I know of at least one that has self-reported as positive. (If you are a member of the group, you can find it in the sheet listed there. Due to the request of privacy & usage of the information on that sheet by the curators, I will not post it here myself.) I also think that spreadsheet is not a great place to see what the incidence of the gene is across breeds, considering that the group itself is largely populated by warmblood breeders.
While I think the incidence in thoroughbreds is relatively low, @Laurierace pointed out an excellent thing of note from this study: 17 of 716 randomly selected horses were found to be carriers. That rounds out to a rough 2.4%. For a closed studbook, the fact that it exists at all (and even from such a small sampling, is at 2.4%) is a significant find. That said, I think that to get a much more comprehensive idea of the numbers, we need to look at promoting awareness of this inside the race industry and see testing occur on a much broader scale.
So you must test your TB mares as well as your WB mares before breeding to any WFFS carrier and never breed to any stallion whose connections refuse to test or release the results.
This I think is an excellent takeaway and agree with Laurierace 100x over.
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I was thinking that this forum had made progress in the ‘be kind’ area and posts had become more civil and helpful. Guess Endlessclimb is still relatively new - but even so…We should add this to Petey Pie’s pet peeves thread?
True, in journalism it is normal to spell out initials the first time they are used in an article.
Also, I did not know what it meant, either, even though I am far from inexperienced or ignorant, thanks.
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You see, the acronym is, in fact, defined in not one, but BOTH of the OP’s links to scientific studies. The OP is presumably not a journalistic expert, but apparently it was too “annoying” for Petey Pie to click the link in the OP, which is literally the first thing they saw.
Instead of doing that logical thing, they typed up a whole response as to why it’s too annoying to do that logical thing.
Petey Pie could have asked what it meant. They could have clicked the (2!!) links in the OP. They could have googled it separately. Instead, they chose to be a jerk about it.
Yeah, I’ll call that spade a spade.
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Perhaps for you the ‘logical thing’ is to spend your time looking.
My response to something I don’t know what something means is often to just move on to, in this case, another thread. If the writer doesn’t care enough about their topic to make sure it is explained and/or intriguing for the reader, I probably don’t care enough to waste my time looking… 
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Okay Petey Pie found it annoying. The only one toddler stomping on this thread is you. You’re not calling anything a spade. You are being rude for no reason. Let it go.
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Who’d have thunk you’d show up?
Hello pot. How are you?
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I’m curious after reading the study, do carriers of WFFS have more lameness issues or break down more frequently than non-carriers? I’m not speaking strictly to TBs but in breed populations with high percentages of carriers.
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There is zero evidence that carriers have any more or different lameness issues than clear horses.
That said, to my knowledge there are no real studies on this, outside of this thread which, as already stated, it not a lot of horses, and a breed that is thought to have a very small % of carriers to begin with.
Based on the summarization of the study (thanks for that! :yes:) this seems like a “duh, but if someone’s paying…” study, in that there’s absolutely no reason to think that FFS (because it really shouldn’t be called WFFS anymore) would have been in a higher % of horses at Santa Anita than any other track.
As for the original scuffle - really? Take responsibility for your own actions. Don’t get all worked up over someone for not defining things that were assumed to be known (and WFFS was a HUGE topic here for a while, so it was not remotely a stretch to think those interested, would know, and those who didn’t know, might not be all that interested, or would at least ask some questions).
If you have no idea what it is, look it up, or just say “I don’t know what that is, can you give a brief description?”. I think Edre handled that very well :yes:
If someone wants to wade into a scientific discussion, it’s not anyone else’s responsibility to make sure any and all jargon are fully understood by everyone present. If you don’t know, ask. It really IS that simple.
Nobody on a forum like this is required to make sure everyone possibly reading knows the details of every acronym or layman’s term (Ace, bute, etc). I can’t imagine anyone on the Health Care forum would be “required” to type out “Polysaccharide Storage Myopathy”, with a link to or a typed description of what that is, every time they started a thread on PSSM.
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Now I’m really curious as to why they chose to look at this. Aside from curiosity of course and scientist look at all manner of things. Just seems rather out of the blue if FF carriers (thank you for the correction JB) having a disproportionate amount of lameness issues or more prone to break downs.
I forgot some of my thoughts on the study issues:
I don’t know that we’ll ever had a comprehensive, statistically significant study on whether or not carriers have any increased risk for injuries. Why? There are just SO many variable when it comes to injuries - conformation, training, footing, things that happen in the pasture, nutrition, age-related wear and tear, and even just a bad step.
Across all the disciplines that carriers are involved in, I just don’t think it’s possible to look at enough horses who are carriers, account for all other factors that lead to injuries, and follow them through their careers (or only look at those who have had a long enough career already), and determine anything. Too many variables. Too many horses. Too much legwork.
The Santa Anita track breakdowns have been a source of a great deal of frustration, finger-pointing, excuses, and ridiculous “changes”. To me (and I fully know I don’t have all details) this seems to be based on just trying to find something other than the track itself as the cause of the greatly increased number of breakdowns there. The timing of the report coming out seems in line with how long it would have taken to perform the study.
Nobody has anything but speculation that FFS carriers COULD be more prone to injury. There’s nothing out there now - nothing - that even suggests it might be an issue. But since it is a connective tissue disorder, and since we know that HERDA (link for those who have no idea what it is :winkgrin: ) carriers DO have physical changes to their tendon structure, it’s not a leap to wonder IF there could be increased risks with FFS carriers.
Even then, while we do know that HERDA tendons do have changes that suggest they might not stand up to intense use as well, there is still no proof it’s a problem in the real world.
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I agree it stemmed from the break downs at Santa Anita. I just thought it would be a shot in the dark considering a very low percentage of TBs are carriers. That in turn made me curious about horse breeds where it is more common.
@Denali6298, currently it is warmbloods that have the highest incidence of the allele (at an estimated 9-11%). No research has yet been published indicating that having one copy of the mutation is detrimental to a horse (though likewise, prior to this research, no studies had indicated the opposite either). Anecdotally, you can look at significant and well-known carrier stallions (such as Donnerhall or Balou du Rouet) who have large numbers of offspring that compete at high levels of sport (and often, for a very long time). Donnerhall son Don Principe (a known carrier) is notable for his long competition career & soundness throughout it. Likewise, Wolkenstein II, Rubignon, and Londonderry can serve as similar examples.
That said, earlier this year there were two articles on horseraceinsider that imprecated (W)FFS for the Santa Anita breakdowns. I can’t access either article on the site, but I found where I cited it - one notable quote was “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.” One article was titled “Mutant Gene Causes Bleeding and Breakdowns” which of course, was a reach considering no studies had been completed at that time.
If research hadn’t already been being conducted in regards to the mutation & the SA breakdowns prior to these articles being released, I imagine it was a catalyst that made it a necessity to look into. That said, I believe the UC Davis team was already working on it prior to these articles.
Ultimately, (W)FFS is not a “smoking gun” for racetrack breakdowns. Now that research has begun down this path, I hope it will continue. This study focused on the frequency of the allele in racing populations (identifying one carrier among the 22 who experienced catastrophic breakdown) and concluded that the number of carriers was not higher than the controls group (as it would be if the carrier horses were more likely to experience breakdown). I would like to see research progress forward (increasing sample sizes would be a great first step) so we can continue to expand our understanding and education.
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So they’re saying FFS is a death sentence? :rolleyes:
And they’re saying that the use of OsPhos and Tildren on FFS horses makes them a ticking time bomb?
Now that research has begun down this path, I hope it will continue. This study focused on the frequency of the allele in racing populations (identifying one carrier among the 22 who experienced catastrophic breakdown) and concluded that the number of carriers was not higher than the controls group (as it would be if the carrier horses were more likely to experience breakdown).
wouldn’t they need to start looking at all racing carriers, to see if their incidences of breakdowns is higher than the overall average, and higher than the population of racing non-carriers? I mean, the % of race-bred TBs who even make it to the track is not that high.
Considering the (theorized) low % of carriers in the breed, and the very large number of TBs racing at all levels, I don’t see how 1 track, and just 700 horses, can prove or disprove anything.
What scenarios and details am I missing? (and I realize there are probably several).
Considering the fact that both articles (both were written in a similar vein, high on dramatized language, low on science and evidence) have been removed from the platform I am assuming their authors are unwilling to back or defend the claims they made therein… I wish I had saved the articles completely rather than significant quotes… Be that as it may, I think that study at least does a good job directly addressing the claims that were posited in these.
As far as the conclusion this study comes to…I see that they actually did look at multiple tracks. Their case study group are the 22 who experienced significant breakdown, and then they compared it to a control group (same track, same season). After that comparison was made they compared “an older cohort of horses (Cohort B; n = 185) that raced during the same season as the cases, but at racetracks across the United States, the number of carriers was not higher compared to the controls, as might be expected if heterozygous WFFS horses were more prone to injury.” They also do compare non-racing thoroughbreds (to see if the allele frequency was different in the non-racing population - it was not).
They do specify that they only studied cases (breakdowns) from one specific track though. The rest of the sampling it seems was to get a more concrete idea of the representation of the mutation among thoroughbreds. (“While cases from a single racetrack were analysed, the low allele frequency in each of the cohorts and in the combined data set makes it highly unlikely that this PLOD1 variant plays a role in catastrophic breakdown” - I read this as saying if the gene were responsible for breakdowns then of the initial 22 studied, there would be more carriers represented.)
That said, I do agree - I would like to see breakdowns from more tracks be tested, in particular - and I’d be curious to see not just the catastrophic breakdowns tested, but those horses who experience injury/get pulled up (but end up being rehabbed/etc). I have no idea how many thoroughbreds race each year…presumably thousands? And I know the JC is the second largest registration in North America (and DNA is required for registration). There’s a wealth of data there that can be tapped into, if the research gets funded and people progress with it… Hopefully, we see that happening.
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What I do know is necropsies are performed after any death at the track. The TB industry is leading in research compared to other horse sports. There is a wealth of knowledge to be found studying racehorses. It’s why we have the advances in veterinarian medicine we do.
That said, if someone wanted to do a study on breakdowns and FFs it would be better, in my non-scientist head, to study the horses it impacts the most which is not TBs. Alas, as JB pointed out that would be a huge undertaking .
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I think there are a few limitations to undertaking a big study that focuses on the relationship between (W)FFS and catastrophic injury (hopefully that would generate more than just a few hundred samples) in a discipline outside of racing.
- Racing is already isolating a number of variables. You know you’re only going to be looking at thoroughbreds (closed book). No other sport has that advantage.
- There are only two sports that I can think of that really experience significant breakdowns (racing - of any variant, admittedly - and eventing). Some of the major dressage and showjumping sires have been found to be carriers, but by and far we don’t see catastrophic breakdowns in those disciplines.
- Variations in performance level (while I know there’s different lengths of racing and different surfaces, the mechanics of racing are the same regardless of what race you are in - the same cannot be said for showjumping or dressage, unless you specifically focus your sampling on just horses competing at a certain level, which is going to severely limit the sample size you can acquire).
Some quick noodling. The Grayson-Jockey Cub Foundation is a very old foundation whose goal is to fund research through grants (but not do the actual research).
The 2019 allotment of $1,338,858 will fund eight new projects at seven universities, nine continuing projects, and three career development awards. The 2019 slate of research brings Grayson-Jockey Club Research Foundation’s totals since 1983 to more than $27.5 million to underwrite 366 projects at 44 universities.
There is one study which is currently (2019) in the second year of a 2 year grants which
An Atlas of gene regulation in the horse
Currently there are no projects which are specifically researching FFS and a possible relationship with TB breakdowns. There are 3 projects relating to preventing and finding fetlock issues along with other projects relating to injuries of TB in general.
I don’t disagree that the variables in Hunters, Jumpers, Dressage, and Eventing, can make things extremely difficult to normalize.
But even in TB racing, there are so many different variables, from stereotypically poor hoof care (follow TB racing enough and you see the very common long toe/low heel situation), the conditions of tracks (the footing material itself, then the conditions of the training and racing days), the methods of training (ie some trainers are known for appreciably more breakdowns than others), the fact that most don’t get a lot of turnout once in training, and other things that directly relate to soundness.
I still think it will never be done, I don’t think it CAN be done 
