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 physical interactions behind cognitive variation are arguably the most studied and elusive aspects of human diversity. Despite the HBD community’s enormous interest in the mind, I find that many of the modern theories they propagate are lacking conceptual rigor. Within this thesis I will attempt the following: 1) To persuade the audience that my conception of particular mental phenomena is more precise than or at least endorses the most epistemically accurate contemporary hypotheses. And 2) To lay out a simple yet reliable framework for future HBDers to base new ideas on by giving biological explanations of particular psychological phenomena. For this purpose alone you can treat this article as a short summarization of the extensive research into our concept of consciousness, as such I will not be covering any of this in extreme detail, neither will I be covering every single aspect of the mind, but it will of course be accompanied by studies and papers that will elucidate these concepts further for anyone who is interested.
Philosophy of mind
First, I think it’s appropriate to cover the philosophical grounds of my views. It should be no surprise that Physicalism/Naturalism is the most dominant position among philosophers within that domain (Bourget and Chalmers, 2013). The number is even greater if you consider scientists as philosophers (which they are). These figures are expected because Physicalism is the most parsimonious explanatory model for how our world works. So what is Physicalism? At the basic level, Physicalism is the belief that our world is a result of physical laws. I cannot highlight the entirety of this debate, the intricacy of the subjects within this article could span the length of multiple textbooks. I will delve more into this in future posts. Instead, I’m going to simply rebut what I believe are common fallacies that underlie dualistic thinking.
The arguments I have read tend to follow similar patterns in their reasoning. The one we will discuss first is the intensional fallacy. Dualist arguments that suffer from this flaw are presented in the following format:
P1: X (usually the mind) has property A
P2: Y (usually the brain/body or just physical entities in general) has property B
P3: Leibniz law which states: Necessarily, for anything, x, and anything, y, x is identical to y if and only if for any property x has, y has, and for any property y has, x has.
C1: X is not Y
From the onset this doesn’t seem that fallacious, and of course some would even argue the intensional fallacy cannot apply here, as leibniz law is not dependent on what someone knows but the properties a target may exhibit. This is incorrect, knowing the different properties the entity may possess by definition requires knowledge and subsequently a thinker. To see why this argument is ultimately fallacious, observe the following syllogism:
P1: Water is knowable with the unaided eye
P2: H2O is unknowable with the unaided eye
P3: leibniz law
C1: Water is not H2O
Descartes, Ross, and arguments on the unity of consciousness tend to all commit this fallacy. We could replace the subjects and their properties with that of neon and boron and the conclusion would be true, the problem is that discrepancies between the descriptions of physical and mental states (or any concept) does not necessarily entail that the two cannot be identical in reference. To make definitive statements on the mind’s characteristics requires an identification of the mechanisms that catalyze such functions. Physicalists have this luxury, Dualists do not. This idea is echoed (actually I’m the echo) by Kant (1781) in his 2nd paralogism of his Critique of Pure Reason (Kitcher, 1990) This brings me to the second fallacy: ad ignorantiam. We know a lot about the mind, Philosophy, Art, History, Literature, Psychology, Neuroscience, etc. What seems to be the crux of the issue is how subjectivity arises from objectivity. I am not charging any particular Dualist argument with this fallacy. Instead, I believe this fallacy pervades Dualism as a whole. It usually goes:
P1: Despite Physicalism’s explanatory power, it hasn’t explained the phenomenological character of experience.
P2: Since Physicalism cannot explain this particular aspect it cannot be a tenable model for our world
C1: Dualism is the only tenable position
What makes this a fallacious argument is that the proponent is essentially asking you to “prove him wrong”. Phenomenology is a difficult concept to ground in physical structures simply because of the sheer complexity behind it. Donald davidson even advocated Dual Aspect Monism as a solution to this perceived indeterminism (more on stochasticity later). Despite the debate on the aforementioned subject, if Dualists accept interactionism (which they have to), positing an “ectoplasmic” nature to mental states is pure ad hoc. This brings me to the final fallacy I will discuss: begging the question. If Physicalists can account for these qualities then any Dualist argument against Physicalism already presupposes the need for Dualism. If Physicalism cannot account for said phenomena then these criticisms could cut both ways. More on Dualism and its presumed fallacies.
Nature of the system
These following sections won’t be new or helpful to anyone versed in current literature on neuroscience or similar fields. This is simply a reference point for those less knowledgeable on the subject. Usually, when you read on the Nervous system, authors will refer to its descriptions with computer and engineering metaphors (Furber and Temple, 2007). This article will do the same, but for conceptual clarity I will stress that the brain is not a computer. Yes, it’s true that computers are the closest thing to a brain that we’ve engineered, but it is a biological organ that has been crafted by millions of years of sloppy evolution. As obvious as that is, let it serve as a reminder to not to take the metaphors too seriously. Despite my previous views, the brain is not a parallel system. There aren’t actual physical boundaries that could represent independence. Subsequently, the brain and the mind cannot be modular as modularity also requires independence. The NS and its parts is in fact parallel if you consider each neuron as its own processor with each synaptic cleft as a physical boundary (though you could arguably still contest the independence). Unfortunately, this is not what Scientists of the mind refer to when they use these terms. Cognitive scientists and Psychologists refer to more complex interactions, and as a result many of their computational models could be labelled parallel. Their divisions are more abstract, the subject of this article is a more empirically grounded level of function.
If anything the brain is an integrated memory system. Which is to say that it is dependent upon neighboring receivers to produce certain behaviors and actions. An integrated system has the same potential as a parallel one, as it can run multiple operations simultaneously (Born 2001). I find integration a better description of our nervous system because it allows for the dependency we clearly witness. Compartmentalization of the cerebral hemispheres is arbitrary. As you can see from the previous video, simple observation indicates that there are no real anatomical boundaries except possibly sulci. However, this would still be against the interests of the consensus. Despite this, localization can still be realized through averaging the enormous variation in functionality (Sporns, Tononi, and Kotter, 2005). Localization is still tricky to realize, as the brain is a biological construct with a general purpose function. This implies that neuronal activity of the same tasks can vary in individuals day by day. There exists a tug and pull between minimization of cost and maximization of growth and adaptation. This is how the brain retains plasticity via a “winner takes all” scenario while simultaneously allowing arborization of localized functionality to solidify (Barbey, 2018). These functions are carried out by populations of neurons. This is because there is no specificity (except maybe some kind of spatial tendency) in regard to the connections between individual neurons. It should be noted that this is not in reference to variation over time. The plasticity of individual neuronal connections and the categorical selection of pathways that groups of neurons take is determined by a multitude of factors that can be coherently expressed, so a lack of specificity is not equivalent to indeterminism in this context. RaceRealist has an interesting article that could explain the stochasticity of low level connectivity. This link will also be helpful to those interested in how this connectivity is realized. As far as the connectivity on the population level goes, there is considerable determinism that shapes the probabilistic nature of cognition (Dold et al., 2018).
This is possibly the most important aspect of consciousness, as it is an accumulation of our memories that help formulate how we perceive and establish ourselves. Alzheimers is a type of dementia that affects memory which can slowly make its carrier lose themselves over time. Our memories are completely dependent on external stimuli. Sub-mechanisms of neural plasticity are responsible for this function and can be carried out in multiple ways. Synaptic plasticity is the most commonly discussed aspect of neuroplasticity. Nonsynaptic Plasticity is newer to the field of neuroscience but works synergistically with the former to carry out key mechanisms involving memory and learning (Tully, Hennig, and Lansner, 2014). Simply put, learning a new skill requires locally specific neurons and their glial modulators to strengthen or weaken their connections with each other. The more you carry out these tasks the stronger these connections become, and subsequently the easier it becomes to perform said tasks. Your eyes, ears and skin are sensory organs that transfer information to your brain where it is integrated, which then catalyzes a motor response (most of the time). The world we model around us completely relies on the information from these organs. Because of this, the brain can be said to be experience dependent. Hence, why the brain is a memory system above all else.
There is considerable debate how memories are stored or retrieved. These traces of memories are called engrams. The most prevalent theory is that the patterns of neurons that were initiated when a memory was solidified are what reactivate when a memory is retrieved. These patterns all happen to be a part of a redundant circuitry, just in case if an engram is wiped out it can still be reformed by using alternative pathways. This is important to note, because this means our brains do not perfectly recall information, they reconstruct it. One counter (though they may coincide with each other) to this theory is the possibility that memory is stored in DNA or RNA through epigenetic changes (Bedecarrats, Chen, Pearce, Cai, Glanzman, 2018). In this study, the researchers were able to transfer memories from a trained slug to an untrained one by injecting it with RNA of the former. Usually the criticism against this study has to do with the supposed “conflation” of memory with the response showcased by the untrained Aplysia (an example being Mattei, 2018). This is an obfuscation from a distinction without a difference. In reality, this effect probably explains how instincts become ingrained within organisms over evolutionary time. The difference is simply the complexity involved and it’s quite possible both mechanisms are responsible for the propagation of memories. Refer to Abraham, Jones, and Glanzman, 2019 for further information on the topic.
In my opinion, emotions are probably the hardest aspect for laymen to conceptualize properly. At the most basic level emotions are simply a type of interoception (Critchley, Garfinkel, 2018). Interoception is the brain’s ability to receive information on the internal state of its physiological systems which allows it to maintain homeostasis. These fluctuations in physiology can be triggered by exogenous stimuli and depending on cultural/social differences these stimuli will have varying responses from the individual (Barrett, 2017). Those specific factors are very important as some studies and experiments have showcased that different emotions can have incredibly similar physiological responses. A frequently cited example is Dutton and Aron, 1974. Not only can different emotions have nearly the same physiological effects there are also overlapping physiological effects for different emotions! However, there is enough consistency that localization is reliable (Nummenmaa, Glerean, Hari, Hietanen, 2013). To give an example that many HBDers would probably relate to. Let’s say the sight of interracial sex angers me. The external input (interracial sex) is recieved by sensory organs (my eyes) and then because of accompanying mental dispositions (like racism) it triggers physiological responses like increased heart beat, higher blood pressure, your brain becomes flooded with catecholamines giving you a burst of energy, your muscles tense, breathing becomes more rapid, etc. This holistic process is itself what we refer to as emotion.
Now emotions are an important part of our decision making processes. You literally cannot make decisions without emotions. As emotions not only dictate the type of decisions we make, they also influence which path we choose when confronted with choice. Cold logic is far more subjective than most people would even realize. This brings forth a new question: What is the relationship between intelligence and emotional intelligence?
Before discussing this we need to first make it clear what exactly it is we’re talking about. Pumpkinperson recognizes that EQ is a very vague concept that isn’t distinguished well from others in his 2016 article. He states that: “And Goleman ruined his whole construct by not distinguishing between people who are smart at emotions (i.e. a master manipulator), and those who just have good emotions (someone who doesn’t feel the need to overeat).” The latter definition is closer to what we will be using. I believe the former is more akin to what we know of as “social intelligence”. For the sake of this post we will be defining it specifically as the ability to regulate and recognize one’s emotions, as I believe attributing any more to the concept will render it indistinguishable from Theory of Mind. Instead it would be more accurate to say that SQ and EQ are subsidiary abilities to TOM.
Since we’ve more or less established that emotions are a type of interoception it seems the best way to answer the previous question is to find exactly what the relationship between interoception and IQ is. To find this out we need to understand how one goes about quantifying this construct. Garfinkel, Seth, Barrett, Suzuki, Critchley, 2015 do just this by making the distinction between subjective and objective measurements of interoception and how both are required to make accurate assessment of one’s EQ (see table one for detailed examples). Now of course the authors cited never mention EQ once in the paper, but I believe conceptually what they are measuring is incredibly similar if not identical to EQ. For example, Garfinkel et al, 2016 found that people with higher anxiety had poorer abilities to accurately gauge their respiratory functions. This connection is further corroborated by some studies indicating that IQ and EQ overlap heavily in the neural networks that create said properties (Barbey, Colom, Grafman, 2012). Our own Racerealist provided considerable evidence that the mediating factor behind racial differences in aggression was education, not testosterone: “However, as I’ve noted last year (and as Alvarado, 2013 did as well), young black males with low education have higher levels of testosterone which is not noticed in black males of the same age group but with more education (Mazur, 2016). Since blacks of a similar age group have lower levels of testosterone but are more highly educated then this is a clue that education drives aggression/testosterone/violent behavior and not that testosterone drives it.
Mazur (2016) also replicated Assari, Caldwell, and Zimmerman’s (2014) finding that “Our model in the male sample suggests that males with higher levels of education has lower aggressive behaviors. Among males, testosterone was not associated with aggressive behaviors.”” This all seems to imply that both EQ and IQ are heavily integrated with one another. In fact, intelligence may be required to regulate one’s emotions and that this creates a feedback loop where emotional issues cause intellectual issues and vice versa. This of course has effects on the racial level that I will delve into in another blog post.
What exactly is intelligence? Pumpkinperson and I usually define it as the mental ability to adapt and I imagine most people would agree, but there is no actual agreed upon definition and I tend to see great variation when reading upon the subject. Truthfully, most variations are semantic rather than conceptual. Macdonald & Woodley, 2016 refer to intelligence as novel problem solving. They state: “Intelligence is usually distinguished from learning which subsumes a variety of mechanisms that allow the organism to take advantage of temporary regularities in its environment – paradigmatically classical and operant conditioning….Intelligence, on the other hand, assumes no environmental regularities – even temporary ones – nor does it refer to learning how to achieve a goal by observing others who have already solved the problem. Rather, as stated in Jerison’s definition, there is the implication that the organism has a goal and is integrating its knowledge in order to solve problems.” I see this definition the most in regards to Evolutionary Biology, and while it is not that different from Pumpkin and I’s definition, notice that we already established earlier that no aspect of cognition can be independent of one’s previous experience. So “novel problem solving” is a nonsensical term. Subsequently one cannot define mental constructs as being separate from the cultural/environmental conditions they are situated in because said mental constructs cannot develop or exist without input from these exogenous factors. Intelligence is holistically catalyzed, so terms like innate, novel, or potential cannot be accurate descriptors for this concept.
Unfortunately, intelligence is almost always coextensive with these terms. These types of issues can cause all sorts of conceptual misunderstandings in discourse on the subject. For example a common criticism thrown at intelligence testing is the idea that they are culturally biased. Now these types of critiques are appropriate when in reference to more menial aspects of cultural differences like how the Japanese read right to left instead of left to right like Americans, or how the former tends to think more collectively than the latter. However, when you divorce the idea of “culture free potential” and “intelligence” from one another it becomes clear that intelligence is not really distinguishable from the application of cultural knowledge. Obviously it doesn’t take some sort of genius to see the fallacy in trying to give a Ugandan who only speaks his native tongue and has never ventured outside of his country the Weschler in english and then call him stupid when he inevitably fails, but that is not what’s happening. The truth of the matter is that East Asians consistently score higher on Intelligence and academic achievement tests than do westerners whom the tests are supposedly biased in favor of.
Ultimately, since human environments are their culture (Fuentes, 2018) and intelligence is the cognitive expression of your imprinted culture it may controversially imply that some cultures are just superior to others. Now of course you can’t impose any idea of “superiority” without first defining a reference point. So if intelligence is simply the mental ability to adapt then what is a good hallmark of intelligence? Innovation for one, and as most HBDers are aware, 1st world countries like South Korea and Germany have the highest levels of Innovation. Historically, western societies have also had the most instances of technological innovation. Even Physical Anthropologists use technological complexity( among other things) to deduce differences in intelligence between species of hominins (of course there are some exceptions). So some cultures are superior at producing innovation and concurrently are better at fostering the development of intelligence than others.
Originally I was planning on dedicating this section to the supposed construct validity of IQ tests which are currently the most accurate measures we have of intelligence. However, recently I came across what I believe is the single best critique(some may disagree) of IQ that I’ve read (Garrison, 2004). Garrison states in his section on validity: “In traditional psychometric theory, validity is defined as the degree to which a test measures what it claims to measure. I want to first point out the oddity of this formulation. For example, how does the reader respond to this: my ruler is valid to the degree to which it measures length? Is it normal practice to begin ruler validation by asking this seemingly circular question? Rulers by definition measure length. Note as well that by asking what a test measures the assumption that something is being measured goes unchallenged.” Notice, Garrison correctly points out the absurdity of construct validity as a sort of litmus test on whether a test supposedly measures what it purports to. Its circularity renders the use of construct validity in this way as fallacious and simultaneously charges of its supposed lack of construct validity (like Richardson, Norgate, 2015) are critically impotent.
In Garrison’s section on the “Scientific status of Psychometry” he states: “ The development of measurement has generally progressed from classification (qualities), to topology (comparisons) to metrication (measurements) (Berka, 1983). Classification concepts such as “cold” become topological when comparisons are used, such as colder than . . . . Thus they “enable us, not only to establish the sameness (or difference), but also to mutually compare at least two objects which possess a given property and, consequently, to arrange them into a sequence” (Berka, 1983, p. 6). he then goes on to claim that IQ tests only satisfy the first two criteria: “For example, norm-referenced achievement tests offer results in terms of percentile ranks, not delineations of what a student does or does not know about a given field of study, let alone diagnoses of the cause of difficulty. Put another way, scoring in the 70th percentile only indicates how well one did relative to the norm; it does not indicate 70 percent of required material was mastered. Thus the test remains at the topological level,” and because of this “The same problem exists with so-called measures of ability. Nash (1990) contends that norm-referenced ability tests only provide rank order information. “Students are ranked, in effect, by their ability to correctly answer test items, but it is inaccurate to argue that their ‘cognitive ability’ is therefore being measured” (Nash, 1990, p. 63).”. Of course this idea is false for reasons already iterated earlier in this post. Does answering test items correctly not require cognitive ability? However, Garrison believes that because “The validity discourse about test score meaning relative to testing purpose is based on value not residing in things or phenomenon themselves, but in their relation to subjects. Length, however, is a property of an object.” IQ tests are actually assessments of social value not measurements. First I need to clarify that there is a distinction between Criterion-referenced tests (CRT) and Norm-referenced tests (NRT), IQ is an example of the latter, and the former is indeed a measurement of a students knowledge in a particular field, not simply a comparison to the rankings of other students. Garrison may be correct in saying that because of this, IQ is just an assessment but scores on NRTs will highly predict those on CRTs and vice versa. So this distinction may matter little to the practical utility of IQ tests. But maybe I’m wrong, maybe its norm referencing isn’t the only reason it’s “just an assessment” and maybe the CRT’s don’t provide extra corroboration to these tests. Even If IQ is just an “assessment” instead of a “measurement” why does that matter? Moreover, even if it’s just an assessment of social value…so what? Do we not value the skills that are learned in school? Should we prioritize something else? Does he believe this subjectivity makes something less scientific? All definitions are inherently circular and thus are subjectively created. If we define this social value as intelligence is it not an ‘“assessment” of intelligence? What does this dichotomy really matter to the overall purpose of these tests?
In this article we’ve clarified what intelligence is, what emotions are, how both of these are catalyzed biologically. I’ve also cleared up logical misconceptions and criticisms on the subjects in the process: IQ is not something that is coextensive with innate potential and consciousness is not a biological mystery (at least in the sense of what it is). Furthermore, a lot of these ideas are not compatible with the consensus within HBD circles. If HBD wants to be taken seriously it needs to either address these issues and inconsistencies or get used to being treated like it’s astrology.
I’m going to go ahead and end this paper here. Simply because we’re already around 4,000 words and I’m sure I’ve bored half of you to death in the process. In the next part I’ll be going more into depth on the racial differences in EQ, what a culture neutral (not culture-free) IQ test may look like, our concept of personality, and the evolution of intelligence.
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.
I have been an avid reader and interested in astronomy/space ever since I could remember. I remember really loving Stephen Hawking and his documentaries on black holes. I would read anything I could find on constellations and stars. From there I went on to reading sci-fi. I then recall seeing The Martian Chronicles by Ray Bradbury and from then on I had become interested in sci-fi writing. But, as I grew older, I drifted away from sci-fi and now only read non-fiction. Then when I got older I got into ‘HBD’ (chronicled here) and along with it evolution—but, unlike other ‘HBDers’ I became enamored with the work of Gould, while some of my favorite books come from him. Gould wrote a lot about evolutionary contingency—the degree to which an outcome could be different. Evolutionary contingency is a big topic in philosophy of biology, and Bradbury has a great short story on this type of contingency.
Ray Bradbury is an interesting author—one who has many short stories and regular books. One of my favorite stories from Bradbury is one called A Sound of Thunder which chronicled a time machine company who let people go back in time to hunt any animal they’d like—if you want to take down the ancestor of a whale before it became aquatic, just name the place and they will send you there. They were told to only stay on the path laid out by the time machine company—animals they could shoot were marked with red paint, presumably those animals would have died anyway so killing them would not change any outcomes. The text from Bradbury is worth quoting in full, as it wonderfully captures the thought of evolutionary contingency:
He indicated a metal path that struck off into green wilderness, over streaming swamp, among giant ferns and palms. “And that,” he said, “is the Path, laid by Time Safari for your use, It floats six inches above the earth. Doesn’t touch so much as one grass blade, flower, or tree. It’s an anti-gravity metal. Its purpose is to keep you from touching this world of the past in any way. Stay on the Path. Don’t go off it. I repeat. Don’t go off. For any reason! If you fall off, there’s a penalty. And don’t shoot any animal we don’t okay.”
“Why?” asked Eckels.
They sat in the ancient wilderness. Far birds’ cries blew on a wind, and the smell of tar and an old salt sea, moist grasses, and flowers the color of blood.
“We don’t want to change the Future. We don’t belong here in the Past. The government doesn’t like us here. We have to pay big graft to keep our franchise. A Time Machine is finicky business. Not knowing it, we might kill an important animal, a small bird, a roach, a flower even, thus destroying an important link in a growing species.”
“That’s not clear,” said Eckels.
“All right,” Travis continued, “say we accidentally kill one mouse here. That means all the future families of this one particular mouse are destroyed, right?”
“And all the families of the families of the families of that one mouse! With a stamp of your foot, you annihilate first one, then a dozen, then a thousand, a million, a billion possible mice!”
“So they’re dead,” said Eckels. “So what?”
“So what?” Travis snorted quietly. “Well, what about the foxes that’ll need those mice to survive? For want of ten mice, a fox dies. For want of ten foxes a lion starves. For want of a lion, all manner of insects, vultures, infinite billions of life forms are thrown into chaos and destruction. Eventually it all boils down to this: fifty-nine million years later, a caveman, one of a dozen on the entire world, goes hunting wild boar or saber-toothed tiger for food. But you, friend, have stepped on all the tigers in that region. By stepping on one single mouse. So the caveman starves. And the caveman, please note, is not just any expendable man, no! He is an entire future nation. From his loins would have sprung ten sons. From their loins one hundred sons, and thus onward to a civilization. Destroy this one man, and you destroy a race, a people, an entire history of life. It is comparable to slaying some of Adam’s grandchildren. The stomp of your foot, on one mouse, could start an earthquake, the effects of which could shake our earth and destinies down through Time, to their very foundations. With the death of that one caveman, a billion others yet unborn are throttled in the womb. Perhaps Rome never rises on its seven hills. Perhaps Europe is forever a dark forest, and only Asia waxes healthy and teeming. Step on a mouse and you crush the Pyramids. Step on a mouse and you leave your print, like a Grand Canyon, across Eternity. Queen Elizabeth might never be born, Washington might not cross the Delaware, there might never be a United States at all. So be careful. Stay on the Path. Never step off!”
“I see,” said Eckels. “Then it wouldn’t pay for us even to touch the grass?”
“Correct. Crushing certain plants could add up infinitesimally. A little error here would multiply in sixty million years, all out of proportion. Of course maybe our theory is wrong. Maybe Time can’t be changed by us. Or maybe it can be changed only in little subtle ways. A dead mouse here makes an insect imbalance there, a population disproportion later, a bad harvest further on, a depression, mass starvation, and finally, a change in social temperament in far-flung countries. Something much more subtle, like that. Perhaps only a soft breath, a whisper, a hair, pollen on the air, such a slight, slight change that unless you looked close you wouldn’t see it. Who knows? Who really can say he knows? We don’t know. We’re guessing. But until we do know for certain whether our messing around in Time can make a big roar or a little rustle in history, we’re being careful. This Machine, this Path, your clothing and bodies, were sterilized, as you know, before the journey. We wear these oxygen helmets so we can’t introduce our bacteria into an ancient atmosphere.”
This passage from Bradbury wonderfully illustrates evolutionary—historical—contingency. Things could have been different—this is the basis of the contingency argument. The universe does not repeat itself—if we were to replay the tape of life we would get a completely different outcome—Lane (2015) states maybe octopi would rule the earth? We could replay the tape of life, have it go exactly as it did to lead up to today, change ONE SEEMINGLY MINISCULE THING (say, stepping on a bug that did not die) which would then cascade throughout history leading to a change in the future. Evolution is full of passive trends, with no indication that—for example with body plans—that there is a drive to become more complex—it is passive (Gould, 1996: 207):
All the tests provide evidence for a passive trend and no drive to complexity. McShea found twenty-four cases of significant increases or decreases in comparing the range of modern descendants with an ancestor (out of a potential sample of ninety comparisons, or five groups of mammals, each with six variables measured in each of three ways; for the other comparison, average descendants did not differ significantly from ancestors). Interestingly, thirteen of these significant changes led to decreases in complexity, while only nine showed an increase. (The difference between thirteen and nine is not statistically significant, but I am wryly amused, given all traditional expectation in the other direction, that more comparisons show increasing rather than decreasing complexity.
Gould first put forth his contingency argument in Wonderful Life—any replay would be different then the next. Gould critiqued the increasing complexity claim, arguing that diversification is always accompanied by decimation—once a mass extinction (say, an asteroid impact) occurs, there will then be subsequent diversification after the decimation.
We have no idea why certain organisms persisted over others after periods of decimation—and ‘adaptation’ to environments cannot be the whole story. Out of all of Gould’s writing that I have read in my life, this passage is one of my favorites as it perfectly captures the problem at hand:
Wind the tape of life back to Burgess times, and let it play again. If Pikaia does not survive in the replay, we are wiped out of future history—all of us, from shark to robin to orangutan. And I don’t think that any handicapper, given Burgess evidence as known today, would have granted very favorable odds for the persistence of Pikaia.
And so, if you wish to ask the question of the ages—why do humans exist?—a major part of the answer, touching those aspects of the issue that science can treat at all, must be: because Pikaia survived the Burgess decimation. This response does not cite a single law of nature; it embodies no statement about predictable evolutionary pathways, no calculation of probabilities based on general rules of anatomy or ecology. The survival of Pikaia was a contingency of “just history.” I do not think that any “higher” answer can be given, and I cannot imagine that any resolution could be more fascinating. We are the offspring of history, and must establish our own paths in this most diverse and interesting of conceivable universes—one indifferent to our suffering, and therefore offering us maximal freedom to thrive, or to fail, in our own chosen way. (Gould, 1989: 323)
Contingency is about counterfactuals—what could have happened, what could have been, or what would have been had some certain condition changed, with everything before that occurring as usual. Bradbury’s A Sound of Thunder wonderfully illustrates the contingency of the evolutionary process—change one seemingly small, minuscule thing in the past and this could snowball and cascade to huge changes in the future—we may never have existed or we would have existed but have been radically different. If we could go back in time and, say, crush a butterfly and see the changes it would have made, we could say that the event that caused the future to change was the crushing of that butterfly—this could have, eventually, led to the non-existence of a certain group of people or a certain group of animals which would have radically changed the outcome of the world—both the natural and human world.
So, if we could replay life’s tape from the very beginning, I do believe that life as we know it would be different—for if we played it from the beginning, we could have a scenario as described by Bradbury—everything could go exactly the same with one small seemingly minuscule change snowballing into a world that we would barely recognize.
The concept of “race” stretches back as long as human civilization. The concept of “racism” also stretches back just as far with it—they seem to be intertwined. There is a consensus, though, the term was constructed during the European Age of Exploration. This claim though, is false. The concept actually goes back at least 5,000 years. By looking at the art and reading the myths of these ancient civilizations, we can see that the social constructivist claim about race—that it is a recent creation—is false. They also described their physical features and also attempted to explain behavioral differences between races based on the limited knowledge they had in their day.
Sarich and Miele (2004) state that the PBS documentary on race—which is largely the main reason why they wrote their book Race: The Reality of Human Difference—claimed that race is a human invention and that since we create it we can then “unmake it.” We can look at art from ancient civilizations and see that they did sort people into groups based on their skin color and other physical characters. Each civilization, of course, thought itself and its racial features to be ‘superior’ to the others they encountered. The ancients used the set of observable features to describe what we now call “races.”
Our first trip on this long journey to understand the history of race is India. The earliest hints of what would become the caste system were written around 5kya. In the Rig Veda, a description of the Arya(n) invasion in the Indus valley where a dark-skinned people lived. The god of the Arya(n)s Indra “is described as “blowing away with supernatural might from earth and from the heavens the black skin which Indra hates” (Gossett, 1997: 3-4). They also called these dark-skinned people “Anasahs” which meant “the noseless people.” They then describe Indra killing all of the dark-skinned people and conquering the Indus for the Arya.
Sarich and Miele (2004: 47-48) note that the peoples that Indra hated were called Dasas—broad-nosed worshippers of the phallus. Even when Alexander the Great’s army reached India and described the Indians in the south of the country as some of the darkest people they have seen, they still made the distinction between Indians and Africans—by their hair type—so this tells us that race is more than ‘skin deep’ to the Greeks. Race, then, was known for thousands of years BEFORE the Age of Exploration.
We can look to ancient China, too, to see instances of racial descriptions and then racism along with it. For instance, a Chinese writer described yellow-haired, blue-eyed people from a distant province, “who greatly resembeled monkeys from whom they are descended” (Gossett, 1997: 4). Another Chinese legend describes differences between themselves and a brabarian tribe. A Chinese emperor stated that he would give his daughter to whomever slayed the chieftan he was having problems with. Then, the palace dog comes back with the head of the chieftan. The emperor did not go back on his word; he gave the dog his daughter and the resulting children were “fond of living in high altitudes and averse to plains” (Gossett, 1997: 4).
Like other civilizations, the ancient Han Chinese regarded other groups they came into contact with as barbarians. They were especially taken aback by the odd appearance of one group, the Yuehzi, because of their hairy, white, ruddy skin and their prominent noses, which the Chinese likened to those of monkeys.
The Han Chinese applied the term “Hu” to barbarians like the Yuehzi who had “deep eye sockets, prominent noses, and beards.” But they did not apply it to the Qiang, another barbarian group, who had a Mongoloid appearance and among whom some of the Yuezhi lived. Both groups were denigrated as uncivilized and inferior to the Chinese, but the Qiang were deemed to belong to the same racial stock, whereas the Yuezhi were viewed as being part of a very different stock, not only barbarian but ugly and monkey-like to boot.
The Egyptians used a color-coding system—red (themselves), yellow (for their eastern enemies), black (Africans), and white (those from the north). The Eygptians also accurately depicted Africans as early as the third century BCE, describing them exactly how 19th-century European anthropologists would. Below is a picture of how the Egyptians depicted these groups.
There is, also, an interesting bit about colorism—discrimination based on skin color—here:
Color prejudice, says one writer, depended on which ethnic group held sway. When the lighter-skinned Egyptians were dominant they referred to the darker group as “the evil race of Ish.” On the other hand, when the darker-skinned Egyptians were in power, they resorted to calling the lighter-skinned people “the pale, degraded race of Arvad.” (Gossett, 1997: 4)
The Jews are some of the oldest peoples on earth, so they should then have some stories about their encounters with different races. One of the oldest, thought to be first, racist sayings was asked by the prophet Jeremiah who said “Can the Ethiopian change his skin or the leopard his spots?” The Jews are said to have ‘invented’ anti-black racism (Gossett, 1997: 5; Sarich and Miele, 2004), but this has been contested (Goldenberg, 1998). Take the full text from Gossett on Ham:
The most famous example of racism among the Jews is found in the legends which greew up concerning Ham, the son of Noah. The account in Genesis tells us of Ham’s expressing contempt for his father because Noah had become drunk and was lying in a naked stupor. Noah’s other sons had covered their father’s nakedness, averting their eyes. Noah blessed the descendants of Shem and Japeth, his other sons, but cursed the descendants of Ham. There is some confusion in the account in Genesis because it is not clear whether the curse was to be visited upon Ham or upon Canaan, Ham being a later insertion. Nothng is said in Genesis about the descendants of either Ham or Canaan being Negroes. This idea is not found untl the oral traditions of the Jews were collected in the Babylonian Talmud from the second century to the sixth centry A.D. In this source, the descendants of Ham are said to be cursed by being black. In the Talmud, there are several contradictory legends concerning Ham—onoe that God forbade anyone to have sexual relations on the Ark and Ham disobeyed this command. Another story is that Ham was cursed with blackness because he resented the fact that his father desired to have a fourth son. To prevent the birth of a rival heir, Ham is said to have castrated his father. Elsewhere in the Talmud, Ham’s descendants are depicted as being led into captivity with their buttocks uncovered as a sign of degredation.
Greeks and Romans
The Greeks and the Romans are really interesting. Being near the intersection of the Medditerranean, they would have seen many different races of people—and this is reflected in their art and legends. The Greek myth of Phaethon, for example, shows that the Greeks knew that skin color was a function of climate.
In the story, Phaethon asked his father to drive the sun chariot, using it only for the day. He could not control the chariot so it came to close to the earth in some regions, burning the people there while for the people in the north he drove too far away from the earth, ligtening their skin. Greek and Roman myths, in fact, show exactly how things change and that if we had a different reference point—like the Greeks and Romans did—we would then create different theories of ‘intelligence’:
“The nations inhabiting the cold places and those of Europe are full of spirit but somewhat deficient in intelligence and skill, so that they continue comparatively free, but lacking in political organization and the capacity to rule their neighbors. The peoples of Asia on the other hand are intelligent and skillful in temperament, but lack spirit, so that they are in continuous subjection and slavery. But the Greek race participates in both characters, just as it occupies the middle position geographically, for it is both spirited and intelligent; hence it continues to be free and to have very good political institutions, and to be capable of ruling all mankind if it attains constitutional unity.” (Pol. 1327b23-33, my italics)
Views of direct environmental influence and the porosity of bodies to these effects also entered the military machines of ancient empires, like that of the Romans. Offices such as Vegetius (De re militari, I/2) suggested avoiding recruiting troops from cold climates as they had too much blood and, hence, inadequate intelligence. Instead, he argued, troops from temperate climates be recruited, as they possess the right amount of blood, ensuring their fitness for camp discipline (Irby, 2016). Delicate and effemenizing land was also to be abandoned as soon as possible, according Manilius and Caesar (ibid). Probably the most famous geopolitical dictum of antiquity reflects exactly this plastic power of laces: “soft lands breed soft men”, according to the claim that Herodotus attributed to Cyrus. (Meloni, 2017: 41-42)
The Roman historian Vitruvius “attributed the keen intelligence of his countrymen to the rarity of the atmosphere and to the heat. The less fortunate northern peoples, “being enveloped in a dense atmosphere, and chilled by moisture from the obstructing air … have but a sluggish intelligence”” (Gossett, 1997: 7). How convenient—people at the time thought they were ‘superior’ to others and then attempted to justify it on the basis of environmental—eventually evolutionary—differences. However, the Greek theory of humors. Such accounts, though, only speak to how the Greeks thought that the environment shaped individuals, not shared traits of the group. Such differences were thought to be almost immediately reversible. They believed that one could take a person who grew up in another environment who, therefore, had a different temperment which could be changed by switching his environment.
Thus if there were, say, a microregion of Germany where “Asiatic” environmental conditions prevailed, a person who settled in that microregion would end up with Asian attributes. Thus, humoral accounts of human diversity focused on the way environments shape individuals, rather than the way populations share traits. (Smith, 2016: 85)
The Greeks and the Romans, ironically, seemed to be really big on environmentalism—the thesis that environment drives the proliferation of traits and that changing the environment can change ones phenotypic traits. While this is not wholly true, there is a kernel of truth here.
Sarich and Miele (2004: 51) describe different ancient scholar’s writings on their observations of racial differences:
The most detailed surviving description of the racially denning characteristics of black Africans from the classical world appears in The Moretum, a poem attributed to Virgil (circa 1st century AD). A female character named Scybale. is described as “African in race—her hair tightly curled, lips thick, color dark, chest broad, breasts pendulous, belly somewhat pinched, legs thick, and feet broad and ample.” In his book Blacks in Antiquity: Ethiopians in the Greco-Roman Experience, Frank M. Snowden comared the description with portrayls by twentieth-century anthropologists E. A Hootn and M. J Herskovits. For example, Hootn described the “outstanding features of the ancient specialized Negro division of manking” as “narrow heads and wide noses, thick lips and thin legs, protruding jaws and receding chins, integument rich in pigment but poor in hairy growth, flat feet and round foreheads, tiny curls and big smiles.”
Snowden concluded: “While the author of The Moretum was writing poetry, not anthropology,” his description of the distinguishing racial characteristics of black Africans “is good anthropology; in fact, the ancient and modern phraseology is so similar that the modern might be considered a translation of the ancient” (emphasis added).
I’m sure most have heard the popular ‘myth’ that God burnt blacks by cooking them too long. Come to find out, there is a real basis for this myth. The Native Americans thought that white people weren’t baked enough, blacks were baked too much and they were—like Goldilocks—juuuuust right:
Earthmaker made the world with trees and fields, with rivers, lakes, and springs, and with hills and valleys. It was beautiful. However, there weren’t any humans, and so one day he decided to make some.
He scooped out a hole in a stream bank and lined the hole with stones to make a hearth, and he built a fire there. Then he took some clay and made a small figure that he put in the hearth. While it baked, he took some twigs and made tongs. When he pulled the figure out of the fire and had let it cool, he moved its limbs and breathed life into it, and it walked away. Earthmaker nonetheless realized that it was only half-baked. That figure became the white people.
Earthmaker decided to try again, and so he made another figure and put it on the hearth. This time he took a nap under a tree while the figure baked, and he slept longer than he intended. When he pulled the second figure out of the fire and had let it cool, he moved its limbs and breathed life into it, and it walked away. Earthmaker realized that this figure was overbaked, and it became the black people.
Earthmaker decided to try one more time. He cleaned the ashes out of the hearth and built a new fire. Then he scooped up some clay and cleaned it of any twigs or leaves, so that it was pure. He made a little figure and put it on the hearth, and this time he sat by the hearth and watched carefully as the figure baked. When this figure was done, he pulled it out of the fire and let it cool. Then he moved its limbs and breathed life into it, and it walked away. This figure was baked just right, and it became the red people. (A Potawatomi Story)
The first peoples to describe Africans in a racist manner was not Europeans, it was the Arabs—Islamics. They held slaves long before Europeans; they even castrated their slaves. Jahiz of Basra described Africans as “people of black color, flat noses, kinky hair.”…despite their dimness, their boundless stupidity, their crude prceptions and their evil dispositions” is how Jahiz of Basra described Africans. Ibn Khaldun stated “The only people who accept slavery are the Negroes, owing to their low degree of humanity and their proximity to the animal stage.” Nasir al-Din Tusi stated “Many have observed that the ape is more teachable than the Zanji [African].” (All quotes from Sarich and Miele, 2004: 60).
What this little tour of the concept of race throughout history tells us one thing: The concept ‘race’ is not a European invention—races were not socially constructed in 1492. They were constructed thousands of years in the past by many different peoples who had different explanations for the racial differences they had observed. While some of them, for their time, are great explanations for the observed differences, there was an element of racial prejudice, even all of those thousands of years ago. Yes, race is partly socially constructed (as evidenced here) but that social construction has a real, biological basis behind it.
It is obvious that the concept of ‘race’ and ‘racism’ went hand-in-hand all throughout antiquity. It is only today, it seems, that we can attempt to use the concept of race without having any ‘racist’ undertones. Though, the tour we went on proves one thing: race exists and was known to have existed for thousands of years.