In the pursuit of additional energy and condition many horses are subject to the intermittent feeding of concentrates, containing high levels of non-structural carbohydrate. Restrictions on forage intake, either through stabling, competing or just loss of appetite during hard training, can also be a feature of this lifestyle, all of which is highly contrary to how the equine digestive tract has evolved to function.
Knottenbelt acknowledges the stark contrast: “In our undoubted wisdom we have decided that horses do not eat what nature intended, in the way nature intended, and set out to feed horses in a way which could never be construed as natural. Unfortunately, the penalty for extra performance and extra condition is invariably sub optimal GI tract health and increased prevalence of GI disease.”
How GI tract issues develop
Concentrate feed requires markedly less chewing when compared to forage intake of equal quantity. As a result, the production of salivary bicarbonate to buffer acidic gastric ingesta is restricted, and periods of time can occur where the stomach is empty. The naturally continuous secretion of gastric acid becomes, in effect, “excessive” when there is little or no food to soak it up. As a result, the gastric mucosa, and specifically the non-glandular mucosa, becomes exposed for longer periods to this acid, increasing the risk of inflammation and lesion development. Knottenbelt explains, “The horse has evolved to eat low quality forage and survive, but requires a defined feeding strategy to maximise this.” Maximising forage intake through ad lib trickle feeding ensures a constant supply to buffer excessive gastric acidity, and also helps to meet behavioural needs of the horse.
The problems with modern feeding and management are, however, not limited to the stomach. The horse generates upwards of 60% of its energy needs from microbial and bacterial fermentation of forage within the hindgut. This hindgut microbiota exists in a delicate balance and can easily become disturbed when environmental, dietary or even pharmaceutically derived changes occur. When conditions create a decline in pH within the hindgut, a disbiosis, or “bacterial inversion,” develops. This describes the proliferation of pathogenic bacteria, lactic acid production and destruction of beneficial forage-fermenting bacteria. In this process, endotoxins are released which reduce the integrity of the colonic mucosa and infiltrate the vascular system to potentially cause systemic disease.
A significant cause of hindgut disbiosis in performance horses, again, stems from feeding non-structural carbohydrate. The horse possesses a limited capacity to break down starch, due to minimal production of pancreatic alpha amylase. If starch intake exceeds the current recommendations, set at a maximum of 1g starch/kg bodyweight/meal, the likelihood of “starch overload” is increased. Should starch fail to be fully broken down in the small intestine, it will reach the hindgut and ferment with deleterious effects on the microbiota.
Is starch a necessary evil?
For horses in hard work, the supplementation of some non-structural carbohydrate to the diet can increase muscle glycogen concentrations and thus improve performance potential. Knottenbelt advises “that if high quality diets are necessary, they need to be of an appropriate type that encourages chewing, salivation, promote gastric acidity control and secretion, intestinal motility and digestion of soluble materials in the small intestine.” Further, horses may benefit from additional digestive support to help normalise gut function under effectively “abnormal conditions” and aid effective utilisation, and digestion of feed.
Often overlooked effects of ulcer medications
The use of acid suppressing medications have become ubiquitous in the management of the performance horse, but much overlooked is the role gastric acid plays within the normal digestive process, including activation of certain digestive enzymes. Knottenbelt emphasizes this: “Exposure to gastric acid is a completely normal event in the process of digestion, otherwise – from an evolutionary perspective – the horse would not produce any!” He goes on to caution that “continued suppression of gastric acid will inevitably result in alteration of the intestine or function. Optimal health of the equine gastrointestinal tract is highly reliant on sufficient salivary secretions, acidity in the stomach and hindgut bacterial digestion.” Aberrations of these factors, particularly long term, will undoubtedly have a negative impact on how the tract functions and its overall health. Should acid suppressing therapy be unavoidable, hindgut nutritional support is paramount to avoid the development of downstream issues, and long-term preventative measures should be implicated as soon as possible.
With limitations in accurately diagnosing hindgut pathology, the exact prevalence of hindgut inflammation and ulceration anti-mortem can be difficult to determine. However, Knottenbelt has clearly observed its potential reach during post-mortem examinations at the vet school. In finding significant hindgut pathology in a high proportion of apparently asymptomatic horses, Knottenbelt suggests that “symptomatic horses may be the tip of the iceberg”. Early screening to detect potential issues is key, both to implement swift changes to feed and management before symptoms arise, and from a welfare aspect.
Knottenbelt concludes: “GI conditions are largely a result of modern management and domestication, so we therefore have a responsibility to research them and devise strategies to detect them at an earlier stage, and implement ways to prevent them in the long term.”
Emma Hardy is the European Marketing Manager for Freedom Health, makers of the SUCCEED Equine digestive programme. For more information about SUCCEED visit, http://www.succeed-equine.co.uk/