The Fructans Debate

There has been an interesting discussion on EE about magnesium and spring grass, as is often the case someone put forward the 'trouble with grass is fructans' argument, and referenced research to support this point.  

I recently attended the laminitis awareness seminar, during this seminar various research was talked about and one of the nutritionists from Dodson and Horrell (who was actually refreshingly non salesy) put forward a counter argument or at least explained why the research did not necessarily prove what it was trying to prove.

I thought this raised an interesting point about having to take research findings in the context of real life, it is very easy to read something and understand it to be the truth, taking it on face value, when actually this would never apply to you or your horse.

I am signed up to the Equine Science Archives which is an excellent resource and very good value for money for a years access.  The following two extracts are taken from their publications in 2010.

Laminitis Latest (Chris Pollit research)

"The discovery that fructans can be used experimentally to induce laminitis has allowed him to examine the changes that occur in the foot in the early stages of the disease. Alimentary overload with oligo-fructan is a valid experimental model for inducing acute laminitis. He points out that using oligo-fructan (OF) to induce laminitis in experimental horses has advantages over the previously used method of giving a large dose of starch. OF given at 10g/kg predictably causes laminitis every time. But the signs are less severe than with the starch model and none of the animals have to be killed." 

"An extract of Streptococcus bovis, the bacteria that multiply dramatically in the large intestine in response to fructan, has a similar effect. However, Pollitt has not yet been able to prove that toxins released by the bacteria actually reach the laminae to be able to have their effect. "We`ve never been able to show any bacterial product at the lamellar zone so far."

What I understand from this research is that if the horse ingests enough fructan (10g/Kg) it will reliably result in laminitis.  We can induce laminitis by introducing fructan but the gut bacteria proliferation in response to the fructan is as yet unproven to directly impact on the laminae.  So we still have no idea how something that impacts on the gut, also effects the feet.

Contrast this to Dr Hollands analysis of Pollits research (Article entitled Laminitis Awareness):

"Experiments have shown that giving large meals of starch or fructans can cause laminitis. Large amounts of these carbohydrates suddenly arriving in the horse’s large intestine disrupt the normal population of bacteria in the gut, leading to a cascade of inflammatory and toxic events.

However, Dr Hollands, nutritionist at Dodson and Horrell, explained that this process is unlikely to be involved in the majority of cases of pasture-associated laminitis.  

Firstly, grass contains little starch. Of the pasture plants commonly found in the UK, only clover has significant amounts of starch. Grasses store glucose that they can’t use straight away as fructans. 

It has been shown that laminitis can be induced by giving a large bolus of fructan  (5g-12.5g fructan/kg body weight).  That’s about 3.75kg fructan for a 500kg horse.

How much fructan would a horse eat when grazing? Grass contains higher levels of fructan during the winter. Mixed pasture might contain 150g fructan/kg dry matter of grass in the winter (compared with 6.6g/kg in the summer). If a 500kg horse eats an amount of grass equivalent to 2.5% of his body weight, (12.5kg), his total intake of fructans would be about 1.9kg.

So the full daily intake falls short of the levels that have been shown to cause laminitis. And what’s more, as horses are “trickle feeders”, that fructan intake is spread out over 24 hours. So even in the winter when the fructan levels in the grass are highest, the horse is only likely to eat something like 50g fructan/hour.  In the summer the figure is likely to be about 5g fructan an hour - a thousand times less than the amount needed to cause laminitis.

What’s more, recent work has shown that fructans are fermented in the small intestine, and so are even less likely to reach the hindgut in sufficient quantities to cause food-induced laminitis.

So how does grass cause laminitis? “We need to move away from thinking about individual components of the diet “ Dr Hollands suggested. “In the end it is the calories that are the main risk factor.”

From this explanation of Pollits research I now believe that in my horses world it would be very difficult for them to consume the amounts of fructan that Pollit had to introduce to trigger laminitis, in fact in the summer, they would be consuming 1000 times less fructan than Pollit had used.

So, what do I see in my own horses?  In my experience my horses cope best with a minimal grass diet which means I restrict them both in terms of slowing down their grass consumption rate (by a grazing muzzle) and by keeping them on a sparse paddock so they have to work harder to get the grass.  The sparse paddock contains the 'stressed' grass which is generally believed to produce more fructan than older tall stemmy grass.  Because however they are restricted their overall calorie intake is reduced, they are also moving around more to get the grass so their energy expenditure is higher.  Personally I think I come down on the side of Dr Hollands and that it is far more important to be concerned about overall calorie intake than fructan.