Equine Gastric Ulcers: What's Actually Happening in the Stomach
Equine gastric ulcers are often discussed as a feeding issue. They’re a physiology issue first.
Unlike humans, horses produce stomach acid continuously, whether they are eating or not. This is important because horses evolved to graze for most of the day, not to consume intermittent meals.
The equine stomach is divided into two distinct regions: the squamous (upper) portion and the glandular (lower) portion. These tissues differ both structurally and functionally, understanding that difference is key to understanding ulcer development.
The squamous region does not have the same protective mechanisms as the lower stomach. It lacks a substantial mucus barrier and bicarbonate secretion, making it more vulnerable to acid exposure. This is where we commonly see “acid splash” ulcers, particularly in performance horses.
The glandular region is normally protected by a mucosal barrier and bicarbonate secretion. Ulcers in this region are not simply the result of acid exposure but rather the breakdown of the protective mechanisms. Glandular disease is more complex, and research in this area remains more limited compared to squamous ulcers.
Continuous acid production alone does not cause ulcers. Ulcers develop when the stomach’s protective mechanisms fail and acid exposure exceeds the tissue’s ability to defend itself.
What contributes to ulcer development?
Ulcers tend to develop when the balance between acid exposure and protection is disrupted. Several factors can shift this balance.
Fasting intervals. When forage intake pauses, acid production does not. Without continuous chewing and saliva buffering, the squamous region is exposed to increasingly acidic conditions.
Exercise. During exercise, increased abdominal pressure can force acidic stomach contents upward into the more vulnerable squamous region. This effect is amplified when the stomach is relatively empty.
Diet composition. High-starch meals may increase volatile fatty acid production, which are byproducts of carbohydrate fermentation within the gastrointestinal tract. In combination with an already acidic environment, these compounds can contribute to injury of the squamous mucosa.
Stress. Physiological stress may impair the integrity and regeneration of the glandular mucosa. Elevated cortisol levels can alter blood flow and reduce the stomach’s ability to maintain its protective barrier. When protective mechanisms are compromised in the presence of continuous acid secretion, ulceration becomes more likely.
Bacterial involvement. Unlike in humans, there is currently no evidence that Helicobacter pylori plays a role in equine gastric ulcer disease.
When ulcers are suspected, veterinary involvement is important to ensure appropriate diagnosis and treatment. Gastric ulcers can significantly damage the stomach lining, and medical therapy is often necessary to support proper healing.
If ulcers reflect an imbalance between acid exposure and protective mechanisms, prevention focuses on restoring that balance. I’ll explore this topic in a future post.