The following two articles are very informative and important to have as background whether or not you know that your horse has ulcers.
Ulcers |
by Madalyn Ward, DVM |
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Much of the attention on treating ulcers has been focused on a new and expensive drug to treat ulcers. While I am not an advocate of treating ulcers with drugs, I am excited to see more focus put on this common condition. As many of my clients know, I put a huge emphasis on the digestive tract for a wide variety of complaints. Many recent magazine articles are discussing specifically ulceration of the equine stomach. These ulcers can be easily visualized with the aid of a two-meter long flexible endoscope. I would like to suggest that ulcers or erosions are just as likely to occur throughout the intestinal tract. Breakdowns in the intestinal lining leads to a serious condition known as leaky gut syndrome. More on that later. Gastric UlcersThe lining of the horse's stomach is made up of a glandular and non-glandular (squamous) portion. The glandular portion covers the lower two-thirds while the squamous mucosa covers the upper one third.Most ulcer problems will develop in the non-glandular lining because it has little protection against the acid which is produced in the lower portion of the stomach. The exceptions to this are the ulcers caused by toxicity from non-steroidal anti-inflammatory drugs such as ButeT and BanamineT. These ulcers occur in the glandular portion of the stomach because NSAIDs block the release of prostaglandin. Prostaglandin is one of the agents the body depends on to protect the glandular lining of the stomach from the hydrochloric acid and pepsin that it secretes. Clinical SignsBoth adult horses and foals are susceptible to gastric ulceration. In the adult horse, clinical signs include diminished appetite, colic, frequent pawing, weight loss and poor performance. A classic sign is a horse who eats the grain portion of his diet slowly if at all, but eats hay readily. Horses with gastric ulcers will often be back sore since the acupuncture association point for the stomach is in the muscle adjacent to the spine at the level of the thoraco lumbar junction. Clinical signs in foals include colic, pot bellied appearance, teeth grinding, and excessive salivation.
Pastured, grazing horses rarely develop gastric ulcers, however when
these same horses are brought into stalls and intermittently fasted they
develop ulcers with in five to seven days. Thoroughbred racehorses in
training appear to be the most at-risk population, which has led
researchers to conclude strenuous exercise may cause a temporary
decrease in blood supply to the stomach. Another possible explanation
for the increased incidence in racehorses is management. Most racehorses
in training stand in a twelve by twelve stall for twenty-three hours a
day with little to no contact with other horses. It is also common
practice to feed racehorses large portions of grain and a minimum amount
of hay. Even if hay is offered free choice, horses will eat less of it
if the grain portion of the diet is meeting their caloric needs. It is
also common practice to give racehorses frequent doses of NSAIDs both
for injury and "prophylactically". All these factors alone or combined
may account for the increased incidence of gastric ulcers in racehorses.
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The Latest on Ulcers |
by Madalyn Ward, DVM |
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At the 2006 Holistic Veterinary Conference, Dr. Scott Carter gave a lecture on gastric and colonic ulcers. So much of the research has focused on gastric ulcers and their treatment but Dr. Carter also shared research on colonic ulcers. A study of the post-mortem findings in 500 horses revealed that 63% of performance horses had colonic ulcers. We have come to understand many of the causes of gastric ulcers, such as infrequent feedings, high starch diets, and exercise causing the acid in the lower protected portion of the stomach to move into the upper, non protected portion. We also know the connection of non-steroidal anti-inflammatory drugs which decrease prostaglandin production and therefore decrease the production of protective mucous to line the intestinal walls. For gastric ulcers, treatments have been mostly focused on buffering the stomach acid or decreasing its production. Dr. Carter’s research indicates that while these treatments have been somewhat effective in treating and preventing stomach ulcers they have actually increased the imbalance in the rest of the digestive tract and in many cases been responsible for increasing the presence of colonic ulcers. To understand what is happening we need to review the function of the stomach and small intestine in the digestive process. The glandular portion of the stomach in the horse produces acid on a continuous basis. It also produces digestive enzymes and mucous which protects it from the actions of the acid and digestive enzymes. The equine stomach is small and food does not normally stay in the stomach long before it is passed to the small intestine. The small intestine is also relatively short and food moves quickly to the large intestine where fermentation of fiber occurs. The digestion of starch occurs in the stomach and small intestine by the actions of stomach acid and digestive enzymes produced in the stomach, and pancreatic enzymes released into the small intestine. Bacteria in the small intestine also contribute to the correct breakdown of starch. All of this starch digestion is highly dependant on the correct pH. The problem with the current treatments for ulcers is that the focus is on decreasing or buffering stomach acid which raises the pH in the stomach and small intestine. When the pH is raised to above four the digestive enzymes stop functioning and the population of healthy starch digesting bacteria in the small intestine decreases. Now undigested starch is moving into the small intestine with few beneficial bacteria. There is always a small number of harmful bacteria lurking about, without healthy bacteria to keep them in check and a higher pH environment, they thrive and they begin to ferment rather than digest the starch. The small intestine is not designed for fermentation and the harmful substances produced damage the intestinal lining producing ulcerations. The toxins produced by fermentation of starches greatly stress the liver when they are picked up by the blood vessels going from the intestines to the liver. Some of these toxins also find their way into the bloodstream directly through damage to the intestinal lining. Now we have the remaining starch that was not digested or fermented being dumped into the cecum portion of the large intestine. The cecum is designed for the fermentation of fiber, not starch, and it also depends on pH for proper function. The lactic acid produced by the starch fermentation lowers the pH in the large intestine which kills the beneficial fiber fermenting bacteria and protozoa. Continued production of lactic acid and other harmful substances effectively shuts down fiber digestion and causes ulcerations and damage to the intestinal lining of the cecum and colon. About the Author Madalyn Ward, DVM, owns Bear Creek Veterinary Clinic in Austin,
Texas. She is certified in Veterinary Homeopathy and Equine Osteopathy.
Memberships include American Veterinary Medical Association, American
Association of Equine Practitioners, American Holistic Veterinary
Medical Association, Texas Veterinay Medical Association and the Academy
of Veterinary Homeopathy. She has authored several books and publishes
the monthly newsletter, “Holistic Horsekeeping.” |
