HORSES grasp their food using a combination of the lips, tongue, and teeth. After chewing and mixing with saliva, it is swallowed into the esophagus where it travels to the stomach. The esophagus connects to the stomach at an oblique angle, preventing the ability to vomit. In an adult horse, the esophagus is around 4–5 feet in length with little reflux capability, and so proper maintenance of healthy teeth is critical to ensure that food is chewed correctly.
The stomach is a relatively small part of the entire digestive system (10%) and an average sized horse (1000 lbs) has a stomach with a capacity of 4–5 gallons. The primary function of the stomach is to add gastric acid and secrete enzymes to facilitate the breakdown of food, while regulating its passage into the small intestine.
The stomach constantly secretes acid as it is designed to work with a small and continuous flow of high fiber from the constant grazing on grass. A critical role of the acid produced by the stomach is to kill potentially harmful microorganisms in the feed, reducing the potential for infection. On an empty stomach however, the acid can penetrate the protective mucus layer and attack the cells beneath, causing ulcers to form.
Food may only remain in the stomach for around 15 minutes before being passed through to the small intestine. The stomach functions at its best when containing around 2 gallons because it empties when two thirds full — whether the enzymes have completed processing the food or not — and this may prevent complete digestion. A continuous supply of forage or several small feedings is therefore preferable to one or two large meals each day.
The stomach is covered by two lining tissues: squamous and glandular. The squamous area covers the upper third section of the stomach and the glandular area covers the bottom two thirds. The upper section of the stomach is more susceptible to ulceration as it lacks the acidic protections found in the glandular area. The majority of glandular lesions are found within the pyloric antrum (where food leaves the stomach and enters the small intestine.)
Once food leaves through the pylorus, it passes into the first portion of the small intestine (duodenum). Although less frequently found, ulcers can also occur in the duodenum and in the esophagus. The majority of duodenal ulcers occur in foals. The small intestine has a capacity of around 10–12 gallons and is the primary digestive organ, with the majority of digestion taking place in the duodenum. Most of the nutrients are absorbed through the walls of the small intestine and into the bloodstream, where it is distributed throughout the body. Feed typically requires 30–90 minutes to pass through the small intestine and into the large intestine.
The large intestine, or hindgut, comprises around two thirds of the digestive system and consists of the cecum, large and small colons, rectum, and anus. Ulcers also frequently occur in the hindgut and have been shown to affect more than half of performance horses. Hindgut ulcers frequently occur alongside gastric ulcers. In contrast with the foregut where digestion is primarily the result of enzymatic action, digestion in the hindgut is largely microbial, performed by billions of bacteria.
The first section of the large intestine is the cecum, which holds around 7–8 gallons wherein bacteria will spend around 7 hours breaking down the feed through fermentation. The cecum is a cul-de-sac pouch with both its entrance and exit at the top of the organ. The bacteria in the cecum are slow to adapt to the different chemical structure of new feedstuffs, taking about three weeks to develop a microbial population that can digest a new feed and maintain a normal flow. Because of this, compaction and colic may occur if a large amount of dry feed is consumed without sufficient liquid or if there is a sudden change in diet.
Microbial digestion continues to take place once feed passes from the cecum to the large colon (holding up to 20 gallons) where it may stay for 2–3 days before passing to the small colon. The small colon holds around 5 gallons and primarily acts to reclaim any excess moisture and return it to the body. This process produces fecal balls of undigested feed that are finally passed through the rectum (around 1 foot long) and expelled through the anus.
Equine Gastrointestinal Tract
Studies have consistently shown that equine gastrointestinal ulcers are extremely common. However, while many studies have looked for breed, age, or gender specific associations, overall they suggest that environmental factors such as duration and intensity of exercise outweigh any such effects. Equine gastric and hindgut ulcers are a common cause of colic and decreased performance, resulting in a range of behavioral and physical changes. Jeremiah’s Ulcer Repulser™ treats, soothes, and protects the entire gastrointestinal tract.
Studies show equine gastric ulcers affect:
37% of untrained racehorses, rising to 93% after 2–3 months of training (Hammond et al., 1986; Murray et al., 1989, 1996; Vatistas et al., 1999; Begg & O'Sullivan, 2003).
37% of pleasure horses (Murray et al., 1996).
58% of show horses (McClure et al., 1999).
50% of foals (Murray, 1999).
40% of Western performance Quarter horses (Bertone, 2000).
44% of Standardbred racehorses, rising to 87% in training (Rabuffo et al., 2002).
56.5% of horses in endurance competition, show jumping, dressage, or western performance (Hartmann & Frankey, 2003).
67% of horses competing in endurance rides (Neito et al., 2004).
66.6% of pregnant and 75.9% of nonpregnant broodmares (le Jeuine et al., 2009).
11% of rarely competed horses, predominantly used in a home environment (Chameroy et al., 2006).
48% of endurance horses during interseason, rising to 93% during the competition season (Tamzali et al., 2011).
72% of Thoroughbred racehorses with squamous ulcers and 25% with glandular ulcers (Sykes et al., 2018).
Some possible warning signs of equine gastric ulcers are:
- A change in attitude — Is your horse more nervous than usual or less willing to perform? Does he seem grouchy or “out of it” for no apparent reason? Behavioral changes: nervousness, aggression, and self-mutilation, may be a clinical sign of equine gastric ulcers (McClure et al., 1999; Andrews et al., 1999; Nicol et al., 2002; McDonnell, 2008).
- Does your horse appear to be preoccupied or unable to concentrate?
- Is your horse less sociable than previously, or more needy?
- Has your horse developed new or worsened barn manners?
- Bruxism — Does your horse frequently grind his teeth, crib, or lash out in any way? (Bell et al., 2007)
A horse cribbing on a tree stump.
- Picky eating — Is he eating as much as he normally does for the amount of work he’s accomplishing? Is he leaving any of his feed uneaten? Conversely, is your horse suddenly ravenous, seeming to demand more food? Poor appetite or ‘picky eating’ is commonly associated with equine ulcers (Murray et al., 1989; Andrews et al., 1999; Vatistas et al., 1993; Bezdeková et al., 2008).
- Dullness — Is your horse generally lackluster and seemingly without energy?
- Decreased performance — Is your horse not as “fluid” as normal? Could his usually fine movement, speed or scope, be described as below average?
- Weight loss — Has your horse dropped weight or has girth size changed? (Murray et al., 1989; Andrews et al., 1999; Dionne et al., 2003)
- Colic — Is your horse showing signs of low-grade colic, a persistent mild discomfort that may cause him to turn his head toward his flank, lie down excessively, paw, or fail to finish a meal? 83% of horses with recurrent colic (Murray, 1990) and 49% with acute colic have gastric ulcers (Dukti et al., 2006).
- A decline in body condition — Is your horse’s coat not quite as sleek and shiny as it once was? (Vatistas et al., 1999)
- Does your horse have loose stools or constipation? Chronic diarrhea has long been associated with equine gastric ulcers (Murray et al., 1989; Andrews et al., 1999).
- Does your horse have mild or severe anemia?
- Does your horse stretch more often than usual to urinate?
- Has your horse begun to lose hair, particularly facial hair?
- Has your horse shortened its stride, particularly on the right rear? This is often one sign of a hindgut ulcer.
- Is your foal doing poorly? 50% of foals develop gastric ulcers within the first few months of life (Murray, 1999).
However, many horses with gastric ulcers will not demonstrate any clinical signs (Andrews et al., 1999; Bell et al., 2007; Lutherson et al., 2009).
Potential causes, and risk factors:
Intense exercise is perhaps the most common risk factor: horses can develop significant stomach ulceration within as little as 8 days of heavy training (Murray et al., 1996; Orsini, 2000; Lester, 2004; Chameroy et al., 2006; Jonsson & Egenvall, 2006).
Show horses with a nervous disposition are more likely to have gastric ulcers than quiet or normally behaved horses (McClure et al., 1999).
Stressful events such as transportation (McClure et al., 2005) and stall confinement increases the risk of developing ulcers (Murray & Eichorn, 1996).
Playing the radio in the barn continuously for several hours increases the risk of ulceration, with talk radio increasing the risk by 3.6 times and music by 2.8 times (Lester et al., 2008).
Horses trained in urban areas are 3.9 times more likely to have gastric ulcers. A lack of direct contact with other horses and solid barriers instead of rails are also risk factors (Lester et al., 2008).
Horses without access to water in their paddock are more than 2.5 times more likely to develop gastric ulcers (Luthersson et al., 2009).
The use of NSAIDs (e.g., bute) have the potential to cause gastric ulcers, however this is usually related to the use of high dosages or frequent administration (Monreal et al., 2004; Reed et al., 2006).
Use of electrolyte supplements increases the risk of developing gastric ulcers (Holbrook et al., 2005).
High-grain, low-hay diets have been shown to increase the incidence of ulcers (Hammond et al., 1986), whereas free access to good quality pasture and a diet containing alfalfa hay can reduce the likelihood (Nadeau et al., 2000; Lybbert et al., 2007).
Large, high starch meals should be avoided in horses prone to gastric ulceration (Taharaguchi et al., 2004; Boswinkel et al., 2007). High starch diets empty from the stomach more slowly and are fermented, resulting in increased acid levels. High starch diets also tend to reflect a high cereal intake and more fluid gastric contents that may promote acid splashing (Argenzio, 1999; Lorenzo-Figueras & Merritt, 2002).
Feeding beet pulp as an additional source of fiber has been shown to decrease the risk of gastric ulcers (Pedersen et al., 2018).
Whereas feed deprivation, i.e., more than 6 hours without food increases the risk of ulcers (Murray & Grady, 2002).
Horses with bowel, liver, and esophageal lesions have a higher prevalence of gastric ulcers (Sandin et al., 2000).
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