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.