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Do Genes and Polymorphisms Explain the Differences between Eastern and Western Societies?

2150 words

In 2012, biologist Hippokratis Kiaris published a book titled Genes, Polymorphisms, and the Making of Societies: How Genetic Behavioral Traits Influence Human Cultures. His main point is that “the presence of different genes in the corresponding people has actually dictated the acquisition of these distinct cultural and historical lines, and that an alternative outcome might be unlikely” (Kiaris, 2012: 9). This is a book that I have not seen discussed in any HBD blog, and based on the premise of the book (how it purports to explain behavioral/societal outcomes between Eastern and Western society) you would think it would be. The book is short, and he speaks with a lot of determinist language. (It’s worth noting he does not discuss IQ at all.)

In the book, he discusses how genes “affect” and “dictate” behavior which then affects “collective decisions and actions” while also stating that it is “conceivable” that history, and what affects human decision-making and reactions, are also “affected by the genetic identity of the people involved” (Kiaris, 2012: 11). Kiaris argues that genetic differences between Easterners and Westerners are driven by “specific environmental conditions that apparently drove the selection of specific alleles in certain populations, which in turn developed particular cultural attitudes and norms” (Kiaris, 2012: 91).

Kiaris attempts to explain the societal differences between the peoples who adopted Platonic thought and those who adopted Confucian thought. He argues that differences between Eastern and Western societies “are not random and stochastic” but are “dictated—or if this is too strong an argument, they are influenced considerably—by the genes that these people carry.” So, Kiaris says, “what we view as a choice is rather the complex and collective outcome of the influence of people’s specific genes combined with the effects of their specific environment … [which] makes the probability for rendering a certain choice distinct between different populations” (Kiaris, 2012: 50).

The first thing that Kiaris discusses (behavior wise) is DRD4. This allele has been associated with miles migrated from Africa (with a correlation of .85) along with novelty-seeking and hyperactivity (which may cause the association found with DRD4 frequency and miles migrated from Africa (Chen et al, 1999). Kiaris notes, of course, that the DRD4 alleles are unevenly distributed across the globe, with people who have migrated further from Africa having a higher frequency of these alleles. Europeans were more likely to have the “novelty-seeking” DRD7 compared to Asian populations (Chang et al, 1996). But, Kiaris (2012: 68) wisely writes (emphasis mine):

Whether these differences [in DRD alleles] represent the collective and cumulative result of selective pressure or they are due to founder effects related to the genetic composition of the early populations that inhabited the corresponding areas remains elusive and is actually impossible to prove or disprove with certainty.

Kiaris then discusses differences between Eastern and Western societies and how we might understand these differences between societies as regards novelty-seeking and the DRD4-7 distribution across the globe. Westerners are more individualistic and this concept of individuality is actually a cornerstone of Western civilization. The “increased excitability and attraction to extravagance” of Westerners, according to Kiaris, is linked to this novelty-seeking behavior which is also related to individualism “and the tendency to constantly seek for means to obtain satisfaction” (Kiaris, 2012: 68). We know that Westerners do not shy away from exploration; after all, the West discovered the East and not vice versa.

Easterners, on the other hand, are more passive and have “an attitude that reflects a certain degree of stoicism and makes life within larger—and likely collectivistic—groups of people more convenient“. Easterners, compared to Westerners, take things “the way they are” which “probably reflects their belief that there is not much one can or should do to change them. This is probably the reason that these people appear rigid against life and loyal, a fact that is also reflected historically in their relatively high political stability” (Kiaris, 2012: 68-69).

Kiaris describes DRD4 as a “prototype Westerner’s gene” (pg 83), stating that the 7R allele of this gene is found more frequently in Europeans compares to Asians. The gene has been associated with increased novelty-seeking, exploratory activity and human migrations, along with liberal ideology. These, of course, are cornerstones of Western civilization and thought, and so, Kiaris argues that the higher frequency of this allele in Europeans—in part—explains certain societal differences between the East and West. Kiaris (2012: 83) then makes a bold claim:

All these features [novelty-seeking, exploratory activity and migration] indeed tend to characterize Westerners and the culutral norms they developed, posing the intriguing possibility that DRD4 can actually represent a single gene that can “predispose” for what we understand as the stereotypic Western-type behavior. Thus, we could imagine that an individual beating the 7-repeat allele functions more efficiently in Western society while the one without this allele would probably be better suited to a society with Eastern-like structure. Alternatively, we could propose that a society with more individuals bearing the 7-repeat allele is more likely to have followed historical lines and choices more typical of a Western society, while a population with a lower number (or deficient as it is the actual case with Easterners) of individuals with the 7-repeat allele would more likely attend to the collective historical outcome of Eaasterners.

Kiaris (2012: 84) is, importantly, skeptical that having a high number of “novelty-seekers” and “explorers” would lead to higher scientific achievement. This is because “attempts to extrapolate from individual characteristics to those of a group of people and societies possess certain dangers and conceptual limitations.

Kiaris (2012: 86) says that “collectivistic behavior … is related to the activity of serotonin.” He then goes on to cite a few instances of other polymorphisms which are associated with collective behavior as well. Goldman et al (2010) show ethnic differences in the and alleles (from Kiaris, 2012: 86):

sandlallele

It should also be noted that populations (Easterners) that had a higher frequency of the allele had a lower prevalence of depression than Westerners. So Western societies are more likely to “suffer more frequently from various manifestations of depression and general mood disorders than those of Eastern cultures (Chiao & Blizinsky, 2010)” (Kiaris, 2012: 89).

As can be seen from the table above, Westerners are more likely to have the allele than Easterners, which should subsequently predict higher levels of happiness in Western compared to Eastern populations. However, “happiness” is, in many ways, subjective; so how would one find an objective way to measure “happiness” cross-culturally? However, Kiaris (2012: 94) writes: “Intuitively speaking, though, I have to admit that I would rather expect Asians to be happier, in general, than Westerners. I cannot support this by specific arguments, but I think the reason for that is related to the individualistic approach of life that the people possess in Western societies: By operating under individualistic norms, it is unavoidably stressful, a condition that operates at the expense of the perception of individuals’ happiness.”

Kiaris discusses catechol-O-methyltransferase (COMT), which is an enzyme responsible for the inactivation of catecholamines. Catecholamines are the hormones dopamine, adrenaline, and noradrenaline. These hormones regulate the “fight or flight” function (Goldstein, 2011). So since catecholamines play a regulatory role in the “fight or flight” mechanism, increased COMT activity results in lower dopamine levels, which is then associated with better performance.

“Warriors” and “worriers” are intrinsically linked to the “fight or flight” mechanism. A “warrior” is someone who performs better under stress, achieves maximal performance despite threat and pain, and is more likely to act efficiently in a threatening environment. A “worrier” is “someone that has an advantage in memory and attention tasks, is more exploratory and efficient in complex environments, but who exhibits worse performance under stressful conditions (Stein et al., 2006)” (Kiaris, 2012: 102).

Kiaris (2012: 107) states that “at the level of society, it can be argued that the specific Met-bearing COMT allele contributes to the buildup of Western individualism. Opposed to this, Easterners’ increased frequency of the Val-bearing “altruistic” allele fits quite well with the construction of a collectivistic society: You have to be an altruist at some degree in order to understand the benefits of collectivism. By being a pure individualist, you only understand “good” as defined and reflected by your sole existence.

So, Kiaris’ whole point is thus: there are differences in polymorphic genes between Easterners and Westerners (and are unevenly distributed) and that differences in these polymorphisms (DRD4, HTT, MAOA, and COMT) explain behavioral differences between behaviors in Eastern and Western societies. So the genetic polymorphisms associated with “Western behavior” (DRD4) are associated with increased novelty-seeking, tendency for financial risk-taking, distance of OoA migration, and liberal ideology. Numerous different MAOA and 5-HTT polymorphisms are associated with collectivism (e.g., Way and Lieberman, 2006 for MAOA and collectivism). The polymorphism in COMT more likely to be found in Westerners predisposes for “worrier’s behavior”. Furthermore, certain polymorphisms of the CHRNB3 gene are more common in all of the populations that migrated out of Africa, which predisposed for leaders—and not follower—behavior.

Trait Gene Allele frequency
Novelty seeking DRD4 7-repeat novelty seeking allele more common in the West
Migration DRD4 7-repeat allele is associated with distance from Africa migration
Nomads/settlers DRD4 7-repeat allele is associated with nomadic life
Political ideology DRD4 7-repeat allele is more common in liberals
Financial risk taking DRD4 7-repeat allele is more common in risk takers
Individualism/Collectivism HTT s allele (collectivistic) of 5-HTT is more common in the East
Happiness HTT l allele has higher prevalence in individuals happy with their life
Individualism/Collectivism MAOA 3-repeat allele (collectivistic) more common in the East)
Warrior/Worrier COMT A-allele (worrier) more common in the West
Altruism COMT G-allele (warrior) associated with altruism
Leader/Follower CHRBN3 A-allele (leader) more common in populations Out-of-Africa

The table above is from Kiaris (2012: 117) who lays out the genes/polymorphisms discussed in his book—what supposedly shows how and why Eastern and Western societies are so different.

Kiaris (2012: 141) then makes a bold claim: “Since we know now that at least a fraction (and likely more than that) of our behavior is due to our genes“, actually “we” don’t “know” this “now”.

The takeaways from the book are: (1) populations differ genetically; (2) since populations differ genetically, then genetic differences correlated with behavior should show frequency differences between populations; (3) since these populations show both behavioral/societal differences and they also differ in genetic polymorphisms which are then associated with that behavior, then those polymorphisms are, in part, a cause of that society and the behavior found in it; (4) therefore, differences in Eastern and Western societies are explained by (some) of these polymorphisms discussed.

Now for a simple rebuttal of the book:

“B iff G” (behavior B is possible if and only if a specific genotype G is instantiated) or “if G, then necessarily B” (genotype G is a sufficient cause for behavior B). Both claims are false; genes are neither a sufficient or necessary cause for any behavior. Genes are, of course, a necessary pre-condition for behavior, but they are not needed for a specific behavior to be instantiated; genes can be said to be difference makers (Sterelny and Kitcher, 1988) (but see Godfrey-Smith and Lewontin, 1993 for a response). These claims cannot be substantiated; therefore, the claims that “if G, then necessarily B” and “B iff G” are false, it cannot be shown that genes are difference makers in regard to behavior, nor can it be shown that particular genes or whatnot.

Conclusion

I’m surprised that I have not come across a book like this sooner; you would expect that there would be a lot more written on this. This book is short, it discusses some good resources, but the conclusions that Kiaris draws, in my opinion, will not come to pass because genes are not neccesary nor sufficient cause of any type of behavior, nor can it be shown that genes are causes of any behavior B. Behavioral differences between Eastern and Western societies, logically, cannot come down to differences in genes, since they are neither necessary nor sufficient causes of behavior (genes are neccessary pre-conditions for behavior, since without genes there is no organism, but genes cannot explain behavior).

Kiaris attempts to show how and why Eastern and Western societies became so different, how and why Western societies are dominated by “Aristotle’s reason and logic”, while Eastern lines of thought “has been dominated by Confucious’s harmony, collectivism, and context dependency” (Kiaris, 2012: 9). While the book is well-written and researched (he talks about nothing new if you’re familiar with the literature), Kiaris fails to prove his ultimate point: that differences in genetic polymorphisms between individuals in different societies explain how and why the societies in question are so different. Though, it is not logically possible for genes to be a necessary nor sufficient cause for any behavior. Kiaris talks like a determinist, since he says that “the presence of different genes in the corresponding people has actually dictated the acquisition of these distinct cultural and historical lines, and that an alternative outcome might be unlikely” (Kiaris, 2012: 9), though that is just wishful thinking: if we were able to start history over again, things would occur differently, “the presence of different genes in the corresponding people” be dammed, since genes do not cause behavior.

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Racial Differences in Physical Functioning

1350 words

Assessing physical functioning is important. Such simple tests—such as walk, stand, and sit tests—can predict numerous things. “Testing” defines one’s abilities after being given a set of instructions. Racial differences exist and, of course, both genetic and environmental factors play a part in health disparities between ethnies in America. Minorities report lower levels of physical activity (PA) than whites, this—most often—leads to negative outcomes, but due to their (average) physiology, they can get away with doing “less” than other ethnies. In this article, I will look at studies which talk about racial differences in physical functioning, what it means, and what can be done about it.

Racial differences in physical functioning

Racial differences in self-rated health at similar levels of health exist (Spencer et al, 2009). Does being optimistic or pessimistic about health effect one’s outcomes? Using 2,929 HABC (Health, Aging, and Body Composition) participants, Spencer et al (2009) examined the relationship between self-rated health (SRH) and race, while controlling for demographic, psychosocial and physical health factors. They found that whites were 3.7 times more likely than blacks to report good SRH.

Elderly blacks were more likely to be less educated, reported lower satisfaction with social support, and also had lower scores on a physical battery test than whites. Further, black men and women were less likely to report that walking a quarter mile was “easy”, implying that (1) they have no endurance and (2) weak leg muscles.

Blacks were also more likely to report higher personal mastery:

Participants were asked whether they agreed or disagreed with the following statements: “ I often feel helpless in dealing with the problems of life ” and “ I can do just about anything I really set my mind to do, ” with response categories of disagree strongly, disagree somewhat, agree somewhat, and agree strongly. (Spencer et al, 2009: 90)

Blacks were also more likely to report higher BMI and more chronic health conditions than whites. White men, though, were more likely to report higher global pain, but were older than black men in the sample. When whites and blacks of similar physical functioning were compared, whites were more likely to report higher SRH. Health pessimists were found to be at higher risk of poor health.

Vazquez et al (2018) showed that ‘Hispanics’ were less likely to report having mobility limitations than whites and blacks even after adjustment for age, gender, and education. Blacks, compared to non-‘Hispanic’ whites were more likely to have limitations on activities of daily living (ADL) and instrumental activities of daily living (IADL) For ADL limitations, questions like “Do participant receive help or supervision with personal care such as bathing, dressing, or getting around the house because of an impairment or a physical or mental health problem?” and for IADLs “Does participant receive help or supervision using the telephone, paying bills, taking medications, preparing light meals, doing laundry, or going shopping?” (Vazquez et al, 2018: 4). They also discuss the so-called “Hispanic paradox” (which I discussed), but could not come to a conclusion on the data they acquired. Nonetheless, ‘Hispanic’ participants were less likely to report mobility issues; blacks were more likely than whites to report significant difficulties with normal activities of daily living.

Araujo et al (2010) devised a lower-extremities chair test: how quickly one can stand and sit in a chair; along with a walking test: the time it takes to walk 50 feet. Those who could not complete the chair test were given a score of ‘0’. Overall, the composite physical function (CPF) score for blacks was 3.45, for ‘Hispanics’ it was 3.66, and for whites, it was 4.30. This shows that older whites were stronger—in the devised tests—and that into older age whites are more likely to not need assistance for everyday activities.

This is important because differences in physical functioning between blacks and whites can explain differences in outcomes one year after having a stroke (Roth et al, 2018). This makes sense, knowing what we know about stroke, cognitive ability and exercise into old age.

Shih et al (2005) conclude:

a nationally representative study of the US population, indicate that among older adults with arthritis: (1) racial disparities found in rates of onset of ADL [activities of daily living] limitations are explained by differences in health needs, health behaviors, and economic resources; (2) there are race-specific differences in risk factors for the onset of ADL limitations; and (3) physical limitations are the most important risk factor for onset of ADL limitations in all racial and ethnic groups.

Safo (2012) showed that out of whites, blacks and “Hispanics”, blacks reported the most (low back) pain, worse role functioning score and overall physical functioning score. Lavernia et al (2011) also found that racial/ethnic minorities were more likely to report pain and have lower physical functioning after having a total knee arthroplasty (TKA) and total hip arthroplasty (THA). They found that blacks and ‘Hispanics’ were more likely to report pain, decreased well-being, and have a lower physical functioning score, which was magnified specifically in blacks. Blacks were more likely to report higher levels of pain than whites (Edwards et al, 2001Campbell and Edwards, 2013), while Kim et al (2017) showed that blacks had lower pain tolerance and higher pain ratings. (Read Pain and Ethnicity by Ronald Wyatt.)

Sarcopenia is the loss of muscle tissue which is a natural part of the aging process. Sarcopenia—and sarcopenic obesity (obesity brought on by muscle loss due to aging)—shows racial/ethnic/gender differences, too. “Hispanics” were the most likely to have sarcopenia and sarcopenic obesity and blacks were least likely to acquire those two maladies (Du et al, 2018). They explain why sarcopenic obesity may be higher in ‘Hispanic’ populations:

One possibility to explain the higher rates of sarcopenia and SO in the Hispanic population could be the higher prevalence of poorly controlled chronic disease, particularly diabetes, and other health conditions.

[…]

We were surprised to find that Hispanic adults had higher rates of sarcopenia and SO [sarcopenic obesity]. One possible explanation could be the disparity in mortality rates among ethnic populations. Populations that have greater survival rates may live longer even with poorer health and thus have greater chance of developing sarcopenia. Alternatively, populations which have lower survival rates may not live long enough to develop sarcopenia and thus may identify with lower prevalence of sarcopenia. This explanation appears to be supported by the results of our study and current mortality statistics; NH Blacks have the highest mortality rate, followed by NH Whites, and lastly Hispanics.

Differences in physical activity could, of course, lead to differences in sarcopenic obesity. Physical activity leads to an increase in testosterone in lifelong sedentary men (Hayes et al, 2017), while those who had high physical activity compared to low physical activity were more likely to have high testosterone, which was not observed between the groups that were on a calorie-restricted diet (Kumagai et al, 2016). Kumagai et al (2018) also showed that vigorous physical exercise leads to increases in testosterone in obese men:

We demonstrated that a 12-week aerobic exercise intervention increased serum total testosterone, free testosterone, and bioavailable testosterone levels in overweight/obese men. We suggest that an increase in vigorous physical activity increased circulating testosterone levels in overweight/obese men.

(Though see Hawkins et al, 2008 who show that only SHGB and DHT increased with no increase in testosterone.)

So, clearly, since exercise can increase testosterone levels in obese subjects, and higher levels of testosterone are associated with lower levels of adipose tissue; since adequate levels of steroid hormones are needed for lower levels of adipose tissue (Mammi et al, 2012), then since exercise increases testosterone and higher levels of testosterone lead to lower levels of adipose tissue, if physical activity is increased, then levels of obesity and sarcopenic obesity should decrease in those populations.

Conclusion

Racial differences in physical functioning exist; these differences in physical functioning that exist have grave consequences for certain events, especially after a stroke. Differences in physical functioning/activity cause differences in sarcopenia/sarcopenic obesity in different ethnies. This can be ameliorated by targeting at-risk groups with certain outreach. This type of research shows how differences in lifestyle between ethnies cause differences in physical activity between ethnies as the years progress.

(Also read Evolving Human Nutrition: Implications for Public Healthspecifically Chapter 8 on socioeconomic status and health disparities for more information on how and why differences like this persist between ethnies in America.)

Problems with Evolutionary Psychology

2350 words

Evolutionary Psychology (EP) is a discipline which purports to explain mental and psychological traits as adaptations—functional products of “natural selection”—which are genetically inherited/transmitted. Its main premises is that the human mind can be explained by evolution through natural selection; that the mind is “modular”—called the “massive modularity hypothesis” (see Pinker, 1997). EP purports that the mind is “a cluster of evolved information-processing mechanisms” with its main goal being “to characterize these Darwinian algorithms” (Sterelny and Griffiths, 1999: 336). The problem with EP, though, is that many of the “theories/hypotheses” are just speculation—what is termed “just-so stories” (Gould and Lewontin, 1979; Richardson, 2007; Nielsen, 2009Fodor and Piattelli-Palmarini, 2010). In this article, I will discuss the massive modularity hypothesis, adaptationism, and the promises that EP makes as a whole.

Massive Modularity

The massive modularity hypothesis (MMH) proposes that the modules “for” mental processing evolved in response to “natural selection” (Samuels, 1998). To evolutionary psychologists, the mind is made up of different modules that were “selected for” different mental abilities. So, to evolutionary psychologists like Tooby and Cosmides, Pinker et al, much of human psychology is rooted in the Pleistocene (i.e., Tooby and Cosmides’ 5th Principle that “our modern skulls house a stone age mind“) . Evolutionary psychologists propose that the mind is made up of different, genetically influenced, modules that which were specifically selected as to help our ancestors solve domain-specific problems.

Two principle arguments exist for the MMH. Argument (1)—called the optimality argument—is:

  1. There are adaptive problems in every environment; different adaptive problems in different environments require different solutions, and different solutions can be implemented by functionally distinct modules.
  2. Adaptive problems are selective pressures; for each unique pressure faced in the original evolutionary environment (OEE), there is a unique module which was selected to solve those—and only those—specific adaptive problems.
  3. Selective mechanisms can produce highly specialized cognitive modules.
  4. Therefore, since different adaptive problems require different solutions and different solutions can be implemented by functionally distinct modules, then there must exist differing modules in the human mind which were selected for in virtue of their contribution to fitness.

Or the argument could be:

  1. Domain-specific processes exist
  2. These processes arose due to evolution
  3. Therefore these domain-specific processes that arose due to evolution have a genetic basis

Tooby and Cosmides claim that, distinct modules for certain adaptive problems in distinct environments are superior at solving different problems, rather than a general-purpose cognitive module. They argue that selection can produce different modules in the mind “for” different adaptive problems. Tooby and Cosmides put their argument in their own words as:

(1) As a rule, when two adaptive problems have solutions that are incompatible or simply different, a single solution will be inferior to two specialized solutions

(2) .. . domain-specific cognitive mechanisms . . . can be expected to systematically outperform (and hence preclude or replace) more general mechanisms

(3) Simply to survive and reproduce, our Pleistocene ancestors had to be good at solving an enormously broad array of adaptive problems—problems that would defeat any modern artificial intelligence system. A small sampling include foraging for food, navigating, selecting a mate, parenting, engaging in social exchange, dealing with aggressive threat, avoiding predators, avoiding pathogenic contamination, avoiding naturally occurring plant toxins, avoiding incest and so on

(4) [Therefore] The human mind can be expected to include a large number of distinct, domain-specific mechanisms (quoted from Samuels, 1998: 585-586)

Clearly, the assumption from Tooby and Cosmides is that specific modules for certain adaptive problems in the OEE are superior to general-purpose modules. Samuels (1998: 586) writes:

In the case of psychological traits, in order to use optimality considerations with any confidence one needs to know (a) what features were being optimized by the evolutionary process and (b) what range of phenotypes were available to natural selection. As a matter of fact, however, we have little knowledge about either of these matters.

Samuels (1998) thusly concludes that “the endorsement of the Massive Modularity Hypothesis by evolutionary psychologists is both unwarranted and unmotivated.” (Also see Prinz, 2006.)

The key point of the MMH is that, according to Tooby and Cosmides, we would expect that the mind consists of different modules which are “designed” to solve domain-specific problems. If we know what type of adaptive situations happened to our ancestors then we should be able to construct the evolution of a trait by knowing its current functional use and “working backwards”—what is termed “reverse engineering”—inferring “function” from “cause” (see Richardson, 2007: chapter 2); inferring effect from relevant causes (see Richardson, 2007: chapter 3) and disentangling historical ancestry from history and structure (see Richardson, 2007: chapter 4).

As for their second argument:

  1. It is impossible for human psychology—that contains nothing but general-purpose mechanisms—to have evolved since such a system cannot be adaptive.
  2. Such a system cannot possibly have solved the adaptive problems faced by our ancestors in the evolutionary past.
  3. Therefore, the mind cannot possibly have evolved general-purpose mechanisms and had to have evolved different mental modules in order to carry out different tasks.

They defend the argument by stating that the domain-dependence of different errors is a cause of the evolution of different modules of the mind; that information for crucial adaptive behavior cannot be learned by using only domain-specific systems; and that many adaptive problems are highly complex and unlikely to have been solved by general-purpose modules. Therefore, the mind must be modular since this can account for domain-specific problems—while, according to Tooby and Cosmides, general-purposed modules cannot. The argument, though, fails to provide us with any reason to accept the claim that the mind is made up of mostly—or is all made up of—Darwinian modules which were kept around since they were targets of selection.

Clearly, evidence for the modularity of mind is lacking—as is the evidence that reverse engineering “works” for the purpose intended.

Lloyd (1999: 224) writes that:

Given these difficulties – well-known especially since Konrad Lorenz and Nico Tinbergen’s pioneering experiments on animal behavior – it is not scientifically acceptable within evolutionary biology to conclude that, because a given pattern of responses contributes to evolutionary success, then there is some ‘organ’ (or part of the brain) producing such a pattern, that is therefore an adaptation (see Williams 1966). This is because the ‘organ’ or ‘module’ may not actually exist as a biologically real trait, and even if it does, its current function may or may not be the same as the past function(s).

Sterelny and Griffiths (1999: 342) write that “… evolutionary psychology has bought into an oversimplified view of the relationship between an evolving population and its environment, and has prematurely accepted a modular conception of the mind.

False dichotomies

Tooby and Cosmides (1992) coined the phrase “Standard Social Science Model” (SSSM) in order to differentiate their EP model (the “integrated causal model”; ICM) from the SSSM. According to Tooby and Cosmides (1992), the basis of the SSSM is to employ complete general-purpose cognitive modules and to deny any type of nativist modules whatsoever. Therefore, according to Tooby and Cosmides’ characterization of their so-called “opposition”, interesting differences between groups—and, of course, individuals—are due completely to cultural conditioning with absolutely no nativist elements since there are only general-purpose modules. Differences between individuals, according to the SSSM, are cultural products—differences in socialization cause individual differences.

Richardson (2007:179) writes:

Tooby and Cosmides’ portrayal [of the SSSM] is very effective. It is also a piece of sophistry, offering a false dichotomy between a manifestly untenable view and their own. The alternative is one that sees no differences between individuals and no biological contribution to individual or social development. I think no serious figure embraces that view, since, perhaps, John Watson in the early twentieth century.

Tooby and Cosmides also say that “There is no small irony in the fact that [the[ Standard Social Science MOdel’s hostility to adaptationist approaches is often justified through the accusation that adaptationist approaches purportedly attribute important differences between individuals, races and classes to genetic differences. In actuality, adaptationist approaches offer the explanation for why the psychic unity of humankind is genuine and not just an ideological fiction” (1992, 79).

Furthermore, David Buss claims that “Natural selection is the only prospect for explaining human nature” (Richardson, 2007: 182). (Whatever “human nature” is. See Nagel’s 2012 Mind and Cosmos for arguments that the mind cannot possibly have been naturally selected since evolutionary biology is a physical theory and Fodor and Pitatelli-Palmarini’s 2010 book What Darwin Got Wrong for the argument against natural selection as an explanatory mechanism in regard to trait fixation.)

Problems with the adaptationist paradigm

Adaptationism is a research programme in which, according to the Stanford Encyclopedia of Philosophy, ““adaptationists” view natural selection among individuals within a population as the only important cause of the evolution of a trait; they also typically believe that the construction of explanations based solely on natural selection to be the most fruitful way of making progress in evolutionary biology and that this endeavor addresses the most important goal of evolutionary biology, which is to understand the evolution of adaptations.” 

Though numerous problems exist with this programme, not least the claim that most—or all—important phenotypic traits are the product of evolution by natural selection. In their book Sex and Death: An Introduction to Philosophy of Biology, Sterelny and Griffiths (1999: 351) write:

Adaptive explanation is an inference from the current phenotype of an organism to the problems that organism faced in its evolutionary past. Obviously, that inference will be problematic if we do not have an accurate description of the current phenotype and its adaptive significance—of the solution that evolution actually produced. The inference from current adaptive importance to adaptation is problematic enough even when the adaptive and phenotypic claims on which it is based are uncontroversial (13.1). The inference is still more problematic when the nature of the phenotype and its adaptive importance are yet to be established.

This is not the main problem with the paradigm, though. The main problem is that all of these theories/hypotheses are “just-so stories”—“… an adaptive scenario, a hypothesis about what a trait’s selective history might have been and hence what its function may be” (Sterelny and Griffiths, 1999: 61). I’d also add that just-so stories are stories that cannot be independently verified of the data that they purport to explain—that is, there is no observation that can disconfirm the adaptationist “hypothesis”, and the only data that “proves” the hypothesis is the data it purports to explain. EP hypotheses are not testable. Therefore EP hypotheses are just-so stories.

Sterelny and Griffiths (1999: 338) “… agree with the central idea of evolutionary psychology, namely, that we should look for the effects of natural selection on the psychological mechanisms that explain our behaviors, rather than on those behaviors themselves.” I disagree, since it is not possible that “psychological mechanisms” can be selected.

What is the relationship between environment and adaptation? First, we need to think of some “problems” that exist in the environment. One example is mate choice: Should one be faithful to their partner? When should one abandon their old partner? When should they help their kin find partners? When and how should one punish infidelity? This problem, pretty obviously, is evidence against the idea that adaptations are explained by the problem to which the adapted trait is the solution (see David Buller’s 2005 book Adapting Minds for strong critiques against “reverse engineering”). If—and only if—a single cognitive device exists that guides a creature’s behavior with respect to the issues of mate choice, the issue is then a single-domain, not multi-domain, problem, while there are different aspects of the same problem (see the questions above). The existence of said module explains why we think of mate choice as a single problem.

Sterelny and Griffiths (1999: 342) are hopeful in EP’s quest to discover our shared “human nature”, “But both the objective and subjective obstacles to carrying out this program remain serious.” The adaptationist programme, however, is unfalsifiable. “Particular adaptive stories can be tested, as we discuss below, but Gould and Lewontin argue that this does not test the idea of adaptationism itself. Whenever a particular adaptive story is discredited, the adaptationist makes up a new story, or just promises to look for one. The possibility that the trait is not an adaptation is never considered” (Sterelny and Griffiths, 1999: 237).

Adaptationist explanations (EP is—mostly—nothing but adaptationist explanation) are not scientific since they cannot be falsified—EP hypotheses are not falsifiable, nor do they generate testable predictions. They only explain the data it purports to explain—meaning that all EP adaptationist explanations are just-so stories. (Also see Kaplan, 2002 for arguments against the adaptationist paradigm.)

Conclusion

Even those who are sympathetic to the EP research programme, rightly, point out the glaring flaws in the programme. These flaws—in my opinion—cannot be overcome. EP will always be “plausible and speculatuve ” just-so stories that purport to explain the evolution of what, supposedly, are traits that were “selected for” in virtue of their contribution to fitness in the OEE. However, we do not (and cannot) know what the OEE was like—we would need a time machine. It is not possible for us to know the selective pressures that occurred on our ancestors in the OEE. We do know that increased reproductive efficiency in the current-day is not evidence that said trait was adaptive and selected in the OEE.

The mind is not modular; Tooby and Cosmides proposed a false dichotomy (their ICM vs SSSM) which is not valid (no one is a “blank slatist”, whatever that is); and the adaptationist paradigm is nothing but speculative just-so stories.

  1. For EP to be a valid research programme, EP hypotheses must generate testable, falsifiable predictions.
  2. EP cannot generate testable, falsifiable predictions (the hypotheses are inherently ad hoc).
  3. Therefore, EP is not a valid research programme.

There is no reason at all to accept any just-so story since these adaptive explanations cannot produce evidence that the trait was not a byproduct, due to genetic drift etc. Therefore EP is not a scientific enterprise; it only tells “plausible”, speculative stories just-so stories “… I view evolutionary psychology as more speculation than science. The conclusion I urge is, accordingly, skeptical. Speculation is just that: speculation. We should regard it as such. Evolutionary psychology as currently practiced is often speculation disguised as results. We should regard it as such” (Richardson, 2007: 25). This is the view that should be accepted in the mainstream, since there can be no evidence for the speculative stories of EP.

Three Arguments for the Existence of Race: Establishing Population Groups as Races

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At least three arguments establish the existence and reality of biological race:

Argument (1) from Michael Hardimon’s (2017) bookRethinking Race: The Case for Deflationary Realism” (The Argument for the Existence of Minimalist Races, see Chapters 2, 3, and 4):

The conditions of minimalist racehood are as follows:

(C1) a group, is distinguished from other groups of human beings by patterns of visible physical features

(C2) [the] members are linked be a common ancestry peculiar to members of that group, and

(C3) [they] originate from a distinctive geographic location (Hardimon, 2017: 31).

This is the argument to prove the existence of minimalist races:

P1) There are differences in patterns of visible physical features which correspond to geographic ancestry
P2) These patterns are exhibited between real groups, existing groups (i.e., individuals who share common ancestry)
P3) These real, existing groups that exhibit these physical patterns by geographic ancestry satisfy the conditions of minimalist race
C) Therefore race exists and is a biological reality

Argument (2) from Michael Hardimon’s (2017) book “Rethinking Race: The Case for Deflationary Realism” (The Argument for the Existence of Populationist Races, see Chapters 5 and 6):

P1) The five populations demarcated by Rosenberg et al (2002) are populationist races; K = 5 demarcates populationist races.
P2) Populationist race=minimalist race.
P3) If populationist race=minimalist race, then everything from showing that minimalist races are a biological reality carries over to populationist races.
P4) Populationist races capture differences in genetic variation between continents and this genetic variation is responsible for the distinctive patterns of visible physical features which correspond to geographic ancestry who belong to biological lines of descent which were initiated by geographically isolated founding populations.
C) Therefore, since populationist races=minmalist races, and visible physical features which correspond to geographic ancestry are genetically transmitted by populations who belong to biological lines of descent, initiated by reproductively isolated founding populations, then populationist races exist and are biologically real.

Argument (3) from Quayshawn Spencer’s (2014) paper “A Radical Solution to the Race Problem” (The argument for the Existence of Blumenbachian Populations):

P1) The term “race” in America refers to biologically real entities; when speaking of race in America, Americans defer to the US Census Bureau who defers to the Office of Management and Budget (OMB).
P2) The OMB refers to race as “sets of” categories, while considering “races” to have 5 members, which correspond to the five major geographic regions.
P3) Rosenberg et al show that, at K = 5, meaningful, though small (~4.3 percent) genetic variation exists between continental-populations
C) Since Americans defer to the US Census Bureau who defers to the OMB, and the OMB refers to race as “sets of” categories which then correspond to five clusters found by Rosenberg et al’s (2002) analysis, race (what Spencer, 2014 terms “Blumenbachian populations”) must exist, though “race” is both socially constructed and biologically real.

Put another way, Spencer’s (2014) argument could also be:

P1) The US meaning of “race” is a referent, which refers to the discourse used by the US Census Bureau; the US Census Bureau refers to the discourse used by the Office of Management and Budget (OMB).
P2) The referent of “race”, in US ontology, refers to a set of human population groups, not a biological kind (sets of human population groups as denoted by the OMB), which refer to “Africans”, “Caucasians”, “East Asians”, “Native Americans”, and Pacific Islanders/Oceanians.
P3) The US meaning of race is both biologically real and socially constructed; Americans refer to real, existing groups when they talk about race.
C) If the US meaning of race is a referent which refers to the discourse used by the US Census Bureau and they refer to the OMB who discuss “sets of” population groups, then when Americans talk about race they talk about Blumenbachian partitions, since race is both biologically real and socially constructed.

The claim “Race exists” is now established. Note how Argument (1) establishes the claim that “races” are real, existing groups who are phenotypically distinct populations with differing geographic ancestry. Note how Argument (2) establishes the claim that populationist race = minimalist race and that “races” are a group of populations that exhibit a distinctive pattern of genetically transmitted phenotypic characters which then correspond to that group’s geographic ancestry who belong to a biological line of descent which was initiated by a geographically separated and reproductively isolated founding population. (This definition of “race” a subdivision of Homo sapiens is the best I’ve come across so far.) Finally, note how Argument (3) establishes the claim that race, in the American sense, is both biologically real and socially constructed. All three arguments are sound and logically valid.

Now, which groups fall into which of the five racial categories?

Caucasians

Caucasians denote a wide-range of groups; Europeans, MENA (Middle Eastern/North African) peoples, Indians are a very diverse group, racially speaking, with “Caucasoids”, “Mongoloids” and “Australoids” (Australoids would mean Pacific Islander/Oceanian) (see Kashyap et al, 2006 for an overview of ethnic, linguistic and geographic affiliations of Indians in the study). Ashkenazi Jews are taken to be a specific race in today’s modern racial ontology, however, Ashkenazi Jews do not exhibit a distinctive pattern of genetically transmitted phenotypic characters which then correspond to their geographic ancestry; they do represent a “geographically isolated and reproductively isolated founding population”, but the fact that they do not exhibit a distinctive pattern of genetically transmitted phenotypic characters means they are not a race, according to Arguments (1) and (2). Ashkenazi Jews are Caucasian, and not their own race. Of course, skin color does not denote race, it is only one marker to use to infer which groups are races.

Africans

Africans comprise all of Sub-Saharan Africa. Africa has the most genetic diversity in the human species (see Campbell and Tishkoff, 2010). Africans, in general, have long, slim bodies with a broad nose, dark skin, kinky hair (lip size is different based on the ethny in question). There are over 3,000 different ethnic groups in Africa, who all comprise the same race. Now, since Africans have the most genetic diversity this does not necessarily mean that they are so phenotypically distinct that there are tens, hundreds, thousands of races on the continent. One only needs to refer back to Arguments (1) and (2) to see that brash claims that “all Xs are Ys” don’t make any sense—especially with the arguments laid out above.

East Asians

East Asians denote a minimalist and populationist race (Arguments (1) and (2)) and Blumenbachian partition (Argument (3)). East Asians denote, obviously, those that derive from East Asia (Chinese, Japanese, Koreans, Vietnamese). These peoples are relatively short, on average, have a distinct yellow-ish tint to their skin (which is why they are sometimes called “yellow”), epicanthic folds and shorter limbs (more likely to have the endomorphic phenotype).

Native Americans

Native Americans are derived from a Siberian population that crossed the Bering Land Bridge about 14kya. They then spread throughout the Americas, becoming the “Natives” we know today. They are what used to be termed “red” people, due to their skin color. Native Americans are derived from Siberians, who share affinities with East Asians. (This will be discussed in further depth below.) They have black hair, and dark-ish skin. Populations that lived in the Americans pre-1492 expansion are part of the Native American racial grouping.

Pacific Islanders/Oceanians

The last racial grouping are Pacific Islanders. Spencer (2014: 1032) writes that we can define Oceanians (Pacific Islanders):

as the most inclusive human population born from East Asians in Oceania (Sahul and the Pacific Islands) and from the original human inhabitants of Oceania. Since Sahul was a single landmass composed of present-day Australia, New Guinea, and Tasmania 50,000–60,000 years ago, when humans first inhabited it, and since we know that the original human inhabitants of Oceania interbred to create modern Oceanians, and since temporal parts of populations are genealogically connected, it should be the case that most Oceanians have genealogical connections to the original peoples of some Pacific island. The only Oceanians who will not will be individuals who became Oceanian from interbreeding alone and Oceanians descended from indigenous peoples of Sahul but not indigenous peoples of a Pacific island (e.g., Aboriginal Australians). The final source of evidence comes from counterfactual cases. [Pacific Islanders and Australian Aborigines share a deep ancestry, see McEvoy et al, 2010.]

A group is in race X, if and only if they share a pattern of visible physical features and common geographic ancestry. If they do not share a pattern of visible physical features which correspond to common geographic ancestry then they do not constitute a race. Keep this in mind for the next two sections.

Are Oceanians black?

One claim that gets tossed around a lot (by black nationalists) is the claim that Oceanians are black due to their skin color, certain phenotypic traits. But this could just as easily be explained by convergent evolution, not that they are, necessarily, the same racial grouping. If this were true, then Australian Aborigines would be black, by proxy, since Australian Aborigines and Oceanian are the same race. The claim, though, holds no water. Just because two groups “look similar” (which I do not see), it does not follow that they are the same race, since other conditions need to be met in order to establish the claim that two separate groups belong to the same race.

Are Native Americans Mongoloid?

Lastly is the claim that Native Americans do not denote an actual racial grouping, they are either Mongoloid or a sub-race of Mongoloids.

Many authors throughout history have presumed that Native Americans were Mongoloid. Franz Boas, for example, said that the Maya Indians were Mongoloid, and that, American populations had features the most similar to Mongoloids, so they are thusly Mongoloid. Wikipedia has a great overview of the history of the “Mongoloid” terminology, with examples from authors throughout history. But that is irrelevant. Native Americans genetically transmit heritable phenotypic characters which correspond with their geographic ancestry and are genetically and geographically isolated population groups.

Although the claim that “Native Americans are Mongoloid” has been echoed for hundreds of years, a simple argument can be erected to take care of the claim:

P1) If Native Americans were East Asian/Mongoloid, then they would look East Asian/Mongoloid.
P2) Native Americans don’t look East Asian/Mongoloid, they have a distinct phenotype which corresponds to their geographic ancestry (See Hardimon’s minimalist/populationist race concepts).
C) Therefore, Native Americans are not East Asian/Mongoloid.

Establishing the claim that Native Americans are not East Asian/Mongoloid is simple. Some authors may make the claim that since they look similar (whatever that means, they don’t look similar to me), that they, therefore according to Arguments (1) and (2) they are a separate race and not a sub-race of East Asians/Mongoloids; Argument (3) further establishes the claim that they are a separate race on the basis that they form a distinct cluster in clustering analyses (Rosenberg et al, 2002) and since, Americans defer to the US Census Beureau and the US Census Beureau defers to the OMB who discusses sets of populations, then when Americans talk about race they talk about Native Americans as separate from East Asians/Mongoloids, since, according to Arguments (1) and (2) they have a distinct phenotype.

Generally, they have distinct skin colors (of course, skin color does not equal race, but it is a big tell), they have similar black, straight hair. But they are, in my opinion, just too phenotypically distinct to call them the same race as Mongoloids/East Asians. For the claim “Native Americans and Mongoloids/East Asians” to be true, they would need to satisfy P1 in Argument (1) and P4 in Argument (2). Native Americans do not satisfy P1 in Argument (1) nor do they satisfy P4 in Argument (2). Therefore, Native Americans are not Mongoloid/East Asian.

Conclusion

The claim “Race exists and is a biological reality” is clearly established by three sound, valid arguments—two from Hardimon (2017; chapters 2-6) and one from Spencer (2014). These arguments show, using the latest of genetic clustering studies, that races, as classicly defined, do indeed, exist and that our old views of race hundreds of years ago were, largely, correct. These arguments establish the existence of the old folk-racial categories. Races have distinct phenotypes which are genetically transmitted and are correlated with geographic ancestry. Some may make certain claims that “Oceanians are black” or “Native Americans are Mongoloid”, but these claims do not hold. These two groups in question are phenotypically distinct, and they come from unique geographic locations, therefore they are not a part of the races that some purport them to be.

The Black-White Bench Press Study

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Blacks vs whites: which race is stronger? Unfortunately, actual studies on actual strength lifts between races are few and far between (and if there are any comparisons between races it’s on an ancillary movement such as quadricep extension; for example see Goodpaster et al 2006). There is, though, one study comparing whites and blacks on a major lift: the bench press. The paper is littered with many problems, most of which make me not able to take the paper seriously. I’ve written about this paper in the past but this article will be much more comprehensive.

When searching for racial comparisons in physical strength, Boyce et al (2014) is one of the only papers one would come across looking at racial differences in strength in one specific (main) lift. The authors used a longitudinal design: they had the police officers’ bench press numbers during their first week on the force and then had data 12.5 years later to assess racial and gender differences in the bench press. They assessed strength scores on the bench press, bench press/lean mass, as well as bench press/body mass.

The assessed 327 police officers: 30 women (13 black, 17 white) and 297 males (41 black and 238 white). Officers that could not be classified as either white or black were removed from the sample. Average number of years between the test at recruitment and later into their career was 12.5 years +/- 2 years while the mean age at the initial recruitment was 26.4 years +/- 3.4 years. The officers were mostly college-educated and were low-middle to upper-middle class.

When the recruits were considered for the job, they had their body mass, percent body fat (with skinfold calipers, which will be covered below) and did a 1RM (one-rep max) on the bench press to assess physical strength. The physical fitness battery (for incoming officers) was as follows (in order): body fat, sit-and-reach flexibility (to see how flexible one is in their lower body/hamstrings), 1RM bench press, and finally a 1.5-mile run. For in-service officers, they had their body fat tested, a treadmill test, bench press, muscular endurance (either curls or sit-ups; curls are a contraindicative exercise if used with a straight bar while sit-ups are contraindicative since they put unneeded strain on the lower back).

All groups, when combined after 12.5 years, had significant mean gains in strength which were accompanied by gains in body mass, percent fat mass, and lean mass. Black men, at initial recruitment, weighed 187 pounds and benched 210 pounds; white men weighed 180 pounds and benched 185 pounds. Black men benched 1.12 times their body weight whereas white men benched 1.027 times their body weight. At the follow-up assessment, black males weighed 223 pounds and benched 240 pounds. White males weighed 205 pounds and benched 215 pounds. Black males benched 1.07 times their body weight whereas white males benched 1.05 times their body weight. (To find out what percentage of body weight one lifts, take weight lifted and divide it by the weight of the individual.)

Black women, on the other hand at initial recruitment, weighed 130 pounds and benched 85 pounds whereas white women weighed 127 pounds and benched 82 pounds. Black women benched .653 times their body weight whereas white women benched .645 times their body weight. At the follow-up assessment, black women weighed 151 pounds and benched 98 pounds whereas white women weighed 141 pounds and benched 90 pounds. Black women benched .649 times their body weight at the follow-up whereas white women benched .638 times their body weight.

So there was no real difference between black and white female recruits/officers but there was a difference between black and white male recruits/officers. Of course, due to higher levels of testosterone and other hormones compared to women, the males had a changed much more significantly from the initial recruitment. Figures 1 and 2 from Boyce et al (2014: 146) are important too:

strrace

strrace2

Since the study was done over 12.5 years and the individuals were in their mid-20s at initial recruitment, then this study is anomalous since the individuals gained strength and lean mass well into their 30s. Testosterone begins to decrease starting at age 25, though it is not a foregone conclusion that this occurs; age-related declines in testosterone are not inevitable. It just seems that this is the case since, around one’s mid-20s, life changes happen (marriage, kids) which then may cause lifestyle changes (weight gain and the onset of depression). Most of the testosterone decline can be explained by smoking, obesity, depression and other health factors (Shi et al, 2013). So if these officers had good nutrition—and I do not see why they did not—then they can, in effect, bypass most of the so-called age-related declines in testosterone (which is also related to marriage, having children and obesity; Gray, 2011; Pollet, Cobey, and van der Meij, 2013; Mazur et al, 2013).

Gains in lean mass are related to gains in strength, and so, since there was considerable body mass gain and, consequently, lean mass gain, then overall bench pressing strength should have pretty much substantially increased. The strength gains, though, were negated when they divided the weight lifted by the weight of the lifters (pound-for-pound strength, which is what matters more). Black males had the greatest body mass gain over the 12.5 year period, which subsequently corresponded to a decrease in strength on the bench press.

Over the 12.5 year period, black males gained 36 pounds whereas white males gained 25 pounds. Although black males gained more weight over the 12.5 year period—and loss on bench press/body mass—blacks were still very slightly stronger than whites (1.07 compared to 1.05) which is not significant. Black and white females, on the other hand, had no real differences in any of the scores that Boyce et al (2014) did. Furthermore, black and white women, in this study, had similar strength gains and body mass/lean mass gains. Of course, this is a self-selected sample: black women are consistently noted to carry more fat mass than white women (see Rahman et al, 2009).

Both black and white males increased in the bench press throughout the 12.5 year period compared to black and white females, which is due to them being men (higher levels of testosterone and other hormones, larger muscle cross-section area; Miller et al, 1993). The groups who were stronger when they were hired remained the strongest at the follow-up. So, Boyce et al (2014) conclude, the bench press is able to be used as an assessor of upper-body strength since blacks actually, according to their study, are stronger than whites so, therefore, “an upper body strength test such as a bench press will have little adverse impact on blacks, a racially protected group” (Boyce et al, 2014: 148). Though, for women, since they are not as physically strong as men, this will have an “adverse impact on female recruit and incumbent officers, a gender protected group, no matter if they are black or white” (Boyce et al, 2014: 148).

Now time for a few pitfalls (one of which is not the fault of the investigators): height was not assessed; skin-fold calipers were used to assess body fat; and a Smith machine bench press was used.

Height: Due to an ongoing investigation on the Charlotte Mecklenburg Police Department (for apparently discriminating against certain recruits on the basis of height), the height of the officers at recruitment and the follow-up were not noted. This is a problem. If height were known (along with a few more anthropometric variables), then we can infer who had the somatotype that is conducive to bench pressing. In lieu of no height data, we cannot infer this. It is easier for people with shorter limbs to bench press, since the bar has a shorter path to travel, compared to people with longer arms who have to move the weight a further distance. Blacks are more likely to have longer arms and, as I have argued, this would impede them in strength when bench pressing and overhead pressing but will help in the deadlift since they have longer arms and a shorter torso, it is easier for people with this soma to deadlift due to their body proportions.

Skin-fold calipers: Body fat was assessed using skin-fold calipers. Blacks have thinner skin folds than whites, and so since they have thinner skin folds than whites, and the formula for assessing body fat from skin-folds is based on whites, then, it has been argued, that black males need their own BMI scale since they have thinner skin folds and differing levels of fat-free body mass (Vickery, Cureton, and Collins, 1988; Wagner and Heyward, 2000). So since the levels of body fat were off for blacks, then Boyce et al’s (2014) bench press/lean mass is useless since body fat was not assessed correctly. (I know that using calipers is cheaper and easier than sending everyone for a DXA scan, but the difference in body composition between blacks and whites should be known so that, at least when it comes to fat comparisons between different races, bad methods don’t get used and parroted.) Since there are well-known differences in skinfolds as they relate to body fat percentage/lean mass regarding blacks and whites, it’s, again, safe to toss out that part of the study (regarding weight moved/lean mass), since there are huge flaws in regard to assessing body fat through use of conventional measures in blacks compared to whites.

Smith machine bench press: This is, perhaps, one of the most important pitfalls. I can think of a few reasons why this machine was used: (1) you don’t really need to teach someone how to get into proper position to grab the bar. (2) the bar is on a set path, and so people with different anthropometric measures may be uncomfortable while using the machine (which would then affect overall strength). (3) Saeterbakken, Tillaar, and Fimland (2011) assessed three different chest press exercises: the Smith machine bench press, the barbell bench press, and the dumbbell bench press. Those in the study had the highest 1RM on the bench press, followed by the Smith machine and finally were the weakest on dumbbell bench press. The biceps brachii is used for stabilization, and they found that EMG activity in the biceps brachii increased with stability requirements (dumbbell > barbell > Smith). This is due to the fact that, on the two exercises that are not assisted, the muscles need to stabilize the free weight. Since you’re using more muscles to stabilize the weight, then, theoretically, you can move more weight. EMG activity was the same regarding the pectoralis major and anterior deltoids but was different in the triceps and biceps brachii. The prime movers (agonists) of the bench press are the anterior deltoids, triceps, and pecs/serratus. Therefore, the antagonists are the posterior deltoids, the biceps, and the lats/rhomboids.

1rmbp

The load lifted on the bench press was three percent higher than on the Smith machine. Since stability requirements are low with the Smith, and the bar is on a set path that cannot be changed, then, theoretically, one should be able to move more weight on the Smith machine (which is my personal experience and the experience of many people I have worked with) compared to the dumbbell and regular bench press. Though, the load lifted on the bench press was about three percent higher than on the Smith machine bench press. The activity of the pectoralis and the anterior deltoid was lower on the eccentric phase (think the negative portion of the lift) when compared to dumbbell and barbell pressing, which is, again, explained by lack of stabilizing muscles used on the Smith machine bench press. So this small study (n=12) shows that there are differences in 1RM between the three lifts studied and that there are differences in the neuromuscular activity of the flexor/extensor muscles of the arm, but showing no difference in the prime movers of the lift (such as the pectoralis major). In the descending phase of the lift, there was less EMG activation, which indicates that a greater neural drive is needed for the eccentric phase of the lift.

The Smith machine used in Boyce et al (2014) was an Atlantis Angled Smith Machine E-155, which I have used personally (and have had hundreds of people use). In my personal experience, weight moved on the Smith is considerably different when compared to a regular bench press, due to the fact that one does not have to stabilize the bar with certain muscles. I will keep an eye out for more Smith machine/bench press/dumbbell press studies in the future, but, from personal experience, one is able to lift more on a Smith than a regular bench.

Conclusion

This is one of the only studies of its kind: assessing racial differences in strength on a major lift. Boyce et al (2014) found that, although blacks had a sharper decrease in pound-for-pound strength, they still kept their slight strength advantage over the 12.5 year period. Both black and white women had similar strength levels and gains in strength and lean mass over the 12.5 year period. Lean mass gain over the period was related to strength gains on the bench; but, as pointed out, they did not correctly assess lean mass for blacks, since calipers (used to test skin folds) are not useful for blacks in the case of figuring out lean mass/body fat levels (Vickery et al, 1988; Wagner and Heyward, 2000).

This study is useless to me. Blacks are not stronger than whites; anthropometric variables play a huge role in strength differences and, due to these differences, blacks are not stronger than whites on certain lifts, as I have documented.

Race, Body Fat, and Skin Folds

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Racial differences in body fat are clear to the naked eye: black women are more likely to carry more body fat than white women; Mexican American women are more likely to carry more body fat than white women, too. Different races/ethnies/genders of these races/ethnies have different formulas to assess body fat through the use of skin-folds. The sites to grasp the skin is different based on gender and race.

Body mass index (BMI) and waist circumference is overestimated in blacks, which means that they need different formulas to assess their BMI and adiposity/lean mass. Race-specific formulas/methods are needed to assess body fat and, along with it, disease risk, since blacks are more likely to be obese (black women, at least, it’s different with black American men with more African ancestry, see below). The fact of the matter is, when matched on a slew of variables, blacks had lower total and abdominal fat mass than whites.

This is even noted in Asian, black and white prepubertal children. He et al (2002) show that sex differences in body fat distribution are present in children who have yet to reach puberty and the differences in body fat in Asians is different than that from blacks and whites which also varies by sex. Asian girls had greater gynoid fat by DXA scan only, with girls having greater gynoid fat than boys. Asian girls had lower adjusted extremity fat and gynoid fat compared to white and black girls. Though, Asian boys had a lower adjusted extremity by fat as shown by DXA (a gold standard in body fat measurement) when compared to whites, but greater gynoid fat than whites and blacks.

Vickery, Cureton, and Collins, (1988)Wagner and Heyward (2000), and Robson, Bazin, and Soderstrom (1971) show that there are considerable body composition differences between blacks and whites. These differences in body composition come down to diet, of course, but there is also a genetic/physiologic component there as well. Combining the known fact that skin-fold testing is not conducive to a good estimate, black American men with more African ancestry are less likely to be obese.

Vickery, Cureton, and Collins (1988) argue that, if accurate estimates of body fat percentages are to be obtained, race-specific formulas need to be developed and used as independent variables to assess racial differences in body fat percentage. Differences in muscularity don’t seem to account for these skinfold differences, nor does greater mesomorphy. One possible explanation for differences in skinfold thickness is that blacks may store most of their body fat subcutaneously. (See Wagner and Heyward, 2000 for a review on fat patterning and body composition in blacks and whites.)

The often-used Durnin-Womersley formula which is used to predict body fat just from skin folds. However, “The 1974 DW equations did not predict %BF(DXA) uniformly in all races or ethnicities” (Davidson et al, 2011). Truesdale et al (2016) even show that numerous formulas used to estimate percent body fat are flawed, even some formulas used on different races. Most of the equations tested showed starkly different conclusions. But, this is based on NHANES data and the only data they provide regarding skin-folds is the tricep and subscapular skinfold so there may still be more problems with all of the equations used to assess body fat percentage between races. (Also see Cooper, 2010.)

Klimentidis et al (2016) show that black men—but not black women—seem to be protected against obesity and central adiposity (fat gain around the midsection) and that race negatively correlated with adiposity. The combo of male gender and West African ancestry predicted low levels of adiposity compared to black Americans with less African ancestry. Furthermore, since black men and women have—theoretically—the same SES, then cultural/social factors would not play as large a role as genetic factors in explaining the differences in adiposity between black men and black women. Black men with more African ancestry had a lower WHR and less central adiposity than black men with less African ancestry. If we assume that they had similar levels of SES and lived in similar neighborhoods, there is only one reason why this would be the case.

Klimentidis et al (2016) write:

One interpretation is that AAs are exposed to environmental and/or cultural factors that predispose them to greater obesity than EAs. Possibly, some of the genes that are inherited as part of their West-African ancestry are protective against obesity, thereby “canceling out” the obesifying effects of environment/culture, but only in men. Another interpretation is that genetic protection is afforded to all individuals of African descent, but this protection is overwhelmed by cultural and/or other factors in women.

Black men do, as is popularly believed, prefer bigger women over smaller women. For example, Freedman et al (2004) showed that black American men were more likely to prefer bigger women. Black American men “are more willing to idealize a woman
of a heavier body size, with more curves, than do their White American counterparts” (Freedman et al, 2004: 197). It is then hypothesized that black American men find these figures attractive (figures with “more curves” (Freedman et al, 2004: 197)) to protect against eating pathologies, such as anorexia and bulimia. So, it has been established that black men have thinner skin folds than whites which leads to skewed lean mass/body fat readings and black men with more African ancestry are less likely to be obese. These average differences between races, of course, contribute to differing disease acquisition.

I have covered differences in body fat in a few Asian ethnies and have come to the obvious conclusion: Asians, at the same height, weight etc as whites and blacks, will have more adipose tissue on their bodies. They, too, like blacks and whites, have different areas that need to be assessed for skin folds to estimate body fat.

Henriques (2016: 29) has a table on the equations for calculating estimated body density from skin fold measures from various populations. Of interest are the ones on blacks or ‘Hispanics‘, blacks or athletes and blacks and whites. (The table is provided from NSCA, 2008 so the references are not in the back of the text.)

For black and ‘Hispanic’ women aged 18-55 years, the sites to use for skin-folds are the chest, abdomen, triceps, subscapular, suprailiac, midaxillary, and the thigh. For blacks or athletes aged 18-61 years, the sites to use are the same as before (but a different equation is used for body fat estimation). For white women or anorexic women aged 18-55, the sites used are just triceps, suprailiac and the thigh. For black and white boys aged 6-17, only the triceps and the calf is used. It is the same for black and white girls, but, again, a different formula is used to assess body fat (Henriques, 2016: 29).

Morrison et al (2012) showed that white girls had a higher percent body fat when compared to black girls at ages 9-12 but every age after, black girls had higher percent body fat (which is related to earlier menarche in black girls since they have higher levels of body fat which means earlier puberty; Kaplowitz, 2008). Black girls, though, had higher levels of fat in their subscapular skin folds than white girls at all ages.

So, it seems, there are population-/race-specific formulas that need to be created to better assess body fat percentage in different races/ethnies and not assume that one formula/way of assessing body fat should be used for all racial/ethnic groups. According to the literature (some reviewed here and in Wagner and Heyward, 2000), these types of formulas are sorely needed to better assess health markers in certain populations. These differences in body fat percentage and distribution then have real health consequences for the races/ethnies in question.

Just-so Stories: FOXP2

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FOXP2 is a so-called “gene for” language. The gene is a transcription factor—meaning that it controls the activity of other genes. Thus, changes to FOXP2 will have changes to other genes as well. Thus, the evolution of language in humans was thought to have hinged on mutations on the FOXP2 gene. Humans that have a single-point mutation in FOXP2 “have impaired speech and grammer, but not impaired language comprehension” (Mason, et al, 2018: 403). This gene is found in numerous mammals (e.g., chimpanzees, gorillas, orangutans, rhesus macaques, and mice) but none of those mammals speak. This gene, then, is expressed in the areas of the brain that affects motor functioning, which includes the coordination needed to create words.

Mice and humans at the FOXP2 gene only differ by 3 amino acids. Only one amino acid difference exists between gorillas, chimps, mice, and macaques, who all have identical amino acid sequences on FOXP2. Furthermore, two more amino acid sequences differ between humans and the sequences which is shared by chimpanzees, gorillas, and macaques. Thus, the difference of two amino acids between humans and other primates appears to have made it possible for language to evolve. Evidence exists for strong selective pressures for the two FOXP2 mutations which allow the brain, larynx, and mouth to coordinate to produce speech. These two altered amino acids may change the ability of FOXP2 transcription factor to be phosphorylated—proteins are either activated by phosphorylation or deactivated by dephosphorylation, or the reverse.

Mason et al (2018: 403) write:

Comparative genomics efforts are now extending beyond primates. A role for FOXP2 in songbird singing and vocal learning has been proposed. Mice communicate via squeaks, with lost young mice emitting high-pitched squeaks, FOXP2 mutations leave mice squeakless. For mice and songbirds, it is a stretch to claim that FOXP2 is a language gene—but it is likely needed in the neuromuscular pathway to make sounds.

FOXp2

Above is Figure 18.17 from Mason et al (2018: 403). They write:

Comparisons  of synonymous and nonsynonymous changes in mouse and primate FOXP2 genes indicate that changing two amino acids in the gene corresponds to the emergence of human language. Black bars represent synonymous changes; gray bars represent nonsynymous changes.

But is that the whole story? Is FOXP2 really a “gene for” language? New results call this hypothesis into question.

In their paper No Evidence for Recent Selection at FOXP2 among Diverse Human Populations, Atkinson et al (2018) did not find evidence for recent positive or balancing selection. Atksinson et al (2018) conclude that they:

do not find evidence that the FOXP2 locus or any previously implicated site within FOXP2 is associated with recent positive selection in humans. Specifically, we demonstrate that there is no evidence that the original two amino-acid substitutions were targeted by a recent sweep limited to modern humans <200 kya as suggested by Enard et al. (2002) … Any modified function of the ROI does not appear to be related to language, however, as modern southern African populations tolerate high minor allele frequencies with no apparent consequences to language faculty. We do not dispute the extensive functional evidence supporting FOXP2’s important role in the neurological processes related to language production (Lai et al., 2001, MacDermot et al., 2005, Torres-Ruiz et al., 2016). However, we show that recent natural selection in the ancestral Homo sapiens population cannot be attributed to the FOXP2 locus and thus Homo sapiens’ development of spoken language.

So the two mutations in exon 7 of FOXP2 weren’t selected and are not responsible for human language. Most likely the accelerated rate is due to loss of function (LoF) (null allele).

The gene was originally discovered in a family that had a history of speech and language disorders (Lai et al, 2001). This “speech gene” was also found in Neanderthals in 2007 (see Krasue et al, 2007). Thus, the modifications to FOXP2 occurred before humans and Neanderthals diverged.

So Atkinson et al (2018) found that the so-called sweep on FOXP2 >200KYA was a statistical artifact which was caused by lumping Africans together Caucasians and other populations. Of course, language is complicated and no one single gene will explain the emergence of human language.

This is a just-so story—that is, an ad hoc hypothesis. Humans had X, others didn’t have X or had a different form of X; therefore X explains human language faculties.

Atkinson et al’s (2018)results represent a substantial revision to the adaptive history of FOXP2, a gene regarded as vital to human evolution.

High evolutionary constraint among taxa but variability within Homo sapiens is compatible with a modified functional role for this locus in humans, such as a recent loss of function.

Therefore, this SNP must not be necessary for language function as both alleles persist at high frequency in modern human populations. Though perhaps obvious, it is important to note that there is no evidence of differences in language ability across human populations. (Atkinson et al, 2018)

This is another just-so story (Gould and Lewontin, 1976Lloyd, 1999Richardson, 2007; Nielsen, 2009) that seems to have bitten the dust. Of course, the functionality of FOXP2 and its role in the neurologic processes related to language; what is disputed (and refuted) is the selectionist just-so story. Selectionist explanations are necessarily ad-hoc. Thus, recent natural selection in our species cannot be attributed to FOXP2, and along with it, our language capabilities.

There is a similar objection, not for FOXP2 and selectionist hypotheses, but for the Lactase gene. Nielsen (2009) puts it succinctly:

The difference in lactose intolerance among human geographic groups, is caused by a difference in allele frequencies in and around the lactase gene (Harvey et al. 1998; Hollox et al. 2001; Enattah et al. 2002; Poulter et al. 2003). … This argument is not erected to dispute the adaptive story regarding the lactase gene, the total evidence in favor of adaptation and selection related to lactose tolerance is overwhelming in this case, but rather to argue that the combination of a functional effect and selection does not demonstrate that selection acted on the specific trait in question. … Although the presence of selection acting on genes underlying a phenotypic trait of interest does help support adaptive stories, it does not establish that selection acted directly on the specific trait of interest.

Even if there were evidence of positive selection of FOXP2 in humans, we cannot logically state that selection acted on the FOXP2 locus; functional effects and selection do not demonstrate that “selection” acted on that trait. Just-so stories (ad hoc hypotheses) “sound good”, but that’s only because they are necessarily true—one can have all the data they want, then they can think up any adaptive story to explain the data and the story will be necessarily true. Therefore, selectionist hypotheses are inherently ad hoc.

In conclusion, another selectionist hypothesis bites the dust. Nevermind the fact that, if FOXP2 were supposedly “selected-for”, there would still be the problem of free-riders (Fodor and Piattelli-Palmarini, 2010). That is, “selection” cannot “select-for” fitness-enhancing traits if/when they are coextensive with other traits—there is no way for selection to distinguish between coextensive traits and thus, it does not explain trait fixation (in this case, the fixation of FOXP2). Ad-hoc hypotheses are necessarily true—that is, they explain the data they purport to explain and only the data they purport to explain. These new results show that there is no support for positive selection at the FOXP2 locus.

Natural Selection is not an Explanatory Mechanism

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Darwin proposed, back in 1859, that species arose due to natural selection—the pruning of deleterious genetic variations in a population, which led to the thinking that the “inherent design” in nature, formerly thought to be due to a designer (“God”) was due to a force Darwin called “natural selection” (NS). The line of reasoning is thus: (1) two individuals of the same population are mostly the same genetically/phenotypically, but have small differences between them, and one of the small differences is a difference in a trait needed for survival. (2) But both traits can contribute to fitness, how does NS ‘know’ to select for either coextensive trait? Now think about two traits: trait T and trait T’. What would explain the fixation of either trait in the population we are discussing? NS is not—cannot—be the mechanism of evolution.

In 2010, philosopher Jerry Fodor and cognitive scientist Massimo Piattelli-Palmarini, wrote a book titled “What Darwin Got Wrong“, which argued that NS is not a causal mechanism in regard to the formation of new species. Their argument is (pg 114):

  1. Selection-for is a causal process.
  2. Actual causal relations aren’t sensitive to counterfactual states of affairs: if it wasn’t the case that A, then the fact that it’s being A would have caused its being B doesn’t explain its being the case that B.
  3. But the distinction between traits that are selected-for and their free-riders turns on the truth (or falsity) of relevant counterfactuals.
  4. So if T and T’ are coextensive, selection cannot distinguish the case in which T free-rides on T’ from the case that T’ free-rides on T.
  5. So the claim that selection is the mechanism of evolution cannot be true.

This argument is incredibly strong. If it is true, then NS cannot be the mechanism by which evolution occurs; NS is not—nor can it be—the mechanism of evolution. So, regarding the case of two traits that are coextensive with each other, it’s not possible to ascertain which trait was selected-for and which trait was the free-rider. NS cannot distinguish between two locally coextensive traits, so, therefore, it is not an explanatory mechanism and does not explain the evolution of species, contra Darwin. It cannot be the mechanism that connects phenotypic variation with fitness variation.

The general adaptationist argument is: “(1) the claim that evolution is a process in which creatures with adaptive traits are selected and (2) the claim that evolution is a process in which creatures are selected for their adaptive traits” (Fodor and Piattelli-Palmarini, 2010: 13). Darwinists are committed to inferring (2) from (1), though it is fallacious. It is known as the intensional fallacy.

Due to the intensionality of “select-for” and “trait”, one cannot infer from ‘Xs have trait t and Xs were selected’ to ‘Xs were selected for having trait t’” (Fodor and Piattelli-Palmarini, 2010: 139). How does one distinguish from a trait that was selected-for and a free-rider that hitched a ride on the truly adaptive trait for the organism in question? The argument provided above shows that it is not possible. “Darwinists have a crux about free-riding because they haven’t noticed the intensionality of selection-for and the like; and when it is brought to their attention, they haven’t the slightest idea what to do about it” (Fodor and Piattelli-Palmarini, 2010: 16).

No observation can show whether or not trait T or T’ was selected-for in virtue of its contribution to fitness in a given population; favoring one story over another in regard to the adaptation of a trait in question, therefore, does not make any logical sense due to the problem of free-riders (and, also, favoring one story over another is due to bias for the like of the specific adaptive just-so story in question). For if two traits are coextensive—meaning that traits coincide with one another—then how can NS—which does not have a mind—‘know’ to “select-for” whichever trait contributes to fitness in the population in question? Breeders are the perfect example.

Breeders have minds and can therefore select for certain traits and against undesirable traits; however, of course, since NS does not have a mind, this is not the case when it comes to naturally selected traits (so-called), since NS does not have a mind. NS cannot explain the distribution of phenotypic traits throughout the world; there is no agent of NS nor are there ‘laws of selection’, therefore NS is not an explanatory mechanism. Explanations based on NS are based only on correlations with traits and fitness, not on causes themselves (this critique can be extended to numerous other fields, too). The problem with relying only on correlations between traits and fitness is two-fold: (1) the trait in question can be irrelevant to fitness and (2) the trait in question can be a free-rider.

Creatures have traits that increase fitness because they were selected-for, the story goes. NS explains why the creature in question has trait T, which increases fitness in environment E. One can then also make the claim that the selection of the trait in question was due to the increased fitness it gave the creature. However, if this claim is made, “then the theory of natural selection would reduce to a trait’s being a cause of reproductive success [which then] explains its being a cause of reproductive success which explains nothing (and isn’t true).

So since genetically-linked traits are coextensive with an infinitude of different possible outcomes, then the hypothesis that trait X is an adaptation is underdetermined by all possible observations, which means that NS cannot explain how and why organisms have the traits they do, since NS cannot distinguish between two coextensive traits, since NS lacks a mind and agency.

NS can be said to be an explanation if and only if two conditions are met: (1) if NS can be understood as acting on counterfactuals and (2) if NS can be said to be acting on any physical evolutionary laws.

(1) A counterfactual is an “if-clause”, which is contrary to a fact. A counterfactual is a statement that cannot be true, for example, “I hear but I have no ears” or “I see but I have no eyes.” Thus, if it were possible for NS to be an explanation for the continuance of a specific trait that is linked to other traits (that is, they are coextensive) in a given population, it would need to—necessarily—invoke a counterfactual about NS. It would need to be the case that the trait in question would still be selected for in the absence of free-riders. As an example from Fodor and Piattelli-Palmarini (2010: 103) a heart pumps blood (what it was selected-for) and makes pumping sounds (its linked free-rider). Thus, if the pumping of blood and the sound that blood-pumping makes were not coextensive, then the pumping, not the pumping sounds, get selected for.

There is a huge problem, though. Counterfactuals are intentional statements; they refer to concepts found in our minds, not any physical things. NS does not have a mind and thus lacks the ability to “select-for” since “selecting-for” is intentional. Therefore NS does not act on counterfactuals; it is blind to the fact of counterfactuals since it does not have a mind.

(2) It does not seem likely that there are “laws of selection”. Clearly, the adaptive value of any phenotype depends on the environment that the organism is in. Fodor and Piattelli-Palmarini (2010: 149) write (emphasis theirs):

The problem is that it’s unlikely that there are laws of selection. Suppose that P1 and P2 are coextensive but that, whereas the former is a property that affects fitness, the latter is merely a correlate of a property that does. The suggestion is that all this comes out right if the relation between P1 and fitness is lawful, and the relation between P2 and fitness is not. …it’s just not plausible that there are laws that relate phenotypic traits per se to fitness. What (if any) effect a trait has on fitness depends on what kind of phenotype is embedded in, and what ecology the creature that has the trait inhabits. This is to say that, if you wish to explain the effects that a phenotypic trait has on a creature’s fitness, what you need is not its history of selection but its natural history. And natural history offers not laws of selection but narrative accounts of causal chains that lead to the fixation of phenotypic traits. Although laws support counterfactuals, natural histories do not; and, as we’ve repeatedly remarked, it’s counterfactual support on which distinguishing the arches from the spandrels depends.

There is, too, a simple example regarding coextensive traits and selection. Think of the lactase gene. It is well-known that we humans are adapted to drink milk—and the cause is gene-culture coevolution that occurred at around the time of cow domestication (Beja-Perreira et al, 2003; Gerbalt et al, 2011). No one disputes the fact that gene-culture coevolution is how and why we can drink milk. But what people do dispute is the adaptive just-so story (Gould and Lewontin, 1976; Lloyd, 1999; Richardson, 2007) that was made to explain how and why the trait went to fixation in certain human populations. Nielsen (2009) writes (emphasis mine):

The difference in lactose intolerance among human geographic groups, is caused by a difference in allele frequencies in and around the lactase gene (Harvey et al. 1998; Hollox et al. 2001; Enattah et al. 2002; Poulter et al. 2003). The cause for the difference in allele frequencies is primarily natural selection emerging about the same time as dairy farming evolved culturally (Bersaglieri et al. 2004). Together, these observations lead to a compelling adaptive story of natural selection favoring alleles causing lactose tolerance. But even in this case we have not directly shown that the cause for the selection is differential survival due to an ability/inability to digest lactose. We must acknowledge that there could have been other factors, unknown to us, causing the selection acting on the region around the Lactase gene. Even if we can argue that selection acted on a specific mutation, and functionally that this mutation has a certain effect on the ability to digest lactose, we cannot, strictly speaking, exclude the possibility that selection acted on some other pleiotropic effect of the mutation. This argument is not erected to dispute the adaptive story regarding the lactase gene, the total evidence in favor of adaptation and selection related to lactose tolerance is overwhelming in this case, but rather to argue that the combination of a functional effect and selection does not demonstrate that selection acted on the specific trait in question.

Selection could have acted on a free-rider that is coextensive with the lactase gene, and just because “the story fits the data” well (that’s a necessary truth; of course the story can fit the data because any story can be formulated for any data) does not mean that it is true, that the reason for trait T is reason R since they “fit the data so well.”

Of course, this holds for EP, evolutionary anthropology, and my favorite theory for the evolution of human skin color, the vitamin D hypothesis. I do not, of course, deny that light skin is needed in order to synthesize vitamin D in climates with low UVB; that is a truism. What is denied is the fact that selection acted on light skin (and its associated/causal genes); what is denied is the combination of functional effect and selection. Just-so stories are necessarily true; they, of course, fit any data because one can formulate any story to fit any data points they have. Thus, Darwinists are just storytellers who have a bunch of data; there is no way to distinguish between the selection of a trait because it increased fitness and the selection of a free-rider that is “just there” that does not increase fitness, but the thing that increases fitness is what the free-rider “rode in on.”

NS is not and cannot be an explanatory mechanism. Darwinism has already been falsified (Jablonka and Lamb, 2005; Noble, 2011; Noble, 2012; Noble, 2017) and so, this is yet another nail-in-the-coffin for Darwinism. The fact that traits that are coextensive means that NS would have to “know” which trait to act on; NS cannot “know” which of the coextensive traits to act on (because it has no mind) and, NS cannot be a general mechanism that connects phenotypic variation to variation in fitness. NS does not explain the evolution of species, nor can NS distinguish between two locally coextensive traits—traits T and T’—because NS has no agency and does not have a mind. Therefore NS is not an explanatory mechanism. Just invoking NS to explain the continuance of any trait fails to explain the survival of the trait because NS cannot distinguish between traits that enhance an organism’s fitness and free-riders which are irrelevant to survival but are coextensive with the selected-for trait, as long as the traits in question are coextensive.

P1) If there is selection for T but not T’, various counterfactuals must be true.
P2) If the counterfactuals are true, then NS must be an intentional-agent, or there must be laws about “selection-for”.
P3) NS is mindless.
P4) There are no laws for “selection-for”.
∴ It is false that selection for T but not T’ occurs in a population.

One then has two choices:

(1) Argue that NS has a mind and therefore that it can “select for” certain traits that are adaptable in a given population of organisms in the environment in question. “Select-for” implies intention. Intentional acts only occur in organisms with minds. Intentional states are only possible if something has a mind. Humans are the only organisms with minds. Humans are the only organisms that can act intentionally. NS does not have a mind. (Animal breeder’s are an example that can select-for desirable traits and against undesirable traits because animals breeder’s are humans and humans can act intentionally.) Therefore NS does not act intentionally since it does not have a mind. I don’t think anyone would argue that NS has a mind and acts intentionally as an agent, therefore P3 is true.

(2) Argue that there are laws for “selection-for” phenotypic traits related to fitness. But it’s not possible that there are laws that relate to the selection of a phenotype, per se, in a given population. The effect of a trait depends on the ecology of the organism in question as well as its natural history. Therefore, to understand the effects of a phenotypic trait on the fitness of an organism we must understand its natural history, not its selection history (so-called). Therefore P4 is true.

There are no laws for “selection-for”, nor does NS have a mind that can select a trait that lends to an organism’s fitness and not a trait that’s just correlated with the trait in question

The Concepts of Racialist Race and Socialrace

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I have chronicled Hardimon’s minimalist and populationist race concepts in a few different articles. They show that race is a biological reality. The arguments that show that race exists are sound. Hardimon, unlike Spencer, distinguishes social from biological concepts of race. For Spencer, race is both a social and biological concept. For Hardimon, race is either a biological or social concept which is why he delineates the social concept from the biological concepts. The two concepts—racialist race and socialrace—are similar, and because they are similar they will both be discussed in the same article.

The racialist concept of race

The racialist concept of race is the first concept of race that Hardimon (2017) defines. He sets out six things that need to be true of human genetics, in his eyes, for the racialist concept of race to be true:

(a) The fraction of human genetic diversity between populations must exceed the fraction of diversity between them.

(b) The fraction of human genetic diversity within populations must be small.

(c) The fraction of diversity between populations must be large.

(d) Most genes must be highly differentiated by race.

(e) The variation in genes that underlie obvious physical differences must be typical of the genome in general.

(f) There must be several important genetic differences between races apart from the genetic differences that underlie obvious physical differences.

Note: (b) says that racialist races are genetically racially homogeneous groups; (c)-(f) say that racialist races are distinguised by major biological differences.

Call (a)-(f) the racialist concept of race’s genetic profile. (Hardimon, 2017: 21)

The racialist race concept, as opposed to the populationist and minimalist race concepts, propose to rank races on traits such as intelligence, morals, and cultural characters to different races. Though, he does strawman the racialist concept (which would be the HBD concept of race, I’d say) because he says things like “To be a member of a particular race would be to be a particular person who is disposed to behave in certain ways. Because of this, if racialist races existed, race would constitute a very significant kind.” This statement aside, though, race does not constitute a very significant kind, it constitutes a modest biological kind.

If one condition for the racialist concept of race is said to be that of an essence of different races, then the racialist concept of race is surely false. This is due to population thinking. Population thinking is a type of thinking that maintains that there is no single way in which genotypes are expressed by genotypes. Thus, there is no phenotypic or genotypic property that could play the role of racial essence. “Since there are no biological essences, there are no racialist race essences, and since there are no racialist race essences, there are no racialist races. The existence of racialist races is incompatible with a broad structural principle of biology” (Hardimon, 2017: 20).

Hardimon has many arguments against the existence of racialist races, including:

The corresponding argument against the truth of the racialist concept of race is that science has not found it to be the case that members of the groups thought to be racialist races share a very large number of important properties by virtue of which they count as members of such groups. Nor does it seem likely that science will find that members of groups thought to be racialist races share a very large number of such properties. The results of Lewontin’s 1972 study and Rosenberh and colleague’s 2002 study strongly suggest that it is extremely unlikely that there are many important genetic differences between races apart from the genetic differences that underlie the obvious physical differences. (pg 24)

Another argument he puts for is that if racialist races exist, then the races would be sharply distinguished between phenotypic and genotypic characteristics. Though, since most of the variation between human races are clinal, he argues, “human populations are not sharply distinguished from one another along a broad range of phenotypic and genotypic dimensions. It follows from this that there are no racialist races” (pg 25).

Hardimon also says that, if racialist races did indeed exist, human populations would be sharply divided by skin color, yet they aren’t. These differences between races are continuous and vary between populations, thus racialist races do not exist. He also says since genetic variation in Homo sapiens is nonconcordant “there are no racialist races” (pg 25).

The likelihood that racialist races exist is especially low relative to the available alternative hypotheses, which indlude the hypothesis that there are no races, period, and the hypothesis that, whereas racialist races do not exist, minimalist races do exist. It is safe to conclude that there are no racialist races, period. (pg 25)

The racialist race concept lacks scientific respectability, it does not represent any “facts of the matter“, and it “supports and legalizes domination” (Hardimon, 2017: 62). It is therefore, socially constructed in a pernicious sense. Racialist races are both ideological and social constructions which then purport to pick out biological kinds.

The concept of socialrace

Socialrace is simply defined as the nonracialist concept of social groups that are taken to be racialist races. Socialraces refer to:

(1) a social group that is taken to be a racialist race,
(2) the social position is occupied by a particular social group that is a socialrace, or
(3) the system of social positions that are socialraces. (Hardimon, 2017: 131)

Socialraces are social groups that are taken or thought to be racialist races. Thus, they are wrongly taken to be racialist races. The two concepts socialrace and racialist race are similar—they both are hierarchical. Since socialrace is a social reality, then it must play a role in our everyday social lives.

Hardimon discusses many things regarding socialrace that many readers—myself included, on some of the things—would disagree with. For instance, he states that “institutional racism”. Hardimon claims that institutional racism “obtains when and where socialrace obtains” (pg 133).

He argues that socialrace is “inter alia a relation of power“, and so the institution is also characterized “by the unequal distribution of social goods such as liberty and opportunity, income and wealth, and the bases of self-respect. Socialrace is a system of advantages (purportedly) based on racialist race” (Hardimon, 2017: 133).

He then argues that differences in socialrace are associated with differences in life outcomes of the socialraces. Thus, “the belief that people are members of a biological race . . . is essential to the social construction of races” (Bernard Boxill, quoted in Hardimon, 2017: 133). Of course, the belief that people are members of a biological race is essential to the social construction of races, because the biological correlate of these socially constructed racial groups is the minimalist concept of race.

Socialrace, of course, has a biological correlate. That biological correlate is minimalist races. Minimalist races can be understood through the populationist race concept. Of course, saying that socialrace has a biological correlate in minimalist race does not necessarily mean that there are corresponding minimalist races for every socialrace. For example, “Hispanics/Latinos” can be said to be a socialrace, but they do not have a corresponding minimalist race because they do not genetically transmit distinct phenotypic characters which correspond to geographic ancestry. Using this terminology, the Irish were, at one point, a socialrace, whereas the Jews are treated as a socialrace today, when they are a subrace of the Caucasian race (they are not their own separate race, that’s like saying the British or Germans are a separate race). Minimalist race then appears to be a necessary condition for socialraces because they pick out real patterns of distinct physical features which correspond to geographic ancestry.

Socialraces, though, do not need to exhibit patterns of visible physical features; even if no such differences existed, groups could still be socialraces, for instance, social classes and other groups can be constructed to be socialraces. The concept of socialrace is a distinctive “race” concept (Hardimon, 2017: 139). Thus, the concept of socialrace is a distinctive concept and it is needed (because it discusses social realities). The idea of a social system based on the racialist concept of race can, therefore, said to be the idea of socialrace (Hardimon, 2017: 140).

Socialrace is clearly separate from the term ‘race’, and so, it is not a ‘race’ concept like the other three concepts, it is distinct with the “socialrace” moniker. This is how we show that, when talking about races in a social sense, there are differences between this concept and the scientific minimalist and populationist race concepts. One can think of it this way: the socialrace concept of race can be of use for sociologists and others whereas the minimalist and populationist concepts of race can be useful for biologists and population geneticists.

Whether or not a group is counted as a socialrace is contingent on whether or not the group in question is treated as a socialrace by the larger society. So, in this sense, “Hispanics/Latinos” can be said to be a socialrace, but, remember, they do not have a corresponding minimalist (populationist) race.

One is “properly” counted a member of a socialrace SR if one in fact satisfies the socially accepted criteria in the correlative putative racialist race. Thus, for example, a person belongs to the socialrace black (in the United States) if he or she has any identifiable sub-Saharan African ancestry because he or she satisfies accepted US criteria for bring a member of the racialist race black.

To “pass” (for example, for white) in a system of socialrace is to be taken to be white (to satisfy the socially accepted criteria for whiteness) despite the dact that one does not satisfy those criteria (for example, by virtue of possesion of “one drop” of “black blood”). The possibility of “passing” (in a given society) points to an important variable in the practical significance of socialrace membership. An individual counts as a member of a socialrace cimply by virtue of satisfying the socially accepted criteria for membership in the corresponding racialist race. Socialrace membership is itself a real social status with real social consequences. In the case of the socialrace black, subjection to antiblack racism is a standing possibility. But the actial practical signifigance of membership in a socialrace will vary with the degree to which the individual is subject to the norms associated with the racialist race to which the individual is taken to belong. (Hardimon, 2017: 144)

Socialraces are a real, social reality. They have a biological correlate in minimalist races and are taken to be racialist races, but racialist races do not exist therefore socialraces are social, not biological, in nature, even though the minimalist race concept can be said to be its biological correlate.

My contention is that the concept I have reflectively uncovered is aleeady in general circulation without being fully recognized as the concept that it is. I have endeavered to make it possible to get a proper hold on the concept and to secure an adequate reflective understanding of its content. If the reader thinks that my account of the concept SOCIALRACE captures a notion she or he has already been using, so much the better. I hope to have clarified that concept. As for the word ‘socialrace’, my hope is that it catches on, that its dissemenation promotes understanding of the phenomenon of socialrace, and that this in turn contribubtes to the dismantling of the latter’s existence.

Hardimon says that the concept of SOCIALRACE can help us better grasp the phenomenon of socialrace. Socialrace is real and illusory, it has “real causal powers (for example, causing people’s death) and that is illusory insofar that it appears to be racialist race” (Hardimon, 2017: 172). Socialraces exist and are a significant social reality, especially since socially determined categories can make biological realities (Kaplan, 2010).

When discussing socialraces, we can say that Jews are sometimes taken to be a socialrace (although they are a part of the Caucasian race) as are Arabs (who are also Caucasian, and thusly not a separate race from Europeans or Jews). However, the US Census Bureau categories take these groups to be “white”; that is the socialgroup “white” in the United States.

Regarding the black socialrace, they comprise numerous “Hispanic/Latino” populations (such as many Dominicans, some Puerto Ricans, Nicaraguans and other Latin American countries with high African admixture). Australian Aborigines and Pacific Islanders can be said to be part of the black socialrace in America, too. The fact of the matter is, socialrace in America just pretty much chooses features that people “think” go with race A, and if they see similar-looking people from two different continents, they will assume that they are part of the same race (as is the case with Aborigines and Pacific Islanders being black, even though they are a distinct group; McEvoy et al, 2010Spencer, 2014).

Lastly, are Asians. In America, “Asians” are taken to be just East Asians (though in the UK when they talk about “Asians” in their police statistics or in the news, they most probably mean Pakistanis. They are not wrong, they are on the Asian continent. However, that is to mislead the people into thinking that what people term Asian (East Asians) are committing the crimes or whatnot, when it’s Pakistanis. The socialrace of Asian in America comprises East and South Asians (some would include Indians, too but they are Caucasian). The socialraces closely mirror Rushton’s three main races, but they are arbitrary, putting populations into groups where they do not belong.

Conclusion

As can be seen, the concepts of socialrace and racalist race are similar. These two concepts are needed to understand each other. Most people, when talking about race, discuss the socialrace concept so it would do them some good to read up more on the concept itself. The racialist concept of race purports to pick out biological kinds and then rank them on a hierarchy in a slew of different traits (which are not physical). Racialist races also purport that racial essences exist, but since essences as a whole do not exist, then racial essences do not exist either. Further, since genetic variation in Homo sapiens is nonconcordant, racialist races do not exist.

Socialrace is simple. Most likely, however you’ve thought about race throughout your life is the socialrace concept. It has a biological correlate in minimalist races. For socialraces to exist, there must be distinctive visible patterns of visible physical features which correspond to geographic ancestry. Thus, minimalist race is a necessary condition for socialrace. Socialrace is a social reality. And if socialrace is a social reality, then it must play a role in our everyday lives.

When these two concepts are looked at together, we can see how and why both of the concepts have been around for as long as they have: they purport to pick out a biological kind, a distinct biological kind. Racialist races do not exist, but just because racialist races do not exist does not mean that socialraces do not exist, because even if, say, minimalist or populationist races did not exist, the concept of socialrace would still be important because socially determined categories can make biological realities (Kaplan, 2010).

DNA is not a “Blueprint”

2200 words

Leading behavior geneticist Robert Plomin is publishing “Blueprint: How DNA Makes Us Who We Are” in October of 2018. I, of course, have not read the book yet. But if the main thesis of the book is that DNA is a “code”, “recipe”, or “blueprint”, then that is already wrong. This is because presuming that DNA is any of the three aforementioned things marries one to certain ideas, even if they themselves do not explicitly state them. Nevertheless, Robert Plomin is what one would term a “hereditarian”, meaning that he believes that genes—more than environment—shape an individual’s psychological and other traits. (That’s a false dichotomy, though.) In the preview for the book at MIT Press, they write:

In Blueprint, behavioral geneticist Robert Plomin describes how the DNA revolution has made DNA personal by giving us the power to predict our psychological strengths and weaknesses from birth. A century of genetic research shows that DNA differences inherited from our parents are the consistent life-long sources of our psychological individuality—the blueprint that makes us who we are. This, says Plomin, is a game-changer. It calls for a radical rethinking of what makes us who were are.

Genetics accounts for fifty percent of psychological differences—not just mental health and school achievement, but all psychological traits, from personality to intellectual abilities. Nature defeats nurture by a landslide.

Plomin explores the implications of this, drawing some provocative conclusions—among them that parenting styles don’t really affect children’s outcomes once genetics is taken into effect. Neither tiger mothers nor attachment parenting affects children’s ability to get into Harvard. After describing why DNA matters, Plomin explains what DNA does, offering readers a unique insider’s view of the exciting synergies that came from combining genetics and psychology.

I won’t get into most of these things today (I will wait until I read the book for that), but this will be just an article showing that DNA is, in fact, not a blueprint, and DNA is not a “code” or “recipe” for the organism.

It’s funny that the little blurb says that “Nature defeats nurture by a landslide“, because, as I have argued at length, nature vs nurture is a false dichotomy (See Oyama, 1985, 20001999Moore, 2002; Schneider, 2007; Moore, 2017). Nature vs nurture is the battleground that the false dichotomy of genes vs environment is fought on. However, it makes no sense to partition heritability estimates if it is indeed true that genes interact with environment—that is, if nature interacts with nurture.

DNA is also called “the book of life”. For example, in her book The Epigenetics Revolution: How Modern Biology Is Rewriting Our Understanding of Genetics, Disease, and Inheritance, Nessa  Carey writes that “There’s no debate that the DNA blueprint is a starting point” (pg 16). This, though, can be contested. “But the promise of a peep into the ‘book of life’ leading to a cure for all diseases was a mistake” (Noble, 2017: 161).

Developmental psychologist and cognitive scientist David S. Moore concurs. In his book The Developing Genome: An Introduction to Behavioral Epigenetics, he writes (pg 45):

So, although I will talk about genes repeatedly in this book, it is only because there is no other convenient way to communicate about contemporary ideas in molecular biology. And when I refer to gebe, I will be talking about a segment or segments of DNA containing sequence information that is used to help construct a protein (or some other product that performs a biological function). But it is worth remembering that contemporary biologists do not mean any one thing when they talk about “genes”; the gene remains a fundementally hypothetical concept to this day. The common belief that there are things inside of us that constitute a set of instructions for building bodies and minds—things that are analogous to “blueprings” or “recipes”—is undoubedtly false. Instead, DNA segements often contain information that is ambiguous, and that must be edited or arranged in context-dependent ways before it can be used.

Still, other may use terms like “genes for” trait T. This, too, is incorrect. In his outstanding book Making Sense of Genes, Kostas Kamporakis writes (pg 19):

I also explain why the notion of “genes for,” in the vernacular sense, is not only misleading but also entirely inaccurate and scientifcally illegitamate.

[…]

First, I show that genes “operate” in the context of development only. This means that genes are impllicated in the development of characters but do not determine them. Second, I explain why single genes do not alone produce characters or disease but contribute to their variation. This means that genes can account for variation in characters but cannot alone explain their origin. Third, I show that genes are not the masters of the game but are subject to complex regulatory processes.

Genes can only be seen as passive templates, not ultimate causes (Noble, 2011), and they cannot explain the origin of different characters but can account for variation in physical characters. Genes only “do” something in the context of development; they are inert molecules and thusly cannot “cause” anything on their own.

Genes are not ‘for’ traits, but they are difference-makers for traits. Sterelny and Griffiths (1999: 102), in their book Sex and Death: An Introduction to Philosophy of Biology write:

Sterelny and Griffiths (1988) responded to the idea that genes are invisible to selection by treating genes as difference makers, and as visible to selection by virtue of the differences they make. In doing so, they provided a formal reconstruction of the “gene for” locution. The details are complex, but the basic intent of the reconstruction is simple. A certain allele in humans is an “allele for brown eyes” because, in standard environments, having that allele rather than alternatives typically available in the population means that your eyes will be brown rather than blue. This is the concpet of a gene as a difference maker. It is very important to note, however, that genes are context-sensitive difference makers. Their effects depend on the genetic, cellular, and other features of their environment.

(Genes can be difference makers for physical traits, but not for psychological traits because no psychophysical laws exist, but I’ll get to that in the future.)

Note how the terms “context-sensitive” and “context-dependent” continue to appear. The DNA-as-blueprint statement presumes that DNA is context-independent, but we cannot divorce genes—whatever they are—from their context, since genes and environment, nature and nurture, are intertwined. (And it is even questioned if ‘genes’ are truly units of inheritance, see Fogle, 1990. Fogle, 2000 also argues to dispense with the concept of “gene” and that biologists should be using terms like intron, promoter region, and exon. Nevertheless, there is a huge disconnect with the term “gene” in molecular biology and classical genetics. Keller 2000 argues that there are still uses for the term “gene” and that we should not dispense with the term. I believe we should dispense with it.)

Susan Oyama (2000: 77) writes in her book The Ontogeny of Information:

Though a plan implies action, it does not itself act, so if the genes are a blueprint, something else is the constructor-construction worker. Though blueprints are usually contrasted with building materials, the genes are quite easily conceptualized as templates for building tools and materials; once so utilized, of course, they enter the developmental process and influence its course. The point of the blueprint analogy, though, does not seem to be to illuminate developmental processes, but rather to assume them and, in celebrating their regularity, to impute cognitive functions to genes. How these functions are exercised is left unclear in this type of metaphor, except that the genetic plan is seen in some peculiar way to carry itself out, generating all the necessary steps in the necessary sequence. No light is shed on multiple developmental possibilities, species-typical or atypical.

The Modern Synthesis is one of the causes for the genes-as-blueprints thinking; the Modern Synthesis has causation in biology wrong. Genes are not active causes, but they are passive templates, as argued by many authors. They, thus, cannot “cause” anything on their own.

In his 2017 book Dance to the Tune of Life: Biological Relativity, Denis Noble writes (pg 157):

As we saw earlier in this chapter, these triplet sequences are formed from any combination of the four bases U, C, A and G in RNA and T, C, A and G in DNA. They are often described as a genetic ‘code’, but it is important to understand that this usage of the word ‘code’ carries overtones that can be confusing.

A code was originally an intentional encryption used by humans to communicate. The genetic ‘code’ is not intentional in that sense. The word ‘code’ has unfortunately reinforced the idea that genes are active and even complete causes, in much the same was as a computer is caused to follow the instructions of a computer program. The more nuetral word ‘template’ would be better. Templates are used only when required (activated); they are not themselves active causes. The active causes lie within the cells themselves since they determine the expression patterns for the different cell types and states. These patterns are comminicated to the DNA by transcrption factors, by methylation patterns and by binding to the tails of histones, all of which influence the pattern and speed of transcription of different parts of the genome. If the word ‘instruction’ is useful here at all, it is rather that the cell instructs the genome. As Barbara McClintock wrote in 1984 after receiving her Nobel Prize, the genome is an ‘organ of the cell’, not the other way around.

Realising that DNA is under the control of the system has been reinforced by the discovery that cells use different start, stop and splice sites for producing different messenger RNAs from a single DNA sequence. This enables the same sequence to code different proteins in different cell types and under different conditions [here’s where context-dependency comes into play again].

Representing the direction of causality in biology the wrong way round is therefore confusing and has far-reaching conseqeunces. The causality is circular, acting both ways: passive causality by DNA sequences acting as otherwise inert templates, and active causality by the functional networks of interactions that determine how the genome is activated.

This takes care of the idea that DNA is a ‘code’. But what about DNA being a ‘blueprint’, that all of the information is contained in the DNA of the organism before conception? DNA is clearly not a ‘program’, in the sense that all of the information to construct the organism exists already in DNA. The complete cell is also needed, and its “complex structures are inherited by self-templating” (Noble, 2017: 161). Thus, the “blueprint” is the whole cell, not just the genome itself (remember that the genome is an organ of the cell).

Lastly, GWA studies have been all the rage recently. However, there is only so much we can learn just from association studies, before we need to turn to the physiological sciences for functional analyses. Indeed, Denis Noble (2018) writes in a new editorial:

As with the results of GWAS (genome-wide association studies) generally, the associations at the genome sequence level are remarkably weak and, with the exception of certain rare genetic diseases, may even be meaningless (13, 21). The reason is that if you gather a sufficiently large data set, it is a mathematical necessity that you will find correlations, even if the data set was generated randomly so that the correlations must be spurious. The bigger the data set, the more spurious correlations will be found (3).

[…]

The results of GWAS do not reveal the secrets of life, nor have they delivered the many cures for complex diseases that society badly needs. The reason is that association studies do not reveal biological mechanisms. Physiology does. Worse still, “the more data, the more arbitrary, meaningless and useless (for future action) correlations will be found in them” is a necessary mathematical statement (3).

Nor does applying a highly restricted DNA sequence-based interpretation of evolutionary biology, and its latest manifestation in GWAS, to the social sciences augur well for society.

It is further worth noting that there is no privileged level of causation in biological systems (Noble, 2012)—a priori, there is no justification to privilege one system over another in regard to causation, so saying that one level of the organism is “higher” than another (for instance, saying that genes are, and should be, privileged over the environment or any other system in the organism regarding causation) is clearly false, since there is upwards and downwards causation, influencing all levels of the system.

In sum, it is highly misleading to refer to DNA as “blueprints”, a “code”, or a “recipe.” Referring to DNA in this way means that one presumes that DNA can be divorced from its context—that it does not work together with the environment. As I have argued in the past, association studies will not elucidate genetic mechanisms, nor will heritability estimates (Richardson, 2012). We need physiological testing for these functional analyses, and association studies like GWAS and even heritability estimates don’t tell us this type of information (Panofsky, 2014). So, it seems, that what Plomin et al are looking for that they assume are “in the genes”, are not there, because they use a false model of the gene (Burt, 2015; Richardson, 2017). Genes are resources—templates to be used by and for the system—not causes of traits and development. They can account for differences in variation, but cannot be said to be the origin of trait differences. Genes can be said to be difference makers, but knowing whether or not they are difference makers for behavior, in my opinion, cannot be known.

(For further information on genes and what they do, reach Chapters Four and Five of Ken Richardson’s book Genes, Brains, and Human Potential: The Science and Ideology of Intelligence. Plomin himself seems to be a reductionist, and Richardson took care of that paradigm in his book. Lickliter (2018) has a good review of the book, along with critiques of the reductionist paradigm that Plomin et al follow.)

Jean Baptiste Lamarck

Eva Jablonka

Charles Murray

Arthur Jensen

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