I have written on this topic for over a decade but continue to encounter many questions and comments that are based on misinformation.
For this discussion I am going to define a normal hind gut as one that is functioning normally – normal manure in normal amounts, no excess gas or bloating, normal gut sounds on examination, no abdominal pain (colic), healthy weight for the amount of food being consumed – although other things can affect weight.
Subtle behavioral signs of trouble include tail swishing or docking, kicking back or at the belly with ears pinned, looking at the flank. Sensitivity to touch or pressure (e.g. girth), gait disturbance or lameness are **not** signs of gut disturbance especially with no other signs of intestinal disorder. [Note: Subtle behavioral changes have been documented with starch feeding but that was a diet of almost 50% barley!]
The disorders du jour are acidosis and hind gut ulcers – both nonexistent the way many people are thinking of them. You may have read about horses having behavioral or movement issues related to “sublinical acidosis” but subclinical by definition means no observable signs.
The pH of the hind gut varies depending on diet. There are no acid secreting cells and material entering from the stomach and small intestine is alkaline. Diets with high levels of simple sugar and starch reaching the hind gut naturally cause a more acidic environment because of the way they are fermented. There are no consequences of this unless pH drops low enough to damage the intestinal lining, at which point you see fever, colic, sepsis, diarrhea and laminitis in extreme cases. The important point here is that acidosis does not, and cannot, occur on diets with reasonable levels of starch and simple sugars. It takes very large amounts to produce enough acidosis to cause clinical signs and those signs include fever and diarrhea.
You may have seen claims subclinical acidosis is related to stereotypical behavior like cribbing, wood-chewing and weaving. There are zero actual studies looking at degree of acidosis and stereotypical behavior. One study found high grain feeding during weaning increased cribbing but this could not be differentiated from low forage access and long periods with nothing to chew on for distraction. A study of 743 young racehorses on two tracks found a connection between using wood shavings and stereotypical behavior but no influence by % of grain and forage fed. Similarly, other studies have found a decrease with more frequent meal feeding but not by composition of the diet.
A supplement manufacturer has reported high prevalence of hind gut “ulcers” based on observations made on horses going through slaughter houses. This entity does not appear in any veterinary medicine or pathology textbooks except for colonic ulcerations caused by phenylbutazone use.
A subsequent study lead by Kerbyson in the UK examined 56 horses euthanized for reasons unrelated to the GI tract and looked for idiopathic (no obvious cause) colonic ulcers. They found 21% had ulcerations clearly related to parasites or sand. Only 5% had ulceration with no obvious visible cause (? autoimmune disease, ? phenylbutazone use) which is a far cry from the 63% the original survey reported. In fact, the supplement manufacturer’s website has since switched from mention of “colonic ulcers” to the hind gut being the site of various specific GI pathologies such as parasites.
Once mistaken information has been widely circulated it is difficult to get rid of it but the time has come to stop worrying about hind gut acidosis or ulcers – and buying supplements to address them.
Eleanor Kellon, VMD