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Ulcers and Lecithin – Digestion and Your Horse



vets with horse

Let’s Eat!

Horses have  evolved to eat  many small meals per day, almost on a continual  basis. Even though the horse’s stomach is  only 8 percent of digestive tract (eight quarts  or two gallons), the emptying time of the stomach  can be a mere twelve minutes and the rate  of passage through the small intestine one  foot per minute. The small volume of the stomach  and the rapid passage of food to the small  intestine is the reason that horses can and are  designed to eat almost continuously. Gastric  pH can drop lower than 2 soon after a horse  stops consuming food and the stomach will  continue to produce strong acid even if food is  not present.

Concentrate feeding can inadvertently  contribute to ulcer formation by its influence  on increasing serum gastric levels, lowering  the horse’s roughage intake and reducing  the amount of time spent eating. Imposed  feed deprivation, such as in colic management  cases, can result in erosion and ulceration of  the gastric mucosa as well.  In the case of racehorses, they are  often not fed immediately prior to training or  racing. This could result in a significant  increase in stomach acidity. Also, horses can  become excited during training and racing, further  lowering gastric pH. These influences  contribute to  gastric ulceration

Studies  show that the  greater the  degree of  training activity,  the increased  severity of  gastric lesions.   Further,  lesions were  induced and maintained in thoroughbred horses  during simulated training, using a diet of  coastal Bermuda and concentrate.   Although  Dr. N. J. Vatistas stopped short of recommending  all racehorses in training receive gastric  ulcer treatment, he indicated, “The truth  may not be far from that”.   Adult horses with ulcers exhibit a  combination of poor appetite, dullness, attitude changes,  decreased performance,  poor  body condition,  rough hair coat, weight loss and colic.

Ulcer Formation Mechanism  Gastric ulceration in horses results  from an imbalance between offensive factors,  e.g. acid and pepsin, and defensive factors  such as mucus, bicarbonate, prostaglandins,  mucosal blood flow and epithelial restitution.  Most of these ulcers occur in the fundic portion  of the stomach, which has a phospholipid rich,  protective epithelial layer. Disruption of this  barrier (mucous, surface-active phospholipids)  is initial to the destruction of the stomach’s  surface epithelium. Because most domesticated  horses do not feed constantly like nature  designed them to, excess acid can ulcerate  this protective layer. Unless the mucous lining  is strong enough to withstand the powerful  acids produced  here, ulcers  often develop.

Management  of Equine  Gastric Ulcers  Various therapeutic  protocols  have been suggested  for the  control of equine  gastric ulcers.  These include  antacids, (think of products such Tums and  Rolaids) and H2 acidblockers such as the  pharmaceutical products Pepsid and Prilosec.   These treatments will reduce acid in the fundic  portion of the stomach and will reduce the  occurrence of ulcers, but there may be unintended  negative consequences from these  treatments. Stomach acid is an extremely  important component of the initial stage of the  digestive process. If in this initial stage of  digestion there is not adequate acid present to  break down food, it will pass into the small  intestine only partially digested. The nutrients  won’t be in a form that can be absorbed in the  small intestine and the horse will not be adequately  nourished.  There is a better way to protect the  horse from and treat gastric ulcers. When the  horse is given lecithin as a nutritional supplement  to his normal diet, the acid in the fundic  portion of the stomach immediately breaks it  down into a mix of reactive phospholipids. The  phospholipids in lecithin are both hydrophilic  and hydrophobic and interact with the cell  membranes of the mucosal epithelium to  strengthen the mucosa. Research has shown  that lecithin not only treats the symptoms of  equine ulcers, it cures the ulcers as well by  making the stomach lining stronger at the cellular  membrane level. The beneficial effects of  a diet supplemented with lecithin also  enhance the rest of the digestive tract. There has been much research to substantiate  this. They also observed horses fed  lecithin had reduced levels of excitability and  anxiety that was attributed to the healing of  gastric ulcers.

Summary  A well-studied health condition in  horses is gastric ulcers. The presence of these  ulcers is associated with poor  condition, irritability and poor  performance. Treatment  options such as reducing stomach  acid production is expensive  and can disrupt the normal  digestive process by not allowing  the food to begin its initial  breakdown as nature intended.  A less expensive and more  effective treatment is to give  horses a nutritional supplement  of lecithin. It strengthens the  epithelial lining of the stomach  treating and preventing gastric ulcers and  allow for the proper absorption of nutrients in  the small intestine.  Lecithin has proven a valuable natural  supplement for horses to treat and prevent  gastric ulcers. Lecithin granules can be  added quickly and easily to a horse’s daily  feed ration or to almost any homemade horse  treat recipe. Horse treats containing lecithin  given between feedings and after training can  help protect the stomach from the damaging  affects of excess acid which is a natural occurrence  in horses.

Special thanks to the contributions of Dr. Craig Russett,  Ph.D in Animal Nutrition.  References:  Geor.R.j. and Papich (1990). Medical therapy for gastrointestinal  ulceration in foals. Comp. Cont. Edu.  Pract. Vet. 12:403-412.  Ghyczy,M., E. Hoff; J. Garzib (1996). Gastric mucosa  protection by phosphatidylcholine (PC) Presented at:  The 7th International Congress on Phospholipids,  Brussels, Belgium.  Jones, W.E. (1999). Equine gastric ulcer syndrome. J.  Equine Vet. Sci. 19:296-306.  Murray, M.J.; C.M. Murray, H.J. Sweeney, J. Weld,  N.J. Digby Wingfield and S.J Stoneham (1996). The  prevalence of gastric ulcers in foals in Ireland and  England: An edoscopic survey. Equine Vet. J.  28(5):368-374.  Russett, J.C. (1997). Lecithin applications in animal  feeds. Specialty Products Research Notes. LEC-D-56.  Traub, J.L.; A.M. Gallina, B.D. Grant, S.M. Reed, P.R.  Gavin and L.M. Paulsen (1983). Phenylututazone toxicosis  in the foal. Am. J. Vet. Res. 44:1410-1418.  Vatitstas, N.J.; Snyder, G. Carlson, B. Johnson, R.M.  Arthur, Thurmond, and K.C.K. Lloyd (1994).  Epidemiological study of gastric ulceration in the  Thoroughbred racehorse: 202 horses 1992-1993. 40th  AAEP Convention Proceedings. pp 125-126.  Wright, B. (1999). Equine digestive tract structure and  function. Ontario Ministry of Agriculture.

[published in Performance Horse Digest, Volume 2, Issue 2.]

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