Letters to the Editor

Why has coeliac disease increased in Swedish children?

W pracy przedstawiono aktualne zalecenia dotyczące karmienia naturalnego i żywienia uzupełniającego niemowląt oraz sposób realizacji tych zaleceń w różnych krajach. Omówiono wyniki badań, które być może będą podstawą do wprowadzenia zmian w żywieniu (skład mleka modyfikowanego, czas wprowadzenia do diety glutenu). Zwrócono uwagę na znaczenie żywienia w krótko- i długoterminowym kształtowaniu zdrowia, w tym także na rolę zwyczajów i nawyków żywieniowych.

The paper presents a review of current recommendations for breastfeeding and complementary nutrition in infancy as well as diversity of nutritional practices and managements held in various countries. Results of recently published studies are reported to summarize and reconsider possible future directions in early human nutrition and dietary intakes in childhood (e.g. composition of infant formulae, new concepts for dietary gluten implementation in infants). A role of nutrition and nutritional habits in pediatrics has been described and associations between nutrition during growth and health consequences in later life have been discussed.

Extensive biological and epidemiologic research has documented compelling benefits for breastfed infants. Human milk provides nutrients and energy for rapid growth and development, protective factors against infection, and biochemical messages that enhance the development of the gastrointestinal tract and host defense.

The remarkable antimicrobial and immunomodulating effects of human milk described elsewhere in this issue contribute to health during the period the infant is breastfeeding. This article examines the hypothesis that breastfeeding may have long-term protective effects against chronic disease in children. Alternatively, artificial feeding, or the absence of breastfeeding, may increase the risk for chronic disease. Many studies have found the incidence and duration of breastfeeding to be lower among children with chronic disease than among children without chronic disease. The purposes of this article are to review the literature on whether artificial feeding carries an increased risk for certain chronic diseases, to explore the possible explanations for reported findings, and to suggest a reasonable approach at this time for pediatricians in clinical practice.

The literature reporting investigations of the association between infant feeding practices and chronic disease has expanded dramatically since 1984 when Borch-Johnsen and colleagues reported that the risk of type 1 diabetes, or insulin-dependent diabetes mellitus (IDDM), was higher among children who were not breastfed for at least 3 months.¹⁷ Since the publication of this first article tying infant feeding to IDDM, more than 100 articles examining this hypothesis have been published. In addition, other studies have considered whether artificial feeding increases the risk for celiac disease, inflammatory bowel disease, childhood cancer, atopic disease,⁶⁴ multiple sclerosis,⁸⁵ Henoch-Schönlein's purpura,⁸⁴ obesity,¹⁰⁹ and cardiovascular disease.⁸⁷ Some of these chronic diseases are more difficult to study than IDDM because they are rare or because their etiologies are complex and poorly understood. Thus, IDDM has a highly developed literature, but childhood cancer has a meager one, and the rare condition Henoch-Schönlein purpura has only a single article.⁸⁴ IDDM, celiac disease, childhood cancer, and inflammatory bowel disease will be covered in this article.

L'âge de début des symptômes et le type de présentation clinique de la maladie cæliaque ont souvent été reliés it l'âge de l'introduction du gluten dans l'alimentation. Il a aussi été montré que l'allaitement maternel retarde le début de la maladie.

Patients et méthodes. - Dans cette étude rétrospective portant sur 169 cas de maladie cæliaque, nous analysons la contribution respective de ces deux paramètres dans la détermination de l'âge de début des symptômes.

Résultats. - Dans notre population, la durée moyenne de l'allaitement maternel a été de 9,6 mois (± 8,9) et l'âge moyen à l'introduction du gluten de 5,6 mois (± 3,2). L'âge moyen de début de la maladie était de 15 mois (± 8,7) et le dé1ai moyen séparant l'introduction du gluten et le début de 9,5 mois (± 7,8). Les deux variables gluten et allaitement maternel étaient fortement corrélées à l'âge de début (r = 0,47 et 0,40, respectivement). Seule la variable allaitement maternel était corrélée à la variable dé1ai (r = 0,33). L'analyse de régression multiple montre que ces deux variables influençaient de manière indépendante l'âge de début, avec des coefficients de régression de 0,90 ± 0,2 et 0,26 ± 0,07. En revanche, seule la variable allaitement maternel influençait la variable délai, avec un coefficient de régression de 0,26 ± 0,07.

Discussion. - Notre étude confirme l'effet indépendant de I'allaitement matemel dans la detérmination de l'âge de début. L'allaitement maternel joue un rôle protecteur indirect en retardant l'introduction du gluten et un rôle protecteur direct en augmentant le délai entre l'introduction du gluten et le début de la maladie cæliaque.

Conclusion. - Un allaitement maternel prolongé, au moins jusqu'à la fin du 6^e mois, et l'introduction retardée du gluten, au moins à partir du 5^e mois, retardent de manière significative le début de la maladie. L'introduction du gluten doit être progressive et sous protection de l'allaitement maternel. L'introduction du gluten 2 mois avant le sevrage retarde de manière significative l'âge de debut de la maladie.

Background. - Age at onset and clinical presentation of celiac disease have often been related to the age of gluten introduction into the diet. It has also been shown that breast feeding delays the onset of the disease.

Patients and methods. - This retrospective study attempts to evaluate the respective contributions of these two parameters in the determination of the age at onset of the symptoms in celiac Tunisian children.

Results. - One-hundred-sixty-nine children were studied. Mean duration of breast feeding in our population was 9.6 ± 8.9 months and mean age of gluten introduction was 5.6 ± 3.2 months. The mean age at onset of the disease was 15 ± 8.7 months and mean latency time between gluten introduction and onset of the disease was 9.5 ± 7.8 months. Both variables, duration of breast feeding and age at gluten introduction were strongly correlated to the age at onset of the disease (r = 0.47 and 0.40, respectively). Only breast feeding was correlated to the variable latency time (r = 0.33). Stepwise multiple regression analysis showed that the two variables independently influenced the age at onset with coefficients of regression of 0.90 ± 0.20 and 0.26 ± 0.07, respectively. Only breast feeding influenced the latency time with a coefficient of regression equal to 0.26 ± 0.07.

Discussion. - Our study confirms the independent effect of breast feeding in the determination of the age at onset of the disease. Breast feeding has two effects: an indirect effect, by delaying the introduction of gluten, and a direct effect, by increasing the latency time between gluten introduction and onset of the disease.

Conclusion. - Prolonged breast feeding, at least until the 6th month, and gluten introduction started at least at the 5th month of life, significantly delay the onset of the disease. Gluten introduction should be done progressively and under breast feeding protection. Introduction of gluten 2 months before weaning has a protective effect.

Gliadin-protein interaction and its relationship to the pathogenesis hypotheses of celiac disease was investigated. Wheat germ agglutinin was not immunodetected in gliadin preparations. Peptic-tryptic gliadin digest was used to study the gliadin-protein interactions by crossed immunoelectrophoresis and affinity blotting. Biotinylated gliadin digest interacted with IgG and bovine serum albumin but not with several glycoproteins. Since albumin and IgG light chains are not glycosylated, this interaction is not lectin-like, neither completely immunological because of recognition of the IgG Fc fraction. Immobilized and boiled IgG was not recognized by gliadin digest as a lectin. Gliadin digest fractions from T-gel chromatography reduced the fluorescence intensity of cis-parinaric acid bound to albumin. The gliadin-protein interaction is not lectin-like or completely immunological but hydrophobic. Hydrophobicity of gliadins may contribute to the pathogenic events that result in celiac disease.