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Screening for type 1 diabetes genetic risk in newborns of continental Italy. Primary prevention (Prevefin Italy)--preliminary data.

Introduction Type 1 diabetes mellitus (T1DM) is one of themost serious and frequent chronic diseases in childrenwith incidence rates increasing in many parts of theworld (1-3).The young age of the patients, the need for long-term insulin therapy and the high prevalence of com-plications account for the great social impact ofT1DM. For these reasons, the discovery of new stra-tegies to prevent T1DM would affect public healthdeeply (4).It is proposed that T1DM is precipitated by envi-ronmental factors, operating in a genetically suscepti-ble host to initiate a destructive islet β-cell specific au-toimmune process (5). In fact T1DM is caused by au-toimmune destruction of the β-cells of the pancreas.Numerous T1DM susceptibility loci have been identi-fied on the entire genome, but the greatest geneticcontribution is provided by the polymorphism of theHLA class II genes (DRB1, DQA1 and DQB1) (6).In the prodromic phase of the islet autoimmuneprocess there are increased blood levels of autoantibo-dies against islet cell antigens, such as insulin (IAA),glutamic acid decarboxylase (GADA) and protein ty-rosine-phosphatase (IA-2A) (5). These autoantibo-dies do not play a direct role in the destruction ofβ-cells, but they can be considered as a marker of theautoimmune response against pancr eatic islets. Recentstudies show a 20% prevalence of anti-β-cell autoan-tibodies in high-risk subjects at 24 months of age (7).The autoimmune process against islet cells causesa gradual impairment of β-cell function, which canoccur at different times in different subjects.The finaloutcome is the decline of insulin secretion, which canbe demonstrated by metabolic tests (8).The reasons why only some genetic susceptibleindividuals proceed to diabetes have not been comple-tely explained. Several theories have been proposed toexplain the way utilized by some factors in activatingautoimmunity against β-cells (5). A great number ofenvironmental factors have been investigated as thepossible triggers of autoimmune response against β-cells: 1) viral infections (e.g. Coxsackievirus andCMV); 2) early infant diet (e.g. breastfeeding versusearly introduction of cow milk components); 3) toxins(n-nitroso derivatives) and 4) vitamin D deficiency.Early intake of cow milk proteins – above all β-casein – has been reported as a risk factor for T1DMin high genetic risk subjects.Although cow milk β-ca-sein molecular str ucture is diff erent from human β-ca-sein, its sequence is homologue to some pancreas β-cell autoantigens. Furthermore, a cell-mediated im-mune response against β-casein has been demonstra-ted in most patients with recent onset T1DM (9, 10).Vitamin D deficiency seems to play a crucial rolein the development of β-cell autoimmunity,as vitaminD acts as an immunosuppressive agent, by reducing