Blacks vs whites: which race is stronger? Unfortunately, actual studies on actual strength lifts between races are few and far between (and if there are any comparisons between races it’s on an ancillary movement such as quadricep extension; for example see Goodpaster et al 2006). There is, though, one study comparing whites and blacks on a major lift: the bench press. The paper is littered with many problems, most of which make me not able to take the paper seriously. I’ve written about this paper in the past but this article will be much more comprehensive.
When searching for racial comparisons in physical strength, Boyce et al (2014) is one of the only papers one would come across looking at racial differences in strength in one specific (main) lift. The authors used a longitudinal design: they had the police officers’ bench press numbers during their first week on the force and then had data 12.5 years later to assess racial and gender differences in the bench press. They assessed strength scores on the bench press, bench press/lean mass, as well as bench press/body mass.
The assessed 327 police officers: 30 women (13 black, 17 white) and 297 males (41 black and 238 white). Officers that could not be classified as either white or black were removed from the sample. Average number of years between the test at recruitment and later into their career was 12.5 years +/- 2 years while the mean age at the initial recruitment was 26.4 years +/- 3.4 years. The officers were mostly college-educated and were low-middle to upper-middle class.
When the recruits were considered for the job, they had their body mass, percent body fat (with skinfold calipers, which will be covered below) and did a 1RM (one-rep max) on the bench press to assess physical strength. The physical fitness battery (for incoming officers) was as follows (in order): body fat, sit-and-reach flexibility (to see how flexible one is in their lower body/hamstrings), 1RM bench press, and finally a 1.5-mile run. For in-service officers, they had their body fat tested, a treadmill test, bench press, muscular endurance (either curls or sit-ups; curls are a contraindicative exercise if used with a straight bar while sit-ups are contraindicative since they put unneeded strain on the lower back).
All groups, when combined after 12.5 years, had significant mean gains in strength which were accompanied by gains in body mass, percent fat mass, and lean mass. Black men, at initial recruitment, weighed 187 pounds and benched 210 pounds; white men weighed 180 pounds and benched 185 pounds. Black men benched 1.12 times their body weight whereas white men benched 1.027 times their body weight. At the follow-up assessment, black males weighed 223 pounds and benched 240 pounds. White males weighed 205 pounds and benched 215 pounds. Black males benched 1.07 times their body weight whereas white males benched 1.05 times their body weight. (To find out what percentage of body weight one lifts, take weight lifted and divide it by the weight of the individual.)
Black women, on the other hand at initial recruitment, weighed 130 pounds and benched 85 pounds whereas white women weighed 127 pounds and benched 82 pounds. Black women benched .653 times their body weight whereas white women benched .645 times their body weight. At the follow-up assessment, black women weighed 151 pounds and benched 98 pounds whereas white women weighed 141 pounds and benched 90 pounds. Black women benched .649 times their body weight at the follow-up whereas white women benched .638 times their body weight.
So there was no real difference between black and white female recruits/officers but there was a difference between black and white male recruits/officers. Of course, due to higher levels of testosterone and other hormones compared to women, the males had a changed much more significantly from the initial recruitment. Figures 1 and 2 from Boyce et al (2014: 146) are important too:
Since the study was done over 12.5 years and the individuals were in their mid-20s at initial recruitment, then this study is anomalous since the individuals gained strength and lean mass well into their 30s. Testosterone begins to decrease starting at age 25, though it is not a foregone conclusion that this occurs; age-related declines in testosterone are not inevitable. It just seems that this is the case since, around one’s mid-20s, life changes happen (marriage, kids) which then may cause lifestyle changes (weight gain and the onset of depression). Most of the testosterone decline can be explained by smoking, obesity, depression and other health factors (Shi et al, 2013). So if these officers had good nutrition—and I do not see why they did not—then they can, in effect, bypass most of the so-called age-related declines in testosterone (which is also related to marriage, having children and obesity; Gray, 2011; Pollet, Cobey, and van der Meij, 2013; Mazur et al, 2013).
Gains in lean mass are related to gains in strength, and so, since there was considerable body mass gain and, consequently, lean mass gain, then overall bench pressing strength should have pretty much substantially increased. The strength gains, though, were negated when they divided the weight lifted by the weight of the lifters (pound-for-pound strength, which is what matters more). Black males had the greatest body mass gain over the 12.5 year period, which subsequently corresponded to a decrease in strength on the bench press.
Over the 12.5 year period, black males gained 36 pounds whereas white males gained 25 pounds. Although black males gained more weight over the 12.5 year period—and loss on bench press/body mass—blacks were still very slightly stronger than whites (1.07 compared to 1.05) which is not significant. Black and white females, on the other hand, had no real differences in any of the scores that Boyce et al (2014) did. Furthermore, black and white women, in this study, had similar strength gains and body mass/lean mass gains. Of course, this is a self-selected sample: black women are consistently noted to carry more fat mass than white women (see Rahman et al, 2009).
Both black and white males increased in the bench press throughout the 12.5 year period compared to black and white females, which is due to them being men (higher levels of testosterone and other hormones, larger muscle cross-section area; Miller et al, 1993). The groups who were stronger when they were hired remained the strongest at the follow-up. So, Boyce et al (2014) conclude, the bench press is able to be used as an assessor of upper-body strength since blacks actually, according to their study, are stronger than whites so, therefore, “an upper body strength test such as a bench press will have little adverse impact on blacks, a racially protected group” (Boyce et al, 2014: 148). Though, for women, since they are not as physically strong as men, this will have an “adverse impact on female recruit and incumbent officers, a gender protected group, no matter if they are black or white” (Boyce et al, 2014: 148).
Now time for a few pitfalls (one of which is not the fault of the investigators): height was not assessed; skin-fold calipers were used to assess body fat; and a Smith machine bench press was used.
Height: Due to an ongoing investigation on the Charlotte Mecklenburg Police Department (for apparently discriminating against certain recruits on the basis of height), the height of the officers at recruitment and the follow-up were not noted. This is a problem. If height were known (along with a few more anthropometric variables), then we can infer who had the somatotype that is conducive to bench pressing. In lieu of no height data, we cannot infer this. It is easier for people with shorter limbs to bench press, since the bar has a shorter path to travel, compared to people with longer arms who have to move the weight a further distance. Blacks are more likely to have longer arms and, as I have argued, this would impede them in strength when bench pressing and overhead pressing but will help in the deadlift since they have longer arms and a shorter torso, it is easier for people with this soma to deadlift due to their body proportions.
Skin-fold calipers: Body fat was assessed using skin-fold calipers. Blacks have thinner skin folds than whites, and so since they have thinner skin folds than whites, and the formula for assessing body fat from skin-folds is based on whites, then, it has been argued, that black males need their own BMI scale since they have thinner skin folds and differing levels of fat-free body mass (Vickery, Cureton, and Collins, 1988; Wagner and Heyward, 2000). So since the levels of body fat were off for blacks, then Boyce et al’s (2014) bench press/lean mass is useless since body fat was not assessed correctly. (I know that using calipers is cheaper and easier than sending everyone for a DXA scan, but the difference in body composition between blacks and whites should be known so that, at least when it comes to fat comparisons between different races, bad methods don’t get used and parroted.) Since there are well-known differences in skinfolds as they relate to body fat percentage/lean mass regarding blacks and whites, it’s, again, safe to toss out that part of the study (regarding weight moved/lean mass), since there are huge flaws in regard to assessing body fat through use of conventional measures in blacks compared to whites.
Smith machine bench press: This is, perhaps, one of the most important pitfalls. I can think of a few reasons why this machine was used: (1) you don’t really need to teach someone how to get into proper position to grab the bar. (2) the bar is on a set path, and so people with different anthropometric measures may be uncomfortable while using the machine (which would then affect overall strength). (3) Saeterbakken, Tillaar, and Fimland (2011) assessed three different chest press exercises: the Smith machine bench press, the barbell bench press, and the dumbbell bench press. Those in the study had the highest 1RM on the bench press, followed by the Smith machine and finally were the weakest on dumbbell bench press. The biceps brachii is used for stabilization, and they found that EMG activity in the biceps brachii increased with stability requirements (dumbbell > barbell > Smith). This is due to the fact that, on the two exercises that are not assisted, the muscles need to stabilize the free weight. Since you’re using more muscles to stabilize the weight, then, theoretically, you can move more weight. EMG activity was the same regarding the pectoralis major and anterior deltoids but was different in the triceps and biceps brachii. The prime movers (agonists) of the bench press are the anterior deltoids, triceps, and pecs/serratus. Therefore, the antagonists are the posterior deltoids, the biceps, and the lats/rhomboids.
The load lifted on the bench press was three percent higher than on the Smith machine. Since stability requirements are low with the Smith, and the bar is on a set path that cannot be changed, then, theoretically, one should be able to move more weight on the Smith machine (which is my personal experience and the experience of many people I have worked with) compared to the dumbbell and regular bench press. Though, the load lifted on the bench press was about three percent higher than on the Smith machine bench press. The activity of the pectoralis and the anterior deltoid was lower on the eccentric phase (think the negative portion of the lift) when compared to dumbbell and barbell pressing, which is, again, explained by lack of stabilizing muscles used on the Smith machine bench press. So this small study (n=12) shows that there are differences in 1RM between the three lifts studied and that there are differences in the neuromuscular activity of the flexor/extensor muscles of the arm, but showing no difference in the prime movers of the lift (such as the pectoralis major). In the descending phase of the lift, there was less EMG activation, which indicates that a greater neural drive is needed for the eccentric phase of the lift.
The Smith machine used in Boyce et al (2014) was an Atlantis Angled Smith Machine E-155, which I have used personally (and have had hundreds of people use). In my personal experience, weight moved on the Smith is considerably different when compared to a regular bench press, due to the fact that one does not have to stabilize the bar with certain muscles. I will keep an eye out for more Smith machine/bench press/dumbbell press studies in the future, but, from personal experience, one is able to lift more on a Smith than a regular bench.
This is one of the only studies of its kind: assessing racial differences in strength on a major lift. Boyce et al (2014) found that, although blacks had a sharper decrease in pound-for-pound strength, they still kept their slight strength advantage over the 12.5 year period. Both black and white women had similar strength levels and gains in strength and lean mass over the 12.5 year period. Lean mass gain over the period was related to strength gains on the bench; but, as pointed out, they did not correctly assess lean mass for blacks, since calipers (used to test skin folds) are not useful for blacks in the case of figuring out lean mass/body fat levels (Vickery et al, 1988; Wagner and Heyward, 2000).
This study is useless to me. Blacks are not stronger than whites; anthropometric variables play a huge role in strength differences and, due to these differences, blacks are not stronger than whites on certain lifts, as I have documented.
Racial differences in body fat are clear to the naked eye: black women are more likely to carry more body fat than white women; Mexican American women are more likely to carry more body fat than white women, too. Different races/ethnies/genders of these races/ethnies have different formulas to assess body fat through the use of skin-folds. The sites to grasp the skin is different based on gender and race.
Body mass index (BMI) and waist circumference is overestimated in blacks, which means that they need different formulas to assess their BMI and adiposity/lean mass. Race-specific formulas/methods are needed to assess body fat and, along with it, disease risk, since blacks are more likely to be obese (black women, at least, it’s different with black American men with more African ancestry, see below). The fact of the matter is, when matched on a slew of variables, blacks had lower total and abdominal fat mass than whites.
This is even noted in Asian, black and white prepubertal children. He et al (2002) show that sex differences in body fat distribution are present in children who have yet to reach puberty and the differences in body fat in Asians is different than that from blacks and whites which also varies by sex. Asian girls had greater gynoid fat by DXA scan only, with girls having greater gynoid fat than boys. Asian girls had lower adjusted extremity fat and gynoid fat compared to white and black girls. Though, Asian boys had a lower adjusted extremity by fat as shown by DXA (a gold standard in body fat measurement) when compared to whites, but greater gynoid fat than whites and blacks.
Vickery, Cureton, and Collins, (1988), Wagner and Heyward (2000), and Robson, Bazin, and Soderstrom (1971) show that there are considerable body composition differences between blacks and whites. These differences in body composition come down to diet, of course, but there is also a genetic/physiologic component there as well. Combining the known fact that skin-fold testing is not conducive to a good estimate, black American men with more African ancestry are less likely to be obese.
Vickery, Cureton, and Collins (1988) argue that, if accurate estimates of body fat percentages are to be obtained, race-specific formulas need to be developed and used as independent variables to assess racial differences in body fat percentage. Differences in muscularity don’t seem to account for these skinfold differences, nor does greater mesomorphy. One possible explanation for differences in skinfold thickness is that blacks may store most of their body fat subcutaneously. (See Wagner and Heyward, 2000 for a review on fat patterning and body composition in blacks and whites.)
The often-used Durnin-Womersley formula which is used to predict body fat just from skin folds. However, “The 1974 DW equations did not predict %BF(DXA) uniformly in all races or ethnicities” (Davidson et al, 2011). Truesdale et al (2016) even show that numerous formulas used to estimate percent body fat are flawed, even some formulas used on different races. Most of the equations tested showed starkly different conclusions. But, this is based on NHANES data and the only data they provide regarding skin-folds is the tricep and subscapular skinfold so there may still be more problems with all of the equations used to assess body fat percentage between races. (Also see Cooper, 2010.)
Klimentidis et al (2016) show that black men—but not black women—seem to be protected against obesity and central adiposity (fat gain around the midsection) and that race negatively correlated with adiposity. The combo of male gender and West African ancestry predicted low levels of adiposity compared to black Americans with less African ancestry. Furthermore, since black men and women have—theoretically—the same SES, then cultural/social factors would not play as large a role as genetic factors in explaining the differences in adiposity between black men and black women. Black men with more African ancestry had a lower WHR and less central adiposity than black men with less African ancestry. If we assume that they had similar levels of SES and lived in similar neighborhoods, there is only one reason why this would be the case.
Klimentidis et al (2016) write:
One interpretation is that AAs are exposed to environmental and/or cultural factors that predispose them to greater obesity than EAs. Possibly, some of the genes that are inherited as part of their West-African ancestry are protective against obesity, thereby “canceling out” the obesifying effects of environment/culture, but only in men. Another interpretation is that genetic protection is afforded to all individuals of African descent, but this protection is overwhelmed by cultural and/or other factors in women.
Black men do, as is popularly believed, prefer bigger women over smaller women. For example, Freedman et al (2004) showed that black American men were more likely to prefer bigger women. Black American men “are more willing to idealize a woman
of a heavier body size, with more curves, than do their White American counterparts” (Freedman et al, 2004: 197). It is then hypothesized that black American men find these figures attractive (figures with “more curves” (Freedman et al, 2004: 197)) to protect against eating pathologies, such as anorexia and bulimia. So, it has been established that black men have thinner skin folds than whites which leads to skewed lean mass/body fat readings and black men with more African ancestry are less likely to be obese. These average differences between races, of course, contribute to differing disease acquisition.
I have covered differences in body fat in a few Asian ethnies and have come to the obvious conclusion: Asians, at the same height, weight etc as whites and blacks, will have more adipose tissue on their bodies. They, too, like blacks and whites, have different areas that need to be assessed for skin folds to estimate body fat.
Henriques (2016: 29) has a table on the equations for calculating estimated body density from skin fold measures from various populations. Of interest are the ones on blacks or ‘Hispanics‘, blacks or athletes and blacks and whites. (The table is provided from NSCA, 2008 so the references are not in the back of the text.)
For black and ‘Hispanic’ women aged 18-55 years, the sites to use for skin-folds are the chest, abdomen, triceps, subscapular, suprailiac, midaxillary, and the thigh. For blacks or athletes aged 18-61 years, the sites to use are the same as before (but a different equation is used for body fat estimation). For white women or anorexic women aged 18-55, the sites used are just triceps, suprailiac and the thigh. For black and white boys aged 6-17, only the triceps and the calf is used. It is the same for black and white girls, but, again, a different formula is used to assess body fat (Henriques, 2016: 29).
Morrison et al (2012) showed that white girls had a higher percent body fat when compared to black girls at ages 9-12 but every age after, black girls had higher percent body fat (which is related to earlier menarche in black girls since they have higher levels of body fat which means earlier puberty; Kaplowitz, 2008). Black girls, though, had higher levels of fat in their subscapular skin folds than white girls at all ages.
So, it seems, there are population-/race-specific formulas that need to be created to better assess body fat percentage in different races/ethnies and not assume that one formula/way of assessing body fat should be used for all racial/ethnic groups. According to the literature (some reviewed here and in Wagner and Heyward, 2000), these types of formulas are sorely needed to better assess health markers in certain populations. These differences in body fat percentage and distribution then have real health consequences for the races/ethnies in question.
FOXP2 is a so-called “gene for” language. The gene is a transcription factor—meaning that it controls the activity of other genes. Thus, changes to FOXP2 will have changes to other genes as well. Thus, the evolution of language in humans was thought to have hinged on mutations on the FOXP2 gene. Humans that have a single-point mutation in FOXP2 “have impaired speech and grammer, but not impaired language comprehension” (Mason, et al, 2018: 403). This gene is found in numerous mammals (e.g., chimpanzees, gorillas, orangutans, rhesus macaques, and mice) but none of those mammals speak. This gene, then, is expressed in the areas of the brain that affects motor functioning, which includes the coordination needed to create words.
Mice and humans at the FOXP2 gene only differ by 3 amino acids. Only one amino acid difference exists between gorillas, chimps, mice, and macaques, who all have identical amino acid sequences on FOXP2. Furthermore, two more amino acid sequences differ between humans and the sequences which is shared by chimpanzees, gorillas, and macaques. Thus, the difference of two amino acids between humans and other primates appears to have made it possible for language to evolve. Evidence exists for strong selective pressures for the two FOXP2 mutations which allow the brain, larynx, and mouth to coordinate to produce speech. These two altered amino acids may change the ability of FOXP2 transcription factor to be phosphorylated—proteins are either activated by phosphorylation or deactivated by dephosphorylation, or the reverse.
Mason et al (2018: 403) write:
Comparative genomics efforts are now extending beyond primates. A role for FOXP2 in songbird singing and vocal learning has been proposed. Mice communicate via squeaks, with lost young mice emitting high-pitched squeaks, FOXP2 mutations leave mice squeakless. For mice and songbirds, it is a stretch to claim that FOXP2 is a language gene—but it is likely needed in the neuromuscular pathway to make sounds.
Above is Figure 18.17 from Mason et al (2018: 403). They write:
Comparisons of synonymous and nonsynonymous changes in mouse and primate FOXP2 genes indicate that changing two amino acids in the gene corresponds to the emergence of human language. Black bars represent synonymous changes; gray bars represent nonsynymous changes.
But is that the whole story? Is FOXP2 really a “gene for” language? New results call this hypothesis into question.
In their paper No Evidence for Recent Selection at FOXP2 among Diverse Human Populations, Atkinson et al (2018) did not find evidence for recent positive or balancing selection. Atksinson et al (2018) conclude that they:
do not find evidence that the FOXP2 locus or any previously implicated site within FOXP2 is associated with recent positive selection in humans. Specifically, we demonstrate that there is no evidence that the original two amino-acid substitutions were targeted by a recent sweep limited to modern humans <200 kya as suggested by Enard et al. (2002) … Any modified function of the ROI does not appear to be related to language, however, as modern southern African populations tolerate high minor allele frequencies with no apparent consequences to language faculty. We do not dispute the extensive functional evidence supporting FOXP2’s important role in the neurological processes related to language production (Lai et al., 2001, MacDermot et al., 2005, Torres-Ruiz et al., 2016). However, we show that recent natural selection in the ancestral Homo sapiens population cannot be attributed to the FOXP2 locus and thus Homo sapiens’ development of spoken language.
So the two mutations in exon 7 of FOXP2 weren’t selected and are not responsible for human language. Most likely the accelerated rate is due to loss of function (LoF) (null allele).
The gene was originally discovered in a family that had a history of speech and language disorders (Lai et al, 2001). This “speech gene” was also found in Neanderthals in 2007 (see Krasue et al, 2007). Thus, the modifications to FOXP2 occurred before humans and Neanderthals diverged.
So Atkinson et al (2018) found that the so-called sweep on FOXP2 >200KYA was a statistical artifact which was caused by lumping Africans together Caucasians and other populations. Of course, language is complicated and no one single gene will explain the emergence of human language.
This is a just-so story—that is, an ad hoc hypothesis. Humans had X, others didn’t have X or had a different form of X; therefore X explains human language faculties.
Atkinson et al’s (2018) “results represent a substantial revision to the adaptive history of FOXP2, a gene regarded as vital to human evolution.”
High evolutionary constraint among taxa but variability within Homo sapiens is compatible with a modified functional role for this locus in humans, such as a recent loss of function.
Therefore, this SNP must not be necessary for language function as both alleles persist at high frequency in modern human populations. Though perhaps obvious, it is important to note that there is no evidence of differences in language ability across human populations. (Atkinson et al, 2018)
This is another just-so story (Gould and Lewontin, 1976; Lloyd, 1999; Richardson, 2007; Nielsen, 2009) that seems to have bitten the dust. Of course, the functionality of FOXP2 and its role in the neurologic processes related to language; what is disputed (and refuted) is the selectionist just-so story. Selectionist explanations are necessarily ad-hoc. Thus, recent natural selection in our species cannot be attributed to FOXP2, and along with it, our language capabilities.
There is a similar objection, not for FOXP2 and selectionist hypotheses, but for the Lactase gene. Nielsen (2009) puts it succinctly:
The difference in lactose intolerance among human geographic groups, is caused by a difference in allele frequencies in and around the lactase gene (Harvey et al. 1998; Hollox et al. 2001; Enattah et al. 2002; Poulter et al. 2003). … This argument is not erected to dispute the adaptive story regarding the lactase gene, the total evidence in favor of adaptation and selection related to lactose tolerance is overwhelming in this case, but rather to argue that the combination of a functional effect and selection does not demonstrate that selection acted on the specific trait in question. … Although the presence of selection acting on genes underlying a phenotypic trait of interest does help support adaptive stories, it does not establish that selection acted directly on the specific trait of interest.
Even if there were evidence of positive selection of FOXP2 in humans, we cannot logically state that selection acted on the FOXP2 locus; functional effects and selection do not demonstrate that “selection” acted on that trait. Just-so stories (ad hoc hypotheses) “sound good”, but that’s only because they are necessarily true—one can have all the data they want, then they can think up any adaptive story to explain the data and the story will be necessarily true. Therefore, selectionist hypotheses are inherently ad hoc.
In conclusion, another selectionist hypothesis bites the dust. Nevermind the fact that, if FOXP2 were supposedly “selected-for”, there would still be the problem of free-riders (Fodor and Piattelli-Palmarini, 2010). That is, “selection” cannot “select-for” fitness-enhancing traits if/when they are coextensive with other traits—there is no way for selection to distinguish between coextensive traits and thus, it does not explain trait fixation (in this case, the fixation of FOXP2). Ad-hoc hypotheses are necessarily true—that is, they explain the data they purport to explain and only the data they purport to explain. These new results show that there is no support for positive selection at the FOXP2 locus.
Darwin proposed, back in 1859, that species arose due to natural selection—the pruning of deleterious genetic variations in a population, which led to the thinking that the “inherent design” in nature, formerly thought to be due to a designer (“God”) was due to a force Darwin called “natural selection” (NS). The line of reasoning is thus: (1) two individuals of the same population are mostly the same genetically/phenotypically, but have small differences between them, and one of the small differences is a difference in a trait needed for survival. (2) But both traits can contribute to fitness, how does NS ‘know’ to select for either coextensive trait? Now think about two traits: trait T and trait T’. What would explain the fixation of either trait in the population we are discussing? NS is not—cannot—be the mechanism of evolution.
In 2010, philosopher Jerry Fodor and cognitive scientist Massimo Piattelli-Palmarini, wrote a book titled “What Darwin Got Wrong“, which argued that NS is not a causal mechanism in regard to the formation of new species. Their argument is (pg 114):
- Selection-for is a causal process.
- Actual causal relations aren’t sensitive to counterfactual states of affairs: if it wasn’t the case that A, then the fact that it’s being A would have caused its being B doesn’t explain its being the case that B.
- But the distinction between traits that are selected-for and their free-riders turns on the truth (or falsity) of relevant counterfactuals.
- So if T and T’ are coextensive, selection cannot distinguish the case in which T free-rides on T’ from the case that T’ free-rides on T.
- So the claim that selection is the mechanism of evolution cannot be true.
This argument is incredibly strong. If it is true, then NS cannot be the mechanism by which evolution occurs; NS is not—nor can it be—the mechanism of evolution. So, regarding the case of two traits that are coextensive with each other, it’s not possible to ascertain which trait was selected-for and which trait was the free-rider. NS cannot distinguish between two locally coextensive traits, so, therefore, it is not an explanatory mechanism and does not explain the evolution of species, contra Darwin. It cannot be the mechanism that connects phenotypic variation with fitness variation.
The general adaptationist argument is: “(1) the claim that evolution is a process in which creatures with adaptive traits are selected and (2) the claim that evolution is a process in which creatures are selected for their adaptive traits” (Fodor and Piattelli-Palmarini, 2010: 13). Darwinists are committed to inferring (2) from (1), though it is fallacious. It is known as the intensional fallacy.
“Due to the intensionality of “select-for” and “trait”, one cannot infer from ‘Xs have trait t and Xs were selected’ to ‘Xs were selected for having trait t’” (Fodor and Piattelli-Palmarini, 2010: 139). How does one distinguish from a trait that was selected-for and a free-rider that hitched a ride on the truly adaptive trait for the organism in question? The argument provided above shows that it is not possible. “Darwinists have a crux about free-riding because they haven’t noticed the intensionality of selection-for and the like; and when it is brought to their attention, they haven’t the slightest idea what to do about it” (Fodor and Piattelli-Palmarini, 2010: 16).
No observation can show whether or not trait T or T’ was selected-for in virtue of its contribution to fitness in a given population; favoring one story over another in regard to the adaptation of a trait in question, therefore, does not make any logical sense due to the problem of free-riders (and, also, favoring one story over another is due to bias for the like of the specific adaptive just-so story in question). For if two traits are coextensive—meaning that traits coincide with one another—then how can NS—which does not have a mind—‘know’ to “select-for” whichever trait contributes to fitness in the population in question? Breeders are the perfect example.
Breeders have minds and can therefore select for certain traits and against undesirable traits; however, of course, since NS does not have a mind, this is not the case when it comes to naturally selected traits (so-called), since NS does not have a mind. NS cannot explain the distribution of phenotypic traits throughout the world; there is no agent of NS nor are there ‘laws of selection’, therefore NS is not an explanatory mechanism. Explanations based on NS are based only on correlations with traits and fitness, not on causes themselves (this critique can be extended to numerous other fields, too). The problem with relying only on correlations between traits and fitness is two-fold: (1) the trait in question can be irrelevant to fitness and (2) the trait in question can be a free-rider.
Creatures have traits that increase fitness because they were selected-for, the story goes. NS explains why the creature in question has trait T, which increases fitness in environment E. One can then also make the claim that the selection of the trait in question was due to the increased fitness it gave the creature. However, if this claim is made, “then the theory of natural selection would reduce to a trait’s being a cause of reproductive success [which then] explains its being a cause of reproductive success which explains nothing (and isn’t true).”
So since genetically-linked traits are coextensive with an infinitude of different possible outcomes, then the hypothesis that trait X is an adaptation is underdetermined by all possible observations, which means that NS cannot explain how and why organisms have the traits they do, since NS cannot distinguish between two coextensive traits, since NS lacks a mind and agency.
NS can be said to be an explanation if and only if two conditions are met: (1) if NS can be understood as acting on counterfactuals and (2) if NS can be said to be acting on any physical evolutionary laws.
(1) A counterfactual is an “if-clause”, which is contrary to a fact. A counterfactual is a statement that cannot be true, for example, “I hear but I have no ears” or “I see but I have no eyes.” Thus, if it were possible for NS to be an explanation for the continuance of a specific trait that is linked to other traits (that is, they are coextensive) in a given population, it would need to—necessarily—invoke a counterfactual about NS. It would need to be the case that the trait in question would still be selected for in the absence of free-riders. As an example from Fodor and Piattelli-Palmarini (2010: 103) a heart pumps blood (what it was selected-for) and makes pumping sounds (its linked free-rider). Thus, if the pumping of blood and the sound that blood-pumping makes were not coextensive, then the pumping, not the pumping sounds, get selected for.
There is a huge problem, though. Counterfactuals are intentional statements; they refer to concepts found in our minds, not any physical things. NS does not have a mind and thus lacks the ability to “select-for” since “selecting-for” is intentional. Therefore NS does not act on counterfactuals; it is blind to the fact of counterfactuals since it does not have a mind.
(2) It does not seem likely that there are “laws of selection”. Clearly, the adaptive value of any phenotype depends on the environment that the organism is in. Fodor and Piattelli-Palmarini (2010: 149) write (emphasis theirs):
The problem is that it’s unlikely that there are laws of selection. Suppose that P1 and P2 are coextensive but that, whereas the former is a property that affects fitness, the latter is merely a correlate of a property that does. The suggestion is that all this comes out right if the relation between P1 and fitness is lawful, and the relation between P2 and fitness is not. …it’s just not plausible that there are laws that relate phenotypic traits per se to fitness. What (if any) effect a trait has on fitness depends on what kind of phenotype is embedded in, and what ecology the creature that has the trait inhabits. This is to say that, if you wish to explain the effects that a phenotypic trait has on a creature’s fitness, what you need is not its history of selection but its natural history. And natural history offers not laws of selection but narrative accounts of causal chains that lead to the fixation of phenotypic traits. Although laws support counterfactuals, natural histories do not; and, as we’ve repeatedly remarked, it’s counterfactual support on which distinguishing the arches from the spandrels depends.
There is, too, a simple example regarding coextensive traits and selection. Think of the lactase gene. It is well-known that we humans are adapted to drink milk—and the cause is gene-culture coevolution that occurred at around the time of cow domestication (Beja-Perreira et al, 2003; Gerbalt et al, 2011). No one disputes the fact that gene-culture coevolution is how and why we can drink milk. But what people do dispute is the adaptive just-so story (Gould and Lewontin, 1976; Lloyd, 1999; Richardson, 2007) that was made to explain how and why the trait went to fixation in certain human populations. Nielsen (2009) writes (emphasis mine):
The difference in lactose intolerance among human geographic groups, is caused by a difference in allele frequencies in and around the lactase gene (Harvey et al. 1998; Hollox et al. 2001; Enattah et al. 2002; Poulter et al. 2003). The cause for the difference in allele frequencies is primarily natural selection emerging about the same time as dairy farming evolved culturally (Bersaglieri et al. 2004). Together, these observations lead to a compelling adaptive story of natural selection favoring alleles causing lactose tolerance. But even in this case we have not directly shown that the cause for the selection is differential survival due to an ability/inability to digest lactose. We must acknowledge that there could have been other factors, unknown to us, causing the selection acting on the region around the Lactase gene. Even if we can argue that selection acted on a specific mutation, and functionally that this mutation has a certain effect on the ability to digest lactose, we cannot, strictly speaking, exclude the possibility that selection acted on some other pleiotropic effect of the mutation. This argument is not erected to dispute the adaptive story regarding the lactase gene, the total evidence in favor of adaptation and selection related to lactose tolerance is overwhelming in this case, but rather to argue that the combination of a functional effect and selection does not demonstrate that selection acted on the specific trait in question.
Selection could have acted on a free-rider that is coextensive with the lactase gene, and just because “the story fits the data” well (that’s a necessary truth; of course the story can fit the data because any story can be formulated for any data) does not mean that it is true, that the reason for trait T is reason R since they “fit the data so well.”
Of course, this holds for EP, evolutionary anthropology, and my favorite theory for the evolution of human skin color, the vitamin D hypothesis. I do not, of course, deny that light skin is needed in order to synthesize vitamin D in climates with low UVB; that is a truism. What is denied is the fact that selection acted on light skin (and its associated/causal genes); what is denied is the combination of functional effect and selection. Just-so stories are necessarily true; they, of course, fit any data because one can formulate any story to fit any data points they have. Thus, Darwinists are just storytellers who have a bunch of data; there is no way to distinguish between the selection of a trait because it increased fitness and the selection of a free-rider that is “just there” that does not increase fitness, but the thing that increases fitness is what the free-rider “rode in on.”
NS is not and cannot be an explanatory mechanism. Darwinism has already been falsified (Jablonka and Lamb, 2005; Noble, 2011; Noble, 2012; Noble, 2017) and so, this is yet another nail-in-the-coffin for Darwinism. The fact that traits that are coextensive means that NS would have to “know” which trait to act on; NS cannot “know” which of the coextensive traits to act on (because it has no mind) and, NS cannot be a general mechanism that connects phenotypic variation to variation in fitness. NS does not explain the evolution of species, nor can NS distinguish between two locally coextensive traits—traits T and T’—because NS has no agency and does not have a mind. Therefore NS is not an explanatory mechanism. Just invoking NS to explain the continuance of any trait fails to explain the survival of the trait because NS cannot distinguish between traits that enhance an organism’s fitness and free-riders which are irrelevant to survival but are coextensive with the selected-for trait, as long as the traits in question are coextensive.
P1) If there is selection for T but not T’, various counterfactuals must be true.
P2) If the counterfactuals are true, then NS must be an intentional-agent, or there must be laws about “selection-for”.
P3) NS is mindless.
P4) There are no laws for “selection-for”.
∴ It is false that selection for T but not T’ occurs in a population.
One then has two choices:
(1) Argue that NS has a mind and therefore that it can “select for” certain traits that are adaptable in a given population of organisms in the environment in question. “Select-for” implies intention. Intentional acts only occur in organisms with minds. Intentional states are only possible if something has a mind. Humans are the only organisms with minds. Humans are the only organisms that can act intentionally. NS does not have a mind. (Animal breeder’s are an example that can select-for desirable traits and against undesirable traits because animals breeder’s are humans and humans can act intentionally.) Therefore NS does not act intentionally since it does not have a mind. I don’t think anyone would argue that NS has a mind and acts intentionally as an agent, therefore P3 is true.
(2) Argue that there are laws for “selection-for” phenotypic traits related to fitness. But it’s not possible that there are laws that relate to the selection of a phenotype, per se, in a given population. The effect of a trait depends on the ecology of the organism in question as well as its natural history. Therefore, to understand the effects of a phenotypic trait on the fitness of an organism we must understand its natural history, not its selection history (so-called). Therefore P4 is true.
There are no laws for “selection-for”, nor does NS have a mind that can select a trait that lends to an organism’s fitness and not a trait that’s just correlated with the trait in question
Leading behavior geneticist Robert Plomin is publishing “Blueprint: How DNA Makes Us Who We Are” in October of 2018. I, of course, have not read the book yet. But if the main thesis of the book is that DNA is a “code”, “recipe”, or “blueprint”, then that is already wrong. This is because presuming that DNA is any of the three aforementioned things marries one to certain ideas, even if they themselves do not explicitly state them. Nevertheless, Robert Plomin is what one would term a “hereditarian”, meaning that he believes that genes—more than environment—shape an individual’s psychological and other traits. (That’s a false dichotomy, though.) In the preview for the book at MIT Press, they write:
In Blueprint, behavioral geneticist Robert Plomin describes how the DNA revolution has made DNA personal by giving us the power to predict our psychological strengths and weaknesses from birth. A century of genetic research shows that DNA differences inherited from our parents are the consistent life-long sources of our psychological individuality—the blueprint that makes us who we are. This, says Plomin, is a game-changer. It calls for a radical rethinking of what makes us who were are.
Genetics accounts for fifty percent of psychological differences—not just mental health and school achievement, but all psychological traits, from personality to intellectual abilities. Nature defeats nurture by a landslide.
Plomin explores the implications of this, drawing some provocative conclusions—among them that parenting styles don’t really affect children’s outcomes once genetics is taken into effect. Neither tiger mothers nor attachment parenting affects children’s ability to get into Harvard. After describing why DNA matters, Plomin explains what DNA does, offering readers a unique insider’s view of the exciting synergies that came from combining genetics and psychology.
I won’t get into most of these things today (I will wait until I read the book for that), but this will be just an article showing that DNA is, in fact, not a blueprint, and DNA is not a “code” or “recipe” for the organism.
It’s funny that the little blurb says that “Nature defeats nurture by a landslide“, because, as I have argued at length, nature vs nurture is a false dichotomy (See Oyama, 1985, 2000, 1999; Moore, 2002; Schneider, 2007; Moore, 2017). Nature vs nurture is the battleground that the false dichotomy of genes vs environment is fought on. However, it makes no sense to partition heritability estimates if it is indeed true that genes interact with environment—that is, if nature interacts with nurture.
DNA is also called “the book of life”. For example, in her book The Epigenetics Revolution: How Modern Biology Is Rewriting Our Understanding of Genetics, Disease, and Inheritance, Nessa Carey writes that “There’s no debate that the DNA blueprint is a starting point” (pg 16). This, though, can be contested. “But the promise of a peep into the ‘book of life’ leading to a cure for all diseases was a mistake” (Noble, 2017: 161).
Developmental psychologist and cognitive scientist David S. Moore concurs. In his book The Developing Genome: An Introduction to Behavioral Epigenetics, he writes (pg 45):
So, although I will talk about genes repeatedly in this book, it is only because there is no other convenient way to communicate about contemporary ideas in molecular biology. And when I refer to gebe, I will be talking about a segment or segments of DNA containing sequence information that is used to help construct a protein (or some other product that performs a biological function). But it is worth remembering that contemporary biologists do not mean any one thing when they talk about “genes”; the gene remains a fundementally hypothetical concept to this day. The common belief that there are things inside of us that constitute a set of instructions for building bodies and minds—things that are analogous to “blueprings” or “recipes”—is undoubedtly false. Instead, DNA segements often contain information that is ambiguous, and that must be edited or arranged in context-dependent ways before it can be used.
Still, other may use terms like “genes for” trait T. This, too, is incorrect. In his outstanding book Making Sense of Genes, Kostas Kamporakis writes (pg 19):
I also explain why the notion of “genes for,” in the vernacular sense, is not only misleading but also entirely inaccurate and scientifcally illegitamate.
First, I show that genes “operate” in the context of development only. This means that genes are impllicated in the development of characters but do not determine them. Second, I explain why single genes do not alone produce characters or disease but contribute to their variation. This means that genes can account for variation in characters but cannot alone explain their origin. Third, I show that genes are not the masters of the game but are subject to complex regulatory processes.
Genes can only be seen as passive templates, not ultimate causes (Noble, 2011), and they cannot explain the origin of different characters but can account for variation in physical characters. Genes only “do” something in the context of development; they are inert molecules and thusly cannot “cause” anything on their own.
Genes are not ‘for’ traits, but they are difference-makers for traits. Sterelny and Griffiths (1999: 102), in their book Sex and Death: An Introduction to Philosophy of Biology write:
Sterelny and Griffiths (1988) responded to the idea that genes are invisible to selection by treating genes as difference makers, and as visible to selection by virtue of the differences they make. In doing so, they provided a formal reconstruction of the “gene for” locution. The details are complex, but the basic intent of the reconstruction is simple. A certain allele in humans is an “allele for brown eyes” because, in standard environments, having that allele rather than alternatives typically available in the population means that your eyes will be brown rather than blue. This is the concpet of a gene as a difference maker. It is very important to note, however, that genes are context-sensitive difference makers. Their effects depend on the genetic, cellular, and other features of their environment.
(Genes can be difference makers for physical traits, but not for psychological traits because no psychophysical laws exist, but I’ll get to that in the future.)
Note how the terms “context-sensitive” and “context-dependent” continue to appear. The DNA-as-blueprint statement presumes that DNA is context-independent, but we cannot divorce genes—whatever they are—from their context, since genes and environment, nature and nurture, are intertwined. (And it is even questioned if ‘genes’ are truly units of inheritance, see Fogle, 1990. Fogle, 2000 also argues to dispense with the concept of “gene” and that biologists should be using terms like intron, promoter region, and exon. Nevertheless, there is a huge disconnect with the term “gene” in molecular biology and classical genetics. Keller 2000 argues that there are still uses for the term “gene” and that we should not dispense with the term. I believe we should dispense with it.)
Susan Oyama (2000: 77) writes in her book The Ontogeny of Information:
“Though a plan implies action, it does not itself act, so if the genes are a blueprint, something else is the constructor-construction worker. Though blueprints are usually contrasted with building materials, the genes are quite easily conceptualized as templates for building tools and materials; once so utilized, of course, they enter the developmental process and influence its course. The point of the blueprint analogy, though, does not seem to be to illuminate developmental processes, but rather to assume them and, in celebrating their regularity, to impute cognitive functions to genes. How these functions are exercised is left unclear in this type of metaphor, except that the genetic plan is seen in some peculiar way to carry itself out, generating all the necessary steps in the necessary sequence. No light is shed on multiple developmental possibilities, species-typical or atypical.“
The Modern Synthesis is one of the causes for the genes-as-blueprints thinking; the Modern Synthesis has causation in biology wrong. Genes are not active causes, but they are passive templates, as argued by many authors. They, thus, cannot “cause” anything on their own.
In his 2017 book Dance to the Tune of Life: Biological Relativity, Denis Noble writes (pg 157):
As we saw earlier in this chapter, these triplet sequences are formed from any combination of the four bases U, C, A and G in RNA and T, C, A and G in DNA. They are often described as a genetic ‘code’, but it is important to understand that this usage of the word ‘code’ carries overtones that can be confusing.
A code was originally an intentional encryption used by humans to communicate. The genetic ‘code’ is not intentional in that sense. The word ‘code’ has unfortunately reinforced the idea that genes are active and even complete causes, in much the same was as a computer is caused to follow the instructions of a computer program. The more nuetral word ‘template’ would be better. Templates are used only when required (activated); they are not themselves active causes. The active causes lie within the cells themselves since they determine the expression patterns for the different cell types and states. These patterns are comminicated to the DNA by transcrption factors, by methylation patterns and by binding to the tails of histones, all of which influence the pattern and speed of transcription of different parts of the genome. If the word ‘instruction’ is useful here at all, it is rather that the cell instructs the genome. As Barbara McClintock wrote in 1984 after receiving her Nobel Prize, the genome is an ‘organ of the cell’, not the other way around.
Realising that DNA is under the control of the system has been reinforced by the discovery that cells use different start, stop and splice sites for producing different messenger RNAs from a single DNA sequence. This enables the same sequence to code different proteins in different cell types and under different conditions [here’s where context-dependency comes into play again].
Representing the direction of causality in biology the wrong way round is therefore confusing and has far-reaching conseqeunces. The causality is circular, acting both ways: passive causality by DNA sequences acting as otherwise inert templates, and active causality by the functional networks of interactions that determine how the genome is activated.
This takes care of the idea that DNA is a ‘code’. But what about DNA being a ‘blueprint’, that all of the information is contained in the DNA of the organism before conception? DNA is clearly not a ‘program’, in the sense that all of the information to construct the organism exists already in DNA. The complete cell is also needed, and its “complex structures are inherited by self-templating” (Noble, 2017: 161). Thus, the “blueprint” is the whole cell, not just the genome itself (remember that the genome is an organ of the cell).
Lastly, GWA studies have been all the rage recently. However, there is only so much we can learn just from association studies, before we need to turn to the physiological sciences for functional analyses. Indeed, Denis Noble (2018) writes in a new editorial:
As with the results of GWAS (genome-wide association studies) generally, the associations at the genome sequence level are remarkably weak and, with the exception of certain rare genetic diseases, may even be meaningless (13, 21). The reason is that if you gather a sufficiently large data set, it is a mathematical necessity that you will find correlations, even if the data set was generated randomly so that the correlations must be spurious. The bigger the data set, the more spurious correlations will be found (3).
The results of GWAS do not reveal the secrets of life, nor have they delivered the many cures for complex diseases that society badly needs. The reason is that association studies do not reveal biological mechanisms. Physiology does. Worse still, “the more data, the more arbitrary, meaningless and useless (for future action) correlations will be found in them” is a necessary mathematical statement (3).
Nor does applying a highly restricted DNA sequence-based interpretation of evolutionary biology, and its latest manifestation in GWAS, to the social sciences augur well for society.
It is further worth noting that there is no privileged level of causation in biological systems (Noble, 2012)—a priori, there is no justification to privilege one system over another in regard to causation, so saying that one level of the organism is “higher” than another (for instance, saying that genes are, and should be, privileged over the environment or any other system in the organism regarding causation) is clearly false, since there is upwards and downwards causation, influencing all levels of the system.
In sum, it is highly misleading to refer to DNA as “blueprints”, a “code”, or a “recipe.” Referring to DNA in this way means that one presumes that DNA can be divorced from its context—that it does not work together with the environment. As I have argued in the past, association studies will not elucidate genetic mechanisms, nor will heritability estimates (Richardson, 2012). We need physiological testing for these functional analyses, and association studies like GWAS and even heritability estimates don’t tell us this type of information (Panofsky, 2014). So, it seems, that what Plomin et al are looking for that they assume are “in the genes”, are not there, because they use a false model of the gene (Burt, 2015; Richardson, 2017). Genes are resources—templates to be used by and for the system—not causes of traits and development. They can account for differences in variation, but cannot be said to be the origin of trait differences. Genes can be said to be difference makers, but knowing whether or not they are difference makers for behavior, in my opinion, cannot be known.
(For further information on genes and what they do, reach Chapters Four and Five of Ken Richardson’s book Genes, Brains, and Human Potential: The Science and Ideology of Intelligence. Plomin himself seems to be a reductionist, and Richardson took care of that paradigm in his book. Lickliter (2018) has a good review of the book, along with critiques of the reductionist paradigm that Plomin et al follow.)
The debate on what type of diet in regard to macronutrient differences rages on. Should we eat high carb, low fat (HCLF)? Or low carb, high fat (LCHF) or something in between? The answer rests on, of course, the type of diets that our ancestors ate—both immediate and in the distant past. In the 1990s, a frozen human was discovered in the Otzal mountains, which gave him the name “Otzi man.” About 5,300 years ago, he was frozen in the mountains. The contents of his stomach have been analyzed in the 27 years since the discovery of Otzi, but an in-depth analysis was not possible until now.
A new paper was published recently, which analyzed the stomach contents of Otzi man (Maixner et al, 2018). There is one reason why it took so long to analyze the contents of his stomach: the authors state that, due to mummification, his stomach moved high up into his rib cage. The Iceman was “omnivorous, with a diet consisting both of wild animal and plant material” (Maixner et al, 2018: 2). They found that his stomach had a really high fat content, with “the presence of ibex and red deer” (pg 3). He also “consumed either fresh or dried wild meat“, while “a slow drying or smoking of the meat over the fire would explain the charcoal particles detected previously in the lower intestine content.“(pg 5).
The extreme alpine environment in which the Iceman lived and where he have been found (3,210 m above sea level) is particularly challenging for the human physiology and requires optimal nutrient supply to avoid rapid starvation and energy loss . Therefore, the Iceman seemed to have been fully aware that fat displays an excellent energy source. On the other hand, the intake of animal adipose tissue fat has a strong correlation with increased risk of coronary artery disease . A high saturated fats diet raises cholesterol levels in the blood, which in turn can lead to atherosclerosis. Importantly, computed tomography scans of the Iceman showed major calcifications in arteria and the aorta indicating an already advanced atherosclerotic disease state . Both his high-fat diet and his genetic predisposition for cardiovascular disease  could have significantly contributed to the development of the arterial calcifications. Finally, we could show that the Iceman either consumed fresh or dried meat. Drying meat by smoking or in the open air are simple but highly effective methods for meat preservation that would have allowed the Iceman to store meat long term on journeys or in periods of food scarcity. In summary, the Iceman’s last meal was a well-balanced mix of carbohydrates, proteins, and lipids, perfectly adjusted to the energetic requirements of his high-altitude trekking. (Maixner et al, 2018: 5)
They claim that “the intake of animal adipose tissue fat has a strong correlation with increased risk of coronary artery disease“, of course, citing a paper that the AHA is involved in (Sacks et al, 2017) which says that “Randomized clinical trials showed that polyunsaturated fat from vegetable oils replacing saturated fats from dairy and meat lowers CVD.” This is nonsense, because dietary fat guidelines have no evidence (Harcombe et al, 2016; Harcombe, Baker, and Davies, 2016; Harcombe, 2017). Saturated fat consumption is not even associated with all-cause mortality, type II diabetes, ischemic stroke, CVD (cardiovascular disease) and CHD (coronary heart disease) (de Sousa et al, 2015).
Thus, if anything, what contributed to Otzi man’s arterial calcification seems to be grains/carbohydrates (see DiNicolantonio et al, 2017), not animal fat. Fats, at 9 kcal per gram, were better for Otzi to consume, as he got more kcal for his buck; eating a similar portion in carbohydrates, for example, would have meant that Otzi would have had to spend more time eating (since carbs have less than half the energy that animal fat does). Since his stomach had ibex (a type of goat) and red deer, it’s safe to say that many of his meals consisted mainly of animal fat, protein with some cereals and plants thrown in (he was an omnivore).
We can then contrast the findings of Otzi’s diet with that of Neanderthals. It has been estimated that, during glacial winters, Neanderthals would have consumed around 74-85 percent of their diet from animal fat when there were no carbohydrates around, with the rest coming from protein (Ben-Dor, Gopher, and Barkai, 2016). Furthermore, based on contemporary data from polar peoples, it is estimated that Neanderthals required around 3,360 to 4,480 kcal per day to winter foraging and cold resistance (Steegmann, Cerny, and Holliday, 2002). The upper-limit for protein intake for Homo sapiens is 4.0 g/bw/day while for erectus it is 3.9 g/bw/day (Ben-Dor et al, 2011), and so this shows that Neanderthals consumed a theoretical upper-maximum of protein due to their large body size. So we can assume that Neanderthals consumed somewhere near 3800 kcal per day. The average Neanderthal is said to have consumed about 292 grams of protein per day, or 1,170 kcal (with a lower end of 985 kcal and an upper end of 1,170 at the high end) (Ben-Dor, Gopher, and Barkai, 2016: 370).
Then if we further assume that Neanderthals consumed no carbohydrates during glacial winters, that leaves protein as the main source of energy, since the large game the Neanderthals hunted were not around. Thus, Neanderthals would have consumed between 2,812 and 3,230 kcal from animal fat with the rest coming from protein. We can also put this into perspective. The average American man consumes about 100 grams of protein per day, while consuming 2,195 kcal per day (Ford and Dietz, 2013). For these reasons, and more, I argued that Neanderthals were significantly stronger than Homo sapiens, and this does have implications for racial differences in athletic ability.
In sum, the last meal of Otzi man is now known. Of course, this is a case of n = 1, so we should not draw too large a conclusion from this, but it is interesting. I don’t see why the composition of the diets of any of Otzi’s relatives would have been any different (or that the contents of his normal diet would have been any different). He ate a diet high in animal fat like Neanderthals, but unlike Neanderthals, they ate a more cereal-based diet which may have contributed to Otzi’s CVD and arterial calcification. We can learn a lot about ourselves and our ancestors through the analysis of their stomach contents (if possible) and teeth (if possible), and maybe even genomes (Berens, Cooper, and Lachance, 2017) because if we learn what they ate then we can maybe begin to shift dietary advice to a more ‘natural’ way and avoid diseases of civilization. But, we have not had time to adapt to the new obesogenic environments we have constructed for ourselves. It’s due to this that we have an obesity epidemic, and by studying the diets of our ancestors, we can then begin to remedy our obesity and other health problems.
JP Rushton was a highly controversial psychologist professor, teaching at the University of Western Ontario for his entire career. In the mid-1980s, he proposed that evolution was “progressive” and that there was a sort of “hierarchy” between the three races that he termed “Mongoloid, Caucasoid, and Negroid” (Rushton, 1985). His theory was then strongly criticized scientists from numerous disciplines (Lynn, 1989; Cain, 1990; Weizmann et al, 1990; Anderson, 1991; Graves, 2002). Rushton responded to these criticisms (Rushton, 1989; Rushton, 1991; Rushton, 1997; though it’s worth noting that Rushton never responded to Graves’ 2002 critiques). (Also see Rushton’s and Graves’ debate.) Copping, Campbell, and Muncer (2014) write that “high K scores were related to earlier sexual debut and unrelated to either pubertal onset or number of sexual partners. This suggests that the HKSS does not reflect an underlying “K dimension.”“, which directly contradicts Rushton’s racial r/K proposal.
There is a now a new critique of Rushton’s theory out now, by Edward Dutton, English anthropologist, with a doctorate in religious studies, just published at the end of last month (Dutton, 2018). I ordered the book the day after publication and it took three weeks to get to my residence since it came from the UK. I finally received it on Friday. It’s a small book, 143 pages sans acknowledgments, references and the index, and seems well-written and researched from what I’ve read so far.
Here is the plan of the book:
Accordingly, in this chapter [Chapter One], we will begin by getting to grips with the key concepts of intelligence and personality. This part is primarily aimed at non-specialist readers or those who are sceptical of the two concepts [it’s really barebones; I’m more than ‘sceptical’ and it did absolutely nothing for me]. In Chapter Two, we will explore Rushton’s theory in depth. Readers who are familiar with Life History Theory may wish to fast forward through to the section on the criticisms of Rushton’s model. I intend to be as fair to his theory as possible, in a way so few of the reviewers were when he presented it. I will respond to the many fallacious criticisms of it, all of which indicate non-scientific motives [what about Rushton? Did he have any non-scientific motives?]. However, I will show that Rushton is just as guilty of these kinds of techniques as his opponents. I will also highlight serious problems with his work, including cherry picking, confirmation bias, and simply misleading other researchers. In Chapter Three, we will explore the concept of ‘race’ and show that although Rushton’s critics were wrong to question the concept’s scientific validity, Rushton effectively misuses the concept, cherry-picking such that his concept works. In Chapter Four, we will explore the research that has verified Rushton’s model, including new measures which he didn’t examine. We will then, in Chapter Five, examine the concept of genius and look at how scientific geniuses tend to be highly intelligent r-strategists, though we will see that Rushton differed from accepted scientific geniuses in key ways.
In Chapter Six, we will find that Rushton’s theory itself is problematic, though not in the ways raised by his more prominent critics. It doesn’t work when it comes to a key measure of mental stability as well as to many other measures, specifically preference for oral sex, the desire to adopt non-related children, the desire to have pets, and positive attitudes to the genetically distant. It also doesn’t work if you try to extend it to other races, beyond the three large groups he examined [because more races exist than Rushton allows]. In Chapter Seven, with all the background, we will scrutinize Rushton’s life up until about the age of 30, while in Chapter Eight, we will follow Rushton from the age of 30 until his death. I will demonstrate the extent to which he was a highly intelligent r-strategist and a Narcissist and we will see that Rushton seemingly came from a line of highly intelligent r-strategists. In Chapter Nine, I will argue that for the good of civilization those who strongly disagree with Rushton must learn to tolerate people like Rushton. (Dutton, 2018: 12-13).
On the back of the book, he writes that Rushton had “two illegitimate children including one by a married black woman.” This is intriguing. Could this be part of Rushton’s motivation to formulate his theory (his theory has already been rebutted by numerous people, so speculating on motivations in lieu of new information seems apt)?
“But on this basis, it could be argued that my critique of Rushton simply gives ammunition to emotionally-driven scientists and their friends in the media. However, it could be countered that my critique only goes to show that it is those who are genuinely motivated by the understanding of the world — those who accept empirical evidence, such as with regard to intelligence and race — who are prepared to critique those regarded as being ‘on their side.’ And this is precisely because they are unbiased and thus do not think in terms of ‘teams.’”
Dutton argues that “many of the criticisms leveled against Rushton’s work by mainstream scientists were actually correct” (pg 13). This is a truism. One only need to read the replies to Rushton, especially Anderson (1991) to see that he completely mixed up the theory. He stated ‘Negroids’ were r-strategists and ‘Mongoloids’ were K-strategists, but this reasoning shows that he did not understand the theory—or, if anything, he knowingly attempted to obfuscate the theory in order to lend stronger credence to his own theory (and personal biases).
The fatal flaw for Rushton’s theory is that, if r/K selection theory did apply to human races, that ‘Mongoloids’ would be r-strategists while ‘Negroids’ would be K-strategists. This is because “Rushton’s own suggested agents of natural selection on African populations imply that African populations have had a strong history of K-selection, as well as the r-selection implied by “droughts”” (Anderson, 1991: 59). As for Mongoloids, “Rushton lists many traits of Mongoloid peoples that are thought to represent adaptation to cold. Cold weather acts in a density-independent fashion (adaptations to cold improve survival in cold weather regardless of population density); cold weather is normally an agent of r-selection” (Anderson, 1991: 59). Rushton’s own arguments imply that ‘Negroids’ would have had more time to approach their environmental carrying capacity and experience ‘K-selecting’ pressures.
Thus, Rushton’s claim about the empirical ordering of life history and behavioural traits in the racial groups exactly contradicts general predictions that follow from his own claims about their ancestral ecology and the r/K model (Boyce, 1984; MacArthur, 1972; MacArthur & Wilson, 1967; Pianka, 1970; Ricklefs, 1990, p. 577). (Specific predictions from the model could be made only about individual populations after careful study in their historical habitat, as I have pointed out above). (Anderson, 1991: 59) [And it is not possible, because the populations in question should be living in the environment that the selection is hypothesized to have occurred. That, of course, is not possible today.]
Though, near the end of the book, Dutton writes that (pg 148) that “Rushton was not a scientific genius. As we have discussed, unlike a scientific genius, his models had clear deficiencies, he cherry-picked data to fit his model, and he was biased in favor of his model. However, Rushton was a highly original scientist who developed an extremely original and daring theory: a kind of artistic-scientist genius combination.”
The final paragraph of the book, though, sums up the whole book up well. Dutton talks about when Jared Taylor introduces Rushton at one of his American Renaissance conferences (February 25th, 2006):
‘Well, thank you very much and . . . eh . . . and thank you Jared for . . . erm . . . putting on another wonderful conference.’ Rushton was reserved, yet friendly and avuncular. ‘Eh . . . it’s a great honor to be the after dinner speaker; to be elevated up like this.’ He was certainly elevated up. Taylor had even remarked that ‘in a sane and civilized world’ Rushton’s work would have ‘worldwide acclaim.’ Rushton’s audience admired him, trusted him . . . They weren’t familiar with him at all.
All in all, to conclude this little mini-review, I would recommend picking up this book as it’s a great look into Rushton’s life, the pitfalls of his theory (and for the new work and other variables that Dutton shows showed Rushton’s M>C>N ‘hierarchy’). Rushton’s work, while politically daring, did not hold up to scientific scrutiny, since the model was beginning to be abandoned in the late 70s (Graves, 2002), with most scientists completely dismissing the model in the early 90s. Commenting on r/K selection, Stearns (1992: 206) writes that “This explanation was suggestive and influential but incorrect” (quoted in Reznick et al, 2002), while Reznick et al (2002: 1518) write that “The r- and K-selection paradigm was replaced by new paradigm that focused on age-specific mortality (Stearns 1976, Charlesworth 1980).” Rushton’s model, while it ‘made sense with the data’, was highly flawed. And even then, it doesn’t matter that it ‘made sense’ with the data, since Rushton’s theory is one large just-so story (Gould and Lewontin, 1976; Lloyd, 1999; Richardson, 2007; Nielsen, 2009; see also Pigliucci and Kaplan, 2000 and Kaplan, 2002
How much admixture does it take for one race to no longer exist? The answer to the question is intuitive, and using Hardimon’s (2017) minimalist race concept, it is also easily answerable on logical grounds. For example, the answer to the question will show that the “one-drop rule” (that “one drop” of “black blood” makes one black) doesn’t make logical sense. These kinds of holdovers are from the racialist concept. Racialist races do not exist, therefore the concept of the “one-drop rule” does not either, since there are no facts of the matter the two concepts explain.
The maintenance of the races that current exist depend on, at the moment, social barriers to reproduction, such as racism, segregation, differences in culture and class, role segregation and racial discrimination. Thus, social isolation is important for the maintenance of the current races. Social isolation, like geographic isolation (i.e., oceans, mountains, deserts, etc.) impedes racial interbreeding and thus ensures the continuation of the genetic transmission of distinct patterns of visible physical features which correspond to geographic ancestry.
Social isolation mechanisms have been in effect for hundreds of years, which began with the advent of African slavery to the New World. Laws against miscegenation existed in some states (Phillips, Odunlami, and Bonham, 2007), which is part of the reason why it’s (an unspoken) taboo to racially intermarry and bear children with someone not of their own race. Due to this, the few interracial unions that did produce children were specifically barred—in the eyes of society—to only be able to have children with others of their same socialrace at the lower ends of the social hierarchy.
Social isolation mechanisms have ensured the continuation of human races after the discovery of the New World when the geographic isolation mechanisms began breaking down due to exploring new lands. These isolating mechanisms on the populace ensured little admixture in the European population, but compared to European Americans, African Americans have a higher percentage of the opposite admixture. Understanding racial admixture and the genetic transmission of distinct visible physical features which correspond to geographic ancestry is extremely important to understanding when races “disappear” due to inbreeding.
Therefore, social isolation—ever since 1492—and the laws/rules that came after the breakdowns of geographic isolation between races still ensured the existence of the races as we know them today. Social factors acted as de facto physical barriers that impeded the races from breeding, thusly keeping their visible physical features intact, which means keeping their racial phenotype intact since races are defined—most importantly—on the basis of visible physical features. Social isolation can, clearly, be just about as “strong” as geographic isolation, since the social repercussions of interracial unions may exile them from the groups they were in. Thus, people would be wary of interracial unions, even if—as it seems—our culture in America seems to be swaying towards inclusivity in regard to interracial relationships, people still generally associate with and date people who look like themselves and their parents (see below).
How Much Admixture?
How much admixture can one race take before said race ceases to exist? Since C 1 (a group is distinguished from another group on the basis of distinct visible physical features) doesn’t require sharp lines between said visible physical features, C 2 (members linked by peculiar ancestry) also doesn’t require that all of the ancestors of Rs (races) be Rs.
The best possible example for an answer to the question of “How much admixture?” is simple. Think of Europeans (a subrace of the Caucasian race). When Europeans interbreed with non-Europeans, they begin to lose their distinct pattern of visible physical features which correspond to their geographic ancestry. Thus, in the case of Europeans, the answer to the question of “How much admixture?”, meaning “How much interbreeding can the European subrace take before it is “bred out” of existence?” is, of course, not too much.
Think of a union between a black woman and white man (using the social race designation; their populationist race is African and Caucasian, respectively). The child the woman bears will share some of her physical features, but barely. The baby will look more like the non-European parent, but of course, a baby who is the product of the union between an African and European will share features with both parents, and thus, the baby can “roughly fit the pattern” of a minimalist race. We can easily explain this: mixed-race individuals can err, physically, to one minimalist race over another because they are the products of individuals who do fit the patterns (of visible physical features which correspond to geographic ancestry).
Contrary to the alarmist claims heard in the media and from the altright, trends in interracial marriages do not indicate that minimalist (populationist) races are coming to an end (in this case, the white (social) race).
It is true that in the modoern (post-1492) world there is vastlty more racial interbreeding than there was before 1492. And if one is referring to the very long run, then races are almost certainly on their way out. But it is one thing to say that the human races will cease to exist at some point in the distant future and quite another to say that they are likely to disappear anytime soon. It is by no means clear that we are in an epistemic position to make the latter claim.
Contrary to what some writers suggest, recent trends in racial intermarriage in the United States do not indivate the imminent end of populationist (or minimalist) races. 5 The skyrocketing rates of intermarriage in this country notwithstanding, it remains true that the vast majority of Americans continue to marry within their own conventionally designated racial group. Despite the remarkable fact that the multiracial, multi-ethnic Americans have apparently become the fastest-growing demographic group in the United States, their numbers are still swamped by individuals who are members of a single continental-level minimalist races. 6 I don’t think that the significant fraction of DNA traceable to “Europeans” in most black Americans, and the small but real fraction of DNA traceable to “Africans” in white Americans, makes the end of the populationist (or minimalist) race significantly more imminent.
There is no evidence of which I am aware indicating that the rate at which racial interbreeding in the United States (or anywhere else) is occurring is one that would lead to the elimination of all racial differences—a situation in which no two groups could be distinguished on the basis of patterns of visible physical corresponding to differences in geographic ancestry—in the near future. To sum up: the increase frequency of encountering individuals of mixed racial ancestry does not mean that the concept of race is going to go out of business anytime soon. (Hardimon, 2017: 122)
Yaeger et al (2009) show that, in their sample, self-identification as African American is a reliable indicator of ancestry. Their findings also “suggest that self-reported race and ancestry can predict ancestral clusters, but do not reveal the extent of admixture.” Thus, self-identified race—even in the presence of admixture as is the case with African Americans—can show the racial category that an individual belongs to (based on their ancestry).
Hardimon (2017: 49) articulates a simple rule that employs the minimalist concept of race:
If both parents of an individual belong to one particular racial group R, that individual will belong to R.
What happens, however, if one parent belongs to R1 and the other parent belongs to R2. The minimalist concept of race does not say. Still less does it tell us what one’s race is if one’s grandparents belongs to an R1, another to R2, another to R3, and another to R4. This is a further respect in which the minimalist race concept is vague.
Particular conceptions of race (for example, the infamous “one-drop rule”) may specify the race of the individuals of “mixed” parentage, but the minimalist concept of race does not. The idea that a genune concept of race must specify the race of each individual is a hangover from the racialist race concept. Recall here that the minimalist racehood is not defined in terms of the characteristics of the individuals who belong to races. It is defined in terms of characteristics of groups.
So, the minimalist concept of race is vague, just like the populationist concept. But we can make one claim on the answer to the question “How much admixture?”: “Once a race loses its specific phenotype due to racial interbreeding, then the race ceases to exist.”
The one drop rule (also known as the law of hypodescent), is a form of racial essentialism (Perez and Hirschman, 2009), which states that “one drop” of another, inferior (on the basis of racialist races) race’s blood denotes him to the inferior race in the social hierarchy. The one drop rule was created back during the slave days and signified who could breed with who, on the basis of how “pure” their blood was. It was, and still is today, a way for race deniers to deny the existence of race.
The one-drop rule stated that anyone with one black ancestor was classified as black (Pauker et al, 2009). That is, his position on the socialrace hierarchy (a hierarchy since it’s based on the false racialist race concept) is based on the fact that he has one black ancestor. Due to this, and other differing amounts of admixture in certain ethnic groups and other social groups taken to be races, people have—fallaciously—stated that races do not exist since the unions of two separate races “erases” one, or both, of the races in question.
This rule helped to ensure the maintenance of populationist races, since society frowned upon interracial marriage. This, obviously, was a social custom. The Jim Crow laws helped to ensure the maintenance of the physical characteristics of the races in question, though the laws were enacted to ensure the “racial purity” (whatever that is) of the European race, it helped to ensure lower amounts of admixture in black Americans. Thus, black Americans would be expected to self-identify as black (Liebler and Zacher, 2017).
Liebler and Zacher (2017)‘s data “supports the notion that this “rule” has some power even today, as there are almost 30 times as many people reporting that they are racially black with American Indian ancestry (weighted N=522,607) as there are people reporting American Indian race with black ancestry (weighted N=16,226).” Bryc et al (2015) show that, despite the expectations of the one drop rule “individuals identify roughly with the majority of their genetic ancestry.”
Most people in one sample that had less than 20 percent African ancestry identified as white. In the US, “Latinos” (a social-race) were estimated to have 65.1 percent European, 6.2 percent African, and 18.6 percent Native American DNA. Overall, 3.5 percent of European Americans had 1 percent or more African ancestry, while 1.4 percent of self-reported European Americans had were estimated to carry at least 2 percent African ancestry (Bryc et al, 2015).
Importantlty, Guo et al (2014) write:
The one-drop rule represents an important case in which social context trumps bio-ancestry. When asked to classify into a single race, most individuals with 30 % to 60 % African ancestry self-report as black; virtually all respondents with >60 % African ancestry self-classify as black. In contrast, a substantially higher proportion of European ancestry is “required” to self-classify or to be classified by an interviewer as white than the proportion of African ancestry necessary to self-classify or be classified as black. However, when given the option of identifying as multiracial, the majority of individuals with 40 % to 60 % African ancestry in both ROOM and Add Health and substantial proportions of individuals with >60 % African ancestry in ROOM stopped self-classifying as only black and primarily chose a multiracial classification.
“The infamous one-drop rule is peculiar to this country [America] but it is a feature of the American conception of race, not the minimalist concept of race.” (Hardimon, 2017: 56) The one-drop rule is a clear tell to how the socialrace concept acts. It is an essentialist concept, which means that it is necessarily racialist—since “one drop” of black blood makes one black—according to the rule.
The Maintenance of Races
It is possible that one society could take social measures to ensure the existence of their specific racial phenotype (that is, the existence of their minimalist race or subrace). Such a society would have to grapple with the moral and ethical underpinnings of such measures to ensure the maintenance of their phenotype (see Glannon, 2001’s book Genes and Future People for an extensive review of the moral, political, social, and ethical implications of human genetic engineering). This could also include genetic modification, though sound arguments exist that show that the way most people view genetic modification depends on a “strong view” of genetic determinism, which is false (Resnick and Vorhaus, 2006). However, it is possible that, through the will of the people in the society, that social isolation can lead to a de facto “physical” isolation through the social norms of the society in question.
However, since the races as they currently are are in no danger of non-existence, such measures, while they would (presumably) work, do not need to be taken. Such measures, though, do not need to be taken, since most people want to court with others who look like themselves, and those who are more likely to look like themselves are people of their own ethny, which is to say, people of their own populationist race. Thus, social measures to ensure the maintenance of races do not need to be taken.
As noted above, certain concepts from the days of the one drop rule are still in effect today, as a holdover from the days of Jim Crow and before. Some of these holdover concepts, though, help to maintain the races we know today. However, there is a possibility that our populationist races, too, have benefits socially constructed. Hardimon (2017: 126) writes (emphases his):
If populationist races exist, the role human action plays in their maintenance is rather more pronounced then the role it played in their genesis. Insofar as social norms and practices prohibiting or discouraging intermarriage have been the primary mechanisms preventing racial interbreeding since 1492, the maintenance of the separation has been intentional: this outcome is the very point of the discriminatory activity and practices in question. There is thus an especially strong sense in which, if populationist races exist, populationist race has been socially constructed since 1492.
Hardimon (2017: 126) goes on to say that the maintenance of populationist races “is not a natural process outside of human control”, nor is it “immutable or inalterable“, while “its existence is not an invariant, unchangeable,”natural” fact” and “The continued existence of populationist races, if it is a fact, is a fact within our power to change.” Thus, if populationist races exist (and they do), they exist by virtue of existing in nature.
So the races are not in danger of non-existence anytime soon, since the percentage of interracial unions are not too high compared to those who marry within their populationist races. The maintenance of populationist races comes down to—and will come down to, as long as humans are around—to social policies, whether enacted by state/country governments or the people themselves, sans any laws on miscegenation.
It has been said that we are attracted to people “who look like us“, “who look like our parents“, and “‘who are more similar to ourselves“. This means—NECESSARILY—that people are more likely to be attracted to people of their own race/ethnic group. People “who look like us” are co-ethnics and people of the same racial background; people who “look like our parents”, are, again, people who would share the same geographic ancestry. Since the physical features that delineate races are genetically transmitted from parent to offspring, then, people are more likely to be attracted to people of their same race. Finally, “people more similar to ourselves” doesn’t necessarily mean “people more racially/ethnically similar to ourselves”, since, of course, there are many other things that individuals have in common other than their race/ethnic group. However, it has been established that we are attracted more to people who share more similar genes than ourselves (Rushton,1997, 1998; Sebro et al, 2017). Thus, logically, since we are attracted to people who look like ourselves and our parents, we are attracted to people of our own ethnicity/race, as a matter of fact.
The question “How much admixture does it take for one race to no longer exist” is answered simply once the term “RACE” is defined: the amount of admixture it takes for one race to be “bred out” of existence is proportional to the amount of admixture it takes for one race’s physical features which correspond to geographic ancestry which are exhibited by the real group in question (this case being a subrace of a minimalist/populationist race). Europeans can’t take “much”, if any, other admixture, otherwise the traits that make Europeans European (which are, of course, not mutually exclusive to them, but the traits they—and their ethnies—exhibit are distinct) will disappear and so one of the Caucasian subraces will disappear as well. Social isolation, at the moment, is maintaining the races as we know them—and will far into the foreseeable future (there is no evidence that they will disappear anytime soon). “Violations” of the one drop rule abound, but they mean little to the minimalist/populationist concepts of race since the visible physical features which distinguish the races remain intact.
The fact that people are more attracted to people who look like themselves and their parents is an implicit way of saying that people are more attracted to people who are physically similar to themselves—that is, racially/ethnically similar to themselves—and shows that the races will not be going anywhere for the foreseeable future.
Human races will continue to exist as long as the social barriers that impede racial interbreeding remain. (Of course, if these social barriers did not exist, a majority of people still would court people who look like themselves and their families.) This is evidence that, contra social laws that impede or frown upon interracial marriages, we do not need such laws/rules because people stick to their own anyway. Therefore, the races are not in danger of disappearing anytime soon.
Over at the blog Anthropology 365 the author—Adam Johnson, biocultural anthropologist—wrote an article titled Populations, Race, and The Sorites Paradox, in which he argues that, since there are no “clear lines” and they are “wuzzy”, we cannot say where one race ends and another begins, therefore race does not exist. His whole argument is largely just the continuum fallacy—that since we cannot show where one race, in this instance, ends and another begins, therefore, race does not exist. This reasoning, however, is very flawed.
The beginning of his article is concerned with laying out the sorites paradox. Imagine zero grains of sand, then continuously add grains of sand, 1, 5, 10, 100, 1000, etc. When does the heap become a pile of sand? Johnson attempts to use this logic regarding races and populations: where does one population end and another begin? (You already know where this is headed; it seems that this is the ‘argument’ that gets the most play nowadays when it comes to race-denialism and racial eliminativism when there are better, non-fallacious, arguments out there to attack the concept of race in our ontology. Using the old and tired “continuum fallacy” no longer makes sense because the objection that “Race does not exist because we cannot tell where one race ends and another begins” has been responded to numerous times, most recently (and forcefully) by philosophers of race Michael Hardimon and Quayshawn Spencer.)
He defines “population”, stating that—in biocultural anthropology—that a population is simply a group of like kinds that interbreed with each other which are separated by geographic barriers. Nothing wrong with that—it’s true. He then makes the huge leap in logic to a within-country comparison (America), showing two arbitrarily circled “populations” on the east and west coasts of America. He admits the circles are “arbitrary”, then adds another purple circle in the middle, and finally a green and purple circle in between the original circles, signifying five populations (the image can be seen below).
He says that “It is often impossible to draw neat boundaries around a group”, but I am aware of no author making any claim that it IS possible (and easy) to draw neat boundaries around groups. To do so, you only need simple conditions; and if there is any deviation out of those conditions, then the population in question do not fit the definition of what you were constructing and they can thus be removed. Johnson says “where does yellow end and purple begin?” since there is so much overlap between all five colors in this image. He says that this reasoning shows how “crude” the concept of population is regarding the accepted definition: a group of like kinds that can interbreed but are geographically separated.
One who denies Hardimon’s (2017) 3 conditions for to establish that populations are minimalist races (C1. visible patterns of distinct physical features which correspond to geographic ancestry; C2. that the members in this group are linked by a common ancestry; and C3. they must originate from a distinct geographic location) may then take to this idea that these arbitrarily drawn circles which are supposed to be “populations” (to Johnson) are then races; but Johnson never left any conditions, only a vague definition. One could argue that two of those clusters satisfy C1-C3 (that the cluster in question shares visible patterns of distinct physical features which correspond to geographic ancestry [the people who, say, make up one town in one of the arbitrarily drawn circles may have different visible patterns of distinct physical features which correspond with their ‘geographic ancestry’], that the members are linked by a common ancestry [the town they now live in, say], and they derive from a distinct geographic location [the arbitrarily drawn circle is a distinct geographic location].
However, for one to say that C1 holds for these arbitrarily drawn circles, they have to stretch the definition in order to accept random populations within a country. They then need to say that C2 refers to any type of “common ancestry” of a certain town; and that C3 then shows that they derive from a distinct geographic location. However, in regard to C2 and C3, one who would attempt such an argument would be equivocating on “geographic ancestry” and “distinct geographic location”, thusly claiming that an infinitude of races exist because the conditions are vague. While I do admit that minimalist concept is vague, in my view, it does not allow for one to equivocate on certain words used in the argument to show that any and all arbitrary populations can be called “races”; it does not work like that because there are distinctive conditions that must be met before further thinking on whether or not a population in question is a “race” or not.
Johnson then quotes Scientific American writer John Terrel who writes in his article “Plug and Play” Genetics, Racial Migrations and Human History:
“Distinguishing between races and populations is effectively making a distinction without a difference. If this comes across as sounding crazy to you, then tell me this. What is a population? How can you tell whether you are “inside” a population or “outside” it? How many of them are there “out there” in the real world? How many did there used to be? More than today, or fewer? (Now substitute in these simple questions the word “race.” Doesn’t make much difference, right?)”
What is a population? Good question. The definition left by Johnson above is alright, but we can refine it. I can simply cite Michael Hardimon’s definition of “populationist race” (Hardimon, 2017: 99; my emphasis):
“A race is a subdivision of Homo sapiens—a group of populations that exhibits a distinctive pattern of genetically transmitted phenotypic characters that corresponds to the group’s geographic ancestry and belongs to a biological line of descent initiated by a geographically separated and reproductively isolated founding population.”
Using this definition of race, a race is a group of populations that exhibits a distinctive pattern of genetically transmitted phenotypic characters that corresponds to the groups’ geographic ancestry. Thus, with “population” having a much more non-vague definition, we can then begin to look for populations that exist in reality (not arbitrarily demarcated “populations” like Johnson did—using arbitrary circles as population groups in America).
Now that population is defined, what about the next question: “How can you tell whether you are “inside” a population or “outside” it?” Since we now have a better grasp of what “population” means in this context, then this question is simple to answer. You can tell whether you are “inside”‘ or “outside” a population by looking in a mirror and then thinking about any “population” as defined above. It really is that simple. However, it is hard when “population” is defined so vaguely, and so you get flaws in reasoning like the one from Johnson.
Now that we know that we can tell whether or not we are “inside” or “outside” a population, his next question is: “How many of them are there “out there” in the real world?” According to the definition presented by Hardimon above, there are 5 current races in the human subspecies. That’s the number of races that are ““out there” in the real world” (as opposed to a possible world we can imagine—which is not the topic of contention).
Now that we know how many of “them” [races] exist, the next questions are: “How many did there used to be? More than today, or fewer?” I won’t pretend to know the answer to this question, but I will say one thing: the number of races that used to exist in the past comes down to the number of populations that exhibit a distinctive pattern of visible physical features which are genetically transmitted by geographically and reproductively isolated founding populations. Though, the number of races that “used to” exist is irrelevant to the fact that races exist today and the number of races that do exist today.
Johnson then claims that we, in the West, have a “long history” of constructing different races. And while this is true, this does not go against the claim that biological racial realism is true. Johnson says that “We homogenized entire continents of people into essential “types” and used the assumptions intrinsic to those types to make grand statements about the “natural” divisions in the human species and the value and meaning associated.” Well, these “entire homogenized continents of people” DO fit into “types”—though they are not “essential”; there are “natural” divisions within the human species BUT one does not have to put value and meaning onto the existence of these populations that we call ‘races’, since they are based solely on distinct pattern of genetically transmitted characters which then correspond with the group’s geographic ancestry.
“Anthropology has since moved on from it’s [sic] assumption that the human species is divided up into natural kinds“, Johnson writes. It seems that Johnson is ignorant to the work of Hardimon (2017) and his racial typology using the minimalist concept of race along with its “scientific equivalent” the populationist race concept. Minimalist races are a biological kind “if only a modest one” (Hardimon, 2017: 91), and so, just because “Anthropology has since moved on from it’s [sic] assumption that the human species is divided up into natural kinds” DOES NOT MEAN THAT there are no “kinds” within the human species. The argument for the existence of minimalist races establishes the claim that the human species is, in fact, divided up into kinds:
P1) There are differences in patterns of visible physical features which correspond to geographic ancestry
P2) These patterns are exhibited between real groups, existing groups (i.e., individuals who share common ancestry)
P3) These real, existing groups that exhibit these physical patterns by geographic ancestry satisfy conditions of minimalist race
C) Therefore race exists and is a biological reality
Minimalist races exist and are biologically real; if minimalist races exist, then populationist races exist; populationist race is the “scientization” of minimalist race; minimalist races entail kinds, and so since minimalist races entail kinds then so do populationist races; therefore both concepts speak to kinds within the human species and their biological reality.
Either way, we can also accept that anthropology has moved away from the assumption that the human race is divided into kinds and not have to give up the argument for the existence of race. Instead of arguing that human races are “kinds” as Hardimon (2017) does, Spencer (2014) argues that since Americans defer to the US Census Bureau regarding race, the must be referring to biologically real groups. The US Census Bureau defers to the Office of Management and Budget. The OMB discusses “sets of” populations. K= 5 delineates populations that Americans refer to when referring to race. So since Americans defer to the Census Bureau and the Census Bureau defers to the OMB, when we Americans talk about race, we talk about proper names for population groups as denoted by the OMB—even though ‘race’ looks like a ‘kind’ term, according to Spencer (2014: 1028) “its current use in US racial discourse is that of a proper name. It is a term that rigidly designates a particular set of “population groups.” This means that race is a particular, not a kind.”
So, there are two sound arguments for the existence of race (the argument for the existence of populationist races from Hardimon and the argument for the existence of Blumenbachian partitions—which both use the same population genetics paper (Rosenberg et al, 2002) to buttress their claims that their “kinds” (Hardimon, 2017) and “partitions” (Spencer, 2014) exist in reality.
Lastly, Johnson cites Galanter et al (2012) who genotyped “populations” throughout South America:
He then states that we have a bunch of South American populations here, all with differing amounts of admixture (which, of course, coincide with three of the five populationist races). He pretty much says, “How can we draw neat circles around these populations to call them “populations”, and what about those other populations not sampled in the analysis?” It makes no sense; when you’re just drawing circles anywhere on any map and then claiming that they are “populations” that satisfy a vague criteria/definition, then you don’t understand any of the newer arguments put forth by philosophers on the existence and reality of racial population groups.
He concludes the article simply:
To conclude, it’s always important to parse in our assumptions and take into account that our levels of analysis (the unit we are studying) may not represent reality. When we equivocate levels of analysis with levels of reality when examining human diversity, as Terrell says, we end up making a distinction between race and populations with no real difference. However, if we understand that the “population(s)” of interest are not reflections of reality, but merely constructed entities that represents an amalgamated web of kinship, political, biological, economic, and random histories at a particular time and place, we can avoid the trap of racial thinking (without using ‘race’) that some scholars fall in to.
He seems to be conflating two concepts here: how we view these visible physical features which correspond to geographic ancestry (our socialview of these populations) and their actual existence completely removed from our social conventions. Yes, socialraces are groups that are taken to be racialist races (that is to say, they are taken to have a specific essence particular to that race and only that race); but the concept of socialrace—the types of social values we give to these populations (think that the minimalist concept of race denotes certain social groups on the basis of distinct visible patterns which correspond to geographic ancestry; the socialrace concept is a good concept since it presents a way of thinking about (1) social groups that are taken to be races (such as ‘Latinos’/’Hispanics’); (2) the social positions that the social groups occupy; and (3) the systems of social structure of which those positions are parts (Hardimon, 2017: 139).
The “populations of interest”, are, indeed, of interest because they pick out what ‘we already know to be’ races.
Races, then, are both socially and biologically constructed. The minimalist concept of race shows the phenotypes that the socialrace concept chooses out when denoting a population its socialrace status in a given society. It shows that there are both biological and social underpinnings to racial categories—that is, there is both a “biological” and “social” realm to race in our ontology, and if we want to understand both ontologies, then we must first think of the consequences of thinking of “race” as only a biological concept and only a social concept and then—after we have thought of “race” as a biological and social concept on its own—we can think of “race” as both a social and biological phenomenon because that’s the best way to describe race in out ontology.
I find it funny how Johnson brings up “population thinking”; but I am probably thinking of it in a different way then he was in his article. When he brings up “population thinking” he wants you to think in terms of his definition of “population”, which pretty much means any group he circles is deemed a population, and thus, since there is no easy way to delineate populations from each other, therefore race does not exist (we must be eliminativist about race). Though when I think of the term “population thinking”, I think of Ernst May’s use of the phrase populationist thinking is more apt: “populationist thinking” is directly opposed to “typological thinking”: “populationist thinking” holds that there are no intrinsic “biological essences”, nor any property—or set of properties—that all, and only all, members of a population share.
For the populationist “all organisms and organic phenomena are composed of unique features and can be described in collectively only in statistical terms. Individuals, or any kind of biological entities, form populations of which we can determine the artihmetic mean and the statistics of variation. Averages are merely statistical abstractions. . . . For the typologist the type (eidos) is real and the variation is an illusion, while for the populationist the type (average is an abstraction and only the variation is real (Mayr, 1976; quoted in Hardimon, 2017: 20).
For example, “Caucasian” is a valid taxonomic category when discussing populationist races. One classified as “Caucasian” might have absolutely none of the genotypic or phenotypic markers associated with “Caucasian-ness”; that is, population thinking does not assume that any one genotype or phenotype is essential to any one population. Thus, there are no intrinsic properties that all members of a race—and only members of that race—share.
To conclude, contrary to the claims of Johnson and Terrel, race does exist and there are reasons why we should accept the existence of these population groups we call races. Johnson largely uses the old and tired continuum fallacy—the fallacy of the beard, whichever name you like—to attempt to argue that “race” does not exist. But he did not even state any conditions on what “population” entails; he just drew random, overlapping circles proclaiming “Ha! Where does X color end and Y color begin!!??” This type of thinking, though, is fallacious, as can be seen. It is completely possible to delinate races on the basis of visible physical features which correspond to geographic ancestry.
Articles like Johnson’s and Terrel’s are easy to come by: they just adopt a racial eliminativist stance on race (that it should be removed from our ontology entirely). They use fallacies like the continuum fallacy to show that since there is no clear ‘genetic line’ (see my article You Don’t Need Genes to Delineate Race) separating so-called races, therefore races do not exist (we must then take an eliminativist approach to race). I’m of the belief that the answer to the question “Does race exist?” will be—and only can be—answered by philosophers of race. We know that geographic variation exists—however small it may be. We know that we can distinguish continental populations on the basis of visible physical features. From there, it’s only a short bit of reasoning to reason, correctly, that race exists and is a biological reality (as the arguments in Spencer, 2014 and Hardimon, 2017 attest to).