Screen shot of the Equine Veterinary Journal’s new release of laminitis research.

The laminitis research community has released a huge volume of free work intended to set the record straight on all things laminitis, as of 2012.

Science papers released online often cost $35 per paper, beyond the budget of many a laminitis-poor horse owner. This “virtual” collection of papers released through the Equine Veterinary Journal is a gift. A big thank you to this publication and all those researchers who contributed their time and knowledge.

The release includes the full text and references of these papers and costs nothing. You don’t even have to log in or leave an email address, though no one would mind, I’m sure.

The material is written by all the big names in laminitis research: James Belnap, Chris Pollitt, Philip Johnson, James Orsini, etc.

Note that this is a very large body of work. I downloaded the provided PDFs (as far as I can tell, you have to download each individual PDF, as opposed to downloading the whole thing in one take — compiling all the papers into one PDF might have made it too large to download). I then made the mistake of printing the PDFs, and I used up maybe half a ream of paper.

Also, note that this material is written using a lot of scientific language, even though the editor states upfront that the purpose of this release is to combat the fact that much of the freely available material published online for horse owners “lacks rigor and quality.” So, these papers are for the average horse owner, but many words will be unfamiliar.

I’ve been reading science papers since 2007, and my first attempt seemed hopeless. I stopped at every new word to look it up, and it took me several days to get through one paper written by someone whom I consider very easy to understand in person. But this is how laminitis researchers write. My advice to anyone who wants to read these papers is perhaps to skip over something at first if it’s causing you great difficulty, because the more you read the material, the more familiar you will get with the terms. When you go back to a paper a second time, it will make more sense.

The takeaway message I see in the early going of my reading is as follows:

Scientists now consider there to be three forms of laminitis. The disease can be caused by sepsis (gastrointestinal injury), endocrine disease (insulin-resistance and Cushing’s disease) or excessive weight bearing. There may be some overlap between the forms based on the horse’s situation, but the changes in the foot are different for each.

There is much work to be done in studying each form. However, there is also a small glimmer of hope on the treatment front.

The paper titled “Progress toward effective prevention and therapy for laminitis” says these differences in the various forms of laminitis make it hard to target a failed process in the hoof and come up with a therapeutic intervention.

However, it also raises the possibility of reversing laminitis. It says new evidence suggests that the laminae do attain the ability to remodel, but this has been absent in the laminitic hoof, and it may be caused by reduced activity of p63, a regulator of epidermal stem cells. It suggests that transplantation of these stem cells from unaffected regions of the horse may have regenerative therapeutic potential for laminitic horses.

I talked to someone in the stem cell lab at Rood & Riddle Equine Hospital in Lexington, Ky., in May 2011 right before I put down my mare Angel, and, at that time, the rate of success for stem cells was not good, and I felt as if the trip alone would kill Angel, and the success rate at the time didn’t warrant trying, even if the monetary challenges could be overcome. I do not have any details on what the lab was using in terms of stem cells at that time. I’m guessing that this new development may bring stem cells to the forefront as a treatment.

As for new details on those various laminitic models:

The sepsis model includes carbohydrate overload and excess fructan scenarios. In the paper titled “Sepsis-related laminitis,” it gives a good explanation of the process: Excess starch arrives in the large intestine and is digested by intestinal bacteria, which results in a severe drop in intestinal pH, an ensuing die off of Gram-negative organisms and a moderate to severe enterocolitis, or inflammation of the colon and small intestine. This leads to injury to the mucosal barrier and absorption of numerous substances, including bacterial toxins. For years, people thought the bacterial toxins, called endotoxins, were the culprit. But this paper says experimental infusions of endotoxins did not result in lamellar failure, so investigators are looking for other trigger factors absorbed from the compromised gastrointestinal tract.

For the endocrine form of the disease, the paper titled “Endocrinological aspects of the pathophysiology of equine laminitis” raises some interesting points. Inducing laminitis in horses and ponies results in serum insulin concentrations much higher than those commonly associated with Cushing’s disease and some cases of pasture-associated endocrine-related laminitis, and it says “similarly high serum insulin concentrations have been documented in recurrently laminitic ponies in the absence of clinical signs of laminitis, such that very high serum insulin concentrations alone are not necessarily laminitis-inducing.” And, even more interesting to me, the feet of the ponies induced with the insulin form of laminitis showed a lack of basement membrane disintegration. Instead, the feet showed apoptosis (programmed cell death) and mitosis (cell division). Thus, these feet do not fall apart in the same manner as in the carbohydrate overload model or the naturally occurring disease. The paper says that debate continues over whether insulin resistance is associated with increased or decreased blood flow in the feet, and insulin resistance’s association with inflammation in the laminitic horse is also unclear. It says studies suggest that excess glucose does not play a role in insulin-induced laminitis.

It talks about identifying horses with insulin resistance. One study on a group of ponies combining five diagnostic tests did not result in higher diagnostic accuracy than individual tests of insulin or leptin. Leptin is a peptide secreted by adipose tissue. I’m not aware of ever having a leptin test done on my horses. The mention of that as a test was a surprise to me.

It says that phenomenal efforts by scientists have increased knowledge about this form of the disease dramatically over the last few years, but those efforts have probably generated as many questions as answers. And it closes with an interesting summary: “It should be remembered that not all laminitis-prone animals are obese and/or insulin resistant, not all obese animals are insulin resistant and not all insulin resistant animals are laminitis-prone.”

Perhaps the opening line of the support limb laminitis paper says a mouthful: “Supporting limb laminitis is a veritable dark hole when it comes to our goal of completely understanding the pathogenesis and therefore the prevention of all types and clinical presentations of laminitis.” However, if you read further, progress is being made on understanding how the laminae fail in this model. That is good news.

There is much to explore in these papers, and a quick study on my part can’t begin to cover the research included. Hopefully, the release of this information will move research forward in a meaningful way. Again, we should all be grateful for this information being given to us online at no charge. Thank you, Equine Veterinary Journal.