There is one thing about the topic of equine gastric ulcers that I am clear on -- the more I learn about it, the more I realize we don't know. For horses with severe ulcers, most studies have shown that omeprazole works extremely well, and should be used as a treatment. However, there are downsides. Daily treatment with omeprazole is not only costly, but there are other questions that arise with its use, such as whether or not a horse receiving omeprazole daily is in violation of the AERC drug policy if its use is discontinued within 24 hours of a ride.

Omeprazole works by stopping stomach acid -- an important function of the stomach -- which aids in destroying bacteria that could cause intestinal tract infections such as salmonella. The altered pH of the stomach may not kill viruses and fungi. Stomach acid is also necessary to digest protein. The undigested protein moves through the cecum and large bowel, where fermentation can cause bloating, discomfort and foul-smelling manure.

Prolonged acid suppression in humans causes vitamin B12 malabsorption. Further human studies have shown an increase in acid production following treatment. Omeprazole has been shown to significantly delay gastric emptying in humans, and there are several other potentially serious side effects.

If we use the drug to cure a horse's ulcers, but don't change any of the management issues that are causing the ulcers, we could face the possibility of having to maintain the equine on omeprazole daily for the competitive life of the horse or possibly having to retire the horse from competition. Because preventing ulcers is preferable to treating ulcers, careful horse management is essential.

Functional considerations

Adult horses secrete up to seven or eight gallons of gastric acid per day -- more than six cups an hour. This is continuous and independent of feed intake. One major cause of gastric ulcers in horses is prolonged exposure of the stomach to high acid levels. The equine stomach is designed for constant feed intake, which provides something for the acid to "work on," therefore using up the acid.

Just 10% of the horse's digestive system capacity is made up of the stomach. The upper compartment of the stomach, which isn't resistant to acids, accounts for about 80% of equine gastric ulcers. The lower compartment only incurs 20% of equine gastric ulcers because it has more intrinsic protective properties.

Emptying of the stomach takes 30 minutes for a liquid meal, while complete emptying after a meal of hay can take up to 24 hours. When a horse grazes all day, the roughage he consumes absorbs a considerable amount of digestive acid, keeping the level within the stomach low. In addition, a horse's saliva has an acid-neutralizing effect. As a result, the amount of acid that accumulates in a horse's stomach declines when he's eating and increases when he's not.

Colonic ulcers

In a study conducted by Frank Pellegrini, DVM, 63% of horses involved in competition sports -- ranging from dressage to racing -- suffered from colonic ulceration.

Pellegrini's work confirmed the findings of earlier studies, showing that 87% of horses have gastric ulcers (ulcers of the stomach). When combined with his findings on the lesser-understood issue of colonic ulcers, however, Pellegrini's study yielded some new information. He found that 54% of performance horses suffered from both gastric and colonic ulcers. Further, Pellegrini's study showed that 97% of performance horses had some type of ulceration.

"This research suggests that ulceration in the colon may be to blame for the low-grade anemia, colic and other conditions seen frequently in high performance horses," said Pellegrini. "Most importantly, it brings into focus the need for further research on the direct causes of colonic ulcers and how exactly they affect the horse."

Unfortunately, no treatment now available can cure them. Omeprazole, used for gastric ulcers, was formulated for the specific conditions found inside the stomach and will not positively affect the delicate colonic environment. "A dietary supplement intended to maintain optimum digestive tract health may be the best solution to preventing colonic ulcers before they negatively affect performance and attitude in the horse," said Pellegrini.

Causes of ulcers

Possible ulcer symptoms

Keeping a healthy gut

One approach to promoting overall digestive tract health involves the use of non-testable, natural foodstuffs to heal the intestinal tract and support good health throughout this critical system. Here are some substances and how they may work to help keep the horse's gut healthy:

-- Beta glucan is a dietary fiber found in oats and barley that has been shown to slow down the movement of feed through the gut, allowing excess starches to be digested before they enter the colon. Beta glucan is also a powerful immune stimulant, encouraging the horse's immune system to attack any bacteria that might otherwise enter an ulcer.

-- Polar lipids, found in specially processed oat oil, help to protect the lining of the gut. Polar lipids are emulsifiers -- they help water and oil to mix -- and help certain oil-soluble vitamins, such as A, D, E and K, to be absorbed by the gut.

-- Glutamine is a natural amino acid that may help the gut renew and heal itself. It is "conditionally essential," ­meaning that the body cannot produce enough of this amino acid when it is undergoing stressful situations, such as heavy competition training. Glutamine assists the cells of the gut to grow close together, keeping out dangerous microorganisms.

-- Threonine is an essential amino acid, meaning that the body doesn't produce enough on its own, so it must be supplied in the feed. Threonine is needed for the creation of mucus which lines the stomach and intestines, protecting them from acidic digestive juices.

-- Yeast sugars called mannan oligosaccharides (MOS for short) help the immune system to get rid of bad bacteria and absorb toxins so they can be safely excreted.

Prevention and recommendations

-- Respect the function of the gut!

-- Turn horses out as much as possible so they can graze.

-- Don't feed a lot of grain.

-- If grain must be fed in large amounts, divide feedings so that no more than three pounds is given at any one time.

-- Avoid prolonged periods of fasting. Ulcers can develop within 10 to 12 hours when horses have no access to feed.

-- Keep roughage available at all times. Horses need to eat continuously.

-- Provide free-choice grass hay at all times.

-- Feed frequent small meals -- optimum is four times a day.

-- Place feed bins on the ground. Horses chew and swallow more efficiently when their heads are down and the throat is extended.

-- Use steam-extruded feeds which have been processed in such a way that eating is slower, resulting in more chewing, increased saliva production and higher saliva bicarbonate levels.

-- Match your horse with a job he enjoys to which he is well-suited.

-- Gradually increase training schedule.

-- Ride conservatively until you know your horse handles competition.

-- Provide daily probiotics if your horse is in training or confined due to injury or illness, as recommended by your vet.

-- Provide as much exercise and entertainment as possible.

-- Avoid frequent or long-term use of non-steroidal anti-inflammatory agents.

-- Tapeworm infestation can mimic symptoms of ulcers. Be sure to use a dewormer that gets rid of tapeworms.

-- Add 1/4 cup of corn oil to your horse's diet daily.

-- A high-energy feed, bananas also contain high levels of phos­pho­lipids that can assist in lining the horse's stomach and preventing acid damage to the stomach.

-- Papayas are another natural way to help horses with ulcers. Papain stimulates the appetite, soothes membranes of the esophagus and stomach and quiets inflammatory bowel disorders. Raw papain is used medically for enzyme replacement in pancreatic insufficiency and has anti-microbial, anthelmintic and anti-ulceratial effects.

-- Horse owners have reported anecdotally that a cup of aloe vera juice twice a day helped decrease their horse's ulcer symptoms.

-- Horses should be fed no less than 50% (and preferably >70%) of their dry matter intake as long dry hay or pasture.

-- Feed a small amount of alfalfa (two to three pounds once or twice daily). Alfalfa's calcium may buffer stomach acid.

-- Keep your horse at a good body weight and body condition score.

Ulcer research

Almost all research has been on non-endurance horses. When race horses were studied, well over 90% had ulcers. The incidence of ulcers in endurance horses is nearer 50%, probably because of the closer relationship between horse and caregiver, along with management practices that are shown to be less likely to cause ulcers. Following are summaries of two recent research projects focusing on endurance horses. (For further information on Dr. Barney Fleming's study, see Vet Forum, October 2005.)

Prevalence of gastric ulcers in endurance horses, a preliminary report (J.E. Nieto et. al., 2004). Gastric endoscopy was performed at the end of a 50 or 80 km endurance ride. Gastric ulceration was evident in 67% of the horses, with ulcers on the squamous region of the stomach found in 57% of the horses and active bleeding of the glandular mucosa in 27%. Three horses (10%) had lesions only on the glandular mucosa. Values of albumin, creatinine and glucose were higher in horses without gastric lesions. The degree of ulceration in endurance horses is less severe than has been reported in Thoroughbred race horses in active training. Incidence of gastric ulcers in active endurance horses (Barney Fleming, DVM, 2005). A study that looked at 92 horses in eight states. All equines were actively involved in endurance riding and were between rides, in order to eliminate the horses that simply showed signs of gastritis from the event itself. Forty-seven (51%) had some degree of ulcers (grade 1, 2 or 3). Thirty-one (33.7%) showed grade 2 and 3 ulcers which are considered clinical lesions. Eleven (11.96%) of the horses had grade 3 bleeding ulcers.

Conclusions

Some horses may need to receive medication and veterinary care in order to heal and prevent ulcers. Many horse owners cannot afford medication costing $500 to $1000 or more each month in order to keep their horse competing. Prevention need not be expensive, and may often be easily accomplished with careful horse management. Remember that every horse is an individual and what works for one may not work for another.

One other consideration is for the horse's general well-being. David Scott, Ph.D, an EGUS researcher at the University of California, Los Angeles, says, "I suggest that unless the animal is showing signs of distress and appears happy and healthy despite having a positive endoscopy for gastric ulcer, do nothing. If the animal is suffering by all means use Gastrogard and withhold the drug prior to competition. The drug should clear the blood in a few days."

For owners questioning their own horse's ulcer risk, Dr. Scott recommends, "If your animals seem happy and healthy, don't have them scoped since what you don't know won't bother you or the horse."

Additional research

All but the last two listed projects as well as Pellegrini's work above were done on other than endurance horses. When race horses were studied well over 90% had ulcers. The incidence of ulcers in Endurance horses is as low as 50%, probably because of the closer relationship between horse and care giver along with management practices that are shown to be less likely to cause ulcers.

Benefits of Corn Oil Supplementation. Ponies fed a free-choice hay diet for 5 weeks, which was followed by 5 weeks of the same diet supplemented with 45 mL of corn oil daily. The study concluded that corn oil supplementation may be an effective and inexpensive way to increase the protective properties of equine glandular gastric mucosa. (Cargile JL et al. 2004)

Effects of exercise on gastric volume and pH in the proximal portion of the stomach of horses. Increased intra-abdominal pressure during intense exercise in horses causes gastric compression, pushing acidic contents into the proximal, squamous-lined region of the stomach. Increased duration of acid exposure directly related to daily duration of exercise may be the reason that squamous lesions tend to develop or worsen when horses are in intensive training programs. (Lorenzo-Figueras M et al. 2003)

Prevalence of gastric ulcers in show horses. Gastric ulceration was detected in 58% of the horses. Horses with a nervous disposition were more likely to have ulceration than quiet or behaviorally normal horses. Horses with gastric ulceration had significantly lower RBC counts and hemoglobin concentrations than those without ulceration. (McClure SR et al. 1999)

Do age or sex matter? One study on 224 Standardbred racehorses in training concluded that although there was little association between age and prevalence of ulcers, there was an association between age and severity of ulcers. Most 2-year-old horses (57.7%) had an ulcer score of 0 or 1. In all other age groups, most (58% to 82.61%) of horses had an ulcer score of 2 or 3. Although overall prevalence of ulceration was comparable among sex groups, the relative risk for gastric ulceration increased with age in castrated males, whereas it decreased in females and sexually intact males. (Rabuffo TS et al.. 2002)

Gastric ulcers in Standardbred racehorses: prevalence, lesion description, and risk factors. The number of lesion sites (P < .0001) and poor body condition (P < .0001) were significantly associated with lesion scores. Gastric ulcers are highly prevalent in Standardbred racehorses. Furthermore, actively racing horses and trotters are more likely to have gastric ulcers. Also, poor body condition in Standardbred racehorses may be an indication that gastric ulcers are present and that lesion scores are high. The cause-and-effect relationship between poor body condition and the presence of gastric ulcers is unclear. (Dionne RM et al. 2003)

Evaluation of urine sucrose concentration for detection of gastric ulcers in horses. Urine sucrose concentration appears to be a reliable but imperfect indicator of gastric squamous ulcers in horses. Sucrose permeability testing may provide a simple, noninvasive test to detect and monitor gastric ulcers in horses. (O'Conner et al. 2004)

Effects of intramuscular omeprazole on gastric acid secretion in horses over a twenty-four hour period. Due to the simplicity of the administration technique and the higher biological availability, intramuscular administration may offer a practical and less expensive way of treating gastric ulcers in horses. (Sandin A et al. 1999)

Effects of intermittent feed deprivation, intermittent feed deprivation with ranitidine administration, and stall confinement with ad libitum access to hay on gastric ulceration in horses. Severe ulceration of the gastric squamous epithelial mucosa, caused by excess acidity, can develop rapidly in horses deprived of feed or not consuming feed. Suppression of gastric acidity with the histamine type-2 receptor antagonist ranitidine effectively minimized the area of ulceration caused by feed deprivation. Compared with being turned out to pasture, stall confinement alone appears to be an important factor in the development of gastric ulcers in horses, probably as a result of altered eating behavior. (Murray MJ et al 1996)

Gastric ulcers in horses: a comparison of endoscopic findings in horses with and without clinical signs. Gastroendoscopic examinations were performed on 187 horses, ranging from one to 24 years. Eighty-seven horses had clinical problems including chronic, recurrent colic for seven or more days (25), one or more episodes of colic within the previous seven days (13), or acute colic (10), diminished appetite (53), poor bodily condition (40), and/or chronic diarrhea (9). One hundred horses that had no signs of gastrointestinal problems were examined as part of a gastroendoscopic survey. Lesions observed in the squamous fundus, squamous mucosa adjacent to the margo plicatus along the greater curvature, glandular fundus, and the squamous mucosa along the lesser curvature were scored on a scale of 0-4, with 0 representing no lesions and 4 representing the most severe lesions. The mean endoscopic scores for the squamous fundus, margo plicatus and lesser curvature were significantly greater (P < 0.001) in horses with clinical signs than those without signs. This was because of the greater number of horses with lesions in the symptomatic group (80/87) compared to those without signs (52/100), and the greater severity of lesions in the horses with clinical signs. Of the horses, 74 were in race training. There was a significantly (P < 0.01) greater prevalence and severity of lesions at all sites except the glandular fundus in horses in training compared to those not in training, and in the horses in training with clinical signs (n = 37) compared to those in training without clinical signs (n = 37). (Murray MJ et al. 1989)

Comparison of endoscopic, necropsy and histology scoring of equine gastric ulcers. Only 1/23 horses had glandular ulcers observed via endoscopic examination whereas, 6/23 horses had glandular ulcers at necropsy and on histopathology. The prevalence of EGUS is high in stalled yearling horses. The endoscopist may underestimate the number of gastric ulcers and may not be able accurately to predict the severity or depth of those ulcers present in the nonglandular equine stomach. Furthermore, the endoscopist may miss glandular gastric ulcers. (Andrews FM et al 2002)

Evaluation of diet as a cause of gastric ulcers in horses. An alfalfa hay-grain diet induced significantly higher pH and VFA concentrations in gastric juice than did bromegrass hay. However, number and severity of nonglandular squamous gastric lesions were significantly lower in horses fed alfalfa hay-grain. An alfalfa hay-grain diet may buffer stomach acid in horses. (Nadeau JA et al. 2000)

Histological characteristics of induced acute peptic injury in equine gastric squamous epithelium. Erosions and ulcers were induced in equine gastric squamous epithelium using a feed deprivation protocol that results in prolonged increased gastric acidity. Specimens of normal gastric mucosa and mucosa with lesions created after 48 and 96 h of feed deprivation were compared for characteristics associated with angiogenesis and mucosal proliferation. These findings demonstrate that processes that promote ulcer healing begin soon after peptic injury and that they progress even with repeated peptic injury. Furthermore, our findings support observations that gastric ulcers often heal without medical intervention, and the theory that medications that reduce gastric acidity do not initiate healing, but rather facilitate ulcer healing by providing a microenvironment that is optimal for healing to proceed. (Murray MJ et al. 2001)

References