The Rise of Childhood Type 1 Diabetes

When did the increase begin?
A steep rise in the incidence of childhood diabetes occurred in many populations over the latter part of the 20th century.


The rise in childhood diabetes can be traced back to the middle of the 20th century. Although it is important not to overinterpret limited data, there is some suggestion that a rising incidence first became apparent in countries with the highest current rates of diabetes and reached lower incidence populations in a later, staggered mattered.

It is crucial to identify long-term changes in the behavior of diabetes as an evolving disease rather than try to explain why they occurred. Some implications of this analysis do however deserve brief consideration. To begin with, a rising incidence in a stable population implies an etiological role for environmental factors. Since there is also good evidence for a long silent gap between initial exposure and onset of disease, factors modulating the rate at which the disease process unfolds may also be relevant.

Genetic susceptibility will determine the probability of an unwanted outcome to the initial exposure, but additional environmental factors, possibly interacting with other genetic influences, may well modulate the rate of progression.

Many attempts have been made to explain the rise of childhood type 1 diabetes over the past 30 years. A common starting point has been the assumption that something new has entered the childhood environment, and early nutrition or infection have seemed the most promising areas of enquiry. The leading hypotheses have related to early exposure to cow’s milk or to enterovirus infection. Despite a wealth of indirect evidence, we still lack proof that either plays a major role in causation of the disease, and it has been plausibly argued that both exert their influence via modulation of the developing mucosal immune system. Breast-feeding patterns do not reflect changes in the incidence of childhood diabetes.

The alternative possibility is that protective factors have been lost from the childhood environment. The hygiene hypothesis, initially developed to explain the parallel rise of asthma and allergy, argues that exposure to a range of infective agents in early childhood is necessary for successful maturation of the neonatal immune repertoire.

Type 2 diabetes has appeared earlier in successive generations and now presents in teenagers. Although this trend mimics genetic anticipation, it is environmentally mediated, since increasing obesity within the population as a whole means that genetically susceptible individuals develop the disease earlier than they would in a less permissive environment. Has a comparable process, possibly with quite unrelated causes, occurred in type 1 diabetes?

In conclusion, the quest to understand type 1 diabetes has largely been driven by the mechanistic approach, which has tried to characterize the disease in terms of defining molecular abnormalities. Given the complexity and diversity of biological systems, it seems increasingly likely that the mechanistic approach will need to be supplemented by a more ecological concept of balanced competition between complex biological processes, a dynamic interaction with more than one possible outcome.