Transcript:

[0:06]

I’m Scott Cieslar, a nutritionist with Mad Barn. Today we’re talking about ulcers in horses — equine gastric ulcer syndrome (EGUS). We’ll cover what it is, prevalence, causes and risk factors, symptoms, diagnosis, management, and a bit on treatment.

[0:56]

What is EGUS? Ulcers occur in the stomach and, more rarely, lesions can occur in the small intestine or hindgut. The most common site is the non-glandular region, from excessive exposure to acid. Horses are chronic secretors of stomach acid; if the stomach sits empty and isn’t buffered, acid reaches the non-glandular region and causes lesions. There may be a bacterial component, but in horses it’s typically the acid exposure.

[1:33]

Prevalence

Rates are very high in racehorses. Thoroughbreds often show severe lesions on endoscopy; Standardbreds also have high rates but lesions tend to be smaller. Other performance horses (barrel racing, show jumping, etc.) also have a high incidence. Younger horses are more susceptible than older horses.

[2:13]

Causes

Horses continuously secrete acid. When they aren’t eating, acid production continues. In people, ulcers are largely due to Helicobacter pylori; in contrast, horses living naturally and grazing don’t tend to get ulcers, pointing to management as the driver.

[2:48]

Risk factors

• Management & social stress: Limited grazing/turnout; moving horses between groups; changes in herd hierarchy (dropping in the pecking order).
• Inadequate forage: Long gaps without forage.
• Exercise context & routines: Trailering, stall time, frequent changes, and other stressors around training/competition.
• Grain/starch feeding: Higher-starch rations have been implicated.
• Confinement, separation/isolation, and feed deprivation increase risk.

[4:11]

Diagnosis

Endoscopic evaluation is the only way to be 100% sure for gastric ulcers.

• Anemia / plasma proteins: No strong correlation with ulcers.
• Fecal occult blood test: A positive suggests bleeding somewhere (stomach or hindgut) and has reasonable accuracy; a negative does not rule out ulcers.

[5:34]

Management

• Aim for a more natural pattern: horses should be eating 16–18 hours/day. Use slow feeders/hay nets to prolong eating, especially for overweight horses.
• Increase grazing time to boost saliva flow and help buffer the stomach.
• Reduce starch/grain. Many performance horses don’t need as much starch as they’re fed. Improve hay quality first; if grain is needed, smaller meals more than three times/day are better.
• Use non-starch energy: non-forage fiber sources and added fat where appropriate.
• Forage type: Compared with bermudagrass, alfalfa has, in some cases, improved ulcer scores. Use modest amounts and keep the whole diet balanced; avoid feeding pure alfalfa all day.
• Avoid irritants: Avoid NSAIDs when possible. Do not use hypertonic electrolyte pastes — concentrated salts can sit in the stomach and damage tissue.

[8:47]

Treatment (acid suppression & rebound)

• Raise gastric pH: Proton pump inhibitors (e.g., omeprazole) and H2-receptor antagonists (e.g., ranitidine) effectively block acid secretion.
• High recurrence after stopping: If causes persist, ulcers often return. Acid rebound can occur when medication or buffers are withdrawn.

[11:00]

Considerations when raising pH

Stomach acid helps kill pathogens and activate pepsinogen → pepsin for protein digestion. Raising pH can reduce protein digestion so that more protein reaches the hindgut, leading to abnormal fermentations and problems there. You may help the stomach short-term while creating hindgut issues.

[12:09]

Supplements

• Many products claim efficacy; few have clinical research behind them.
• Label dressing: Example: glutamine is often listed at very low amounts despite the diet and body providing much more; benefits are seen only at higher levels, not token doses.
• Buffers/antacids: Provide temporary relief but may be followed by rebound.
• Alfalfa: Often associated with improved ulcer scores when included sensibly.
• Oils: Prefer omega-3–rich options (e.g., flax, fish oil); avoid high omega-6 oils like corn oil.
• Probiotics: Some Lactobacillus species can inhibit pathogenic bacteria and may aid healing.

[15:57]

Endoscopic evaluation (examples)

Example 1: yellow, plaque-like changes from continuous acid insult in the non-glandular region; some lesions along the line can heal relatively quickly. Example 2 (Standardbred): “red, angry” non-glandular region near where acid is produced and the esophagus enters.

Key point: The severity on scope does not reliably match clinical signs — some horses look bad clinically but scope mildly, and vice versa.

[19:24]

Hindgut disturbance

Excess starch escaping small-intestinal digestion lowers hindgut pH, reduces fiber digestion, and allows “bad bugs” to proliferate. Hindgut acidosis can lead to toxin production, leaky gut, colic, and laminitis.

[20:15]

Grains & digestibility

Pre-cecal starch digestibility varies by grain and processing. Oats are highly digested in the small intestine; corn sends more starch to the hindgut, especially if not well processed. Similar concerns apply to protein: raising gastric pH reduces protein digestion, so more protein reaches the hindgut.

[21:43]

Meal size

Larger grain meals increase fecal acidity. Even around 1 kg of corn can raise acids in some horses. There’s individual variation, so keep meals small and frequent.

[24:58]

Q&A: Can ulcers heal by changing management alone?

Yes. Remove the cause and many ulcers resolve over time (e.g., lay-offs/turnout). Note: for scoping, feed is often withheld ~12 hours; that deprivation can itself start hyperkeratosis, so timing should be consistent. Severe cases may have slow gastric emptying, making scoping difficult and sometimes affecting medication strategies.

[27:20]

Medication notes

Commercial omeprazole products (e.g., GastroGard) use special coating to get through the stomach. If feed remains in the stomach too long, that coating can be compromised; severe cases sometimes require higher dosing. With prolonged use, bile reflux and glandular ulcers can occur in some horses.

[28:18]

Follow-up example

After about 60 days of treatment, the previously red, inflamed region looked much improved. A clinic asked for an after-GastroGard feeding approach to limit recurrence; that led to a product used post-omeprazole.

[29:08]

What “Visceral” is used for

Used primarily for gastric ulcers (with some hindgut support). Typical plan: complete omeprazole/GastroGard, then start this and wean off over ~2 weeks to limit acid rebound; continue while the stressor persists and remove when it’s gone.

[29:55]

What’s in it (overview)

A combination of components (e.g., lecithin, probiotics, glutamine, and soothing herbs) aimed at protecting the stomach surface and supporting turnover. It’s not just a probiotic; it’s a multi-component formula.

[30:52]

Preventive use

Some use it preventively during training down or show season, especially if the horse has a history of ulcers. It isn’t meant to be fed forever; it’s less expensive than GastroGard/omeprazole, but the goal is to fix management and discontinue when no longer needed.