Editorial Commentary
Why Do Black Americans Have Higher Prevalence
of Hypertension?
An Enigma Still Unsolved
Flávio D. Fuchs
See related article, pp 383–389
S tudies 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 demon-
strates 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, protect-
ing them from fatal salt-depletive diseases during the stormy
Atlantic passage, such as diarrhea and vomiting.5 This con-
dition would induce hypertension when they and their de-
scendants 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 Ameri-
cans. Kao et al6 and Kopp et al7 reported an association
between a genetic variation of the MYH9 region on chromo-
some 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
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 ffuchs@hcpa.ufrgs.br
(Hypertension. 2011;57:379-380.)
© 2011 American Heart Association, Inc.
Hypertension is available at http://hyper.ahajournals.org
DOI: 10.1161/HYPERTENSIONAHA.110.163196
379
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 re-
mains unknown, particularly with regard to differences in the
renal handling of sodium between normotensive black sub-
jects 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
380 Hypertension March 2011
blacks (1.88 [95% CI: 1.53 to 2.32]) compared with non-
Hispanic whites, despite adjustment for a large number of
potential confounders, including race/ethnicity, age, sex,
education, insurance status, financial status, general health
status, functional status, body mass index, diabetes mellitus,
smoking status, physical activity, and sodium, fiber, alcohol,
and total daily calorie intake. The rate of blood pressure
control was similar in non-Hispanic whites and in Mexican
Americans. In an analysis restricted to individuals with
hypertension, the authors included adherence to medications
to the full model, and the degree of control remained poorer
for non-Hispanic blacks (odds ratio: 1.49 [95% CI: 1.12 to
1.98]) in comparison with non-Hispanic whites. Redmond et
al11 rightly concluded that racial/ethnic disparities in blood
pressure control were not explained by differences in health
behaviors that they identified within the data collected by the
NHANES. Nonetheless, measurement bias of some health
behaviors cannot be fully discarded.
Nutritional aspects, in particular, seem to be more impor-
tant, because in the NHANES 2003–2006, nutrients were
identified by just one 24-hour dietary recall. At least the
record of 3 days or the use of validated food-frequency
questionnaires are nowadays recommended to better establish
individual dietary patterns. A lower adherence to a Dietary
Approaches to Stop Hypertension–like pattern of diet by
black Americans, a diet that has been associated with lower
prevalence of hypertension,12 may have been missed by the
1-day questionnaire. The authors were not able to investigate
the frequency of consumption of dairy products, and they
used fiber content as a proxy for ingestion of fruits and
vegetables.
The evaluation of adherence to treatment is another poten-
tial source of bias. Hypertensives classified as nonadherent
were those who answered “yes” to the question, “Because of
your high blood pressure/hypertension, have you ever been
told to take prescribed medicine?” and “no” to the question,
“Are you now taking prescribed medicine?” Evaluation of
adherence to treatment has been a complex issue, and an
unknown proportion of participants may have been misclas-
sified by the criteria used in this analysis. Other potential
biases, such as occupational-related physical activity, expo-
sure to psychosocial stressors, discrimination, socioeconomic
position in early life, social networks, and other unknown
confounders, which may vary by ethnic background, were not
investigated in the NHANES.
And where are we going now? Redmond et al11 recom-
mend that future research should further assess the relation-
ships of gene-environment interactions, job-related stress,
racism, and other psychosocial factors to racial/ethnic dispar-
ities in the prevalence of hypertension. In other words, they
are saying what has been repeatedly stated by articles on the
subject, that the enigma over the reasons for the higher
prevalence and lower rate of control of hypertension among
black Americans still remains to be deciphered.
Sources of Funding
This study was supported, in part, by the National Institute of
Science and Technology for Health Technology Assessment–Na-
tional Council for Scientific and Technological Development/Brazil.
Disclosures
None.
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