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Race and Menarche

1100 words

Back in 2016 I wrote about racial differences in menarche and how there is good evidence that leptin is a strong candidate for the cause in my article Leptin and its Role in the Sexual Maturity of Black Girls (disregard the just-so stories). Black girls are more likely to hit puberty at a younger age than white girls. Why? One reason may be that leptin may play a role in the accelerated growth and maturation of black girls, since there was a positive relationship between leptin concentration and obesity in black girls (Wagner and Heyward, 2000). When girls start to develop at younger and younger ages, a phrase you hear often is “It’s the chemicals in the food” in regard to, for example, early breast development on a young, pre-teen girl.

Black girls are more likely to be obese than white girls (Freedman et al, 2000) and it is thought that body fat permits the effects of earlier menarche due to leptin being released from the adipocyte (fat cell) (Salsberry, Reagen, and Pajer, 2010). Freedman et al (2000) showed that black girls experienced menarche 3 months earlier than white girls on average, while over a 20 year period the median age decreased by 9.5 months. There is also evidence of earlier thelarche (breast development) in black girls, which was mediated by gonadotropin (Cabrera et al, 2014). Wong et al (1998) found that circulating serum leptin levels were correlated with earlier menarche in black girls which was related to body fatness and age but lessened after fat mass, maturation and physical fitness. There is a ton of evidence that exists that body fatness is related to obesity and, as I said above, the mechanism is probably fat cells releasing leptin, permitting earlier menarche (see Kaplowitz, 2008). Higher levels of body fat cause earlier menarche; earlier menarche does not cause higher levels of body fat. The evidence is there that leptin indeed plays the permissive role to allow a girl to enter into puberty earlier, and that this is how and why black girls enter menarche earlier than white girls.

So when fat mass increases, so does leptin; when leptin increases, girls have puberty at an earlier age (Apter, 2009). Black girls have higher levels of circulating leptin than white girls (Ambrosious et al, 1998). So knowing the relationship between leptin and obesity and how fat cells release leptin into the body permissing earlier puberty, we can confidently say that leptin is a major cause of earlier pubertal development in black girls. Total body fat correlates with fasted leptin (Ebenibo et al, 2018).

Siervogel et al (2003) write:

A negative relationship between age at menarche, BMI and body fatness in girls has been shown [636465]. It is still unclear, however, whether increased early childhood adiposity induces an earlier onset of puberty, if rapid maturation and early puberty induce an increase in body fat later in life, or whether both of these phenomena occur.

The average age of menarche in black girls was 12 years of age whereas for white girls it was 12.5 (Regan et al, 2013). Since we now know the causes of earlier menarche, we can talk about ultimate causation.

Since menarche is correlated with obesity and circulating leptin levels, then food quality would be an easy culprit to look at.

Deardorff et al (2014) write:

Three sets of findings stood out. One, grandmother’s lower education was related to later menarche for Black girls. Two, mother’s unmarried status (at birth and age 7) was associated with earlier menarche for Hispanics and Whites, but not for Blacks. Three, family income at child’s birth was related to earlier menarche for Blacks and Hispanics, but not Whites.

Lower family income at birth was associated with earlier menarche for Blacks (and to some extent for Hispanics), but not for white girls.

Deardorff et al’s (2014) study suggests that social determinants of health can be intervened upon and differences in pubertal timing can be ameliorated since they are driven by social factors.

Black children have higher levels of insulino-glucose ratios than white children, even after adjusting for confounds (Wong et al, 1999). There were similar findings when comparing normal-weight black and white girls matched for age, bone age, weight, and BMI. Black girls also had higher levels of insulin than white girls. Black girls grow faster than white girls beginning at 2 years of age, with the cause hypothesized to be “higher serum insulin concentrations in healthy African American girls suppress the hepatic production of IGFBP-1, which results in higher circulating concentrations of free IGF-I, contributing to the accelerated growth observed in African American girls compared with their white counterparts” (Wong et al, 1999: 297).

Wong et al (1999) found that black girls were older and more sexually mature than white girls according to the Tanner stages of development (using pubic hair as a measure). Even after adjusting for age, black girls were still more sexually mature, heavier, and had higher levels of fat-free mass. Both serum insulin levels and serum concentrations of IGF-1 were significantly higher in black girls compared to white girls. Even after they controlled for differences in pubic hair development and fat mass, the differences in IGF-1 and IGFBP-1 remained significant. So black girls in this study had higher levels of IGF-1 and insulin than white girls.

This is significant because higher levels of IGF-1 at age 8 are associated with earlier menarche in girls (Thankamoney et al, 2012). Earlier menarche is related to higher levels of adiposity, as noted above, and the mechanism for earlier menarche is fat cells releasing insulin which has a permissive effect on menarche. Further, there is evidence that lower levels of circulating growth hormones are related to delayed menarche (Circo, 2014).

IGF-1 is a protein “coded for” by the IGF-1 gene (Hoppener et al, 1985). IGF-1 is molecularly similar to insulin (Laron, 2001). This makes sense. Body fat cannot be stored unless insulin is high; since they are molecularly similar, they both cause growth, albeit in different ways.

In conclusion, there is strong evidence that body fatness is related to earlier menarche, with the mechanism being fat cells releasing leptin which has a permissive effect on pubertal development. Further evidence indicates that circulating hormones like insulin and IGF-1 also have permissive effects on pubertal development. Black girls are more likely to be obese than white girls. Black girls are more likely to have higher levels of circulating hormones like IGF-1 and insulin than white girls. Thus, a cause—a major cause in my opinion—for earlier menarche in black girls compared to white girls is higher levels of body fat and higher levels of circulating hormones like IGF-1 and insulin which have a permissive effect on menarche.


Racial Differences in the Palmaris Longus

1050 words

There are many physical differences between racial/ethnic groups. Some of these differences are obvious to the naked eye, others much less so. One racial difference that exists is variation in having a tendon called the palmaris longus (PL). This muscle rests between the flexor carpi radialis and the flexor carpi urinalis. The radius and ulna are bones in the forearm. The radius supports the lateral (thumb) side of the hand whereas the ulna supports the medial (pinky) side; they enable wrist rotation. To see if you have the tendon, take your pinky and touch it to your thumb. If you have the tendon you should see it poking out of your wrist. Fourteen percent of the population lacks the PL, but there is considerable variation by race. These differences, of course, have should be taken into account when doing a tendon graph operation.

The action that the PL performs is flexing the wrist; the origin is the medial epicondyle of the humerus; it inserts in the palmar aponeurosis and flexor rentinaculum of the hand. The antagonist muscles are extensor carpi radialis brevis, extensor carpi radialis longus, and extensor carpi urinalis.

There are unilateral (affecting one side of the body) differences in the variation of this tendon along with bilateral (affecting both sides of the body) differences. There is differential absence of the tendon depending on which hand is dominant (Eric et al, 2011). The tendon also has been found to contribute to the strength of thumb abuction (Gangata, Ndou, and Louw, 2013). However, it has been shown that whether or not one has the PL or not does not contribute to grip/pinch strength (Sebastin et al, 2005).

Soltani et al (2012) followed patients at hand surgery clinics LA county +University of Southern California Medical Center and Keck Medical Center of the University of Southern California. Their objective was to observe the variation in the PL in regard to race, sex and ethnicity (indeed, they placed people into races based on the US Census designations; see Spencer, 2014, they excluded mixed-race people from the ethnicity part of the analysis). They wanted to see the extent that the PL was missing and whether or not it was bilateral or unilateral. They evaluated a group of 516 multi-ethnic individuals while age, race, ethnicity and sex was accounted for. They then administered the Schaeffer test:



Obviously, this only works with lean individuals. So obese patients needed to get an ultrasound to ascertain whether or not they had the tendon.

In their sample of 516, 415 were Caucasian, 55 were African American, 35 were Asian and 11 were mixed race. The age range was 12-94, while an even number of men and women were tested (288, 288). Soltani et al (2012) write:

There were no differences in the absence of the PL based on laterality. The right side was absent in 11.8% and left 12.0% of the time (see Table 1). Further, there were no differences in the absence of the PL based on gender,  value 0.369 (see Table 2). Ethnically, there was no difference in the absence of the PL between White (non-Hispanic) and White (Hispanic) patients, with prevalence of 14.9% and 13.1%, respectively. However, African American (4.5%) and Asian (2.9%) patients had significantly fewer absences of the PL than the Hispanic reference group.

They then write in the discussion that this has implications for plastic surgery—this anatomic variation between the races has implications for surgery:

This is information that should be taken into account preoperatively when planning surgical algorithms in treating tendon injuries or palsy. The PL is one such option as a tendon transfer for opponensplasty in restoring intrinsic function in cases of recurrent median nerve injury. If the PL is absent on the affected side, it is important to know preoperatively to plan using another donor muscle such as the extensor indicis proprius. In our study, the African American population had a statistically significantly lower rate of absent PL (4.5%), which is radically different than previously published reports from Nigeria, where the absence rates were much higher (31%). This could be due to the ethnic heterogeneity of the African American population of the United States compared to the Nigerian population. Nevertheless, the PL is present in high likelihood in this particular ethnic group which bodes well for using the PL in a surgical scenario. The PL is used quite frequently in cases of secondary tendon reconstruction, and it is useful for the surgeon to be aware of that issue preoperatively for surgical safety and efficiency in harvesting the tendon graft. The patient needs to be aware of the location of possible surgical incisions for tendon harvesting. Further, the surgeon should examine all possible tendon donors preoperatively, and one’s suspicion might be heightened by knowing the patient’s ethnicity. This is particularly important for the White population which in our study had the highest rates of absence, in both the Hispanic and non-Hispanic subsets. The surgeon must be aware in these patients that it is more likely that the PL might be absent. Thus, in Caucasian patients, it is particularly important to have a thorough examination of possible tendon donor sites.

Touching on the point of there being no difference between having or not having a PL and grip/pinch strength: we should not expect that, since whites dominate strength competitions (and the Chinese powerlifters are no slouches either, look at some videos of them). So, just because whites have a higher prevalence of not having the tendon does not mean that they do not have a strong hand grip. Indeed, senior blacks did have a stronger hand grip than whites (Araujo et al, 2010), but the PL is not the cause of the slightly higher hand grip strength (this was seen in a Turkish study; Setin et al, 2013). However, tennis players need a strong grip and the PL is more likely to be found in elite tennis players over the recreational athletes (Vercruyssen, Scafoglieri, and Cattrysse, 2016). But Nekkanti et al (2018) conclude that “There was no statistically significant correlation between agenesis of PL and the mean hand grip. Right-handed dominant individuals had a higher incidence of PL.”

In sum, this is tendon varies by race/ethnicity/sex/handedness like many other traits. understanding these differences will lead to a better understanding of plastic surgery in regard to the tendon. There is a racial difference, but it is of no functional relevance in regard to hand grip/power/strength sports.

Is Diet and Exercise Eugenic?

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Eugenics can be defined as “the science of improving a human population by controlled breeding to increase the occurrence of desirable heritable characteristics.” Though, in his book Genetic Ethics: An Introduction, Farrelly (2018: 30) cites Bertrand Russel’s definition of eugenics. Eugenics is “the attempt to improve the biological character of a breed by deliberate methods adopted to that end.” So, eugenics does not have to be ‘bad’, if it is morally justifiable and defensible, if they treat all people as free and equal (which most eugenic movements in the past have not done. See my article Eugenics and the State for a history of eugenics and the policies that arose from it.)

Dieting (defined as “what one eats”, not the other commonly-used definition “when one is in caloric restriction under TDEE”) and exercise change the expression of genes in the genome. For example, mature skeletal muscle can adapt to numerous stressors—indeed, if it could not, then we would not be able to choose to gain (or lose) muscle mass. Exercise induces the activity of certain genes (Vissing, Anderson, and Schjerling, 2005). One study on endurance athletes showed that there are pronounced effects of gene expression on exercised and non-exercised muscles (Catoire et al, 2012). One study showed that the ingestion of glucose during exercise decreases the gene expression of genes associated with fatty acid metabolism (Civitarese et al, 2005). Numerous epigenetic changes are also induced by exercise (Ntanasis-Stathopoulos, Tzanninis, and Koutsilieris, 2013). Miyamoto-Mikami et al (2018) showed that young men who participated in high-intensity intermittent exercise training showed that 79 genes had an elevated expression whereas 73 genes were significantly reduced.

Williams and Neufer (1996) show that long-term responses in regard to adaptations in regard to a specific exercise “require changes in gene expression, mediated by changes in the rate of transcription of specific genes and in the rate of synthesis of
specific proteins.” Further, diet and exercise can change the transcriptional properties of skeletal muscle, which induce further physiological changes (Hargreaves and Cameron-Smith, 2002). There is even preliminary evidence that diet and exercise affects the epigenome over several generations (Barres and Zierath, 2016). Since changes occur to the epigenome due to environmental stressors, and exercise is an environmental stressor, it follows that exercise, too, can change the epigenome.

People visit the gym to change their biology. Since people visit the gym to change their biology, are they involved in “self-eugenics”? I would say yes, going with the definition from Russell quoted above. That one wants to change their biology means that they are most likely not currently happy with the way their biological phenotype currently is. So they visit the gym, begin a diet (defined here as “caloric restriction”) in order to change their biological phenotype since they are not happy with it. Methods like diet and exercise seek to improve the biological character of a breed through deliberate methods, and so, fall under the umbrella of “eugenics.”

But there is a difference between this type of “eugenics” and methods commonly thought of when “eugenics” are discussed. “When eugenic measures exemplify moral and epistemic virtue rather than vice, they are morally obligatory rather than simply morally permissible” (Farrelly, 2018: 42). Prescribing (a sensible) diet and exercise to a populace can and will improve their health; further, educating people on the right and wrong things to eat (“right and wrong things to eat” in regard to their current goals) and how these things we eat affect our physiology is not morally objectionable nor is it coercive.

Think of the eugenic policies I discussed in my article on eugenics and the State. The policies discussed (such as forced sterilization, infanticide, forced contraceptive measures, and selective breeding) are immoral: the State is attempting to force its ideals on the populace, and so it can be argued that it is immoral since individual autonomy is taken away (or attempted to be taken away). On the other hand, prescribing diet and exercise is not eugenic in this manner: it’s just a prescription, what one should do if they would like to live their life to the highest quality. This includes staying away from highly processed and refined foods (carbs) and other, “non-natural” foodstuffs. This is only a suggestion based on the current state of nutritional knowledge; if one wants to live the best-possible life then they should diet and exercise.

On the other hand, we can take a State-measure and, using the definition in this article from Russell, can say that this measure is eugenic, but its similarities to what is being argued here is irrelevant, since I am arguing for education, not forcing people to do something (though I will state my views on this matter at the end, which I still honestly think about since it conflicts with some of my views.)

Back in the beginning of this decade, then-mayor of NYC Michael Bloombergproposed [a] regulation that would bar food service establishments from selling certain sugary drinks in containers larger than sixteen ounces” in an effort to “reduce the city’s obesity rate.” When this law was proposed, I was all for it. People cannot make decisions for themselves, because when they do, they make the “wrong” (in regard to, what I would assume to be what people try to achieve—a healthy lifestyle) decisions, and so, I thought that a policy like this was a good idea, because who the hell needs a 64 oz. Big Gulp soda (which could have up to 700 kcal in the cup) from 7-11? Why would someone need to down almost 2 liters of soda in one go? Note that, I would assume, the individual would not be caught dead drinking out of a 2-liter bottle of soda (though I have seen quite a lot of people do so, even early in the morning). But there is no problem using the cup since its size is kind of deceptive—deceptive in the manner that it does not look like the 2-liter bottle of (family-sized) soda.

I loved this proposal when it was announced. It would, I thought, attempt to address one aspect of our obesity problem (since nearly 40 percent of all of the added sugars we consume come from sugary drinks). Back then, I was more libertarian in my politics, but I thought that the policy was a good idea, even though it conflicted with my views on politics. I now do not believe we should take these types of measures—I believe that education is sufficient, along with getting rid of food deserts which hamper the ability of those in those deserts to get access to good, high-quality food (which affects certain races over others; National Research Council, 2009).

The view held by Bloomberg, and now current NYC mayor Bill Deblasio, is an example of a policy that would take away one’s choice to drink what they would like. Bloomberg’s rationale was that, if people wanted more of the drink, then they can go over and refill their cup so that they can see what and how much they are actually drinking. This, on its face, is sensible. If one wants to drink the same amount they would have drank in, say, a 64 oz. Big Gulp, they can keep refilling their cup in order to get the same amount of liquid they would have gotten in the bigger cup. But, what if someone wants a 64 oz. Big Gulp? What about a 128 oz. Ultra Big Gulp? A 256 oz. Super Ultra Big Gulp? Is there anywhere we should draw this line? Should we?

In any case, I have shown that exercise and diet is “eugenic” in the sense of Russel’s definition. But it is not “eugenic” in the sense of, in my opinion, what most people mean when they discuss “eugenics”: taking away one’s individual autonomy to do what they want, forcing them to do something. (Though, they are not being told they cannot drink sugary drinks, they are being told that there is a size limit on how big their cup is; they would be forced to drink a sugary drink in a small cup.)

Bloomberg’s proposed measure is quite obviously eugenic since it “attempt[s] to improve the biological character of a breed by deliberate methods adopted to that end.” Is the health of the populace more important than individual autonomy to be able to buy their 256 oz. Super Ultra Big Gulp? Or is one’s ability to freely drink their 256 oz. Ultra Big Gulp more important? If it can be shown that this policy would reduce the number of obese people in the City, should it be attempted?

These are important (moral) questions to answer. I am honestly undecided here; this issue is incredibly complex. Though, we do know one thing: exercise and diet is “eugenic” in Russel’s sense, and the measures exemplify moral and epistemic virtue so it is not like “State-forced” eugenics of old. Whether or not there is a negative connotation to “eugenics” depends on whether or not it pursues sound and morally justifiable aims. Therefore, though prescribing diet and exercise is eugenic since they both influence the epigenome and gene expression (along with it falling under Russel’s definition of eugenics), it is not eugenic in a negative sense, since there are sound and morally justifiable aims in prescribing diet and exercise to the population at large.

Race as a Genuine Kind

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Race realism can be defined as the belief that our racial categories pick out real kinds in nature. Picking out real kinds in nature is a necessary condition for race realism to be true. I’ve extensively covered Hardimon’s (2017) and Spencer’s (2014) arguments on the existence of race. They definitively prove that, all though there is a social/cultural dimension to race, biological racial realism is true, since our racial categories truly do pick out real kinds in nature.

In the philosophy of race, questions such as “What is race?” and “Is race biological?” are asked. Philosophers of race use many tools at their disposal to attempt to answer these and other questions regarding the metaphysics of race. Four main views on race exist: racial anti-realism, the belief that race does not exist; race realism, the belief that race is real; social constructivism, the belief that race is a social construct; and biological racial realism, the belief that race is biologically real (Spencer, 2011).

Note that social constructivists about race are race realists; they believe that race is real but that it is strictly a social reality. Racial anti-realists take the belief that race does not exist at all; so those who make the claim that social constructivists about race say that race is not real, they really mean to say that racial anti-realists claim that race is not real. People hear the phrase “social construct” and automatically assume that that individual is attempting to argue that race is not real. But social constructivists about race do believe that race is real—that is, they are race realists, but only in a social, not biological, manner.

Spencer (2011: 9) argues that genuine kinds are kinds that contribute to long-term scientific progress, meaning that genuine kinds are “a valid kind in a well-ordered SRP [scientific research program].” Spencer (2011: 9) states that valid kinds in an SRP are “useful for playing an epistemic role of scientific kinds in that SRP, as well as a kind that is adequately epistemically justified in its SRP” while also stating that “ a valid kind in an SRP must be useful for playing an epistemic role of scientific kinds in its SRP.” Kinds are valid in SRPs when they can help scientists generate observations for understanding the natural world. Genuine kinds can be epistemically useful without being inductively useful.

Genuine kinds can be epistemically real or just a human (social) construct. Genuine kinds are real enough to use in scientific research—because they tell us just enough about the world to be epistemically useful in a SRP. That a kind is genuine means that it is “real enough” to be used in scientific research.

Now let’s look at Spencer’s argument that biological racial realism should mean “race is a genuine kind in biology”:

(1) The meaning of ‘biological racial realism’ in the race debate should be a metaphysically minimal interpretation of important scientific kindhood that also does the most justice to what counts as an important scientific kind.

(2) A “metaphysically minimal” interpretation of important scientific kindhood is one that does not adopt unnecessary and contentious metaphysical assumptions.

(3) The interpretation of important scientific kindhood that does the most justice to what counts as an important scientific kind is the one that best captures epistemically important scientific kinds—or ‘EIS kinds’ for short.

(4) The candidates for important scientific kindhood in the race debate are naturalo kinds, naturali kinds, naturalu kinds, naturalp kinds, realp biological kinds, reali biological kinds, and genuine kinds.

(5) No kind of kind in the race debate is both metaphysically minimal and does a better job of capturing EIS kindhood than genuine kinds.

(6) Therefore, the meaning of ‘biological racial realism’ in the race debate should be ‘race is a genuine kind in biology’.

This argument provided by Spencer establishes the fact that biological racial realism in the race debate should be ‘race is a genuine kind in biology.’ Now that I have laid out that an entity being biologically real in the race debate is not whether or not it is objective but whether it is epistemically justified in a biological research program, I will now turn to other author’s views on biological racial realism.

The topic on “Race as a Biological Kind” on PhilPapers states that:

One option is to say that one’s ancestor is a member of race X in virtue of sharing similar phenotypic, or observable, properties specific to other members of one’ s reproductively isolated breeding population.  A second option is to say that one’s ancestor is a member of race X in virtue of sharing similar genotypic, or genetic, properties specific to other members of one’s reproductively isolated breeding population.

While “… ancestral relations among reproductively isolated breeding populations and either genotypic or phenotypic properties is one way to develop a naturalistic account of race.” Note how this is almost, to the tee, Hardimon’s (2017) populationist race concept.

Andreason (2000) writes that “Most constructivists assume that biological realism and social constructivism are incompatible views about race; I argue that the two conceptions can be compatible.” Indeed, the claim that race is a social construct of a biological reality is a tempting view to take (and one I take to myself). That we socially construct groups does not mean that there is no biological reality to them, as Spencer (2014) shows with his Blumenbachian partitions. The claim that race is a social construct of a biological reality is completely at ends with the claim that race is purely social/political (as Dorothy Roberts argues) and the claim that race is purely biological. Though, we cannot separate ‘social/political’ and ‘biological’ terminology from our ontology. We must use both in conjunction in order to tease out what ‘race’ truly means. Stating that race is a social construct and only a social construct betrays the biology behind race. Stating that race is only biological betrays the social aspects of race. (Though, Hardimon (2017) has one race concept—the minimalist race concept—in which there is nothing ‘social’ about his proposed concept of race.)

Hardimon has four concepts of race: (1) the racialist concept of race—the claim that significant intellectual and moral differences exist between races (which he dispatched in his book); (2) the minimalist concept of race—the claim that groups that exhibit patterns of visible physical features which correspond to geographic ancestry satisfy the conditions of minimalist race; (3) the populationist race concept of race (the scientization of the minimalist race concept)—the claim that “race is a subdivision of Homo sapiens—a group of populations that exhibits a distinctive pattern of genetically transmitted phenotypic characters that corresponds to the group’s geographic ancestry and belongs to a biological line of descent initiated by a geographically separated and reproductively isolated founding population” (Hardimon, 2017: 99); and (4) the socialrace concept of race—the claim that race is a social, not biological, reality, and that society constructs what ‘race’ is.

Our racial categories pick out real kinds in nature, therefore race realism is true. This is established by both Hardimon (2017) and Spencer (2014), who discuss Rosenberg et al’s (2002) paper on the existence of population clusters deemed continental-level minimalist races by Hardimon (2017) and Blumenbachian partitions by Spencer (2014). Both arguments provided by Hardimon and Spencer are sound—they answer numerous objections that critics bring up to argue against Rosenberg et al’s (2002) study and other’s interpretation of what they say.

This article discusses Rosenberg et al (2002), and has this to say about the Kalash (the sixth cluster in that Rosenberg et al (2002) found):

The sixth population which is composed entirely of members of the Kalash, an isolated population in central Pakistan, is omitted by Wade on the grounds it “makes no genetic or geographic sense”. But the Kalash have a significant degree of genetic isolation from others, comparable in magnitude to that of other groups such as Native Americans. Moreover, they all live in the same place.

This is nonsense. That Structure labels a population as genetically distinct does not entail that that population is a continental-level minimalist race. That Structure picks out the Kalash as a genetically distinct group does not undercut Hardimon’s (2017) arguments on the existence of continental-level minimalist races. So, both K=6 and K=5 show that continental-level minimalist races are genetically structured (Hardimon, 2017: 88). (Further responses to critiques of Rosenberg et al can be found here and in Hardimon, 2017, chapter 5 and Spencer, 2014.)

Lastly, I’ll take some time to respond to commenter Oliver D. Smith’s objections to cranial measures and geographic ancestry.

Smith cited Sierp and Henneberg’s (2015) paper Can ancestry be consistently determined from the skeleton? in which the authors show that “no one individual was identified as belonging to only one ‘racial class’” (Sierp and Henneberg, 2015: 23). I don’t find this to be a problem. If we take Hardimon’s minimalist and populationist race concepts, the three conditions that need to be satisfied to delineate races are differences in phenotype which correspond to geographic ancestry, geographic location, and geographic ancestry. The critique from Sierp and Henneberg (2015) only counts against one parameter—if that—which are skulls. When delineating races, we don’t only look at skulls (one visible physical feature), we look at the whole suite of traits that make a “race” “racial.” Therefore, Sierp and Henneberg’s (2015) critique has no bearing on Hardimon’s (2017) or Spencer’s (2014) arguments.

Is race a genuine kind in biology? Do our racial categories pick out real kinds in nature? The answer to both questions is “yes.” Race is a genuine kind in biology since it captures EIS kindhood; our racial categories do pick out real kinds in nature, as shown by Spencer (2014) and his Blumenbachian partitions. Hardimon’s and Spencer’s arguments are definitive: biological racial realism is true.

(i) If biological racial realism is true, then our racial categories would have to pick out real kinds in nature.
(ii) Our racial categories pick out real kinds in nature.
(iii) Therefore, biological racial realism is true.

Just-so Stories: Christianity

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Storytelling in religions is ubiquitous. Storytelling can be found in all religions for myriad reasons, including—but not limited to—(1) the passing of traditions; (2) how the mores of the society in question should be structured (Wuthnow, 2011); (3) bringing people into the religion by creating origin myths, and so on. In short, the function of religious storytelling has numerous primary directives, but one of the most important is answering why questions (Braustein, 2012) (i.e., “Why are we here?”, “Why do we do X?”), not how questions (i.e., “How did we get here?”). Thus, the importance of religious storytelling seems to be obvious: religious storytelling serves its function in virtue of explaining why questions which were formulated by a human mind. It also, for billions of people around the world, grounds morality in an objective reality given to Man by God.

If religious storytelling can answer how questions, then, it is proposed, we can believe these stories as evidence that the religions in question are true. However, there is much pushback in believing these religious stories. Religious stories are what can be termed “just-so stories”, which amount to hypotheses which offer “little in the way of independent evidence to suggest that it is actually true” (Law, 2016). It is for this reason that we cannot—nor should we—accept any religious just-so stories: they lack sufficient evidence for belief, other than what they purport to explain. In this article, I will discuss certain just-so stories and Christianity—how they fail to successfully argue what they purport to but still serve important (moralistic) functions. Religion and language/writing are deeply intertwined, and so, understanding how and why we speak and write along with the history of civilization will help us to better understand how and why we tell these kinds of stories.

Religion has been around as long as agriculture (Peoples, Duda, and Marlowe, 2016), and so, if we understand the co-evolution of both of these variables, then we may understand how and why these types of stories have persisted through the ages. Storytelling—in a religious manner—is a way to ground a certain group’s morals in something objective. This is one very important reason that religious storytelling has persisted. For example, Christians argue that Jesus rose from the dead in 3 days and that God created the universe we live in, and so on. These two claims, though, are just-so stories since there is no independent evidence for the claims. There are other more important functions to Christian storytelling other than believing in the ultimate truths of the purported claims.

Stories have many functions—one of the many functions is to give purpose to one’s life. Yet another function is to guide how one lives their lives using stories that were created thousands of years ago. Storytelling in Christianity is a large topic—one that is held dear to many people. What are some of the stories and are there any independent reasons to believe them?

Creationists—those who believe that a Supreme Being created everything we see around us—use the Bible and its stories as evidence that evolution is false and Creationism is true. One prominent Creationist is Dr. Bo Kirkwood who wrote The Evolution Delusion: A Scientific Study of Creation and Evolution (Kirkwood, 2016). In the book, he attempts to use Christian storytelling to attempt to discredit the fact of evolution. He makes many questionable claims including “God’s fingerprints are seen by observing his finely tuned universe” (Kirkwood, 2016: 210). This is a perfect example of a just-so story—make a claim that has no evidence to support it, the only evidence to support it is the claim (that “God’s fingerprints are seen by observing his finely tuned universe”).

No evidence exists that the universe is “God’s fingerprints … finely tuned” the universe, and so it is a just-so story. The arguments pushed by Creationists such as Kirkwood (2016) do not make any testable predictions. The Big Bang theory, however, does make testable predictions and is, therefore, not a just-so story. Note how Kirkwood’s (2016) claim have no independent evidence to back them—that God “finely tuned” the universe is one of the ultimate just-so stories. It’s literally based off of faith and no evidence. Nothing can falsify the claim that God “finely tuned” the universe, and so we should disregard claims like this from Creationists. Kirkwood’s (2016) claims that the universe is “finely tuned” by God is an attempt to argue that there is a Creator of the universe we live in, and so we should dispense with evolutionary thinking and embrace the Creator, God. Kirkwood (2016) believes that, if evolutionary theory can be disproven by appealing to claims that God “finely tuned” the universe, then more people would believe God’s Word and society would start trending in a more religious, Christian trajectory.

Just because claims from Creationists are false does not mean that religious storytelling has no use—no function—in the modern day (or even thousands of years ago when they were first formulated) One of the most important functions for storytelling in Christianity is the grounding of objective morality. Most of the stories told in the Bible have a moralistic message that it wants to convey. Do this, not that, because God is watching and this objective morality is grounded by God. These stories, then, got passed down through each successive generation and eventually became got sorted into what is now the Bible during the Council of Nicaea.

One of the best examples of morality in the Bible—and the stories that accompany it—is Romans 13: 8-10, where it is stated that, many of the Commandments can be summed up succinctly as “Love does no harm to a neighbor. Therefore, love is the fulfillment of the law” (New International Version). The Ten Commandments were given to Moses by God – they were given to Moses to give to the Israelites in order to guide them to live good, moral lives. So, if “… whoever loves others has fulfilled the law” (New International Version), and those who follow the Ten Commandments have fulfilled the law by loving—not harming—their neighbors, then those who follow the story that Moses was given the Commandments by God are living a moral life and therefore these stories help people in our societies live moral lives. That these stories help billions of Christians live moral lives does not speak to the truth of the claim that these Commandments were given to Moses by God, though. That is irrelevant. The most important thing here is that these stories help others live moral lives. (Quite obviously, the stories are not sufficient to live a moral life, since there are non-religious people who do so.)

Religious storytelling—irrespective of the truth of the stories—is clearly important in our societies. They help people with certain moral quandaries, to live their lives a certain way because they believe that someone is watching them. If these stories help people live good, moral lives, then it does not matter if the ultimate claims of the stories are true or not. Therefore, Christian storytelling has very important functions for how our current societies function which is why Christian storytelling has persisted through the ages, even if the claims are false.

Strength and Neuromuscular Coordination

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PumpkinPerson (PP) has some weird—and uneducated—views regarding strength and coordination, which, of course, implies that he has no understanding of what “coordination” truly is. He seems to have convinced himself that coordination weightlifting does not require coordination (neuromuscular coordination; hereafter NMC—the ability of the central nervous system—CNS—to control muscles). That view is patently ridiculous. In this article, I will explain the logic behind the fact that strength and power exercises, in particular, NEED a high NMC, and without a high NMC, the athlete in question cannot perform to their highest potential.

PP wrote about an “athletic g factor” to attempt to liken it to the “g factor” regarding “intelligence” tests, but I’m not worried about that comparison (IQ is boring to me now). What I am worried about are his outlandish claims regarding what he believes regarding strength and NMC. PP cited Jensen’s Bias in Mental Testing where Jensen cited a correlation matrix in which “all of [the] correlations were positive“, writing that he’s “not sure why some commenters think weight lifting requires coordination when the correlation between strength (hand grip, chinning) and coordination (Pursuit rotor tacking, Mirror star tracing) is zero” (PP; Physical Coordination).

Well, “some commenters” have actual experience in what he is talking about, so, forgive me if I don’t believe the claims that, in my opinion, he pulled out of thin air. Take chin-ups. Imagine a case of someone attempting to chin-up that does not have high NMC. Since they were not coordinated, do you think they would be able to do a controlled rep in order to complete one rep? Or would their body be all over the place, flailing around since they do not have the mind-muscle (MMC) connection required to complete the lift. Now take his other example, hand grip. On its face, one might assume that this requires no NMC. But think about the process of gripping something tightly. If the muscles in the forearm, for example, are not adequately trained, then, in all lifts involving forearm strength (a great majority of which involve at least some type of forearm strength) will not be able to be performed properly, since the individual in question does not have the NMC required to properly do the exercise in question.

PP then says that when he “lift weights, [he doesn’t] feel like [he’s] using coordination.” This proves two things to me: (1) PP does not know how to lift properly, and then (2) follows that he does not know about the MMC.

The MMC is where the mind and the body “meet.” Acetylcholine functions as a neurotransmitter. This neurotransmitter “communicates” with the muscles in the body to cause a contraction. This contraction, then, causes the action of voluntary muscle movement. (I had an A&P professor explain to me that, out of the whole textbook he taught out of, one of the only things in the textbook that we could choose to do was move the body—contract muscles and cause movement). So when acetylcholine is released, it latches onto muscle fibers and causes muscle contractions.

We can put the MMC in this way: imagine doing a movement such as a bicep curl. One is not actively attempting to use the proper levers in order to properly lift the weight. On the other hand, if one is actively thinking about the muscles being used in the movement, then they are using the connection—they are strengthing their MMC and, in turn, developing the proper NMC which is required in order to properly lift weights and get the most returns possible from your time spent lifting.

20190220_153711 (1)

The above diagram I drew is the process by which muscle action occurs. In my recent article on fiber typing and metabolic disease, I explained the process by which muscles contract:

But the skeletal muscle will not contract unless the skeletal muscles are stimulated. The nervous system and the muscular system communicate, which is called neural activiation—defined as the contraction of muscle generated by neural stimulation. We have what are called “motor neurons”—neurons located in the CNS (central nervous system) which can send impulses to muscles to move them. This is done through a special synapse called the neuromuscular junction. A motor neuron that connects with muscle fibers is called a motor unit and the point where the muscle fiber and motor unit meet is callled the neuromuscular junction. It is a small gap between the nerve and muscle fiber called a synapse. Action potentials (electrical impulses) are sent down the axon of the motor neuron from the CNS and when the action potential reaches the end of the axon, hormones called neurotransmitters are then released. Neurotransmitters transport the electrical signal from the nerve to the muscle.

So action potentials (APs) are carried out at the junction between synapses. So, regarding acetylcholine, when it is released, it binds to the synapses (a small space which separates the muscle from the nerve) and it then binds onto the receptors of the muscle fibers. Now we know that, in order for a muscle to contract, the brain sends the chemical message (acetylcholine) across synapses which then initiates movement. So, as can be seen from the diagram above, the MMC refers to the chemo-electric connection between the motor cortex, the cortico-spinal column, peripheral nerves and the neuromuscular junction. A neuromuscular junction is a synapse formed by the contact between a motor neuron and a muscle fiber. This is why beginners in the gym get stronger in the first 8 weeks or so of training—there has not been enough time for muscle to adequately grow in that time span. Thus, when people lift weights correctly, what they are doing is training their NMC—and their mind—to be able to adequately perform these types of actions in a safe, controlled manner.

How is NMC measured? It’s not simple to measure it, and in reality, the most feasible way to “measure it” in real life situations without the use of a lab is to just see one’s progress while they progress through higher and higher weights from their starting weights and they learn to perform the exercise in question safely. But a more empirical measure used in order to measure NMC are electromyography (EMG) tests. In fact, this test is THE MEASURE used to measure NMC, since all of the relevant variables in question (some seen in the above diagram) are tested. EMGs are used for numerous reasons, mostly in order to test for types of motor diseases which affect muscle action. There is also a related measure here: a nerve conduction study. This measures the speed and strength of signals traveling between two synapses, and so, the better one’s nerve conduction is in regard to muscle action, the higher their NMC is and, therefore, the better they will be able to perform any certain lift. So, for example, we can say that one’s NMC increased and the cause was resistance training if their EMG tests increase.

Imagine an Olympic lifter going to snatch 400 pounds. Would any sane person bet that they have low NMC (i.e., a low rate of firing between synapses as measured by an EMG)? A claim such as this would be quite preposterous—individuals like Olympic lifters clearly have trained both their bodies and minds in order to lift to the best of their abilities. And if they did NOT have high NMC (i.e., a higher rate of firing between synapses), then the weight would wobble and ultimately fall, causing the lifter serious injury. But, of course, we do not see that, since strength and NMC are closely related.

I now have some examples of studies which looked into this matter (that thinking about the action one is performing activates the primary muscles used in the movement in question), which will definitely put PP’s claims to rest for good.

Neuromuscular coordination is needed, for example, to be able to “squat lift” correctly (meaning, pick up a load from a squatting start and lift it; Scholz, Millford, and McMillan, 1995). Our understanding of how this occurs has greatly increased in 30 some-odd years since our technology has improved.

Now, take the MMC. We can simply define it as “One focusing on using the muscles in question to perform the lift.Calatayud et al (2016) studied 18 resistance-trained men on a 1RM (one-rep max) bench press. Each individual in the study participated in 2 sessions: one to determine their 1RM and another experimental session. Calatayud et al (2016) attempted to control for as many factors as possible in order to attempt to see if the baseline changed at all. For example, all measures were made by the same two investigators; all measures were taken in the same facility; all participants participated in the same warm-up mobility drills prior to performing the lift; all participants performed the lift in the exact same manner they performed the two aforementioned sessions (same technique and body position, i.e., suicide grip and powerlifting technique).

They found that (1) higher levels of EMG activity lead to moving more weight; (2) the men could “selectively activate pectoralis and triceps muscles during the
bench press when this exercise is performed at low intensities
” (Calatayud et al, 2016), at moderate intensities; (3) that focusing on one muscle (i.e., triceps brachii over pec major) did not hamper activation in one over the other; and (4) a threshold exists between 60-80 percent existed for muscle activation. Thus, experienced resistance-trained men can actively increase activity in certain muscles when cued to focus on those certain muscles.

Snyder and Fry (2012) studied 11 D-III football players on the bench press while recording EMG activity. They found that, when verbal cues were given to focus on the chest muscles, EMG increased by 22 percent, but when verbally cued to focus on the triceps, the pec major returned to baseline (though this does not mean, of course, that performance was hampered), while EMG activity increased by 26 percent. However, in-line with the findings from Calatayud et al (2016), when 80% 1RM were tested, EMG activity in the triceps remained unchanged, implying that there is a threshold.

The results of this study show that trained subjects can alter the participation of muscles in both moderate and higher-intensity multijoint resistance training exercises in response to verbal instructions, because both TB and PM activities were increased selectively in response to 2 different sets of instructions at 50% 1RM and 80% 1RM. This indicates that verbal instructions from trainers, therapists, and coaches are likely to have a measurable effect on muscle involvement, although it is unclear how generalizable this effect might be to all training exercises. Previous research from our laboratory (23) indicated that untrained subjects performing a lat pull-down at 30% max isometric load could respond to verbal instructions to increase back muscle involvement by increasing latissimus dorsi activity while maintaining proper form and similar speed of movement. The subjects in that study increased latissimus dorsi activity by 17.6%, whereas in the current study, verbal instruction resulted in a 22.3% increase from baseline at 50% 1RM for PM and a 25.6% increase for TB. However, antagonist activity was not measured by Snyder and Leech (23), and it was possible that the subjects activated antagonist muscles to offset additional force produced by agonist muscles. This study addressed this possibility, but no changes were seen in antagonist muscle activity with verbal instructions. The question of the effect of higher testing loads was also addressed by this study, and it was found that at 50% 1RM, the subjects were capable of altering muscle participation of both the horizontal adductors and the elbow extensors, but at 80% 1RM, only the horizontal adductors were affected. (Snyder and Fry, 2012)

If the activity of a muscle as measured by EMG is increased, then we can say that, for all intents and purposed, that NMC is high. One who is not familiar with a lift will have low NMC, that is, the firing will be low compared to someone with high NMC. Quite clearly, verbal instruction to focus on certain muscles can better activate them, and, using EMG, we can say that they have high NMC if the firing between synapses is fast.

Rutherford and Jones (1986) write that “It is concluded that a large part of the improvement in the ability to lift weights was due to an increased ability to coordinate other muscle groups involved in the movement such as those used to stabilise the body.” How weird is that… While Kim, Lockhart, and Roberto (2009) in their sample of elderly individuals found that “Strength gain by exercise training plays a role in the improved coordination of other fixator muscles necessary for body support while performing daily tasks such as cooking, gardening, reaching for an object, and walking, and in gaining more coordinated contractions between agonist and antagonist muscle groups leading to greater net force in the imposing movements.” Finally, Dahab and McCambridge (2009) found that strength training in kids improves the number and coordination of active neurons along with the firing rate pattern. This is important because the number and coordination of active neurons along with the rate of firing pattern influences—very strongly—NMC and how coordinated they will be.

In conclusion, it is quite obvious that PP does not know what he is talking about and only writes what sounds good in his head without having an adequate understanding of anatomy and physiology, NMC, MMC, APs and the like. These types of confusions can be cleared up by having an adequate understanding of anatomy and physiology and knowing how and why muscle actions are done, where they begin and where they end. Clearly, the claim that weight lifting requires no coordination is false.

JP Rushton, Richard Lynn, Satoshi Kanazawa, and Michael Hart: the Just-so Storytellers

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The four men in the title are, in my opinion, the biggest just-so storytellers in the “HBD” movement. These four men have written numerous journal articles and books pushing their just-so stories—making a career out of storytelling. We have Rudyard Kipling’s Just So Stories for Little Children, well Rushton, Lynn, Kanazawa, and Hart (RLKH) told Just-so Stories for Adults—like all EP is. Either way, RLKH have quite the following—those who would defend their just-so stories—and if you deny and question them, you’re “denying evolution” and are “no better than a creationist.” Well, too bad for them, rejecting just-so stories means nothing of the sort.

So even though humans as a species are incredibly K selected, some believe that some humans are more K selected than others.  In other words, while some men have numerous sexual partners and father lots of illegitimate babies with different mothers, other men are more nerdy, and father very few children with only one woman, but they make sure those children are well parented and provided for.

When men first evolved in the warm hospitable tropics some 200,000 years ago, survival was relatively easy, so instead of natural selection (survival of the fittest), genetic fitness was determined by who could get the most women (sexual selection).  As a result, men with the biggest muscles, highest testosterone, best social skills, most charisma and sexual abilities, were the most successful at passing on their genes.  But as the ice age emerged and humans moved North, passing on genes became more about natural selection and less about sexual selection.  What good is it to be a great pick up artist if you can’t survive the winter long enough to mate? (PumpkinPerson; Why women hate nerdy men)

When asked “why white women didn’t evolve to prefer nerds,” PumpkinPerson writes that “cold climate women evolved to be submissive so their preferences were prehistorically irrelevant.” More and more just-so stories. That’s all “HBD” is: a collection of just-so stories.

Sexual selection is a subset of “natural selection” but there is one important difference: humans have minds and thus, humans can *attempt to* “select-for” traits, but each trait is coextensive with an infinitude of traits which throws a wrench in the notion. There is no such thing as “natural selection (Fodor and Piatteli-Palmarini, 2010).

The above just-so story, personally, is one of my favorites, in the top ten, at least. This type of just-so story was popularized by Rushton and his r/K selection theory (read the rebuttal here; I also have many rebuttals of Anonymous Conservatives just-so stories, his attempted revival of Rushton’s storytelling). Africans, like PP claimed above, evolved in hotter, harsher environments, and so had to have more progeny in order to ensure reproductive success. On the other hand, when Man out of Africa, he encountered colder temperatures and, it is said, had to have fewer children in order to ensure that the children were looked after.

According to Richard Lynn, then, this migration into colder climates caused a decrease in colder climates due to a shift to “K strategy”, which then “selected-for” lower testosterone (Lynn, 1990). In Lynn (1990), he claims that differences in PCa (prostate cancer) are evidence for the claim that blacks have higher levels of testosterone than whites, which drives behavioral differences between the races. He then assumes that these differences have an evolutionary origin between the races, and that migrating into colder climates caused a decrease in testosterone in Europeans compared to Africans. However, one large mistake that Lynn (1990) makes is assuming that testosterone levels today have any bearing on testosterone levels thousands of years ago.

Claims that PCa are caused by higher levels of testosterone are ubiquitous in the “HBD” literature. But, as I have covered in the past, there is no reason to be scared of the hormone testosterone (read my most extensive review here); testosterone does not cause aggression and it does not cause PCa (Stattin et al, 2003).

One of the most oft-cited studies on the matter of T differences between blacks and whites is a small, highly methodologically/conceptually flawed study by Ross et al (1986). I have documented numerous flaws with the study.

So Lynn, in his 1990 just-so story shown above, claims that, due to colder temperatures, children would have needed more attention. Giving more attention would have meant having fewer children. This was done, he claims, through shifting to K strategy. So then, a decrease in testosterone was how to achieve this “K adaptation”, and achieving this “K adaptation” was through a reduction in T levels which subsequently, according to Lynn, brought “about a lowering of sexual drive and behaviour” (Lynn, 1990: 1205).

Note how Lynn’s claims in this paper *completely rest on* differences in prostate cancer between races. He uses these differences due to the assumption that high levels of testosterone contribute to differences in prostate cancer. This claim is false.

One of my favorites is from Rushton and Templer (2012) who attempt to show that the melanocortin system modulates aggression and sexuality in humans. I wrote a response to it, and, of course, one of the main culprits is our old friend testosterone. The hypothesis put forth is, of course, another just-so story. Nevermind the fact that Rushton and Templer show no understanding of endocrinology. We have a great understanding of the melanocortin system and what it does in humans (see Cone, 2006), but, unfortunately for Rushton and Templer, none of the review discusses the fringe ideas they put forth. Rushton and Templer showed that they do not understand human physiology, much less the melanocortin system.

Lynn (2013) even claims that testosterone has an effect on human penis length between races, citing a study on… rats. RATS!! THAT is the standard of evidence that Lynn has for attempting to prove his fringe just-so stories.

These just-so stories pushed by Rushton (1997), Lynn (2006), and Hart (2007) lack independent evidence—we don’t have a time machine to verify their claims. So they’re just-so stories. I rebutted all 3 of these psycho-logists’ claims in this article on how black women do not have higher levels of T than white women. I did, indeed, used to push all types of just-so stories when I was a more hard-core “HBDer”, but I’ve since learned the errors of my ways and have stopped telling just-so stories See exhibit A, defending Kanazawa’s just-so stories.

I wrote:

“To be blunt, black women look more like men than women due to their higher levels of testosterone.”

I can’t believe some of the stuff that I used to write/believe… I have, of course, since seen the error of my ways (in more than one way, as can be evidenced by my view changes over the past two years).

Anyway, these types of claims are easily put to rest by reading Mazur’s (2016) analysis of testosterone and honor culture.

“There is no indication of inordinately high T among young black women with low education.”

“The pattern [high testosterone] is not seen among teenage boys or among females.”

So, quite clearly, PumpkinPerson’s just-so storytelling, as popularized by RLKH, has no backing in reality—these psycho-logists told nothing but just-so stories. “But the stories are consistent with the data!”, one may attempt to say. Well, to that, I would say the stories are selected to be consistent with the data; how parsimonious a just-so story is with any current data is irrelevant since one can spin any type of story they want to fit with any data point they have. This is put succinctly by Smith (2016) in his paper Explanations for adaptations, just-so stories, and limitations on evidence in evolutionary biology:

“An important weakness in the use of narratives for scientific purposes is that the ending is known before the narrative is constructed. … [Just-so stories] are always consistent with the observations because they are selected to be so.”

The method known as “inference to best explanation” is not a solution to these problems. … Some just-so stories should not be told.

Now, put this to the stories of RLKH, and it will become clear that all they are doing is storytelling—telling just-so stories for adults. These types of stories are inherently ad hoc and generate no testable predictions. It doesn’t matter that they “agree with the data”, since one can construct any type of narrative to agree with the data—that’s a fact.

It’s no surprise that people still, to this day, attempt to defend RLKH’s just-so storytelling—it is rooted in the Darwinian paradigm of natural selection, after all. However, appealing to an imaginary force (natural selection) which shaped traits over thousands of years is literally telling just-so stories—there is no evidence for the claim other than evidence the story purports to explain—nevermind the fact that the trait in question could have moved to fixation by other methods than “selection.” (See Samir Okasha’s (2018) book Agents and Goals in Evolution for a critique of Darwin’s view of “natural selection” with an “agent” behind it, guiding the process—Mother Nature.) Thus, RLKH et al are nothing but Darwinian just-so storytellers—and anyone who defends them as being “purveyors of truth”, people who get “shouted down” for attempting to “speak the truth” are no better than the just-so storytellers themselves.

Dorothy Roberts on Race as a Political Entity

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I recently bought Dorothy Roberts’ Fatal Invention: How Science, Politics and Big Business Re-create Race in the Twenty-First Century (2011) (it was $1.99 in the nook store, couldn’t pass it up), which, how the title of the book explains, discusses how race is recreated today using methods of the past as well as methods of the future. One of her main claims is that race is a political entity. Now, while I don’t disagree here (there are of course social aspects to what we call “races”), she completely rides against biological racial realism (eg Spencer, 2014; Hardimon, 2017). Her concept, though, is similar to Hardimon’s (2017) socialrace concept, and it is already a part of Spencer’s Blumenbachian partitions (since race is both biologically and socially constructed in the American view of race). While I do not believe that you need genes to delineate race, Roberts also goes on the attack on Rosenberg et al (2002), who both Hardimon and Spencer cite to buttress their arguments on the reality of biological races.

Race is not a biological category that is politcally charged. It is a political category that has been disguised as a biological one. (Roberts, 2011: 14)

Note how this is extremely similar to Hardimon’s socialrace concept. In Hardimon’s concept, socialraces have a biological correlate: minimalist races. Hardimon’s concept says, for example, that “Hispanics/Latinos” are socialraces but they are a group that do not have a corresponding minimalist race—because “Hispanics/Latinos” are a mixture of different races. Race IS a biological category that has been politically charged: Groups look different; groups that look different share geographic ancestry; groups that look different that share geographic ancestry are derived from the same geographic location; therefore race is a biological category and is therefore politically charged (one reason) since people do not like the out-group—people that look different from themselves.

This distinction is important because many people misinterpret the phrase “race is socially constructed” to mean that the biological category of race has a social meaning, so that each society interprets differently what is means to belong to a biological race. According to this view, first we are born into  a race, and then our society determines the consequences of this natural inheritance. There is, then, no contradiction between seeing race as both biological and socially constructed. (Roberts, 2011: 14)

There, actually, IS NO CONTRADICTION between seeing race as socially and biologically constructed. Racial categories pick out real kinds in nature—which is what “biological racial realism” means. Since our racial categories pick out real kinds in nature, then, when it comes to society and social construction, whatever is believed about certain races in that society will be socially constructed. You can’t, for example, call a Nigerian Caucasian (see more on this below) because it does not make any sense.

Roberts then goes on (p. 14-15) about how “human beings do not fit the zoological definition of race” since a “biological race is a population of organisms that can be distinguished from other populations in the same species based on differences in inherited traits.” And so, since no human groups have this high degree of genetic differentiation, there are no human races, but only one human race.

Though Hardimon (2017: 99) articulates the best definition of race I have come across:

A race is a subdivision of Homo sapiens—a group of populations that exhibits a distinctive pattern of genetically transmitted phenotypic characters that corresponds to the group’s geographic ancestry and belongs to a biological line of descent initiated by a geographically separated and reproductively isolated founding population.

So we know that (1) populations exhibit distinctive features; (2) these populations that exhibit these distinctive features correspond to that population’s geographic ancestry, (3) these populations that exhibit these distinctive features which correspond to geographic ancestry belong to a biological line of descent which was initiated by reproductive isolated and geographically separated founding populations; so (4) race exists.

We know race is a political grouping because it has its political roots in slavery and colonialism, it has served its political function over the four hundred years since its inceptio, and its boundary lines—how many there are and who belongs to each one—have shifted over time and across nations to suit those political purposes. Who qualifiies as white, black, and Indian has been the matter of countless rule changes and judicial decisions. These racial reclassifications did not occur in response to scientific advances in human biology, but in response to sociopolitical imperatives. They reveal that was is being defined, orgainzed, and interpreted is a political relationship and not an innate classification. (Roberts, 2011: 15)

We can take this two ways here: (1) point out that Roberts is conflating minimalist/populationist races with socialraces (which is exactly what she is describing to the tee). Yes, since race is partly social, then, based on the social attitudes of people which do change over time. Then, in that society, certain groups who were barred from being in another group may be allowed “into” the group. This does not mean that race is not biological. “Oh the Irish were considered “not white” at one point in time, therefore race doesn’t exist since groups can exit group A and become group B based on sociopolitical inclinations.” This, of course, goes over the distinctive phenotypic differences between groups with peculiar geographic ancestry. THAT is what defines race; what Roberts is discussing is important, since race is partly political, but it is not the whole story.

In addition to the grotesque lynchings that terrorized blacks throughout the South, an especially brutal form of reenslavement was the false imprisonment of thousands of black men who were then leased to white farmers, entrepreneurs, and corporations as a source of cheap labor.

It is in this accute distinction that between the political status of whites and blacks, this way of governing the power relationship between them, that we find the origins of race. Colonial landowners inherited slavery as an ancient practive, but they invented race as a modern system of power. They employed Aristotle’s concept of natural slaves and natural rulers to define permanent features of black and white people. Race separated human beings into two fundamentally distinct groups: those who were indelibly born to be lifelong servants and those who were born to be their masters. Race radically transformed not only what it meant to be enslaved, but what it meant to be free. (Roberts, 2011: 23)

Let’s accept Roberts’ argument here that the political status of whites and blacks was a way to govern the power relationship between them: so what? That group A subjugated group B and attempted to justify it with X, Y, and Z doesn’t mean that group A and group B are not biological races—it just means that group A subjugated group B and, in the future, there were social repercussions (which is also a part of the phenomenon of race as a partly social construct).

Roberts then discusses the Census (p. 31-35) and how ever-changing racial definitions undermine the claim that biological racial realism is true. In Spencer’s argument, the US meaning of “race” is just a referent, “specifically the referent of US racial discourse” (Spencer, 2014: 1027). This is because, in America, race-talk is tied to the census. We Americans are familiar with the racial groupings on the census since they are not only in use on the census but numerous other institutions. Spencer (2014) then discusses how we can use “phonetic cues alone (e.g., African American Vernacular English), surnames alone (e.g., “Chen”), first names alone (e.g., “Lakisha”), and visual cues alone (e.g., a person’s face)” (Spencer, 2014: 1027) to know someone’s race. Therefore, according to Spencer, the discourse used in the census is the discourse used nation-wide.

But the census does not set what “race” means on these forms: the OMB (Office of Management Budgeting) does. The OMB refers to race as a “set” of populations, and so this leads Spencer to believe that the “sets” of populations that the OMB is referring to are whites, blacks, Asians, Pacific Islanders, and American Indians. So race is a particular, not a kind as Hardimon argues.

Roberts then argues against the “new racial science”, most forcefully, against Rosenberg et al (2002). She brings up the usual discourse “…the number of genetic clusters is dictated by the computer user, not the computer program” (Roberts, 2011: 74). Roberts says that the clusters are “arbitrary.” Roberts says that Rosenberg et al’s (2002) study failed to verify 18th-century racial typology, but it did confirm what we have known since Lewontin’s (1972) analysis: that there is more genetic variation within races than between them. About 93-95 percent of human genetic variation was found to be within race whereas 5-7 percent of human genetic variation was found to be between groups.

Roberts says that the clusters are “arbitrary.” This is a common critique, but it is irrelevant. The five populations found by Structure are genetically structured—they are meaningfully demarcated on the basis of genetic markers (Hardimon, 2017: 88). Roberts also discusses the K = 6 run, which identified the Kalash people.

The fact that structure represents a population as genetically distinct does not entail that the population is a race. Nor is the idea that populations corresponding to the five major geographic areas are minimalist races undercut by the fact that structure picks out the Kalash as a genetically distinct group. Like the K=5 graph, the K=6 graph shows that modulo our assumption, continental-level races are genetically structured” (Hardimon, 2017: 88).

The five clusters identified by Rosenberg et al (2002) represent continental-level minimalist races so the five populations which correspond to the major geographic locations throughout the world are continental-level minimalist races. So it is, in fact, possible to place individuals into different their continental-level minimalist race without knowing anything about the race or ancestry of the individuals from which the microsatellites were drawn. Rosenberg et al (2002) studied the populations based on language, culture, and geography, not skin color or race.

It is true that Rosenberg et al (2002) found 4.3 percent of the overall human genetic variation to be between races—but this does not ride against claims from biological racial realists. The genetic variation is enough to say that we have partitions at K = 5.

“People are born with ancestry that comes from their parents but are assigned a race” is how Camara Jones, a research director at the Centers for Disease Control (CDC) explains it. (Roberts, 2011: 77)

People are assigned races based on the ethnicity/ancestry of the parents. A Nigerian would not be assigned to the Asian race, since the Nigerian has none of the features which make “Asians” Asian.

This is very simple: if both parents belong to race R, then the child will be race R as well. If parent 1 belongs to R1 and so does parent 2, then the child will belong to R1 as well (since the parents have distinct physical features which correspond with geographic ancestry and their ancestors derived from a distinct geographic location. So, since people are born with ancestry that comes from their parents, then they are assigned their PARENT’S race; they are not assigned A race, as if one can assign any individual to any race. But what if one parent belongs to R1 and the other belongs to R2? Hardimon’s minimalist concept is vague here; it only shows that races exist, it does not say which populations are races. If an individual’s parents belong to R1 and R2, then that individual is mixed race. The existence of mixed race people, of course, does not rail against the existence of biological races.

In sum, Roberts does make some good points (in what I have read of the book so far), but she gets it wrong on race. Hardimon and Spencer have both defended the methodology/concepts used by Rosenberg et al (2002) and in doing so, they successfully argued for the existence of biological races—though their two viewpoints differ. That race is, in part, socially (politically) constructed is irrelevant. What Roberts does not understand is that these socially constructed groups (“white”, “black”) still, very much so, capture biological differences between them. That they are socialraces does not mean that they DO NOT have different physical features which correspond to geographic ancestry. The socialrace concept (which Roberts espouses in her book) is separate from Hardimon’s other scientific race concepts. But it is already inherent in Spencer’s, since his Blumenbachian partitions are social constructs of a biological reality. You don’t need genes to delineate races and minimalist races exist and are biologically real.

(I will cover other things from her book as I get to them. I will discuss race and medicine at length.)

Just-So Stories: The Slavery Hypertension Hypothesis

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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!” (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.


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.

Muscle Fibers, Obesity, Cardiometabolic Disorders, and Race

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The association between muscle fiber typing obesity and race is striking. It is well-established that blacks have a higher proportion of type II skeletal muscle fibers than whites and these higher proportions of these specific types of muscle fibers lead to physiological differences between the two races which then lead to differing health outcomes between them—along with differences in athletic competition. Racial differences in health are no doubt complex, but there are certain differences between the races that we can look at and say that there is a relationship here that warrants further scrutiny.

Why is there an association between negative health outcomes and muscle phsyiology? The answer is very simple if one knows the basics of muscle physiology and how and why muscles contract (it is worth noting that out of a slew of anatomic and phsyiologic factors, movement is the only thing we can consciously control, compare to menstration and other similar physiologic processes which are beyond our control). In this article, I will describe what muscles do, how they are controlled, muscle physiology, the differences in fiber typing between the races and what it means for health outcomes between them.

Muscle anatomy and physiology

Muscle fiber number is determined by the second trimester. Bell (1980) noted that skeletal muscle fiber in 6 year olds is not different from normal adult tissue, and so, we can say that between the time in the womb and age 6, muscle fiber type is set and cannot be changed (though training can change how certain fibers respond, see below).

Muscle anatomy and physiology is interesting because it shows us how and why we move the way we do. Tendons attach muscle to bone. Attached to the tendon is the muscle belly. The muscle belly is made up of facsicles and the fascicles are made up of muscle fibers. Muscle fibers are made up of myofibrils and myofibrils are made up of myofilaments. Finally, myofilaments are made up of proteins—specifically actin and myosin, this is what makes up our muscles.


(Image from here.)

Muscle fibers are encased by sarcolemma which contains cell components such as sarcoplasm, nuclei, and mitochondria. They also have other cells called myofibrils which contain myofilaments which are then made up of actin (thin filaments) and mysoin (thick filaments). These two types of filaments form numerous repeating sections within a myofibril and each repeating section is known as a sarcomere. Sarcomeres are the “functional” unit of the muscle, like the neuron is for the nervous system. Each ‘z-line’ denotes another sarcomere across a myofibril (Franzini-Armstrong, 1973; Luther, 2009).

Other than actin and myosin, there are two more proteins important for muscle contraction: tropomyosin and troponin. Tropomyosin is found on the actin filament and it blocks myosin binding sites which are located on the actin filament, and so it keeps myosin from attaching to muscle while it is in a relaxed state. On the other hand, troponin is also located on the actin filament but troponin’s job is to provide binding sites for calcium and tropomyosin when a muscle needs to contract.

So the structure of skeletal muscle can be broken down like so: epymyseum > muscle belly > perimyseum > fascicle > endomyseum > muscle fibers > myofibrils > myofilaments > myosin and actin. Note diagram (C) from above; the sarcomere is the smallest contractile unit in the myofibril. According to sliding filament theory (see Cook, 2004 for a review), a sarcomere shortens as a result of the ‘z-lines’ moving closer together. The reason these ‘z-lines’ converge is because myosin heads attach to the actin filament which asynchronistically pulls the actin filament across the myosin, which then results in the shortening of the muscle fiber. Sarcomeres are the basic unit controlling changes in muscle length, so the faster or slower they fire depends on the majority type of fiber in that specific area.

But the skeletal muscle will not contract unless the skeletal muscles are stimulated. The nervous system and the muscular system communicate, which is called neural activiation—defined as the contraction of muscle generated by neural stimulation. We have what are called “motor neurons”—neurons located in the CNS (central nervous system) which can send impulses to muscles to move them. This is done through a special synapse called the neuromuscular junction. A motor neuron that connects with muscle fibers is called a motor unit and the point where the muscle fiber and motor unit meet is callled the neuromuscular junction. It is a small gap between the nerve and muscle fiber called a synapse. Action potentials (electrical impulses) are sent down the axon of the motor neuron from the CNS and when the action potential reaches the end of the axon, hormones called neurotransmitters are then released. Neurotransmitters transport the electrical signal from the nerve to the muscle.

Muscle fiber types

The two main categories of muscle fiber are type I and type II—‘slow’ and ‘fast’ twitch, respectively. Type I fibers contain more blood cappilaries, higher levels of mitochondria (which transforms food into ATP) and myoglobin which allows for an improved delivery of oxygen. Since myoglobin is similar to hemoglobin (the red pigment which is found in red blood cells), type I fibers are also known as ‘red fibers.’ Type I fibers are also smaller in diameter and slower to produce maximal tension, but are also the most fatigue-resistant type of fiber.

Type II fibers have two subdivisions—IIa and IIx—based on their mechanical and chemical properties. Type II fibers are in many ways the opposite of type I fibers—they  contain far fewer blood cappilaries, mitochondria and myoglobin. Since they have less myoglobin, they are not red, but white, which is why they are known as ‘white fibers.’ IIx fibers have a lower oxidative capacity and thusly tire out quicker. IIa, on the other hand, have a higher oxidative capacity and fatigue slower than IIx fibers (Herbison, Jaweed, and Ditunno, 1982; Tellis et al, 2012). IIa fibers are also known as intermediate fast twitch fibers since they can use both anarobic and aerobic metabolism equally to produce energy. So IIx fibers are a combo of I and II fibers. Type II fibers are bigger, quicker to produce maximal tension, and tire out quicker.

Now, when it comes to fiber typing between the races, blacks have a higher proportion of type II fibers compared to whites who have a higher proportion of type I fibers (Ama et al, 1986; Ceaser and Hunter, 2015; see Entine, 2000 and Epstein, 2014 for reviews). Higher proportions of type I fibers are associated with lower chance of cardiovascular events, whereas type II fibers are associated with a higher risk. Thus, “Skeletal muscle fibre composition may be a mediator of the protective effects of exercise against cardiovascular disease” (Andersen et al, 2015).

Now that the basics of muscle anatomy and physiology are apparent, hopefully the hows and whys of muscle contraction and what different muscle fibers do are becoming clear, because these different fibers are distributed between the races in uneven frequencies, which then leads to differences in sporting performance but also differents in health outcomes.

Muscle fibers and health outcomes

We now know the physiology and anatomy of muscle and muscle fiber typing. We also know the differences between each type of skeletal muscle fiber. Since the two races do indeed differ in the percentage of skeletal muscle fiber possessed on average, we then should find stark differences in health outcomes, part of the reason being these differences in muscle fiber typing.

While blacks on average have a higher proportion of type II muscle fibers, whites have a higher proportion of type I muscle fibers. Noting what I wrote above about the differences between the fiber types, and knowing what we know about racial differences in disease outcomes, we can draw some inferences on how differences in muscle fiber typing between races/individuals can then affect disease seriousness/acquisition.

In their review of black-white differences in muscle fiber typing, Ceaser and Hunter (2015) write that “The longitudinal data regarding the rise in obesity indicates obesity rates have been highest among non-Hispanic Black women and Hispanic women.” And so, knowing what we know about fiber type differences between races and how these fibers act when they fire, we can see how muscle fiber typing would contribute to differences in disease acquisition between groups.

Tanner et al (2001) studied 53 women (n=28, lean women; and n=25, obese women) who were undergoing an elective abdominal surgery (either a hysterectomy or gastric bypass). Their physiologic/anatomic measures were taken and they were divided into races: blacks and whites, along with their obesity status. Tanner et al found that the lean subjects had a higher proportion of type I fibers and a lower proportion of type IIx fibers whereas those who were obese were more likely to have a higher proportion of type IIb muscle fibers.

Like other analyses on this matter, Tanner et al (2001) showed that the black subjects had a higher proportion of type II fibers in comparison to whites who had a higher proportion of type I fibers (adiposity was not taken into account). Fifty-one percent of the fiber typing from whites was type I whereas for blacks it was 43.7 pervent. Blacks had a higher proportion of type IIx fibers than whites (16.3 percent for whites and 23.4 for blacks). Lean blacks and lean whites, though, had a similar percentage of type IIx fibers (13.8 percent for whites and 15 percent for blacks). It is interesting to note that there was no difference in type I fibers between lean whites and blacks (55.1 percent for whites and 54.1 percent for blacks), though muscle fibers from obese blacks contained far fewer type I fibers compared to their white counterparts (48.6 percent for whites and 34.5 for blacks). Obese blacks’ muscle fiber had a higher proportion of type IIx fibers than obese whites’ fiber typing (19.2 percent for whites and 31 percent for blacks). Lean blacks and lean whites had a higher proportion of type I fibers than obese blacks and obese whites. Obese whites and obese blacks had more type IIx fibers than lean whites and lean blacks.

So, since type II fibers are insulin resistant (Jensen et al, 2007), then they should be related to glucose intloerance—type II diabetes—and blacks with ancestry from West Africa should be most affected. Fung (2016, 2018) shows that obesity is a disease of insulin resistance, and so, we can bring that same rationale to racial differences in obesity. Indeed, Nielsen and Christensen (2011) hypothesize that the higher prevalence of glucose intolerance in blacks is related to their lower percentage of type I fibers and their higher percentage of type II fibers.

Nielsen and Christensen (2011) hypothesize that since blacks have a lower percentage of type I fibers (the oxidative type), this explains the lower fat oxidation along with lower resting metabolic rate, sleeping metabolic rate, resting energy expenditure and Vo2 max in comparison to whites. Since type I fibers are more oxidative over the glycolitic type II fibers, the lower oxidative capacity in these fibers “may cause a higher fat storage at lower levels of energy intake than in individuals with a higher oxidative capacity” (Nielsen and Christensen, 2011: 611). Though the ratio of IIx and IIa fibers are extremely plastic and affected by lifestyle, Nielsen and Christensen do note that individuals with different fiber typings had similar oxidative capacity if they engaged in physical activity. Recall back to Caesar and Hunter (2015) who note that blacks have a lower maximal aerobic capacity and higher proportion of type II fibers. They note that lack of physical activity exacerbates the negative effects that a majority type II fibers has over majority type I. And so, some of these differences can be ameliorated between these two racial groups.

The point is, individuals/groups with a higher percentage of type II fibers who do not engage in physical activity have an even higher risk of lower oxidative capacity. Furthermore, a higher proportion of type II fibers implies a higher percentage of IIx fibers, “which are the least oxidative fibres and are positively associated with T2D and obesity” (Nielsen and Christensen, 2011: 612). They also note that this may explain the rural-urban difference in diabetes prevalance, with urban populations having a higher proportion of type II diabetics. They also note that this may explain the difference in type II diabetes in US blacks and West African natives—but the reverse is true for West Africans in the US. There is a higher rate of modernization and, with that, a higher chance to be less physically active and if the individual in question is less physically active and has a higher proportion of type II fibers then they will have a higher chance of acquiring metabolic diseases (obesity is also a metabolic disease). Since whites have a higher proportion of type I fibers, they can increase their fat intake—and with it, their fat oxidation—but this does not hold for blacks who “may not adjust well to changes in fat intake” (Nielsen and Christensen, 2011: 612).

Nielsen and Christensen end their paper writing:

Thus, Blacks of West African ancestry might be genetically predisposed to T2D because of an inherited lower amount of skeletal muscle fibre type I, whereby the oxidative capacity and fat oxidation is reduced, causing increased muscular tissue fat accumulation. This might induce skeletal muscle insulin resistance followed by an induced stress on the insulin-producing beta cells. Together with higher beta-cell dysfunction in the West African Diaspora compared to Whites, this will eventually lead to T2D (an overview of the ‘skeletal muscle distribution hypothesis’ can be seen in Figure 2).


Lambernd et al (2012) show that muscle contractions eliminated insuin resistance by blocking pro-inflammatory signalling pathways: this is the mechanism by which physical activity decreases glucose intolerance and thusly improves health outcomes—especially for those with a higher proportion of type II fibers. Thus, it is important for individuals with type II fibers to exercise, since sedentariness is associated with an age-related insulin resistance due to impaired GLUT4 utilization (Bunprajun et al, 2013).

(Also see Morrison and Cooper’s (2006) hypothesis that “reduced oxygen-carrying capacity induced a shift to more explosive muscle properties” (Epstein, 2014: 179). Epstein notes that the only science there is on this hypothesis is one mouse and rat study showing that low hemoglobin can “induce a switch to more explosive muscle fibers” (Epstein, 2014: 178), but this has not been tested on humans to see if it would hold. If this is tested on humans and if it does hold, then that would lend credence to Morrison’s and Cooper’s (2006) hypothesis.)


Knowing what we know about muscle anatomy and physiology and how muscles act we can understand the influence the different muscle types have on disease and how they contribute to disease variation between race, sex and the individual level. Especially knowing how type II fibers act when the individual in question is insulin resistant is extremely important—though it has been noted that individuals who participate in aerobic exercise decrease their risk for cardiometabolic diseases and can change the fiber distribution difference between IIx and IIa fibers, lowering their risk for acquiring cardiometabolic diseases (Ceaser and Hunter, 2015).

Thinking back to sarcomeres (the smallest contractile unit in the muscle) and how they would act in type II fibers: they would obviously contract much faster in type II muscles over type I muscles; they would then obviously tear faster than type I muscles; since type II muscles are more likely to be insulin resistant, then those with a higher proportion of type II fibers need to focus more on aerobic activity to “balance out” type IIx and IIa fibers and decrease the risk of cardiometabolic disease due to more muscle contractions (Lambernd et al, 2012). Since blacks have a higher proportion of type II fibers and are more likely to be sedentary than whites, and since those who have a higher proportion of type II fibers are more likely to be obese, then it is clear that exercise can and will ameliorate some of the disparity in cardiometabolic diseases between blacks and whites.