Over the past 20 years, the incidence of type-2 diabetes in the western world has increased dramatically, a pattern that parallels closely the rising incidence of obesity and (by implication) that of insulin resistance . Furthermore, age at presentation has been falling, such that the incidence of type-2 diabetes in American adolescents has increased 10-fold and in Japanese school children 36-fold within a generation . Rather strikingly,
the same pattern of increasing incidence and younger age at presentation has occurred for type-1 diabetes over the same time period.
Several studies in Europe show a doubling in incidence of type-1 diabetes over the last generation, with a clear shift of presentation to younger age groups [39, 40] although the data are largely restricted to children and adolescents. The incidence of type-1 diabetes has been highest around puberty in all populations studied [41, 42]. The earlier peak in girls is consistent with their earlier maturation . The association between type-1 diabetes and puberty has never been satisfactorily explained, but may once again be an expression of insulin resistance. The hormonal changes of puberty (particularly the rise in growth hormone) place demands on insulin production that already damaged islets may be unable to meet. Again, BMI rises rapidly during puberty, and with it insulin resistance  (fig. 2).
If this latter were the correct explanation, the accelerator hypothesis would predict a correspondingly earlier presentation of diabetes as the BMI previously associated with puberty is reached at a progressively younger age. Tuomilehto et al.  have reported how, over recent years, the age-at-onset curve for diabetes has risen to include most of early childhood, all but losing its peripubertal peak. Others have shown independently that weight gain early in childhood is associated with a higher risk of early type-1 diabetes [46, 47] and the same appears to be true for type-2 . Most recently, the Childhood Diabetes in Finland Study Group has reported that a relative o tr>
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