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Answering Common “Criticisms” of the Theory of African American Offending
4150 words
Introduction
Back in September I published an article arguing that since the theory of African American offending (TAAO) makes successful novel predictions and hereditarian explanations don’t, that we should accept the TAAO over hereditarian explanations. I then published a follow-up arguing that crime is bad and racism causes crime so racism is bad (and I also argued that stereotypes lead to self-fulfilling prophecies which then cause the black-white crime gap). The TAAO combines general strain theory, social control theory, social disorganization theory, learning theory, and low self control theory in order to better explain and predict crime in black Americans (Unnever, 2014).
For if a theory makes successful novel predictions, therefore that raises the probability that the theory is true. Take T1 and T2. T1 makes successful novel predictions. T2 doesn’t. So if T1 and T2 both try to explain the same things, then it’s only logical to accept T1 over T2. That’s the basis of the argument against hereditarian explanations of crime—the main ones all fail. Although some attempt at a theory has been made integrating hereditarian explanations (Ellis’ 2017 evolutionary neuroandrogenic theory), it doesn’t make any novel predictions. I’ve recently argued that that’s a death knell for hereditarian theories—there are no novel predictions of any kind for hereditarianism.
But since I published my comparison of the successes of the TAAO over hereditarian explanations, I’ve come across a few “responses” and they all follow the same trend: “What about Africa, Britain, and other places where blacks commit more crime? Why doesn’t racism cause other groups to commit more crime?” or “So blacks don’t have agency?” or “Despite what you argued against hereditarian explanations what about as-of-yet-to-be-discovered genes or hormonal influences that lead to higher crime in blacks compared to whites?” or “What about IQ and it’s relationship to crime?” or “What control groups are there for TAAO studies?” or “The black-white crime gap was lower during Jim Crow, how is this possible if the TAAO is true?” or “Unnever and Gabbidon are just making excuses for blacks with their TAAO” or “The so-called ‘novel predictions’ you reference aren’t novel at all.” I will answer these in turn and then provide a few more novel predictions of the TAAO.
“What about Africa, Britain, and other places where blacks commit more crime? Why doesn’t racism cause other groups to commit more crime?“
For some reason, TAAO detractors think this is some kind of knock-down questions for the TAAO and think that they disprove it. These are easily answered and they don’t threaten the theory at all.
For one, the theory of AFRICAN AMERICAN offending is irrelevant places that… Aren’t America. It’s a specific theory to explain why blacks commit crime at a higher rate IN AMERICA, therefore other countries are irrelevant. There would need to be a specific theory of crime for each of those places and contexts. So this question doesn’t hurt the theory. So going off of the first question, the answer to the second question also addresses it—it’s a theory that’s specifically formulated to explain and predict crime in a certain population in a certain place.
For two, why would a theory that’s specifically formulated to explain crime using the unique experiences of black Americans matter for other American groups? Blacks went through 400 years of slavery and then after that went through segregation and Jim Crow, so why would it mean anything that other groups face discrimination but then don’t have higher rates of crime compared to the average? Since the theory has specific focus on understanding the unique experiences and dynamics of crime in the black American population, it’s obvious that asking about other groups is just irrelevant. Other racial and ethnic groups aren’t the primary focus—since it aims to address historical and contemporary factors that lead to higher crime in the black American population. It’s in the name of the theory—so why would other racial groups matter? Unnever and Gabbidon (2011: 37) even explicitly addressed this point:
Our work builds upon the fundamental assumption made by Afrocentists that an understanding of black offending can only be attained if their behavior is situated within the lived experiences of being African American in a conflicted, racially stratified society. We assert that any criminological theory that aims to explain black offending must place the black experience and their unique worldview at the core of its foundation. Our theory places the history and lived experiences of African American people at its center. We also fully embrace the Afrocentric assumption that African American offending is related to racial subordination. Thus, our work does not attempt to create a “general” theory of crime that applies to every American; instead, our theory explains how the unique experiences and worldview of blacks in America are related to their offending. In short, our theory draws on the strengths of both Afrocentricity and the Eurocentric canon.
“So blacks don’t have agency?”
The theory doesn’t say that blacks lack agency (the capacity to make decisions and choices) at all. What the theory does say is that systemic factors like racism, socioeconomic disparities, and historical and contemporary marginalization can influence one’s choices and opportunities. So while individuals have agency, their choices are shaped by the social context they find themselves in. So if one has a choice to do X or ~X but they physical CAN’T do X, then they do not have a choice—they have an illusion of choice. The TAAO acknowledges that choices are constrained by poverty, racism, and social inequity. So while blacks—as all humans do—have agency, some “choices” are constrained, giving the illusion of choice. Thus, constraints should also be considered while analyzing why blacks offend more. This, too, is not a knock-down question.
“Despite what you argued against hereditarian explanations what about as-of-yet-to-be-discovered genes or hormonal influences that lead to higher crime in blacks compared to whites?”
Over the years I’d say I’ve done a good job of arguing against hereditarian theories of crime. (Like testosterone increasing aggression and blacks having higher levels of testosterone, the AR gene, and MAOA.) They’re just not tenable. The genetic explanation makes no sense. (Talk about disregarding agency…) But one response is that we could find some as-of-yet-to-be-discovered genes, gene networks, or neurohormonal influences which explain the higher crime rates in black Americans. This is just like the “five years away” claim that hereditarians love to use. We just need to wait X amount of years for the magic evidence, yet five years never comes since five years away is always five years away.
“What about IQ and it’s relationship to crime?”
Of course the IQ-ists love this question. The assumption is that lower IQ people are more likely to commit crime. So low is means more crime and high IQ means less crime. Ignoring the fact that IQ is not a cause of anything but an outcome of one’s life experiences, we know that the correlation between IQ and crime is -0.01 within family (Frisell, Pawitan, and Langstrom, 2012). So that, too, is an irrelevant question. The relationship just isn’t there.
“What control groups are there for TAAO studies?”
Other than the first question about why don’t other groups who experience racism commit more crime and what about blacks in other countries, this one takes the cake. The TAAO doesn’t need control groups in TAAO tests since it focuses specifically on understanding the unique factors that contribute to crime in America. So instead of comparing different racial or ethnic groups, the TAAO seeks to identify and analyze specific historical, social, and systemic factors which shape the experiences and behaviors of black Americans within the context of American society.
“The black-white crime gap was lower during Jim Crow, why? How is this possible if the TAAO is true?”
Between 1950 and 1963, non-whites made up 11 percent of the US population, 90 percent of which were black. In 1950 for whites the murder rate was 2 to 3 deaths per 100,000 while for non-whites the rate was 28 deaths per 100,000 (28 times the US average) which then fell to 21 per 100,000 in 1961 which was still about 8 times that of the white murder rate while the rate raised again between 1962 and 1964 (Langberg, 1967). Langan (1992) showed a steady increase in the incarcerated black population from 1926 (21 percent) to 1986 (44 percent). But demographic factors account for this, like increases in the sentencing of blacks, the increase in the black population, and increase on black arrest rates—furthermore, there is evidence for increased discrimination between 1973 and 1982 that would explain the 70s-80s incarceration rates (Harding and Winship, 2016). Harding and Winship also showed that differential population growth can account for one-third of the increase in the prison population difference while the rest can be accounted for by differences in sentencing and arrest rates between 1960 and 1980. So the black population increased more in states that had higher incarceration rates. Nonetheless, the TAAO isn’t supposed to retroactively explain trends.
Therefore, the disparity between whites and blacks remained, even pre-1964. This question, too, isn’t a knockdown for the TAAO either. These questions that are asked when one is provided with the successful novel predictions of the TAAO are just cope since hereditarian explanations don’t make novel predictions and their explanations fail (like the ENA theory).
“Unnever and Gabbidon are just making excuses for blacks with their TAAO.”
This is not what they’re doing with their theory at all. A theory is a well-substantiated explanation of some aspect of the natural word that’s based on observation, empirical data, and evidence. They provide testable hypotheses that can be empirically tested. They also make predictions based on their proposed explanations. Predictive capacity is a hallmark of scientific theories. And it’s clear and I’ve shown that the TAAO makes successful novel predictions. Therefore the ability of a theory to make predictions—especially risky and novel ones—lends credibility to the validity of the theory.
The claim that the TAAO is a mere excuse for black crime is ridiculous. Because if that’s true, then all theories of crime are excuses for criminal activity. The TAAO should be evaluated on its predictive power—it’s ability to make successful novel predictions. Claims that the theory is a mere “excuse” for black crime is ridiculous, especially since the theory makes successful novel predictions. It’s clearly a valuable framework for understanding black crime in America.
“The so-called ‘novel predictions’ you reference aren’t novel at all”
We need to understand what the TAAO actually is. It’s a theory of crime that considers the African American “peerless” worldview. “Peerless” means “incomparable.” They have the worldview they do due to the 400 years of slavery and oppression like Jim Crow laws and segregation. Therefore, to explain black crime we need to understand the peerless African American experience. That’s a main premise of the theory. So the TAAO has one main premise, and it’s from this premise that the predictions of the TAAO are derived.
The peerless worldview of African Americans This premise recognizes the unique historical, contemporary, social, and cultural experiences of African Americans including their experiences of racial discrimination, social marginalization, and racial identity. This premise, then, lays the key groundwork for understanding black crime. This core premise of the TAAO then centers the theory within the context of the African American experience. Each of the predictions below are derived from the core premise of the TAAO—that of the peerless worldview of African Americans without relying on the predictions as premises used for the construction of the theory. Each of the predictions follows from the core premise, and they reflect how the African American experiences of racial discrimination, social marginalization and racial identity influence their likelihood of experiencing racial discrimination. Unnever and Gabbidon gave many arguments and references that this is indeed the case. The predictions, then, weren’t used as premise to construct the TAAO but they indeed are derived from—indeed they emerge from—the foundational experiences of African Americans and then serve as testable hypotheses which are derived from that understanding.
Thus, the predictions follow from the TAAO and they are derived from the foundational premise of the TAAO, without being used in the construction of the theory itself, qualifying as novel predictions according to Musgrave (1988): “a predicted fact is a novel fact for a theory if it was not used to construct that theory — where a fact is used to construct a theory if it figures in the premises from which that theory was deduced” and Beerbower: “the purpose of science is to enable accurate predictions and that, in fact, science cannot actually achieve more than that...The test of an explanatory theory, therefore, is its success at prediction, at forecasting. This view need not be limited to actual predictions of future, yet to happen events; it can accommodate theories that are able to generate results that have already been observed or, if not observed, have already occurred...it must have some reach beyond the data used to construct the theory“
More novel predictions of the TAAO
Therefore, since the TAAO has success in its predictions and hereditarian ones don’t (they don’t even make any novel predictions), it’s only rational to accept the theory that makes successful novel predictions over the one that doesn’t. The only reason one would accept the hereditarian explanations over the TAAO is due to bias and ignorance (racism), since the TAAO is a much more robust theory that actually has explanatory AND predictive power. So the issue here is quite clear—since we know the causes of black crime due to the successful novel predictions that the TAAO generates, then there are clear and actionable things we can do to try to mitigate the crime rate. This is something that hereditarian theories don’t do, most importantly because they don’t make any novel predictions. Since the TAAO makes successful risky novel predictions—predictions that, if they didn’t hold, they would then refute the theory—and since the predictions hold, then the theory is more likely to be true than not. The TAAO not only accommodates, but it makes predictions, and we can’t say the same for hereditarianism.
The issue is that so-called “race-neutral” theories of crime need to assume that racial discrimination isn’t a cause of black American offending because this would then limit it only to black Americans. Therefore race-neutral theories of crime don’t have the same predictive and explanatory power as a race-centric theory of crime—which is what the TAAO is. It’s clear that: the TAAO makes successful novel predictions, the predictions aren’t used as premises in the TAAO, the TAAO is a race-centric, country-specific theory of crime (and not a general theory of crime), racism and stereotypes don’t explain offending for non-African Americans, the theory doesn’t say that blacks lack agency, IQ doesn’t explain crime within families, and cope from hereditarians that one day we will find genes or neurohormonal influences which lead to crime in black Americans is just cope. It’s clear that the TAAO is the superior theory of crime because it does what scientific theories are supposed to do: successfully predict novel facts of the matter, something that hereditarianism just does not do which is why I’m justified in calling it a racist movement. Basically since there are unique characters of a demographic that require perspectives that are solely related to that group, then we need group-centric theories of crime due to the unique experiences of thsg group, and this is what the TAAO does.
Now that I’ve answered common criticisms of the TAAO, I have a few more successful novel predictions of the theory. In my original article I cited 3 novel predictions, how they followed from the theory, and then the references that confirmed the predictions:
(Prediction 1) Black Americans with a stronger sense of racial identity are less likely to engage in criminal behavior than black Americans with a weak sense of racial identity. How does this prediction follow from the theory? TAAO suggests that a strong racial identity can act as a protective factor against criminal involvement. Those with a stronger sense of racial identity may be less likely to engage in criminal behavior as a way to cope with racial discrimination and societal marginalization. (Burt, Simons, and Gibbons, 2013; Burt, Lei, and Simons, 2017; Gaston and Doherty, 2018; Scott and Seal, 2019)
(Prediction 2) Experiencing racial discrimination increases the likelihood of black Americans engaging in criminal actions. How does this follow from the theory? TAAO posits that racial discrimination can lead to feelings of frustration and marginalization, and to cope with these stressors, some individuals may resort to committing criminal acts as a way to exert power or control in response to their experiences of racial discrimination. (Unnever, 2014; Unnever, Cullen, and Barnes, 2016; Herda, 2016, 2018; Scott and Seal, 2019)
(Prediction 3) Black Americans who feel socially marginalized and disadvantaged are more prone to committing crime as a coping mechanism and have weakened school bonds. How does this follow from the theory? TAAO suggests that those who experience social exclusion and disadvantage may turn to crime as a way to address their negative life circumstances. and feelings of agency. (Unnever, 2014; Unnever, Cullen, and Barnes, 2016)
(Prediction 4) Black people who experience microaggreesions and perceive injustices in the criminal justice system are more likely to engage in serious and violent offending. How does this follow from the theory? Experiences of racial discrimination and marginalization can lead to negative emotions like anger and depression among black people. These negative emotions, which are then exacerbated by microaggreesions and perceptions of injustice in the criminal justice system, may increase the likelihood of engaging in serious and violent offending as a coping mechanism or means of asserting power. But, again, those with a stronger racial identity may be more resilient to the effect of discrimination (Isom, 2015).
(Prediction 5) Black Americans who perceive a lack of opportunity for socioeconomic advancement due to systemic barriers are more inclined to engage in criminal activity as a means of economic survival and social mobility. How does this follow from the theory? Perceptions of limited opportunities and systemic injustices can drive individuals to engage in criminal behaviors as a response to inequality (Vargas, 2023).
The fact that the TAAO generates these novel and successful predictions is evidence that we should accept the theory.
We also know that perceptions of criminal injustice predict offending (Bouffard and Piquero, 2013), we know that blacks are more likely than whites to perceive criminal injustice (Brunson and Weitzer, 2009) and we know that there are small differences among blacks and their perception of criminal injustice (Unnever, Gabbidon, and Higgins, 2011). So knowing this, more blacks should offend, right? Wrong. The vast majority of blacks don’t offend even though they share the same belief about the injustices of the criminal justice system. So how can we explain that? “Positive ethnic-racial socialization buffers the effect of weak school bonds on adolescent substance use and adult offending” (Gaston and Doherty, 2018). So the discrimination that black Americans have erodes their trust in social institutions like the school system, and then these weakened school bonds then increase the risk of offending.
Supporting a major tenet of TAAO and prior research on the protective ability of ethnic-racial socialization, the analyses showed that Black males who received positive ethnic-racial socialization messages in childhood develop resilience to the criminogenic effect of weak school bonds and face a lower risk for offending over the life course. (Gaston and Doherty, 2018)
One factor that is salient in the TAAO is racial subordination. We know that black people don’t commit crime because they are black, but we know that their offending is related to socio-environmental context like poverty, bad schools (while racism and stereotypes weaken school bonds blacks have, which makes them more likely to offend), broken families, and lead exposure (Butler, 2010) of which the TAAO addresses. We also know that there is no such thing as a “safe” level of lead exposure and that the relationship between lead and crime is robust and replicated across different countries and cultures. We also know that blacks were used as an experiment of sorts, where they were knowingly exposed to lead paint in subsidized homes.
This environmental racism (Washington, 2019), then, is another aspect of the racial subordination of blacks. And from 1976 to 2005, blacks were 7 times more likely than whites to commit murder. The fact of the matter is, the black-white murder gap has been large for over 100 years. And in discussing environmental racism, Unnever and Gabbidon (2011: 188) are explicit about the so-called genetic hypothesis of crime: “We want to be perfectly clear that our argument in no way is related to the thesis that there is a genetic cause to African American offending.” Therefore, this question doesn’t strike the heart of the TAAO and is just an attempt at evading the successful novel predictions the theory generates.
Conclusion
I’ve shown that the common “criticisms” of the TAAO are anything but and are easily answered. I then gave more successful predictions of the TAAO. It’s quite clear that one should accept the TAAO over hereditarian explanations. We also know that black isolation is a predictor of crime as well—even in 1996 blacks accounted for over 50 percent of murders and two-thirds of robberies (Shihadeh and Flynn, 1996). In 2020, blacks were six times more likely to be arrested for murder than whites. We also know that the belief by blacks in the violent stereotype predicts their offending and their adherence to the stereotype predicts crime and self control (Unnever, 2014). Therefore, a kind of stereotype threat arises here and has effects during police encounters like wkth height (Hester and Gray, 2018)(Najdowski, Bottoms, and Goff, 2015; Strine, 2018; Najdowski, 2012, 2023) , with one argument that race stereotypes track ecology, not race, (Williams, 2023) (just like for IQ; Steele and Aronson, 1995; Thames et al, 2014). We know that stereotype threats weaken school bonds and that weakened school bonds are related to offending, therefore we can infer that stereotype threats lead to an increase in crime (Unnever and Gabbidon, 2011).
Unnever and Gabbidon were quite clear and explicit in their argument and the hypotheses and predictions they made based on their theory. So when tested, if they were found not to hold then the theory would be falsified. But the theories held under empirical examination. Unnever and Gabbidon (2011: 98) were explicit in their theory and what it meant:
Put simply, we hypothesize that the probability of African American offending increases as blacks become more aware of toxic stereotypes, encounter stereotype threats, and are discriminated against because of their race. Our theory additionally posits that these forms of racism impact offending because they undermine the ability of African Americans to develop strong ties with conventional institutions. The extant literature indicates that stereotype threats and personal experiences of racial discrimination negatively impact the strength of the bonds (attachment, involvement, commitment) that black students have with their schools (Smalls, White, Chavous, and Sellers, 2007; Thomas, Caldwell, Faison, and Jackson, 2009). And, the research is clear; weak social bonds increase the probability of black offending (Carswell, 2007).
The worldview shared by black Americans is a consequence of the experience they and their ancestors had in America. This then explains their offending patterns, and why they commit more crime than whites. The socio-historical context that the TAAO looks to explain black crime is robust. Since the TAAO is successful in what it sets out to do, then, I wouldn’t doubt that there should be other race-centric theories of crime that try to explain and predict offending in those populations. The empirical successes of the TAAO’s predictions attest to the fact that other theories of crime for other races would be fruitful in predicting and explaining crime in those groups.
Hereditarians dream of having a theory that enjoys the empirical support that the TAAO has. The fact that the TAAO makes successful novel predictions and hereditarianism doesn’t is reason enough to reject hereditarian explanations and accept the TAAO. Accepting a theory that makes novel predictions is rational since it speaks to the theory’s predictive power. So by generating predictions that were previously unknown or untested and them confirming them through empirical evidence, the theory therefore shows its ability to predict and anticipate real-world phenomena. This then strengthens confidence in the theory’s underlying principles which provides a framework for understanding complex phenomena. Further, the ability of a theory to make such predictions suggests that the theory is robust and adaptable, meaning that it’s capable of accommodating new data while refining our understanding over time.
Hereditarians would love nothing more than to reduce black criminality to their genes or hormones, but reality tells a different story, and it’s one where the TAAO exists and makes successful novel predictions.
HBD and (the Lack of) Novel Predictions
2250 words
a predicted fact is a novel fact for a theory if it was not used to construct that theory — where a fact is used to construct a theory if it figures in the premises from which that theory was deduced. (Musgrave, 1988; cf Mayo, 1991: 524)
Introduction
Previously I demonstrated that the HBD movement is a racist movement. I showed this by arguing that it perfectly tracks with John Lovchik’s definition of racism, which is where “racism is a system of ranking human beings for the purpose of gaining and justifying an unequal distribution of political and economic power.” There is, however, a different issue—an issue that comes from the philosophy of science. So a theory is scientific if and only if it is based on empirical evidence, subject to falsifiability and testability, open to modification or rejection based on further experimentation or observation and—perhaps most importantly—is capable of generating novel predictions, where a novel prediction goes beyond existing knowledge and expectation and can be verified through empirical testing.
Here I will show that HBD doesn’t make any novel predictions, and I will also discuss one old attempt at showing that it does and that it is an example of a degenerative research programme. Effectively, I will argue that contrary to what is claimed, HBD is a degenerating research programme.
On so-called novel predictions
HBD and evolutionary psychology falls prey to the same issues that invalidate both of them. They both rely on ad hoc and post hoc storytelling. In a previous article on novel predictions, I stated:
A risky, novel prediction refers to a prediction made by a scientific theory or hypothesis that goes beyond what is expected or already known within an existing framework (novelness). It involves making a specific claim about a future observation or empirical result that, if confirmed, would provide considerable evidence in support of the scientific theory or hypothesis.
So EP and HBD are cut from the same cloth. John Beerbower (2016) puts the issue succinctly:
At this point, it seems appropriate to address explicitly one debate in the philosophy of science—that is, whether science can, or should try to, do more than predict consequences. One view that held considerable influence during the first half of the twentieth century is called the predictivist thesis: that the purpose of science is to enable accurate predictions and that, in fact, science cannot actually achieve more than that. The test of an explanatory theory, therefore, is its success at prediction, at forecasting. This view need not be limited to actual predictions of future, yet to happen events; it can accommodate theories that are able to generate results that have already been observed or, if not observed, have already occurred. Of course, in such cases, care must be taken that the theory has not simply been retrofitted to the observations that have already been made—it must have some reach beyond the data used to construct the theory.
HBDers promote the tenets that intelligence (IQ), along with behavior and socioeconomic outcomes are strongly associated with genetic differences among individuals and groups. They also use the cold winter theory (CWT) to try to intersect these tenets and show how they evolved over time. According to the CWT, the challenges of surviving in colder climates such as the need to hunt, plan ahead, and cooperate exerted selective pressures which favored genes which fostered higher intelligence in populations that inhabited these regions. I have previously shown years back that the CWT lacks novel predictive power, and that there are devastating response to the CWT which show the invalidity of the theory. Rushton used it in his long-refuted r/K selection theory for human races. Further, for example Jablonski and Chaplin (2000) successfully predicted that “multiple convergences of light skin evolved in different modern human populations and separately in Neanderthals” (Chaplin and Jablonski, 2009: 457). This was a successfully predicted novel fact, something that HBD doesn’t do.
Urbach (1974) (see Deakin, 1976 for response) in criticizing “environmentalism” and contrasting it with “hereditarianism”, claimed that hereditarianism made novel predictions. He also claimed that the “hard core” of the hereditarian research programme was that (1) cognitive ability of all people is due to general intelligence and individual and (2) group differences are due to heredity. We know that (1) is false, since general intelligence is a myth and we know that (2) is false since group differences are due to environmental factors since Jensen’s default hypothesis is false (along with the fact that Asians are a selected population). Further Urbach (1974: 134-135) writes that 4 novel facts of hereditarianism are “(i) of the degree of family resemblances in IQ, (ii) of IQ-related social mobility, (iii) of the distribution of IQ’s, and (iv) of the differences in sibling regression for American Negroes and whites.”
But the above aren’t novel predictions.
(i) Hereditarianism predicts that intelligence has a significant hereditary component, leading to similarities in IQ scores among family members. (Nevermind the fact that environments are inherited by these family members as well.) The prediction appears specific, but it’s not novel in the framework of hereditarianism. The idea that IQ is heritable and that family members share similarities in IQ has been a main tenet of hereditarianism for decades, even in 1974 at the time of publication of Urbach’s paper,rather than offering a new or unexpected insight.
(ii) Hereditarianism also suggests that differences in IQ also have implications for social mobility, with people with higher IQs having a greater change for more upward social mobility. This, too, isn’t novel within the hereditarian framework since even in 1974 and the decades before then this was known.
(iii) Hereditarianism also predicts that IQ scores follow a normal distribution, with a majority of people clustering around the middle. This, too, isn’t a novel prediction, since even Binet unconsciously built his test to have a normal distribution (Nash, 1987: 71). (Also note that Binet knew that his scales weren’t measures but thought that for practical measures they were; Michell, 2012.) Terman constructed his test to also have it. Urbach (1974: 131) states that “even if researchers had set out to obtain a particular distribution of IQ’s, there was no divine guarantee that their efforts would have been successful.” But we know that the process of building a normal distribution is done by choosing only items that conform to the normal distribution are selected, since items most are likely to get right are kept while on both ends items are also kept. In their psychometrics textbook, Rusk and Golombok (2009: 85) state that “it is common practice to carry out item analysis in such a way that only items that contribute to normality are selected.” Jensen (1980: 71) even stated “It is claimed that the psychometrist can make up a test that will yield any kind of score distribution he pleases. This is roughly true, but some types of distributions are much easier to obtain than others.”
(iv) Lastly, hereditarianism predicts that differences in sibling regression or the extent to which sibling IQ scores deviate from the population mean could vary between racial and ethnic groups. The prediction seems specific, but it reflects assumptions of genetic influences on psychological trait—which already were assumptions of hereditarian thought at that time and even today. Thus, it’s not a new or unexpected insight.
Therefore, the so-called novel predictions referenced by Urbach are anything but and reflect existing assumptions and concepts in the field at the time of publication, or he’s outright wrong (as is the case with the normal distribution).
Modern day hereditarians may claim that the correlation between genetics and IQ/educational attainment validates their theories and therefore counts as novel. However, the claim that genes would correlate with IQ has been a central tenet in this field for literally 100 years. Thus, a prediction that there would be a relationship between genes and IQ isn’t new. Nevermind the fact that correlations are spurious and meaningless (Richardson, 2017; Richardson and Jones, 2019) along with the missing heritability problem. Also note that as sample size increase, so to does the chance for spurious correlations, (Calude and Longo, 2016). The hereditarian may also claim that predicting group differences in IQ based on genetic and environmental factors is a novel prediction. Yet again, the idea that these contribute to IQ has been known for decades. The general prediction isn’t novel at all.
So quite obviously, using the above definition of “novel fact” from Musgrave, HBD doesn’t make any novel predictions of previously unknown facts not used in the construction of the theory. The same, then, would hold true for an HBDer who may say something along the lines of “I predict that a West African descendant will win the 100m dash at the next Olympics.” This doesn’t qualify as a novel prediction of a novel fact, either. This is because it relies on existing knowledge related to athletics and racial/ethnic demographics. It’s based in historical data and trends of West African descendants having been successful at previous 100m dash events at the Olympics. Therefore, since it’s not a novel insight that goes beyond the bounds of the theory, it doesn’t qualify as “novel” for the theory.
Why novel predictions matter
Science thrives on progress, so without theories/hypotheses that make novel predictions, a scientific program would stagnate. The inability of hereditarianism to generate risky, novel predictions severely limits it’s ability in explaining human behavior. Novel predictions also provide opportunities for empirical testing, so without novel predictions, hereditarianism lacks the opportunity for rigorous empirical testing. But a proponent could say that whether or not the predictions are novel, there are still predictions that come to pass based on hereditarian ideas.
Without novel prediction, hereditarianism is confined to testing hypotheses that are well-known or widely accepted in the framework or the field itself. This then results in a narrow focus, where researchers merely confirm their pre-existing beliefs instead of challenging them. Further, constantly testing beliefs that aren’t novel leads to confirmation bias where researchers selectively seek out what agrees with them while ignoring what doesn’t (Rushton was guilty of this with his r/K selection theory). Without the generation of novel predictions, hereditarianism lacks innovation. Lastly, the non-existence of novel predictions raises questions about the progressiveness of the framework. True scientific progress is predicated on the formulation of testing novel hypotheses which challenge existing paradigms. Merely claiming that a field generates testable and successful novel predictions and therefore that field is a progressive one is unfounded.
Thus, all hereditarianism does is accommodate, there is no true novel predictive power from it. So instead of generating risky, novel predictions that could potentially falsity the framework, hereditarians merely resort to post-hoc explanations, better known as just-so stories to fit their preconceived notions about human behavior and diversity. HBD claims are also vague and lack the detail needed for rigorous testing—the neck isn’t stuck out far enough for where if the prediction fails that the framework would be refuted. That’s because the predictions are based on assumptions they already know. Thus, HBD is merely narrative construction, and we can construct narratives about any kind of trait we observe today have the story conform with the fact that the trait still exists today. Therefore hereditarianism is in the same bad way as evolutionary psychology.
I have previously compared and contrasted hereditarian explanations of crime with the Unnever-Gabbidon theory of African American offending (TAAO) (Unnever and Gabbidon, 2011). I showed how hereditarian explanations of crime not only fail, but that hereditarian explanations lack novel predictive power. On the other hand, Unnever and Gabbidon explicitly state hypotheses and predictions which would follow from. The TAAO, and when they were tested they were found to hold validating the TAAO.
Conclusion
In this discussion I have tried to show that hereditarian/HBD theories make no novel predictions. They are merely narrative construction. The proposed evolutionary explanation for racial differences in IQ relying on the CWT is ad hoc, meaning it’s a just-so story. Lynn even had to add in something about population size and mutation rates since Arctic people, who have the biggest brain size, don’t have the highest IQ which is nothing more than special pleading.
Urbach’s (1974) four so-called novel predictions of hereditarianism are anything but, since they are based on assumptions already held by hereditarianism. They represent extensions or reformulation of existing assumptions, while also relying on retrospective storytelling.
I have provided a theory (the TAAO) which does make novel predictions. If the predictions wouldn’t have held, then the theory would have been falsified. However, tests of the theory found that they hold (Burt, Simons, and Gibbons, 2013; Unnever, 2014; Unnever, Cullen, and Barnes, 2016; Herda, 2016, 2018; Burt, Lei, and Simons, 2017; Gaston and Doherty, 2018; Scott and Seal, 2019). The hereditarian dream of having the predictive and explanatory power that the TAAO does quite obviously fails.
Therefore, the failure of hereditarianism to produce successful, risky novel predictions should rightly raise concerns about its scientific validity and the scientific credibility of the program. So the only rational view is to reject hereditarianism as a scientific enterprise, since it doesn’t make novel predictions and it’s merely, quite obviously, a way to make prejudices scientific. Clearly, based on what a novel prediction of a novel fact entails, HBD/hereditarian theory doesn’t make any such predictions of novel facts.
Racism Disguised as Science: Why the HBD Movement is Racist
2600 words
Introduction
Over the last 10 years or so, claims from the human biodiversity (HBD) movement have been gaining more and more traction. Proponents of HBD may say something like “we’re not racists, we’re ‘Noticers'” (to use Steve Sailer terminology – more on him below). The thing is, the HBD movement is a racist movement for the following reasons: it promotes and justifies racial hierarchies, inequities, is justified by pseudoscience, and it’s historical connections to the eugenics movement which sought to use pseudoscientific theories of racial superiority to justify oppression and discrimination.
But ever since 1969, Arthur Jensen and others have tried to intellectualize such a position, the discussion around racism has moved on to things like not only overt examples of racism but to systemic inequities along with unconscious biases which perpetuate racial hierarchies. But despite a veneer of scientific objectivity, the underlying motivation appears to be that of upholding some groups as “better” and others “worse.” This is like when hereditarians like Rushton tried to argue in the 90s that they can’t be racist since they say Asians (who are a selected population) are better than whites who are better than blacks on trait X. We know that views on Asians have changed over the years, for example with the use of the term “Mongoloid idiot.” Nonetheless, it’s obvious that the HBD movement purports a racial hierarchy. Knowing this, I will show how HBD is a racist movement.
Why HBD is racist
I have previously provided 6 definitions of racism. In that article I discussed how racism “gets into the body” and causes negative health outcomes for black women. I have since written more about why racism and stereotypes are bad since they cause the black-white crime gap through the perpetuation of self-fulfilling prophecies and they also cause psychological and physiological harm.
One of the definitions of “racism” I gave came from John Lovchik in his book Racism: Reality Built on a Myth (2018: 12), where he wrote that “racism is a system of ranking human beings for the purpose of gaining and justifying an unequal distribution of political and economic power.” Using this definition, it is clear that the HBD movement is a racist movement since it attempts to justify this ranking or human beings to justify and gain different kinds of power. This definition from Lovchik encompasses both systemic racism and overt acts of discrimination.
HBD proponents believe they we can delineate races not only based on physical appearance but also genetic differences. This is inherent in their system of ranking. But I think the same. Spencer’s (2014, 2021) OMB race theory (to which I hold to) states that race is a referent denoting a proper name to population groups. But that’s where the similarities end; OMB race theory is nothing like HBD. The key distinction between the two is in the interpretation of said differences. While both perspectives hold that population groups can be sorted into distinct groups, there is a divergence in their intentions and conclusions regarding the significance of said racial categorization.
Spencer’s OMB race theory emphasizes the declination of races based on physical differences as well as genetic ones using K=5 and how the OMB defines race in America—as a proper name for population groups. But Spencer (2014: 1036) explicitly states that his theory has no normative conclusion in it, since “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.” So the theory focuses solely on genetic ancestry without any normative judgements or hierarchical ranking of the races.
Conversely, the HBD movement, despite also genetically delineating races, differs in the application and interpretation of the evidence. Unlike Spencer’s OMB race theory, HBD states that genetic differences between groups contribute to differences in intelligence, social outcomes and behavior. HBD proponents use genetic analyses like GWAS to show that a trait has some kind of genetic influence and that, since there is a phenotypic difference in the trait between certain racial groups that it then follows that there is a genetic difference between certain racial groups when it comes to the phenotypic trait in question.
So this distinction that I have outlined shows the principle ways in which OMB race theory is nothing like HBD theory. So while both ideas involve genetic delineation of races, Spencer’s doesn’t support racist ideologies or hierarchical rankings among the races while the HBD movement does. Thus, the distinction shows the relationship between genetic analysis, racism and racial categorization is nuanced and that, just because one believes that human races exist, it doesn’t necessarily follow that they are a racist.
Furthermore, the attribution of social outcomes/inequality to biological/genetic differences is yet another reason why HBD is racist. They argue that most differences (read: outcomes/inequalities) between groups can come down mostly to genes, still leaving room for an environmental component. (This is also one of Bailey’s 1997 hereditarian fallacies.) It is this claim that socially-valued differences between groups are genetic in nature which then leads to systemic discrimination. So by attributing differences in outcome and resources, to biological differences, HBD attempts to perpetuate and legitimate systemic discrimination against certain racial groups. “It’s in their genes, nothing can be done.” Therefore, by ranking humans based on race and attributing differences in outcomes between groups—in part—to biological differences, the HBD movement justifies and perpetuates systemic discrimination against certain races, making HBD a racist movement.
Eugenic thinking arose in the late 1800s and began to be put into action in the 1900s. From sterilization to certain people deemed inferior, to advocating the enhancement of humanity through selective breeding of certain groups of people, some of the ideas from the eugenics movement are inherent in HBD-type thinking. The HBD movement then emerged as a more “respectable” iteration of the eugenics movement and they draw on similar themes. But why does this connection matter? It matters since the historical connection between the two shows how such pernicious thinking can penetrate social thought.
Lastly the HBD movement relies on pseudoscience. They often distort or misrepresent scientific findings. Most obvious is J. P. Rushton. In his discussion of Gould’s (1978) reanalysis of Morton’s skull collection, Rushton miscited Gould’s results in a way that jived with Rushton’s racial hierarchies (Cain and Vanderwolf, 1990). Rushton also misrepresented the skull data from Beals et al (1984). Rushton is the perfect example of this, since he misrepresented and ignored a ton of contrary data so that his theory could be more important. Rushton’s cherry-picking, misrepresentation of data, and ignoring contrary evidence while not responding to devestating critiques (Anderson, 1991; Graves 2002a, b) show this perfectly. This is the perfect example of confirmation bias.
They also rely on simplistic and reductionist interpretation of genetic research. By doing this, they also perpetuate stereotypes which can then have real-world consequences, like people committing horrific mass murder (the Buffalo shooter made reference to such genetic studies, which is why science communication is so important).
In his 2020 book Human Diversity the infamous Charles Murray made a statement about inferiority and superiority in reference to classes, races, and sexes, writing:
To say that groups of people differ genetically in ways that bear on cognitive repertoires (as this book does) guarantees accusations that I am misusing science in the service of bigotry and oppression. Let me therefore state explicitly that I reject claims that groups of people, be they sexes or races or classes, can be ranked from superior to inferior. I reject claims that differences among groups have any relevance to human worth or dignity.
Seeing as Chuck is most famous for his book The Bell Curve, this passage needs to be taken in context. So although he claims to reject such claims of inferiority and superiority, his previous work has contributed to such notions, and thus, it is implicit in his work. Furthermore, the language he used in the passage also implies hierarchical distinctions. When he made reference to “groups of people [who] differ genetically in ways that bear on cognitive repertoires“, there is a subtle suggestion that groups may possess inherent advantages or disadvantages in cognitive ability, thusly implying a form of hierarchy.
Murray’s work has been used by alt-right and white nationalist groups, and we know that white nationalist groups use such information for their own gain (Panofsky, Dasgupta, and Iturriaga, 2020; Bird, Jackson, and Winston, 2023). Panofsky and his coauthors write that “the claims that genetics defines racial groups and makes them different, that IQ and cultural differences among racial groups are caused by genes, and that racial inequalities within and between nations are the inevitable outcome of long evolutionary processes are neither new nor supported by science (either old or new). They’re the basic, tired evergreens of ancient racist thought.“
Next we have Steve Sailer. He may claim that he is merely observing (or as he says “Noticing”) and discussing empirical data. So his focus on racial differences and how they are driven mainly by genetic differences aligns with Lovchik’s definition of racism, since it involves the ranking of races based on perceived genetic differences, in both IQ and crime. Therefore, by emphasizing these differences and their purported implications for socially-relevant traits and their so-called implications for social hierarchies, Sailer’s work can be seen as justifying social inequalities and therefore justifying systemic discrimination.
Lastly, we have Bo Winegard’s Aporia Magazine essay titled What is a racist? In the article he forwards 5 definitions (while giving a 10-point scale, I will bracket the score he gives each):
Flawed:
1: Somebody who believes that race is a real, biological phenomenon and that races are different from each other. [1/10]
2: Somebody who believes that some races have higher average socially desirable traits such as intelligence and self-control than others. [3/10]3: Somebody who treats members of one race differently from members of another race. [5/10]
Plausible:
4: Somebody who dislikes members of other races. [8/10]
5: Somebody who advocates for differential treatment under the law for different races. [10/10]
Note that the first 2 encompass what, for the purposes of this article, I call racist in the HBD parlance. Nonetheless, I have tried to sufficiently argue that those 2 do constitute racism and I think I have shown how. In the first, if it is used to justify and legitimate social hierarchies, it is indeed racist. For the second, if someone holds the belief that races differ on socially values traits and that it is genetically caused, then it could perpetuate racist stereotypes and the continuation of racist ideologies. The third and fourth constitute racial discrimination. These 2 could also be known as hearts and minds racism, which operate at the level of individual beliefs, attitudes, and behavior. But the fifth definition that Bo forwarded is the most interesting one, since it has certain implications.
About the fifth definition, Bo wrote that (my emphasis) “a racist is somebody who advocates for differential treatment under the law for different races, [it] is the most incontrovertible and therefore paradigmatic definition of racist that I can imagine.” This is interesting. If it is not able to be denied, disputed, and serves as a typical example of the referent of racism, then this has implications for the views of certain hereditarians and the people they ran with.
We know that Jensen ran with actual racists and that he lent his name to their cause. (Jackson, 2022; see also Jackson and Winston, 2020 for a discussion). We know that hereditarians, despite their protestations, ignore evolutionary theory (Roseman and Bird, 2023). Nonetheless, we know that there is no support for the hereditarian hypothesis (Bird, 2021). But the issue here is the fifth definition that Bo said isn’t indisputable.
In his 2020 article Research on group differences in intelligence: A defense of free inquiry, philosopher Nathan Cofnas noted that hereditarians call for a kind of “tailored training program“, which John Jackson took to be “a two-tiered education system.” Although Cofnas didn’t say it, he cited hereditarians who DID say it. Thus, he showed how they ARE racists. And Cofnas states that we can’t know what would happen if race differences in intelligence would be found to have a genetic basis. But I argued before that since the hereditarian hypothesis is false and if we believe it is true then it could—and has—caused harm, so we should thusly ban IQ tests. Nonetheless, Cofnas’ passage in his article can be seen as racist under Lovchik’s definition, since he advocates for tailored training programs, which could result in unequal distribution of resources and further entrench inequities based on genetic differences between groups in their so-called intelligence which hereditarians argue is partly genetic in nature.
Prominent hereditarians Shockley and Cattell said some overtly racist things, Cattell even creating a religion called “Beyondism” (Tucker, 2009). Shockley called for the voluntary sterilization of black women (Thorp, 2022) and proposed a sterilization plan to pay anyone with an IQ a sum of money to get sterilized. I have also further documented the eugenic thinking of IQists and criminologists. It seems that this field is and has been a hole for racists ever since it’s inception.
Conclusion
Throughout this discussion, I have argued that the HBD movement is a racist one. Most importantly, a lot of their research was bankrolled by the Nazi Pioneer Fund. So financial support from a racist organization is pivotal in this matter, since these researchers were doing work that would justify the conclusions of the racist Fund (see Tucker 1996, 2002). So since the Fund had a history of funding research into eugenics, and of promoting research which could—implicitly—be seen as justification for racial superiorityp and inferiority, and therefore attempting to justify existing inequities.
Relying on John Lovchik’s definition of racism, I’ve shown how the HBD movement is a racist movement since it seeks to justify existing inequalities between racial groups and since it is a system of ranking human beings. I’ve also shown that mere belief in the existence of race isn’t enough for one to be rightly called a racist, since theories of race like Spencer’s (2014) OMB race theory is nothing like HBD theory since it doesn’t rank the races, nor does it argue that the genetic differences between races are causal for the socially important differences that hereditarians discuss. Racism isn’t only about individual attitudes, but also about systemic structures and institutional practices which perpetuate racial hierarchies and inequities.
I showed how, despite his protestations, Murray believes that races, classes, and sexes can be ranked—which is a form of hierarchy. I also showed how Steve “The Noticer” Sailer is a racist. Both of these men’s views are racist. I then discussed Winegard’s definitions, showing that they are all good definitions of the term under discussion. I then turned to how Jensen ran with racist Nazis and how Cofnas cited researchers who called for tailored training programs.
That the HBD movement promotes the idea that differences in socially valued traits are genetic in nature through pseudoscientific theories along with the fact that it quite obviously is an attempt at justifying a human hierarchy of socially valued traits means that there is no question about it—the HBD movement is a racist movement.
(P1) If the HBD movement promotes and justifies racial hierarchies and inequities, then it is a racist movement.
(P2) The HBD movement promotes and justifies racial hierarchies and inequities.
(C) So the HBD movement is a racist movement.
The Rockefeller Foundation’s Failure in Finding a General Intelligence Factor in Dogs
2000 words
Introduction
Hereditarians have been trying to prove the existence of a genetic basis of intelligence for over 100 years. In this time frame, they have used everything from twin, family and adoption studies to tools from the molecular genetics era like GCTA and GWAS. Using heritability estimates, behavior geneticists claim that since intelligence is highly heritable, that there must thusly be a genetic basis to intelligence controlled by many genes of small effect, meaning it’s highly polygenic.
In his outstanding book Misbehaving Science, Panofsky (2014) discusses an attempt funded by the Rockefeller Foundation (RF) at showing a genetic basis to dog intelligence to prove that intelligence had a genetic basis. But it didn’t end up working out for them—in fact, it showed the opposite. The investigation which was funded by the RF showed quite the opposite result that they were looking for—while they did find evidence of some genetic differences between the dog breeds studied, they didn’t find evidence for the existence of a “general factor of intelligence” in the dogs. This issue was explored in Scott and Fuller’s 1965 book Genetics and the Social Behavior of the Dog. These researchers, though, outright failed in their task to discover a “general intelligence” in dogs. Modern-day research also corroborates this notion.
The genetic basis of dog intelligence?
This push to breed a dog that was highly intelligent was funded by the Rockefeller Foundation for ten years at the Jackson Laboratory. Panofsky (2014: 55) explains:
Over the next twenty years many scientists did stints at Jackson Laboratory working on its projects or attending its short courses and training programs. These projects and researchers produced dozens of papers, mostly concerning dogs and mice, that would form much of the empirical base of the emerging field. In 1965 Scott and John Fuller, his research partner, published Genetics and the Social Behavior of the Dog. It was the most important publication to come out of the Jackson Lab program. Scott and Fuller found many genetic differences between dog breeds; they did not find evidence for general intelligence or temperament. Dogs would exhibit different degrees of intelligence or temperamental characteristics depending on the situation. This evidence of interaction led them to question the high heritability of human intelligence—thus undermining a goal of the Rockefeller Foundation sponsors who had hoped to discredit the idea that intelligence was the product of education. Although the behavioral program at Jackson Laboratory declined after this point, it had been the first important base for the new field.
Quite obviously this was the opposite result of what they wanted—dog intelligence was based on the situation and therefore context-dependent.
Scott and Fuller (1965) discuss how they used to call their tests “intelligence tests” but then switched to calling them “performance tests”, “since the animals
seemed to solve their problems in many ways other than through pure thought or
intellect” (Scott and Fuller 1965: 37), while also writing that “no evidence was found for a general factor of intelligence which would produce good performance on all tests” (1965, 328). They also stated that they found nothing like the general intelligence factor in dogs like that is found in humans (1965: 472) while also stating that it’s a “mistaken notion” to believe in the general intelligence factor (1965: 512). They then conclude, basically, that situationism is valid for dogs, writing that their “general impression is that an individual from any dog breed will perform well in a situation in which he can be highly motivated and for which he has the necessary physical capacities” (1965: 512). Indeed, Scott noted that due to the heritability estimates of dog intelligence Scott came to the conclusion that human heritability estimates “are far too high” (quoted in Paul, 1998: 279). This is something that even Schonemann (1997) noted—and it’s “too high” due to the inflation of heritability due to the false assumptions of twin studies, which lead to the missing heritability crisis. One principle finding was that genetic differences didn’t appear early in development, which were then molded by further experience in the world. Behavior was highly variable between individuals and similar within breeds.
The results were quite unexpected but scientifically exciting. During the very early stages of development there was so little behavior observed that there was little opportunity for genetic differences to be expressed. When the complex patterns of behavior did appear, they did not show pure and uncontaminated effects of heredity. Instead, they were extraordinarily variable within an individual and surprisingly similar between individuals. In short, the evidence supported the conclusion that genetic differences in behavior do not appear all at once early in development, to be modified by later experience, but are themselves developed under the influence of environmental factors and may appear in full flower only relatively late in life. (Scott and Fuller, 1965)
The whole goal of this study by the Jackson Lab was to show that there was a genetic basis to intelligence in dogs and that they therefore could breed a dog that was intelligent and friendly (Paul, 1998). They also noted that there was no breed which was far and above the best at the task in question. Scott and Fuller found that performance on their tests was strongly affected by motivational and emotional factors. They also found that breed differences were strongly influenced by the environment, where two dogs from different breeds became similar when raised together. We know that dogs raised with cats showed more favorable disposition towards them (Fox, 1958; cf Feuerstein and Terkel, 2008, Menchetti et al, 2020). Scott and Fuller (1965: 333) then concluded that:
On the basis of the information we now have, we can conclude that all breeds show about the same average level of performance in problem solving, provided they can be adequately motivated, provided physical differences and handicaps do not affect the tests, and provided interfering emotional reactions such as fear can be eliminated. In short, all the breeds appear quite similar in pure intelligence.
The issue is that by believing that heritability shows anything about how “genetic” a trait is, one then inters that there has to be a genetic basis to the trait in question, and that the higher the estimate, the more strongly controlled by genes the trait in question is. However, we now know this claim to be false (Moore and Shenk, 2016). More to the point, the simple fact that IQ shows higher heritability than traits in the animal kingdom should have given behavioral geneticists pause. Nonetheless, it is interesting that this study that was carried out in the 1940s showed a negative result in the quest to show a genetic basis to intelligence using dogs, since dogs and humans quite obviously are different. Panofsky (2014: 65) also framed these results with that of rats that were selectively bred to be “smart” and “dumb”:
Further, many animal studies showed that strain differences in behavior were not independent of environment. R. M. Cooper and J. P. Zubek’s study of rats selectively bred to be “dull” and “bright” in maze-running ability showed dramatic differences between the strains in the “normal” environment. But in the “enriched” and especially the “restricted” developmental environments, both strains’ performance were quite similar. Scott and Fuller made a similar finding in their comparative study of dog breeds: “The behavior traits do not appear to be preorganized by heredity. Rather a dog inherits a number of abilities which can be organized in different ways to meet different situations.” Thus even creatures that had been explicitly engineered to embody racial superiority and inferiority could not demonstrate the idea in any simple way
Psychologist Robert Tryon (1940) devised a series of mazes, ran rats through them and then selected rats that learned quicker and slower (Innis, 1992). These differences then seemed to persists across these rat generations. Then Searle (1949) discovered that the so-called “dumb” rats were merely afraid of the mechanical noise of the maze, showing that Tryon selected for—unknowingly—emotional capacity. Marlowitz (1969) then concluded “that the labels “maze-bright” and “maze-dull” are inexplicit and inappropriate for use with these strains.”
Dogs and human races are sometimes said to be similar, in which a dog breed can be likened to a human race (see Norton et al, 2019). However, dog breeds are the result of conscious human selection for certain traits which then creates the breed. So while Scott and Fuller did find evidence for a good amount of genetic differences between the breeds they studied, they did not find any evidence of a genetic basis of intelligence or temperament. This is also good evidence for the claim that a trait can be heritable (have high heritability) but have no genetic basis. Moreover, we know that high levels of training improve dog’s problem solving ability (Marshall-Pescini et al, 2008, 2016). Further, perceived differences in trainability are due to physical capabilities and not cognitive ones (Helton, 2008). And in Labrador Retrievers, post-play training also improved training performance (Affenzeller, Palme, and Zulch, 2017; Affenzeller, 2020). Dogs’ body language during operant conditioning was also related to their success rate in learning (Hasegawa, Ohtani, and Ohta, 2014). We also know that dogs performed tasks better and faster the more experience they had with them, not being able to solve the task before seeing it demonstrated by the human administering the task (Albuquerque et al, 2021). Gnanadesikan et al (2020) state that cognitive phenotypes seem to vary by breed, and that these phenotypes have strong potential to be artificially selected, but we have seen that this is an error. Morrill et al (2022) found no evidence that the behavioral tendencies of certain breeds reflected intentional selection by humans but could not discount the possibility.
Conclusion
Dog breeds have been used by hereditarians for decades as a model for that of intelligence differences between human races. The analogy that dog breeds and human races are also similar has been used to show that there is a genetic basis for human race, and that human races are thusly a biological reality. (Note that I am a pluralist about race.) But we have seen that in the 40s the study which was undertaken to prove a hereditary basis to dog intelligence and then liken it to human intelligence quite obviously failed. This then led one of the authors to conclude—correctly—that human heritability estimates are inflated (which has led to the missing heritability problem of the 2000s).
Upon studying the dogs in their study, they found that there was no general factor of intelligence in these dogs, and that the situation was paramount in how the dog would perform on the task in question. This then led Scott to conclude that human heritability estimates are too high, a conclusion echoed by modern day researchers like Schonemann. The issue is, if dogs with their numerous breeds and genetic variation defy a single general factor, what would that mean for humans? This is just more evidence that “general intelligence” is a mere myth, a statistical abstraction. There was also no evidence for a general temperament, since breeds that were scared in one situation were confident in another (showing yet again that situationism held here). The failure of the study carried out by the RF then led to the questioning of the high heritability of human intelligence (IQ), which wasn’t forgotten as the decades progressed. Nonetheless, this study casted doubt on the claim that intelligence had a genetic basis.
Why, though, would a study of dogs be informative here? Well, the goal was to show that intelligence in dogs had a hereditary component and that thusly a kind of designer dog could be created that was friendly and intelligent, and this could then be likened to humans. But when the results were the opposite of what they desired, the project was quickly abandoned. If only modern-day behavioral geneticists would get the memo that heritability isn’t useful for what they want it to be useful for (Moore and Shenk, 2016)
Racial Differences in Motor Development: A Bio-Cultural View of Motor Development
3050 words
Introduction
Psychologist J. P. Rushton was perhaps most famous for attempting to formulate a grand theory of racial differences. He tried to argue that, on a matrix of different traits, the “hierarchy” was basically Mongoloids > Caucasoids > Negroids. But Rushton’s theory was met with much force, and many authors in many of the different disciplines in which he derived his data to formulate his theory attacked his r/K selection theory also known as Differential K theory (where all humans are K, but some humans are more K than others, so some humans are more r than others). Nonetheless, although his theory has been falsified for many decades, did he get some things right about race? Well, a stopped clock is right twice a day, so it wouldn’t be that outlandish to believe that Rushton got some things right about racial differences, especially when it comes to physical differences. While we can be certain that there are physical differences in groups we term “racial groups” and designate “white”, “black”, “Asian”, “Native American”, and “Pacific Islander” (the five races in American racetalk), this doesn’t lend credence to Rushton’s r/K theory.
In this article, I will discuss Rushton’s claims on motor development between blacks and whites. I will argue that he basically got this right, but it is of no consequence to the overall truth of his grand theory of racial differences. We know that there are physical differences between racial groups. But that there are physical differences between racial groups doesn’t entail that Rushton’s grand theory is true. The only entailment, I think, that can be drawn from that is there is a possibility that physical differences between races could exist between them, but it is a leap to attribute these differences to Rushton’s r/K theory, since it is a falsified theory on logical, empirical and methodological grounds. So I will argue that while Rushton got this right, a stopped clock is right twice a day but this doesn’t mean that his r/K theory is true for human races.
Was Rushton right? Evaluating newer studies on black-white motor development
Imagine three newborns: one white, one black and the third Asian and you observe the first few weeks of their lives. Upon observing the beginnings of their lives, you begin to notice differences in motor development between them. The black infant is more motorically advanced than the white infant who is more motorically advanced than the Asian infant. The black infant begins to master movement, coordination and dexterity showing a remarkable level of motoric dexterity, while the white infant shows less motoric dexterity than the black infant, and the Asian infant still shows lower motoric dexterity than the white infant.
These disparities in motor development are evidence in the early stages of life, so is it genetic? Cultural? Bio-cultural? I will argue that what explains this is a bio-cultural view, and so it will of course eschew reductionism, but of course as infants grow and navigate through their cultural milieu and family lives, this will have a significant effect on their experiences and along with it their motoric development.
Although Rushton got a lot wrong, it seems that he got this issue right—there does seem to be differences in precocity of motor development between the races, and the references he cites below in his 2000 edition of Race, Evolution, and Behavior—although most are ancient compared to today’s standards—hold to scrutiny today, where blacks walk earlier than whites who walk earlier than Asians.
Rushton (2000: 148-149) writes:
Revised forms of Bayley’s Scales of Mental and Motor Development administered in 12 metropolitan areas of the United States to 1,409 representative infants aged 1-15 months showed black babies scored consistently above whites on the Motor Scale (Bayley, 1965). This difference was not limited to any one class of behavior, but included: coordination (arm and hand); muscular strength and tonus (holds head steady, balances head when carried, sits alone steadily, and stands alone); and locomotion (turns from side to back, raises self to sitting, makes stepping movements, walks with help, and walks alone).
Similar results have been found for children up to about age 3 elsewhere in the United States, in Jamaica, and in sub-Saharan Africa (Curti, Marshall, Steggerda, & Henderson, 1935; Knobloch & Pasamanik, 1953; Williams & Scott, 1953; Walters, 1967). In a review critical of the literature Warren (1972) nonetheless reported evidence for African motor precocity in 10 out of 12 studies. For example, Geber (1958:186) had examined 308 children in Uganda and reported an “all-round advance of development over European standards which was greater the younger the child.” Freedman (1974, 1979) found similar results in studies of newboms in Nigeria using the Cambridge Neonatal Scales (Brazelton & Freedman, 1971).
Mongoloid children are motorically delayed relative to Caucasoids. In a series of studies carried out on second- through fifth-generation Chinese-Americans in San Francisco, on third- and fourth-generation Japanese-Americans in Hawaii, and on Navajo Amerindians in New Mexico and Arizona, consistent differences were found between these groups and second- to fourth-generation European-Americans using the Cambridge Neonatal Scales (Freedman, 1974, 1979; Freedman & Freedman, 1969). One measure involved pressing the baby’s nose with a cloth, forcing it to breathe with its mouth. Whereas the average Chinese baby fails to exhibit a coordinated “defense reaction,” most Caucasian babies turn away or swipe at the cloth with the hands, a response reported in Western pediatric textbooks as the normal one.
On other measures including “automatic walk,” “head turning,” and “walking alone,” Mongoloid children are more delayed than Caucasoid children. Mongoloid samples, including the Navajo Amerindians, typically do not walk until 13 months, compared to the Caucasian 12 months and Negro 11 months (Freedman, 1979). In a standardization of the Denver Developmental Screening Test in Japan, Ueda (1978) found slower rates of motoric maturation in Japanese as compared with Caucasoid norms derived from the United States, with tests made from birth to 2 months in coordination and head lifting, from 3 to 5 months in muscular strength and rolling over, at 6 to 13 months in locomotion, and at 15 to 20 months in removing garments.
Regarding newer studies on this matter, there are differences between European and Asian children in the direction that Rushton claimed. Infants from Hong Kong displayed a difference sequence of rolling compared to Canadian children. There does seem to be a disparity in motoric development between Asian and white children (Mayson, Harris, and Bachman, 2007). These authors do cite some of the same studies like the DDST (which is currently outdated) which showed how Asian children were motorically delayed compared to white children. And although they put caution on their findings of their literature review, it’s quite clear that this pattern exists and it is a bio-cultural one. So they conclude their literature review writing “the literature reviewed suggests differences in rate of motor development among children of various ethnic origins, including those of Asian and European descent” and that “Limited support suggests also that certain developmental milestones, such as rolling, may differ between infants of Asian and European origin.” Further, cultural practices in northern China—for example, lying them on their backs on sandbags—stall the onset of walking in babies sitting, crawling, and walking by a few months (Karasik et al, 2011).
This is related to the muscles that are used to roll from a supine to prone position and vice versa. Since some Asian children spend a longer time in apparatuses that aren’t conducive to growing a strong muscular base to be able to roll from the supine to prone position, to crawl and eventually walk, this is the “cultural” in the “bio-cultural” approach I will argue for.
One study on Norwegian children found that half of the children were waking by 13 months (the median) while 25 percent were walking by 12 months and 75 percent were walking by 14 months (Storvold, Aarethun, and Bratberg, 2013). One reason for the delayed response time could be supine sleeping, which was put into effect during the Back to Sleep program to mitigate causes of death from SIDS. Although it obviously saved tens of thousands of infant lives, it came at a cost of slightly stunted motoric development. It also seems that there is poor predictive value for infant milestones such as walking when it comes to health (Jenni et al, 2012).
Black Caribbean, black African and Indian infants were less likely to show delays in gross motor milestones compared to white infants. But Pakistani and Bangladeshi infants were more likely to be delayed in motoric development and communicative gestures, which was partly attributed to socio-cultural factors (Kelly et al, 2006). Kelly et al (2006: 828) also warn against genetic conclusions based on their large findings of difference between white and African and Caribbean infants:
The differences we observed between Black African and Black Caribbean compared with White infants are large and remain unaffected after adjusting for important covariates. This makes it tempting to conclude that the remaining effect must be a consequence of genetic differences. However, such a conclusion would be prematurely drawn. First, we have not included the measurement of genetic factors in our analysis, and, therefore, the presence of such effects cannot be demonstrated. Second, speculating on such effects should only be done alongside recognition that the model we have been able to test contains imperfect measurement.
It has also been observed that black and white children achieved greater mastery of motoric ability (locomotor skills) compared to Asian children but there was no difference by age group (Adeyemi-Walker et al, 2018). It was also found that infants with higher motor development scores had a lower weight weight relative to their length as they grew. So it was found that delayed motor development was associated with higher weight relative to length (Shoaibi et al, 2018). Black infants are also more motorically advanced and this is seen at up to two years of age (Malina, 1988) while black children perform better on tests of motor ability than white children (Okano et al, 2001). Kilbride et al (1970) also found that Baganda infants in Uganda showed better motoric ability than white American children. Campbell and Heddeker (2001) also showed that black infants were more motorically advanced than infants of other races.
It is clear that research like this blows up the claim that there should be a “one-size fits all” chart for motoric development in infants and that there should be race-specific milestones. This means that we should throw out the WEIRD assumptions when it comes to motoric development of infants (Karasik et al, 2011). They discuss research in other cultures where African, Caribbean and Indian caregivers massage the muscles of babies, stretch their limbs, toss them in their air, sit them up, and walk with them while helping them which then shapes their muscles and has them learn the mind-muscle connections needed to be able to learn how to eventually walk. And it also seems that random assignment to exercise excelerates how quickly an infant walks. White infants also sit at 6 months while black infants sit at 4 months. Nonetheless, it is clear that culture and context can indeed shape motoric development in groups around the world.
A bio-cultural view of motor development
When it comes to biological influences on motor development, sex and age are two important variables (Escolano-Perez, Sanchez-Lopez, and Herrero-Nivela, 2021). Important to this, of course, is that the individual must be normal, and they must have a normal brain with normal vision and spatial skills. They must be able to hear (to eventually follow commands and hear what is going on in their environment to change their course of action if need be). Further, the child’s home environment and gestational age influence different portions of motoral development (Darcy, 2022). After infants begin crawling, their whole world changes and they process visual motion better and faster, being able to differentiate between different speeds and directions, so a stimulating environment for the infant can spur the development of the brain (Van der Meer and Van der Weel, 2022). Biological maturation and body weight also affect motor development. Walking develops naturally, but walking and motor competence need to be nurtured for the child to reach their full potential; lower motor competence is related to higher body weight (Drenowatz and Greier, 2019).
One study on Dutch and Israeli infants even found—using developmental niche construction—that “infant motor development indeed is at least partly culturally constructed [which] emphasizes the importance of placing infant motor development studies into their ‘cultural cradle‘ (Oudgeneong, Atun-Eni, and Schaik, 2020). Gross motor development—rolling over, crawling, alternating kicks, moving from lying to sitting, and having tummy time—is recognized by the WHO. Further, children from different cultures have different experiences, which also could lead to, for example, not doing things that are conducive to the development of gross motor development (Angulo-Barroso et al, 2010). Moreover, motor development is embodied, enculturated, embedded, and enabling (Adolph and Hoch, 2020). It is also known that differences in the cultural environment “have a non-negligible effect on motor development” (Bril, 1986). Motor development also takes place in physical environments and is purposive and goal-directed (Hallemans, Verbeque, and de Walle, 2020).
So putting this all together, we have conceptualized motor development as a dynamic process which is influenced by a complex interplay of biological and cultural factors (Barnes, Zieff, and Anderson, 1999). Biological factors like sex, age, health, sensory abilities, and socio-cultural factors like home environment and developmental niches explain motor development and differences in them between individuals. The cultural differences, though, can impede motoral development, and not allow one to reach milestones they would have otherwise reached in a different cultural environment, just like if one couldn’t hear or see would have trouble reaching developmental milestones.
Children of course grow up in cultural environments and contexts and so they are culturally situated. So what this means is that both the cultural and social environment the child finds themselves in will of course then influence their physical and mental development and lead them to their milestones they hit which is dictated by the normal biology they have which then is allowed by the socio-cultural environment they are born into. So we have the bio-cultural view on motor development, and beyond the cultural environment the child finds themselves in, the interactions they have between parents and caregivers—more knowledgeable others—can be pertinent to their motor development and reaching of developmental milestones. Cultural practices and expectations could emphasize certain milestones over others and then guide the child towards the trajectory. So the framework recognizes that normal biology and sensory perceptions are needed for the development of normal motor development, but that cultural and social differences in that context will spur motor development in the child who finds themselves in different cultures.
Conclusion
Was Rushton right about this? Yes, I think he was. The recent literature on the matter speaks to this. But that doesn’t mean that his r/K selection theory is true. There are differences in motor development between races. But what is interesting is the interaction between biological and cultural factors that spur motor development. The question of black motor precocity, however, is a socio-political question, since science is a social convention influenced by the values of the scientist in question. Now, to the best of my knowledge, Rushton himself never carried out studies on this, he just collated them to use them for his racial trait matrix. However, it’s quite clear that Rushton was politically politically and socially motivated to prove that his theory was true.
But physical differences between the races are easy enough to prove, and of course they are due to biological and cultural interactions. There are differences in skin color and their properties between blacks and whites (Campiche et al, 2019). There is a 3 percent center of mass difference between blacks and whites which explains why each race excels at running and swimming (Bejan, Jones, and Charles, 2010). There are differences in body composition between Asians and whites which means, at the same BMI, Asians would have thicker skin folds and higher body fat than whites (Wang et al, 1994; WHO expert consultation, 2004; Wang et al, 2011). Just like at the same BMI, blacks have lower body fat and thinner skin folds than whites (Vickery, Cureton, and Collins, 1988; Wagner and Heyward, 2000; Flegal et al, 2010). There are differences in menarche and thelarche between blacks and whites (Wagner and Heyward, 2000; Kaplowitz, 2008; Reagan et al, 2013; Cabrera et al, 2014; Deardorff et al, 2014; ). There are differences in anatomy and physiology and somatotype between blacks and whites and these differences would explain how the races would perform on the big four lifts. There are interesting and real physical differences between races.
So obviously, what is considered “normal” is different in different cultures, and motor development is no different. So just like I think we should have different BMI and skin fold charts for different races, so too should we have different developmental milestones for different races and cultures. The discussion here is clear, since what is “average” and “normal” is different based on race and culture. Like for instance, black babies begin walking around 11 months, white babies around 12 months and Native American babies at 13 months. So while parents may be worried that their child didn’t hit a certain developmental milestone like walking, sitting, rolling, taking a bio-cultural approach will assuage these worries.
Nonetheless, while Rushton was right about race and motor development, we need to center his research project in context. He was clearly motivated, despite the numerous and forceful critiques of his framework, to prove that he was right. But the continuance of Rushton pushing his theory up until his death shows me that he was quite obviously socially and politically motivated, contrary to what he may have said.
We have approached this paper from the stance that science is a social activity, with all observations influenced by, as well as reflective of, the values of scientists and the political leanings of the sociocultural context within which research is conducted. We suggest that when questions of group difference are pursued in science, awareness of how the categories themselves have been shaped by social and historical forces, as well as of the potential effects on society, is important. (Barnes, Zieff, and Anderson, 1999)
“Missing Heritability” and Missing Children: On the Issues of Heritability and Hereditarian Interpretations
3100 words
“Biological systems are complex, non-linear, and non-additive. Heritability estimates are attempts to impose a simplistic and reified dichotomy (nature/nurture) on non-dichotomous processes.” (Rose, 2006)
“Heritability estimates do not help identify particular genes or ascertain their functions in development or physiology, and thus, by this way of thinking, they yield no causal information.” (Panofsky, 2016: 167)
“What is being reported as ‘genetic’, with high heritability, can be explained by difference-making interactions between real people. In other words, parents and children are sensitive, reactive, living beings, not hollow mechanical or statistical units.” (Richardson, 2022: 52)
Introduction
In the world of behavioral genetics, it is claimed that studies of twins, adoptees and families can point us to the interplay between genetic and environmental influences on complex behavioral traits. To study this, they use a concept called “heritability”—taken from animal breeding—which estimates the the degree of variation in a phenotypic trait that is due to genetic variation amongst individuals in the studied population. But upon the advent of molecular genetic analysis after the human genome project, something happened that troubled behavioral genetic researchers: The heritability estimates gleaned from twin, family and adoption studies did not match the estimates gleaned from the molecular genetic studies. This then creates a conundrum—why do the estimates from one way of gleaning heritability don’t match to other ways? I think it’s because biological models represent a simplistic (and false) model of biological causation (Burt and Simon, 2015; Lala, 2023). This is what is termed “missing heritability.” This raises questions that aren’t dissimilar to when a child dissappears.
Imagine a missing child. Imagine the fervor a family and authorities go through in order to find the child and bring them home. The initial fervor, the relentless pursuit, and the agonizing uncertainty constitute a parallel narrative in behavioral genetics, where behavioral geneticists—like the family of a missing child and the authorities—find themselves grappling with unforseen troubles. In this discussion, I will argue that the additivity assumption is false, that this kind of thinking is a holdover from the neo-Darwinian Modern Synthesis, that hereditarians have been told for decades that heritability just isn’t useful for what they want to do, and finally “missing heritability” and missing children are in some ways analogous, but that there is a key difference: The missing children actually existed, while the “missing heritability” never existed at all.
The additivity assumption
Behavioral geneticists pay lip service to “interactions”, but then conceptualize these interactions as due to additive heritability (Richardson, 2017a: 48-49). But the fact of the matter is, genetic interactions create phantom heritability (Zuk et al, 2012). When it comes to the additive claim of heritability, that claim is straight up false.
The additive claim is one of the most important things for the utility of the concept of heritability for the behavioral geneticist. The claim that heritability estimates for a trait are additive means that the contribution of each gene variant is independent and they all sum up to explain the overall heritability (Richardson 2017a: 44 states that “all genes associated with a trait (including intelligence) are like positive or negative charges“). But in reality, gene variants aren’t independent effects, they interact with other genes, the environment and other developmental resources. In fact, violations of the additivity assumption are large (Daw, Guo, and Harris, 2015).
Gene-gene, gene-environment, and environmental factors can lead to overestimates of heritability, and they are non-additive. So after the 2000s with the completion of the human genome project, these researchers realized that the genetic variants that heritability they identified using molecular genetics did not jive with the heritability they computed from twin studies from the 1920s until the late 1990s and then even into the 2020s. So the expected additive contribution of heritability fell short in actually explaining the heritability gleaned from twin studies using molecular genetic data.
Thinking of heritability as a complex jigsaw puzzle may better help to explain the issue. The traditional view of heritability assumes that each genetic piece fits neatly into the puzzle to then complete the overall genetic picture. But in reality, these pieces may not be additive. They can interact in unexpected ways which then creates gaps in our understanding, like a missing puzzle piece. So the non-additive effects of gene variants which includes interactions and their complexities, can be likened to missing pieces in the heritability puzzle. The unaccounted-for genetic interactions and nuances then contribute to what is called “missing heritability.” So just as one may search and search for missing puzzle pieces, so to do behavioral geneticists search and search for the “missing heritability”.
So heritability assumes no gene-gene and gene-environment interaction, no gene-environment correlation, among other false or questionable assumptions. But the main issue, I think, is that of the additivity assumption—it’s outright false and since it’s outright false, then it cannot accurately represent the intricate ways in which genes and other developmental resources interact to form the phenotype.
If heritability estimates assume that genetic influences on a trait are additive and independent, then heritability estimates oversimplify genetic complexity. If heritability estimates oversimplify genetic complexity, then heritability estimates do not adequately account for gene-environment interactions. If heritability does not account for gene-environment interactions, then heritability fails to capture the complexity of trait inheritance. Thus, if heritability assumes that genetic influences on a trait are additive and independent, then heritability fails to capture the complexity of trait inheritance due to its oversimplified treatment of genetic complexity and omission of gene-environment interactions.
One more issue, is that of the “heritability fallacy” (Moore and Shenk, 2016). One commits a heritability fallacy when they assume that heritability is an index of genetic influence on traits and that heritability can tell us anything about the relative contribution of trait inheritance and ontogeny. Moore and Shenk (2016) then make a valid conclusion based on the false belief that heritability us anything about the “genetic strength” on a trait:
In light of this, numerous theorists have concluded that ‘the term “heritability,” which carries a strong conviction or connotation of something “[in]heritable” in the everyday sense, is no longer suitable for use in human genetics, and its use should be discontinued.’31 Reviewing the evidence, we come to the same conclusion. Continued use of the term with respect to human traits spreads the demonstrably false notion that genes have some direct and isolated influence on traits. Instead, scientists need to help the public understand that all complex traits are a consequence of developmental processes.
“Missing heritability”, missing children
Twin studies traditionally find heritability to be estimated between 50 and 80 percent for numerous traits (eg Polderman et al, 2015; see Joseph’s critique). But as alluded to earlier, molecular studies have found heritabilities of 10 percent or lower (eg, Sniekers et al, 2017; Savage et al, 2018; Zabaneh et al, 2018). This discrepancy between different heritability estimates using different tools is what is termed “missing heritability” (Mathhews and Turkheimer, 2022). But the issue is, increasing the sample sizes will merely increase the chance of spurious correlations (Calude and Longo, 2018), which is all these studies show (Richardson, 2017b; Richardson and Jones, 2019).
This tells me one important thing—behavioral geneticists have so much faith in the heritability estimates gleaned from twin studies that they assume that the heritability is “missing” in the newer molecular genetic studies. But if something is “missing”, then that implies that it can be found. They have so much faith that eventually, as samples get higher and higher in GWAS and similar studies, that we will find the heritability that is missing and eventually, be able to identify genetic variants responsible for traits of interest such as IQ. However I think this is confused and a simple analogy will show why.
When a child goes missing, it is implied that they will be found by authorities, whether dead or alive. Now I can liken this to heritability. The term “missing heritability” comes from the disconnect between heritability estimates gleaned from twin studies and heritability estimates gleaned from molecular genetic studies like GWAS. So the implication here is, since twin studies show X percent heritability (high heritability), and molecular genetic studies show Y percent heritability (low heritability) – which is a huge difference between estimates between different tools – then the implication is that there is “missing heritability” that must be explained by rare variants or other factors.
So just like parents and authorities try so hard to find their missing children, so to do behavioral geneticists try so hard to find their “missing heritability.” As families endure anguish as they try to find their children, this is then mirrored in the efforts of behavioral geneticists to try and close the gap between two different kinds of tools that glean heritability.
But there is an important issue at play here—namely the fact that missing children actually exist, but “missing heritability” doesn’t, and that’s why we haven’t found it. Although some parents, sadly, may never find their missing children, the analogy here is that behavioral geneticists will never find their own “children” (their missing heritability) because it simply does not exist.
Spurious correlations
Even increasing the sample sizes won’t do anything, since the larger the sample size, the bigger chance for spurious correlations, and that’s all GWAS studies for IQ are (Richardson and Jones, 2019), while correlations with GWAS are inevitable and meaningless (Richardson, 2017b). Denis Noble (2018) puts this well:
As with the results of GWAS (genome-wide association studies) generally, the associations at the genome sequence level are remarkably weak and, with the exception of certain rare genetic diseases, may even be meaningless (13, 21). The reason is that if you gather a sufficiently large data set, it is a mathematical necessity that you will find correlations, even if the data set was generated randomly so that the correlations must be spurious. The bigger the data set, the more spurious correlations will be found (3). The current rush to gather sequence data from ever larger cohorts therefore runs the risk that it may simply prove a mathematical necessity rather than finding causal correlations. It cannot be emphasized enough that finding correlations does not prove causality. Investigating causation is the role of physiology.
Nor does finding higher overall correlations by summing correlations with larger numbers of genes showing individually tiny correlations solve the problem, even when the correlations are not spurious, since we have no way to find the drugs that can target so many gene products with the correct profile of action.
The Darwinian model
But the claim that there is a line that goes from G (genes) to P (phenotype) is just a mere holdover from the neo-Darwinian modern synthesis. The fact of the matter is, “HBD” and hereditarianism are based on reductionistic models of genes and how they work. But the reality is, genes don’t work how they think they do, reality is much more complex than they assume. Feldman and Ramachandran (2018) ask “Missing compared to what?”, effectively challenging the “missing heritability” claim. As Feldman and Ramachandran (2018) ask, would Herrnstein and Murray have written The Bell Curve if they believed that the heritability of IQ were 0.30? I don’t think they would have. In any case, such a belief in the heritability of IQ being between 0.4 and 0.8 shows the genetic determinist assumptions which are inherent in this type of “HBD” genetic determinist thinking.
Amusingly, as Ned Block (1995) noted, Murray said in an interview that “60 percent of the intelligence comes from heredity” and that that heritability is “not 60 percent of the variation. It is 60 percent of the IQ in any given person.” Such a major blunder from one of the “intellectual spearheads” of the “HBD race realist” movement…
Behavioral geneticists claim that the heritability is missing only because sample sizes are low, and as sample sizes increase, the missing heritability based on associated genes will be found. But this doesn’t follow at all since increasing sample sizes will just increase spurious hits of genes correlated with the trait in question but it says absolutely nothing about causation. Nevertheless, only a developmental perspective can provide us mechanistic knowledge and so-called heritability of a phenotype cannot give us such information because heritability isn’t a mechanistic variable and doesn’t show causation.
Importantly, a developmental perspective provides mechanistic knowledge that can yield practical treatments for pathologies. In contrast, information about the “heritability” of a phenotype—the kind of information generated by twin studies—can never be as useful as information about the development of a phenotype, because only developmental information produces the kind of thorough understanding of a trait’s emergence that can allow for successful interventions. (Moore 2015: 286)
The Darwinian model and it’s assumptions are inherent in thinking about heritability and genetic causation as a whole and are antithetical to developmental, EES-type thinking. Since hereditarianism and HBD-type thinking are neo-Darwinist, it then follows that such thinking is inherent in their beliefs, assumptions, and arguments.
Conclusion
Assumptions of heritability simply do not hold. Heritability, quite simply, isn’t a characteristic of traits but it is a characteristic of “relationships in a population observed in a particular setting” (Oyama, 1985/2000). Heritability estimates tell us absolutely nothing about development, nor the causes of development. Heritability is a mere breeding statistic and tells us nothing at all about the causes of development or whether or not genes are “causal” for a trait in question (Robette, Genin, and Clerget-Darpoux, 2022). It is key to understand that heritability along with the so-called “missing heritability” are based on reductive models of genetics that just do not hold, especially with newer knowledge that we have from systems biology (eg, Noble, 2012).
The assumption that heritability estimates tell us anything useful about genetics, traits, and causes along with a reductive belief in genetic causation for the ontogeny of traits has wasted millions of dollars. Now we need to grapple with the fact that heritability just doesn’t tell us anything about genetic causes of traits, but that genes are necessary, not sufficient, causes for traits because no genes (along with other developmental resources) means no organism. Also coming from twin, family and adoption studies are Turkheimer’s (2000) so-called “laws of behavioral genetics.” Further, the falsity of the EEA (equal environments assumption) is paramount here, and since the EEA is false, genetic conclusions from such studies are invalid (Joseph et al, 2015). There is also the fact that heritability is based on a false biological model. The issue is that heritability rests on a “conceptual model is unsound and the goal of heritability studies is biologically nonsensical given what we now know about the way genes work” (Burt and Simons, 2015: 107). What Richardson (2022) terms “the agricultural model of heritability” is known as false. In fact, the heritability of “IQ” is higher than any heritability found in the animal kingdom (Schonemann, 1997). Why this doesn’t give any researcher pause is beyond me.
Nonetheless, the Darwinian assumptions that are inherent in behavioral genetic, HBD “race realist” thinking are false. And the fact of the matter is, increasing the sample size of molecular genetic studies will only increase the chances of spurious correlations and picking up population stratification. So, it seems that using heritability to show genetic and environmental causes is a bust and has been a bust ever since Jensen revived the race and IQ debate in 1969, along with the subsequent responses that Jensen received against his argument which then led to the 1970s as being a decade in which numerous arguments were made against the concept of heritability (eg, Layzer, 1974).
It has also been pointed out to racial hereditarians for literally decades that heritability is is a flawed metric (Layzer, 1974; Taylor, 1980; Bailey, 1997; Schonemann, 1997; Guo, 2000; Moore, 2002; Rose, 2006; Schneider, 2007; Charney, 2012, 2013; Burt and Simons, 2015; Panofsky, 2014; Joseph et al, 2015; Moore and Shenk, 2016; Panofsky, 2016; Richardson, 2017; Lerner, 2018). These issues—among many more—lead Lerner to conclude:
However, the theory and research discussed across this chapter and previous ones afford the conclusion that no psychological attribute is pre-organized in the genes and unavailable to environmental influence. That is, any alleged genetic difference (or “inferiority”) of African Americans based on the high heritability of intelligence would seem to be an attribution built on a misunderstanding of concepts basic to an appropriate conceptualization of the nature–nurture controversy. An appreciation of the coaction of genes and context—of genes↔context relations—within the relational developmental system, and of the meaning, implications, and limitations of the heritability concept, should lead to the conclusion that the genetic-differences hypothesis of racial differences in IQ makes no scientific sense. (Lerner, 2018: 636)
That heritability doesn’t address mechanisms and ignores genetic factors, along with being inherently reductionist means that there is little to no utility of heritability for humans. And the complex, non-additive, non-linear aspects of biological systems are attempts at reducing biological systems to their component parts, (Rose, 2006), making heritability, again, inherently reductionist. We have to attempt to analyzed causes, not variances (Lewontin, 1974), which heritability cannot do. So it’s very obvious that the hereditarian programme which was revived by Jensen (1969)—and based on twin studies which were first undertaken in the 1920s—is based on a seriously flawed model of genes and how they work. But, of course, hereditarians have an ideological agenda to uphold, so that’s why they continue to pursue “heritability” in order to “prove” that “in part”, racial differences in many socio-behavioral traits—IQ included—are due to genes. But this type of argumentation quite clearly fails.
The fact of the matter is, “there are very good reasons to believe gene variations are at best irrelevant to common disorders and at worst a distraction from the social and political roots of major public health problems generally and of their unequal distribution in particular” (Chaufan and Joseph 2013: 284). (Also see Joseph’s, 2015 The Trouble with Twin Studies for more argumentation against the use of heritability and it’s inflation due to false assumptions along with arguments against “missing heritability.”) In fact, claims of “missing heritability” rest on “genetic determinist beliefs, a reliance on twin research, the use of heritability estimates, and the failure to seriously consider the possibility that presumed genes do not exist” (Joseph, 2012). Although it has been claimed that so-called rare variants explain the “missing heritability” (Genin, 2020), this is nothing but cope. So the heritability was never missing, it never existed at all.
Hypertension, Brain Volume, and Race: Hypotheses, Predictions and Actionable Strategies
2300 words
Introduction
Hypertension (HT, also known as high blood pressure, BP) is defined as a BP of 140/90. But more recently, the guidelines were changed making HT being defend as a BP over 130/90 (Carey et al, 2022; Iqbal and Jamal, 2022). One 2019 study showed that in a sample with an age range of 20-79, 24 percent of men and 23 percent of women could be classified as hypertensive based on the old guidelines (140/90) (Deguire et al, 2019). Having consistent high BP could lead to devestating consequences like (from the patient’s perspective) hot flushes, dizziness, and mood disorders (Goodhart, 2016). However, one serious problem with HT is the issue that consistently high BP is associated with a decrease in brain volume (BV). This has been seen in two systematic reviews and meta-analyses (Alosco et al, 2013; Beauchet et al, 2013; Lane et al, 2019; Alateeq, Walsh and Cherbuin, 2021; Newby et al, 2022) while we know that long-standing hypertension has deleterious effects on brain health (Salerno et al, 1992). However, it’s not only high BP that’s related to this, it’s also lower BP in conjuction with lower pulse pressure (Muller et al, 2010; Foster-Dingley, 2015). So what this says to me is that too much or too little blood flow to the brain is deleterious for brain health.I will state the hypothesis and then I will state the predictions that follow from it. I will then provide three reasons why I think this relationship occurs.
The hypothesis
The hypothesis is simple: high BP (hypertension, HT) is associated with a reduced brain volume. This relationship is dose-dependent, meaning that the extent and duration of HT correlates with the degree of BV changes. So the hypothesis suggests that there is a relationship—an association—between HT and brain volume, where people with HT will be more likely to have decreased BVs than those who lack HT—that is, those with BP in the normal range.
The dose-dependent relationship that has been observed (Alateeq, Walsh and Cherbuin, 2021), and this shows that as HT increases and persists over time, the effects of decreased BV become more pronounced. This relationship suggests that it’s not a binary, either-or situation, present or absent situation, but that it varies across a continuum. So people with shorter-lasting HT will have fewer effects than those with constant and consistent elevated BP and they will then show subsequent higher decreases in BV. This dose-dependent relationship also suggests that as BP continues to elevate, the decrease in BV will worsen.
This dose-dependent relationship implies a few things. The consequences of HT on BV aren’t binary (either or), but are related to the severity of HT, how long one has HT, and at what age they have HT and that it varies on a continuum. For instance, people with mild or short-lasting HT would experience smaller reductions in BV than those that have severe or long-standing HT. The dose-dependent relationship also suggests that the longer one has HT without treatment, the more severe and worse the reduction in BV will be if it is uncontrolled. So as BP continues to elevate, it may lead to a gradual reduction in BV. So the relationship between HT and BV isn’t uniform, but it varies based on the intensity and duration of high BP.
So the hypothesis suggests that HT isn’t just a risk factor for cardiovascular disease, but it’s also a risk factor for decreased BV. This seems intuitive, since the higher one’s BP, the more likely it is that there is the beginnings of a blockage somewhere in the intricate system of blood vessels in the body. And since the brain is a vascular organ, then by decreasing the amount of blood flowing to it, this then would lead to cell death, white matter lesions which would lead to a smaller BV. One newer study showed, with a sample of Asians, whites, blacks, and “Latinos” that, compared to those with normal BP, those who were transitioning to higher BP or already had higher BP had lower brain connectivity, decreased cerebral gray matter and frontal cortex volume, while this change was worse for men (George et al, 2023). Shang et al (2021) showed that HT diagnosed in early and middle life but not late life was associated with decreased BV and increased risk of dimentia. This, of course, is due to the slow cumulative effects of HT and it’s effects on the brain. While Power et al (2016) “The pattern of hypertension ~15 years prior and hypotension concurrent with neuroimaging was associated with smaller volumes in regions preferentially affected by Alzheimer’s disease.” But not only is BP relevant here, so is the variability of BP at night (Gutteridge et al, 2022; Yu et al, 2022). Alateeq, Walsh and Cherbuin (2021) conclude that:
Although reviews have been previously published in this area, they only investigated the effects of hypertension on brain volume [86]. To the best of our knowledge, this study’s the first systematic review with meta-analysis providing quantitative evidence on the negative association between continuous BP and global and regional brain volumes. Our results suggest that heightened BP across its whole range is associated with poorer cerebral health which may place individuals at increased risk of premature cognitive decline and dementia. It is therefore important that more prevention efforts be directed at younger populations with a greater focus on achieving optimal BP rather than remaining below clinical or pre-clinical thresholds[5].
One would think that a high BP would actually increase blood flow to the brain, but HT actually causes alterations in the flow of blood to the brain which leads to ischaemia and it causes the blood-brain barrier to break down (Pires et al, 2013). Essentially, HT has devestating effects on the brain which could lead to dimentia and Alzheimer’s (Iadecola and Davisson, 2009).
So the association between HT and decreased BV means that individuals with HT can experience alterations in BV in comparison to those with normal BP. The hypothesis also suggests that there are several mechanisms (detailed below), which may lead to various physiological and anatomic changes in the brain, such as vascular damage, inflammation and tissue atrophy.
The mechanisms
(1) High BP can damage blood vessels in the brain, which leads to reduced blood flow. This is called “cerebral hypoperfusion.” The reduced blood flow can deprive the cells in the brain of oxygen and nutrients, which cause them to shrink or die which leads to decreased brain volume (BV). Over time, high BP can damage the arteries, making them less elastic
(2) Over a long period of time having high BP, this can cause hypertensive encephalopathy, which is basically brain swelling. A rapid increase in BP could over the short term increase BV, but left untreated it could lead to brain damage and atrophy over time.
And (3) Chronically high BP can lead to the creation of white matter lesions on the brain, and the lesions are areas of damaged brain tissue which could result in microvascular changes caused by high BP (hypertension, HT). Thus, over time, the accumulation of white matter lesions could lead to a decrease in brain volume. HT can contribute to white matter lesions in the brain, which are then associated with cognitive changes and decreased BV, and these lesions increase with BP severity.
So we have (1) cerebral hypoperfusion, (2) hypertensive encephalopathy, and (3) white matter lesions. I need to think/read more on which of these could lead to decreased BV, or if they all actually work together to decrease BV. We know that HT damages blood vessels, and of course there are blood vessels in the brain, so it then follows that HT would decrease BV.
I can also detail a step-by-step mechanism. The process beings with consistently elevated BP, which could be due to various factors like genetics, diet/lifestyle, and underlying medical conditions. High BP then places increased strain on the blood vessels in the body, including those in the brain. This higher pressure could then lead to structural change of the blood vessels over time. Then, chronic HT over time can lead to endothelial dysfunction, which could impair the ability of blood vessels to regulate blood flow and maintain vessel integrity. The dysfunction can result in oxidative stress and inflammation.
Then as a response to prolonged elevated BP, blood vessels in the brain could undergo vascular remodeling, which involves changes im blood vessel structure and thickness, which can then affect blood flow dynamics. Furthermore, in some cases, this could lead to something called cerebral small vessel disease which involves damage to the small blood vessels in the brain including capillaries and arterioles. This could impair delivery of oxygen and nutrients to brain tissue which could lead to cell death and consequently a decrease in BV. Then reduced blood flow along compromised blood vessel integrity could lead to cerebral ischaemia—reduced blood supply—and hypoxia—reduced oxygen supply—in certain parts of the brain. This can then result in neural damage and eventually cell death.
Then HT-related vascular changes and cerebral small vessel disease can trigger brain inflammation. Prolonged exposure to neural inflammation, hypoxia and ischemia can lead to neuronal atrophy, where neurons shrink and lose their functional integrity. HT can also increase the incidence of white matter lesions in the brain which can be seen in neuroimages, which involve areas of white matter tissue which become damaged. Finally, over time, the cumulative effects of the aforementioned processes—vascular changes, inflammation, neural atrophy, and white matter changes could lead to a decrease in BV. This reduction can manifest as brain atrophy which is then observed in parts of the brain which are susceptible and vulnerable to the effects of HT.
So the step-by-step mechanism goes like this: elevated BP —> increased vascular strain —> endothelial dysfunction —> vascular remodeling —> cerebral small vessel disease —> ischemia and hypoxia —> inflammation and neuroinflammation —> neuronal atrophy —> white matter changes —> reduction in BV.
Hypotheses and predictions
H1: The severity of HT directly correlates with the extent of BV reduction. One prediction would be that people with more severe HT would exhibit greater BV decreases than those with moderate (less severe) HT, which is where the dose-dependent relationship comes in.
H2: The duration of HT is a critical factor in BV reduction. One prediction would be that people with long-standing HT will show more significant BV changes than those with recent onset HT.
H3: Effective BP management can mitigate BV reduction in people with HT. One prediction would be that people with more controlled HT would show less significant BV reduction than those with uncontrolled HT.
H4: Certain subpopulations may be more susceptible to BV decreases due to HT. One prediction is that certain factors like age of onset (HT at younger age), genetic factors (some may have certain gene variants that make them more susceptible and vulnerable to damage caused by elevated BP), comorbities (people with diabetes, obesity and heart problems could be at higher risk of decreased BV due to the interaction of these factors), ethnic/racial factors (some populations—like blacks—could be at higher risk of having HT and they could be more at risk due to experiencing disparities in healthcare and treatment.
The hypotheses and predictions generated from the main proposition that HT is associated with a reduction in BV and that the relationship is dose-dependent can be considered risky, novel predictions. They are risky in the sense that they are testable and falsifiable. Thus, if the predictions don’t hold, then it could falsify the initial hypothesis.
Blacks and blood pressure
Due to this, for populations like black Americans, this is significant. About 33 percent of blacks have hypertension (Peters, Arojan, and Flack, 2006), while urban blacks are more likely to have elevated BP than whites (Lindhorst et al, 2007). Though Non, Gravlee, and Mulligan (2012) showed that racial differences in education—not genetic ancestry—explained differences in BP in blacks compared to whites. Further, Victor et al (2018) showed that in black male barbershop attendees who had uncontrolled BP, that along with medication and outreach, this lead to a decrease in BP. Williams (1992) cited stress, socioecologic stress, social support, coping patterns, health behavior, sodium, calcium, and potassium consumption, alcohol consumption, and obesity as social factors which lead to increased BP.
Moreover, consistent with the hypothesis discussed here (that chronic elevated BP leads to reductions in BV which lead to a higher chance of dementia and Alzheimer’s), it’s been shown that vulnerability to HT is a major determinate in the risk of acquiring Alzheimer’s (Clark et al, 2020; Akushevic et al, 2022). It has also been shown that “a lifetime of racism makes Alzheimer’s more common in black Americans” and consistent with the discussion here since racism is associated with stress which is associated with elevated BP, then consistent events of racial discrimination would lead to consistent and elevated BP which would then lead to decreased BV and then a higher chance of acquitting Alzheimer’s. But, there is evidence that blood pressure drugs (in this case telmisartan) reduce the incidence of Alzheimer’s in black Americans (Zhang et al, 2022) while the same result was also seen using antihyperintensive medications in blacks which led to a reduction in incidence of dementia (Murray et al, 2018), which lends credence to the discussed hypothesis. Stress and poverty—experiences—and not ancestry could explain higher rates of dementia in black Americans as well. Thus, since blood pressure could explain higher rates of dementia in black populations, this then lends credence to the discussed hypothesis.
Conclusion
The evidence that chronic elevated BP leads to reductions in BV are well-studied and the mechanisms are well-known. I discussed the hypothesis that chronically elevated BP leads to reduced blood flow to the brain which decreases BV. I then discussed the mechanisms behind the relationship, and then hypotheses and predictions that follow from them. Lastly, I discussed the well-known fact that blacks have higher rates of BP, and also higher rates of dementia and Alzheimer’s, and linked the fact that they have higher rates of BP to those maladies.
So by catching chronically elevated BP in the early ages, since the earlier one has high BP the more likely they are to have reduced brain volume and the associated maladies, we can then begin to fight the associated issues before they coalesce, since we know the mechanisms behind them, along with the fact that blood pressure drugs and antihypertensive medications decrease incidences of dementia and Alzheimer’s in black Americans.
IQ, Achievement Tests, and Circularity
2150 words
Introduction
In the realm of educational assessment and psychometrics, a distinction between IQ and achievement tests needs to be upheld. It is claimed that IQ is a measure of one’s potential learning ability, while achievement tests show what one has actually learned. However, this distinction is not strongly supported in my reading of this literature. IQ and achievement tests are merely different versions of the same evaluative tool. This is what I will argue in this article: That IQ and achievement tests are different versions of the same test, and so any attempt to “validate” IQ tests based not only on other IQ tests, achievement tests and job performance is circular, I will argue that, of course, the goal of psychometrics in measuring the mind is impossible. The hereditarian argument, when it comes to defending their concept and the claim that they are measuring some unitary and hypothetical variable, then, fails. At best, these tests show one’s distance from the middle class, since that’s the where most of the items on the test derive from. Thus, IQ and achievement tests are different versions of the same test and so, they merely show one’s “distance” from a certain kind of class-specific knowledge (Richardson, 2012), due to the cultural and psychological tools one must possess to score well on these tests (Richardson, 2002).
Circular IQ-ist arguments
IQ-ists have been using IQ tests since they were brought to America by Henry Goddard in 1913. But one major issue (one they still haven’t solved—and quite honestly never will) was that they didn’t have any way to ensure that the test was construct valid. So this is why, in 1923, Boring stated that “intelligence is what intelligence tests test“, while Jensen (1972: 76) said “intelligence, by definition, is what intelligence tests measure.” However, such statements are circular and they are circular because they don’t provide real evidence or explanation.
Boring’s claim that “intelligence is what intelligence tests test” is circular since it defines intelligence based on the outcome of “intelligence tests.” So if you ask “What is intelligence“, and I say “It’s what intelligence tests measure“, I haven’t actually provided a meaningful definition of intelligence. The claim merely rests on the assumption that “intelligence tests” measure intelligence, not telling us what it actually is.
Jensen’s (1976) claim that “intelligence, by definition, is what intelligence tests measure” is circular for similar reasons to Boring’s since it also defines intelligence by referring to “intelligence tests” and at the same time assumes that intelligence tests are accurately measuring intelligence. Neither claim actually provides an independent understanding of what intelligence is, it merely ties the concept of “intelligence” back to its “measurement” (by IQ tests). Jensen’s Spearman’s hypothesis on the nature of black-white differences has also been criticized as circular (Wilson, 1985). Not only was Jensen (and by extension Spearman) guilty of circular reasoning, so too was Sternberg (Schlinger, 2003). Such a circular claim was also made by Van der Mass, Kan, and Borsboom (2014).
But Jensen seemed to have changed his view, since in his 1998 book The g Factor, he argues that we should dispense with the term “intelligence”, but curiously that we should still study the g factor and assume identity between IQ and g… (Jensen made many more logical errors in his defense of “general intelligence”, like saying not to reify intelligence on one page and then a few pages later reifying it.) Circular arguments have been identified in not only Jensen’s writings Spearman’s hypothesis, but also in using construct validity to validate a measure (Gordon, Schonemann; Guttman, 1992: 192).
The same circularity can be seen when discussions of the correlation between IQ and achievement tests is brought up. “These two tests correlate so they’re measuring the same thing”, is an example one may come across. But the error here is assuming that mental measurement is possible and that IQ and achievement tests are independent of each other. However, IQ and achievement tests are different versions of the same test. This is an example of circular validation, which occurs when a test’s “validity” is established by the test itself, leading to a self-reinforcing loop.
IQ tests are often validated with other older editions of the test. For example, the newer version of the S-B would be “validated” against the older version of the test that the newer version was created to replace (Howe, 1997: 18; Richardson, 2002: 301), which not only leads to circular “validation”, but would also lead to the same assumptions from the older test constructors (like Terman) which would still then be alive in the test itself (since Terman assumed men and women should be equal in IQ and so this assumption is still there today). IQ tests are also often “validated” by comparing IQ test results to outcomes like job performance and academic performance. Richardson and Norgate (2015) have a critical review of the correlation between IQ and job performance, arguing that it’s inflated by “corrections”, while Sackett et al, 2023 show “a mean observed validity of .16, and a mean corrected for unreliability in the criterion and for range restriction of .23. Using this value drops cognitive ability’s rank among the set of predictors examined from 5th to 12th” for the correlation between “general cognitive ability” and job performance.
But this could lead to circular validation, in that if a high IQ is used as a predictor of success in school or work, then success in school or work would be used as evidence in validating the IQ test, which would then lead to a circular argument. The test’s validity is being supported by the outcome that it’s supposed to predict.
Achievement tests are destined to see what one had learned or achieved regarding a certain kind of subject matter. Achievement tests are often validated by correlating test scores with grades or other kinds of academic achievement (which would also be circular). But if high achievement test scores are used to validate the test and those scores are also used as evidence of academic achievement, then that would be circular. Achievement tests are “validated” on their relationship between IQ tests and grades. Heckman and Kautz (2013) note that “achievement tests are often validated using other standardized achievement tests or other measures of cognitive ability—surely a circular practice” and “Validating one measure of cognitive ability using other measures of cognitive ability is circular.” But it should also be noted that the correlation between college grades and job performance 6 or more years after college is only .05 (Armstrong, 2011).
Now what about the claim that IQ tests and achievement tests correlate so they measure the same thing? Richardson (2017) addressed this issue:
For example, IQ tests are so constructed as to predict school performance by testing for specific knowledge or text‐like rules—like those learned in school. But then, a circularity of logic makes the case that a correlation between IQ and school performance proves test validity. From the very way in which the tests are assembled, however, this is inevitable. Such circularity is also reflected in correlations between IQ and adult occupational levels, income, wealth, and so on. As education largely determines the entry level to the job market, correlations between IQ and occupation are, again, at least partly, self‐fulfilling
The circularity inherent in likening IQ and achievement tests has also been noted by Nash (1990). There is no distinction between IQ and achievement tests since there is no theory or definition of intelligence and how, then, this theory and definition would be likened to answering questions correctly on an IQ test.
But how, to put first things first, is the term ‘cognitive ability’ defined? If it is a hypothetical ability required to do well at school then an ability so theorised could be measured by an ordinary scholastic attainment test. IQ measures are the best measures of IQ we have because IQ is defined as ‘general cognitive ability’. Actually, as we have seen, IQ theory is compelled to maintain that IQ tests measure ‘cognitive ability’ by fiat, and it therefore follows that it is tautologous to claim that IQ tests are the best measures of IQ that we have. Unless IQ theory can protect the distinction it makes between IQ/ability tests and attainment/ achievement tests its argument is revealed as circular. IQ measures are the best measures of IQ we have because IQ is defined as ‘general cognitive ability’: IQ tests are the only measures of IQ.
The fact of the matter is, IQ “predicts” (is correlated with) school achievement since they are different versions of the same test (Schwartz, 1975; Beaujean et al, 2018). Since the main purpose of IQ tests in the modern day is to “predict” achievement (Kaufman et al, 2012), then if we correctly identify IQ and achievement tests as different versions of the same test, then we can rightly state that the “prediction” is itself a form of circular reasoning. What is the distinction between “intelligence” tests and achievement tests? They both have similar items on them, which is why they correlate so highly with each other. This, therefore, makes the comparison of the two in an attempt to “validate” one or the other circular.
I can now argue that the distinction between IQ and achievement tests is nonexistent. If IQ and achievement tests are different versions of the same test, then they share the same domain of assessing knowledge and skills. IQ and achievement tests contain similar informational content on them, and so they can both be considered knowledge tests—class-specific knowledge. IQ and achievement tests share the same domain of assessing knowledge and skills. Therefore, IQ and achievement tests are different versions of the same test. Put simply, if IQ and achievement tests are different versions of the same test, then they will have similar item content, and they do so we can correctly argue that they are different versions of the same test.
Moreover, even constructing tests has been criticized as circular:
Given the consistent use of teachers’ opinions as a primary criterion for validity of the Binet and Wechsler tests, it seems odd to claim then that such tests provide “objective alternatives to the subjective judgments of teachers and employers.” If the tests’ primary claim to predictive validity is that their results have strong correlations with academic success, one wonders how an objective test can predict performance in an acknowledged subjective environment? No one seems willing to acknowledge the circular and tortuous reasoning behind the development of tests that rely on the subjective judgments of secondary teachers in order to develop an assessment device that claims independence of those judgments so as to then be able to claim that it can objectively assess a student’s ability to gain the approval of subjective judgments of college professors. (And remember, these tests were used to validate the next generation of tests and those tests validated the following generation and so forth on down to the tests that are being given today.) Anastasi (1985) comes close to admitting that bias is inherent in the tests when he confesses the tests only measure what many anthropologists would called a culturally bound definition of intelligence. (Thorndike and Lohman, 1990)
Conclusion
It seems clear to me that almost the whole field of psychometrics is plagued with the problem of inferring causes from correlation and using circular arguments in an attempt to justify and validate the claim that IQ tests measure intelligence by using flawed arguments that relate IQ to job and academic performance. However this idea is very confused. Moreover, circular arguments aren’t only restricted to IQ and achievement tests, but also in twin studies (Joseph, 2014; Joseph et al, 2015). IQ and achievement tests merely show what one knows, not their learning potential, since they are general knowledge tests—tests of class-specific knowledge. So even Gottfredson’s “definition” of intelligence fails, since Gottfredson presumes IQ to be a measure of learning ability (nevermind the fact that the “definition” is so narrow and I struggle to think of a valid way to operationalize it to culture-bound tests).
The fact that newer versions of tests already in circulation are “validated” against other older versions of the same test means that the tests are circularly validated. The original test (say the S-B) was never itself validated, and so, they’re just “validating” the newer test on the assumption that the older one was valid. The newer test, in being compared to its predecessor, means that the “validation” is occuring on the other older test which has similar principles, assumptions, and content to the newer test. The issue of content overlap, too, is a problem, since some questions or tasks on the newer test could be identical to questions or tasks on the older test. The point is, both IQ and achievement tests are merely knowledge tests, not tests of a mythical general cognitive ability.
Examining Misguided Notions of Evolutionary “Progress”
2650 words
Introduction
For years, PumpkinPerson (PP) has been pushing an argument which states that “if you’re the first branch, and you don’t do anymore branching, then you’re less evolved than higher branches.” This is the concept of “more evolved” or the concept of evolutionary progress. Over the years I have written a few articles on the confused nature of this thinking. PP seems to like the argument since Rushton deployed a version of it for his r/K selection (Differential K) theory, which stated that “Mongoloids” are more “K evolved” than “Caucasians” who are more “K evolved” than “Negroids”, to use Rushton’s (1992) language. Rushton posited that this ordering occurred due to the cold winters that the ancestors of “Mongoloids” and “Caucasoids” underwent, and he theorized that this led to evolutionary progress, which would mean that certain populations are more advanced than others (Rushton, 1992; see here for response). It is in this context that PP’s statement above needs to be carefully considered and analyzed to determine its implications and relevance to Rushton’s argument. It commits the affirming the consequent fallacy, and assuming the statement is true leads to many logical inconsistenties like there being a “most evolved” species,
Why this evolutionary progress argument is fallacious
if you’re the first branch, and you don’t do anymore branching, then you’re less evolved than higher branches.
This is one of the most confused statements I have ever read on the subject of phylogenies. This misconception, though, is so widespread that there have been quite a few papers that talk about this and talk about how to steer students away from this kind of thinking about evolutionary trees (Crisp and Cook, 2004; Baum, Smith, and Donovan, 2005; Gregory, 2008; Omland, Cook, and Crisp, 2008). This argument is invalid since the concept of “evolved” in evolutionary trees doesn’t refer to a hierarchical scale, where higher branches are “more evolved” than lower branches (which are “less evolved”). What evolutionary trees do is show historical relationships between different species, which shows common ancestry and divergence over time. So each branch represents a lineage and all living organisms have been evolving foe the same amount of time since the last common ancestor (LCA). Thus, the position of a branch on the tree doesn’t determine a species’ level of evolution.
The argument is invalid since it incorrectly assumes that the position of the branch on a phylogeny determines the evolution or the “evolutionary advancement” of a species. Here’s how I formulate this argument:
(P1) If you’re the first branch on the evolutionary tree and you don’t do any more branching, then you’re less evolved than higher branches.
(P2) (Assumption) Evolutionary advancement is solely determined by the position on the tree and the number of branches.
(C) So species represented by higher branches on the evolutionary tree are more evolved than species represented by lower branches.
There is a contradiction in P2, since as I explained above, each branch represents a new lineage and every species on the tree is equally evolved. PP’s assumption seems to be that newer branches have different traits than the species that preceded it, implying that there is an advancement occurring. Nevertheless, I can use a reductio to refute the argument.
Let’s consider a hypothetical scenario in which this statement is true: “If you’re the first branch and you don’t do any more branching, then you’re less evolved than higher branches.” This suggests that the position of a species on a phylogeny determines its level of evolution. So according to this concept, if a species occupies a higher branch, it should be “more evolved” than a species on a lower branch. So following this line of reasoning, a species that has undergone extensive branching and diversification should be classified as “more evolved” compared to a species that has fewer branching points.
Now imagine that in this hypothetical scenario, we have species A and species B in a phylogeny. Suppose that species A is the first branch and that it hasn’t undergone any branching. Conversely, species B, which is represented on a higher branch, has experienced extensive branching and diversification, which adheres to the criteria for a species to be considered “more evolved.” But there are logical implications for the concept concerning the positions of species A and species B on the phylogeny.
So according to the concept of linear progression which is implied in the original statement, if species B is “more evolved” than species A due to its higher branch position, it logically follows that species B should continue to further evolve and diversify. This progression should lead to new branching points, as each subsequent stage would be considered “more evolved” than the last. Thus, applying the line of reasoning in the original statement, it suggests that there should always be a species represented on an even higher branch than species B, and this should continue ad infinitim, with no endpoint.
The logical consequence of the statement is that an infinite progression of increasingly evolved species, each species being represented by a higher branch than the one before, without any final of ultimate endpoint for a “most evolved” species. This result leads to an absurdity, since it contradicts our understanding of evolution as an ongoing and continuous process. The idea of a linear and hierarchical progression of a species in an evolutionary tree culminating in a “most evolved” species isn’t supported by our scientific understanding and it leads to an absurd outcome.
Thus, the logical implications of the statement “If you’re the first branch and you don’t do any more branching, then you’re less evolved than higher branches” leads to an absurd and contradictory result and so it must be false. The concept of the position of a species on an evolutionary tree isn’t supported by scientific evidence and understanding. Phylogenies represent historical relationships and divergence events over time.
(1) Assume the original claim is true: If you’re the first branch and you don’t do any more branching, then you’re less evolved than higher branches.
(2) Suppose species A is the first branch and undergoes no further branching.
(3) Now take species B which is in a higher branch which has undergone extensive diversification and branching, making it “more evolved”, according to the statement in (1).
(4) But based on the concept of linear progression implied in (1), species B should continue to evolved and diversity even further, leading to new branches and increased evolution.
(5) Following the logic in (1), there should always be a species represented on an even higher branch than species B, which is even more evolved.
(6) This process should continue ad infinitim with species continually branching and becoming “more evolved” without an endpoint.
(7) This leads to an absurd result, since it suggests that there is no species that could be considered “more evolved” or reach a final stage of evolution, contradicting our understanding of evolution as a continuous, ongoing process, with no ultimate endpoint.
(8) So since the assumption in (1) leads to an absurd result, then it must be false.
So the original statement is false, and a species’ position on a phylogeny doesn’t determine the level of evolution and the superiority of a species. The concept of a linear and hierarchical progression of advancement in a phylogeny is not supported by scientific evidence and assuming the statement in (1) is true leads to a logically absurd outcome. Each species evolves in its unique ecological context, without reaching a final state of evolution or hierarchical scale of superiority. This reductio ad absurdum argument therefore reveals the fallacy in the original statement.
Also, think about the claim that there are species that are “more evolved” than other species. This implies that there are “less evolved” species. Thus, a logical consequence of the claim is that there could be a “most evolved” species.
So if a species is “most evolved”, it would mean that that species has surpassed all others in evolutionary advancement and there are no other species more advanced than it. Following this line of reasoning, there should be no further branching or diversification of this species since it has already achieved the highest level of evolution. But evolution is an ongoing process. Organisms continously adapt to and change their surroundings (the organism-environment system), and change in response to this. But if the “most evolved” species is static, this contradicts what we know about evolution, mainly that it is continuous, ongoing change—it is dynamic. Further, as the environment changes, the “most evolved” species could become less suited to the environment’s conditions over time, leading to a decline in its numbers or even it’s extinction. This would then imply that there would have been other species that are “more evolved.” (It merely shows the response of the organism to its environment and how it develops differently.) Finally, the idea of a “most evolved” species implies an endpoint of evolution, which contradicts our knowledge of evolution and the diversification of life one earth. Therefore, the assumption that there is a “most evolved” species leads to a logical contradiction and an absurdity based on what we know about evolution and life on earth.
The statement possesses scala naturae thinking, which is also known as the great chain of being. This is something Rushton (2004) sought to bring back to evolutionary biology. However, the assumptions that need to hold for this to be true—that is, the assumptions that need to hold for this kind of tree reading to even be within the realm of possibility is false. This is wonderfully noted by Gregory (2008) who states that “The order of terminal noses is meaningless.” Crisp and Cook (2004) also state how such tree-reading is intuitive and this intuition of course is false:
Intuitive interpretation of ancestry from trees is likely to lead to errors, especially the common fallacy that a species-poor lineage is more ‘ancestral’ or ‘diverges earlier’ than does its species-rich sister group. Errors occur when trees are read in a one-sided way, which is more commonly done when trees branch asymmetrically.
There are several logical implications of that statement. I’ve already covered the claim that there is a kind of progression and advancement in evolution—a linear and hierarchical ranking—and the fixed endpoint (“most evolved”). Further, in my view, this leads to value judgments, that some species are “better” or “superior” to others. It also seems to ignore that the branching signifies not which species has undergone more evolution, but the evolutionary relationships between species. Finally, evolution occurs independently in each lineage and is based on their specific histories and interactions between developmental resources, it’s not valid to compare species as “more evolved” than others based on the relationships between species on evolutionary trees, so it’s based on an arbitrary comparison between species.
Finally, I can refute this using Gould’s full house argument.
P1: If evolution is a ladder of progress, with “more evolved” species on higher rungs, then the fossil record should demonstrate a steady increase in complexity over time.
P2: The fossils record does not shit a steady increase in complexity over time.
C: Therefore, evolution is not a ladder of progress and species cannot be ranked as “more evolved” based on complexity.
P1: If the concept of “more evolved” is valid, then there would be a linear and hierarchical progression in the advancement of evolution, wjtcertsin species considered superior to others based on their perceived level of evolutionary change.
P2: If there a linear and hierarchical progression of advancement in evolution, then the fossil record should demonstrate a steady increase in complexity over time, with species progressively becoming more complex and “better” in a hierarchical sense.
P3: The fossils record does not show a steady increase in complexity over time; it instead shows a diverse and branching pattern of evolution.
C1: So the concept of “more evolved” isn’t valid, since there is an absence of a steady increase in complexity in the fossil record and this refutes the notion of a linear and hierarchical progression of advancement in evolution.
P4: If the concept of “more evolved” is not valid, then there is no objective hierarchy of superiority among species based in their positions on an evolutionary tree.
C2: Thus, there is no objective hierarchy of superiority among species based on their positions on an evolutionary tree.
There is one final fallacy contained in that statement: it affirms the consequent. This logical fallacy takes the form of: If P then Q, P is true so Q is true.” Even if the concept of “more evolved” were valid, just because a species doesn’t do any more branching doesn’t mean it’s less evolved. So this reasoning is as follows: If you’re the first branch and you don’t do anymore branching, then you’re less evolved than higher branches (If P and Q, then R). It affirms the consequent like this: You didn’t do anymore branching (Q), so this branch has to be less evolved than the higher branches (R). It incorrectly infers the consequent Q (not doing anymore branching) as a sufficient condition for the antecedent P (being the first branch), which leads to the flawed conclusion (R) that the species is less evolved than higher branches. Just because a species doesn’t do anymore branching doesn’t mean it’s less evolved than another species. There could be numerous reasons why branching didn’t occur and it doesn’t directly determine evolutionary status. The argument infers being less evolved from doing less branching, which affirms the consequent. If a species doesn’t do anymore branching then that branch is less evolved than a higher branch. So since the argument affirms the consequent, it is therefore invalid.
Conclusion
Reading phylogenies in such a manner—in a way that would make one infer the conclusion that evolution is progressive and that there are “more evolved” species—although intuitive is false. Misconceptions like this along with many others while reading evolutionary trees are so persistent that much thought has been put into educating the public on right and wrong ways to read evolutionary trees.
As I showed in my argument ad absurdums where I accepted the claim as true, it leads to logical inconsistenties and goes against everything we know about evolution. Evolution is not progressive, it’s merely local change. That a species changes over time from another species doesn’t imply anything about “how evolved” (“more or less”) it is in comparison to the other. Excising this thinking is tough, but it is doable by understanding how evolutionary trees are constructed and how to read them correctly. It further affirms the consequent, leading to a false conclusion.
All living species have spent the same amount of time evolving. Branching merely signifies a divergence, not a linear scale of advancement. Of course one would think that if evolution is happening and one species evolves into another and that this relationship is shown on a tree that this would indicate that the newer species is “better” in some way in comparison to the species it derived from. But it merely suggests that the species faced different challenges which influenced its evolution; each species adapted and survived in its own unique evolutionary ecology, leading to diversification and the formation of newer branches on the tree. Evolution does not follow a linear path of progress, and there is no inherent hierarchy of superiority among species based on their position on the evolutionary tree. While the tree visually represents relationships between species, it doesn’t imply judgments like “better” or “worse”, “more evolved” or “less evolved.” It merely highlights the complexity and diversity of all life on earth.
Evolution is quite obviously not progressive, and even if it were, we wouldn’t see evolutionary progression from reading evolutionary trees, since such evolutionary relationships between species can be ladderized or not, with many kinds of different branches that may not be intuitive to those who read evolutionary trees as showing “more evolved” species, they nevertheless show a valid evolutionary relationship.
When Will Bo Winegard Understand What Social Constructivists Say and Don’t Say About Race?: Correcting Bo’s Misconceptions About Social Constructivism
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For years it seems as if Bo Winegard—former professor (his contract was not renewed)—does not understand the difference between social constructivism about race (racial constructivism refers to the same thing as social constructivism about race so I will be using these two terms interchangeably) and biological realism about race. It seems like he assumes that racial constructivists say that race isn’t real. But if that were true, how would it make sense to call race a social concept if it doesn’t exist? It also seems to me like he is saying that social constructs aren’t real. Money and language are social constructs, too, so does that mean they aren’t real? It doesn’t make sense to say that.
Quite obviously, if X is a social convention, then X is real, albeit a social reality. So if race is a social convention, then race is real. However, Bo’s ignorance to this debate is seen perfectly with this quote from a recent article he wrote:
Some conservative social constructionists and culture-only theorists (i.e., non race realists) have pushed back against the excesses of racial progressivism
In this article, Bo (rightly) claims that hereditarianism is a subset of race realism (I make a distinction between psychological and racial hereditarianism). But where Bo goes wrong is in not making the distinction between biological and social racial realism, as for example Kaplan and Winther (2014) did. Kaplan and Winther’s paper is actually the best look into how the concepts of bio-genomic cluster/racial realism, socialrace, and biological racial realism are realist positions about race. The AAPA even stated a few years back that “race has become a social reality that structures societies and how we experience the world. In this regard, race is real, as is racism, and both have real biological consequences. Membership in socially-defined (racial) groups can have real-life impacts themselves even if there are no biological races in the human species (Graves, 2015). That is: The social can and does become biological (meaning that the social can manifest itself in biology).
Bo’s ignorance can be further seen with this quote:
there is an alternative position: race realism, which argues that people use the concept of race for the same reason that they use the concept of species or sex
And he also wrote a tweet while explaining his “moderate manifesto”, again pushing the same misconception that social constructivists about race aren’t realists about race:
(2) Modern elite discourse contends that race is illusory, a kind of reified figment of our social imagination. BUT, it also contends that we need to promote race-conscious policies to rectify past wrongs. Race is unreal. But some “races” deserve benefits.
… I should note that race, like many other categories, is partially a social construct. But that does not mean that it’s not real.
Bo makes claims like “race is real”, as if social constructivists don’t think that race is real. That’s the only way for social constructivists to be about race. I think Bo is talking about racial anti-realists like Joshua Glasgow, who claim that race is neither socially nor biologically real. But social constructivists and biological racial realists (this term gets thorny since it could refer to a “realist” like Rushton or Jensen, who have no solid grounding in their belief in race or it could refer to philosophers like Michael Hardimon (like his minimalist/populationist, racialist and socialrace concepts) and Quayshawn Spencer (his Blumenbachian partitions), are both realists about race, but in different ways. Kaplan and Winther’s distinctions are good to set these 2 different camps a part and distinguish between them while still accepting that they are both realists.
I don’t think Bo realizes the meandering he has been doing for years discussing this concept. Race is partially a social construct, but race is real (which hereditarians believe), yet social constructivists about race are talking about something. They are talking about a referent, where a referent for race here is a property name for a set of human population groups (Spencer, 2019). The concept of race refers to a social something, thus it is real since society makes it real. Nothing in that entails that race isn’t real. If Bo made the distinction between biological and social races, then he would be able to say that social constructivists about race believe that race is real (they are realists about race as a social convention), but they are anti-realists about biological races.
Social constructivists are anti-realists about biological races, but they hold that the category RACE is a social and not biological construct. I addressed this issue in my article on white privilege:
If race doesn’t exist, then why does white privilege matter?
Lastly, those who argue against the concept of white privilege may say that those who are against the concept of white privilege would then at the same time say that race—and therefore whites—do not exist so, in effect, what are they talking about if ‘whites’ don’t exist because race does not exist? This is of course a ridiculous statement. One can indeed reject claims from biological racial realists and believe that race exists and is a socially constructed reality. Thus, one can reject the claim that there is a ‘biological’ European race, and they can accept the claim that there is an ever-changing ‘white’ race, in which groups get added or subtracted based on current social thought (e.g., the Irish, Italians, Jews), changing with how society views certain groups.
Though, it is perfectly possible for race to exist socially and not biologically. So the social creation of races affords the arbitrarily-created racial groups to be in certain areas on the hierarchy of races. Roberts (2011: 15) states that “Race is not a biological category that is politically charged. It is a political category that has been disguised as a biological one.” She argues that we are not biologically separated into races, we are politically separated into them, signifying race as a political construct. Most people believe that the claim “Race is a social construct” means that “Race does not exist.” However, that would be ridiculous. The social constructivist just believes that society divides people into races based on how we look (i.e., how we are born) and then society divides us into races on the basis of how we look. So society takes the phenotype and creates races out of differences which then correlate with certain continents.
So, there is no contradiction in the claim that “Race does not exist” and the claim that “Whites have certain unearned privileges over other groups.” Being an antirealist about biological race does not mean that one is an antirealist about socialraces. Thus, one can believe that whites have certain privileges over other groups, all the while being antirealists about biological races (saying that “Races don’t exist biologically”).
Going off Kaplan and Winther’s distinction, there are 3 kinds of racial realism: bio-genomic/cluster realism, biological racial realism, and social constructivism about race (socialraces). These three different racial frameworks have one thing in common: they accept the reality of race, but they merely disagree as to the origins of racial groups. Using these distinctions set forth by Kaplan and Winther, we can see how best to view different racial concepts and how to apply them in real life. Kaplan and Winther (2014: 1042) “are conventionalists about bio-genomic cluster/race, antirealists about biological race, and realists about social race.” And they can state this due to the distinction they’ve made between different kinds of racial realism. (Since I personally am a pluralist about race, all of these could hold under certain contexts, but I do hold that race is a social construct of a biological reality, pushing Spencer’s argument.)
Biological race isn’t socialrace
These 2 race concepts are distinct, where one talks about how race is viewed in the social realm while the other talks about how race is viewed in the biological realm. There is of course the view that race is a social construct of a biological reality (a view which I hold myself).
Biological race refers to the categorization of humans based on genetic traits and ancestry (using this definition, captures the bio-genomic/cluster realism as well). So if biological and socialrace were equivalent concepts, then it would mean that genetic differences that define different racial groups would map onto similar social consequences. So if two people from different racial groups are biologically different, then their social experiences and opportunities in society should also differ. Obviously, the claim here is that if two concepts are identical, then they should produce the same outcomes. But socialrace isn’t merely a reflection of biological race (as race realists like Murray, Jensen, Lynn, an Rushton hold to). Socialrace has been influenced by cultural, social, and political factors and so quite obviously it is socially constructed (constructed by society, the majority believe that race is real, so that makes it real).
There are of course social inequalities related to different racial groups. People of different socialraces find themselves treated differently while experiencing different things, and this then results in disparities in opportunity, privileges and disadvantages. These disparities can be noted in healthcare, criminal justice, education, employment and housing—anywhere individuals from a group can face systemic barriers and discrimination. People from certain racial groups may experience lower access to quality education, reduced job opportunities, increased chance of coming into contact with the law, how they are given healthcare, etc. Sin s these disparities persist even after controlling for SES, this shows how race is salient in everyday life.
The existence of social disparities and inequalities between racial groups shows that socialrace cannot be determined by biological factors. It is instead influenced by social constructs, historical context, and power dynamics in a society. So differences in societal consequences indicate the distinction between the two concepts. Socialrace isn’t a mere extension of biological race. Biological differences can and do exist between groups. But it is the social construction and attribution of meaning to these differences that have shaped the lived experiences and outcomes of individuals in society. So by recognizing that race isn’t solely determined by biology, and by recognizing that socialrace isn’t biological race and biological race isn’t social race (i.e., they are different concepts), we can have a better, more nuanced take on how we socially construct differences between groups. (Like that of “Hispanics/Latinos.) Having said all that, here’s the argument:
(P1) If biological and socialrace are the same, then they would have identical consequences in society regarding opportunities, privileges, and disadvantages
(P2) But there are disparities in opportunities, privileges, and disadvantages based on socialrace in various societies.
(C) So biological race and socialrace aren’t the same.
The claim that X is a social construct doesn’t mean that X is imaginary, fake, or unreal. Social constructs have real, tangible impacts on society and individuals’ lives which influences how they are perceived and treated. Further, historical injustices and systemic racism are more evidence that race is a social construct.
Going back to the distinction between three types of racial realism from Kaplan and Winther, what they phrase biological racial realism (Kaplan and Winther, 2014: 1040-1041):
Biological racial realism affirms that a stable mapping exists between the social groups identified as races and groups characterized genomically or, at least, phenomically.2 That the groups are biological populations explains why the particular social groups, and not others, are so identified. Furthermore, for some, but by no means all, biological racial realists, the existence of biological populations (and of the biologically grounded properties of their constituent individuals) explains and justifies at least some social inequalities (e.g., the “hereditarians”; Jensen 1969; Herrnstein and Murray 1995; Rushton 1995; Lynn and Vanhanen 2002). [This is like Hardimon’s racialist race/socialrace distinction.]
Quite obviously, distinguishing between the kinds of racial realism here points out that biological racial realists are of the hereditarian camp, and so race is an explanation for certain social inequalities (IQ, job market outcomes, crime). Social constructivists, however, have argued that what explains these differences is the social, historical, and political factors (see eg The Color of Mind).
(P1) If race is a social construct, then racial categories are not fixed and universally agreed-upon.
(P2) If racial categories are not fixed and universally agreed-upon, then different societies can define race differently.
(C1) So if race is a social construct, then different societies can define race differently.
(P3) If different societies can define race differently, then race lacks an inherent and biological basis.
(P4) Different societies do define race differently (observation of diverse racial classifications worldwide).
(C2) Thus, race lacks and inherent and biological basis.
(P5) If race lacks and inherent and biological basis, then race is a social construct.
(P6) Race lacks an inherent and biological basis.
(C3) Therefore, race is a social construct.
Premise 1: The concept of race varies across place and time. For example, we once had the one drop rule, which stated that any amount of “black blood” makes one black irregardless of their appearance or background. But Brazil has a more fluid approach to racial classification, like pardo and mullato. So this shows that racial categories aren’t fixed and universally agreed-upon, since race concepts in the US and Brazil are different. It also shows that race categories can change on the basis of social and cultural context and, in the context of Brazil, the number of slaves that were transported there.
Premise 2: Racial categories were strictly enforced in apartheid South Africa and people were placed into groups based on arbitrary criteria. Though this classification system differs from the caste system in India, where caste distinctions are based on a social hierarchy, not racial characteristics, which shows how different societies have different concepts of identity and social distinctions (how and in what way to structure their societies). So Conclusion 1 then follows: The variability in racial categorization across societies shows that the concept of race is not fixed, but is shaped by societal norms and beliefs.
Premise 3: Jim Crow laws and the one drop rule show how racial categorization can shift depending on the times and what is currently going on in the society in question. The example of Jim Crow laws show that historical context and social norms dictated racial classification and the boundary between races. Again, going back to the example of Brazil is informative to explain the point. The Brazilian racial system encompasses a larger range of racial groups which were influenced by slavery and colonization and the interactions between European, African, and indigenous peoples. So this shows how racial identity can and has been shaped by historical happenstance along with the intermixing or racial and ethnic groups.
Premise 4: As I already explained, Brazil and South Africa recognize a broader range of racial categories due to their historical circumstances and diverse social histories and dynamics. So Conclusion 2 follows, since these examples show that race doesn’t have a fixed, inherent and objective biological basis; it shows that race is shaped by social, historical, and cultural contexts.
Premise 5: So due to the variability in racial categorization historically and today, and the changing of racial boundaries in the past. For instance, Irish and Italian Americans were seen as different races in the 1900s, but over time as they assimilated into American society, racial categories began to blur and they then became part of the white race. Racial categories in Brazil are based on how the person is perceived, which leads to multiple different racial groups. Apartheid South Africa has 4 classifications: White, Black, Colored (mixed race) and Indian. These examples highlight the fact that based on changing social conventions and thought, how race can and does change with the times based on what is currently going on in the society in question. This highlights the fluid nature of racial categories. The argument up until this point has provided evidence for Premise 6, so Conclusion 3 follows: race is a social construct. Varying racial categories in different societies across time and place, the absence of an objective biological basis to race, along with the influence of historical, cultural, and social factors all point to the conclusion that race is a social construct.
Conclusion
Quite obviously, there is a distinction between biological and social race. The distinction is important, if we want to reject a concept of biological race while still stating that race is real. But hereditarians like Bo, it seems, don’t understand the distinction at hand. Bo, at least, isn’t alone in being confused about race concepts and their entailments. Murray (2020) stated:
Advocates of “race is a social construct” have raised a host of methodological and philosophical issues with the cluster analyses. None of the critical articles has published a cluster analysis that does not show the kind of results I’ve shown.
But social constructivists need to do no such thing. Why would they need to produce a cluster analysis that shows opposite results to what Murray claims? This shows that Murray doesn’t understand what social constructivists believe. Of course, equating race and biology is the MO of hereditarians, since they argue that some social inequalities between races are due to genetic differences between races.
Social constructivists talking about something real—a dynamic and evolving concept which has profound consequences for society. Rejecting the concept of biological races doesn’t entail that the social constructvist doesn’t believe that human groups don’t differ genetically. It does entail that the genetic diversity found in humans groups doesn’t necessitate the establishment of rigid and fixed racial categories. So in rejecting biological racial realism, social constructivists embrace the view that racial classifications are fixated by social, cultural, and historical contingencies. The examples I’ve given in this article show how racial categorization has changed based on time and place, and this is because race is a social construct.
I should note that I am a pluralist about race, which is “the view that there’s a plurality of natures and realities for race in the relevant linguistic context” (Spencer, 2019: 27), so “there is no such thing as a global meaning of ‘race’ (2019 : 43). The fact that there is no such thing as a global meaning of race entails that different societies across time and place will define racial groups differently, which we have seen, and so race is therefore a social construct (and I claim it is a social construct of a biological reality). Hereditarians like Bo don’t have this nuance, due to their apparent insistence that social constructivists are a kind of anti-realist about race as a whole. This claim, as I’ve exhaustively shown, is false. Different concepts of race can exist with each other based on context, leading to complex and multifaceted understandings of race and it’s place in society.
The second argument I formalized quite obviously gets at the distinction between biological and social racial realism shows the distinction between the two—I have defended the premises and have given examples on societies in different time and place that had different views of the racial groups in this country. This, then, shows that race is a social construct and that social constructivists about race are realists about race—since they are talking about something that has a referent.
NotPoliticallyCorrect 