INTERPLAY · Interplay between genetic determinants of glycaemia, type 2 diabetes and cardiovascular disease in interaction with dietary and lifestyle factors

Interplay between genetic determinants of glycaemia, type 2 diabetes and cardiovascular disease in interaction with dietary and lifestyle factors

Type 2 diabetes is a global public health crisis comprising a major, growing cause of morbidity and premature death. Efforts to prevent worldwide diabetes and its disabling and life-threatening complications, such as coronary artery diseases are now at the forefront of global public health concerns. The disease is a consequence of obesogenic lifestyles, acting upon the backdrop of genetic predisposition, and the scaling number of individuals affected by diabetes over the past few decades is more likely linked to rapid lifestyle transition rather than inherited changes. However, adverse lifestyles do not always cause diabetes, and healthy lifestyles are not ubiquitously protective. Why people develop diabetes? Why individuals with diabetes experience different clinical complications? What is the role of glycaemia on and related complications? Can we use data generated during the last decade to better understand diabetes and to ultimately better prevent, treat, or cure the disease? Our research proposal took advantage of genetic data to gain insights into the complex physiological relationship between blood glucose and the risk of coronary artery disease. We provided evidence that increased glucose is a causal factor leading to increased risk of cardiovascular disease, and that this increased risk is independent from the risk conferred by other processes that are also present in the context of diabetes. These findings support the notion that close monitoring of glycemia, especially among individuals at increased genetic risk, might be a beneficial intervention to reduce cardiovascular events. Results from our research program represent now the most comprehensive evidence on the interplay between genetic and lifestyle factors in diabetes. We showed that both genetic predisposition and dietary quality were each associated with the development of type 2 diabetes, and that a lifestyle intervention improves cardiometabolic risk factors regardless of genetic risk. These results indicate that genetic risk alone does not seem to explain variable response to diabetes preventive interventions. Notwithstanding, the important public health message these findings convey: future studies, integrating genetics and other biological markers such as epigenomics, metabolomics, and metagenomics, are likely to be necessary to facilitate the integration of genomics information into clinical and public health practice. The time to conduct such integrative studies has come, and Dr. Merino is well positioned to work on complementary multi-omics studies given his gained expertise.

Data: CORDIS, © European Union