A substantial proportion of obese individuals does not present cardiometabolic complications such as diabetes, hypertension, or dyslipidemia. Some, but not all, prospective studies observe similar risk of cardiovascular events and all-cause mortality among individuals with this so-called “metabolically healthy obese” (MHO) phenotype, compared to the metabolically healthy normal weight or metabolically healthy non-obese phenotypes. Compared to the metabolically unhealthy obese (MUO) phenotype, MHO is often characterized by a more favourable inflammatory profile, less visceral fat, less infiltration of macrophages into adipose tissue, and smaller adipocyte cell size. Tipping the inflammation balance in adipose tissue might be particularly important for metabolic health in the obese. While the potential role of genetic predisposition or lifestyle factors such as diet in the MHO phenotype is yet to be clarified, it is well known that diet affects inflammation profile and contributes to the functionality of adipose tissue. This review will discuss genetic predisposition and the molecular mechanisms underlying the potential effect of food on the development of the metabolic phenotype characteristic of obesity.This article is protected by copyright. All rights reserved