TrendsCow's milk and type I diabetes: the gut immune system deserves attention
Section snippets
Epidemiological aspects
Since 1984, 23 case control studies on breast-feeding, diet and type 1 diabetes have been performed, a sizeable proportion of which did not link early exposure to cow's milk constituents with type 1 diabetes but rejected this hypothesis8. An unresolved problem with these studies is that breast-feeding and dietary data based on a mother's recall responses many years later might be unreliable and even biased by the knowledge that a child later developed diabetes (J. Norris, Denver, CO). These
Candidate diabetogens in cow's milk
Cow's milk contains (in decreasing quantities) α-casein, β-casein, β-lactoglobulin, γ-casein, α-lactalbumin, gammaglobulin, albumin and many hormonal constituents such as insulin, macrophage colony-stimulating factor (M-CSF) or transforming growth factor β (TGF-β). Interestingly, in some studies, patients with recent-onset type 1 diabetes showed a higher degree of humoral and cellular immune responses against milk components than controls (usually not HLA matched). When considering the
A wider perspective and the role of gut mucosa
A comprehensive review of the data led to the conclusion that there is no unique property of cow's milk with regard to the pathogenesis of type 1 diabetes. First, cow's milk-containing diets have been associated with other ‘autoimmune’ diseases in man such as multiple sclerosis12, and have been shown to induce mild rheumatoid arthritis in rabbits13. Further, because the MHC associations of the three diseases are different, it is highly unlikely that the same mimicry epitope of milk proteins is
Conclusions
Animal models provide compelling evidence of a dietary control of autoimmune diabetes, whereas a similar role in man is yet to be determined. It appears that there is nothing unique about cow's milk but that many different sources of complex proteins might be diabetogenic, as judged from animal and some epidemiological studies. Critical factors are probably the immunoregulatory state of the gut and whether encounter of dietary antigens leads to an oral tolerance response or to sensitization and
Acknowledgements
We thank all participants of the symposium for their contribution and apologize for not being able to acknowledge all of the significant contributions to the discussion. We are grateful to all speakers at the symposium, to S. Flohé and N. Schloot for reading the manuscript, and to M. Ganz of Roche Diagnostics for organizing the symposium.
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The Symposium ‘Cow's Milk and Diabetes’ was held at Barcelona, Spain, on 7 September 1998.