animal health consulting
The amine hypothesis
high-protein diets and behavioural problems in horses
Christine King BVSc, MANZCVS (equine), MVetClinStud
What do we know?
How much of this hypothesis can I prove?
Here is what is already known in horses, based largely on research into laminitis, digestive disorders such as colic, and the gut microbial community.
1. High-NSC diets increase hindgut acidity. That is, they ↓ pH in the hindgut.
In case you skipped or slept through chemistry class in high school, pH is a paradoxical or counterintuitive thing: the lower the pH, the greater the acidity of a solution.
That's because the pH scale extends from 1 (extremely acidic) to 14 (extremely alkaline or basic); 7 is neutral (neither acidic nor alkaline).
Hindgut pH in horses is generally slightly acidic (pH in the mid- to high-6s), even in horses on high-fibre diets. That's because the generation of beneficial short-chain fatty acids (SCFA) from the microbial fermentation of dietary fibre creates a slightly acidic environment. The caecum and colon are well equipped to handle this slight acidity.
However, with high-grain diets and with experimental starch or oligofructose overload, hindgut pH may drop into the high- or even the low-5s.
As each whole number on the pH scale represents a 10-fold difference from the one before, even these seemingly small changes in hindgut pH (e.g., from 6.8 to 5.8) represent huge changes in acidity of the hindgut contents — and correspondingly huge changes in the microbial community as the more acid-sensitive species are inhibited or even killed.
But to make this already-convoluted journey easier to follow, I'll stick with the term acidic rather than refer to pH.
The microbial fermentation of nonstructural carbohydrates (NSC) that 'spilled over' from the small intestine into the caecum and colon increases the acidity of the hindgut contents.
By how much depends on the amount of NSC in a single meal, or in a short space of time in horses on pasture full-time. For example, in a German study I'll discuss in a bit, the researchers estimated the amount of NSC the horses on pasture would have consumed in the past 2 hours.
This study showed one other thing that is important to this discussion: there was an astonishing amount of individual variation among the four horses in the pasture group, and even in the hay-fed group.
Before I go on, we have some good data on the spillover threshold for dietary starch (2 g starch/kg bwt/meal). But we're still only guessing about the thresholds for the other components of NSC: simple sugars, oligosaccharides, and fructans.
Here's a reminder about which plant carbs contribute to a feed's NSC content.
Like starch, simple sugars can be broken down ('hydrolysed') by the horse's digestive enzymes and absorbed directly into the bloodstream from the small intestine. However, the other NSCs cannot; they can only be broken down by acid in the stomach and by microbial fermentation.
As to that, the German study I promised examined carbohydrate digestion in the horse's stomach. That alone is remarkable; we're not used to thinking that carbohydrate digestion might begin in the horse's stomach. (In fact, it begins in the mouth, with secretion of the starch-degrading enzyme, amylase, in the horse's saliva.)
The study measured the various plant 'sugars' and fibres in the horse's feed and in the horse's stomach after a meal. The researchers examined four different diets: pasture, hay, and hay + oats at two levels of starch intake.[14]
I was most interested in what happened in the four horses on pasture full-time, and particularly what happened with the fructan portion of the pasture, which in this study included oligosaccharides and fructan polysaccharides (so, OF+fructans).
The fructan content of the pasture at this point in the study was quite low, 4.4% DM. That's similar to the OF+fructan content of the autumn and winter pasture my equine guinea pigs have been on: 3.5% in autumn and 4.2% in winter.
Take a look at what happened to the fructan portion of the pasture in the stomach:
Table of Contents
5. The (failed) amine–laminitis hypothesis
6. The amine–behaviour hypothesis
7. What do we know?
© Christine M. King, 2026. All rights reserved.
First published on 31 August, 2026. Last updated 08 September, 2026.
This section continues on the next page. Click on the 'Read on...' link below the Table of Contents.
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Reference
[14] Bachmann M, Schusser GF, Wensch-Dorendorf M, et al. Carbohydrate digestion in the stomach of horses grazed on pasture, fed hay or hay and oats. Journal of Equine Veterinary Science, 2024; 141: 105152.
Figure 7 (a). Fructan loss (digestion) in the stomach of four horses on pasture full-time. Each horse is represented by a different coloured line. In this study, 'fructans' included both oligosaccharides and polysaccharides.[14]
Although there were only four horses in this group, the fate of the fructans in their pasture ranged from a drop of less than 5% (negligible digestion) to the digestion of almost 90% of the fructans consumed in the past 2 hours.
Calculating an average for this small group of horses would be pointless — and misleading. The real take-away from this graph is that only some horses have a lot of spillover of fructans into their small intestine, and ultimately into their hindgut. In three of the four horses, more than 70% of the fructans eaten were broken down in the stomach, presumably by a combination of gastric acid and microbial fermentation.
A similar thing happened in the eight horses fed hay. In this group, the fructan content of the various hays ranged from 0.7% DM to 6.6% DM. Fructan digestion in the stomach ranged from zero to 87%.
Figure 7 (b). Fructan loss (digestion) in the stomach of eight horses fed hay. Each horse is represented by a different coloured line. Four different hays were fed, each with a different fructan content, with two horses on each hay. In this study, 'fructans' included both oligosaccharides and polysaccharides.[14]
This study may go some way toward explaining why deliberate starch or oligofructose overload in experimental studies does not invariably cause laminitis in horses. There's usually one or two horses in the group that 'resist' succumbing to carbohydrate overload. I have long found these individuals — these 'white crows' — fascinating. Alas, I appear to be alone in wondering what makes them different, more resilient. Generally, they are merely an annoyance to the researchers who are trying to induce the disease in order to study it.
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In short, there is a tremendous amount of individual variation among horses in response to NSC intake. Not all horses respond alike to the same NSC intake. Why is that? It's because no two horses have exactly the same gut microbial community.
Whatever the threshold is for spillover of the various NSC components into the hindgut, these two things are true:
Spillover is inevitable when dietary NSC is high enough in that horse.
It invitably causes an increase in hindgut acidity.
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