Cardiovascular disease (CVD) causes 12.4 million deaths annually, most (9.6 million) occurring in developing countries. Hypertension, the most common CVD, arises within the context of obesity, but the underlying mechanisms remain obscure. Obesity and salt intake are two important risk factors for hypertension and are the focus of this paper. Traditional African populations show a low prevalence of hypertension, but hypertension is more common in migrant African populations in the West than in other ethnic groups. One explanation is genetic, but no causative gene has been confidently identified. Nongenetic susceptibilities such as fetal programming are an alternative explanation. Hypothetically, fetal programming induced by transient stimuli permanently alters fetal structure and function at the cellular, organ and whole-body levels. Birth weight is inversely related to blood pressure and hypertension risk, suggesting that susceptibility to hypertension risk factors such as obesity and salt sensitivity are themselves programmed. In support of this hypothesis, obesity (especially central obesity) is also inversely related to size at birth. Likewise, salt sensitivity might derive from undernutrition in utero, reducing the nephron number and resetting the pressure-natriuresis curve rightward. However, no robust human data or evidence of enhanced salt sensitivity among African-origin populations exist. In the United States, blacks have a greater prevalence of low birth weight than whites, suggesting that the higher prevalence of hypertension among blacks is related to fetal programming. Nevertheless, we need to be scrupulous in ascribing risk to the myriad other confounders of this relationship, including environmental and behavioral correlates of ethnicity, before concluding that excess risk of hypertension in Africans is programmed in utero.