Horse stomach ulcers are remarkably common, affecting an estimated 70% or more of performance horses and even Thoroughbred mares living at pasture. The causes range from diet and feeding schedules to exercise intensity, medications, and confinement stress. Unlike human ulcers, bacteria don’t appear to play a significant role. Instead, equine ulcers are driven primarily by how a horse’s unique stomach anatomy interacts with modern management practices.
Two Types of Ulcer, Two Different Causes
A horse’s stomach has two distinct lining types, and each develops ulcers through a different mechanism. The upper portion is lined with squamous tissue, similar to the lining of the esophagus. It has no built-in protection against acid. The lower portion is glandular tissue that naturally produces acid and has a mucus barrier to protect itself.
Ulcers in the upper squamous region (called Equine Squamous Gastric Disease, or ESGD) happen when acid splashes onto tissue that wasn’t designed to handle it. Anything that increases acid exposure to this vulnerable upper lining, whether it’s diet, fasting, or exercise, raises the risk.
Ulcers in the lower glandular region (called Equine Glandular Gastric Disease, or EGGD) are less well understood. This tissue normally sits in a highly acidic environment with a pH between 1 and 3, so the problem isn’t acid exposure itself. Instead, something causes the protective mucus-and-bicarbonate barrier to break down. Most glandular ulcers appear near the pylorus, the narrow exit of the stomach. Researchers have not yet pinpointed a single cause for this breakdown, though medications and stress are suspected contributors.
Diet and Feeding Schedule
Horses produce stomach acid continuously, not just when they eat. In the wild, they graze for 16 to 18 hours a day, so there’s almost always food in the stomach to absorb that acid. Modern feeding schedules, typically two or three meals a day with hours of empty stomach in between, create long windows where acid has nothing to work on except the stomach lining.
Forage does double duty as protection. Chewing hay or grass stimulates saliva production, and horse saliva contains bicarbonate, a natural acid buffer. Fibrous material also forms a mat in the stomach that physically separates the acidic liquid below from the squamous tissue above. When hay intake drops or meals are spaced too far apart, both of these protective effects disappear.
High-grain and high-starch diets compound the problem. When large amounts of starch reach the stomach, bacteria ferment it and produce lactic acid and volatile fatty acids. These byproducts add to the damage already being caused by hydrochloric acid. The combination is worse than acid alone, because the fermentation products help acid penetrate deeper into the squamous cells, accelerating ulcer formation. Specific risk factors identified in the research include lower hay provision, fewer meals per day, and higher grain and starch intake.
Exercise and the Acid Splash Effect
Intense exercise is one of the most consistent risk factors for squamous ulcers, and the mechanism is surprisingly physical. At any gait faster than a walk, the horse’s abdominal muscles contract and compress the stomach. This increased pressure pushes the acidic contents upward and dorsally, splashing them onto the unprotected squamous lining in the upper stomach.
This “splash effect” explains why racehorses and high-level sport horses have some of the highest ulcer rates. The more intense and frequent the exercise, the more often acid reaches tissue it shouldn’t touch. Even horses in moderate work can develop ulcers this way if their stomachs are relatively empty during exercise, since there’s less forage to act as a buffer between the acid pool and the squamous region.
Pain Medications and NSAIDs
Non-steroidal anti-inflammatory drugs, particularly phenylbutazone (commonly called “bute”), are a well-known cause of gastric ulcers in horses. These drugs work by blocking an enzyme called COX-1, which is involved in producing prostaglandins. Prostaglandins stimulate the production of protective mucus in the glandular stomach lining. When that mucus layer thins out, the tissue becomes vulnerable to its own acid.
This mechanism primarily affects the glandular region, since that’s where the mucus barrier matters most. Horses that are hospitalized face a particularly high risk because they’re often given NSAIDs for pain while simultaneously fasting before procedures, creating a double hit of reduced mucosal protection and unabsorbed stomach acid.
Confinement, Transport, and Stress
Stall confinement and transportation both raise cortisol levels in horses, and both are linked to ulcer development. In one study of mares, half the horses developed new or worsened squamous ulcers after a period of confinement alone, with some progressing to moderate-grade lesions along the lesser curvature of the stomach.
The connection between stress and ulcers likely involves several overlapping factors. Confined horses eat less forage, which removes the buffering effect of saliva and the protective fiber mat. They also can’t engage in their natural near-constant grazing behavior, leaving the stomach empty for longer stretches. Social isolation adds psychological stress on top of the dietary disruption. Transportation combines all of these, adding vibration, balance demands, and the physical compression of the abdomen during movement.
Why Bacteria Aren’t the Culprit
In humans, the bacterium Helicobacter pylori is a primary driver of stomach ulcers. Horse owners sometimes assume the same applies to their animals, but research has consistently found otherwise. No Helicobacter species has been associated with glandular gastric disease in horses, and broader studies looking at the full bacterial community in the equine stomach found no single species, phylum, or genus linked to ulcer development. Equine ulcers are fundamentally a management and environment problem, not an infectious one.
Reducing Ulcer Risk Through Feeding
Because so many ulcer causes trace back to acid exposure on an empty or poorly buffered stomach, the most effective prevention strategies center on how and what a horse eats. Continuous or near-continuous access to forage is the single most protective factor. Horses with ready access to hay or pasture for the majority of the day maintain a more stable stomach environment, with more saliva production and a physical fiber barrier between acid and the squamous lining.
Alfalfa hay offers additional benefit because of its naturally higher calcium and protein content, both of which help buffer stomach acid. Feeding a small amount of alfalfa before exercise can help reduce the splash effect by raising stomach pH and adding bulk. Reducing grain meals in favor of forage-based calories lowers the amount of fermentable starch reaching the stomach. When grain is necessary, splitting it into smaller, more frequent meals limits the amount of starch available for bacterial fermentation at any one time.
For horses in heavy training, competing, or traveling frequently, the combination of dietary adjustments with awareness of exercise timing and stress management covers the broadest range of ulcer causes. Feeding hay before riding, minimizing time spent with an empty stomach, and keeping stall confinement as brief as practical all directly address the mechanisms that damage the stomach lining.