Yet another study reaffirms direct link between depression and type 2 diabetes development

A causal positive association from depression to type 2 diabetes, with evidence of mediation by BMI was found in a recent study published in Diabetes Care Journal, a peer-reviewed medical journal by the American Diabetes Association. The researchers also performed a multi-phenotype GWAS (MP-GWAS) of the two diseases, highlighting seven shared loci that target nearby genes in several target tissues.

Type 2 diabetes is a disease characterized by chronic hyperglycemia, while depression is its frequent comorbidity, potentially because of shared risk factors. It has been shown that depression, even at subclinical levels, increases the risk of incident type 2 diabetes by 25–60% . whereas others have shown that type 2 diabetes increases the risk of depression by 40–60%.

Depression is a common comorbidity of type 2 diabetes. The team assessed the causal relationships and shared genetics between them.

To identify shared genetics, the study authors performed; 1) genome-wide association studies (GWAS) separately and 2) multiphenotype GWAS (MP-GWAS) of type 2 diabetes (19,344 case subjects, 463,641 control subjects) and depression using major depressive disorder (MDD) and self-reported depressive symptoms in the UK Biobank. They analyzed expression quantitative trait locus (eQTL) data from public databases to identify target genes in relevant tissues.

The results highlighted the importance to prevent type 2 diabetes at the onset of depressive symptoms and the need to maintain a healthy weight in the context of its effect on depression and type 2 diabetes comorbidity.

Reference: Jared G. Maina, Zhanna Balkhiyarova, Arie Nouwen, Igor Pupko, Anna Ulrich, Mathilde Boissel, Amélie Bonnefond, Philippe Froguel, Amna Khamis, Inga Prokopenko, Marika Kaakinen; Bidirectional Mendelian Randomization and Multiphenotype GWAS Show Causality and Shared Pathophysiology Between Depression and Type 2 Diabetes. Diabetes Care 1 September 2023; 46 (9): 1707–1714. (https://doi.org/10.2337/dc22-2373)