Due to the outright failure in linking testosterone to differences in racial genetics, prostate cancer (PCa) and aggression, those who would still claim genetic or biological causation for differences in PCa incidence and aggression/crime which would then be linked to race needed to search other avenues for their long-awaited discovery and mechanism for the proposed relationships. This is where the AR (androgen receptor) gene comes in. The AR gene allows the creation of androgen receptors, and this is where androgen “dock”, if you will, allowing the physiological system to use it to carry out what it needs to. In this article, I will discuss the AR gene, CAG repeats, aggression, PCa, a just-so story and finally what may explain the differences in PCa acquisition and aggression between races, not appealing to genes.
Though, hereditarianism is concerned with the so-called biological/genetic transmission of socially-desired traits and also genetic causation of socially-undesired traits, due to the fall of the testosterone-causes-aggressive-behavior paradigm, surely some other biological mechanism could explain why blacks have higher rates of aggression, crime and PCa along with testosterone? Surely, if testosterone isn’t driving the relationship, it would somehow be implicated with it, through some other mechanism in some other kind of way? This is where the androgen receptor gene (AR gene) comes into play. So since CAG repeat length is assumed to be related to androgen receptor sensitivity, and since one report states that lower CAG repeats are associated with aggression (Simmons and Roney, 2011), this is where the hereditarian looks to next for their proposed relationships between testosterone, aggression and PCa. Simmons and Roney also, similarly to Rushton’s r/K, claim that “shorter AR-CAG repeats would have been beneficial for males inhabiting tropical regions because this genetic trait would have encouraged an androgenic response, reportedly along with higher testosterone levels” (Oubre, 2020: 293). Just-so stories all the way down.
Racial differences in AR geneand aggression/PCa
Such claims that the AR polymorphism followed racial lines and was correlated with PCa incidence began to appear in the late 1990s (eg, Giovannuci et al, 1997; Pettaway, 1999). It has been shown that the number of CAG repeats on the AR gene is related to heightened activity on the androgen receptor, and that blacks are more likely to have fewer CAG repeats on the AR gene (Sartor et al, 1997; Platz et al, 2000; Bennett et al, 2002; Gilligan et al, 2004; Ackerman et al, 2013). (But also see Gilligan et al (2004), Lange et al, (2008), and Sun and Lee (2013) for contrary evidence to these claims.) African populations have shorter CAG repeats than non-African populations on the AR gene (Samtal et al, 2022), and since carriers or short CAG repeats had a higher incidence of PCa (Weng et al, 2017; Qin et al, 2022), then this would be the next-best spot to look after the testosterone/PCa/aggression hypothesis failed so spectacularly. But since “Androgen receptor (AR) mediates the peripheral effects of testosterone” (Tirabassi et al, 2015), this has been a new haven for the hereditarian to go to and look for their relationship between aggression and biology.
Fewer CAG repeats has been linked to self-reported aggression (Mettman et al, 2014; Butovskaya et al, 2015; Fernandez-Castillo and Cormand, 2016). Though unfortunately for hereditarian theorists, they also need to look elsewhere, since the number of CAG repeats wasn’t related to aggressive behavior in men nor in women (Valenzuela et al, 2022). Vermeer (2010) found no relationship between CAG repeats and adolescent risk-taking, depression, dominance, or self-esteem. These findings are contrary to other claims, such as this from Geniole et al (2019): “Testosterone thus appears to promote human aggression through an AR-related mechanism“. Rajender et al (2008) showed that rapists and murders had fewer CAG repeats than controls (18.44 repeats, 17.59 repeats, and 21.19 repeats respectively). This is significant due to what was referenced above about testosterone modulating human aggression through an androgen receptor mechanism. Butovskaya et al (2012) also found no relationship between the AR gene and any of the aggression subscales they used.
Since shorter CAG repeats on the AR gene were also related to the severity of PCa incidence (Giovannuci et al, 1997), then what explains the 2 times higher incidence of PCa in blacks compared to whites and 3 to 4 times higher incidence in Asians (Hinata and Fujisawa, 2022; Yamoah et al, 2022) should be related to AR gene and CAG repeats. (Though shorter CGN repeats don’t increase PCa risk in whites and blacks; Li et al, 2017.) However, when blacks and whites had similar preventative care, differences almost entirely vanished (Dess et al, 2019; Yamoah et al, 2022). Lewis and Cropp (2020) have a good review of PCa incidence in blacks. Thus, external—not internal—factors influenced mortality rates, and even though there may be some biological factors that cause either a higher incidence of PCa or survival once it metastatizes, that doesn’t preclude the possibility of inequities on healthcare which cause this relationship (Reddick, 2018). But how can we explain this in an evolutionary context, either recently or in the deep past? Don’t worry, the just-so storytellers have us covered.
Just-so stories and androgenreceptors
Urological surgeon William Aiken (2011), publishing in the prestigious journal Medical Hypotheses “speculated” that slaves thsg survived the Middle Passage were more sensitive to androgens, which would then protect them from the conditions they found themselves in on the slave ships during the Passage. This, he surmised, is why African descendants are way disproportionately represented in sprinting records and why, then, blacks have a higher incidence of PCa than whites. Aiken (2011: 1122) explains the “reasoning” behind his hypothesis:
This hypothesis emerged from an exploration of the possible interplay between historical events and biological mechanisms resulting in the similarity in the disproportionate racial and geographic distributions in seemingly unrelated phenomena such as sprinting ability and prostate cancer. The hypothesis is equally a synthesis of the interpretations of observations of a disparate nature such as the high incidence and mortality rates of prostate cancer amongst men of African descent in the Americas while West Africans residing in urban West African centre’s have a lower prostate cancer incidence and mortality [2], the 3-fold greater prostate cancer incidence in Afro-Trinidadians compared to Indo Asian-Trinidadians despite exposure to largely similar environmental conditions [5], the improvement in athletic sprinting performance observed when athletes take anabolic steroids [3], the observation that both sprinting ability and prostate cancer are related to specific hand patterns which in turn are related to antenatal exposure to high testosterone levels [6,7], the observation that prostate cancer is androgen-dependent and undergoes involution when testosterone is inhibited or withdrawn [4], the observation that West Africans born in West Africa are under-represented amongst the elite sprinters [1] despite their relatively large populations and despite West Africa being the region of origin of the ancestors of today’s elite sprinters and finally the observation that prostate cancer is related to androgen receptor responsiveness which in turn is related to its CAG-repeat length [8].
One of Aiken’s predictions is that black Americans and Caribbean blacks should have lower shorter CAG repeats than the populations of descent in Africa. Unfortunately for him, West Africans seem to have shorter CAG repeats than descendants of the Middle Passage (Kittles et al, 2001). Not least, neither of the two predictions he proposed to explain the relationship are risky or novel. By risky prediction I mean a hypothesis that would disprove the overarching hypothesis should the relationship not hold under scrutiny. By novel fact I mean a predicted fact that’s not used in the construction of the hypothesis. Quite clearly, Aiken’s hypothesis doesn’t meet this criteria, and so it is a just-so story.
But such fantastical, selection-type stories have been in the media relatively recently. Like Oprah’s and Dr. Oz’s assertions that blacks that survived the Middle Passage did so in virtue of their ability to retain salt during the voyage which then, today, leads to higher incidences of hypertension. This is known as the slavery hypertension hypothesis(Lujan and DiCarlo, 2018) and is, of course, also a just-so story. Just like the just-so story cited above, those Africans who took the voyage across the sea had some kind of advantage which explained why they survived and, consequently, explained relationships between maladies in their descendants. These types of stories—no matter how well-crafted—are nothing more than stories that explain what they purport to explain with no novel evidence that would raise the probability of the hypothesis being true.
Aggression
Aggression is related to crime, in that it is surmised that more aggressive individuals would then commit more crimes. I’ve noted the failure of hereditarian explanations over the years, so what do I think best explains the relationship between aggression and crime and, ultimately, criminal activity? Well, since crime is an action, it is therefore irreducible. I would propose a kind of situationism in explaining this.
Situational action theory (SAT) (eg Wilkstrom, 2010, 2019) is a cousin of situationism, and is a kind of moral action theory, placing the agent in situations (environments) which then would lead to criminal action as a discourse to take. “The core principle of SAT is that crime is ultimately the outcome of certain ‘kinds of people’ being exposed to certain ‘kinds of situations’” (Messner, 2012). For instance, a good example of this would be for black Americans. Mazur’s (2016)honor culture hypothesis states that blacks who are constantly vigilant for threats to their status and self have higher rates of testosterone in virtue of the fact that aggression increases testosterone.
So this would then be an example of the kind of relationship that SAT would look for. So SAT and the honor culture hypothesis are interactionist in that they recognize the interaction between the agent and the environment (situations) the agent finds themselves in. Violence is merely situational action (Wikstrom and Treiber, 2009), so to explain a violent crime, we need to know the status of the agent and the environment that the crime occurred in, along with the victim and motivating factors for the action in question. The fact of the matter is, actions are irreducible and what is irreducible isn’t physical, so physical (biological) explanations won’t work here. Further, the longer that people stay in criminogenic environments, the more likely they are to commit crime, due to the situations they find themselves in. Thus, a kind of analytic criminology should be employed to discover how and why crimes occur (Wikstrom and Kroneberg, 2022). Considerations in biology should not be looked at when talking about actions and their causes.
Prostate cancer
I have discussed this in the past: What best explains the incidences in PCa between races is diet. For instance, blacks have lower rates of vitamin D than other races (Guiterrez et al, 2022; Thamattoor, 2021). People with lower levels of vitamin D are more likely to acquire PCa, and those with the lowest levels of vitamin D were more likely to have aggressive PCa (Xie et al, 2017). Since consuming high IUs of vitamin D seems to stave off PCa (Khan and Parton, 2004; Naier-Shalliker et al, 2021), and since there seems to be a dose-response relationship between vitamin D consumption and PCa mortality (Song et al, 2018) along wkth vitamin D seeming to reverse low-grade PCa (Samson, 2015), it stands to reason that the higher incidences of PCa in blacks in comparison to whites are due to socio-environmental dietary factors. We don’t need any assumed biological/genetic factors in order to explain the relationship when we know the etiology of PCa.
But as can be seen, again, the relationships between the proposed explanations in order to continue pushing their biological/genetic theories of PCa and aggression linked with testosterone and race also fails. Rushton’s r/K theory, for instance, implicated testosterone as a “master switch” (Rushton, 1999). Attempted reductions to biology were also seen in (the now-retracted) Rushton and Templer (2012) (see responses here and here). Reductions to biology quite clearly fail, but that doesn’t deter the hereditarian from pushing the racist theory that genes and biology explain the poor outcomes of blacks.
(Note: I don’t believe in an afterlife and I’m not a theist.)
What do Americans think about the existence of an afterlife and what are the differences between races?
What do Americans think about the existence of an afterlife—of heaven and hell? The existence of an afterlife to American citizens is clear—more Americans believe in heaven but not in hell, per Pew. But 26% of the respondents didn’t believe in either heaven or hell. But those who did not believe in heaven or hell but did believe in an afterlife were asked to describe their views:
Respondents who believe in neither heaven nor hell but do still believe in an afterlife were given the opportunity to describe their idea of this afterlife in the form of an open-ended question that asked: “In your own words, what do you think the afterlife is like?”
Within this group, about one-in-five people (21%) express belief in an afterlife where one’s spirit, consciousness or energy lives on after their physical body has passed away, or in a continued existence in an alternate dimension or reality. One respondent describes their view as “a resting place for our spirits and energy. I don’t think it’s like the traditional view of heaven but I’m also not sure that death is the end.” And another says, “I believe that life continues and after my current life is done, I will go on in some other form. It won’t be me, as in my traits and personality, but something of me will carry on.”
Blacks were slightly more likely to believe in heaven over whites, though a super majority of both races do believe in heaven, while way more blacks than whites believed in the existence of hell. Others professed less-widely-held views on the afterlife, like existing as a spirit, consciousness, or energy in the afterlife. Those who believe state that heaven is free from earthly matters, such as suffering while in hell it is the opposite—hell is nothing but eternal suffering, not due to any fire and brimstone, but because it is eternal separation from God. America is, to my surprise, still a very superstitious country when it comes to God and Satan and the existence of heaven and hell. People believe that their prayers can be answered and that interactions between the living and the dead are possible. Black Americans are more likely to believe that their prayers can be directly answered in comparison to white Americans (83 percent compared to 65 percent, respectively) , while 67 percent of Americans think it’s possible. Black Americans also believe that revelations from a higher power are possible in comparison to white Americans (85 percent and 66 percent, respectively), while black Americans are more likely to believe that they have experienced contact from a higher power compared to white Americans (53 percent compared to 25 percent, respectively).
Moreover, black men over age 50 who attend church had a 47 percent reduction in all-cause mortality compared to those who did not attend (Bruce et al, 2022), so there seems to be a protective effect that occurs due to attending church services (Assari and Lankarani, 2018; Carter-Edwards et al, 2018; Majee et al, 2022). It has been found that blacks consistently report lower odds of having depression, and the answer is probably due to attending religious services (Reese et al, 2012). However, when it comes to church attendance, for white women their attendance at church is either nonexistent or protective when it comes to body mass while for black women consistent relations between church attendance and body mass have been shown (Godbolt et al, 2018). Given the fact that black women have been consistently more likely to be obese than white women since at least the late 80s and 90s (Gillum, 1987; Kumanyika, 1987; Allison et al, 1997) and today (Tilghman, 2003; Johnson et al, 2012; Agyemang and Powell-Wiley, 2014; Tucker et al, 2021), this finding is not surprising. But the effects of racism can not only explain the higher rates of obesity in black women (Cozier et al, 2014), it could also explain the higher rates of “weathering” of black women’s bodies (Geronimus et al, 2006).
Nevertheless, blacks are more likely to be religious and report religious experiences in comparison to whites, and blacks are also more likely to be religious in comparison to the general US population. Why may blacks be more religious than whites? This is a question I will try to answer in the future.
The ultimate answer to your question is found in Revelation 21-22 which describes the new heaven and earth. In Revelation 21:24 we are told that people from the various nations will be in heaven. That is, those who believe in Jesus Christ and follow Him will live there for eternity. But the culture of heaven will be God’s culture. Everything is new. Heaven and earth will be new. The old will have disappeared and the new will have come. Sin will be gone and racial prejudices and alliances will be gone.
The difference between heaven and hell is that in heaven—that is, in the new heaven and new earth—there will be perfect racial and ethnic harmony, but in hell, racial and ethnic animosities will reach their fullest fury and last forever.
So what is RACE? In my view, race is a suite of physical characteristics which are demarcated by geographic ancestry, as argued by Hardimon and Spencer. So if race is physical, then if a thing isn’t physical—that is, if a thing is immaterial—then there would be no way to identify which racial group they were a part of while they were alive. If we take the afterlife to be a situation in which a person has died but they then exist again as a disembodied soul/mind, then there can’t possibly be races in heaven, since what identified the person as part of a racial group (the physical) doesn’t exist anymore.
In the book The Myth of an Afterlife, Drange (2015: 329-330) articulates what he calls the nonidentificationargument, where it is inconceivable for a person to be identified if they are bodiless, and if they are bodiless and race is a property of physical bodies, then it would follow that there wouldn’t be races in heaven since disembodied souls, by definition, lack physical bodies—there would be no way for the identities of people to be established, and so if people’s identities cannot be established, then it follows that their racial identities cannot be established either.
Bodiless people would have no sense organs and no body of any sort.
Therefore, they could not feel anything by touch or see or hear anything (in the most common senses of “see” and “hear”).
Thus, if they were to have any thoughts about who they are, then they would have no way to determine for sure that the thoughts are (genuine) memories, as opposed to mere figments of imagination.
So, bodiless people would have no way to establish their own identities.
Also, there would be no way for their identities to be established by anyone else.
Hence, there would be no way whatever for the identities of bodiless people to be established.
But for a person to be in an afterlife at all, it is conceptually necessary for his or her identity to be capable of being established.
It follows that a totally disembodied personal afterlife is not conceivable.
Drange’s argument is against a certain conception of the afterlife, mainly if it is one where souls are disembodied, it follows that there would be no way to identify them, and so it follows that there would be no races in heaven, since race is a physical property of humans and their bodies. But there are different ways of looking at the possibility of races in heaven, depending on which theory of race one holds to.
Nathan Placencia (2021) argues that whether or not races exist in heaven depends on which philosophy of race you hold to, but he does make the positive claim that there may be racial identities in heaven. For racial constructivists, since race exists merely due to social conventions and racialization, then race wouldn’t exist. For the racial skeptic, since race doesn’t exist as a biological category, then races don’t exist. That is, since racial naturalism is false, then races of any kind cannot exist, where racial naturalism is basically like the hereditarian conception (or non-conception, if you will) of race (see Kaplan and Winther, 2015). Racial naturalists argue that race is grounded in genetically-mediated biological differences. I am of course sympathetic to the view, though I do hold that race is a social construct of a biological reality and I am a pluralist about race. The last conception that Placencia discusses is that of deflationary realism, where race is genetically-grounded but not itself normatively important (Hardimon, 2017). So Placencia claims that for the racial constructivists and skeptics, races won’t exist in heaven while for the deflationary realist, the “answer is maybe” on whether or not race will exist in heaven which then of course depends on what the resurrected heavenly bodies would look like.
Believers in heaven state that Believers will have new, physical bodies in heaven. But Jesus wasn’t immediately recognizable to his followers, though they did come to know that it was actually him after spending time with him. So theists of course then believe that we get new physical bodies in heaven but that we would look different than we did while we had a physical, earthly existence. Certain chapters in Revelations (21:4, 22:4) talk about God wiping away tears and a name appearing on their foreheads, so this then implies that there would be new, physical bodies in heaven. But now the question is, would heavenly bodies fall under racial lines as we currently understand them in this life? The question is obviously unanswerable, but certain texts in the Bible after Jesus’ resurrection state that he did look different than he did while he was alive in earth.
Baker-Hytch (2021: 182) argues that “the new creation is depicted as an everlasting reality whose human inhabitants from all nations will have resurrection bodies that—after the pattern of Jesus’ resurrection body—neither age nor die and that will partake in shared pleasures such as eating and drinking together.” So there is a trend in Christian and theistic thought that in heaven, we will all have new heavenly bodies and not exist as mere disembodied souls. But talk of new heavenly bodies faces an issue—if they are bodies in the sense that we think of bodies now, the bodies that we inhabit now, then would they grow old, decay and eventually die? Would God then give us new heavenly bodies? It would stand to reason that, if God is indeed all-powerful and all-knowing, then he would have thought these issues through and so heavenly bodies wouldn’t have the same properties as physical, earthly bodies and so they wouldn’t get older, die and eventually decay.
Conclusion
If the afterlife is completely disembodied, then it follows that race wouldn’t exist in the afterlife, since there would be no way for the identities of persons to be established, and thusly there would be no way for the race of the disembodied soul to be established. Most theists contend that we will have new, heavenly bodies in heaven, but whether or not they would look the same as the former earthly bodies is up in the air, since Jesus after his resurrection apparently looked different, since it states in the Bible that it took some time for Jesus’ followers to recognize him. So, if Heaven exists, will there be races? The concept RACE is a physical one. So if there are disembodied souls in heaven, and they have no physical bodies, then races won’t exist in heaven.
I obviously am a realist about race who holds to radical pluralism about racial kinds—there can be many concepts of race which are true and are context-dependent. Though I do not believe in an afterlife, I do believe that if an afterlife is nothing but disembodied souls living in heaven wkth God, then it follows that there won’t be races in heaven since there are no physical bodies on which to ground racial ontologies. On the other hand, if what most theists contend is true—that we get new heavenly bodies after our death and entrance into the afterlife—whether or not race would exist in heaven is questionable and it depends on which concept of RACE one holds to. If one is a constructivist or skeptic (AKA eliminativist or anti-realist) about race, then race wouldn’t exist in heaven as race is due to social conventions and the concept of racialization of groups as races. But if one is a deflationary realist about race (which I myself am), then the answer to the question of whether or not races would exist in heaven is maybe.
Nevertheless, whether or not one believes in the existence of an afterlife is slightly drawn on racial lines, with blacks being more likely to believe in an afterlife compared to whites, while are more likely to believe that their prayers can be directly answered and that they can talk to a higher power in comparison to whites.
So depending on how races get squared away in heaven upon receiving new heavenly bodies, it is unknown whether or not races will exist in heaven.
A mutation can be said to be directed if it arises due to the needs of the developing organism, and they occur at higher frequencies if it is beneficial (Foster, 2000; Saier et al, 2017). If there is some sort of stress, then an adaptive mutation would occur. The existence of this kind of mechanism has been debated in the literature, but its existence spells trouble for neo-Darwinian theory, whose proponents claim that mutations are random and then “selected-for” in virtue of their contributions to fitness. Indeed, this concept challenges a core tenet of neo-Darwinism (Sarkar, 1991). I will argue that directed mutation/non-random mutation/stress-directed adaptation (DM, directed mutation for short) spells trouble for the neo-Darwinian paradigm.
The issue at hand
The possibility of DMs were argued for by Cairns, Overbaugh, and Miller (1988), where they argue that environmental pressure can cause adaptive changes to genes that would be beneficial to the organism. This then spurred a long debate about whether or not such mutations were possible (see Sarkar, 1991; Fox Keller, 1992; Brisson, 2003; Jablonka and Lamb, 2014). Although Cairns, Overbaugh, and Miller were wrong—that is, they were not dealing with mutations that were due to the environmental disturbances they posed (Jablonka and Lamb, 2014: 84)—their paper did bring up the possibility that some mutations could be a direct consequence of environmental disturbances which would then be catapulted by the homeodynamic physiology of the organism.
Recently, strong support for directed mutation has emerged, not for point mutations as independently proposed by Cairns, Hall and their collaborators, but for transposon-mediated mutations (12, 13). If accepted by the scientific community, this concept could advance (or revise) our perception of evolution, allowing increased rates of mutational change in times of need. But this concept goes against the current dogma that states that mutations occur randomly, and only the beneficial ones are selected for (14, 15). The concept of directed mutation, if established, would require the reversal of a long accepted precept.
This is similar to the concept of phenotypic plasticity. It is the phenomenon of a given genotype expressing different phenotypes due to environmental factors. This concept is basically a physiological one. When talking about how plastic a phenotype is, its relation to the physiology of the organism is paramount. We know that physiological changes are homeodynamic. That is, changes in physiology are constantly happening due to the effects of the environment the organism finds itself in. For example, acute changes in heart rate occur due to what happens in the environment, like say a predator chase it’s prey. The heart rates of both predator and prey increases as blood flow increases due to stress hormones. I will discuss phenotypic plasticity on its own in the future, but for now I will just note that genetic and environmental factors influence the plasticity of phenotypes (Ledon-Rettig and Ragsdale, 2021) and that phenotypic plasticity and development play a role in evolution (West-Eberhard, 2003, 2005; Wund, 2015
The fact of the matter is, phenotypic plasticity is directly related to the concept of directed mutation, due to DM being a largely physiological concept. I will argue that this refutes a central Darwinian premise. Namely that since directed mutations are possible, then they are not random. If they are not random, then due to what occurs during the development of an organism, a directed mutation could be adaptive. This, then, is the answer to how phenotypic traits become fixed in the genome without the need for natural selection.
Directed mutations
Sueoka (1988) showed that basically all organisms are subject to directed mutations. It has been noted by mathematicans that on a purely random mutational model, that there would not be enough time to explain all of the phenotypic diversity we see today (Wright, 2000). Doubt is placed on three principles of neo-Darwinism: mutations occur independently of the environment the organism is in (this is empirically false); mutations are due to replication errors (this is true, but not always the case) and mutation rates are constant (Brisson, 2003).
One of the main claims of the neo-Darwinian paradigm is that mutations occur at random, and the mutation is selected-for or against based on its relationship to fitness. Fodor’s argument has refuted the concept of natural selection, since “selection-for” is an intensional context and so can’t distinguish between correlated traits. However, we know now that since physiology is sensitive to the environment, and since adaptive changes to physiology would occur not only in an organism but during its development, it then follows that directed mutations would be a thing, and so they wouldn’t be random as neo-Darwinian dogma would claim.
In her review Stress-directed adaptive mutations and evolution, Wright (2004) concludes:
In nature, where cell division must often be negligible as a result of multiple adverse conditions, beneficial mutations for evolution can arise in specific response to stressors that target related genes for derepression. Specific transcription of these genes then results in localized DNA secondary structures containing unpaired bases vulnerable to mutation. Many environmental stressors can also affect supercoiling and [stress-directed mutation] directly.
But what are the mechanisms of DMs? “Mechanism” in this meaning would “refer to the circumstances affecting mutation rates” (Wright, 2000). She also defines what “random” means in neo-Darwinian parlance: “a mutation is random if it is unrelated to the metabolic function of the gene and if it occurs at a rate that is undirected by specific selective conditions of the environment.” Thus, the existence of DMs would then refute this tenet of neo-Darwinism. Two of the mechanisms of such DMs are transcriptional activation and supercoiling. Transcriptional activation (TA) can cause changes to single-stranded DNA (ssDNA) and also supercoiling (the addition of more coils onto DNA). TA can be caused by either derepression (which is a mechanism which occurs due to the absence of some molecule) or induction (the activation of an inactive gene which then becomes transcribed). Thus, knowing this, “genetic derepression may be the only mechanism by which particular environmental conditions of stress target specific regions of the genome for higher mutation rates (hypermutation)” (Wright, 2000). Such responses rely on a quick response, and this is due to the plastic phenotypes of the organism which then allow such DMs to occur. It then follows that stress-induced changes would allow organisms to survive in new environments, without a need for neo-Darwinian “mechanisms”—mainly natural selection. Thus, the biochemical mechanism for such mutations is transcriptional activation. Such stress-directed mutation could be seen as “quasi-Lamarckian” (Koonin and Wolf, 2009).
In nature, nutritional stress and associated genetic derepression must be rampant. If mutation rates can be altered by the many variables controlling specific, stress-induced transcription, one might reasonably argue that many mutations are to some extent directed as a result of the unique metabolism of every organism responding to the challenges of its environment. (Wright, 2000)
No longer can we think about mutation solely in terms of random failures in DNA maintenance and repair. We now know that stress conditions can affect the operation of the enzyme systems that are responsible for maintaining and repairing DNA, and parts of these systems sometimes seem to be coupled with regulatory elements that control how, how much, and where DNA is altered.
Jablonka and Lamb present solid evidence that mutations are semi-directed. Such mutations, as we have seen, are able to be induced by the environment in response to stress, which is due to our plastic, homeodynamic physiology. They discuss “four dimensions” of evolution which are DNA, epigenetic, behavioral and cultural. Their works (including their Epigenetic Inheritance and Evolution: The Lamarckian Dimension; see Jablonka and Lamb, 2015) provide solid evidence and arguments against the neo-Darwinian view of evolution. The fact of the matter is, there are multiple inheritance systems over and above DNA, which then contribute to nonrandom, directed mutations. The fact of the matter is, Lamarckism wasn’t wrong and Jablonka and Lamb have strongly argued for that conclusion. Epigenetics clearly influences evolution, and this therefore vindicates Lamarckism. Epigenetic variation can be inherited too (Jablonka and Lamb, 1989). Since phenotypic plasticity is relevant in how organisms adapt to their environment, then epigenetic mechanisms contribute to evolution (Ashe, Colot, and Oldroyd, 2021). Such changes that arise due to epigenetic mechanisms can indeed influence mutation (Meyer, 2015), and I would say—more directly—that certain epigenetic mechanisms play a part in how an adaptive, directed mutation would arise during the development of an organism. Stochastic epigenetic variation can indeed become adaptive (Feinberg and Irizarry, 2010).
Non-random mutations have been known to be pretty ubiquitous (Tsunoyama, Bellgard, and Gojobori, 2001). This has even been shown in the plant Arabidopis (Monroe et al, 2022), which shows that basically, mutations are not random (Domingues, 2023). A similar concept to DMs is blind stochasticity. Noble and Noble (2017, 2018; cf Noble, 2017) have shown that organisms harness stochastic processes in order to adapt to the environment—to harness function. A stochastic process is a state of a system that cannot be predicted even knowing the current state of said system.
Even all the way back in 1979, such changes were beginning to be noticed by evolutionists, such as Ho and Saunders (1979) who write that variations in the phenotype
are produced by interactions between the organism and the environment during development. We propose, therefore, that the intrinsic dynamical structure of the epigenetic system itself, in its interaction with the environment, is the source of non-random variations which direct evolutionary change, and that a proper study of evolution consists in the working out of the dynamics of the epigenetic system and its response to environmental stimuli as well as the mechanisms whereby novel developmental responses are canalized.
The organism participates in its own evolution (as considerations from niche construction show), and “evolutionary novelties” can and do arise nonrandomly (Ho, 2010). This is completely at-odds with the neo-Darwinian paradigm. Indeed, the creators of the Modern Synthesis ignored developmental and epigenetic issues when it came to formulating their theory. Fortunately, in the new millennium, we have come to understand and appreciate how development and evolution occur and how dynamic the physiological system itself truly is.
There have been critical takes on the concept of DM (Lenski and Mittler, 2003; Charlesworth, Barton, and Charlesworth, 2017; see Noble and Shapiro, 2021 for critique), like for example Futuyama (2017) who claims that DM is “groundless.” However, James Shapiro’s (1992; 2013, 2014) concept of natural genetic engineering states that cells can restructure their genomes so this “means viewing genetic change as a coordinated cell biological process, the reorganization of discrete genomic modules, resulting in the formation of new DNA structures” (Shapiro, 1993). DNA is harnessed by and for the physiological system to carry out certain tasks. Since development is self-organizing and dynamic (Smith and Thelen, 2003; Saetzler, Sonnenschein, and Soto, 2012) and since development is spurred on by physiological processes, along with the fact that physiology is sensitive to the goings-on of the environment that the developing organism finds itself in, then it follows that mutations can and would arise due to need, which would refute claims from neo-Darwinians who claim that mutations arise due to chance and not need.
Conclusion
It is clear that mutations can be (1) adaptive and (2) environmentally-induced. Such adaptive mutations, clearly, arise due to need and not chance. If they arise due to need and not chance, then they are directed and adaptive. They are directed by the plastic physiology of the organism which constructs the phenotype in a dialectical manner, using genes as its passive products, not active causes. This is because biological causation is multi-leveled, not one-way (Noble, 2012). There is also the fact of the matter that “genetic change is far from random and often not gradual” (Noble, 2013).
As can be seen in this discussion, adaptive, directed mutations are a fact of life, and so, one more domino of neo-Darwinism has fallen. Berkley claims that “The genetic variation that occurs in a population because of mutation is random“; “mutations are random“, but as we’ve seen here, this is not the case. Through the biological process of physiology and its relationship to the ebbs and flows of the environment, the organism’s phenotype that is being constructed by the self-organizing system can respond to changes in the cellular and overall environment and thusly direct changes in the phenotype and genes which would then enhance survival due to the environmental insult.
Lamarckism has been vindicated over the past 25 or so years, and it’s due to a better understanding of epigenetic processes in evolution and in the developing organism. Since what Lamarck is known for is the claim that the environment can affect the phenotype in a heritable manner, and since we now know that DNA is not the only thing inherited but epigenetically-modified DNA sequences are too, it follows that Lamarck was right. What we need to understand development and evolution is the Extended Evolutionary Synthesis, which does make novel predictions and predictions that the neo-Darwinian paradigm doesn’t (Laland et al, 2015).
Such directed changes in the genome which are caused by the physiological system due to the plastic nature of organismal construction refute a main premise of the neo-Darwinian paradigm. This is the alternative to neo-Darwinian natural selection, as Fodor noted in his attack on neo-Darwinism:
The alternative possibility to Darwin’s is that the direction of phenotypic change is very largely determined by endogenous variables. The current literature suggests that alterations in the timing of genetically controlled developmental processes is often the endogenous variable of choice; hence the ‘devo’ in ‘evo-devo’.
Darwin got quite a bit wrong, and it’s of no fault of his own. But those who claim that Darwin discovered mechanisms or articulated the random process of mutations quite obviously need to update their thoughts in the new millennium on the basis of new information informed by systems biologists and epigeneticists. The process of the construction of organisms is dynamic and self-organizing, and this is how phenotypic traits become fixed in populations of organisms. Plasticity is in fact a major driver of evolution along with the concept of genetic assimilation, which results in the canalization of the plastic trait which then eliminates the plastic response from the environment (Sommer, 2020). Phenotypic plasticity can have adaptive traits arise, but natural selection can’t be the mechanism of evolution due to Fodor’s considerations. Development can lead to evolution, not only evolution leading to development (West-Eberhard, 2003). In fact, development in many cases precedes evolution.
Hereditarians champion Asians (specifically East Asians) as proof of their gene-centric worldview—that their genetic constitution allows their stellar performance in educational and life outcomes. However, scholars have noted for decades that Asians are a specially selected group—using what is known as “hyper-selectivity” or “educational selectivity.” Immigrants that are more likely to have a college degree compared to those in their native country and their host nation; they bring over different kinds of class tools that then help their progeny in the next generation. This selectivity gives the children of immigrants—whether it be 1.5 generation (children that emigrated during adolescence) or second generation children—a better “starting point”, and, along with the cultural tools, allows them to succeed in America. In this article, I will describe the process of immigration of certain Asian groups to America, and then I will argue that what explains their success today is not genes as hereditarians try to argue, but the selectivity of the population in question and then I will argue against the hereditarian position.
Although they seem dissimilar, educational and hyper-selectivity share some common ground. Immigrant selectivity describes the fact that those who emigrate are not a random sample of the population from which they derive, but they have better educational accolades than those that stayed behind (Borjas, 1987; Borjas, Kauppinen, and Poutvaara, 2018; Sporlein and Kristen, 2019). There is then the concept of negative selection, too (contrasted with positive selection, which is what educational and hyper-selectivity are). There is both a positive and negative selection occurring, and immigrants are indeed a self-selected group with selection also occurring for unobserved traits (Aydemir, 2003). Indeed, migrants to less equal countries like the US are positively selected (Parry et al, 2017) and those that do migrate are more skilled, ambitious, and motivated (Cattaneo, 2007). Immigrants are in general more educated than those who do not migrate, but this differs depending on country of origin (Feliciano, 2005) while economic migrants are favorably self-selected (Chiswick, 1999).
From immigrant yellow peril to model minority
Asian immigration to the United States has been occurring in large numbers since the 1860s. During that time, Chinese immigrants wanted to escape the horrid situation in China and try their luck in the California gold rush and they had aspirations to return to China after they had made some money. They mostly came from the Guangdong province in China (Jorae, 2009). This was the first wave of Asian immigration to America. Between 1882 and 1943 the US government severely restricted the immigration of the Chinese into America since they were emigrating to work on the transcontinental railroad, and they passed the legislation so native-born Americans could get the jobs (Zellar, 2003; Gates, 2017). (It’s also worth noting that immigrant labor between 1880s and 1920s was a necessary condition for the industrial revolution; Hirschman and Mogford, 2009.) The first exclusionary act was the act of May, 6 1882, and it had lasting negative effects until at least the 1940s (Long et al, 2022). Chinese immigrants then began a “revolving door system” where young workers replaced older workers (Chew, Leach, and Liu, 2018). In 1885, the first Chinese-only school was opened. So in 1892 the second piece of legislation—the Geary Act—was passed, which was a further exclusionary tactic. Porteus and Babcock (1926: 37) noted how by 1888 that the Chinese in Hawaii “had infiltrated every trade and occupation in the islands.” It was then in 1942 where FDR repealed these two legislations on the Chinese.
But perceptions on the Chinese began to change. From being known as “the yellow peril” in the late 19th to early 20th century, a Gallup poll in 1942 stated that the Chinese were “hardworking, honest, brave, religious, intelligent, and practical” while in that same poll, the Japanese were described as “treacherous, sly, cruel, and warlike.” This of course speaks to the xenophobic attitudes of Americans at the time, and further speaks to the kind of “villain of the week” mentality.
The second wave of Asian immigration was the Japanese and the became the new source of cheap labor after the Chinese in the early 20th century. They were treated as the Chinese were treated previously, and due to a “gentleman’s agreement” between Japan in America in 1908, Japan limited migration of Japanese to America to non-laborers (Hirschman and Wong, 1987: 6). But the immigration act of 1924—the Johnson Reed Act—even barred Asian immigration from countries from which it previously allowed. Nevertheless, previous attitudes on the Chinese and Japanese show one important thing—that racist ideals toward a group of people can and do change over the years.
When it comes to the Taiwanese, they had already secured a spot in America by having a large amount of Taiwanese immigrants that who had college degrees before 1965. After the Hart-Cellar act was passed they stayed in the country and then sponsored their highly educated family members to America, and so this is an explanation for why there is hyper-selectivity (Model, 2017).
From a “peril” and “treacherous and warlike” to “hardworking, honest and intelligent” in mere decades. Americans in the early 20th century, in fact, looked at Asians back then as blacks are looked at today, with similar claims made about genital and brain size to Asians back then.
Asians are said to be “model minorities” today, due to their educational attainment and higher incomes. Lee and Zhou (2015: 31-32) state three things about “model minority” status:
(1) It overlooks the fact that Asians aren’t a monolith and comprise many different ethnic groups that don’t have the same model outcomes.
(2) It has been used to claim that “race doesn’t matter” in America since Asians can apparently make it in America despite non-white status.
(3) It pits Asian Americans against other minorities.
It has been said that the model minority stereotype “masks a history of discrimination“, “holds Asian Americans back at work” and that it “hurts us all.” I will explain higher educational attainment below, but when it comes to higher incomes, Asian families are more likely to live in extended (auxiliary) families which contribute to the income of the household (Reyes, 2019). Asian American families have an average of 3.5 people, which makes them larger than the average US family. As Jennifer Lee notes:
High household incomes among Asian Americans can also be explained by “the fact that some live in multi-generational homes with more than one person earning an income,” said Jennifer Lee, a sociology professor at the University of California at Irvine, and co-author of the book “The Asian-American Achievement Paradox.” “You have parents, grandparents, an aunt, some children.”
Nevertheless, the history of Asians in America—whether it’s when they first arrived and the racism they faced or today being seen as “model minorities”, is suggestive as to why they are so successful in America today. They are so successful because it’s not merely any kind of people of the country in question that emigrate, it’s a specific kind of people with specific outlooks and qualifications. This, in effect, then explains the how and why of Asian academic achievement.
Hyper-selectivity and the Asian American experience
Hyper-selectivity refers to the “higher percentage of college graduates among immigrants compared to non-migrants from their country of origin, and a higher percentage of college graduates compared to the host country” (Lee and Zhou, 2015: 15). This selective process began in the 1960s, and the federal policies themselves select a particular kind of entrant into the country (Juun, 2007; Ho, 2017; Model, 2017). Asians in America can be said to be a “middleman minority” (Hirschman and Wong, 1987), where a “middleman minority” refers to “minority entrepreneurs who mediate between the dominant and subordinate group” (Douglas and Saenz, 2008; see also Bonacich, 1973). It is an occupational pattern rather than a status (Lou, 1988). Lee and Rong (1988) seek explanations of Asian educational success in terms of family structure, along with middleman and niche theories of migration.
Some would uphold a culturalist thesis—that what explains exceptional educational outcomes for Asians would be their culture. For example, Asian Americans study about one hour more per day than whites (Tang, 2021), though one 2011 analysis found that Asians spent more time studying and doing homework—Asians spent 13 hours per week studying while whites only studies for 5. Asian Americans spend significantly more time studying than other racial groups (Ramey and Shao, 2017). When it comes to homework, black students spent 36 minutes on homework, “Hispanic” students spent 50 minutes, white students spent 56 minutes, and Asians spent 2 hours and 14 minutes doing homework, while they also spent more time on other supplementary educational tasks (Dunachik and Park, 2022). Asian American parents were also more likely to spend 20 minutes with their children helping with their homework (Garcia, 2013).
Some would state that this is due to an “Asian culture”, but reality tells a different story. The hyper-selectivity of Asians explains this, and their successes cannot be reduced to their culture. Lee and Zhou (2017) state that “Asian immigrants to the United States are hyper-selected, which results in the transmission and recreation of middle-class specific cultural frames, institutions, and practices, including a strict success frame as well as an ethnic system of supplementary education to support the success frame for the second generation.” Yiu (2013) notes that Chinese in Spain have much lower educational attainment and ambitions in comparison to other ethnies in Spain. Merely twenty percent of Chinese youth were enrolled in post-secondary school, while 40 percent of all youths and 30 percent of all immigrants were (Yiu, 2013).
Context matters. And the ambitions of a group of people would then depend on national context. This is what Noam (2014) found for the Chinese in the Netherlands—where Chinese Americans accept the cultural values of high educational attainment, Chinese Dutch oppose them:
In the United States and the Netherlands the second-generation Chinese approach their ethnocultural values regarding education in dissimilar ways—either accepting or opposing them—yet they both adjust them to their national context.
What is termed the “immigrant paradox” is stronger in Asian and African than other immigrants (Crosnoe and Turley, 2017). Tran et al (2018) note how likely a certain immigrant group would be to have a higher degree in comparison to those in their country of origin:
Among the population age twenty-five and older, first-generation immigrants reported significantly higher percentages of having a bachelor’s degree or higher than their nonmigrant counterparts in respective home countries. This achievement gap is most striking between Chinese nonmigrants and Chinese immigrants in the United States, but also substantial for the other three groups. Only 3.6 percent of nonmigrant Chinese reported having a college education, but 52.7 percent of immigrant Chinese held a bachelor’s degree. This hyper-selectivity ratio of 17:1 between immigrant and nonmigrant means that Chinese immigrants were disproportionately well educated relative to non-migrants. This ratio is about 8:1 for Asian Indians. This gap is also quite stark among Nigerians. Immigrant Nigerians (63.8 percent) were six times more likely than their nonmigrant counterparts to report having a bachelor’s degree or more (11.5 percent). Their hyper-selectivity ratio is about 6:1. Similarly, 23.5 percent of immigrant Cubans reported having a college degree relative to only 14.2 percent of nonmigrant Cubans, a gap of 9 percent. Among Armenians, the corresponding gap is about 10 percent.
Genetic and cultural hypotheses have been contrasted in an attempt to explain why Asian Americans excel over and above whites. Sue and Okazaki (1990) take a structuralist interpretation—they argue that Asians believe that education is paramount for social mobility. Lynn (1991) rejects Sue and Okazaki’s relative functionalism hypothesis, though it should be noted that hereditarian beliefs about genes and IQ are highly suspect and, frankly, do not work. There is also the fact that, as Sue and Okazaki (1990: 48), note that “Lynn failed to take into account the fact that the Japanese samples tended to have higher socioeconomic standing and a higher representation of urban than rural children than did the American samples from which the norms were constructed.” (Also see Sautman, 1994 and Yee, 1992: 111.) Sue and Okazaki showed that Asians differed from white Americans on one question—they were more likely than white Americans to believe that success in life was related to school success, and this is consistent with the Lee and Zhou account.
In Lynn’s (1991) reply to Sue and Okazaki, he notes that their relative functionalism hypothesis has to be dismissed, but he did not discount the role of motivation, staying longer in school and doing more homework. He then—in typical Lynn style—claims that these traits have high heritability and so a genetic hypothesis should not be discounted. Sue and Okazaki (1991) responded, discussing Lynn’s views on CWT, Asian adoptees, and what he says about their relative functionalism hypothesis. In any case, Lynn’s reply is in no way satisfactory, since his belief that genes contribute to IQ scores (that IQ is genetically mediated) is false. Nevertheless, Flynn showed that when IQ is held constant, that when compared with whites, that “Asian’s achievements exceed those of Whites by a huge amount.”
PumpkinPerson claims, using the Coleman report (Coleman, 1966) that “the incredible scores of Oriental Americans is not at all explained by selective immigration” and that he “decided to compare them in the first grade before environment has had much time to cause differences.” I will take both if these claims in turn.
(1) This is false. While selection wasn’t really a thing for Chinese immigrants, it has been noted that the children of Chinese immigrants during the Exclusion period had “greater human capital than those of unrestricted immigrants, despite restricted immigrants having lower skill” which “suggests particularly strong intergenerational transmission of skill among Chinese immigrants of the exclusion era” (Chen, 2015). It is a truism that the Chinese of this time period were not selected in the nature that Asian immigrants are today, but discrimination did lead to their assimilation (Chen and Xie, 2020). Indeed, second-generation Chinese Americans attending American schools had good schooling (Djang, 1935: 101). And for Japanese Americans, Hirschman and Wong (1986: 9) point out:
Another important feature of Asian immigration was the educational selectivity of different streams of immigrants. While the educational composition of recent Asian immigrants has been extraordinary (Chen 1977; North 1974; Pernia 1976), this was not always the case. Most of the early Asian immigrants to the United States, like their counterparts from Europe, arrived with only minimal educational qualifications. The important exception was early Japanese immigrants. Data from the 1960 Census show that Japanese immigrants, above age 65 in 1960, had a median eight years of schooling-comparable to the figure for the white population of the same age (U.S. Bureau of the Census 1963a, 1963c). This finding is corroborated by earlier studies which report a very selective pattern of Japanese immigration to the United States, particularly to the mainland (Ichihashi 1932; Kitano 1976; Petersen 1971; Strong [1934] 1970).
(2) The home environment before first-grade does have a large effect on outcomes (e.g., Brooks-Gunn et al, 1996). Of course exposure to different kinds of things in the household would explain certain outcomes later in life, such as test scores.
In the book Temperament and Race, Porteus and Babcock (1926: 119-120) discussed the racial rankings of grades by one researcher, with the following chart, showing similar findings to Coleman:
They also discussed the Thorndike Examination of High School Graduates in Hawaii from 1922-1923, that the Chinese and Japanese scored below whites but this could be seen as them not having full English proficiency. Chun (1940: 35) showed that “Anglo Saxons” has Binet IQs of 100, and IQs of 87 and 85 for the Chinese and Japanese respectively, and this is similar to what Porteus and Babcock (1926) showed for Chinese and Japanese too. This also could be due to low English proficiency. Chun (1940) also shows that there were a large amount of schools for the Chinese as well. Coupled with the fact that immigrants aren’t a random sample of the population from which they derive, selection therefore explains these values. It’s quite clear that the Chinese had good education since the 1880s with the introduction of Chinese schools on the mainland and in Hawaii, and along with the fact that Japanese immigrants had education on par with whites at the time, of course the selectivity of the population along with the education they got clearly mattered.
When it comes to Asian immigration post-1965, “The new preference system allowed highly skilled professionals, primarily doctors, nurses, and engineers from Asian countries, to immigrate and eventually to sponsor their families” (Hirschman 2015), while the Act resulted in a majority of nurses that came from Asia (Rockett et al, 1989; Masselink and Jones, 2015). Erika Lee notes in The Making of Asian America (2017: 287):
As in the past, Asian immigrants are highly regulated by immigration laws, but the emphasis of U. S. Laws in admitting family-sponsored immigrants and professional, highly skilled individuals has meant that the majority of New arrivals from to join family already here and bring a different set of educational and professional skills than earlier immigrants.”
Hsin and Xie (2014) showed that, rather than “cognitive ability” and sociodemographics, higher academic effort explains the Asian-White achievement gap. They argue that beliefs in academic effort along with immigrant status explains the relationship. Teachers have higher, more positive expectations for Asian students, and that such positive stereotypes will further influence their excelling, which is a pygmalion effect (Hsin and Xie, 2014). And so, the Asian-White achievement gap can be explained by higher academic effort, not IQ or SES, it’s driven by the Asian-White difference in academic effort. I don’t see an issue using teacher ratings, since teacher ratings have shown an even higher correlation between the accuracy of teacher’s assessments and IQ, at .65 as one study notes (Hoge and Coladarci, 1989) while a newer analysis showed a correlation of .80 (Kaufmann, 2019). Lee (2014) described why Asians have higher academic effort in comparison to Americans:
differences in the cultural frame and the resources used to support it help to explain why the children of some Asian immigrant groups get ahead, despite their socioeconomic disadvantage.
Studies show that Asian-American youth are less psychologically adjusted (32) and socially engaged (33) in school than their white peers. They may experience more conflict in relationships with parents because of the high educational expectations their parents place on them (32). Asian-American youth are under pressure to meet extraordinarily high standards because they consider other high achieving coethnics, rather than native-born whites, to be their reference group (7).
Even low-SES Asians have a high drive to succeed in academics, having work ethic similar to the white and Asian middle-class, and one attempted explanation is due to Confucian values (Liu, and Xie, 2016). Though Lee and Zhou (2020) have successfully argued against this claim, stating that second generation Chinese in Spain do not have such high educational attainment in Spain (Yiu, 2013), refuting the reduction of educational attainment to Confucian beliefs of Asians, since other Asian immigrants that do not share such Confucian beliefs are also hyper-selected. And while Asian American parents do hold higher educational expectations for their children in comparison to white American parents (Kao, 1995), this too is consistent with the Lee and Zhou account.
In a series of papers, Sakamoto (2017) and Sakamoto and Wang (2020) try to argue against the hyper-selectivity thesis. Sakamoto and Wang, I think, underestimate the importance of hyper-selectivity in explaining Asian educational achievements. They argue that cultural factors explain Asian American success, while Zhou and Lee (2017) argue that it’s due to selective migration patters that favor highly-able immigrants. Sakamoto and Wang claim that cultural factors explain the most about Asian achievement, but Zhou and Lee state that cultural factors alone cannot account for their achievement—cultural factors like Confucianism. While individual effort does play a role, as Hsin and Xie (2014) argue, of course cultural and structural factors also play a role, the argument given by Sakamoto and Wang can be refuted by the following argument:
(1) If selective migration is a significant factor in explaining the success of Asian Americans, then class background can’t be the sole explanation of their success. (2) Selective migration is a significant factor that explains the success of Asian Americans. (3) But Sakamoto and Wang claim that class background is basically the only reason for higher Asian American achievement. Since (3) contradicts (2) and (2) is true, then we can reject (3). Thus, the argument in Sakamoto and Wang does not refute the argument in Zhou and Lee.
Further, not all Asian immigrants enjoy the same level of success, since other Asian immigrants (like South Asians) are less likely to have selective migratory patterns than East Asians. Therefore, this shows that selective migration, and not culture, is paramount in explaining Asian American academic achievement. Hyper-selectivity on its own does not set the stage for Asian American achievement, but it does set the stage for the remaking of cultural practices which then forster educational success. Culture does matter, but not in the way that most conceptualize it. Sakamoto and Wang do not refute Zhou and Lee, since Zhou and Lee (2017: 8) provide evidence that “culture has structural roots and that cultural patterns emerge from structural circumstances of contemporary immigration.”
Hereditarian explanations of Asian educational achievement
For decades, hereditarians have argued that Asian educational achievements in contrast to whites’ are due to their “cognitive ability” (“IQ”), which is genetically mediated, on the basis of heritability estimates. For instance, hereditarians use data from transracial adoptees to try to argue that genetic differences cause differences in IQ between Asians and whites and then whites and blacks. However, this can be explained by adoptions’ beneficial effects for IQ and the Flynn effect (Thomas, 2017).
Hereditarians claim that since they argue for East Asian superiority, that they therefore are not racists. Sautman (1994: 80) noted how since hereditarians claim that they since they speak of East Asians being superior to whites, they therefore show a lack of bias in their assessment of racial differences:
In clustering East Asians and whites as genetically-favored and Africans, Southeast Asians and others as disfavored, Western race theorists use East Asians as a “racial wedge” against other non-whites. They argue that highlighting East Asian, not white, superiority shows an absence of bias. Thus, a criminologist who legs putatively higher crime rates of US blacks to r-strategy reproduction, underscores that he is “not a member of the least criminal racial group” (i.e. East Asians). A professor of management writes that whites will feel more comfortable in recognizing black inferiority if they know that East Asians outscore whites on IQ tests. a British journalist has queried “If they [East Asians] can be cleverer than we are, why can’t we be cleverer than some other group?”
[Herrnstein, Murray and Rushton] used this representation of whites as more cognitively advanced than blacks but less than Asians to silence those critics who insisted that the race researchers’ findings were ethnically self-serving. Rushton thus posed the question, “If my work was motivated by racism, why would I want Asians to have bigger brains than whites?” … it became useful to tout the Asians’ cognitive superiority but only so long as whites remained above blacks in the cognitive hierarchy.
The phrase “Mongoloid idiot” was coined, due to supposed similarities between Asians and people with Down syndrome. Along with being a sexual danger to white women, this then corresponded with how they were perceived—race scientists concluded that they had smaller brains than whites. This is noted in Lieberman’s (2001) Table 1 on the ever-changing skull size differences between the races.
The hierarchy changed right as East Asia began to modernize and have an economic boom (Lieberman, 2001). So we go from racism against East Asians, naming syndromes after them, saying they have small brains and large penises, to model minorities, high IQ, larger brains, lower sexual drive and booming economies. This speaks to the contextual-dependence of such claims, and that attitudes toward certain groups do indeed change over time.
To attempt to explain IQ and other differences between races, Lynn proposed that the harshness of cold winters shaped the cognitive skills of Europeans and East Asians over millenia, and that this explains why Asians score higher than whites and whites over blacks (Lynn, 1991, 2006a: 135-136, 2019; Rushton, 1997: 228-230, 2012). Many issues with these just-so stories and evolutionary theories (r/K theory) have been levied, showing that they merely “explain” observations, with no novel predictions, nevermind the anthropological misunderstandings from Lynn, Rushton, Jensen, and Kanazawa. Lynn (1991) attempted to show that children from Hong Kong showed higher reaction times and had higher IQs than British children, which he interpreted as having a neurological basis. Though, due to omissions and misinterpretations of data, we cannot accept Lynn’s conclusions (Thomas, 2011).
On that same note, the Chinese are notorious for cheating on standardized tests, they are cheating on the SAT, GRE, and other examinations, and they pay up to $6000 to have people take tests for them. There was, also, a large UCLA cheating ring which was recently busted. There is also the fact that the OECD allows China to administer the PISA in select regions, so the claim cannot be made that PISA results are representative of China. There is also the fact that the Chinese have what is called a “hukuo system” which is a tool for controlling migration from rural to urban areas. And so, even though some children may for example attend school in Shanghai, when it comes to for hukuo, they must return to their province of origin. It’s clear that the Chinese game standardized tests. They are cheating the PISA system by being selective on the students they administer the test to in Shanghai by doing hukuo.
Lynn (2010) argued that it was unnecessary to contribute the success of East Asians to Confucian values (this is true), and that IQ explains East Asian success in math and science. Though, what does explain their success is their selectivity, not their IQ. Lynn (2006a: 89) claimed that “The Chinese and Japanese who emigrated to the United States in the second half of the nineteenth century were largely peasants who came to do unskilled work on the construction of the railways and other building work.” While this is true to a point, it’s irrelevant and skirts around the fact that, as Hirschman and Wong noted, Japanese immigrants had educational parity with whites before the 1960s and the fact that Chinese laborers were indeed selected and this also affected their children in a positive manner.
In a now-retracted paper, Rushton (1992) opined that one “theoretical possibility” to explain why Asians have more “K” traits compared to “r” traits (see Anderson, 1991 for critique), is that evolution is progressive and that Asians are “more “advanced”” than are other groups. But the fact of the matter is, evolution isn’t progressive. Nevertheless, Rushton (1995) attempted to defend his arguments from Yee (1992) by saying the same old, bringing up Lynn’s study on reaction time and IQ (refuted by Thomas) along with Jensen’s (refuted by Sautman). He brings up the “evidence” from transracial adoption studies (see Thomas, 2017). Rushton then brings up brain size, talking about the larger brains of Asians (see above from Lieberman on how this seems to change with the times). Rushton then discusses “other variables”, like his crime data (refuted by Cernovsky and Littman, 2019), testosterone, and twinning (see Allen et al, 1992). This is all beside the point that Gorey and Cryns (1995) showed that any behavioral differences between Rushton’s three races can be explained by environment while Peregrine, Ember, and Ember (2003) showed no cross-cultural statistical support for Rushton’s theory.
To the hereditarian, Asians are upheld to say that they are not racists, since why would a racist state that Asians are “better” than whites? This, though, gives hereditarians cover. Nevertheless, the arguments used by hereditarians for Asian academic achievement and IQ fail, since they rely on numerous false assumptions and arguments.
Conclusion
Immigration in the past was mixed between positive and negative selection, but today is largely positive (Abramitzky and Boustan, 2017). In recent years, Asian immigrants were more highly selected than non-Asian immigrants (Huang, 2022). Asians have been the largest percentage of immigrants since 2009 (National Academy of Science, 2018). Lynn (2006a: 97) claims that “environmentalists do not offer any explanation for the consistently high IQ of East Asians, and it is doubtful whether any credible environmental explanation can be found.” But this claim fails since hyper-selectivity explains Asian educational achievements over whites.
The study of race differences, then, is completely political (Jackson, 2006). Since science is a social activity, then one’s political leanings and values would influence the science they seek out to do (Barnes, Zieff, and Anderson, 1999). This is wonderfully illustrated by the claims of hereditarians about Asians who are just using them as a cover to peddle racist inferiority tropes about blacks.
I have described how Asians have come in waves to America over the past 150 years. I have also shown how most immigrants today, and specifically Asians, are positively selected. I have further described a process of selection in certain Asians during the early 1900s. The hyper-selectivity thesis explains Asian American achievement, due to what hyper-selectivity is and the processes that they go through. I then explained how hereditarians attempt to use Asians as a cover for their racism, but their arguments are invalid and rely on numerous false assumptions. Having said all of that, here are the arguments:
The hyper-selectivity thesis does not ignore challenges faced by working class and lower-income Asians, it merely highlights unique characters of the Asian American experience which allow them to overcome economic barriers and then achieve high levels of academic and economic success. It also does not ignore the role of racism and discrimination, but it suggests that even in the face of this, they have unique characteristics due to their selectivity that still enable them to highly achieve. And it is supported by a large body of empirical and theoretical evidence which shows the robustness of the phenomenon across different contexts and time periods. Thus, the thesis is of value to understanding the Asian American experience in the United States. Furthermore, we can reject the genetic hypothesis of Lynn, as Sue and Okazaki have successfully argued. Having said all that, I have formalized the arguments made in this article.
P1: If the unique cultural and socioeconomic resources of Asian American immigrants have allowed them to achieve high levels of success, then hyper-selectivity is true.
P2: Empirical evidence shows that Asian immigrants and their children have achieved high levels of success, outperforming other racial and ethnic groups in the US in education and income.
C: Thus, the hyper-selectivity thesis is true.
P1: If Asian American immigrants possess unique cultural and socioeconomic resources which allow them to receive high levels of success, then hyper-selectivity is true.
P2: If Asian American immigrants have achieved high levels of success in the US, then they possess unique cultural and socioeconomic resources.
C: Thus, if Asian American immigrants have high levels of success in the US, then hyper-selectivity is true.
Now let me connect these two arguments:
P1: If hyper-selectivity is true, then the academic achievements of Asian Americans is not due solely to socioeconomic Status.
P2: If the academic achievements of Asian Americans isn’t solely due to socioeconomic status, then the achievement gap between groups cannot be fully explained by socioeconomic status (but it can be explained by effort, not cognitive ability).
P3: Hyper-selectivity is true (see arguments above).
C: Thus the achievement gap between Asians and other races cannot be fully explained by socioeconomic status (1, 2, and 3)
P4: (Using addition) Overwhelming evidence shows that Asian Americans outperform other races in America, regardless of socioeconomic status.
C2: So hyper-selectivity remains the best explanation of Asian American academic success, despite critics who state it’s solely due to socioeconomic status (2, 3, and 4 using addition).
Steatopygia is an extreme accumulatation of large amounts of fat on the buttocks, and is also known as obesity in the coccyx (Wallner et al, 2022). “Steato” means “fat” and “pygia” means “buttocks” in Greek. This body type is claimed to be “common in women of the Khoi tribe or ‘Hottentots’ and is considered an aspect of beauty” (Todd, 2010). Steve Sabol, writing for The Genetic Literacy Project, opines that steatopygia could be “the ancestral state of the human lineage.” Steatopygia in the Khoisan has been written about since around the 1600s. This trait has been linked with primitiveness, since it was first noted in the Khoisan (Hudson et al, 2008; Fox, 2020: 16) and has also been observed in the San, the pygmies of Central Africa and the Ong of the Andaman Islands (Shepherd, 2017). Shattock (1909) also notes steatopygous artworks throughout antiquity. Francis Galton noted that while he was too ashamed to ask a Khoisan woman to measure her, he stood back with a pocket ruler and calculated the width and breadth of her buttocks (Hudson, 2004: 326) A few hypotheses have been proposed to explain why Khoisan women are more likely to have this condition, which will be reviewed below.
Perhaps the most famous woman to be afflicted with this condition is Sarah Baartman. Though the date of her birth is contested, she was probably born between the 1770s and 1789. She lived on a farm which belonged to South African colonialist David Fourie, who had settled the land that Baartman’s family lived on. Then, after his death, her clan was broken up and sold to various different people. One free black man took possession of Sarah, and due to his massive debt, began showing off Sarah’s enlarged buttocks which was due to steatopygia, showing her off to British soldiers. She was an exotic dancer for soldiers who were in the infirmary, while men would be able to touch her and even have sex with her if they paid. Then in 1810 she set sail for England with the freed black that bought her and a Scottish physician who thought that she would be better off than being a sideshow for mere soldiers on their deathbed. Racial theories at the time linked fatness to blackness and thinness to whiteness. In fact, fatness as pertains to black bodies had not been seen as anything bad until the Enlightenment, since fatter bodies used to be seen as beautiful to Europeans of that time. This then changed when fatness was linked to racial inferiority. Fatness was a negative racial trait first, before it was medically linked with negative outcomes (Lyons and Lyons, 2004: 31-33; Strings, 2019: 86-87, 94; Stahl, 2018; Nanda, 2019; see Carlan, 2020, Jennings, 2020, Sturgis, 2020, and Davis, 2021 for reviews). After Baartman’s death, her body was kept on display at the French Natural History Museum before being repatriated back to her home of South Africa in 2002. Indeed, Khoisan skeletal remains were seen as valuable due to their steatopygia (Botha and Steyn, 2016).
fat phobia is not based on health concerns. What I found in my research is that in the West, it’s actually rooted in the trans-Atlantic slave trade and Protestantism. In the trans-Atlantic slave trade, colonists and race scientists suggested that black people were sensuous and thus prone to sexual and oral excesses. Protestantism encouraged temperance in all pleasures, including those of the palate. By the early 19th century, particularly in the U.S., fatness was deemed evidence of immorality and racial inferiority.
De Villiers (1961) states that the Bushman’s lumbar curve is flatter than other races, and that since they have lower levels of subcutaneous fat, their steatopygia is more pronounced. She notes a small correlation between “butterfly labia” and steatopygia, with an r of .3223. She also states that there is no evidence that the large labia in Khoi women are artificial (I take this to mean that they weren’t stretched), but we now know this is not the case. She ascertained the degree of steatopygia by measuring “the horizontal distance between the apex of the lumbar curvature and a vertical plane touching the most posteriorly projecting point of the buttocks” (de Villiers, 1961: 226) So she noted a 3 to 4.5 inch distance in adults before middle age.
Steatopygia is claimed to be adaptive in warmer climates, or as an adaptation to food stress (Tobias, 1961 and also see Tobias’ discussion with Boyd and Richerson, 1996; see Hudson et al, 2008 for work on steatopygia figurines from the Jomon period in Japan, and they argue that it was adaptive due to food shortages, just like Tobias). Tobias (1961) notes that steatopygia has been observed in Bushwomen throughout Africa, though it can’t be seen as an adaptation to water storage but it could have been an adaptation for fat and protein storage. It has even been claimed—on the basis of one picture of an Andamanese woman with steatopygia—that it was helped them carry their children and that the fat reserves allowed women to carry more body fat for times of famine. This is how ridiculous adaptationist claims are. Tobias (1971: 147) proposed that steatopygia was due to the effects of cultural and natural selection:
The stronger the cultural pressures, the more drastic would be the cultural selection of certain qualities deemed desirable.
But there is no evidence for this hypothesis (Montagu, 1966) (nevermind novel evidence). Froment (2001) states that steatopygia could be a genetic adaptation to food storage.
Even as early as 1919 it was stated that:
Evidence is not presented to show that peoples in which steatopygia is common (it appears to be nowhere universal) are any more able than others to withstand famine, or that among the Hottentots the women on the whole suffer less than the men during scarcity of food. On the other hand it is well known that races in which this character does not occur have accustomed themselves to unfavorable food conditions. (Miller, 1919: 201)
steatopygia is principally an adaptation to the unique habitat in which the Bushman has evolved, a habitat of great heat and aridity necessitating an adaptive reduction in general body fat in order to permit rapid heat loss, while maintaining a sufficient amount of fat for normal metabolic purposes, especially in an environment which may grow very cold at night. Hence, the reduction of general body fat and its relegation to an unobtrusive part of the body, where it serves as a depot for general utilization by the body.
The claim that steatopygia is adaptive could be seen as basically what is known as the “thrifty gene hypothesis”. The hypothesis states that fat storage was positively selected for in hunter-gatherer populations (Sugden et al, 2018)—this is also similar to the nutritional reserve hypothesis (Low, 1987). Even John Baker in his book Race (Baker, 1971:318) states that it is improbable that the large buttocks of these women is due to a kind of storage for famine, since they most likely did not evolve in the area.
An entailment of the hypothesis could be that men found steatopygous women attractive, and since the fat stores conferred a survival advantage, and since men liked it, then it continued to be passed on. The observations of the hump of a camel and excess fat in the ass of a desert sheep is said to be analogous to steatopygia in Khoisan women (Findlay, 1959). But Tobias (1961: 34) explicitly rejects this notion, stating that it’s an adaptation due to a hunter-gatherer economy, and that the fat stores are for fats and protein, also claiming that sexual and cultural selection worked with natural selection to enhance these features. Krut and Singer (1963: 181) also state that “there is no preference on the part of the males for steatopygous women.”
Basically the hypothesis is that fat storage is a vertebrate adaptation in response to times of famine and low food storage and so, since it was an adaptive trait and seen as beautiful, it continued to be preserved in certain lineages. It is even estimated that H. erectus had 66% higher daily energy needs than austrolopithecene with it being almost 100% higher in lactating erectus compared to austrolopithecene. Then the higher demand for energy could have led to higher fat storages, which could then explain the incidence of steatopygia in Khoisan women (Kuipers et al, 2012).
In Race Differences in Intelligence, Lynn (2006: 50) also repeats the famine hypothesis, while also stating:
The genitalia of the Bushmen are unique among the human races. Bushmen have penises that stick out horizontally, while Bushwomen have prominent minor labia that descend about 3 inches below the vagina. The adaptive advantages of these characteristics are unknown.
“Penises that stick out horizontally” may mean “semi-erect penises”, but I cannot find any reliable source of information for this claim. While there was an older comparison between bonobos, apes, and Bushmen comparing their “semi-erect penises” (Gordon, 1998: 41), this seems to me to be nothing more than a racist conjecture in an attempt to paint Africans as “closer to apes”, so of course Lynn repeated it. It was also claimed that as a Bushman become more admixed, they would then begin to have a “droopier penis”, and so one could ascertain a Bushman’s admixture on the basis of his “droopier penis” (Gordon, 1998: 38). Nevermind this panglossian claim from Lynn that the “adaptive advantages” for the traits are unknown, as if every trait needs to have an adaptive reason that it still exists today. The semi-erect penis claim, it seems, is merely an old, repeated claim with no evidentiary basis.
There is also the “Hottentot apron” (also known as the tablier; de Villiers, 1961) which is an elongation of the labia. This was noted in medical textbooks, but describing Khoi women was removed in subsequent editions (Hayes and Temple-Smith, 2022). The black body has clearly been fetishized (Villani, 2022). In any case, the labia minora is stretched by some African people, and has been seen to be stretched up to 20cm, with this being known as type 4 genital mutilation (Puppo, 2010; also see Koster and Price, 2008). It has even been argued that “contemporary cosmetic labiaplasty is highly invested in a colonial sexual imaginary, by which the aesthetic valuation of the labia is linked to the construction and maintenance of racial hierarchies” (Nurka, 2018; James, 2021).
So paranoid and yet fascinated were many white males with the notion of the stallion-like sexual performance of black males that at the turn of the twentieth century, it was not uncommon for those white southerners who lynched black males to mutilate their poor victims’ genitals and castrate them as well. David M. Friedman, in A Mind of Its Own: A Cultural History of the Penis, documents not merely the Western obsession with the black man’s penis but also the macabre lengths to which such fear and envy can go. He identified ritual castration as the final act of the lynch mob, explaining: “To really kill a black man, you first had to kill his penis.”6 Friedman devoted an entire chapter in his book to the ways in which white fears of sexual competition with black males had translated into a strange but enduring fetishism about the black male organ. (Hilliard, 2012: 72)
The racist hyper-sexualization of black women and men has its roots in colonialism (Holmes, 2016), and black women are dehumanized and hyper-sexualized more than white women, being compared more to objects and animals (Anderson et al, 2018). Basically, black women are objectified more than white women are.
Conclusion
Claims that any trait T are adaptive are merely just-so stories. That is, they are merely ad hoc hypotheses and no novel evidence can be provided in support for the hypothesis that would raise the probability of the trait being an adaptation. It is not confirmation of a hypothesis that a trait merely exists, since the hypothesis attempts to explain why the trait exists in the first place. Gould and Lewontin (1979) warned about assuming that traits are adaptations, and even said that once one adaptive story has been shown to be false that they would then erect another story in an attempt to show that the trait is an adaptation without ever contemplating that the trait is not an adaptation.
So Lynn’s wondering of the adaptive reasons of Khoisan steatopygia, “horizontal penises”, and enlarged labia are merely nothing more than the thoughts of a panglossian. “The trait exists so it MUST have an adaptive function.” And while there are a few different adaptive hypotheses for steatopygia, there is no way to distinguish it from being an adaptation or a byproduct. That is, a byproduct hypothesis would be just as valid as an adaptation hypothesis, due to the linkage of traits. But we need independent evidence in order to be justified in believing that T is an adaptation. That is, we need a novel fact of the matter that was unknown before the formation of the hypothesis. And if there is no novel fact, then the hypothesis is a just-so story. It’s merely circular reasoning. In fact, Lynn’s and Rushton’s obsession with penis size is merely due to their obsession with proving—whether they deny it or not—racial superiority and inferiority.
PumpkinPerson, using his long-outdated belief that evolution is progressive using evolutionary trees, claims—using a Y-chromosome tree—that the Bushman are at the bottom of the tree and “are believed to have absolutely colossal sexual characteristics” which is “consistent with Rushton’s theory that less advanced populations are more r selected.” “Rushton’s theory” meaning the long-dead Differential-K theory also known as r/K selection theory. PP here is just repeating the claim that these traits are “primitive”, since they are “older” and the traits are presumably not seen in “younger” populations, and is like the claim cited above from Sabol where he states that steatopygia is an ancestral state of the human lineage. The claim is, of course, ridiculous.
The fact of the matter is, there is no good evidence (by “good evidence” I mean independent evidence) that steatopygia is an adaptation, along with the other supposed adaptationist claims from the last 100 or so years. One can think of a multitude of different stories that explain the evolution of one single trait, but that isn’t good enough, as can be seen. Independent, novek evidence, is needed to raise the probability of the state of affairs being true, and I’m at a loss of thinking of any kind of novek facts generated from any of the steatopygia-as-adaptation hypothesis. These hypotheses were formulated due to the sexualization of Africans, which has of course continued to today with the claims of Rushton, Lynn, Kanazawa, Hart, and Templer. However, their just-so stories—along with the ones about sexual characteristics having an adaptive function—hold no water.
It is claimed that genes (DNA sequences) have a special, privileged role in the development of all traits. But once we understand what genes do and their role in development, then we will understand that the role ascribed to genes by gene-selectionists and hereditarians outright fails. Indeed, the whole “nature vs nurture” debate implies that genes determine traits and that it’s possible to partition the relative contributions to traits in a genetic and environmental way. This, however, is far from reality (like heritability estimates).
DST isn’t a traditional scientific theory—it is more a theoretical perspective on developmental biology, heredity, and evolution, though it does make some general predictions (Griffiths and Hochman, 2015). But aspects of it have been used to generate novel predictions in accordance with the extended evolutionary synthesis (Laland et al, 2015).
Development is a process of multiple interacting sources.
Context sensitivity and contingency
Development depends on the current state of the organism.
Extended inheritance
An organism inherits resources from the environment in addition to genes.
Development as a process of construction
The organism helps shape its own environment, such as the way a beaver builds a dam to raise the water level to build a lodge.
Distributed control
Idea that no single source of influence has central control over an organism’s development.
Evolution as construction
The evolution of an entire developmental system, including whole ecosystems of which organisms are parts, not just the changes of a particular being or population.
Genes (DNA sequences) as resources and outcomes
Hereditarians have a reductionist view of genes and what they do. Genes, to the hereditarian, are causes of not only development but of traits and evolution, too. However the hereditarian is sorely mistaken—there is no a priori justification for treating genes as privileged causes over and above other developmental resources (Noble, 2012). I take Noble’s argument there to mean that strong causal parity is true—where causal parity means that all developmental resources are on par with each other, with no other resource having primacy over another. They all need to “dance in tune” with the “music of life” to produce the phenotype, to borrow Noble’s (2006, 2017) analogy. Hereditarian dogma also has its basis in the neo-Darwinian Modern Synthesis. The modern synthesis has gotten causality in biology wrong. Genes are, simply put, passive, not active, causes:
Genes, as DNA sequences, do not of course form selves in any ordinary sense. The DNA molecule on its own does absolutely nothing since it reacts biochemically only to triggering signals. It cannot even initiate its own transcription or replication. … It would therefore be more correct to say that genes are not active causes; they are, rather, caused to give their information by and to the system that activates them. The only kind of causation that can be attributed to them is passive, much in the way a computer program reads and uses databases. (Noble, 2011)
These ideas, of course, are also against the claim that genes are blueprints or recipes, as Plomin (2018) claims in his most recent book (Joseph, 2022). This implies that they are context-independent; we have known for years that genes are massively context-sensitive. The line of argument that hereditarians push is that genes are context-insensitive, that is they’re context-independent. But since DNA is but one of the developmental resources the physiological system uses to create the phenotype, this claim fails. Genes are not causes on their own.
Behavioral geneticist and evolutionary psychologist J. P. Rushton (1997: 64) claims that a study shows that “genes are like blueprints or recipes providing a template for propelling development forward to some targeted endpoint.” That is, Rushton is saying that there is context-independent “information” in genes, and that genes, in essence, guide development toward a targeted endpoint. Noah Carl (2019) claims that the hereditarian hypothesis “states that these differences [in cognitive ability] are partly or substantially explained by genetics.” When he says the differences are “partly or substantially explained by genetics”, he’s talking about “cognitive ability” being caused by genes. The claim that genes cause (either partly or substantially) cognitive ability—and all traits, for that matter—fails and it fails since genes don’t do what hereditarians think they do. (Nevermind the conceptual reasons.) These claims are laughable, due to what Noble, Oyama, Moore and Jablonka and Lamb have argued. It is outright false that genes are like blueprints or recipes. Rushton’s is reductionist in a sociobiology-type way, while Plomin’s is reductionist in a behavioral genetic type way.
In The Dependent Gene, David Moore (2002: 81) talks about the context-dependency of genes:
Such contextual dependence renders untenable the simplistic belief that there are coherent, long-lived entities called “genes” that dictate instructions to cellular machinery that merely constructs the body accordingly. The common belief that genes contain context-independent “information”—and so are analogous to “blueprints” or “recipes”—is simply false.
Genes are always expressed in context and cannot be divorced from said context, like hereditarians attempt using heritability analyses. Phenotypes aren’t “in the genes”, they aren’t innate. They develop through the lifespan (Blumberg, 2018).
Causal parity and hereditarianism
Hereditarianism can be said to be a form of genetic reductionism (and mind-brain identity). The main idea of reductionism is to reduce the whole to the sum of its parts and then analyze those parts. Humans (the whole) are made up of genes (the parts), so to understand human behavior, and humans as a whole, we must then understand genes, so the story goes.
Cofnas (2020) makes several claims regarding the hereditarian hypothesis and genes:
But if we find that many of the same SNPs predict intelligence in different racial groups, a risky prediction made by the hereditarian hypothesis will have passed a crucial test.
…
But if work on the genetics and neuroscience of intelligence becomes sufficiently advanced, it may soon become possible to give a convincing causal account of how specific SNPs affect brain structures that underlie intelligence (Haier, 2017). If we can give a biological account of how genes with different distributions lead to race differences, this would essentially constitute proof of hereditarianism. As of now, there is nothing that would indicate that it is particularly unlikely that race differences will turn out to have a substantial genetic component. If this possibility cannot be ruled out scientifically, we must face the ethical question of whether we ought to pursue the truth, whatever it may be.
Haier is a reductionist of not only the gene variety but the neuro variety—he attempts to reduce “intelligence” to genes and neurology (brain physiology). I have though strongly criticized the use of fMRI neuroimaging studies regarding IQ; cognitive localizations in the brain are untenable (Uttal, 2001, 2011) and this is because mind-brain identity is false.
Cofnas asks “How can we disentangle the effects of genes and environment?” and states the the behavioral geneticist has two ways—correlations between twins and adoptees and GWAS. Unfortunately for Cofnas, twin and adoption studies show no such thing (see Ho, 2013), most importantly because the EEA is false (Joseph, 2022a, b). GWAS studies are also fatally confounded (Janssens and Joyner, 2019) and PGS doesn’t show what behavioral geneticists need it to show (Richardson, 2017, 2022). The concept of “heritability” is also a bunk notion (Moore and Shenk, 2016). (Also see below for further discussion on heritability.) At the end of the day, we can’t do what the hereditarian needs to be done for their explanations to hold any water. And this is even before we look at the causal parity between genes and other developmental resources. Quite obviously, the hereditarian hypothesis is a gene-centered view, and it is of course a reductionist view. And since it is a reductionist, gene-centered view, it is then false.
Genetic, epigenetic, and environmental factors operate as a system to form the phenotype. Since this is true, therefore, both genetic and epigenetic determinism is false (also see Wagoner and Uller, 2015). It’s false because the genes one is born with, or develops with, don’t dictate or determine anything, especially not academic achievement as hereditarian gene-hunters would so gleefully claim. And one’s early experience need not dictate an expected outcome, since development is a continuous process. Although, that does not mean that environmental maladies that one experiences during childhood won’t have lasting effects into adulthood due to possibly affecting their psychology, anatomy or physiology.
The genome is responsive, that is, it is inert before it is activated by the physiological system. When we put DNA in a petri dish, it does nothing. It does nothing because DNA cannot be said to be a separate replicator from the cell (Noble, 2018). So genes don’t do anything independent of the context they’re in; they do what they do DUE TO the context they’re in. This is like Gottlieb’s (2007)probabilistic epigenesis, where the development of an organism is due to the coaction of irreducible bidirectional biological and environmental influences. David S. Moore, in The Developing Genome: An Introduction to Behavioral Epigenetics states this succinctly:
Genes—that is, DNA segments—are always influenced by their contexts, so there is never a perfect relationship between the presence of a gene and the ultimate appearance of a phenotype. Genes do not determine who we become, because nongenetic factors play critical roles in trait development; genes do what they do at least in part because of their contexts.
What he means by “critical roles in trait development” is clear if one understands Developmental Systems Theory (DST). DST was formulated by Susan Oyama (1985) in her landmark book “The Ontogeny of Information. In the book, she argues that nature and nurture are not antagonistic to each other, they are cooperative in shaping the development of organisms. Genes do not play a unique informational role in development. Thus, nature vs. nurture is a false dichotomy—it’s nature interacting with nurture, or GxE. This interactionism between nature and nurture—genes and environment—is a direct refutation of hereditarianism. What matters is context, and the context is never independent from what is going on during development. Genes aren’t the units of selection, the developmental system is, as Oyama explains in Evolution’s Eye:
If one must have a “unit” of evolution, it would be the interactive developmental system: life cycles of organisms in their niches. Evolution would then be change in the constitution and distribution of these systems (Oyama, 2000b)
Genes are important, of course, for the construction of the organism—but so are other resources. Without genes, there would be nothing for the cell to read to initiate transcription. However, without the cellular environment, we wouldn’t have DNA. Lewontin puts this wonderfully in the introduction to the 2000 edition of Ontogeny:
There are no “gene actions” outside environments, and no “environmental actions” can occur in the absence of genes. The very status of environment as a contributing cause to the nature of an organism depends on the existence of a developing organism. Without organisms there may be a physical world, but there are no environments. In like manner no organisms exist in the abstract without environments, although there may be naked DNA molecules lying in the dust. Organisms are the nexus of external circumstances and DNA molecules that make these physical circumstances into causes of development in the first place. They become causes only at their nexus, and they cannot exist as causes except in their simultaneous action. That is the essence of Oyama’s claim that information comes into existence only in the process of Ontogeny. (2000, 15-16)
Genes aren’t causes on their own, they are resources for development. And being resources for development, they have no privileged level of causation over other developmental resources, such as “methylation patterns, membrane templates, cytoplasmic gradients, centrioles, nests, parental care, habitats, and cultures” (Griffiths and Stotz, 2018). All of these things, and more of course, need to work in concert with each other.
Indeed, this is the causal parity argument—the claim that genes aren’t special developmental resources, that they are “on par” with other developmental resources (Griffiths and Gray, 1994; Griffiths and Stotz, 2018). Gene knockout studies show that the loss of a gene can be compensated by other genes—which is known as “genetic compensation.” None of the developmental resources play a more determinative role than other resources (Noble, 2012; Gamma and Liebrenz, 2019). This causal parity, then, has implications for thinking about trait ontogeny.
The causal parity of genes and other developmental factors also implies that genes cannot constitute sufficient causal routes to traits, let alone provide complete explanations of traits. Full-blown explanations will integrate various kinds of causes across different levels of organizational hierarchy, and across the divide between the internal and the external. The impossibly broad categories of nature vs. nurture that captured the imagination of our intellectual ancestors a century ago are no longer fit for the science of today. (Gamma and Liebrenz, 2019)
Oyama (2000a 40) articulates the casual parity thesis like this:
What I am arguing for here is a view of causality that gives formative weight to all operative influences, since none is alone sufficient for the phenomenon or for any of its properties, and since variation in any or many of them may or may not bring about variation in the result, depending on the configuration of the whole.
The ‘parity thesis’ is the claim that if some role is alleged to be unique to nucleic acids and to justify relegating nongenetic factors to a secondary role in explaining development, it will turn out on closer examination that this role is not unique to nucleic acids, but can be played by other factors.
Genes are necessary pre-conditions for trait development, just as the other developmental resources are necessary pre-conditions for trait development. No humans without genes—this means that genes are necessary pre-conditions. If genes then humans—this implies that genes are sufficient for human life, but they are but one part of what makes humans human, when all of the interactants are present, then the phenotype can be constructed. So all of the developmental resources interacting are sufficient.
The nature vs. nurture dichotomy can be construed in such a way that they are competing explanations. However, we now know that the dichotomy is a false one and that the third way—interactionism—is how we should understand development. Despite hereditarian protestations, DST/interactionism refutes their claims. The “information” in the genes, then, cannot explain how organisms are made, since information is constructed dialectically between the resources and the system. There are a multiplicity of causal factors that are involved in this process, and genes can’t be privileged in this process. Thus the phrase “genetic causation” isn’t a coherent concept. Moreover, DNA sequences aren’t even coherent outside of cellular context (Noble, 2008).
In The Ontogeny of Information Oyama pioneered the parity argument, or the ‘parity thesis’, concerning genetic and environmental causes in development (see also Griffiths and Gray 1994; Griffiths and Gray 2005; Griffiths and Knight 1998; Stotz 2006; Stotz and Allen 2012). Oyama relentlessly tracked down failures of parity of reasoning in earlier theorists. The same feature is accorded great significance when a gene exhibits it, only to be ignored when a non-genetic factor exhibits it. When a feature thought to explain the unique importance of genetic causes in development is found to be more widely distributed across developmental causes, it is discarded and another feature is substituted. Griffiths and Gray (1994) argued in this spirit against the idea that genes are the sole or even the main source of information in development. Other ideas associated with ‘parity’ are that the study of development does not turn on a single distinction between two classes of developmental resources, and that the distinctions useful for understanding development do not all map neatly onto the distinction between genetic and non-genetic.
Shea (2011) tries to argue that genes do have a special role, and that is to transport information. Genes are, of course, inherited, but so is every other part of the system (resources). Claiming that there is information “in the genes” is tantamount to saying that there is a special role for DNA in development. But, as I hope will be clear, this claim fails due to the nature of DNA and its role in development.
This line of argument leads to one clear conclusion—genes are followers, they are not leaders; most evolution begins with environmentally-mediated phenotypic change, and then genetic changes occur (West-Eberhard, 2003). Ho and Saunders (1979) state that variation in organisms is constructed during development due to an interaction between genetic and non-genetic factors. That is, they follow what is needed to do by the developmental system, they aren’t leading development, they are but one party in the whole symphony of development. Development can be said to be irreducible, so we cannot reduce development to genes or anything else, as all interactants need to be present for development to be carried out. Since genes are activated by other factors, it is incoherent to talk of “genetic causes.” Genes affect the phenotype only when they are expressed, and other resources, too, affect the phenotype this is, ultimately, an argument genes against as blueprints, codes, recipes, or any other kind of flowery language one can used to impute what amounts to intention to inert DNA.
Even though epigenetics invalidates all genetic reductionism (Lerner and Overton, 2017), genetic reductionist ideas still persist. They give three reasons why genetic reductionist ideas still persist despite the conceptual, methodological, and empirical refutations. (1) Use of terms like “mechanism”, “trait”, and “interaction”; (2) constantly shifting to other genes once their purported “genes for” traits didn’t workout; and (3) they “buried opponents under repetitive results” (Panofsky, quoted in Lerner and Overton, 2017). The fact of the matter is, there are so many lines of evidence and argument that refute hereditarian claims that it is clear the only reason why one would still be a hereditarian in this day and age is that they’re ignorant—that is racist.
Genes, that is, are servants, not masters, of the development of form and individual differences. Genes do serve as templates for proteins: but not under their own direction. And, as entirely passive strings of chemicals, it is logically impossible for them to initiate and steer development in any sense. (Richardson, 2016)
DST and hereditarian behavioral genetics
I would say that DST challenges three claims from hereditarian behavioral genetics (HBG hereafter):
(1) The claim that we can neatly apportion genes and environment into different causes for the ontogeny of traits;
(2) Genes are the only thing that are inherited and that genes are the unit of selection and a unique—that is, special and privileged cause over and above other resources;
(3) That genes vs environment, blank skate vs human nature, are a valid dichotomy.
(1) HBG needs to rely on the attempting to portion out causes of traits into gene and environmental causes. The heritability statistic presumes additivity, thy is, it assumes no interaction. This is patently false. Charney (2016) gives the example of schizophrenia—it is claimed that 50 percent of the heritability of schizophrenia is accounted for by 8000 genes, which means that each SNP accounts for 1/8000 of the half of the heritability. This claim is clearly false, as genetics aren’t additive, and the additivity assumption precludes the interaction of genes with genes, and environment, which create new interactive environments. Biological systems are not additive, they’re interactive. Heritability estimates, therefore, are attempts at dichotomizing what is not dichitomizable (Rose, 2005).
An approach that partitions variance into independent main effects will never resolve the debate because, by definition, it has no choice but to perpetuate it. (Goldhaber, 2012)
This approach, of course, is the approach that attempts to partition variance into G and E components. The assumption is that G and E are additive. But as DST theorists have argued for almost 40 years, they are not additive, they are interactive and so not additive, therefore heritability estimates fail on conceptual grounds (as well as many others). Heritability estimates have been—and continue to today—been at the heart of the continuance of the nature vs nurture distinction, the battle, if you will. But if we accept Oyama’s causal parity argument—and due to the reality of how genes work in the system, I see no reason why we shouldn’t—then we should reject hereditarianism. Hereditarians have no choice but to continue the false dichotomy of nature vs nurture. Their “field” depends on it. But despite the fact that the main tool for the behavioral geneticist lies on false pretenses (twin and adoption studies), they still try to show that heritability estimates are valid in explaining trait variation (Segalowitz, 1999; Taylor, 2006, 2010).
(2) More than genes are inherited. Jablonka and Lamb (2005) argue that there are four dimensions—interactants—to evolution: genetic, epigenetic, behavioral, and symbolic. They show the context-dependency of the genome, meaning that genotype does not determine phenotype. What does determine the phenotype, as can be seen from the discussion here, is the interacting of developmental resources in development. Clearly, there are many other inheritance systems other than genes. There is also the fact that the gene as popularly conceived does not exist—so it should be the end of the gene as we know it.
(3) Lastly, DST throws out the false dichotomy of genes and environment, nature and nurture. DST—in all of its forms—rejects the outright false dichotomy of nature vs nurture. They are not in a battle with each other, attempting to decide who is to be the determining factor in trait ontogeny. They interact, and this interaction is irreducible. So we can’t reduce development to genes or environment (Moore, 2016) Development isn’t predetermined, it’s probabilistic. The stability of phenotypic form isn’t found in the genes (Moore and Lickliter, 2023)
Conclusion
Genes are outcomes, not causes, of evolution and they are not causes of trait ontogeny on their own. The reality is that strong causal parity is true, so genes cannot be regarded as a special developmental resource from other resources—that is, genes are not privileged resources. Since they are not privileged resources, we need to, then, dispense with any and all concepts of development that champion genes as being the leader of the developmental process. The system is, not genes, with genes being but one of many of the interactants that shape phenotypic development.
By relying on the false narrative that genes are causes and that they cause not only our traits but our psychological traits and what we deem “good” and “bad”, we would then be trading social justice for hereditarianism (genetic reductionism).
These recommended uses of bad science reinforce fears of institutionalized racism in America and further the societal marginalization of minority groups; these implications of their recommendations are never publicly considered by those who promulgate these flawed extensions of counterfactual genetic reductionism. (Lerner, 2021)
Such [disastrous societal] applications can only rob people of life chances and destroy social justice. Because developmental science has the knowledge base to change the life course trajectories of people who are often the targets of genetic reductionist ideas, all that remains to eradicate genetic reductionism from scientific discussion is to have sufficient numbers of developmental scientists willing to proclaim loudly and convincingly that the naked truth is that the “emperor” (of genetic reductionism) has no clothes. (Lerner, 2021: 338)
Clearly, hereditarians need the nature vs nurture debate to continue so they can push their misunderstandings about genes ans psychology. However, given our richer understanding of genes and how they work, we now know that hereditarianism is untenable, and DST conceptions of the gene and development as a whole have led us to that conclusion. Lerner (2017) stated that as soon as the failure of one version of genetic reductionism is observed, another one pious up—making it like a game of whack-a-mole.
The cure to hereditarian genetic reductionism is a relational developmental systems (RDS) model. This model has its origins with Uri Bronfenbrenner’s ecological systems theory (Bronfenbrenner and Ceci, 1994; Ceci, 1996; Patel, 2011; Rosa and Tudge, 2013. Development is about the interacting and relation between the individual and environment, and this is where RDS theory comes in. Biology, physiology, culture, and history are studied to explain human development (Lerner, 2021). Hereditarian ideas cannot give us anything like what models derived from developmental systems ideas can. An organism-environment view can lead to a more fruitful, and the organism and environment are inseparable (Jarvilehto, 1998; Griffiths and Gray, 2002). And it is for these reasons, including many, many more, that hereditarian genetic reductionist ideas should become mere sand in the wind.
Having said all that, here’s the argument:
P1: If hereditarianism is true, then strong causal parity is false.
Science is concerned with studying physical processes and phenomena. So anything that isn’t physical (like the mind/consciousness) can’t studied by science. I have made manysound arguments for this conclusion. However, we can go deeper. Here is the argument:
(1) Mind is first-personal and subjective.
(2) But science is third-personal and objective.
So (3) it follows that science (a third-personal objective endeavor) can’t study mind (first-personal subjective states).
I will defend these both premises and the conclusion in this article.
Defending the premises
Premise (1) The existence of a first-person perspective (FPP) is necessary and sufficient for consciousness. It is this first-person perspective that we are experiencing, as I write this article and as you read it. A first-person view is subjective experience. Each human has their own special access to their own minds that is “private.” By “private”, I mean it is only accessible to them, the agent, and not accessible to anyone else. If it’s not accessible to anyone else, and another observer would be a third-person observer, then it isn’t accessible by the methods of science. Further, the pronoun “I” denotes an FPP. When we refer to ourselves, we say “I.” “I did that.” “I will do that.” “I have done that.” All of these considerations point to one thing: Consciousness is a subjective state in which agents experience sensations and feelings, and the world around them.
The FPP is the first person perspective of “I”—and by that I mean the experience that we all have every day of our lives. It’s how we ourselves experience the world around us. By “subjective” I mean simply that which belongs to the thinking subject. Subjective states can be said to be intentional states. Intentional states are normative and so irreducible to the physical. So subjective knowledge is—private—knowledge of one’s first-personal states, their beliefs, goals, and desires.
Premise (2) When I say “Science is third-personal”, I mean that there is an observer—on the outside, deliberating on things, viewing things. They are using their first-personal subjective experience to do science, which is in the third person. The mind, apparently, is just the electro-chemistry of the brain—basically the mind is what the brain does. However, mind isn’t identical to brain. Yes, scientists can study the brain since it is made up of physical parts, and neurophysiologists can study the states of the brain. Of course we use our first-personal subjective states to scientifically study what is third-personal. But this need not license the conclusion that since we can study the brain using neuroscience then we can study the mind using neuroscience since M and P are not identical. M is subjective, while P is objective. Lavazza and Robinson (2014) explain this perfectly:
Another set of arguments that present an apparently unanswerable objection to a materialist view is grounded in the fact that every item in an entirely material world would admit of third-person description. Every item would be accessible to the third-person viewpoint and would be amenable to description based on what is revealed to that viewpoint. The problem for the materialist view is that any such description will fail to capture what is accessible only to a first-person viewpoint and thus necessarily will omit the very centre of a person’s world; more specifically, it will omit the self, understood as the subject of conscious states as well as much of the intentional content of those states. As David Lund maintains, third-person information about oneself (knowledge of oneself by description) seems indeed to be neither necessary nor sufficient for consciousness of oneself. It is not sufficient, for (in first-person terms) I would be unable to see that the third-person information is information about me unless I were already aware of myself in a first-person way. But in the materialist view, it would have to be sufficient.
Conclusion I have successfully defended both premises, and so the conclusion that science (third-personal) cannot study mind (first-personal) follows. Of course there is the field of neuroscience where we study the brain’s physiology. Neuroscience contains 2 assumptions—(1) that the mind is physical; and (2) that the brain (or some aspect of the CNS) is sufficient for the mind, that is, we are our brains. The goal, then, is to attempt to discover the sufficient conditions of consciousness; basically the brain produces the mind and there are parts of the mind which are reducible to or identical to parts of the brain. The physical enables conscious experience—that is, it is a dependency condition. But dependency conditions are not sufficient conditions. The ultimate claim, then, is that phenomenal experience is identical to, reducible to, or sufficient from neural activity. Neuroscience neither has the skills nor methods to study the mind—being a science and third-personal, it can only study the physical and so it studies the brain, and the CNS, not the mind. There are organs that have specific processes that we can study, like the stomach and digestion, or the lung and breathing, or the heart and blood circulation. So then it would follow that we study the brain for mind, as neuroscientists assume. But the claim clearly fails (Manzotti and Moderato, 2014).
Francis Crick—one of the discoverers of DNA along with James Watson and Rosalind Franklin— in his book The Astonishing Hypothesis said that humans are
“Just a bunch of neurons…You, your joys, and your sorrows, your memories and your ambitions, your sense of personal identity and free will, are in fact no more than the behaviour of a vast assembly of nerve cells and their associated molecules.”
Of course neurons and everything else that makes up the brain is necessary for the mind but necessariness isn’t sufficientness and it definitely isn’t identity, so Crick’s claim is false.
Richard Dawkins in 1976 argued that humans are mere gene-machines, that is, humans exist merely to propagate selfish genes. But selfishness is a property of organisms (so that’s a mereological fallacy), his idea isn’t even testable by Dawkins’ own admission and DNA can’t be regarded as separate from the cell (Noble, 2011, 2018).
The attempt from Crick to reduce human mental life to mere neurons and by Dawkins to reduce human social life to being for “selfish genes” clearly fail. The most important part, I think, is that they are reductive perspectives, and reductionism is false, so their claims are false. These two claims are attempts at using science to explain the mind and (what appear to be, for Dawkins) intentionality (from his selfish genes), and they obviously fail.
Conclusion
A similar argument is made by Lynne Rudder Baker, where she gives an argument she calls “the master argument”: (1) All phenomena can be explained by science. (2) All science is constructed exclusively from a third-personal view. So (3) All phenomena can be explained with a third-personal view. (Also see Baker, 2007.)
Obviously it’s valid, but is it sound? No, it isn’t, since the first premise is obviously false—mind cannot be explained by a third-personal perspective.
Scientific naturalism is clearly false, since it cannot explain all phenomena like the mind since the mind isn’t physically/ontologically reducible. So, again, as many other arguments have established and entailed, we are not fully physical and, due to this, science can’t explain all aspects of humans. Two substances exist, one first-personal, subjective and private, and the other objective and public. So we should accept that there is an irreducible aspect of human constitution that science simply cannot study, as hard as they try. Thus, the limits of science are clear—Science CANNOT explain everything.
It has been commonly stated in hereditarian circles that by increasing aid to Africa, then we would be merely helping their demographic explosion. In 2020, the average adolescent fertility in Sub-Saharan Africa (SSA) rate was 98 births per 1000 girls. Birthrates in most African countries are very high, and to some, the claim is that if we give aid to these countries then they will continue to have more children as they have the means to do so. Though high birthrates in SSA are “concentrated among vulnerable groups where progress is oftenpoorest” (Neal et al, 2020). This worry however, has no basis in reality. In this article, I will provide a few studies looking at the relationship between economic aid and decreasing birthrates. This, then, refutes the (racist) worries of people like Steve Sailer who warn that by increasing aid to Africa we are then helping their population explosion. However, what is borne out by data in countries where this has occurred, if there are sufficient family planning methods, the birthrate will decrease—not increase—with monetary aid to poor African countries.
What is hunger?
Hunger is a feeling of discomfort or weakness; having a desire or craving for food or having pain that is caused by lack of food. There is malnutrition (a condition caused by a diet that has insufficient nutrients for normal functioning), undernourishment (where the food one does eat does not give enough kcal for normal functioning), and starvation (a state of the body caused by long-term lack of food or nutrients). Hunger is a self-reported notion, and so, we would then need to indirectly measure physical variables that are associated with being well-fed or not. Like measuring one’s blood for the lack of certain nutrients, measuring the foods they do eat and ascertaining the macro-nutrient content of what they eat, measuring their height and weight and comparing it to a representative sample, checking to see if there are micro-nutrient deficiencies (Conway, 2012).
But what causes hunger? Inequality/inequities and poverty cause hunger. Indeed, we have enough food to feed 10 billion people—the world produces enough food to feed 1.5 times the world population, but people making $2 a day cannot afford the food (Holt-Giminez et al, 2012) while 828 million people per day go hungry. About 14 million children suffer from acute malnutrition, 45 percent of child deaths around the world are due to hunger and it’s causes, and 700 children die per day due to dirty water, unhygienic water sources, and hunger. So we DO have the food to feed these people, what they DON’T have is the money to feed themselves and their families due to the pittance wages they receive. The year 2022 has been called “a year of unprecedented hunger” by the World Food Programme.
estimated that between 720 and 811 million people went hungry in 2020. High costs and low affordability also mean billions cannot eat healthily or nutritiously. Considering the middle of the projected range (768 million), 118 million more people were facing hunger in 2020 than in 2019 – or as many as 161 million, considering the upper bound of the range.
In 1974, the Food and Agriculture Organization of the United Nations (FAO) began reporting on the number of people that faced hunger issues. They define hunger as:
an uncomfortable or painful physical sensation caused by insufficient consumption of dietary energy. It becomes chronic when the person does not consume a sufficient amount of calories (dietary energy) on a regular basis to lead a normal, active and healthy life. For decades, FAO has used the Prevalence of Undernourishment indicator to estimate the extent of hunger in the world, thus “hunger” may also be referred to as undernourishment.
Hunger is related to food insecurity, where food insecurity is when one is unable to procure items for nourishment due either to availability or lack of monies to procure foodstuffs that would lead to normal development. The FAO also has a measure of food insecurity prevalence of undernourishment (PoU) along with the prevalence of moderate or severe food insecurity in a population based on the food insecurity experience scale (FIES) which estimates how prevalent food insecurity is in a population down to the household or individual level which is ascertained through interviews with the populace.
Now that I have defined hunger, how we indirectly measure hunger (with its physical correlates) and the troubling future we have with hunger across the world, we can now turn to the claim that aid to poor countries will increase their birthrates. This claim has been made a lot by many different groups, and it certainly is a logical claim to make, but what does the data say in countries where such an intervention did occur? Did their population increase even after aid was given to them? Or did their population decrease as they got aid? The answer to this question will be the answer to the question in Africa as we continue to reach the fabled year of 2050 when their population is expected to reach 5 times its present size by the year 2050 in one 1988 estimate (Yanagishita, 1988) to 4 projections based on different assumptions (Haub, 1997), to certain African countries increasing even past 2100 (Ezeh, Kissling, and Singer, 2020). Africa is quickly urbanizing (Veary et al, 2019), and since urbanization decreases fertility rates (Yi and Vaupel, 1989; White et al, 2008; Martine, Alves, and Cavenaghi, 2013; Lerch, 2019), I would hedge my bet that the population growth in Africa—if ample aid is provided since aid to developing countries decreases, not increases, a country’s population—will be far lower than predicted, nevermind the fact that the assumption would be that the population would increase linearly.
Food security and population growth
In his 2010 book One Billion Hungry: Can We Feed the World?, Gordon Conway (2010) writes about the claim that aid to Africa will increase the African population. He cites a study stating that giving developing populations more food is a self-defeating policy since it will cause their population to increase. He writes:
Nevertheless, the fertility rate decline has not been universal. In many Sub-Saharan countries fertility rate declines have stalled at rates over 5.0 after gradually decreasing for several years.25 The reasons are complex, but a common feature appears to be the decreased funding for family planning programs. According to data from thirty-one countries, on average 30 percent of women in Sub-Saharan Africa have an unmet need for modern family planning methods, a proportion that has not declined in the last decade.26 In nineteen of these countries, it is as high as nearly 50 percent. If fertility were to remain constant at current levels, the population of less-developed regions would increase to 9.8 billion in 2050 instead of the projected 7.9 billion.27
A popular misconception is that providing the developing countries with more food will serve to increase populations; in other words, it is a self-defeating policy.28 The more food women have, the more children they will have and the greater will be their children’s survival, leading to population growth, so goes the argument. However, the experience of the demographic transition described above suggests the opposite. As people become more prosperous, which includes being better fed and having lower child mortality, the fewer children women want. Providing they then have access to family planning methods, the fertility rates will drop and the population will cease to grow.29
In Kenya and Tanzania, fertility has declined for the most educated women and in certain other regions. In Uganda, while fertility levels remain at the pre-transition state, there is a decrease in fertility for specific demographics of women—the most educated and urbanized, along with those in the raster region of the country. In Zimbabwe, though fertility rates continue to fall, it isn’t falling for women with less than a secondary education and in certain regions. This is yet more data that speaks to the claim that as locals urbanize and get more educated, the fertility levels begin to decrease.
Since 30 percent of women in SSA have an unmet need for family planning, by educating them on the need for family planning along with readily accessible contraceptives, ensuring that contraceptives become a permanent part of family planning, and taking action to remove barriers that hinder family planning, we can then help those 30 percent of women plan for families and therefore birth rates will decrease. It is therefore imperative that we roll out programs that would teach people how to plan for families and that would mean educating them on contraceptive use and, as I will explain below, give aid to them, since when people become more prosperous, the birth rate will decrease since they have more children since their death rates are so high.
The authors claim in this paper that experimental and correlational data state that as food production increases, so too will the population that is receiving that food, as they will then be unfettered by the ravenous issues that affect their death rates. They would then be able to have as many children as they want, so the story goes. However, as I will go into below, this is not what we have seen when aid and family planning have been to countries that so sorely needed it.
Foster and Rosenzwieg showed that although female literacy rose to 81 percent in India from 1981-1999, they found no evidence that the increase in female literacy had an effect on decreasing the birthrate in India. The Green Revolution in India led to increased growth and the ability to diversify their occupations. This, in turn, made child-rearing more expensive which then led to a subsequent decrease in the birthrate. Their results do show that the decrease in fertility was driven by an increase in wages for Indian women. They, furthermore, found evidence that health centers (like hospitals) were associated with a decrease in fertility. Foster and Rosenzwieg, thus, “have clearly demonstrated that economic incentives have mattered greatly for the decline in rural fertility in India” (Desai, 2006).
Gertler and Molyneux show that the dramatic decrease in fertility in Indonesia between 1982 to 1987 was due to the increased use in contraceptives along with the increased demand of contraceptives. They found that improvements in women’s education along with an increase in wages for both men and women were responsible for 45 to 60 percent of the decline, and this was driven by contraceptive use. Further, 75 percent of the decline was due to contraceptive use, while 87 percent of the use in contraceptives was due to increased wages and education. They therefore showed that increasing education and wages were responsible for 65 percent of the fertility decline.
Poston and Gu showed that structural development had strong negative effects on fertility, and that family planning has a negative effect on fertility. Basically, SES factors led to a decrease in the birthrate in China. In urban Chinese areas, family planning is higher than in rural areas where fertility is higher, which then licenses the conclusion that family planning decreases birthrates (Poston, 2008). Limieng, Shatalova, and Kalabikhina (2022) show that the higher the per capita GDP, the lower the fertility rate is.
Conclusion
The studies reviewed here show that as people become more well-off, given that they have access to family planning methods, their population will then begin to decrease. There is though, as is the case with China, a fine line to walk through where the population will get too old and not enough younger people will be around, as is the case in Asia already (Goh, 2005). SSA lies at one end of the spectrum—increased fertility due to lack of family planning, low education, low contraceptive use, and low income—while Asian countries like China represent the other side of the spectrum—decreased fertility, higher contraceptive use, and a higher GDP which then leads to a decrease in fertility. Very clearly, there is a middle-ground where a population can be well-off and sustain a population when they have the resources to do so.
Why are birthrates so high in five African countries?
The major factors driving population growth in these countries include low contraceptive use, high adolescent fertility rates and a prevalence of polygamous marriages. There’s also the low education status of women, low to poor investment in children’s education, and factors related to religion and ideas.
The use of modern contraceptives is generally low across sub-Saharan Africa. The overall prevalence is 22%. In the Democratic Republic of Congo, however, the uptake of short-acting contraceptives is at 8.1%. In Nigeria, it is at 10.5%. The uptake in Ethiopia is 25%, in Tanzania it’s 27.1% and in Egypt 43%.
For long-acting family planning methods, apart from Egypt with over 20% uptake, the other four countries driving population growth in the region recorded very poor uptake. This low uptake will logically lead to a population explosion.
Some of the factors associated with high contraceptive use in Africa are women’s education, exposure to news and mass media, good economic status and urban residency.
Investing in women’s health, furthermore, leads to “strong intergenerational spillover effects” which then encourages economic development, which would then further decrease the birthrate (Bloom, Kuhn, and Pretnner, 2018). This is borne out in Kenya, Zimbabwe, and Botswana where women had higher levels of education and subsequent decreases in child mortality (Ramirez, Tania and Stewart, 1997). There is also evidence that declining fertility explained a bit less than one-third of the decrease in poverty in rural India in the years 1987 and 1988 and 1993 and 1994 (Dupta and Dubey, 2003). Reducing infant and child mortality also decreases fertility and increases schooling (Kalemli-Ozcan, 2000).
When locales are food secure, then they will have a lower child mortality rate, ceteris paribus and malnutrition is a large driver of this relationship (Bain et al, 2019). Household food insecurity along with dietary diversity is associated with “stunting” (low height for one’s expected age) in SSA (Gassara et al, 2021). So the claim that aid—whether it’s monetary or foodstuffs—will increase the population exponentially is obviously false.
So for people like Steve Sailer who look at current demographic trends using the UN’s data, calling it “the world’s most important graph“, the literature shows that, as Africa urbanizes, becomes more educated, has access to family planning and contraceptives, that their population will decrease. So, by giving aid and education, the population in Africa won’t increase, it will actually DECREASE. We have the means to feed the world on the basis of the food we already produce, it is we just need to educate propel, provide aid to them in all shapes and forms, and then people will have fewer children when they are food secure and have access to contraceptives along with education about them.
Thus, the answer to the question “Will aid to Africa increase the African population?” is a big “No.”
To be an agent is to be a being with the capacity to act. To be able to act one must be able to intend. To be able to intend one must have a mind. But nonhuman animals lack minds. So nonhuman animals don’t act, they merely behave. This does not mean that nonhuman animals should not be treated with any value, indeed since we are moral beings and act morally, we should treat non-minded organisms as best we can. In my view, the capacity to act is what sets humans apart from the rest of the animal kingdom. That is, humans are the only animals with minds and the capacity to act and reason, and this is because humans are the only animals with language. So this is what makes humans special and unique—it is what sets humans apart from the rest of the animal kingdom. This is the conclusion that I will mount this in this article.
Language and propositional attitudes
Perhaps the most well-known philosopher to deny agency to animals is philosopher of mind Donald Davidson (1975, 1982). In his paper Rational Animals, Davidson (1982) basically argued that no organism can think or have a reason to do X if they have no concept of belief, so nonhuman animals are incapable of thought or reason, therefore nonhuman animals lack minds and they do not act. Davidson’s argument is a modern-day Descartes “animals are automata” argument.
Davidson argues that in order to have a belief, the organism needs to have a concept of belief and that in order to have a concept of belief then the organism must have language—they must be able to state their intentions, beliefs, and desires. Davidson (1982: 322-323) puts this well:
The version of the thesis which I want to promote needs to be distinguished from various related versions. I don’t, for example, believe that thinking can be reduced to linguistic activity. I find no plausibility in the idea that thoughts can be nomologically identified with, or correlated with, phenomena characterized in physical or neurological terms. Nor do I see any reason to maintain that what we can’t say we can’t think. My thesis is not, then, that each thought depends for its existence on the existence of a sentence that expresses that thought. My thesis is rather that a creature cannot have a thought unless it has language. In order to be a thinking, rational creature, the creature must be able to express many thoughts, and above all, be able to interpret the speech and thoughts of others.
If a thing is said to have propositional attitudes, if a thing lacks language, how can it be said to have propositional attitudes, where a propositional attitude is an intentional state “about” something? Language is important here because the contents of intentional states are propositions. So if an organism can’t talk, then it can’t have propositional attitudes, that is it can’t have intentional states.
I think Davidson’s argument in Rational Animals successfully shows that animals lack minds and therefore do not act. I have reformed it:
If X is to have a belief, then X has to have the concept of belief. If X has the concept of belief, then X has language. If X doesn’t understand or speak a language, then X cannot have beliefs. Belief is necessary for thought/reasoning. So nonhuman animals don’t think/reason. So nonhuman animals lack mind.
The argument can also be put into premise and conclusion form like this:
(1) To be able to think, an organism must have a full range of propositional attitudes (PAs). (2) Having a full range of PAs rests on having language. (3) Nonhuman animals lack language. (4) So nonhuman animals lack PAs. (5) So, nonhuman animals don’t think. (6) So nonhuman animals lack mind.
The argument as formulated is valid and, I think, it’s obviously sound. Since animals lack language and this is an empirical fact, then they cannot have PAs so they therefore do not think. Nonhuman animals do not utter words, since they lack language.
Action and behavior
What nonhuman animals DO is behave (Stroecker, 2009)—where behavior is due to antecedent conditions. I have made the distinction between “action” and “behavior” quite simple. Goals and reasons distinguish action from behavior. Action is goal-oriented and done for reasons, whereas behavior is a reaction due antecedent conditions—the organism behaves due to causal stimuli. This can be said to be a form of Descartes’ view of animals as automata—that they are material beings without minds. Humans, he held, are both material and immaterial—the mind being immaterial and the body being material. Descartes showed that nonhuman animal behavior is akin to the automatic behaviors in humans—where “behavior” is a result of antecedent conditions and not goal-directed. This argument by analogy from Descartes shows that nonhuman animal behavior is reflexive, and so they cannot think and they can be rightly said to be automata (Thomas, 2020).
Brenick and Webster (2000: 147) wonderfully articulate the distinction between action and behavior, and once this distinction is made clear, it is quite obvious that the claim “animals don’t act, they merely behave” is true.
Teleology, the reader is reminded, involves goals or lures that provide the reasons for a person acting in a certain way. It is goals or reasons that establish action from simple behavior. On the other hand the concept of efficient causation is involved in the concept of behavior. Behavior is the result of antecedent conditions. The individual behaves in response to causal stimuli or antecedent conditions. Hence, behavior is a reaction to what already is—the result of a push from the past to do something in the present. In contrast, an action aims at the future. It is motivated by a vision of what can be.
The best example is being hit with a mallet in the knee by a doctor which tests the L2, L3 and L4 segments of the spinal cord. Try as they might, if the doctor hits them in the right spot—assuming they have no issues with their L2, L3, and L4 segments of their spinal cord—the knee will jerk up which indicates no issues with those spinal cord segments. The knee jerking is due to an antecedent condition. Now think of that same movement being done as an exercise, the knee extention on an exercise machine. There is conscious thought to be the knee in accordance with the exercise to work the targeted muscles. This, therefore, is an action, since there this is goal-driven and performed for a reason—to work out the specified muscles of the exercise. This of course occurred for a reason, but it was an intention by the doctor, not the individual who was getting his patellar reflex tested.
(1) If nonhuman animals had the capacity to act, then they could make decisions based on their own preferences, goals, and beliefs.
(2) Nonhuman animals cannot make decisions on their own preferences, goals and beliefs (they don’t have a concept of BELIEF).
(3) Therefore nonhuman animals can’t act.
I can also make the claim and give an argument that animals aren’t moral agents and so they cannot be concerned with “right” or “wrong” since they lack language and thusly a mind.
For X to be moral, they need to be concerned with “right” or “wrong.” For X to have those concepts, they must have a language and therefore a mind. Nonhuman animals lack language. Nonhuman animals lack mind. Therefore nonhuman animals lack morals.
For animals to be said to have thought, they must be able to think about words using a language, but they cannot do so since they lack language and so they lack propositional attitudes. So animals lack the ability to intend to do things, they merely react to what occurs to them (they “behave”).
Human language is compositional and referential (Pagel, 2017). Humans (and Neanderthals) also share a derived TF (transcription factor) of FOXP2—FOXP2 has been claimed to be a “language gene”, though, as Mason et al (2018: 403) rightly state, “FOXP2 is likely needed in the neuromuscular pathway to make sounds.” But in 2018, a paper was published—No Evidence for Recent Selection of FOXP2 among Diverse Human Populations (Atkinson et al, 2018)—where the authors show that “natural selection” can’t be attributed to FOXP2 and therefore the development of human language, meaning it’s a just-so story. So there is no support for positive selection of the FOXP2 locus.
Apes like Koko and Nim Chimpsky, it is claimed, can use sign language and construct sentences using sign language when they want something. However, it is now known that 92% of Ally’s (Nim’s brother) and all of Koko’s signs were signed before they signed their “thoughts” (Terrace et al, 1979: 899). Thus, these apes don’t understand what they’re doing, they don’t have the desire for what they are claimed to be signing, they are just doing what their handlers tell them to do. And there is still no evidence that nonhuman animals possess a theory of mind (ToM) (Penn and Povinelli, 2007).
I would say that in order for nonhuman animals to have a ToM, they must have the concept of belief. But, as Davidson (1982) has shown, they can’t have a concept of belief since they lack language so they can’t have a ToM. There is, furthermore, no good evidence that human babes under the age of 3 and nonhuman animals cannot attribute beliefs or mental states (Burge, 2018). Though, of course, human babies grow and eventually do acquire this ability, they are not born rational, they need to acquire it through experience. They can do this because they have human brains which is a necessary pre-condition for mindedness. The same cannot be said for nonhuman animals, though.
My view that animals don’t act and they merely behave may be a fringe one, but one author holds this view, too. In Why Animals Can’t Act, Stroecker (2009) argues that animals don’t act, but they do behave. Agency, to Stroecker (2009: 267):
is a skill that is dependent on a highly sophisticated, social practice, the practice of public practical deliberation. Only because we are raised in this practice and moreover because we have internalized it can we be expected to do whatever it is that is arguably the best and in turn can our doings be explained on the basis of this particular skill.
Conclusion
The argument that has been mounted here shows that for an organism to be able to think, it must have propositional attitudes and therefore language. The claim that one must possess language in order to have beliefs and thusly propositional attitudes is the strongest claim against animal minds and rationality. This view I articulated is called “lingualism”—the claim that agency is confined to language utterers, thusly agency is confined to humans since to be an agent one must have a mind and humans are the only animals with minds.
The discussion here shows that since nonhuman animals lack language, they lack belief and they ability to have beliefs about beliefs. And since they lack language, they lack propositional attitudes. So nonhuman animals aren’t moral agents, they lack minds, and since they lack minds they cannot think and so they cannot be rational and cannot be said to be agents.
So what sets humans apart from the animal kingdom—that is, what makes humans special and distinct from the animal kingdom—is the capacity for language, and along with it thought, action, and agency, that is, the ability to act intentionally and not merely due to antecedent conditions. Language, action, and mind are what makes us unique and special—but this is not a theistic claim. So, at the end of the day, the ultimate claim is that our minds are what make us unique in the animal kingdom, since other animals lack mind.
“Race” is a heavy topic. It influences many aspects of our daily lives, and in some cases, it even influences people to carry out heinous acts on groups of people deemed “inferior.” Such thoughts of “inferiority” of groups deemed (racialized as) races comes from horribly interpreting scientific studies, and in some cases, it is outright stated by the authors themselves, albeit using flowery language (eg Rushton, 2000). People that believe in the reality of race are called “race realists”, whether or not they hold a biological or social view of race.
On the socialrace side, social groups are racialized as races. “Social identities are contextual to historical and cultural elements.” “Racialization” is “the process through which groups come to be understood as major biological entities and human lineages, formed due to reproductive isolation, in which membership is transmitted through biological descent” (Hochman, 2019). Thinking about the root words for “racialization”, the two words are “racial formation.” Thus, when a group becomes racialized, it becomes a race based on societal expectations and thought.
“Hispanics” are an easy example to illustrate this case. In daily American discourse, people speak of “Hispanics”, “Spanish” people, and “Latinos/Latin Americans.” There are 33 Latin American countries to which this designation can be assigned to. In any case, what I term the “HLS distinction” (Hispanic, Latin American, Spanish distinction) is clearly a social designation and not a biological one. The group is an amalgamation of different peoples with differing amount ancestry to different countries of the world. “Hispanics” in some studies (eg Risch et al, 2002) don’t cluster in their own cluster (which would be taken to be a race, given that one has an argument for the claim), since they are an amalgam of different racial groups, it makes sense that they “clustered variously with the other groups.” Thus, “HLSs” are a social, not biological, kind.
Race concepts
Since “HBDers” call themselves “race realists” too, there needs to be a distinction between those who believe what I term “psychological race realism”—the claim that the psychological differences between the races are genetically transmitted and reduced to physical things—and regular old race realism—the claim that race exists as a social construct of a biological reality. Kaplan and Winther (2014) distinguish between bio-genomic/cluster race realism (the claim that race is real on the basis of genomic clusters from studies using programs like STRUCTURE); biological race realism affirms a kind of one-to-one mapping between social groups and clusters in DNA studies (though this not need be the case); and social race realism which is the racialization of social groups. They are anti-realists about biological race, but conventionalists about bio-genomic/cluster race. I think this is a good avenue to take, since the main program that psychological hereditarians push cannot ever be logically viable due to the irreducibility of the mental. (The “HBD” (Human Biological Diversity type racial realism is what I term psychological racial realism, while the type of racial realism I push is bio-genomic/cluster realism.)
In 2017, philosopher of race Michael Hardimon published his Rethinking Race: The Case for Deflationary Realism. In the book, Hardimon distinguishes between four race concepts: racialist races, in which it’s proponents attempt to rank-order racialized groups in socially-valued traits. Racialist races are socially constructed groups which then purport to pick out biological kinds. However, the concept of racialist race does not refer to any group in the world, genetic variation in Homo sapiens is nonconcordant, human variation is clinal, that is human groups aren’t sharply distinguished between one another on the basis of genomic data. Socialraces are groups taken to be racialist races, the social position taken by a group said to be a socialrace, or the system of positions that are social races (Hardimon, 2017: 131). So these two concepts need to be grouped together since they are hierarchical, though they need not be correlated with each other that strongly—one can be an anti-realist about biological races but be a realist about social races. This is why there is no contradiction in saying that biological race isn’t real but socialraces are. Socialraces also have a biological correlate, and these are what Hardimon terms “minimalist races”, which I will describe below.
Step 1. Recognize that there are differences in patterns of visible physical features of human beings that correspond to their differences in geographic ancestry.
Step 2. Observe that these patterns are exhibited by groups (that is, real existing groups).
Step 3. Note that the groups that exhibit these patterns of visible physical features correspond to differences in geographical ancestry satisfy the conditions of the minimalist concept of race.
The minimalist race concept does not state which populations are races, it just states that race exists. Hardimon’s populationist race concept (PRC) does, though. Although we don’t need genes to delineate race, using new technologies can and does help us to elucidate the existence of races. However, if minimalist races are populationist races, then the kind minimalist race equals populationist race. So if minimalist races are real, then so are populationist races.
Since 2014 in his paper A Radical Solution to the Race Problem, philosopher of race and science Quayshawn Spencer has been tinkering with an argument he now calls “the identity argument” (which I will provide below). The Office of Management and Budget has guidelines for the classification of people on the US census, being White, Black, Native American, Pacific Islander and Asian. The OMB never calls race a kind or a category, but they do refer to races as a set of categories or a proper name for population groups (Spencer, 2014). Spencer (2019a: 113) makes and defends 3 claims in regard to his OMB race theory:
(3.7) The set of races in OMB race talk is one meaning of ‘race’ in US race talk.
(3.8) The set of races in OMB race talk is the set of human continental populations.
(3.9) The set of human continental populations is biologically real.
In Spencer’s (2022) chapter in Remapping Race in a Global Context, A metaphysical mapping problem for race theorists and human population geneticists, Spencer has—in my opinion—articulated the best version of his OMB race argument.
Spencer’s identity argument
Of course, in the discussion of STRUCTURE and how many clusters it is told to construct from genomic data, the program is merely doing whag the human tells it to do. However, the five populations that come out in K= 5 “are genetically structured … which is to say, meaningfully demarcated solely on the basis of genetic markers” (Hardimon, 2017: 88). Hardimon (2017: 85) calls these clusters” continental-level minimalist races” whereas Spencer (2022: 278) calls these “the human continental populations” or “Blumenbachian partitions” (Spencer, 2014: 1026).
K = 5 shows 5 human continental populations which are robust and have been replicated numerous times. The 5 human continental populations are Africans, Caucasians, East Asians, Native Americans, and Oceanians. K = 5 corresponds to the racial scheme used by the OMB, and by scientists and Americans in daily life. Human continental populations and OMB races correspond one-to-one in the following way: African, black; Caucasian, white; East Asian, Asian; Native American, American Indian; and Oceanian, Pacific Islander. So there is a metaphysical relation between the human continental populations in K = 5 and the OMB races. Spencer states that “identity” is what is exemplified between K = 5 and OMB races, and he then constructed this argument he calls “the identity thesis”:
(2.1) The identity thesis is true if, in OMB race talk, ‘American Indian,’ ‘Asian’, ‘Black’, ‘Pacific Islander,’ and ‘White’ are singular terms, and ‘American Indian’ means Native American, ‘Asian’ means East Asian, ‘Black’ means African, ‘Pacific Islander’ means Oceanian, and ‘White’ means Caucasian.
(2.2) In OMB race talk, the first conjunct in (2.1)’s antecedent is true.
(2.3) In OMB race talk, the second conjunct in (2.1)’s antecedent is true.
(2.4) So, the identity thesis is true.
(2.1) is true since the antecedent analytically entails the consequent; (2.2) is true based on the OMB’s intentions when they when coining the race terms, that is to provide a common language across US agencies; (2.3) is true since human continental populations are the best choices for the meanings of the OMB race terms—they posit referents which are part of the semantic content of the OMB race terms; it therefore follows that the conclusion (2.4) logically follows so the argument is deductively valid and I think it is sound.
Spencer (2019a) professes to be a radical pluralist about race—that is, there are many different race concepts for certain contexts based on American race talk. The referent “race” is merely a proper name for a set of human population groups. Race is therefore a social construct of a biological reality.
Conclusion
Race is meaningful in American social discourse—call it race talk. We should not be eliminativist about race, since there is medical relevance for certain groups deemed races. That is, we shouldn’t eliminate the concept RACE from our vocabulary, since it has a referent. RACE is a social construct of a biological reality. It must be said, though, that many people believe that since X is a social construct then X is therefore not real or doesn’t exist. But this line of thinking can be easily countered. Money is a social construct, so does that mean that money doesn’t exist so money isn’t real? No—the example perfectly shows the fallacious thinking of those who think that social constructivists are claiming that since X is socially constructed then X is not real. This couldn’t be further from the truth since social constructivists about race are realists about race. Pluralism about race is true—that is, there are many natures and realities for race based on the relevant context (Spencer, 2019: 27).
Lastly, these theories of race I have shown here do not license the claims that realists about racialist races or biological racial realists (as termed by Kaplan and Winther) have about these groups. While Hardimon distinguishes between the four concepts of race, Spencer’s concept and then argument tried to argue that race is a social construct of a biological reality.
Nevertheless, I do worry that politically right-winged people—for example, Charles Murray—might try to misuse my research for their own purposes. I’m also worried about the educational research that shows learning about human genetic differences in racial terms—for instance, lactase persistence alleles—increases racist attitudes among the learners.
Spencer took care of the first part as early as his 2014 paper and has reiterated it since—the DNA evidence that elucidates the reality of human races are on noncoding DNA, so Spencer (2014: 1036) states:
Nothing in Blumenbachian race theory entails that socially important differences exist among US races. This means that the theory does not entail that there are aesthetic, intellectual, or moral differences among US races. Nor does it entail that US races differ in drug metabolizing enzymes or genetic disorders. This is not political correctness either. Rather, the genetic evidence that supports the theory comes from noncoding DNA sequences. Thus, if individuals wish to make claims about one race being superior to another in some respect, they will have to look elsewhere for that evidence.
Although I am a pluralist about race, the race concept I think best shows the reality of race is Spencer’s as he holds race to be a social construct of a biological reality in his OMB race theory. And we can easily see that RACE is a social construct of a biological reality with Spencer’s identity thesis by looking at the mapping between K = 5 and the OMB—the social part is the OMB designations of races, whereas the biological part are the clusters that appear in K = 5.
My thinking on race has changed a lot over the years. I used to be against the claim that race is a social construct. Though, if you know that being a social constructivist about race means that you don’t need to be an antirealist about the concept RACE as a whole, then you can state “Race is a social construct of a biological reality”, where “biological reality” means the concept RACE has some biological grounding, as seen in K = 5 STRUCTURE studies. RACE is an idea invented by people, which is the “social construct” claim. Thus, we impute racial categories onto people (the social construct part of the argument) and the racial categories we impute onto people have a biological grounding (as seen by K = 5).
P1: If RACE is a social construct of a biological reality, then RACE is not an inherent characteristic of the individual.
P2: If RACE is not an inherent characteristic of the individual, then one’s RACE is designated by the society they live in.
C: Thus, if RACE is a social construct of a biological reality, then one’s RACE is designated by the society they live in.
NotPoliticallyCorrect 