Increasing evidence that enteroviruses are "linked to" (not "cause of") type 1 diabetes

Children with type 1 diabetes are nearly 10 times as likely to have a particular viral infection than children without diabetes. This news is based on a high-quality review of the findings of 26 studies that assessed how common an enterovirus infection is among people with and without type 1 diabetes. The enterovirus group of viruses includes polio and coxsackie viruses, which are believed to be the viruses most likely linked to type 1 diabetes. The review findings indicate a clear relationship, with the odds of having an enterovirus infection in people with type 1 diabetes almost 10 times greater than in unaffected individuals. However, as the researchers importantly note, the review cannot prove that the virus causes diabetes as the studies cannot confirm that infection occurred before the onset of diabetes. This research supports previous studies that have identified enteroviruses as being linked to type 1 diabetes. There is now a need to assess the relationship between the virus and diabetes over time to determine whether there really is a cause-and-effect relationship between the two.
Source: NHS Choices

Original paper:
Enterovirus infection and type 1 diabetes mellitus: systematic review and meta-analysis of observational molecular studies. BMJ 2011; 2011; 342:d35

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One Response to Increasing evidence that enteroviruses are "linked to" (not "cause of") type 1 diabetes

  1. Dr Rick Bennett says:

    Yes this association is not novel observation. Many pathogens are linked to the onset of disease in the near or long term. The notion of microbial cause and effect is simplistic and narrow. These kind of pathogen host interactions are a systems question and will not be resolved by linear analysis and thinking. The days of simple microbe host interactions as Koch postulated were mostly identified long ago. The kinds of diseases that confront us today will require the construction of a complex system to include microbial genetics, host genetics and epigenetics and host specific immune responses and timing. Even this model is simplistic and when applied to a large population the variances will be so great that clear multi variant associations will be only slowly revealed. Nonetheless we need to start the modeling ASAP. Yet who is funding this kind of work.?

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