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 l and s alleles (from Kiaris, 2012: 86):
It should also be noted that populations (Easterners) that had a higher frequency of the s 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 l 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.
|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.
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.
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, 2001; Campbell 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.
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 Health, specifically Chapter 8 on socioeconomic status and health disparities for more information on how and why differences like this persist between ethnies in America.)
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, 2009; Fodor and Piattelli-Palmarini, 2010). In this article, I will discuss the massive modularity hypothesis, adaptationism, and the promises that EP makes as a whole.
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:
- 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.
- 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.
- Selective mechanisms can produce highly specialized cognitive modules.
- 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:
- Domain-specific processes exist
- These processes arose due to evolution
- 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.
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:
- It is impossible for human psychology—that contains nothing but general-purpose mechanisms—to have evolved since such a system cannot be adaptive.
- Such a system cannot possibly have solved the adaptive problems faced by our ancestors in the evolutionary past.
- 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.”
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.)
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.
- For EP to be a valid research programme, EP hypotheses must generate testable, falsifiable predictions.
- EP cannot generate testable, falsifiable predictions (the hypotheses are inherently ad hoc).
- 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.