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Cow's milk and immune-mediated diabetes
1German Diabetes Research Institute at the University of Düsseldorf, Auf'm Hennekamp 65, 40225 Düsseldorf, Germany.
Insights
Early cow's milk formula exposure is debated for type 1 diabetes risk. While some studies suggest a link, others show no association, indicating complex factors influence autoimmune disease development.
Area of Science:
- Immunology
- Endocrinology
- Gastroenterology
Background:
- Cow's milk-based infant formulas have been hypothesized to increase the risk of type 1 diabetes mellitus (T1DM) and other immune-mediated diseases.
- Epidemiological studies and animal models suggest cow's milk proteins might be diabetogenic, but evidence remains inconclusive.
- The gut-associated immune system and oral tolerance mechanisms are increasingly recognized as crucial in autoimmune disease development.
Purpose of the Study:
- To critically evaluate the association between early cow's milk exposure and the development of type 1 diabetes mellitus.
- To explore the role of cow's milk proteins and other dietary factors in modulating autoimmune responses and oral tolerance.
Main Methods:
- Review of epidemiological studies in humans examining early infant feeding practices and T1DM risk.
- Analysis of animal models investigating the diabetogenic potential of cow's milk proteins compared to other dietary proteins.
- Examination of evidence regarding the gut-associated immune system, oral tolerance, and influencing factors like breast milk, microbiota, and infections.
Main Results:
- Conflicting evidence exists regarding the association between early cow's milk formula exposure and T1DM risk; some studies show no link.
- In animal models, cow's milk proteins demonstrate modest diabetogenic effects, with wheat or soy proteins inducing higher rates of autoimmune diabetes.
- Disturbed oral tolerance, influenced by factors like breast milk, gut microbiota, and infections, is implicated in autoimmune disease pathogenesis.
Conclusions:
- The role of cow's milk proteins in T1DM development is complex and not definitively established.
- Cow's milk proteins may contribute to autoimmunity through epitope mimicry or by disrupting oral tolerance via bioactive peptides.
- Dietary regulation of autoimmunity extends beyond cow's milk to other dietary proteins, highlighting the intricate interplay between diet and immune health.
Abstract:
Cow's milk-based infant formulas and cow's milk consumption in childhood have been suggested to promote the development of type 1 diabetes mellitus and other immune-mediated or neurological diseases. Epidemiological studies in man have led to the hypothesis that introduction of cow's milk-based infant formula within the first 3 months of life is associated with increased risk of type 1 diabetes mellitus. Furthermore, in animal models of type 1 diabetes mellitus, cow's milk proteins have been proven to be 'diabetogenic'. However, the issue seems far from being resolved. Several epidemiological studies and, more importantly, the first prospective trials did not show an association between early exposure to cow's milk and type 1 diabetes mellitus. In animal models, cow's milk proteins are modestly and variably diabetogenic, wheat or soybean proteins in the diet cause higher rates of autoimmune diabetes. In both man and rodents there is increasing evidence that the gut-associated immune system plays a major role in disease development, probably because of disturbed oral tolerance mechanisms. Oral tolerance depends on immunological homeostasis and normal maturation of the gut. These factors are influenced by growth factors and cytokines from breast milk, normal bacterial colonization, infections and diet. All these factors have been proposed as risk factors for type 1 diabetes mellitus. Hence, cow's milk proteins may provide mimicry epitopes relevant in autoimmunity, as well as destabilizing oral tolerance mechanisms by biologically active peptides. The concept of dietary regulation of autoimmunity does not apply only to cow's milk protein, but also to other dietary proteins.