There is evidence that people with food intolerance have more leaky gut walls than healthy individuals – so they let more undigested food molecules through. This has major health implications which will be considered later, but how does the gut become more leaky in the first place?
Inflammation, produced by immune attack, can make the gut wall more leaky. One source of inflammation is disease – any gut infection that produces diarrhoea may inflame the gut wall. In babies, such infections are often the start of food intolerance.
Alternatively, foods themselves might provoke inflammation of the gut wall, if there is a localized allergic response to them. This is not something that most allergists would agree with – they see IgE/mast cell reactions to foods (see p29) as being all-or-nothing affairs which produce immediate and unmistakable symptoms. The idea that there might be a small-scale, localized IgE reaction, whose main effect is to make the gut more permeable, is not widely accepted. The main evidence in its favour is the effect of a drug, sodium cromoglycate, on some patients with food intolerance.
The effects of this drug have mainly been studied in migraine patients. If such patients undertake an elimination diet, a large proportion of them get better and can then identify one or more foods which provoke their symptoms. Each time a culprit food is eaten it will provoke a migraine -but not if sodium cromoglycate is given in advance. Sodium cromoglycate is
known to stabilize mast cells and prevent them from releasing their inflammatory mediators. And the drug is not absorbed from the gut in any appreciable quantity. So the logical conclusion is that it prevents reactions to culprit foods by blocking mast-cell reactions in the gut wall.
There is a third way in which the gut wall might be made more leaky. We all produce a special type of IgA antibody called secretory IgA or SIgA. The production of SIgA is stimulated by the Peyer’s patches, and it pours out into the gut, where it binds to its target antigen. By binding to antigens, and locking them into immune complexes, SIgA effectively makes them much bigger. The bigger they are the more difficult it is for them to pass through the gut wall. So SIgA reduces the number of food molecules that cross the gut wall – and the number of microbes, because SIgA is made to these as well. Like IgA in the blood, SIgA does not cause any inflammation.
There is some evidence that people with food intolerance have less SIgA than healthy people. However, there are patients who have severe deficiencies of SIgA, and, although they are ill in other ways, they show no more signs of food sensitivity than the population at large. This suggests that SIgA deficiency alone is not enough to cause food intolerance.
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