There are two instances in which diet can play a role in the development of laminitis. The first is commonly known as ‘grain overload,’ where a horse or pony escapes from its stall, breaks into the feed room and eats far more grain than it should (anything more than 3 kg in one feeding can be risky). In this situation, excessive starches and sugars in the grains are insufficiently digested in the small intestine (where normal amounts of starch and sugar would be broken down to glucose and absorbed), and reach the large intestine. Here, the microbial population is suddenly overloaded with a novel substrate for them to ferment. They produce excessive gasses and acids (which can contribute to colic), altering the ecosystem and killing off microbes (in turn releasing harmful toxins), and resulting in the production of compounds called vasoactive amines. The absorption of these vasoactive amines and toxins into the bloodstream reach the hoof, where they break down the basolateral membranes of the lamina and can ultimately cause laminitis. Pasture-associated laminitis is similar, where either high sugars in the grasses, or specialized sugars called fructans, accumulate in the grass.
The other theory involves the horse’s metabolic system. Elevated concentrations of insulin in the blood can trigger laminitis, although the mechanism is not well understood. A horse can develop elevated concentrations of insulin in their blood when they develop insulin resistance, where insulin fails to regulate glucose concentrations and therefore more and more insulin is produced by the body. Insulin resistance can develop in horses that consume too much starch and sugar from high grain meals or pasture on a regular basis, are obese, or are genetically predisposed (easy keepers, ponies and some horse breeds).
Management for Prevention
Laminitis prevention includes dietary evaluation and restriction of starch and sugar, monitoring body weight and condition, regulating pasture access and making sure grain bins are kept tightly closed!