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(Hypertension. 1998;32:817-819.)
© 1998 American Heart Association, Inc.

Statement of Opinion

Is There a Racial Predisposition to Hypertension?

Christopher J. O'Donnell; ; William B. Kannel

From the National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham (C.J.O'D., W.B.K.); the Department of Preventive Medicine, Boston Medical Center, Boston University School of Medicine (W.B.K.); the Cardiology Division, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston (C.J.O'D.), Mass.

Correspondence to William B. Kannel, Framingham Heart Study, 5 Thurber St, Framingham, MA 01702. E-mail esta@fram.nhlbi.nih.gov

Key Words: hypertension, essential • race • genetics

Cooper and Kaufman call attention to the difficulty of evaluating racial predisposition to disease.¹ They correctly point out that "racial" predisposition to pathology is usually taken to imply the existence of an inborn genetic flaw and that there are inherent weaknesses in efforts to date to infer genetic effects from observed phenotypes. It is indeed hazardous, and very likely erroneous, to draw etiologic inferences from observational investigation of racial differences in the prevalence of hypertension. This difficulty results in part because the "exposure," ie, race or ethnicity, is an inherent trait that is extremely difficult to measure or even define and in part because the outcome, hypertension, is a complex phenotype. Furthermore, observational studies only provide clues to pathogenesis (implying "guilt by association") and not definitive evidence. Observational epidemiology has never claimed to provide definitive information on the "cause" of disease, using instead the term "risk factor" to describe the observed relationship. However, arguments regarding the existence or absence of racial or ethnic differences must also consider the large body of human genetic research in rarer Mendelian forms of diseases, some of which have been described as being largely restricted to single racial or ethnic populations. It also seems fair to note that if it were not for the data suggesting a familial aggregation of hypertension, as well as a "racial" vulnerability to development and sequelae of hypertension, there would be little enthusiasm for testing these hypotheses by the more definitive currently available molecular genetic techniques.

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