Can we slow the rising incidence of childhood-onset autoimmune diabetes? The overload hypothesis.
Overload of the beta cell, mediated by a variety of mechanisms, may sensitise it to immune damage and apoptosis, and thus accelerate ongoing autoimmune processes leading to its destruction. Environmental risk determinants that may exert such overload effects include insulin resistance due to excess fat cell accumulation, and increased insulin requirement due to a high growth rate, physical stress (infection, inflammation) or psychological stress. The increasing incidence of childhood diabetes, and the shift to younger age at onset, is unlikely to be driven by environmental risk factors that have been associated with initiation of autoimmunity, e.g. virus infections or early infant feeding. Risk factors that may accelerate beta cell destruction have shown a steady increase in the population, and are more plausible causes of such a pattern of change. Child growth, weight and birthweight are well-established estimates of community wealth and increase in most countries of Europe. Overfeeding of children early in life leads to both accelerated growth and weight, and even a moderate excess of child growth, not necessarily associated with obesity, is associated with risk of type 1 diabetes. New, safe and effective immune-modulating drugs for possible arrest of the autoimmune process may become available in time, but in the interim these accelerating factors may be targeted. Public health programmes for pregnant mothers and young families, aiming at changing overfeeding and the sedentary lifestyle of the children would be preferable to other alternatives. Interventions such as these would be safe and could potentially influence future risks of type 1 and type 2 diabetes and other major threats to adult health.
Dahlquist
G
G
Department of Clinical Sciences, Paediatrics, Umea University Hospital, S-90185 Umea, Sweden. gisela.dahlquist@pediatri.umu.se
D017668:Age of Onset; D002648:Child; D003922:Diabetes Mellitus, Type 1 / Q000196:embryology / Q000453:epidemiology*; D006801:Humans; D015994:Incidence; D008954:Models, Biological; D011236:Prediabetic State / Q000453:epidemiology