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Action and behavior are distinct concepts, although in common lexicon they are used interchangeably. The two concepts are needed to distinguish what one intends to do and what one reacts to and how they react. In this article, I will explain the distinction between the two and how and why people get it wrong when discussing the two concepts—since using them interchangeably is inaccurate.
Actions are intentional; they are done for reasons (Davidson, 1963). Actions are determined by one’s current intentional state and they then act for reasons. So, in effect, the agent’s intentional states cause the action, but the action is carried out for reasons. Actions are that which is done by an agent, but stated in this way, it could be used interchangeably with behavior. The Wikipedia article on “action” states:
action is an intentional, purposive, conscious and subjectively meaningful activity
So actions are conscious, compared to behaviors which are reflexive and unconscious—not done for reasons.
Davidson (1963: 685) writes:
Whenever someone does something for a reason, therefore, he can be characterized as (a) having some sort of pro attitude toward actions of a certain kind, and (b) believing (or knowing, perceiving, noticing, remembering) that his action is of that kind.
So providing the reason why an agent did A requires naming the pro-attitude—beliefs paired with desires—or the related belief that caused the agent’s action. When I explain behavior, this will become clear.
Behavior is different: behavior is a reaction to a stimulus and this reaction is unconscious. For example, take a doctor’s office visit. Hitting the knee in the right spot causes the knee to jerk up—doctors use this test to test for nerve damage. It tests the L2, L3, and L4 segments of the spinal cord, so if there is no reflex, the doctor knows there is a problem.
This is done without thought—the patient does not think about the reflex. This then shows how and why action and behavior are distinct concepts. Here’s what occurs when the doctor hits the patient’s knee:
When the doctor hits the knee, the patient’s thigh muscle stretches. When the thigh muscle stretches, a signal is then sent along the sensory neuron to the spinal cord where it interacts with a motor neuron which goes to the thigh muscle. The muscle then contracts which causes the reflex. (Recall my article on causes of muscle movement.)
So this, compared to consciously taking a step—consciously jerking your leg in the same way as a doctor expects the patellar reflex—is what distinguishes one from the other—what distinguishes action from behavior. Sure, the behavior of the patellar reflex occurred for a reason—but it was not done consciously by the agent so it is therefore not an action.
Perhaps it would be important at this point to explain the differences between action, conduct, and behavior, because we have used these three terms in the discussion of caring. …
Teleology, the reader is reminded, involves goals or lures that provide the reasons for a person actingin a certain way. It is goals or reasons that establish action from simple behavior. On the other hand the concept of efficient causation is involved in the concept of behavior. Behavior is the result of antecedentconditions. The individual behaves in response to causal stimuli or antecedent conditions. Hence, behavior is a reaction to what already is—the result of a push from the past to do something in the present. In contrast, an action aims at the future. It is motivated by a vision of what can be. (Brencick and Webster, 2000: 147)
This is also another thing that Darwin got wrong. He believed that instincts and reflexes are inherited—this is not wrong since they are behaviors and behaviors are dispositional which means they can be selected. However, he believed that before they were inherited as instincts and reflexes, they were intentional acts. As Badcock (2000: 56) writes in Evolutionary Psychology: A Critical Introduction:
Darwin explicitly states this when he says that ‘it seems probable that some actions, which were at first performed consciously, have become through habit and association converted into relex actions, and are now firmly fixed and inherited.’
This is quite obviously wrong, as I have explained above; instead of “reflexive actions”, Darwin meant “reflexive behaviors”. So, it seems that Darwin did not grasp the distinction between “action” and “behavior” either.
We can then form this simple argument, take cognition:
This is a natural outcome of what has been argued here, due to the distinction between action and behavior. So when we think of “cognition” what comes to mind? Thinking. Thinking is an action—so thinking (cognition) is intentional. Intentionality is “the power of minds and mental states to be about, to represent, or to stand for, things, properties and states of affairs.” So, when we think, our minds/mental states can represent, stand for things, properties and states of affairs. Therefore, cognition is intentional. Since cognition is intentional and behavior is dispositional, it directly follows that cognition cannot be responsible for behavior.
Thinking is a mental activity which results in a thought. So if thinking is a mental activity which results in a thought, 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 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 particular belief; when they commit themselves to an answer they have formulated a new belief.
Beliefs are propositional attitudes: believing p involves adopting the belief attitude to proposition p. So, cognition is thinking: a mental process that results in the formation of a propositional belief. When one acquires a propositional attitude by thinking, a process takes place in stages. Future propositional attitudes are justified on earlier propositional attitudes. So cognition is thinking; thinking is a mental state of considering a particular view (proposition).
Therefore, thinking is an action (since it is intentional) and cannot possibly be a behavior (a disposition). Something can be either an action or a behavior—it cannot be both.
Let’s say that I have the belief that food is downtown. I desire to eat. So I intend to go downtown to get some food. While the cause is the sensation of hunger. This chain shows how actions are intentional—how one intends to act.
Furthermore, using the example I explained above, how a doctor assesses the patellar reflex is a behavior—it is not an action since the agent himself did not cause it. One could say that it is an action for the doctor performing the reflexive test, but it cannot be an action for the agent the test is being done on—it is, therefore, a behavior.
I have explained the difference between action and behavior and how and why they are distinct. I gave an example of action (cognition) and behavior (patellar reflex) and explained how they are distinct. I then gave an argument showing how cognition (an action) cannot possibly be responsible for behavior. I showed how Darwin believed (falsely) that actions could eventually become behaviors. Darwin pretty much stated “Actions can be selected and eventually become behaviors.” This is nonsense. Actions, by virtue of being intentional, cannot be selected, even if they are done over and over again, they do not eventually become behaviors. On the other hand, behavior, by virtue of being dispositional, can be selected. In any case, I have definitively shown that the two concepts are distinct and that it is nonsense to conflate the terms.
Construct validity for IQ is fleeting. Some people may refer to Haier’s brain imaging data as evidence for construct validity for IQ, even though there are numerous problems with brain imaging and that neuroreductionist explanations for cognition are “probably not” possible (Uttal, 2014; also see Uttal, 2012). Construct validity refers to how well a test measures what it purports to measure—and this is non-existent for IQ (see Richardson and Norgate, 2014). If the tests did test what they purport to (intelligence), then they would be construct valid. I will show an example of a measure that was validated and shown to be reliable without circular reliance of the instrument itself; I will show that the measures people use in attempt to prove that IQ has construct validity fail; and finally I will provide an argument that the claim “IQ tests test intelligence” is false since the tests are not construct valid.
Jung and Haier (2007) formulated the P-FIT hypothesis—the Parieto-Frontal Intelligence Theory. The theory purports to show how individual differences in test scores are linked to variations in brain structure and function. There are, however, a few problems with the theory (as Richardson and Norgate, 2007 point out in the same issue; pg 162-163). IQ and brain region volumes are experience-dependent (eg Shonkoff et al, 2014; Betancourt et al, 2015; Lipina, 2016; Kim et al, 2019). So since they are experience-dependent, then different experiences will form different brains/test scores. Richardson and Norgate (2007) state that such bigger brain areas are not the cause of IQ, rather that, the cause of IQ is the experience-dependency of both: exposure to middle-class knowledge and skills leads to a better knowledge base for test-taking (Richardson, 2002), whereas access to better nutrition would be found in middle- and upper-classes, which, as Richardson and Norgate (2007) note, lower-quality, more energy-dense foods are more likely to be found in lower classes. Thus, Haier et al did not “find” what they purported too, based on simplistic correlations.
Now let me provide the argument about IQ test experience-dependency:
Premise 1: IQ tests are experience-dependent.
Premise 2: IQ tests are experience-dependent because some classes are more exposed to the knowledge and structure of the test by way of being born into a certain social class.
Premise 3: If IQ tests are experience-dependent because some social classes are more exposed to the knowledge and structure of the test along with whatever else comes with the membership of that social class then the tests test distance from the middle class and its knowledge structure.
Conclusion 1: IQ tests test distance from the middle class and its knowledge structure (P1, P2, P3).
Premise 4: If IQ tests test distance from the middle class and its knowledge structure, then how an individual scores on a test is a function of that individual’s cultural/social distance from the middle class.
Conclusion 2: How an individual scores on a test is a function of that individual’s cultural/social distance from the middle class since the items on the test are more likely to be found in the middle class (i.e., they are experience-dependent) and so, one who is of a lower class will necessarily score lower due to not being exposed to the items on the test (C1, P4)
Conclusion 3: IQ tests test distance from the middle class and its knowledge structure, thus, IQ scores are middle-class scores (C1, C2).
Still further regarding neuroimaging, we need to take a look at William Uttal’s work.
Uttal (2014) shows that “The problem is that both of these approaches are deeply flawed for methodological, conceptual, and empirical reasons. One reason is that simple models composed of a few neurons may simulate behavior but actually be based on completely different neuronal interactions. Therefore, the current best answer to the question asked in the title of this contribution [Are neuroreductionist explanations of cognition possible?] is–probably not.”
Uttal even has a book on meta-analyses and brain imaging—which, of course, has implications for Jung and Haier’s P-FIT theory. In his book Reliability in Cognitive Neuroscience: A Meta-meta Analysis, Uttal (2012: 2) writes:
There is a real possibility, therefore, that we are ascribing much too much meaning to what are possibly random, quasi-random, or irrelevant response patterns. That is, given the many factors that can influence a brain image, it may be that cognitive states and braib image activations are, in actuality, only weakly associated. Other cryptic, uncontrolled intervening factors may account for much, if not all, of the observed findings. Furthermore, differences in the localization patterns observed from one experiment to the next nowadays seems to reflect the inescapable fact that most of the brain is involved in virtually any cognitive process.
Uttal (2012: 86) also warns about individual variability throughout the day, writing:
However, based on these findings, McGonigle and his colleagues emphasized the lack of reliability even within this highly constrained single-subject experimental design. They warned that: “If researchers had access to only a single session from a single subject, erroneous conclusions are a possibility, in that responses to this single session may be claimed to be typical responses for this subject” (p. 708).
The point, of course, is that if individual subjects are different from day to day, what chance will we have of answering the “where” question by pooling the results of a number of subjects?
That such neural activations gleaned from neuroimaging studies vary from individual to individual, and even time of day in regard to individual, means that these differences are not accounted for in such group analyses (meta-analyses). “… the pooling process could lead to grossly distorted interpretations that deviate greatly from the actual biological function of an individual brain. If this conclusion is generally confirmed, the goal of using pooled data to produce some kind of mythical average response to predict the location of activation sites on an individual brain would become less and less achievable“‘ (Uttal, 2012: 88).
Clearly, individual differences in brain imaging are not stable and they change day to day, hour to hour. Since this is the case, how does it make sense to pool (meta-analyze) such data and then point to a few brain images as important for X if there is such large variation in individuals day to day? Neuroimaging data is extremely variable, which I hope no one would deny. So when such studies are meta-analyzed, inter- and intrasubject variation is obscured.
The idea of an average or typical “activation region” is probably nonsensical in light of the neurophysiological and neuroanatomical differences among subjects. Researchers must acknowledge that pooling data obscures what may be meaningful differences among people and their brain mechanisms. THowever, there is an even more negative outcome. That is, by reifying some kinds of “average,” we may be abetting and preserving some false ideas concerning the localization of modular cognitive function (Uttal, 2012: 91).
So when we are dealing with the raw neuroimaging data (i.e., the unprocessed locations of activation peaks), the graphical plots provided of the peaks do not lead to convergence onto a small number of brain areas for that cognitive process.
… inconsistencies abount at all levels of data pooling when one uses brain imaging techniques to search for macroscopic regional correlates of cognitive processes. Individual subjects exhibit a high degree of day-to-day variability. Intersubject comparisons between subjects produce an even greater degree of variability.
The overall pattern of inconsistency and unreliability that is evident in the literature to be reviewed here again suggests that intrinsic variability observed at the subject and experimental level propagates upward into the meta-analysis level and is not relieved by subsequent pooling of additional data or averaging. It does not encourage us to believe that the individual meta-analyses will provide a better answer to the localization of cognitive processes question than does any individual study. Indeed, it now seems plausible that carrying out a meta-analysis actually increases variability of the empirical findings (Uttal, 2012: 132).
So since reliability is low at all levels of neuroimaging analysis, it is very likely that the relations between particular brain regions and specific cognitive processes have not been established and may not even exist. The numerous reports purporting to find such relations report random and quasi-random fluctuations in extremely complex systems.
Construct validity (CV) is “the degree to which a test measures what it claims, or purports, to be measuring.” A “construct” is a theoretical psychological construct. So CV in this instance refers to whether IQ tests test intelligence. We accept that unseen functions measure what they purport to when they’re mechanistically related to differences in two variables. E.g, blood alcohol and consumption level nd the height of the mercury column and blood pressure. These measures are valid because they rely on well-known theoretical constructs. There is no theory for individual intelligence differences (Richardson, 2012). So IQ tests can’t be construct valid.
The accuracy of thermometers was established without circular reliance on the instrument itself. Thermometers measure temperature. IQ tests (supposedly) measure intelligence. There is a difference between these two, though: the reliability of thermometers measuring temperature was established without circular reliance on the thermometer itself (see Chang, 2007).
In regard to IQ tests, it is proposed that the tests are valid since they predict school performance and adult occupation levels, income and wealth. Though, this is circular reasoning and doesn’t establish the claim that IQ tests are valid measures (Richardson, 2017). IQ tests rely on other tests to attempt to prove they are valid. Though, as seen with the valid example of thermometers being validated without circular reliance on the instrument itself, IQ tests are said to be valid by claiming that it predicts test scores and life success. IQ and other similar tests are different versions of the same test, and so, it cannot be said that they are validated on that measure, since they are relating how “well” the test is valid with previous IQ tests, for example, the Stanford-Binet test. This is because “Most other tests have followed the Stanford–Binet in this regard (and, indeed are usually ‘validated’ by their level of agreement with it; Anastasi, 1990)” (Richardson, 2002: 301). How weird… new tests are validated with their agreement with other, non-construct valid tests, which does not, of course, prove the validity of IQ tests.
IQ tests are constructed by excising items that discriminate between better and worse test takers, meaning, of course, that the bell curve is not natural, but forced (see Simon, 1997). Humans make the bell curve, it is not a natural phenomenon re IQ tests, since the first tests produced weird-looking distributions. (Also see Richardson, 2017a, Chapter 2 for more arguments against the bell curve distribution.)
Finally, Richardson and Norgate (2014) write:
In scientific method, generally, we accept external, observable, differences as a valid measure of an unseen function when we can mechanistically relate differences in one to differences in the other (e.g., height of a column of mercury and blood pressure; white cell count and internal infection; erythrocyte sedimentation rate (ESR) and internal levels of inflammation; breath alcohol and level of consumption). Such measures are valid because they rely on detailed, and widely accepted, theoretical models of the functions in question. There is no such theory for cognitive ability nor, therefore, of the true nature of individual differences in cognitive functions.
That “There is no such theory for cognitive ability” is even admitted by lead IQ-ist Ian Deary in his 2001 book Intelligence: A Very Short Introduction, in which he writes “There is no such thing as a theory of human intelligence differences—not in the way that grown-up sciences like physics or chemistry have theories” (Richardson, 2012). Thus, due to this, this is yet another barrier against IQ’s attempted validity, since there is no such thing as a theory of human intelligence.
In sum, neuroimaging meta-analyses (like Jung and Haier, 2007; see also Richardson and Norgate, 2007 in the same issue, pg 162-163) do not show what they purport to show for numerous reasons. (1) There are, of course, consequences of malnutrition for brain development and lower classes are more likely to not have their nutritional needs met (Ruxton and Kirk, 1996); (2) low classes are more likely to be exposed to substance abuse (Karriker-Jaffe, 2013), which may well impact brain regions; (3) “Stress arising from the poor sense of control over circumstances, including financial and workplace insecurity, affects children and leaves “an indelible impression on brain structure and function” (Teicher 2002, p. 68; cf. Austin et al. 2005)” (Richardson and Norgate, 2007: 163); and (4) working-class attitudes are related to poor self-efficacy beliefs, which also affect test performance (Richardson, 2002). So, Jung and Haier’s (2007) theory “merely redescribes the class structure and social history of society and its unfortunate consequences” (Richardson and Norgate, 2007: 163).
In regard to neuroimaging, pooling together (meta-analyzing) numerous studies is fraught with conceptual and methodological problems, since a high-degree of individual variability exists. Thus, attempting to find “average” brain differences in individuals fails, and the meta-analytic technique used (eg by Jung and Haier, 2007) fails to find what they want to find: average brain areas where, supposedly, cognition occurs between individuals. Meta-analyzing such disparate studies does not show an “average” where cognitive processes occur, and thusly, cause differences in IQ test-taking. Reductionist neuroimaging studies do not, as is popularly believed, pinpoint where cognitive processes take place in the brain, they have not been established and they may not even exist.
Nueroreductionism does not work; attempting to reduce cognitive processes to different regions of the brain, even using meta-analytic techniques as discussed here, fail. There “probably cannot” be neuroreductionist explanations for cognition (Uttal, 2014), and so, using these studies to attempt to pinpoint where in the brain—supposedly—cognition occurs for such ancillary things such as IQ test-taking fails. (Neuro)Reductionism fails.
Since there is no theory of individual differences in IQ, then they cannot be construct valid. Even if there were a theory of individual differences, IQ tests would still not be construct valid, since it would need to be established that there is a mechanistic relation between IQ tests and variable X. Attempts at validating IQ tests rely on correlations with other tests and older IQ tests—but that’s what is under contention, IQ validity, and so, correlating with older tests does not give the requisite validity to IQ tests to make the claim “IQ tests test intelligence” true. IQ does not even measure ability for complex cognition; real-life tasks are more complex than the most complex items on any IQ test (Richardson and Norgate, 2014b)
Now, having said all that, the argument can be formulated very simply:
Premise 1: If the claim “IQ tests test intelligence” is true, then IQ tests must be construct valid.
Premise 2: IQ tests are not construct valid.
Conclusion: Therefore, the claim “IQ tests test intelligence” is false. (modus tollens, P1, P2)
Michael Hardimon published Rethinking Race: The Case for Deflationary Realism last year (Hardimon, 2017). I was awaiting some critical assessment of the book, and it seems that at the end of March, some criticism finally came. The criticism came from another philosopher, Joshua Glasgow, in the journal Mind (Glasgow, 2018). The article is pretty much just arguing against his minimalist race concept and one thing he brings up in his book, the case of a twin earth and what we would call out-and-out clones of ourselves on this twin earth. Glasgow makes some good points, but I think he is largely misguided on Hardimon’s view of race.
Hardimon (2017) is the latest defense for the existence of race—all the while denying the existence of “racialist races”—that there are differences in mores, “intelligence” etc—and taking the racialist view and “stripping it down to its barebones” and shows that race exists, in a minimal way. This is what Hardimon calls “social constructivism” in the pernicious sense—racialist races, in Hardimon’s eyes, are socially constructed in a pernicious sense, arguing that racialist races do not represent any “facts of the matter” and “supports and legalizes domination” (pg 62). The minimalist concept, on the other hand, does not “support and legalize domination”, nor does it assume that there are differences in “intelligence”, mores and other mental characters; it’s only on the basis of superficial physical features. These superficial physical features are distributed across the globe geographically and these groups are real and exist who show these superficial physical features across the globe. Thus, race, in a minimal sense, exists. However, people like Glasgow have a few things to say about that.
Glasgow (2018) begins by praising Hardimon (2017) for “dispatching racialism” in his first chapter, also claiming that “academic writings have decisively shown why racialism is a bad theory” (pg 2). Hardimon argues that to believe in race, on not need believe what the racialist concept pushes; one must only acknowledge and accept that there are:
1) differences in visible physical features which correspond to geographic ancestry; 2) these differences in visible features which correspond to geographic ancestry are exhibited between real groups; 3) these real groups that exhibit these differences in physical features which correspond to geographic ancestry satisfy the conditions of minimalist race; C) therefore race exists.
This is a simple enough argument, but Glasgow disagrees. As a counter, Glasgow brings up the “twin earth” argument. Imagine a twin earth was created. On Twin Earth, everything is exactly the same; there are copies of you, me, copies of companies, animals, history mirrored down to exact minutiae, etc. The main contention here is that Hardimon claims that ancestry is important for our conception of race. But with the twin earth argument, since everything, down to everything, is the same, then the people who live on twin earth look just like us but! do not share ancestry with us, they look like us (share patterns of visible physical features), so what race would we call them? Glasgow thusly states that “sharing ancestry is not necessary for a group to count as a race” (pg 3). But, clearly, sharing ancestry is important for our conception of race. While the thought experiment is a good one it fails since ancestry is very clearly necessary for a group to count as a race, as Hardimon has argued.
Hardimon (2017: 52) addresses this, writing:
Racial Twin Americans might share our concept of race and deny that races have different geographical origins. This is because they might fail to understand that this is a component of their race concept. If, however, their belief that races do not have different geographical origins did not reflect a misunderstanding of their “race concept,” then their “race concept” would not be the same concept as the concept that is the ordinary race concept in our world. Their use of ‘race’ would pick out a different subject matter entirely from ours.
and on page 45 writes:
Glasgow envisages Racial Twin Earth in such a way that, from an empirical (that is, human) point of view, these groups would have distinctive ancestries, even if they did not have distinctive ancestries an sich. But if this is so, the groups [Racial Twin Earthings] do not provide a good example of races that lack distinctive ancestries and so do not constitute a clear counterexample to C(2) [that members of a race are “linked by a common ancestry peculiar to members of that group”].
C(2) (P2 in the simple argument for the existence of race) is fine, and the objections from Glasgow do not show that P(C)2 is false at all. The Racial Twin Earth argument is a good one, it is sound. However, as Hardimon had already noted in his book, Glasgow’s objection to C(2) does not rebut the fact that races share peculiar ancestry unique to them.
Next, Glasgow criticizes Hardimon’s viewpoints on “Hispanics” and Brazilians. These two groups, says Glasgow, shows that two siblings with the same ancestry, though they have different skin colors, would be different races in Brazil. He uses this example to state that “This suggests that race and ancestry can be disconnected” (pg 4). He criticizes Hardimon’s solution to the problem of race and Brazilians, stating that our term “race” and the term in Brazil do not track the same things. “This is jarring. All that anthropological and sociological work done to compare Brazil with the rest of the world (including the USA) would be premised on a translation error” (pg 4). Since Americans and Brazilians, in Glasgow’s eyes, can have a serious conversation about race, this suggests to Glasgow that “our concept of race must not require that races have distinct ancestral groups” (pg 5).
I did cover Brazilians and “Hispanics” as regards the minimalist race concept. Some argue that the “color system” in Brazil is actually a “racial system” (Guimaraes 2012: 1160). While they do denote race as ‘COR’ (Brazilian for ‘color), one can argue that the term used for ‘color’ is ‘race’ and that we would have no problem discussing ‘race’ with Brazilians, since Brazilians and Americans have similar views on what ‘race’ really is. Hardimon (2017: 49) writes:
On the other hand, it is not clear that the Brazilian concept of COR is altogether independent of the phenomenon we Americans designate using ‘race.’ The color that ‘COR’ picks out is racial skin color. The well-known, widespread preference for lighter (whiter) skin in Brazil is at least arguably a racial preference. It seems likely that white skin color is preferred because of its association with the white race. This provides a reason for thinking that the minimalist concept of race may be lurking in the background of Brazilian thinking about race.
Since ‘COR’ picks out racial skin color, it can be safely argued that Brazilians and Americans at least are generally speaking about the same things. Since the color system in Brazil pretty much mirrors what we know as racial systems, demarcating races on the basis of physical features, we are, it can be argued, talking about the same (or similar) things.
Further, the fact that “Latinos” do not fit into Hardimon’s minimalist race concepts is not a problem with Hardimon’s arguments about race, but is a problem with how “Latinos” see themselves and racialize themselves as a group. “Latinos” can count as a socialrace, but they do not—can not—count as a minimalist race (such as the Caucasian minimalist race; the African minimalist race; the Asian minimalist race etc), since they do not share visible physical patterns which correspond to differences in geographic ancestry. Since they do not exhibit characters that demarcate minimalist races, they are not minimalist races. Looking at Cubans compared to, say, Mexicans (on average) is enough to buttress this point.
Glasgow then argues that there are similar problems when you make the claim “that having a distinct geographical origin is required for a group to be a race” (pg 5). He says that we can create “Twin Trump” and “Twin Clinton” might be created from “whole cloth” on two different continents, but we would still call them both “white.” Glasgow then claims that “I worry that visible trait groups are not biological objects because the lines between them are biologically arbitrary” (pg 5). He argues that we need a “dividing line”, for example, to show that skin color is an arbitrary trait to divide races. But if we look at skin color as an adaptation to the climate of the people in question (Jones et al, 2018), then this trait is not “arbitrary”, and the trait is then linked to geographic ancestry.
Glasgow then goes down the old and tired route that “There is no biological reason to mark out one line as dividing the races rather than another, simply based on visible traits” (pg 5). He then goes on to discuss the fact that Hardimon invokes Rosenberg et al (2002) who show that our genes cluster in specific geographic ancestries and that this is biological evidence for the existence of race. Glasgow brings up two objections to the demarcation of races on both physical appearance and genetic analyses: picture the color spectrum, “Now thicken the orange part, and thin out the light red and yellow parts on either side of orange. You’ve just created an orange ‘cluster’” (pg 6), while asking the question:
Does the fact that there are more bits in the orange part mean that drawing a line somewhere to create the categories orange and yellow now marks a scientifically principled line, whereas it didn’t when all three zones on the spectrum were equally sized?
I admit this is a good question, and that this objection would indeed go with the visible trait of skin color in regard to race; but as I said above, since skin color can be conceptualized as a physical adaptation to climate, then that is a good proxy for geographic ancestry, whether or not there is a “smooth variation” of skin colors as you move away from the equator or not, it is evidence that “races” have biological differences and these differences start on the biggest organ in the human body. This is just the classic continuum fallacy in action: that X and Y are two different parts of an extreme; there is no definable point where X becomes Y, therefore there is no difference between X and Y.
As for Glasgow’s other objection, he writes (pg 6):
if we find a large number of individuals in the band below 62.3 inches, and another large grouping in the band above 68.7 inches, with a thinner population in between, does that mean that we have a biological reason for adopting the categories ‘short’ and ‘tall’?
It really depends on what the average height is in regard to “adopting the categories ‘short’ and ‘tall’” (pg 6). The first question was better than the second, alas, they do not do a good job of objecting to Hardimon’s race concept.
In sum, Glasgow’s (2018) review of Hardimon’s (2017) book Rethinking Race: The Case for Deflationary Realism is an alright review; though Glasgow leaves a lot to be desired and I do think that his critique could have been more strongly argued. Minimalist races do exist and are biologically real.
I am of the opinion that what matters regarding the existence of race is not biological science, i.e., testing to see which populations have which differing allele frequencies etc; what matters is the philosophical aspects to race. The debates in the philosophical literature regarding race are extremely interesting (which I will cover in the future), and are based on racial naturalism and racial eliminativism.
(Racial naturalism “signifies the old, biological conception of race“; racial eliminativism “recommends discarding the concept of race entirely“; racial constructivism “races have come into existence and continue to exist through “human culture and human decisions” (Mallon 2007, 94)“; thin constructivism “depicts race as a grouping of humans according to ancestry and genetically insignificant, “superficial properties that are prototypically linked with race,” such as skin tone, hair color and hair texture (Mallon 2006, 534); and racial skepticism “holds that because racial naturalism is false, races of any type do not exist“.) (Also note that Spencer (2018) critiques Hardimon’s viewpoints in his book as well, which will also be covered in the future, along with the back-and-forth debate in the philosophical literature between Quayshawn Spencer (e.g., 2015) and Adam Hochman (e.g., 2014).)
Steroids get a bad reputation. It largely comes from movies and people’s anecdotal experiences and repeating stories they hear from the media and other forms of entertainment, usually stating that there is a phenomenon called ‘roid rage’ that makes steroid users violent. Is this true? Are any myths about steroids true, such as a shrunken penis? Are there ways to off-set it? Steroids and their derivatives are off-topic for this blog, but it needs to be stressed that there are a few myths that get pushes about steroids and what it does to behavior, its supposed effects on aggression and so forth.
With about 3 million AAS (ab)users (anabolic-androgenic steroids) in America (El Osta et al, 2016), knowing the effects of steroids and similar drugs such as Winny (a cutting agent) would have positive effects, since, of course, athletes mostly use them.
This is, perhaps, one of the most popular. Though the actual myth is that AAS use causes the penis to shrink (which is not true), in reality, AAS use causes the testicles to shrink by causing the Leydig cells to decrease natural testosterone production which then decreases the firmness and shape of the testicles which then results in a loss of size.
In one study of 772 gay men using 6 gyms between the months of January and February (and you need to think of the type of bias there that those people who are ‘Resolutioners’ would be more likely to go to the gym those months), a questionnaire was given to the men. 15 .2 percent of the men had used, with 11.7 percent of them injecting within the past 12 months. HIV positive men were more likely to have used in the past compared to negative men (probably due to scripts). Fifty-one percent of them reported testicular atrophy, and they were more likely to report suicidal thoughts (Bolding, Sherr, and Elford, 2002). They conclude:
One in seven gay men surveyed in central London gyms in 2000 said they had used steroids in the previous 12 months. HIV positive men were more likely to have used steroids than other men, some therapeutically. Side effects were reported widely and steroid use was associated with having had suicidal thoughts and feeling depressed, although cause and effect could not be established. Our findings suggest that steroid use among gay men may have serious consequences for both physical and mental health.
Of course, those who (ab)use substances have more psychological problems than those who do not. Another study of 203 bodybuilders found that 8 percent (n = 17) found testicular atrophy (for what it’s worth, it was an internet survey of drug utilization) (Perry et al, 2005). Another study found that out of 88 percent of individuals who abused the drug complained of side-effects of AAS use, about 40 percent described testicular atrophy (Evans, 1997), while testicular atrophy was noted in about 50 percent of cases (sample size n = 24) (Darke et al, 2016).
One study of steroid users found that only 17 percent of them had normal sperm levels (Torres-Calleja et al, 2001), this is because exogenous testosterone will result in the atrophy of germinal cells which cause a decrease in spermatogenesis. Though, too, increased AAS (ab)use later into life may lead to infertility later in life. Knuth et al (1989) also studied 41 bodybuilders with an average age of 26.7. They went through a huge laundry list of different types of steroids they have taken over their lives. Nineteen of the men were still using steroids at the time of the investigation (group I), whereas 12 of them (group II) stopped taking steroids 3 months prior, while 10 of them (group III) stopped steroid use 4 to 24 months prior.
They found that only 5 of them had sperm counts below the average of 20 million sperm per square ml, while 24 of the bodybuilders showed these symptoms. No difference between group I and II was noticed and group III (the group that abstained from use for 4 to 24 months) largely had sperm levels in the normal range. So, the data suggests that even in cases of severe decrease of sensitivity to androgens due to AAS (ab)use, spermatogenesis may still continue normally in some men, even when high levels of androgens are administered exogenously, while even after prolonged use it seems it is possible for sperm levels to go back to the normal range (Knuth et al 1989).
Aggression and crime
Now it’s time for the fun part and my reason for writing this article. Does (ab)using steroids cause someone to go into an uncontrollable rage, a la the Incredible Hulk when they inject themselves with testosterone? The media has latched into the mind of many, with films and TV shows showing the insanely aggressive man who has been (ab)using AAS. But how true is this? A few papers have shown that this phenomenon is indeed true (Konacher and Workman, 1989; Pope and Katz, 1994), but how true is it on its own, since AAS (ab)users are known to use multiple substances???
Konacher and Workman (1989) is a case study done on one man who had no criminal history, who began taking AASs three months before he murdered his wife, and they conclude that AAS can be said to be a ‘personality changer’. Piacetino et al (2015) conclude in their review of steroid use and psychopathology in athletes that “AAS use in athletes is associated with mood and anxiety disturbances, as well as reckless behavior, in some predisposed individuals, who are likely to develop various types of psychopathology after long-term exposure to these substances. There is a lack of studies investigating whether the preexistence of psychopathology is likely to induce AAS consumption, but the bulk of available data, combined with animal data, point to the development of specific psycho-pathology, increased aggressiveness, mood destabilization, eating behavior abnormalities, and psychosis after AAS abuse/dependence.” I, too, would add that since most steroid abuse are polysubstance abusers (they use multiple illicit drugs on top of AAS), that the steroids per se are not causing crime or aggressive behavior, it’s the other drugs that the steroid (ab)user is also taking. And there is evidence for this assertion.
Lundholm et al (2015) showed just that: that AAS (ab)use was confounded with other substances used while the individual in question was also taking AAS. They write:
“We found a strong association between self-reported lifetime AAS use and violent offending in a population-based sample of more than 10,000 men aged 20-47 years. However, the association decreased substantially and lost statistical significance after adjusting for other substance abuse. This supports the notion that AAS use in the general population occurs as a component of polysubstance abuse, but argues against its purported role as a primary risk factor for interpersonal violence. Further, adjusting for potential individual-level confounders initially attenuated the association, but did not contribute to any substantial change after controlling for polysubstance abuse.“
Even The National Institute of Health (NIH) writes: “In summary, the extent to which steroid abuse contributes to violence and behavioral disorders is unknown. As with the health complications of steroid abuse, the prevalence of extreme cases of violence and behavioral disorders seems to be low, but it may be underreported or underrecognized.” We don’t know whether steroids cause aggression or more aggressive athletes are more likely to use the substance (Freberg, 2009: 424). Clearly, the claims of steroids causing aggressive behavior and crime are overblown and there has yet to be a scientific consensus on the matter. A great documentary on the matter is Bigger, Stronger, Faster, which goes through the myths of testosterone while chronicling the use of illicit drugs in bodybuilding and powerlifting.
This, too, was even seen in one study where men were administered supraphysiologic doses of testosterone to see its effects on muscle size and strength since it had never been tested; no changes in mood or behavior occurred (Bhasin et al, 1996). Furthermore, injecting individuals with supraphysiological doses of testosterone as high as 200 and 600 mg per week does not cause heightened anger or aggression (Tricker et al, 1996; O’Connor et, 2002). Testosterone is one of the most abused AASs around, and if a heightened level of T doesn’t cause crime, nor can testosterone levels being higher this week compared to last seem to be a trigger for crime, we can safely disregard any claims of ‘roid rage’ since they coincide with other drug use (polysubstance abuse). So since we know that supraphysiologic doses of testosterone don’t cause crime nor aggression, we can say that AAS use, on its own (and even with other drugs) does not cause crime or heightened aggression since aggression elevates testosterone secretion, testosterone doesn’t elevate aggression.
One review also suggests that medical issues associated with AAS (ab)use are exaggerated to deter their use by athletes (Hoffman and Ratamess, 2006). They conclude that “Existing data suggest that in certain circumstances the medical risk associated with anabolic steroid use may have been somewhat exaggerated, possibly to dissuade use in athletes.”
Racial differences in steroid use
Irving et al (2002) found that 2.1 percent of whites used steroids, whereas 7.6 percent of blacks did; 6.1 percent of ‘Hispanics’ use them within the past 12 months, and a whopping 14.1 percent of Hmong Chinese used them; 7.9 percent of ‘other Asians’ used them, and 3,1 percent of ‘Native Americans’ did with 11.3 percent of mixed race people using them within the past 12 months to gain muscle. Middle schoolers were more likely to use than high schoolers, while people from lower SES brackets were more likely to use than people in higher SES brackets.
Stilger and Yesalis (1999: 134) write (emphasis mine):
Of the 873 high school football players participating in the study, 54 (6.3%) reported having used or currently using AAS. Caucasians represented 85% of all subjects in the survey. Nine percent were African-American while the remainder (6%) consisted of Hispanics, Asian, and other. Of the AAS users, 74% were Caucasian, 13% African American, 7% Hispanic, and 3% Asian, x2 (4,854 4) 4.203, p 4 .38. The study also indicated that minorities are twice as likely to use AAS as opposed to Caucasians. Cross tabulated results indicate that 11.2% of all minorities use/used AAS as opposed to 6.5% of all Caucasians (data not displayed).
One study even had whites and blacks reporting the same abuse of steroids in their sample (n = 10,850 ‘Caucasians’ and n = 1,883 black Americans), with blacks reporting, too, lower levels of other drug abuse (Green et al, 2001). Studies indeed find higher rates of drug use for white Americans than other ethnies, in college (McCabe et al, 2007). Black Americans also frequently underreport and lie about their drug use (Ledgerwood et al, 2008; Lu et al, 2001). Blacks are also more likely to go to the ER after abusing drugs than whites (Drug Abuse Warning Network, 2011). Bauman and Ennett (1994) also found that blacks underreport drug use whereas whites overreport.
So can we really believe the black athletes who state that they do not (ab)use AAS? No, we cannot. Blacks like about any and all drug use, so believing that they are being truthful about AAS (ab)use in this specific instance is not called for.
Like with all things you use and abuse, there are always side-effects. Though, the media furor one hears regarding AAS and testosterone (ab)use are largely blown out of proportion. The risks associated with AAS (ab)use are ‘transient’, and will subside after one discontinues using the drugs. Blacks seem to take more AAS than whites, even if they do lie about any and all drug use. (And other races, too, seem to use it at higher rates than whites.) Steroid use does not seem to be ‘bad’ if one knows what they’re doing and are under Doctor’s supervision, but even then, if you want to know the truth about AAS, then you need to watch the documentary Bigger, Stronger, Faster. I chalk this up to the media themselves demonizing testosterone itself, along with the ‘toxic masculinity’ and the ‘toxic jock effect‘ (Miller, 2009; Miller, 2011). Though, if you dig into the literature yourself you’ll see there is scant evidence for AAS and testosterone (ab)use causing crime, that doesn’t stop papers like those two by Miller talking about the effects of ‘toxic jocks’ and in effect, deriding masculine men and with it the hormone that makes Men men: testosterone. If taken safely, there is nothing wrong with AAS/testosterone use.
(Note: Doctor’s supervision only, etc)
A recent paper was published on the origins of Native Americans titled Terminal Pleistocene Alaskan genome reveals first founding population of Native Americans (Moreno-Mayar et al, 2018). An infant genome was studied and it was found that group of people the infant belonged to was similar to modern Native Americans but not a direct ancestor. The infant’s group and modern Native Americans share the same common ancestors, however. This, of course, supports the hypothesis that Native Americans are descended from Asian migrants.
The infant is also related to both North and South Natives, which implies they’re descended from a single migration. (Though I am aware of a hypothesis that states that there were three waves of migration into the Americas from Beringia, along with back migrations from South America back into Asia.)
Moreno-Mayar et al (2018) write in the abstract: “Our findings further suggest that the far-northern North American presence of northern Native Americans is from a back migration that replaced or absorbed the initial founding population of Ancient Beringians.” And they conclude (pg 5):
The USR1 results provide direct genomic evidence that all Native Americans can be traced back to the same source population from a single Late Pleistocene founding event. Descendants of that population were present in eastern Beringia until at least 11.5 ka. By that time, however, a separate branch of Native Americans had already established itself in unglaciated North America, and diverged into the two basal groups that ultimately became the ancestors of most of the indigenous populations of the Americas.
This is a highly interesting paper which shows that, as we’ve known for decades, that the ancestors of the Native Americans crossed the Bering Land Bridge around 11 kya. Though, my reason for writing this article is not for this very interesting paper, but the ‘conclusions’ that people that people are drawing from it.
Of course, whenever a study like this gets published you get a whole slew of people who read the popular articles on the matter and don’t read the actual journal article. The problem here is that some people took the chance to attempt to say that this paper showed that the origins of Man were in Europe, not Africa as can be seen in the tweet below.
“…represent a growing body of evidence being discovered across the world that suggests the origins of the human race may have been Europe and not Africa as once believed.”
So I read the paper, read it again and even cntrl f’d it and didn’t see the phrase. So where did the phrase come from?
I did some digging and I found the source for the quote, which, of course, was not in the Nature article. The quote in question comes from an article titled Scientists discover DNA proving original Native Americans were White. Oh, wow. Isn’t that interesting? Maybe he read a different paper then I did.
The author stated that the infant was “more closely related to modern white Europeans“, though of course this too wasn’t stated anywhere in the article. He also quoted an evolutionary biologist who stated “This is a new population of Native Americans — the white Native American.” Wow, this is interesting. Now let’s look at what else this author writes:
Working with scientists at the University of Alaska and elsewhere, Willerslev compared the genetic makeup of the baby, named Xach’itee’aanenh t’eede gaay or “sunrise child-girl” by the local community, with genomes from other ancient and modern people. They found that nearly half of the girls DNA came from the ancient North Europeans who lived in what is no Scandinavia. The rest of her genetic makeup was a roughly even mixed of DNA now carried by northern and southern Native Americans. Using evolutionary models, the researchers showed the ancestors of the first Native Americans started to emerge as a distinct population about 35,000 years ago.
Isn’t that weird? This is nowhere in the original article. So I did some digging and what do I find? I found that the author of this article literally plagiarized almost word for word from another article from The Guardian!
Working with scientists at the University of Alaska and elsewhere, Willerslev compared the genetic makeup of the baby, named Xach’itee’aanenh t’eede gaay or “sunrise child-girl” by the local community, with genomes from other ancient and modern people. They found that nearly half of the girls DNA came from the ancient north Eurasians who lived in what is now Siberia. The rest of her genetic makeup was a roughly even mixed of DNA now carried by northern and southern Native Americans.
Using evolutionary models, the researchers showed the ancestors of the first Native Americans started to emerge as a distinct population about 35,000 years ago.
This is not only an example of straight up plagiarism, the author of the other article literally only switched “Siberia” with “Scandinavia” and “ancient north Eurasians” with “ancient North Europeans”. Ancient north Eurasians are NOT WHITE! Where do you gather this from?! There is NO INDICATION that they were ‘ancient north Europeans!
In sum, if you ever see articles like this that purport to show that Native Americans were white European and that it supposedly calls the OoA model into question, always ALWAYS check the claims and don’t fall for plagiarist bullshit. This is truly incredible that not only did the author literally copy and past a full article, he also snipped a few words to fit the narrative he was pushing! I will be notifying the author of the Guardian article of this plagiarism. You can check it out yourself, read the first article cited above then read the Guardian article. Do people really think they can get away with literally plagiarizing and article like that word for word?
This article is on a whole other level compared to the claims that modern Man began in Europe and that a few teeth upend the OoA model. This guy didn’t even read the paper, it seems like he read the Guardian article and then copy and pasted it and changed a few words for his own ‘gain’ to ‘show’ that the first Native Americans were white. There is no way that one can interpret this paper in this manner if they’ve truly read and understood it. Always, always read original journal articles and, if you must read popular science articles then read it from a reputable website, not kooky websites with an agenda to push who literally plagiarize other people’s work. You can tell who’s gullible and who’s not just by what they say about new papers that can possibly be misinterpreted.
Ryan Faulk, like most IQ-ists, believes that the correlation with job performance and IQ somehow is evidence for its validity. He further believes that because self- and peer-ratings correlate with one’s IQ scores that that is further evidence for IQ’s validity.
Well too bad for Faulk, correlations with other tests and other IQ tests lead to circular assumptions. The first problem, as I’ve covered before, is that there is no agreed-upon model or description of IQ/intelligence/’g’ and so therefore we cannot reliably and truthfully state that differences in ‘g’ this supposed ‘mental power’ this ‘strength’ is what causes differences in test scores. Unfortunately for Ryan Faulk and other IQ-ists, again, coming back to our good old friend test construction, it’s no wonder that IQ tests correlate around .5—or so is claimed—with job performance, however IQ test scores correlate at around .5 with school achievement, which is caused by some items containing knowledge that has been learned in school, such as “In what continent is Egypt?” and Who wrote Hamlet?” and “What is the boiling point of water?” As Ken Richardson writes in his 2017 book Genes, Brains, and Human Potential: The Science and Ideology of Intelligence (pg 85):
So it should come as no surprise that performance on them [IQ tests] is associated with school performance. As Robert L. Thorndike and Elizabeth P. Hagen explained in their leading textbook, Educational and Psychological Measurement, “From the very way in which the tests were assembled [such correlation] could hardly be otherwise.”
So, obviously, neither of the two tests determine independently that they measure intelligence, this so-called innate power, and because they’re different versions of the same test there is a moderate correlation between them. This goes back to item analysis and test construction. Is it any wonder, then, why correlations with IQ and achievement increase with age? It’s built into the test! And while Faulk does cite high correlations from one of Schmidt and Hunter’s meta-analyses on the subject, what he doesn’t tell you is that one review found a correlation of .66 between teacher’s assessment and future achievement of their students later in life (higher than the correlation with job performance and IQ) (Hoge and Coladarci, 1989.) They write (pg 303): “The median correlation, 0.66, suggests a moderate to strong correspondence between teacher judgments and student achievement.” This is just like what I quoted the other day in my response to Grey Enlightenment where I quoted Layzer (1972) who wrote:
Admirers of IQ tests usually lay great stress on their predictive power. They marvel that a one-hour test administered to a child at the age of eight can predict with considerable interest whether he will finish college. But as Burt and colleagues have clearly demonstrated, teachers subjective assessments afford even more reliable predictors. This is almost a truism.
So the correlation of .5 between occupation level and IQ is self-fulfilling, which are not independent measures. In regard to the IQ and job performance correlation, which I’ve discussed in the past, studies in the 70s showed much lower correlations, between .2 and .3, which Jensen points out in The g Factor.
The problem with the so-called validity studies carried out by Schmidt and Hunter, as cited by Ryan Faulk, is that they included numerous other tests that were not IQ tests in their analysis like memory tests, reading tests, the SAT, university admission tests, employment selection tests, and a variety of armed forces tests. “Just calling these “general ability tests,” as Schmidt and Hunter do, is like reducing a diversity of serum counts to a “general. blood test” (Richardson, 2017: 87). Of course the problem with using vastly different tests is that they tap into different abilities and sources of individual differences. The correlation between SAT scores and high school grades is .28 whereas the correlation between both the SAT and high school grades and IQ is about .2. So it’s clearly not testing the same “general ability” that’s being tested.
Furthermore, regarding job performance, it’s based on one measure: supervisor ratings. These ratings are highly subjective and extremely biased with age and halo effects seen with height and facial attractiveness being seen to sway judgments on how well one works. Measures of job performance are unreliable—especially from supervisors—due to the assumptions and biases that go into the measure.
Do IQ tests test neural processes? Not really. One of the most-studied variables is reaction time. The quicker they react to a stimulus, supposedly, the higher their IQ is in average as they are quicker to process information, the story goes. Detterman (1987) notes that other factors other than ‘processing speed’ can explain differences in reaction time, including but not limited to, stress, understanding instructions, motivation to do said task, attention, arousal, sensory acuity, confidence, etc. Khodadadi et al (2014) even write “The relationship between reaction time and IQ is too complicated and reveal a significant correlation depends on various variables (e.g. methodology, data analysis, instrument etc.).” Complex cognition in real life is also completely different than the simple questions asked in the Raven (Richardson and Norgate, 2014).
It is easy to look at the puzzles that make up IQ tests and be convinced that they really do test brain power. But then we ignore the brain power thst nearly everyone displays in their everyday lives. Some psychologists have noticed thst people who stumble over formal tests of cognitive can bangle highly complex problems in their real lives all the time. As Michael Eysenck put it in his well-known book Psychology, “There is an apparent contradiction between our ability to deal effectively with out everyday environment and our failure to perform well on many laboratory reasoning tasks.” We can say the same about IQ tests.
Real-life problems combine many more variables that change over time and interact. It seems that the ability to do pretentious problems in a pencil-and-paper (or computer) format, like IQ test items, is itself a learned, if not-so-complex skill. (Richardson, 2017: 95-96)
Finally, Faulk cites studies showing that how intelligent people and their peers rates themselves and others predicted how well they did on IQ tests. This isn’t surprising. Since they correlate with academic achievement at .5 then if one is good academically then they’d have a high test score more often than not. That friends rate friends high and they end up matching scores is no surprise either as people generally group together with other people like themselves and so therefore will have similar achievements. That is not evidence for test validity though!! See Richardson and Norgate (2015) “In scientific method, generally, we accept external, observable differences as a valid measure of an unseen function when we can mechanistically relate differences in one to diffences in the other …” So even Faulk’s attempt to ‘validate’ IQ tests using peer- and self-ratings of ‘intelligence’ (whatever that is) falls on its face since its not a true measure of validity. It’s not construct validity. (EDIT: Psychological constructs are validated ‘by testing whether they relate to measures of other constructs as specified by theory‘ (Strauss and Smith, 2009). This doesn’t exist for IQ therefore IQ isn’t construct valid.)
In sum, Faulk’s article leaves a ton to be desired and doesn’t outright prove that there is validity to IQ tests because, as I’ve shown in the past, validity for IQ is nonexistent, though some have tried (using correlations with job performance as evidence) but Richardson and Norgate (2015) take down those claims and show that the correlation is between .2 and .3, not the .5+ cited by Hunter and Schmidt in their ‘validation studies’. The criteria laid out by Faulk does not prove that there is true construct validity to IQ tests and due to test construction, we see these correlations with educational achievement.
The word ‘construct’ is defined as “an idea or theory containing various conceptual elements, typically one considered to be subjective and not based on empirical evidence.” Whereas the word ‘validity’ is defined as “the quality of being logically or factually sound; soundness or cogency.” Is there construct validity for IQ tests? Are IQ tests tested against an idea or theory containing various conceptual elements? No, they are not.
Cronbach and Meehl (1955) define construct validity, which they state is “involved whenever a test is to be interpreted as a measure of some attribute or quality which is not “operationally defined.”” Though, the construct validity for IQ tests has been fleeting to investigators. Why? Because there is no theory of individual IQ differences to test IQ tests on. It is even stated that “there is no accepted unit of measurement for constructs and even fairly well-known ones, such as IQ, are open to debate.” The ‘fairly well-known ones’ like IQ are ‘open to debate’ because no such validity exists. The only ‘validity’ that exists for IQ tests is correlations with other tests and attempted correlations with job performance, but I will show that that is not construct validity as is classicly defined.
Construct validity can be easily defined as the ability of a test to measure the concept or construct that it is intended to measure. We know two things about IQ tests: 1) they do not test ‘intelligence’ (but they supposedly do a ‘good enough job’ so that it does not matter) and 2) it does not even test the ‘construct’ that it is intended to measure. For example, the math problem ‘1+1’ is construct valid regarding one’s knowledge and application of that math problem. Construct validity can pretty much be summed up as the proof that it is measuring what the test intends…but where is this proof? It is non-existent.
Richardson (1998: 116) writes:
Psychometrists, in the absence of such theoretical description, simply reduce score differences, blindly to the hypothetical construct of ‘natural ability’. The absence of descriptive precision about those constructs has always made validity estimation difficult. Consequently the crucial construct validity is rarely mentioned in test manuals. Instead, test designers have sought other kinds of evidence about the valdity of their tests.
The validity of new tests is sometimes claimed when performances on them correlate with performances on other, previously accepted, and currently used, tests. This is usually called the criterion validity of tests. The Stanford-Binet and the WISC are often used as the ‘standards’ in this respect. Whereas it may be reassuring to know that the new test appears to be measuring the same thing as an old favourite, the assumption here is that (construct) validity has already been demonstrated in the criterion test.
Some may attempt to say that, for instance, biological construct validity for IQ tests may be ‘brain size’, since brain size is correlated with IQ at .4 (meaning 16 percent of the variance in IQ is explained by brain size). However, for this to be true, someone with a larger brain would always have to be ‘more intelligent’ (whatever that means; score higher on an IQ test) than someone with a smaller brain. This is not true, so therefore brain size is not and should not be used as a measure of construct validity. Nisbett et al (2012: 144) address this:
Overall brain size does not plausibly account for differences in aspects of intelligence because all areas of the brain are not equally important for cognitive functioning.
For example, breathalyzer tests are construct valid. There is a .93 correlation (test-retest) between 1 ml/kg bodyweight of ethanol in 20, healthy male subjects. Furthermore, obtaining BAC through gas chromatography of venous blood, the two readings were highly correlated at .94 and .95 (Landauer, 1972). Landauer (1972: 253) writes “the very high accuracy and validity of breath analysis as a correct estimate of the BAL is clearly shown.” Construct validity exists for ad-libitum taste tests of alcohol in the laboratory (Jones et al, 2016).
There is a casual connection between what one breathes into the breathalyzer and his BAC that comes out of the breathalyzer and how much he had to drink. For example, for a male at a bodyweight of 160 pounds, 4 drinks would have him at a BAC of .09, which would make him unfit to drive. (‘One drink’ being 12 oz of beer, 5 oz of wine, or 1.25 oz of 80 proof liquor.) He drinks more, his BAC reading goes up. Someone is more ‘intelligent’ (scores higher on an IQ test), then what? The correlations obtained from so-called ‘more intelligent people’, like glucose consumption, brain evoked potentials, reaction time, nerve conduction velocity, etc have never been shown to determine higher ‘ability’ to score higher on IQ tests. That, too, would not even be construct validation for IQ tests, since there needs to be a measure showing why person A scored higher than person B, which needs to hold one hundred percent of the time.
Another good example of the construct validity of an unseen construct is white blood cell count. White blood cell count was “associated with current smoking status and COPD severity, and a risk factor for poor lung function, and quality of life, especially in non-currently smoking COPD patients. The WBC count can be used, as an easily measurable COPD biomarker” (Koo et al, 2017). In fact, the PRISA II test has white blood cell count in it, which is a construct valid test. Even elevated white blood cell count strongly predicts all-cause and cardiovascular mortality (Johnson et al, 2005). It is also an independent risk factor for coronary artery disease (Twig et al, 2012).
A good example of tests supposedly testing one thing but testing another is found here:
As an example, think about a general knowledge test of basic algebra. If a test is designed to assess knowledge of facts concerning rate, time, distance, and their interrelationship with one another, but test questions are phrased in long and complex reading passages, then perhaps reading skills are inadvertently being measured instead of factual knowledge of basic algebra.
Numerous constructs have validity—but not IQ tests. It is assumed that they test ‘intelligence’ even though an operational definition of intelligence is hard to come by. This is important, as if there cannot be an agreement on what is being tested, how will there be construct validity for said construct in question?
Richardson (2002) writes that Detterman and Sternberg sent out a questionnaire to a group of theorists which was similar to another questionnaire sent out decades earlier to see if there was an agreement on what ‘intelligence’ is. Twenty-five attributes of intelligence were mentioned. Only 3 were mentioned by more than 25 percent of the respondents, with about half mentioning ‘higher level components’, one quarter mentioned ‘executive processes’ while 29 percent mentioned ‘that which is valued by culture’. About one-third of the attributes were mentioned by less than 10 percent of the respondents with 8 percent of them answering that intelligence is ‘the ability to learn’. So if there is hardly any consensus on what IQ tests measure or what ‘intelligence’ is, then construct validity for IQ seems to be very far in the distance, almost unseeable, because we cannot even define the word, nor actually test it with a test that’s not constructed to fit the constructors’ presupposed notions.
Now, explaining the non-existent validity of IQ tests is very simple: IQ tests are purported to measure ‘g’ (whatever that is) and individual differences in test scores supposedly reflect individual differences in ‘g’. However, we cannot say that it is differences in ‘g’ that cause differences in individual test scores since there is no agreed-upon model or description of ‘g’ (Richardson, 2017: 84). Richardson (2017: 84) writes:
In consequence, all claims about the validity of IQ tests have been based on the assumption that other criteria, such as social rank or educational or occupational acheivement, are also, in effect, measures of intelligence. So tests have been constructed to replicate such ranks, as we have seen. Unfortunately, the logic is then reversed to declare that IQ tests must be measures of intelligence, because they predict school acheivement or future occupational level. This is not proper scientific validation so much as a self-fulfilling ordinance.
Construct validity for IQ does not exist (Richardson and Norgate, 2015), unlike construct validity for breathalyzers (Landauer, 1972) or white blood cell count as a disease proxy (Wu et al, 2013; Shah et al, 2017). So, if construct validity is non-existent, then that means that there is no measure for how well IQ tests measure what it’s ‘purported to measure’, i.e., how ‘intelligent’ one is over another because 1) the definition of ‘intelligence’ is ill-defined and 2) IQ tests are not validated against agreed-upon biological models, though some attempts have been made, though the evidence is inconsistent (Richardson and Norgate, 2015). For there to be true validity, evidence cannot be inconsistent; it needs to measure what it purports to measure 100 percent of the time. IQ tests are not calibrated against biological models, but against correlations with other tests that ‘purport’ to measure ‘intelligence’.
(Note: No, I am not saying that everyone is equal in ‘intelligence’ (whatever that is), nor am I stating that everyone has the same exact capacity. As I pointed out last week, just because I point out flaws in tests, it does not mean that I think that people have ‘equal ability’, and my example of an ‘athletic abilities’ test last week is apt to show that pointing out flawed tests does not mean that I deny individual differences in a ‘thing’ (though athletic abilities tests are much better with no assumptions like IQ tests have.))
Different races have different morphology/somatype. Therefore, we can reason that different races would fare better or worse at a certain lift depending on their limb length, such as leg length, arm length, torso length and so on. How do somatypic differences lead to differences in strength between the races on the Big Four lifts? The four lifts I will cover are bench press, deadlift, squat and overhead press.
East Asians have higher levels of body fat (for instance the Chinese, Wang et al, 2011) and have lower BMIs, yet higher levels of body fat (Wang et al, 1994). This, along with their somatype are part of the reason why they excel in some strength sports. Since East Asians have a smaller stature, averaging about 5 feet 8 inches, with shorter arms and legs. Thinking about how the ancestors of the East Asians evolved, this makes sense: they would have needed to be shorter and have shorter limbs as it is easier to warm a body with a smaller surface area. Therefore, while squatting they have a shorter path to travel with the bar on their back. East Asians would strongly excel at the squat, and if you watch these types of competitions, you’d see them strongly overrepresented—especially the Chinese.
African-Americans are descended from West African slaves, and so they have longer, thinner limbs with lower amounts of body fat on average (especially if they have more African ancestry), which is a classic sign of a mesomorphic phenotype. They do also skew ecto, which is useful in the running competitions they dominate (in the case of West Africans and descendants and certain tribes of Kenyans and Ethiopians). Either way, due to their long limbs and a short torso, they have to travel further with the weight therefore here they suffer and wouldn’t be as strong as people who have a long torso with shorter limbs.
Like East Asians, Europeans have similar morphology—skewing ectomorphic, the somatype that dominates strength competitions. Having a long torso with shorter limbs and more type I than type II fibers, they would then be able to lift more, especially since these competitors keep a high body fat percentage. Again, like with East Asians, there is a biomechanical advantage here and due to their higher levels of body fat and endomorphic somatype along with shorter limbs, they would be able to move more weight on the squat, especially more than African-Americans. Biomechanics is key when it comes to evaluating different groups’ morphology when attempting to see who would be stronger on average.
The deadlift is pretty straightforward: bending down and deadlifting the weight off of the ground. Key anatomic differences between the races dictate who would be better here. East Asians, with shorter limbs and a longer torso the bar has to travel a further path, compared to someone with longer limbs and shorter torso. Though, someone with short limbs and a short torso would also have a biomechanical advantage in pulling, it is nothing like if one has long arms and a short torso.
Here is where they would shine. Their anatomy is perfect for this lift. Since they have longer limbs and a shorter torso, the bar has a shorter path to travel to reach the endpoint of the lift. At the set-up of the lift, they already have a biomechanical advantage and they can generate more power in the lift due to their leverage advantage. The deadlift favors people with a long torso, short femurs, and long arms, and so it would favor African-Americans. (Their long arms off-sets their short torsos, though the bar would still have to travel further, they still would have the ability to move more weight.)
European Americans would have the same biomechanical problems as East Asians, but not as much since they have a taller stature. It is well-known in the world of weightlifting that having shorter, ‘T-rex arms’ impedes strength on the lift, since speaking from an anatomic viewpoint, they are just not built for it. No style of deadlift (the sumo or conventional) suits people with short arms, and so they are already at a biomechanical disadvantage. Relative to African-Americans, European Americans have ‘T-rex arms’ and therefore they would suffer at pulling exercises—deadlift included.
The overhead press is where people with shorter arms would excel. Thus, East Asians would be extremely strong pushers. Say the bar starts at the top of their chest, the path of the bar to the lockout would be shorter than if someone had longer arms. The size of the trapezius muscles also comes into play here, and people with larger trapezius muscles have a stronger press. The East Asians short stature and therefore shorter limbs is perfect for this lift and why they would excel.
African-Americans would suffer at the overhead press for one reason: their long limbs, mainly their arms. The bar has a further path to travel and thus strength would be impeded. Indeed, people not built for pressing have long arms, long torsos, and long legs. Performing the full range of motion, African-Americans would have less strength than East Asians and European Americans.
Again, due to similar morphology as East Asians, they, too, would excel at this lift. Since the lift is completed when the arms lock out, those with shorter arms would be able to move more weight and so what hurts them on the deadlift helps on pressing movements like the overhead press.
Lastly, the bench press. East Asians would excel here as well since they have shorter arms and the bar would have a shorter path to travel. Notice anything with bar movement? That’s a key to see which group would be stronger on average: looking at the average morphology of the races and then thinking about how the lift is performed, you can estimate who would be good at which lift and why. The bench press would favor someone with a shorter stature and arms, and they’d be able to lift more weight. (I personally have long arms compared to my body and my bench press suffers compared to my deadlift.) However, Caruso et al (2012) found that body mass is a more important predictor of who would excel at the bench press. East Asians have a higher body fat percentage, and therefore would be stronger on average in the lift.
Here, too, African-Americans will suffer. Like with the overhead press, the bar has a further path to travel. They also have less body fat on average and that would also have the bar travel more, having the individual put more exertion into the lift compared to someone who had shorter arms. The longer your arms are in a pushing exercise, the further the bar has to travel until lockout. Thus you can see that people with longer arms would suffer in the strength department compared to people with shorter arms, but this is reversed for pulling exercises like the deadlift described above. (There is also a specific longitudinal study on black-white differences in bench press which I will cover in the ‘Objections‘ section.)
Again, like with East Asians due to similar somatype, European Americans, too, would excel at this lift. They are able to generate more pound-for-pound power in the lift. The bar also has a shorter path to travel and since the people who compete in these competitions also have higher levels of body fat, then the bar has less of a distance to travel, thus increasing the amount of force the muscle can generate. Limb size/body mass/somatype predict how races/individuals would do on specific lifts.
One of the main objections that some may have is that one longitudinal study on black and white police officers found that blacks were stronger than whites at the end of the study (Boyce et al, 2014). However, I heavily criticized this paper at the beginning of the year and for good reason: heights of the officers weren’t reported (which is not the fault of the researchers but of an ongoing lawsuit at that department since people complained that they were discriminating against people based on height). The paper is highly flawed, but looking at it on face value someone who does not have the requisite knowledge they would accept the paper’s conclusions at face value. One of the main reasons for my criticism of the paper is that the bench press was tested on a Smith machine, not a barbell bench press. Bench pressing on the Smith machine decreases stability in the biceps brachii (Saterbakken et al, 2011) but there is similar muscle recovery between different bench presses in trained men (Smith, barbell, and dumbbell) (Ferreira et al, 2016). This does not affect my overall critique of Boyce et al (2014) however, since you can move more weight than you would normally be able to, along with the machine being on one plane of motion so everyone has to attempt to get into the same position to do the lift and we know how that is ridiculous due to individual differences in morphology.
Some may point to hand-grip tests, which I have written about in the past, and state that ‘blacks are stronger’ based on hand-grip tests. Just by looking at the raw numbers you’d say that blacks had a stronger grip. However, to get an idea of the strength differences pound-for-pound there is a simple formula: weight lifted/bodyweight=how strong one is pound-for-pound on a certain exercise. So using the values from Araujo et al (2010), for blacks we have a grip strength of 89.826 with an average weight of 193 pounds. Therefore pound-for-pound strength comes out to .456. On the other hand, for Europeans, they had an average grip strength of 88.528 pounds with an average weight of 196 pounds, so their pound-for-pound grip strength is about .452, which, just like African-Americans is almost half of their body weight. One must also keep in mind that these hand-grip studies are done on older populations. I have yet to come across any studies on younger populations that use the big four lifts described in this article and seeing who is stronger, so inferences are all that we have.
Further, Thorpe et al (2016) also show how there is an association between household income and grip-strength—people who live in homes with higher incomes have a stronger grip, with blacks having a stronger grip than whites. Thorpe et al (2016) showed that black women had a stronger grip strength than white women, whereas for black men they only had a stronger grip than white men at the highest SES percentile. This could imply nutrient deficiencies driving down their ability for increases grip strength, which is a viable hypothesis. Although Thorpe et al (2016) showed that black men had a stronger grip strength, these results conflict with Haas, Krueger, and Rohlfson (2012) though the disparities can be explained by the age of both cohorts.
Nevertheless, grip strength—as well as overall strength—is related to a higher life expectancy (Ruiz et al, 2008; Volkalis, Haille, and Meisinger, 2015). If blacks were stronger—and this is being debated with studies like hand-grip—then we should expect to see black men living longer than white men, however, we see the opposite. Black men die earlier than white men, and it just so happens that the diseases that are correlated with strength and mortality are diseases that blacks are more likely to get over whites. One should think about this if they’re entertaining the idea that blacks have an inherent strength advantage over whites.
Others may argue that since chimpanzees have a higher proportion of type II fibers and that’s one reason why they are stronger than us by 1.35 times (O’Neill et al, 2017) and have the ability to rip our faces off. Of course, other factors are at play here other than the chimps’ fast twitch fiber content. Of course, one must also think of the chimpanzee’s way smaller stature when discussing their overall strength. It’s not just their type II fibers, but how much smaller they are which gives them the ability to generate more force pound-for-pound in comparison to humans. So this is a bad example to attempt to show that blacks are stronger than whites based solely on the composition of the muscle fibers.
Finally, back in July I argued that Neanderthals would be stronger than Homo sapiens due to their morphology and a wide waist. This, of course, has implications for strength differences between the races. People with a wider waist would have the ability to generate more power. Blacks have a higher center of gravity due to longer limbs whereas whites and Asians have lower centers of gravity due to a longer torso. Along with climatic conditions, the Neanderthal diet also contributed to their wide waist and thorax, which would then help with strength. Therefore, this has implications for racial differences in strength. We can replace Europeans with Neanderthals and Homo sapiens with Africans and the relationship would still hold. This is yet more proof that blacks are not stronger than whites. This article also contributes to the argument I laid out in my article on how racial differences in muscle fiber typing predict differences in elite sporting competition. Morphology/somatype is the final piece of the puzzle; without the correct morphology, it’d be really hard for someone to become an elite athlete in a certain field if they do not have the correct morphology.
Looking at the big four lifts, the advantage goes to European Americans and East Asians. This is due to their average somatype and morphology. The only lift that Africans would excel at is the deadlift and this is due to their morphology—mainly their long arms. People with longer arms excel at pulling exercises whereas people with shorter arms excel at pushing exercises. Hand-grip strength studies show blacks having a higher grip strength than whites, however in one study if you see who is stronger pound-for-pound, the differences are insignificant. The longitudinal bench press study is highly flawed due to numerous confounds and is therefore unacceptable to assess strength and race. The fact that chimpanzees have a higher proportion of type II fibers compared to humans is also irrelevant. Chimpanzees have a smaller stature and they can, therefore, generate way more power pound-for-pound. Attempting to replace Africans with chimpanzees in this scenario doesn’t make sense because Africans have longer limbs than Europeans and would, therefore, generate less force pound-for-pound. Overall strength is related to mortality; stronger people live longer and have fewer maladies than weaker people. This too lends credence to my argument that whites are stronger than blacks.
American Renaissance published an article the other day titled “Is ‘Racism’ Killing Black People?” and, for the most part, I largely agree with it. However, there are a few faults in it that I need to address.
First, off, as the article rightly noted, it’s not only perceived ‘racism’ that is the cause for these health disparities, but stress from other blacks as well. Gregory Hood (the author of the AmRen article) cites a new study showing that blacks who move out of the ‘hood’ see a subsequent decrease in BP (Kershaw et al, 2017). They followed 2,290 people 974 were men and 1,306 were women. This is data collected from the CARDIA study which has helped us to understand racial disparities in all types of different health outcomes. Blacks who lived in high segregation neighborhoods had higher levels of SBP (systolic blood pressure), and saw a decrease in their SBP when they moved to less segregated neighborhoods. The authors conclude that “policies that reduce segregation may have meaningful health benefits.” What kind of policies will ‘reduce segregation’? Most races/ethnic groups group together in an area, so I don’t see how this would happen.
In regards to the argument on black maternal mortality and ‘racism’, I think it’s much more nuanced. Black women are 2 to 6 times more likely to die giving birth than white women; while the leading causes of maternal death in black women is pregnancy-induced hypertension, and embolism (Chang et al, 2003), though reasons for the mortality rate are not explainable at present (Flanders-Stepans, 2002). Further, in regards to preeclampasia, women who get pregnant at younger ages are more likely to acquire the disease while pregnant, and blacks and other non-whites are more likely to get pregnant at younger ages than whites (Main et al, 2015).
However, there are ways to reduce maternal mortality in black women. In a RCT undertaken between the years of 1990-2011 in Memphis, Tennesee, black women were followed with their live-in children and placed into one of four groups: “treatment 1 (transportation for prenatal care [n = 166]), treatment 2 (transportation plus developmental screening for infants and toddlers [n = 514]), treatment 3 (transportation plus prenatal/postpartum home visiting [n = 230]), and treatment 4 (transportation, screening, and prenatal, postpartum, and infant/toddler home visiting [n = 228])” (Olds et al, 2014). They conclude that pre- and post-natal care greatly reduces maternal/infant mortality in black women, “living in highly disadvantaged settings.”
Further, the racial disparity in post-term neonates is largely driven by “CHD among term infants with US-born mothers is driven predominately by the postneonatal survival disadvantage of African-American infants” (Collins et al, 2017). Though, as can be seen in the study by Olds et al (2014), pre- and post-natal care can greatly reduce both infant and maternal mortality.
Stress can also be measured in pregnant women by measuring the level of blood cortisol (Gillespie et al, 2017). They show that, independent of adulthood stress, stress during childhood may shape birth timing, with cortisol being the biological mediator. This may be an explanation for what Gregory Hood notes. He states in his article that there has to be an explanation for why black women birth earlier, and while I am sympathetic to biological models ala Rushton (1997), Gillespie et al (2017) drive a hard argument that stress during childhood using cortisol as a biological mediator makes a lot of sense.
There are a few studies that attest to pre- and post-natal care having a large effect on the morality of black women, and that having the carers being black women seems to have a positive effect (Guerra-Reyes and Hamilton, 2017). They conclude that “Recognition, support, and increasing the number of African-American midwives and birth assistants is vital in tackling health inequalities.” In regards to infant mortality rate (IMR), 18 states will achieve racial equality by 2050 if current trends from 1999-2013 hold (Joedrecka et al, 2017).
Now for the main reason I decided to write this: the ‘Hispanic’ paradox. This paradox is that for the past twenty years, ‘Hispanics’ with low SES have similar or better health outcomes than whites (Franzini, Ribble, and Keddie, 2001). However, more recent analyses show that the ‘Hispanic’ paradox does not exist, mostly due to methodological problems and migrant selectivity (Crimmins et al, 2007; Teruya and Bazargan-Hezeji, 2013) and was not noticed in Chile either (Cabiesies, Tunstall, and Pickett, 2013). There is no migrant selectivity in regards to smoking, however (Fenelon, 2013, 2016).
Studies which advocate the validity of the Immigrant Paradox are countered by those which report specific, negative physical and mental health outcomes, and higher rates of substance use, especially among immigrant adolescents. Findings may also be compromised by fundamental methodological concerns such as migrant health selectivity, and approaches that consider only selectively healthy groups. Moreover, the Immigrant Paradox’s benefits do not appear to extend evenly and consistently to all races, ethnicities and subgroups. Similarly, the Hispanic Paradox does not protect consistently across all Latino ethnicities, age groups and genders, with Puerto Ricans and Cubans in particular found to enjoy fewer health advantages.
This is good evidence that the people who migrate to America are healthier, and that the symptoms of low SES show in their children, but not in them because they are a self-selected population. There is no ‘Hispanic’ paradox (Smith and Bradshaw, 2006; Schoenthaler, 2016). Even a new meta-analysis on this ‘paradox’ states “Immigrant children and youth suffer from an immigrant mortality disadvantage” (Shor, Roelfs, and Vamg, 2017).
Lastly, Gregory Hood brings up stress and suicide, stating that if blacks were really more stressed than whites then blacks would have higher rates of suicide, but some studies show that whites have a higher rate of suicidal ideation, while others do not show this (Perez-Rodriguez et al, 2010). Though, as Balis and Postolache (2010) show, studies show that while there is conflicting evidence in regards to racial/ethnic differences in suicide, whites still attempt it the most. However, suicide for young black Americans is on the rise. Ahmedani et al (2016) show that “Nearly 27% of White individuals made a mental health visit versus less than 20% of Asian, Hawaiian/Pacific Islander, and Black individuals in this period. Within 4 weeks, all visits and mental health visits remained most common for White individuals (67.3% and 47.4%, respectively) and least common among Asian individuals (52.8% and 31.9%, respectively). Within 52-weeks, more than 90% made any visit. Alaskan Native/Native American (81.5%) and White individuals (79.5%) made mental health visits 10–25% more often than other groups.” However, at least in Fulton County, Georgia, black suicide decedents were less likely to report depression than white suicide decedents (Abe et al, 2008).
However, for whites, as noted in this 1982 New York Times article, suicidal feelings “reflects feelings of loneliness and hopelessness, which can be greater factors as one grows older; for instance, after loved ones have died” whereas for older white men, loss of status may be a cause, which would not be that prevalent in lower SES ethnicities. The article seems to implicate loss of status as a main cause for higher rates of suicide in white Americans, and states that as other, lower SES ethnies attain higher status, that suicide rates would rise for them as well.
Another cause could be prescription drugs, for instance in the Northeast which has been hit hard by the opiate/heroin crisis which leads to more white deaths. Robert Putnam puts this on “the links between poverty, hopelessness and health” and states that the suicide rate has declined for two groups, black males and males over the age of 75. Further, “divorce, economic strain, or political repression are often characterized as suicide risks.” Cheng et al (2010) show that “A high level of identification with one’s ethnic group was associated with lower rates of suicide attempts.” So, it seems that if one keeps their status, and has a high level of identification with their ethnic group, whites would then be protected against suicidal ideation. Nonmetropolitan counties also have higher rates of suicide than metropolitan counties (Ivey-Stephenson et al, 2017). People who livee in rural counties are less likely to seek help for mental problems (Carpenter-Song and Snell-Rood, 2016). Whites are also more likely to live in rural areas. This could explain higher rates of suicide in whites, along with loss of status, depression and drug use.
In conclusion, the ‘Hispanic’ paradox doesn’t exist; whites attempt/commit suicide more due to loss of status and since most whites live in rural areas, they do not seek help for their mental health problems which then leads to suicide. In regards to black maternal mortality/infant mortality rates, if they have midwives present during and after the birth, mortality rates have decreased. If these trends continue, there will be racial equality in terms of maternal/infant mortality in 18 states. The AmRen article was good and well written, but there were a few huge flaws. The author assumed that since the ‘Hispanic paradox’ exists, that this should have one disregard the effects of, say, stress on blood pressure in black Americans, as I have discussed in the past. But since the ‘Hispanic’ paradox does not exist, then you cannot say that (perceived) discrimination and ‘racism’ is not a cause for higher rates of mortality in blacks compared to whites.
I was alerted to an article on the website (Ir)”RationalWiki” which in their own words “critique[s] and challenge[s] pseudoscience and the anti-science movement, explore[s] authoritarianism and fundamentalism, and analyze[s] how these subjects are handled in the media.” Unfortunately, it seems like the one who wrote this article (and is still adding to it) just selectively read certain articles and quote mined them.
The article on this website about me is an unfair mischaracterization of my views. Quotes will follow from the article with my comments.
In the opening paragraph they write:
NotPoliticallyCorrect is an Alt-right blog that promotes racialist pseudoscience and white nationalism; the owner posts as RaceRealist using the euphemism “racial realist” coined by the white supremacist J. P. Rushton who is extensively quoted on the blog.
- I’m not alt-right nor am I a white nationalist.
- I don’t promote ‘racialist pseudoscience’ nor do I promote ‘white nationalism’.
- Correct, Rushton did coin the term ‘race realist’, but he was not a ‘white supremacist’.
They continue, quoting an article of mine that I wrote almost two years ago titled Non-Western People are Abnormal to Our Society. I still stand by everything that I wrote in that article.
A racist crank obsessed with controversial topics such as race and IQ and eugenics, RaceRealist argues in a 2016 blog essay “Non-Western People are Abnormal to Our [Western] Societies” and its comments that “MENA” and “SSA’s” (i.e. people from the Middle-East, North Africa and Sub-Saharan Africa) as well as other non-Westerners are somehow abnormal to the US and Europe:
They then quote me:
MENA and SSA people are abnormal to Western societies. It’s clear that, on average, full-on acclimation is not possible.
One only needs to look at what is occurring in Western European countries to see that, on average, this is true.
In the same essay, RaceRealist goes on to post crude racism, such as “Negros” are biologically inferior:
Quoting me writing:
The same can be said for Negros[sic] in America as well. They are deviant, dysfunctional, they cause distress in our country and finally, they pose a danger to us, our families and societies as a whole. Just like those immigrants we have come into our countries who cannot assimilate because it’s not in their biology.
Except everything I wrote here was logically sound (last sentence notwithstanding). Look at the 4 d’s of abnormal psychology (which is the next quote they provide):
The “4 d’s of abnormality” and how they relate to our culture and the current culture/biology of those non-Western immigrants coming into our country is extremely telling. It’s clear that those people cannot assimilate into our societies because of differing biology and differing locations in which they evolved in. We chose our environments based on our biology. Environment increasingly depends on their genes, rather than being the cause of their exogenous behavior.
The 4 d’s of abnormality are deviance, dysfunction, distress and danger. Everything I wrote and then provided examples for in regards to the 4 d’s of abnormality are sound.
You can read my article Diversity in the Social Context for more evidence for this argument.
They then quote my article The Evolution of Jewish Nepotism writing:
RaceRealist is an anti-Semite who dislikes Ashkenazi Jews, accusing them of “derogating other ethnicities”; when discussing Ashkenazi Jews, he bizarrely maintains their higher average IQ is partly a product of “breeding with beautiful Roman women a few thousand years ago”, for which there exists no evidence.
I admit it is conjecture. Evidence exists for Jewish men migrating to Rome to mate with Roman women (Atzmon et al, 2010). I never stated that I ‘dislike Ashkenazi Jews’. In regards to the derogation, it’s true. Close-knit ethnic groups derogate the out-group (Sampasivam et al, 2016). Further, oxytocin promotes human ethnocentrism, which caused in-group favoritism and out-group derogation (Drew et al, 2010). In-groups derogate out-groups. Read the literature.
And the final thing the page shows is my tweet saying that “I finally made it on (Ir)”RationalWiki””:
to which they wrote:
Just because I have the numbers “88” in my handle doesn’t make me “alt-right” nor does it make me a “white nationalist.” I thought about changing it, then I realized that it’s good to weed out the people who aren’t serious about discussion and just look for things to discredit people that are meaningless to the conversation at hand. It tells you a lot about someone when they bring up irrelevant things. I’m not a white nationalist, nor am I an alt-righter. Just because I write about politics rarely and use them as an example (like in my article The Rise of Ethnocentrism and the Alt-Right: The Rebirth of Selfish Genes which I also disavow now that I realize that ‘selfish genes’ are a metaphor; Noble, 2011; Noble, 2013; Noble et al, 2014).
Take a look at the tags it tagged the article with: “Alt-righters, Pseudoscience, Racists, Internet kooks, Psuedoscience promoters, Alt-right, Internet Hate Sites.” Not an alrighter, I don’t push psuedoscience, I’m not a ‘racist’ (whatever that means). If you don’t like what I write, respond to any article you disagree with and explain why with logical, rational arguments. This piece is garbage and mischaracterizes my views using selective quotations (which, even then, failed to prove their point. No, numbers after a username are not evidence).
All in all, this article is garbage. It says that Rushton is ‘extensively quoted’, which is true for what I wrote in the beginning of this blog’s history, but not so for the past, say, 18 months. Rushton has been the target of my attacks on penis size, testosterone, and my personal favorite, r/K selection theory. But sure, go and dig in the archives for old articles to quote mine. This article written about me is dumb, doesn’t characterize my views correctly (calls me a ‘white nationalist’ and ‘alt-righter’). Selectively quote certain articles, assert that Rushton is ‘extensively quoted’ when I hardly discuss him anymore and when I do it’s about testosterone/to rebut him. (Ir)RationalWiki should think about reading a bit of my blog before characterizing me as something I’m not.
For the record, I don’t care about politics. I am not alt-right. I am not a white nationalist. I’m not an anti-semite. This will be updated to cover whatever else they decide to write about me. Hopefully it’s at least a bit closer to reality next time, because this article sucks.