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The cold winter theory (CWT) is a theory that purports to explain why those whose ancestors evolved in colder climes are more “intelligent” than those whose ancestors evolved in warmer climes. Popularized by Rushton (1997), Lynn (2006), and Kanazawa (2012), the theory—supposedly—accounts for the “haves” and the “have not” in regard to intelligence. However, the theory is a just-so story, that is, it explains what it purports to explain without generating previously unknown facts not used in the construction of the theory. PumpkinPerson is irritated by people who do not believe the just-so story of the CWT writing (citing the same old “challenges” as Lynn which were dispatched by McGreal):
The cold winter theory is extremely important to HBD. In fact I don’t even understand how one can believe in racially genetic differences in IQ without also believing that cold winters select for higher intelligence because of the survival challenges of keeping warm, building shelter, and hunting large game.
The CWT is “extremely important to HBD“, as PP claims, since there needs to be an evolutionary basis for population differences in “intelligence” (IQ). Without the just-so story, the claim that racial differences in “intelligence” are “genetically” based crumbles.
Well, here is the biggest “challenge” (all other refutations of it aside) to the CWT. Notions of which population are or are not “intelligent” change with the times. The best example is what the Greeks—specifically Aristotle—wrote about the intelligence of those who lived in the north. Maurizio Meloni, in his 2019 book Impressionable Biologies: From the Archaeology of Plasticity to the Sociology of Epigenetics captures this point (pg 41-42; emphasis his):
Aristotle’s Politics is a compendium of all these ideas [Orientals being seen as “softer, more delicate and unwarlike” along with the structure of militaries], with people living in temperate (mediocriter) places presented as the most capable of producing the best political systems:
“The nations inhabiting the cold places and those of Europe are full of spirit but somewhat deficient in intelligence and skill, so that they continue comparatively free, but lacking in political organization and the capacity to rule their neighbors. The peoples of Asia on the other hand are intelligent and skillful in temperament, but lack spirit, so that they are in continuous subjection and slavery. But the Greek race participates in both characters, just as it occupies the middle position geographically, for it is both spirited and intelligent; hence it continues to be free and to have very good political institutions, and to be capable of ruling all mankind if it attains constitutional unity.” (Pol. 1327b23-33, my italics)
Views of direct environmental influence and the porosity of bodies to these effects also entered the military machines of ancient empires, like that of the Romans. Offices such as Vegetius (De re militari, I/2) suggested avoiding recruiting troops from cold climates as they had too much blood and, hence, inadequate intelligence. Instead, he argued, troops from temperate climates be recruited, as they possess the right amount of blood, ensuring their fitness for camp discipline (Irby, 2016). Delicate and effemenizing land was also to be abandoned as soon as possible, according Manilius and Caesar (ibid). Probably the most famous geopolitical dictum of antiquity reflects exactly this plastic power of places: “soft lands breed soft men”, according to the claim that Herodotus attributed to Cyrus.
Isn’t that weird, how things change? Quite obviously, which population is or is not “intelligent” is based on the time and place of the observation. Those in northern Europe, who are purported to be more intelligent than those who live in temperate, hotter climes—back in antiquity—were seen to be less intelligent in comparison to those who lived in more temperate, hotter climes. Imagine stating what Aristotle said thousands of years ago in the present day—those who push the CWT just-so story would look at you like you’re crazy because, supposedly, those who live in and evolved in colder climes had to plan ahead and faced a tougher environment in comparison to those who lived closer to the equator.
Imagine we could transport Aristotle to the present day. What would he say about our perspectives on which population is or is not intelligent? Surely he would think it ridiculous that the Greeks today are less “intelligent” than those from northern Europe. But that only speaks to how things change and how people’s perspectives on things change with the times and who is or is not a dominant group. Now imagine that we can transport someone (preferably an “IQ” researcher) to antiquity when the Greeks were at the height of their power. They would then create a just-so story to justify their observations about the intelligence of populations based on their evolutionary history.
Anatoly Karlin cites Galton, who claims that ancient Greek IQ was 125, while Karlin himself claims IQ 90. I cite Karlin’s article not to contest his “IQ estimates”—nor Galton’s—I cite it to show the disparate “estimates” of the intelligence of the ancient Greeks. Because, according to the Greeks, they occupied the middle position geographically, and so they were both spirited and intelligent compared to Asians and northern Europeans.
This is similar to Wicherts, Boorsboom, and Dolan (2010) who responded to Rushton, Lynn, and Templer. They state that the socio-cultural achievements of Mesopotamia and Egypt stand in “stark contrast to the current low level of national IQ of peoples of Iraq and Egypt and that these ancient achievements appear to contradict evolutionary accounts of differences in national IQ.“ One can make a similar observation about the Maya. Their cultural achievements stand in stark contrast to their “evolutionary history” in warm climes. The Maya were geographically isolated from other populations and they still created a writing system (independently) along with other cultural achievements that show that “national IQs” are irrelevant to what the population achieved. I’m sure an IQ-ist can create a just-so story to explain this away, but that’s not the point.
Going back to what Karlin and Galton stated about Greek IQ, their IQ is irrelevant to their achievements. Whether or not their IQ was 120-125 or 90 is irrelevant to what they achieved. To the Mesopotamians and Egyptians, they were more intelligent than those from northern climes. They would, obviously, think that based on their achievements and the lack of achievements in the north. The achievements of peoples in antiquity would paint a whole different picture in regard to an evolutionary theory of human intelligence—and its distribution in human populations.
So which just-so story (ad hoc hypothesis) should we accept? Or should we just accept that which population is or is not “intelligent” and capable of constructing militaries is contingent based on the time and the place of the observation? Looking at “national IQs” of peoples in antiquity would show a huge difference in comparison to what we observe today about the “national IQs” (supposedly ‘intelligence’) of populations around the world. In antiquity, those who lived in temperate and even hotter climes had greater achievements than others. Greeks and Romans argued that peoples from northern climes should not be enlisted in the military due to where they were from.
These observations from the Greeks and Romans about who and who not to enlist in the military, along with their thoughts on Northern Europeans prove that perspectives on which population is or is not “intelligent” is contingent based on the time and place. This is why “national IQs” should not be accepted, not even accounting for the problems with the data (Richardson, 2004; also see Morse, 2008; also see The Ethics of Development: An Introduction by Ingram and Derdak, 2018). Seeing the development of countries/populations in antiquity would lead to a whole different evolutionary theory of the intelligence of populations, proving the contingency of the observations.
Different groups of people eat different things. Different groups of people also differ genetically. What one eats is part of their environment. So, there is a G and E (genes and environment) interaction between races/ethnies in regard to the shape of their teeth. Yes, one can have a different shape to their teeth, on average, compared to their co-ethnics if they eat different things from them as that is one thing that shapes the development of teeth.
It is very difficult to ascertain the race of an individual through their dentition, but there are certain dental characters which can lead to the identification of race. Rawlani et al (2017) show that there are differences in the dentition of Caucasians, Negroids, Mongoloids and Australoids.
One distinct difference that Monogloid teeth have is having a “shovel” or “scoop” appearance. They also have larger incisors than Caucasoids, while having shorter anatomic roots with better-developed trunks. Caucasoids had a “v” shape to their teeth, while their anterior teeth were “chisel shaped”; 37 percent of Caucasoids had a cusp on the carabelli cusp. Rawlani et al (2017) also note that one study found that 94 percent of Anglo-Saxons had four cusps compared to five for other races. Australoids had a larger arch size (but relatively smaller anterior teeth), which accommodates larger teeth. They have the biggest molars of any race; the mesiodistal diameter of the first molar is 10 percent larger than white Americans and Norweigian Lapps. Negroids had smaller teeth with more spacing, they are also less likely to have the Carabelli cusp and shovel incisors. They are more likely to have class III malocclusion (imperfect positioning of the teeth when the jaw is closed) and open bite. Blacks are more likely to have bimaxillary protrusion, though Asians do get orthodontic surgery for it (Yong-Ming et al, 2009).
Rawlani et al’s (2017) review show that there are morphologic differences in teeth between racial groups that can be used for identification.
When it comes to the emergence of teeth, American Indians (specifically Northern Plains Indians) had an earlier emergence of teeth compared to whites and blacks. American Indian children had a higher rate of dental caries, and so, since their teeth appear at an earlier age compared to whites and blacks, they had more of a chance for their teeth to be exposed to diets high in sugar and processed foods along with lack of oral hygiene (Warren et al, 2016).
Older blacks had more decayed teeth than whites in one study (Hybels et al, 2016). Furthermore, older blacks were more likely than older whites to self-report worse oral hygeine; blacks had a lower number of teeth than whites in this study—which was replicated in other studies—though differences in number of teeth may come down to differences in access to dental care along with dental visits (Huang and Park, 2016). One study even showed that there was unconscious racial bias in regard to root canal treatments: whites were more likely to get root canals (i.e., they showed a bias in decision-making favoring whites), whereas blacks were more likely to get the tooth pulled (Patel et al, 2018).
Kressin et al (2003) also show that blacks are less likely to receive root canals than whites, while Asians were more likely, which lends further credence to the claim of unconscious racial bias. So just like unconscious bias affects patients in regard to other kinds of medical treatment, the same is true for other doctors such as dentists: they have a racial bias which then affects the care they give their patients. Gilbert, Shewchuk, and Litaker (2006) also show that blacks are more likely to have tooth extractions when compared to other races, but people who went to a practice that had a higher percentage of black Americans were more likely to have a tooth extraction, regardless of the individual’s race. This says to me that, since there is unconscious bias in tooth extraction (root canals), that the more black patients a dentist sees the more it is likely that they would extract the tooth of the patient (regardless of race), since they would do that more often than not due to the number of patients they see that are black Americans.
Otuyemi and Noar (1996) showed that Nigerian children had larger mesio-distal crown diameters compared to Briton children. American blacks are more likely to have hyperdontia (extra teeth in the mouth) compared to whites, and are also more likely to have fourth molars and extra premolars (Harris and Clark, 2008). Blacks have slightly larger teeth than whites (Parciak, 2015).
Dung et al (2019) also note ethnic differences in teeth looking at four ethnic groups in Vietnam:
Our study of 4565 Vietnamese children of four ethnic groups (Kinh, Tay, Thai and Muong) showed that most dental arch indicators in males were statistically significantly higher than those in females.
In comparison to other ethnic groups, 12-year-old Vietnamese children had similar dimensions of the upper and lower intercanine and intermolar width to children in the same age group in South China. However, the average upper posterior length 1 and lower posterior length 1 were shorter than those in Africans (Kenyan) and Caucasian (American blacks aged 12). The 12-year-old Vietnamese have a narrower and shorter dental arch than Caucasian children, especially the maxillary, and they need earlier orthodontic intervention.
The size of the mandible reflects the type of energy ingested: decreases “in masticatory stress among agriculturalists causes the mandible to grow and develop differently” (Cramon-Taubadel, 2011). This effect would not only be seen in an evolutionary context. Cramon-Taubadel (2011) writes:
The results demonstrate that global patterns of human mandibular shape reflect differences in subsistence economy rather than neutral population history. This suggests that as human populations transitioned from a hunter-gatherer lifestyle to an agricultural one, mandibular shape changed accordingly, effectively erasing the signal of genetic relationships among populations.
So it seems like the change from a hunter-gatherer lifestyle to one based on plant/animal domestication had a significant effect on the mandible—and therefore teeth—of a population.
So teeth are a bone, and bones adapt. When an individual is young, the way their teeth, and subsequently jaw, are can be altered by diet. Eating hard or soft foods during adolescence can radically change the shape of the teeth (Liebermann, 2013). The harder the stuff one has to chew on will alter their facial morphology (i.e., their jaw and cheekbones) and, in turn, their teeth. This is because the teeth are bones and any stress put on them will change them. This, of course, speaks to the interaction of G and E (genes and environment). There are genes that contribute to differences in dental morphology between populations, and they impact the difference between ethnic/racial groups.
Further making the differences between these groups is what they choose to eat: the hardness or softness of the food they eat in adolescence and childhood can and will dictate the strength of one’s jaw and shape and strength of their teeth in adulthood, though racial/ethnic identification would still be possible.
Racial differences in dentition come down to evolution (development) and what and how much of the population in question eats. The differences in dentition between these populations are, in a way, dictated by what they eat in the beginning years of life. This critical period may dictate whether or not one has a strong or weak jaw. These differences come down to, like everything else, an interaction between G and E (genes and environment), such as the food one eats as an adolescent/baby which would then affect the formation of teeth in that individual. Of course, in countries that have a super-majority of one ethnic group over another, we can see what diet does to an individual in an ethnic group’s teeth.
There are quite striking differences in dentition between races/ethnic groups, and this can and will (along with other variables) lead to correctly identifying the race of an individual in question.
I have written a few response articles to some of what Thompson has written over the past few years. He is most ridiculous when he begins to talk about nutrition (see my response to one of his articles on diet: Is Diet An IQ Test?). Now, in a review of Angela Saini’s (2019) new book Superior: The Return of Race Science, titled Superior Ideology, Thompson, yet again, makes more ridiculous assertions—this time about bone density as an adaptation. (I don’t care about what he says about race; though I should note that the debate will be settled with philosophy, not biology. Nor do I care about whatever else he says, I’m only concerned with his awful take on anatomy and physiology.)
The intellectually curious would ask: are there other adaptations which are not superficial? How about bone density?
Just-so story incoming.
I’m very familiar with these two papers. Let’s look at them both in turn.
The first study is Racial Differences in Bone Density between Young Adult Black and White Subjects Persist after Adjustment for Anthropometric, Lifestyle, and Biochemical Differences (Ettinger et al, 1997). Now, I did reference this article in my own piece on racial differences in drowning, though only to drive home the point that there are racial differences in bone density. Thompson is outright using this article as “evidence” that it is an adaptation.
In any case, Ettinger et al (1997) state that greater bone density in blacks may be due to differences in calciotropic hormones—hormones that play a major role in bone growth and bone remodeling. When compared with whites “black persons have lower urinary calcium excretion, higher 1,25-dihydroxyvitamin D (1, 25D) level, and lower 25-hydroxyvitamin D (25D) and osteocalcin level (9)” (Ettinger et al, 1997). They also state that bone density can be affected by calcium intake, physical activity, They also state that testosterone (an androgen) may account for racial and gender differences in bone density, writing “Two studies have demonstrated statistically significantly higher serum testosterone level in young adult black men (22) and women (23).”
Oh, wow. What are refs  and ?  is one of my favorites—Ross et al (1986) (read my response). To be brief, the main problems with Ross et al is that assay times were all over the place, along with it being a small convenience sample of 50 blacks and 50 whites. LabTests Online writes that it is preferred to assay in the morning while in a fasted state. In Ross et al, the assay times were between 10 am and 3 pm, which was a “convenient time” for the students. Along with the fact that the sample was small, this study should not be taken seriously regarding racial differences in testosterone, and, thus, racial differences in bone density.
Now what about ? This is another favorite of mine—Henderson et al (1988; of which Ross was a part of). Mazur (2016) shows that black women do not have higher levels of testosterone than white women. Furthermore, this is just like Ellis’ (2017) claims that there is a difference in prenatal androgen exposure, but that claim, too, fails. In any case, testosterone can’t explain differences in bone density between races.
Ettinger et al (1997) showed that blacks had higher levels of bone density than whites in all of the sites they looked at. (Though they also used skin-fold testing, which is notoroiously bad at measuring body composition in blacks; see Vickery, Cureton, and Collins, 1988). However, Ettinger et al (1997) did not claim, nor did they imply that bone density is an adaptation.
Now, getting to the second citation, Hochberg (2007). Hochberg (2007) is a review of differences in bone mineral density (BMD) between blacks and whites. Unfortunately, there is no evidence in this paper, either, that BMD is an adaptation. Hochberg (2007) gives numerous reasons why blacks would have stronger skeletons than whites, and neither is that they are an “adaptation”:
Higher bone strength in blacks could be due to several factors including development of a stronger skeleton during childhood and adolescence, slower loss of bone during adulthood due to reduced rates of bone turnover and greater ability to replace lost bone due to better bone formation. Bell and colleagues reported that black children had higher bone mass than white children and that this difference persisted into young adulthood, at least in men (23,24). Development of a stronger skeleton during childhood and adolescence is dependent on the interaction of genetic and environmental factors, including nutrition and lifestyle factors (25).
Genetic, nutritional, lifestyle and hormonal factors may contribute to differences in rates of bone turnover during adulthood
There are numerous papers in the literature that show that blacks have higher BMD than whites and that there are racial differences in this variable. However, the papers that Thompson has cited are not evidence. That trait T exists and there is a difference in trait T between G1 and G2 does not license the claim that the difference in trait T between G1 and G2 is “genetic.”
Thompson then writes:
Equally, how about differences in glomerular function, a measure of kidney health, for which the scores are adjusted for those of Black African descent, to account for their higher muscle mass? Muscle mass and bone density are not superficial characteristics. In conflicts it would be a considerable advantage to have strong warriors, favouring “hard survival”.
Here’s the just-so story.
Race adjustment for estimating glomerular filtration rate (GFR) is not always needed (Zanocco et al, 2012). Renal function is measured by GFR. Renal function is an indication of the kidney’s functioning. Racial differences in kidney function exist, even in cases where the patients do not have CKD (chronic kidney disease) (Peralta et al, 2011). Black Americans also constitute 35 percent of all patients in America receiving kidney dialysis, despite being only 13 percent of the US population. Blacks do generate higher levels of creatinine compared to whites, and this is due to higher average muscle mass when compared with whites.
There are differences in BMD and muscle mass between blacks and whites which is established by young adulthood (Popp et al, 2017), but the claim that there trait T is an adaptation because trait T exists and there is a difference between G1 and G2 is unfounded. It’s simply a just-so story, using the old EP reverse engineering. The two papers referenced by Thompson are not evidence that the BMD is an adaptation, it only shows that there are racial differences in the trait. That there are racial differences in the two traits does not license the claim that the traits in question are an adaptation as Thompson seems to be claiming. The papers he refers to only note a difference between the two groups; it does not discuss the ultimate etiology of the difference between the groups, which Thompson does with his just-so story.
I recently bought Lamarck’s Revenge by paleobiologist Peter Ward (2018) because I went on a trip and needed something to read on the flight. I just finished the book the other day and I thought that I would give a review and also discuss Coyne’s review of the book since I know he is so uptight about epigenetic theories, like that of Denis Noble and Jablonka and Lamb. In Lamarck’s Revenge, Ward (2018) purports to show that Lamarck was right all along and that the advent of the burgeoning field is “Lamarck’s revenge” for those who—in the current day—make fun of his theories in intro biology classes. (When I took Bio 101, the professor made it a point to bring up Lamarck and giraffe necks as a “Look at this wrong theory”, nevermind the fact that Darwin was wrong too.) I will go chapter-by-chapter, give a brief synopsis of each, and then discuss Coyne’s review.
In the introduction, Ward discusses some of the problems with Darwinian thought and current biological understanding. The current neo-Darwinian Modern Synthesis states that what occurs in the lifetime of the organism cannot be passed down to further generations—that any ‘marks’ on the genome are then erased. However, recent research has shown that this is not the case. Numerous studies on plants and “simpler” organisms refute the notion, though for more “complex” organisms it has yet to be proved. However, that this discussion is even occurring is proof that we are heading in the right direction in regard to a new synthesis. In fact, Jablonka and Lamb (2005) showed in their book Evolution in Four Dimensions, that epigenetic mechanisms can and do produce rapid speciation—too quick for “normal” Darwinian evolution.
Ward (2018: 3-4) writes:
There are good times and bad times on earth, and it is proposed here that dichotomy has fueled a coupling of times when evolution has been mainly through Darwinian evolution and others when Lamarckian evolution has been dominant. Darwinian in good times, Lamarckian in bad, when bad can be defined as those times when our environments turn topsy-turvy, and do so quickly. When an asteroid hits the planet. When giant volcanic episodes create stagnant oceans. When a parent becomes a sexual predator. When our industrial output warms the world. When there are six billion humans and counting.
These examples are good—save the one about when a parent becomes a sexual predator (but if we accept the thesis that what we do and what happens to us can leave marks on our DNA that don’t change it but are passed on then it is OK)—and they all point to one thing: when the environment becomes ultra-chaotic. When such changes occur in the environment, that organism needs a physiology that is able to change on-demand to survive (see Richardson, 2017).
Ward (2018: 8) then describes Lamarck’s three-step process:
First, an animal experienced a radical change of the environment aroujnd it. Second, the initial response to the environmental change was some new kind of behavior by that of the animal (or whole species). Third, the behavioral change was followed by morphological change in subsequent generations.
Ward then discusses others before Darwin—Darwin’s grandfather Erasmus, for instance—who had theories of evolution before Darwin. In any case, we went from a world in which a God created all to a world where everything we see was created by natural processes.
Then in Chapter 2, Ward discusses Lamarck and Darwin and each of their theories in turn. (Note that Darwin did have Lamarckian views too.) Ward discusses the intellectual dual between Lamarck and Georges Cuvier, the father of the field of comparative anatomy—he studied mass extinctions. At Lamarck’s funeral, Cuvier spoke bad about Lamarck and buried his theories. (See Cuvier’s (1836) Elegy of Lamarck.) These types of arguments between academics have been going on for hundreds of years—and they will not stop any time soon.
In Chapter 3 Ward discusses Darwin’s ideas all the way to the Modern Synthesis, discussing how Darwin formulated his theory of natural selection, the purported “mechanism of evolution.” Ward discusses how Darwin at first rejected Lamarck’s ideas but then integrated them into future editions of On the Origin. We can think of this scenario: Imagine any environment and organisms in it. The environment rapidly shifts to where it is unrecognizable. The organisms in that environment then need to either change their behavior (and reproduce) or die. Now, if there were no way for organisms to change, say, their physiology (since physiology is dependent on what is occurring in the outside environment), then the species would die and there would be no evolution. However, the advent of evolved physiologies changed that. Morphologic and physiologic plasticity can and does help organisms survive in new environments—environments that are “new” to the parental organism—and this is a form of Lamarckism (“heritable epigenetics” as Ward calls it).
They studied two (so-called) different species of nautilus—one, nautilus pampilus, widespread across the Pacific and Indian Oceans and two, Nautilus stenomphalus which is only found at the Great Barrier Reef. Pompilus has a hole in the middle of its shell, whereas stenomphalus has a plug in the middle. Both of these (so-called) species have different kinds of anatomy—Pompilus has a hood covered with bumps of flesh whereas stenomphalus‘ hood is filled with projections of moss-like twig structures. So over a thirty-day period, they captured thirty nautiluses and snipped a piece of their tentacles and sequences the DNA found in it. They found that the DNA of these two morphologically different animals was the same. Thus, although the two are said to be different species based on their morphology, genetically they are the same species which leads Ward (2018: 52) to claim “that perhaps there are fewer, not more, species on Earth than science has defined.” Ward (2018: 53) cites a recent example—the fact that the Columbian and North American wooly mammoths “were genetically the same but the two had phenotypes determined by environment” (see Enk et al, 2011).
Now take Ward’s (2018: 58) definition of “heritable epigenetics”:
In heritable epigenetics, we pass on the same genome, but one marked (mark is the formal term for the place that a methyl molecule attaches to one nucleotide, a rung in the ladder of DNA) in such a way that the new organism soon has its own DNA swarmed by these new (and usually unwelcome) additions riding on the chromosomes. The genotype is not changed, but the genes carrying the new, sucker-like methyl molecules change the workings of the organism to something new, such as the production (or lack thereof) of chemicals necessary for our good health, or for how some part of the body is produced.
Chapter 5 discusses different environments in the context of evolutionary history. Environmental catastrophes that lead to the decimation of most life on the planet are the subject—something that Gould wrote about in his career (his concept of contingency in the evolutionary process). Now, going back to Lamarck’s dictum (first an environmental change, second a change in behavior, and third a change in phenotype), we can see that these kinds of processes were indeed imperative in the evolution of life on earth. Take the asteroid impact (K-Pg extinction; Cretaceous-Paleogene) that killed off the dinosaurs and threw tons of soot into the air, blocking out the sun making it effectively night (Schulte et al, 2010). All organisms that survived needed to eat. If the organism only ate in the day time, it would then need to eat at night or die. That right there is a radical environmental change (step 1) and then a change in behavior (step 2) which would eventually lead to step 3.
In Chapter 6, Ward discusses epigenetics and the origins of life. The main subject of the chapter is lateral gene transfer—the transmission of different DNA between genomes. Hundreds or thousands of new genes can be inserted into an organism and effectively change the morphology, it is a Lamarckian mechanism. Ward posits that there were many kinds of “genetic codes” and “metabolisms” throughout earth’s history, even organisms that were “alive” but were not capable of reproducing and so they were “one-offs.” Ward even describes Margulis’ (1967) theory of endosymbiosis as “a Lamarckian event“, which even Margulis accepts. Thus, the evolution of organisms is possible through lateral gene transfer and is another Lamarckian mechanism.
Chapter 7 discusses epigenetics and the Cambrian explosion. Ward cites a Creationist who claims that there has not been enough time since the 500 million year explosion to explain the diversity of body plans since then. Stephen Jay Gould wrote a whole book on this—Wonderful Life. It is true that Darwinian theory cannot explain the diversity of body plans, nor even the diversity of species and their traits (Fodor and Piatelli-Palmarini, 2010), but this does not mean that Creationism is true. If we are discussing the diversification of organismal life after mass extinctions, then Darwinian evolution cannot have possibly played a role in the survival of species—organisms with adaptive physiologies would have had a better chance of surviving in these new, chaotic environments.
It is posited here that four different epigenetic mechanisms presumably contributed to the great increase in both the kinds of species and the kinds of morphologies that distinguished them that together produced the Cambrian explosion as we currently know it: the first, now familiar, methylation; second, small RNA silencing; third, changes in the histones, the scaffolding that dictates the overall shape of a DNA molecule; and, finally, lateral gene transfer, which has recently been shown to work in animals, not just microbes. (Ward, 2018: 113)
Ginsburg and Jablonka (2010) state that “[associative] learning-based diversification was
accompanied by neurohormonal stress, which led to an ongoing destabilization and re-patterning of the epigenome, which, in turn, enabled further morphological, physiological, and behavioral diversification.” So associative learning, according to Ginsburg and Jablonka, was the driver of the Cambrian explosion. Ward (2018: 115) writes:
[The paper by Ginsburg and Jablonka] says that changes of behavior by both animal predators and animal prey began as an “arms race” in not just morphology but behavior. Learning how to hunt or flee; detecting food and mats and habitats at a distance from chemical senses of smell or vision, or from deciphering vibrations coming through water. Yet none of that would matter if the new behaviors and abilities were not passed on. As more animal body plans and the species they were composed of appeared, ecological communities changed radically and quickly. The epigenetic systems in snimals were, according to the authors, “destabilized,” andin reordering them it allowed new kinds of morphology, physiology, and again behavior, ans amid this was the ever-greater use of powerful hormone systems. Seeinf an approaching predator was not enough. The recognition of imminent danger would only save an animal’s life if its whole body was alerted and put on a “war footing” by the flooding of the creature with stress hormones. Poweful enactors of action. Over time, these systems were made heritable and, according to the authors, the novel evolution of fight or flight chemicals would have greatly enhanced survivability and success of early animals “enabled animals to exploit new niches, promoted new types of relations and arms races, and led to adaptive repsonses that became fixed through genetics.”
That, and vision. Brains, behavior, sense organs and hormones are tied to the nervous system to the digestive system. No single adaption led to animal success. It was the integration of these disparate systems into a whole that fostered survivability, and fostered the rapid evolution of new kinds of animals during the evolutionary fecund Cambrian explosion.
So, ever-changing environments are how physiological systems evolved (see Richardson, 2017: Chapters 4 and 5). Therefore, if the environment were static, then physiologies would not have evolved. Ever-changing environments were imperative to the evolution of life on earth. For if this were not the case, organisms with complex physiologies (note that a physiological system is literally a whole complex of cells) would never have evolved and we would not be here.
In chapter 8 Ward discusses epigenetic processes before and after mass extinctions. He states that, to mass extinction researchers, there are 3 ways in which mass extinction have occurred: (1) asteroid or comet impact; (2) greenhouse mass extinction events; and (3) glaciation extinction events. So these mass extinctions caused the emergence of body plans and new species—brought on by epigenetic mechanisms.
Chapter 9 discusses good and bad times in human history—and the epigenetic changes that may have occurred. Ward (2018: 149) discusses the Toba eruption and that “some small group of survivors underwent a behavioral change that became heritable, producing cultural change that is difficult to overstate.” Environmental change leads to behavioral change which eventually leads to change in morphology, as Lamarck said, and mass extinction events are the perfect way to show what Lamarck was saying.
In chapter 10 Ward discusses epigenetics and violence, the star of the chapter being MAOA. Take this example from Ward (2018: 167-168):
Causing violent death or escaping violent death or simply being subjected to intense violence causes significant flooding of the body with a whole pharmacological medicine chest of proteins, and in so doing changes the chemical state of virtually every cell. The produces epigenetic change(s) that can, depending on the individual, create a newly heritable state that is passed on to the offspring. The epigenetic change caused by the fight-or-flight response may cause progeny to be more susceptible to causing violence.
Ward then discsses MAOA (pg 168-170), though read my thoughts on the matter. (He discusses the role of epigenetics in the “turning on” of the gene. Child abuse has been shown to cause epigenetic changes in the brain (Zannas et al, 2015). (It’s notable that Ward—rightly—in this chapter dispenses with the nature vs. nurture argument.)
In Chapter 11, Ward discusses food and famine changing our DNA. He cites the most popular example, that of the studies done on survivors who bore children during or after the famine. (I have discussed this at length.) In September of 1944, the Dutch ordered a nation-wide railroad strike. The Germans then restricted food and medical access to the country causing the deaths of some 20,000 people and harming millions more. So those who were in the womb during the famine had higher rates of disorders such as obesity, anorexia, obesity, and cardiovascular incidences.
However, one study showed that if one’s father had little access to food during the slow growth period, then cardiovascular disease mortality was low. But diabetes mortality was high when the paternal grandfather was exposed to excess food. Further, when SES factors were controlled for, the difference in lifespan was 32 years, which was dependent on whether or not the grandfather was exposed to an overabundance of food or lack of abundance of food just before puberty.
Nutrition can alter the epigenome (Zhang and Kutateladze, 2018), since it can alter the epigenome and the epigenome is heritable, then these changes can be passed on to future generations too.
Ward then discusses the microbiome and epigenetics (read my article for a primer on the microbiome, what it does, and racial differences in it). The microbiome has been called “the second genome” (Grice and Segre, 2012), and so, any changes to the “second genome” can also be passed down to subsequent generations.
In Chapter 12, Ward discusses epigenetics and pandemics. Seeing people die from horrible diseases of course has horrible effects on people. Yes, there were evolutionary implications from these pandemics in that the gene pool was decreased—but what of the effects on the survivors? Methylation impacts behavior and behavior impacts methylation (Lerner and Overton, 2017), and so, differing behaviors after such atrocities can be tagged on the epigenome.
Ward then takes the discussion on pandemics and death and shifts to religion. Imagine seeing your children die, would you not want to believe that there was a better place for them after death to—somewhat—quell your sorrow over their loss? Of course, having an epiphany about something (anything, not just religon) can change how you view life. Ward also discusses a study where atheists had different brain regions activated even while no stimulation was presented. (I don’t like brain imaging studies, see William Uttal’s books and papers.) Ward also discusses the VMAT2 gene, which “controls” mood through the production of the VMAT protein, elevating hormones such as dopamine and serotonin (similar to taking numerous illegal drugs).
Then in Chapter 13 he discusses chemicals and toxins and how they relate to epigenetic processes. These kinds of chemicals and toxins are linked with changes in DNA methylation, miroRNAs, and histone modifications (Hou et al, 2012). (Also see Tiffon, 2018 for more on chemicals and how they affect the epigenome.)
Finally, in Chapter 14 Ward discusses the future of evolution in a world with CRISPR-CAS9. He discusses many ways in which the technology can be useful to us. He discusses one study in which Chinese scientists knocked out the myostatin gene in 65 dog embryos. Twenty-seven of the dogs were born and only two—a male and a female—had both copies of the myostatin gene disrupted. This is just like when researchers made “double-muscle” cattle. See my article ‘Double-Muscled’ Humans?
He then discusses the possibility of “supersoldiers” and if we can engineer humans to be emotionless killing machines. Imagine being able to engineer humans that had no sympathy, no empathy, that looked just like you and I. CRISPR is a tool that uses epigenetic processes and, thus, we can say that CRISPR is a man-made Lamarckian mechanism of genetic change (mimicking lateral gene transfer).
Now, let’s quickly discuss Coyne’s review before I give my thoughts on the book. He criticizes Ward’s article linked above (Coyne admits he did not read the book), stating that his claim that the two nautiluses discussed above being the same species with the same genome and epigenetic forces leading to differences in morphology (phenotype). Take Coyne’s critique of Vandepas, et al, 2016—that they only sequenced two mitochondrial genes. Combosch et al (2017; of which Ward was a coauthor) write (my emphasis):
Moreover, previous molecular phylogenetic studies indicate major problems with the conchiological species boundaries and concluded that Nautilus represents three geographically distinct clades with poorly circumscribed species (Bonacum et al, 2011; Ward et al, 2016). This is been reiterated in a more recent study (Vandepas et al, 2016), which concluded that N. pompilius is a morphologically variable species and most other species may not be valid. However, these studies were predominantly or exclusively based on mitochondrial DNA (mtDNA), an informative but often misleading marker for phylogenetic inference (e.g., Stöger & Schrödl 2013) which cannot reliably confirm and/or resolve the genetic composition of putative hybrid specimens (Wray et al, 1995).
Looks like Coyne did not look hard enough for more studies on the matter. In any case, it’s not just Ward that makes this argument—many other researchers do (see e.g., Tajika et al, 2018). So, if there is no genetic difference between these two (so-called) species, and they have morphological differences, then the possibility that seems likely is that the differences in morphology are environmentally-driven.
Lastly, Coyne was critical of Ward’s thoughts on the heritability of histone modification, DNA methylation, etc. It seems that Coyne has not read the work of philosopher Jan Baedke (see his Google Scholar page), specifically his book Above the Gene, Beyond Biology: Toward a Philosophy of Epigenetics along with the work of sociologist Maurizio Meloni (see his Google Scholar page), specifically his book Impressionable Biologies: From the Archaeology of Plasticity to the Sociology of Epigenetics. If he did, Coyne would then see that his rebuttal to Ward makes no sense as Baedke discusses epigenetics from an evolutionary perspective and Meloni discusses epigenetics through a social, human perspective and what can—and does—occur in regard to epigenetic processes in humans.
Coyne did discuss Noble’s views on epigenetics and evolution—and Noble responded in one of his talks. However, it seems like Coyne is not aware of the work of Baedke and Meloni—I wonder what he’d say about their work? Anything that attacks the neo-Darwinian Modern Synthesis gets under Coyne’s skin—almost as if it is a religion for him.
Did I like the book? I thought it was good. Out of 5 stars, I give it 3. He got some things wrong, For instance, I asked Shea Robinson, author of Epigenetics and Public Policy: The Tangled Web of Science and Politics about the beginning of the book and he directed me to two articles on his website: Lamarck’s Actual Lamarckism (or How Contemporary Epigenetics is not Lamarckian) and The Unfortunate Legacy of Jean-Baptiste Lamarck. The beginning of the book is rocky, the middle is good (discussing the Cambrian explosion) and the end is alright. The strength of the book is how Ward discusses the processes that epigenetics occurs by and how epigenetic processes can occur—and help drive—evolutionary change, just as Jablonka and Lamb (1995, 2005) argue, along with Baedke (2018). The book is a great read, if only for the history of epigenetics (which Robinson (2018) goes into more depth, as does Baedke (2018) and Meloni (2019)).
Lamarck’s Revenge is a welcome addition to the slew of books and articles that go against the Modern Synthesis and should be required reading for those interested in the history of biology and evolution.
In the past, I have written on the subject of HBD and sports (it is a main subject of this blog). I have covered baseball, football, running, bodybuilding, and strength over many articles. Though, I have not covered basketball yet. Black Americans comprised 74.4 percent of the NBA, compared to 19.1 percent of whites (TIDES, 2017). Why do blacks dominate the racial composition of baskeball? Height is strongly related to success in basketball, though whites and blacks are around the same height, with blacks being slightly shorter (blacks being 69.4 inches compared to whites who were 69.8 inches; CDC, 2012). So, why do blacks dominate basketball?
Basketball success isn’t predicated so much on height, rather, limb length plays more of a factor in basketball success. Blacks have longer limbs than whites (Wagner and Heyward, 2000; Bejan, Jones, and Charles, 2010). The average adult man has an arm span about 2.1 inches greater than his height (Nwosu and Lee, 2008), while Monson, Brasil, and Hlusko (2018) state that taller basketball players had a greater height-to-wingspan ratio and they were, therefore, more successful. The Bleacher Report reports that:
The average NBA Player’s wingspan differential came out at 4.3 percent, so anything above that is going to be reasonably advantageous.
So, more successful basketball players have a longer arm span compared to their height, which makes them more successful in the sport. Blacks have longer limbs than whites, even though they are on average the same height. Thus, one reason why blacks are more successful than whites at basketball is due to their somatotype—their long limbs, specifically,
David Epstein (2014: 129) writes in The Sports Gene:
Based on data from the NBA and NBA predraft combines (using only true, shoes-off measurements of players), the Census Bureaum abd the Centers for Disease Control’s National Center for Health Statistics, there is such a premium on extra height for NBA that the probability of an American man between the ages of twenty and forty being a current NBA player rises nearly a full order of magnitude with every two-inch increase in height starting at six feet. For a man between six feet and 6’2”, the chance of his currently being in the NBA is five in a million. At 6’2” to 6’4”, that increases to twenty in a million. For a man between 6’10” and seven feet tall, it rises to thirty-two thousand in a million, or 3.2 percent. An American man who is seven feet tall is such a rarity that the CDC does not even list a height percentile at that stature. But the NBA measurements combined with the curve formed by the CDC’s data suggest that of American men ages twenty to forty who stand seven feet tall, a startling 17 percent of them are in the NBA right now.* Find six honest seven-footers, and one will be in the NBA.
* Many of the men who NBA rosters claim are seven feet tall prove to be an inch or even two inches shorter when measured at the combine with their shows off. Shaquille O’Neal, however, is a true 7’1” with his shoes off.
And on page 132 he writes:
The average arm-span-to-height ratio of an NBA player is 1.063. (For medical context, a ratio greater than 1.05 is one of the traditonal diagnostic criteria for Marfan syndrome, the disorder of the body’s connective tissues that results in elongated limbs.) An average-height NBA player, one who is about 6’7”, has a wingspan of seven feet.
So we can clearly see that NBA players, on average, are freaks of nature when it comes to limb length, having freakish arm length proportions which is conducive to success in basketball.
Why are long limbs so conducive to basketball success? I can think of a few reasons.
(1) The taller one is and the longer one’s limbs are the less likely they are to have a blocked shot.
(2) The taller one is and the longer one’s limbs are is advantageous when performing a lay-up.
(3) The taller one is and the longer one’s limbs are means they can battle for rebounds at better than a shorter man with shorter limbs.
Epstein (2014: 136) also states that the predraft data shows that the average white NBA player is 6’7.5” with a wingspan of 6’10” while the average black NBA player is 6’5.5” with an average wingspan of 6’11”—meaning that blacks were shorter but “longer.” What this means is that blacks don’t play at “their height”—they play as if they were taller due to their wingspan.
Such limb length differences are a function of climate. Shorter, stockier bodies (i.e., an endomorphic somatotype) is conducive to life in colder climes, whereas longer, more narrowbodies (ecto-meso) are conducive to life in the tropics. Endomorphic somas are conducive to life in colder climes because there is less surface area to keep warm—and this is seen by looking at those whose ancestors evolved in cold climes (Asians, Inuits)—shorter, more compact bodies retain more heat. Conversely, ecto-meso somas are conducive to life in hotter, more tropical climes since this type of body dissipates heat more efficiently than endo somas (Lieberman, 2015). So, blacks are more likely to have the soma conducive to basketball success due to where their ancestors evolved.
So, now we have discussed the facts that height and limb length are conducive to success in basketball. Although blacks and whites in America are the same height, they have vastly different average limb lengths, as numerous studies attest to. These average differences in limb length are how and why blacks succeed far better than whites in the NBA.
Athleticism is irreducible to biology (Lewis, 2004), as has been argued in the past. However, that does not mean that there are NOT traits that are conducive to success in basketball and other sports. Both height and limb length are related: more than likely, the taller one is, the longer their limbs are relative to their height. This is what we see in elite NBA players. Height, will, altitude, and myriad other factors combine to create the elite NBA phenotype; height seems to be a necessary—not sufficient—condition for basketball success (since one can be successful at basketball without the freakish heights of the average player). Though, as Epstein wrote in his book, both height and limb length are conducive to success in basketball, and it just so happens that blacks have longer limbs than whites which of course translates over to their domination in basketball.
Contrary to popular belief, though, players coming from broken homes and an impoverished life are not the norm. As Dubrow and Adams (2010) write:
We find that, after accounting for methodological problems common in newspaper data, most NBA players come from relatively advantaged social origins and African Americans from disadvantaged social origins have lower odds of being in the NBA than African American and white players from relatively advantaged origins.
Sports writer Peter Keating writes that:
[Dubrow and Adams] found that among African-Americans, a child from a low-income family has 37 percent lower odds of making the NBA than a child from a middle- or upper-income family. Poor white athletes are 75 percent less likely to become NBA players than middle-class or well-off whites. Further, a black athlete from a family without two parents is 18 percent less likely to play in the NBA than a black athlete raised by two parents, while a white athlete from a non-two-parent family has 33 percent lower odds of making the pros. As Dubrow and Adams put it, “The intersection of race, class and family structure background presents unequal pathways into the league.”
(McSweeney, 2008 also has a nice review of the matter.)
Turner et al (2015) state that black males were more likely to play basketball than whites males. Higher-income boys were more likely to play baseball, whereas lower-income boys were more likely to play basketball. Though, it seems that when it comes to elite basketball success, players seem to come from higher-income homes.
Therefore, to succeed in basketball, one needs height and long limbs to succeed in basketball. Contrary to popular belief, it is less likely for an NBA player to come from a low-income family—they come from middle-class families the most. Indeed, those who come from lower-income families, even if they have the skill, most likely won’t have the money to develop the talent they have. Though there are some analyses which point to basketball being played by lower-income children—and I have no reason to disagree with them—when it comes to professional play, both blacks and whites are less likely to become NBA players if they grew up in poverty.
The limb length differences between blacks and whites which are conducive to sport success are a function of the climate that their ancestors evolved in. Now, although athleticism is irreducible to biology (because biological and cultural factors interact to create the elite athletic phenotype), that does not mean that there are no traits conducive to sporting success. Quite the opposite: A taller player would more often than not beat a shorter player; when it comes to players with the same height and different limb lengths, the one with the longer limbs will stand a better chance at beating the one with shorter limbs. Blacks and whites have different limb lengths, and this explains how and why blacks are more successful at basketball than whites. Cultural and biological factors combine in order to cause what one is good at.
Basketball is huge in the black community (due in part to people gravitating toward what they are good at), and due to this, since blacks have an advantage right out of the gate, they will gravitate more toward the sport and, therefore, height and limb length is a huge reason why black dominate at this sport.
Hoffman et al (2016) questioned laypeople and medical students and residents on a 15-question questionnaire regarding different beliefs people have about racial differences. The point of the questionnaire was to ascertain how people are biased in regard to racial differences in pain and how the bias affects the treatment the individual of the certain racial group. Only two of the questions had anything to do with pain. In this article, I will answer the questions one by one.
1. On average, Blacks age more slowly than Whites.
This one is true (though they rate this question as false). I don’t know why, though, because there are differences between black and white skin and these differences affect the rate of aging between races.
Campiche et al (2019) found that there is a difference in aging regarding skin in different ethnies (the cohorts were French and Mauritanian). The average age was 46 for the French and 56 foe the Mauritanians, and the Mauritanians still looked younger! Campiche et al (2019) write:
The difference in age between our Caucasian and Black African cohorts (median age 46 years vs 56 years) could bring into question the comparisons of the two cohorts. Nevertheless, we mostly found that Caucasians displayed more severe signs of aging than Black Africans which is in line with the common understanding that the onset of aging in fair skin starts earlier than in darkly pigmented skin and that there were differences in the appearance of lip lines and facial pores.
This question is true, contrary to the claims of Hoffman et al (2016).
2. Black people’s nerve-endings are less sensitive than White people’s nerve-endings.
I can find no literature on this matter and the only articles point me to Hoffman et al (2016) and different articles on the matter. I accept the claim as false.
3. Black people’s blood coagulates more quickly–because of that, Blacks have a lower rate of hemophilia than Whites.
Blacks’ blood does clot faster than whites, and part of the cause is differences in the PAR4 gene family (Bray et al, 2013). The reason that blacks’ blood clots faster than whites’ is due to the effects of thrombin, an enzyme that activates the molecule responsible for blood clotting. Blacks do have a lower rate of hemophilia than whites, though, but not by much (13.2 cases/100,000 for whites compared to 11 for blacks) (Soucie, Evatt, and Jackson, 1998). The question is true, contra Hoffman et al (2016).
4. Whites, on average, have larger brains than Blacks.
They stated that this question is false, which is bizarre. I am aware of no literature that attests to the claim that whites do not have larger brains than blacks. Many analyses back the claim that whites have larger brains than blacks (though Nisbett disagrees and states that there are studies that show the contrary but does not leave a citation) (Rushton, 1997). (Though see Race and Brain Size: Blacks Have Bigger Brains for an alternate view.)
5. Whites are less susceptible to heart disease like hypertension than Blacks.
They say this claim is true. And it is. Hypertension (high blood pressure) is a physiological variable which means that social environment can greatly affect it (Williams, 1992). Higher rates of obesity drive this association as well. American blacks have a lower rate of CHD than whites (7.2 compared to 7.8) but this is reversed for women (7.0 compared to 4.6) (Leigh, Alvarez, and Rodriguez, 2016). The CDC, though, says that the rate of heart disease is the same between blacks and whites, at 23.8 percent though (slightly higher than the 23.5 percent average).
6. Blacks are less likely to contract spinal cord diseases like multiple sclerosis.
7. Whites have a better sense of hearing compared with Blacks.
They state that this claim is false. Pratt et al (2009) state that hearing loss is more likely to occur in white over black elderly patients.
8. Black people’s skin has more collagen (i.e., it’s thicker) than White people’s skin.
They state that this claim is false, and it is. That there is no difference in skin thickness between blacks and whites is irrelevant, though. Black skin is more compact, with greater intercellular cohesion (LaRuche and Cesarini, 1992; Rawlings, 2006).
9. Blacks, on average, have denser, stronger bones than Whites.
10. Blacks have a more sensitive sense of smell than Whites; they can differentiate odors and detect faint smells better than Whites.
This claim is false, according to Hofmann et al. And I can find nothing in the literature on the matter so I will accept their claim.
11. Whites have more efficient respiratory systems than Blacks.
They state that this claim is false. However, Schwartz et al (1988) state that “Controlling for sex, age, standing height, and body mass index, blacks had consistently lower levels of lung function for most measures.” This claim seems to be true.
12. Black couples are significantly more fertile than White couples.
They state this claim is false. Wellons et al (2008) state that “black women were more likely to have experienced infertility.” So the claim is in the opposite of what Hoffman et al question.
13. Whites are less likely to have a stroke than Blacks.
They state that this claim is true, and it is. Minorities are more likely to have a stroke than whites. Brevata et al (2005) write that blacks are more likely to have severe strokes than whites. The claim is true.
14. Blacks are better at detecting movement than Whites.
This seems like a bizarre claim. They state that it is false and I will accept it as false since I can find no literature on the matter.
15. Blacks have stronger immune systems than Whites and are less likely to contract colds.
Europeans and Africans have different immune systems. The immune system of black Americans is stronger than whites’. Twenty-four hours after being infected with salmonella and listeria bacteria, researchers found that the white blood cells from black Americans responded quicker than that of the white blood cells from white Americans. The white blood cells from black Americans ridded the infection about three times quicker than the white blood cells from black Americans. They stated that this claim is false, but it appears to be true.
So, by my count, out of the 15 questions asked, 8 of them have a factual basis (with some in the opposite direction), compared to Hoffman et al’s (2016) assertion that only 4 of them are true. In any case, there are a lot of myths about racial differences out there, and some of these questions by Hoffman et al are myths. Though some of them do have a factual basis. I wonder what kind of literature they referred to when asking these questions, because the literature that I am aware of when it comes to some of these matters is different compared to what Hoffman et al (2016) claim. Racial/ethnic differences do, obviously, exist but there are many myths involved with them.
There are many superficial physical differences between the races. But differences in pain sensitivity would be one that is not really “superficial”, as you can’t really see it (you can see someone’s reaction to pain, but not see it). “Pain” is defined as physical discomfort caused by injury. There are some myths about pain differences between racial groups, that still persist today. And these myths have bad consequences.
For example, Hoffman et al (2016) state that “people assume a priori that blacks feel less pain than do whites.” Hoffman et al (2016) carried out two studies: (1) using a between-participants design, laymen were asked to assess the pain of white and black subjects and (2) again using a between-participants design, they asked students and medical doctors to assess pain between blacks and whites. In (2) they asked these 15 questions:
1. On average, Blacks age more slowly than Whites.
2. Black people’s nerve-endings are less sensitive than White
3. Black people’s blood coagulates more quickly–because of
that, Blacks have a lower rate of hemophilia than Whites.
4. Whites, on average, have larger brains than Blacks.
5. Whites are less susceptible to heart disease like hypertension than Blacks.
6. Blacks are less likely to contract spinal cord diseases like
7. Whites have a better sense of hearing compared with Blacks.
8. Black people’s skin has more collagen (i.e., it’s thicker) than
White people’s skin.
9. Blacks, on average, have denser, stronger bones than Whites.
10. Blacks have a more sensitive sense of smell than Whites;
they can differentiate odors and detect faint smells better
11. Whites have more efficient respiratory systems than Blacks.
12. Black couples are significantly more fertile than White couples.
13. Whites are less likely to have a stroke than Blacks.
14. Blacks are better at detecting movement than Whites.
15. Blacks have stronger immune systems than Whites and are
less likely to contract colds.
(I’ll cover these questions in a future article.)
Here is the table showing the respondents’ answers to the questions:
So they established that whites with no medical training hold false beliefs about black-white differences that then carry over to pain management. They showed in study 2 that medical students’ and residents’ apparently false beliefs about racial differences in the questions they answered showed bias in the accuracy of the recommended pain treatments. Hoffman et al (2016) conclude that:
The present work sheds light on a heretofore unexplored source of racial bias in pain assessment and treatment recommendations within a relevant population (i.e., medical students and residents), in a context where racial disparities are well documented (i.e., pain management). It demonstrates that beliefs about biological differences between blacks and whites—beliefs dating back to slavery—are associated with the perception that black people feel less pain than do white people and with inadequate treatment recommendations for black patients’ pain.
(See also the Psychology Today article on the matter.)
Similarly, Hollingshead et al (2016) reported that subjects, regardless of race, rated the white person more sensitive to pain and more likely to report pain than the black person. Whites reported that they were less pain sensitive and less likely to report pain than their peers. Blacks reported that they were more sensitive to pain while reporting more pain than their peers.
Interestingly, Trawalter, Hoffman, and Waytz (2012) state that black NFL players are more likely to play in a subsequent game than whites when injured, and that, as found in many other studies, blacks are more likely to feel less pain than whites. However, what the literature really shows is the opposite: blacks are more likely to feel pain than whites.
Kim et al (2017) showed that blacks, “Hispanics” and Asians had lower pain tolerance, higher pain ratings and greater temporal sensation of pain. They also showed that blacks had lower pain tolerance and higher pain ratings but no differences in pain threshold.
Blacks report greater pain regarding AIDs, glaucoma, migraine, headache, jaw pain, postoperative pain, joint pain and many other types of pain compared to whites (Green et al, 2003; Klonoff, 2009). Riley III et al’s (2002) results indicate that blacks show a stronger link between pain and emotions than whites. Obana and Davis (2016) showed that Native Hawaiian/Pacific Islander male and females reported higher pain scores than whites when it came to joint pain (but they were not significant). Bolen et al (2010) showed that work limitation, severe joint pain, and arthritis-attributable activity were higher for non-“Hispanic” blacks, “Hispanics” and multiracial people compared to non-“Hispanic” whites. Even American Indians, Alaskan natives, and Aboriginal Canadians had a higher prevalence of pain and pain symptoms than Americans (Jimenez et al, 2011).
Chan et al (2011) surveyed older Singaporeans. They found that Malay people had lower pain sensitivity compared to Chinese people, and that Indians reported greater pain sensitivity when compared with Malay and Chinese people. Australian women rated menstrual pain higher and lasting 36 percent longer than Chinese women (Zhu et al, 2010).
When it comes to potential mechanisms, physiological mechanisms are hypothesized by Campbell and Edwards (2012) who write:
For example, in comparison to non-Hispanic whites, African–Americans have reduced nociceptive flexion reflex thresholds ; the nociceptive flexion reflex is an electrophysiological, spinally mediated reflex, which is not amenable to voluntary control or subject to issues of response bias that plague self-report of pain experiences. This finding suggests that the observed ethnic differences in pain are unlikely to be fully explainable by sociocultural influences and hints that neurobiological processes may contribute to such differences.
Mossey (2011) shows that “Racial/ethnic minorities consistently receive less adequate treatment for acute and chronic pain than non-Hispanic whites, even after controlling for age, gender, and pain intensity.” Martinez et al (2014) showed that when it comes to colorectal and lung cancer, mixed-race individuals and blacks are more likely to report higher pain severity than whites. (Also see Shavers, Bakos, and Sheppard, 2010.)
All of the literature points in the opposite direction of the myths about pain sensitivity in regard to race: blacks feel more pain than whites and are more likely to have a lower pain tolerance. So the myths people hold about differences in pain between racial groups (mostly blacks and whites) are false. Pain is a subjective experience. And there will be differences in pain thresholds between individuals and racial groups and the causes may be both sociocultural and physiological in nature. However, this bias (in the wrong direction) speaks to what I wrote about last night: physician bias when it comes to blacks and other minorities.
Barr (2014: 183-184) writes:
Based to a certain extent on the attention given to his earlier publication, Todd moved to a faculty position with the Emory University School of Medicine, in Atlanta, Georgia. There he was able to essentially repeat his earlier study, this time examining persons coming tothe emergency room of a large, inner-city community hospital in Atlanta that was affiliated with Emory (Todd et al, 2000). He evaluated the medical records of 217 individuals coming to the emergency room over a 40-month period for treatment of an isolated long-bone fracture. Given the racial makeup of Atlanta, these included 127 blacks and 90 whites. They found that
- 54 of the blacks (43 percent) received no medication for pain during their treatment
- 23 of the whites (26 percent) received no medication for pain during their treatment
As with the earlier study in Los Angeles involving whites and Hispanics, in this study, the blacks were nearly twice as likely to receive no pain medication while in the emergency room. With this study, the authors were keenly aware of the importance of documenting the extent to which the patients expressed painful symptoms. By thoroughly reviewing the medical records of these patients, they found that 54 percent of blacks and 59 percent of whites had a notation in their medical record that they had expressed painful symptoms. The nearly twofold difference in withholding pain medication in blacks and whites was because the doctor didn’t order the medication, not because the patient didn’t want the medication.
This, again, speaks to physician bias when it comes to race in a medical context. Race is a useful tool in medicine, but to hold biases in the complete opposite direction that they exist in is wrong. This study—and many others—speak to the type of bias that physicians have against minorities in a medical context. Understanding that the differences in pain are actually the opposite from what is commonly believed by both laypeople and medical doctors is important: if blacks feel more pain than whites regarding the same injuries and they are not getting the care needed, then this speaks to physician bias. What Barr showed was that blacks were treated at the emergency room based on their ethnicity. This is wrong. Race/ethnicity is a useful tool in medicine, but to outright use it as an assumption for numerous factors makes no sense and could cause more harm than good.
Using race in a medical context is a good thing. But using race in a medical context using essentialist, outdated views about race is wrong and can lead to many horrible outcomes. Of course, using race in this context can and does lead to certain things being discovered over others. For instance, if one’s race is assumed to be “driving” one’s illness (i.e., that one has a disease that that race/ethny is more likely to have), then race can and is a good marker to use—specifically geographic ancestry. However, when it comes to things like pain management, this obviously leads to false ideas about how different groups manage and feel pain.
Views about racial differences in pain affect both laypeople and medical doctors. These views can be and are harmful. The literature points to the case being the opposite of what is believed by people: blacks have lower pain tolerance and higher pain ratings than whites. These types of differences are also found between many other races and ethnic groups. The causes could be both sociocultural and physiological. A person’s response to pain depends on their unique physiology, life experiences, ethnicity and other factors. Understanding how and why physicians are biased toward how blacks feel pain is important, along with addressing the other biases that they have about other minorities when it comes to a medical context. Race and ethnicity are important tools for medicine, but these are some of the ways that the concepts can be used with nothing good coming out of it.
I’m currently reading Health Disparities in the United States: Social Class, Race, Ethnicity and Health by medical doctor and sociologist Donald Barr. In the book, he chronicles differences in health between races and ethnies, talks about the concepts of race used and cites well-known studies to people who read this blog, and he also shows that doctors are—either conscious or not—biased against minorities in certain medical contexts.
In Chapter 1 discusses the fact that, although Americans spend the most money on health care, Americans have a lower life expectancy and higher infant mortality rate than all other developed countries, showing the association in social inequality and health across all income levels and education. In Chapter 2, he asks the question “What is health?”, discussing many concepts of what “health” is. In Chapter 3, he defines “socioeconomic status” and shows the link between poor health and poor SES. In Chapter 4, he discusses the link between inequality and poor health, introducing the concept of “allostatic load”, which is the physiologic response to being in a spot of social disadvantage.
In Chapter 5, he looks at different race concepts, since it is a main premise of the book. In Chapter 6, he shows that minorities are more likely to be in a position of low SES. He asks, if minorities of the same SES as whites are consistently found to be of lower health than whites of the same SES, is it because those with poor health tend to be minorities, that they tend to have lower SES or both? In Chapter 7, he asks the same questions while focusing on children. In Chapter 8, he examines disparities in access to healthcare, showing that even when minorities have the same insurance and doctors that minorities still face worse health outcomes (he shows that they either do not receive appropriate healthcare or receive lower-quality care). In Chapter 9, he shows that physicians treat blacks and other minorities differently, albeit unconsciously. In Chapter 10, he discusses when—if ever—a physician would be justified in using racial/ethnic categories. And in Chapter 11, he states that not all of these disparities need to be eliminated.
In Chapter 2, Barr (2014: 45) presents this table, showing rates of illness and selective rates of death between States in America. Obviously, the one to look at that is different than the others is Mississippi. Mississippi is 37.5% black.
Wow, I wonder why Mississippi has such a high rate of obesity, diabetes, and hypertension (high blood pressure). Must be all of those obesity, diabetes and hypertension genes (HBDer).
Obesity and diabetes
The first thing to look at is median income. It is substantially lower in Mississippi compared to California, Iowa, and New York. About 23 million people in America live one mile from a supermarket, while black Americans are about half as likely to have access to supermarkets while “Hispanics” are about a third likely to have access to them (New York Law School Racial Justice Project, 2012). So when it comes to those who have to travel more than a mile for fresh fruit and vegetables, they have poorer health (Stack, 2015). So combine lower median income, along with food deserts and one can start to see how minorities have poorer health due in part to their SES. In short, living in a food desert can affect public health.
Blacks are the most obese ethnic group in America, and this relationship is largely driven by black women. Now, it’s not weird that women have higher levels of body fat than men, since women it is needed for physiological functioning. Though, there is something weird here: Black American men with more African ancestry are less likely to be obese (Klimentidis et al, 2016). Since black women and black men in America are in the same economic bracket, there must be something in the West African male physiology that “protects” them against central adiposity, though variation in social, environmental and cultural factors may play a role as well. In any case, the more West African ancestry American blacks have, the less likely they are to be obese. Klimentidis et al’s (2016) study “suggests that there are specific genetic variants and physiological mechanism(s) that differ among West African and European populations.”
Obesity affects more ethnies in America than others: non-Hispanic blacks and “Hispanics” are more likely to be obese than non-“Hispanic” whites and Asians (Hales et al, 2017). This could be due to, in part, to the variation in supermarket access and access to good foods—the concept of food deserts. Look at any low-income area near you. You’ll see a majority of corner stores with cheap, garbage food. The lack of ability to buy good food (along with the education to know what to buy and when to buy it) can explain differences in obesity rates—obviously not all. Obesity is related with diabetes, and sinec the relationship is so strong, the term “diabesity” was coined.
Eating cheap, processed carbohydrates spikes insulin. Repeated insulin spikes over time leads to type II diabetes and, eventually, obesity too. One can be skinny and have diabetes (a phenomenon known as thin on the outside, fat on the inside “TOFI”). However, since both diseases are co-morbid, we need to look at them in similar contexts. The higher rates of obesity can help to explain the higher rates of diabetes and hypertension—since those who are obese have higher blood pressure (Aronow, 2017).
Minorities are more likely to develop type II diabetes (Tuchman, 2011), and the cause of this is access to high-quality foods. But racial differences in obeisty and SES do not fully explain the higher rates of type II diabetes in black Americans; being a black American is a strong, independent factor for developing type II diabetes and this is compounded by low SES (Brancati et al, 1996). Zizi et al (2016) showed that both long and short black sleepers have an increased risk of developing type II diabetes. There are racial differences in sleep, with blacks having higher durations of long and short sleep compared to whites (Adenekan et al, 2013).
Now let’s look at hypertension (blood pressure). Blood pressure is a physiological variable. Since it is a physiological variable, it can and does respond to social/environmental contexts. So blood pressure can be affected by social contexts, too. For example, Williams (1992) cites stress, socioecologic stress, social support, coping patterns, health behavior, sodium and more for reasons why blacks have higher BP than whites. Dressler (1991) shows that the struggle to maintain a middle-class lifestyle is related to higher levels of BP. Similarly, Keith and Herring (1991) show that skin color is a strong predictor of occupational status and that darker-skinned blacks in America are twice as likely to experience racial discrimination than lighter-skinned blacks. This, too, can help to account for higher levels of BP between the races. In any case, Williams (1992) shows, definitively, that the causes of black-white differences in BP lie in the social environment.
Similarly, Non, Gravlee, and Mulligan (2012) show that racial disparities in BP are explained by education, and not genetic ancestry. They show that the association between BP and education was much stronger for blacks than for whites. Their results also 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.” People who face discrimination could, and do, have higher levels of BP due to the stress they feel due to the discrimination. (Note that I take no sides on whether the discrimination is real or imagined, because even if it were imagined, it still leads to real physiologic consequences.)
Do note that there is a just-so story to explain how and why blacks have higher levels of blood pressure than whites: The Slavery Hypertension Hypothesis (Lujan and Dicarlo, 2018). This has all of the hallmarks of a just-so story posited by evolutionary psychologists. The story goes like this: Black slaves who were on the way to America in the Middle Passage had genes that favored better salt retention. So it is noted that black Americans have higher rates of BP than whites, and then they work backward and attempt to posit the best story possible to explain the current-day observation. This is the usual method evolutionary psychologists use—the method of reverse engineering, the inference from function to cause. So (1) note that blacks have higher levels of BP than whites; (2) infer the function to cause (blacks with genes that favored salt retention were more likely to survive; so (3) this is why blacks have higher rates of BP than whites. Though the explanation fails, since education, and not genetic ancestry, explains the difference in BP between blacks and whites (Non, Gravlee, and Mulligan, 2012). One only needs to understand the intricacies of physiology and how our physiological systems respond to what occurs in the greater environment.
So, obesity can explain both the higher rates of diabetes and higher rates of blood pressure, with differences in the immediate social environment explaining the rest of the differences in blood pressure between blacks and whites. (Note that heart disease deaths are directly related to hypertension. Heart disease affects blacks more than whites.)
In Race, Medicine, and Epigenetics: How the Social Becomes Biological, I shortly discussed breast cancer in black women:
Black women are more likely to die from breast cancer, for example, and racism seems like it can explain a lot of it. They have less access to screening, treatment, care, they receive delays in diagnoses, along with lower-quality treatment than white women. But “implicit racial bias and institutional racism probably play an important role in the explanation of this difficult treatment” (Hardimon, 2017: 166). Furthermore, black women are more than twice as likely to acquire a type of breast cancer called “triple negative” breast cancer (Stark et al, 2010; Howlader et al, 2014; Kohler et al, 2015; DeSantis et al, 2019). Of course, this could be a relevant race-related genetic difference in disease.
Now note the infant mortality rate between the states: the infant mortality rate in Mississippi is 9.7%. Smith et al (2018) show that black women are at a higher rate of having their infant die at birth. Pre-term births are related to low birth weights, and they both are related to infant mortality. Matoba and Collins (2017) write:
In the United States, African-American infants have significantly worse infant mortality than white infants. Individual risk factors alone do not explain this persistent gap, just as they did not explain the disparity in preterm birth and low birth weight. Recent studies in social determinants provide insight into the contribution of community and environmental factors to the racial disparity. Select community-level factors are potential, but partial, determinants of the racial disparity. Interpersonal and institutionalized racism is an important, and increasingly recognized, stressor for African-American women with damaging consequences to maternal and child health.
The Guardian ran a recent story on infant mortality and race, positing racism as a cause of the disparity. In any case, the social environment can and does play a part in everything discussed here today since the social can and does become biological. Part of the reason why Mississippi has a way higher rate of years of potential life lost (10,214 compared to 5500-5900 for Iowa, New York, and California) is that rates of infant mortality are higher in Mississippi. So the median age of death is 75. If an infant dies at one year of age, then that is 74 years of life lost. Therefore it is not surprising that the State with the highest level of infant mortalities has a higher number of years of potential life lost. Further, one 2017 review found that segregation was associated with increased risk of preterm birth and low birth weight for blacks (Mehra, Boyd, and Ickovis, 2017)
Note how Mississippi has lower rates of asthma. This is explained by the fact that Mississippi is more rural than, say New York. Rates of asthma are associated with living in a metropolitan area (Frazier et al, 2012; Malik, Kumar, and Frieri, 2012). (Note that blacks and other races have higher rates of asthma than other races.)
The lower one’s position is on the social hierarchy the lower their probability of staying healthy and having a high life expectancy; when people have the same type of health insurance and are treated for the same disease in the same hospital by the same doctor, that minority groups get worse health care, either not receiving it or receiving lower standards of quality in care. What could account for such disparities? I asked PumpkinPerson the question, and he said:
1) EGI: Doctors put more effort into saving coethnics: she looks like my italian grandma. I’ll make sure she gets the best medicine.
2) IQ: low IQ populations don’t understand the doctor’s advice and damage their health
3) r/K: some populations have faster life history so don’t live as long, even with good medical care
If (1), then the doctors need to be named, shamed, and have their medical licenses revoked. If (2), then they need better education (since IQ is just an index of middle-class knowledge). (3) is completely irrelevant, since it doesn’t make sense for humans and the concept is long-dead in ecology. In any case, PumpkinPerson danced around the true cause: differences in healthcare brought about by unconscious bias (of which (1) may be a cause). But positing (1) as a cause completely misses the point (and is the usual HBDer reductionism to genes causing most/if not all things). It’s the usual HBD/Rushtonian reductionism to genes. That’s all the HBD worldview reduces to: genes/IQ.
In any case, Reschovsky and O’Malley (2008: 229, 230)
Our results indicate that the minority makeup of physicians’ patient panels is associated with greater reports from physicians of difficulties providing high-quality care. At least some of this relationship appears to be explained by the lower resources flowing to high-minority practices.
The results of this study suggest that racial and ethnic disparities in primary health care are in part systemic in nature, and the lower resources flowing to physicians treating more minority patients are a contributing factor.
Thus, bias—whether conscious or unconscious—by physicians can explain how and why there are differences in health outcomes between people that have the same health insurance and doctor. Barr (2014: 168) states that “for black Americans, where a person lives sems to be associated with access to primary care, the quality of available hospital care, and the quality of available home care.” Barr shows that blacks receive a different level of care for a wide-range of diseases and illnesses compared to whites. For instance, Smedley et al (2003) write that “some evidence suggests that bias, prejudice, and stereotyping on the part of healthcare providers may contribute to differences in care.” Quite clearly, there is racial bias against minorities and it does seem to affect healthcare, whether or not it is intended or unintended (conscious or unconscious) (Williams and Rucker, 2000). Bird and Clinton (2001: 255) write:
Race and class-based structuring of the U.S. health delivery system has combined with other factors, including physicians’ attitudes—perhaps legacies conditioned by their participation in slavery and creation of the scientific myth of black biological and intellectual inferiority—to create a medical-social, health system cultural, and health delivery environment which contributes to the propagation of racial health disparities, and, ultimately, the health system’s race and class dilemma.
Blacks are more likely to take the advice of physicians, and to use the needed services, such as preventative care and are less likely to delay seeking care when the physician is of their own race (Saha et al, 2000; LaVeist, Nuru-Jeter, and Jones, 2008).
Blacks are more likely to perceive racism in healthcare and when they are able to choose their own doctors, they are more satisfied with their level of care (Chen et al, 2005). Chapman, Kaatz, and Carnes (2013) show that increasing awareness of implicit bias in healthcare can lower such disparities, stating that having more black doctors will alleviate such problems since they are less likely to be biased. Having a black doctor lead to more effective care for black men. Quite clearly, the race of the doctor matters for implicit biases and minority doctors lead to more effective healthcare for minorities, since they are less likely to be affected by racial biases. Minorities trust the healthcare system less than whites (Boulware et al, 2003). Black and white physicians even agree that race is a medically relevant data point, but do not agree on why (Bonham et al, 2009).
The table presented by Barr is telling. He purported to show that on certain indices of health, certain states fair worse than others. Rates of illness and rates of death between different states (with differing ethnic compositions) were compared. Using national data, he showed that Mississippi has the highest rates of death and illness (sans asthma). Social factors can and do account for the differences in hypertension between blacks and whites (and States); food deserts (lack of access to good food) can explain higher rates of obesity and diabetes and also higher rates of blood pressure between the races (and States with a higher percentage of certain racial/ethnic groups). Of course, physiological variables are affected by the social environment, so we have to look at differences in the social environment between groups to see how and why there are differences in any physiological variable we look at.
Doctors, whether consciously or not, treat minority patients differently and there is evidence that this leads to differences in health outcomes between ethnic groups in America. PP’s hypotheses don’t cut it (the only one that does it his “EGIs”, but that explanation fails; the cause is bias by the doctors but “EGIs” have nothing to do with the bias). In any case, there are social and cultural reasons why there are such health disparities between States and races/ethnies. Understanding the causes behind them can and will lead to closing the gap between them. The social can and does become biological, and this is the perfect way to show this. There are ways to lower the disparities in a medical context, and education seems to be one of them—for both patient and doctor.
Some states are healthier than others based on objective measures of health and mortality, and understanding the reasons why can and will decrease these differences.
The following will not all be anthropologists by trade or certification, but each carved their own little niche the distorts research. I will address them in way that reflects the weird way they are all connected.
Bruce Fenton: So thanks to RR, I’ve learned how he once peddled crap such as “giants“, among other things. Needless to say, that answered alot of my questions I had after taking apart his article on his book a while back.
Jeffery Schwarz and John Grehan: Now, to be fair, these guys deserve somewhat more credit in their premise, that is regarding the morphological links with orangutans and humans. It has some basis in how humans evolved, originally being arboreal and not knuckle walking. However, their approach of preferring inheritance based on external morphology over coding DNA and overall genetics has been criticized again, and again, and again, and again.
For clarification, I found them from an Indian study on Hominid development in Fenton’s spurces, which focused on bipedalism. It noted an “Asian hypothesis” of human origins. Technically, Grehan proposed an African-Asian distribution, and as of now Schwarz’s actual hominid data currently works with OOA as a base model while adjusting it. So it doesn’t support Fenton even if Orangutans were the actual ancestors of humans.
It’s worth mentioning as well, the commenter “Marc” in the Grehan link is a crank as well, but not for today.
Shi Huang: Shi Huang here is the only other major researcher I know of who has actually produced any notable difference in the Human-Chimp clade finding, on top of rejecting OOA.
The implications however stray further from the Cann study than Fenton’s. In fact, if you read the link on phenotypic association of human populations…it’s kind demonstrates the futility of using external phenotypes.
Overall, his theory on Africans being Denisovan and Neanderthal admixed humans doesn’t align with Haplogroup associations touched upon previously in my Fenton article linked to Dienekes, the nature of the East African cluster mentioned in my article on modern Africans with A and B y chromosomes making up the majority of Eurasian affiliated Nilotics, and my previous article on the post Neanderthal substructure making up the majority of African genetics.
Now compare all of these inferences, to this-
Fossils or traits indicating AMH migration from East Asia into Africa or Europe have
been noted before. First, native Africans such as Khoisans are well known to have certain East Asian features such as shoveling teeth, epicanthic fold, and lighter skins. Mbuti pygmies look very much like the Andamanese. The much lower frequency of shoveling teeth in African fossils and Khoisan relative to ancient and modern Chinese suggests that this type of teeth could only originate in China with its African presence due to migration. The type of shoveling teeth found in Neanderthals and Pleistocene Homo from Atapuerca-Sima de los Huesos may either be a different type from that of Asians and Africans or come from early disposal of Homo from Asia to Europe (Martinon-Torres et al., 2007; Wolpoff, 1996). Second, a combination of three features has been noted to be region-specific to China fossils with lower frequency also found in North Africa: a non-depressed nasal root, non-projecting perpendicularly oriented nasal bones and facial flatness (Brauer and Stringer, 1997). Third, Dali man of China (~250,000 years ago) had lower upper facial index and flat nasomolar angle, but these two modern features only first
appeared in Europe in Cro Magnons (Xinzhi Wu, personal communication).
I’ll admit I’m no expert in genomics, but having at least looking over the Dali paper and comparing it to this, I think anyone else who has sense and had done the same would come to the same conclusion as I would to dismiss this paper as the leaps and assertions it makes are vast and at times amateur. Wu Xinzhi apparantly read this himself, but recalling his own paper and work he was much more cautious and more involved in this kind of data. As particular as his theory was, it never devolved into statements like this.
That humans have been a single species for more than ~2 myr is consistent with the
unique feature of being human, i.e., creativity, which could be defined as constant creation of novelty. Intentionally made and constantly improved knife type stone tools, first appeared 2.3- 2.8 myr ago, may be beyond the capabilities of non-humans and mark the first appearance of creativity in life on Earth.
The appearance of modern humans should be accompanied by new technologies just as
the knife type stone tools were associated with the first appearance of the genus Homo. A technology just one step more advanced than stone tools is pottery making. Consistent with our model, the earliest pottery making intended for practical usage was found in Hunan and the neighboring Jiangxi in South China at 18,000-20,000 years ago (Boaretto et al., 2009; Wu et al., 2012). While future investigations could extend the time even earlier, one should not expect a new technology to appear simultaneously with the first appearance of AMH since it would take time for the first modern humans to grow into a large enough population to be able to invent new cultures. It is also remarkable to note that the next new invention after pottery, rice or agriculture, also likely came from Hunan (Zhang and Yuan, 1998). Both the link to his blog post on OOA and this slightly dismissal post on his work shows an ardent defender of his, one that should be very familiar.
German Dziebel: It only takes a short cross-reference to see his BS. Basically, he’s pushing some sort of hypothesis that undermines the divergences of Pygmies and Bantu farmers. This basically mean ignoring the conclusions from his own sources on genetics, here, and here. He confuses the pygmy phenotype, which is shown to be independent, with the pygmy genetic cluster. This is disingenuous to anyone familiar with the topic. He is correct that they are not genetically unrelated due to the geneflow, which accounts for language, but his proposal to explain this primarily on recent splits is contradicted by full genetic research tackling the matter.
On the Shi Huang paper, he says that the Chinese lack the possibility of “bias” Americans feel to support OOA based on guilt of African American discrimination. Perhaps, yet that doesn’t explain Manzi on the Ceprano skull, nor does that explain this paper showing Chinese lacking the substructure expected from the more popular idea of regional continuity, which actually shows bias on behalf on the Chinese to push a theory. Likewise, Wu Xinzhi who proposed the hypothesis even stated it wasn’t mutually exclusive with OOA.
I’ve been saving this as an article concept due to how amazing it was to come across each of them twice after what started as a simple cross reference. This shouldn’t, however, be read as someone who is against changes to the mainstream, but as someone with actual scrutiny on scientific stances. I can accept the meaningfulness of Orangutans, Australians, and Chinese archaic humans in modern human origins.
In my absence a lot has occurred in researching African substructure since the Ballito boy paper a while back.
I’ve somewhat touched upon this subject previously in two relevant articles, one of which I will provide a short update on regarding “cranks” in population history, including Bruce Fenton, in the future.
The structure of this article will be outlining the general and particular ancestral groups linked to modern Sub-Saharans, briefly putting them in context of OOA, and attempting to approximate them in the form of fossilized specimens. The ancestry analysis will start from the most recent data to the most ancient data discussed (that is shortly before the Holocene towards the branching of H. sapiens from other relatives from H. Ergaster from about 0.5-1 mya) as it will only be more complex from then on.
The first layer will be the finding from the Mahgreb remains that date about 18k, showing profile that is approximately two thirds Near Eastern hunter gatherer, 1 third Sub-Saharan but showing no particular affiliation to a modern sample. It is only slightly shifted towards the Hadza, perhaps suggesting the ancient Eastern African cluster that preceded Basal Eurasian. This shows two things, one the antiquity of back migration to Africa and the oldest DNA sample that is directly linked to modern Sub-Saharans. This could possibly be part of a previous human culture, which may have been part of the migration that lead to modern West Africans. I, however, hesitate to suggest they are direct ancestors. It provides an rough portrait of ancient North Africa nonetheless, a location I particularly figured to be relevant for clues on modern sub-saharans given the different geography of North Africa at the time of the “Wet Sahara“.
The next finding is the break-down of DNA among Western (Yoruba and Mende), Eastern (Nilotic), and Southern (Khoi-San) Africans. The findings show that, in accordance to the Ballito Boy study, Western Africans are a mixture of Ancient East Africans and Basal African Sapiens, Khoi-Sans are derived from the basal Branch at around 250k-300k, and Nilotics are mostly of the 70k-80k branch. However, what it shows is that these populations exchanged genes, particularly between Eastern and Southern Africans. In the case of West Africans, the Yoruba more so then the Mende. I suspect that this could explain the Igbo from the African Genome project showing signs of hunter-gatherers that are more like the Khoi-San than Pygmies at low percentages.
Archaic DNA is where it gets interesting however. I’ve already discussed the 140k-150k admixture event that lead to modern variation of MCU7, but two canididates have came up. One, predictably by this point, is an archaic human ancestry at about 8% in Yoruba, using the same methods to detect 2% archaic DNA in pygmies, dated around 460k-540k , roughly after the divergence of Sapiens from Neanderthals based on another study. The first study however distinguished it from that of the Pygmies, which seems to be older according to this study. The dating of the Pygmy’s admixture is also set around 30k, while the same study dates that of the average Sub-Saharan at 9k. Likewise the TMRCA is place at around 2.9 based on one of the Loci, this seems to align nicely to the age of the MCU7 phylogeny in Africans compared to that of Eurasian Archaics. This is however older than the admixture found in Hammer’s study, suggesting late Erectus. This can be resolved by the conclusion of Hsieh’s study. That is, archaic admixture in Africa was found to be weak, though continuous. This could mean that while penetrating new ecosystems, Hominid interaction what short but often, accumulating alot of layers in small degrees, preserved due to advantageous traits as seen in Neanderthal’s immune system genes. These genes were in turn a trait of the common ancestor that Sapiens lost.
It is therefore possible that archaic admixture could contain different archaic admixture within it based on this behavior. A previous study’s results of loci with ages similar to that of the Neanderthal divergence in hunter gatherers supports this, being somewhat intermediate between MCU7 population and the Basal African. This particular one, however, may very well be tied to a larger finding.
A revised study finds archaic African admixture prior to the split, yet it isn’t African exclusive and seems to have occurred prior to the OOA split. It is only a preprint, but it aligns with what we may have assumed given how long archaic and modern linegaes have mixed. However, as opposed to the continuous flow inferred from pygmies, this particular event was strong and rapid. The researchers likewise note on page 4, though against models of an TMRCA after that of Neanderthals, do not rule it out as a scenario in African substructure. This acknowledges the point made by Razib awhile ago that substructure in Africa reflects the complex development of hominids there. This even pertains to even the Sapiens specific line.
I will now briefly outline the following fossils relevant to modern African population substructure. At the most diverge, early homo found at the Ishango area. I would like to mention that I doubt it mated with Sapiens directly, as the sediment analysis would suggest. Rather, I believe this specimen would genetically contain the variant of genes multiple studies have found to be under selection in African hunter-gathers. The Late Erectus found in Hammer or the Rhodesiensis-like specimen in the initial ghost population models for the Yoruba and Mende I believe were the actual populations that interacted with Humans while possibly carrying these genes.
Late Erectus, or Ergaster, then is represented by Tighenif or Rabat. The latter species can be presented by Bodo or Kabwe. The Kabwe, however, seems to be within Erectus s.l based on internal anatomy than a Petralona equivalent to Sapiens as Bodo is suggested. That is, relative to Bodo or Florisbad, it lacks specializations towards Sapiens. The Ceprano studies however show it nonetheless to be more within the range of overall morphology towards Middle Pleistocene Hominids rather than Ergaster.
(Edit: The Post- LCA admixture could be represented by the two specimens above as well, and I would likewise add a Sapiens Intermediate as well, Florisbad. This status seems to have been replicated here, here, here, here and here. The similar Eliye Springs skull bridges the gap towards Sapiens.)
The next specimen would be the Ceprano skull, the best morphological node for the species Sapiens, Neanderthal, and Denisovans for their LCA. This is significant as it thoroughly rebukes Fenton by his first mistake, dismissing the morphological data in Western Eurasia and Africa. It is shown to be distant from Asian Erectus and seems to represent a “Homo Erectus Sensu Lato” that developed derived traits that would be continued into a trajectory seen in Africa. This is supported by Mounier’s analysis that hypothesized the LCA to be closer to African than European samples. Likewise, his analysis with Manzi shows Erectus/Ergaster tendencies in morphology in partiuclar areas rather than Neanderthal. Manzi also acknowledges a potential morphological link in Africa as well. Therefore we can attribute the LCA detected in DNA in Africans and non Africans by the revised preprint to the above specimen.
(Edit: Manzi has additionally, without confusion, located such an African ancestor to the Hiedelbergensis morphology of Ceprano at the Gombere site.)
Basal Humans, likely the migratory population 148k years ago, would be presented by the Iwo Eleru skull. Jm8 mentions of their relation to similar specimen and DNA sequences found. Likewise, they seem to be responsible for A00.
My previous article has previously mentioned the resulting phenotypic diversity in Modern Africans by way of their skulls. However, I will briefly touch upon some recent examples from my bin of sources.
Lukena Hill Crania 20k: Similar to late Pleistocene North Africans, rare morphology in modern samples. Best represents pre-holocene humans prior to gracilization along with 33k Nazlet Khater. The latter skull could likewise conform to Khoi-san ancestry prior to Gracilization in the Holocene.
Nakuru IX: Odd skull with not much literature, somewhere from southern Africa and dated around 17k, yet aligns with Bantu. This book, which provides a very close continuum in morphology that I’ve been following, dates it as Holocene with some Khoi-san samples. This suggest that at some point it was re-grouped.
Concluding remarks, I have left out alot of other significant details that could give direction in what to investigate in future findings. I encourage that readers go over the original articles themselves to notice other significant findings, such as the relevant positively selected features associated with them. I, may likewise, touch upon the sequences of morphology, paleo-environments, and archaeology in the future. For the time being, we have acquired both game-changing evidence of ancient substructure and a refined continuum of homo evolution in recent years.