Race and medicine is a tendentious topic. On one hand, you have people like sociologist Dorothy Roberts (2012) who argues against the use of race in a medical context, whereas philosopher of race Michael Hardimon thinks that we should not be exclusionists about race when it comes to medicine. If there are biological races, and there are salient genetic differences between them, then why should we disregard this when it comes to a medically relevant context? Surely Roberts would agree that we use her socio-political concept of race when it comes to medicine, but not treat them like biological races. Roberts is an anti-realist about biological races, whereas Hardimon is not—he recognizes that there is a minimalist and social aspect to race which are separate concepts.
In his book Rethinking Race: The Case for Deflationary Realism, Hardimon (2017, Chapter 8) discusses race and medicine after discussing and defending his different race concepts. If race is real—whether socially, biologically, or both—then why should we ignore it when it comes to medical contexts? It seems to me that many people would be hurt by such a denial of reality, and that’s what most people want to prevent, and which is the main reason why they deny that races exist, so it seems counterintuitive to me.
Hardimon (2017: 161-162; emphasis his) writes:
If, as seems to be the case, the study of medically relevant genetic variants among races is a legitamate project, then exclusionism about biological race in medical research—the view that there is no place for a biological concept of race in medical research—is false. There is a place for a biological concept of race in the study of medically relevant genetic variants among races. Inclusionism about biological race in medical research is true.
So, we should not be exclusionists (like Roberts), we should be inclusionists (like Hardimon). Sure, some critics would argue that we should be looking at the individual and not their racial or ethnic group. But consider this: Imagine that an individual has something wrong and standard tests do not find out what it is. The doctor then decides that the patient has X disease. They then treat X disease, and then find out that they have Y disease that a certain ethnic group is more likely to have. In this case, accepting the reality of biological races and its usefulness in medical research would have caught this disease earlier and the patient would have gotten the help they needed much, much sooner.
Black women are more likely to die from breast cancer, for example, and racism seems like it can explain a lot of it. They have less access to screening, treatment, care, they receive delays in diagnoses, along with lower-quality treatment than white women. But “implicit racial bias and institutional racism probably play an important role in the explanation of this difficult treatment” (Hardimon, 2017: 166). Furthermore, black women are more than twice as likely to acquire a type of breast cancer called “triple negative” breast cancer (Stark et al, 2010; Howlader et al, 2014; Kohler et al, 2015; DeSantis et al, 2019). Of course, this could be a relevant race-related genetic difference in disease.
We should, of course, use the concepts of socialrace when discussing the medical effects of racism (i.e., psychosocial stress) and the minimalist/populationist race concepts when discussing the medically relevant race-related genetic diseases. Being eliminativist about race doesn’t make sense—since if we deny that race exists at all and do not use the term at all anymore, there would be higher mortality for these “populations.” Thus, we should use both of Hardimon’s terms in regard to medicine and racial differences in health outcomes as both concepts can and will show us how and why diseases are more likely to appear in certain racial groups; we should not be eliminativists/exclusionists about race, we should be inclusionists.
Hardimon discusses how racism can manifest itself as health differences, and how this can have epigenetic effects. He writes (pg 155-156):
As philosopher Shannon Sullivan explains, another way in which racism may be shown to influence health is by causing epigenetic changes in the genotype. It is known that changes in gene expression can have durable and even transgenerational effects on health, passing from parents to their children and their children’s children. This suggests that the biological dimensions of racism can replicate themselves across more than one generation through epigenetic mechanisms. Epigenetics, the scientific study of such changes, explains how the process of transgenerational biological replication of ill health can occur without changes in the underlying DNA sequence.
If such changes to the DNA sequences can be transmitted to the next generation in the developmental system, then that means that the social can—and does—has an effect on our biology and that it can be passed down through subsequent generations. It is simple to explain why this makes sense: for if the developing organism was not plastic, and genes could not change based on what occurs in the environment for the fetus or the organism itself, then how could organisms survive when the environment changes if the “genetic code” of the genome were fixed and not malleable? For example, Jasienska (2009) argues that:
… the low birth weight of contemporary African Americans not only results from the difference in present exposure to lifestyle factors known to affect fetal development but also from conditions experienced during the period of slavery. Slaves had poor nutritional status during all stages of life because of the inadequate dietary intake accompanied by high energetic costs of physical work and infectious diseases. The concept of ‘‘fetal programming’’ suggests that physiology and metabolism including growth and fat accumulation of the developing fetus, and, thus its birth weight, depend on intergenerational signal of environmental quality passed through generations of matrilinear ancestors.
If the environmental quality—i.e., current environmental quality—is “known” by the developing fetus through cues from the mother’s nutrition, stress etc, then a smaller body size may be adaptive in that certain environment and the organism may survive with fewer resources due to smaller body size. In any case, I will discuss this in the future but it was just an example of a possible epigenetic modification on current slaves. I, personally, have noticed that a lot of blacks are really skinny and have really low body fat—who knows, maybe this could be part of the reason why?
This is something that sociologist Maurizio Meloni (2018) calls “the postgenomic body”—the fact that biology is malleable through what occurs in our social lives. So not only is the human brain plastic, but so is the epigenome and microbiome, which is affected by diet and lifestyle—along with what we do and what occurs to us in our social lives. So our social lives, in effect, can become embodied in our epigenome and passed down to subsequent generations. Similar points are also argued by Ulijaszek, Mann, and Elton (2012). (Also see my article Nutrition, Development, Epigenetics, and Physical Plasticity.)So in effect, environments are inherited too, and so, therefore, the environments that we find ourselves in are, in effect, passed down through the generations. Meloni (2018) writes:
On the other hand, by re-embedding the individual within a wider lineage of ancestral experiences and reconfiguring it as a holobiontic assemblage, it may literally dissolve the subject of emancipation. Moreover, the power of biological heredity may be so expanded (as it includes potentially any single ancestral experience) to become stronger than in any previous genetic view. Finally, the several iterations of plasticity that emerge from this genealogy appear so deeply racialized and gendered that it is difficult to quickly turn them into an inherently emancipatory concept. Even as a concept, plasticity has an inertial weight and viscosity that is the task of the genealogist to excavate and bring into view.
Thus, current biological states can be “tagged” and therefore be epigenetically transmitted to future generations. Think about it in this way: if epigenetic tags can be transmitted to the next generation then it would be presumed that that environment—or a similar one—would be what newer generations would be born in. Thus, the plasticity of the organism would help it in life, especially the immediate plasticity of the organism in the womb. Likewise, Kuzawa and Sweet (2008) argue:
that environmentally responsive phenotypic plasticity, in combination with the better-studied acute and chronic effects of social-environmental exposures, provides a more parsimonious explanation than genetics for the persistence of CVD disparities between members of socially imposed racial categories.
Of course, if we look at race as both a biological and social category (i.e., Spencer, 2014), then this is not surprising that differences in disease acquisition can persist “between members of socially imposed racial categories.” Phenotypic plasticity is the big thing here, as noted by many authors who write about epigenetics. If the organism is plastic (if it can be malleable and change depending on external environmental cues), then disease states can—theoretically—be epigenetically passed to future generations. This is just like Jasienska’s (2009, 2013, Chapter 5) argument that the organism—in this case, the fetus—can respond to the environmental quality that it is developing in and, therefore, differences in anatomy and physiology can and do occur based on the plasticity of the organism.
Lastly, Jan Badke, author of Above the Gene, Beyond Biology: Toward a Philosophy of Epigenetics (Baedke, 2018), argues that, since the gene-centered view of biology has been upended (i.e., Jablonka and Lamb, 2005; Noble, 2006, 2011, 2012, 2017) for a postgenomic view (Richardson and Stevens, 2015). Genes are not closed off from the environment; all organisms, including humans, are open systems and so, there are relationships between the environment, developmental system, and the genome which affect the developing organism. Baedke and Delgado (2019) argue that the “colonial shadow … biologicizes as well as racializes social-cultural differences among human groups.” Since every race faces specific life challenges in its environment, therefore, each race shows a “unique social status that is closely linked to its biological status.” Thus, differing environments, such as access to different foods (i.e., the effects of obesifying foods) and discrimination can and are passed down epigenetically. Baedke and Delgado (2019: 9) argue that:
… both racial frameworks nutrition plays a crucial role. It is a key pathway over which sociocultural and environmental difference are embodied as racial difference. Thus, belonging to a particular race means having a particular biosocial status, since races include two poles – a social status (e.g., class, socio-economic status) and a biological status (disease susceptibility) – which are closely interlinked. Against this background, human populations in Mexico become an exemplar of types of bodies that are not only relocated to a destabilizing modernized world in which they suffer from socio-economic deprivation. What is more, they become paradigmatic primitive bodies that are unbalanced, biologically deprived, and sick. In short, in these recent epigenetic studies poor places and lifestyles determine poor bodies, and vice versa.
In sum, accepting the reality of race—both in a minimalist/populationist biological manner and social manner—can and will help us better understand disease acquisition and differing levels of certain diseases between races. Recognizing the minimalist/populationist concepts of race will allow us to discover genetic differences between races that contribute to variation in different diseases—since genes do not alone outright cause diseases (Kampourakis, 2017: 19). Being eliminativist/exclusionist about race does not make sense, and it would cause much more harm than good when it comes to racial disease acquisition and mortality rates.
Furthermore, acknowledging the fact that the social dimensions of race can help us understand how racism manifests itself in biology (for a good intro to this see Sullivan’s (2015) book The Physiology of Racist and Sexist Oppression, for even if the “oppression” is imagined, it can still have very real biological effects that could be passed onto the next generation—and it could particularly affect a developing fetus, too). It seems that there is a good argument that the effects of slavery could have been passed down through the generations manifesting itself in smaller bodies; these effects also could have possibly manifested itself in regard to obesity in Latin America post-colonialism. Gravlee (2009) and Kaplan (2010) also argue that the social, too, manifests itself in biology.
(For further information on how the social can and does become biological see Meloni’s (2019) book Impressionable Biologies: From the Archaeology of Plasticity to the Sociology of Epigenetics, along with Meloni (2014)‘s paper How biology became social, and what it means for social theory. Reading Baedke’s and Meloni’s arguments on plasticity and epigenetics should be required before discussing these concepts.)
I’m watching Mystery Diagnosis right now, and I heard the narrator say that lupus is three times more common in African Americans than Caucasian Americans. (The woman was black.) So let’s look into it.
Lupus is a long-term autoimmune disease where the body’s immune system becomes hyperactive and attacks healthy tissue. It can damage any part of the body, skin cells, joints, organs. Many symptoms of lupus exist, like kidney inflammation, swelling, and damage to the blood, heart, joints, and lungs. No cure exists for lupus, though there are ways to minimize inflammation through diet and lifestyle.
Lupus is two to three times more likely to occur in women of color—blacks, Hispanics/Latinos, Native Americans, and others—compared to white Americans. Somers et al (2014) state that lupus affects 1 in 537 black women, “with black patients experiencing earlier age at diagnosis, >2-fold increases in SLE incidence and prevalence, and increased proportions of renal disease and progression to ESRD as compared to white patients.” However, Somers et al (2016) note that medical records may be poor or missing while the reliability of diagnosis is low for non-whites and non-blacks. They also note that race and ethny data in the US is based on self-ID for the parents and child on the birth certificate, but self-ID has almost a perfect relationship with geographic ancestry (i.e., race) (Tang et al, 2005).
Guillermo et al (2017: 7) write that:
Ethnicity is a biological and social construct, including not only genetic ancestry, but also cultural characteristics (language, religion, values, social behaviors, country of origin) yet it is an arbitrary definition . Race is oftentimes used interchangeable with ethnicity but it mainly refers to the biological features of groups of people. Given that there are differences in the clinical characteristics and prognosis among different populations, it is worth evaluating the impact of race/ethnicity in SLE. Genetic ancestry influences the risk for the incidence of SLE; for example, Amerindian ancestry is associated with an increased number of risk alleles for SLE , and also with an early age at onset , Amerindian and African ancestry are associated with a higher risk for kidney involvement [122,123] and European ancestry with a lower risk .
First, let’s look at ref , which is McKenzie and Crowcroft (1994), who Guillermo et al (2017) cite as saying that ethnicity is “an arbitrary definition.” They note that some researchers use Blumenbach’s terms (see Spencer, 2014). They claim that modern definitions class Asians as Caucasian or black … what? They state that modern definitions classify Asians as black because “all disadvantaged groups [are] “black populations,”
[since] the experience of racism is paramount.” This is ridiculous on so many levels.
In any case, Southern Europeans are more likely to have a higher risk of renal involvement, and antibody production but along with that a lower risk of discoid rash whereas Western Europeans while Ashkenazi Jews “seem to be protected from neurologic manifestations” (see Richman et al, 2009). Asians and Native Americans in Canada are less likely to have manifestations than Africans; a type of lupus known as cutaneous vasculitis is more common in Native Americans from Canada, while Asians from Canada had a lower rate of serotisis and arthritis compared to Caucasians, Native Americans and African descendants (Peschken et al, 2015). However, Peschken et al (2015) note that while ethnicity was not that strong a predictor of damage accrual, low income was.
Kidney involvement is a major factor in the development of lupus (Bagamant and Fu, 2009), while it is more frequent in “Hispanics”, African-descendants, and Asians. Further, “Hispanics” and blacks are more likely to have end-stage renal failure than whites (Ricardo et al, 2015). When it comes to lupus nephritis—inflammation of the kidneys caused by lupus—“Hispanics” also have a better response to mycophenolate mofetil, which is an immunosuppressive drug that prevents organ rejection (Appel et al, 2009). After the onset of the disease, the disease declines slowly in “Hispanics”, then Africans, and finally fastest in whites. There also seems to be an SES factor in the aetiology of the disease. Sule and Petri (2005) write that “Socioeconomic status can have a major impact on SLE disease manifestations and mortality, independent of ethnicity“, while saying that association with SES is all over the place, with there being no relationship with SES and lupus acquisition.
Vila et al (2003) studied “Hispanics” from Texas and Puerto Rico. They noted that those from Texas accrued more damage than those from Puerto Rico. This is not surprising. “Hispanics” are not a homogenous group (they are a socialrace with no minimalist correlate, they have differing admixture from all over; “Hispanics” can be of any race. Vila et al (2007: 362) note that:
This diversity appears to be areflection of the great variability that exists between these populations with regards to their genetic, environmental and sociodemographic backgrounds.
“Hispanics” from the southeast part of America are different ethnically than those from the southeast.
Blacks and “Hispanics” have a higher rate of mortality than whites, but these differences disappear once SES is accounted for (Ward, Pyun, and Studenski, 1995; Kasitanon, Magder, and Petri, 2006; Fernandez et al, 2007). There could be some genetic differences between races/ethnies that contribute to disease differences between them. But as Kampourakis (2017: 19) notes in his book Making Sense of Genes:
… genes do not alone produce characters or disease but contribute to their variation. This means that genes can account for variation in characters but cannot alone explain their origin.
In sum, there is a wide range of differences between races and ethnies when it comes to lupus. Is the main cause environmental or genetic? Neither, as genes and environment interact to form disease (and any other) phenotypes. So if one at-risk minority group has a low SES, that may be a risk factor. The fact that there are ethnic differences in response to autoimmune drugs when it comes to certain forms of lupus is interesting. The wide range of ethnic differences in the acquisition of the disease is interesting, with Ashkenazi Jews seemingly protected from the disease. In any case, there are racial/ethnic differences in the acquisition of this disease and to better treat those with this disease—and any other—we need to be realists about race, whether it’s biological or social, since there are very real disease and mortality outcomes between them.
JP Rushton’s career was pretty much nothing but peddling bullshit. In the beginning of his career, he was a social learning theorist. He published a book Altruism, Socialization, and Society (Rushton, 1980). I bought the book a few years back when I was still a hardcore Rushton defender to see what he wrote about before he started pushing IQ and evolutionary theories about human races and I thought it was pretty good. In any case, Rushton got a lot wrong. So much so, that his career was, in my opinion, wasted peddling bullshit. Rushton was shown to be wrong time and time again on r/K theory and cold winter theory; Rushton was shown to be wrong time and time again on his crime theorizing; and Rushton’s and Jensen’s papers on the causes of the black-white IQ gap rest on a misunderstanding of heritability. In this piece, I will cover those three subjects.
Recently, two new papers have appeared that have a bone to pick with Rushton: One by Flynn (2019) and the other by Cernovsky and Litman (2019). Flynn discusses Rushton’s claims on the method of correlated vectors, his cold winter theory (that Asians and Europeans were subjected to harsher climates which led to higher levels of intelligence and therefore IQ) and his misuse of regression to the mean. He also discussed how the black-white IQ gap is environmental in nature (which is the logical position to hold, since IQ tests are tests of middle-class knowledge and skills (Richardson, 2002) and they are not construct valid).
Cold Winters Theory
Rushton theorized that, due to exposure to harsher environments, that Europeans and East Asians evolved to be more intelligent than Africans who stayed in the, what I assume to be, less harsh environments of Africa (Rushton, 1985). This is Rushton’s “Differential K theory.” Flynn (2019) writes that he “can supply an evolutionary scenario for almost any pattern of current IQ scores.” And of course, one can do that with any evolutionary adaptive hypothesis.
Even Frost (2019) admits that “there is no unified evolutionary theory of human intelligence, other than the general theory of evolution by natural selection.” But since “natural selection” is not a mechanism (Fodor, 2008; Fodor and Piattelli-Palmarini, 2010), then it cannot explain the evolution of intelligence differences, nevermind the fact that, mostly, these claims are pushed by differences in non-construct valid IQ test scores.
In any case, Rushton’s theory is a just-so story.
Judith Anderson (1991) refuted Rushton’s hypothesis on ecological grounds. Rushton asserted that Africans were r-selected whereas Asians and Europeans were more K-selected. Rushton, however, did not even use alpha-selection, which is selection for competitive ability. So r- and K selection is based on density-independence and density-dependence. K-selection is expected to favor genotypes that persist at high densities—increasing K—whereas r-selection is expected to favor genotypes that increase more quickly at low densities—increasing r. Alpha-selection can also occur at high or low population densities but is more likely in high densities. Though alpha-selection “favours genotypes that, owing to their negative effects on others, often reduce the growth rate and the maximum population size” (Anderson, 1991: 52). I further discussed the huge flaws with Rushton’s r/K model here. So Rushton’s theory fails on those grounds, along with many others.
When it came to race, Rushton was a lumper, not a splitter. What I mean by these terms is simple: lumpers lump together Native Americans with East Asians and Pacific Islanders with Africans while splitters split them into further divisions. Why was Rushton a lumper? Because it fit more with his theory, of course. I remember back when I was a Rushton-ist, and I was, too, a lumper, that to explain away the low IQs of Native Americans—and in turn their achievements—was that they still had their intelligence from the cold winters and that’s when they did their achievements. Then, as they spent more time in hotter climates, they became dumber. In any case, there is no justification for lumping Native Americans with East Asians. Looking through Rushton’s book, he gives no justification for his lumping, so I can only assume that it is bias on his part. Now I will justify the claim that splitting is better than lumping. (Rushton also gave no definition of race, and according to Cernovsky and Litman (2019: 54), Rushton “failed to provide any scientific definition of race …”
Race is both a social and biological construct. I can justify the claim that Natives and East Asians are distinct races in one way here: ask both groups if the other is the same race. What do you think the answer will be? Now, onto genetics.
Spencer (2014) discusses the results from Tishkoff et al (2009), saying that when they added 134 ethnic groups to the ones found in the HDGP sample of 52, the K=5 partition clustered Caucasians, Mongoloids, and three distinct sets of Africans. Mongoloids, in this case, being East Asians, Native Americans, and Oceanians. But Tishkoff et al oversampled African ethnic groups. This, though, does not undercut my argument: of course when you oversample ethnic groups you will get the result of Tishkoff et al (2009) and since Africans were oversampled, the populations more genetically similar were grouped into the same cluster, which, of course, does not mean they are the same race.
Census racial discourse is just national racial discourse. The census uses defers to the OMB to define race. How does the OMB define race? The OMB defines “race” as “sets of” populations. Race in US racial discourse designates a set of population groups, thus, race is a particular, not a kind.
I can then invoke Hardimon’s (2017) argument for the existence of minimalist races:
1 There are differences in patterns of visible physical features which correspond to geographic ancestry.
2 These patterns are exhibited between real groups.
3 These groups that exhibit these physical patterns by geographic ancestry satisfy conditions of minimalist race.
C Race exists.
Now we can say:
1 If Native Americans and East Asians are phenotypically distinct, then they are different races.
2 Native Americans and East Asians are phenotypically distinct.
C Therefore Native Americans and East Asians are different races.
Rushton arbitrarily excluded data that did not fit his theory. How dishonest. Cernovsky and Litman (2019) write:
When Rushton presented crime statistics derived from 2 Interpol Yearbooks as allegedly supporting his thesis that Negroids are more crime inclined than Caucasoids, he arbitrarily excluded disconfirmatory data sets. When all data from the same two Interpol Yearbooks are re-calculated, most of the statistically significant trends in the data are in the direction opposite to Rushton’s beliefs: Negroids had lower crime rates than Caucasoids with respect to sexual offenses, rapes, theft, and violent theft or robbery, with most correlation coefficients exceeding .60. While we do not place much credence in such Interpol statistics as they only reproduce information provided by government officials of different countries, our re-analysis indicated that Rushton excluded data that would discredit his theory.
Further throwing a wrench into Rushton’s assertions is his claim that Mongoloids constitutes both East Asians and Native Americans. Well, Central America has some of the highest crime rates in the world—even higher than in some African countries. What is the ad-hoc justification for explaining away this anomaly if they truly are the same race? If they are the same race, why is the crime rate so much higher in Central America? Surely, Rushton’s defenders would claim something along the lines of recent evolution towards X, Y, and Z. But then I would say, then on what basis are they the same race? No matter what Rushton’s defenders say, they are boxed into a corner.
Lastly, Rushton and Jensen (2005) argued, on the basis of heritability estimates, and twin studies, that the black-white IQ gap is largely genetic in nature. But there are a few problems. They rely largely on a slew of trans-racial adoption studies, all of which have been called into question (Thomas, 2017). IQ tests, furthermore, are not construct valid (Richardson and Norgate, 2015; Richardson, 2017). Heritability estimates also fail. This is because, in non-controlled environments these stats do not tell us much, if anything (Moore and Shenk, 2016). Likewise, Guo (2000: 299) concurs, writing “it can be argued that the term ‘heritability’, which carries a strong conviction or connotation of something ‘heritable’ in everyday sense, is no longer suitable for use in human genetics and its use should be discontinued.” (For more arguments against heritability, read Behavior Genetics and the Fallacy of Nature vs Nurture.)
Rushton and Jensen (2005) also relied on the use of twin studies, however, all of the assumptions that researchers use to attempt to immunize their arguments from refutation are circular and ad hoc; they also agree that MZs experience more similar environments than DZs, too (Joseph et al, 2014; Joseph, 2016, see a summary here; Richardson, 2017). In any case, the fact that G and E interact means that heritability estimates are, in effect, useless in humans. Farm animals are bred in highly controlled environments; humans are not. Thus, we cannot—and should not—accept the results of twin studies; they cannot tell us whether or not genes are responsible for any behavioral trait.
There was a lot that Rushton got wrong. His cold winters theory is a just-so story; East Asians and Native Americans are not the same race; heritability estimates are not a measure of how much genes have to do with phenotypic variation within or between groups; IQ tests are not construct valid; r/K selection theory was slayed as early as 1991 and then again in 2002 (Graves, 2002); twin studies are not informative when it comes to how much genes influence traits, they only measure environmental similarity; and finally, Rushton omitted data that did not fit his hypothesis on racial differences in crime.
It’s sad to think that one can spend a career—about 25 years—spewing nothing but pseudoscience. One of the only things I agree with him on is that races are real—but when it comes to the nuances, I disagree with him, because there are five races, not three. Rushton got a lot wrong, and I do not know why anyone would defend him, even when these glaring errors are pointed out. (For a good look into Rushton’s lies, see Dutton’s (2018) book J. Philippe Rushton: A Life History Perspective and my mini-review on the book.)
I was watching the show Ancient Aliens a while back (I don’t believe it, it’s great for a good laugh now and then, though) and I recall them “theorizing” that Asians are aliens—specifically due to the Dropa stones. So I was searching Google for some information on it, and I discovered this article Race, Citizenship, and the Politics of Alien Abduction; Or, Why Aliens do not Abduct Asian Americans (Tromly, 2017).
Tromly argues that alien abductions are a specific cultural—national—phenomenon and that certain groups, mainly Asian Americans, are excluded from these so-called abductions. Surely, most readers are familiar with the most famous of all alien abductions—the case of Betty and Barney Hill (Barney Hill was a black man). One night, they were driving down the road. And all of a sudden, they woke up in their car and many hours had elapsed (a concept known as “missing time“). They then went to a hypnotizer and underwent hypnosis. They then described many experiments that the aliens carried out on them. In any case, I’m not going to discuss the so-called abduction here, but this is one case—one of the most famous—of a minority being abducted.
Tromly argues that the notion of alien visitors elicits collectivity in humans—that, of course, all national, racial, and social differences would be put aside in the event of a hostile alien invasion and we would attempt to quell the alien threat. Think War of the Worlds. Indeed, Stephen Hawking argued that we should not attempt to contact aliens. His reasoning was simple: When Europeans came to the Americas in the late 1400s, with their superior technology, they subjugated the natives. Of course, if aliens from far, far away came to earth, they would be far more technologically superior to us—leaps and bounds ahead of the technological superiority when Europeans and Native Americans are compared. So this type of alien invasion, Tromley argues, would spur humans’ “species-consciousness”
Tromly (2017: 278) writes:
According to this paradigm, abductees are traumatized to the point that nationality becomes irrelevant. Describing the trauma of his own abduction in his bestselling book Communion, Whitley Strieber writes, “I was reduced to raw biological response. It was as if my forebrain had been separated from the rest of my system, and all that remained was a primitive creature, in effect the ape out of which we evolved long ago” (18).
So, Tromly then cites psychiatrist John Mack who argues that abductees are not self-selected and that they come from all walks of life. He is pretty much saying that, to the aliens, there is no one type of person that is more desireable to the aliens and therefore no one group is more worthy of visitation than any other. Further, he is arguing that, whatever differences exist between these diverse people, they are equal in one thing: their visitations by alien visitors.
Tromly (2017: 280) then writes:
Lowe argues that this ideal of political membership comes at the cost of specific individuation: “In being represented as citizen within the political sphere… the subject is ‘split off’ from the unrepresentable histories of situated embodiment that contradict the abstract form of citizenship” (2). These inadmissible “particularities” include “race, national origin, locality, and embodiment [that] remain largely invisible within the political sphere” (2). It is useful to revisit Mack’s presentation of the abduction community in light of Lowe’s observations, because his catalogue of abductees is typical of the discourse in that it defines abductees solely in terms of class and profession—in effect, Mack’s example of the diversity of abductees is underwritten by an assumption of sameness. Because he fails to mention other types of difference on the assumption that they are irrelevant, Mack excludes these differences and, ironically, his demonstration of the diversity of the abductee community becomes subtly exclusionary.
Alien abduction, if you keep up with this kind of thing, is pretty obviously racially exclusive: most abductees are white Americans. Though, of course, believers in alien abductions claim that this accurately reflects the racial demographics of America—with whites being the majority racial group.
Tromly then describes a re-telling of the Betty and Barney Hill saga, where the couple he describes are still an inter-racial couple, but the wife remembers the alien abduction, whereas the husband recalls does not remember it, he recalls the night as normal. This story is written by Asian American writer Peter Ho. So when the wife sees a blue alien light, the husband sees blue police lights—implying that alien abductions and police stops are, in a way, coeval. The wife wants to tell the story—the abduction story—since it can be looked at in a broader national context whereas the husband does not want to—since what he recalls of that night was not a night of alien abduction but a night of being stopped by the police. Eventually, the husband gives in to his wife, who was continuously nagging him to “remember’ the abduction. So he “recalled” one under hypnosis, and a completely different one while he dreamed.
Tromly (2017: 287) writes:
The significance of the Asian American abductee’s absence is shaped, in part, by how abduction in general is understood. Accepting accounts of abduction as true accounts of events that have taken place would require hypothesizing about why aliens might be more interested in some ethnicities than others. To understand accounts of abduction as imagined stories that emerge from anxiety, hysteria, or trauma might suggest that these narratives are not a useful avenue for the expression of the concerns of Asian Americans. … Of course, linguistic barriers may be a reason that a certain segment of the Asian American community cannot participate in the textual spread of the abduction phenomenon. (Many abductees recall repressed memories of abduction after reading texts by Hopkins or Strieber.) However, a more compelling reason for their exclusion is that Asian Americans, or the associations they typically bear in popular discourse, disrupt the logic of the abduction narrative.
Great point! What if the aliens can only telepathically communicate with English-speaking people, therefore they are the only ones that get abucted—and not Asian Americans?
Tellingly, Asianness is sometimes used to mark the otherness of extraterrestrial aliens—Strieber, for example, describes the otherworldly features of an alien with whom he comes in contact through a comparison with “Asian” features: “its eyes are slanted, more than an Oriental’s eyes” (60).9 However, rather than focusing on the possible racial connotations of physical descriptions of aliens, it is more productive to examine the similarities between descriptions of alien characteristics and long-standing Asian American stereotypes. Whether they are conceptualized as a threat to humanity or an advanced and enlightened race, aliens that abduct are almost always described as being deliberate, dispassionate, and, needless to say, technologically adept.
Of course, this is where the observation from Ancient Aliens comes from: popular accounts of the aliens are that they are short, physically weak and frail-looking, and, most notably, have slanted eyes. Asians fit this description, too. So, one can see the parallel here: Asians are technologically adapt, as are the aliens. Asians, too, are looked at as being an enlightened race. This, too, pushes the Asian stereotypes—the “yellow peril” stereotype—where Asians want to come to America and take American resources, and the “model minority”—the claim that Asians are what other minorities should strive to be—because they excel “through technological sophistication, emotionless drive” (Tromly, 2017: 288), while they are extremely productive, what I assume aliens would be like.
In any case, it seems that alien abductees are actually more likely to be white. I was watching Ancient Aliens last April and they were discussing certain characteristics of abductees—pretty much like Tromly was, without mentioning race. What they mentioned, though, was pretty funny: abductees were more likely to have rH negative blood along with having a higher percentage of green and hazel eyes. I took two pictures of the screen when it came on:
Wow, how interesting, what a disparity. So it seems, that along with not targetting minorities at the same rate as whites, they are targeting a group of people that are more likely to have green eyes and rH negative blood. Then, someone appeared on the screen and then stated that since hazel and green eyes and RH negative blood are due to mutations, that the aliens either created it or they have a special interest in it. They were talking about a “genetic component” to alien abductions. Seems like even being abducted by aliens is “genetic”, too. Wow, what isn’t “genetic” nowadays?
This article wasn’t that serious; I just found this today and read it, and I had a few laughs. While it is interesting that only white Americans seem to be the subjects of alien abductions and the like—and minorities seem to be overlooked—I don’t think it’s anything like Tromly says. Though obviously, I would say that since the aliens are not abducting Asian Americans and aliens look similar to Asians (small bodies, almond-shaped eyes, and weak and frail-looking bodies) and it is hypothesized by Ancient Astronaut “theorists” that aliens are humans from the future, the conclusion is simple to see: these aliens abducting humans are Asians from the future and they’re not abducting Asians because they are looking for different genes and other physiological and anatomic differences, and since they are descended from Asians then why would they abduct them? Checkmate, Ancient Aliens deniers.
Barnett argues in The Waning of Materialism that for any pair of conscious beings, it is impossible for that pair itself to be conscious. I punch myself and feel pain; You punch yourself and feel pain. But our pair wouldn’t feel a thing. Thus, pairs of people are incapable of experiencing pain. This is what Barnett call’s “The Datum.” He posits six explanations for explaining “The Datum”:
(1) Pairs of people lack a sufficient number of sufficient parts; (2) Pairs of people lack immediate parts of standing in the right sorts of relations to the other and the environment; (3) pairs of people lack the immediate parts of the right kinds of nature; (4) pairs of people are not structures, they are unstructured collections of two parts; (5) some combination of 1-4; and (6) pairs of people are not simple.
Let’s take (1): Imagine that each human on earth is in severe pain, while the collection of people is experiencing pure bliss. This is untenable. Thus, no matter how large, a collection of people cannot be the subject of experience. So pairs of people do not have a sufficient number of immediate parts and thusly do not explain “The Datum.”
Now let’s take (2): Let’s say that scientists shrink you and I down into someone else’s brain, me being the left hemisphere and you being the right hemisphere. Then someone punches the person we have been implanted as their hemispheres; they then react. We then stimulate neurons and the person defends themselves, putting their hands up in defense. We do just what that person’s hemispheres would have done. So we function just like a regular brain. So now you and I have a new relation: is it conscious? You and I may remain conscious, but arethe pair conscious? No. Thus, pairs of people lack the right parts necessary to stand in the right sorts of relations to themselves and the environment and therefore do not explain “The Datum.”
Now let’s take (3): Let’s say I tell you that I have two objects—(a) and (b)—in mind. You, clearly, need more information to conclude that (a) and (b) are conscious, but you don’t need more information to conclude that the pair—comprised of (a) and (b)—is conscious. We know a priori that pairs of things are not conscious; pairs of, say, TVs, rocks, shoes, beds, are not conscious. So, that any pair—(a) and (b)—may be conscious is absurd is not evidence that the two alone are not conscious.
Now let’s take (4): We can know by reflection that the pair comprising (a) and (b) are not conscious. We know a priori that pairs of things are collections while conscious beings are structures. Collections exist iff whenever the comprisal of what makes up the collections exist; a structure of things exists iff the things in question exist in relation to a certain structure. So consider the atoms in the threads in my pillow as a collection and my pillow as a structure. So if we were to disperse the atoms in the thread making up my pillow out into space, the atoms would still exist but my pillow would not. So are pairs of people incapable of having experience because they are not structures? Let’s now return to (2), when you and I were placed in someone’s brain as their hemispheres. So unlike the pair, the system (brain) is a structure and it would cease to exist if you and I were removed from the individual’s brain, though the pair that you and I form would not. However, the system of people is not a candidate for the subject of experience than the pair that constitutes the system. So the idea that pairs of people are incapable of experience since they are not structures does not explain “The Datum.”
Now let’s take (5): Maybe “The Datum” is not explained by (1)-(4). Maybe some combination of the 4 explains “The Datum.” Maybe pairs of people aren’t conscious because it is a collection which results from the existence of two people; maybe a conscious being is a structure comprised of many cells, organs, standing with one another and the environment they are in certain causal dependent relations. So human bodies which are physical structures that are comprised of organs, cells, blood, etc, are conscious; the differences between human bodies are captured in (1)-(4); the four hypotheses do not explain “The Datum” alone; so some combination of (1)-(4) must explain “The Datum.” So let’s go back to (1). If we consider 7 billion people—and not a pair—then we know that no matter the number of people, that collection is not, itself, conscious. Now take (2), but on a larger—societal—level. If everyone in that society has a similar goal and aims for those goals, are they conscious? No; the claim that they are is absurd. Sure, the society functions just as human brain functions, but is that society—itself—conscious? No. Now take (3), but imagine that every neuron in your head was replaced by a mini-man. Thus, if we shift our attention to the number of mini-men in the head to the structure they comprise, it does not make any difference: (1)-(3) does not explain “The Datum.” Finally, let’s take (4). Imagine that your brain was sliced in half and dispersed into vats. Then those hemispheres are halved—while radio transmitters are placed in your hemispheres (preserving communication with the CNS)—and so on and so forth, until each of your neurons sits in its own individual vat. Now imagine that each neuron is paired up with an individual and the neuron gets a break, with the individual then carrying out the function of the specific neuron, Now, what concerns us is whether or not ‘you’ are identical to the scattered parts of what used to comprise ‘you’ and the system that controls your body. Certain times, billions of people operating billions of radio transmitters are operating the system; other days its billions of neurons operating billions of radio transmitters. So these billions of objects which still interact with your nervous system interact with your nervous system just like your brain used to when it was confined to its skull. So whether or not these billions of people that comprise your radio transmitters that control your scattered neurons is irrelevant; what matters is whether the system itself is a subject of experience—and it is not. So no combination of (1)-(4) explains “The Datum.”
Now, finally, let’s take (6): Are pairs of people not qualified from being conscious because they aren’t simple? In all 4 of the hypotheses, composite entities are presented and we ask whether or not the entity may be conscious. Whether or not the entity in question has 2, 100, 100,000, 100,000,000,000 parts is irrelevant. What does matter—however—is whether or not the posited entities presented are a composite. So there is absurdity in the idea that they are identical to a subject of any experience. The only hypotheses that rival this preceding explanation are (1)-(4), but they are inadequate. So simplicity best explains “The Datum.”
So conscious beings must be simple. We are not simple particles, so Barnett’s argument is an argument against materialism. So correlations between our mental states and our brain states do not give reason to identify ourselves with our brains. Therefore we are not our brains.
I am simple. I contain no proper parts (there is no such thing as “half an *I*”). However, my brain contains proper parts. Therefore I am not my brain.
Adapting Minds, Evolutionary Psychology as Maladapted Psychology, and Getting Darwin Wrong—Books Against Evolutionary Psychology
Years ago I wanted to be an Evolutionary Psychologist. After I discovered the work of Lynn, Rushton, Jensen, Kanazawa et al, I was fascinated by the subject of Evolutionary Psychology (EP). Thankfully, I did not go down that route (I went into health sciences). I was enthralled by the work of those that claimed that our psychology reflects adaptations to the Pleistocene EEA (environment of evolutionary adaptedness; or OEE, original evolutionary environment). However, little did I know, these types of hypotheses were just-so stories—ad hoc explanations. They are ad hoc since they are made “for this” reason—i.e., noticing the existence of trait T.
Three books shaped my views on EP: Adapting Minds: Evolutionary Psychology and the Persistent Quest for Human Nature (Buller, 2006), Evolutionary Psychology as Maladapted Psychology (Richardson, 2007), and Getting Darwin Wrong: Why Evolutionary Psychology Won’t Work (Wallace, 2010). These three books are solid. Each one is different, but they all have the same theme: They are against the Santa Barbara School of EP, started by Tooby, Cosmides, and Barkow.
This is one of my favorite books by the philosopher of science David Buller. In the book, Buller distinguishes between “evolutionary psychology” and “Evolutionary Psychology”, the latter being the school of thought pushed by Pinker, Tooby and Cosmides, and Buss. On pages 3-4, Buller (2006) writes:
Initially, I was completely captivated by evolutionary psychology, and I was certain that it was providing a deep and accurate understanding of human mentality and behavior. But after six months’ research, it was unclear to me how everything that went by the name “evolutionary psychology” fit together, and I began having serious doubts about many of the confident claims made by evolutionary psychologists (such as Mooris’s claim that “research has proved” that the majority of sperm in an ejaculate function as sperm warriors). A year’s research later, it was clear to me that there were distinctly different lines of research being conducted under the “evolutionary psychology” label, and I became convinced that the line of research had garnered the most attention, both within academia and throughout the popular media, was wrong in almost every detail. This book emerged as my effort to sort the promising from the wrongheaded lines of research. Accordingly, I originally intended to write a book about the “strong” and the “weak” evolutionary psychology. As the project evolved, however, I found that there was too much to be said about the problems with the “weak” evolutionary psychology, and the project consequently became a critique of evolutionary psychology.
But at many junctures, I felt that I didn’t want to go public with a critique of evolutionary psychology. For, as my research progressed, I became disheartened over the scarcity of reasoned intellectual exchange regarding evolutionary psychology. I found that published criticism of evolutionary psychology typically contained more vitriol than serious analysis of the claims made by evolutionary psychologists, and I didn’t want to be associated with that.
I can see how he was captivated by EP. Initially, I was too, since I believed that it actually had something to say about the evolution of our psychology.
Buller then makes a solid point on page 6:
Accordingly, the rhetoric sets up the following dichotomy: Either you accept biology, in which case you must accept the claim of evolutionary psychologists, or you don’t. Critics have thus been portrayed as necessarily committed to scientifically empty theories from the social sciences, to some form of postmodernist relativism, or to creationism [which is ironic, since EP and creatonism are nothing but just-so stories]. No one who truly accepts evolution, the rhetoric goes, can seriosuly question any of the specific claims of evolutionary psychology.
Each chapter of the book focuses on specific programmes that EPists push: Chapter 1 is about Evolution; Chapter 2 is about Mind; Chapter 3 is about Adaptation; Chapter 4 is about Modularity; Chapter 5 is about Mating; Chapter 6 is about Marriage; Chapter 7 is about Parenthood; and Chapter 8 is about “Human Nature.”
I’m just now reading through the book again, and it’s damn good. It gives a nice critical eye to the claims made by Buss, Pinker, Tooby and Cosmides et al.. Of course, there are critics of EP who decry the claim that we are evolved animals, so that critique isn’t without (some) merit. However, EPists make similarly idiotic claims:
All too often I found evolutionary psychologists dismissing their critics as “antiscientific,” “politically correct postmodernists,” or closeted creationists. Any skepticism about the claims of evolutionary psychology was typically portrayed as a product of dogmatic indoctrination in the social sciences, and the attendant belief that all of human psychology is the product of “socialization,” or else as evidence of a commitment to the “superstitious” belief that humans somehow managed to “transcend” the evolutionary process. Indeed, many critics have been dismissed as simply not wanting to accept the implications of the fact that humans evolved just like beasts in the field. (Buller, 2006: 5)
These types of claims are, though, ridiculous. Critiquing an abortive research programme does not make one “antiscientific” in any way.
Buller’s book is solid and really attacks the EP orthodoxy along with popular accounts of EP. I highly recommend it to anyone who wants to read a well-reasoned critique of all of the popular concepts of EP, which EPists push as “the truth.”
Getting Darwin Wrong
Getting Darwin Wrong is written by psychologist Brendan Wallace. He explicitly states that the book is not about the nature-nurture debate; it is not about whether we should use Darwinian thinking to help understand the human mind; nor is it about other recent attempts—such as sociobiology—to apply Darwinian thinking to human psychology. Though, what the book is about, of course, is EP. It is, specifically, like Buller’s and Richardson’s books, about the books written by Pinker, Tooby and Cosmides et al..
So: why another book discussing EP? To begin with, it might well be thought wise to write a book after the initial storm [of controversy] has died down. Far too much of the initial discussion created mich heat but threw little light on the basic claims of EP, but led instead to a situation where various terms of abuse (‘relativist’, ‘determinist’, ‘reductionist’) were thrown about, without much thought being given to defining these terms, or deciding whether or not EP (or its opponents) were guilty of the myriad intellectual ‘sins’ of which they were accused. Moreover, there was a (to my mind) reprehensible tendency to inder political tendencies from the various scientific theories proposed. EP has political connotations of course: all scientific theories (including those of theoretical physics) have political implications. But it’s grossly unfair to argue that just because a theory might lead to ‘right wing’ (or ‘left wing’) conclusions that therefore it must be rejected. As an old philosophy lecturer once told us as fresh eyed undergraduates in our first years at University: if something has been proven to be true, you just have to accept it, whether you like its implications or not. ‘It makes me feel bad, therefore it is false’ is not an argument.
I, of course, agree with this. Though, funnily enough, people I have debated EP with have accused me of having political motivations for denying EP just-so stories. What is most funny about those accusations, though, is that if I DID have political motivations regarding EP, I WOULD accept EP just-so stories, as a lot of them line-up with political beliefs that I hold. It seems that people cannot fathom that one can be on the right and reject the storytelling of EPists.
Wallace attacks three views of EP: the “information processing”—“… the idea that human cognition consists mainly (or exlclusively) of the processing of information” (Wallace, 2010: 7), the theory of cognitivism—“… the belief that cognition is the manipulation of symbols by rules or algorithms” (Wallace, 2010: 7), and computationalism, “… the belief that the human brain is (or can be usefully compared to) a digital computer” (Wallace, 2010: 7).
So the argument of this book is (I think) novel and quite simple. It is this. Evolutionary Psychology is NOT (as it is normally taken to be) an unproblematic adaption of Darwinian theory to the science of psychology. Instead, EP is an adaption of a specific ‘school’ of psychology: that of cognitivism (or the ‘information processing view of human cognition’ or ‘computationalism’). Essentially EP is an attempt to reinterpret and restate the basic precepts of cognitivism within a Darwinian framework.
This seems like a controversial argument but actually, a careful reading of the seminal works of Cosmides, Tooby, Pinker and other associated with EP shows that they have always been fairly clear about what EP really is, and what they are trying to do. I will also attempt to show that Cosmides et al. were forced to adopt their cognitivist position because of certain assumptions they began with about what psychology is and should be, and that these assumptions themselves are by no means unproblematic. (Wallace, 2010: 8-9)
In one of the major themes of the book, Wallace attacks the massive modularity hypothesis (MMH) that EPists push. According to EP, the mind is made up of different modules which evolved for specific tasks in our OEE. However, as I have noted before, the arguments erected in favor of this view fail.
Getting Darwin Wrong is the most different of the three books discussed today, and I like it as a solid history into the underpinnings of EP and its assumptions.
Evolutionary Psychology as Maladapted Psychology
The final book I will discuss is Evolutionary Psychology as Maladapted Psychology by the philosopher of science Robert Richardson. It is most similar to Buller’s book, in that it specifically attacks EP theories, whereas Wallace’s book shows the history of EP and how and why the assumptions underpinning them are false. Richardson, like Buller, attacks the just-so stories of Pinker, Tooby and Cosmides, and Buss. He shows, for instance, that so-called “evolved fears” of snakes and spiders are baseless. (Indeed, there is good evidence that these are learned fears.)
Richardson discusses the aims of EP, reverse engineering, adaptation, massive modularity and Tooby and Cosmides’ integrated causal model (ICM) vs their version of what social ‘scientists’ believe—the standard social science model (SSSM). He notes how they have erected a false dichotomy between an untenable view and their own, so that others would accept their own view.
The structure of his book is as follows (Richardson, 2007: 51):
The heart of this book is organized around three different approaches toward empirically evaluating evolutionary explanations. These include what is called “reverse engineering” (chap. 2); another alternative is to infer the effect from the relevant causes, an approach that reflects the dynamic perspective of much of evolutionary biology (chap. 3); finally I will turn to analyses designed to disentangle history from structurem which depends on disentangling historical ancestry (chap. 4). I believe that the later analyses are the most powerful.
One of the strengths of his book is the forcefulness of his analyses of EP claims. For example, his discussion of so-called evolved fears of snakes and spiders is particularly strong:
On this view, at least some human fears (but not all) are given explanations in evolutionary terms. So a fear of snakes or spiders, like our fear of strangers and heights, serves to protect us from dangers. Having observed that snakes and spiders are always scary, and not only to humans, but other primates, Steven Pinker (1997: 386) says “The common thread is obvious. These are the situations that put our evolutionary ancestors in danger. Spiders and snakes are often venomous, especially in Africa…. Fear is the emotion that motivated our ancestors to cope with the dangers they were likely to face” (cf. Nesse 1990). This is a curious view, actually. Spiders offer very little risk to humans, aside from annoyance. Most are not even venomous. There are perhaps eight species of black widow, one of the Sydney funnel web, six cases of brown recluses in North and South America, and one of the red banana spider in Latin America. These do present varying amounts of risk to humans. They are not ancestrally in Africa, our continent of origin. Given that there are over 37,000 known species of spiders, that’s a small percentage. The risk from spiders is exaggerated. The “fact” that they are “always scary” and the explanation of this fact in terms of the threat they posed to our ancestors is nonetheless one piece of lore of evolutionary psychology. Likeways, snakes have a reputation among evolutionary psychologists that is hardly deserved. In Africa, some are truly dangerous, but by no means most. About one quarter of species in Uganda pose a threat to humans, though there is geographic variability. It’s only in Australia—hardly our point of origin—that the majority of snakes are venomous. Any case for an evolved fear of snakes would need to be based on the threat from a minority. In this case too, the threat seems exaggerated. There is a good deal of mythology in the anecdotes we are offered. It is not altogether clear how the mythology gets established, but it is often repeated, with scant evidence. (Richardson, 2007: 28)
It is important to note that, for example in chimps, fear of snakes is learned (socially), since captive chimps show no fear to snakes (Anderson, 2018). See also Ehrlich (2003: 89) who notes that this fear of snakes is not found in New Guinea natives, where one would assume that it would be found if the claims from Pinker hold.
Richardson attacks the false dichotomy pushed by Tooby and Cosmides (1992), writing:
Tooby and Cosmides’ portrayal [of the SSSM] is very effective. It is also a piece of sophistry, offering a false dichotomy between a manifestly untenable view and their own. The alternative is one that sees no differences between individuals and no biological contribution to individual or social development. I think no serious figure embraces that view, since, perhaps, John Watson in the early twentieth century.
Tooby and Cosmides also say that “There is no small irony in the fact that [the] Standard Social Science MOdel’s hostility to adaptationist approaches is often justified through the accusation that adaptationist approaches purportedly attribute important differences between individuals, races and classes to genetic differences. In actuality, adaptationist approaches offer the explanation for why the psychic unity of humankind is genuine and not just an ideological fiction” (1992, 79).
Of course, if one puts for an untenable view with their own, theirs will then be accepted.
Lastly, Richardson (2007: 73) attacks one of Buss’s hypotheses:
We begin by assessing differences between men and women in terms of their sexual attitudes. Let’s suppose, contrary to fact, that we actually have reasonable gauges of these differences. Buss uses the evidence to conclude that there are sexual differences, notes the consistency of this with some evolutionary models, and infers that our ancestors not only actually behaved in a way that reflects the differences in our attitudes, but that there were selective pressures to behave. These differences in attitude are supposed to reflect some deeper underlying differences in mating strategies. The mating strategies are taken in turn to reflect some fundamental biological imperative. This argument is put forth without citing evidence concerning, say, group structure, which would certainly be relevant. It is put forth without so much as information concerning group size. It is put forth without information concerning similarities between ancestral and current group structures, mating structures, or group sizes. It is, of course, put forth without evidence concerning actual mating behavior, or the differences supposed to exist in ancestral groups. From all this, and less, we infer that there is an evolutionary and adaptive explanation of the differences between the sexes. That conclusion, in turn, allows Buss to interpret the evidence in a way that he thinks somehow makes evolutionary sense. If this is the way the argument works, then it is a case of reverse engineering. But it is not a very compelling case of reverse engineering.
EP, since its inception in the early 90s, has been the subject of numerous debates. I, personally, reject EP on the grounds that no EP hypothesis can be independently verified. However, contrary to my views, Richardson, Buller, and Wallace are hopeful in the EP paradigm, though they strongly criticize it. For example, Richardson (2007: 25) writes that he “views evolutionary psychology as more speculation than science” and that “It does not warrant our acceptance“, so “Evolutionary psychology as currently practiced is often speculation disguised as results. We should regard it as such.” I agree with this—speculation is not science. Just-so stories are not science.
In any case, all three of these books, if read with an open mind, will have one become extremely skeptical of EP, and, hopefully, reject the abortive research programme since it cannot do what it purports to.
(Ir)RationalWiki (IW) is a Wikipedia-style website, where anyone can edit or create an article on whatever they’d like. They are a left-leaning website, so they, of course, don’t like what they consider to be “right-wingers.” Many “HBDers” have IW articles on them, notable hbdchick, JayMan (though it seems like his article was deleted), Emil Kirkegaard, Anatoly Karlin, and even a new one on the philosopher of biology Nathan Cofnas (see his response here). When I discovered my own article on IW, I laughed, since it grouped me in with “Frogs and Swastikas, AltRight.” Well, I think that the “Pepe the frog” meme is idiotic and childish, and I’m not a Nazi (National Socialist).
In any case, I recently looked at the page and discovered that they finally edited it to reflect my new views. My views changed around April/May 2017 due to two books: DNA is not Destiny: The Remarkable, Completely Misunderstood Relationship Between You and Your Genes (Heine, 2017) and Genes, Brains, and Human Potential: The Science and Ideology of Intelligence (Richardson, 2017). I would say that before reading these two books that I was a “genetic determinist.” However, Richardson’s work lead me to the work of Denis Noble, Jablonka and Lamb, Susan Oyama, and David Moore and the philosophy of developmental systems theory (DST). My deterministic views (and outdated views on genes and the physiological system) were then cured.
In any case, here is what the new edit says about me now:
RaceRealist started out as a supporter of hereditarianism racist theories about IQ and a fanboy of Richard Lynn and Arthur Jensen, but later to his credit rejected these views. Instead however of giving up all his racialist beliefs, he still defends racialism, albeit minus the IQ pseudoscience. The latter has led to him to be criticised as still being a racist but using a deceptive motte and bailey strategy of trying to present himself as a more moderate non-hereditarian “race realist” when he still retains the old racist IQ beliefs about inferior black people in private. Furthermore, despite claiming to have changed his views on the latter – all his old pro-hereditarianism posts on his blog are still up alongside background photos of white supremacists.
The first sentence is true; I did start out as supporter of hereditarianism. When I discovered the work of people like Rushton, Lynn, Kanazawa, and Jensen I thought “Wow, this all makes so much sense and explains why our societies are stratified the way they are.” Though, as mentioned above, I did change my views.
Yes, I do “still defend racialism”, but a softer, non-hereditarian view of human races (Spencer, 2014, Hardimon 2017). These types of arguments about race are non-hereditarian, non-hierarchical. I do agree that “IQ science” is psuedoscience, but the claim that “I still retain [my] old racist IQ beliefs about inferior black people in private” are completely unfounded. How does whoever wrote this know what views I hold in private? Further, they claimed that I “rejected [those] views” in reference to hereditarianism (Jensenism) but then they say that “I still retain [my] old racist IQ beliefs about inferior black people in private”? How does that make any sense?
Further, I have explicitly stated that the terms “superior” and “inferior” are strictly anatomic terms and, outside of that context, make no sense. The head is superior to the feet; the feet is inferior to the head. It seems that the author of this did not read my article Blumenbachian Partitions and Minimalist Races where I explicitly state:
Biological racial realism (the fact that race exists as a biological reality) is true, however, just like with Hardimon’s minimalist races, they do not denote “superiority”, “inferiority” for one race over another. Most importantly, Blumenbachian populations do not denote those terms because the genetic evidence that is used to support the Blumenbachian partition use noncoding DNA. (It should also be noted that the terms “superior” and “inferior” are nonsensical, when used outside of their anatomic contexts. The head is the most superior part of the human body, the feet are the most inferior part of the human body. This is the only time these terms make sense, thus, using the terms outside of this context makes no sense.)
Yes I have changed my “views on the latter [hereditarianism]”, and no, I will not remove my “old pro-hereditarianism posts” on my blog. I leave them up to show the evolution of my views over time. My blog is almost four years old, and half of the time I was a staunch hereditarian/genetic determinist and the other half I discarded those views and embraced the philosophy of DST.
In any case, the race debate is a philosophical, not biological, one; genetic variation exists between human populations which no one denies. The question “What is race?” is strictly a philosophical question and so, after that question is answered, it follows that the argument about the existence of race is then philosophical. Holding views on racial realism (the claim that our racial categories pick out real kinds in nature; Smith, 2015; 43). Therefore, the views that I hold on race are not scientific, but philosophical.
Re my views on immigration: yes I did write that non-western people are abnormal to our societies (fun fact: I wrote that as a paper for an Abnormal Psychology course, and I got an A). I do still hold that immigration should be restricted/completely halted, though it should not be based on IQ testing, as I once argued in the past. I agree that these views that I once held are idiotic. Looking back at what I wrote and used to believe in the past, I believed a lot of bullshit and pseudoscience. I openly admit that my former prejudices drove my old beliefs. However, as noted earlier (and in the past), I rejected those kinds of genetic determinist “racist” views after discovering the philosophy of DST and reading Richardson and Heine.
A final note on my politics: I support closed borders, I support capitalism and I am a nationalist. I don’t care about what people do in private, just don’t bring it out on the streets. I would say that I am somewhat of a libertarian, and while I do hold some “AltRight” views, I would not self-identify as an alt-righter.
In sum, (Ir)RationalWiki is a joke of a website with how they attack individuals who do use their real names. I’m just some anon guy with a blog and Twitter account. They libel people with mined quotes and don’t reflect their views correctly. In any case, yes my views have changed, and no, it’s not some “cover” for my old views. I do not still hold those same beliefs “in private” (how would whoever wrote this know what views I hold in private? It’s idiotic). I’m not “AltRight”, nor have I ever been.
I’ve written on steroid use between blacks and whites last year, but it was a smaller part of an article concerning the misconceptions people have on steroids and what they do (responding to the hysteria that the media and the like discuss with their claims of “roid rage”). I cited some studies showing that blacks use more drugs than whites; that blacks are more likely to lie about drug-use than whites; and that blacks are more likely to use steroids than whites (indeed, minorities were twice as likely to use steroids compared to whites in one study). (It is also worth noting that “roid rage” is a myth; AAS use is associated with other drug use, which explains the relationship. See Lundholm et al, 2015. For further information on this matter, see the documentary Bigger, Stronger, Faster.)
Steroids are synthetic hormones—lab-made hormones that mimic the so-called “male hormone” testosterone. Though the term “steroid” is misleading; what is being discussed are androgenic anabolic steroids (AAS), since, for example, estrogen is a steroid and does not have the muscle-building and recovery properties of AAS. The term “anabolic” refers to muscle-building whereas the term “androgenic” refers to the increase in male sexual characters. AAS abuse is associated with tendon ruptures, a lower incidence of prostate hypertrophy, anxiety, depression, and a decreased libido (Bagge et al, 2017). Furthermore, the negative effects of AAS (ab)use cause cardiovascular problems, dyslipedemia—which may impact vascular functioning, ventricular arrhythmias while training, hypertension, etc. (Goldman and Basaria, 2018). Further negative effects include raised cholesterol, hair thinning, sterility, and decreased hormone levels. Croaker (2017) notes that AAS use is prevalent throughout high school and collegiate sports, though “When the desired outcome is achieved, the results are always short lived.”
Individuals use steroids for myriad reasons—despite the well-known adverse effects. A few considered are: (1) to become better at sports; (2) to increase muscle mass (which then relates to increased recovery time so the individual can train more); and (3) they are administered a script by their primary care doctor because their testosterone levels are low for their age range. In any case, in this article, I will discuss (1) and (2).
Whichever way the racial differences in AAS use go, we can all agree on one thing: in young men, they most likely want to become better athletes. AAS use is associated with shorter recovery times (
How can you tell if any individual is using steroids? It’s very simple. An increase in upper-body mass, most notably the shoulders and traps. The reason for this is that there are more androgen receptors in the shoulders and so they respond better to the flood of synthetic hormone.
AAS (ab)use is pretty prevalent throughout America. For example, Blashill et al (2017) write that “Black, Hispanic, and White sexual minority boys reported misuse at approximately 25%, 20%, and 9%, respectively.” “Sexual minorities” refers to sexual identity and the sex of the sexual partner. “Whites” were those who said they were not “Hispanic” and were white; “blacks” were those who said that they were not “Hispanic” and were black; while “Hispanics” were those who identified as a “Hispanic” ethnicity while marking down another race. (Note that “white” and “black” are socialraces.)
The (ab)use of AAS particularly affects homosexual minorities. Blashill et al (2017) write:
Sexual orientation health disparities in anabolic steroid misuse disproportionally affect Black and Hispanic sexual minority adolescent boys …
Blashill et al (2017) conclude from the results of their study that the (ab)use of AAS by sexual minorities may be due to “muscularity-oriented body image concerns.” I have heard (albeit, anecdotally) that a lot of homosexuals use AAS in order to look good so they would fall under (2).
The Child Trends Data Bank writes that “There are no significant differences in use of steroids in the past 12 months when comparing whites, blacks, and Hispanics.”
Hua and Braddock (2008: 29) write that “White males reported higher prevalence of steroid use than Black males, and sport participation served as a protective factor, but only for Black males.” They conclude that:
Specifically, our results show that sport participation served as a protective factor, but only for Black males. Sports active black male adolescents reported lower rates of steroid use than Black males who were not involved in sports.
So, it seems that sport participation is protective for blacks in regard to steroid use. However, black males lie about drug use more than white males, and so, I don’t see why we should accept the conclusions of this study. I also find it hard to believe that sport participation would be protective against AAS use. Intuitively, you would expect it to cause more AAS use.
The Journal of Ethics states that AAS (ab)use was higher in white (6.2%) and “Hispanic” students (7.2%) than black students (3.6%).
Irving et al (2002) state that 2.1% of white males 7.6 percent of black males, 6.1% of “Hispanic” males, 14.8% of Hmong males, 7.9% of “other Asian”, 3.1% of Native Americans, and 11.3% of mixed race males reported AAS use. Whereas 0.5% of white females, 4.3% of black girls, 0.9% of “Hispanic” girls, 8.9% of Hmong girls, 3% of “other Asian” girls, 4.7% of Native American girls, and 4.1% of mixed race girls used steroids. Here is table 1 from Irving et al (2002):
Low SES individuals were more likely to (ab)use AAS than high SES individuals in both sexes. Middle schoolers were more likely than high schoolers. (Where are they getting the AAS? Their parents? Older siblings?)
Irving et al noted that the male AAS users were least satisfied with their shoulders (we can’t all be so lucky). Fortunately for them, as noted above, the shoulders have the most androgen receptors in the body and so their shoulders will grow. However, other than not being satisfied with their shoulders, body image was not associated with AAS use in males. Female AAS users, more so than non-AAS users, were more likely to report that they used AAS to for “weight and shape.” Further, sport players were more likely than non-sport players to use AAS—as expected. In a nutshell, AAS use is associated with poor markers of physical health—most importantly because many individuals wanted to lose weight (most likely fat mass). It should be noted that those who were dissatisfied with their bodies were less knowledgable about nutrition, so to amleiorate some of this, nutrition should be taught earlier in schools.
I can’t think of any reasons why, however, Hmong males and females would be using AAS more than other ethnies. However, Irving et al (2002: 251) write:
One finding regarding the demographic characteristics of steroid users in our sample is worth noting. Steroid use was more common in non-Caucasian respondents (both male and female), with particularly high rates among Hmong participants. Initially, we were puzzled by this result and questioned its validity. However, in consultation with community informants from social service agencies that work with southeast Asian youth in the Minneapolis/St. Paul area, we were told by some informants that the “word on the street” was the Hmong youth were attempting to “bulk up” physically, by working out and using steroids. One possible explanation for this finding is that, as fairly recent immigrants (most Hmong immigrated to the U.S. in the past 20 years), Hmong youth may be “bulking up” to gain status in a culture that emphasizes physical appearance, including weight, shape, and physical strength. This interpretation is supported by anthropological research wherein exposure to western ideals of beauty and eating habits is followed by increases in weight and shape preoccupation and disordered eating practices among individuals from non-western cultures. On the other hand, it is possible that Hmong youth may have misinterpreted the question.
So if the Hmong did not misunderstand the question, it is possible, for example, that they were getting bullied (due to being new immigrants) and decided to take AAS in order to get bigger to stop the bullying.
Stilger et al (1999) note that (my emphasis):
Of the 873 high school football players participating in the study, 54 (6.3%) reported having used or currently using AAS. Caucasians represented 85% of all subjects in the survey. Nine percent were African-American while the remainder (6%) consisted of Hispanics, Asian, and other. Of the AAS users, 74% were Caucasian, 13% African American, 7% Hispanic, and 3% Asian, x2 (4,854 4) 4.203, p 4 .38. The study also indicated that minorities are twice as likely to use AAS as opposed to Caucasians. Cross tabulated results indicate that 11.2% of all minorities use/used AAS as opposed to 6.5% of all Caucasians (data not displayed).
Lastly, Green et al (2001) note that whites and blacks used AAS at the same rate, though the n = 10,850 Caucasians while for African Americans the n = 1,883.
However, unless a study notes that the participants’ blood was assayed, why should we believe the results when it’s been noted that blacks underreport and lie about drug use more than whites (Bauman and Ennett (1994); Ledgerwood et al, 2008; Lu et al, 2001)?
In sum, many studies report different results. I would say that the difference is due to cultural/social differences based on where the studies were carried out. The mixed results of these studies points to one thing: AAS use is prevalent throughout school life, and since it starts so young with many people, older siblings seem to be getting it for them. Sexual minorities are more likely to use than whites and this seems to come down to body image; Hmong seem more likely to use than non-Hmong; and the racial differences seem to hold with females as well.
Steve Stewart-Williams wrote an article for Nautilus yesterday titled Nurture Alone Can’t Explain Male Aggression. He begins the article by describing a bank robber who shoots and kills a bank teller and then takes police on a high-speed chase where he finally gets killed. Then it is revealed that the bank robber had an extensive criminal history. Oh, it was a male. “you weren’t being sexist“, he writes, “you were playing the odds.” Most men aren’t violent, but most violent individuals are men. Stewart-Williams then discusses a recent article published by The New York Times titled It’s Dangerous to Be a Boy, with the headline (emphasis mine) “They smoke more, fight more and are far more likely to die young than girls. But their tendency to violence isn’t innate.” I will discuss the use of the term “innate” further down.
Stewart-Williams then states, going off the headline quoted above, that the statement means that “sex differences in aggression come entirely from the environment: from culture rather than biology, nurture rather than nature.” Nevermind the false dichotomy here, let’s finish up discussing the gist of the article before getting onto what’s wrong with it. He then states that biology matters as well, and that the claim that male violence isn’t “innate” is the “Nurture Only” position, while we know that “Biology matters as well.” This seems to be the strawman that all evolutionary psychologists battle with: Anyone who disagrees with EP claim C is a “blank slatist” (this phrase taken care of by Robert Richardson in Evolutionary Psychology as Maladapted Psychology); but due to the interaction of nature and nurture, genes and environment, you can’t partition them into percentages—as is done with heritability estimates (see Moore and Shenk, 2016).
So these sex differences in aggression are noticed in all cultures. What could explain this? Stewart-Williams then discusses the Eagly and Woods’ (2016) social role theory of sex differences. They agree—of course—that there are sex differences in aggression and crime found throughout all cultures on earth, but the cause of domination is due to the effect of evolved differences in body size—men being bigger, stronger, and faster than women while women are smaller, weaker, and slower than men. So this proposed hypothesis states that the psychological differences found throughout all cultures is due to physical sex differences.
“Why wouldn’t natural selection create psychological sex differences as well as physical ones?“, Stewart-Williams writes. Well the answer to this question is that there are no psychophysical laws so psychological traits/mental abilities can’t be selected. Then there is the fact that natural selection is not an explanatory mechanism since it cannot explain trait fixation because there are no laws of selection for trait fixation (Fodor, 2008; Fodor and Piatteli-Palmarini, 2010).
Stewart-Williams writes “Some argue that, even if culture doesn’t create the aggression sex difference out of nothing, it does still amplify a relatively trivial inborn difference.” This is ridiculous: “culture doesn’t create the sex difference out of nothing”, however, small differences between males and females can be magnified by culture (Eliot, 2009). Note that this is a developmental perspective, and that developmental systems theory (DST) is completely at-ends with Evolutionary Psychology.
Is it just a coincidence that this alleged surge in socialization comes at the same time as the massive surge in circulating testosterone that accompanies puberty in males?
I see he is implying that circulating testosterone levels explain differences in aggression between males and females and that this also explains aggression as well. Though, as I have documented, the claim is false.
Stewart-Williams than writes:
The socialization hypothesis offers no particular reason to expect this. But the decline in violence coincides almost perfectly with the decline in testosterone found in men throughout the adult years, and mirrors the decline found in males of other species. Once again, this is much easier to explain in evolutionary than in sociocultural terms.
How interesting to bring this up. I’m sure most have heard the claim that testosterone levels begin to decrease at around age 25-30 (a decrease in total T of 1-2 percent per year after age 30). Though, note that age-range. What major life events occur during that time for most men? Marriage, children (some bouts of depression). Smoking, too, explains some of it. Shi et al (2013) write:
The annual decline in T (−0.8% per year) is similar to that reported from longitudinal cohort studies in the United States (17), Denmark (36), and Australia (16). The current study strongly suggests that the decline in T is not an inevitable part of aging, which is consistent with a recent cross-sectional study of 325 men 40 years and older self-reporting very good or excellent health (37). Our data show that variability in the change in T is largely explained by smoking behavior and intercurrent changes in health status, particularly obesity, depression, the overall burden of chronic disease, and marital status.
Though, predominantly, the biggest culprit to decreasing testosterone is obesity. Further, smokers have higher levels of testosterone than non-smokers (Wang et al, 2013). This is because smoking cessation causes fat mass to accumulate, and higher fat mass is associated with lower testosterone levels.
In any case, Stewart-Williams continues to talk about the “Nurture Only” (“blank slate”) position. He discusses how human males commit around 95 percent of crime while being 79 percent of homicide victims. He then states that male chimpanzees commit 92 percent of “chimpicides” while male chimps are 72 percent of those who are killed. So if he will use chimps as an example for an “innate” tendency, then I’ll use something on chimps to prove the point that it’s not testosterone that causes aggression, as Stewart-Williams is implying.
In The Trouble with Testosterone, Sapolsky (1997) discusses five chimpanzees. The chimpanzees were then allowed to form a hierarchy, 1-5. Number 3 pushed his weight around on numbers 4 and 5 but was subservient to numbers 1 and 2. Number three was taken and then injected with testosterone. He then began engaging in more aggressive behavior, which would confirm the hypothesis that testosterone causes aggression, right? Wrong. Sapolsky (1997) writes:
So even though small fluctuations in the levels of the hormone don’t seem to matter much, testosterone still causes aggression. But that would be wrong. Check out number 3 more closely. Is he now raining aggression and terror on any and all in the group, frothing in an androgenic glaze of indiscriminate violence. Not at all. He’s still judiciously kowtowing to numbers 1 and 2 but has simply become a total bastard to number 4 and 5. This is critical: testosterone isn’t causing aggression, it’s exaggerating the aggression that’s already there.
Now let’s get to the problem with the term “innate”: It’s an empty term. It’s a term that people use when they don’t want to think about the development of the trait in question. For example, the term “innate” is thought by numerous researchers today to be driven “by” genes. It is assumed that “innate traits” are “non-malleable.” Maybe the assumption is that only genes are needed for the culmination of trait X. Or maybe the assumption is that a trait is “innate” iff it is fully genetically influenced. Though, there is a problem there, too. What does it mean for something to be “genetically influenced”? What a priori justification exists to privilege genes over any other developmental variables? There is none. Noble’s (2012; 2017) argument rears its head whenever the discussion of “genetic traits” comes up: it’s nonsensical to talk about, since, in a multi-level complex biological system, pinpointing one level is useless since they all interact.
However, Bateson and Mameli (2007) dispense with the term “innate”. They write that “Over-used metaphors from engineering such as ‘‘hardwiring’’ and ‘‘pre-programming’’ applied globally to the outcome of development fail to capture the character of the processes and once again invite the mistaken view that they can be contrasted with their opposites. We believe that a thorough investigation of developmental processes has been hindered by indiscriminate use of the labels ‘‘innate’’ and ‘‘acquired.’’”
So the next time you see a marvelous and complex behavior—such as a border collie herding sheep or birds flying south for the winter—try to resist the temptation to label it as instinctive, hardwired, genetic, or innate. By foregoing a label and digging deeper, you will open yourself to consideration of the myriad of factors that shape who we are and why we behave the way we do.
In sum, Stewart-Williams does not understand endocrinology (positing evolutionary explanations for T decreases at around the mid-20s in comparison to socio-cultural ones); he does not understand that socialization in male and female babies makes small gaps wider (Eliot, 2009); he does not understand (though he only implied this and did not outright claim it) that testosterone does not cause violence/aggression/crime. Evolutionary Psychologists really need to get a clue. Positing evolutionary explanations (i.e., just-so stories when they cannot be independently verified of the data they purport to explain) does not lend itself to any kind of explanation for why a certain trait persists in the modern world. Lastly (though he did not make the claim here), the terms “innate” and “genetic” are baseless and empty and do not give us any new information about the trait in question.