Hereditarianism is the theory that differences in psychology between individuals and groups have a ‘genetic’ or ‘innate’ (to capture the thought before the ‘gene’ was conceptualized) cause to them—which therefore would explain the hows and whys of, for example, the current social hierarchy. The term ‘racism’ has many referents—and using one of the many definitions of ‘racism’, one could say that the hereditarian theory is racist since it attempts to justify and naturalize the current social hierarchy.
In what I hope is my last word on the IQ/hereditarian debate, I will provide three conceptual arguments against hereditarianism: (1) psychologists don’t ‘measure’ any’thing’ with their psychological tests since there is no object of measurement, no specified measured object, and measurement unit for any specific trait; only physical things can be measured and psychological ‘traits’ are not physical so they cannot be measured (Berka, 1983; Nash, 1990; Garrison, 2009); (2) there is no theory or definition of “intelligence” (Lanz, 2000; Richardson, 2002; Richardson and Norgate, 2015; Richardson, 2017) so there can be no ‘measure’ of it, the example of temperature and thermometers will be briefly mentioned; (3) the logical impossibility of psychophysical reduction entails that mental abilities/psychological traits cannot be genetically inherited/transmitted; and (4) psychological theories are influenced by the current problems/going-on in society as well as society influencing psychological theories. These four objections are lethal to hereditarianism, the final showing that psychology is not an ‘objective science.’
(i) The Berka/Nash measurement objection
The Berka/Nash measurement objection is simply: if there is no specified measured object, object of measurement or measuring unit for the ‘trait’, then no ‘thing’ is truly being ‘measured’ as only physical things can be measured. Nash gives the example of a stick—the stick is the measured object, the length of the stick is the object of measurement (the property being measured) and inches, centimeters etc are the measuring units. Being that the stick is in physical space, its property can be measured—its length. Since psychological traits are not physical (this will also come into play for (ii) as well) nor do they have a physical basis, there can be no ‘measuring’ of psychological traits. Indeed, since scaling is accepted by fiat to be a ‘measure’ of something. This, though, leads to confusion, especially to psychologists.
The most obvious problem with the theory of IQ measurement is that although a scale of items held to test ‘intelligence’ can be constructed, there are no fixed points of reference. If the ice point of water at one atmosphere fixes 276.16 K, what fixes 140 points of IQ? Fellows of the Royal Society? Ordinal scales are perfectly adequate for certain measurements. Moh’s scale of scratch hardness consists of ten fixed points from talc to diamond, and is good enough for certain practical purposes. IQ scales (like attainment test scales) are ordinal scales, but this is not really to the point, for whatever the nature of the scale it could not provide evidence for the property IQ or, therefore, that IQ has been measured. (Nash, 1990: 131)
In first constructing its scales and only then preceding to induce what they ‘measure’ from correlational studies, psychometry has got into the habit of trying to do what cannot be done and doing it the wrong way round anyway. (Nash, 1990: 133)
The fact of the matter is, IQ tests don’t even meet the minimal theory of measurement since there is no—non-circular—definition of what this ‘general cognitive ability’ even is.
(ii) No theory or definition of intelligence
This also goes back to Nash’s critique of IQ (since there can be no non-circular definition of what “IQ tests” purport to measure): There is no theory or definition of intelligence therefore there CAN BE no ‘measure’ of it. Imagine saying that you have measured temperature without a theory behind it. Indeed, I have explained in another article that although IQ-ists like Jensen and Eysenck emphatically state that the ‘measuring’ of ‘intelligence’ with “IQ tests” is “just like” the measuring of temperature with thermometers, this claim fails as there is no physical basis to psychological traits/mental abilities so they, therefore, cannot be measured. If “intelligence” is not like height or weight, then “intelligence”‘ cannot be measured. “Intelligence” is not like height or weight. Therefore, “intelligence” cannot be measured.
We had a theory and definition of temperature and then the measuring tool was constructed to measure our new construct. The construct of temperature was then verified independently of the instrument used to originally measure it, with the thermoscope which then was verified with human sensation. Thus, temperature was verified in a non-circular way. On the other hand, “intelligence tests” are “validated” circularly, if the tests correlate highly with other older tests (like Terman’s Stanford-Binet), it is held that the new test ‘measures’ the construct of ‘intelligence’—even if none of the previous tests have themselves been validated!
Therefore, this too is a problem for IQ-ists—their scale was first constructed (to agree with the social hierarchy, no less; Mensh and Mensh, 1991) and then they set about trying to see what their scales ‘measure’ with correlational studies. But we know that since two things are correlated that doesn’t mean that one causes the other—there could be some unknown third variable causing the relationship or the relationship could be spurious. In any case, this conceptual problem, too, is a problem for the IQ-ist. IQ is nothing like temperature since temperature is an actual physical measure that was verified independently of the instrument constructed to measure the construct in the first place.
Claims of individuals as ‘intelligent’ (whatever that means) or not are descriptive, not explanatory—it is the reflection of one’s current “ability” (used loosely) in relation to their current age norms (Anastasi; Howe, 1997).
(iii) The logical impossibility of psychophysical reduction
I will start this section off with two (a priori) arguments:
Anything that cannot be described in material terms using words that only refer to material properties is immaterial.
The mind cannot be described in material terms using words that only refer to material properties.
Therefore the mind is immaterial; materialism is false.
If physicalism is true then all facts can be stated using a physical vocabulary.
But facts about the mind cannot be stated using a physical vocabulary.
So physicalism is false.
(Note that the arguments provided are valid, and I hold them to be sound thus an objector would need to reject then refute a premise.)
Therefore, if all facts cannot be stated using a physical vocabulary and if the mind cannot be described in material terms using words that only refer to material properties, then there can, logically, be no such thing as ‘mental measurement’—no matter what IQ-ists try to tell you.
Different physical systems can give rise to different mental phenomena—what is known as the argument from multiple realizability. Thus, since psychological traits/mental states are multiply realizable, then it is impossible for psychology to reduce to mental kinds to reduce to physical kinds—the mental kind can be realized by multiple physical states. Psychological states are either multiply realizable or they are type identical to the physio-chemical states of the brain. That is a kind of mind-brain identity thesis—that the mind is identical to the states of the brain. Although they are correlated, this does not mean that the mind is the brain or that the mind can be reduced to physio-chemical states, as Putnam’s argument from multiple realizability concludes. If type-physicalism is true, then it must be true that every and all mental properties can be realized in the same exact way. But, empirically, it is highly plausible that mental properties can be realized in multiple ways. Therefore, type-identity theory is false.
Psychophysical laws are laws connnecting mental abilities/psychological traits with physical states. But, as Davidson famously argued in his defense of Anomalous Monism, there can be no such laws linking mental and physical events. There are no mental laws therefore there can be no scientific theory of mental states. Science studies the physical. The mental is not physical. Thus, science cannot study the mental. Indeed, since there are no bridge laws that link the mental and physical and the mental is irreducible to and underdetermined by the physical, it then follows that science cannot study the mental. Therefore, a science of the mind is impossible.
Further note that the claim “IQ is heritable” reduces to “thinking is heritable”, since the main aspect of test-taking is thinking. Thinking is a mental activity which results in a thought. If thinking is a mental activity which results in a thought, then what is a thought? A thought is a mental state of considering a particular idea or answer to a question or committing oneself to an idea or an answer. These mental states are, or are related to, beliefs. When one considers a particular answer to a question, they are paving the way to holding a certain belief. So when they have committed themselves to an answer, they have committed themselves to a new belief. Since beliefs are propositional attitudes, believing p means adopting the belief attitude that p. So, since cognition is thinking, then thinking is a mental process that results in the formation of a propositional belief. Thus, since thinking is related to beliefs and desires (without beliefs and desires we would not be able to think), then thinking (cognition) is irreducible to physical/functional states, meaning that the main aspect of test-taking (thinking) is irreducible to the physical thus physical states don’t explain thinking which means the main aspect of (IQ) test-taking is irreducible to the physical.
(iv) Reflexivity in psychology
In this last section, I will discuss the reflexivity—circularity—problem for psychology. This is important for psychological theorizing since, to its practitioners, psychology is seen to be an ‘objective science.’ If you think about psychology (and science) and how it is practiced, it (they) investigates third-personal, not first-personal, states. Thus, there can be no science of the mind (what psychology purports to be) and psychology can, therefore, not be an ‘objective science’ as the hard sciences are. The ‘knowledge’ that we attain from psychology comes from, obviously, the study of people. As Wade (2010: 5) notes, the knowledge that people and society are the object of study “creates a reflexivity, or circular process of cause and effect, whereby the ‘objects’ of study can and do change their behavior and ideas according to the conclusions that their observers draw about their behavior and ideas.”
It is quite clear that such academic concepts do not arise independently—in the history of psychology, it has been used in an attempt to justify the current social hierarchy of the time (as seen in 1900s America, Germany, and Britain). Psychological theories are influenced by current social goings-on. Thus, it is influenced by the bias of the psychologists in question. “The views, attitudes, and values of psychologists influence the claims they make” (Jones, Elcock, and Tyson, 2011: 29).
… scientific ideas did not develop in a vacuum but rather reflected underlying political or economic trends. 15
The current social context influences the psychological discourse and the psychological discourse influences the current social context. The a priori beliefs that one holds will influence what they choose to study. An obvious example being, hereditarian psychologists who believe there are innate differences in ‘IQ’ (they use ‘IQ’ and ‘intelligence’ interchangeably as if there is an identity relation) will undertake certain studies in order to ‘prove’ that the relationship they believe to be true holds and that there is indeed a biological cause to mental abilities within and between groups and individuals. Do note, however, that we have the data (blacks score lower on IQ tests) and one must then make an interpretation. So we have three possible scenarios: (1) differences in biology cause differences in IQ; (2) differences in experience cause differences in IQ; or (3) the tests are constructed to get the results the IQ-ists want in order to justify the current social hierarchy. Mensh and Mensh (1991) have succinctly argued for (3) while hereditarians argue for (1) and environmentalists argue for (2). While it is indeed true that one’s life experiences can influence their IQ scores, we have seen that it is logically impossible for genes to influence/cause mental abilities/psychological traits.
The only tenable answer is (3). Such relationships, as noted by Mensh and Mensh (1991), Gould (1996), and Garrison (2009), between test scores and the social hierarchy are interpreted by the hereditarian psychologist thusly: (1) our tests measure an innate mental ability; (2) if our tests measure an innate mental ability, then differences in the social hierarchy are due to biology, not environment; (3) thus, environmental differences cannot account for what is innate between individuals so our tests measure innate biological potential for intelligence.
The [IQ] tests do what their construction dictates; they correlate a group’s mental worth with its place in the social hierarchy. (Mensh and Mensh, 1991)
Richards (1997) in his book on racism in the history of psychology, identified 331 psychology articles published between 1909 (the first conceptualization of the ‘gene’, no less) and 1940 which argued for biology as a difference-maker for psychological traits while noting that 176 articles for the ‘environment’ side were published in that same time period.
Note that the racist views of the psychologists in question more than likely influenced their research interests—they set out to ‘prove’ their a priori biases. Indeed, they even modeled their tests after such biases. Tests that were constructed that agreed with their a priori pre-suppositions on who was or was not intelligence was kept whereas those that did not agree with those notions were thrown out (as noted by Hilliard, 2012). This is just as Jones, Elcock, and Tyson (2011: 67) note with the ‘positive manifold’ (‘general intelligence’):
Subtests within a battery of intelligence tests are included n the basis of them showing a substantial correlation with the test as a whole, and tests which do not show such correlations are excluded.
From this, it directly follows that psychometry (and psychology) are not sciences and do not ‘measure’ anything (returning to (i) above). What psychometrics (and psychology) do is attempt to use their biased tests in order to sort individuals into where they ‘belong’ on the social hierarchy. Standardized testing (IQ tests were one of the first standardized tests, along with the SAT)—and by proxy psychometrics—is NOT a form of measurement. The hierarchy that the tests ‘find’ is presupposed to exist and then constructed into existence using the test to ‘prove’ their biases ‘right.’
Indeed, Hilliard (2012) noted that in South Africa in the 1950s that there was a 15-point difference in IQ between two white cultural groups. Rather than fan flames of political tension between the groups, the test was changed in order to eliminate the difference between the two groups. The same, she notes, was the case regarding IQ differences between men and women—Terman eliminated such differences by picking and choosing certain items that favored one group and balanced them out so that they scored near-equally. These are two great examples from the 20th century that demonstrate the reflexivity in psychology—how one’s a priori biases influence what they study and the types of conclusions they draw from data.
Psychology, at least when it comes to racial differences in ‘IQ’, is being used to confirm pre-existing prejudices and not find any ‘new objective facts.’ “… psychology [puts] a scientific gloss on the accepted social wisdom of the day” (Christian, 2008: 5). This can be seen with a reading into the history of “IQ tests” themselves. The point is, that psychology and society influence each other in a reflexive—circular—manner. Thus, psychology is not and cannot be an ‘objective science’ and when it comes to ‘IQ’ the biases that led to the bringing of the tests to America and concurrently social policy are still—albeit implicitly—believed today.
Psychology originally developed in the US in the 19th century in order to attempt to fix societal problems—there needed to be a science of the mind and psychology purported to be just that. They, thusly, needed a science of ‘human nature’, and it was for this reason that psychology developed in the US. The first US psychologists were trained in Germany and then returned to the US and developed an American psychology. Though, do note that in Germany psychology was seen as the science of the mind while in America it would then turn out to be the science of behavior (Jones, Elcock, and Tyson, 2011). This also does speak to the eugenic views held by certain IQ-ists in the 20th and into the 21st century.
In Nazi Germany, Jewish psychologists were purged since their views did not line-up with the Nazi regime.
Psychology appealed to the Nazi Party for two reasons: because psychological theory could be used to support Nazi ideology, and because psychology could be applied in service to the state apparatus. Those psychologists who remained adapted their theories to suit Nazi ideology, and developed theories that demonstrated the necessary inferiority of non-Aryan groups (Jones and Elcock, 2001). These helped to justify actions by the state in discriminating against, and ultimately attempting to eradicate, thse other groups. (Jones, Elcock, and Tyson (2011: 38-39)
These examples show that psychology is influenced by society but also that society influences psychological theorizing. Clearly, what psychologists choose to study, since society influences psychology, is a reflection of a society’s social concerns. In the case of IQ, crime, etc, the psychologist attempts to naturalize and biologicize such differences in order to explain them as ‘innate’ or ‘genetic’. The rise of IQ tests in America, too, also coincided with the worry that ‘national intelligence’ was declining and so, the IQ test would need to be used to ‘screen’ prospective immigrants. (See Richardson, 2011 for an in-depth consideration on the tests and conditions that the testees were exposed to on Ellis Island; also see Gould, 1996.)
(i) The Berka/Nash measurement objection is one of the most lethal arguments for IQ-ists. If they cannot state the specified measured object, the object of measurement, and the measuring unit for IQ then they cannot say that any’thing’ is being ‘measured’ by ‘IQ tests.’ This then brings us to (ii). Since there is no theory or definition of what is being ‘measured’, and if the tests were constructed first before the theory, then there will necessarily be a built-in bias to what is being ‘measured’ (namely, so-called ‘innnate mental potential’). (iii) Since it is logically impossible for psychology to reduce to physical structure, and since all facts cannot be stated using a physical vocabulary nor can the mind be described using material terms that only refer to material properties, then this is another blow to the claim that psychology is an ‘objective science’ and that some’thing’ is being ‘measured’ by their tests (constructed to agree with their a priori biases). And (iv) The bias that is inherent in psychology (for both the right and the left) influences the practitioners’ theorizing and how they interpret data. Society has influenced psychology (and psychology has influenced the society) and we only need to look at America and Nazi Germany in the 20th century to see that this holds.
The relationship between psychology and society is inseparable—it is a truism that what psychologists choose to study and how and why they formulate their conclusions will be influenced by the biases they already hold about society and how and why it is the way it is. For these reasons, psychology/psychometry are not ‘sciences’ and hereditarianism is not a logically sound position. Hereditarianism, then, stays what it was when it was formulated—a racist theory that attempts to bilogicize and justify the current social hierarchy. Thus, one should not accept that psychologists ‘measure’ any’thing’ with their tests; one should not accept the claim that mental abilities can be genetically transmitted/inherited; one should not accept the claim that psychology is an objective ‘science’ due to the reflexive relationship between psychology and society.
The arguments given show why hereditarianism should be abandoned—it is not a scientific theory, it just attempts to naturalize biological inequalities between individuals and groups (Mensh and Mensh, 1991; Gould, 1996; Garrison, 2009). Psychometrics (what hereditarians use to attempt to justify their claims) is, then, nothing more than a political ring.
The term ‘racism’ has many definitions. What does it mean for a person to be a ‘racist’? What does it mean for a person to have ‘racist beliefs’? What does the term ‘racism’ refer to? The answers to these questions then will inform the next part—what does racism have to do with stress and physiology?
What is ‘racism’?
Racism has many definitions, so many—and so many for uses in different contexts—that it has been argued, for example by those in the far-right, that it is, therefore, a meaningless term. However, just because there are many definitions of the term, it does not then mean that there is no referent for the term we use. A referent is a thing that is signified. In this instance, what is the referent for racism? I will provide a few on-hand definitions and then discuss them.
In Part VI of The Oxford Handbook of Race and Philosophy (edited by Naomi Zack, 2016) titled Racisms and Neo-Racisms, Zack writes (pg 469; my emphasis):
Logically, it would seem as though ideas about race would have to precede racism. But the subject of racism is more broad and complicated than the subject of race, for at least these two historical reasons. First, the kind of prejudice (prejudged cognitions and negative emotions) and discrimination (treating people differently on the grounds of group identities) that constitute racism have a longer history than the modern idea of race, for instance in European anti-Semitism. And second, insofar as modern ideas of race have been in the service of the dominant interests in international and internal interactions, these ideas of race are ideologies that have devalued non-white groups. That is, ideas of race are themselves already inherently racist.
In philosophy, racism has been treated as attitudes and actions of individuals that affect nonwhites unjustly and social structures and institutions that advantage whites and disadvantage nonwhites. The first is hearts-and-minds or classic racism, for instance the use of stereotypes and harmful actions by whites against people of color, as well as negative feelings about them. The second is structural racism, for instance the use of stereotypes or institutional racism, for instance, the facts of how American blacks and Hispanics are, compared to whites, worse off on major measures of human well-being, such as education, income, family wealth, health, family stability, longevity, and rates of incarceration.
John Lovchik in his book Racism: Reality Built on a Myth (2018: 12) notes that “racism is a system of ranking human beings for the purpose of gaining and justifying an unequal distribution of political and economic power.” Note that using this definition, “hereditarianism” (the theory that individual differences between groups and individuals can be reduced to genes; I will give conceptual reasons why hereditarianism is false as what I hope is my final word on the debate) is a racist theory as it attempts to justify the current social hierarchy. (The reason why IQ tests were first brought to America and created by Binet and Simon; see The History and Construction of IQ Tests and The Frivolousness of the Hereditarian-Environmentalist IQ Debate: Gould, Binet, and the Utility of IQ Testing.) This is why hereditarianism saw its resurgence with Jensen’s infamous 1969 paper. Indeed, many prominent hereditarians have held racist beliefs, and were even eugenicists espousing eugenic ideas.
Headley (2000) notes a few definitions of racism—motivational, behavioral, and cognitive racism. Motivational racism is “the infliction of unequal consideration, motivated by the desire to dominate, based on race alone“; behavioral racism is “failure to give equal consideration, based on the fact of race alone”; and cognitive racism is “unequal consideration, out of a belief in the inferiority of another race.”
I have presented six definitions of racism—though there are many more. Now, for the purposes of this article, I will present my own: the ‘inferiorization’ of a racialized group which is then used to explain disparities in things like IQ test scores, social class/SES, education differences, personality, etc. Now, knowing what we know about physiological systems and how they react to the environment around them—the immediate environment and the social environment—how does this then relate to stress and physiology?
Racism, stress, and physiology
Now that we know what racism is, having had a rundown of certain definitions of ‘racism’, I will now discuss the physiological effects such stances could have on groups racialized as ‘races’ (note that I am using socialraces in this article; recall that social constructivists about race need to be realists about race).
The term ‘weathering’ refers to the body’s breaking down due to stress over time. Such stressors can come from one’s immediate environment (i.e., pollution, foodstuffs, etc) or their social environment (a demanding job, how one perceives themselves and how people react to them). So as the body experiences more and more stress it becomes more and more ‘weathered’ which then leads to heightened risk for disease in stressed individuals/populations.
Allostatic states “refer to altered and sustained activity levels of the primary mediators (e.g., glucocorticosteroids) that integrate energetic and associated behaviours in response to changing environments and challenges such as social interactions, weather, disease, predators and pollution” (McEwen, 2005). Examples of allostatic overload such as acceleration of atherosclerosis, hypertension (HTN), stroke, and abdominal obesity (McEwen, 2005) are more likely to be found in the group we racialize as ‘black’ in America—particularly women (Gillum, 1987; Gillum and Hyattsville, 1996; Barnes, Alexander, and Staggers, 1997; Worral et al, 2002; Kataoka et al, 2013).
Geronimus et al (2006) set to find out whether or not the heightened rate of stressors (e.g., racism, environmental pollution, etc) can explain why black bodies are more ‘weathered’ than white bodies. They found that such differences were not explained by poverty, indicating that it even affects well-off blacks. Allostatic load refers to heightened hormonal production in response to stressors. We know that physiological is homeodynamic and therefore changes based on the immediate environment and social environment (for example, when you feel like you’re about to get into a fight, your heart rate increases and you get ready to ‘fight or flight’).
Experiencing racism (environmental stimuli; real or imagined, the outcome is the same) is associated with increased blood pressure (HTN). So if one experiences racism they will them experience an increase in blood pressure, as BP is a physiological variable (Armstead et al, 1987; McNeilly et al, 1995; see Doleszar et al, 2018 for a review). The concept of weathering, then, shows that racial health disparities are, in fact, racist health disparities (Sullivan, 2015: 106). Racism, then, contributes to higher levels of allostasis and, along with it, higher levels of certain hormones associated with higher allostasis.
One way to measure biological age is by measuring the length of telomeres. Telomeres are found at the ends of chromosomes. Since telomere lengths shorten with age (Shammas, 2012), those with shorter telomeres are ‘biologically older’ than those of the same age with longer telomeres. Geronimus et al (2011) showed that black women had shorter telomeres than white women, which was due to subjective and objective stressors (i.e., racism). Black women in the age group 49-55 were 7.5 years ‘older’ than white women. Thus, they had an older physiological age compared to their chronological age. It is known that direct contact with discriminatory events is associated with poor health outcomes. Harrell, Hall, and Taliaferro (2003) note that:
“…physiological set points and the mechanisms governing them are not fixed. External stressors can permanently alter physiological functioning. Racism increases the volume of stress one experiences and may contribute directly to the physiological arousal that is a marker of stress-related diseases.
Social factors can, indeed, influence physiology and there is a wealth of information on how the social becomes biological and how environmental (social) factors influence physiological systems. Forrester et al (2019) replicated Geronimus’ findings, showing that blacks have a higher ‘biological age’ than whites and that psychosocial factors affect blacks more than whites. Simons et al (2020) also replicated Geronimus’ findings, showing that persistent exposure to racism was associated with higher rates of inflammation in blacks which then predicted higher rates of disease in blacks compared to whites. Such discrimination can help to explain differences in birth outcomes (e.g., Jasienska, 2009), stress, inflammation, obesity, stroke rates, etc in blacks compared to whites (Molnar, 2015).
But what is the mechanism by which higher allostatic load scores contribute to negative outcomes and shorter telomeres indicating a higher biological age? When one feels that they are being discriminated against, the sympathetic nervous system activates due to chronic stress and along with it HPA dysfunction. What this means is that there is a loss of the anti-inflammatory effects of cortisol—it becomes blunted. This then increases oxidative stress and inflammation. Thus, the inflammatory processes result in cardiovascular disease and immune and metabolic dysfunction. The HPA axis monitors and responds to stress—allostatic load. When stress hormones are released, the adrenal gland is targeted. When it receives a signal from the pituitary gland, it pumps epinephrine and norepinephrine into the body, causing our hearts to beat faster, causing us to breathe more deeply—what is known as ‘fight or flight.’ Cortisol is also released and is known as a stress hormone, but when the stressful event is over, all three hormones return to baseline. Thus, the higher amount of stress hormones in circulation indicates higher levels of allostatic load—higher levels of stress in the individual in question. We know that blacks have higher levels of allostatic load (i.e., stress-related hormones) than whites (Duru et al, 2012). Barr (2014: 71-72) writes:
Imagine, though, that before the allostatic load has a chance to return to its baseline level, another stressor is sensed by the hypothalamus. The allostatic load will once again increase to the plateau level. Should the perception of stressors be ongoing, the allostatic load will not have the chance to ever fully recharge, and the adrenal gland will be producing an ongoing stream of stress response hormones. The body will experience chronic elevation in its allostatic load. […] A person experiencing repeated stressors, without the opportunity for intervals that are relatively stress-free, will experience a chronically elevated allostatic load, with higher than normal levels of circulating stress response hormones.
What these studies show, then, is that race is a cause of health inequalities, but it’s not inherent in biology but due to social factors that influence the physiology of the individual in question. The term ‘racism’ has many referents, and using one of them identifies ‘hereditarianism’ as a racist ideology (it is inherently ideological). These overviews of studies show that racial health inequalities are due, in part, to perceived discrimination (racism) thus they are racist health disparities. We know that physiology is a dynamic system that can respond to what occurs in the immediate environment—even the social environment (Williams, 1992). Thus, what explains part of the health inequalities between races is perceived discrimination—racism—and how it affects the body’s physiological systems (HPA axis, HTN, etc) and telomeres.
The Bajau spleen size and better-living-through-evolution story is also a reminder that since the dawn of the theory of evolution, humans have been incredibly creative in coming up with evolutionary and hence genetic narratives and explanations for just about every human trait that can be measured. This effort recycles from time to time and is again reaching a peak in an era when it is possible to quickly and cheaply “genotype” human populations. (Joyner, Boros, and Fink, 2018: 524-525)
Yesterday on Twitter Matt Yglesias—Vox blogger—tweeted out a 2018 paper in which the authors argue that ‘natural selection’ explained the bigger spleens of the Bajau and, consequently, how they could hold their breaths for such a long time (Ilardo et al, 2018). The main claim of the paper is that ‘natural selection’ ‘selected-for’ larger spleens which then increases how much oxygen can be stored. The point of the study was to find out if their exceptional diving abilities had a ‘genetic basis.’ Thankfully, though, a group of physiologists looked into the claims of Ilardo et al (2018) and found their main claims wanting (Joyner, Boros, and Fink, 2018). That’s how easy it is for selectionists: Notice a trait; then work backward and attempt to formulate the best story you can (see Smith, 2016).
These diving capabilities are similar to high-altitude hypoxia—indeed the authors assume that there was an adaptation for breath-hold diving. They compared some Bajau people (n=59) and close neighbors who did not—the Saluan (n=34)—really interact with the water environment. So, using a portable ultrasound machine, they photographed the spleens of the two groups and noted a “clear visual difference” between Bajau spleens and Saluan spleens. The Bajau had spleens about 40-50 cc bigger than the Saluan.
These results suggest a physiological difference between the Bajau and the Saluan that is not solely attributable to a plastic response of the spleen to diving activity. While other unknown environmental factors could potentially explain the observed difference between the groups, genetic factors remain a possibility.
So big spleens mean big breath-diving ability. And big spleens were an object of selection. So breath-diving was therefore selected for—so the just-so story goes. But, “a slightly larger spleen is almost certainly not the most important [part of diving] from a physiological perspective” (Joyner, Boros, and Fink, 2018: 524). They then found ‘genes for’ big spleens and they then formulated their just-so story. Accompanying evidence was the fact that deep-diving animals have bigger spleens, so since the Bajau have bigger spleens, this then would mean that the bigger spleens then allows for better breath-diving. Joyner, Boros, and Fink (2018: 525) write:
The general idea is that, like blood doping in cyclists, bigger spleens that contract would give the Bajau divers a boost of oxygen-carrying red cells that would make them more successful at underwater-based hunting and gathering. Thus, spleen size was selected for via evolution over the last 1,000 years or so. A few simple back-of-the-envelope calculations about oxygen stores are instructive. A 40 cc bigger spleen that was all red cells and contracted completely with diving might give the Bajau 20 milliliters of extra oxygen. That is about 1% or less of the oxygen stored in the body and lungs of healthy humans.
Joyner and colleagues then go on to note other ethnies who perform similar breath-dives, while also noting that the Bajau routinely perform dives at 5-10 meters for 30 seconds, which while impressive, is something that fit people can do if they train their lung capacity.
Of note, in the famous Japanese and Korean breath-hold divers who have been studied for decades, repeated descents of this depth and duration don’t cause oxygen levels in the blood to fall much (Schagatay, Lodin-Sundstrom, and Abrahamsson 2011; Stanek et al. 1993). Second, repeated dives of this duration with brief periods of rest only cause whole-body oxygen consumption to rise to the level seen during a brisk walk or slow jog (Craig and Medd 1968). This is hardly the sort of maximum efforts made by deep-diving seals, competitive breath-hold divers, and blood-doping cyclists. The extra oxygen from a slightly larger spleen could easily be generated by a slightly larger breath prior to starting the dive.
It is incredibly easy to think up just-so stories for anything you notice (e.g., my just-so story on Mesoamerican human sacrifices). The Bajau learn to do breath-dive like that—it is an acquired ability. ALL human traits are experience-dependent and plastic, but obviously not to the same degrees.
The spleen is a blood filter. Being a blood filter, if it can filter MORE blood by being bigger, then it will give the individual whose spleen it is an advantage at certain tasks. It sits upper-left part of the abdomen and is protected by the rib cage while also being a place for blood cell storage (Pernar and Tavakkoli, 2019). The spleen acts as a reservoir of oxygen storing “‘thick blood’ rich in cells” so that when the diving animal the oxygen levels are stressed, the body has the reservoir of extra oxygen (Milton, 2004). Esperson et al (2002) also note how the spleen acts as a reservoir of red blood cells, while the contraction of the spleen causes extra hemoglobin production after exposure to diving events.
When a diver submerges their body in the water, two things happen: bradycardia—slower heart rate and vasoconstriction—the narrowing of arteries. The increase in water pressure further causes blood shift—an extension of vasoconstriction which allows us to dive deeply and the spleen effect—meaning that the spleen of divers shrinks which then releases the stored RBCs into the body, allowing for prolonged diving. So, if we look at this in regard to the Bajau, their large spleen shrinks and since their spleen is large due to the number of RBCs it has, it would then follow that as they deep-dive the spleen would shrink (known as splenic contraction) causing the release of the RBCs into the body, allowing for the deep-diving phenotype. Thus, without the blood shift and spleen effect, divers would not be able to dive to such deep depths. (See Gooden, 1994.) The mammalian dive response has, also, been hypothesized to be a reflex to preserve life (Panneton, 2013).
Bajau and, for example, Tibetan environments are similar in that the Bajau spend time in low-oxygen environments (the water) and so do the Tibetans (the mountains). But the Tibetans are constantly exposed to this effect; the Bajau need to be in the water for this effect to occur.
Lastly, the “HBDers” in the comments on Yglesias’ tweet said the same ol’ predictable things. Such as “human spleen growth is complex and due to what the stereotypes of a group’s spleen size are”; “of course it’s true!”; “variation in spleen size within groups is greater than variation in spleen size within groups”; “spleens are a social construct”; “evolution only happened in humans below the neck”; etc. These are the same ol’ sayings that come out from “HBDers” whenever a finding like this comes out. And, you can tell that they are ignorant to the anatomy/physiology of this stuff. They just jump on anything that they can say “HBD is real!!” as if anyone denies that humans are biologically diverse (like when the Rushton retraction came ‘it doesn’t mean that HBD isn’t true!). They move and weave different definitions of ‘HBD’ to fit their needs.
Such storytelling can be done for any trait, as noted by Smith (2016). One can think up selectionist stories and competing ideas for the evolution of traits, but without a way of ajudicating between two stories. One of the best definitions of just-so stories I am aware of is from Not in Our Genes (Lewontin, Rose, and Kamin, 1984: 258-262) cited in Smith (2016). Just-so stories:
predicate a genetically determined contrast in the past…unstated assumption that genes may arise with any arbitrarily complicated action needed by the theory…insulated from any possibility of being contradicted by fact…. If one is allowed to invent genes with arbitrary complicated effects on phenotype and then to invent adaptive stories about the unrecoverable past of human history, all phenomena, real and imaginary, can be explained.
So what happens when a physiologist looks into “HBD” claims? They are found very, very wanting.
I’ve been writing on this blog since June 15th, 2015. Back then, I held staunch hereditarian beliefs. Rushton’s views on testosterone were enticing to me, especially his theoretical article with Templer (Rushton and Templer, 2012). When I first read it I thought “Oh, justification for my prior beliefs about blacks and crime.” Then, when I started studying anatomy and physiology, I reread the paper and thought “Wow who gave the OK to publish this mess?”
So in February of 2018 I published a critique of the article, Do pigmentation and the melanocortin system modulate aggression and sexuality in humans as they do in other animals? A Response to Rushton and Templer (2012). I critiqued many of the claims in their article; its biggest weakness completely handwaving the warnings of Ducrest et al (2008) that human populations “are therefore not expected to consistently exhibit the associations between melaninbased coloration and the physiological and behavioural traits reported in our study.” Rushton and Templer dodged this by saying that we should compare African and European crime rates and that we do, indeed, see that Africans commit more crimes than whites and Africans have darker skin than whites so this is sort of “preliminary evidence” for the relationship in human races.
However, unfortunately for Rushton, Cernovsky and Litmann (2019) reanlyzed the INTERPOL crime data:
When all data from the same two Interpol Yearbooks are re-calculated, most of the statistically significant trends in the data are in the direction opposite to Rushton’s beliefs: Negroids had lower crime rates than Caucasoids with respect to sexual offenses, rapes, theft, and violent theft or robbery, with most correlation coefficients exceeding .60. While we do not place much credence in such Interpol statistics as they only reproduce information provided by government officials of different countries, our re-analysis indicated that Rushton excluded data that would discredit his theory.
So, if we accept the INTERPOL data—as Rushton did—then we would be justified in saying that the proposed relationships and causal pathways do not hold.
Then at the end of October the Twitter account @evopsychgoogle wrote a long thread with a strong, in-depth critique of the arguments and sources in Rushton and Templer (2012). He then published his critique as a letter to the editor of Personality and Individual Differences (PaID). In the letter, he exposes the shoddy logic of Rushton and Templer, while showing their misreadings of sources and misunderstanding of pleiotropy. Their main point in the paper is that LHT may explain why dark-skinned individuals are more violent, mature faster, etc while they also argue that the melanocortin system is a physiological coordinator of LH traits and skin color.
Testosterone production is a simple bodily process—to quote myself from November, 2017:
There are five simple steps to testosterone production: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone (Leydig cells produce testosterone in the presence of luteinizing hormone) (Saladin, 2010: 137). Testosterone is a steroid and so there are no ‘genes for’ testosterone.
Cells in the testes need to take cholesterol and then convert it into testosterone with the luteinizing hormone. According to Rushton and Templer, the result of this bodily process is part of the reason why blacks are more violent than whites—they have higher levels of testosterone and testosterone causes aggression/violence. Surely, Rushton and Templer were aware of Rohrmann et al (2007) who showed no difference in testosterone between blacks and whites. Surely Rushton and Templer were aware of all of the research that I cited in what I would call my ‘master article’ on race, testosterone, prostate cancer, and aggression. Rushton and Templer, quite obviously on a review of the literature, are misleading their readers.
Thankfully this paper has only been cited 15 times in the past 8 years since it was published. Evolution, presumably, accounts for the differences in death, AIDS rate, testosterone, lower life expectancy, etc. One recent citation can be found in the textbook Race and Crime (Gabiddon and Greene, 2018, 5th edition) in a discussion about Rushton’s r/K selection theory and causes for Rushton’s proposed relationship. They write (pg 122-123):
As with all theories, there have been several criticisms of the r/K selection theory. First, Rushton generally underemphasizes sociological factors. Most of his cross-national comparisons point strictly to numbers, without taking into account variables such as socioeconomic status, and other important sociological variables (Whihte, 2018). Second, in the 21st century, there are few “pure” races, especially in the United States, as noted in Chapter 1. White sexual aggression against Black females during the slave era produces countless mixed-race offspring. Therefore, the rigorous adherence to the Black-White-Asian split is problematic. Finally, if Rushton;s theory were true, what would explain White aggression as early colonizers and their current involvement in wars and violence across the globe? In contrast to Rushton’s theory, Bradley (1978) argued that, as a result of migration to colder regions, since the beginning of humanity, Whites have been the global aggressors.
So, testosterone does not cause aggression and it does not cause crime; the melanocortin system does not work in such a way that works for Rushton and Templer’s theory (Cone, 2006).
Hilliard (2012: 73) stated that “No evidence shows that racism motivated Rushton” while Dutton (2018) stated the same, interviewing Rushton’s ex-wife (whom he had an illegitimate black son with). But, knowing what we know about testosterone and Rushton’s views on blacks and whites, knowing about his (false) views on testosterone and race (while citing old, flawed studies like Ross et al) we can call into question the claim that Rushton had no racial animus. @evopsychgoogle also brought up the fact that COIs and funding sources were not brought up (this being Rushton’s final paper before his death and the fact that he was the head of the Pioneer Fund at the time means we don’t have to ask where the funding came from). Rushton and Templer should have never been published in the first place.
Lastly, Clark et al (2020) argued that ‘intelligence’ as ‘measured‘ by ‘IQ tests’ modulates the relationship between religiosity and crime at a country-wide level. They, of course, used Lynn’s global ‘IQ’ data. Though, there were many critiques of the paper and the data used in it (see here, here, and here) and Clark et al decided to finally retract their paper due to the problems of Lynn’s dataset. So, if they retracted due to the problems with Lynn’s dataset, does that mean that other papers that relied on Lynn’s shoddy work (e.g., Richardson, 2004; Morse, 2008) should be retracted too? Ebbeson (2020) notes the flawed ‘IQ estimates’ used in Clark (2020), noting the small, unrepresentative child samples used, along with showing that their dataset leads to “notions” which “are incompatible with psychological science” so “all conclusions drawn from these data are invalid.”
Clark et al “lost confidence in their findings” since “the homicide data have limitations that call [their] findings into question” while “The IQ data … have much more serious issues.” “Serious” is an understatement. To quote Ebbeson (2020)
For example, in the ‘NIQ_QNWSAS’ dataset, several African, South Asian and Central American countries have an average IQ below 50, such as Nepal (national IQ: 43.0), Sierra Leone (national IQ: 45.1), Guatemala (national IQ: 47.7) and Gambia (national IQ: 49.8) These estimates would seem to suggest that a majority of the population in these countries are moderately, severely, or profoundly cognitively impaired. (cf. Table 1). This notion is incompatible with psychological science and there is no doubt that these estimates are wrong.
All in all, this is not a good week for “HBD”—Rushton is being exposed for the know-nothing about physiology that he is, and Lynn’s ‘national IQ’ numbers are getting the scrutiny they finally deserve. So, I hold, if Clark et al was retracted for those reasons, we need to retract ALL papers that relied on Lynn’s ‘national IQ data.’ People may cry ‘censorship! HBD is dead!’, but ‘HBD’ (what I would term psychological hereditarianism) has been long dead. Rushton and Templer’s paper should have never been published but it’s better late than never that it is finally getting retracted. If you’re saying that Rushton and Templer got retracted for “political reasons” then it’s clear that you did not read either of the two existing critiques of the paper.
I started this blog almost 5 years ago. Currently (excluding this one), there are 480 articles on this blog. Searching my blog name “notpoliticallycorrect.me” on Google Scholar leads to two citations—one on “IQ” and obesity and the other on inclusionism about race when it comes to medicine. These two cites pretty much perfectly show my views and their change in the past 5 years since the creation of this blog. I will discuss both papers that cited me in turn.
In the journal Social and Human Sciences. Domestic and Foreign Literature (a sociology journal), a 2016 article I published (back in my “HBD” days titled “Race, Obesity, Poverty, and IQ, writing:
income and education (which in the latter case presumably correlates with IQ levels). They have the highest prevalence of type 2 diabetes. In terms of ethnicity, overweight indicators are as follows: 67.3% for whites, 75.6% for African Americans and 77.9% for Latinos. Summing up all this, we obtain, in the words of the authors of the study, “politically incorrect conclusions”: African Americans and Hispanics are more at risk of living in poverty, have lower IQ, higher rates of obesity and a chance of developing diabetes; The main factor in these correlations is the IQ level (Race, obesity, poverty and IQ, 2016).
Almost four years later (after my views have undergone a significant change) I would draw different conclusions. Blacks are 51% more likely to be obese than whites (Lincoln, Abdou, and Lloyd, 2016) with the cause being a multitude of factors. Though it seems that black American men with more African ancestry may be protected against central adiposity (Klimentidis et al, 2016). Racial disparities in obesity are due to an interaction of a multitude of factors (Byrd, Toth, and Stanford, 2018). Interestingly, black kids with obesity don’t perceive themselves as obese (Lankarani and Assani, 2018), which, presumably, is due to higher rates of obesity in the black population. Black girls are more likely to have an earlier menarche than white giris (e.g., Freedman et al, 2000) and it is because black girls are more likely to be obese than white girls which is due to the effects of leptin being permissive for menarche, from the higher levels of body fat in black girls (Salsberry, Reagen, and Pajer, 2010).
We must look to social determinants of health to understand why certain non-white populations are more likely to be obese than others. Looking at “IQ” as causal for obesity—which I used to believe—obscures much more than it helps. We can look to epigenetic effects, for example, regarding biological explanations of obesity (Krueger and Reithner, 2016), for instance high BMI in black women being related to saliva-based DNA methylation, which is used as a marker for aging (Li et al, 2019). Even perceived racism (it does not have to be actual) can have physiologic effects on black women, heigtening cortisol levels, leading to a heigtened obesity risk (Mwendwa et al, 2016).
In any case, it’s cool that I got cited but uncool that it was something that I don’t believe anymore.
The second citation comes from Rossi (2020: 13) in the journal Social Science Information titled New avenues in epigenetic research about race: Online activism around reparations for slavery in the United States citing my article Race, Medicine, and Epigenetics: How the Social Becomes Biological:
Consequently, social scientists’ opinions about epigenetic research dealing with race and slavery have sometimes been scrutinized by blog authors. For example, the article untitled [sic] ‘Race, medicine, and epigenetics: How the social becomes biological’ published in 2019 on the blog Notpoliticallycorrect features a long discussion on whether race could be seen as a viable variable to discuss the epigenetics of trauma, especially relating to slavery in the US.14 After summarizing the views of legal scholar and sociologist Dorothy Roberts, who has argued repeatedly in her works against the use of the concept of race in biomedical sciences, the author sides with philosophers Michael Hardimon and Shannon Sullivan, who are both enthusiastic about the inclusion of race to discuss genetics and epigenetics:
Race and medicine is a tendentious topic. On one hand, you have people like sociologist Dorothy Roberts (2012) who argues against the use of race in a medical context, whereas philosopher of race Michael Hardimon thinks that we should not be exclusionists about race when it comes to medicine. If there are biological races, and there are salient genetic differences between them, then why should we disregard this when it comes to a medically relevant context? [. . .] So, we should not be exclusionists (like Roberts), we should be inclusionists (like Hardimon). [. . .] Furthermore, acknowledging the fact that the social dimensions of race can help us understand how racism manifests itself in biology (for a good intro to this see Sullivan’s (2015) book The Physiology of Racist and Sexist Oppression, for even if the ‘oppression’ is imagined, it can still have very real biological effects that could be passed onto the next generation – and it could particularly affect a developing fetus, too). It seems that there is a good argument that the effects of slavery could have been passed down through the generations manifesting itself in smaller bodies.
Relying also on Jasienska’s research, the author of this blog post therefore dismissed the idea that race should not be applied to the medical field, while using the words and legitimacy of humanities scholars such as Hardimon and Sullivan to back up their claims. These contributions show the way journalists and various blog authors write about epigenetics by mixing together scientific articles in various fields (the social sciences, philosophy, psychiatry, social work) in an effort to bring more legitimacy to the topic. This process highlights the ways in which lay circles produce new connections between various papers and texts dealing with epigenetics, no matter how different their fields of expertise may be.
This shows a very sharp contrast with my current views and my older views on race and obesity. Before, thinking that obesity was “determined” by IQ (e.g., Kanazawa, 2012; Kanazawa, 2014) was an error—people with low “IQs” are more likely to be in poverty and have less access to good foods, along with the abundance of fast food restaurants in areas with a higher concentration of blacks (James et al, 2014). Black women, for instance, have a lower RMR than white women (Gannon, DiPietro, and Poehlman, 2000)
These two articles of mine that were cited (on similar issues, no less) show the evolution of my views over the past four or so years in between the publication of the two articles on this blog. This is a good case study on how the one can view the aetiology of one thing completely different based on the types of views they previously held. The views of obesity and race I hold now are much more complex than the reductive “it’s genes/IQ” kind of guy that I used to be. A more holistic view of obesity disparities, factoring in access to food (food swamps/deserts), income, location etc is more informative than looking just to “IQ” or “genes for” obesity—because even if “genes for” obesity exist and even if “genes for” obesity are distributed unevenly across races, the predominant determinant of weight will be activity level/caloric consumption, which is based on SES and other factors—not “IQ” or “obesity genes.” The social does become biological, and it does have consequences for obesity disparities between and within races.
The other day on Twitter, Davide Piffer made the claim that North and South Italians are “two different races” and that the North is “governed by morons from the South.” What would make him say that North and South Italians “are two different races”? Well, a new study was just published which looked into the genetic divergence of North and South Italians. It seems that Piffer is saying that the fact that North and South Italians are genetically distinct means that they are races. But this is an error in reasoning—it is fallacious to believe that just because two groups are genetically distinct that they are therefore races.
Sazzini et al (2020) show evidence that North and South Italians genetically diverged after the last glacial maximum (LGM). They state that there was “adaptive evolution” at “insulin-related loci” from Italian regions with temperate climates. The state that climatic factors differentiated those from the North and those from the South. The “adaptations” that those in the North have protect them from:
… we proposed climate-related selective pressures as potential factors having influenced adaptive evolution at insulin-related genes especially in the ancestors of Northern Italians. By regulating glucose homeostasis, adiposity, and thermogenesis in response to high-calorie diets adopted to cope with energetically demanding environmental conditions, these adaptive events might have also contributed to make people from Northern Italy less prone to develop T2D and obesity despite the challenging nutritional context imposed by modern lifestyles. Conversely, possible adaptations against pathogens and modulation of melanogenesis in response to high UV radiation are supposed to have played a role in reduced susceptibility of people from Southern Italy respectively to immunoglobulin-A nephropathy and skin cancers. Finally, multiple adaptive processes evolved by the overall Italian population, but having resulted more pronounced in people from the southern regions of the peninsula, were found to have the potential to secondarily modulate the longevity phenotype. Therefore, by pinpointing genetic determinants underlying biological adaptation of Italian population clusters in response to locally diverging environmental contexts, the present study succeeded in disclosing also valuable biomedical implications of such evolutionary events.
What they did was select 39 unrelated genomes, representative of the known genetic differences in Italian the Italian population, and then compare the differences 35 populations from all over Europe. They found divergence between the two occurred between 12 and 19 kya—they presume that the so-called “adaptations” for North Italians, being “adapted” to lower temperatures and higher-kcal food, and the so-called “adaptations” for South Italians being adapted to warmer climes, so they have “genes to protect against” skin cancer and pathogens—while gene variants ‘related’ to longer life were also showed changes in those genes.
The press release, though, cautions against adaptive conclusions:
The authors caution that although correlations may be drawn between evolutionary adaptations and current disease prevalence among populations, they are unable to prove causation, or rule out the possibility that more recent gene flow from populations exposed to diverse environmental conditions outside of Italy may have also contributed to the different genetic signatures seen between northern and southern Italians today.
While this is an interesting study (and it does need to reign back its ‘adaptive conclusions’), it does not show that North and South Italians are different races. If they are different races, how does it go? Is there a single North Italian race and a single South Italian race? Or are North Italians Caucasian, while South Italians would be African? Are there 5, 6, or 7 races in Piffer’s racial schema?
Like all hereditarians, he just assumes the existence of race—if this and that population are genetically distinct, then they must be races. Wow, how compelling an argument to show that races exist. But if North and South Italians are a different race on the basis of genetic differentiation, then so are East and West Germans (Nelis et al, 2009), North and South Germans (Heath et al, 2008), Southeast and Northwest Dutch (Lao et al, 2013), North and South Dutch (Byrne et al, 2020), Northern and Southern Swedes (Humphreys et al, 2011), East and West Fins (Kerminen et al, 2017), etc. Using genetic differentiation as a basis to show which population is or is not a race logically leads one down this path. Why not 7 billion races? Each individual is unique? Oh, wait: He would say something about “breeding populations” probably—and that’d be good because he would then be stating conditions for racehood, not just assuming their existence on the basis of genetic differentiation. Though, the claim would still fail.
Piffer has let his mask slip before—back in March he called immigrants to Italy “gorillas”, then saying that “Gorillas are nobler” because they would not take beds from the sick, since this was when Corona was really heating up in Italy. This is similar to what the “World’s Smartest Man” Christopher Langan said about gorillas and immigration. There seems to be a relationship between idiotic sayings about gorillas and immigration and racism… hmm…
In any case, the fact that North and South Italians are genetically distinct populations in no way, shape, or form, is evidence that they are different races. For if it is, then there are many, many races—even in countries with the same group of people, if we are to understand race how Piffer seems to understand it (any type of genomic differentiation between populations makes them races). So is each family on earth a different race? This is the kind of conclusion that Piffer’s lazy thinking leads to. Piffer is just like Murray—if populations cluster in genomic analyses then those population clusters are races. Two hereditarians—two assumptions that fail, since if we take them to their logical conclusion, there are more races than is traditionally stated. Piffer, it seems, just sees a group he is clearly biased agains (South Italians), sees they are distinct genomically from the North, and then says “Aha! these morons from the South who are governing us are just a different race than we are!” Clinal differences in skin color, too, don’t ‘prove’ that North and South Italians are a different race.
Too bad for Piffer, reality is different than in his own biased world. Italy is over two thousand years old—and the people in the North and the South belong to the same race. Piffer’s ‘research’ into the “IQs” of North and South Italians (Lynn, 2010; Piffer and Lynn, 2014; see Cornoldi et al, 2010; D’Amico et al, 2011; Robinson, Saggino, and Tommasi, 2011; Danielle and Malanima, 2011; Cornoldi, Giofre, and Martini, 2013; in any case, is (and has been) suspect—but now we know that he has other motivations than just iScience!
(Note: The Italianthro blog has a ton of information on Italy, its peopling, “IQ”, and other things. Check the blog out.)
Bans against consanguinity have been around for thousands, of years, though they differ by degree and culture. The Greeks had no single name for it, a similar term not appearing until around the 9th century—for instance, classic Athenian law stated that children of the same father could marry—i.e., a half-brother and half-sister (Ager, 2005). But what were some of the original reasons why they were banned—eugenic considerations or cultural/closeness reasons? Why were people banned from having a partner that was too close to them? Throughout history, different cultures obviously had different practices. The Roman Catholic Church, Pharaonic and Ptolemic Egypt, ancient Iran, all had different practices, for different reasons, on close marriage to relatives. The ban on first-cousin marriage appeared in American law around the time of the Civil War—clearly, then, the cousin-marriage ban in America was not based on the eugenics movement, though it was eugenic in nature (Paul and Spencer, 2008). Though there was debate on the matter during the Progressive Era (Wilson).
Schneider addressed sexual and matrimonial prohibitions among the Yapese in an early article (1957), but he developed his approach in a volume devoted to the subject of incest (1976). It was in the latter that he presented his culturalist views on the topic, making the important point that ‘the most frequent confusion found in the literature in my experience is the confusion between the question of the origin of the prohibition on incest and the question of why it is maintained long after the conditions which may account for its origin have passed’(Schneider 1976: 156). He went on to argue that ‘the incest prohibition is not universal’, supporting this affirmation with the cases of brother–sister marriages of Pharaonic and Ptolemaic Egypt, the ‘apparent lack’ of an incest prohibition in ancient Iran, and the marriages between members of the royal family of Hawaii as analysed by Marshall Sahlins (Schneider 1976: 154). None of these relations would be considered as incestuous for the native people. He also insisted on the inclusion of kin other than nuclear kin in the different prohibitions that Europeans identify as incestuous, on the importance of elements such as food for determining who a person can and cannot have sexual relations with and on cases in which incest includes non-sexual behaviour. He then proposed equating incest with the idea of acting ‘ungrammatically’ in a given cultural code (Schneider 1976: 167). Thus, for Schneider, a priori deﬁnitions of incest based on a Western tendency to relate kinship to sexual intercourse and the birth of a child should be avoided. Rather, he argued, we should adopt a cultural and symbolic approach towards each case. [See also Scheidel, 1997 for more information on sibling and half-sibling marriage in Roman Egypt. They did this to keep the throne in the family; Galton, 1998]
But the Romans were the first to dissuade consanguineous marriages when Emperor Claudius married his niece Agrippina in the middle of the 1st century. Then, in the middle of the fifth century, which the Roman Catholic Church eventually picked up, with the Pope citing passages in Leviticus to justify the banning of marriages with close kin (Bittles, 2009). (I should bring up the ‘Hajnal line’ now, but I’ll save that for an article by itself. In the meantime, read Steinbach, Kuhnt, and Knull, 2016 where they show that by taking marriage rate, divorce rate, step-families, and single-parent prevalence into account, we cannot use the ‘Hajnal line’ to explain differences between East and West Europe”; see also who argue that Szolyysek and Ogorek, 2019 who show that when regional populations cluster on familial traits that they lie outside of the ‘line’, which calls into questions the conclusions of Hajnal and his acolytes.)
When it comes to these cases, the ban on close marriages was not to have healthy children—and therefore attempt to prevent the types of problems that arise through the marriage of a close relative if they conceive a child—the ban was to avoid relationships that lacked difference on a bio-social level. One example here would be in certain Muslim communities. Children who shared the same wet nurse—a nurse who breastfeeds for parents—were banned from having any kind of relations later in life as they were known as ‘milk-siblings’:
Children who have been regularly breastfed (three to five or more times) by the same woman are considered “milk-siblings” and are prohibited from marrying each other. It is forbidden for a man to marry his milk mother (wet nurse) or for a woman to marry her milk mother’s husband.
In Leviticus 18:6-18, Deuteronomy 22:30, and Deuteronomy 27:2-23 the authors spake against marriage with close (blood) relatives while in Leviticus 20:11-21 along with the prohibitions against relations with blood kin, even your uncle’s wife was out of the question (the unrelated wife). When it comes to the Roman Catholic Church banning cousin marriage, however, there is a debate as to what the impetus for the ban was: was it due to eugenic considerations or to ban the marriage of two close individuals, no matter their relatedness status? MacKellar and Bechtel (2014: 62) write:
It is likely, however, that the basis for this prohibition on consanguinity [in the Roman Catholic Church] was not a concern for eugenic considerations. The condemnation of affinity, such as marrying a step-daughter (cannon 1092) and marrying an adopted child or sibling (cannon 1094) implies that these codes were again drafted on the basis of avoiding sexual relationships between people who were considered too similar or who had something ‘overly in common.’
Parkes (2005) notes that even marriage between a godparent and godchild was banned in Christian communities. I grew up Roman Catholic and I, too, would not marry my Godmother (who is my fourth cousin). MacKellar and Bechtel (2014: 63) do note that the Christian Church even banned relationships between, say, student and teacher to prevent “sexual corruption and abuse. These sexual restrictions were not, therefore, drafted to protect progeny from inheritable disorders but were similar to those that prevent relationships between teachers and their pupils or doctors with their patients. These relationships were prohibited even though it may have been certain that no child would ever be born.
Chinese cousin marriage prohibitions are interesting. First cousins could marry eac other if they did not have the same surname but if they had the same surname they were barred from marriage, as Wong (2017) notes that “The old Chinese system is a patriarchal system, where children take the surname of the father. In this patriarchal system, first cousins of the same surname could not marry. First cousins, with different surnames, could marry.”
Many Asian ethnies have the same or similar surnames. So, on that basis, it is interesting to note that in Korea, for example, much cultural shame is brought on people who choose to marry and have the same last name. It is so taboo that family and friends question their loved ones who date a person with their same last name. The New York Times has an interesting story from the mid-90s about Koreans and dating/marrying an individual with the same last name:
It should be a time of celebration. K. H. Lee and his girlfriend have fallen in love and want to get married soon to start a new life together.
But Mr. Lee, a 31-year-old civil servant, and his fiancee face a battle against Korean history that threatens to bring their love to ruin: they have the same last name. Even his friends disapprove of his plans.
“I can feel them asking, ‘Do you really have to do this?'” said Mr. Lee, who, who would not disclose his full given name or his girlfriend’s because the issue is so delicate. “Even if it were allowed by law, if the relatives found out, the whole family would be shamed because we have a strong sense of face.” Not being able to marry a person with the same family name is a special burden in South Korea, where 22 percent of South Korea’s 44 million people are named Kim. The figure leaps to 55 percent after adding in Park, Lee, Choi, and Chong.
The NYT story also notes an interesting bit of Korean folklore about this ban:
According to folklore, the practice was brought over from China in the 14th century, after a Korean messenger, named Lee, visited China. His Chinese host asked him his wife’s name, and upon hearing that it was also Lee, the Chinese supposedly replied: “Ah! You’re not an aristocrat. You’re a commoner!” When the messenger returned, he relayed the story to the Korean emperor, who immediately declared a ban against same-clan marriages.
Dating people with the same last name in South Korea is such a taboo that some people even attempt to find out their perspective SO’s last name discretely. The practice, to them is cultural as of now since presumably, marriage and children with one with the same last name won’t lead to any birth defects.
We have been marrying/conceiving children with close relatives since time immemorial. Though, different peoples have different reasons for shunning consanguineous marriages—some cultural, some biological, some both. The Greeks banned it in some instances, but allowed it in others. In Islam, children who are “milk-siblings” cannot marry. Asians (who are likely to share names with their own ethny, and even sometimes another Asian of a different ethny) have some interesting considerations on cousin marriages—it being so engrained in their culture that some will not talk to someone if they share their last name. The considerations of banning consanguineous marriages by the Church, though, could go both ways—it could be due to banning marriages between people who are ‘related’ socially, and not genetically.
The history of cousin marriage—along with the banning/allowing it throughout history, along with how different peoples handle the situation shows exactly how humans individuate through culture.
Sudden Infant Death Syndrome (SIDS) has a long history—almost as long as human civilization (Raven, 2018). The term was coined in 1969 to bring attention to children who died in the postnatal period (Kinney and Thach, 2012; Duncan and Byard, 2018). About 95 percent of SIDS cases occur within the first 6 months of life, happening around the 4-6 months mark (Fleming, Blair, and Pease, 2015). The syndrome is associated with the sleep period, presumed to have begun with the transition from sleep to waking (Kinney and Thach, 2012) The prone sleeping position, along with smoking, is said to increase the incidence of SIDS (Ramirez, Ramirez, and Anderson, 2018). Due to a campaign in the mid-90s, though (called the back-to-sleep campaign), it has been estimated that SIDS deaths have decreased by 50 percent, saving thousands of infant lives (Kinney and Thach, 2012).
But, those infants who die from SIDS may also have a problem with the part of their brain that controls waking/sleeping:
Infants who die from SIDS may have a problem with the part of the brain that helps control breathing and waking during sleep. If a baby is breathing stale air and not getting enough oxygen, the brain usually triggers the baby to wake up and cry to get more oxygen.
So, if a baby’s brain is not getting enough oxygen, its brain will have it wake up and cry in an attempt to rid itself of “stale oxygen”—this is one other purpose that crying serves—which then gets the baby more oxygen to its brain.
As can be imagined, acute rises in CO2 levels occur when an individual is unable to expel CO2, such as in the setting of an airway obstruction that might occur when an individual is lying prone in a crib or bed perhaps with a pillow and bedclothes covering the nose and mouth. It has been proposed that such a rise in CO2 would activate arousal circuitry in a normal baby to wake the baby up, cause them to cry out, summoning a caregiver who would come to their aid, and ostensibly correct the airway blockage to allow resumption of normal breathing [16,20,31]. It has been proposed, among other possibilities, that there is an impaired CO2-arousal system in SIDS-susceptible babies such that when they rebreathe CO2 as described above, they do not arouse, and thus do not cry out, and the blockage is not corrected [16,32]. They thus become acidotic and hypoxic and ultimately succumb.
So, if a babe’s airway gets blocked, for instance by a pillow or toy, they wake, cry out for attention and their caregiver comes to solve the problem or they change their laying position. But in SIDS cases, this does not occur. Why? Buchanan argues that those who succumb to sudden deaths like SIDS have screwy serotonin receptors—they ensure that blood oxygen and CO2 levels are healthy. But some of these infants may have brains that don’t allow them to detect the CO2 and blood oxygen levels—when the body may be suffocating. SIDS victims are usually found face-down in their cribs. But, there are no biomarkers for SIDS (Haynes, 2018). The SIDS diagnosis is only given after all other causes of death are ruled out—this is why SIDS is so mysterious. Genetic mutations have been posited as a cause (Männikkö et al, 2018), as has a pregnant mother smoking during pregancy, leading to a doubled risk of SIDS (Anderson et al, 2019).
But the best prevention against SIDS is nonprone sleeping—having the baby sleep on its back. The efficacy of this approach since the 1990ss has been noted (Gibson et al, 1992; de Luca and Hinide, 2016) while “Achieving recommended prenatal care and infant vaccinations, as well as reductions in maternal tobacco and substance use, has the potential to further reduce rates of SIDS and should be given as much attention as safe sleep advice in SIDS risk reduction campaigns” (Hauck and Tanabe, 2017: e289). The back-to-sleep program, though, has been associated with a decrease in motor development from the infant sending time in the supine position along with the strong possibility of developing plagiocephaly—which causes a “flat head” due to being placed in similar positions while the infant’s skull is soft and still developing (Miller et al, 2011). It has also been estimated that if it was known that the advice to place infants on their stomachs to sleep led to SIDS, then we “might have prevented over 10 000 infant deaths in the UK and at least 50 000 in Europe, the USA, and Australasia” (Gilbert et al, 2005: 884).
But the history of SIDS in America is a lot more sinister—rather than children dying from ‘natural causes’ (SIDS), in the 1970s, it was hypothesized by one SIDS researcher that SIDS was ‘genetic’ and ‘transmissible’ on the basis of one family who, unfortunately, had experienced this tragedy more than once.
This leads us to the story of Waneta Hoyt, who is the subject of this article.
Hoyt and Steinschneider: Genes vs environment
Horrible tragedies befell a woman from New York named Waneta Hoyt—five of her children had mysteriously died due to SIDS between the years of 1965-1971.
Waneta killed her first child, Eric who was three-months-old. SIDS is a diagnosis that is arrived at through a process of elimination—rule out all other causes at a young age (under 1) and the cause is then SIDS. But, the thing is, when an autopsy is performed on the infant, there is no difference between what would be said to be SIDS deaths and a light smothering.
After Waneta murdered her first child, she was cold and distant but it was not noticed. It was reported that she would never hold her children as a loving mother would, keeping them quite far from her. But it wasn’t until three years later that she, again, murdered. But this time it was two of her children—her two-year-old son and six-week-old daughter. The murders that Waneta were committing were wrongfully diagnosed as being due to SIDS.
This caught the attention of renowned SIDS researcher Alfred Steinschneider who had a clinic in which he specialized in caring for infants who were thought to be high-risk for SIDS. Steinschneider wanted to watch Waneta’s fourth child in his sleeping ward, in an attempt to prevent what he thought was due to SIDS. So, when he heard of Waneta’s story, he reached out to her to monitor her daughter, Molly.
The nurses at Steinschneider’s clinic, though, became suspicious of Waneta when she was at the clinic since she was cold and distant to Molly—she would not show her any affection. Steinschneider’s nurses emphatically told Steinschneider that it was Waneta who was murdering her children. Steinschneider shot back, and sent Molly home anyway. In an interview on the television program Deadly Women called Mothers Who Kill, one of the nurses who watched Molly before she was discharged by Steinschneider said:
And then about a quarter to eleven when we were getting ready to go off duty I said ‘Joyce, what do you think, do you think she’s still alive?’ Of course when I came on duty the next day she was dead.
Forty-eight hours later, on Thursday, June 4, Steinschneider scheduled Molly for her third discharge. By now, the nurses were speaking more openly about their suspicions. “I just know something’s going to happen,” Corrine Dower said to Thelma. “One of these times she’s going to do it.” Corrine was scornful of Steinschneider. “If he had any brains at all he would have seen that she didn’t want the baby,” she would say years later. “You can tell in the grocery store if a person cares about their child. We were just disgusted with Steinschneider.” (book excerpt from How Two Baby Deaths Led to a Misguided SIDS Theory)
Presumably, since this was Waneta’s fourth time experiencing the tragedy of SIDS, Steinschneider did not think that Waneta could be involved—but his nurses knew the truth. It was when Waneta had her fifth child that Steinschneider thought he would make his breakthrough in his research. Steinschneider was so convinced that the baby’s were dying due to SIDS, and he thought that if he could monitor Waneta’s new baby as much as possible, that he may figure out why babies die from SIDS.
Steinschneider believes that SIDS is hereditary—passed on through genes. The fifth child was watched at Steinschneider’s clinic and when Steinschneider discharged him—in an attempt to prove his theory—his nurses protested. Then, shortly after, Waneta called Steinschneider saying that it had happened again—her fifth child had mysteriously died.
After the death of Waneta’s fifth child, Steinschneider published his paper Prolonged Apnea and the Sudden Infant Death Syndrome: Clinical and Laboratory Observations arguing that SIDS was caused largely by hereditary sleep apnea (Steinschneider, 1972). By 1997, Steinschneider’s paper was the most-cited paper in the SIDS literature (Bergman, 1997). It was due to Steinschneider’s research, though, that parents began using sleep monitors to monitor their children’s sleep so they could be alerted in case their child had sleep apnea.
Steinschneider cared more about his research and theory of SIDS and sleep apnea over what was striking him right in the face—Waneta was responsible for the deaths of her five children. Steinschneider’s 1972 paper was cited and used for 22 years, until it was found upon an in-depth look into Steinschneider’s paper that what was clear to Steinschneider’s nurses and not him was true—Waneta was responsible for the deaths of her children. Steinschneider’s paper, in any case, concluded that SIDS is a genetic disorder and it was thusly inherited. And Waneta’s case, it seems, lent credence to his hypothesis. Steinschneider gave Waneta the perfect alibi—her woes were caused by a genetic disease and there was nothing that could have been done to prevent it.
Waneta was convicted in 1995 of five counts of murder and sentenced to 75 years in prison—therefore refuting Steinschneider’s theory. Three years after her sentence, though, Waneta died in prison of cancer. The case of Waneta Hoyt allowed mothers to kill their children in this specific way (a light smothering) for almost a quarter of a century.
Norton saw history repeating itself in the reluctance of many factors to face the fact that some deaths attributed to SIDS were homicides. She agreed with the bulk of SIDS research, which pointed to apnea, or the cessation of breathing, as the final pathway to death. But there were many causes of apnea, not all of them natural. An adult could place a hand or a pillow over an infant’s nose and mouth and stop the child from breathing. The pressure needed to smother an infant often left no telltale signs, Norton explained.
“There is no way for the pathologist at autopsy to distinguish between homicidal smothering and SIDS,” she concluded.
Norton worried that homicides were being passed off as SIDS because many doctors held the erroneous belief that SIDS ran in families. They ignored large-scale studies that had shown no genetic tendency toward SIDS. Flouting conventional wisdom, Norton warned that the sudden, unexplained death of a SIDS victim’s sibling should be treated as a possible homicide.
When Waneta was convicted, letters to the editor were sent about Steinschneider’s paper. The short correction to the paper chronicles, interestingly, a letter to the editor of the journal Pediatrics, who published the Steinschneider paper
“But the paper indicated a more sinister possibility to Dr. John F. Hick of Minnesota. In a letter to the journal, he wrote that the case offered “circumstantial evidence suggesting a critical role for the mother in the death of her children.” (See below.)
But his warning was dismissed, until Mr. Fitzpatrick read the paper 15 years later.
“The medical records described two happy, healthy, perfectly normal kids,” he said. “It convinced me that these children were murdered.”
Hick’s letter to Pediatrics says:
In reporting two siblings who succumbed to “sudden infant death syndrome,” Steinschneider exposes an unparalleled family chronicle of infant death.’ Of five children, four died in early infancy and the other died without explanation at age 28 months. Prolonged apnea is proposed as the common denominator in the deaths, yet the author leaves many questions relevant to the fate of these children unanswered.
In her signed confession, Waneta said that she smothered her five children because their screaming made her “feel useless”, though Waneta later stated that she only said that to stop the police from questioning her. Steinschneider, like another motivated-reasoner J.P. Rushton, ignored data that did not fit his theory of sleep-apnea-induced-SIDS—specifically how Waneta acted around her children while at his clinic and the thoughts of his own nursing staff telling him not to discharge the Hoyt infants.
Waneta recalled her strangling of her children—specifically Julie:
”They just kept crying and crying. . . . I just picked up Julie and I put her into my arm, in between my arm and my neck like this . . . and I just kept squeezing and squeezing and squeezing.”
Steinschneider’s testimony during Waneta’s trial, however, is very interesting. Reported by the New York Times, Steinschneider attempted to defend his patient Waneta against claims that she had murdered her children:
Autopsies were done,” he said, speaking of Molly. “They could not find a known cause of death.”
This, Dr. Steinschneider said, “by definition” is SIDS.
But under intense cross-examination. Dr. Steinschneider conceded that he could not remember — and did not record — crucial details from the medical histories of the two infants, whom he had hospitalized for observation soon after birth. In each case, the parents had reported that the baby was having difficulty breathing and that its older siblings had died mysteriously.
The doctor also acknowledged concluding that Molly and Noah had died of SIDS without knowing how thoroughly the authorities had probed the “death scene” for evidence of other causes, including murder.
It is said—even by the prosecutor on her case—that Waneta suffered from Munchausen by proxy (Firstman and Talan, 1996)—which is the intentional cause of illness, usually on children, in order for the mother to elicit sympathy for others (Gehlawat et al, 2015). In cases like this, mothers who have the Munchausen syndrome will suffocate their children and then rush them to the hospital—they get the satisfaction of inflicting pain and then the satisfaction of getting cared for for the so-called mysterious death of their baby. One study of 51 sleep apnea monitorings found that about 40 percent of the program treated infants who had apnea that seemed to be induced by the parent; this was inferred from the fact that once the infants were admitted to the hospital, the doctors found no signs of apnea (Light and Sheridan, 1990).
One doctor even took it upon himself to place cameras in his practice in order to monitor parents that were suspected of abusing their children. Thirty-nine infants were monitored—thirty-three infants were being abused by their parents, what’s more is that some of the infants in this study who were identified in the video also had a sibling who mysteriously died from SIDS (Southall et al, 1997). What the study shows is that these parents were suffocating their children, causing their breathing problems and that they most likely have gotten away with infanticide before. Another case involved a mother taking her daughter to eleven different hospitals, but none of them found anything wrong with the girl and she ended up dying under suspicious circumstances (Hassler, Zamorski, and Weirich, 2007).
We now know that Steinschneider ignored contrary evidence to his theory of genetically-induced sleep apnea causing SIDS which apparently ran in families, and since he brushed off his nursing staff telling him that Waneta was acting strangely around her two children that he had admitted into his clinic, he could have saved their lives. But Steinschneider’s genetic determinist theory was more important than seeing what was clear as day to his staff and even others who read his 1972 paper—a mother was strangling her own infants.
SIDS has a long history, dating back to biblical times. But, in the modern-era, erroneous theories on the causes of SIDS were pushed while other, more obvious causes were disregarded in favor of a grand genetic theory of SIDS causation. Waneta and Steinschneider both helped each other out: Steinschneider (unknowingly) helped Waneta evade detection for 22 years while Waneta lent credence to the hypothesis that Steinschneider was developing. The fact that, at the time of their first meeting, three of Waneta’s children had died in almost the same fashion pointed to a genetic, inherited cause in Steinschneider’s eyes.
At the time of publication of The Death of Innocents, Steinschneider still continues to defend his now-discredited theory and still lobbies for the use of infant sleep monitors. Of course, since he testified FOR Waneta, despite the mounting evidence against her, he could be seen as an accomplice, however weakly. But this case shows one thing that should be well-known—researchers become attached to their pet hypotheses/theories and will ignore contrary evidence if it is brought to their attention. Firstman and Talman estimate that between 5 and 10 percent of SIDS cases are actually homicides. (But see Milroy and Kepron, 2017.)
Steinschneider created the SIDS disease on the basis of Waneta’s story—and a multi-million dollar industry then appeared due to his paper—it’s all to save infants, buy these sleep apnea monitors. But there were two children that Steinschneider did not—could not—save: He could have saved those babies, if not for his genetic determinist beliefs on SIDS causation. Had Steinshneider looked at the more obvious answer to the problem which was right in front of his face, he may have seen that Waneta suffered from Munchausen by Proxy, and, as evidenced from the references above, those who suffer from the disease act out exactly how Waneta did—by strangling their children with the cause of death being blamed on SIDS.
The Hoyt-Steinschneider case is a warning—don’t jump so quickly to implicate heredity in the ontology of X, especially when other, more obvious, tells are right there in front of you.