Dr. Raymond Geor, a veterinarian and researcher at the College of Veterinarian Medicine at Michigan State University, gave one of the first presentations I heard at the Mid-Atlantic Nutrition Conference. His talk had big 6-syllable scientific terms- all delivered with the measured pace of a scientist. He packs a lot of information in his talk, and as a layperson I usually come away thinking, “What was he talking about?”
I am fortunate to have a tape recorder to help me keep track of the stuff I miss. The more I listen to his talk, the more I can skate around the moguls of language and studies: And the more I can see the landscape he is describing. There were no bunny slopes in sight; the good doctor took us to the top of the Matterhorn and it was an hour’s speed race the whole way down to the end.
The verbal description of his talk was only two paragraphs long. It stated that there are anecdotal impressions by veterinarians of a relationship between obesity, insulin resistance, equine metabolic syndrome and laminitis. The second paragraph stated Geor would review the current diet and nutrition management for reducing the risk of laminitis in these animals.
We start with a wee background from last year where Dr. Nicholas Frank gave a presentation that I summarize as “ Obesity in a horse is a good clinical sign that you are courting problems.” This is where Geor picks up and in a nice way says- it has been noted that the observable characteristic of obesity often indicates a predisposition for pasture-induced laminitis in horses. This, then, would be the laminitic phenotype. These horses seem to respond to changes in dietary and environmental conditions differently than other members of their herd.
We were also reminded of the fact that at the heart of laminitis is inflammation that disrupts life in the laminae resulting in its death and, in some cases, severe coffin bone rotation and the demise of the horse as well. Furthermore, there is a pretty good hunch that there is a connection between a pasture-induced laminitis episode and disturbance in the animal’s hind-gut brought on by rapidly fermenting carbohydrates that in some way (death of microbes, toxin release, gut leakage?) causes an inflammatory response in the horse that takes it over the threshold into laminitis.
Currently there are three main theories scientists are working on.
- there is an underlying inflammatory condition in these horses and ponies.
- Insulin toxcity
- A perfect storm of multiple colliding factors
Why would a fat horse or pony be more susceptible to laminitis? Ah-ha. That’s a good question that has no answers. But, there have been some recent discoveries in other species (us humans for one) that merit consideration (and therefore research) for the equine species.
It would seem that fat, once thought of as a simple collection of storage cells, actually is ALIVE! ( the monster within- I sense a movie in all of this.) Adipose tissue is very metabolically active. It regulates things like pro-inflammatory cytokines, which makes the scientist wonder if the obese horse is in a constant metabolic state of systemic inflammation. If so it would be easy enough to understand why anything that would contribute more inflammation would tip the horse over the laminitic threshold.
In other species fat seems to have a pretty strong affect on insulin. Interestingly insulin actually has two pathways, one is use (sensitivity) and the other is production. Fat appears to decrease the use of insulin while increasing the production of it with the result that there ends up being a large concentration of insulin in the blood stream (hyperinsulinemia.) That’s a very bad thing for the circulation and results in vaso-constriction: in other words tissue (such as the laminae) starvation and death.
Then there is the perfect storm theory, fat, inflammation, insulin, gut mobility, gut bio-environment, gut motility, gut permeability, forage composition factors other than carbohydrates, genetics, climate, life-style. Whew. Oh, and what about the obese mom that predisposes her foal to metabolic disorders? Happens in humans – could the same be true in horses?
And here’s my own wild card questions. How about how the whole digestion process works in these laminitic phenotypes. Does their system empty slower or faster than their healthy counterparts? There is always talk of the role of GI micro-organisms in creating laminitis.
Well, perhaps the genetic pre-disposition component is the foal eating mom’s bacteria laden feces.Mom could have “laminitis-making-bacteria” in her GI track. Maybe it’s not a gene, maybe it’s being in a stall with predisposed, obese, laminitic mom and the foal’s natural and needed coprophagia.
So many of these conditions are tightly intertwined that it will be a galactic challenge to investigate. And, of course, there is very little money to support this research.
I have an insulin resistant horse and another overweight pony. After listening to Geor’s presentation I renewed my efforts to reduce their weight as I have seen and heard the devastation of laminitis.
And, personally, I’m going on a diet lest I become even more inflammatory in my remarks.