Why do black Americans have higher prevalence of hypertension?: an enigma still unsolved.

Studies have consistently reported a higher prevalence of hypertension in blacks than in whites, a main reason for the higher incidence of cardiovascular disease in blacks.1 The long list of putative causes for this higher prevalence suggests that the real reasons are still unknown. Biological differences in the mechanisms of blood pressure control or in the environment and habits of whites and blacks are among the potential causes. The higher prevalence of hypertension in blacks living in the United States instead of Africa2 demonstrates that environmental and behavioral characteristics are the more likely reasons for the higher prevalence in blacks living in the United States. They could act directly or by triggering mechanisms of blood pressure increase that are dormant in blacks living in Africa. Kaplan and Victor3 listed 18 genotypes and intermediate phenotypes that were implicated with an increase of blood pressure in blacks. A higher sensitivity to alcohol could be added to that list.4 Some of these mechanisms, such as a higher renal retention of sodium by blacks, are attractive. The “slavery hypertension hypothesis” states that the higher prevalence of hypertension among blacks could have resulted from an enhanced ability to conserve salt by slaves, protecting them from fatal salt-depletive diseases during the stormy Atlantic passage, such as diarrhea and vomiting.5 This condition would induce hypertension when they and their descendants consumed the much higher sodium content in American compared with African foods. This hypothesis is hard to confirm or refute. The association between genetic traits and renal outcomes has been reported in black Americans versus white Americans. Kao et al6 and Kopp et al7 reported an association between a genetic variation of the MYH9 region on chromosome 22 with focal segmental glomerulosclerosis, a condition previously attributed to “hypertensive nephrosclerosis” and found much more frequently in black patients with end-stage renal disease than in whites with end-stage renal disease. The attributable risk for carriage of this MYH9 haplotype was found in 74% of blacks and in only 4% of whites with focal segmental glomerulosclerosis. More recently, using much more complete genomic sequences, Tzur et al8 reported missense mutations in the APOL1 gene, which neighbors the MYH9 gene on chromosome 22 in patients with focal segmental glomerulosclerosis. These genetic defects may account for the higher propensity of blacks to develop end-stage renal disease, which may then induce hypertension, rather than hypertension being responsible for the renal damage. Nonetheless, the possible role of these or other genetic defects in the large majority of blacks without focal segmental glomerulosclerosis or end-stage renal disease remains unknown, particularly with regard to differences in the renal handling of sodium between normotensive black subjects living in Africa and the United States. Differences in exposure to the environment and habits between blacks and whites have also been proposed to explain their differential prevalence of hypertension. Many potential reasons have been reported, such as socioeconomic status, dietary habits, social network, stress, and health behaviors. Among the consequences of differential dietary habits, excess adiposity emerges as a natural candidate to explain the higher prevalence of hypertension in blacks, who have a 51% greater prevalence of obesity than whites.9 Nonetheless, excess of adiposity does not fully account for the higher prevalence of hypertension in blacks. Based on data of National Health and Nutrition Examination Survey (NHANES) III, Okosun et al10 demonstrated that the population-attributable fraction of hypertension attributed to abdominal obesity was 24.9% in black men and 15.9% in black women. The risk of black ethnicity for hypertension persisted after adjustment for abdominal obesity and other confounders: the odds ratios in black men were 1.80 (95% CI: 1.54 to 2.11) and in black women 2.70 (95% CI: 2.07 to 3.28). There is no conclusive evidence that other nutritional factors could explain the higher prevalence of hypertension in blacks. In this issue of Hypertension, Redmond et al11 present the results of an analysis of the data from the NHANES 2001– 2006 survey, a nationally representative cohort of US adults, aiming to identify health behaviors that could explain the high prevalence and lower rate of hypertension control among black people. They found that the rate of blood pressure control was worse among non-Hispanic blacks (27.4% with uncontrolled blood pressure) compared with non-Hispanic whites (17.0%) and Mexican Americans (20.2% with uncontrolled blood pressure). Odds ratios for poorly controlled blood pressure were higher in non-Hispanic The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association. From the Division of Cardiology, Hospital de Clínicas de Porto Alegre, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil. Correspondence to Flávio D. Fuchs, Serviço de Cardiologia, Sala 2061, Hospital de Clínicas de Porto Alegre, Ramiro Barcelos, 2350, 90.035-903, Porto Alegre, RS, Brazil. E-mail [email protected] (Hypertension. 2011;57:379-380.) © 2011 American Heart Association, Inc.