, Volume 50, Issue 8, pp 1571-1575
Date: 20 Jun 2007

To boldly go—or to go too boldly? The accelerator hypothesis revisited

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There’s many a beautiful hypothesis slain by an ugly fact

T. H. Huxley

Biological science notoriously leads us into a world of increasing complexity, and concepts that purport to rearrange familiar observations into a new and simpler pattern therefore merit careful consideration. Such is the accelerator hypothesis, proposed by Terry Wilkin [1]. In this issue of Diabetologia, Wilkin provides a brief review of his hypothesis, and explores some of its implications for the classification of diabetes [2].

The accelerator hypothesis proposes that the conditions we call types 1 and 2 diabetes are for practical purposes one and the same. Whilst conceding that the aetiology of beta cell damage may differ, the hypothesis postulates that superimposed insulin resistance then drives both forms of diabetes down the same pathway to end-stage beta cell failure. The difference between the two types of diabetes lies in their rate of progression, which is determined by three accelerators. First comes consti