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Blacks have higher BP on average than whites. Why? One popular explanation is the Slavery Hypertension Hypothesis (SHH). The SHH is a hypothesis which posits 2 things: (1) that those living in the African climate were subject to limited water and salt, and dehydration so, a higher sodium-retention mechanism evolved in those populations to retain salt, which also leads to hypertension; and (2) during the Middle Passage there were high amounts of vomiting, diarrhea, heat, and little salt and so surviving slaves were “selected for” salt conserving water and salt. Then, when they reached the plantations, due to low water, copious sweating, and intense work, there were additional selective pressures which “selected for” water and salt conservation.
This hypothesis is so popular, that it was even pushed by Oprah, when Dr. Mehmet Oz asked Oprah why blacks have higher BP than whites. Lujan and DiCarlo (2018) write:
During a May 2007 Oprah show, Dr. Mehmet Oz asked Oprah, “Do you know why African-Americans have high blood pressure?” Oprah promptly replied that Africans who survived the slave trade’s Middle Passage “were those who could hold more salt in their bodies.” To which Dr. Oz exclaimed, “That’s perfect!” (64, 71). According to Dr. Oz and Oprah, African-Americans today are afflicted by hypertension at higher rate than whites because of genes passed on by their ancestors, genes that favored salt retention and that, in turn, cause high blood pressure (Fig. 1) (71). [They are implying that genetic ancestry is associated with BP; see below.]
Lujan and DiCarlo (2018) state that when individuals were “salt-loaded”, normal salt-resistant individuals retained just as much sodium in their bodies as salt-sensitive individuals. Salt-resistant individuals retain as much salt as salt-sensitive individuals—but they did not develop hypertension.
Furthermore, available evidence suggests that the difference in salt-sensitivity between African-Americans and Caucasians (European-Americans) is significantly smaller than what the Slavery Hypertension Hypothesis suggests. In fact, Chrysant and colleagues (14) were unable to find differences in the blood pressure response to salt by race, age, sex, or body weight. Thus salt sensitivity is not a racial problem, but rather a human problem, and the generalization that blacks are salt sensitive and whites are not should be discarded (14). It is important to note that measurements of salt retention in humans have come into serious question (50).
The hypothesis, as explained above, explains the data it purports to explain and only the data it purports to explain and is, therefore, a just-so story. Using the definition from Sterelny and Griffiths (1999: 61), a just-so story is “an adaptive scenario, a hypothesis about what a trait’s selective history might have been and hence what its function may be.”
So, the just-so story goes, that Africans in Africa—and those who survived the Middle Passage—had genes which favored better salt retention, and so, they were “selected for” which lead to an increased chance of survival in the low-salt, low-water, high-heat environment. The hypothesis is clearly ad hoc – notice that African-descended people have higher rates of blood pressure and then work backward. What in their recent or past history, could have lead to these high rates of hypertension in today’s societies.
This method is the usual EP reverse engineering method—strongly criticized by philosophers of science Robert Richardson (2007) and David Buller (2005)—which is “the inference from function to cause” (Richardson, 2007: 51). The just-so storytellers then work backward from a data point and “reason” how the trait became fixated in a particular population. So the formulators of the SHH wanted to infer function from cause—what the function of higher African BP was.
So the just-so story in question was formulated, which leads to genetic essentialist and determinist views—that genes are “causing” and were “selected for”—to explain the data they wanted to explain. But it makes no testable predictions, so it’s a just-so story. The hypothesis is inherently ad hoc—the “justification” for the hypothesis was reasoned backward from a fact we know today—that blacks have higher BP—and the “speculation” was provided as if it were true—which has permeated into the media, as can be seen above.
There are more sensible explanations for differences in hypertension between blacks and whites (I use those terms since they are socialraces). Genetic determinists would always go to the genes as an explanation for differences in any trait X. However, there is no reason to posit genetic differences between population groups as evidence for the differences in the causes of the trait in question. There are more sensible explanations for the BP disparity between blacks and whites.
Williams (1992) cites social factors as much more important than genetic factors in the etiology of hypertension – stress, social support, coping patterns, health behavior, sodium, calcium, and potassium consumption, alcohol consumption, and obesity. Citing these environmental factors that raise BP is critical—the human body’s physiology is adaptive and so, it can adapt to differing environments based on the reactions of the individual in that environment. This, of course, holds for nutrition as well. Nutrition most definitely affects BP – nutrition also affects rates of obesity (obviously). Blacks are more likely to be lower SES. Since blacks are more likely to be lower SES, they have higher rates of obesity which lead to higher rates of BP, too.
But one of the most important factors here is education. If people don’t know something, then they won’t do it. If they are taught ways to reduce symptom X, there is a higher chance of them reducing symptom X because they are better-armed with the knowledge against it. Knowing that all of these different environmental factors influence BP, then this points to a main culprit: education. Non, Gravlee, and Mulligan (2012) argue that it’s not ancestry that explains hypertension, but differences in education.
Non, Gravlee, and Mulligan (2012) analyzed both environmental and genetic factors which lead to hypertension. Thy found that in the black sample, systolic BP and mean arterial pressure (MAP) were higher among those who had a HS diploma or lower, but found no differences by education in the white sample.
So black men were predicted to have a higher SBP, then white men, black women and finally white women, across all levels of education. SBP declined most sharply in black men and women compared to white men and women.
Genetic ancestry was not associated with BP among black Americans, but there was a significant association between education and BP. Education is, of course, not too good a measure of the social environment. Even using this measure, significant reductions in BP were found. Genetic ancestry is supposed to be associated BP in virtue of the ancestral environment of black Americans, along with supposed selection pressures which occurred on the Middle Passage. So if genetic ancestry isn’t associated, then the hypothesis is discarded.
Non, Gravlee, and Mulligan’s (2012) results support the “minority poverty hypothesis” because “the worst blood pressures were predicted for people who faced the double burden of being less educated and identifying as African American.” The minority poverty hypothesis is “The idea is that black people who live in poverty are uniquely disadvantaged in attaining good health because of the combination of poverty and race” (Hall, Humphreys, and Ruseski, 2015: 5).
Because genetic ancestry was estimated from only 294 loci, and a large set of populations across Africa, which may not be best for representing the West African ancestry of black Americans (Note how this is the population in question in the theory we are discussing). So an analysis focusing just on West African populations may change the relationship. Education was their only measure of the social environment, but other measures of the social environment, like “residential segregation, psychosocial stress, and everyday discrimination” may fully account for higher levels of BP in black Americans. Of course, further there needs to be further study to see whether it is the education per se that causes the differences in BP or if education serves only as a marker for other aspects of the social environment.
The evidence that education accounts for a lot of the variation in differences in BP between blacks and whites is strong. If it is other aspects of the social environment, and not education per se, then there is something in that environment that does not elicit the physiological response that leads to higher BP. We can also, of course, liken this to the Mazur’s (2016) honor culture hypothesis—the hypothesis “that young men’s participation in the honor culture of poor black neighborhoods has the effect of elevating T.” This is due to the adaptiveness of our physiological systems and how it adapts to the environment based on environmental cues.
There was one recent study where they found that “Among black male barbershop patrons with uncontrolled hypertension, health promotion by barbers resulted in larger blood-pressure reduction when coupled with medication management in barbershops by specialty-trained pharmacists” (Victor et al, 2018). This, of course, makes sense. If one is made aware of anything wrong with them, then they will be more likely to seek help for their ailments.
Victor et al (2018) write:
Because black men with hypertension often have multiple cardiovascular risk factors,37 marked reductions in blood pressure — if sustained with the use of our approach and then initiated more widely — might reduce the high rates of hypertension-related disability and death among black men with hypertension in the United States.11
Since three out of four black men have high blood pressure by the time they are 55, then if this can and does hold for the long-term, then this would help many individuals.
Seventy-eight barber shops enrolled in the program. The n was 319 men who had a SBP of 140 mm or higher from 52 black-owned barber shops. The intervention increased doctor visits and anti-hypertensive medications (which I disagree with). Pharmacists were placed in the shop and checked the BP of black men who entered (barbers were also trained to measure BP). Reductions of 21.6 and 14.9 SBP and DBP respectively were seen. 63 percent of those who participated achieved a normal BP whereas 12 percent of those in the control group did so. This, clearly, is another way in which education can lower BP in this population.
This is a great idea—and if further study confirms that this works, it should begin to be implemented elsewhere. The most important factor is outreach—getting the information to people and teaching them how to reduce it on their own through lifestyle modifications. And since outreach is related to educating people on a certain topic, then this, too, falls under the—somewhat large—umbrella of “education.”
In sum, the SHH is a just-so story and doesn’t explain why blacks have higher rates of BP than whites. Genetic ancestry seems to not explain hypertension rates between blacks and whites. Social environment changes and outreach can lower BP disparities between populations. If one understands the intricacies of physiology, then they would understand the physiological responses to different environmental/social stimuli.