Type 1 Diabetes

A common blood pressure drug is showing new promise to help treat and cure type 1 diabetes.

Overall prevalence of diabetes may have increased, but undiagnosed diabetes may be declining.

Research finds differences in type 1 diabetes in children versus teens.

New study shows recent improvement in years of life lost.

In industrialized countries, 20–40% of T1DM patients younger than 20 years present with diabetic ketoacidosis. After adjusting for age, gender, ethnicity, diabetes type, and family history of diabetes, diabetic ketoacidosis at diagnosis was associated with lower family income, less desirable health insurance coverage, and lower parental education. Younger children present with more severe symptoms at diagnosis, because children younger than 7 years old have lost on average 80% of the islets, compared to 60% in those 7–14 years old and 40% in those older than 14 years.

Twin and family studies indicate that genetic factors alone cannot explain the etiology of T1DM. Seasonality, increasing incidence and epidemics of T1DM as well as numerous ecological, cross-sectional and retrospective studies suggest a critical role of environmental factors, such as infections with certain viruses (especially enteric infections in early life) and effects of early childhood diet. Natural history studies that follow children at increased risk of T1DM provide the best opportunity to study environmental triggers.

In part 2 of this exclusive interview, Dr. Aaron Vinik shares an update on INGAP research.

The first large-scale studies of the prediction of T1DM relied upon the detection of cytoplasmic islet cell autoantibodies (ICA) assays based on indirect immunofluorescence. High titer cytoplasmic ICA is most often associated with the presence of multiple islet autoantibodies and therefore a high risk of progression to diabetes.

Type 1A diabetes results from a chronic autoimmune destruction of the pancreatic beta cells, probably initiated by exposure of a genetically susceptible individual to some environmental agent(s). This preclinical period is marked by the presence of autoantibodies to pancreatic beta-cell antigens such as insulin, GAD65 (Glutamic Acid Decarboxylase), ICA512 (called also IA-2) or ZnT8 (Zinc Transporter 8), and precedes the onset of hyperglycemia by a few years.

β-cell centric classification of diabetes puts focus on single common denominator of all types.