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The Conceptual Impossibility of Hereditarian Intelligence
3650 words
Introduction
For more than 100 years—from Galton and Spearman to Burt, Jensen, Rushton, Lynn and today’s polygenic score enthusiasts—hereditarian thinkers have argued that general intelligence is a unitary, highly heritable biological trait and that observed individual and group level differences in IQ and it’s underlying “g” factor primarily reflect genetic causation. The Bell Curve brought such thinking into the mainstream from obscure psychology journals, and today hereditarian behavioral geneticists claim that 10 to 20 percent of the variance in education and cognitive performance has been explained by GWA studies (see Richardson, 2017). The consensus is that intelligence within and between populations is largely genetic in nature.
While hereditarianism is empirically contested and morally wrong, the biggest kill-shot is that it is conceptually impossible, and one can use many a priori arguments from philosophy of mind to show this. Donald Davidson’s argument against the possibility of psychophysical laws, Kripke’s reading of Wittgenstein, and Nagel’s argument from indexicality can be used to show that hereditarianism is a category error. Ken Richardson’s systems theory can then be used to show that g is an artifact of dynamic systems (along with test construction), and Vygotsky’s cultural-historical psychology shows that higher mental functions (which hereditarians try to explain biologically) originate as socially scaffolded, inter-mental processes mediated by cultural tools and interactions with more knowledgeable others, not individual genetic endowment.
Thus, these metaphysical, normative, systemic, developmental and phenomenological refutations show that hereditarianism is based on a category mistake. Ultimately, what hereditarianism lacks is a coherent object to measure—since psychological traits aren’t measurable at all. I will show here how hereditarianism can be refuted with nothing but a priori logic, and then show what really causes differences in test scores within and between groups. Kripke’s Wittgenstein and the argument against the possibility of psychophysical laws, along with a Kim-Kripke normativity argument against hereditarianism show that hereditarianism just isn’t a logically tenable position. So if it’s not logically tenable, then the only way to explain gaps in IQ is an environmental one.
I will begin with showing that no strict psychophysical laws can link genes/brain states to mental kinds, then demonstrating that even the weaker functional-reduction route collapses at the very first step because no causal-role definition of intentionality (intelligence) is possible. After that I will add the general rule following considerations from Kripke’s Wittgenstein and then add it to my definition of intelligence, showing that rule-following is irreducibly normative and cannot be fixed by any internal state and that no causal-functional definition is possible. Then I will show that the empirical target of hereditarianism—the g factor—is nothing more than a statistical artifact of historically contingent, culturally-situated rule systems and not a biological substrate. These rule systems do not originate internally, but they develop as inter-mental relations mediated by cultural tools. Each of these arguments dispenses with attempted hereditarian escapes—the very notion of a genetically constituted, rank-orderable general intelligence is logically impossible.
We don’t need “better data”—I will demonstrate that the target of hereditarian research does not and cannot exist as a natural, measurable, genetically-distributed trait. IQ scores are not measurements of a psychological magnitude (Berka, 1983; Nash, 1990); no psychophysical laws exist that can bridge genes to normative mental kinds (Davidson, 1979), and the so-called positive manifold is nothing more than a cultural artifact due to test construction (Richardson, 2017). Thus, what explains IQ variance is exposure to the culture in which the right rules are used regarding the IQ test.
Psychophysical laws don’t exist
Hereditarianism implicitly assumes a psychophysical law like “G -> P.” Psychophysical laws are universal, necessary mappings between physical states and mental states. To reduce the mental to the physical, you need lawlike correlations—whenever physical state P occurs, mental state M occurs. These laws must be necessary, not contingent. They must bridge the explanatory gap from the third-personal to the first-personal. We have correlations, but correlations don’t entail identity. If correlations don’t entail identity, then the correlations aren’t evidence of any kind is psychophysical law. So if there are no psychophysical laws, there is no reduction and there is no explanation of the mental.
Hereditarianism assumes type-type psychophysical reduction. Type-type identity posits that all instances of a mental type correspond to all instances of a physical type. But hereditarians need bridge laws—they imply universal mappings allowing reduction of the mental to the measurable physical. But since mental kinds are anomalous, type-type reduction is impossible.
Hereditarians claim that genes cause g which then cause intelligence. This requires type-type reduction. Intelligence kind = g kind = physical kind. But g isn’t physical—it’s a mathematical construct, the first PC. Only physical kinds can be influenced by genes;nonphysical kinds cannot. Even if g correlates with brain states, correlation isn’t identity. Basically, no psychophysical laws means no reduction and therefore no mental explanation.
If hereditarianism is true, then intelligence is type-reducible to g/genes. If type-reduction holds, then strict psychophysical laws exist. So if hereditarianism is true, then strict psychophysical laws exist. But no psychophysical laws exist, due to multiple realizablilty and Davidson’s considerations. So hereditarianism is false.
We know that the same mental kind can be realized in different physical kinds, meaning that no physical kind correlates one-to-one necessarily with a mental kind. Even if we generously weaken the demand from strict identity to functional laws, hereditarian reduction still fails (see below).
The Kim-Kripke normativity argument
Even the only plausible route to mind-body reduction that most physicalists still defend collapses a priori for intentional/cognitive states because no causal-functional definition can ever capture the normativity of meaning and rule following (Heikenhimo, 2008). Identity claims like water = h2O only work because the functional profile is already reducible. Since the functional profile of intentional intelligence is not reducible, there is no explanatory bridge from neural states to the normativity of thought. So identity claims fail—this just strengthens Davidson’s conclusions. Therefore, every reductionist strategy that could possibly license the move from “genetic variance -> variation in intelligence” is blocked a priori.
(1) If hereditarianism is true, then general intelligence as a real cognitive capacity must be reducible to the physical domain (genes, neural states, etc).
(2) The only remaining respectable route to mind-body reduction of cognitive/intentional processes is Kim’s three-step functional-reduction model.
(C1) So if hereditarianism is true, then general intelligence must he reducible to Kim’s three-step functional-reduction model.
(3) Kim-style reduction requires—as its indispensable first step—an adequate causal-functional definition of the target property (intelligence, rule-following, grasping meaning, etc) that preserves the established normative meaning of the concept without circularly using mental/intentional vocabulary in the definiens.
(4) Any causal-functional definition of intentional/cognitive states necessarily obliterates the normative distinction between correct and incorrect application (Kripke’s normativity argument applied to mental content).
(C2) Therefore, no adequate causal-functional definition of general intelligence is possible, even in principle.
(5) If no adequate causal-functional definition is possible, then Kim-style functional reduction of general intelligence is impossible.
(C3) So Kim-style functional reduction of general intelligence is impossible.
(C4) So hereditarianism is false.
A hereditarian can resist Kim-Kripke in 4 ways but each fails. (1) They can claim intelligence need not be reducible, but then genes cannot causally affect it, dissolving hereditarianism into mere correlation. (2) They can reject Kim-style reduction in factor of non-reductive or mechanistic physicalism, but these views still require functional roles and collapse under Kim’s causal exclusion argument. (3) They can insist that intelligence has a purely causal-functional definition (processing efficiency or pattern recognition), but such definitions omit the normativity of reasoning and therefore do no capture intelligence at all. (4) They can deny that normativity matters, but removing correctness conditions eliminates psychological content and makes “intelligence” unintelligible, destroying the very trait hereditarianism requires. Thus, all possible routes collapse into contradiction or eliminativism.
The rule-following argument against hereditarianism
Imagine a child who is just learning to add. She adds 68+57=125. We then say that she is correct. Why is 125 correct and 15 incorrect? It isn’t correct because she feels sure, because someone who writes 15 could be just as sure. It isn’t correct because her brain lit up in a certain way, because the neural pattern could also belong to someone following a different rule. It isn’t correct because all of her past answers, because all past uses were finite and are compatible with infinitely many bizzare rules that only diverge now. It isn’t correct because of her genes or any internal biological state, because DNA is just another finite physical fact inside of her body.
There is nothing inside of her head, body or genome that reaches out and touches the difference between correct and incorrect. But the difference is real. So where does it lie? It lives outside of her in the shared community practices. Correctness is a public status, not a private possession. Every single thing that IQ tests reward—series completion, analogies, classification, vocabulary, matrix reasoning—is exactly this kind of going on correctly. So every single point on an IQ test is an act whose rightness is fixed in the space of communal practice. What we call “intelligence” exists only between us—between the community, society and culture in which an individual is raised.
Intelligence is a normative ability. To be intelligent is to go on in the same way, to apply concepts correctly, to get it right when solving new problems, reasoning, understanding analogies, etc. So intelligence = rule-following (grasping and correctly applying abstract patterns).
Rule following is essentially normative—there is a difference between seeming right and being right. Any finite set of past performances is compatible with an infinite set of many rules. No fact about an individual—neither physical nor mental content—uniquely determines the rule they are following. So no internal state fixes the norm. Thus, rule following cannot be constituted by internal/genetic states. No psychophysical law can connect G to correct rule following (intelligence).
Therefore rule-following is set by participation in a social practice. Therefore, normative abilities (intelligence, reasoning, understanding) are socially, not genetically, constituted. So hereditarianism is logically impossible.
At its core, intelligence is the ability to get it right. Getting it right is a social status conferred by participation in communal practices. No amount of genetic or neural causation can confer that status—because no internal state can fix the normative fact. So the very concept of “genetically constituted general intelligence” is incoherent. Therefore, hereditarianism is logically impossible.
(1) H -> G -> P
Hereditarianism -> genes/g -> normative intelligence
(2) P -> R
Normative intelligence -> correct rule-following.
(3) R -> ~G
Rule following cannot be fixed by internal physical/mental states.
So ~(G -> P)
So ~H.
The Berka-Nash measurement objection
This is a little-known critique of psychology and IQ. First put forth in Karel Berka’s 1983 book Measurement: It’s Concepts, Theories, and Problems, and then elaborated on in Roy Nash’s (1990) Intelligence and Realism: A Materialist Critique of IQ.
If hereditarianism is true, then intelligence must be a measurable trait (with additive structure, object, and units) that genes can causally influence via g. If intelligence is measurable, then psychophysical laws must exist to map physical causes to mental kinds. But no such measurability or laws exist. Thus, hereditarianism is false.
None of the main, big-name hereditarians have ever addressed this type of argument. (Although Brand et al, 2003 did attempt to, their critique didn’t work and they didn’t even touch the heart of the matter.) Clearly, the argument shows that hereditarian psychology is weak to such critique. The above argument shows that IQ is quasi-quantification, without an empirical object, no structure, or lawful properties
The argument for g is circular
“Subtests within a battery of intelligence tests are included n the basis of them showing a substantial correlation with the test as a whole, and tests which do not show such correlations are excluded.” (Tyson, Jones, and Elcock, 2011: 67)
g is defined as the common variance of pre-selected subtests that must correlate. Subtests are included only if they correlate. A pattern guaranteed by construction cannot be evidence of a pre-existing biological unity. So g is a tautological artifact, not a natural kind that genes can cause.
Hereditarians need g to be a natural kind trait that genes can act upon. But g is an epiphenomenal artifact due to test construction produced by current covariation of culturally specific cognitive tasks in modern school societies. Artifacts of historically contingent cultural ecologies are not natural kind traits. So g is not a natural kind. So hereditarianism is false.
The category error argument
Intelligence is a first-person indexical act. g is a third-person statistical abstraction. There can be no identity between a phenomenonal act and a statistical abstraction. So g cannot be intelligence—no reduction is possible.
There is no such thing as genetically constituted general intelligence since intelligence is a rational normative competence, the g factor is an epiphenomenal artifact of a historically contingent self-organizing cultural-cognitive ecology, and higher psychological functions originate as social relations mediated by cultural tools which only later appear individual. Hereditarianism tries to explain a normative status with causal mechanisms, a dynamic cultural artifact with a fixed trait, and an inter-mental function with intra-cranial genetics.
g is a third-person statistical construct. Intelligence, as a psychological trait, consists of first-person indexical cognitive acts. Category A – third-person, impersonal (g, PGS, allele frequencies, brain scans). Category B – first-person, subjective, experiential).
Genetic claims assert that differences in g (category A) are caused by differences in genes and that this then explains differences in intelligence (category B). For such claims to be valid, g (category A) must be identical to intelligence (category B). But g has no first-person phenomenology meaning no one experiences using g, while intelligence does. So g (category A) cannot be identical to intelligence (category B).
Thus, claiming genes cause differences in g which then explain group differences in intelligence commits a category error, since a statistical artifact is equated with a lived, psychological reality.
A natural-kind trait must be individuated independent of the measurement procedure. g is individuated only by the procedure (PC1 extracted from tests chosen for their intercorrelations). Therefore, g is not a natural-kind trait. Only natural kinds can plausibly be treated as biological traits. Thus, g is not a biological trait.
Combining this argument with the Kim-Kripke normativity argument shows that hereditarians don’t just reify a statistical abstraction, they try to reduce a normative category into a descriptive one.
Vygotsky’s social genesis of higher functions
Higher psychological functions originate as social relations mediated by cultural tools which only later appear individual. If hereditarianism is true, then higher psychological functions originate as intra-individual genetic endowments. A function cannot originate both as inter-mental social relations and as intra-individual genetic endowments. So hereditarianism is false.
Intelligence is not something a sole individual possesses—it is something a person achieves within a cultural-historical scaffold. Intelligence is not an individual possession that cab be ranked by genes, it is a first-person indexical act that is performed within, and made possible by, that social scaffold.
Ultimately, Vygotsky’s claim is ontological, not merely developmental. Higher mental functions are constituted by social interaction and cultural tools. Thus, their ontological origin cannot be genetic because the property isn’t intrinsic, it’s relational. No amount of intra-individual genetic variation can produce a relational property.
Possible counters
“We don’t need reduction, we only need prediction/causal inference. We’re only showing genes -> brains -> test scores.” If genes or polygenic scores causally explain the intentional-level fact that someone got question 27 right, there must be a strict law covering the relation. There is none. All they have is physical-physical causation—DNA -> neural firing -> finger movement. The normative fact that the movement was the correct one is never touched by any physical law.
“Intelligence is just “whatever enables success on complex cognitive tasks—we can functionalize it that way and avoid normativity.” This is the move that Heikenhimo (2008) takes out. Any causal-role description of “getting it right on complex tasks” obliterates the distinction between getting it right and merely producing behavior that happens to match. The normativity argument shows you can’t define “correct application” in purely causal terms without eliminativism or circularity.
“g is biologically real because it correlates with brain volume, reaction time, PGSs, etc.” Even if every physical variable perfectly correlated with getting every Raven item right, it still wouldn’t explain why one pattern is normatively correct and another isn’t. The normative status is anomalous and socially constituted. Correlation isn’t identity and identity is impossible.
“Heritability is just a population statistic.” Heritability presupposes that the trait is well-defined and additive in the relevant population. The Berka-Nash measurement objection shows that IQ (and any psychological trait) is not quantitatively-structured trait with a conjoint measurement structure. Without that, h2 is either undefined or meaningless.
Even then, the hereditarian can agree with the overall argument I’ve mounted here and say something like: “Psychometrics and behavioral genetics have replaced the folk notion of intelligence with a precise, operational successor concept: general cognitive ability as indexed by the first principle component of cognitive test variance. This successor concept is quantitative, additive, biologically real and has non-zero heritability. We aren’t measuring the irreducibly normative thing you’re talking about; we’re measuring something else that is useful and genetically influenced.” Unfortunately, this concept fails once you ask what justifies treating the first PC as a causal trait. As soon as you claim it causes anything at the intentional-level (higher g causes better reasoning, generic variance causes higher g which causes higher life success), they are back to needing psychophysical laws or a functional definition that bridges the normative gap. If they then retreat to pure physical prediction, they have then abandoned the claim that genes cause intelligence differences. Therefore, this concept is either covertly normative (and therefore irreducible), or purely descriptive/physical (therefore being irrelevant to intelligence.)
A successor concept can replace a folk concept if and only if it preserves the explanatorily relevant structure. But replacing “intelligence” with “PC1 of test performance” destroys the essential normative structure of the concept. Therefore, g cannot serve as a scientific successor to the concept of intelligence.
“We don’t need laws, identity, or functional definitions. Intelligence is a real pattern in the data. PGSs, brain volume, reaction time, educational attainment and job performance all compress onto a single and robust predictive dimension. That dimension is ontologically real in exactly the same way as temperature is real in statistical mechanics even before we had microphysical reduction. The heritability of the pattern is high. Therefore genes causally contribute to the pattern. g, the single latent variable, compresses performance across dozens of cognitive tests, predicts school grades, job performance, reaction time, brain size, PGSs with great accuracy. This compression is identical across countries, decades, and test batteries. So g is as real as temperature.” This “robust, predictive pattern” is real only as conformity to culturally dominant rule systems inside modern test-taking societies. The circularity of g still rears its head.
Conclusion
Hereditarianism rests on the unspoken assumption that general intelligence is a natural-kind, individual-level, biologically-caused property that can be lawfully tied to, or functionality defined in terms of, genes and brain states. Davidson shows there are no psychophysical laws; Kim-Kripke show even functional definitions are impossible; Kripke-Wittgenstein show that intelligence is irreducibly normative and holistic; Richardson/Vygotsky show that g is a cultural artifact and that higher mental faculties are born inter-mental;
Because IQ doesn’t measure any quantitatively-structured psychological trait (Berka-Nash), and no psychophysical laws exist (Davidson), the very notion of additive genetic variance contributing to variance in IQ is logically incoherent – h2 is therefore 0.
Hereditarianism requires general intelligence to be (1) a natural-kind trait located inside the skull (eg Jensen’s g), (2) quantitatively-structured so that genetic variance components are meaningful, (3) reducible—whether by strict laws or functional definition—to physical states that genes can modulate, and (4) the causal origin of correct rule-following on IQ tests. Every one of these requirements is logically impossible: no psychophysical laws exist (Davidson), no functional definitions of intentional states is possible (Heikenhimo), rule-following is irreducibly normative and socially constituted (Kripke-Wittgenstein), IQ lacks additive quantitative structure (Berka, Nash, Michell, Richardson) higher mental functions originate as social relations (Vygotsky).
Now I can say that: Intelligence is the dynamic capacity of individuals to engage effectively with their sociocultural environment, utilizing a diverse range of cognitive abilities (psychological tools), cultural tools, and social interactions, and realized through rule-governed pra gives that determine the correctness of reasoning, problem solving and concept application.
Differences in IQ, therefore, aren’t due to differences in genes/biology (no matter what the latest PGS/neuroimaging study tells you). They show an individual’s proximity to the culturally and socially defined practices on the test. So from a rule-following perspective, each test item has a normatively correct solution, determined by communal standards. So IQ scores show the extent to which someone has internalized the relevant, culturally-mediated rules, not a fixed, heritable mental trait.
So the object that hereditarians have been trying to measure and rank by race doesn’t and cannot exist. There is no remaining, respectable position for the hereditarian to turn to. They would all collapse into the same category error: trying to explain a normative, inter-mental historically contingent status with intra-cranial causation.
No future discovery—no better PGSs, no perfect brain scan, no new and improved test battery—can ever rescue the core hereditarian claim. Because the arguments here are conceptual. Hereditarianism is clearly a physicalist theory, but because physicalism cannot accommodate the normativity and rule following that constitute intelligence, the hereditarian position inherits physicalism’failure, making it untenable. Hereditarianism needs physicalism to be true. But since physicalism is false, so is hereditarianism.
(1) If hereditarianism is true then general intelligence must be a quantitatively-structured, individual-level, natural-kind trait that is either (a) linked by strict psychophysical laws or (b) functionally reducible to physical states genes can modulate.
(2) No such trait is possible since no psychophysical laws exist (Davidson), no functional reduction of intentional/normative states is possible (Kim-Kripke normativity argument), and rule-following correctness is irreducibly social and non-quantitative (Wittgenstein/Kripke, Berka, Nash, Michell, Richardson, Vygotsky).
(C) Therefore, hereditarianism is false.
Gould’s Argument Against the “General Factor of Intelligence”
2050 words
Introduction
In his 1981 book The Mismeasure of Man, Stephen Jay Gould mounted a long, historical argument, against scientific racism and eugenics. A key point to the book was arguing against the so-called “general factor of intelligence” (GFI). Gould argued that the GFI was a mere reification—an abstraction treated as a concrete entity. In this article, I will formalize Gould’s argument from the book (that g is a mere statistical abstraction), and that we, therefore, should reject the GFI. Gould’s argument is one of ontology—basically what g is or isn’t. I have already touched on Gould’s argument before, but this will be a more systematic approach in actually formalizing the argument and defending the premises.
Spearman’s g was falsified soon after he proposed it. Jensen’s g is an unfalsifiable tautology, a circular construct where test performance defines intelligence and intelligence explains performance. Geary’s g rests on an identity claim: that g is identical to mitochondrial functioning and can be localized to ATP, but it lacks causal clarity and direct measurability to elevate it beyond a mere correlation to a real, biologically-grounded entity.
Gould’s argument against the GFI
In Mismeasure, Gould attacked historical hereditarian figures as reifying intelligence as a unitary, measurable entity. Mainly attacking Spearman’s Burt, Gould argued that since Spearman saw positive correlations between tests that, therefore, there must be a GFI to explain test intercorrelations. Spearman’s GFI is the first principle component (PC1), which Jensen redefined to be g. (We also know that Spearman saw what he wanted to see in his data; Schlinger, 2003.) Here is Gould’s (1981: 252) argument against the GFI:
Causal reasons lie behind the positive correlations of most mental tests. But what reasons? We cannot infer the reasons from a strong first principal component any more than we can induce the cause of a single correlation coefficient from its magnitude. We cannot reify g as a “thing” unless we have convincing, independent information beyond the fact of correlation itself.
Using modus tollens, the argument is:
(P1) If g is a real, biologically-grounded entity, then it should be directly observable or measurable independently of statistical correlations in test performance.
(P2) But g is not directly observable or measurable as a distinct entity in the brain or elsewhere; it is only inferred from factor analysis of test scores.
(C) So g is not a real biologically-grounded entity—it is a reification, an abstraction mistaken for a concrete reality.
(P1) A real entity needs a clear, standalone existence—not just a shadow in data.
(P2) g lacks this standalone evidence, it’s tied to correlations.
(C) So g isn’t real; it’s reified.
Hereditarians treat g as quantifiable brainstuff. That is, they assume that it can already be measured. For g to be more than a statistical artifact, it would need to have an independent, standalone existence—like an actual physical trait—and not merely just be a statistical pattern in data. But Gould shows that no one has located where in the brain this occurs—despite even Jensen’s (1999) insistence about g being quantifiable brainstuff:
g…[is] a biological [property], a property of the brain
The ultimate arbiter among various “theories of intelligence” must be the physical properties of the brain itself. The current frontier of g research is the investigation of the anatomical and physiological features of the brain that cause g.
…psychometric g has many physical correlates…[and it] is a biological phenomenon.
Just like in Jensen’s infamous 1969 paper, he wrote that “We should not reify g as an entity…since it is only a hypothetical construct“, but then he contradicted himself 10 pages later writing that g (“intelligence”) “is a biological reality and not just a figment of social conventions.” However, here are the steps that Jensen uses to infer that g exists:
(1) If there is a general intelligence factor “g,” then it explains why people perform well on various cognitive tests.
(2) If “g” exists and explains test performance, the absence of “g” would mean that people do not perform well on these tests.
(3) We observe that people do perform well on various cognitive tests (i.e., test performance is generally positive).
(4) Therefore, since “g” would explain this positive test performance, we conclude that “g” exists.
Put another way, the argument is: If g exists then it explains test performance; we see test performance; therefore g exists. Quite obviously, it seems like logic wasn’t Jensen’s strong point.
But if g is reified as a unitary, measurable entity, then it must be a simple, indivisible capacity which uniformly underlies all cognitive abilities. So if g is a simple, indivisible capacity that uniform underlies all cognitive abilities, then it must be able to be expressed as a single, consistent property unaffected by the diversity of cognitive tasks. So if g is reified as a unitary, real entity, then it must be expressed as a single cognitive property unaffected by the diversity of cognitive tasks. But g cannot be expressed as a single, consistent property unaffected by the diversity of cognitive tasks, so g cannot be reified as a unitary, real entity. We know, a priori, that a real entity must have a nature that can be defined. Thus, if g is real then it needs to be everything (all abilities) and one thing (a conceptual impossibility). (Note that step 4 in my steps is the rectification that Gould warned about.) The fact of the matter is, the existence of g is circularly tied to the test—which is where P1 comes into play.
“Subtests within a battery of intelligence tests are included n the basis of them showing a substantial correlation with the test as a whole, and tests which do not show such correlations are excluded.” (Tyson, Jones, and Elcock, 2011: 67)
This quote shows the inherent circularity in defining intelligence from a hereditarian viewpoint. Since only subtests that correlate are chosen, there is a self-reinforcing loop, meaning that the intercorrelations merely reflect test design. Thus, the statistical analysis merely “sees” what is already built into the test which then creates a false impression of a unified general factor. So using factor analysis to show that a general factor arises is irrelevant—since it’s obviously engineered into the test. The claim that “intelligence is what IQ tests measure” (eg Van der Maas, Kan, and Borsboom, 2014) but the tests are constructed to CONFIRM a GFI. Thus, g isn’t a discovered truth, it’s a mere construct that was created due to how tests themselves are created. g emerges from IQ tests designed to produce correlated subtest scores, since we know that subtests are included on the basis of correlation. The engineering of this positive manifold creates g, not as a natural phenomenon, but as a human creation. Unlike real entities which exist independently of how we measure them, g’s existence hinges on test construction which then stripes it of its ontological autonomy.
One, certainly novel, view on the biology supposedly underlying g is Geary’s (2018, 2019, 2020, 2021) argument that mitochondrial functioning—specifically the role of mitochondrial functioning in producing ATP through oxidative phosphorylation—is the biological basis for g. Thus, since mitochondria fuel cellular processes including neuronal activity, Geary links that efficiency to cognitive performance across diverse tasks which then explains the positive manifold. But Geary relies on correlations between mitochondrial health and cognitive outcomes without causal evidence tying it to g. Furthermore, environmental factors like pollutants affect mitochondrial functioning which means that external influences—and not an intrinsic g—could drive the observed patterns. Moreover, Schubert and Hagemann (2020) showed that Geary’s hypothesis doesn’t hold under scrutiny. Again, g is inferred from correlational outcomes, and not observed independently. Since Geary identifies g with mitochondrial functioning, he assumes that the positive manifold reflects a single entity, namely ATP efficiency. Thus, without proving the identity, Geary reifies a correlation into a thing, which is what Gould warned about not doing. Geary also assumes that the positive manifold demands a biological cause, making it circular (much like Jensen’s g). My rejection of Geary’s hypothesis hinges on causality and identity—mitochondrial functioning just isn’t identical with the mythical g.
The ultimate claim I’m making here is that if psychometricians are actually measuring something, then it must be physical (going back to what Jensen argued about g having a biological basis and being a brain property). So if g is what psychometricians are measuring, then g must be a physical entity. But if g lacks a physical basis or the mental defies physical reduction, then psychometrics isn’t measuring anything real. This is indeed why psychometrics isn’t measurement and, therefore, why a science of the mind is impossible.
For something to exist as a real, biological entity, it must exhibit real verifiable properties, like hemoglobin and dopamine, and it must exhibit specific, verifiable properties: a well-defined structure or mechanism; a clear function; and causal powers that can be directly observed and measured independently of the tools used to detect it. Clearly, these hallmarks distinguish real entities from mere abstractions/statistical artifacts. As we have seen, g doesn’t meet the above criteria, so the claim that g is a biologically-grounded entity is philosophically untenable. Real biological entities have specific, delimited roles, like the role of hemoglobin in the transportation of oxygen. But g is proposed as a single, unified factor that explains ALL cognitive abilities. So the g concept is vague and lacks the specificity expected of real biological entities.
Hemoglobin can be measured in a blood sample but g can’t be directly observed or quantified outside of the statistical framework of IQ test correlations. Factor analysis derives g from patters of test performance, not from an independent biological substrate. Further, intelligence encompasses distinct abilities, as I have argued. g cannot coherently unify the multiplicity of what makes up intelligence, without sacrificing ontological precision. As I argued above, real entities maintain stable, specific identities—g’s elasticity, which is stretched to explain all cognition—undermines it’s claims to be a singular, real thing.
Now I can unpack the argument like this:
(P1) A concept is valid if, and only if, it corresponds to an independently verifiable reality.
(P2) If g corresponds to an independently verifiable reality, then it must be directly measurable or observable beyond the correlations of IQ test scores.
(P3) But g is not directly observable beyond the correlations of IQ test scores; it is constructed through the deliberate selection of subtests that correlate with the overall test.
(C1) Thus g does not correspond to an independently verifiable reality.
(C2) Thus, g is not a valid concept.
Conclusion
The so-called evidence that hereditarians have brought to the table to infer the existence of g for almost 100 years since Spearman clearly fails. Even after Spearman formulated it, it was quickly falsified (Heene, 2008). Even then, for the neuroreductionist who would try to argue that MRI or fMRI would show a biological basis to the GFI, they would run right into the empirical/logical arguments from Uttal’s anti-neuroreduction arguments.
g is not a real, measurable entity in the brain or biology but a reified abstraction shaped by methodological biases and statistical convenience. g lacks the ontological coherence and empirical support of real biological entities. Now, if g doesn’t exist—especially as an explanation for IQ test performance—then we need an explanation, and it can be found in social class.
(P1) If g doesn’t exist then psychometricians are showing other sources of variation.
(P2) The items on the test are class-dependent.
(P3) If psychometricians are showing other sources of variation and the items on the tests are class-dependent, then IQ score differences are mere surrogates for social class.
(C) Thus, if g doesn’t exist then IQ score differences are mere surrogates for social class.
We don’t need a mysterious factor to explain the intercorrelations. What does explain it is class—exposure to the item content of the test. We need to dispense with a GFI, since it’s conceptual incoherence and biological implausibility undermine it’s validity as a scientific construct. Thus, g will remain a myth. This is another thing that Gould got right in his book, along with his attack on Morton.
Gould was obviously right about the reification of g.
The Developmental Systems Argument Against Hereditarianism
2000 words
“Genetic determinism can be described as the attribution of the formation of traits to genes, where genes are ascribed more causal power than what scientific consensus suggests” Gerick et al (2017)
Defining hereditarianism and DST
Hereditarianism has many entailments, but a main one is that genes are necessary and sufficient for phenotypes. Hereditarianism can be defined succinctly as: the belief that human traits, behaviors, and capabilities are predominantly or solely caused by genetic inheritance, with the environment being negligible. So this belief implies that genes are necessary (without the specific genes, the trait wouldn’t appear) and sufficient (the genes in question can alone account for the appearance of the trait without significant environmental influence). So if genes are sufficient for phenotypes, then we could predict one’s phenotype from one’s genotype. (It’s also reductionist and deterministic). That a form of genetic determinism is taught in schools (Jamieson and Radick, 2017) is one reason why this hereditarian view must be fought.
But if development is understood as the dynamic interaction between genes, environment, and developmental products where no single factor dominates in the development of an organism (the DST view), then a view that assumes the primacy of one of the developmental resources (hereditarianism and it’s assumption about genes), then this leads to a logical incompatibility and incoherence. Since certain things are true about organismal development, then hereditarianism cannot possibly be true. I have made a similar argument to this before, but I have not formalized it in this way. Since we know that development is context-dependent, and we know that hereditarianism assumes the context-independence of genes, we can rightly assume that hereditarianism is false. Furthermore, since hereditarianism assumes no or negligible developmental plasticity, then that’s another reason to reject it. Here’s the argument:
(1) Hereditarianism (H) implies genetic determinism (GD).
(2) GD implies negligible developmental plasticity (DP).
(3) But DP isn’t negligible.
(C) Therefore H is false.
H=hereditarianism
GD=genetic determinism
D=developmental plasticity/environmental influence
(1) H->GD
(2) GD->¬D
(3) D
(C) ∴¬H
Under the assumption that hereditarianism is a species of genetic determinism, and DST is a context-dependent account of development: If DST is accurate, then hereditarianism is false. We know that traits aren’t genetically determined, so DST is accurate. Therefore, hereditarianism must be false.
Hereditarians have tried paying lip service to the interactionist/developmental systems view (as I showed here and here), but by definition, hereditarianism discounts interactionism since even their main tool (the heritability estimate) assumes no interaction between genes and environment (whereas the interaction between genes and environment is inherent in the DST philosophy).
We know that genes are not sole determinants of phenotypes, but they are one of many interacting developmental resources, which refutes the often unstated assumption that genes are blueprints or recipes for development. Hereditarianism doesn’t and can’t account for the fact that the environment can enable, contain, and alter genetic expression. Therefore, a holistic—and not reductionist—view of development is one we should accept. The hereditarian view of development is clearly untenable.
Below is an argument I’ve constructed that relies on the argument in Noble (2011) for genes as passive causes:
(1) If genes are passive information carriers, then they do not initiate biological processes independently.
(2) Genes do not initiate their own transcription or replication; they react to triggering signals within a biological system.
(3) Therefore, genes are passive information carriers.
(4) If something is a passive information carrier, it cannot be considered an active cause of biological processes.
(5) So if genes are passive information carriers, then genes cannot be considered an active cause of biological processes.
Noble’s biological relativity argument
Hereditarianism assumes a privileged level of causation (genes are the privileged resource of development). But we know—a priori—that there is no privileged level of causation in biological systems (Noble’s 2012 biological relativity argument). So hereditarianism must be false. Here’s the argument:
We know the biological systems are characterized by multiple interacting levels molecular, cellular, organismal, environmental) where each level can influence each other in a dynamic way. So no single level has a causal priority over another. In biological systems, causation is understood as the process by which one event or state leads to another. So for there to be a privileged level of causation in biological systems, one level would need to be inherently more deterministic or controlling of others, independent of the context that the developing organism is situated. But each level of biological organization (from genes to the ecosystem of the organisms) is interdependent where changes at one level can only be understood in relation to changes at other levels (genetic expression is influenced by cellular conditions, which are then affected by organismal health and environmental factors).
So no level of biological organization operates independently or can dictate outcomes without influence or interaction with other levels. Even what may seem like so-called “genetic causes” require the cell to read the context-dependent information in the gene. So there is a feedback loop where influences are not unidirectional but reciprocal. While genes can influence protein synthesis, the need for proteins can regulate gene expression through feedback mechanisms. Therefore, a priori, there is no privileged level of causation in biological systems, since each level is part of an integrated system where causation is distributed and context-dependent, not localized to any one of the levels of biological organization.
See these references for more on how genes are necessary, passive causes but not sufficient causes. These references attest to how genes are looked at today in systems biology, not using a reductionist viewpoint. Oyama, 2000; Moore, 2001; Shapiro, 2013; Kampourakis, 2017; Richardson, 2017, 2020, 2021, 2022; Baverstock, 2021; McKenna, Gawne, and Nijhout, 2022. But here is the gist:
“Active causation” is when X causes or initiates an event to occur, whereas “passive causation” is when X is causes to do something or forced to do something by something else or another situation/event. Both Baverstock and Noble argue that genes (DNA sequences) are passive causes, meaning they don’t initiate the causation of traits. Baverstock also argued that the phenotype plays an active role in morphogenesis and evolution, causing changes in processes (which is similar to West-Eberhard’s and Lerner’s views conceptualizing genes as followers, not leaders, in the evolutionary process).
Noble also argues that genes aren’t active, but rather passive causes, since they merely react to the signals from what is occurring in the developmental system and the environment (which, in this case is conceptualized differently in different contexts for the purpose of this argument like the uterine environment, the environments that get created through the interactions of gene products, gene and gene interactions and gene environment interactions which are ultimately caused by the physiological system). He then ultimately, using Shapiro’s “read write genome argument”, argued that the only kind of causation that can be attributed to genes is passive, in the same way that computer programs read and use databases.
Using Oyama’s concept of “information”, it’s not a property of biological things, but is a relational, contextual concept, arguing that is constructed by the history of the developmental system, while information then emerged through the irreducible interactions which are ultimately caused by the self-organizing developmental system; she calls this “constructive interactionism.”
Over the last 40 years since the publication of Oyama’s developmental systems theory and the subsequent strengthening of her view, we’ve come to find out that genes (and genotypes) aren’t causes in and of themselves, and that genes are mere inert molecules, outside of the living cell. So if the cell activates a gene, then the gene transcribes information (remembering how “information” is conceptualized in Oyama’s DST; this premise establishes a causal relationship between the cell and a gene, with the cell activating the gene since the cell is the active cause and the gene is the passive one). If the gene transcribes its information (of which then ontogeny of information is relational and contextual, emerging through the irreducible actions of the developmental resources), then it produces a protein. So if the cell activates a gene, then it produces a protein (the cell being the active cause and the gene and the protein being passive causes).
“But genes load the gun and environment pulls the trigger”
This is a phrase I’ve heard quite a bit, and I think it’s wrong due to what I’ve outlined above. It’s still deterministic and it looks at genes as active causes. The “genes load the gun” part of the phrase assumes that genes have an active role in initiating biological potentials. But we know that genes are acted on by cellular and environmental context, which then dictates genetic expression. It also assumes linear causation, in a one-way, cause-and-effect sequence.
The claim that the environment merely “pulls the trigger” assumes that there is already an inherent “information” that’s in the genes, which is why that’s a genetic determinist claim. It also minimizes the environment to an activator rather than a co-creator of biological outcomes. So using Oyama’s concept of information as something constructed through developmental interactions emphasizes that the environment doesn’t merely activate what’s already there, it also participates in the very construction of biological information and the ontogeny of traits. It also presumes that genes store all relevant information, but we know that it’s dynamically-shaped, using—but not limited to—genes as passive causes. Basically, biological information is an emergent property of biological systems, not a preexisting genetic code.
Furthermore, since we know that the phenotype plays an active role in morphogenesis and evolution, we know that the outcome (the phenotype) isn’t just a result of genetic loading followed by environmental activation. The phenotype actively contributes to shaping genetic expression and evolutionary trajectories. So if genes are activated by the cell and the broader physiological system, then the idea of genes loading anything independently falls apart. Genes are read or used by the physiological system to carry out certain processes in a context-dependent nanner, not setting the stage, but responding to it.
Conclusion
The role of genes in biological systems and causation as discussed by Noble, Richardson, Oyama, Moore, West-Eberhard, Baverstock, Shapiro and others directly refutes the hereditarian/genetic determinist view of what genes do in biological systems. Genes aren’t the primary architects of biological outcomes; instead genes are seen as passive components within a dynamic, interactive system.
By definition, hereditarianism assumes that genes are necessary and sufficient for causes for phenotypes (genes are the primary drivers of trait ontogeny and development). By definition, DST holds that development is an emergent property of a system where genes are just one component among many influencing factors. If development were primarily determined by genetics, then it would contradict the foundational tenet of DST, that development results from interdependent influences. So since hereditarianism and DST are mutually exclusive in their core assertions about the role of genetics in development, hereditarianism cannot be true since we know that a priori there is no privileged level of causation in biological systems.
So quite clearly hereditarianism fails on conceptual, logical, and empirical grounds. The work that’s been done over the past 50 years in biology—both conceptually and empirically—shows that the old way of viewing genes and their role in organismal development just doesn’t work anymore. Biological outcomes are not merely due to genetic blueprints but are dynamically-shaped outcomes, constructed through the irreducible interactions of multiple levels and resources, which then renders hereditarianism simplistic and outdated in the face of modern biological understanding. Noble’s biological relativity argument is a powerful argument that has direct implications for hereditarianism, and the strengthening of the argument from Baverstock and McKenna, Gawne, and Nijhout definitively show the emptiness in any kind of assumptions that genes are active cause of biological processes. Thus, we should ridicule hereditarian views of the gene and what it does in development. It’s simply an untenable view that one cannot logically defend in the face of the conceptual and empirical work on biological systems.
Therefore, to be a hereditarian in 2025 is to show that one does not understand current biological thinking.
Answering Common “Criticisms” of the Theory of African American Offending
4150 words
Introduction
Back in September I published an article arguing that since the theory of African American offending (TAAO) makes successful novel predictions and hereditarian explanations don’t, that we should accept the TAAO over hereditarian explanations. I then published a follow-up arguing that crime is bad and racism causes crime so racism is bad (and I also argued that stereotypes lead to self-fulfilling prophecies which then cause the black-white crime gap). The TAAO combines general strain theory, social control theory, social disorganization theory, learning theory, and low self control theory in order to better explain and predict crime in black Americans (Unnever, 2014).
For if a theory makes successful novel predictions, therefore that raises the probability that the theory is true. Take T1 and T2. T1 makes successful novel predictions. T2 doesn’t. So if T1 and T2 both try to explain the same things, then it’s only logical to accept T1 over T2. That’s the basis of the argument against hereditarian explanations of crime—the main ones all fail. Although some attempt at a theory has been made integrating hereditarian explanations (Ellis’ 2017 evolutionary neuroandrogenic theory), it doesn’t make any novel predictions. I’ve recently argued that that’s a death knell for hereditarian theories—there are no novel predictions of any kind for hereditarianism.
But since I published my comparison of the successes of the TAAO over hereditarian explanations, I’ve come across a few “responses” and they all follow the same trend: “What about Africa, Britain, and other places where blacks commit more crime? Why doesn’t racism cause other groups to commit more crime?” or “So blacks don’t have agency?” or “Despite what you argued against hereditarian explanations what about as-of-yet-to-be-discovered genes or hormonal influences that lead to higher crime in blacks compared to whites?” or “What about IQ and it’s relationship to crime?” or “What control groups are there for TAAO studies?” or “The black-white crime gap was lower during Jim Crow, how is this possible if the TAAO is true?” or “Unnever and Gabbidon are just making excuses for blacks with their TAAO” or “The so-called ‘novel predictions’ you reference aren’t novel at all.” I will answer these in turn and then provide a few more novel predictions of the TAAO.
“What about Africa, Britain, and other places where blacks commit more crime? Why doesn’t racism cause other groups to commit more crime?“
For some reason, TAAO detractors think these are some kind of knock-down questions for the TAAO and think that they disprove it. These are easily answered and they don’t threaten the theory at all.
For one, the theory of AFRICAN AMERICAN offending is irrelevant places that… Aren’t America. It’s a specific theory to explain why blacks commit crime at a higher rate IN AMERICA, therefore other countries are irrelevant. There would need to be a specific theory of crime for each of those places and contexts. So this question doesn’t hurt the theory. So going off of the first question, the answer to the second question also addresses it—it’s a theory that’s specifically formulated to explain and predict crime in a certain population in a certain place.
For two, why would a theory that’s specifically formulated to explain crime using the unique experiences of black Americans matter for other American groups? Blacks went through 400 years of slavery and then after that went through segregation and Jim Crow, so why would it mean anything that other groups face discrimination but then don’t have higher rates of crime compared to the average? Since the theory has specific focus on understanding the unique experiences and dynamics of crime in the black American population, it’s obvious that asking about other groups is just irrelevant. Other racial and ethnic groups aren’t the primary focus—since it aims to address historical and contemporary factors that lead to higher crime in the black American population. It’s in the name of the theory—so why would other racial groups matter? Unnever and Gabbidon (2011: 37) even explicitly addressed this point:
Our work builds upon the fundamental assumption made by Afrocentists that an understanding of black offending can only be attained if their behavior is situated within the lived experiences of being African American in a conflicted, racially stratified society. We assert that any criminological theory that aims to explain black offending must place the black experience and their unique worldview at the core of its foundation. Our theory places the history and lived experiences of African American people at its center. We also fully embrace the Afrocentric assumption that African American offending is related to racial subordination. Thus, our work does not attempt to create a “general” theory of crime that applies to every American; instead, our theory explains how the unique experiences and worldview of blacks in America are related to their offending. In short, our theory draws on the strengths of both Afrocentricity and the Eurocentric canon.
“So blacks don’t have agency?”
The theory doesn’t say that blacks lack agency (the capacity to make decisions and choices) at all. What the theory does say is that systemic factors like racism, socioeconomic disparities, and historical and contemporary marginalization can influence one’s choices and opportunities. So while individuals have agency, their choices are shaped by the social context they find themselves in. So if one has a choice to do X or ~X but they physical CAN’T do X, then they do not have a choice—they have an illusion of choice. The TAAO acknowledges that choices are constrained by poverty, racism, and social inequity. So while blacks—as all humans do—have agency, some “choices” are constrained, giving the illusion of choice. Thus, constraints should also be considered while analyzing why blacks offend more. This, too, is not a knock-down question.
“Despite what you argued against hereditarian explanations what about as-of-yet-to-be-discovered genes or hormonal influences that lead to higher crime in blacks compared to whites?”
Over the years I’d say I’ve done a good job of arguing against hereditarian theories of crime. (Like testosterone increasing aggression and blacks having higher levels of testosterone, the AR gene, and MAOA.) They’re just not tenable. The genetic explanation makes no sense. (Talk about disregarding agency…) But one response is that we could find some as-of-yet-to-be-discovered genes, gene networks, or neurohormonal influences which explain the higher crime rates in black Americans. This is just like the “five years away” claim that hereditarians love to use. We just need to wait X amount of years for the magic evidence, yet five years never comes since five years away is always five years away.
“What about IQ and it’s relationship to crime?”
Of course the IQ-ists love this question. The assumption is that lower IQ people are more likely to commit crime. So low is means more crime and high IQ means less crime. Ignoring the fact that IQ is not a cause of anything but an outcome of one’s life experiences, we know that the correlation between IQ and crime is -0.01 within family (Frisell, Pawitan, and Langstrom, 2012). So that, too, is an irrelevant question. The relationship just isn’t there.
“What control groups are there for TAAO studies?”
Other than the first question about why don’t other groups who experience racism commit more crime and what about blacks in other countries, this one takes the cake. The TAAO doesn’t need control groups in TAAO tests since it focuses specifically on understanding the unique factors that contribute to crime in America. So instead of comparing different racial or ethnic groups, the TAAO seeks to identify and analyze specific historical, social, and systemic factors which shape the experiences and behaviors of black Americans within the context of American society.
“The black-white crime gap was lower during Jim Crow, why? How is this possible if the TAAO is true?”
Between 1950 and 1963, non-whites made up 11 percent of the US population, 90 percent of which were black. In 1950 for whites the murder rate was 2 to 3 deaths per 100,000 while for non-whites the rate was 28 deaths per 100,000 (28 times the US average) which then fell to 21 per 100,000 in 1961 which was still about 8 times that of the white murder rate while the rate raised again between 1962 and 1964 (Langberg, 1967). Langan (1992) showed a steady increase in the incarcerated black population from 1926 (21 percent) to 1986 (44 percent). But demographic factors account for this, like increases in the sentencing of blacks, the increase in the black population, and increase on black arrest rates—furthermore, there is evidence for increased discrimination between 1973 and 1982 that would explain the 70s-80s incarceration rates (Harding and Winship, 2016). Harding and Winship also showed that differential population growth can account for one-third of the increase in the prison population difference while the rest can be accounted for by differences in sentencing and arrest rates between 1960 and 1980. So the black population increased more in states that had higher incarceration rates. Nonetheless, the TAAO isn’t supposed to retroactively explain trends.
Therefore, the disparity between whites and blacks remained, even pre-1964. This question, too, isn’t a knockdown for the TAAO either. These questions that are asked when one is provided with the successful novel predictions of the TAAO are just cope since hereditarian explanations don’t make novel predictions and their explanations fail (like the ENA theory).
“Unnever and Gabbidon are just making excuses for blacks with their TAAO.”
This is not what they’re doing with their theory at all. A theory is a well-substantiated explanation of some aspect of the natural word that’s based on observation, empirical data, and evidence. They provide testable hypotheses that can be empirically tested. They also make predictions based on their proposed explanations. Predictive capacity is a hallmark of scientific theories. And it’s clear and I’ve shown that the TAAO makes successful novel predictions. Therefore the ability of a theory to make predictions—especially risky and novel ones—lends credibility to the validity of the theory.
The claim that the TAAO is a mere excuse for black crime is ridiculous. Because if that’s true, then all theories of crime are excuses for criminal activity. The TAAO should be evaluated on its predictive power—it’s ability to make successful novel predictions. Claims that the theory is a mere “excuse” for black crime is ridiculous, especially since the theory makes successful novel predictions. It’s clearly a valuable framework for understanding black crime in America.
“The so-called ‘novel predictions’ you reference aren’t novel at all”
We need to understand what the TAAO actually is. It’s a theory of crime that considers the African American “peerless” worldview. “Peerless” means “incomparable.” They have the worldview they do due to the 400 years of slavery and oppression like Jim Crow laws and segregation. Therefore, to explain black crime we need to understand the peerless African American experience. That’s a main premise of the theory. So the TAAO has one main premise, and it’s from this premise that the predictions of the TAAO are derived.
The peerless worldview of African Americans This premise recognizes the unique historical, contemporary, social, and cultural experiences of African Americans including their experiences of racial discrimination, social marginalization, and racial identity. This premise, then, lays the key groundwork for understanding black crime. This core premise of the TAAO then centers the theory within the context of the African American experience. Each of the predictions below are derived from the core premise of the TAAO—that of the peerless worldview of African Americans without relying on the predictions as premises used for the construction of the theory. Each of the predictions follows from the core premise, and they reflect how the African American experiences of racial discrimination, social marginalization and racial identity influence their likelihood of experiencing racial discrimination. Unnever and Gabbidon gave many arguments and references that this is indeed the case. The predictions, then, weren’t used as premise to construct the TAAO but they indeed are derived from—indeed they emerge from—the foundational experiences of African Americans and then serve as testable hypotheses which are derived from that understanding.
Thus, the predictions follow from the TAAO and they are derived from the foundational premise of the TAAO, without being used in the construction of the theory itself, qualifying as novel predictions according to Musgrave (1988): “a predicted fact is a novel fact for a theory if it was not used to construct that theory — where a fact is used to construct a theory if it figures in the premises from which that theory was deduced” and Beerbower: “the purpose of science is to enable accurate predictions and that, in fact, science cannot actually achieve more than that...The test of an explanatory theory, therefore, is its success at prediction, at forecasting. This view need not be limited to actual predictions of future, yet to happen events; it can accommodate theories that are able to generate results that have already been observed or, if not observed, have already occurred...it must have some reach beyond the data used to construct the theory“
More novel predictions of the TAAO
Therefore, since the TAAO has success in its predictions and hereditarian ones don’t (they don’t even make any novel predictions), it’s only rational to accept the theory that makes successful novel predictions over the one that doesn’t. The only reason one would accept the hereditarian explanations over the TAAO is due to bias and ignorance (racism), since the TAAO is a much more robust theory that actually has explanatory AND predictive power. So the issue here is quite clear—since we know the causes of black crime due to the successful novel predictions that the TAAO generates, then there are clear and actionable things we can do to try to mitigate the crime rate. This is something that hereditarian theories don’t do, most importantly because they don’t make any novel predictions. Since the TAAO makes successful risky novel predictions—predictions that, if they didn’t hold, they would then refute the theory—and since the predictions hold, then the theory is more likely to be true than not. The TAAO not only accommodates, but it makes predictions, and we can’t say the same for hereditarianism.
The issue is that so-called “race-neutral” theories of crime need to assume that racial discrimination isn’t a cause of black American offending because this would then limit it only to black Americans. Therefore race-neutral theories of crime don’t have the same predictive and explanatory power as a race-centric theory of crime—which is what the TAAO is. It’s clear that: the TAAO makes successful novel predictions, the predictions aren’t used as premises in the TAAO, the TAAO is a race-centric, country-specific theory of crime (and not a general theory of crime), racism and stereotypes don’t explain offending for non-African Americans, the theory doesn’t say that blacks lack agency, IQ doesn’t explain crime within families, and cope from hereditarians that one day we will find genes or neurohormonal influences which lead to crime in black Americans is just cope. It’s clear that the TAAO is the superior theory of crime because it does what scientific theories are supposed to do: successfully predict novel facts of the matter, something that hereditarianism just does not do which is why I’m justified in calling it a racist movement. Basically since there are unique characters of a demographic that require perspectives that are solely related to that group, then we need group-centric theories of crime due to the unique experiences of thsg group, and this is what the TAAO does.
Now that I’ve answered common criticisms of the TAAO, I have a few more successful novel predictions of the theory. In my original article I cited 3 novel predictions, how they followed from the theory, and then the references that confirmed the predictions:
(Prediction 1) Black Americans with a stronger sense of racial identity are less likely to engage in criminal behavior than black Americans with a weak sense of racial identity. How does this prediction follow from the theory? TAAO suggests that a strong racial identity can act as a protective factor against criminal involvement. Those with a stronger sense of racial identity may be less likely to engage in criminal behavior as a way to cope with racial discrimination and societal marginalization. (Burt, Simons, and Gibbons, 2013; Burt, Lei, and Simons, 2017; Gaston and Doherty, 2018; Scott and Seal, 2019)
(Prediction 2) Experiencing racial discrimination increases the likelihood of black Americans engaging in criminal actions. How does this follow from the theory? TAAO posits that racial discrimination can lead to feelings of frustration and marginalization, and to cope with these stressors, some individuals may resort to committing criminal acts as a way to exert power or control in response to their experiences of racial discrimination. (Unnever, 2014; Unnever, Cullen, and Barnes, 2016; Herda, 2016, 2018; Scott and Seal, 2019)
(Prediction 3) Black Americans who feel socially marginalized and disadvantaged are more prone to committing crime as a coping mechanism and have weakened school bonds. How does this follow from the theory? TAAO suggests that those who experience social exclusion and disadvantage may turn to crime as a way to address their negative life circumstances. and feelings of agency. (Unnever, 2014; Unnever, Cullen, and Barnes, 2016)
(Prediction 4) Black people who experience microaggreesions and perceive injustices in the criminal justice system are more likely to engage in serious and violent offending. How does this follow from the theory? Experiences of racial discrimination and marginalization can lead to negative emotions like anger and depression among black people. These negative emotions, which are then exacerbated by microaggreesions and perceptions of injustice in the criminal justice system, may increase the likelihood of engaging in serious and violent offending as a coping mechanism or means of asserting power. But, again, those with a stronger racial identity may be more resilient to the effect of discrimination (Isom, 2015).
(Prediction 5) Black Americans who perceive a lack of opportunity for socioeconomic advancement due to systemic barriers are more inclined to engage in criminal activity as a means of economic survival and social mobility. How does this follow from the theory? Perceptions of limited opportunities and systemic injustices can drive individuals to engage in criminal behaviors as a response to inequality (Vargas, 2023).
The fact that the TAAO generates these novel and successful predictions is evidence that we should accept the theory.
We also know that perceptions of criminal injustice predict offending (Bouffard and Piquero, 2013), we know that blacks are more likely than whites to perceive criminal injustice (Brunson and Weitzer, 2009) and we know that there are small differences among blacks and their perception of criminal injustice (Unnever, Gabbidon, and Higgins, 2011). So knowing this, more blacks should offend, right? Wrong. The vast majority of blacks don’t offend even though they share the same belief about the injustices of the criminal justice system. So how can we explain that? “Positive ethnic-racial socialization buffers the effect of weak school bonds on adolescent substance use and adult offending” (Gaston and Doherty, 2018). So the discrimination that black Americans have erodes their trust in social institutions like the school system, and then these weakened school bonds then increase the risk of offending.
Supporting a major tenet of TAAO and prior research on the protective ability of ethnic-racial socialization, the analyses showed that Black males who received positive ethnic-racial socialization messages in childhood develop resilience to the criminogenic effect of weak school bonds and face a lower risk for offending over the life course. (Gaston and Doherty, 2018)
One factor that is salient in the TAAO is racial subordination. We know that black people don’t commit crime because they are black, but we know that their offending is related to socio-environmental context like poverty, bad schools (while racism and stereotypes weaken school bonds blacks have, which makes them more likely to offend), broken families, and lead exposure (Butler, 2010) of which the TAAO addresses. We also know that there is no such thing as a “safe” level of lead exposure and that the relationship between lead and crime is robust and replicated across different countries and cultures. We also know that blacks were used as an experiment of sorts, where they were knowingly exposed to lead paint in subsidized homes.
This environmental racism (Washington, 2019), then, is another aspect of the racial subordination of blacks. And from 1976 to 2005, blacks were 7 times more likely than whites to commit murder. The fact of the matter is, the black-white murder gap has been large for over 100 years. And in discussing environmental racism, Unnever and Gabbidon (2011: 188) are explicit about the so-called genetic hypothesis of crime: “We want to be perfectly clear that our argument in no way is related to the thesis that there is a genetic cause to African American offending.” Therefore, this question doesn’t strike the heart of the TAAO and is just an attempt at evading the successful novel predictions the theory generates.
Conclusion
I’ve shown that the common “criticisms” of the TAAO are anything but and are easily answered. I then gave more successful predictions of the TAAO. It’s quite clear that one should accept the TAAO over hereditarian explanations. We also know that black isolation is a predictor of crime as well—even in 1996 blacks accounted for over 50 percent of murders and two-thirds of robberies (Shihadeh and Flynn, 1996). In 2020, blacks were six times more likely to be arrested for murder than whites. We also know that the belief by blacks in the violent stereotype predicts their offending and their adherence to the stereotype predicts crime and self control (Unnever, 2014). Therefore, a kind of stereotype threat arises here and has effects during police encounters like wkth height (Hester and Gray, 2018)(Najdowski, Bottoms, and Goff, 2015; Strine, 2018; Najdowski, 2012, 2023) , with one argument that race stereotypes track ecology, not race, (Williams, 2023) (just like for IQ; Steele and Aronson, 1995; Thames et al, 2014). We know that stereotype threats weaken school bonds and that weakened school bonds are related to offending, therefore we can infer that stereotype threats lead to an increase in crime (Unnever and Gabbidon, 2011).
Unnever and Gabbidon were quite clear and explicit in their argument and the hypotheses and predictions they made based on their theory. So when tested, if they were found not to hold then the theory would be falsified. But the theories held under empirical examination. Unnever and Gabbidon (2011: 98) were explicit in their theory and what it meant:
Put simply, we hypothesize that the probability of African American offending increases as blacks become more aware of toxic stereotypes, encounter stereotype threats, and are discriminated against because of their race. Our theory additionally posits that these forms of racism impact offending because they undermine the ability of African Americans to develop strong ties with conventional institutions. The extant literature indicates that stereotype threats and personal experiences of racial discrimination negatively impact the strength of the bonds (attachment, involvement, commitment) that black students have with their schools (Smalls, White, Chavous, and Sellers, 2007; Thomas, Caldwell, Faison, and Jackson, 2009). And, the research is clear; weak social bonds increase the probability of black offending (Carswell, 2007).
The worldview shared by black Americans is a consequence of the experience they and their ancestors had in America. This then explains their offending patterns, and why they commit more crime than whites. The socio-historical context that the TAAO looks to explain black crime is robust. Since the TAAO is successful in what it sets out to do, then, I wouldn’t doubt that there should be other race-centric theories of crime that try to explain and predict offending in those populations. The empirical successes of the TAAO’s predictions attest to the fact that other theories of crime for other races would be fruitful in predicting and explaining crime in those groups.
Hereditarians dream of having a theory that enjoys the empirical support that the TAAO has. The fact that the TAAO makes successful novel predictions and hereditarianism doesn’t is reason enough to reject hereditarian explanations and accept the TAAO. Accepting a theory that makes novel predictions is rational since it speaks to the theory’s predictive power. So by generating predictions that were previously unknown or untested and them confirming them through empirical evidence, the theory therefore shows its ability to predict and anticipate real-world phenomena. This then strengthens confidence in the theory’s underlying principles which provides a framework for understanding complex phenomena. Further, the ability of a theory to make such predictions suggests that the theory is robust and adaptable, meaning that it’s capable of accommodating new data while refining our understanding over time.
Hereditarians would love nothing more than to reduce black criminality to their genes or hormones, but reality tells a different story, and it’s one where the TAAO exists and makes successful novel predictions.
HBD and (the Lack of) Novel Predictions
2250 words
a predicted fact is a novel fact for a theory if it was not used to construct that theory — where a fact is used to construct a theory if it figures in the premises from which that theory was deduced. (Musgrave, 1988; cf Mayo, 1991: 524)
Introduction
Previously I demonstrated that the HBD movement is a racist movement. I showed this by arguing that it perfectly tracks with John Lovchik’s definition of racism, which is where “racism is a system of ranking human beings for the purpose of gaining and justifying an unequal distribution of political and economic power.” There is, however, a different issue—an issue that comes from the philosophy of science. So a theory is scientific if and only if it is based on empirical evidence, subject to falsifiability and testability, open to modification or rejection based on further experimentation or observation and—perhaps most importantly—is capable of generating novel predictions, where a novel prediction goes beyond existing knowledge and expectation and can be verified through empirical testing.
Here I will show that HBD doesn’t make any novel predictions, and I will also discuss one old attempt at showing that it does and that it is an example of a degenerative research programme. Effectively, I will argue that contrary to what is claimed, HBD is a degenerating research programme.
On so-called novel predictions
HBD and evolutionary psychology falls prey to the same issues that invalidate both of them. They both rely on ad hoc and post hoc storytelling. In a previous article on novel predictions, I stated:
A risky, novel prediction refers to a prediction made by a scientific theory or hypothesis that goes beyond what is expected or already known within an existing framework (novelness). It involves making a specific claim about a future observation or empirical result that, if confirmed, would provide considerable evidence in support of the scientific theory or hypothesis.
So EP and HBD are cut from the same cloth. John Beerbower (2016) puts the issue succinctly:
At this point, it seems appropriate to address explicitly one debate in the philosophy of science—that is, whether science can, or should try to, do more than predict consequences. One view that held considerable influence during the first half of the twentieth century is called the predictivist thesis: that the purpose of science is to enable accurate predictions and that, in fact, science cannot actually achieve more than that. The test of an explanatory theory, therefore, is its success at prediction, at forecasting. This view need not be limited to actual predictions of future, yet to happen events; it can accommodate theories that are able to generate results that have already been observed or, if not observed, have already occurred. Of course, in such cases, care must be taken that the theory has not simply been retrofitted to the observations that have already been made—it must have some reach beyond the data used to construct the theory.
HBDers promote the tenets that intelligence (IQ), along with behavior and socioeconomic outcomes are strongly associated with genetic differences among individuals and groups. They also use the cold winter theory (CWT) to try to intersect these tenets and show how they evolved over time. According to the CWT, the challenges of surviving in colder climates such as the need to hunt, plan ahead, and cooperate exerted selective pressures which favored genes which fostered higher intelligence in populations that inhabited these regions. I have previously shown years back that the CWT lacks novel predictive power, and that there are devastating response to the CWT which show the invalidity of the theory. Rushton used it in his long-refuted r/K selection theory for human races. Further, for example Jablonski and Chaplin (2000) successfully predicted that “multiple convergences of light skin evolved in different modern human populations and separately in Neanderthals” (Chaplin and Jablonski, 2009: 457). This was a successfully predicted novel fact, something that HBD doesn’t do.
Urbach (1974) (see Deakin, 1976 for response) in criticizing “environmentalism” and contrasting it with “hereditarianism”, claimed that hereditarianism made novel predictions. He also claimed that the “hard core” of the hereditarian research programme was that (1) cognitive ability of all people is due to general intelligence and individual and (2) group differences are due to heredity. We know that (1) is false, since general intelligence is a myth and we know that (2) is false since group differences are due to environmental factors since Jensen’s default hypothesis is false (along with the fact that Asians are a selected population). Further Urbach (1974: 134-135) writes that 4 novel facts of hereditarianism are “(i) of the degree of family resemblances in IQ, (ii) of IQ-related social mobility, (iii) of the distribution of IQ’s, and (iv) of the differences in sibling regression for American Negroes and whites.”
But the above aren’t novel predictions.
(i) Hereditarianism predicts that intelligence has a significant hereditary component, leading to similarities in IQ scores among family members. (Nevermind the fact that environments are inherited by these family members as well.) The prediction appears specific, but it’s not novel in the framework of hereditarianism. The idea that IQ is heritable and that family members share similarities in IQ has been a main tenet of hereditarianism for decades, even in 1974 at the time of publication of Urbach’s paper,rather than offering a new or unexpected insight.
(ii) Hereditarianism also suggests that differences in IQ also have implications for social mobility, with people with higher IQs having a greater change for more upward social mobility. This, too, isn’t novel within the hereditarian framework since even in 1974 and the decades before then this was known.
(iii) Hereditarianism also predicts that IQ scores follow a normal distribution, with a majority of people clustering around the middle. This, too, isn’t a novel prediction, since even Binet unconsciously built his test to have a normal distribution (Nash, 1987: 71). (Also note that Binet knew that his scales weren’t measures but thought that for practical measures they were; Michell, 2012.) Terman constructed his test to also have it. Urbach (1974: 131) states that “even if researchers had set out to obtain a particular distribution of IQ’s, there was no divine guarantee that their efforts would have been successful.” But we know that the process of building a normal distribution is done by choosing only items that conform to the normal distribution are selected, since items most are likely to get right are kept while on both ends items are also kept. In their psychometrics textbook, Rusk and Golombok (2009: 85) state that “it is common practice to carry out item analysis in such a way that only items that contribute to normality are selected.” Jensen (1980: 71) even stated “It is claimed that the psychometrist can make up a test that will yield any kind of score distribution he pleases. This is roughly true, but some types of distributions are much easier to obtain than others.”
(iv) Lastly, hereditarianism predicts that differences in sibling regression or the extent to which sibling IQ scores deviate from the population mean could vary between racial and ethnic groups. The prediction seems specific, but it reflects assumptions of genetic influences on psychological trait—which already were assumptions of hereditarian thought at that time and even today. Thus, it’s not a new or unexpected insight.
Therefore, the so-called novel predictions referenced by Urbach are anything but and reflect existing assumptions and concepts in the field at the time of publication, or he’s outright wrong (as is the case with the normal distribution).
Modern day hereditarians may claim that the correlation between genetics and IQ/educational attainment validates their theories and therefore counts as novel. However, the claim that genes would correlate with IQ has been a central tenet in this field for literally 100 years. Thus, a prediction that there would be a relationship between genes and IQ isn’t new. Nevermind the fact that correlations are spurious and meaningless (Richardson, 2017; Richardson and Jones, 2019) along with the missing heritability problem. Also note that as sample size increase, so to does the chance for spurious correlations, (Calude and Longo, 2016). The hereditarian may also claim that predicting group differences in IQ based on genetic and environmental factors is a novel prediction. Yet again, the idea that these contribute to IQ has been known for decades. The general prediction isn’t novel at all.
So quite obviously, using the above definition of “novel fact” from Musgrave, HBD doesn’t make any novel predictions of previously unknown facts not used in the construction of the theory. The same, then, would hold true for an HBDer who may say something along the lines of “I predict that a West African descendant will win the 100m dash at the next Olympics.” This doesn’t qualify as a novel prediction of a novel fact, either. This is because it relies on existing knowledge related to athletics and racial/ethnic demographics. It’s based in historical data and trends of West African descendants having been successful at previous 100m dash events at the Olympics. Therefore, since it’s not a novel insight that goes beyond the bounds of the theory, it doesn’t qualify as “novel” for the theory.
Why novel predictions matter
Science thrives on progress, so without theories/hypotheses that make novel predictions, a scientific program would stagnate. The inability of hereditarianism to generate risky, novel predictions severely limits it’s ability in explaining human behavior. Novel predictions also provide opportunities for empirical testing, so without novel predictions, hereditarianism lacks the opportunity for rigorous empirical testing. But a proponent could say that whether or not the predictions are novel, there are still predictions that come to pass based on hereditarian ideas.
Without novel prediction, hereditarianism is confined to testing hypotheses that are well-known or widely accepted in the framework or the field itself. This then results in a narrow focus, where researchers merely confirm their pre-existing beliefs instead of challenging them. Further, constantly testing beliefs that aren’t novel leads to confirmation bias where researchers selectively seek out what agrees with them while ignoring what doesn’t (Rushton was guilty of this with his r/K selection theory). Without the generation of novel predictions, hereditarianism lacks innovation. Lastly, the non-existence of novel predictions raises questions about the progressiveness of the framework. True scientific progress is predicated on the formulation of testing novel hypotheses which challenge existing paradigms. Merely claiming that a field generates testable and successful novel predictions and therefore that field is a progressive one is unfounded.
Thus, all hereditarianism does is accommodate, there is no true novel predictive power from it. So instead of generating risky, novel predictions that could potentially falsity the framework, hereditarians merely resort to post-hoc explanations, better known as just-so stories to fit their preconceived notions about human behavior and diversity. HBD claims are also vague and lack the detail needed for rigorous testing—the neck isn’t stuck out far enough for where if the prediction fails that the framework would be refuted. That’s because the predictions are based on assumptions they already know. Thus, HBD is merely narrative construction, and we can construct narratives about any kind of trait we observe today have the story conform with the fact that the trait still exists today. Therefore hereditarianism is in the same bad way as evolutionary psychology.
I have previously compared and contrasted hereditarian explanations of crime with the Unnever-Gabbidon theory of African American offending (TAAO) (Unnever and Gabbidon, 2011). I showed how hereditarian explanations of crime not only fail, but that hereditarian explanations lack novel predictive power. On the other hand, Unnever and Gabbidon explicitly state hypotheses and predictions which would follow from. The TAAO, and when they were tested they were found to hold validating the TAAO.
Conclusion
In this discussion I have tried to show that hereditarian/HBD theories make no novel predictions. They are merely narrative construction. The proposed evolutionary explanation for racial differences in IQ relying on the CWT is ad hoc, meaning it’s a just-so story. Lynn even had to add in something about population size and mutation rates since Arctic people, who have the biggest brain size, don’t have the highest IQ which is nothing more than special pleading.
Urbach’s (1974) four so-called novel predictions of hereditarianism are anything but, since they are based on assumptions already held by hereditarianism. They represent extensions or reformulation of existing assumptions, while also relying on retrospective storytelling.
I have provided a theory (the TAAO) which does make novel predictions. If the predictions wouldn’t have held, then the theory would have been falsified. However, tests of the theory found that they hold (Burt, Simons, and Gibbons, 2013; Unnever, 2014; Unnever, Cullen, and Barnes, 2016; Herda, 2016, 2018; Burt, Lei, and Simons, 2017; Gaston and Doherty, 2018; Scott and Seal, 2019). The hereditarian dream of having the predictive and explanatory power that the TAAO does quite obviously fails.
Therefore, the failure of hereditarianism to produce successful, risky novel predictions should rightly raise concerns about its scientific validity and the scientific credibility of the program. So the only rational view is to reject hereditarianism as a scientific enterprise, since it doesn’t make novel predictions and it’s merely, quite obviously, a way to make prejudices scientific. Clearly, based on what a novel prediction of a novel fact entails, HBD/hereditarian theory doesn’t make any such predictions of novel facts.
Racism Disguised as Science: Why the HBD Movement is Racist
2600 words
Introduction
Over the last 10 years or so, claims from the human biodiversity (HBD) movement have been gaining more and more traction. Proponents of HBD may say something like “we’re not racists, we’re ‘Noticers'” (to use Steve Sailer terminology – more on him below). The thing is, the HBD movement is a racist movement for the following reasons: it promotes and justifies racial hierarchies, inequities, is justified by pseudoscience, and it’s historical connections to the eugenics movement which sought to use pseudoscientific theories of racial superiority to justify oppression and discrimination.
But ever since 1969, Arthur Jensen and others have tried to intellectualize such a position, the discussion around racism has moved on to things like not only overt examples of racism but to systemic inequities along with unconscious biases which perpetuate racial hierarchies. But despite a veneer of scientific objectivity, the underlying motivation appears to be that of upholding some groups as “better” and others “worse.” This is like when hereditarians like Rushton tried to argue in the 90s that they can’t be racist since they say Asians (who are a selected population) are better than whites who are better than blacks on trait X. We know that views on Asians have changed over the years, for example with the use of the term “Mongoloid idiot.” Nonetheless, it’s obvious that the HBD movement purports a racial hierarchy. Knowing this, I will show how HBD is a racist movement.
Why HBD is racist
I have previously provided 6 definitions of racism. In that article I discussed how racism “gets into the body” and causes negative health outcomes for black women. I have since written more about why racism and stereotypes are bad since they cause the black-white crime gap through the perpetuation of self-fulfilling prophecies and they also cause psychological and physiological harm.
One of the definitions of “racism” I gave came from John Lovchik in his book Racism: Reality Built on a Myth (2018: 12), where he wrote that “racism is a system of ranking human beings for the purpose of gaining and justifying an unequal distribution of political and economic power.” Using this definition, it is clear that the HBD movement is a racist movement since it attempts to justify this ranking or human beings to justify and gain different kinds of power. This definition from Lovchik encompasses both systemic racism and overt acts of discrimination.
HBD proponents believe they we can delineate races not only based on physical appearance but also genetic differences. This is inherent in their system of ranking. But I think the same. Spencer’s (2014, 2021) OMB race theory (to which I hold to) states that race is a referent denoting a proper name to population groups. But that’s where the similarities end; OMB race theory is nothing like HBD. The key distinction between the two is in the interpretation of said differences. While both perspectives hold that population groups can be sorted into distinct groups, there is a divergence in their intentions and conclusions regarding the significance of said racial categorization.
Spencer’s OMB race theory emphasizes the declination of races based on physical differences as well as genetic ones using K=5 and how the OMB defines race in America—as a proper name for population groups. But Spencer (2014: 1036) explicitly states that his theory has no normative conclusion in it, since “the genetic evidence that supports the theory comes from noncoding DNA sequences. Thus, if individuals wish to make claims about one race being superior to another in some respect, they will have to look elsewhere for that evidence.” So the theory focuses solely on genetic ancestry without any normative judgements or hierarchical ranking of the races.
Conversely, the HBD movement, despite also genetically delineating races, differs in the application and interpretation of the evidence. Unlike Spencer’s OMB race theory, HBD states that genetic differences between groups contribute to differences in intelligence, social outcomes and behavior. HBD proponents use genetic analyses like GWAS to show that a trait has some kind of genetic influence and that, since there is a phenotypic difference in the trait between certain racial groups that it then follows that there is a genetic difference between certain racial groups when it comes to the phenotypic trait in question.
So this distinction that I have outlined shows the principle ways in which OMB race theory is nothing like HBD theory. So while both ideas involve genetic delineation of races, Spencer’s doesn’t support racist ideologies or hierarchical rankings among the races while the HBD movement does. Thus, the distinction shows the relationship between genetic analysis, racism and racial categorization is nuanced and that, just because one believes that human races exist, it doesn’t necessarily follow that they are a racist.
Furthermore, the attribution of social outcomes/inequality to biological/genetic differences is yet another reason why HBD is racist. They argue that most differences (read: outcomes/inequalities) between groups can come down mostly to genes, still leaving room for an environmental component. (This is also one of Bailey’s 1997 hereditarian fallacies.) It is this claim that socially-valued differences between groups are genetic in nature which then leads to systemic discrimination. So by attributing differences in outcome and resources, to biological differences, HBD attempts to perpetuate and legitimate systemic discrimination against certain racial groups. “It’s in their genes, nothing can be done.” Therefore, by ranking humans based on race and attributing differences in outcomes between groups—in part—to biological differences, the HBD movement justifies and perpetuates systemic discrimination against certain races, making HBD a racist movement.
Eugenic thinking arose in the late 1800s and began to be put into action in the 1900s. From sterilization to certain people deemed inferior, to advocating the enhancement of humanity through selective breeding of certain groups of people, some of the ideas from the eugenics movement are inherent in HBD-type thinking. The HBD movement then emerged as a more “respectable” iteration of the eugenics movement and they draw on similar themes. But why does this connection matter? It matters since the historical connection between the two shows how such pernicious thinking can penetrate social thought.
Lastly the HBD movement relies on pseudoscience. They often distort or misrepresent scientific findings. Most obvious is J. P. Rushton. In his discussion of Gould’s (1978) reanalysis of Morton’s skull collection, Rushton miscited Gould’s results in a way that jived with Rushton’s racial hierarchies (Cain and Vanderwolf, 1990). Rushton also misrepresented the skull data from Beals et al (1984). Rushton is the perfect example of this, since he misrepresented and ignored a ton of contrary data so that his theory could be more important. Rushton’s cherry-picking, misrepresentation of data, and ignoring contrary evidence while not responding to devestating critiques (Anderson, 1991; Graves 2002a, b) show this perfectly. This is the perfect example of confirmation bias.
They also rely on simplistic and reductionist interpretation of genetic research. By doing this, they also perpetuate stereotypes which can then have real-world consequences, like people committing horrific mass murder (the Buffalo shooter made reference to such genetic studies, which is why science communication is so important).
In his 2020 book Human Diversity the infamous Charles Murray made a statement about inferiority and superiority in reference to classes, races, and sexes, writing:
To say that groups of people differ genetically in ways that bear on cognitive repertoires (as this book does) guarantees accusations that I am misusing science in the service of bigotry and oppression. Let me therefore state explicitly that I reject claims that groups of people, be they sexes or races or classes, can be ranked from superior to inferior. I reject claims that differences among groups have any relevance to human worth or dignity.
Seeing as Chuck is most famous for his book The Bell Curve, this passage needs to be taken in context. So although he claims to reject such claims of inferiority and superiority, his previous work has contributed to such notions, and thus, it is implicit in his work. Furthermore, the language he used in the passage also implies hierarchical distinctions. When he made reference to “groups of people [who] differ genetically in ways that bear on cognitive repertoires“, there is a subtle suggestion that groups may possess inherent advantages or disadvantages in cognitive ability, thusly implying a form of hierarchy.
Murray’s work has been used by alt-right and white nationalist groups, and we know that white nationalist groups use such information for their own gain (Panofsky, Dasgupta, and Iturriaga, 2020; Bird, Jackson, and Winston, 2023). Panofsky and his coauthors write that “the claims that genetics defines racial groups and makes them different, that IQ and cultural differences among racial groups are caused by genes, and that racial inequalities within and between nations are the inevitable outcome of long evolutionary processes are neither new nor supported by science (either old or new). They’re the basic, tired evergreens of ancient racist thought.“
Next we have Steve Sailer. He may claim that he is merely observing (or as he says “Noticing”) and discussing empirical data. So his focus on racial differences and how they are driven mainly by genetic differences aligns with Lovchik’s definition of racism, since it involves the ranking of races based on perceived genetic differences, in both IQ and crime. Therefore, by emphasizing these differences and their purported implications for socially-relevant traits and their so-called implications for social hierarchies, Sailer’s work can be seen as justifying social inequalities and therefore justifying systemic discrimination.
Lastly, we have Bo Winegard’s Aporia Magazine essay titled What is a racist? In the article he forwards 5 definitions (while giving a 10-point scale, I will bracket the score he gives each):
Flawed:
1: Somebody who believes that race is a real, biological phenomenon and that races are different from each other. [1/10]
2: Somebody who believes that some races have higher average socially desirable traits such as intelligence and self-control than others. [3/10]3: Somebody who treats members of one race differently from members of another race. [5/10]
Plausible:
4: Somebody who dislikes members of other races. [8/10]
5: Somebody who advocates for differential treatment under the law for different races. [10/10]
Note that the first 2 encompass what, for the purposes of this article, I call racist in the HBD parlance. Nonetheless, I have tried to sufficiently argue that those 2 do constitute racism and I think I have shown how. In the first, if it is used to justify and legitimate social hierarchies, it is indeed racist. For the second, if someone holds the belief that races differ on socially values traits and that it is genetically caused, then it could perpetuate racist stereotypes and the continuation of racist ideologies. The third and fourth constitute racial discrimination. These 2 could also be known as hearts and minds racism, which operate at the level of individual beliefs, attitudes, and behavior. But the fifth definition that Bo forwarded is the most interesting one, since it has certain implications.
About the fifth definition, Bo wrote that (my emphasis) “a racist is somebody who advocates for differential treatment under the law for different races, [it] is the most incontrovertible and therefore paradigmatic definition of racist that I can imagine.” This is interesting. If it is not able to be denied, disputed, and serves as a typical example of the referent of racism, then this has implications for the views of certain hereditarians and the people they ran with.
We know that Jensen ran with actual racists and that he lent his name to their cause. (Jackson, 2022; see also Jackson and Winston, 2020 for a discussion). We know that hereditarians, despite their protestations, ignore evolutionary theory (Roseman and Bird, 2023). Nonetheless, we know that there is no support for the hereditarian hypothesis (Bird, 2021). But the issue here is the fifth definition that Bo said isn’t indisputable.
In his 2020 article Research on group differences in intelligence: A defense of free inquiry, philosopher Nathan Cofnas noted that hereditarians call for a kind of “tailored training program“, which John Jackson took to be “a two-tiered education system.” Although Cofnas didn’t say it, he cited hereditarians who DID say it. Thus, he showed how they ARE racists. And Cofnas states that we can’t know what would happen if race differences in intelligence would be found to have a genetic basis. But I argued before that since the hereditarian hypothesis is false and if we believe it is true then it could—and has—caused harm, so we should thusly ban IQ tests. Nonetheless, Cofnas’ passage in his article can be seen as racist under Lovchik’s definition, since he advocates for tailored training programs, which could result in unequal distribution of resources and further entrench inequities based on genetic differences between groups in their so-called intelligence which hereditarians argue is partly genetic in nature.
Prominent hereditarians Shockley and Cattell said some overtly racist things, Cattell even creating a religion called “Beyondism” (Tucker, 2009). Shockley called for the voluntary sterilization of black women (Thorp, 2022) and proposed a sterilization plan to pay anyone with an IQ a sum of money to get sterilized. I have also further documented the eugenic thinking of IQists and criminologists. It seems that this field is and has been a hole for racists ever since it’s inception.
Conclusion
Throughout this discussion, I have argued that the HBD movement is a racist one. Most importantly, a lot of their research was bankrolled by the Nazi Pioneer Fund. So financial support from a racist organization is pivotal in this matter, since these researchers were doing work that would justify the conclusions of the racist Fund (see Tucker 1996, 2002). So since the Fund had a history of funding research into eugenics, and of promoting research which could—implicitly—be seen as justification for racial superiorityp and inferiority, and therefore attempting to justify existing inequities.
Relying on John Lovchik’s definition of racism, I’ve shown how the HBD movement is a racist movement since it seeks to justify existing inequalities between racial groups and since it is a system of ranking human beings. I’ve also shown that mere belief in the existence of race isn’t enough for one to be rightly called a racist, since theories of race like Spencer’s (2014) OMB race theory is nothing like HBD theory since it doesn’t rank the races, nor does it argue that the genetic differences between races are causal for the socially important differences that hereditarians discuss. Racism isn’t only about individual attitudes, but also about systemic structures and institutional practices which perpetuate racial hierarchies and inequities.
I showed how, despite his protestations, Murray believes that races, classes, and sexes can be ranked—which is a form of hierarchy. I also showed how Steve “The Noticer” Sailer is a racist. Both of these men’s views are racist. I then discussed Winegard’s definitions, showing that they are all good definitions of the term under discussion. I then turned to how Jensen ran with racist Nazis and how Cofnas cited researchers who called for tailored training programs.
That the HBD movement promotes the idea that differences in socially valued traits are genetic in nature through pseudoscientific theories along with the fact that it quite obviously is an attempt at justifying a human hierarchy of socially valued traits means that there is no question about it—the HBD movement is a racist movement.
(P1) If the HBD movement promotes and justifies racial hierarchies and inequities, then it is a racist movement.
(P2) The HBD movement promotes and justifies racial hierarchies and inequities.
(C) So the HBD movement is a racist movement.
The Rockefeller Foundation’s Failure in Finding a General Intelligence Factor in Dogs
2000 words
Introduction
Hereditarians have been trying to prove the existence of a genetic basis of intelligence for over 100 years. In this time frame, they have used everything from twin, family and adoption studies to tools from the molecular genetics era like GCTA and GWAS. Using heritability estimates, behavior geneticists claim that since intelligence is highly heritable, that there must thusly be a genetic basis to intelligence controlled by many genes of small effect, meaning it’s highly polygenic.
In his outstanding book Misbehaving Science, Panofsky (2014) discusses an attempt funded by the Rockefeller Foundation (RF) at showing a genetic basis to dog intelligence to prove that intelligence had a genetic basis. But it didn’t end up working out for them—in fact, it showed the opposite. The investigation which was funded by the RF showed quite the opposite result that they were looking for—while they did find evidence of some genetic differences between the dog breeds studied, they didn’t find evidence for the existence of a “general factor of intelligence” in the dogs. This issue was explored in Scott and Fuller’s 1965 book Genetics and the Social Behavior of the Dog. These researchers, though, outright failed in their task to discover a “general intelligence” in dogs. Modern-day research also corroborates this notion.
The genetic basis of dog intelligence?
This push to breed a dog that was highly intelligent was funded by the Rockefeller Foundation for ten years at the Jackson Laboratory. Panofsky (2014: 55) explains:
Over the next twenty years many scientists did stints at Jackson Laboratory working on its projects or attending its short courses and training programs. These projects and researchers produced dozens of papers, mostly concerning dogs and mice, that would form much of the empirical base of the emerging field. In 1965 Scott and John Fuller, his research partner, published Genetics and the Social Behavior of the Dog. It was the most important publication to come out of the Jackson Lab program. Scott and Fuller found many genetic differences between dog breeds; they did not find evidence for general intelligence or temperament. Dogs would exhibit different degrees of intelligence or temperamental characteristics depending on the situation. This evidence of interaction led them to question the high heritability of human intelligence—thus undermining a goal of the Rockefeller Foundation sponsors who had hoped to discredit the idea that intelligence was the product of education. Although the behavioral program at Jackson Laboratory declined after this point, it had been the first important base for the new field.
Quite obviously this was the opposite result of what they wanted—dog intelligence was based on the situation and therefore context-dependent.
Scott and Fuller (1965) discuss how they used to call their tests “intelligence tests” but then switched to calling them “performance tests”, “since the animals
seemed to solve their problems in many ways other than through pure thought or
intellect” (Scott and Fuller 1965: 37), while also writing that “no evidence was found for a general factor of intelligence which would produce good performance on all tests” (1965, 328). They also stated that they found nothing like the general intelligence factor in dogs like that is found in humans (1965: 472) while also stating that it’s a “mistaken notion” to believe in the general intelligence factor (1965: 512). They then conclude, basically, that situationism is valid for dogs, writing that their “general impression is that an individual from any dog breed will perform well in a situation in which he can be highly motivated and for which he has the necessary physical capacities” (1965: 512). Indeed, Scott noted that due to the heritability estimates of dog intelligence Scott came to the conclusion that human heritability estimates “are far too high” (quoted in Paul, 1998: 279). This is something that even Schonemann (1997) noted—and it’s “too high” due to the inflation of heritability due to the false assumptions of twin studies, which lead to the missing heritability crisis. One principle finding was that genetic differences didn’t appear early in development, which were then molded by further experience in the world. Behavior was highly variable between individuals and similar within breeds.
The results were quite unexpected but scientifically exciting. During the very early stages of development there was so little behavior observed that there was little opportunity for genetic differences to be expressed. When the complex patterns of behavior did appear, they did not show pure and uncontaminated effects of heredity. Instead, they were extraordinarily variable within an individual and surprisingly similar between individuals. In short, the evidence supported the conclusion that genetic differences in behavior do not appear all at once early in development, to be modified by later experience, but are themselves developed under the influence of environmental factors and may appear in full flower only relatively late in life. (Scott and Fuller, 1965)
The whole goal of this study by the Jackson Lab was to show that there was a genetic basis to intelligence in dogs and that they therefore could breed a dog that was intelligent and friendly (Paul, 1998). They also noted that there was no breed which was far and above the best at the task in question. Scott and Fuller found that performance on their tests was strongly affected by motivational and emotional factors. They also found that breed differences were strongly influenced by the environment, where two dogs from different breeds became similar when raised together. We know that dogs raised with cats showed more favorable disposition towards them (Fox, 1958; cf Feuerstein and Terkel, 2008, Menchetti et al, 2020). Scott and Fuller (1965: 333) then concluded that:
On the basis of the information we now have, we can conclude that all breeds show about the same average level of performance in problem solving, provided they can be adequately motivated, provided physical differences and handicaps do not affect the tests, and provided interfering emotional reactions such as fear can be eliminated. In short, all the breeds appear quite similar in pure intelligence.
The issue is that by believing that heritability shows anything about how “genetic” a trait is, one then inters that there has to be a genetic basis to the trait in question, and that the higher the estimate, the more strongly controlled by genes the trait in question is. However, we now know this claim to be false (Moore and Shenk, 2016). More to the point, the simple fact that IQ shows higher heritability than traits in the animal kingdom should have given behavioral geneticists pause. Nonetheless, it is interesting that this study that was carried out in the 1940s showed a negative result in the quest to show a genetic basis to intelligence using dogs, since dogs and humans quite obviously are different. Panofsky (2014: 65) also framed these results with that of rats that were selectively bred to be “smart” and “dumb”:
Further, many animal studies showed that strain differences in behavior were not independent of environment. R. M. Cooper and J. P. Zubek’s study of rats selectively bred to be “dull” and “bright” in maze-running ability showed dramatic differences between the strains in the “normal” environment. But in the “enriched” and especially the “restricted” developmental environments, both strains’ performance were quite similar. Scott and Fuller made a similar finding in their comparative study of dog breeds: “The behavior traits do not appear to be preorganized by heredity. Rather a dog inherits a number of abilities which can be organized in different ways to meet different situations.” Thus even creatures that had been explicitly engineered to embody racial superiority and inferiority could not demonstrate the idea in any simple way
Psychologist Robert Tryon (1940) devised a series of mazes, ran rats through them and then selected rats that learned quicker and slower (Innis, 1992). These differences then seemed to persists across these rat generations. Then Searle (1949) discovered that the so-called “dumb” rats were merely afraid of the mechanical noise of the maze, showing that Tryon selected for—unknowingly—emotional capacity. Marlowitz (1969) then concluded “that the labels “maze-bright” and “maze-dull” are inexplicit and inappropriate for use with these strains.”
Dogs and human races are sometimes said to be similar, in which a dog breed can be likened to a human race (see Norton et al, 2019). However, dog breeds are the result of conscious human selection for certain traits which then creates the breed. So while Scott and Fuller did find evidence for a good amount of genetic differences between the breeds they studied, they did not find any evidence of a genetic basis of intelligence or temperament. This is also good evidence for the claim that a trait can be heritable (have high heritability) but have no genetic basis. Moreover, we know that high levels of training improve dog’s problem solving ability (Marshall-Pescini et al, 2008, 2016). Further, perceived differences in trainability are due to physical capabilities and not cognitive ones (Helton, 2008). And in Labrador Retrievers, post-play training also improved training performance (Affenzeller, Palme, and Zulch, 2017; Affenzeller, 2020). Dogs’ body language during operant conditioning was also related to their success rate in learning (Hasegawa, Ohtani, and Ohta, 2014). We also know that dogs performed tasks better and faster the more experience they had with them, not being able to solve the task before seeing it demonstrated by the human administering the task (Albuquerque et al, 2021). Gnanadesikan et al (2020) state that cognitive phenotypes seem to vary by breed, and that these phenotypes have strong potential to be artificially selected, but we have seen that this is an error. Morrill et al (2022) found no evidence that the behavioral tendencies of certain breeds reflected intentional selection by humans but could not discount the possibility.
Conclusion
Dog breeds have been used by hereditarians for decades as a model for that of intelligence differences between human races. The analogy that dog breeds and human races are also similar has been used to show that there is a genetic basis for human race, and that human races are thusly a biological reality. (Note that I am a pluralist about race.) But we have seen that in the 40s the study which was undertaken to prove a hereditary basis to dog intelligence and then liken it to human intelligence quite obviously failed. This then led one of the authors to conclude—correctly—that human heritability estimates are inflated (which has led to the missing heritability problem of the 2000s).
Upon studying the dogs in their study, they found that there was no general factor of intelligence in these dogs, and that the situation was paramount in how the dog would perform on the task in question. This then led Scott to conclude that human heritability estimates are too high, a conclusion echoed by modern day researchers like Schonemann. The issue is, if dogs with their numerous breeds and genetic variation defy a single general factor, what would that mean for humans? This is just more evidence that “general intelligence” is a mere myth, a statistical abstraction. There was also no evidence for a general temperament, since breeds that were scared in one situation were confident in another (showing yet again that situationism held here). The failure of the study carried out by the RF then led to the questioning of the high heritability of human intelligence (IQ), which wasn’t forgotten as the decades progressed. Nonetheless, this study casted doubt on the claim that intelligence had a genetic basis.
Why, though, would a study of dogs be informative here? Well, the goal was to show that intelligence in dogs had a hereditary component and that thusly a kind of designer dog could be created that was friendly and intelligent, and this could then be likened to humans. But when the results were the opposite of what they desired, the project was quickly abandoned. If only modern-day behavioral geneticists would get the memo that heritability isn’t useful for what they want it to be useful for (Moore and Shenk, 2016)
Racial Differences in Motor Development: A Bio-Cultural View of Motor Development
3050 words
Introduction
Psychologist J. P. Rushton was perhaps most famous for attempting to formulate a grand theory of racial differences. He tried to argue that, on a matrix of different traits, the “hierarchy” was basically Mongoloids > Caucasoids > Negroids. But Rushton’s theory was met with much force, and many authors in many of the different disciplines in which he derived his data to formulate his theory attacked his r/K selection theory also known as Differential K theory (where all humans are K, but some humans are more K than others, so some humans are more r than others). Nonetheless, although his theory has been falsified for many decades, did he get some things right about race? Well, a stopped clock is right twice a day, so it wouldn’t be that outlandish to believe that Rushton got some things right about racial differences, especially when it comes to physical differences. While we can be certain that there are physical differences in groups we term “racial groups” and designate “white”, “black”, “Asian”, “Native American”, and “Pacific Islander” (the five races in American racetalk), this doesn’t lend credence to Rushton’s r/K theory.
In this article, I will discuss Rushton’s claims on motor development between blacks and whites. I will argue that he basically got this right, but it is of no consequence to the overall truth of his grand theory of racial differences. We know that there are physical differences between racial groups. But that there are physical differences between racial groups doesn’t entail that Rushton’s grand theory is true. The only entailment, I think, that can be drawn from that is there is a possibility that physical differences between races could exist between them, but it is a leap to attribute these differences to Rushton’s r/K theory, since it is a falsified theory on logical, empirical and methodological grounds. So I will argue that while Rushton got this right, a stopped clock is right twice a day but this doesn’t mean that his r/K theory is true for human races.
Was Rushton right? Evaluating newer studies on black-white motor development
Imagine three newborns: one white, one black and the third Asian and you observe the first few weeks of their lives. Upon observing the beginnings of their lives, you begin to notice differences in motor development between them. The black infant is more motorically advanced than the white infant who is more motorically advanced than the Asian infant. The black infant begins to master movement, coordination and dexterity showing a remarkable level of motoric dexterity, while the white infant shows less motoric dexterity than the black infant, and the Asian infant still shows lower motoric dexterity than the white infant.
These disparities in motor development are evidence in the early stages of life, so is it genetic? Cultural? Bio-cultural? I will argue that what explains this is a bio-cultural view, and so it will of course eschew reductionism, but of course as infants grow and navigate through their cultural milieu and family lives, this will have a significant effect on their experiences and along with it their motoric development.
Although Rushton got a lot wrong, it seems that he got this issue right—there does seem to be differences in precocity of motor development between the races, and the references he cites below in his 2000 edition of Race, Evolution, and Behavior—although most are ancient compared to today’s standards—hold to scrutiny today, where blacks walk earlier than whites who walk earlier than Asians.
Rushton (2000: 148-149) writes:
Revised forms of Bayley’s Scales of Mental and Motor Development administered in 12 metropolitan areas of the United States to 1,409 representative infants aged 1-15 months showed black babies scored consistently above whites on the Motor Scale (Bayley, 1965). This difference was not limited to any one class of behavior, but included: coordination (arm and hand); muscular strength and tonus (holds head steady, balances head when carried, sits alone steadily, and stands alone); and locomotion (turns from side to back, raises self to sitting, makes stepping movements, walks with help, and walks alone).
Similar results have been found for children up to about age 3 elsewhere in the United States, in Jamaica, and in sub-Saharan Africa (Curti, Marshall, Steggerda, & Henderson, 1935; Knobloch & Pasamanik, 1953; Williams & Scott, 1953; Walters, 1967). In a review critical of the literature Warren (1972) nonetheless reported evidence for African motor precocity in 10 out of 12 studies. For example, Geber (1958:186) had examined 308 children in Uganda and reported an “all-round advance of development over European standards which was greater the younger the child.” Freedman (1974, 1979) found similar results in studies of newboms in Nigeria using the Cambridge Neonatal Scales (Brazelton & Freedman, 1971).
Mongoloid children are motorically delayed relative to Caucasoids. In a series of studies carried out on second- through fifth-generation Chinese-Americans in San Francisco, on third- and fourth-generation Japanese-Americans in Hawaii, and on Navajo Amerindians in New Mexico and Arizona, consistent differences were found between these groups and second- to fourth-generation European-Americans using the Cambridge Neonatal Scales (Freedman, 1974, 1979; Freedman & Freedman, 1969). One measure involved pressing the baby’s nose with a cloth, forcing it to breathe with its mouth. Whereas the average Chinese baby fails to exhibit a coordinated “defense reaction,” most Caucasian babies turn away or swipe at the cloth with the hands, a response reported in Western pediatric textbooks as the normal one.
On other measures including “automatic walk,” “head turning,” and “walking alone,” Mongoloid children are more delayed than Caucasoid children. Mongoloid samples, including the Navajo Amerindians, typically do not walk until 13 months, compared to the Caucasian 12 months and Negro 11 months (Freedman, 1979). In a standardization of the Denver Developmental Screening Test in Japan, Ueda (1978) found slower rates of motoric maturation in Japanese as compared with Caucasoid norms derived from the United States, with tests made from birth to 2 months in coordination and head lifting, from 3 to 5 months in muscular strength and rolling over, at 6 to 13 months in locomotion, and at 15 to 20 months in removing garments.
Regarding newer studies on this matter, there are differences between European and Asian children in the direction that Rushton claimed. Infants from Hong Kong displayed a difference sequence of rolling compared to Canadian children. There does seem to be a disparity in motoric development between Asian and white children (Mayson, Harris, and Bachman, 2007). These authors do cite some of the same studies like the DDST (which is currently outdated) which showed how Asian children were motorically delayed compared to white children. And although they put caution on their findings of their literature review, it’s quite clear that this pattern exists and it is a bio-cultural one. So they conclude their literature review writing “the literature reviewed suggests differences in rate of motor development among children of various ethnic origins, including those of Asian and European descent” and that “Limited support suggests also that certain developmental milestones, such as rolling, may differ between infants of Asian and European origin.” Further, cultural practices in northern China—for example, lying them on their backs on sandbags—stall the onset of walking in babies sitting, crawling, and walking by a few months (Karasik et al, 2011).
This is related to the muscles that are used to roll from a supine to prone position and vice versa. Since some Asian children spend a longer time in apparatuses that aren’t conducive to growing a strong muscular base to be able to roll from the supine to prone position, to crawl and eventually walk, this is the “cultural” in the “bio-cultural” approach I will argue for.
One study on Norwegian children found that half of the children were waking by 13 months (the median) while 25 percent were walking by 12 months and 75 percent were walking by 14 months (Storvold, Aarethun, and Bratberg, 2013). One reason for the delayed response time could be supine sleeping, which was put into effect during the Back to Sleep program to mitigate causes of death from SIDS. Although it obviously saved tens of thousands of infant lives, it came at a cost of slightly stunted motoric development. It also seems that there is poor predictive value for infant milestones such as walking when it comes to health (Jenni et al, 2012).
Black Caribbean, black African and Indian infants were less likely to show delays in gross motor milestones compared to white infants. But Pakistani and Bangladeshi infants were more likely to be delayed in motoric development and communicative gestures, which was partly attributed to socio-cultural factors (Kelly et al, 2006). Kelly et al (2006: 828) also warn against genetic conclusions based on their large findings of difference between white and African and Caribbean infants:
The differences we observed between Black African and Black Caribbean compared with White infants are large and remain unaffected after adjusting for important covariates. This makes it tempting to conclude that the remaining effect must be a consequence of genetic differences. However, such a conclusion would be prematurely drawn. First, we have not included the measurement of genetic factors in our analysis, and, therefore, the presence of such effects cannot be demonstrated. Second, speculating on such effects should only be done alongside recognition that the model we have been able to test contains imperfect measurement.
It has also been observed that black and white children achieved greater mastery of motoric ability (locomotor skills) compared to Asian children but there was no difference by age group (Adeyemi-Walker et al, 2018). It was also found that infants with higher motor development scores had a lower weight weight relative to their length as they grew. So it was found that delayed motor development was associated with higher weight relative to length (Shoaibi et al, 2018). Black infants are also more motorically advanced and this is seen at up to two years of age (Malina, 1988) while black children perform better on tests of motor ability than white children (Okano et al, 2001). Kilbride et al (1970) also found that Baganda infants in Uganda showed better motoric ability than white American children. Campbell and Heddeker (2001) also showed that black infants were more motorically advanced than infants of other races.
It is clear that research like this blows up the claim that there should be a “one-size fits all” chart for motoric development in infants and that there should be race-specific milestones. This means that we should throw out the WEIRD assumptions when it comes to motoric development of infants (Karasik et al, 2011). They discuss research in other cultures where African, Caribbean and Indian caregivers massage the muscles of babies, stretch their limbs, toss them in their air, sit them up, and walk with them while helping them which then shapes their muscles and has them learn the mind-muscle connections needed to be able to learn how to eventually walk. And it also seems that random assignment to exercise excelerates how quickly an infant walks. White infants also sit at 6 months while black infants sit at 4 months. Nonetheless, it is clear that culture and context can indeed shape motoric development in groups around the world.
A bio-cultural view of motor development
When it comes to biological influences on motor development, sex and age are two important variables (Escolano-Perez, Sanchez-Lopez, and Herrero-Nivela, 2021). Important to this, of course, is that the individual must be normal, and they must have a normal brain with normal vision and spatial skills. They must be able to hear (to eventually follow commands and hear what is going on in their environment to change their course of action if need be). Further, the child’s home environment and gestational age influence different portions of motoral development (Darcy, 2022). After infants begin crawling, their whole world changes and they process visual motion better and faster, being able to differentiate between different speeds and directions, so a stimulating environment for the infant can spur the development of the brain (Van der Meer and Van der Weel, 2022). Biological maturation and body weight also affect motor development. Walking develops naturally, but walking and motor competence need to be nurtured for the child to reach their full potential; lower motor competence is related to higher body weight (Drenowatz and Greier, 2019).
One study on Dutch and Israeli infants even found—using developmental niche construction—that “infant motor development indeed is at least partly culturally constructed [which] emphasizes the importance of placing infant motor development studies into their ‘cultural cradle‘ (Oudgeneong, Atun-Eni, and Schaik, 2020). Gross motor development—rolling over, crawling, alternating kicks, moving from lying to sitting, and having tummy time—is recognized by the WHO. Further, children from different cultures have different experiences, which also could lead to, for example, not doing things that are conducive to the development of gross motor development (Angulo-Barroso et al, 2010). Moreover, motor development is embodied, enculturated, embedded, and enabling (Adolph and Hoch, 2020). It is also known that differences in the cultural environment “have a non-negligible effect on motor development” (Bril, 1986). Motor development also takes place in physical environments and is purposive and goal-directed (Hallemans, Verbeque, and de Walle, 2020).
So putting this all together, we have conceptualized motor development as a dynamic process which is influenced by a complex interplay of biological and cultural factors (Barnes, Zieff, and Anderson, 1999). Biological factors like sex, age, health, sensory abilities, and socio-cultural factors like home environment and developmental niches explain motor development and differences in them between individuals. The cultural differences, though, can impede motoral development, and not allow one to reach milestones they would have otherwise reached in a different cultural environment, just like if one couldn’t hear or see would have trouble reaching developmental milestones.
Children of course grow up in cultural environments and contexts and so they are culturally situated. So what this means is that both the cultural and social environment the child finds themselves in will of course then influence their physical and mental development and lead them to their milestones they hit which is dictated by the normal biology they have which then is allowed by the socio-cultural environment they are born into. So we have the bio-cultural view on motor development, and beyond the cultural environment the child finds themselves in, the interactions they have between parents and caregivers—more knowledgeable others—can be pertinent to their motor development and reaching of developmental milestones. Cultural practices and expectations could emphasize certain milestones over others and then guide the child towards the trajectory. So the framework recognizes that normal biology and sensory perceptions are needed for the development of normal motor development, but that cultural and social differences in that context will spur motor development in the child who finds themselves in different cultures.
Conclusion
Was Rushton right about this? Yes, I think he was. The recent literature on the matter speaks to this. But that doesn’t mean that his r/K selection theory is true. There are differences in motor development between races. But what is interesting is the interaction between biological and cultural factors that spur motor development. The question of black motor precocity, however, is a socio-political question, since science is a social convention influenced by the values of the scientist in question. Now, to the best of my knowledge, Rushton himself never carried out studies on this, he just collated them to use them for his racial trait matrix. However, it’s quite clear that Rushton was politically politically and socially motivated to prove that his theory was true.
But physical differences between the races are easy enough to prove, and of course they are due to biological and cultural interactions. There are differences in skin color and their properties between blacks and whites (Campiche et al, 2019). There is a 3 percent center of mass difference between blacks and whites which explains why each race excels at running and swimming (Bejan, Jones, and Charles, 2010). There are differences in body composition between Asians and whites which means, at the same BMI, Asians would have thicker skin folds and higher body fat than whites (Wang et al, 1994; WHO expert consultation, 2004; Wang et al, 2011). Just like at the same BMI, blacks have lower body fat and thinner skin folds than whites (Vickery, Cureton, and Collins, 1988; Wagner and Heyward, 2000; Flegal et al, 2010). There are differences in menarche and thelarche between blacks and whites (Wagner and Heyward, 2000; Kaplowitz, 2008; Reagan et al, 2013; Cabrera et al, 2014; Deardorff et al, 2014; ). There are differences in anatomy and physiology and somatotype between blacks and whites and these differences would explain how the races would perform on the big four lifts. There are interesting and real physical differences between races.
So obviously, what is considered “normal” is different in different cultures, and motor development is no different. So just like I think we should have different BMI and skin fold charts for different races, so too should we have different developmental milestones for different races and cultures. The discussion here is clear, since what is “average” and “normal” is different based on race and culture. Like for instance, black babies begin walking around 11 months, white babies around 12 months and Native American babies at 13 months. So while parents may be worried that their child didn’t hit a certain developmental milestone like walking, sitting, rolling, taking a bio-cultural approach will assuage these worries.
Nonetheless, while Rushton was right about race and motor development, we need to center his research project in context. He was clearly motivated, despite the numerous and forceful critiques of his framework, to prove that he was right. But the continuance of Rushton pushing his theory up until his death shows me that he was quite obviously socially and politically motivated, contrary to what he may have said.
We have approached this paper from the stance that science is a social activity, with all observations influenced by, as well as reflective of, the values of scientists and the political leanings of the sociocultural context within which research is conducted. We suggest that when questions of group difference are pursued in science, awareness of how the categories themselves have been shaped by social and historical forces, as well as of the potential effects on society, is important. (Barnes, Zieff, and Anderson, 1999)
“Missing Heritability” and Missing Children: On the Issues of Heritability and Hereditarian Interpretations
3100 words
“Biological systems are complex, non-linear, and non-additive. Heritability estimates are attempts to impose a simplistic and reified dichotomy (nature/nurture) on non-dichotomous processes.” (Rose, 2006)
“Heritability estimates do not help identify particular genes or ascertain their functions in development or physiology, and thus, by this way of thinking, they yield no causal information.” (Panofsky, 2016: 167)
“What is being reported as ‘genetic’, with high heritability, can be explained by difference-making interactions between real people. In other words, parents and children are sensitive, reactive, living beings, not hollow mechanical or statistical units.” (Richardson, 2022: 52)
Introduction
In the world of behavioral genetics, it is claimed that studies of twins, adoptees and families can point us to the interplay between genetic and environmental influences on complex behavioral traits. To study this, they use a concept called “heritability”—taken from animal breeding—which estimates the the degree of variation in a phenotypic trait that is due to genetic variation amongst individuals in the studied population. But upon the advent of molecular genetic analysis after the human genome project, something happened that troubled behavioral genetic researchers: The heritability estimates gleaned from twin, family and adoption studies did not match the estimates gleaned from the molecular genetic studies. This then creates a conundrum—why do the estimates from one way of gleaning heritability don’t match to other ways? I think it’s because biological models represent a simplistic (and false) model of biological causation (Burt and Simon, 2015; Lala, 2023). This is what is termed “missing heritability.” This raises questions that aren’t dissimilar to when a child dissappears.
Imagine a missing child. Imagine the fervor a family and authorities go through in order to find the child and bring them home. The initial fervor, the relentless pursuit, and the agonizing uncertainty constitute a parallel narrative in behavioral genetics, where behavioral geneticists—like the family of a missing child and the authorities—find themselves grappling with unforseen troubles. In this discussion, I will argue that the additivity assumption is false, that this kind of thinking is a holdover from the neo-Darwinian Modern Synthesis, that hereditarians have been told for decades that heritability just isn’t useful for what they want to do, and finally “missing heritability” and missing children are in some ways analogous, but that there is a key difference: The missing children actually existed, while the “missing heritability” never existed at all.
The additivity assumption
Behavioral geneticists pay lip service to “interactions”, but then conceptualize these interactions as due to additive heritability (Richardson, 2017a: 48-49). But the fact of the matter is, genetic interactions create phantom heritability (Zuk et al, 2012). When it comes to the additive claim of heritability, that claim is straight up false.
The additive claim is one of the most important things for the utility of the concept of heritability for the behavioral geneticist. The claim that heritability estimates for a trait are additive means that the contribution of each gene variant is independent and they all sum up to explain the overall heritability (Richardson 2017a: 44 states that “all genes associated with a trait (including intelligence) are like positive or negative charges“). But in reality, gene variants aren’t independent effects, they interact with other genes, the environment and other developmental resources. In fact, violations of the additivity assumption are large (Daw, Guo, and Harris, 2015).
Gene-gene, gene-environment, and environmental factors can lead to overestimates of heritability, and they are non-additive. So after the 2000s with the completion of the human genome project, these researchers realized that the genetic variants that heritability they identified using molecular genetics did not jive with the heritability they computed from twin studies from the 1920s until the late 1990s and then even into the 2020s. So the expected additive contribution of heritability fell short in actually explaining the heritability gleaned from twin studies using molecular genetic data.
Thinking of heritability as a complex jigsaw puzzle may better help to explain the issue. The traditional view of heritability assumes that each genetic piece fits neatly into the puzzle to then complete the overall genetic picture. But in reality, these pieces may not be additive. They can interact in unexpected ways which then creates gaps in our understanding, like a missing puzzle piece. So the non-additive effects of gene variants which includes interactions and their complexities, can be likened to missing pieces in the heritability puzzle. The unaccounted-for genetic interactions and nuances then contribute to what is called “missing heritability.” So just as one may search and search for missing puzzle pieces, so to do behavioral geneticists search and search for the “missing heritability”.
So heritability assumes no gene-gene and gene-environment interaction, no gene-environment correlation, among other false or questionable assumptions. But the main issue, I think, is that of the additivity assumption—it’s outright false and since it’s outright false, then it cannot accurately represent the intricate ways in which genes and other developmental resources interact to form the phenotype.
If heritability estimates assume that genetic influences on a trait are additive and independent, then heritability estimates oversimplify genetic complexity. If heritability estimates oversimplify genetic complexity, then heritability estimates do not adequately account for gene-environment interactions. If heritability does not account for gene-environment interactions, then heritability fails to capture the complexity of trait inheritance. Thus, if heritability assumes that genetic influences on a trait are additive and independent, then heritability fails to capture the complexity of trait inheritance due to its oversimplified treatment of genetic complexity and omission of gene-environment interactions.
One more issue, is that of the “heritability fallacy” (Moore and Shenk, 2016). One commits a heritability fallacy when they assume that heritability is an index of genetic influence on traits and that heritability can tell us anything about the relative contribution of trait inheritance and ontogeny. Moore and Shenk (2016) then make a valid conclusion based on the false belief that heritability us anything about the “genetic strength” on a trait:
In light of this, numerous theorists have concluded that ‘the term “heritability,” which carries a strong conviction or connotation of something “[in]heritable” in the everyday sense, is no longer suitable for use in human genetics, and its use should be discontinued.’31 Reviewing the evidence, we come to the same conclusion. Continued use of the term with respect to human traits spreads the demonstrably false notion that genes have some direct and isolated influence on traits. Instead, scientists need to help the public understand that all complex traits are a consequence of developmental processes.
“Missing heritability”, missing children
Twin studies traditionally find heritability to be estimated between 50 and 80 percent for numerous traits (eg Polderman et al, 2015; see Joseph’s critique). But as alluded to earlier, molecular studies have found heritabilities of 10 percent or lower (eg, Sniekers et al, 2017; Savage et al, 2018; Zabaneh et al, 2018). This discrepancy between different heritability estimates using different tools is what is termed “missing heritability” (Mathhews and Turkheimer, 2022). But the issue is, increasing the sample sizes will merely increase the chance of spurious correlations (Calude and Longo, 2018), which is all these studies show (Richardson, 2017b; Richardson and Jones, 2019).
This tells me one important thing—behavioral geneticists have so much faith in the heritability estimates gleaned from twin studies that they assume that the heritability is “missing” in the newer molecular genetic studies. But if something is “missing”, then that implies that it can be found. They have so much faith that eventually, as samples get higher and higher in GWAS and similar studies, that we will find the heritability that is missing and eventually, be able to identify genetic variants responsible for traits of interest such as IQ. However I think this is confused and a simple analogy will show why.
When a child goes missing, it is implied that they will be found by authorities, whether dead or alive. Now I can liken this to heritability. The term “missing heritability” comes from the disconnect between heritability estimates gleaned from twin studies and heritability estimates gleaned from molecular genetic studies like GWAS. So the implication here is, since twin studies show X percent heritability (high heritability), and molecular genetic studies show Y percent heritability (low heritability) – which is a huge difference between estimates between different tools – then the implication is that there is “missing heritability” that must be explained by rare variants or other factors.
So just like parents and authorities try so hard to find their missing children, so to do behavioral geneticists try so hard to find their “missing heritability.” As families endure anguish as they try to find their children, this is then mirrored in the efforts of behavioral geneticists to try and close the gap between two different kinds of tools that glean heritability.
But there is an important issue at play here—namely the fact that missing children actually exist, but “missing heritability” doesn’t, and that’s why we haven’t found it. Although some parents, sadly, may never find their missing children, the analogy here is that behavioral geneticists will never find their own “children” (their missing heritability) because it simply does not exist.
Spurious correlations
Even increasing the sample sizes won’t do anything, since the larger the sample size, the bigger chance for spurious correlations, and that’s all GWAS studies for IQ are (Richardson and Jones, 2019), while correlations with GWAS are inevitable and meaningless (Richardson, 2017b). Denis Noble (2018) puts this well:
As with the results of GWAS (genome-wide association studies) generally, the associations at the genome sequence level are remarkably weak and, with the exception of certain rare genetic diseases, may even be meaningless (13, 21). The reason is that if you gather a sufficiently large data set, it is a mathematical necessity that you will find correlations, even if the data set was generated randomly so that the correlations must be spurious. The bigger the data set, the more spurious correlations will be found (3). The current rush to gather sequence data from ever larger cohorts therefore runs the risk that it may simply prove a mathematical necessity rather than finding causal correlations. It cannot be emphasized enough that finding correlations does not prove causality. Investigating causation is the role of physiology.
Nor does finding higher overall correlations by summing correlations with larger numbers of genes showing individually tiny correlations solve the problem, even when the correlations are not spurious, since we have no way to find the drugs that can target so many gene products with the correct profile of action.
The Darwinian model
But the claim that there is a line that goes from G (genes) to P (phenotype) is just a mere holdover from the neo-Darwinian modern synthesis. The fact of the matter is, “HBD” and hereditarianism are based on reductionistic models of genes and how they work. But the reality is, genes don’t work how they think they do, reality is much more complex than they assume. Feldman and Ramachandran (2018) ask “Missing compared to what?”, effectively challenging the “missing heritability” claim. As Feldman and Ramachandran (2018) ask, would Herrnstein and Murray have written The Bell Curve if they believed that the heritability of IQ were 0.30? I don’t think they would have. In any case, such a belief in the heritability of IQ being between 0.4 and 0.8 shows the genetic determinist assumptions which are inherent in this type of “HBD” genetic determinist thinking.
Amusingly, as Ned Block (1995) noted, Murray said in an interview that “60 percent of the intelligence comes from heredity” and that that heritability is “not 60 percent of the variation. It is 60 percent of the IQ in any given person.” Such a major blunder from one of the “intellectual spearheads” of the “HBD race realist” movement…
Behavioral geneticists claim that the heritability is missing only because sample sizes are low, and as sample sizes increase, the missing heritability based on associated genes will be found. But this doesn’t follow at all since increasing sample sizes will just increase spurious hits of genes correlated with the trait in question but it says absolutely nothing about causation. Nevertheless, only a developmental perspective can provide us mechanistic knowledge and so-called heritability of a phenotype cannot give us such information because heritability isn’t a mechanistic variable and doesn’t show causation.
Importantly, a developmental perspective provides mechanistic knowledge that can yield practical treatments for pathologies. In contrast, information about the “heritability” of a phenotype—the kind of information generated by twin studies—can never be as useful as information about the development of a phenotype, because only developmental information produces the kind of thorough understanding of a trait’s emergence that can allow for successful interventions. (Moore 2015: 286)
The Darwinian model and it’s assumptions are inherent in thinking about heritability and genetic causation as a whole and are antithetical to developmental, EES-type thinking. Since hereditarianism and HBD-type thinking are neo-Darwinist, it then follows that such thinking is inherent in their beliefs, assumptions, and arguments.
Conclusion
Assumptions of heritability simply do not hold. Heritability, quite simply, isn’t a characteristic of traits but it is a characteristic of “relationships in a population observed in a particular setting” (Oyama, 1985/2000). Heritability estimates tell us absolutely nothing about development, nor the causes of development. Heritability is a mere breeding statistic and tells us nothing at all about the causes of development or whether or not genes are “causal” for a trait in question (Robette, Genin, and Clerget-Darpoux, 2022). It is key to understand that heritability along with the so-called “missing heritability” are based on reductive models of genetics that just do not hold, especially with newer knowledge that we have from systems biology (eg, Noble, 2012).
The assumption that heritability estimates tell us anything useful about genetics, traits, and causes along with a reductive belief in genetic causation for the ontogeny of traits has wasted millions of dollars. Now we need to grapple with the fact that heritability just doesn’t tell us anything about genetic causes of traits, but that genes are necessary, not sufficient, causes for traits because no genes (along with other developmental resources) means no organism. Also coming from twin, family and adoption studies are Turkheimer’s (2000) so-called “laws of behavioral genetics.” Further, the falsity of the EEA (equal environments assumption) is paramount here, and since the EEA is false, genetic conclusions from such studies are invalid (Joseph et al, 2015). There is also the fact that heritability is based on a false biological model. The issue is that heritability rests on a “conceptual model is unsound and the goal of heritability studies is biologically nonsensical given what we now know about the way genes work” (Burt and Simons, 2015: 107). What Richardson (2022) terms “the agricultural model of heritability” is known as false. In fact, the heritability of “IQ” is higher than any heritability found in the animal kingdom (Schonemann, 1997). Why this doesn’t give any researcher pause is beyond me.
Nonetheless, the Darwinian assumptions that are inherent in behavioral genetic, HBD “race realist” thinking are false. And the fact of the matter is, increasing the sample size of molecular genetic studies will only increase the chances of spurious correlations and picking up population stratification. So, it seems that using heritability to show genetic and environmental causes is a bust and has been a bust ever since Jensen revived the race and IQ debate in 1969, along with the subsequent responses that Jensen received against his argument which then led to the 1970s as being a decade in which numerous arguments were made against the concept of heritability (eg, Layzer, 1974).
It has also been pointed out to racial hereditarians for literally decades that heritability is is a flawed metric (Layzer, 1974; Taylor, 1980; Bailey, 1997; Schonemann, 1997; Guo, 2000; Moore, 2002; Rose, 2006; Schneider, 2007; Charney, 2012, 2013; Burt and Simons, 2015; Panofsky, 2014; Joseph et al, 2015; Moore and Shenk, 2016; Panofsky, 2016; Richardson, 2017; Lerner, 2018). These issues—among many more—lead Lerner to conclude:
However, the theory and research discussed across this chapter and previous ones afford the conclusion that no psychological attribute is pre-organized in the genes and unavailable to environmental influence. That is, any alleged genetic difference (or “inferiority”) of African Americans based on the high heritability of intelligence would seem to be an attribution built on a misunderstanding of concepts basic to an appropriate conceptualization of the nature–nurture controversy. An appreciation of the coaction of genes and context—of genes↔context relations—within the relational developmental system, and of the meaning, implications, and limitations of the heritability concept, should lead to the conclusion that the genetic-differences hypothesis of racial differences in IQ makes no scientific sense. (Lerner, 2018: 636)
That heritability doesn’t address mechanisms and ignores genetic factors, along with being inherently reductionist means that there is little to no utility of heritability for humans. And the complex, non-additive, non-linear aspects of biological systems are attempts at reducing biological systems to their component parts, (Rose, 2006), making heritability, again, inherently reductionist. We have to attempt to analyzed causes, not variances (Lewontin, 1974), which heritability cannot do. So it’s very obvious that the hereditarian programme which was revived by Jensen (1969)—and based on twin studies which were first undertaken in the 1920s—is based on a seriously flawed model of genes and how they work. But, of course, hereditarians have an ideological agenda to uphold, so that’s why they continue to pursue “heritability” in order to “prove” that “in part”, racial differences in many socio-behavioral traits—IQ included—are due to genes. But this type of argumentation quite clearly fails.
The fact of the matter is, “there are very good reasons to believe gene variations are at best irrelevant to common disorders and at worst a distraction from the social and political roots of major public health problems generally and of their unequal distribution in particular” (Chaufan and Joseph 2013: 284). (Also see Joseph’s, 2015 The Trouble with Twin Studies for more argumentation against the use of heritability and it’s inflation due to false assumptions along with arguments against “missing heritability.”) In fact, claims of “missing heritability” rest on “genetic determinist beliefs, a reliance on twin research, the use of heritability estimates, and the failure to seriously consider the possibility that presumed genes do not exist” (Joseph, 2012). Although it has been claimed that so-called rare variants explain the “missing heritability” (Genin, 2020), this is nothing but cope. So the heritability was never missing, it never existed at all.
Hypertension, Brain Volume, and Race: Hypotheses, Predictions and Actionable Strategies
2300 words
Introduction
Hypertension (HT, also known as high blood pressure, BP) is defined as a BP of 140/90. But more recently, the guidelines were changed making HT being defend as a BP over 130/90 (Carey et al, 2022; Iqbal and Jamal, 2022). One 2019 study showed that in a sample with an age range of 20-79, 24 percent of men and 23 percent of women could be classified as hypertensive based on the old guidelines (140/90) (Deguire et al, 2019). Having consistent high BP could lead to devestating consequences like (from the patient’s perspective) hot flushes, dizziness, and mood disorders (Goodhart, 2016). However, one serious problem with HT is the issue that consistently high BP is associated with a decrease in brain volume (BV). This has been seen in two systematic reviews and meta-analyses (Alosco et al, 2013; Beauchet et al, 2013; Lane et al, 2019; Alateeq, Walsh and Cherbuin, 2021; Newby et al, 2022) while we know that long-standing hypertension has deleterious effects on brain health (Salerno et al, 1992). However, it’s not only high BP that’s related to this, it’s also lower BP in conjuction with lower pulse pressure (Muller et al, 2010; Foster-Dingley, 2015). So what this says to me is that too much or too little blood flow to the brain is deleterious for brain health.I will state the hypothesis and then I will state the predictions that follow from it. I will then provide three reasons why I think this relationship occurs.
The hypothesis
The hypothesis is simple: high BP (hypertension, HT) is associated with a reduced brain volume. This relationship is dose-dependent, meaning that the extent and duration of HT correlates with the degree of BV changes. So the hypothesis suggests that there is a relationship—an association—between HT and brain volume, where people with HT will be more likely to have decreased BVs than those who lack HT—that is, those with BP in the normal range.
The dose-dependent relationship that has been observed (Alateeq, Walsh and Cherbuin, 2021), and this shows that as HT increases and persists over time, the effects of decreased BV become more pronounced. This relationship suggests that it’s not a binary, either-or situation, present or absent situation, but that it varies across a continuum. So people with shorter-lasting HT will have fewer effects than those with constant and consistent elevated BP and they will then show subsequent higher decreases in BV. This dose-dependent relationship also suggests that as BP continues to elevate, the decrease in BV will worsen.
This dose-dependent relationship implies a few things. The consequences of HT on BV aren’t binary (either or), but are related to the severity of HT, how long one has HT, and at what age they have HT and that it varies on a continuum. For instance, people with mild or short-lasting HT would experience smaller reductions in BV than those that have severe or long-standing HT. The dose-dependent relationship also suggests that the longer one has HT without treatment, the more severe and worse the reduction in BV will be if it is uncontrolled. So as BP continues to elevate, it may lead to a gradual reduction in BV. So the relationship between HT and BV isn’t uniform, but it varies based on the intensity and duration of high BP.
So the hypothesis suggests that HT isn’t just a risk factor for cardiovascular disease, but it’s also a risk factor for decreased BV. This seems intuitive, since the higher one’s BP, the more likely it is that there is the beginnings of a blockage somewhere in the intricate system of blood vessels in the body. And since the brain is a vascular organ, then by decreasing the amount of blood flowing to it, this then would lead to cell death, white matter lesions which would lead to a smaller BV. One newer study showed, with a sample of Asians, whites, blacks, and “Latinos” that, compared to those with normal BP, those who were transitioning to higher BP or already had higher BP had lower brain connectivity, decreased cerebral gray matter and frontal cortex volume, while this change was worse for men (George et al, 2023). Shang et al (2021) showed that HT diagnosed in early and middle life but not late life was associated with decreased BV and increased risk of dimentia. This, of course, is due to the slow cumulative effects of HT and it’s effects on the brain. While Power et al (2016) “The pattern of hypertension ~15 years prior and hypotension concurrent with neuroimaging was associated with smaller volumes in regions preferentially affected by Alzheimer’s disease.” But not only is BP relevant here, so is the variability of BP at night (Gutteridge et al, 2022; Yu et al, 2022). Alateeq, Walsh and Cherbuin (2021) conclude that:
Although reviews have been previously published in this area, they only investigated the effects of hypertension on brain volume [86]. To the best of our knowledge, this study’s the first systematic review with meta-analysis providing quantitative evidence on the negative association between continuous BP and global and regional brain volumes. Our results suggest that heightened BP across its whole range is associated with poorer cerebral health which may place individuals at increased risk of premature cognitive decline and dementia. It is therefore important that more prevention efforts be directed at younger populations with a greater focus on achieving optimal BP rather than remaining below clinical or pre-clinical thresholds[5].
One would think that a high BP would actually increase blood flow to the brain, but HT actually causes alterations in the flow of blood to the brain which leads to ischaemia and it causes the blood-brain barrier to break down (Pires et al, 2013). Essentially, HT has devestating effects on the brain which could lead to dimentia and Alzheimer’s (Iadecola and Davisson, 2009).
So the association between HT and decreased BV means that individuals with HT can experience alterations in BV in comparison to those with normal BP. The hypothesis also suggests that there are several mechanisms (detailed below), which may lead to various physiological and anatomic changes in the brain, such as vascular damage, inflammation and tissue atrophy.
The mechanisms
(1) High BP can damage blood vessels in the brain, which leads to reduced blood flow. This is called “cerebral hypoperfusion.” The reduced blood flow can deprive the cells in the brain of oxygen and nutrients, which cause them to shrink or die which leads to decreased brain volume (BV). Over time, high BP can damage the arteries, making them less elastic
(2) Over a long period of time having high BP, this can cause hypertensive encephalopathy, which is basically brain swelling. A rapid increase in BP could over the short term increase BV, but left untreated it could lead to brain damage and atrophy over time.
And (3) Chronically high BP can lead to the creation of white matter lesions on the brain, and the lesions are areas of damaged brain tissue which could result in microvascular changes caused by high BP (hypertension, HT). Thus, over time, the accumulation of white matter lesions could lead to a decrease in brain volume. HT can contribute to white matter lesions in the brain, which are then associated with cognitive changes and decreased BV, and these lesions increase with BP severity.
So we have (1) cerebral hypoperfusion, (2) hypertensive encephalopathy, and (3) white matter lesions. I need to think/read more on which of these could lead to decreased BV, or if they all actually work together to decrease BV. We know that HT damages blood vessels, and of course there are blood vessels in the brain, so it then follows that HT would decrease BV.
I can also detail a step-by-step mechanism. The process beings with consistently elevated BP, which could be due to various factors like genetics, diet/lifestyle, and underlying medical conditions. High BP then places increased strain on the blood vessels in the body, including those in the brain. This higher pressure could then lead to structural change of the blood vessels over time. Then, chronic HT over time can lead to endothelial dysfunction, which could impair the ability of blood vessels to regulate blood flow and maintain vessel integrity. The dysfunction can result in oxidative stress and inflammation.
Then as a response to prolonged elevated BP, blood vessels in the brain could undergo vascular remodeling, which involves changes im blood vessel structure and thickness, which can then affect blood flow dynamics. Furthermore, in some cases, this could lead to something called cerebral small vessel disease which involves damage to the small blood vessels in the brain including capillaries and arterioles. This could impair delivery of oxygen and nutrients to brain tissue which could lead to cell death and consequently a decrease in BV. Then reduced blood flow along compromised blood vessel integrity could lead to cerebral ischaemia—reduced blood supply—and hypoxia—reduced oxygen supply—in certain parts of the brain. This can then result in neural damage and eventually cell death.
Then HT-related vascular changes and cerebral small vessel disease can trigger brain inflammation. Prolonged exposure to neural inflammation, hypoxia and ischemia can lead to neuronal atrophy, where neurons shrink and lose their functional integrity. HT can also increase the incidence of white matter lesions in the brain which can be seen in neuroimages, which involve areas of white matter tissue which become damaged. Finally, over time, the cumulative effects of the aforementioned processes—vascular changes, inflammation, neural atrophy, and white matter changes could lead to a decrease in BV. This reduction can manifest as brain atrophy which is then observed in parts of the brain which are susceptible and vulnerable to the effects of HT.
So the step-by-step mechanism goes like this: elevated BP —> increased vascular strain —> endothelial dysfunction —> vascular remodeling —> cerebral small vessel disease —> ischemia and hypoxia —> inflammation and neuroinflammation —> neuronal atrophy —> white matter changes —> reduction in BV.
Hypotheses and predictions
H1: The severity of HT directly correlates with the extent of BV reduction. One prediction would be that people with more severe HT would exhibit greater BV decreases than those with moderate (less severe) HT, which is where the dose-dependent relationship comes in.
H2: The duration of HT is a critical factor in BV reduction. One prediction would be that people with long-standing HT will show more significant BV changes than those with recent onset HT.
H3: Effective BP management can mitigate BV reduction in people with HT. One prediction would be that people with more controlled HT would show less significant BV reduction than those with uncontrolled HT.
H4: Certain subpopulations may be more susceptible to BV decreases due to HT. One prediction is that certain factors like age of onset (HT at younger age), genetic factors (some may have certain gene variants that make them more susceptible and vulnerable to damage caused by elevated BP), comorbities (people with diabetes, obesity and heart problems could be at higher risk of decreased BV due to the interaction of these factors), ethnic/racial factors (some populations—like blacks—could be at higher risk of having HT and they could be more at risk due to experiencing disparities in healthcare and treatment.
The hypotheses and predictions generated from the main proposition that HT is associated with a reduction in BV and that the relationship is dose-dependent can be considered risky, novel predictions. They are risky in the sense that they are testable and falsifiable. Thus, if the predictions don’t hold, then it could falsify the initial hypothesis.
Blacks and blood pressure
Due to this, for populations like black Americans, this is significant. About 33 percent of blacks have hypertension (Peters, Arojan, and Flack, 2006), while urban blacks are more likely to have elevated BP than whites (Lindhorst et al, 2007). Though Non, Gravlee, and Mulligan (2012) showed that racial differences in education—not genetic ancestry—explained differences in BP in blacks compared to whites. Further, Victor et al (2018) showed that in black male barbershop attendees who had uncontrolled BP, that along with medication and outreach, this lead to a decrease in BP. Williams (1992) cited stress, socioecologic stress, social support, coping patterns, health behavior, sodium, calcium, and potassium consumption, alcohol consumption, and obesity as social factors which lead to increased BP.
Moreover, consistent with the hypothesis discussed here (that chronic elevated BP leads to reductions in BV which lead to a higher chance of dementia and Alzheimer’s), it’s been shown that vulnerability to HT is a major determinate in the risk of acquiring Alzheimer’s (Clark et al, 2020; Akushevic et al, 2022). It has also been shown that “a lifetime of racism makes Alzheimer’s more common in black Americans” and consistent with the discussion here since racism is associated with stress which is associated with elevated BP, then consistent events of racial discrimination would lead to consistent and elevated BP which would then lead to decreased BV and then a higher chance of acquitting Alzheimer’s. But, there is evidence that blood pressure drugs (in this case telmisartan) reduce the incidence of Alzheimer’s in black Americans (Zhang et al, 2022) while the same result was also seen using antihyperintensive medications in blacks which led to a reduction in incidence of dementia (Murray et al, 2018), which lends credence to the discussed hypothesis. Stress and poverty—experiences—and not ancestry could explain higher rates of dementia in black Americans as well. Thus, since blood pressure could explain higher rates of dementia in black populations, this then lends credence to the discussed hypothesis.
Conclusion
The evidence that chronic elevated BP leads to reductions in BV are well-studied and the mechanisms are well-known. I discussed the hypothesis that chronically elevated BP leads to reduced blood flow to the brain which decreases BV. I then discussed the mechanisms behind the relationship, and then hypotheses and predictions that follow from them. Lastly, I discussed the well-known fact that blacks have higher rates of BP, and also higher rates of dementia and Alzheimer’s, and linked the fact that they have higher rates of BP to those maladies.
So by catching chronically elevated BP in the early ages, since the earlier one has high BP the more likely they are to have reduced brain volume and the associated maladies, we can then begin to fight the associated issues before they coalesce, since we know the mechanisms behind them, along with the fact that blood pressure drugs and antihypertensive medications decrease incidences of dementia and Alzheimer’s in black Americans.
NotPoliticallyCorrect 