Poor early nutrition has varying effects on subsequent cardiometabolic disease (CMD) rates. Fetal and neonatal periods are critical for the development and growth of the systems involved in CMD. The increased rates of hypertension, metabolic syndrome, diabetes mellitus type 2, renal failure and heart failure observed nowadays in Latin America could be the result of the discrepancy between the nutritional environment during fetal and early life and the adult environment. This discrepancy causes a mismatch between the fetal programming of the subject and its adult circumstances created by the imposition of new life styles. The two largest international studies on cardiovascular risk factors for a first myocardial infarction (INTERHEART) and stroke (INTERSTROKE) demonstrated that in Latin America the factor with the highest attributable population risk was abdominal obesity. The conflict between the earlier programming and the later presence of abdominal obesity produced a higher sensitivity of this population to develop a state of low-degree inflammation, insulin resistance and the epidemic of CMD to lower levels of abdominal adiposity. The relative roles played by genetic and environmental factors and the interaction between the two are the still subjects of great debate. We have reviewed the relationship between maternal malnutrition, early growth restriction, epigenetic adaptations, and the later occurrence of abdominal obesity and CMD in Latin America.