Frank Andrews is a graduate of Washington State University College of Veterinary Medicine. He completed an equine medicine and surgery residency atAndrews with horse The Ohio State University and is Board Certified in Large Animal Internal Medicine. After 20 years at the University of Tennessee College of Veterinary Medicine as Professor and Section Chief, he is currently LVMA Equine Committee Professor and Director of the Equine Health Studies Program at Louisiana State University School of Veterinary Medicine.

Equine gastric ulcer syndrome (EGUS) is a condition in horses characterized by ulcers in the terminal esophagus, proximal (squamous) stomach, distal (glandular) stomach, and proximal duodenum [1]. Diagnosis of EGUS is based on history, clinical signs, endoscopic examination, and response to treatment. All ages and breeds of horses are susceptible to EGUS, and current pharmacologic strategies focus on blocking gastric acid secretion and increasing stomach pH, which creates a permissive environment for ulcer healing.  However, long-term treatment with pharmacologic agents is expensive and requires frequent daily handling of the horse.  Recently, nutritional and dietary management factors have been identified to play an important role in gastric ulcers in horses.  Thus, diet and nutritional management can be employed as an adjunct and follow-up to pharmacologic therapy to decrease ulcer severity and recurrence. This review focuses on nutritional and dietary factors that have been implicated to cause EGUS and how the horse diet can be managed to lessen ulcer severity and prevent recurrence of EGUS.  Highlighted in this review are the basic anatomy and physiology of the equine stomach, current feed management practices that put the horse at risk for EGUS, and dietary strategies that can decrease ulcer severity and prevent recurrence once ulcers are successfully treated.

 Anatomy and gastric acid secretion
Horses are predisposed to gastric ulcers because of their compound stomach. The majority (80%) of ulcers occur in the proximal-third of the stomach, which is lined by non-glandular stratified squamous epithelia. The distal two-thirds of the stomach are lined by glandular mucosa that secrete protective mucus and bicarbonate, as well as hydrochloric acid (HCl), and pepsinogen for digestion [2].  This glandular region also has an extensive capillary network and undergoes rapid restitution of epithelium when injured. Approximately 20% of ulcers occur in this region, and many heal rapidly without therapeutic intervention. The nonglandular squamous mucosa is predisposed to acid injury because it lacks this substantial protective mucus and bicarbonate layer [3].

Horses are continuous gastric HCl secretors, and acid exposure is thought to be the primary cause of EGUS [4]. Gastric acid secretion is stimulated by gastrin, histamine, and acetylcholine from the Vagus nerve. However, other acids (volatile fatty acids [VFA], bile acids [BA], and lactic acid [LA]) and enzymes (pepsin) found in the stomach also contribute to an acidic environment and low stomach pH. A recent study found that horses have a lower pH in the proximal stomach during early morning (1:00 to 9:00 AM), which suggests a circadian pattern for gastric acid secretion [5].  Prolonged exposure of the proximal stomach to a low pH environment is the likely cause of EGUS and is similar to gastroesophageal reflux disease (GERD) in humans.

Synergistic action between VFA, LA, BA, and HCl may cause acid damage to the non-glandular mucosa of the stomach, leading to EGUS [6, 7, 8]. Both HCl alone and in combination with VFA (pH ≤ 4.0) byproducts of grain fermentation by resident stomach bacteria have been shown to inhibit non-glandular stomach mucosal cell sodium transport, resulting in cell swelling and eventual ulceration. The ulcerogenic effects of VFAs were dose-dependent, and the severity of the damage was related to VFA carbon chain length [7, 8, 9]. However, a recent study showed that D- and L- lactic acids, also byproducts of bacterial fermentation of grain, when exposed to the non-glandular stomach mucosa in vitro in an acid environment, did not significantly alter barrier function or sodium transport through the tissues, when compared to VFA with similar PKa [10].  Thus, the role of LA in the cause of EGUS needs further investigation.

Bile acids, on the other hand, were shown to increase non-glandular mucosal cell permeability to hydrogen ions, which eventually leads to ulceration [6].  However, the effects of BA in EGUS are questionable because they usually come from less acidic duodenal reflux and are non-ulcergenic at a pH >4 [11]. Also, the proteolytic enzyme pepsinogen, which is cleaved to pepsin at a pH<4, may act synergistically with HCl to result in acid damage. Thus, while HCl and stomach pH have been incriminated as the main causes of EGUS, it is likely that a combination of HCl, organic acids, and pepsin act to cause injury to the gastric mucosa, causing EGUS.

Risk factors and Clinical Signs of EGUS
While acid injury has been implicated in the cause of EGUS, several risk factors for its development have also been identified and clinical signs consistent with EGUS have been identified  

Exercise intensity
Horses involved in training and racing are at high risk to develop EGUS [14]. In fact, current prevalence figures show that 60% to 90% of performance horses have EGUS.  A recent study showed that horses running on a high-speed treadmill have increased abdominal pressure and decreased stomach volume [15]. The authors' speculated that this activity allowed contraction of the stomach, resulting in reflux of the acid from the glandular mucosa into the non-glandular mucosa, leading to injury. Therefore, daily exercise may increase the exposure of the non-glandular mucosa to acid, explaining the increased prevalence of gastric ulcers in horses in training. Furthermore, an increase in serum gastrin concentration has been shown to occur in exercising horses [16]. This increase in serum gastrin may increase glandular HCl secretion, which, in turn, may lead to acid damage.

A recent study showed that sodium transport in the non-glandular mucosa was down-regulated in horses ≥ 5 years of age (the age of most racehorses) compared to horses > 5 years of age [17]. The inability of the non-glandular mucosal cells to up-regulate sodium transport may predispose them to cell swelling and eventual ulceration, which may be why young horses are more susceptible to EGUS.

Intermittent vs. continuous feeding
Horses grazing at pasture have a decreased prevalence of EGUS.  During grazing, there is a continuous flow of saliva and ingesta that buffer stomach acid; stomach pH is ≥ 4.0 for a large portion of the day. On the other hand, when feed is withheld from horses before racing or as with stabled horses, gastric pH drops rapidly, and the non-glandular mucosa is exposed to an acid environment. However, a recent study showed that pastured pregnant and non-pregnant mares had a high prevalence of gastric ulcers [18]. The high prevalence of gastric ulcers in these pastured mares may be because horses consume less forage during evening hours than during daytime hours, which may result in less saliva production and a low pH environment in the proximal stomach. A recent study by Husted et al. [5] showed that proximal stomach pH was lower in the early morning hours (1:00 am to 9:00 am) regardless of housing (paddock or stable). This may be why both pastured and stabled horses are susceptible to EGUS, albeit by varying degrees. Still, intermittent feeding has been shown to cause and increase the severity of non-glandular ulcers in horses, and this concept has been used as a model to consistently produce EGUS in research settings [19-21].

Stall confinement
Alongside feeding practices, stall confinement has been implicated as a risk factor for EGUS.  However, a recent study showed that neither proximal nor ventral stomach pH changed significantly in horses housed in stalls alone, housed in stalls with a companion, or housed in a grass paddock [6].  Here again, pH in the proximal stomach was lower during the early morning hours regardless of housing, and feed intake was lowest during these hours.  Thus, other factors in stabled horses may also increase their risk of developing EGUS.  For example, stabled horses are bolus fed (two large meals daily).  These meals are traditionally high in grains and consumed rapidly, which leads to a decrease in saliva production and less buffering of stomach contents.  Also, high grain diets may be fermented by resident stomach bacteria to VFA, which in an acid environment may lead to ulceration [7-9, 22]. 

High concentrate diets
Size and composition of grain in the diet is thought to have a profound effect on risk for developing EGUS.  Serum gastrin concentrations are highest in horses fed high concentrate diets. These diets are high in digestible carbohydrates, which are fermented by resident bacteria, resulting in the production of VFA.  In the presence of low stomach pH (≤ 4), VFA cause acid damage to the non-glandular squamous mucosa [7-9, 22]. However, in a recent study, horses fed Alfalfa hay and a pelleted concentrate diet had lower gastric ulcer scores than horses fed Coastal Bermuda hay [23]. Furthermore, a previous study showed that horses fed Alfalfa hay and grain had a higher stomach pH and lower ulcer scores when compared to horses fed Brome grass hay without grain [22]. In this study, the authors speculated that calcium and protein, both high in the Alfalfa hay-grain diet, buffered stomach contents, resulting in a protective effect on the non-glandular mucosa. Thus, Alfalfa hay when fed with or without concentrates may have a protective and anti-ulcer effect in horses.

Clinical signs of EGUS
Clinical signs associated with EGUS are numerous but often vague. Therefore, ulcers are more commonly diagnosed in horses showing clear clinical signs [1, 24, 25]. In Thoroughbred horses in race training, gastric ulcers are associated with poor performance, poor hair coat, picky eating, and colic. Gastric ulcers were identified in 88% to 92% of horses with a client complaint of conditions associated with ulcers or horses showing subtle signs of poor health, compared to 37% to 52% identification in horses not showing symptoms. In addition to an increased prevalence of ulcer diagnosis in clinically affected horses, the severity of ulceration may be correlated with the severity of the symptoms.

Diagnosis of EGUS requires a thorough history, physical examination, and a minimum data base.  Identifying risk factors and clinical signs are helpful in making a diagnosis; however, gastroscopy is the only definitive diagnosis for gastric ulcers currently available.  Standing gastroscopy procedures have been described in detail elsewhere in the literature and require at least a 2 meter endoscope to visualize the non-glandular mucosa and margo plicatus and a 2.5m to 3m endoscope to visualize the pylorus and proximal duodenum in most adult horses [26, 27].  Use of a gastric ulcer scoring system allows clinicians to compare gastroscopic findings, monitor healing of ulcers, and evaluate efficacy of treatment [1, 28].

Currently there are no hematologic or biochemical markers to diagnose EGUS.  However, a recent report showed that horses with gastric ulcers had lower red blood cell (RBC) counts and hemoglobin concentrations than horses that did not have gastric ulcers [29].  Some horses with EGUS may be slightly anemic or hypoprotenemic, but in this authors' experience, although RBC and hemoglobin concentrations may be low, they are rarely outside normal reference ranges.

In a recent study, a fecal occult blood test (FOBT) was also found to be helpful in diagnosis of EGUS [31]. The positive predictive value of the FOBT in horses with EGUS was 90%; however, the negative predictive value was only 17%, suggesting that horses with a positive FOBT are likely to have a gastric ulcer. In an attempt to improve the negative predictive value of the FOBT, investigators developed another test (SUCCEED Equine Fecal Blood Test) that uses specific equine monoclonal antibodies to both albumin and hemoglobin in an easy-to-use kit. A recent report published in the company bulletin [32,33] showed a greatly improved predictive value of the negative test (72%), but the predictive value of a positive test was slightly lower (77%). Thus, this new test may be helpful in diagnosing EGUS in horses, but should be used as part of a complete work-up. A false positive FOBT may also result if a recent rectal examination has been performed or if the horse has a protein losing enteropathy.

Unfortunately, laboratory techniques provide only presumptive diagnostic evidence of EGUS; therefore if gastroscopy is not available and ulcers are strongly suspected, it may be worthwhile to start empirical treatment and observe for resolution of clinical signs.  If the horse does not respond to treatment, referral to a facility with a gastroscope is indicated.

Management of EGUS
Pain relief, healing, and prevention of secondary complications are the primary goals of anti-ulcer therapy and management recommendations.  The mainstay of pharmacologic treatment of EGUS is to increase stomach pH and suppress HCl acid secretion.  Because of the high recurrence rate, effective acid control should be followed by nutritional and dietary management strategies to prevent ulcer recurrence.

Pharmacologic therapy
Once EGUS is diagnosed, therapy should be initiated to achieve the above goals.  Some EGUS lesions heal spontaneously, but the majority require pharmacologic therapy to heal, especially while horses remain in athletic training [1, 34, 35]. the most accepted strategy to treat EGUS is acid suppressive therapy.  Currently, omeprazole (Gastrogard) is the only Food and Drug Administration-approved product for prevention of recurrence and treatment of EGUS.  However, other pharmacological therapies have been used to treat EGUS with mixed success.

Duration of pharmacologic treatment
 It is difficult to predict how long a non-glandular or glandular gastric ulcer will take to heal, but the initial recommended treatment time for most anti-ulcer medications is 28 days.  However, management changes in addition to pharmacologic therapy may speed the healing of ulcers.  For example, after a feed deprivation model of ulcer induction, ulcers were healed or nearly healed in horses after 9 days of pasture turnout [20], whereas Thoroughbred horses treated with omeprazole while still in training took longer to heal: 57%, 67%, and 77% healing after 14, 21, and 28 days of treatment, respectively [35]. Horses with spontaneous occurring ulcers in a field trial treated with omeprazole showed 86% healing after 28 days of treatment [36, 37]. We recommend endoscopic examination after 14 days of omeprazole therapy to determine if the ulcers are healed.  If the gastric ulcers are healed, the dose can be reduced (1 mg/kg, PO, q24h) to prevent recurrence of ulcers while the horse remains in race training [38].  If the ulcers are still present, the full 28-day course of omeprazole should be followed and the horse further evaluated after that time.  When endoscopy is not available, horses should be treated for at least 28 days.  It should be noted that clinical signs might resolve before complete healing has taken place. Signs of poor appetite, colic, or diarrhea will usually resolve within a few days after initiating treatment, and the horse is expected to make improvements in body condition and attitude within 2 to 3 weeks [39]. Histamine type 2 antagonist therapy should be continued for at least 28 days, but healing may take longer than 40 days and may not be as effective as treatment with omeprazole paste [40].

In general it may take longer to treat large ulcers, more severe ulcers, and ulcers in the non-glandular mucosa [41]. In cases where clinical signs have resolved and the risk factors for ulcer development are low, spontaneous healing of ulcers may occur without further treatment. However, spontaneous healing does not usually occur in horses that continue intensive training, and ulcers may re-occur in those successfully treated if therapy is discontinued [35, 38]. If clinical signs attributed to EGUS have not resolved after 48 hours of treatment, the diagnosis or therapy should be re-considered.

Environmental, nutritional and dietary management of EGUS
Pharmacologic therapy may be necessary to heal both glandular and non-glandular gastric ulcers in horses, but once pharmacologic therapy is discontinued, the ulcer will likely quickly return if management changes are not instituted.  Environmental, nutritional, and dietary management can be initiated during therapy to help facilitate ulcer healing and ultimately prevent ulcer recurrence. As mentioned before, intense or long-duration exercise, stall confinement, and diet are risk factors for EGUS.  Therefore, managing these risk factors can decrease severity and prevent ulcer recurrence.

Modification of exercise intensity and duration
In horses, intense exercise, racing, and race training has been shown to contribute to worsening of non-glandular gastric ulcers compared to horses kept at pasture or not in training.  Also, endurance exercise has been shown to play a role in the cause of EGUS in horses.  In one study, 67% of horses competing in 50- and 80-mile endurance rides had gastric ulcers [42].  In addition, repeated oral administration of hypertonic replacement electrolyte solutions to these horses was shown to increase the number and severity of gastric ulcers [43].  Thus, these oral hypertonic electrolyte replacement products should be used with caution in exercising horses.

Pasture turnout
One study found that even giving a horse in a stall ad lib grass hay did not improve ulcers, while horses maintained on pasture rarely had gastric ulcers [44, 45]. Therefore, pasture turnout is the best dietary method of controlling gastric ulcers. However, management of the diet fed to stalled horses can be modified to decrease the risk of ulcer. Current dietary recommendations include providing continuous feeding of good quality grass and/or alfalfa hay.  Sweet feed should be kept to a minimum, and grains like barley or oats can be substituted to decrease its fermentation to VFAs.

Eliminate bolus feeding and increase forage and fiber
Another effective method to decrease EGUS is to feed a high forage diet continuously.  Stabled horses are frequently fed two large meals daily, which results in lower saliva production and increases the rate and extent of intragastric fermentation and the gastric emptying rate. Diet composition, meal size, and feeding frequency have been identified to contribute to the cause of gastric ulcers in horses.  In humans, ingestion of a high protein meal is a stimulus for the release of gastrin and subsequent release of gastric acid [44].  In the horse, one study showed that the ingestion of a grain meal resulted in a higher gastrin stimulus than grass hay [45]. Horses fed hay versus withholding feed had similar acid output, but higher gastric pH. It was theorized that the salivary bicarbonate and the buffering effect of the hay were responsible for the higher pH.

The composition and frequency of feeding forage is important in preventing EGUS. In addition to providing constant access to feed to buffer gastric acidity, modifying the diet may help prevent ulcers. Although the gastric juice VFA concentrations were higher in horses fed an alfalfa/grain diet, they had higher gastric juice pH and lower ulcer scores than the same horses fed Brome grass hay [22]. In that study, no gastric hormones were measured, and it was hypothesized that the calcium in the alfalfa hay could have a direct effect on gastric secretions or that the protein was acting as a buffer for the pH. In a rat model, a diet of 2% calcium inhibited basal gastric secretion but not secretions in response to histamine stimulation [46]. Therefore, providing constant access to alfalfa hay will likely help to raise gastric pH [22, 23].

Horses fed straw as the only forage available were 4.4 times more likely to have a gastric ulcer severity score ≥ 2 (out of 5) compared to hay feeding [47].  Also, horses fed straw were 5.7 times more likely to have a gastric ulcer severity score of ≥ 2, compared to haylage feeding.  Also, horses fed > 2 g/kg body weight (BW) of starch per day were likely to have a 2-fold increase in gastric ulcer severity score of  ≥ 2. Although the absolute fiber and grain requirements have not been determined for horses, current recommended levels of long-stem, high quality forage are at 1.0-1.5 kg per 100kg of BW and 0.5 kg per 100 kg BW concentrates [9, 48]. Straw should not be fed as a sole source of forage!

Decrease size and increase frequency of concentrate feeding
Serum gastrin concentrations are high in horses fed high concentrate diets [45].  Gastrin is the only hormone known to stimulate secretion of hydrochloric acid, and rations that contain more readily available nutrients, such as pellets and sweet feed, produce a significant increase in postpranial gastrin concentrations.  In particular, grain feeding was shown to delay gastrin secretion, which corresponded to an increase in gastric acid secretion after the stomach had emptied the grain contents [49].

Also, high concentrate diets are high in hydrolysable or water soluble carbohydrates.  Hydrolysable carbohydrates are readily fermented by resident stomach bacteria, resulting in the production of VFAs, which, in the presence of a low stomach pH (≤ 4), cause damage to the NG squamous mucosa [7-9, 22].

The size of the grain meal may also affect the extent of intragastric fermentation, thereby affecting VFA production [50].  Métayer et al. compared the gastric emptying rates in horses fed a small (300g/100 BW) vs. large (700g/100 BW) high starch concentrate.  Although the calculated rate of gastric emptying (g/min) was higher with the large meal, gastric emptying in terms of percent of the original meal was much slower.  Therefore, when horses are fed large, starch rich meals, intragastric fermentation and VFA fermentation may be favored because of the large amount of fermentable carbohydrates and the longer retention time within the stomach.  In the same study, when comparing the high and low starch meals, gastric emptying was significantly faster for horses consuming a meal lower in starch than one high in starch.  Larger meal size and higher starch content were associated with gastric emptying in terms of percent of total original meal.  A recent study showed that when grain was fed at 0.5 kg/100 kg BW, VFA concentrations were below threshold values for causing damage to nonglandular mucosa [9]. Thus, grain or concentrates should not be fed in excess of 0.5 kg/100 kg BW every 6 hours.

Antibiotics vs. probiotics
Helicobacter pylori and other Helicobacter species have not been shown to cause EGUS, although Helicobacter DNA has been isolated from the glandular and non-glandular stomach mucosa in horses [51,52]. Instead, other resident, acid-tolerant bacteria (E. coli, Lactobacillus, and Streptococcus) are suspected contributors to EGUS, and a large population of these bacteria was isolated from the gastric contents of horses fed various diets in one study [53]. In rats, which have a compound stomach similar to horses, bacteria (E. Coli) rapidly colonized acetic acid-induced stomach ulcers and impaired ulcer healing [54]. In this study, oral antibiotic treatment with streptomycin and/or penicillin suppressed bacterial colonization of the ulcer and markedly accelerated ulcer healing compared to placebo-treated controls. Also, oral administration of lactulose resulted in increases Lactobacillus growth and colonization of the ulcer bed. In a recent study in horses with spontaneously occuring gastric ulcers, an antibiotic (trimethoprim suphadimidine) or a probiotic preparation containing Lactobacillus agilis, L. salivarius, L. equi, Streptococcus equinus, and S. bovis administered orally decreased ulcer number and severity compared to untreated controls [55]. These data suggest that resident stomach bacteria are important in maintenance and progression of non-glandular gastric ulcers in horses. Treatment with antibiotic and/or probiotic preparations may facilitate ulcer healing after 2 weeks of treatment, with the full effect occuring after 4 weeks of treatment. Thus, antibiotic treatment may be indicated in horses with chronic non-responsive gastric ulcers, but more importantly, probiotic preparations containing Lactobacillus and Streptococcus may be helpful in prevention of gastric ulcers or may be used as an adjunct to pharmacologic treatment.

Dietary supplements
A plethora of dietary supplements on the market for horses boast efficacy in treatment and prevention of gastric ulcers. However, many of these products have not been tested in the horse, and to date, very little scientific evidence exists on their efficacy. Below are several supplements that have some scientific testing or have ingredients that have been shown to be helpful in ulcer treatment and prevention.

Seabuckthorn berry extract
There is an increasing interest in the use of herbs and berries that may have therapeutic application in humans and animals.  Berries and pulp from the seabuckthorn plant (Hippophae rhamnoides) are high in vitamins, trace minerals, amino acids, antioxidants and other bioactive substances and have been used successfully to treat mucosal injury, including decubital ulcers, burns and stomach and duodenal ulcers in humans [56, 57]. In addition, seabuckthorn berries have been shown to successfully treat and prevent acetic acid-induced gastric ulcers in rats [58]. A recent study was completed to evaluate the efficacy of seabuckthorn berry pulp and extract (3 ounces fed twice daily; SeaBuck Complete, Seabuck, LLC, Midvale, UT) on the treatment and prevention of gastric ulcers in horses [59]. This preparation of seabuckthorn berries did not significantly decrease non-glandular gastric ulcer scores in eight treated horses, compared to the untreated controls; however, this preparation prevented an increase in gastric ulcer scores following an alternating feed deprivation, ulcer induction model, compared to untreated control horses, which had a significant increase in gastric ulcer scores. Also, gastric ulcer scores in seven of the eight seabuckthorn berry-treated horses either stayed the same or decreased compared to just two of the eight untreated controls.  Although this preparation of seabuckthorn berry did not heal ulcers in these horses, it may be efficacious in the prevention or worsening of non-glandular gastric ulcers in horses during times of stress.

EGUSIN 250 (Pellet) and SLH (Powder)
EGUSIN® (Centaur, Inc., Kansas City, KS, USA) is a dietary supplement which contains two antacids (immediate and long acting), lecithin (phospholipid), and pectin, as well as micro-milled whole oats (groats), which contains Beta-glucan-gels, insoluble oats fibers, polar lipids and natural antioxidants.  These ingredients help protect the stomach from the damaging effects of stomach acid and against generation of oxygen free radicals.  In a study performed at LSU, EGUSIN® fed horses had fewer and less severe ulcers after 5 weeks of feeding when compared to untreated controls.  There was no alteration in blood pH in horses in this study and stomach pH remained low and did not change significantly over the treatment periods.

Calcium carbonate supplements (Neigh-Lox)
Many supplements on the market contain calcium carbonate, a primary component of human antacid preparations (Tums; Rolaids). These products contain varying concentrations of calcium carbonate and various other herbs and coating agents.  The author (FMA) performed a small study with an antacid preparation containing calcium carbonate (Neigh-Lox, Kentucky Performance Products, Versailles, KY) to determine efficacy in treatment and prevention of gastric ulcers in horses (Frank M. Andrews, DVM, MS, Knoxville, TN, unpublished data, 2001).  In that study, four healthy horses were fed hay and a small amount of grain top-dressed with 4 ounces of this calcium carbonate supplement twice daily for 3 weeks. There was no significant difference in gastric ulcer scores between control horses and treated horses; however, gastric juice pH remained ≥ 4 for 2 hours after feeding, when compared to control horses.  Also, in an in vitro study, this supplement, when added to acid damaged stomach tissue, resulted in recovery of sodium transport. Thus, these data suggest that calcium carbonate preparations may have some efficacy in maintaining mucosal integrity, but may need to be fed more frequently than twice daily to prevent EGUS.

Oils (corn oil, rice bran oil)
Dietary fats delay gastric emptying time in humans and other species [60]. In contrast to most species, gastric emptying rates are slower in horses fed a high carbohydrate diet, compared to horses fed a high fat diet, although these rates were not statistically significant [61]. However, gastric relaxation was significantly greater in horses fed the high carbohydrate diet compared to horses fed the high fat diet. Supplementation of dietary fat may not have a profound effect on gastric emptying in horses. However, in another study [62], ponies fed dietary corn oil (45 mL, orally, once daily) by dose syringe with gastric cannulas had a significantly lower gastric acid output and increased prostaglandin concentration in gastric juice. The authors conclude that corn oil supplementation could be an economical approach to the therapeutic and prophylactic management of glandular ulcers in horses, especially those associated with the use of non-steroidal antiinflammatory drugs. In contrast to the previous study, results from an evaluation of the anti-ulcerogenic properties of corn oil, refined rice bran oil and crude rice bran oil showed no statistical differences in non-glandular ulcer scores between the treatment groups [63].  However, glandular ulcers were rare in these horses. Horses were fed the oil (8 ounces, once daily, mixed in grain) for 6 weeks. In this model, dietary oils did not prevent non-glandular gastric ulcers in these horses, suggesting that dietary oils may not be useful in treatment or prevention of non-glandular ulcers, but may be helpful in treatment or prevention of glandular ulcers.

Concentrated electrolyte pastes or solutions
Repeated oral administration of hypertonic replacement electrolyte solutions, commonly given to endurance horses, has been shown to increase the number and severity of gastric ulcers [43].  Thus, these products should be used with caution in horses and may be best given after exercise with feed to minimize their effects on the gastric mucosa.

1. If gastric ulcers are diagnosed by your veterinarian, then initiate effective pharmacologic treatment (GastroGard or Ranitidine) to heal the ulcers.
2. Provide a minimum of 1 to 1.5 kg/100 kg BW of long stem, high quality forage free-choice throughout the day and night.
3. Feed alfalfa hay or a mixture of alfalfa hay to help buffer stomach acid.
4. Feed grain and concentrates sparingly.  Give no more than 0.5 kg/100 kg BW of grain or grain mixes (such as sweet feed), and do not feed grain meals less than 6 hours apart.  Weigh all grains before giving.
5. Try corn oil or other tested dietary supplements (Seabuckthorn berry, EGUSIN 250 or SLH, or Zinpro performance minerals) to prevent recurrence of ulcers
6. Fee hypertonic electrolyte pastes or supplements after exercise mixed with a small amount of grain (see 4 above).
7. Consider therapeutic or preventative doses of effective pharmacologic agents (GastroGard or Ranitidine) in horses that are performing high intensity exercise, traveling, or in a high-stress situation.

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