1Grupo Vilano, Fundación Cardiovascular de Colombia, Floridablanca, Colombia; 2Facultad de Medicina Universidad de Santander (UDES), Bucaramanga, Colombia; and 3Grupo de Investigación en Cirugía Pediatría, Fundación Cardiovascular de Colombia, Floridablanca, Colombia.
Disclosure: The authors have no conflicts of interest.
*Address for correspondence: Calle 155a #23-58, 3 Piso, Research Institute, Fundación Cardiovascular de Colombia, Floridablanca, Colombia. E-mail: firstname.lastname@example.org.
The prevalence of cardiovascular diseases (CVD) and diabetes mellitus type 2 (DM 2) is decreasing in developed countries despite the increase in the percentage of subjects with obesity and other well-recognized cardiovascular risk factors. In contrast, the recent transition of the economic model experienced by developing countries, characterized by the adoption of a Western lifestyle, that we have named “socioeconomic pathology,” has led to an increase in the burden of CVD. It has been demonstrated that conventional cardiovascular risk factors in developed and developing countries are the same. Why then does the population of developing countries currently have a higher incidence of CVD than that of developed countries if they share the same risk factors? We have proposed the existence of a higher susceptibility to the development of systemic inflammation at low levels of abdominal obesity in the population of developing countries and the consequent endothelial dysfunction, insulin resistance, DM 2, and CVD. In contrast, an important percentage of obese people living in developed countries have a healthy phenotype and low risk of developing CVD and DM 2. Human epidemiologic studies and experimental dietary interventions in animal models have provided considerable evidence to suggest that nutritional imbalance and metabolic disturbances early in life may later have a persistent effect on an adult's health that may even be transmitted to the next generations. Epigenetic changes dependent on nutrition could be key in this evolutionary health behavior, acting as a buffering system, permitting the adaptation to environmental conditions by silencing or increasing the expression of certain genes.