Infant feeding patterns

Whether breastfeeding protects from or early introduction of supplementary foods causes type 1 diabetes, remains unsolved, although these aspects of the diet have received more research attention than many other areas in the etiology of type 1 diabetes (Virtanen & Knip 2003). Findings from prospective studies with enough statistical power are awaited.

Putative protecting effects of breastfeeding could be due to protection against infections provided by breast milk through, for example, secretory IgA antibodies and enhancement of the infant's own immune responses, increased beta-cell proliferation (Juto 1985), or delayed exposure to foreign food antigens. Breast milk contains cytokines and growth factors, which affect the maturation of the gut-associated lymphoid tissue (GALT) (Srivastava et al. 1996).

An early introduction of cow's milk-based infant formulas and other cow's milk products may increase the risk of type 1 diabetes according to case-control evidence, although the results remain inconclusive (Virtanen et al. 1991; Virtanen & Knip 2003). An early introduction of cow's milk or a short exclusive breastfeeding were not related to early stages of beta-cell autoimmunity in birth cohort studies of individuals with increased genetic risk of type 1 diabetes (Norris et al. 1996; Couper et al. 1999; Hummel et al. 2000; Kimpimaki et al. 2001; Norris et al. 2003; Ziegler et al. 2003), but inversely to the development of four type 1 diabetes-associated autoantibodies out of the four studied (Kimpimaki et al. 2001). The findings from a pilot study of the only randomised trial available suggest that beta-cell autoimmunity can be prevented or delayed by giving hydrolysed infant formula instead of regular cow's milk-based one (Akerblom et al. 1999).

Several theories try to explain the putative diabetogenicity of cow's milk (Knip & Akerblom 1998). Early immunisation to bovine insulin may be related to the development of beta-cell autoimmunity (Vaarala et al. 1999). Abnormal tolerance development has been observed in those infants who develop early signs of beta-cell autoimmunity (Vaarala et al. 1999). The putative diabetes-promoting effects of dietary antigens may be mediated through GALT. Food proteins may induce beta-cell autoimmunity also because of changes in gut permeability due to microbial infections. Greater weight gain related to greater intake of energy has been observed in infant formula-fed compared with breastfed infants from 3 months of age (Heinig et al. 1993). By increasing insulin demand, increased weight gain caused by supplementary feeding could be a contributory factor in the development of diabetes. An early exposure to cow's milk and rapid growth in infancy were both independent risk factors of childhood type 1 diabetes in one case-control series (Hyppanen et al. 1999).

Recently, it was suggested that exposure to gluten-containing cereals and rice at the age of 4 to 6 months would protect from development of early beta-cell autoimmunity compared to earlier or later exposure (Norris et al. 2003). German birth cohort findings related early gluten exposure to development of early beta-cell autoimmunity (Ziegler et al. 2003).

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