1. Messages
  2. Hay Question; now long, LONG post about ESC, WSC, etc

Re: Hay Question; now long, LONG post about ESC, WSC, etc

janieclougher@...
 

Hi, Karen - Yes, there is a lot to this group!  The good news is that there is a ton of information here,  it is somewhat easier to find than on the usual forums, and the posts are monitored for being evidence-based advice and information.  The bad news is that there is a LOT of information here, and Yahoo is a bit of a bugger to navigate.

There is still an ongoing myth about WSC, fructans and laminitis.  Dr. Kellon eloquently addresses this in the essay "Fall Laminitis":

https://uckeleequine.wordpress.com/2014/08/16/fall-laminitis/

Dr. Gustafson has a truly fab explanation of this, in the last post of this thread:

https://groups.yahoo.com/neo/groups/EquineCushings/conversations/topics/198272

And here is the link to the file about fructans:

https://groups.yahoo.com/neo/groups/EquineCushings/files/Fructans/

You are on your way to helping your horse, by ruling in or out PSSM. Good for you doing both tests - I know way too many people who only do the one (easy and cheaper test); then say the horse doesn't have PSSM.

 There is more to being "off" than PSSM, as you know (see below, after the endless paragraphs about WSC and fructans)

Short version: New information shows that ESC and starch are what we need to monitor.  ESC + starch need to be below 10% combined, but starch itself should be no more than 4.5% (3.5% for sensitive horses). (new being in the last 15 or so years on this list - the last couple of years in mainstream info) WSC includes fructans, which have been shown to be a non-issue. For PSSM horses, one must be careful not only to have low ESC and starch, but not to have buckets of fat; excess fat in the diet can actually cause or exacerbate insulin resistance.

Long version:

Dr. Pollitt,in 1996, started publishing data concerning laminitis in horses.  At that time, there was very little good understanding of the underlying mechanisms and pathology of laminits, and, I am sorry to say, pretty much all laminitis was grouped into 6 main categories: carbohydrate overload; pasture-associated laminitis (really vague and not well-understood); severe infection/endotoxemia; supporting limb; toxic (black walnut etc); idiopathic (out-of-the-blue, unknown cause). That meant all laminitis was considered to be the same, and have the same pathology.  Not helpful!

Pasture-associated laminitis and idiopathic laminitis shared the fact that there was absolutely no smoking gun to account for the issue.  Lots of horses get tossed onto pasture, and don't get laminitis.  Winter laminitis manifestly does not involve lush green grass.

Dr. Pollitt was able to show that a fructan overdose resulted in laminitis. He used stomach-tubed, big doses of inulin fructans, from chicory root. These types of fructans are not prevalent in pasture, nor do horses ingest them in such massive, bolus-type quantities. Still, it was a good start to trying to decipher the laminits conundrum, and it gave insights into how to treat laminitis from a feed-room break-in.

http://www.ncbi.nlm.nih.gov/pubmed/8565952

Sadly, the popular press got hold of that and ran with it.  It has since been shown, over and over again, that fructans can only cause laminitis in the case of a massive overdose, which also results in fever, diarrhea, and obvious systemic illness.  Especially in North America, there is not enough fructan in all the pasture in the whole continent to cause this. Other researchers, including Pollitt, have now looked at hyperinsulinemia as a cause of laminitis:

http://www.ncbi.nlm.nih.gov/pubmed/8565952

Here are a list of Dr. Pollitt's many publications: you can see that the fructan over-dose has been superseded by new data:

http://www.ncbi.nlm.nih.gov/pubmed


So..... what is the culprit?  One study in Finland  indicated that 89% of all laminitic horses admitted to their hospital suffered laminits as a result of an endocrine issue: insulin resistance (equine metabolic syndrome, hyperinsulinemia) and/or Cushing's disorder (PPID) (full disclosure  - small sample size of 36 horses over 16 months).

http://www.ncbi.nlm.nih.gov/pubmed/21696910

Fructans are not, I say again, NOT, sugars. They are a complex carbohydrate, and cannot be digested by mammals. They can be digested by bacteria, as in ruminant's rumens, rabbit's and horse's cecums, and camelid's magic weird stomach systems.(not sure where elephants and hippos fit in here). Fructans are food for bacteria.

If you overwhelm the bacteria in the fermenting chambers of the above mammals, you will get a major bacterial die-off, a shift in bacterial species, hind-gut acidosis in horses and rabbits, rumen acidosis in ruminants,  systemic illness, and, if there are hooves present, laminitis.  Any huge influx of carbs can do this, hence the common sequel of laminitis after a feed-room break-in.

Most laminitis does not occur  because of feed-room break-ins, retained placenta, severe infection, Lyme disease etc.  Most laminitis occurs because of hyperinsulinemia and/or PPID.  This includes most pasture-associated laminitis.

The insulin-resistant horse (ditto PPID horse) can look completely and utterly normal (even though they have a low-grade, smoldering laminitis), right up until something tips them over the edge into frank laminitis.  Early signs are very, very subtle: apparent back pain; difficulty in turning, which might be thought due to arthritis in older horses; reluctance to move forward; tender feet on gravel; general grumpiness when being ridden. All of these can occur when there is low-grade foot pain. Many of these signs are attributed to "bad attitude" or training issues. There may or may not be signature rings on the hooves. In the PPID horse, often the very first sign of PPID is unexplained autumn laminitis, "out of the blue", when the normal seasonal rise of ACTH is exaggerated.

This brings us to one of the cornerstones of the protocol that Dr. Kellon has developed: Diagnosis.  If your horse has foot-pain, is "off", stiff, or has obvious laminitis, the diagnosis is key.  The beginning is to get your veterinarian out.  Pull blood to determine if there is PPID or IR (go here for more info:  https://groups.yahoo.com/neo/groups/EquineCushings/files/2%20%20Diagnosis%20Diet%20Trim/ )

Get your veterinarian to do a full lameness exam, most importantly including regional limb blocks.  If your vet blocks a foot, or both front feet, and the horse goes sound, that is hugely important information. If none of the limb blocks do much of anything, then you know you are dealing with overall muscle or axial skeletal pain, or a neurological issue.

This was likely just a tad more than you had really wanted to hear (original innocent question about hay).  All the info on this list, once digested, will help you to help your horse to optimal health.














 






Join main@ECIR.groups.io to automatically receive all group messages.