News from ADA 2019

Please let me share some news from the ADA in San Francisco where Lars Krogvold and myself are enjoying a lot of good science and exciting news in diabetes, networking and social interaction with international and national colleagues.


We learned on Friday from the D2D study that vitamin D 4000 U/d did not prevent the development of type 2 diabetes in 2600 subjects with prediabetes. The results are important and support the prevention study previously published from Tromsoe, and also our own study published in Diabetes Care in 2017 where we could not detect any effect of vitamin D to patients with type 2 diabetes and low levels of vitamin D at baseline on insulin secretion or insulin resistance.


On Saturday, Sturan F. Grant from Children’s hospital, Philadelphia gave a talk on TCF7L2 - A genetic window into the course and management of type 1 and type 2 diabetes. It is well known that a genetic polymorphism in the TCF7L2 is the strongest genetic risk markers for Type 2 diabetes, and it has been confirmed in a number of population from all around the world. However, it is less clear in Asian population, because the allele frequency for the most important variant rs 7903146 is much lower there. Research has also showed that this polymorphism is also associated to response to lifestyle intervention in the DPP study, to the response to SU treatment and to the risk for diabetes in patients with cystic fibrosis.


On Sunday, the findings from the large REWIND study were presented. This is the 5th major cardiovascular outcome study reporting the effects of GLP-1 receptor agonists. In this study, 9901 participants from 24 countries were randomized to dulaglutide once weekly or placebo for a median of 5.4 years. Patients had a mean age of 66 years, 46% were women, mean BMI was 32 and HbA1c was 7.3&. The primary outcome was 3p MACE, and the hazard ratio was 0.88 (p=0.026) for patients in the dulaglutide group compared to the control group. Total mortality was not significantly reduced (HR 0.90), but a renal composite endpoint was (HR 0.85, p=0,0004). The results are published in the Lancet.

Kåre I. Birkeland