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The use of polygenic scores has caused much excitement in the field of socio-genomics. A polygenic score is derived from statistical gene associations using what is known as a genome-wide association study (GWAS). Using genes that are associated with many traits, they propose, they will be able to unlock the genomic causes of diseases and socially-valued traits. The methods of GWA studies also assume that the ‘information’ that is ‘encoded’ in the DNA sequence is “causal in terms of cellular phenotype” (Baverstock, 2019).
For instance it is claimed by Robert Plomin that “predictions from polygenic scores have unique causal status. Usually correlations do not imply causation, but correlations involving polygenic scores imply causation in the sense that these correlations are not subject to reverse causation because nothing changes the inherited DNA sequence variation.”
Take the stronger claim from Plomin and Stumm (2018):
GPS are unique predictors in the behavioural sciences. They are an exception to the rule that correlations do not imply causation in the sense that there can be no backward causation when GPS are correlated with traits. That is, nothing in our brains, behaviour or environment changes inherited differences in DNA sequence. A related advantage of GPS as predictors is that they are exceptionally stable throughout the life span because they index inherited differences in DNA sequence. Although mutations can accrue in the cells used to obtain DNA, like any cells in the body these mutations would not be expected to change systematically the thousands of inherited SNPs that contribute to a GPS.
This is a strange claim for two reasons.
(1) They do not, in fact, imply causation since the scores derived from GWA studies which are associational and therefore cannot show causes—GWA studies are pretty much giant correlational studies that scan the genomes of hundreds of thousands of people and look for genes that are more likely to be in the sample population for the disease/”trait” in question. These studies are also heavily skewed to European populations and, even if they were valid for European populations (which they are not), they would not be valid for non-European ethnic groups (Martin et al, 2017; Curtis, 2018; Haworth et al, 2018).
(2) The claim that “nothing changes inherited DNA sequence variation” is patently false; what one experiences throughout their lives can most definitely change their inherited DNA sequence variation (Baedke, 2018; Meloni, 2019).
But, as pointed out by Turkheimer, Plomin and Stumm are assuming that no top-down causation exists (see, e.g., Ellis, Noble, and O’Connor, 2011). We know that both top-down (downward) and bottom-up (upward) causation exists (e.g., Noble, 2012; see Noble 2017 for a review). Plomin, it seems, is coming from a very hardline view of genes and how they work. A view, it looks like to me, that derives from the Darwinian view of genes and how they ‘work.’
Such work also is carried out under the assumption that ‘nature’ and ‘nurture’ are independent and can therefore be separated. Indeed, the title of Plomin’s 2018 book Blueprint implies that DNA is a blueprint. In the book he has made the claim that DNA is a “fortune-teller” and that things like PGSs are “fortune-telling devices” (Plomin, 2018: 6). PGSs are also carried out based on the assumption that the heritability estimates derived from twin/family/adoption studies tell us anything about how “genetic” a trait is. But, since the EEA is false (Joseph, 2014; Joseph et al, 2015) then we should outright reject any and all genetic interpretations of these kinds of studies. PGS studies are premised on the assumption that the aforementioned twin/adoption/family studies show the “genetic variation” in traits. But if the main assumptions are false, then their conclusions crumble.
Indeed, lifestyle factors are better indicators of one’s disease risk compared to polygenic scores, and so “This means that a person with a “high” gene score risk but a healthy lifestyle is at lower risk than a person with a “low” gene score risk and an unhealthy lifestyle” (Joyner, 2019). Janssens (2019) argues that PRSs (polygenic risk scores) “do not ‘exist’ in the same way that blood pressure does … [nor do they] ‘exist’ in the same way clinical risk models do …” Janssens and Joyner (2019) also note that “Most [SNP] hits have no demonstrated mechanistic linkage to the biological property of interest. By showing mechanistic relations between the proposed gene(s) and the disease phenotype, researchers would, then, be on their way to show “causation” for PGS/PRS.
Nevertheless, Sexton et al (2018) argue that “While research has shown that height is a polygenic trait heavily influenced by common SNPs [7–12], a polygenic score that quantifies common SNP effect is generally insufficient for successful individual phenotype prediction.” Smith-Wooley et al (2018) write that “… a genome-wide polygenic score … predicts up to 5% of the variance in each university success variable.” But think about the words “predicts up to”—this is a meaningless phrase. Such language is, of course, causal when they—nor anyone else—has shown that such scores are indeed casual (mechanistically).
What these studies are indexing are not causal genic variants for disease and other “traits”, they are showing the population structure of the population sampled in question (Richardson, 2017; Richardson and Jones, 2019). Furthermore, the demographic history of the sample in question can also mediate the stratification in the population (Zaidi and Mathieson, 2020). Therefore, claims that PGSs are causal are unfounded—indeed, GWA studies cannot show causation. GWA studies survive on the correlational model—but, as has been shown by many authors, the studies show spurious correlations, not the “genetics” of any studied “trait” and they, therefore, do not show causation.
One further nail-in-the-coffin for hereditarian claims for PGS/PRS and GWA studies is due to the fact that the larger the dataset (the larger the number of datapoints), there will be many more spurious correlations found (Calude and Longo, 2017). When it comes to hereditarian claims, this is relevant to twin studies (e.g., Polderman et al, 2015) and GWA studies for “intelligence” (e.g., Sniekers et al, 2017). It is entirely possible, as is argued by Richardson and Jones (2019) that the results from GWA studies “for intelligence” are entirely spurious, since the correlations may appear due to the size of the dataset, not the nature of it (Calude and Longo, 2017). Zhou and Zao (2019) argue that “For complex polygenic traits, spurious correlation makes the separation of causal and null SNPs difficult, leading to a doomed failure of PRS.” This is troubling for hereditarian claims when it comes to “genes for” “intelligence” and other socially-valued traits.
How can hereditarians show PGS/PRS causation?
This is a hard question to answer, but I think I have one. The hereditarian must:
(1) provide a valid deductive argument, in that the conclusion is the phenomena to be explained; (2) provide an explanans (the sentences adduced as the explanation for the phenomenon) that has one lawlike generalization; and (3) show the remaining premises which state the preceding conditions have to have empirical content and they have to be true.
An explanandum is a description of the events that need explaining (in this case, PGS/PRS) while an explanans does the explaining—meaning that the sentences are adduced as explanations of the explanans. Garson (2018: 30) gives the example of zebra stripes and flies. The explanans is Stripes deter flies while the explanandum is Zebras have stripes. So we can then say that zebras have stripes because stripes deter flies.
Causation for PGS would not be shown, for example, by showing that certain races/ethnies have higher PGSs for “intelligence”. The claim is that since Jews have higher PGSs for “intelligence” then it follows that PGSs can show causation (e.g., Dunkel et al, 2019; see Freese et al, 2019 for a response). But this just shows how ideology can and does color one’s conclusions they glean from certain data. That is NOT sufficient to show causation for PGS.
PGSs cannot, currently, show causation. The studies that such scores are derived from fall prey to the fact that spurious correlations are inevitable in large datasets, which also is a problem for other hereditarian claims (about twins and GWA studies for “intelligence”). Thus, PGSs do not show causation and the fact that large datasets lead to spurious correlations means that even by increasing the number of subjects in the study, this would still not elucidate “genetic causation.”
Ranking human worth on the basis of how well one compares in academic contests, with the effect that high ranks are associated with privilege, status, and power, does suggest that psychometry is best explored as a form of vertical classification and attending rankings of social value. (Garrison, 2009: 36)
Binet and Simon’s (1916) book The Development of Intelligence in Children is somewhat of a Bible for IQ-ists. The book chronicles the methods Binet and Simon used to construct their tests for children to identify those children who needed more help at school. In the book, they describe the anatomic measures they used. Indeed, before becoming a self-taught psychologist, Binet measured skulls and concluded that skull measurements did not correlate with teacher’s assessment of their students’ “intelligence” (Gould, 1995, chapter 5).
In any case, despite Binet’s protestations that Gould discusses, he wanted to use his tests to create what Binet and Simon (1916: 262) called an “ideal city.”
It now remains to explain the use of our measuring scale which we consider a standard of the child’s intelligence. Of what use is a measure of intelligence? Without doubt one could conceive many possible applications of the process, in dreaming of a future where the social sphere would be better organized than ours; where every one would work according to his own aptitudes in such a way that no particle force should be lost for society. That would be the ideal city. It is indeed far from us. But we have to remain among the sterner and matter-of-fact realities of life, since we here deal with practical experiments which are the most commonplace realities.
Binet disregarded his skull measurements as a correlate of ‘intelligence’ since they did not agree with teacher’s ratings. But then Binet and Simon (1916: 309) discuss how teachers assessed students (and gave an example). This is then how Binet made sure that the new psychological ‘measure’ that he devised related to how teachers assessed their students. Binet and Simon’s “theory” grouped certain children as “superior” and others as “inferior” in ‘intelligence’ (whatever that is), but did not pinpoint biology as the cause of the differences between the children. These groupings, though, corresponded to the social class of the children.
Thus, in effect, what Binet and Simon wanted to do was to organize society along a system of class social class lines while using his ‘intelligence tests’ to place the individual where they “belonged” on the hierarchy on the basis of their “intelligence”—whether or not this “intelligence” was “innate” or “learned.” Indeed, Binet and Simon did originally develop their scales to distinguish children who needed more help in school than others. They assumed that individuals had certain (intellectual) properties which then related to their class position. And that by using their scales, they can identify certain children and then place them into certain classes for remedial help. But a closer reading of Binet and Simon shows two hereditarians who wanted to use their tests for similar reasons that they were originally brought to America for!
Binet and Simon’s test was created to “separate natural intelligence and instruction” since they attempted to ‘measure’ the “natural intelligence” (Mensh and Mensh, 1991). Mensh and Mensh (1991: 23) continue:
Although Binet’s original aim was to construct an instrument for classifying unsuccessful school performers inferior in intelligence, it was impossible for him to create one that would do only that, i.e., function at only one extreme. Because his test was a projection of the relationship between concepts of inferiority and superiority—each of which requires the other—it was intrinsically a device for universal ranking according to alleged mental worth.
This “ideal city” that Binet and Simon imagine would have individuals work to their “known aptitudes”—meaning that individuals would work where their social class dictated they would work. This was, in fact, eerily similar to the uses of the test that Goddard translated and the test—the Stanford-Binet—that Terman developed in 1916.
Binet and Simon (1916: 92) also discuss further uses for their tests, irrespective of job placement for individuals:
When the work, which is here only begun, shall have taken its definite character, it will doubtless permit the solution of many pending questions, since we are aiming at nothing less than the measure of intelligence; one will this know how to compare the different intellectual levels not only according to age, but according to sex, social condition, and to race; applications of our method will be found useful to normal anthropology, and also to criminal anthropology, which touches closely upon the study of the subnormal, and will receive the principle conclusion of our study.
Binet, therefore, had similar views to Goddard and Terman, regarding “tests of intelligence” and Binet wanted to stratify society by ‘intelligence’ using his own tests (which were culturally biased against certain classes). Binet’s writings on the uses of his tests, ironically, mirrored what the creators of the Army Alpha and Beta tests believed. Binet believed that his tests could select individuals that were right for the role they would be designated to work. Binet, nevertheless, contradicted himself numerous times (Spring, 1972; Mensh and Mensh, 1991).
This dream of an “ideal city” was taken a step further when Binet’s test was brought and translated to America by Goddard and used for selecting military recruits (call it an “ideal country”). They would construct the test in order to “ensure” the right percentages of “the right” people who would be in their spot that was designated to them on the basis of their intelligence.
What Binet was attempting to do was to mark individual social value with his test. He claimed that we can use his (practical) test to select people for certain social roles. Thus, Binet’s dream for what his tests would do—and were then further developed by Goddard, Yerkes, Terman, et al—is inherent in what the IQ-ists of today want to do. They believe that there are “IQ cutoffs”, meaning that people with an IQ above or below a certain threshold won’t be able to do job X. However, the causal efficacy of IQ is what is in question along with the fact that IQ-ists have certain biases that they construct into their tests that they believe are ‘objective.’ But where Binet shifted from the IQ-ists of today and his contemporaries was that he believed that ‘intelligence’ is relative to one’s social situation (Binet and Simon, 1916: 266-267).
It is ironic that Gould believed that we could use Binet’s test (along with contemporary tests constructed and ‘validated’—correlated—with Terman’s Stanford-Binet test) for ‘good’; this is what Binet thought he would be done. But then, when the hereditarians had Binet’s test, they took Binet’s arguments to a logical conclusion. This also has to do with the fact that the test was constructed AND THEN they attempted to ‘see’ what was ‘measured’ with correlational studies. The ‘meaning’ of test scores, thusly, is seen after the fact with—wait for it—correlations with other tests that were ‘validated’ with other (unvalidated) tests.
This comes back to the claim that the mental can be ‘measured’ at all. If physicalism is false—and there are dozens of (a priori) arguments that establish this fact— and the mental is therefore irreducible to the physical, then psychological traits—and with it the mind—cannot be measured. It then follows that the mind cannot be measured. Further, rankings are not measures (Nash, 1990: 63), therefore, ability and achievement tests cannot be ‘measures’ of any property of individuals or groups—the object of measurement is the human and this was inherent in Binet’s original conception of his test that the IQ-ists in America attempted with their restrictions on immigration in the early 1900s.
This speaks to the fatalism that is inherent in IQ-ism—and was inherent since the creation of the first standardized tests (of which IQ tests are). These tests are—and have been since their inception—attempting to measure human worth and the differences and value between persons. The IQ-ist claims that “IQ tests must measure something.” And this ‘measurement’, it is claimed, is inherent in the fact that the tests have ‘predictive validity.’ But such claims of that a ‘property’ inherent in individuals and groups fails. The real ‘function’ of standardized testing is for assessment, and not measurement.
The “ideal city”, it seems, is just a city of IQ-ism—where one’s social roles are delegated by where they score on a test that is constructed to get the results the constructors want. Therefore, what Binet wanted his tests to do was (and some may ever argue it still is) being used to mark social worth (Garrison, 2004, 2009). Psychometry is therefore a political ring. It is inherently political and not “value-free.” Psychologists/psychometricians do not have an ‘objective science’, as the object of study (the human) can reflexively change their behavior when they know they are being studied. Their field is inherently political and they mark individuals and groups—whether they admit it or not. “Ideal cities” can lead to eugenic thinking, in any case, and to strive for “ideality” can lead to social harms—even if the intentions are ‘good.’
Hereditarianism is the theory that differences in psychology between individuals and groups have a ‘genetic’ or ‘innate’ (to capture the thought before the ‘gene’ was conceptualized) cause to them—which therefore would explain the hows and whys of, for example, the current social hierarchy. The term ‘racism’ has many referents—and using one of the many definitions of ‘racism’, one could say that the hereditarian theory is racist since it attempts to justify and naturalize the current social hierarchy.
In what I hope is my last word on the IQ/hereditarian debate, I will provide three conceptual arguments against hereditarianism: (1) psychologists don’t ‘measure’ any’thing’ with their psychological tests since there is no object of measurement, no specified measured object, and measurement unit for any specific trait; only physical things can be measured and psychological ‘traits’ are not physical so they cannot be measured (Berka, 1983; Nash, 1990; Garrison, 2009); (2) there is no theory or definition of “intelligence” (Lanz, 2000; Richardson, 2002; Richardson and Norgate, 2015; Richardson, 2017) so there can be no ‘measure’ of it, the example of temperature and thermometers will be briefly mentioned; (3) the logical impossibility of psychophysical reduction entails that mental abilities/psychological traits cannot be genetically inherited/transmitted; and (4) psychological theories are influenced by the current problems/going-on in society as well as society influencing psychological theories. These four objections are lethal to hereditarianism, the final showing that psychology is not an ‘objective science.’
(i) The Berka/Nash measurement objection
The Berka/Nash measurement objection is simply: if there is no specified measured object, object of measurement or measuring unit for the ‘trait’, then no ‘thing’ is truly being ‘measured’ as only physical things can be measured. Nash gives the example of a stick—the stick is the measured object, the length of the stick is the object of measurement (the property being measured) and inches, centimeters etc are the measuring units. Being that the stick is in physical space, its property can be measured—its length. Since psychological traits are not physical (this will also come into play for (ii) as well) nor do they have a physical basis, there can be no ‘measuring’ of psychological traits. Indeed, since scaling is accepted by fiat to be a ‘measure’ of something. This, though, leads to confusion, especially to psychologists.
The most obvious problem with the theory of IQ measurement is that although a scale of items held to test ‘intelligence’ can be constructed, there are no fixed points of reference. If the ice point of water at one atmosphere fixes 276.16 K, what fixes 140 points of IQ? Fellows of the Royal Society? Ordinal scales are perfectly adequate for certain measurements. Moh’s scale of scratch hardness consists of ten fixed points from talc to diamond, and is good enough for certain practical purposes. IQ scales (like attainment test scales) are ordinal scales, but this is not really to the point, for whatever the nature of the scale it could not provide evidence for the property IQ or, therefore, that IQ has been measured. (Nash, 1990: 131)
In first constructing its scales and only then preceding to induce what they ‘measure’ from correlational studies, psychometry has got into the habit of trying to do what cannot be done and doing it the wrong way round anyway. (Nash, 1990: 133)
The fact of the matter is, IQ tests don’t even meet the minimal theory of measurement since there is no—non-circular—definition of what this ‘general cognitive ability’ even is.
(ii) No theory or definition of intelligence
This also goes back to Nash’s critique of IQ (since there can be no non-circular definition of what “IQ tests” purport to measure): There is no theory or definition of intelligence therefore there CAN BE no ‘measure’ of it. Imagine saying that you have measured temperature without a theory behind it. Indeed, I have explained in another article that although IQ-ists like Jensen and Eysenck emphatically state that the ‘measuring’ of ‘intelligence’ with “IQ tests” is “just like” the measuring of temperature with thermometers, this claim fails as there is no physical basis to psychological traits/mental abilities so they, therefore, cannot be measured. If “intelligence” is not like height or weight, then “intelligence”‘ cannot be measured. “Intelligence” is not like height or weight. Therefore, “intelligence” cannot be measured.
We had a theory and definition of temperature and then the measuring tool was constructed to measure our new construct. The construct of temperature was then verified independently of the instrument used to originally measure it, with the thermoscope which then was verified with human sensation. Thus, temperature was verified in a non-circular way. On the other hand, “intelligence tests” are “validated” circularly, if the tests correlate highly with other older tests (like Terman’s Stanford-Binet), it is held that the new test ‘measures’ the construct of ‘intelligence’—even if none of the previous tests have themselves been validated!
Therefore, this too is a problem for IQ-ists—their scale was first constructed (to agree with the social hierarchy, no less; Mensh and Mensh, 1991) and then they set about trying to see what their scales ‘measure’ with correlational studies. But we know that since two things are correlated that doesn’t mean that one causes the other—there could be some unknown third variable causing the relationship or the relationship could be spurious. In any case, this conceptual problem, too, is a problem for the IQ-ist. IQ is nothing like temperature since temperature is an actual physical measure that was verified independently of the instrument constructed to measure the construct in the first place.
Claims of individuals as ‘intelligent’ (whatever that means) or not are descriptive, not explanatory—it is the reflection of one’s current “ability” (used loosely) in relation to their current age norms (Anastasi; Howe, 1997).
(iii) The logical impossibility of psychophysical reduction
I will start this section off with two (a priori) arguments:
Anything that cannot be described in material terms using words that only refer to material properties is immaterial.
The mind cannot be described in material terms using words that only refer to material properties.
Therefore the mind is immaterial; materialism is false.
If physicalism is true then all facts can be stated using a physical vocabulary.
But facts about the mind cannot be stated using a physical vocabulary.
So physicalism is false.
(Note that the arguments provided are valid, and I hold them to be sound thus an objector would need to reject then refute a premise.)
Therefore, if all facts cannot be stated using a physical vocabulary and if the mind cannot be described in material terms using words that only refer to material properties, then there can, logically, be no such thing as ‘mental measurement’—no matter what IQ-ists try to tell you.
Different physical systems can give rise to different mental phenomena—what is known as the argument from multiple realizability. Thus, since psychological traits/mental states are multiply realizable, then it is impossible for psychology to reduce to mental kinds to reduce to physical kinds—the mental kind can be realized by multiple physical states. Psychological states are either multiply realizable or they are type identical to the physio-chemical states of the brain. That is a kind of mind-brain identity thesis—that the mind is identical to the states of the brain. Although they are correlated, this does not mean that the mind is the brain or that the mind can be reduced to physio-chemical states, as Putnam’s argument from multiple realizability concludes. If type-physicalism is true, then it must be true that every and all mental properties can be realized in the same exact way. But, empirically, it is highly plausible that mental properties can be realized in multiple ways. Therefore, type-identity theory is false.
Psychophysical laws are laws connnecting mental abilities/psychological traits with physical states. But, as Davidson famously argued in his defense of Anomalous Monism, there can be no such laws linking mental and physical events. There are no mental laws therefore there can be no scientific theory of mental states. Science studies the physical. The mental is not physical. Thus, science cannot study the mental. Indeed, since there are no bridge laws that link the mental and physical and the mental is irreducible to and underdetermined by the physical, it then follows that science cannot study the mental. Therefore, a science of the mind is impossible.
Further note that the claim “IQ is heritable” reduces to “thinking is heritable”, since the main aspect of test-taking is thinking. Thinking is a mental activity which results in a thought. If thinking is a mental activity which results in a thought, then what is a thought? A thought is a mental state of considering a particular idea or answer to a question or committing oneself to an idea or an answer. These mental states are, or are related to, beliefs. When one considers a particular answer to a question, they are paving the way to holding a certain belief. So when they have committed themselves to an answer, they have committed themselves to a new belief. Since beliefs are propositional attitudes, believing p means adopting the belief attitude that p. So, since cognition is thinking, then thinking is a mental process that results in the formation of a propositional belief. Thus, since thinking is related to beliefs and desires (without beliefs and desires we would not be able to think), then thinking (cognition) is irreducible to physical/functional states, meaning that the main aspect of test-taking (thinking) is irreducible to the physical thus physical states don’t explain thinking which means the main aspect of (IQ) test-taking is irreducible to the physical.
(iv) Reflexivity in psychology
In this last section, I will discuss the reflexivity—circularity—problem for psychology. This is important for psychological theorizing since, to its practitioners, psychology is seen to be an ‘objective science.’ If you think about psychology (and science) and how it is practiced, it (they) investigates third-personal, not first-personal, states. Thus, there can be no science of the mind (what psychology purports to be) and psychology can, therefore, not be an ‘objective science’ as the hard sciences are. The ‘knowledge’ that we attain from psychology comes from, obviously, the study of people. As Wade (2010: 5) notes, the knowledge that people and society are the object of study “creates a reflexivity, or circular process of cause and effect, whereby the ‘objects’ of study can and do change their behavior and ideas according to the conclusions that their observers draw about their behavior and ideas.”
It is quite clear that such academic concepts do not arise independently—in the history of psychology, it has been used in an attempt to justify the current social hierarchy of the time (as seen in 1900s America, Germany, and Britain). Psychological theories are influenced by current social goings-on. Thus, it is influenced by the bias of the psychologists in question. “The views, attitudes, and values of psychologists influence the claims they make” (Jones, Elcock, and Tyson, 2011: 29).
… scientific ideas did not develop in a vacuum but rather reflected underlying political or economic trends. 15
The current social context influences the psychological discourse and the psychological discourse influences the current social context. The a priori beliefs that one holds will influence what they choose to study. An obvious example being, hereditarian psychologists who believe there are innate differences in ‘IQ’ (they use ‘IQ’ and ‘intelligence’ interchangeably as if there is an identity relation) will undertake certain studies in order to ‘prove’ that the relationship they believe to be true holds and that there is indeed a biological cause to mental abilities within and between groups and individuals. Do note, however, that we have the data (blacks score lower on IQ tests) and one must then make an interpretation. So we have three possible scenarios: (1) differences in biology cause differences in IQ; (2) differences in experience cause differences in IQ; or (3) the tests are constructed to get the results the IQ-ists want in order to justify the current social hierarchy. Mensh and Mensh (1991) have succinctly argued for (3) while hereditarians argue for (1) and environmentalists argue for (2). While it is indeed true that one’s life experiences can influence their IQ scores, we have seen that it is logically impossible for genes to influence/cause mental abilities/psychological traits.
The only tenable answer is (3). Such relationships, as noted by Mensh and Mensh (1991), Gould (1996), and Garrison (2009), between test scores and the social hierarchy are interpreted by the hereditarian psychologist thusly: (1) our tests measure an innate mental ability; (2) if our tests measure an innate mental ability, then differences in the social hierarchy are due to biology, not environment; (3) thus, environmental differences cannot account for what is innate between individuals so our tests measure innate biological potential for intelligence.
The [IQ] tests do what their construction dictates; they correlate a group’s mental worth with its place in the social hierarchy. (Mensh and Mensh, 1991)
Richards (1997) in his book on racism in the history of psychology, identified 331 psychology articles published between 1909 (the first conceptualization of the ‘gene’, no less) and 1940 which argued for biology as a difference-maker for psychological traits while noting that 176 articles for the ‘environment’ side were published in that same time period.
Note that the racist views of the psychologists in question more than likely influenced their research interests—they set out to ‘prove’ their a priori biases. Indeed, they even modeled their tests after such biases. Tests that were constructed that agreed with their a priori pre-suppositions on who was or was not intelligence was kept whereas those that did not agree with those notions were thrown out (as noted by Hilliard, 2012). This is just as Jones, Elcock, and Tyson (2011: 67) note with the ‘positive manifold’ (‘general intelligence’):
Subtests within a battery of intelligence tests are included n the basis of them showing a substantial correlation with the test as a whole, and tests which do not show such correlations are excluded.
From this, it directly follows that psychometry (and psychology) are not sciences and do not ‘measure’ anything (returning to (i) above). What psychometrics (and psychology) do is attempt to use their biased tests in order to sort individuals into where they ‘belong’ on the social hierarchy. Standardized testing (IQ tests were one of the first standardized tests, along with the SAT)—and by proxy psychometrics—is NOT a form of measurement. The hierarchy that the tests ‘find’ is presupposed to exist and then constructed into existence using the test to ‘prove’ their biases ‘right.’
Indeed, Hilliard (2012) noted that in South Africa in the 1950s that there was a 15-point difference in IQ between two white cultural groups. Rather than fan flames of political tension between the groups, the test was changed in order to eliminate the difference between the two groups. The same, she notes, was the case regarding IQ differences between men and women—Terman eliminated such differences by picking and choosing certain items that favored one group and balanced them out so that they scored near-equally. These are two great examples from the 20th century that demonstrate the reflexivity in psychology—how one’s a priori biases influence what they study and the types of conclusions they draw from data.
Psychology, at least when it comes to racial differences in ‘IQ’, is being used to confirm pre-existing prejudices and not find any ‘new objective facts.’ “… psychology [puts] a scientific gloss on the accepted social wisdom of the day” (Christian, 2008: 5). This can be seen with a reading into the history of “IQ tests” themselves. The point is, that psychology and society influence each other in a reflexive—circular—manner. Thus, psychology is not and cannot be an ‘objective science’ and when it comes to ‘IQ’ the biases that led to the bringing of the tests to America and concurrently social policy are still—albeit implicitly—believed today.
Psychology originally developed in the US in the 19th century in order to attempt to fix societal problems—there needed to be a science of the mind and psychology purported to be just that. They, thusly, needed a science of ‘human nature’, and it was for this reason that psychology developed in the US. The first US psychologists were trained in Germany and then returned to the US and developed an American psychology. Though, do note that in Germany psychology was seen as the science of the mind while in America it would then turn out to be the science of behavior (Jones, Elcock, and Tyson, 2011). This also does speak to the eugenic views held by certain IQ-ists in the 20th and into the 21st century.
In Nazi Germany, Jewish psychologists were purged since their views did not line-up with the Nazi regime.
Psychology appealed to the Nazi Party for two reasons: because psychological theory could be used to support Nazi ideology, and because psychology could be applied in service to the state apparatus. Those psychologists who remained adapted their theories to suit Nazi ideology, and developed theories that demonstrated the necessary inferiority of non-Aryan groups (Jones and Elcock, 2001). These helped to justify actions by the state in discriminating against, and ultimately attempting to eradicate, thse other groups. (Jones, Elcock, and Tyson (2011: 38-39)
These examples show that psychology is influenced by society but also that society influences psychological theorizing. Clearly, what psychologists choose to study, since society influences psychology, is a reflection of a society’s social concerns. In the case of IQ, crime, etc, the psychologist attempts to naturalize and biologicize such differences in order to explain them as ‘innate’ or ‘genetic’. The rise of IQ tests in America, too, also coincided with the worry that ‘national intelligence’ was declining and so, the IQ test would need to be used to ‘screen’ prospective immigrants. (See Richardson, 2011 for an in-depth consideration on the tests and conditions that the testees were exposed to on Ellis Island; also see Gould, 1996.)
(i) The Berka/Nash measurement objection is one of the most lethal arguments for IQ-ists. If they cannot state the specified measured object, the object of measurement, and the measuring unit for IQ then they cannot say that any’thing’ is being ‘measured’ by ‘IQ tests.’ This then brings us to (ii). Since there is no theory or definition of what is being ‘measured’, and if the tests were constructed first before the theory, then there will necessarily be a built-in bias to what is being ‘measured’ (namely, so-called ‘innnate mental potential’). (iii) Since it is logically impossible for psychology to reduce to physical structure, and since all facts cannot be stated using a physical vocabulary nor can the mind be described using material terms that only refer to material properties, then this is another blow to the claim that psychology is an ‘objective science’ and that some’thing’ is being ‘measured’ by their tests (constructed to agree with their a priori biases). And (iv) The bias that is inherent in psychology (for both the right and the left) influences the practitioners’ theorizing and how they interpret data. Society has influenced psychology (and psychology has influenced the society) and we only need to look at America and Nazi Germany in the 20th century to see that this holds.
The relationship between psychology and society is inseparable—it is a truism that what psychologists choose to study and how and why they formulate their conclusions will be influenced by the biases they already hold about society and how and why it is the way it is. For these reasons, psychology/psychometry are not ‘sciences’ and hereditarianism is not a logically sound position. Hereditarianism, then, stays what it was when it was formulated—a racist theory that attempts to bilogicize and justify the current social hierarchy. Thus, one should not accept that psychologists ‘measure’ any’thing’ with their tests; one should not accept the claim that mental abilities can be genetically transmitted/inherited; one should not accept the claim that psychology is an objective ‘science’ due to the reflexive relationship between psychology and society.
The arguments given show why hereditarianism should be abandoned—it is not a scientific theory, it just attempts to naturalize biological inequalities between individuals and groups (Mensh and Mensh, 1991; Gould, 1996; Garrison, 2009). Psychometrics (what hereditarians use to attempt to justify their claims) is, then, nothing more than a political ring.
The Bajau spleen size and better-living-through-evolution story is also a reminder that since the dawn of the theory of evolution, humans have been incredibly creative in coming up with evolutionary and hence genetic narratives and explanations for just about every human trait that can be measured. This effort recycles from time to time and is again reaching a peak in an era when it is possible to quickly and cheaply “genotype” human populations. (Joyner, Boros, and Fink, 2018: 524-525)
Yesterday on Twitter Matt Yglesias—Vox blogger—tweeted out a 2018 paper in which the authors argue that ‘natural selection’ explained the bigger spleens of the Bajau and, consequently, how they could hold their breaths for such a long time (Ilardo et al, 2018). The main claim of the paper is that ‘natural selection’ ‘selected-for’ larger spleens which then increases how much oxygen can be stored. The point of the study was to find out if their exceptional diving abilities had a ‘genetic basis.’ Thankfully, though, a group of physiologists looked into the claims of Ilardo et al (2018) and found their main claims wanting (Joyner, Boros, and Fink, 2018). That’s how easy it is for selectionists: Notice a trait; then work backward and attempt to formulate the best story you can (see Smith, 2016).
These diving capabilities are similar to high-altitude hypoxia—indeed the authors assume that there was an adaptation for breath-hold diving. They compared some Bajau people (n=59) and close neighbors who did not—the Saluan (n=34)—really interact with the water environment. So, using a portable ultrasound machine, they photographed the spleens of the two groups and noted a “clear visual difference” between Bajau spleens and Saluan spleens. The Bajau had spleens about 40-50 cc bigger than the Saluan.
These results suggest a physiological difference between the Bajau and the Saluan that is not solely attributable to a plastic response of the spleen to diving activity. While other unknown environmental factors could potentially explain the observed difference between the groups, genetic factors remain a possibility.
So big spleens mean big breath-diving ability. And big spleens were an object of selection. So breath-diving was therefore selected for—so the just-so story goes. But, “a slightly larger spleen is almost certainly not the most important [part of diving] from a physiological perspective” (Joyner, Boros, and Fink, 2018: 524). They then found ‘genes for’ big spleens and they then formulated their just-so story. Accompanying evidence was the fact that deep-diving animals have bigger spleens, so since the Bajau have bigger spleens, this then would mean that the bigger spleens then allows for better breath-diving. Joyner, Boros, and Fink (2018: 525) write:
The general idea is that, like blood doping in cyclists, bigger spleens that contract would give the Bajau divers a boost of oxygen-carrying red cells that would make them more successful at underwater-based hunting and gathering. Thus, spleen size was selected for via evolution over the last 1,000 years or so. A few simple back-of-the-envelope calculations about oxygen stores are instructive. A 40 cc bigger spleen that was all red cells and contracted completely with diving might give the Bajau 20 milliliters of extra oxygen. That is about 1% or less of the oxygen stored in the body and lungs of healthy humans.
Joyner and colleagues then go on to note other ethnies who perform similar breath-dives, while also noting that the Bajau routinely perform dives at 5-10 meters for 30 seconds, which while impressive, is something that fit people can do if they train their lung capacity.
Of note, in the famous Japanese and Korean breath-hold divers who have been studied for decades, repeated descents of this depth and duration don’t cause oxygen levels in the blood to fall much (Schagatay, Lodin-Sundstrom, and Abrahamsson 2011; Stanek et al. 1993). Second, repeated dives of this duration with brief periods of rest only cause whole-body oxygen consumption to rise to the level seen during a brisk walk or slow jog (Craig and Medd 1968). This is hardly the sort of maximum efforts made by deep-diving seals, competitive breath-hold divers, and blood-doping cyclists. The extra oxygen from a slightly larger spleen could easily be generated by a slightly larger breath prior to starting the dive.
It is incredibly easy to think up just-so stories for anything you notice (e.g., my just-so story on Mesoamerican human sacrifices). The Bajau learn to do breath-dive like that—it is an acquired ability. ALL human traits are experience-dependent and plastic, but obviously not to the same degrees.
The spleen is a blood filter. Being a blood filter, if it can filter MORE blood by being bigger, then it will give the individual whose spleen it is an advantage at certain tasks. It sits upper-left part of the abdomen and is protected by the rib cage while also being a place for blood cell storage (Pernar and Tavakkoli, 2019). The spleen acts as a reservoir of oxygen storing “‘thick blood’ rich in cells” so that when the diving animal the oxygen levels are stressed, the body has the reservoir of extra oxygen (Milton, 2004). Esperson et al (2002) also note how the spleen acts as a reservoir of red blood cells, while the contraction of the spleen causes extra hemoglobin production after exposure to diving events.
When a diver submerges their body in the water, two things happen: bradycardia—slower heart rate and vasoconstriction—the narrowing of arteries. The increase in water pressure further causes blood shift—an extension of vasoconstriction which allows us to dive deeply and the spleen effect—meaning that the spleen of divers shrinks which then releases the stored RBCs into the body, allowing for prolonged diving. So, if we look at this in regard to the Bajau, their large spleen shrinks and since their spleen is large due to the number of RBCs it has, it would then follow that as they deep-dive the spleen would shrink (known as splenic contraction) causing the release of the RBCs into the body, allowing for the deep-diving phenotype. Thus, without the blood shift and spleen effect, divers would not be able to dive to such deep depths. (See Gooden, 1994.) The mammalian dive response has, also, been hypothesized to be a reflex to preserve life (Panneton, 2013).
Bajau and, for example, Tibetan environments are similar in that the Bajau spend time in low-oxygen environments (the water) and so do the Tibetans (the mountains). But the Tibetans are constantly exposed to this effect; the Bajau need to be in the water for this effect to occur.
Lastly, the “HBDers” in the comments on Yglesias’ tweet said the same ol’ predictable things. Such as “human spleen growth is complex and due to what the stereotypes of a group’s spleen size are”; “of course it’s true!”; “variation in spleen size within groups is greater than variation in spleen size within groups”; “spleens are a social construct”; “evolution only happened in humans below the neck”; etc. These are the same ol’ sayings that come out from “HBDers” whenever a finding like this comes out. And, you can tell that they are ignorant to the anatomy/physiology of this stuff. They just jump on anything that they can say “HBD is real!!” as if anyone denies that humans are biologically diverse (like when the Rushton retraction came ‘it doesn’t mean that HBD isn’t true!). They move and weave different definitions of ‘HBD’ to fit their needs.
Such storytelling can be done for any trait, as noted by Smith (2016). One can think up selectionist stories and competing ideas for the evolution of traits, but without a way of ajudicating between two stories. One of the best definitions of just-so stories I am aware of is from Not in Our Genes (Lewontin, Rose, and Kamin, 1984: 258-262) cited in Smith (2016). Just-so stories:
predicate a genetically determined contrast in the past…unstated assumption that genes may arise with any arbitrarily complicated action needed by the theory…insulated from any possibility of being contradicted by fact…. If one is allowed to invent genes with arbitrary complicated effects on phenotype and then to invent adaptive stories about the unrecoverable past of human history, all phenomena, real and imaginary, can be explained.
So what happens when a physiologist looks into “HBD” claims? They are found very, very wanting.
I’ve been writing on this blog since June 15th, 2015. Back then, I held staunch hereditarian beliefs. Rushton’s views on testosterone were enticing to me, especially his theoretical article with Templer (Rushton and Templer, 2012). When I first read it I thought “Oh, justification for my prior beliefs about blacks and crime.” Then, when I started studying anatomy and physiology, I reread the paper and thought “Wow who gave the OK to publish this mess?”
So in February of 2018 I published a critique of the article, Do pigmentation and the melanocortin system modulate aggression and sexuality in humans as they do in other animals? A Response to Rushton and Templer (2012). I critiqued many of the claims in their article; its biggest weakness completely handwaving the warnings of Ducrest et al (2008) that human populations “are therefore not expected to consistently exhibit the associations between melaninbased coloration and the physiological and behavioural traits reported in our study.” Rushton and Templer dodged this by saying that we should compare African and European crime rates and that we do, indeed, see that Africans commit more crimes than whites and Africans have darker skin than whites so this is sort of “preliminary evidence” for the relationship in human races.
However, unfortunately for Rushton, Cernovsky and Litmann (2019) reanlyzed the INTERPOL crime data:
When all data from the same two Interpol Yearbooks are re-calculated, most of the statistically significant trends in the data are in the direction opposite to Rushton’s beliefs: Negroids had lower crime rates than Caucasoids with respect to sexual offenses, rapes, theft, and violent theft or robbery, with most correlation coefficients exceeding .60. While we do not place much credence in such Interpol statistics as they only reproduce information provided by government officials of different countries, our re-analysis indicated that Rushton excluded data that would discredit his theory.
So, if we accept the INTERPOL data—as Rushton did—then we would be justified in saying that the proposed relationships and causal pathways do not hold.
Then at the end of October the Twitter account @evopsychgoogle wrote a long thread with a strong, in-depth critique of the arguments and sources in Rushton and Templer (2012). He then published his critique as a letter to the editor of Personality and Individual Differences (PaID). In the letter, he exposes the shoddy logic of Rushton and Templer, while showing their misreadings of sources and misunderstanding of pleiotropy. Their main point in the paper is that LHT may explain why dark-skinned individuals are more violent, mature faster, etc while they also argue that the melanocortin system is a physiological coordinator of LH traits and skin color.
Testosterone production is a simple bodily process—to quote myself from November, 2017:
There are five simple steps to testosterone production: 1) DNA codes for mRNA; 2) mRNA codes for the synthesis of an enzyme in the cytoplasm; 3) luteinizing hormone stimulates the production of another messenger in the cell when testosterone is needed; 4) this second messenger activates the enzyme; 5) the enzyme then converts cholesterol to testosterone (Leydig cells produce testosterone in the presence of luteinizing hormone) (Saladin, 2010: 137). Testosterone is a steroid and so there are no ‘genes for’ testosterone.
Cells in the testes need to take cholesterol and then convert it into testosterone with the luteinizing hormone. According to Rushton and Templer, the result of this bodily process is part of the reason why blacks are more violent than whites—they have higher levels of testosterone and testosterone causes aggression/violence. Surely, Rushton and Templer were aware of Rohrmann et al (2007) who showed no difference in testosterone between blacks and whites. Surely Rushton and Templer were aware of all of the research that I cited in what I would call my ‘master article’ on race, testosterone, prostate cancer, and aggression. Rushton and Templer, quite obviously on a review of the literature, are misleading their readers.
Thankfully this paper has only been cited 15 times in the past 8 years since it was published. Evolution, presumably, accounts for the differences in death, AIDS rate, testosterone, lower life expectancy, etc. One recent citation can be found in the textbook Race and Crime (Gabiddon and Greene, 2018, 5th edition) in a discussion about Rushton’s r/K selection theory and causes for Rushton’s proposed relationship. They write (pg 122-123):
As with all theories, there have been several criticisms of the r/K selection theory. First, Rushton generally underemphasizes sociological factors. Most of his cross-national comparisons point strictly to numbers, without taking into account variables such as socioeconomic status, and other important sociological variables (Whihte, 2018). Second, in the 21st century, there are few “pure” races, especially in the United States, as noted in Chapter 1. White sexual aggression against Black females during the slave era produces countless mixed-race offspring. Therefore, the rigorous adherence to the Black-White-Asian split is problematic. Finally, if Rushton;s theory were true, what would explain White aggression as early colonizers and their current involvement in wars and violence across the globe? In contrast to Rushton’s theory, Bradley (1978) argued that, as a result of migration to colder regions, since the beginning of humanity, Whites have been the global aggressors.
So, testosterone does not cause aggression and it does not cause crime; the melanocortin system does not work in such a way that works for Rushton and Templer’s theory (Cone, 2006).
Hilliard (2012: 73) stated that “No evidence shows that racism motivated Rushton” while Dutton (2018) stated the same, interviewing Rushton’s ex-wife (whom he had an illegitimate black son with). But, knowing what we know about testosterone and Rushton’s views on blacks and whites, knowing about his (false) views on testosterone and race (while citing old, flawed studies like Ross et al) we can call into question the claim that Rushton had no racial animus. @evopsychgoogle also brought up the fact that COIs and funding sources were not brought up (this being Rushton’s final paper before his death and the fact that he was the head of the Pioneer Fund at the time means we don’t have to ask where the funding came from). Rushton and Templer should have never been published in the first place.
Lastly, Clark et al (2020) argued that ‘intelligence’ as ‘measured‘ by ‘IQ tests’ modulates the relationship between religiosity and crime at a country-wide level. They, of course, used Lynn’s global ‘IQ’ data. Though, there were many critiques of the paper and the data used in it (see here, here, and here) and Clark et al decided to finally retract their paper due to the problems of Lynn’s dataset. So, if they retracted due to the problems with Lynn’s dataset, does that mean that other papers that relied on Lynn’s shoddy work (e.g., Richardson, 2004; Morse, 2008) should be retracted too? Ebbeson (2020) notes the flawed ‘IQ estimates’ used in Clark (2020), noting the small, unrepresentative child samples used, along with showing that their dataset leads to “notions” which “are incompatible with psychological science” so “all conclusions drawn from these data are invalid.”
Clark et al “lost confidence in their findings” since “the homicide data have limitations that call [their] findings into question” while “The IQ data … have much more serious issues.” “Serious” is an understatement. To quote Ebbeson (2020)
For example, in the ‘NIQ_QNWSAS’ dataset, several African, South Asian and Central American countries have an average IQ below 50, such as Nepal (national IQ: 43.0), Sierra Leone (national IQ: 45.1), Guatemala (national IQ: 47.7) and Gambia (national IQ: 49.8) These estimates would seem to suggest that a majority of the population in these countries are moderately, severely, or profoundly cognitively impaired. (cf. Table 1). This notion is incompatible with psychological science and there is no doubt that these estimates are wrong.
All in all, this is not a good week for “HBD”—Rushton is being exposed for the know-nothing about physiology that he is, and Lynn’s ‘national IQ’ numbers are getting the scrutiny they finally deserve. So, I hold, if Clark et al was retracted for those reasons, we need to retract ALL papers that relied on Lynn’s ‘national IQ data.’ People may cry ‘censorship! HBD is dead!’, but ‘HBD’ (what I would term psychological hereditarianism) has been long dead. Rushton and Templer’s paper should have never been published but it’s better late than never that it is finally getting retracted. If you’re saying that Rushton and Templer got retracted for “political reasons” then it’s clear that you did not read either of the two existing critiques of the paper.
Sudden Infant Death Syndrome (SIDS) has a long history—almost as long as human civilization (Raven, 2018). The term was coined in 1969 to bring attention to children who died in the postnatal period (Kinney and Thach, 2012; Duncan and Byard, 2018). About 95 percent of SIDS cases occur within the first 6 months of life, happening around the 4-6 months mark (Fleming, Blair, and Pease, 2015). The syndrome is associated with the sleep period, presumed to have begun with the transition from sleep to waking (Kinney and Thach, 2012) The prone sleeping position, along with smoking, is said to increase the incidence of SIDS (Ramirez, Ramirez, and Anderson, 2018). Due to a campaign in the mid-90s, though (called the back-to-sleep campaign), it has been estimated that SIDS deaths have decreased by 50 percent, saving thousands of infant lives (Kinney and Thach, 2012).
But, those infants who die from SIDS may also have a problem with the part of their brain that controls waking/sleeping:
Infants who die from SIDS may have a problem with the part of the brain that helps control breathing and waking during sleep. If a baby is breathing stale air and not getting enough oxygen, the brain usually triggers the baby to wake up and cry to get more oxygen.
So, if a baby’s brain is not getting enough oxygen, its brain will have it wake up and cry in an attempt to rid itself of “stale oxygen”—this is one other purpose that crying serves—which then gets the baby more oxygen to its brain.
As can be imagined, acute rises in CO2 levels occur when an individual is unable to expel CO2, such as in the setting of an airway obstruction that might occur when an individual is lying prone in a crib or bed perhaps with a pillow and bedclothes covering the nose and mouth. It has been proposed that such a rise in CO2 would activate arousal circuitry in a normal baby to wake the baby up, cause them to cry out, summoning a caregiver who would come to their aid, and ostensibly correct the airway blockage to allow resumption of normal breathing [16,20,31]. It has been proposed, among other possibilities, that there is an impaired CO2-arousal system in SIDS-susceptible babies such that when they rebreathe CO2 as described above, they do not arouse, and thus do not cry out, and the blockage is not corrected [16,32]. They thus become acidotic and hypoxic and ultimately succumb.
So, if a babe’s airway gets blocked, for instance by a pillow or toy, they wake, cry out for attention and their caregiver comes to solve the problem or they change their laying position. But in SIDS cases, this does not occur. Why? Buchanan argues that those who succumb to sudden deaths like SIDS have screwy serotonin receptors—they ensure that blood oxygen and CO2 levels are healthy. But some of these infants may have brains that don’t allow them to detect the CO2 and blood oxygen levels—when the body may be suffocating. SIDS victims are usually found face-down in their cribs. But, there are no biomarkers for SIDS (Haynes, 2018). The SIDS diagnosis is only given after all other causes of death are ruled out—this is why SIDS is so mysterious. Genetic mutations have been posited as a cause (Männikkö et al, 2018), as has a pregnant mother smoking during pregancy, leading to a doubled risk of SIDS (Anderson et al, 2019).
But the best prevention against SIDS is nonprone sleeping—having the baby sleep on its back. The efficacy of this approach since the 1990ss has been noted (Gibson et al, 1992; de Luca and Hinide, 2016) while “Achieving recommended prenatal care and infant vaccinations, as well as reductions in maternal tobacco and substance use, has the potential to further reduce rates of SIDS and should be given as much attention as safe sleep advice in SIDS risk reduction campaigns” (Hauck and Tanabe, 2017: e289). The back-to-sleep program, though, has been associated with a decrease in motor development from the infant sending time in the supine position along with the strong possibility of developing plagiocephaly—which causes a “flat head” due to being placed in similar positions while the infant’s skull is soft and still developing (Miller et al, 2011). It has also been estimated that if it was known that the advice to place infants on their stomachs to sleep led to SIDS, then we “might have prevented over 10 000 infant deaths in the UK and at least 50 000 in Europe, the USA, and Australasia” (Gilbert et al, 2005: 884).
But the history of SIDS in America is a lot more sinister—rather than children dying from ‘natural causes’ (SIDS), in the 1970s, it was hypothesized by one SIDS researcher that SIDS was ‘genetic’ and ‘transmissible’ on the basis of one family who, unfortunately, had experienced this tragedy more than once.
This leads us to the story of Waneta Hoyt, who is the subject of this article.
Hoyt and Steinschneider: Genes vs environment
Horrible tragedies befell a woman from New York named Waneta Hoyt—five of her children had mysteriously died due to SIDS between the years of 1965-1971.
Waneta killed her first child, Eric who was three-months-old. SIDS is a diagnosis that is arrived at through a process of elimination—rule out all other causes at a young age (under 1) and the cause is then SIDS. But, the thing is, when an autopsy is performed on the infant, there is no difference between what would be said to be SIDS deaths and a light smothering.
After Waneta murdered her first child, she was cold and distant but it was not noticed. It was reported that she would never hold her children as a loving mother would, keeping them quite far from her. But it wasn’t until three years later that she, again, murdered. But this time it was two of her children—her two-year-old son and six-week-old daughter. The murders that Waneta were committing were wrongfully diagnosed as being due to SIDS.
This caught the attention of renowned SIDS researcher Alfred Steinschneider who had a clinic in which he specialized in caring for infants who were thought to be high-risk for SIDS. Steinschneider wanted to watch Waneta’s fourth child in his sleeping ward, in an attempt to prevent what he thought was due to SIDS. So, when he heard of Waneta’s story, he reached out to her to monitor her daughter, Molly.
The nurses at Steinschneider’s clinic, though, became suspicious of Waneta when she was at the clinic since she was cold and distant to Molly—she would not show her any affection. Steinschneider’s nurses emphatically told Steinschneider that it was Waneta who was murdering her children. Steinschneider shot back, and sent Molly home anyway. In an interview on the television program Deadly Women called Mothers Who Kill, one of the nurses who watched Molly before she was discharged by Steinschneider said:
And then about a quarter to eleven when we were getting ready to go off duty I said ‘Joyce, what do you think, do you think she’s still alive?’ Of course when I came on duty the next day she was dead.
Forty-eight hours later, on Thursday, June 4, Steinschneider scheduled Molly for her third discharge. By now, the nurses were speaking more openly about their suspicions. “I just know something’s going to happen,” Corrine Dower said to Thelma. “One of these times she’s going to do it.” Corrine was scornful of Steinschneider. “If he had any brains at all he would have seen that she didn’t want the baby,” she would say years later. “You can tell in the grocery store if a person cares about their child. We were just disgusted with Steinschneider.” (book excerpt from How Two Baby Deaths Led to a Misguided SIDS Theory)
Presumably, since this was Waneta’s fourth time experiencing the tragedy of SIDS, Steinschneider did not think that Waneta could be involved—but his nurses knew the truth. It was when Waneta had her fifth child that Steinschneider thought he would make his breakthrough in his research. Steinschneider was so convinced that the baby’s were dying due to SIDS, and he thought that if he could monitor Waneta’s new baby as much as possible, that he may figure out why babies die from SIDS.
Steinschneider believes that SIDS is hereditary—passed on through genes. The fifth child was watched at Steinschneider’s clinic and when Steinschneider discharged him—in an attempt to prove his theory—his nurses protested. Then, shortly after, Waneta called Steinschneider saying that it had happened again—her fifth child had mysteriously died.
After the death of Waneta’s fifth child, Steinschneider published his paper Prolonged Apnea and the Sudden Infant Death Syndrome: Clinical and Laboratory Observations arguing that SIDS was caused largely by hereditary sleep apnea (Steinschneider, 1972). By 1997, Steinschneider’s paper was the most-cited paper in the SIDS literature (Bergman, 1997). It was due to Steinschneider’s research, though, that parents began using sleep monitors to monitor their children’s sleep so they could be alerted in case their child had sleep apnea.
Steinschneider cared more about his research and theory of SIDS and sleep apnea over what was striking him right in the face—Waneta was responsible for the deaths of her five children. Steinschneider’s 1972 paper was cited and used for 22 years, until it was found upon an in-depth look into Steinschneider’s paper that what was clear to Steinschneider’s nurses and not him was true—Waneta was responsible for the deaths of her children. Steinschneider’s paper, in any case, concluded that SIDS is a genetic disorder and it was thusly inherited. And Waneta’s case, it seems, lent credence to his hypothesis. Steinschneider gave Waneta the perfect alibi—her woes were caused by a genetic disease and there was nothing that could have been done to prevent it.
Waneta was convicted in 1995 of five counts of murder and sentenced to 75 years in prison—therefore refuting Steinschneider’s theory. Three years after her sentence, though, Waneta died in prison of cancer. The case of Waneta Hoyt allowed mothers to kill their children in this specific way (a light smothering) for almost a quarter of a century.
Norton saw history repeating itself in the reluctance of many factors to face the fact that some deaths attributed to SIDS were homicides. She agreed with the bulk of SIDS research, which pointed to apnea, or the cessation of breathing, as the final pathway to death. But there were many causes of apnea, not all of them natural. An adult could place a hand or a pillow over an infant’s nose and mouth and stop the child from breathing. The pressure needed to smother an infant often left no telltale signs, Norton explained.
“There is no way for the pathologist at autopsy to distinguish between homicidal smothering and SIDS,” she concluded.
Norton worried that homicides were being passed off as SIDS because many doctors held the erroneous belief that SIDS ran in families. They ignored large-scale studies that had shown no genetic tendency toward SIDS. Flouting conventional wisdom, Norton warned that the sudden, unexplained death of a SIDS victim’s sibling should be treated as a possible homicide.
When Waneta was convicted, letters to the editor were sent about Steinschneider’s paper. The short correction to the paper chronicles, interestingly, a letter to the editor of the journal Pediatrics, who published the Steinschneider paper
“But the paper indicated a more sinister possibility to Dr. John F. Hick of Minnesota. In a letter to the journal, he wrote that the case offered “circumstantial evidence suggesting a critical role for the mother in the death of her children.” (See below.)
But his warning was dismissed, until Mr. Fitzpatrick read the paper 15 years later.
“The medical records described two happy, healthy, perfectly normal kids,” he said. “It convinced me that these children were murdered.”
Hick’s letter to Pediatrics says:
In reporting two siblings who succumbed to “sudden infant death syndrome,” Steinschneider exposes an unparalleled family chronicle of infant death.’ Of five children, four died in early infancy and the other died without explanation at age 28 months. Prolonged apnea is proposed as the common denominator in the deaths, yet the author leaves many questions relevant to the fate of these children unanswered.
In her signed confession, Waneta said that she smothered her five children because their screaming made her “feel useless”, though Waneta later stated that she only said that to stop the police from questioning her. Steinschneider, like another motivated-reasoner J.P. Rushton, ignored data that did not fit his theory of sleep-apnea-induced-SIDS—specifically how Waneta acted around her children while at his clinic and the thoughts of his own nursing staff telling him not to discharge the Hoyt infants.
Waneta recalled her strangling of her children—specifically Julie:
”They just kept crying and crying. . . . I just picked up Julie and I put her into my arm, in between my arm and my neck like this . . . and I just kept squeezing and squeezing and squeezing.”
Steinschneider’s testimony during Waneta’s trial, however, is very interesting. Reported by the New York Times, Steinschneider attempted to defend his patient Waneta against claims that she had murdered her children:
Autopsies were done,” he said, speaking of Molly. “They could not find a known cause of death.”
This, Dr. Steinschneider said, “by definition” is SIDS.
But under intense cross-examination. Dr. Steinschneider conceded that he could not remember — and did not record — crucial details from the medical histories of the two infants, whom he had hospitalized for observation soon after birth. In each case, the parents had reported that the baby was having difficulty breathing and that its older siblings had died mysteriously.
The doctor also acknowledged concluding that Molly and Noah had died of SIDS without knowing how thoroughly the authorities had probed the “death scene” for evidence of other causes, including murder.
It is said—even by the prosecutor on her case—that Waneta suffered from Munchausen by proxy (Firstman and Talan, 1996)—which is the intentional cause of illness, usually on children, in order for the mother to elicit sympathy for others (Gehlawat et al, 2015). In cases like this, mothers who have the Munchausen syndrome will suffocate their children and then rush them to the hospital—they get the satisfaction of inflicting pain and then the satisfaction of getting cared for for the so-called mysterious death of their baby. One study of 51 sleep apnea monitorings found that about 40 percent of the program treated infants who had apnea that seemed to be induced by the parent; this was inferred from the fact that once the infants were admitted to the hospital, the doctors found no signs of apnea (Light and Sheridan, 1990).
One doctor even took it upon himself to place cameras in his practice in order to monitor parents that were suspected of abusing their children. Thirty-nine infants were monitored—thirty-three infants were being abused by their parents, what’s more is that some of the infants in this study who were identified in the video also had a sibling who mysteriously died from SIDS (Southall et al, 1997). What the study shows is that these parents were suffocating their children, causing their breathing problems and that they most likely have gotten away with infanticide before. Another case involved a mother taking her daughter to eleven different hospitals, but none of them found anything wrong with the girl and she ended up dying under suspicious circumstances (Hassler, Zamorski, and Weirich, 2007).
We now know that Steinschneider ignored contrary evidence to his theory of genetically-induced sleep apnea causing SIDS which apparently ran in families, and since he brushed off his nursing staff telling him that Waneta was acting strangely around her two children that he had admitted into his clinic, he could have saved their lives. But Steinschneider’s genetic determinist theory was more important than seeing what was clear as day to his staff and even others who read his 1972 paper—a mother was strangling her own infants.
SIDS has a long history, dating back to biblical times. But, in the modern-era, erroneous theories on the causes of SIDS were pushed while other, more obvious causes were disregarded in favor of a grand genetic theory of SIDS causation. Waneta and Steinschneider both helped each other out: Steinschneider (unknowingly) helped Waneta evade detection for 22 years while Waneta lent credence to the hypothesis that Steinschneider was developing. The fact that, at the time of their first meeting, three of Waneta’s children had died in almost the same fashion pointed to a genetic, inherited cause in Steinschneider’s eyes.
At the time of publication of The Death of Innocents, Steinschneider still continues to defend his now-discredited theory and still lobbies for the use of infant sleep monitors. Of course, since he testified FOR Waneta, despite the mounting evidence against her, he could be seen as an accomplice, however weakly. But this case shows one thing that should be well-known—researchers become attached to their pet hypotheses/theories and will ignore contrary evidence if it is brought to their attention. Firstman and Talman estimate that between 5 and 10 percent of SIDS cases are actually homicides. (But see Milroy and Kepron, 2017.)
Steinschneider created the SIDS disease on the basis of Waneta’s story—and a multi-million dollar industry then appeared due to his paper—it’s all to save infants, buy these sleep apnea monitors. But there were two children that Steinschneider did not—could not—save: He could have saved those babies, if not for his genetic determinist beliefs on SIDS causation. Had Steinshneider looked at the more obvious answer to the problem which was right in front of his face, he may have seen that Waneta suffered from Munchausen by Proxy, and, as evidenced from the references above, those who suffer from the disease act out exactly how Waneta did—by strangling their children with the cause of death being blamed on SIDS.
The Hoyt-Steinschneider case is a warning—don’t jump so quickly to implicate heredity in the ontology of X, especially when other, more obvious, tells are right there in front of you.
In 1969, Arthur Jensen published a bombshell article in the Harvard Educational Review titled How Much Can We Boost IQ and Scholastic Achievement? in which he argued that compensatory education has failed (e.g., Headstart) and it, therefore, should be abandoned. Jensen was a big proponent against school integration due to his research on IQ (Tucker, 2002). Tucker (1998) also argued, “that the supposed significance of the genetic influence on IQ has invariably reflected a particular ideological view of the purpose of education and its relation to the state that is rooted in conservative political thought.” Such ideological leanings of the IQ-ists have been well-noted (Tucker, 2002; Saini, 2019).(Though it should be noted that school integration didn’t cause any negative effects for whites and had many positive effects for blacks, see Nazaryan and Johnson, 2019). Note how the revival of “racial differences in intelligence” in the mainstream occurred after the Civil Rights Act of 1964. Such ideological leanings have been incipient in ‘intelligence’ testing since its inception.
In any case, what was the ultimate goal of such research into racial/class differences in “intelligence”? The original application of what eventually became tests of “intelligence” were to (1) identify those with learning disabilities and (2) shoe-horn people into jobs “for” them—what Binet called his “ideal city.” When IQ tests were brought to America and translated from French to English by Henry Goddard in 1911 and then again by Lewis Terman in 1916. Goddard was hesitant to force sterilization, but he did believe that those his tests designated as “feeble-minded” should not be allowed to bear children.
Proponents of IQ emphatically state that it’s not a “measure of superiority” and that it’s only the critics who believe that, with no evidence for the claim. However, if one reads Jensen’s earliest writings on IQ, they would see that Jensen did, in fact, believe that heritability could estimate one’s “genetic standing” (Jensen, 1970) and that if we continue our welfare policy that we would lead a group toward “genetic enslavement” (Jensen, 1969). Jensen ran with racists, so there is a possibility that he himself held similar types of views to the people he ran with. The following quotes show Jensen’s eugenic thinking:
“Is there a danger that current welfare policies, unaided by eugenic foresight, could lead to the genetic enslavement of a substantial segment of our population?” – Jensen, 1969: 95, How Much Can We Boost IQ and Scholastic Achievement?
“What the evidence on heritability tells us is that we can, in fact, estimate a person’s genetic standing on intelligence from his score on an IQ test.” – Jensen, 1970, Can We and Should We Study Race Difference?
“… the best thing the black community could do would be to limit the birth-rate among the least-able members, which of course is a eugenic proposal.” – A Conversation with Arthur Jensen, American Reinnasance, 1992
In a review of Raymond Cattell’s Beyondism, Richard Lynn stated:
“What is called for here is not genocide, the killing off of the populations of incompetent cultures. But we do need to think realistically in terms of “phasing out” of such peoples.”
I don’t see how he’s not calling for genocide—genocide is the systemic killing of a specific group of people. Eugenic methods are one way to accomplish this. Richard Lynn’s father was a eugenicist, signing his name to a manifesto which asked the question of how the genetic constitution of the world could be improved, per Lynn (see Interview with a pioneer, American Reinassance). Lynn continues:
My father’s interests did give me an early appreciation of the importance of genetics, although I think I would have adopted this position anyway since the evidence is irrefutable for a strong genetic determination of intelligence and educational attainment and a moderate genetic determination of personality. More importantly, my father served as a role model for scientific achievement and has given me the confidence to advance theories that have sometimes been controversial.
Lynn stated that he is “very pessimistic” about the future of the West, due to the immigration of individuals from low IQ countries who have a higher birthrate than Westerners along with the supposed dysgenic fertility that American white women are facing. (See Lynn, 1996, 2001 for a discussion and look into these views.) In Dysgenics, Lynn (1996: 2) writes that he hopes “To make the case that in the repudiation of eugenics an important truth has been lost, and to rehabilitate the argument that genetic deterioration is occurring in Western populations and in most of the developed world.”
Raymond Cattell was also one who believed that certain people should (voluntarily) be sterilized. He created a religion called “Beyondism” in an attempt to accomplish this goal, his research, in fact, served his eugenic and political beliefs (Tucker, 2009). Compassion was seen as evil to Cattell, which is one major way it strays from other religions. Presumably, one is compassionate to those less fortunate and, therefore, the compassion would help one who Cattell deems “genetically inferior” and so compassion is evil since it leads to the propagation of those Cattell deems less fit. Cattell also stated that, from the perspective of Beyondism, the propagation of ‘genetic failures’ is “positively evil” (Tucker, 2009: 136). He also coined the term ‘genthanasia’ which was “phasing out” a “moribund culture … by educational and birth measures, without a single member dying before his time” (Cattell, quoted in Tucker, 2009: 146).
William Shockley “reasoned” that if the problems that blacks face in America are hereditary, then by attempting to halt the reproduction of blacks, there would be less racism against them. Well if there are few people to be racist against, then there would be less racism against those people. Shocking. Further, Shockley wanted to enstate what he called a “Voluntary Sterilization Bonus Plan” where individuals with IQs below 100 would, with each single point below 100, be given $1000—although the plan was never implemented (Hilliard, 2012: 50). He also wanted to institute a sperm bank of ‘geniuses’ (whatever that means) but, he was never told, women did not want the sperm of Shockley’s short, balding self (he was 5’6” weighing 150 pounds)—although he had a ‘high IQ’ (he was rejected as being one of Terman’s Termites)—they wanted the sperm of taller, good-looking men, regardless of their IQ (Hilliard, 2012: 20).
It is worth noting that Shockley precedes Jensen’s thinking on race and IQ—Jensen was in the audience of one of Shockley’s talks in the late ’60s hearing him talk about racial differences in IQ. Psychology was Jensen’s second choice; his first was to be a symphony conductor. Hilliard (2012: 51) describes this:
“When Shockley addressed a meeting of the Center for Advanced Study in the Behavioral Sciences at Stanford in the late 1960s, one member of the audience drawn to his discourse was Arthur R. Jensen, a psychologist who taught at the University of California–Berkeley. Jensen, who had described himself as a “frustrated symphony conductor,” may have had his own reasons for reverencing Shockley’s every word. The younger psychologist had been forced to abandon a career in music because his own considerable talents in that area nevertheless lacked “soul,” or the emotional intensity needed to succeed in so competitive a profession. He decided on psychology as a second choice, carrying along with him a grudge against those American subcultures perceived as being “more expressive” than the white culture from which he sprang. Jensen received his bachelor’s degree in that field from the University of California– Berkeley in 1945.”
Shockley even disowned his son for dating a Costa Rican woman since it would “deteriorate their white gene pool” while describing his children as a “considerable regression”, even though they had advanced degrees. He blamed this ‘genetic misfortune’ on his wife who did not have as high educational attainment as he did (Hilliard, 2012: 49). This man greatly influenced Jensen—and it seems to show in his first writings on IQ—what eventually kicked off the ‘IQ debate’ (which is frivolous) back in the late 1960s. (James Thompson has said that Shockley wouldn’t talk to anyone if he didn’t know their IQ—presumably, because he did not want to talk to anyone ‘lower’ than he. The idiotic ‘thinking’ of eugenic IQ-ists.
Shockley was involved in a car accident, and received a head injury, with colleagues noting that his views on race and eugenics came about after his car accident (Hilliard, 2012: 48). So, it can rightly be argued that if Shockley would never have gotten into a car accident then he would have never had the views he did on race and IQ, meaning that he would not be speaking for Jensen to be in the audience to then eventually write his infamous 1969 paper. So, the current revival of the race-and-IQ debate can be said to be due to Shockly’s influence on Jensen, which is due (in some way) to head injuries sustained during a car accident.
IQ-ists speak of a “genetic deterioration”, what is termed “dysgenics” (the opposite of eugenics). Professor Seymour Itzkoff published The Decline of Intelligence in America (Itzkoff, 1994), arguing that the decline in our country’s “intelligence” is the cause of our economic and political woes. And, while he does not outright discuss eugenics in the book, he states that higher IQ people are not having children and so the national IQ is decreasing—a dysgenic effect. He is also a recipient of funding from the Pioneer Fund, published in Mankind Quarterly, and was one of the 52 signatories of Mainstream Science on Intelligence (Gottfredson, 1997).
The Decline of Intelligence in America was The Bell Curve before The Bell Curve. Itzkoff argued policy proscriptions, including encouraging certain people to breed and certain people not to breed (eugenics without calling it eugenics). Itzkoff stated that welfare policy is one reason why our “intelligence”—as a nation—has declined (see also Jensen, 1969; Lynn, 2001). Itzkoff (1994: 195) states that “Those at the bottom should be humanely persuaded, with generous gifts if deemed appropriate but for one generation only to refrain from conceiving and having children.” So his views are a mixture of Jensen’s, Shockley’s and others. Itzkoff advocates for both positive and negative eugenics for black Americans. I have not seen any IQ-ist discuss Itzkoff’s writings; I will do so in the future.
Philosopher and IQ-ist Jonathon Anomaly (see Winegard, Winegard, and Anomaly, 2020) has a paper in which he ‘defends eugenics’, even stating what we ‘should’ (cautiously) do about public policy in relation to eugenic ideas. He speaks of “undesirable genetic endowment“, while couching his “moral obligation to produce children with the best chance of the best life” (Anomaly, 2018) “through mechanisms of prenatal screening, enshrined in the principle of procreative beneficence and our responsibility to not pass along an “undesirable genetic endowment” (Love, 2018: 4). (See my arguments to discourage such research here and here.) Presumably, like Itzkoff (1994), such policies will be concentrated on the lower classes, of which minority populations are the majority. Robert Wilson (2019), author of The Eugenic Mind Project writes that Anomaly (2018) fails to argue for eugenics, mischaracterizes eugenics, mischaracterizes the scientific consensus, simplifies and misleads on the history, is careless about race and IQ, appealing for moral principles, and no substance linking demography, eugenics and policy recommendations. Anomaly could hardly contain his negative eugenist views; his views being akin to more traditional, negative forms of eugenics” (Wilson, 2019: 74).
In any case, IQ tests were used as a vehicle for sterilization and barring immigrants into America in the 1920s (Swanson, 1995; Gould, 1996; Wilson, 2017; Dolmage, 2018). In his book The Eugenic Mind Project, Wilson (2017) discusses standpoint eugenics—how eugenic policies affected people and their own personal experiences with eugenic policies. In the book, Wilson argues that, to the eugenicists, there are different ‘sorts’ of people that can be distinguished from others. Wilson (2017: 48) writes:
This was not, however, the way of human betterment favored by the applied science of eugenics and that continues to forms [sic] a key part of The Eugenic Mind. Instead, historically eugenicists typically followed Galton in emphasizing that quality was not equally distributed in the kinds of human populations that are regulated by governmental policies and jurisdictional legislation. More specifically, they thought of such populations as being composed of fundamentally distinct kinds of people, with some kinds being of higher quality than others. Some of these sorts of people were to be improved through eugenic policies that encouraged their own reproduction; others were to be eliminated over generational time. The goal of intergenerational human improvement within the eugenics movement was thus achieved by increasing the proportion of higher-quality people in future generations, and this could be achieved in two ways under eugenic logic. Thus, eugenicists historically advocated ideas, laws, policies, and practices either that aimed to maximize the reproduction of higher-quality people—positive eugenics—or that aimed to minimalize the reproduction of lower-quality people. Or both.
A hallmark of The Eugenic Mind, says Wilson, is the distinction between the ‘fit’ and ‘unfit’. Thus, those deemed ‘unfit’ would be sterilized as they are different ‘kinds’ of people. Eugenics is seen as an applied science and so, it attempts to achieve certain goals—the propagation of the ‘fit’ and elimination of the ‘unfit.’ The first IQ tests were constructed with class, so that the test scores mirrored current racial/class divisions, justifying the social hierarchy (Mensh and Mensh, 1991). Thus, using the ‘science of IQ’, we could then identify ‘feeble-minds’ and therefore select them out of the gene pool. What really would be going on here is not selecting out ‘low IQ people’ but selecting out those of lower classes—one of the main reasons these types of views sprang up. A trait was ‘eugenic’ if it fit “folk knowledge characteristic of people” (Wilson, 2017: 70).
Eugenic-type thinking also had its beginnings in criminality, right when the first IQ tests were being constructed by Binet in 1905 (Kuhar and Fatović-Ferenčić, 2012). Lombroso’s thesis of hereditary criminality also gave American eugenicists the platform for sterilization of criminals (Applegate, 2018: 438). But early eugenicists were more concerned over white female ‘morons’ and white lower-status, promiscuous white women being coerced and segregated in order to prevent them from breeding, it even being suggested by “one or two scientists” that the women should live on a farm performing menial tasks and should be sterilized; the eugenicists wanted state control of heredity (Applegate, 2018: 439). Mexican-American men and women were even sterilized in the 1900s (Lira, 2015). Such beliefs seem to be baked-in from political and social prejudices; not any basis in ‘science.’
Eugenicists wished for state control over the “propagation of the mentally incompetent,” whether through mental illness or disability. Ultimately, these beliefs would lead not only to forced detention and isolation, but also to regular affronts to human life and dignity. (Applegate, 2018: 442)
But Dr. Sullivan, the medical officer of Holloway Prison in The Eugenics Review stated that “Criminals, looked at from the eugenic standpoint, cannot be put into any single category; some of them, probably most of them, are of average stock, and become criminal under the influence of their milieu; they do not directly interest the eugenist” (Sullivan, 1909: 119-120). The “hyperincarceration of blacks” is also argued to be eugenic in nature (Oleson, 2016; Jones and Seabrook, 2017). Such race-based segregation, argues Oleson, significantly depresses the birthrate of affected groups—racialized minorities (socialgroups taken to be races, e.g., ‘Hispanics‘ and blacks). So since minority populations are overrepresented in prison and they are less likely to procreate, it then follows that such arguments like Oleson’s (2016) has some weight to it. So this then would have eugenic effects over generational time. Even today, America is still sterilizing prisoners, so, it seems, the legacy of the 20th century has yet to let up.
… the penal code is a eugenic instrument, although until today, it has been without consciousness of this function. And following the results of eugenic science, it can tomorrow widen or narrow the circle of crimes in the end of conducing to the physical and psychic improvement of the race. (Battaglini, 1914)
Hitler, noticing the American sterilization laws and the Immigration Act of 1924, instituted eugenic policies on this basis—yes, the Nazi eugenic movement was largely taken from the then-existing social policy in America at the time. Pioneer Fund president Henry Laughlin, who used data from IQ tests in front of Congress to bar certain immigrants from the United States (Swanson, 1995; Dolmage, 2018). The Nazis and Americans had extensive contact with each other, while Germany modeled their sterilization law after Henry Laughlin’s laws for sterilization in US states (Cornwell, 2001; Black, 2003; see Allen, 2004; Lelliot, 2004; and Weikart, 2006 for reviews; Wittmann, 2004). But it is worth noting that Hitler was not a Darwinian (Richards, 2012, 2013). Hitler’s laws in the early 1930s on eugenics “may have had some resemblance to the most extreme of American state’s laws” (Wittmann, 2004: 19), since he was observing the eugenic programs implemented by certain states (eugenic laws were never federally mandated).
The IQ-ist thinking that IQ tests ‘measure’ intelligence led to eugenic policies and the sterilization of criminals and those with low IQs. Jensen and Shockley were the forefronts of bringing IQ-ism back into the picture, and they both had eugenic views (Shockley being way more radical than Jensen, but it is clear that Shockley was his influence here and that, without Shockley, IQ-ism may not have had the sway it does today. The IQ-ist ideology that has led to eugenic thinking and social policies, race and ‘intelligence’ has been there since its inception and it is clear that it still exists today (Chitty, 2007). Most of the big-name IQ-ists have, either explicitly or implicitly, stated things that can be construed in a eugenic way, and thusly, the main goal of the IQ-ist program is revealed: limit the birthrates of the lower classes, which are mostly minorities.
The eugenics movement in America—which then influenced Nazi policy—was not built on science, nor was it political (even though it aimed to be “applied science”; Wilson, 2017), it was a political movement which was erected to control social groups thought to be inferior to the higher-ups (Quigley, 1995). The link between eugenic thinking and IQ-ism in its history go hand-in-hand and some IQ-ists, even today, still advocate for such social policy based on the results from IQ tests (Herrnstein and Murray, 1994; Itzkoff, 1994).
Such prescriptions from IQ-ists for what ‘should be’ done with low IQ people speak to their bias in the matter. One of the great IQ-ists, so revered, Arthur Jensen was very implicit in his views in the late 1960s and early 70s about what should be done for the black population in America. His predecessors, too, had the same type of eugenic beliefs which then influenced their thoughts and values on crime and ‘intelligence.’ This game that IQ-ists have been playing has been going on for over 100 years; and with the advent of new genetic technology, the IQ-ists can continue their eugenic games, attempting to prevent ‘certain people’ from having children.
These tests, originally devised to correlate group’s places on the social hierarchy, cannot be ‘used for good’, as the point of its inception was to justify current class hierarchies as ‘genetic and immutable.’ These psychologists and criminologists leave their fields of inquiry and then attempt to influence public policy using clearly biased tests, as the history of the field has shown since its inception in the early 1900s. These are yet more reasons why IQ testing should be banned, as no good can come from believing that a group or individual is ‘less intelligent’ than another. The eugenic thinking of IQ-ists and criminologists feed off each other, with the IQ-ist ideas being the catalyst for the eugenic policies that followed.
The history of standardized testing—including IQ testing—has a contentious history. What causes score distributions between groups of people? I stated at least four reasons why there is a test gap:
(1) Differences in genes cause differences in IQ scores;
(2) Differences in environment cause differences in IQ scores;
(3) A combination of genes and environment cause differences in IQ scores; and
(4) Differences in IQ scores are built into the test based on the test constructors’ prior biases.
I hold to (4) since, as I have noted, the hereditarian-environmentalist debate is frivolous. There is, as I have been saying for years now, no agreed-upon definition of ‘intelligence’, since there are such disparate answers from the ‘experts’ (Lanz, 2000; Richardson, 2002).
For the lack of such a definition only reflects the fact that there is no worked-out theory of intelligence. Having a successful definition of intelligence without a corresponding theory would be like having a building without foundations. This lack of theory is also responsible for the lack of some principled regimentation of the very many uses the word ‘intelligence’ and its cognates are put to. Tao many questions concerning intelligence are still open, too many answers controversial. Consider a few examples of rather basic questions: Does ‘intelligence’ name some entity which underlies and explains certain classes of performances1, or is the word ‘intelligence’ only sort of a shorthand-description for ‘being good at a couple of tasks or tests’ (typically those used in IQ tests)? In other words: Is ‘intelligence’ primarily a descriptive or also an explanatorily useful term? Is there really something like intelligence or are there only different individual abilities (compare Deese 1993)? Or should we turn our backs on the noun ‘intelligence’ and focus on the adverb ‘intelligently’, used to characterize certain classes of behaviors? (Lanz, 2000: 20)
Nash (1990: 133-4) writes:
Always since there are just a series of tasks of one sort or another on which performance can be ranked and correlated with other performances. Some performances are defined as ‘cognitive performances’ and other performances as ‘attainment performances’ on essentially arbitrary, common sense grounds. Then, since ‘cognitive performances’ require ‘ability’ they are said to measure that ‘ability’. And, obviously, the more ‘cognitive ability’ an individual posesses the more that individual can acheive. These procedures can provide no evidence that IQ is or can be measured, and it is rather besides the point to look for any, since that IQ is a metric property is a fundamental assumption of IQ theory. It is imposible that any ‘evidence’ could be produced by such procedures. A standardised test score (whether on tests designated as IQ or attainment tests) obtained by an individual indicates the relative standing of that individual. A score lies within the top ten perent or bottom half, or whatever, of those gained by the standardisation group. None of this demonstrates measurement of any property. People may be rank ordered by their telephone numbers but that would not indicate measurement of anything. IQ theory must demonstrate not that it has ranked people according to some performance (that requires no demonstration) but that they are ranked according to some real property revealed by that performance. If the test is an IQ test the property is IQ — by definition — and there can in consequence be no evidence dependent on measurement procedures for hypothesising its existence. The question is one of theory and meaning rather than one of technique. It is impossible to provide a satisfactory, that is non-circular, definition of the supposed ‘general cognitive ability’ IQ tests attempt to measure and without that definition IQ theory fails to meet the minimal conditions of measurement.
These is similar to Mary Midgley’s critique of ‘intelligence’ in her last book before her death What Is Philosophy For? (Midgley, 2018). The ‘definitions’ of ‘intelligence’ and, along with it, its ‘measurement’ have never been satisfactory. Haier (2016: 24) refers to Gottfredson’s ‘definition’ of ‘intelligence, stating that ‘intelligence’ is a ‘general mental ability.’ But if that is the case, that it is a ‘general mental ability’ (g) then ‘intelligence’ does not exist because ‘g’ does not exist as a property in the brain. Lanz’s (2000) critique is also like Howe’s (1988; 1997) that ‘intelligence’ is a descriptive, not explanatory, term.
Now that the concept of ‘intelligence’ has been covered, let’s turn to race and test bias.
Test items are biased when they have different psychological meanings across cultures (He and van de Vijver 2012: 7). If they have different meanings across cultures, then the tests will not reflect the same ‘ability’ between cultures. Being exposed to the knowledge—and correct usage of it—on a test is imperative for performance. For if one is not exposed to the content on the test, how are they expected to do well if they do not know the content? Indeed, there is much evidence that minority groups are not acculturated to the items on the test (Manly et al, 1997; Ryan et al, 2005; Boone et al, 2007). This is what IQ tests measure: acculturation to the the tests’ constructors, school cirriculum and school teachers—aspects of white, middle-class culture (Richardson, 1998). Ryan et al (2005) found that reading and and educational level, not race or ethnicity, was related to worse performance on psychological tests.
Serpell et al (2006) took 149 white and black fourth-graders and randomly assigned them to ethnically homogeneous groups of three, working on a motion task on a computer. Both blacks and whites learned equally well, but the transfer outcomes were better for blacks than for whites.
Helms (1992) claims that standardized tests are “Eurocentric”, which is “a perceptual set in which European and/ or European American values, customs, traditions and characteristics are used as exclusive standards against which people and events in the world are evaluated and perceived.” In her conclusion, she stated that “Acculturation
and assimilation to White Euro-American culture should enhance one’s performance on currently existing cognitive ability tests” (Helms, 1992: 1098). There just so happens to be evidence for this (along with the the studies referenced above).
Fagan and Holland (2002) showed that when exposure to different kinds of information was required, whites did better than blacks but when it was based on generally available knowledge, there was no difference between the groups. Fagan and Holland (2007) asked whites and blacks to solve problems found on usual IQ-type tests (e.g., standardized tests). Half of the items were solvable on the basis of available information, but the other items were solveable only on the basis of having acquired previous knowledge, which indicated test bais (Fagan and Holland, 2007). They, again, showed that when knowledge is equalized, so are IQ scores. Thus, cultural differences in information acquisition explain IQ scores. “There is no distinction between crassly biased IQ test items and those that appear to be non-biased” (Mensh and Mensh, 1991). This is because each item is chosen because it agrees with the distribution that the test constructors presuppose (Simon, 1997).
How do the neuropsychological studies referenced above along with Fagan and Holland’s studies show that test bias—and, along with it test construction—is built into the test which causes the distribution of the scores observed? Simple: Since the test constructors come from a higher social class, and the items chosen for inclusion on the test are more likely to be found in certain cultural groups than others, it follows that the reason for lower scores was that they were not exposed to the culturally-specific knowledge used on the test (Richardson, 2002; Hilliard, 2012).
The [IQ] tests do what their construction dictates; they correlate a group’s mental worth with its place in the social hierarchy. (Mensh and Mensh, 1991)
This is very easily seen with how such tests are constructed. The biases go back to the beginning of standardized testing—the first one being the SAT. The tests’ constructors had an idea of who was or was not ‘intelligent’ and so constructed the tests to show what they already ‘knew.’
…as one delves further … into test construction, one finds a maze of arbitrary steps taken to ensure that the items selected — the surrogates of intelligence — will rank children of different classes in conformity with a mental hierarchy that is presupposed to exist. (Mensh and Mensh, 1991)
Garrison (2009: 5) states that standardized tests “exist to assess social function” and that “Standardized testing—or the theory and practice known as “psychometrics” … is not a form of measurment.” The same way tests were constructed in the 1900s is the same way they are constructed today—with arbitrary items and a presuppossed mental hiearchy which then become baked into the tests by virtue of how they are constructed.
IQ-ists like to say that certain genes are associated with high intelligence (using their GWASes), but what could the argument possibly be that would show that variation in SNPs would cause variation in ‘intelligence’? What would a theory of that look like? How is the hereditarian hypothesis not a just-so story? Such tests were created to justify the hierarchies in society, the tests were constructed to give the results that they get. So, I don’t see how genetic ‘explanations’ are not just-so stories.
1 Blacks and whites are different cultural groups.
2 If (1), then they will have different experiences by virtue of being different cultural groups.is
3 So blacks and whites, being different cultural groups, will score differently on tests of ability, since they are exposed to different knowledge structures due to their different cultures and so, all tests of ability are culture-bound. Knowledge, Culture, Logic, and IQ
Rushton and Jensen (2005) claim that the evidence they review over the past 30 years of IQ testing points to a ‘genetic component’ to the black-white IQ gap, relying on the flawed Minnesota study of twins “reared apart” (Joseph, 2018)—among other methods—to generate heritability estimates and state that “The new evidence reviewed here points to some genetic component in Black–White differences in mean IQ.” The concept of heritability, however, is a flawed metric (Bailey, 1997; Schonemann, 1997; Guo, 2000; Moore, 2002; Rose, 2006; Schneider, 2007; Charney, 2012, 2013; Burt and Simons, 2014; Panofsky, 2014; Joseph et al, 2015; Moore and Shenk, 2016; Panofsky, 2016; Richardson, 2017). That G and E interact means that we cannot tease out “percentages” of nature and nurture’s “contribution” to a “trait.” So, one cannot point to heritability estimates as if they point to a “genetic cause” of the score gap between blacks and whites. Further note that the gap has closed in recent years (Dickens and Flynn, 2006; Smith, 2018).
And now, here is another argument based on the differing experiences that cultural groups experience which then explains IQ score differences (eg Mensh and Mensh, 1991; Manly et al, 1997; Kwate, 2001; Fagan and Holland, 2002, 2007; Cole, 2004; Ryan et al, 2005; Boone et al, 2007; Au, 2008; Hilliard, 2012; Au, 2013).
(1) If children of different class levels have experiences of different kinds with different material; and
(2) if IQ tests draw a disproportionate amount of test items from the higher classes; then
(c) higher class children should have higher scores than lower-class children.
Nature vs nurture can be said to be a debate on what is ‘innate’ and what is ‘acquired’ in an organism. Debates about how nature and nurture tie into athletic ability and race both fall back onto the dichotomous notion. “Athleticism is innate and genetic!”, the hereditarian proclaims. “That blacks of West African ancestry are over-represented in the 100m dash is evidence of nature over nurture!” How simplistic these claims are.
Steve Sailer, in his response to Birney et al on the existence of race, assumes that because those with ancestry to West Africa consistently have produced the most finalists (and winners) in the Olympics that race, therefore, must exist.
I pointed out on Twitter that it’s hard to reconcile the current dogma about race not being a biological reality with what we see in sports, such as each of the last 72 finalists in the Olympic 100-meter dash going all the way back to 1984 nine Olympics ago being at least half sub-Saharan in ancestry.
the abundant data suggesting that individuals of sub-Saharan ancestry enjoy genetic advantages.
For example, it’s considered fine to suggest that the reason that each new Dibaba is fast is due to their shared genetics. But to say that one major reason Ethiopians keep winning Olympic running medals (now up to 54, but none at any distance shorter than the 1,500-meter metric mile because Ethiopians lack sprinting ability) is due to their shared genetics is thought unthinkable.
Sailer’s argument seems to be “Group X is better than Group Y at event A. Therefore, X and Y are races”, which is similar to the hereditarian arguments on the existence of ‘race’—just assume they exist.
The outright reductionism to genes in Sailer’s view on athleticism and race is plainly obvious. That blacks are over-represented in certain sports (e.g., football and basketball) is taken to be evidence for this type of reductionism that Sailer and others appeal to (Gnida, 1995). Such appeals can be said to be implicitly saying “The reason why blacks succeed at sport is due to genes while whites succeed due to hard work, so blacks don’t need to work as hard as whites when it comes to sports.”
There are anatomic and physiological differences between groups deemed “black” and “white”, and these differences do influence sporting success. Even though this is true, this does not mean that race exists. Such reductionist claims—as I myself have espoused years ago—do not hold up. Yes, blacks have a higher proportion of type II muscle fibers (Caesar and Henry, 2015), but this does not alone explain success in certain athletic disciplines.
Current genetic testing cannot identify an athlete (Pitsiladis et al, 2013). I reviewed some of the literature on power genotypes and race and concluded that there are no genes yet identified that can be said to be a sufficient cause of success in power sports.
Just because group A has gene or gene networks G and they compete in competition C does not mean that gene or gene networks G contribute in full—or in part—to sporting success. The correlations could be coincidental and non-functional in regard to the sport in question. Athletes should be studied in isolation, meaning just studying a specific athlete in a specific discipline to ascertain how, what, and why works for the specific athlete along with taking anthropomorphic measures, seeing how bad they want “it”, and other environmental factors such as nutrition and training. Looking at the body as a system will take us away from privileging one part over another—while we also do understand that they do play a role but not the role that reductionists believe.
No evidence exists for DNA variants that are common to endurance athletes (Rankinen et al, 2016). But they do have one thing in common (which is an environmental effect on biology): those born at altitude have a permanently altered ventilatory response as adults while “Peruvians born at altitude have a nearly 10% larger forced vital capacity compared to genetically matched Peruvians born at sea level” (Brutasaert and Parra, 2009: 16). Certain environmental effects on biology are well-known, and those biological changes do help in certain athletic events (Epstein, 2014). Yan et al (2016) conclude that “conclude that the traditional argument of nature versus nurture is no longer relevant, as it has been clearly established that both are important factors in the road to becoming an elite athlete.”
Georgiades et al (2017) go the other way and what they argue is clear in the title of their paper “Why nature prevails over nurture in the making of the elite athlete.” They continue:
Despite this complexity, the overwhelming and accumulating evidence, amounted through experimental research spanning almost two centuries, tips the balance in favour of nature in the “nature” and “nurture” debate. In other words, truly elite-level athletes are built – but only from those born with innate ability.
They use twin studies as an example stating that since heritability is greater than 50% but lower than 100% means “that the environment is also important.” But this is a strange take, especially from seasoned sports scientists (like Pitsiladis). Attempting to partition traits into a ‘nature’ and ‘nurture’ component and then argue that the emergence of that trait is due more to genetics than environment is an erroneous use of heritability estimates. It is not possible—nor is it feasible—to separate traits into genetic and environmental components. The question does not even make sense.
“… the question of how to separate the native from the acquired in the responses of man does not seem likely to be answered because the question is unintelligible.” (Leonard Carmichael 1925, quoted in Genes, Determinism and God, Alexander, 2017)
Tucker and Collins (2012) write:
Rather, individual performance thresholds are determined by our genetic make-up, and training can be defined as the process by which genetic potential is realised. Although the specific details are currently unknown, the current scientific literature clearly indicates that both nurture and nature are involved in determining elite athletic performance. In conclusion, elite sporting performance is the result of the interaction between genetic and training factors, with the result that both talent identification and management systems to facilitate optimal training are crucial to sporting success.
Tucker and Collins (2012) define training as the realization of genetic potential, while DNA “control the ceiling” of what one may be able to accomplish. “… training maximises
the likelihood of obtaining a performance level with a genetically controlled ‘ceiling’, accounts for the observed dominance of certain populations in specific sporting disciplines” (Tucker and Collins, 2012: 6). “Training” would be the environment here and the “genetically controlled ‘ceiling'” would be genes here. The authors are arguing that while training is important, training is just realizing the ‘potential’ of what is ‘already in’ the genes—an erroneous way of looking at genes. Shenk (2010: 107) explains why:
As the search for athletic genes continues, therefore, the overwhelming evidence suggests that researchers will instead locate genes prone to certain types of interactions: gene variant A in combination with gene variant B, provoked into expression by X amount of training + Y altitude + Z will to win + a hundred other life variables (coaching, injuries, etc.), will produce some specific result R. What this means, of course, What this means, of course, is that we need to dispense rhetorically with thick firewall between biology (nature) and training (nurture). The reality of GxE assures that each person’s genes interacts with his climate, altitude, culture, meals, language, customs and spirituality—everything—to produce unique lifestyle trajectories. Genes play a critical role, but as dynamic instruments, not a fixed blueprint. A seven- or fourteen- or twenty-eight-year-old is not that way merely because of genetic instruction.
The model proposed by Tucker and Collins (2012) is pretty reductionist (see Ericsson, 2012 for a response), while the model proposed by Shenk (2010) is more holistic. The hypothetical model explaining Kenyan distance running success (Wilbur and Pitsiladis, 2012) is, too, a more realistic way of assessing sport dominance:
The formation of an elite athlete comes down to a combination of genes, training, and numerous other interacting factors. The attempt to boil the appearance of a certain trait to either ‘genes’ or ‘environment’ and partition them into percentages is an unsound procedure. That a certain group continuously wins a certain event does not constitute evidence that the group in question is a race, nor does it constitute evidence that ‘genes’ are the cause of the outcome between groups in that event. The holistic model of human athletic performance in which genes contribute to certain physiological processes along with training, and other biomechanical and psychological differences is the correct way to think about sport and race. Actually seeing an athlete in motion in his preferred sport is (and I believe always will be) superior to just genetic analyses. Genetic tests also have “no role to play in talent identification” (Webborn et al, 2015).
One emerging concept is that there are many potential genetic pathways to a given phenotype . This concept is consistent with ideas that biological redundancy underpins complex multiscale physiological responses and adaptations in humans . From an applied perspective, the ideas discussed in this review suggest that talent identification on the basis of DNA testing is likely to be of limited value, and that field testing, which is essentially a higher order ‘bioassay’, is likely to remain a key element of talent identification in both the near and foreseeable future . (Joyner, 2019; Genetic Approaches for Sports Performance: How Far Away Are We?)
Athleticism is irreducible to biology (Louis, 2004). Holistic (nature and nurture) will beat the reductionist (nature vs nurture) views; with how biological systems work, there is no reason to privilege one level over another (Noble, 2012), so there is no reason to privilege the gene over the environment, environment over the gene. The interaction of multiple factors explains sport success.
Genetic reductionism refers to the belief that understanding our genes will have us understand everything from human behavior to disease. The behavioral genetic approach claims to be the best way to parse through social and biological causes of health, disease, and behavior. The aim of genetic reductionism is to reduce a complex biological system to the sum of its parts. While there was some value in doing so when our technology was in its infancy and we did learn a lot about what makes us “us”, the reductionist paradigm has outlived its usefulness.
If we want to understand a complex biological system then we shouldn’t use gene scores, heritability estimates, or gene sequencing. We should be attempting to understand how the whole biological system interacts with its surroundings—its environment.
Reductionists may claim that “gene knockout” studies can point us in the direction of genetic causation—“knockout” a gene and, if there are any changes, then we can say that that gene caused that trait. But is it so simple? Richardson (2000) puts it well:
All we know for sure is that rare changes, or mutations, in certain single genes can drastically disrupt intelligence, by virtue of the fact that they disrupt the whole system.
Noble (2011) writes:
Differences in DNA do not necessarily, or even usually, result in differences in phenotype. The great majority, 80%, of knockouts in yeast, for example, are normally ‘silent’ (Hillenmeyer et al. 2008). While there must be underlying effects in the protein networks, these are clearly buffered at the higher levels. The phenotypic effects therefore appear only when the organism is metabolically stressed, and even then they do not reveal the precise quantitative contributions for reasons I have explained elsewhere (Noble, 2011). The failure of knockouts to systematically and reliably reveal gene functions is one of the great (and expensive) disappointments of recent biology. Note, however, that the disappointment exists only in the gene-centred view. By contrast it is an exciting challenge from the systems perspective. This very effective ‘buffering’ of genetic change is itself an important systems property of cells and organisms.
Moreover, even when a difference in the phenotype does become manifest, it may not reveal the function(s) of the gene. In fact, it cannot do so, since all the functions shared between the original and the mutated gene are necessarily hidden from view. … Only a full physiological analysis of the roles of the protein it codes for in higher-level functions can reveal that. That will include identifying the real biological regulators as systems properties. Knockout experiments by themselves do not identify regulators (Davies, 2009).
All knocking-out or changing genes/alleles will do is show us that T is correlated with G, not that T is caused by G. Merely observing a correlation between a change in genes or knocking genes out will tell us nothing about biological causation. Reductionism will not have us understand the etiology of disease as the discipline of physiology is not reductionist at all—it is a holistic discipline.
Lewontin (2000: 12) writes in the introduction to The Ontogeny of Information: “But if I successfully perform knockout experiments on every gene that can be seen in such experiments to have an effect on, say, wing shape, have I even learned what causes the wing shape of one species or individual to differ from that of another? After all, two species of Drosophilia presumably have the same relevant set of loci.”
But the loss of a gene can be compensated by another gene—a phenomenon known as genetic compensation. In a complex bio-system, when one gene is knocked out, another similar gene may take the ‘role’ of the knocked-out gene. Noble (2006: 106-107) explains:
Suppose there are three biochemical pathways A, B, and C, by which a particular necessary molecule, such as a hormone, can be made in the body. And suppose the genes for A fail. What happens? The failure of the A genes will stimulate feedback. This feedback will affect what happens with the sets of genes for B and C. These alternate genes will be more extensively used. In the jargon, we have here a case of feedback regulation; the feedback up-regulates the expression levels of the two unaffected genes to compensate for the genes that got knocked out.
Clearly, in this case, we can compensate for two such failures and still be functional. Only if all three mechanisms fail does the system as a whole fail. The more parallel compensatory mechanisms an organism has, the more robust (fail-safe) will be its functionality.
The Neo-Darwinian Synthesis has trouble explaining such compensatory genetic mechanisms—but the systems view (Developmental Systems Theory, DST) does not. Even if a knockout affects the phenotype, we cannot say that that gene outright caused the phenotype, the system was screwed up, and so it responded in that way.
Genetic networks and their role in development became clear when geneticists began using genetic knockout techniques to disable genes which were known to be implicated in the development of characters but the phenotype remained unchanged—this, again, is an example of genetic compensation. Jablonka and Lamb (2005: 67) describe three reasons why the genome can compensate for the absence of a particular gene:
first, many genes have duplicate copies, so when both alleles of one copy are knocked out, the reserve copy compensates; second, genes that normally have other functions can take the place of a gene that has been knocked out; and third, the dynamic regulatory structure of the network is such that knocking out single components is not felt.
Using Waddington’s epigenetic landscape example, Jablonka and Lamb (2005: 68) go on to say that if you knocked a peg out, “processes that adjust the tension on the guy ropes from other pegs could leave the landscape essentially unchanged, and the character quite normal. … If knocking out a gene completely has no detectable effect, there is no reason why changing a nucleotide here and there should necessarily make a difference. The evolved network of interactions that underlies the development and maintenance of every character is able to accommodate or compensate for many genetic variations.”
“multiple alternative pathways . . . are the rule rather than the exception . . . such pathways can continue to function despite amino acid changes that may impair one intermediate regulator. Our results underscore the importance of systems biology approaches to understand functional and evolutionary constraints on genes and proteins.” (Quoted in Richardson, 2017: 132)
When it comes to disease, genes are said to be difference-makers—that is, the one gene difference/mutation is what is causing the disease phenotype. Genes, of course, interact with our lifestyles and they are implicated in the development of disease—as necessary, not sufficient, causes. GWA studies (genome-wide association studies) have been all the rage for the past ten or so years. And, to find diseases ‘associated’ with disease, GWA practioners take healthy people and diseased people, sequence their genomes and they then look for certain alleles that are more common in one group over the other. Alleles more common in the disease group are said to be ‘associated’ with the disease while alleles more common in the control group can be said to be protective of the disease (Kampourakis, 2017: 102). (This same process is how ‘intelligence‘ is GWASed.)
“Disease is a character difference” (Kampourakis, 2017: 132). So if disease is a character difference and differences in genes cannot explain the existence of different characters but can explain the variation in characters then the same must hold for disease.
“Gene for” talk is about the attribution of characters and diseases to DNA, even thoughit is not DNA that is directly responsible for them. … Therefore, if many genes produce or affect the production of the protein that in turn affects a character or disease, it makes no sense to identify one gene as the gene responsible “for” this character or disease. Single genes do not produce characters or disease …(Kampourakis, 2017: 134-135)
This all stems from the “blueprint metaphor”—the belief that the genome contains a blueprint for form and development. There are, however, no ‘genes for’ character or disease, therefore, genetic determinism is false.
Genes, in fact, are weakly associated with disease. A new study (Patron et al, 2019) analyzed 569 GWA studies, looking at 219 different diseases. David Scott (one of the co-authors) was interviewed by Reuters where he said:
“Despite these rare exceptions [genes accounting for half of the risk of acquiring Crohn’s, celiac and macular degeneration], it is becoming increasingly clear that the risks for getting most diseases arise from your metabolism, your environment, your lifestyle, or your exposure to various kinds of nutrients, chemicals, bacteria, or viruses,” Wishart said.
“Based on our results, more than 95% of diseases or disease risks (including Alzheimer’s disease, autism, asthma, juvenile diabetes, psoriasis, etc.) could NOT be predicted accurately from SNPs.”
It seems like this is, yet again, another failure of the reductionist paradigm. We need to understand how genes interact in the whole human biological system, not reducing our system to the sum of its parts (‘genes’). Programs like this are premised on reductionist assumptions; it seems intuitive to think that many diseases are ’caused by’ genes, as if genes are ‘in control’ of development. However, what is truly ‘in control’ of development is the physiological system—where genes are used only as resources, not causes. The reductionist (neo-Darwinist) paradigm cannot really explain genetic compensation after knocking out genes, but the systems view can. The amazing complexity of complex bio-systems allows them to buffer against developmental miscues and missing genes in order to complete the development of the organism.
Genes are not active causes, they are passive causes, resources—they, therefore, cannot cause disease and characters.