Horse stomach ulcers are caused by acid damaging the stomach lining, but the specific triggers range from diet and feeding schedule to exercise, stress, and pain medications. The condition is remarkably common: prevalence rates in Thoroughbred racehorses run between 66 and 93%, and even horses used for leisure or light riding show rates above 60%. Understanding what drives ulcer formation starts with how the horse’s stomach is built and why it’s so vulnerable.
Two Regions, Two Types of Ulcers
A horse’s stomach has two distinctly different linings divided by a visible ridge called the margo plicatus. The upper portion is covered in squamous tissue, similar to the lining of the esophagus. It’s thin, relatively unprotected, and never meant to sit in acid. The lower portion is glandular tissue that actively produces stomach acid but also secretes a mucus layer to protect itself.
This matters because ulcers in each region develop for different reasons. Squamous ulcers form when acid reaches tissue that has no natural defense against it. Glandular ulcers, by contrast, develop when the lower stomach’s built-in protective mechanisms break down. A horse can have one type, the other, or both at the same time. Squamous ulcers are more common overall, but glandular ulcers can be harder to treat because their causes are less straightforward.
Continuous Acid, Intermittent Feeding
The single biggest driver of squamous ulcers is the mismatch between how a horse’s stomach works and how most horses are fed. Horses produce stomach acid continuously, not just when they eat. In the wild, they graze for 16 or more hours a day, which means food is almost always present to absorb acid and the horse is almost always chewing and producing saliva. Saliva is rich in bicarbonate, a natural acid buffer, and horses produce twice as much saliva when eating forage compared to grain or pellets.
When a horse is fed two meals a day with long gaps in between, acid keeps flowing into an increasingly empty stomach. Research shows that after as little as four hours without food, the pH in the upper stomach drops to consistently acidic levels (below 4). That acid pools against the unprotected squamous lining and begins to erode it. Any period of daytime fasting rapidly increases acid exposure in the upper stomach, making twice-daily feeding schedules one of the most significant risk factors for ulcer development.
Providing forage throughout the day is protective because both the physical presence of hay in the stomach and the saliva generated by chewing act as buffers against acid.
High-Grain Diets Make It Worse
Diets heavy in grain, sweet feed, or other starch-rich concentrates create a more acidic stomach environment through two separate mechanisms. First, bacteria in the gut rapidly ferment sugars and starches, producing volatile fatty acids that add to the overall acid load. Second, grain requires far less chewing than hay or pasture grass, so the horse produces less saliva and for a shorter period of time. The result is more acid and less buffering, a combination that accelerates squamous ulcer formation.
Penn State Extension recommends keeping sugar and starch intake below 1 gram per kilogram of body weight per meal and no more than 2 grams per kilogram per day. For a 1,100-pound (500 kg) horse, that means no more than 500 grams of combined sugar and starch in a single feeding. Many commercial grain mixes exceed this threshold quickly, especially when fed in large meals to meet the calorie demands of performance horses.
Exercise Splashes Acid Upward
Intense exercise is a well-documented cause of squamous ulcers, which explains why racehorses and competition horses have the highest prevalence rates (80 to 100% in horses actively racing). Exercise increases stomach acid production while simultaneously decreasing blood flow to the digestive tract. But the most direct mechanism is physical: when a horse moves at speed, abdominal pressure compresses the stomach and causes acidic fluid to splash upward onto the unprotected squamous lining.
Think of it like a half-full water bottle being shaken. The acid that normally sits in the lower glandular region, where the tissue can handle it, gets pushed into contact with the thin upper lining that has no mucus barrier. Horses in heavier work, whether dressage (85.7% prevalence), steeplechase (86.7%), or racing, consistently show higher ulcer rates than horses in lighter activity.
Pain Medications Damage the Glandular Lining
Non-steroidal anti-inflammatory drugs, commonly called NSAIDs, are one of the primary causes of glandular ulcers. Phenylbutazone (Bute) and flunixin meglumine (Banamine) are the most widely used in horses. These drugs work by blocking enzymes involved in inflammation, but those same enzymes help maintain the protective mucus lining and blood flow in the glandular stomach.
The damage happens through two routes. Systemically, the drug reduces the stomach’s ability to maintain its mucus barrier regardless of how it’s given. Locally, when NSAIDs are given orally, the drug molecules penetrate directly into the surface cells of the stomach lining, become trapped inside them, and cause cell death. Overdosing or prolonged use significantly raises the risk, but even standard doses can contribute to glandular erosion in some horses.
Stress and Management Practices
Environmental stress plays a significant role, particularly in glandular ulcer development. Horses housed individually, managed by multiple handlers, or kept in consistent heavy work show higher rates of glandular disease. The exact biological pathway isn’t fully mapped, but the pattern is clear: the more stressors a horse faces, the more likely its stomach’s natural defenses will falter.
Transport is one of the most potent acute stressors. Researchers found that as little as four hours of trailering induced ulcers in horses that had no ulcers before departure. Transport combines multiple stressors at once: confinement, vibration, temperature changes, social disruption, and fasting. Even when hay is available during travel, many horses choose not to eat, which removes the buffering protection of both forage and saliva right when stress hormones are running highest.
Stall confinement without turnout, frequent changes in routine, and isolation from other horses all contribute to a stress load that can compromise the glandular lining’s ability to protect itself.
How These Causes Overlap
In practice, most horses with ulcers are dealing with several of these factors simultaneously. A typical performance horse might be stalled for most of the day, fed two large grain meals with limited hay, trailered to competitions on weekends, exercised intensely, and given Bute after hard workouts. Each of those factors independently raises ulcer risk. Together, they create conditions where ulcer development is almost inevitable.
This overlap also explains why ulcer management usually requires changes on multiple fronts rather than addressing a single cause. A horse that continues on the same feeding schedule, workload, and housing arrangement will often re-ulcerate even after treatment, because the underlying causes remain in place. The squamous region responds most strongly to dietary and feeding changes, while the glandular region is more influenced by stress reduction and limiting NSAID use.