When and how should gluten be introduced into the infant's diet

Abstract

Coeliac disease (CD), or permanent gluten-sensitiveenteropathy, develops because tolerance to ingestedwheat gluten (gliadins and glutenins) and relatedproteins from wheat rye and barley never develops,or is broken after it has developed. CD is char-acterized by inflammation of the small intestine,resulting in crypt hyperplasia, villous atrophy andflattening of the mucosa. Other characteristics arean increased number of intraepithelial lymphocytes(IELs) and lamina propria lymphocytes, increasedserum concentrations of immunoglobulin A (IgA)antibodies towards gliadin and the autoantigentissue transglutaminase. When gluten is withdrawnfrom the diet the mucosal morphology is restored,the specific antibody levels become normal andsymptoms of the disease disappear (1). CD is anacquired disorder, which can be diagnosed fromearly infancy with classical symptoms such asdiarrhoea, malabsorption and failure to thrive, toadulthood with a wider and more diffuse spectrumof symptoms (2). Poor dietary compliance andundiagnosed disease, which is frequent in adultpopulations, are associated with increased morbid-ity and mortality (3).CD is a chronic inflammatory disease with astrong polygenic component, although most of thegenes involved are still unknown (4). Over 90% ofpatients express the major histocompatibility com-plex (MHC) class II molecule HLA-DQ2 and theremainder usually HLA-DQ8, both of which pre-dispose for the disease (5). Exposure to gluten orcertain peptides thereof, in genetically predisposedindividuals, is a prerequisite for CD development,and once established the disease can be turned onand shut off by introducing gluten into or with-drawing gluten from the diet. CD is associated withan abnormal T-cell-initiated immune response togluten, but the detailed pathogenesis still remains tobe elucidated. The Swedish epidemic of CD withclassical symptoms in children below 2 years of age,which surfaced for a little longer than a decade fromthe mid-1980s, strongly supports an aetiological roleof environmental factors, such as early infantfeeding practices (6, 7), and thus a multifactorialaetiology.Large amounts of gluten: independent riskfactorThe recent Swedish incident case-referent studycontributed to the identification of some of thesecausal environmental risk factors. For the first timethe design of the study allowed assessment of theconsumption of gluten-containing cereals on anindividual level (8). Introduction of gluten-contain-ing foods in large amounts, compared with small ormedium amounts, was an independent risk factorfor CD development [adjusted odds ratio (OR) 1.5,95% confidence interval (CI) 1.1