Don’t let yours be one of them.
Gastric ulceration is virtually ubiquitous among performance horses, occurring in as many as 93% of Thoroughbred racehorses. In addition, up to 60% of other athletic horses also show signs of the disease. The problem is even of great importance in foals, as up to 57% of foal will show ulceration in their first few months of life. YET up to 50% of horses with ulcers do not show any outward signs of the condition!
WHY OH WHY?
There are many environmental and physiological factors that contribute to the appearance of gastric ulcers in horses. The many risk factors for gastric ulceration include chronic use of non-steroidal anti-inflammatory drugs, high-carb feeding, and mechanical compaction of the stomach through high-intensity exercise.
HOW DO WE TREAT this potentially lethal condition?
…..these animals are performing athletic tasks that continually test their performance capabilities, frequently resulting in injuries that must be treated with bute and other NSAIDs (Non-Steroidal Anti-Inflammatory Drugs).
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Such compounds work to reduce inflammation in part by inhibiting the production of pro-inflammatory mediators, including prostaglandin E2 (PGE2). However, while NSAIDs effectively control pain and inflammation, they also inhibit the production of PGE2 in the stomach, leading to increased susceptibility to ulcers. PGE2 is critical in the stomach; it participates in regulation of mucus and bicarbonate secretion that protects the stomach lining from acid. PGE2 also promotes blood flow to the stomach lining, stimulates proliferation of epithelial cells as well as mucosal immune function. NSAIDs also have a direct irritating effect on the gastric lining by acting almost like soap on the mucus layer of the stomach lining. Thus, depletion of PGE2 by NSAIDs can have very negative effects on the stomach and make it vulnerable to damage by acid.
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Are you Feeding an Oink Oink?
Horses are often fed diets that are not consistent with their gastrointestinal anatomy. Their small stomach and large caecum makes horses ideally suited to ‘trickle feeding’ on high-fiber feeds for many hours over the course of a day. But most performance horses are fed more like pigs, with high-carbohydrate diets fed in 2 or 3 large meals. These meal-fed diets are frequently high in soluble carbohydrate and low in long-stem fiber placing considerable stress on a gastrointestinal system not designed to handle them. This feeding method is ideal for creating gastric and duodenal ulcers in horses, as the high-starch feeds reduce pH in the stomach and upper small intestine. Furthermore, since horses are designed to feed continually their stomach produces acid continually, unlike humans that produce acid only when eating. Hence, when we feed our horses only 2 or 3 times a day their stomachs are being continually challenged with acid even when there is no feed inside to buffer the erosive actions of acid.
Training and Environmental Stress
Training for Racing, Barrels or the Grand Prix ring imposes significant stress on horses. Stress hormones (cortisol, epinephrine and norepinephrine) reduce PGE2 production (see above), and also stimulate production of histamine, which directly promotes secretion of gastric acid. This increases the vulnerability of the horse to gastric ulceration.
Foals are often found to have gastric ulcers, predominantly as a result of their physical development. Little stomachs are very prone to injury by acid and enzymes. Shipping of horses and prolonged restraint in stalls may also contribute to ulcer formation.
4 Clinical Signs of gastric ulceration
Clinical signs may vary between horses depending on age and other factors:
- A mature horse may have any of a poor hair coat, “cranky” attitude, poor appetite, or regular bouts of colic.
- A foal may display these symptoms in addition to others including diarrhea, slowed growth rate, grinding of teeth, pot-belly, interrupted nursing and excessive salivation.
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Conventional medical treatment of gastric ulcers in horses usually includes using histamine H2-receptor antagonists, including cimetidine, famotidine and ranitidine or the proton pump inhibitor omeprazole. These treatments have some success in elevating gastric pH and mitigating ulcer formation, but they have a number of well-known limitations: 1) some (eg omeprazole) are effective curative agents, but do not prevent ulcer formation. Furthermore, omeprazole is cost-prohibitive for many horse owners. 2) use of H2-receptor agonists has been associated with gastric yeast infection in as much as 54% of animals using the products. The infection delays ulcer healing and may invade the gastric mucosa causing further clinical disease. Furthermore, some of these drug treatments cannot be given in the days leading up to athletic events or competitions. Therefore, alternative treatment options are frequently sought. Some anecdotal success has been achieved by feeding probiotics (ie. Live-culture yoghurt or commercial probiotics), though solid science to support this observational evidence is lacking.
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An ‘alternative’ ulcer treatment which is supported by substantive science is the use of bioflavonoids. Bioflavonoids are a class of botanical compounds that function as antioxidants, enzyme inhibitors, pigments and light screens. They also are involved with photosensitization, photosynthesis and defense against infection. A growing body of evidence points to a possible connection between plant bioflavonoids and prevention/treatment of gastric ulceration in mammals. A specific ‘flavan’ was reported to be as effective as omeprazole in reducing total gastric secretion, reducing the free and total acids in the gastric secretions, and reducing gastric mucosal histamine. Another flavan reduced indomethacin-induced gastric damage in lab rats by up to 99%. Naringenin, was found to effectively prevent gastric ulceration initiated by absolute alcohol… great news for Vodka drinkers? ;<)
Gastric ulceration is a highly problematic condition affecting the vast majority of performance horses. Even those without obvious clinical signs could be experiencing reduced exercise tolerance and performance, reduced feed efficiency, and gastrointestinal pain due to subclinical ulceration. There are several drug and non-drug treatments available for gastric ulceration including proton pump inhibitors (eg. Omeprazole), H2 receptor agonists (eg. Cimetidine), and at least one plant bioflavonoids based product with evidence of clinical efficacy.
But remember, gastric ulceration is a serious condition that should only be diagnosed and treated under the supervision of a qualified veterinary practitioner; but find one that practices with an open mind!
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