Why Horses Develop Gastric Ulcers: Diet, Stress, and Exercise Explained

Understanding why gastric ulcers develop is fundamental to effective prevention. While both ESGD and EGGD fall under the umbrella of EGUS, the mechanisms responsible for their development differ considerably. 

Acid Exposure and ESGD 

The squamous region of the equine stomach lacks the protective mechanisms found in the glandular mucosa. Exposure to hydrochloric acid and volatile fatty acids can compromise tissue integrity, ultimately leading to ulceration¹. 

High-concentrate diets increase volatile fatty acid production and have been directly linked to ulcer formation¹. 

Why Forage Matters 

Continuous forage intake plays a critical protective role. Horses fed roughage produce approximately twice as much saliva as horses consuming concentrate feeds. Saliva acts as a natural buffer against gastric acidity¹. 

Periods of forage deprivation exceeding six hours significantly increase the risk of ESGD. Horses consuming insufficient roughage are more likely to develop ulcers². 

The Impact of Exercise 

Exercise is a major contributor to ESGD. During trot and gallop, intragastric pressure increases substantially, causing acidic gastric contents to splash onto the unprotected squamous mucosa. 

Experimental studies successfully induced squamous ulcers through race-training simulations alone¹. This helps explain why racing and endurance horses consistently show the highest ulcer prevalence. 

Stress and Gastric Disease 

Stress is increasingly recognized as a contributing factor, particularly in EGGD. Horses with severe glandular disease often demonstrate heightened stress responses and behavioural abnormalities¹. 

Management factors such as multiple caretakers, environmental changes, transport, and training intensity may contribute to stress-associated gastric disease³. 

NSAIDs and Glandular Ulcers 

Unlike ESGD, EGGD is thought to result primarily from compromised mucosal defence mechanisms rather than direct acid injury⁴. 

Non-steroidal anti-inflammatory drugs (NSAIDs), particularly phenylbutazone and flunixin meglumine, can impair mucosal blood flow and contribute to glandular ulcer formation¹. 

Conclusion 

Dietary management, forage availability, exercise intensity, stress, and medication use all contribute to gastric ulcer development. Recognizing these risk factors enables veterinarians and horse owners to implement preventive strategies before clinical disease develops. 

References

1. van den Boom R. Equine gastric ulcer syndrome in adult horses. The Veterinary Journal. 2022 May 1;283:105830. https://doi.org/10.1016/j.tvjl.2022.105830

2. Galinelli N, Wambacq W, Broeckx BJ, Hesta M. High intake of sugars and starch, low number of meals and low roughage intake are associated with Equine Gastric Ulcer Syndrome in a Belgian cohort. Journal of Animal Physiology and Animal Nutrition. 2021 Nov;105:18-23. https://www.researchgate.net/profile/Nicolas-Galinelli/publication/336719348
3. Mönki J, Hewetson M, Virtala AM. Risk factors for equine gastric glandular disease: a case-control study in a Finnish referral hospital population. Journal of veterinary internal medicine. 2016 Jul;30(4):1270-5. https://doi.org/10.1111/jvim.14370