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For many years, researchers have suspected that bacteria, viruses and other micro-organisms play an important role in the development of autoimmune conditions such as type 1 diabetes. This “hygiene hypothesis” postulates that our decreasing exposure to a lower amount of bugs and germs may leave some people more susceptible to autoimmune attacks.

A team of researchers from Yale University in the US have leant further support to this hypothesis by demonstrating that a certain strain of research mice were far more likely to develop type 1 diabetes when raised in a special germ-free environment as opposed to normal laboratory conditions.

It appears that the mice in the germ-free environment were more susceptible because they had not been exposed to a type of harmless bacteria that lives in the human intestine and commonly found on non-sterile services. Previous research into other disorders has shown there to be interactions between intestinal microbes and the immune system and this research suggests that these interactions may be behind why some people develop type 1 diabetes and others do not.

Whilst the US research suggests that exposure to germs is good for us, JDRF-funded researchers in the UK have revealed a very different result. A recent discovery by scientists based in Brighton has found a definitive link between the incidence of type 1 diabetes and infection with common tummy bugs known as enteroviruses.

Researchers examined the pancreas tissue of people who had passed away not long after being diagnosed with type 1 diabetes and compared it with non-diabetic pancreata. They found that the beta cells found in more than half of the diabetic pancreases were infected with enteroviruses. Conversely, enteroviral infection was rare in the non-diabetic pancreas.

In most people, infection by an enterovirus results in symptoms similar to the common cold or gastric upset. This research suggests that it may also be playing a role in the autoimmune process whereby the immune system labels beta cells as ‘foreign’, resulting in type 1 diabetes.

Both these exciting research breakthroughs have given us a significantly greater understanding of what can trigger the onset of type 1 diabetes and may possibly lead to the development of a therapy or vaccine to prevent the condition.

Nature 455(7216):1109-13
Diabetologia 52(6):1143-51

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  1. My son has had Type 1 diabetes from the age of 3. I am neither pro or against the Hygiene hypothesis.

    Further there is the classical "narrow" hygiene hypothesis which states exposure needs to be in the early years of human development and a more general "broader" hygiene hypothesis, which states exposure may be protective at an time and may need to be ongoing.

    However, evidence that any particular bacteria may cause or promote the onset of a disease (type 1 diabetes in this case) is NOT evidence against either the "broad" or "narrow" hygiene hypothesis. I agree that both research cited seem interesting and important, but stating that the JDRF funded research disproves the hygiene hypothesis is misleading, if not an outright lie.

    As anyone who studied high school science should be able to tell, you can not prove a hypothesis or theory, you can only disprove it. Therefor it is important that research that does not actually disprove a hypothesis not be stated as doing so, because once a hypothesis is disproved it needs to be recast in the light of the new information. The more research fails to disprove a hypothesis the more we learn. Both pieces of research, as framed by this article, actually fail to disprove the hypothesis.

    If there is anything in the research that does actually disprove the hygiene hypothesis, this article does not lead one to it.