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This is an archived Horseadvice.com Discussion. The parent article and menus are available on the navigation menu below:
HorseAdvice.com » Diseases of Horses » Endocrine System » Equine Metabolic SynDrOme and Insulin Resistance »
  Discussion on Cause of founder in EMS - simpler than it seems
Author Message
Member:
Wolfydoc

Posted on Thursday, Mar 16, 2006 - 9:30 pm:

Hey there,
I'm going to open a can of worms. Me thinks we may be making the question of why EMS horses founder too complicated. Founder is founder, and the natural hoof care practitioners of the American Asso. of Natural Hoof Care Practitioners firmly believe that founder is caused by DIET, to include all food, supplements, and potentially drugs. It is not caused by obesity per se. Obese horses have an unnatural diet (green grass, grains, sugars like molasses, legumes, and even grass hays high in nonstructural carbohydrates can be the culprits) and likely unnatural feeding practices (set meals, food set in one place), often combined with unnatural lifestyles (confinement to a stall or small paddock, lack of exercise, no herdmates). Experienced practitioners in the AANHCP have seen founder cases time and time again respond ONLY when these factors are addressed, especially diet. Founder-inducing diets happen to also be obesity-inducing; obesity begets EMS in some horses. Diet is at the top of the chain of events, if you will. This is true whether the horse has EMS or not. Barefoot trimming will not fix founder - changing the diet will.

And just as an aside, it's hard to believe that attaching any kind of shoe to a hoof wall that is itself losing its attachments to the coffin bone will do any good. AANHCP practitioners turn chronic founder cases around while barefoot. But that's a discussion that should be under the founder section!
Moderator:
DrO

Posted on Friday, Mar 17, 2006 - 8:56 am:

If I understand you correctly no can of worms that I can see Cynthia, you could be reading from our articles on these subjects from our site, particularly with respect to the importance of diet and treatment. But there are several minor statements you make that do not account for some common observations:
  • If weight were not a significant factor in founder it becomes very hard to explain why the fronts (which bear the lions share of the horses weight) are so much worse effected than the rears.
  • Certainly the highest grain diets I have ever been personally familiar with is the race track where horses may be receiving 15 lbs of grain a day or more. In my stint on the track where we cared for many hundreds of horses I don't remember seeing a single founder over a 6 month period. But these horses are always in a moderate condition.
  • What I call spring grass founders are the most common type in my practice and these have always been hard to explain in horses that are not fat. I think the recent theories on the role of MMProteases are the most consistent thing I have ever seen with what we observe in the field.
The role of unneeded calories, as measured by obesity, and rapidly fermentable calories reaching the cecum accounts for the majority of my founders. The role of insulin insensitivity as a primary cause of founder remains conjectural but is making for some very interesting research. By probing these mechanisms deeply we may find some therapeutic tools for the acute episodes.
DrO
Member:
Wolfydoc

Posted on Tuesday, Apr 4, 2006 - 2:43 am:

Straighten me out DrO. What I was trying to say is that there is not a direct line, mechanical, cause and effect between added weight borne by the hooves, and laminitis/founder. Does that make sense? It's what's in those extra calories that is the problem. Grains, molasses, green grasses, even many dried grass hays contain high amounts of nonstructural carbohydrates - sugars, starches, fructans - that pass essentially undigested into the hindgut to be rapidly fermented. The obesity is a side effect of those excess calories.

Am I off my rocker?

Also, I believe I read in the founder article that the MMP enzymes are produced by bacteria in the gut. Actually, according to Chris Pollitt at the Univ. of Queensland, a leading researcher in laminitis pathophysiology, they are produced in the laminae themselves, and are key players in the normal constantly occurring breakdown and remodeling of the attachments between the epidermal laminae and the basement membrane/dermal laminae, which allows the hoof wall to - in simple terms - slide past the dermal laminae as it grows downward. There is normally a balancing act going on between MMP production and MMP - inhibiting enzymes in the laminae themselves that may go horribly wrong during laminitis, with excess MMP production and activation. Do you have a source stating that bacteria are producing the MMPs that play a role in laminitis? According to Pollitt lamellar tissues affected by laminitis increase their production of MMPs, in response to some circulating trigger factor(s), but we don't know for sure yet exactly what the trigger(s) may be. The one trigger Pollitt has shown, at least in vitro, that increases lamellar MMP activation and causes lamellar separation, is some factor present in cultures of Streptococcus bovis isolated from the equine cecum. But the MMPs are produced IN the laminae, not by the bacteria in the gut. Let me know if I'm not reading my sources correctly.

cindy
Moderator:
DrO

Posted on Tuesday, Apr 4, 2006 - 2:53 pm:

I think that weight is an important component and that this is demonstrated by the common observation that the front feet are worse effected in founder than the back. But it may not be an initiating cause. As for the association between obesity and founder there may be another component besides weight alone or an indication of high laminitic carbohydrates. Many obese horses are insulin resistant and there are some indications that this may have a play in the pathogenesis of some founders.

You are absolutely correct about what is currently known on the pathogenesis from carbohydrate overload and physiology of how hoof walls move down as they grow. Saying the bacteria release the MMProteases (instead of activating their production by means of a as yet unidentified chemical messenger) in the laminae is incorrect. I don't remember if when I wrote that I was taking short hand liberties or if that was left over from the previous version before attending Chris Pollitt's lecture in 2003 at the AAEP and I have just not corrected it. But it will be on the list to fix and thank you for bringing this up.
DrO
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