The gluten riddle – searching for the triggers of coeliac disease
“The fact that patients with coeliac disease now have more food products to choose from is, of course, a good thing. What is less good is that some people cut down on gluten without knowing whether or not they have the disease”, says Carin Andrén Aronsson.
Coeliac disease is not something you have more or less – you either have it, in which case you should follow an entirely gluten-free diet, or you don’t, and if so, it is a bad idea to avoid regular grains, which contain a lot of healthy fibres and minerals.Carin Andrén. Photo: Björn Martinsson
Carin Andrén Aronsson is a dietician and her research colleague Daniel Agardh is a paediatrician. Their goal, among other things, is to try to understand the triggering factor of coeliac disease.
In order to develop coeliac disease, you must eat gluten, and have a certain set of genes. However, these genes are common in Sweden, where we also eat a lot of gluten-rich foods. Still, only about 3 per cent of Swedish children have coeliac disease. Although this is a lot for a chronic autoimmune disease, it does not correspond to the occurrence of the genes concerned and food containing gluten. Therefore, there must be another underlying factor.
“Perhaps the disease is triggered by viral infections, something in the intestinal flora, something in the diet other than gluten, or that the person’s immune system as an infant did not receive the correct stimulus. Or, it’s a combination of several factors…”, says Daniel Agardh.
The researchers’ studies are partially based on the major international TEDDY study*, that monitors children with an elevated hereditary risk of type 1 diabetes and coeliac disease – two diseases that often occur together. The study’s close to 6 000 participants are monitored until they turn 15, during which time detailed records are kept regarding their health and diet.
“The great advantage of TEDDY is that it involves retrieving information long before a child has been diagnosed with an illness. This allows you to see what separates the children who eventually develop diabetes or coeliac disease from those who don’t”, explains Daniel Agardh.
Coeliac disease means that the body’s immune system responds to gluten by attacking the surface of the small intestine. When the intestine is damaged, it becomes more difficult for the body to absorb nutrition and important trace elements, which can lead to osteoporosis, growth disorders, deficiency diseases, etc.
The disease is more common in Sweden than in many other countries, which is believed to be due to both genetics and diet.
“Sweden is a ‘formula and porridge’type of country. We eat a lot of foods that are based on wheat, rye and barley which contain gluten”, says Carin Andrén Aronsson.
In small children, the disease may cause impaired growth, poor appetite and stomach problems. Adults often experience more diffuse symptoms, such as fatigue and depression.
“Many adult patients have repeatedly sought medical attention for several years before they finally learn that their problems are due to coeliac disease. Sometimes the disease remains undetected until the patient is examined for inexplicable fractures, finding that they are due to osteoporosis, which in turn may be caused by a damaged intestine”, says Daniel Agardh.
The genes that involve a risk of coeliac disease can be found in more than 40 per cent of the Swedish population. Therefore, one way would be to test all newborns and, if they are found to have these genes, provide dietary advice to the children’s parents.
The advice would not be about the duration of breastfeeding or when to introduce gluten, as Carin Andrén Aronsson’s research has shown that these factors are not crucial. The amount of gluten, on the other hand, seems to be important: the more gluten an infant receives, the greater the risk of coeliac disease.
“Parents of children carrying risk genes could be advised to go easy on the formula and porridge. It does not mean having the child on an entirely gluten-free diet, but perhaps avoiding giving them flour-based foods with every meal”, she says.
However, in this respect, Daniel Agardh does not completely agree with his colleague.
“Reducing the amount of gluten perhaps will only delay the disease? We still don’t know enough to determine what ultimately triggers it”, he argues.
While a genetic testing of newborns would identify the 40 per cent carrying the particular genes, a general screening later in childhood could identify the 2–3 per cent who actually develop the disease. In recent years, the value of this type of screening has been discussed in medical circles. The main question is whether the advantages – in the form of identifying patients who may be treated – outweigh the disadvantages in terms of societal costs and worry among families.
“But one thing is certain: if a screening is worth doing somewhere in the future, it is here in Sweden. We have both the disease and the right knowledge about it”, says Daniel Agardh.
*TEDDY = The Environmental Determinants of Diabetes in the Young. For more information, visit www.med.lu.se/teddy.