
Researchers have found that horses treated for gastric ulcers could be getting less calcium into the bloodstream than they would normally. Depending on the calcium source, horses treated with omeprazole (such as GastroGard, the FDA-approved medications for the treatment and prevention of equine gastric ulcers) could be digesting 15-20% less calcium than when they’re not on omeprazole.
Over prolonged treatment periods, this could lead to deficiencies if the horse isn’t consuming adequate amounts of calcium, said Joe Pagan, PhD, founder of Kentucky Equine Research (KER), in Versailles.
“The vast majority of commercial feeds include sufficient quantities of calcium for working horses to cover the horse’s calcium needs, even if he’s not digesting the full amount due to omeprazole,” said Pagan. “But that means following the feeding instructions on the labels to be sure the horse is getting the correct ration.”
Horses on hay alone or that receive supplementary commercial feed mixed with oats, for example, might not be getting adequate calcium if they’re also being treated for gastric ulcers. “When they’re already borderline in their calcium intake, omeprazole might make them deficient in calcium by reducing their ability to digest it,” he said.
In their study of Thoroughbred horses working as their own controls, Pagan and his fellow researchers analyzed all sources of calcium intake—including hay, feed, and supplements—as well as the amount of calcium in the horses’ feces. They studied the horses with different combinations of calcium sources, with and without omeprazole treatment, over a total period of 12 weeks.
They found that horses receiving calcium carbonate (produced from limestone)—which is found in most commercial feeds—experienced a 20% reduction in calcium digestibility when treated with omeprazole, Pagan said. Those receiving marine-derived calcium, available as a supplement, had a 15% drop in calcium digestibility. Digestibility is the digestive system’s ability to absorb nutrients from food and into the circulatory system for distribution throughout the body. Nutrients passing through the digestive system without getting picked up through its walls are essentially wasted, Pagan explained.
Calcium dissolves better in acid than in water, he said. Omeprazole reduces acidity in the digestive system, which could explain why horses digest less calcium when on omeprazole, he said.
When the bloodstream is lacking calcium, it can replenish its stock by dipping into its “reservoirs”—the bones, said Pagan. As a result, calcium-deficient horses might experience weakened bones, he said. However, he did not study possible effects on bones in his study.
In addition, it appears that omeprazole can trigger an excess production of a hormone called gastrin, Pagan said. Although more research is necessary, it seems possible that this excess gastrin might, in turn, trigger excess production of parathyroid hormone, which can lead to bone resorption. “It would be interesting to study a large group of horses treated with omeprazole and follow their parathyroid production,” he said.
Parathyroid-related bone resorption could lead to bone weakening and malformation, such as what we see in a disease commonly known as “big head,” or Miller’s disease, said Pagan. “This was common in flour mill horses because they weren’t getting enough calcium in their grain, and they would develop enlarged heads from this secondary hyperparathyroidism,” he said.
In these cases the body pulls calcium from the skull into the bloodstream and replaces the missing bone with fibrous tissue, leading to a larger head.
While omeprazole use is unlikely to cause bone issues in horses on correct rations, it’s important to respect professional recommendations for both omeprazole treatment duration and commercial feeding instructions, Pagan said.