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GeneLifeCard SIGNED

Genetic and lifestyle regulators of cardiometabolic risk in individuals gaining weight

Total Cost €


EC-Contrib. €






Project "GeneLifeCard" data sheet

The following table provides information about the project.


Organization address
address: NORREGADE 10
postcode: 1165

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Denmark [DK]
 Total cost 207˙312 €
 EC max contribution 207˙312 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2020
 Duration (year-month-day) from 2020-09-01   to  2022-08-31


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KOBENHAVNS UNIVERSITET DK (KOBENHAVN) coordinator 207˙312.00


 Project objective

The current obesity pandemic is a major threat to public health systems worldwide. The majority of obesity-related health care costs are due to cardiometabolic impairments such as insulin resistance, dyslipidemia, and hypertension, which increase the risk of type 2 diabetes and cardiovascular disease. However, many obese individuals seem resistant to cardiometabolic complications, the “metabolically healthy obese (MHO)”, while some normal weight individuals suffer from comorbidities similar to the obese. Genetic mechanisms may partly explain this paradox. Recent genome-wide studies have identified multiple genetic loci associated with increased overall body fat and subcutaneous fat deposition but lower cardiometabolic risk. Vice versa, the fat-decreasing alleles at these loci are associated with higher cardiometabolic risk. Some lifestyle factors, such as higher physical activity and smoking, are associated with lower body fat but show directionally opposite effects on cardiometabolic risk. At present, it remains unclear whether genetic predisposition to higher subcutaneous fat storage or healthy lifestyle behaviors may uncouple long-term weight gain from cardiometabolic risk during adulthood. Thus, the primary aim of the present project is to examine whether genetic and lifestyle factors abolish the impact of long-term weight gain on cardiometabolic risk by meta-analyses of five prospective cohorts with repeated measures of body weight and cardiometabolic traits. I will also examine whether these factors predict a MHO status in middle-age and the maintenance of such status over time. My results will provide new biological insights and may enable targeted lifestyle interventions against obesity-related cardiometabolic impairments. Moreover, the project will greatly advance my career by allowing me to learn highly valuable research skills in the area of genetic epidemiology, complementing my previous expertise in the field of cardiovascular epidemiology.

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