Type 1 diabetes—not all in the genes

Abstract The incidence of autoimmune diseases is appreciable and increasing. Type 1 diabetes is one such disease, and is, in part, determined genetically, involving many genes (up to 40 at the last count), but they alone cannot account for the frequency of the disease, indicating that non‐genetic factors are important [Leslie et al., 2004; Weets et al., 2002]. The character of such non‐genetic factors is important to understand since the prevention or modulation of such factors provides a more likely source of a cure for type 1 diabetes. Non‐genetic factors play a major role in causing type 1 diabetes as shown by studies of twins, populations that have migrated, and populations with changing disease incidence [Hermann et al., 2003; Weets et al., 2002]. Disproportionate maternal influences on disease‐risk suggest that critical disease‐inducing environmental events operate very early in life, even in utero [Leslie et al., 2004]. Firm evidence for a role of viral infections in the etiology of type 1 diabetes comes from a recent demonstration that four rare variants of interferon‐producing genes are each associated with a 50% reduction in type 1 diabetes risk [Nejentsev et al., 2009]. Early infant diet affects type 1 diabetes development, while exposure to westernized heat‐processed food could be relevant given the close relationship between disease incidence and the gross national product of European countries [Leslie et al., 2004]. Epigenetic regulation could mediate environmental influences and is a candidate for that elusive “missing heritability” in the pathogenesis of autoimmune diabetes, e.g. in peripheral blood monocyte activation [Beyan et al., 2010]. In summary, epidemiological evidence favors the induction of childhood‐onset type 1 diabetes by an environmental event, possibly a virus or a dietary factor, or both, operating over a finite period in early childhood. J. Med. Virol. 83:1670–1670, 2011. © 2011 Wiley‐Liss, Inc.