Mar. 19, 2013 Countries with lower mortality from infectious disease exhibit higher rates of type 1 diabetes, according to a new study by Dr. A. Abela and Professor S. Fava of the University of Malta. The findings, collating data from three major international studies and presented at the Society for Endocrinology annual conference in Harrogate UK, suggest that the as yet unexplained global rise in type 1 diabetes may be linked to reduced exposure to pathogens in early life.
Type 1 diabetes is caused when the immune system destroys the cells of the pancreas that release insulin, leaving the patient unable to control his own blood sugar. It is estimated to affect around half a million children worldwide, increasing in incidence by an estimated 3% every year. This increase is well documented and is linked to the developed world, but is so far unexplained -- various theories put forward include the 'hygiene hypothesis', which suggests that encounters between the developing immune system and micro-organisms such as bacteria and parasites are part of human evolution and may therefore protect against the development of auto-immunity.
The researchers investigated whether markers of infectious disease burden could be linked to the local incidence of type 1 diabetes. They used data from the World Health Organisation (WHO) DiaMond Project, WHO global burden of disease: 2004 update, and the Alexander Project, to correlate type 1 diabetes incidence by country with mortality from infectious disease and bacterial antibiotic susceptibility (which indicates antibiotic use and thus exposure to bacterial infection).
Type 1 diabetes rates were highest in countries with low mortality from infectious disease. This was true for total mortality from infectious disease (r=-0.35, p=0.008), as well as deaths caused specifically by diarrhea, respiratory disease, tuberculosis, and infections and parasitic disease (all p<0.05). They also found type 1 diabetes rates are significantly associated with the local susceptibility of the bacteria Streptococcus pneumoniae to all antibiotics studied.
This study suggests that there may be an association between type 1 diabetes rates and infectious disease burden. It is possible that the increasing global incidence of type 1 diabetes may be linked to lack of exposure to pathogens during early life. Whilst the data provide support for the hygiene hypothesis they do not prove it: the rise in type 1 diabetes rates is a complex problem and this study is of association only. Other potential contributing factors may show a similar geographical variation to infectious disease burden, as this is linked to the developed world. The authors are keen to use further studies to identify other environmental factors which may predispose to type 1 diabetes.
Study leader Professor Stephen Fava, Consultant in Diabetes and Endocrinology at Mater Dei Hospital, Malta & Associate Professor of Medicine at the University of Malta, said:
"The global rise in type 1 diabetes is an unexplained phenomenon. Many suggest that the exposure, or rather the lack of exposure, to infectious disease when young might be linked to the development of autoimmunity.
"Our data show that type 1 diabetes rates were highest in countries where markers of exposure to infectious disease were lowest. Incidence of type 1 diabetes was significantly linked to mortality from a variety of infectious diseases and to the local susceptibility of a common bacterium to antibiotics.
"These data provide support for the notion that the immune system can somehow become disordered and attack the body's own cells if it is not trained by regular exposure to micro-organisms -- the so called hygiene hypothesis. More research is needed to try to identify other environmental factors that may be linked to the continuing conundrum of rising type 1 diabetes rates."
Other social bookmarking and sharing tools:
- Alexia-Giovanna Abela, Stephen Fava. Association of the incidence of type 1 diabetes with markers of infection and antibiotic susceptibility at country level. Endocrine Abstracts, 2013; : 1 DOI: 10.1530/endoabs.31.P223
Note: If no author is given, the source is cited instead.