The Problem of Equine Gastric Ulcer Syndrome (EGUS) is a really common one. It isn’t just something that affects racehorses who are stabled for most of the time and fed high energy, low fibre diets – although this sort of regime does predispose horses to the problem – and riders and trainers in all disciplines are finding that EGUS is a cause of poor performance and behavioural problems. We don’t know whether the incidence has become more common, or whether our greater understanding and sophisticated diagnostic methods mean it is easier to spot, but whatever the case, we have a better chance of finding strategies to overcome it.
When your horse’s stomach wall has any degree of EGUS (open wound in a hostile, acid environment), you may notice changes for the worse in behaviour, a diminishing appetite with poorer performance, possible weight loss, abdominal tenderness to the touch (which can result in riding, girthing and grooming problems) and possibly excessive salivation, recurrent colic and a lacklustre coat. I write may notice because reportedly 50 per cent of horses with ulcers show no outward signs, so these equine friends suffer in silence… It is mostly a manmade problem caused by the way we feed, train and transport horses, but big improvements in EGUS can be made by increasing a horse’s ability to live more as nature intended.
Is acid to blame?
The diagram shows two opposing forces (red arrows damage vs. green arrows repair). Whilst some research into the bacterium Helicobacter equorum has been done, current veterinary focus is to reduce the amount of acid that is being produced by using drugs such as Tagament, Zantac, or Omaprazole. This creates a temporary less painful, less hostile environment for an ulcer. In the resulting temporarily less acid /more alkaline environment, tissue seeks to repair itself and, if appetite improves, roughage eaten can once again ‘mop up’ acidity adequately. Hopefully, this breaks the vicious cycle. However, the great misnomer in EGUS is ‘increased acidity’ because your horse doesn’t produce more acid than it should!
One of life’s miracles is how the stomach is designed to contain acid. There is a neutral pH (7.0) near the lower oesophageal sphincter (right/top where feed and saliva enter), a near neutral to mildly acidic pH (6.0 – 3.0) near the margo plicatus (dark green border in the middle) and a mildly to extremely acidic pH (4.0 – 1.5) in the glandular region near the pylorus where acid is produced. This last region is the most hostile and most difficult to repair location for an ulcer.
Overall, the design of the stomach copes perfectly with acid until there is impaired mucosal barrier protection – e.g. inadequate mucosal blood supply and/or impaired mucous production. Just how robust the design is, is demonstrated by horses needing to lie down to reach REM sleep. When they do, acidified stomach content covers the ‘vulnerable’ non-glandular wall whilst glandular parietal cells continue to produce hydrochloric acid at a low rate. But, as you know, horses can lie down for up to two hours, so if acid was the villain, how would they be able to? Rather than focus on mainly acid, shouldn’t we accept that a far more likely prelude to EGUS is that your horse is unable to repair and renew its protective squamous epithelium or its glandular epithelium?
Still dubious? Look at a widely known cause of ulcers. Non-Steroid Anti-Inflammatory Drugs (NSAIDs) in longer term use cause damage to the gastroduodenal mucosa via several mechanisms: 1) the topical irritant effect of these drugs on the epithelium, 2) suppression of gastric prostaglandin synthesis, 3) impairment of the barrier properties of the mucosa, 4) reduction of gastric mucosal blood flow and 5) interference with the repair of superficial injury. NSAIDs do not require any change to acidity levels to effect damage, they create a locus minoris resistentiae i.e. a weak spot in the stomach lining that’s no longer able to rise to its normal function of standing up to acidity. Acidity isn’t the chicken, it’s the egg.
Every horse owner and vet knows that raising the pH doesn’t always work, not because the pH didn’t get raised effectively, but because epithelial wound repair wasn’t finished by the time pH was allowed to come down to normal again. The vicious cycle wasn’t broken. Without follow-up gastroscopy, it is difficult to judge whether repair was complete because after all, 50 per cent of horses with ulcers show no outward signs… So why not speed up that healing process, facilitate it and make it happen more robustly with a sustainable abundance of appropriate nutrients? Why not use nutrients to improve the odds of prevention.
What is the flip side of raising the stomach pH?
Although there is no consensus on its involvement, is interesting to note that Helicobacter is known to remain motile for longer in a raised pH, so it can burrow into a stomach wall for longer. Other than that, there is no real issue with short term pH manipulation. However, the same cannot be said for long term pH raising, simply because raising the pH reduces the necessary protection that acid offers your horse against bacteria, potentially harmful microbes that can reside in feed. Raising the pH also hinders its protein-cleaving enzyme pepsin (it hydrolyses peptide bonds), meaning that further along the digestive tract work must be done that should have been done ‘upstream’. Even at half-dosage you change pH (otherwise why do it) and in doing so, less protein happens less via gastric pepsin so more has to be done by pancreatic enzymes and the exopeptidases in the brush border of the small intestine. Take into consideration that research has shown that a horse can develop a gastric lesion in as little as five days. This might suggest that minimising trigger factors (such as carbohydrate load, stress, competition, training, transporting, limiting turnout, box rest, changing routine, anti-inflammatory drugs) remains the best way to manage EGUS whilst also sensibly speeding up epithelial wound healing and restoring the mucosal barrier.
For fullness of information, prostaglandins (PGE2) trigger the production of the protective mucosal barrier by the surface epithelium cells. PGE2s are short term, very locally acting messenger molecules that are made from polyunsaturated omega-6 fatty acid (arachidonic acid) via a cascade of multiple enzymes. A key one of these is mPGES-1 which requires glutathione as an essential cofactor for activity. So… your horse can be short on PGE2 based on deficiency if there is an inability to convert linoleic acid to arachidonic acid (cannot happen if required enzyme delta-6-desaturase lacks magnesium as cofactor, a diet high in refined carbohydrates slows delta-6-desaturase which then decreases production of healthy prostaglandins), or there’s not enough linoleic acid to start with, or because of feeding Aspirin-like drugs which are known to inhibit the function of prostagladins, or because your horse is low on glutathione. Do you see how the availability of nutritional resources have a direct bearing on how well a stomach wall can protect itself? I always refer to nutrient intake, nutrient uptake and nutrient expenditure, well, in respect of glutathione, this is used (nutrient expenditure) to limit the damage a free radical load inflicts. Again it’s a cascade of multiple nutrients cooperating: vitamin C grabs a free radical + passes it onto vitamin E + which passes it on to glutathione so your horse ends up with a less harmful free radical. If your horse’ free radical load is high, its glutathione level will get low… thereby also the mPGES-1 level, and the prostaglandin level that ↓ gastric acid secretion and ↑ gastric mucous secretion.
For fullness of information, a common finding during scoping is Gasterophilus intestinalis (2nd/3rd instar larvae) hibernating in the non-glandular (least acidic) portion of the stomach. These bots burrow into the stomach wall but plug the hole by their own body, so infection can go unnoticed as no symptoms may present. After a deworming programme has killed the larvae, successful repair of the burrow hole depends on the quality/speed of reepitheliazation (green arrow in diagram at the top of this page).
Even in EGUS, carbohydrates crop up. The usual problem is that the total carbohydrate load outpaces how many amylase enzymes are available to cleave them. Carbohydrates affect EGUS in two ways, firstly carbs can ferment already in the stomach and produce Volatile Fatty Acids (VFAs). These penetrate the squamous mucosal tissue of the stomach easily when acid concentrations are high (i.e. pH is low). This causes cell damage, inflammation and ulceration. Since performance horses are fed diets that are high in fermentable carbohydrates, VFAs generated by resident bacteria may contribute to EGUS. Secondly, because carbs fuel blood glucose level, the latter affects systolic and diastolic whole blood viscosity (the shear rate of not just of blood plasma) so that instead of the watery substance blood is supposed to be, blood becomes thicker. Sure enough hydration also affects whole blood viscosity but most stabled horses can drink ad libitum whilst those turned out enjoy grass that contains 80-90 percent water. Remember the reduction of gastric mucosal blood flow NSAID causes? Connect the dots, one factor is how easily nutrients can reach the working cells, notably the surface epithelium. Simply put, if a horse has a higher but not necessarily abnormal blood glucose level, blood viscosity changes, and nooks and crannies of the circulatory bed (such as the epithelial surface circulation) invariably get a poorer nutrient supply as a result. Carbohydrate tolerance thus takes on new importance. Consulting a well-informed, registered (but independent!) equine nutritionist is a very clever action to take.
If constant turnout isn’t an option, then let your horse spend as much time as possible out in the paddock. During stabling and travel provide ad lib forage – gastric acid trickle awaits this ‘mop’ – and if your horse requires a concentrate feed to provide extra energy for work, then choose a feed that’s high in fibre but low in starch and trickle feed in small regular meals. Adding chaff to feed promotes longer chewing time (i.e. more alkaline saliva mixed in) and provides extra fibre. In addition consider supplementing with a pure aloe vera, a herb well known to help digestion. Do however make sure that the aloe vera product you use is made properly, is palatable -exemplary powder in sachets for instance- and is dosed specifically for horses. It would be wise to read frequently asked questions. Helping your horse’ natural ability to repair (the diagram shows the proper term: reepithelialization) is always wise, even if you would go the pH manipulation route. The two approaches do not work against each other. My personal preference has always been to conquer health challenges via natural means, not always achievable for sure, but in the problem of equine gastric ulcer syndrome (EGUS) there is lots of scope for success.
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