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Just-So Stories: The Slavery Hypertension Hypothesis

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1800 words

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!” (6471). 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.

sbp

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.

sbp2

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.

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34 Comments

  1. King meLo says:

    “But it makes no testable predictions”

    How does it not make testable predictions?

    Like

    • RaceRealist says:

      What testable predictions does it make? The story infers function (high BP in blacks) from cause – the cause being the SHH. I’ve shown how the story is false.

      But enlighten me, Melo. What testable predictions does it make? Hell, even the rationale behind the hypothesis is false, as I’ve shown.

      Like

  2. King meLo says:

    “The story infers function (high BP in blacks) from cause – the cause being the SHH.”

    How does that not generate any predictions?

    “But enlighten me, Melo. What testable predictions does it make?

    Well convergent evolution would always be a possible novel prediction. The body is holistic so it would be hard to believ other echnisms would not be affected by this adaptation. I’m not into physiology so I don’t know. Ancient genomic data could be used to determine the frequency at which particular mutations are passed on. There are also methods we can use to deduce what the OEE was when Negroids diverged. I don’t think there is much disagreement that a lot of Africans lived in hot climates.

    “Hell, even the rationale behind the hypothesis is false, as I’ve shown.”

    I never said i agree with the hypothesis.

    Do you think these adaptionist hypotheses are just- so stories?:

    https://www.pnas.org/content/early/2018/12/26/1809046116?collection=#sec-7

    https://journals.plos.org/ploscompbiol/article?id=10.1371/journal.pcbi.1006504#pcbi-1006504-g007

    These aren’t adaptionist theories but tell me what you think of these two? Have you read them?:

    http://www.rgwinther.com/Publications/WintherRG2009PredictionSelectionistEvolTheory.pdf

    https://academic.oup.com/mbe/article/34/8/1863/3804550

    Like

    • RaceRealist says:

      How does that not generate any predictions?

      Because the story was inferred from a fact we know—it explains the data it purports to and it doesn’t make any testable predictions. What testable predictions does it make?

      How are those testable predictions? Well I am into physiology, and I do know.

      All adaptationist hypotheses are just-so stories if they cannot be independently verified.

      The first one is solid. Human physiology is adaptive—that’s not under contention here. What’s under contention are adaptationist hypotheses, and the fact that physiology is adaptive doesn’t make adaptationist hypotheses scientific.

      The brain can be selected but positing what it was “selected for” is a just-so story.

      Methodological adaptationism rests on the flawed assumption that trait X is an adaptation, which the flawed reverse engineering method is then used to reconstruct what a trait “evolved for” (its just-so story). Empirical adaptationism is taken care of by Gould and Lewontin’s Spandrels of San Marco paper. Nevermind the fact that selectionist theory takes NS to be a mechanism—which is false.

      Sarkar’s argument against genomic adaptationism:

      P1 The physical properties of DNA and its cellular environment lead to increased genome size and its baroque structure.
      P2 Genome size is negatively correlated with population size.
      P3 Selection acts against larger genomes.
      P4 Small population sizes prevent the elimination of features selected against unless selection is very strong.
      C Genomes increase in size, diversity, and so on and persist even though selection acts against these features.

      Adaptionism is too flawed to save. It’s been rebutted by numerous authors – just-so stories (selectionist hypotheses) are not science

      Like

    • King meLo says:

      “How are those testable predictions?”

      Well ancient genomics has a long way to go but we can identify selection in the genome as my final source exhibits. Fossils and other ancient deposits give clues as to what the ecosystem was like which allows further insight onto the casual factors of selection. Convergent evolution is always a possible novel prediction as long as the organisms in question are not closely related.

      https://www.giss.nasa.gov/research/briefs/schmidt_01/

      “All adaptationist hypotheses are just-so stories if they cannot be independently verified.”

      The first 3 sources I provide all make risky predictions. They can be independently verified.

      “The first one is solid.”

      The first study? So you do agree that there are scientific adaptionist hypotheses. If this is true we don’t really disagree.

      “What’s under contention are adaptationist hypotheses, and the fact that physiology is adaptive doesn’t make adaptationist hypotheses scientific.”

      Not all Adaptionist hypotheses are equally rigorous in their epistemic and methodological standards. Since independent verification can “save” an Ad hoc(new) hypothesis, you need to explain why all Adaptionist hypotheses cannot be independently verified.

      “The brain can be selected but positing what it was “selected for” is a just-so story.”

      The brain is a general purpose mechanism, it is more than likely a pre-adapted exaptation. The cultural brain hypothesis posits selection for generality.

      “Methodological adaptationism rests on the flawed assumption that trait X is an adaptation,”

      No. It isn’t an assumption if you first test the hypothesis that trait x was a result of positive or negative selection and not genetic drift.

      “which the flawed reverse engineering method is then used to reconstruct what a trait “evolved for” ”

      What is flawed about extrapolating cause from function if selection has already been identified as occurring or have occurred? This would imply it’s function is a direct result of the cause(exogenous factors).

      “Empirical adaptationism is taken care of by Gould and Lewontin’s Spandrels of San Marco paper. ”

      I’m not sure how you think spandrels refute natural selection.

      “Nevermind the fact that selectionist theory takes NS to be a mechanism—which is false.”

      I’m not sure how you think NS has to be a mechanism. I don’t think it is. The mechanisms of selection and the subsequent variation are other organisms and Environmental fluctuations.

      “P1 The physical properties of DNA and its cellular environment lead to increased genome size and its baroque structure.
      P2 Genome size is negatively correlated with population size.
      P3 Selection acts against larger genomes.
      P4 Small population sizes prevent the elimination of features selected against unless selection is very strong.
      C Genomes increase in size, diversity, and so on and persist even though selection acts against these feat”

      P2 is not always true. Also I’d check out my final source as it more or less refutes Neutral theory.

      “Adaptionism is too flawed to save.”

      Adaptionism isn’t a thing. What are you even talking about?

      Like

  3. King meLo says:

    That doesn’t answer the question.

    Ad hoc hypotheses have not made predictions. That doesn’t mean they can’t.

    Like

  4. King meLo says:

    Why do you keep deleting your replies?

    Like

  5. King meLo says:

    You bum me out dude. Grow some nuts. I’m not an unreasonable person

    Like

  6. Racialist says:

    thats bullhshit and you know it. you and that other moron smith, your leftist buddy. all one has to do is read the comments on your posts

    Like

  7. rural african negroes have lower bp than whites.

    what about rural african whites?

    answer: the white farmers of africa have higher bp.

    black american bp is caused by eating shit and low vitamin d and then stress.

    poor white trash has high bp too…

    but in the fraud that is the US, class is not a thing…

    except that it is required of all who have or would have high rank in the US…

    to hate poor people.

    it’s bullshit.

    SYSTOLIC BP IS AS HERITABLE AS IQ IN THE TWIN STUDIES, YET…

    NO ONE NEEDS TO HAVE A RESTING SYSTOLIC BP ABOVE 110.

    JUST LIKE NO ONE NEEDS TO BE FAT.

    THERE ARE NO GOOD REASONS TO SUPPOSE THAT TEST SCORES ARE UN-LIKE BP, ADIPOSITY, INSULIN SENSITIVITY, ETC.

    NONE.

    Like

  8. explaining american negro bp by slavery is like explaining southern italy’s problem with gangsters by catholicism.

    dumb!

    what about black african americans from africa? it’s such a select population.

    AND IF YOU NOTICE THE FAKE LEGERDEMAIN OF “ADJUSTING FOR RELIABILITY” COMES UP WITH A SYSTOLIC BP THAT’S 91% “GENETIC”.

    HBD IS A GAY DEATH CULT.

    Like

  9. i have this theory that dental decay is 100% preventable, but dental wear is not.

    but the means of avoiding decay 100% is not promoted because it would mean the end of dentistry.

    Like

  10. i was right.

    as a matter of fact, barring gum disease, teeth can be treated in such a way that one could eat nothing but panettone and still never have a cavity.

    the downside is black teeth.

    silver diamine flouride makes tooth decay IMPOSSIBLE, but it stains teeth black.

    Like

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