Healthcare Professional Resources

The Environmental Determinants of Islet Autoimmunity (ENDIA) study is Australia’s only pregnancy and birth cohort study looking at the causes of Type 1 Diabetes. Type 1 Diabetes has doubled in incidence in childhood in Australia over the last 20 years. The highest increase in Type 1 Diabetes has been observed in younger children with lower risk genes. This may be explained by our modern pro-inflammatory environment, which has changed over the past two decades.

The unifying hypothesis is that gene-environmental interactions occurring during prenatal and/or postnatal development drive beta-cell destruction and cause islet autoimmunity in children at risk of Type 1 Diabetes.

The specific hypotheses are:

  • The maternal microbiome during pregnancy and lactation differs in composition, diversity and functional products between mothers whose offspring do and do not develop islet autoimmunity and type 1 diabetes.
  • The microbiome differs in composition, diversity and functional products in children who do and do not develop islet autoimmunity and type 1 diabetes during the first 3 years of life.
  • Accelerated weight gain during pregnancy, and accelerated weight gain and insulin resistance during the first 3 years of life, is associated with an increased risk of islet autoimmunity.
  • Innate and adaptive immune function will differ in children who do and do not develop islet autoimmunity and type 1 diabetes during the first 3 years of life.
  • Viral infection during pregnancy and first 3 years of life modified the risk of islet autoimmunity and type 1 diabetes.
  • The expression of genes, proteins and metabolites will differ in children who do and do not develop islet autoimmunity and type 1 diabetes during the first 3 years of life.
  • A system biology approach will reveal a inter-relationships between relevant environmental factors, demonstrating that the microbiome, metabolome and epigenome are condition by prenatal and postnatal environmental exposures including type 1 diabetes, nutrition, weight gain, physical activity and viral infection during pregnancy; and mode of delivery, accelerated weight gain, nutrition, immune function, early fever, antibiotic use and viral infection during early life.

Defining the environmental influences and specific gene-environment interactions that initiate and/or promote destruction of the insulin producing cells in early life could lead to a means of primary prevention before the autoimmune process leading to Type 1 Diabetes begins. Moreover, identifying specific microorganisms and their functional products that alter risk for Type 1 Diabetes will not only define pathogenesis but will allow development of specific biomarkers and provide a potential way of targeting specific therapy.

We aim to study 1400 children (Australia-wide) who have a first degree relative with Type 1 Diabetes to determine interactions between genes and the environment and how they affect the risk of Type 1 Diabetes. Follow up will be during the pregnancy and at 3 monthly intervals until the child is 24 months, then 6 monthly thereafter. The primary outcome measure is persistent islet autoimmunity.

Patients that meet the following criteria may be eligible for ENDIA:

  • Pregnant women with Type 1 Diabetes
  • Women that are pregnant to man with Type 1 Diabetes
  • Pregnant women with an existing child that has Type 1 Diabetes who will be a sibling of the expectant baby
  • Babies less than 6 months of age that have a parent or sibling with Type 1 Diabetes

If you would like more information about the ENDIA study please use the Contact form or email endia@adelaide.edu.au directly and ask for a Resources Pack consisting of study brochures and posters for display in your practice. If helpful, we can arrange for a member of our research team to visit your practice and discuss ENDIA with you.