Our immune system, as we know all too well, is essential for survival and well-being. It can be a mixed blessing; it can protect against infectious disease, but can also have unpleasant effects like allergy and autoimmunity (immunity to the body’s own proteins).
It is vital that it reacts to some things, but just as vital that it should not react to others. It now seems likely that the way in which our immune system responds to our food is much more important than had previously been realized; disturbances in this response may play a crucial role in a variety of diseases including rheumatoid arthritis, migraine and eczema.
We usually tend to think of our skin as our main contact with the outside world but, in fact, it is a pretty successful barrier keeping out most infective agents and foreign molecules; these usually gain access only when the skin has been broken in some way.
By contrast, the whole function of the digestive system is to take things in, on a fairly large scale. Until recently, it was assumed that proteins were absorbed only after being broken down into their constituent amino acids, molecules which are too small to provoke an immune reaction.
It has now been found, however, that quite sizeable protein molecules can cross the intestinal barrier. For several hours after a meal, recognizable proteins, for example, from eggs, milk and wheat, are circulating in the blood. These are foreign proteins and we would expect the immune system to react against them.
Even if only a very small proportion of the food protein crossed the barrier in this form, it represents, potentially, a massive immunological onslaught. For some reason, however, these food proteins normally seem to be tolerated.
It is only when this tolerance is disturbed that there is an immune response. Somehow, the system seems to be able to discriminate between food proteins, which ideally should not provoke an immune response, and other things, which should. Oral vaccines (for example, polio vaccine) and various harmful bugs, which enter via the gut, can still provoke classic immune reactions.
A breakdown in this discriminatory system seems to be a factor in coeliac disease, a particularly unpleasant condition, in which there is an immune reaction to wheat protein (gluten). The lining of the small intestine is damaged, and sufferers are unable to absorb food properly. The symptoms are weight loss, diarrhea and general misery; children with the disease have the pot bellies and sagging buttocks normally associated with famine victims.
A gluten-free diet works like magic, and one of the first things noticed is a change of mood.
The suggestion has been made that diet can help in the control of rheumatoid arthritis; this idea is probably as old as the belief in copper bracelets. Dr Cliona O’Farrelly first became interested in the possibility after reading an article in a magazine.
She had worked on coeliac disease at Trinity College, Dublin, before moving to Sussex to work with Dr Luke Fernandes, a rheumatologist at the Royal Sussex County Hospital. The scientific literature, however, was not encouraging. She found that previous research on the effects of diet had produced mixed results and that there was widespread scepticism among medical people.
Nevertheless, it did seem that these mixed results could be accounted for if diet was important only to some types of rheumatoid arthritis sufferer but not to others. Looking further, she and her colleagues carried out tests on 87 patients and found that just over half of them showed evidence of an immune reaction to wheat or milk protein; 41 of them had raised levels of antibodies to wheat gluten.
Rheumatoid arthritis is an autoimmune disease, a type of disease in which the immune system reacts against the body’s own proteins.
Rheumatic complications are known to occur consequent to other diseases, particularly after infections with bacteria or viruses. For some reason, in rheumatoid arthritis, the immune system makes antibodies (which have been produced against something else); the autoimmune reaction is against the product of another immune reaction.
It seems likely that these two types of antibody react to form complexes which lodge in the joints and that these complexes are attacked by the active cells of the immune system, producing an inflammatory response.
Antibodies are proteins, immunoglobulins, and there are a number of different types, including IgG, IgA and IgM. The rheumatoid factor antibodies are produced against normal IgG antibodies.
For sometime, it has been known that about 75 percent of patients have an IgM rheumatoid factor. More recently, however, another rheumatoid factor, of type IgA, has been found in about 60 percent of patients. IgA is generally associated with mucosal surfaces, such as the lining of the digestive system. In the Sussex study, although only about half the patients showed immune reactions to the dietary proteins, 90 percent of these had rheumatoid factor type IgA.
Therefore, it seems that rheumatoid arthritis sufferers can be divided into two classes, those who give an immune response to dietary protein (about half), and those who do not. Most of those who give an immune response to food, have rheumatoid factor IgA, which may have derived from the gastrointestinal tract. Perhaps these are the only ones who will respond to a manipulation of the diet and this is now being investigated.
At present, no one knows much about the mechanisms which normally maintain tolerance to dietary proteins and how and why they break down. The change from tolerance to an active immune response may be the result of some malfunction or of damage which increases the amount of food protein circulating in the blood.
It seems likely that some cases of rheumatoid arthritis are a secondary consequence of such an unusual response to dietary protein. Wheat protein, because of its tendency to provoke such responses, may have a particularly important role.