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Cold Winter Theory, the Vitamin D Hypothesis and the Prediction of Novel Facts
2400 words
HBDers purport that as one moves further north from Africa that IQ raises as a function of how the population in question needed to survive. The explanation is that as our species migrated out of Africa, more “intelligence” was needed and this is what explains the current IQ disparities across the world: the ancestors of populations evolving in different areas with different demands then changed their “IQs” and this then is responsible for differential national development between nations. Cold winter theory (CWT) explains these disparities.
On the other hand is the vitamin D hypothesis (VDH). The VDH purports to explain why populations have light skin at northern latitudes. As the migration north out of Africa occurred, peoples needed to get progressively lighter in order to synthesize vitamin D. The observation here is that as light skin is selected for in locations where UVB is absent, seasonal or more variable whereas dark skin is selected for where UVB is stronger. So we have two hypotheses: but there is a problem. Only one of these hypotheses makes novel predictions. Predictions of novel predictions are what science truly is. A predicted fact is a novel fact for a hypothesis if it wasn’t used in the construction of the hypothesis (Musgrave, 1988). In this article, I will cover both the CWT and VDH, predictions of facts that each made (or didn’t make) and which can be called “science”.
Cold winter theory
The cold winter theory, formulated by Lynn and Rushton, purports to give an evolutionary explanation for differences in national IQs: certain populations evolved in areas with deathly cold winters in the north, while those who lived in tropical climes had, in comparison to those who evolved in the north, an “easier time to live”. Over time as populations adapted to their environments, differences in ‘intelligence’ (whatever that is) evolved due to the different demands of each environment, or so the HBDers say.
Put simply, the CWT states that IQ differences exist due to different evolutionary pressures. Since our species migrated into cold, novel environments, this was the selective pressure needed for higher levels of ‘intelligence’. On the other hand, humans who remained in Africa and other tropical locations did experience these novel, cold environments and so their ‘intelligence’ stayed at around the same level as it was 70,000 years ago. Many authors hold this theory, including Rushton (1997), Lynn (2006), Hart, (2007) Kanazawa (2008), Rushton and Templer (2012; see my thoughts on their hypothesis here) and Wade (2014). Lynn (2013) even spoke of a “widespreadonsensus” on the CWT, writing:
“There is widespread consensus on this thesis, e.g. Kanazawa (2008), Lynn (1991, 2006), and Templer and Arikawa (2006).”
So this “consensus” seems to be a group of his friends and his own publications. We can change this sentence to ““There is widespread consensus on this thesis, including two of my publications, a paper where the author assumes that the earth is flat: “First, Kanazawa’s (2008) computations of geographic distance used Pythagoras’ theorem and so the paper assumed that the earth is flat (Gelade, 2008).” (Wicherts et al, 2012) and another publication where the authors assume hot weather leads to lower intelligence. Oh yea, they’re all PF members. Weird.” That Lynn (2013) calls this “consensus” is a joke.
What caused higher levels of ‘intelligence’ in those that migrated out of Africa? Well, according to those who push the CWT, finding food and shelter. Kanazawa, Lynn, and Rushton all argue that finding food, making shelter and hunting animals were all harder in Eurasia than in Africa.
One explanation for high IQs of people who evolved recently in northern climes is their brain size. Lynn (2006: 139) cites data showing the average brain sizes of populations, along with the temperatures in that location:
Do note the anomaly with the Arctic peoples. To explain this away in an ad-hoc manner, Lynn (2006: 156-7) writes:
These severe winters would be expected to have acted as a strong selection for increased intelligence, but this evidently failed to occur because their IQ is only 91. The explanation for this must lie in the small numbers of the Arctic Peoples whose population at the end of the twentieth century was only approximately 56,000 as compared with approximately 1.4 billion East Asians.
This is completely ad-hoc. There is no independent verifier for the claim. That the Arcitic don’t have the highest IQs but experienced the harshest temperatures and therefore have the biggest brain size is a huge anomaly, which Lynn (2006) attempts to explain away by population size.
He does not explain why natural selection among Arctic peoples would result in larger brain sizes or enhanced visual memory yet the same evolutionary pressures associated with a cold environment would not also produce higher intelligence. Arctic peoples have clear physical adaptations to the cold, such as short, stocky bodies well-suited to conserving heat.
Furthermore, the argument that Lynn attempts is on the mutations/population size is special pleading—he is ignoring anomalies in his theory that don’t fit it. However, “evolution is not necessary for temperature and IQ to co-vary across geographic space” (Pesta and Poznanski, 2014).
If high ‘intelligence’ is supposedly an adaptation to cold temperatures, then what is the observation that disconfirms a byproduct hypothesis? On the other hand, if ‘intelligence’ is a byproduct, which observation would disconfirm an adaptationist hypothesis? No possible observation can confirm or disconfirm either hypothesis, therefore they are just-so stories. Since a byproduct explanation would explain the same phenomena since byproducts are also inherited, then just saying that ‘intelligence’ is a byproduct of, say, needing larger heads to dissipate heat (Lieberman, 2015). One can make any story they want to fit the data, but if there is no prediction of novel facts then how useful is the hypothesis if it explains the data it purports to explain and only the data it purports to explain?
It is indeed possible to argue that hotter climates need higher levels of intelligence than colder climates, which has been argued in the past (see Anderson, 1991; Graves, 2002; Sternberg, Grigorenko, and Kidd, 2005). Indeed, Sternberg, Grigorenko, and Kidd (2005: 50) write: “post hoc evolutionary arguments … can have the character of ad hoc “just so” stories designed to support, in retrospect, whatever point the author wishes to make about present-day people.” One can think up any “just-so” story to explain any data. But if the “just-so” story doesn’t make any risky predictions of novel facts, then it’s not science, but pseudoscience.
Vitamin D hypothesis
The VDH is simple: those populations that evolved in areas with seasonal, absent, or more variable levels of UVB have lighter skin than populations that evolved in areas with strong UVB levels year-round (Chaplan and Jablonksi, 2009: 458). Robins (2009) is a huge critic of the VDH, though her objections to the VDH have been answered (and will be discussed below).
The VDH is similar to the CWT in that it postulates that the adaptations in question only arose due to migrations out of our ancestral lands. We can see a very strong relationship between high UVB rays and dark skin and conversely with low UVB rays and light skin. Like with the CWT, the VDH has an anomaly and, coincidentally, the anomaly has to do with the same population involved in the CWT anomaly.
Arctic people have dark-ish skin for living in the climate that they do. But since they live in very cold climates then we have a strange anomaly here that needs explaining. We only need to look at the environment around them. They are surrounded by ice. Ice reflects UVB rays. UVB rays hit the skin. Arctic people consume a diet high in vitamin D (from fish). Therefore what explains Arctic skin color is UVB rays bouncing off the ice along with their high vitamin D diet. The sun’s rays are, actually, more dangerous in the snow than on the beach, with UVB rays being 2.5 more times dangerous in the snow than beach.
Evolution in different geographic locations over tens of thousands of years caused skin color differences. Thus, we can expect that, if peoples are out of the conditions where their ancestors evolved their skin color, that there would then be expected complications. For example, if human skin pigmentation is an adaptation to UV rays (Jablonski and Chaplan, 2010), we should expect that, when populations are removed from their ancestral lands and are in new locations with differing levels of UV rays, that there would be a subsequent uptick in diseases caused by vitamin D deficiencies.
This is what we find. We find significant differences in circulating serum vitamin D levels, and these circulating serum vitamin D levels then predict health outcomes in certain populations. This would only be true if sunlight influenced vitamin D production and that skin progressively gets lighter as one moves away from Africa and other tropical locations.
Skin pigmentation regulates vitamin D production (Neer, 1975). This is due to the fact that when UVB rays strike the skin, we synthesize vitamin D, and the lighter one’s skin is, the more vitamin D can be synthesized in areas with fewer UVB rays. (Also see Daraghmeh et al, 2016 for more evidence for the vitamin D hypothesis.)
P1) UV rays generate vitamin D in human skin
P2) Human populations that migrate to climates with less sunlight get fewer UV rays
P3) To produce more vitamin D, the skin needs to get progressively lighter
C) Therefore, what explains human skin variation is climate and UV rays linked to vitamin D production in the skin.
Novel predictions
Science is the generation of novel facts from risky predictions (Musgrave, 1988; Winther, 2009). And so, hypotheses that predict novel facts from risky predictions are scientific hypotheses, whereas those hypotheses that need to continuously backtrack and think up ad-hoc hypotheses are then pseudoscientific. Pseudoscience is simple enough to define. The Stanford Encyclopedia of Philosophy defines it as:
“A pretended or spurious science; a collection of related beliefs about the world mistakenly regarded as being based on scientific method or as having the status that scientific truths now have.”
All theories have a protective belt of ad hoc hypotheses. Theories become pseudoscientific when they fail to make new predictions and must take on more and more ad-hoc hypotheses that have no predictive value. If the ad-hoc hypotheses that are added to the main hypothesis have no predictive value then the new explanations for whichever hypothesis that is in danger of being falsified are just used to save the hypothesis from being refuted and it thus becomes pseudoscience.
In the case of CWT, it makes no prediction of novel facts; it only explains the data that it purports to explain. What is so great about the CWT if it makes no predictions of novel facts and only explains what it purports to explain? One may attempt to argue that it has made some ‘novel’ predictions but the ‘predictions’ that are proposed are not risky at all.
For example, Hart (2007: 417) makes a few “predictions”, but whether or not they’re “risky” or “novel” I’ll let you decide (I think they’re neither, of course). He writes that very few accomplishments will be made by Africans, or Australian or New Guinean Aborigines; members of those groups will not be highly represented in chess; and that major advances in scientific fields will come from those of European ancestry or the “Monglids”, Koreans, Chinese or Japanese.
On the other hand, Hart (2007: 417) makes two more “predictions”: he says that IQ data for Congoid Pygmies, Andaman Islanders, and Bantu-speaking people are few and far between and he believes that when enough IQ testing is undertaken there he expects IQ values between 60 and 85. Conversely, for the Lapps, Siberians, Eskimoes, Mongols and Tibetans, he predicts that IQ values should be between 85-105. He then states that if these “predictions” turn out to be wrong then he would have to admit that his hypothesis is wrong. But the thing is, he chose “predictions” that he knew would come to pass and therefore these are not novel, risky predictions but are predictions that Hart (2007) knows would come to pass.
What novel predictions has the VDH made? This is very simple. The convergent evolution of light skin was predicted in all hominids that trekked out of Africa and into colder lands. This occurred “because of the importance of maintaining the potential for producing pre-vitamin D3 in the skin under conditions of low annual UVB (Jablonski and Chaplin, 2000; Jablonski, 2004)” while these predictions “have been borne out by recent genetic studies, which have demonstrated that depigmented skin evolved independently by different molecular mechanisms multiple times in the history of the human lineage” (Chaplan and Jablonksi, 2009: 452). This was successfully predicted by Chaplan and Jablonski (2000).
The VDH still holds explanatory scope and predictive success; no other agent other than vitamin D can explain the observation that light skin is selected for in areas where there is low, absent or seasonal UVB. Conversely, in areas where there is a strong, year-round presence of UVB rays, dark skin is selected for.
Conclusion
Scientific hypotheses predict novel facts not known before the formulation of the hypothesis. The VDT has successfully predicted novel facts, whereas I am at a loss thinking of a novel fact that the CWT predicted.
In order to push an adaptationist hypothesis for CWT and ‘intelligence’, one must propose an observation that would confirm the adaptationist hypothesis while at the same time disconfirming the byproduct hypothesis. Since byproducts are inherited to, the byproduct hypothesis would predict the same things that an adaptationist hypothesis would. Thus, the CWT is a just-so story since no observation would confirm or disconfirm either hypothesis. On the other hand, the CWT doesn’t make predictions of novel facts, it makes “predictions” that are already known and would not undermine the hypothesis if disproved (but there would always be a proponent of the CWT waiting in the wings to propose an ad-hoc hypothesis in order to save the CWT, but I have already established that it isn’t science).
On the other hand, the VDT has successfully predicted that hominins that trekked out of Africa would have light skin which was then subsequently confirmed by genomic evidence. The fact that strong UVB rays year-round predict dark skin whereas seasonal, absent, or low levels of UVB predict light skin has been proved to be true. With the advent of genomic testing, it has been shown that hominids that migrated out of Africa did indeed have lighter skin. This is independent verification for the VDH; the VDH has predicted a novel fact whereas the CWT has not.
Race and Vitamin D Deficiency
1600 words
Vitamin D is an important “vitamin” (it is really a steroid hormone). It is produced when the skin (the largest organ in the body) is exposed to the sun’s UVB rays (Nair and Maseeh, 2012). So this is one of the only ways to get natural levels of UVB. We can then think that, if a population is outside of its natural evolutionary habitat (the habitat where that skin color evolved), then we should note numerous problems caused by the lack of vitamin D in whichever population is studied outside of a location that doesn’t get the correct amount of UVB rays from the sun.
Black Americans are more likely than other ethnies to be deficient in vitamin D (Harris, 2006; Cosman et al, 2007; Nair, 2012; Forest and Stuhldreher, 2014; Taksler et al, 2014). But, paradoxically, low vitamin D levels don’t cause weaker bones in black Americans (O’Conner et al, 2014). However, like with all hypotheses, there are naysayers. For example. Powe et al (2013) argue that vitamin D tests misdiagnose blacks, that blacks have a form of the vitamin that cells can use called 25-hydroxyvitamin D. They conclude: “Community-dwelling black Americans, as compared with whites, had low levels of total 25-hydroxyvitamin D and vitamin D–binding protein, resulting in similar concentrations of estimated bioavailable 25-hydroxyvitamin D. Racial differences in the prevalence of common genetic polymorphisms provide a likely explanation for this observation.” Though there are a whole host of problems here.
The limitations of Powe et al (2013) striking: it was cross-sectional and observational (like most nutrition studies) so they were unable to predict effects of vitamin-D binding protein on bone fractures; no data on the consumption of vitamin D supplements; measurement of bone turnover markers, urinary calcium excretion and levels of 1,25-dihydroxyvitamin D may explain the effect of VDBP (vitamin D-binding protein) on mineral metabolism; and they relied on a calculation, rather than a measurement of 25-hydroxyvitamin D levels.
Powe et al’s (2013) findings, though, have been disputed. Using different measurement tools from Powe et al (2013), Henderson et al (2015) conclude that “Counter to prior observations by immunoassay, VDBG concentrations did not vary by race.” While Bouillon (2014) writes: In our view, black Americans, as compared with white Americans, have lower levels of not only total 25-hydroxyvitamin D but also free or bioavailable 25-hydroxyvitamin D.” And finally, Hollis and Bikle (2014) write: “Specifically, for any given physically measured level of bio-available 25-hydroxyvitamin D, the authors are overestimating bio-available 25-hydroxyvitamin D by 2 to 2.5 times owing to underestimation of vitamin D–binding protein in blacks.”
Either way, even if what Powe et al (2013) conclude is true, that would not mean that black Americans should not supplement with vitamin D, since many diseases and health problems are associated with low vitamin D intake in blacks, including osteoporosis, cardiovascular disease, cancer, diabetes, and other serious conditions (Harris, 2006). An indirect relationship between low levels of vitamin D and hypertension is also noted (Mehta and Agarwal, 2017). Since there is an indirect relationship between vitamin D levels and hypertension, then we should keep an eye on this because black Americans have some of the highest levels of hypertension in the world (Ferdinand and Armani, 2007; see also Fuchs, 2011).
Vitamin D is, of course, important for skeletal and nonskeletal health (Kennel et al, 2010). So if vitamin D is important for skeletal and nonskeletal health, we should see more diseases in black Americans that imply a lack of this steroid in the body. Although blacks have stronger bones even when deficient in vitamin D, it is still observed that black children who break their forearms have less vitamin D circulating in their blood (Ryan et al, 2011). This observation is borne out by the data, since black children are more likely to be deficient in vitamin D compared to other ethnies (Moore, Murphy, and Hollick, 2005). Since black skin predicts vitamin D deficiency (Thomas and Demay, 2000), it seems logical to give vitamin D supplements to children, especially black children, on the basis that it would help lower incidences of bone fractures, even though blacks have stronger bones than whites.
Furthermore, physiologically “normal” levels of vitamin D differ in blacks compared to whites (Wright et al, 2012). They showed that it is indeed a strong possibility that both whites and blacks have different levels of optimum vitamin D. Wright et al (2012) showed that there is a relationship between 25(OH)D levels and intact parathyroid hormone (iPth); for blacks, the threshold in which there was no change was 20 ng/ml whereas for whites it was 30 ng/ml which suggests that there are different levels of optimal vitamin D for each race, and the cause is due to skin color. Thus, physiologically “normal” levels of vitamin D differ for blacks and whites.
There is also a high prevalence of vitamin D deficiency/insufficiency and asthma in black inner-city youth in Washington DC (Freishtat et al, 2010). We can clearly see that, even though black Americans have stronger bones than white Americans and vitamin D predicts bone strength, the fact that blacks have stronger bones than whites even while being deficient in vitamin D on average does not mean that black Americans should not supplement with vitamin D, since it would ameliorate many other problems they have that are related to vitamin D deficiency.
There are also racial differences in prostate cancer (PCa) acquisition too, and vitamin D deficiency may also explain this disparity (Khan and Partin, 2004; Bhardwaj et al, 2017). I have heavily criticized the explanations that testosterone influences PCa, while having indicated that environmental factors such as diet and vitamin D deficiency may explain a large amount of the gap (Batai et al, 2017; but see Stranaland et al, 2017 for a contrary view). Since low vitamin D is related to prostate cancer, by supplementing with vitamin D, it is possible that levels of PCa may decrease. Kristal et al (2014) show that both high and low levels of vitamin D are associated with PCa.
Evidence also exists that vitamin D levels and hypertension are related. Rostand (2010) proposes a unified hypothesis: an important role exists in vitamin D deficiency and the pathogenesis and maintenance of hypertension in blacks (Rostand, 2010).
(From Rostand, 2010)
Since black Americans are no longer near the equator, their ability to synthesize vitamin D from UVB rays is diminished. This then probably leads the RAS (renin-angiotensin system) and inflammatory cytokine activation which then leads to vascular endothelial dysfunction along with structural changes to the microvasculature, which have been linked to vascular (arterial) stiffness along with increased vascular resistance, and these changes are shown to precede hypertension, which also occurs early in life. So since blacks are deficient in vitamin D, which even starts in the womb (Bodnar et al, 2007; Dawodu and Wagner, 2007; Lee et al, 2007; Khalessi et al, 2015; Seto et al, 2016), and this vitamin D deficiency most likely produces changes in large and small arteries and arterials, this could be the explanation for higher hypertension in black Americans (Rostand, 2010: 1701).
This would be a large environmental mismatch: since the population is displaced from its ancestral homeland, then this causes problems since it is not the environment where their ancestors evolved. So in this case, since black Americans are concentrated in the southeast corner of the United States, this may explain the high rates of vitamin D deficiency and hypertension in the black American community.
People whose ancestors evolved in locations with fewer UVB rays have lighter skin, whereas people whose ancestors evolved in locations with more UVB rays have darker skin. Thus, by placing populations in their opposite evolutionary environment, we can see how and why deleterious effects would occur in the population that is in the mismatched environment. For whites, skin cancer would occur, whereas for blacks, higher rates of hypertension and low birth weights occur.
Looking at levels of vitamin D deficiency in races is a great way to understand the evolution of certain populations. Because if the vitamin D hypothesis is correct, if skin color is an adaptation to UVB rays, with light skin being an adaptation to low UVB while dark skin is an adaptation to high UVB, then we can safely hypothesize about certain problems that would arise in races that are outside of their natural habitats. We have confirmed these hypotheses—black Americans who are outside of the location that their ancestors evolved in are more likely to have deleterious symptoms, and the symptoms are due to differences in vitamin D production, which come down to differences in skin color and how the skin synthesizes vitamin D in low-light environments.
Even though blacks have stronger bones than whites, this does not mean that they do not experience fractures at a high rate—especially children—and since the association was noticed, then by supplementing with vitamin D, this may lower the disparity of these types of injuries.
Since black Americans, compared to their evolutionary history, live in low-light environments, this then explains the how and why of vitamin D deficiency and why blacks need to supplement with vitamin D; no matter if certain studies show that blacks are ‘healthy’ even though they have low levels of vitamin D. If true (which I strongly doubt), that does not mean that black Americans should not supplement with vitamin D, because numerous other maladies are associated with vitamin D intake. This is one aspect where understanding the evolution of our species and the different races in it would lead to better medical care for individuals and ancestral groups that may need special treatment.
It is clear that race and geography should inform vitamin D intake, for if we do this, many diseases that arise can be ameliorated and quality of life can increase for everyone.
Nutrition and Antisocial Behavior
2150 words
What is the relationship between nutrition and antisocial behavior? Does not consuming adequate amounts of vitamins and minerals lead to an increased risk for antisocial behavior? If it does, then lower class people will have commit crimes at a higher rate, and part of the problem may indeed be dietary. Though, what kind of data is there that lends credence to the idea? It is well-known that malnutrition leads to antisocial behavior, but what kind of effect does it have on the populace as a whole?
About 85 percent of Americans lack essential vitamins and minerals. Though, when most people think of the word ‘malnutrition’ and the imagery it brings along with it, they assume that someone in a third-world country is being talked about, say a rail-thin kid somewhere in Africa who is extremely malnourished due to lack of kcal and vitamins and minerals. However, just because one lives in a first-world country and has access to kcal to where they’re “not hungry” doesn’t mean that vitamin and mineral deficiencies do not exist in these countries. This is known as “hidden hunger” when people can get enough kcal for their daily energy needs but what they are eating is lower-quality food, and thus, they become vitamin and nutrient deficient. What kind of effects does this have?
Infants are most at risk, more than half of American babies are at-risk for malnutrition; malnutrition in the postnatal years can lead to antisocial behavior and a lower ‘IQ’ (Galler and Ramsey, 1989; Liu et al, 2003; Galler et al, 2011, 2012a, 2012b; Gesch, 2013; Kuratko et al, 2013; Raine et al, 2015; Thompson et al, 2017). Clearly, not getting pertinent vitamins and minerals at critical times of development for infants leads to antisocial behavior in the future. These cases, though, can be prevented with a good diet. But the preventative measures that can prevent some of this behavior has been demonized for the past 50 or so years.
Poor nutrition leads to the development of childhood behavior problems. As seen in rat studies, for example, lack of dietary protein leads to aggressive behavior while rats who are protein-deficient in the womb show altered locomotor activity. The same is also seen with vitamins and minerals; monkeys and rats who were fed a diet low in tryptophan were reported to be more aggressive whereas those that were fed high amounts of tryptophan were calmer. Since tryptophan is one of the building blocks of serotonin and serotonin regulates mood, we can logically state that diets low in tryptophan may lead to higher levels of aggressive behavior. The role of omega 3 fatty acids are mixed, with omega 3 supplementation showing a difference for girls, but not boys (see Itomura et al, 2005). So, animal and human correlational studies and human intervention studies lend credence to the hypothesis that malnutrition in the womb and after birth leads to antisocial behavior (Liu and Raine, 2004).
We also have data from one randomized, placebo-controlled trial showing the effect of diet and nutrition on antisocial behavior (Gesch et al, 2002). They state that since there is evidence that offenders’ diets are lacking in pertinent vitamins and minerals, they should test whether or not the introduction of physiologically adequate vitamins, minerals and essential fatty acids (EFAs) would have an effect on the behavior of the inmates. They undertook an experimental, double-blind, placebo-controlled randomized trial on 231 adult prisoners and then compared their write-ups before and after nutritional intervention. The vitamin/mineral supplement contained 44 mg of DHA (omega 3 fatty acid docosahexaenoic acid; plays a key role in enhancing brain structure and function, stimulating neurite outgrowth), 80 mg of EPA (eicosapentaenoic acid; n3), and 1.26 g of ALA (alpha-linolenic acid), 1260mg of LA (linolic acid), and 160mg of GLA (gamma-Linolenic acid, n6) and a vegetable oil placebo. (Also see Hibbeln and Gow, 2015 for more information on n3 and nutrient deficits in childhood behavior disorders and neurodevelopment.)
Raine (2014: 218-219) writes:
We can also link micronutrients to specific brain structures involved in violence. The amygdala and hippocampus, which are impaired in offenders, are packed with zinc-containing neurons. Zinc deficiency in humans during pregnancy can in turn impair DNA, RNA, and protein synthesis during brain development—the building blocks of brain chemistry—and may result in very early brain abnormalities. Zinc also plays a role in building up fatty acids, which, as we have seen, are crucial for brain structure and function.
Gesch et al (2002) found pretty interesting results: those who were given the capsules with vitamins, minerals, and EFAs had 26.3 percent fewer offenses than those who got the placebo. Further, when compared with the baseline, when taking the supplement for two weeks, there was an average 35.1 percent reduction in offenses compared to the placebo group who showed little change. Gesch et al (2002) conclude:
Antisocial behaviour in prisons, including violence, are reduced by prisons, are reduced by vitamins, minerals and essential fatty acids with similar implications for those eating poor diets in the community.
Of course one could argue that these results would not transfer over to the general population, but to a critique like this, the observed effect of behavior is physiological; so by supplementing the prisoners’ diets giving them pertinent vitamins, minerals and EFAs, violence and antisocial behavior decreased, which shows some level of causation between nutrition/nutrient/fatty acid deprivation and antisocial behavior and violent activity.
Gesch et al (2002) found that some prisoners did not know how to construct a healthy diet nor did they know what vitamins were. So, naturally, since some prisoners didn’t know how to construct diets with an adequate amount of EFAs, vitamins and minerals, they were malnourished, though they consumed an adequate amount of calories. The intervention showed that EFA, vitamin and mineral deficiency has a causal effect on decreasing antisocial and violent behavior in those deficient. So giving them physiological doses lowered antisocial behavior, and since it was an RCT, social and ethnic factors on behavior were avoided.
Of course (and this shouldn’t need to be said), I am not making the claim that differences in nutrition explain all variance in antisocial and violent behavior. The fact of the matter is, this is causal evidence that lack of vitamin, mineral and EFA consumption has some causal effect on antisocial behavior and violent tendencies.
Schoenthaler et al (1996) also showed how correcting low values of vitamins and minerals in those deficient led to a reduction in violence among juvenile delinquents. Though it has a small n, the results are promising. (Also see Zaalberg et al, 2010.) These simple studies show how easy it is to lower antisocial and violent behavior: those deficient in nutrients just need to take some vitamins and eat higher-quality food and there should be a reduction in antisocial and violent behavior.
Liu, Zhao, and Reyes (2015) propose “a conceptual framework whereby epigenetic modifications (e.g., DNA methylation) mediate the link between micro- and macro-nutrient deficiency early in life and brain dysfunction (e.g., structural aberration, neurotransmitter perturbation), which has been linked to development of behavior problems later on in life.” Their model is as follows: macro- and micro-nutrient deficiencies are risk-factors for psychopathologies since they can lead to changes in the epigenetic regulation of the genome (along with other environmental variables such as lead consumption, which causes abnormal behavior and also epigenetic changes which can be passed through the generations; Senut et al, 2012; Sen et al, 2015) which then leads to impaired brain development, which then leads to externalizing behavior, internalizing behavior and autism and schizophrenia (two disorders which are also affected by the microbiome; Strati et al, 2017; Dickerson, 2017).
Clearly, since the food we eat gives us access to certain fatty acids that cannot be produced de novo in the brain or body, good nutrition is needed for a developing brain and if certain pertinent vitamins, minerals or fatty acids are missing, negative outcomes could occur for said individual in the future due to lack of brain development from being nutrient, vitamin, and mineral deficient in childhood. Further, interactions between nutrient deficiencies and exposure to toxic chemicals may be a cause of a large amount of antisocial behavior (Walsh et al, 1997; Hubbs-Tait et al, 2005; Firth et al, 2017).
Looking for a cause for this interaction between metal consumption and nutrient deficiencies, Liu, Zhao, and Reyes (2015) state that since protein and fatty acids are essential to brain growth, lack of consumption of pertinent micro- and macro-nutrients along with consumption of high amounts of protein both in and out of the womb contribute to lack of brain growth and, at adulthood, explains part of the difference in antisocial behavior. What you can further see from the above studies is that metals consumed by an individual can interact with the nutrient deficiencies in said individual and cause more deleterious outcomes, since, for example, lead is a nutrient antagonist—that is, it inhibits the physiologic actions of whatever bioavailable nutrients are available to the body for us.
Good nutrition is, of course, imperative since it gives our bodies what it needs to grow and develop as we grow in the womb, as adolescents and even into old age. So, therefore, developing people who are nutrient deficient will have worse behavioral outcomes. Further, lower class people are more likely to be nutrient deficient and consume lower quality diets than higher, more affluent classes, though it’s hard to discover which way the causation goes (Darmon and Drewnowski, 2008). Of course, the logical conclusion is that being deficient in vitamins, minerals and EFAs causes changes to the epigenome and retards brain development, therefore this has a partly causal effect on future antisocial, violent and criminal behavior. So, some of the crime difference between classes can be attributed to differences in nutrition/toxic metal exposure that induces epigenetic changes that change the structure of the brain and doesn’t allow full brain development due to lack of vitamins, minerals, and EFAs.
There seems to be a causal effect on criminal, violent and antisocial behavior regarding nutrient deficiencies in both juveniles and adults (which starts in the womb and continues into adolescence and adulthood). However, it has been shown in a few randomized controlled trials that nutritional interventions decrease some antisocial behavior, with the effect being strongest for those individuals who showed worse nutrient deficiencies.
If the relationship between nutrition/interaction between nutrient deficiencies and toxins can be replicated successfully then this leads us to one major question: Are we, as a society, in part, causing some of the differences in crime due to how our society is regarding nutrition and the types of food that are advertised to our youth? Are people’s diets which lead to nutrient deficiencies a driving factor in causing crime? The evidence so far on nutrition and its effects on the epigenome and its effects on the growth of the brain in the womb and adolescence requires us to take a serious look at this relationship. That lower class people are exposed to more neurotoxins such as lead (Bellinger, 2008) and are more likely to be nutrient deficient (Darmon and Drewnowski, 2008; Hackman, Farrah, and Meaney, 2011) then if they were educated on which foods to eat to avoid nutrient deficiencies along with avoiding neurotoxins such as lead (which exacerbate nutrient deficiencies and cause crime), then a reduction in crime should occur.
Nutrition is important for all living beings; and as can be seen, those who are deficient in certain nutrients and have less access to good, whole, nutritious food (who also have an increased risk for exposure to neurotoxins) can lead to negative outcomes. These things can be prevented, it seems, with a few vitamins/minerals/EFA consumption. The effects of sleep, poor diet (which also lead to metabolic syndromes) can also exacerbate this relationship, between individuals and ethnicities. The relationship between violence and antisocial behavior and nutrient deficiencies/the interaction with nutrient deficiencies and neurotoxins is a great avenue for future research to reduce violent crime in our society. Lower class people, of course, should be the targets of such interventions since there seems to be a causal effect—-however small or large—on behavior, both violent and nonviolent—and so nutrition interventions should close some of the crime gaps between classes.
Conclusion
The logic is very simple: nutrition affects mood (Rao et al, 2008; Jacka, 2017) which is, in part, driven by the microbiome’s intimate relationship with the brain (Clapp et al, 2017; Singh et al, 2017); nutrition also affects the epigenome and the growth and structure of the brain if vitamin and mineral needs are not met by the growing body. This then leads to differences in gene expression due to the foods consumed, the microbiome (which also influences the epigenome) further leads to differences in gene expression and behavior since the two are intimately linked as well. Thus, the aetiology of certain behaviors may come down to nutrient deficiencies and complex interactions between the environment, neurotoxins, nutrient deficiencies and genetic factors. Clearly, we can prevent this with preventative nutritional education, and since lower class people are more likely to suffer the most from these problems, the measures targeted to them, if followed through, will lower incidences of crime and antisocial/violent behavior.
“Latinos”, Brazilians, Mixed-Race Individuals and Race Concepts
2050 words
How do “Latinos”, Brazilians, and mixed-race individuals fit into Hardimon’s (2017) differing race concepts (racialist, minimalist, populationist, and socialrace)? It’s easier explaining how “Latinos” fit into this, but mixed-race individuals are a bit trickier (for instance, the minimalist concept of race does not say anything about it and is therefore vague in that respect). This article will discuss these two populations and see where they fit into these categories.
Mixed-race individuals
Mixed-race individuals are tricky to place in these conceptions of race that Hardimon (2017) lays out and defends. For example, minimalist race itself is vague; it does not say which populations/individuals with populational characteristics would be placed, the argument just establishes the biological reality and significance of race. The concept of the “one drop rule” (was a legal) is a social standard in that anyone with “one drop” of “black blood” was deemed black (which, it seems, did well for so-called conceptions of “racial purity” since most white Americans have low amounts of black ancestry; Bryc et al, 2015).
The one drop rule was an attempt to limit racial miscegenation (racial mixing), and it seems to have, for the most part, worked since many white Americans have low to no African ancestry (since 95 percent of white Americans have no African ancestry; Bryc et al, 2015).
Though, as Hardimon (2017: 49) writes, the fact that individuals must have a race is a holdover from the racialist concept; minimalist race, as I’ve covered, is not defined by the features of an individual but is defined by the features of the group said individual belongs to. It is defined in terms of group—not individual—characteristics. So just because individual I doesn’t look like their R but instead looks like an R2, for example, doesn’t make individual I an R2; individual I is still an R even though they look like an R2 since the concept is based on shared group characteristics.
Hardimon doesn’t really discuss mixed-race individuals in his book; there’s only really one note on the subject (and it’s about social race, pg. 209, note 54):
People who are members of more than one socialrace in a socialrace regime that does not recognize mixed race as a racial position will be in the anomalous situation of not having an established socialrace position in society. Having such a position is one way of being a “normal” member of society organized around the institution of socialrace. Not to have such a position is to have no place in the social world along the dimension of socialrace. Hence, perhaps, the pathos of mixed-race individuals seeking social recognition for their distinctive mixed race identity.
Though, in certain (racialist/socialrace) societies, a mixed-race individual would become what the “lower” race is in that society. For instance, if an individual were half white and half black—like the former President of the United States Barack Obama—he would be designated as “black”, as we all know (since he’s the first black President of the United States). This is known as the concept of “hypodescent” and has its basis in Hardimon’s socialrace concept since racial status of the offspring is designated to the parent who has lower “standing” than the majority in said country. So, therefore, the concept of hypodescent is the concept of socialrace in action.
Mixed-race individuals are seen as members of their “lower-status parent group“, which shows how racial constructivism is alive today. One is designated the lower-status of their parent in a hierarchical manner—one way in which the socialrace concept borrows from the racialist race concept in that it is hierarchical.
The researchers found, for example, that one-quarter-Asian individuals are consistently considered more white than one-quarter-black individuals, despite the fact that African Americans and European Americans share a substantial degree of genetic heritage. One Drop Rule Persists—Harvard
Brazil
How does this work in Brazil? Surely this makes problems for racial concepts, right?
Brazilians don’t use the term “race” (raca), but the term “color” (cor). “The reason the word Color (capitalized to call attention to this particular meaning) is preferred to race in Brazil is probably because it captures the continuous aspects of phenotypes” (Parra et al, 2003). Clearly, the conception of “race” (raca) in Brazil comes down to what “color” (cor) one is; and so we should state that Brazilian society is stratified into “colors” and not true “races”. The 1872 Brazilian census created four “color” groups “white, caboclo, black and brown (branco, caboclo (mixed indigenous-European), negro and pardo). These groups were always defined by the same formula: Colour group = members of a pure race + phenotypes of this race in the process of reversion (Guimaraes 1999)” (Guimaraes, 2012: 1157).
Though, distinct from Hardimon (2017), Guimaraes (2012: 1160) argues that the Brazilian color system is, in fact, a racial system:
What makes colour in Brazil a racial term is precisely the fact that the physiognomic traits used by racialists to distinguish different human races became convoluted with the original European system of classification based on shades of skin colour.
Hardimon (2017: 49) writes:
On the other hand, it is not clear that the Brazilian concept of COR is altogether independent of the phenomenon we Americans designate using ‘race.’ The color that ‘COR’ picks out is racial skin color. The well-known, widespread preference for lighter (whiter) skin in Brazil is at least arguably a racial preference. It seems likely that white skin color is preferred because of its association with the white race. This provides a reason for thinking that the minimalist concept of race may be lurking in the background of Brazilian thinking about race.
Someone who is “white” (identifies as white) in Brazil will (most likely) not be white in America; this is due to their differing classification system based on color, which is loosely tied with the minimalist concept, but is distinct from it in that it’s just based largely on the color of one’s skin (one of many requisites for minimalist racehood).
The role of race and color in regard to Brazilian society is complex, biologically, sociologically, and psychologically; but it’s clear that some concept of what we could call a “classical” race concept—however crude—could be said to be in use in Brazil today.
Latinos/Hispanics
The US Census Bureau states that “People who identify their origin as Hispanic, Latino, or Spanish may be of any race.” This is true; just because one derives from a Latin American country does not mean that they are some kind of “Latino” or “Hispanic” race.
Take, as an example, the case of Alberto Fujimori. Alberto Fujimori is the son of Japanese immigrants to Peru, and he eventually ended up becoming the President of Peru. His parents emigrated to Peru and he was born in Lima. Now here’s where things get tricky: is he all of a sudden some new type of “race” called “Hispanic” or “Latino”, all because he was born across the ocean? Is Pope Francis all of a sudden not Italian by ancestry since he was born in Argentina? Are people who are born in Argentina, Chile, and Paraguay with direct ancestry to Germany and Italy all of a sudden no longer German or Italian but some new “Hispanic” or “Latino” race? No! Just because you’re born not in your ancestral home does not mean you “become” whatever society designates that part of the world (in this case “Latin America”). Their race does not change on the basis of where they are born; their individual ancestries can still be traced back to their countries of origin, therefore attempting to “racialize” the terms “Hispanic” or “Latino” do not make any sense.
“Hispanics” do not—and cannot—count as a minimalist race on the basis of one condition: they do not share a single pattern of visible physical features. No one pattern of hair, skin color, lip shape, eye shape etc. They do not share a single geographic origin; they have a mixture of Ancestry from Africa, Europe, and Asia. “Hispanics” can be seen, obviously, as a mixture of minimalist races. “Hispanics” are denied minimalist racehood since they do not exhibit characteristics of minimalist races, which is even echoed, as shown above, by the US Census Bureau.
Hardimon (2017: 39) writes:
To deny that Latinos constitute a race is not to deny that individual Latinos or Latinos as a group can be the targets of racism (for example, owing to skin color). Nor is it to deny that Latinos are often regarded as “racially other” (as differing in some essential humanly important way corresponding to skin color) by members of other racialized groups (for example, Anglos). … Nor is it to deny that they constitute a socialrace in my sense of the term. Still less does it imply that Latinos ought not to aspire to a degree of solidarity connoted by the Spanish word raza.
So “Latinos” can be designated as a socialrace (though socialraces do not always have a mirrored minimalist race), but not as a minimalist race since they do not fit the criteria for minimalist racehood. Many “Latinos” can be said to be mestizos, which are half European (normally of Spanish descent) and half Indian. Still, further, they can be castizos, about three-quarters European and one-quarter Indian. Then you have the “Latino” Carribean countries (Dominican Republic, Cuba, Puerto Rico) with differing amounts of admixture from all over, from different minimalist races. Though, in America, most Dominicans would be counted as “black” under the concept of “hypodescent”—the one drop rule. Many Cubans can be seen to have majority Spanish ancestry, and its the same for Puerto Ricans.
“Latinos/Hispanics” do not constitute a major race (in the minimalist and populationist sense) because they are a mixture of different minimalist races. This does not mean, however, that one designated as “Latino” in America does not have full ancestry to a European country; this is how the concept of “Latino” in America uses the concept of socialrace—it’s only based on the perceived race of the individual (that they derive from a “Latino” country) and that therefore makes them “Latino”, all the while ignoring their actual racial ancestry.
There is even a phrase in Latin America “Mejorar la raza” or “improve the race” by having children with lighter-skinned people since light skin is seen as beautiful in Latin America. They want to better “their race” (even though they—as “Latinos”—don’t have a race), and so they will attempt to have children with lighter and lighter people (i.e., people who have more and more European ancestry) to “improve their race” (i.e., their socialrace) since European features are seen as more beautiful in Latin America.
Most of the ruling class in Latin America is of European descent, while the lower classes are of admixed/unadmixed Indians (coming from differing tribes). This, one can say, is one way that socialrace is used in Latin America.
Conclusion
Brazilians and “Latinos/Hispanics” clearly could have been grouped in the mixed-race category, but each of these subjects has distinct concepts it needed to discuss. The Brazilian concept of “cor” and “raca” are loosely intertwined; they can be said to use aspects of mimimalist races. On the other hand, “Latinos/Hispanics” are not designated minimalist racehood on the basis that they do not share a single pattern of physical features, nor do they share a geographic origin, since the groups that make up “Latinos” (which are minimalist races) are the geographic locations in question. “Latinos/Hispanics” are not minimalist races because they do not exhibit the features of minimalist races.
Mixed-race individuals, regarding the socialrace concept, can be seen to be the “lower” of the races they are admixed with on the social ladder—which is how it is in America (the concept of hypodescent). The existence of mixed-race individuals does not invalidate the concept of race; minimalist racehood is not defined on the basis of individual characters, but on the basis of the characters of the group. Therefore this does not go against the concept of minimalist race.
The concepts of race can definitely survive these anomalies when describing the biological realities of race; some of them can be said to be socialraces for one respect, whereas in reality, they are mixtures of minimalist races. Races exist and the existence of Brazilians (even with their own categorization of races/colors) and “Latinos/Hispanics” and other mixed-race groups/individuals do not rail against any concepts that purport to argue for the existence and biological reality of race.
A Simple Argument for the Existence of Race
1550 words
Race deniers say that there is too small of a genetic distance between races to call the so-called races “races”. They latch on to Lewontin’s 1974 analysis, trumpeting that genetic distance is too small for there to be true “races”. There is, however, a simple way to bypass the useless discussions that would ensue if one cites genetic evidence for the existence of race: just use this simple argument:
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
This argument is simple; anyone who denies this needs to provide a good enough counter-argument, and I’m not aware of any that exist to counter the argument.
P1 shows that there are patterns of visible physical features which correspond to geographic ancestry. This is due to the climates said race evolved in over evolutionary history. Since these phenotypes are not randomly distributed across the globe, but show distinct patterning based on geographic ancestry, we can say that P1 is true; different populations show patterns of different physical features which are not randomly distributed across the globe. Further, since P1 establishes that races are populations that look different from each other, it guarantees that groups like the Amish, social classes etc are not counted as races. P1 further allows a member of a given race to not show the normative physical characters that are characteristic of that race. It further allows for the possibility that individuals from two different races may not differ in their physical characters. These visible physical characters that differ by populations we then call races also need to be heritable to be biological. “Because the visible physical features of race are heritable, the skin color, hair type, and eye shape of children of Rs tend to resemble the skin color, hair type, and eye shape of their parents” (Hardimon, 2017: 35). P1 is true.
P2 shows that these patterns of visible physical features are exhibited between real, existing groups. That is, the groups that exhibit these patterns exist in reality. No one denies this either. Differences in physical features that these real, existing groups exhibit can then be used as proxies for factors in P1. Though, like with which populations figure into this concept, the minimalist race concept doesn’t say—it only establishes the biological existence of races. “In recent years the concept of the continent has come under fire for not being well defined. 59 It is of interest that the formation of the concepts CONTINENT and RACE are roughly coeval. One wonders if the geneses of the two ideas are mutually entwined. Could it be that our idea of continent derives in part from the idea of the habitat of a racial group? Could it be that the idea of a racial group gets part of its content from the idea of a group whose aboriginal home is a distinctive continent? Perhaps the concepts should be thought of as having formed in tandem, each helping to fix the other’s reference” (Hardimon, 2017: 51). Since these real, existing populations that were geographically separated for thousands of years show these visible physical patterns, P2 is true.
P3 follows from the specification of the concept of minimalist race. If these populations that exhibit these distinct visible characters and if they are non-randomly distributed across the globe then this satisfied the argument for the concept of minimalist race. The specification of the minimalist concept of race states that groups satisfy the requisites for the concept by being distinguishable by patterns of visible physical features (P1) and that individuals who share a common ancestry peculiar to them which derive from a distinct geographic location (P2) exist as real groups. Since P1 and P2 are true, P3 follows logically from P1 and P2, which then leads us to the conclusion which is true and establishes the argument for the minimalist concept of race as a sound and valid argument.
C is then the logical conclusion of the three premises: race exists and is a biological reality since the patterns of visible physical features are non-randomly distributed across the globe and are exhibited by real, existing groups. Since all three premises are true and the conclusion is true, it is a valid argument; since the premises are true the argument is sound. No one can—logically—deny the existence of race when presented with this logical proof.
Though notice the argument doesn’t identify which populations are designated as “races” (that’s for another article), the argument just establishes that race exists and it exists as a biological reality. Notice also how this conception of race is sort of like the “racialist concept”, but it takes it down to its barest bones—only taking the normatively important, superficial biological physical features (these features establish minimalist races as biologically existing).
Notice, too, that I did not appeal to any genetic differences between the races, indeed, in my opinion, they are not needed when discussing race. All that is needed when discussing race and whether or not it is a biological reality is asking three simple questions:
1) Are there differences in patterns of visible physical features that correspond to geographic ancestry? Yes.
2) Are these patterns exhibited by real, existing groups? Yes.
3) Do these real, existing groups satisfy conditions of minimalist race? Yes
Therefore race exists.
These three simple questions (just take the premises and ask them as questions) will have one—knowingly or not—admit to the biological reality and existence of race.
Do note, though, nothing in this argument brings up anything about what we “can’t see”, meaning things like “intelligence” or mores of these races. This concept is distinct from the racialist concept in that it does not mention normatively important characters; it does not posit a relationship between visible physical characters and normatively important characters; and it does not “rank” populations on some type of scale. “Also, the conjoint fact that a group is characterized by a distinctive pattern of visible physical characteristics and consists of members who are linked by a common ancestry and originates from a distinctive geographic location is of no intrinsic normative significance. The status of being a minimalist race has no intrinsic normative significance“ (Hardimon, 2017: 32).
Clearly, one does not need to invoke genetic differences to show that race exists as a biological reality. That races differ in patterns of visible physical features which are inherited from the parents and are heritable establishes the biological reality of minimalist race. I really see no way that one could, logically, deny the existence of race given the argument provided in this article. Race exists and is a biological reality and the argument for the existence of minimalist race establishes this fact. Races differ in physiognomy and morphology; these physical differences are non-randomly distributed by geographic ancestry/at the continental level. These populations that show these physical differences share a peculiar ancestry. Knowing these facts, we can safely infer the existence of race. It is the only logical conclusion to come to. Note that the minimalist concept is deflationist—meaning that racialist races do not exist and that this concept enjoys what the racialist concept was supposed to, it is deflationary in the aspect that it takes the normative physical differences from the racialist concept. It is realist since it acknowledges the existence of minimalist race as genetically grounded and relatively superficial but still very significant biological reality of race.
Races can exist as minimalist races and socialraces—no contradiction exists. minimalist race, and its “scientific” companion populationist race (which I will cover in the future) show that there is a well-formulated argument for the existence of race (minimalist race concept) whereas the other concept shows how it is grounded in science and partitions populations to races (populationist concept; both are deflationary). (Read the descriptions of racialist race, minimalist race, populationist race, and socialrace.) You don’t need genes to delineate race; you only need a sound, valid argument based on biological principles. Minimalist races exist.
Race exists and is a biological reality, even if it is ‘socially constructed’ (what isn’t?), our social constructs still correspond to differing breeding populations who share peculiar ancestry and show patterns of visible physical features establish the existence of race.
From Hardimon (2017: 177)
(I also came across a book review from philosopher Joshua Glasgow (Book Review Rethinking Race: The Case for Deflationary Realism, by Michael O. Hardimon. Harvard University Press, 2017. Pp. 240.), author of A Theory of Race (2009) who has some pretty good critiques against Hardimon’s theses in his book, but not good enough. I am going to cover a bit more about these concepts then discuss his article. I will also cover “Latinos” and mixed race people as regards these concepts as well.)
4/19/2018 edit: Two more simple arguments:
(Where P is population, C is continent and T is trait(s)
Population P that evolved in continent C have physical traits T which correspond to C.
Afrocentric Melanist Theorists
2650 words
Extremists exist in every ideology (there are too many to name but take the books March of the Titans (Kemp, 1999) to Testosterone Rex (Fine, 2017) as examples), but some are (in my opinion) more extreme (and funnier and more delusional) than others (even if they’re almost neck and neck). Afrocentrists veer toward the extreme side (as Nordicists veer to the extreme side on the opposite end). But certain beliefs these ideologies have may “sound right” to the uneducated ear, especially when they begin to weave fantastical stories with physiological terminology in order to woo the listener. You see things like “Melanin affects the idea of white supremacy“, but what does this really mean (you will see what it means near the end of this article)? The one saying it may believe it themselves, though it all doesn’t make sense. The extremist views that are more interesting are the Afrocentric ones, though, especially the melanin theory that gets thrown around in Afrocentric circles.
Melanin production
Melanin is produced by melanocytes. Melanin is synthesized from L-tyrosine, with the help of tyrosinase, which is one of the main enzymes for melanin production (Solano, 2014; D’Mello et al, 2016). (See Cone, 2006 for a review of the melanocortin system.) Melanin absorbs energy from UV rays which then dissipate in the body as heat (de Monteallano, 1993). There are three types of melanin: eumelanin (there are two types of eumelanin: brown eumelanin and black eumelanin), pheomelanin (these two are present in the human epidermis; Thody et al, 1991; Solano, 2014) and neuromelanin. Pheomelanin and eumelanin are found in the hair and skin.
Races that live closer to the equator have higher concentrations of melanin in their skin (not neuromelanin, which will be discussed later) which then causes dark skin pigmentation. But everyone on earth has around the same number of melanocytes; skin pigmentation differences come down to differences in UV exposure (for which melanin is useful; and produced due to UV radiation Brenner and Hearing, 2008), disease (albinism and vitiligo), size of melanocytes (see below) and genetic make up.
Europeans and Chinese have about half as much melanin as African and Indian skin types, whereas Africans had the largest melanosomes, followed by the Indians, Mexicans, Chinese, and Europeans, therefore variation in melanosome size may also account for skin variation between races. It’s also interesting to note that people, no matter the skin color, who are born in high UV areas—regardless of ethnicity—have twice as much epidermal melanin compared to people born in low UV areas (Alaluf et al, 2002).
Melanin and pseudoscience
Rushton and Templer (2012) wrongly hypothesized that the melanocortin system modulated sexuality and aggression and humans as they do in animals. The claims made here are may “sound good” to one who isn’t well-versed in the physiology of aggression and sexuality, but to those people, Rushton and Templer’s hypothesis “sounds good enough” and so they believe it without question. On the opposite side, you have black “academics” who believe that melanin gives blacks some type of “greatness” and is the reason for their “natural moves.’ In the book Darwin’s Athletes: How Sport Has Damaged Black America and Preserved the Myth of Race, Hoberman (1997: 89) shortly discusses Afrocentric melanin theorists:
Finally, there are the melanin theorists. a motley collection of pseudo-scientific cranks and better-known members of the black academic demimonde who attended the Fourth Annual World Melanin Conference in Dallas in April 1989—Leonard Jeffries, John Henrik Clarke, Ivan Van Sertima, and others. For these racial biologists, the pigment that makes skin dark is “the Chemical Key to Black Greatness” and accounts for an entire range of superior black aptitudes: “The reason why Black athletes do so well and have these ‘natural moves’ is these melanic tracks in the brainstem tie into the cerrebellum . . . a part of us that controls motor movement (Dr. Richard King). The real signifigance of the melanin theory is that it is the reductio ad absurdum of black racial seperatism, putting its adherents in a de facto alliance with white racists, who have their own reasons to establish separate racial physiologies. Afrocentric science curricula that promote melanin theory have been introduced in a nimber of urban school districts in the United States, thereby doing educational damage to those children who can least afford it.
Note how there are similarities to Rushton and Templer’s (2012) hypothesis on the melanocortin system in darker-pigmented races (mainly blacks since that’s the race they theorized on). But what I find the funniest about melanin theory, as that some Afrocentrists use higher levels of melanin as “physiologic” proof that blacks are “superior athletes” (this can be explained without appealing to melanin). Though do note how the Afrocentric view of melanin and Rushton and Templer’s (2012) view of the melanocortin system and melanin are stark opposites of each other—and they’re both horribly wrong.
Now let’s look at some quotes from some Afrocentric websites.
These quotes are from Suzar’s (1999) book Blacked Out Through Whitewash: Exposing the Quantum Deception/Rediscovering and Recovering Suppressed Melanated (the author cites another book, Melanin: The Chemical Key to Black Greatness by Carol Barnes (1988):
“…your mental processes (brain power) are controlled by the same chemical that gives Black humans their superior physical (athletics, rhythmic dancing) abilities. This chemical…is Melanin!”
Then writing:
The abundance of melanin in Black humans produces a superior organism both mentally and physically. Black infants sit, stand, crawl and walk sooner than whites, and demonstrate more advanced cognitive skills than their white counterparts because of their abundance of melanin. Melanin is the neuro-chemical basis foe what is called “SOUL” in Black people. Melanin refines the nervous system in such a way that messages from the brain reach other areas of the body more rapidly in Black people than in the other. In the same way Blacks excel in athletics, Blacks can excel in all other areas as well (like they did in the past!) once the road blocks are removed.
Notice how this uses Rushton-like data similar to his ‘life history/r/K’ theory of human racial differences. People can have any kind of data they want, but when they start discussing the data then they are leaving the realm of science and are entering the realm of philosophy. They then interpret the data wrong, as evidence for ‘superiority’ in certain traits, and those who are less informed will buy it without question. Do note the similarities to Rushton and Templer’s (2012) hypothesis on the causes for sexual behavior and aggression differences in human races: melanin and the melanocortin system is partly a cause for these racial disparities. You only need a ‘good story’ (a just-so story) that seems like it is a plausible explanation in order to lure someone who’s unsuspecting to pseudo-science. (I would liken melanin to ‘g’ here. Both melanin and ‘g’ are given ‘powers’ that do not exist; but in the case of ‘g’, it doesn’t exist so at least Afrocentrists are discussing an actual hormone, though they are horribly misrepresenting what the actual data on melanin says.)
The most in-depth take-down of Afrocentric melanist theories is from de Mantellano (1993). Afrocentric theory states that black people—and Egyptians because they were black too (they weren’t)—since they have higher levels of melanin in their skin, then this gives them physical and mental superiority over those with less melanin in their skin. They misinterpret (willingly or not) many papers in order to push their pseudo-scientific theories to the ignorant masses (which already is occurring in inner-city schools, widening the already wide science gaps; see de Manteallno, 1992). What Afrocentrists do not understand is that all humans have similar anounts of neuromelanin (which they wrongly conflate with skin melanin), while neuromelanin levels in the brain are also independent of melanin levels in the skin. So the fantastic claims of melanin causing physical and mental ‘superiority’ (whatever that is) for darker-skinned individuals is unfounded.
Further claims from Afrocentrists are that since blacks have more skin melanin then this also means they have more melatonin and beta-melanocyte-stimulating hormone. Melatonin in humans also has no physiological relationship to skin color (de Mantellano, 1993). Lastly, Afrocentric melanists also state, as I have covered before, that Europeans are African albino mutants.
In fact, the claim that whites are just African albino mutants is ridiculous. Whites can produce eumelanin, while albinos can’t. Albinos are also homozygous recessive—since albinism is a Mendelian disorder, one must be homozygous recessive for “the albinism gene” (de Mantellano, 1993: 42). They can mate forever and they will never create offspring with the ability to synthesize melanin. Therefore it is impossible for whites to have been African albinos.
De Mantellano (1993) concludes that the theory is not to be taken seriously (of course) but states that “The idea that there are distinct races and that one is superior to the others is as racist and erroneous when it refers to high melanin levels as it was when it described low melanin levels (the Aryan “master race”)” (pg 54). Of course, no ‘master race’ exists, and the concept of ‘superiority’ has no basis in evolutionary biology, but race exists and is a biological reality. Though that doesn’t mean that any of the Afrocentric claims covered here have any basis—that’s because they conflate neuromelanin and melanin in the skin, even if they didn’t conflate the two they still would not be correct.
The fatal flaw in this type of Afrocentric “reasoning” is that neuromelanin differs in structure, location, and biosynthesis from skin melanin. Afrocentrists assert that neuromelanin and skin melanin are correlated. Though what falsifies this assertion is that albinos have the same amount of neuromelanin in their brains as non-albinos. So all of the purported ‘mental and physical superiority’ that was ’caused by melanin’ makes no sense, because neuromelanin and skin melanin were conflated. Neuromelanin does not even have the physiologic effects that most Afrocentrists believe.
Most Afrocentric melanists also cite individuals who cite…. rat studies and then extrapolate those results to humans. This is dumb. Yes I know the tired old “Humans are animals too!” but just because we’re animals too doesn’t mean that hormones work the same way in all species; it’s just some sort of bland appeal.
Perhaps one of the most amusing parts of de Mantellano (1993) is where he quotes a few prominent Afrocentrists who ‘argue’ that white men are afraid of black men because “Africans have very dominant genes”:
The conspiracy to destroy black youth. . . . It has to do with the fact that in terms of genetics and genes that because Africans have dominant genes that it is very possible for Africans to annihilate the European population. And the best way to prevent the annihilation is to get to the root of the perpetrator who could do that.
And that, of course, would be African men. Because it is men, specifically African men, that start the reproductive process off. For example, in looking at the four possibilities of sexual relationships. Of looking at those four there is only one possibility to produce a European child. If you have an African man with an African woman you will produce a child of color. If you have an African man with a European woman you will also produce a child of color. If you have a European man with an African woman that will also produce a child of color. European men can only produce a child that looks like them when they connect with a European woman. As the result of that, then, European men are very much afraid of African men and the conspiracy is directly centered at them. . . . And that’s that conspiracy is synonymous with the word genocide, and genocide not only is gradual, it is collective (Kunjufu, 1989).[…]
The reason that the Black male . . . is and always has been central to the issue of white supremacy is clarified by the definition of racism as white genetic survival. In the collective white psyche, Black males represent the greatest threat to white genetic survival because only males (of any color) can impose sexual intercourse, and Black males have the greatest genetic potential (of all non-white males) to cause white genetic annihilation. Thus, Black males must be attacked and destroyed in a power system designed to assure white genetic survival. . . . The prevention of white genetic annihilation is pursued through all means, including chemical and biological warfare. Today, the white genetic survival imperative, instead of using chemicals in gas chambers, is using chemicals in the streets-crack, cocaine, ecstasy, PCP, heroin and methadon [sic] (all “designer chemicals”). [Welsing, 1991a: 4]
Other more outlandish ideas are quoted by de Mantellano (1993) too, and all of the claims made about the physiology of melanin, neuromelanin bringing supernatural, physical and mental powers are horribly flawed. These people have no understanding of the physiology of the hormone, nor what they’re really speaking about. These attempted physiological theories to attempt to show racial ‘superiority’ make absolutely no sense if one has a basic understanding of the physiological system.
Claims made by Afrocentrists regarding melanin and neuromelanin range from blacks having more melanin in their muscle cells which is the cause for black athleticism; darker-eyed people having quicker reaction times which was thought to be caused by melanin; melanin centers in the brain being important for controlling and coordination of the body and brain power; to being critical for control of memory, motivation, mental maturation etc; causing altered states of consciousness which then causes black people who attend Church to speak in toungues; helps in the processing of memory; melanin and the pineal gland is at highest functionality in humans; and they conflate skin melanin with neuromelanin, when they are two different hormones (references for these claims can be found in de Montenallo, 1993).
Conclusion
Psuedo-science about melanin is rampant, no matter which side one is on. Both sides make ridiculous assertions and leaps of logic regarding melanin, and I find it very amusing that each group is talking about the same thing while attempting to argue the polar opposite of what the other is arguing. These misconceptions come from no understanding of physiology, to ideological biases, to delusions of ‘superiority’ to just plain ignorance overall. Afrocentrist fairy tales most probably are widening and already-wide science gap between blacks and whites. Of course, race doesn’t really have any bearing on whether or not you’ll believe something, though of course, black kids are more susceptible to believing the fantastical stories and non-understandings of physiology that come from their inner-city teachers who will then indoctrinate them to their ideology.
Correlations between skin pigmentation and neuromelanin are nonexistent. Further, there is no known physiological relationship between melatonin and skin color in humans. Therefore, the assertion that blacks have more melatonin due to their skin color and they then have this physical and mental superiority due to melanin has absolutely no scientific basis (even though those who push these types of theories have absolutely no understanding of the physiology of the hormone they are discussing). Racial pride ‘stories’ are harmful to science education; I don’t see March of the Titans being taught at schools (if I am in error let me know), but Afrocentric melanist theories are?
The most important thing to take note of here is the similarities between Rushton and Templer (2012) and melanists. They mirror each other so well, they are talking about the same exact hormone, but both groups have wildly different conclusions. Rushton and Templer (2012) were driven by the (wrong) hypothesis that testosterone caused aggression and crime and that since a whole slew of animals that had dark pigmentation were aggressive, therefore this should apply to humans too because “Evolution doesn’t stop at the neck”, as most people say. On the other side, we have melanists making wild, almost sci-fi like claims about the power and magic of this one hormone in black bodies and only black bodies. To believe something like that you’d have to be either ignorant or highly biased.
Melanism is clearly untenable, and Afrocentrists who push this ‘theory’ should take a few physiology classes and learn what this hormone does in the human body because they are woefully misinformed, reading books of pseudo-science.
The Weight Loss and Thermodynamics Fallacy
2000 words
Eat less and move more and you will lose weight. That’s the common mantra of everyone around the world because this is what has been repeated for decades. “The First Law of Thermodynamics states that energy can neither be created nor destroyed in an isolated system”. This Law is used in support of the CICO paradigm. But this kind of thinking does not make sense. The First Law only tells us that energy is conserved. That’s it. It says absolutely nothing about weight loss. Does anyone think that it’s weird that we’re given weight loss advice with physics (thermodynamics) and not advice for our physiology? This fallacy, what I term the CICO fallacy, then leads to the second fallacy: that a calorie is a calorie. The implication is this: the body does not discern between what type of macro you choose to ingest, it’s only worried about the amount of energy consumed. But, as I will show, this type of thinking does not work, either.
The First Law of Thermodynamics
The First Law states that energy can neither be created nor destroyed. A positive caloric balance must be associated with weight gain, but where the wrong conclusions come in is when people assume that the positive caloric balance is driving the weight gain. So if the First Law is interpreted correctly, then both conclusions—getting fat makes one consume more energy and consuming more energy makes one fat—are both valid hypotheses. The evidence and observations suggest that getting fat makes one consume more energy. (Jason Fung (2016: 33) writes: “Having studied a full year of thermodynamics in university, I can assure you that neither calories nor weight loss were mentioned even a single time.“)
Obesity researcher Jules Hirsch said to the New York Times:
There is an inflexible law of physics—energy taken in must exactly equal the number of calories leaving the system when fat storage is unchanged. Calories leave the system when food is used to fuel the body. To lower fat content—reduce obesity—one must reduce calories taken in, or increase activity, or both. This is true whether calories come from pumpkins or peanuts or pate de foie gras.
It’s this type of information that has caused the CICO paradigm to continue unabated. However, there are dissenting voices. People like Dr. Jason Fung, Gary Taubes, Zoe Harcombe, Nina Teicholz, Tim Noakes all go against the conventional wisdom regarding obesity and the cause for weight gain.
Another thing that is not taken into account is what occurs in the body when calories are reduced. One important thing to note is that the energy we consume and expend are not independent variables—they are dependent. Therefore, if we lower what we consume, what we expend will then lower as well. If you change one of them, the other will change too. For example, if you exercise more in an attempt to lose more weight you will eat more to compensate. If you eat less to lose more weight, your body’s metabolism will drop to match what the intake is. This is exactly what was seen in the Biggest Loser Study—shockingly lower RMRs in the contestants (see Fothergill et al, 2016). Biological systems are way more complex than to reduce it down to “eat less and move more=weight loss”, and that is easily shown.
Fliers and Maratos-Flier (2007: 74) write in Scientific American:
An animal whose food is suddenly restricted tends to reduce its energy expenditure both by being less active and by slowing energy use in cells, thereby limiting weight loss. It also experiences increased hunger so that once the restriction ends, it will eat more than its prior norm until the earlier weight is attained.
Take this example. Caloric excess in children is positively correlated with height increases. Though the caloric excess is not driving the height increases; they eat because they are growing.
The point that most people miss is the third storage system—fat storage. The three storage systems are kcal in/kcal out and fat storage. Insulin dictates fat storage, in the absence of insulin, the body cannot gain weight. Insulin shuttles fat into the adipocyte which is why insulin is fattening. That’s the point that CICO doesn’t work due to hormonal fluctuations. The most fattening hormone is insulin. The types of foods that elicit the highest insulin response are processed carbohydrates. Therefore, those are the most fattening foods. People who assume CICO state that a calorie is a calorie; that’s wrong.
Imagine a crowded room. The room is getting more crowded, and you ask me why the room is getting more crowded. I say ‘the room is more crowded because more people are entering it than leaving it.’ You say ‘duh, of course that’s true, but why is the room more crowded?’ Saying a room gets crowded because more people are entering than leaving it is redundant; saying that one gets fat because more calories are consumed than burned is redundant, it only says the same thing in two different ways so it is meaningless. Rooms that have more people enter them than leave them will become more crowded since there is no getting around the First Law, right?
Now take that same logic with obesity. Thermodynamics states that if we get fatter then more energy is entering our body than leaving it. Overeating means we’ve consumed more calories than we have expended. It’s tautological.
‘CICO could work’ but that is irrelevant, since what is assumed by the CICOers is that calories are calories; the assumption that once ingested, they go through the same metabolic pathways. This is false. The First Law says nothing about why we get fat. It is irrelevant to human physiology.
Taubes (2007: 293) writes:
Change in energy stores = Energy intake — Energy expenditure
[…]
The first law of thermodynamics dictates that weight gain—the increase in energy stored as fat and lean-tissue mass—will be accompanied by or associated with positive energy balance, but it does not say that it is caused by a positive energy balance—by “a plethora of calories,” as Russel Cecil and Robert Loeb’s 1951 Textbook of Medicine put it. There is no arrow of causality in the equation. It is equally possible, without violating this fundamental truth, for a change in energy stores, the left side of the above equation, to be the driving force in the cause and effect; some regulatory phenomenon could drive us to gai weight, which would in turn cause a positive energy balance—and thus overeating or sedentary behavior. Either way, the calories in will equal the calories out, as they must, but what is the cause in one cause is effect in the other.
And on pg 294:
The alternative hypothesis reverses the causality: we are driven to get fat by “primary metabolic or enzymatic effects,” as Hilde Bruch phrased it, and this fattening process induces the compensatory responses of overeating and/or physical inactivity. We eat more, move less, and have less energy to expend because we are metabolically or hormonally driven to get fat.
All the first law of thermodynamics tells us is that people can’t become more massive without taking in more energy than they expend since people who are heavier contain more energy than people who are lighter. That person has to consume more energy to accommodate said increasing mass. That person also cannot become lighter without expending more energy than they take in. That’s all the First Law tells us: energy is conserved. It says nothing about causation. The First Law literally only says that if something becomes more massive than more energy has to come in than leave. Nothing is said about cause and effect; it only tells us what has to happen if said thing does happen. That’s not causal information.
People only assume that the First Law has any relevance to obesity because of the ‘energy cannot be created nor destroyed’ part. But this shows no understanding of the Law. If you carefully read and understand it, you will see that it gives you absolutely no causal information. You can then reverse the commonly-held mantra—that eating more leads to obesity—to becoming obese leads one to eat more. It’s perfectly logical to reverse it and no Law is broken. People erroneously assume that the Laws of physics dictate weight gain and loss, but in complex metabolic systems, what is ingested is more important than how much is ingested (because we have hormones that let us know when to stop eating—which don’t get released while one eats carbohydrates).
The Second Law of Thermodynamics
The second weight loss fallacy is ‘a calorie is a calorie’, therefore, for weight loss, it doesn’t matter if a majority of my calories comes from fat, carbs or protein; the body will register the calories consumed and will regulate fat stores as dictated by the First Law (supposedly). The fallacy of invoking the First Law of thermodynamics ties directly into the fallacy of the Second Law of Thermodynamics—what the Second Law states is, that variation in metabolic pathways is to be expected, therefore, the mantra “a calorie is a calorie” violates the Second Law as a principle (Feinman and Fine, 2004, 2007).
A diet split of 55:30:15 CHO, fat, protein, yielded 1848 kcal. In fact, thermodynamics does not support the dictum that, all else being equal (i.e., two diets with the same amount of calories, but differing macro splits; one high-fat low carb the other high carb low-fat).
However, in 2004 Zoe Harcombe recalculated the figure from Feinman and Fein (2004) and found it to be wrong. The correct number ended up being 1825 kcal, not 1848 kcal, which strengthened Feinman and Fine’s (2004) point (Harcombe, 2004). She also writes:
I then repeated the calculations for a 10:30:60 high protein diet (keeping fat the same and swapping carbs out and protein in), and the calories available to the body dropped to 1,641. This is incredible. This means that two people can both eat 2000 calories a day and the high carbohydrate person is effectively getting nearly 200 calories more than the high protein person. Anyone still wonder why low-carbohydreate diets have a built in advantage?
So we can see that it’s ridiculous to ignore the thermic effect of food, seeing as it’s 20 percent for protein and 5 percent for CHO.
To put this into perspective, two people eating similar diets (but differing macro splits) only need to out-eat the other by 20 calories per day and that will be enough to gain more weight than the other person. Taubes (2011: 58) writes:
How many calories do we have to consume, but not expend, stashing them away in our fat tissue, to trsnsform ourselves, as many of us do, from lean twenty-five-year-olds to obese fifty-year-olds?
Twenty calories a day.
Twenty calories a day times the 365 days in a year comes to a little more than seven thousand calories stored as fat every year—two pounds of excess fat.
Multiply that by 10 and that’s twenty pounds gained in ten years—all from counting kcal wrong (Aamodt, 2016: 111-112). So with Harcomb’s (2004) example, the damage will be much worse in 10 years. This is all based on the assumption that ‘calories are calories’ which is false, as I have shown.
Conclusion
The CICO paradigm is wrong. Consumption and expenditure are not independent variables, they are dependent. So if you decrease one of them, the other will decrease as well. This is the fatal flaw in the CICO paradigm. The First Law always holds, yes, but it tells us absolutely nothing about obesity or human physiology and is therefore irrelevant. The Second Law is violated when one states that ‘a calorie is a calorie’, but this is demonstrably false. The Second Law states that variation in metabolic pathway efficiency is to be expected. Therefore stating that “a calorie is a calorie” violates the Second Law. This has further implications. Using Taubes’ example of 20 calories per day, if people truly believe the CICO mantra then people eating the same exact number of calories will have different weight gains if the skew of carbs to fat is higher in one than the other. Couple that with what insulin does in the body and this exacerbates the problem.
Stating that thermodynamics has anything to do with weight loss is clearly fallacious.
Behavior Genetics and the Fallacy of Nature vs Nurture
3250 words
People appeal to moderate to high heritability estimates as evidence that a trait is controlled by genes. They then assume that because something has a high heritability then that it must show something about causation. The fact of the matter is, they do not. Heritability estimates assume a false dichotomy of nature vs nurture; it assumes that we can neatly partition genetic from environmental effects. It assumes that the higher a trait’s heritability the more genes control said trait. These are all false. One of the main ways that heritability is estimated is by the CTM (classic twin method). This method, though, has a ton of assumptions poured into it—most importantly, the assumption that DZ and MZ fraternal twins experience roughly equal environments—the equal environments assumption (EEA). Heritability studies are useless for humans; twin studies bias estimates upwards with a whole host of assumptions.
I will show that i) heritability estimates are highly flawed (due to erroneous assumptions); ii) nature vs nurture cannot be separated (like behavior geneticists claim) and so their main tool (the heritability estimate) should be discontinued; iii) genetic reductionism is not a tenable model due to what we now know about how genes work. All three of these reasons are enough to discontinue heritability estimates. If the nature vs nurture debate rests on a fallacy, and this fallacy is used as a vehicle for heritability estimates, then they should be discontinued for humans and only be used for breeding animals where they can control the environment fully (Schonemann, 1997; Moore and Shenk, 2016).
Heritability, twin studies, and equal environments
Back in 2014-2015, there was a debate in the criminological literature that had implications for heritability studies as a whole. Burt and Simons (2014) stated that it was time to get rid of heritability studies. Barnes et al (2015) responded that this was “a de facto form of censorship” (pg 2). Joseph et al (2015) respond to these accusations, writing, “It was good science and not “censorship” when earlier scientists called for ending studies based on craniometry, phrenology, and physiognomy, and any contemporary criminologist calling for the use of astrological charts to predict whether certain people will commit violent crimes would be justifiably ridiculed.” The main thing here, in my opinion, is that heritability estimates are based on an oversimplified (and wrong) model of the gene. Partitioning variance assumes that you can partition how much a trait is influenced by “nature” or “nurture” which is a false dichotomy (Moore, 2002; Schneider, 2007; Moore and Shenk, 2016).
More importantly, no “genes have been found” (I know that’s everyone’s favorite thing to hear) for traits that supposedly have high heritabilities. On page 179 of his book (nook version), Misbehaving Science, Controversy and the Development of Behavior Genetics Panofsky (2014) writes:
Molecular genetics has been a major dissapointment, if not an outright failure, in behavior genetics. Scientists have made many bold claims about genes for behavioral traits or mental disorders only to later retract them or to have them not be replicated by other scientists. Further, the findings that have been confirmed, or not yet falsified, have been few, far between, and small in magnitude.
There seems to be a huge disconnect between heritability estimates gleaned from twin studies and what the actual molecular genetic evidence says. This is because the EEA—that fraternal MZ twins experience roughly similar environments compared to fraternal DZ twins—is false. Fraternal MZ twins end up experiencing more similar environments when compared with fraternal DZ twins. Though most researchers attempt to save face by stating that MZ twins “seek out” and “elicit” their own environments which then makes them more similar compared to DZ twins. However, this is circular logic. The conclusion (that twins experience more similar environments) is in the premise, and therefore it is an invalid argument due to the logical fallacy. (It should also be noted that identical twins’ genes are not identical.)
Heritability studies assume an outdated model of the gene. The flaw regarding heritability estimates is simple: they imply a false dichotomy of nature vs nurture, while also assuming that genes and environment are independent, while the contribution to complex behaviors can be precisely quantified (Charney, 2013). This is one of the most critical parts of the heritability debate. Prenatal environments of DZ twins “can be significantly more stressful than that of DZ twins, and hence a cause of greater stress-related phenotypic concordance, the equal environment assumption will not hold in relation to behavioral phenotypes potentially associated with prenatal stress” (Charney, 2012: 20). This also is cause for concern regarding studies of twins reared apart. While twins are reared apart to eliminate shared environmental confounds, it cannot eliminate perhaps the most important confound of all—the prenatal environment (Moore and Shenk, 2016).
One of the most-cited studies regarding twins reared apart is Bouchard (1990). Though there are a whole slew of problems with this study.
1) You have the huge confound of similar environments before birth.
2) Full details for the MISTRA have never been published, so we don’t know how ‘separated’ the twins were. Though Bouchard et al do say that they were separated between 0 to 48.7 months (table 1) so some pairs spent at least 4 years together. Some of the twins even had reunions and spent a lot of time together.
3) They’re not representative and twins who do sign up for this research are self-selecting. Ken Richardson says in his book (2017, pg 55): “Twins generally tend to be self-selecting in any twin study. They may have responded to advertisements placed by investigators or have been prompted to do so by friends or family, on the grounds that they are alike. Remember, at least some of them knew each other prior to the study. Jay Joseph has suggested that the twins who elected to participate in all twin studies are likely to be more similar to one another than twins who chose not to participate. This makes it difficult to claim that the results would apply to the general population.”
4) And the results aren’t fully reported. Richardson also states that (2017, pg 55) “… of two IQ tests administered in the MISTRA, results have been published for one but not the other. No explanation was given for that omission. Could it be they produced different results?” He even states that attempts to get the data, by researchers like Jay Joseph, have been denied. Why would you refuse to publish, or give to another researcher, your data when asked?
We don’t know the relevant environments, the children’s average age at testing is closer to the biological mother than adopted mother; the biological mother and child will have reduced self-esteem and be more vulnerable to difficult situations, and in this sense they share environments; and conscious or unconscious bias make adopted children different from other family members. Adoption agencies also attempt to put children into similar homes as the biological mother too.
Charney (2012: 25) brings up an important point: “For phenotypes of any degree of complexity, DNA does not contain a determinate genetic program (analogous to the digital code of a computer) from which we can predict phenotype. If DNA were the sole carrier of information relevant to phenotype formation, and contained a genetic program sufficiently determinate that solely by reading it we could predict phenotype, then humans (and all other organisms) would be largely lacking in phenotypic plasticity.” Moore and Shenk (2016) also state that “we inherit developmental resources, not traits.”
1 For twin studies to be valid DZ twins and MZ fraternal twins would have to experience roughly equal environments. 2 Fraternal MZ twins experience much more similar environments than DZ twins. 3 Therefore the EEA is false and no genetic interpretations can be drawn from the data.
Heritability estimates cannot detangle genes and environment, and therefore they should be discontinued or reinterpreted (Joseph et al, 2015). Burt and Simons (2014: 110) also conclude: “Rejecting heritability studies and the false nature–nurture dichotomy and gene-centric model on which they are grounded is a necessary step forward that will pave the way for a reconceptualization of the link between the biological and the social in shaping criminal propensities in ways that are consistent with postgenomic knowledge“. I disagree with Barnes et al (2015) when they say that ending heritability estimates are “a defacto form of censorship“, because if nature vs nurture is a false dichotomy and the gene-centric model that heritability estimates rely on is wrong, then we need to either discontinue or reinterpret the estimates, not saying that ‘this is how much nature contributes to X and this is how much nurture contributes to Y’. (See also Richardson and Norgate, 2005 for more arguments regarding the EEA.)
Sapolsky (2017: 219) writes:
Oh, that’s right, humans. Of all species, heritability scores in humans plummet the most when shifting from a controlled experimental setting to considering the species’ full range of habitats. Just consider how much the heritability score for wearing earrings, with its gender split, has declined since 1958.
Heritability flaws
High heritability estimates have been used as evidence for causation—that genes control a large part of the trait in question. This reasoning, however, is highly flawed. People confuse “heritable” with “inheritable” (Moore and Shenk, 2016). Heritability does not inform us what causes a trait, how much environment contributes to a trait, nor does it tell us the relative influence of genes on a trait. Moore and Shenk (2016) agree with Joseph et al (2015) and Burt and Simons (2014) that heritability studies need to end, but Moore and Shenk’s reasoning slightly differs: they say we should end estimates because people confuse “heritable” with “inheritable”. Likewise, Guo (2000: 299) concurs, writing “it can be argued that the term ‘heritability’, which carries a strong conviction or connotation of something ‘heritable’ in everyday sense, is no longer suitable for use in human genetics and its use should be discontinued.”
Some may say that if a trait turns out to be mildly heritable then we can say that genes have some effect, but we know that genes affect all traits so it seems kind of redundant to have a useless measure that assumes a false dichotomy and relies on an outdated, additive model of the gene.
Rose (2006), too, agrees that heritability estimates imply a false dichotomy of nature vs nurture onto biological systems:
Biological systems are complex, non-linear, and non-additive. Heritability estimates are attempts to impose a simplistic and reified dichotomy (nature/nurture) on non-dichotomous processes.
Likewise, Lewontin (2006) argues we should be analyzing and studying causes, not variance.
There are numerous hereditarian scientific fallacies which include: 1) trait heritability does not predict what would occur when environments/genes change; 2) they’re inaccurate since they don’t account for gene-environment covariation or interaction while also ignoring nonadditive effects on behavior and cognitive ability; 3) molecular genetics does not show evidence that we can partition environment from genetic factors; 4) it wouldn’t tell us which traits are ‘genetic’ or not; and 5) proposed evolutionary models of human divergence are not supported by these studies (since heritability in the present doesn’t speak to what traits were like thousands of years ago) (Bailey, 1997).
Bailey (1997) brings up important arguments against the use of heritability, and even discusses fallacious writing from Rushton on the matter:
Rushton (1995), for example, thinks that if observed differences among the
racial groups that he defines are higher for traits that have high heritability within the groups, the hypothesis of genetically caused differences among the groups is supported.
Bailey (1997) then goes on to discuss three lakes: Otter lake, Welcome lake, and Bark lake. Otter lake has very high primary production, while Bark lake has very little and Welcome lake is somewhere in between (you can see that ‘Otter’, ‘Bark’ and ‘Welcome’ lakes are analogies for ‘Orientals’, ‘Blacks’, and ‘Whites’ as said by Rushton). But there is variation within the lakes, there are high production pockets of water in Bark lake while there are low production pockets of water in Otter lake. All three lakes are visited and measurements are taken. Bailey (1997) states that his conclusion would be that they differ in how much light each receives. Bailey (1997: 131) writes:
If I substitute three groups of people for my lakes, IQ for primary production, and genes for light levels, the fallacy of the slippery scale, as applied to human behaviour genetics, becomes clear. Even if we are sure that there is a difference among groups of people in IQ, and we are sure that IQ has high heritability within
each of the groups (i.e. variation in IQ is largely caused by genetic variation), we can make no inference about the cause of differences in IQ among the groups. The differences might be caused by genetic differences or they might not, but the heritability studies within the groups can’t help us make that judgment.
(Genes don’t cause IQ scores—or behavior—but that’s for another day.)
Heritability estimates for, say, IQ, are higher than any other trait in the animal kingdom. Heritability estimates for animal traits are low—lower than the stratospheric heritability of IQ. For example, heritability estimates of the bodyweight of farm animals is about 30 percent, which is the same for egg and milk production. Body fat in pigs and wool on sheep has a heritability of about 50 percent. But these estimates pale in comparison to the heritability estimates of IQ: estimates have been as high as 80 percent (but Schonemann, 1997 states it’s 60 percent but it’s as high as 80-90 percent today); this heritability estimate for IQ “surpasses almost anything found in the animal kingdom” (Schonemann, 1997: 104).
This high heritability estimate for IQ, of course, comes to us from the highly flawed twin studies discussed above. The reason why farmers and botanists use heritability estimates is that they can perfectly control the environment, and therefore get accurate—or close enough to it—estimates that will help them in their breeding efforts. Conversely, for humans, environments cannot be perfectly controlled and it is, of course, unethical to rear twins, MZ and DZ, in a controlled environment. Proponents of the twin method may say “It doesn’t matter if it’s flawed, it still shows there is a genetic component to trait X!”. But as discussed by Moore and Shenk (2016), that’s irrelevant because genetic factors influence all of our characteristics.
Heritability and causation
In the final section, I will shortly discuss how people fallaciously assume that high heritability estimates imply that a trait is strongly influenced by genetic factors.
In his essay in the book Postgenomics: Perspectives on Biology After the Genome, sociologist Aaron Panofsky (2016: 167; nook version) writes:
Heritability estimates do not help identify particular genes or ascertain their functions in development or physiology, and thus, by this way of thinking, they yield no causal information.
This is important to note: to those who truly believe that heritability estimates tell us anything about causation, how could they, logically, give us causal information if genes that lead to trait variation are not identified (Richardson, 2012)?
Panofsky (2014: 102-103) writes:
Experimental evidence from plants and animals suggest that shapes of the curves cannot inferred in advance and rarely follow the smooth, nonintersecting pattern like in figure 3.2. Thus true causal interpretations of heritability are hopeless and must be abandoned. Behavior geneticists did not claim direct experimental evidence, but they thought these various indirect lines of evidence provided a reasonable set of assumptions that would enable them to interpret heritability scores causally—provided they offer apporopriate, reasonable qualifications.
Graph from Panofsky (2014: 103)
Heritability estimates imply nothing about causation. It is about associations with variance, not identity and causes (Richardson, 2017: 69). A heritability of 0 does not mean that genes do not play a role in the development of form and function and phenotypic variation, it just means that, for whatever reason, there is little correlation between the two.
Scheneider (2007) writes (emphasis mine):
Heritability estimates apply only to groups, and are inherently inapplicable to individuals in any sense. And they do not imply causation. As Moore notes, all of these important limitations have been frequently ignored or minimized.
Reductionism
Heritability estimates imply nothing about causation. Behavior geneticists and others assume that heritability estimates will lead to ‘finding the genes’ that ’cause’ or are ‘associated with’ behavior. Their models are also, of course, extremely reductionist. It is then important to note that genes do not determine behavior. To quote Lerner and Overton (2017: 114):
Data presented in a 2016 special section of the journal Child Development indicate
that “some behaviors may be affected by only slight changes in DNA methylation,
while others may require a larger percent change in methylation; of course, the
effects are also likely bidirectional, with behavior impacting changes in methylation” [Lester et al., 2016, p. 31]. This point is key . It underscores the absurdity of genetic reductionist models: Genes do not determine behavior.
Methylation impacts behavior; behavior impacts methylation. It is the relations between methylation and behavior, not the genes acting as the “command center”, the “executive” of human behavior and development, that constitute the basic role of biology across the developmental course. This is the fatal flaw of reductionist models. Lastly, Lerner and Overton (2017: 145) write (emphasis mine):
That is, with the recent advances in understanding the role of epigenetics and recent research findings supporting this role, it should no longer be possible for any scientist to undertake the procedure of splitting of nature and nurture and, through reductionist procedures, come to conclusions that the one or the other plays a more important role in behavior and development.
[Richardson (2017: 129) also writes: “Note that this environmental source of [epigenetic] variation will appear in the behavioral geneticists twin-study as genetic variation: quite probably another way in which heritability estimates are distorted.”]
Reductionism in biology is fatally flawed. Reductionism, of course, has greatly increased our understanding of biology. However, it is time to move past the false dichotomy of nature vs nurture, and with that, move past heritability estimates since they prop up the fallacy of nature vs nurture. There is no way to separate the two since they are intertwined, but behavior geneticists would like you to believe that by studying twins raised apart will tell you anything about how ‘genetic’ or ‘environmental’ variation in a trait is in a population. Since heritability estimates are gleaned from the highly flawed studies of twins reared apart, a whole host of assumptions is poured in and these estimates are highly inflated, showing that genes influence a trait more than they supposedly do.
Twin studies, and along with it, heritability estimates, are useless for figuring out, and describing, trait variation in humans. The developmental system is more complex than the genetic reductionists (behavior geneticists) would like one to believe. The reductionist model has been heavily attacked in recent years (Regenmortal, 2004; Noble, 2008, 2012, 2015, 2016; Joyner, 2011, b; Joyner and Pederson, 2011).
Nature vs nurture has also shown to be a false dichotomy because the system develops in whichever environment it finds itself in (Oyama, 1985, 1999; 2000; Moore, 2002; Schneider, 2007)
Conclusion
Since the genetic reductionist model is wrong, along with heritability estimates (because of the nature/nurture fallacy), both should be discontinued. One of the main vehicles of these two models—twin studies—should also be discontinued. These fatal flaws of the behavior geneticists’ paradigm should be enough to discontinue these techniques in the study of human development and behavior. Heritability estimates give no causal information and they also use an outdated model of the gene; twin studies assume too many things for it to be a viable model in the discovering how traits manifest (most importantly, twin studies keep the nature/nurture fallacy alive and should be discontinued on that note only, in my opinion); and genetic reductionist models have been shown to be fatally flawed in recent years. We now have a better understanding of what a gene is today (Portin and Wilkins, 2017), and due to this, we should discontinue whatever implies the fallacy of nature vs nurture because it is irrelevant and a false dichotomy. That, alone, should be enough to discontinue twin studies and heritability estimates.
Race Differences in Penis Size Revisited: Is Rushton’s r/K Theory of Race Differences in Penis Length Confirmed?
2050 words
In 1985 JP Rushton, psychology professor at the University of Ontario, published a paper arguing that r/K selection theory (which he termed Differential K theory) explained and predicted outcomes of what he termed the three main races of humanity—Mongoloids, Negroids and Caucasoids (Rushton, 1985; 1997). Since Rushton’s three races differed on a whole suite of traits, he reasoned races that were more K-selected (Caucasoids and Mongoloids) had slower reproduction times, higher time preference, higher IQ etc in comparison to the more r-selected Negroids who had faster reproduction times, lower time preference, lower IQ etc (see Rushton, 1997 for a review; also see Van Lange, Rinderu, and Bushmen, 2017 for a replication of Rushton’s data not theory). Were Rushton’s assertions on race and penis size verified and do they lend credence to his Differential-K claims regarding human races?
Rushton’s so-called r/K continuum has a whole suite of traits on it. Ranging from brain size to speed of maturation to reaction time and IQ, these data points supposedly lend credence to Rushton’s Differential-K theory of human differences. Penis size is, of course, important for Rushton’s theory due to what he’s said about it in interviews.
Rushton’s main reasoning for penis size differences between race is “You can’t have both”, and that if you have a larger brain then you must have a smaller penis; if you have a smaller penis you must have a larger brain. He believed there was a “tradeoff” between brain size and penis size. In the book Darwin’s Athletes: How Sport Has Damaged Black America and Preserved the Myth of Race, Hoberman (1997: 312) quotes Rushton: “Even if you take something like athletic ability or sexuality—not to reinforce stereotypes or some such thing—but, you know, it’s a trade-off: more brain or more penis. You can’t have both.” This, though, is false. There is no type of evidence to imply that this so-called ‘trade-off’ exists. In my readings of Rushton’s work over the years, that’s always something I’ve wondered: was Rushton implying that large penises take more energy to have and therefore the trade-off exists due to this supposed relationship?
Andrew Joyce of the Occidental Observer published an article the other day in defense of Richard Lynn. Near the end of his article he writes:
Another tactic is to belittle an entire area of research by picking out a particularly counter-intuitive example that the public can be depended on to regard as ridiculous. A good example is J. Philippe Rushton’s claim, based on data he compiled for his classic Race, Evolution and Behavior, that average penis size varied between races in accord with the predictions of r/K theory. This claim was held up to ridicule by the likes of Richard Lewontin and other crusaders against race realism, and it is regularly presented in articles hostile to the race realist perspective. Richard Lynn’s response, as always, was to gather more data—from 113 populations. And unsurprisingly for those who keep up with this area of research, he found that indeed the data confirmedRushton’s original claim.
The claim was ridiculed because it was ridiculous. This paper by Lynn (2013) titled Rushton’s r-K life history theory of race differences in penis length and circumference examined in 113 populations is the paper that supposedly verifies Rushton’s theory regarding race differences in penis size, along with one of its correlates in Rushton’s theory (testosterone). Lynn (2013) proclaims that East Asians are the most K-evolved, then come Europeans, while Africans are the least K-evolved. This, then, is the cause of the supposed racial differences in penis size.
Lynn (2013) begins by briefly discussing Rushton’s ‘findings’ on racial differences in penis size while also giving an overview of Rushton’s debunked r/K selection theory. He then discusses some of Rushton’s studies (which I will describe briefly below) along with stories from antiquity of the supposed larger penis size of African males.
Our old friend testosterone also makes an appearance in this paper. Lynn (2013: 262) writes:
Testosterone is a determinant of aggression (Book, Starzyk, & Quinsey, 2001; Brooks & Reddon, 1996; Dabbs, 2000). Hence, a reduction of aggression and sexual competitiveness between men in the colder climates would have been achieved by a reduction of testosterone, entailing the race differences in testosterone (Negroids > Caucasoids > Mongoloids) that are given in Lynn (1990). The reduction of testosterone had the effect of reducing penis length, for which evidence is given by Widodsky and Greene (1940).
Phew, there’s a lot to unpack here. (I discuss Lynn 1990 in this article.) Testosterone does not determine aggression; see my most recent article on testosterone (aggression increases testosterone; testosterone does not increase aggression. Book, Starzyk and Quinsey, 2001 show a .14 correlation between testosterone and aggression, whereas Archer, Graham-Kevan, and Davies 2005 show the correlation is .08). This is just a correlation. Sapolsky (1997: 113) writes:
Okay, suppose you note a correlation between levels of aggression and levels of testosterone among these normal males. This could be because (a) testosterone elevates aggression; (b) aggression elevates testosterone secretion; (c) neither causes the other. There’s a huge bias to assume option a while b is the answer. Study after study has shown that when you examine testosterone when males are first placed together in the social group, testosterone levels predict nothing about who is going to be aggressive. The subsequent behavioral differences drive the hormonal changes, not the other way around.
Brooks and Reddon (1996) also only show relationships with testosterone and aggressive acts; they show no causation. This same relationship was noted by Dabbs (2000; another Lynn 2013 citation) in prisoners. More violent prisoners were seen to have higher testosterone, but there is a caveat here too: being aggressive stimulates testosterone production so of course they had higher levels of testosterone; this is not evidence for testosterone causing aggression.
Another problem with that paragraph quoted from Lynn (2013) is that it’s a just-so story. It’s an ad-hoc explanation. You notice something with data you have today and then you imagine a nice-sounding story to attempt to explain your data in an evolutionary context. Nice-sounding stories are cool and all and I’m sure everyone loves a nicely told story, but when it comes to evolutionary theory I’d like theories that can be independently verified of the data they’re trying to explain.
My last problem with that paragraph from Lynn (2013) is his final citation: he cites it as evidence that the reduction of testosterone affects penis length…..but his citation (Widodsky and Green, 1940) is a study on rats… While these studies can give us a wealth of information regarding our physiologic systems (at least showing us which types of avenues to pursue; see my previous article on myostatin), they don’t really mean anything for humans; especially this study on the application of testosterone to the penis of a rat. See, the fatal flaw in these assertions is this: would a, say, 5 percent difference in testosterone lead to a larger penis as if there is a dose-response relationship between testosterone and penis length? It doesn’t make any sense.
Lynn (2013), though, says that Rushton’s theory doesn’t propose that there is a direct causal relationship between “intelligence”‘ and penis length, but just that they co-evolved together, with testosterone reduction occurring when Homo sapiens migrated north out of Africa they needed to cooperate more so selection for lower levels of testosterone subsequently occurred which then shrunk the penises of Rushton’s Caucasian and Mongoloid races.
Lynn (2013) then discusses two “new datasets”, one of which is apparently in Donald Templer’s book Is Size Important (which is on my to-read list, so many books, so little time). Table 1 below is from Lynn reproducing Templer’s ‘work’ in his book.
The second “dataset” is extremely dubious. Lynn (2013) attempts to dress it up, writing that “The information in this website has been collated from data obtained by research centres and reports worldwide.” Ethnicmuse has a good article on the pitfalls of Lynn’s (2013) article. (Also read Scott McGreal’s rebuttal.)
Rushton attempted to link race and penis size for 30 years. In a paper with Bogaert (Rushton and Bogaert, 1987), they attempt to show that blacks had larger penises than whites who h ad longer penises than Asians which then supposedly verified one dimension of Rushton’s theory. Rushton (1988) also discusses race differences in penis size, citing a previous paper by Rushton and Bogaert, where they use data from Alfred Kinsey, but this data is nonrepresentative and nonrandom (see Zuckermann and Brody, 1988 and Weizmann et al, 1990: 8).
Still others may attempt to use supposed differences in IGF-1 (insulin-like growth factor 1) as evidence that there is, at least, physiological evidence for the claim that black men have larger penises than white men, though I discussed that back in December of 2016 and found it strongly lacking.
Rushton (1997: 182) shows a table of racial differences in penis size which was supposedly collected by the WHO (World Health Organization). Though a closer look shows this is not true. Ethnicmuse writes:
ANALYSIS: The WHO did not study penis sizes. It relied on three separate studies, two of which were not peer-reviewed and the data was included as “Appendix III” (which should have alerted Rushton that this was not an original study). The first study references Africans in the US (not Africa!) and Europeans in the US (not Europe!), the second Europeans in Australia (not Europe!) and the third, Thais.
So it seems to be bullshit all the way down.
Ajmani et al (1985) showed that 385 healthy Nigerians had an average penile length of 3.21 inches (flaccid). Orakwe and Ebuh (2007) show that while Nigerians had longer penises than other ethnies tested, the only statistical difference was between them and Koreans. Though Veale et al (2014: 983) write that “There are no indications of differences in racial variability in our present study, e.g. the study from Nigeria was not a positive outlier.”
Lynn and Dutton have attempted to use androgen differentials between the races as evidence for racial differences in penis size (this is another attempt at a physiological argument to attempt to show the existence of racial differences in penis size). Edward Dutton attempted to revive the debate on racial differences in penis size during a 2015 presentation where he, again, showed that Negroids have higher levels of testosterone than Caucasoids who have higher levels of androgens than Mongoloids. These claims, though, have been rebutted by Scott McGreal who showed that populations differences in androgen levels are meaningless while they subsequently fail to validate Rushton and Lynn’s claims on racial differences in penis size.
Finally, it was reported the other day that condoms from China were too small in Zimbabwe, per Zimbabwe’s health minister. This led Kevin MacDonald to proclaim that this was “More corroboration of race differences in penis size which was part of the data Philippe Rushton used in his theory of r/K selection (along with brain size, maturation rates, IQ, etc.)” This isn’t “more corroboration” for Rushton’s long-dead theory; nor is this evidence that blacks have longer penises. I don’t understand why people make broad and sweeping generalizations. It’s one country in Africa that complained about smaller condoms from a country in East Asia, therefore this is more corroboration for Rushton’s r/K selection theory? The logic doesn’t follow.
Asians have small condoms. Those condoms go to Africa. They complain condoms from China are too small. Therefore Rushton’s r/K selection theory is corroborated. Flawed logic.
In sum, Lynn (2013) didn’t verify Rushton’s theory regarding racial differences in penis size and I find it even funnier that Lynn ends his article talking about “falsification’ stating that this aspect of Rushton’s theory has survived two attempts at falsification, therefore, it can be regarded as a “progressive research program“, though obviously, with the highly flawed “data” that was used, one cannot rationally make that statement. Supposed hormonal differences between the races do not cause penis size differences; even if blacks had levels of testosterone significantly higher than whites (the 19 percent that is claimed by Lynn and Rushton off of one highly flawed study in Ross et al, 1986) they still would not have longer penises.
The study of physical differences between populations is important, but sometimes, stereotypes do not tell you anything, especially in this case. Though in this instance, the claim that blacks have the longest penis lies on shaky ground, and with what evidence we do have for the claim, we cannot logically make the inference (especially not from Lynn’s (2013) flimsy data). Richard Lynn did not “confirm” anything with this paper; the only thing he “confirmed” are his own preconceived notions; he did not ‘prove’ what he set out to.
NotPoliticallyCorrect 