There I was, hooked up to a heart monitor as the doctor zeroed in with needle in hand. It wasn’t a big deal. I was about to be anesthetized for a routine if mildly unpleasant colonoscopy. I wouldn’t even have been consciously aware of being stressed but for the monitor’s tinny, insistent allegrissimo: Clear as a bell, my heart began to race as the needle neared, despite my rational mind.
It was fascinating how completely my subtlest anxiety was reflected in my heart rate. It lasted no longer than a few seconds; the prick was minor, yet my body registered a little internal yelp. I remarked upon it because I had been reviewing statistics showing that African-Americans suffer from chronic hypertension at five to seven times the rate of Americans deemed white. While high blood pressure is not necessarily associated with emotional distress, distress can certainly increase blood pressure.
I do not mean to imply that my little moment of trepidation represented any significant measure of arterial tension. Surely it didn’t rise to the average stress level of getting my seventh grader to finish his homework. Nothing about the situation ranked near the way my temples throb whenever Michael Jackson and O.J. Simpson are compressed into the same sentence.
This line of contemplation began when reading Stephen Dubner’s profile of Harvard economist Roland Fryer in the March 20 New York Times Magazine. Dubner wrote glowingly of “Fryer’s notion that there might be a genetic predisposition at work…heightened when he came across a period illustration that seemed to show a slave trader in Africa licking the face of a prospective slave…. A person with a higher capacity for salt retention might also retain more water and thus increase his chance of surviving. So it might have been that a slave trader would try to select, with a lick to the cheek, the ‘saltier’ Africans…. Africans who did manage to survive the voyage–and who then formed the gene pool of modern African Americans–may have been disproportionately marked by hypertension.”
I do not have room to detail all the ways this is wrong. But for a lucid refutation, see Jay Kaufman’s “The Anatomy of a Medical Myth” at raceandgenomics.ssrc.org/Kaufman/pf; and see “Epidemiology and Society: A Forum on Epidemiology and Global Health,” in Volume 14, No. 1 of the journal Epidemiology, January 2003. The theory Fryer describes, known as “the Slavery Hypothesis,” has been circulating since the early 1980s. It has been consistently refuted. One can start with the obvious–that, as Kaufman puts it, the logic is “exactly backwards, as the ‘saltier’ Africans would be exactly the ones who were not retaining sodium, and therefore…the least able to endure the voyage.” Nor are there data showing a genetic marker for sodium retention. Assuming there were one, it would be misleading to call it, as much of the literature does, a “slavery gene” instead of a “hypertension gene,” according to Robert Pollack, professor of biology at Columbia University. Nor has such a hypothesis accounted for why no populations of West Africans display endemic propensities for hypertension; or why Finns have rates of hypertension comparable to African-Americans; nor has there been any study of whether slave-descended Americans who are light-skinned enough to have “passed” into the white population manifest the same rates of hypertension as their darker-skinned kin.