The genetic contribution to disease pathogenesis in childhood diabetes is greatest in the very young.

Abstract

Epidemiological data are presented to support the hypothesis that the genetic contribution to disease pathogenesis in childhood onset diabetes is greatest in those presenting at a very early age. Analysis of family data from two national surveys of childhood onset Type 1 (insulin-dependent) diabetes (1988 in under 15s: 1992 in under 5s) reveals that children developing diabetes between the ages 1 and 2 years are significantly more likely to have a parental history of Type 1 diabetes than older children. It is proposed that compared with other children, those with very early onset diabetes have either a greater genetic and smaller environmental contribution to the initiation of the autoimmune process leading to Type 1 diabetes: or inherited HLA alleles associated with a more fulminant autoimmune mediated Beta-cell destruction once the process is initiated.