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I’ve been chronicling the VDH recently since it has great explanatory—and predictive—power. Light skin is a clear adaptation to low UVR, while dark skin is a clear adaptation to high UVR. Dark, highly melanized skin confers advantages in high UVR environments, such as protection against DNA damage, and also absorbs sufficient UV for vitamin D production while also protecting against folate depletion. However, when our ancestors migrated out of Africa, dark skin would not cut it in temperate environments with highly variable UV rays. This is where our highly adaptive physiology came into play, ensuring that we survived in highly variable environments. Light skin was important in low UVR environments in order to synthesize ample vitamin D, however, that synthesized vitamin D then conferred numerous other physiological advantages to the cold.
Eighty to ninety percent of the vitamin D required for humans comes from the sun, whereas ten to twenty percent comes from the diet, such as fatty fish, eggs, and dairy products (fortified with vitamin D, of course) (Ajabshir, Asif, and Nayer, 2014). Humans need to rely on high amounts of UV rays for vitamin D synthesis (Carlberg, 2014) other than Arctic peoples. Since dark skin does not synthesize vitamin D as well as light skin, skin gradually lightened as our ancestors migrated out of Africa (Juzeniene et al, 2009). This was then imperative to the physiologic adaptations that then occurred as our physiology had to adapt to novel, colder environments with fewer UV rays.
Sufficient amounts of vitamin D are highly important for the human musculoskeletal system (Wintermeyer et al, 2016), which is extremely important for birthing mothers. Along with the increased vitamin D synthesis in low UV environments, the heightened production of vitamin D conferred numerous other physiologic benefits which then helped humans adapt to colder environments with more varying UVR.
Vasoconstriction occurs when the blood vessels constrict which leads to heightened blood pressure, whereas vasodilation is the dilation of blood vessels which decreases blood pressure. So evolutionarily speaking, we had to have adaptive physiology in order to be able to “switch” back and forth between vasoconstriction and vasodilation, depending on what the current environment needed. Vasodilation, though, most likely had no advantage in high UV environments, and thus must have been an advantage in low UV environments, where it was more likely to be colder and so, when the blood vessels constrict, blood pressure increases and thus, heat loss could be considerably slowed in these environments due to these physiologic adaptations.
The races also differ, along with many other physiologic abilities, in nitric oxide-mediated vasodilation. Vasodilation is the dilation of blood vessels, which increases blood pressure. Mata-Greenwood and Chen (2008) reviewed the relevant literature regarding black/white differences in nitric oxide-dependent vasorelaxation and concluded that nitric oxide vasodilation is reduced in darker-skinned populations. Thus, we can infer that in lighter-skinned populations nitric oxide vasodilation is increased in lighter-skinned populations, which would have conferred a great physiological advantage when it came to colonizing environments with lower UV rays.
VDR and vitamin D metabolizing enzymes are present in adipose tissue. Tetrahydrobiopterin; which acts as a cofactor in the synthesis of nitric oxide and its primary function is as a vasodilator in the blood vessels (meaning that blood pressure is increased, to keep more heat in the cold) (Chalupsky and Cai, 2005). Since vasodilation is the body’s primary response to heat stress, blood flow increases which allows heat to leave the body. Therefore, the human body’s ability regarding vasodilation and vasoconstriction mechanisms were important in surviving areas with varying UVR.
One function of our adipose tissue is the storage of vitamin D, while vitamin D metabolizing enzymes and VDR are also expressed in the adipocyte (Abbas, 2017). With these known actions of vitamin D on adipose tissue, we can speculate that since vitamin D and the VDR are expressed in adipose tissue, it may have exerted a role in the adipose tissue which may have been important for surviving in cold, low UV environments (see below).
Furthermore, since these mechanisms are brought on by short-term changes, we can infer that it would hardly be of any use in high UVR environments and would be critical in temperate environments. So, vasodilation and vasoconstriction have little to no benefit in high UVR environments but seem to be imperative in temperate environments where UVR varies. It’s also likely that vitamin D influences vasodilation by influential nitric oxide synthesis (see Andrukhova et al, 2014) and vasoconstriction by influencing the renin-angiotensin system (Ajabshir, Asig, and Nayer, 2014).
This would have conferred great benefit to our ancestors as they migrated into more temperate and colder climates. You can read this for information on how adaptive our physiology is and why it’s like that. Because we went into numerous new environments and natural selection couldn’t act quickly enough, therefore the human body’s physiology is extremely adaptive.
What this suggests is that as skin lightened and adapted to low UV, the increased synthesis in vitamin D influenced vasodilation by a strong influence on nitric oxide synthase, along with vasoconstriction, implies that it would have been easier to survive in novel environments due to adaptive physiology and skin color, along with body fat reserves and the physiologic effects of vitamin D on adipose tissue. These physiologic adaptations would have been of no to little use in Africa. Thus, they must have been useful after we migrated out of Africa and experienced wildly varying environments—the whole reason why our physiology evolved (Richardson, 2017: chapter 5).
When the human body is exposed to cold, a few things occur: cutaneous vasoconstriction, shivering (Castellani and Young, 2016), “behavioral thermoregulation” (Young, Sawka, and Pandolf, 1996), while the human body can adapt physiologically to the cold (Young, 1994). The physiologic functions that vitamin D and folate in regard to vasodilation and vasoconstriction, there is a great chance that these effects were important in maintaining energy homeostasis in colder climates.
In sum, the evolution of light skin conferred a great survival advantage to our ancestors. This then upped the production of vitamin D synthesis in the body, which where then of utmost importance in regard to the adaptation of the human physiology to colder, lower-UV environments. Without our adaptive physiological systems, we would not have been able to leave Africa into novel environments. We need both behavioral thermoregulation as well as adaptive physiology to be able to survive in novel environments. Thus, the importance of skin lightening in our evolution becomes clearer:
As humans migrated out of Africa, lighter skin was needed to synthesize vitamin D. This was especially important to women, who needed higher amounts of vitamin D, in order to produce enough calcium for lactation and pregnancy—so the babe had enough calcium to grow its skeleton in the womb. With the uptake in vitamin D synthesis, this then allowed more adaptive physiologic changes that occurred due to the cold, and along with vasodilation and vasoconstriction, along with shivering and adapting behaviorally to the new environments, were our ancestors able to survive. Dark skin cannot synthesize vitamin D as well as light skin in low UV environments; this also can be seen with the lowered production of nitric oxide-dependent vasodilation in dark-skinned populations. Thus, vasoconstriction conferred no physiologic benefit in high UV environments, but almost certainly conferred a physiologic benefit in low UV environments.
Skin color differences between the sexes are always discussed in terms of women being lighter than men, but never men being darker than women. This is seen in numerous animal studies (some reviewed by Rushton and Templer, 2012; read rebuttal here; also see Ducrest, Keller, and Roulin, 2008). Though, the colors that evolved on the animal’s fur due to whatever mate choices are irrelevant to the survival capabilities that the fur, feathers etc give to the organism in question. So, when we look at humans, we lost our protective body hair millions of years ago (Lieberman, 2015), and with that, we could then sweat. So since furlessness evolved in the lineage Homo, there was little flexibility in what could occur due to environmental pressures on skin color in Africa. It should be further noted that, as Nina Jablonski writes in her book Living Color: The Biological and Social Meaning of Skin Color (2012, pg 74)
No researchers, by the way, have explored the opposite possibility, that women deliberately selected darker men!
One hypothesis proposes that lighter skin in women first arose as a byproduct due to the actions of differing levels of hormones in the sexes—with men obviously having higher levels of testosterone, making them darker them women. So according to this hypothesis, light-skinned women evolved since men could tell high-quality from low-quality mates as well as measure hormonal status and childbearing potential, which was much easier to do with lighter- than darker-skinned women.
Another hypothesis put forth is that further from the equator, sexual competition between women would have increased for mates since mates were depleted, and so light skin evolved since men found it more beautiful. Thus, women living at higher latitudes were lighter than women living at lower latitudes because men had to go further to hunt which meant they were more likely to die which caused even greater competition between females, lightening their skin even more. And another, related, argument, proposed that light skin in women evolved due to a complex of childlike traits which includes a higher voice, smoother skin and childlike facial features, which then reduced male competition and aggressiveness. But women did not stay around waiting to be provisioned and they got out and gathered, and hunted sometimes, too.
Harris (2005) proposes that light skin evolved due to parental selection—mothers choosing the lightest daughters to survive, killing off the darker ones. All babies are born pale—or at least lacking the amount of pigment they have later in life. So how would parental—mostly maternal—selection have caused selection for lighter skin in girls as Harris (2005) proposes? It’d be a pretty large guessing game.
The role of sexual selection in regard to human skin color, though, has been tested and falsified. Madrigal and Kelly (2007a) tested the hypothesis that skin reflectance should be positively correlated with distance from the equator. It was proposed by other authors that as our ancestors migrated out of Africa, environmental selection relaxed and sexual selection took over. Their data did not lend credence to the hypothesis and falsified it.
Madrigal and Kelly (2007a: 475) write (emphasis mine):
We tested the hypothesis that human sexual dimorphism in skin color should be positively correlated with distance from the equator, a proposal generated by the sexual selection hypothesis. We found no support for that proposition. Before this paper was written, the sexual selection hypothesis was based on stated male preference data in a number of human groups. Here, we focused on the actual pattern of sexual dimorphism. We report that the distribution of human sexual dimorphism in relation to latitude is not that which is predicted by the sexual selection hypothesis. According to that hypothesis, in areas of low solar radiation, there should be greater sexual dimorphism, because sexual selection for lighter females is not counterbalanced by natural selection for dark skin. Our data analysis does not support this prediction.
Though Frost (2007) replied, stating that Madrigal and Kelly (2007a) presumed that sexual selection was equal in all areas. Madrigal and Kelly (2007b) responded, stating that they tested one specific hypothesis regarding sexual selection and found it to be false. Frost (2007) proposed two hypotheses in order to test his version, but, again, no one has proposed that women select darker men, which could be a cause of lighter-skinned women (though sexual selection does not—and cannot—explain the observed gradation in skin color between men and women).
Skin color differences between men and women first arose to ensure women enough calcium for lactation and pregnancies. Since skin pigmentation protects against UVR but also must generate vitamin D, it must be light or dark enough to ensure ample vitamin D production in that certain climate, along with protecting against the UVR in that climate. So women needed sufficient vitamin D, which meant they needed sufficient calcium to ensure a strong skeleton for the fetus, for breastfeeding and for the mother’s own overall health.
However, breastfeeding new babes is demanding on the mother’s body (calcium reserves are depleted four times quicker), and the calcium the babe needs to grow its skeleton comes directly from the mother’s bones. Even a mother deficient in vitamin D will still give calcium to the babe at the expense of her own health. But she then needs to increase her reserves of calcium in order to ensure future pregnancies aren’t fatal for her or her offspring.
Though, at the moment to the best of my knowledge, there are no studies on calcium absorption, vitamin D levels and the recovery of the female skeleton after breastfeeding. (Though n3 fatty acids are paramount as well, and so a mother must have sufficient fat stores; see Lassek and Gaulin, 2008.) Thus, light-skinned women are most likely at an advantage when it comes to vitamin D production: The lighter they are, the more vitamin D and calcium they can produce for more pregnancies. Since light skin synthesizes vitamin D more efficiently, the body could then synthesize and use calcium more efficiently. The body cannot use and absorb calcium unless vitamin D is present. Since the fetus takes calcium from the mother’s skeleton, ample amounts of vitamin D must be present. For ample amounts of vitamin D to be present, the skin must be light enough to ensure vitamin D synthesis which would be needed for calcium absorption (Cashman, 2007; Gallagher, Yalamanchili, and Smith, 2012; Aloia et al, 2013).
Nina Jablonski writes in her book (2012, 77):
Women who are chronically deficient in vitamin D because of successive pregnancies and periods of breastfeeding experience a form of bone degeneration called osteomalacia. This has serious consequences for infants born of later pregnancies and for mothers themselves, who are at greater risk of breaking bones. It makes sense that protection of female health during the reproductive years would be a top evolutionary priority, so we are now investigating whether, in fact, slightly lighter skin in women might be a fairly simple way of ensuring that women get enough vitamin D after pregnancy and breastfeeding to enable their bodies to recover quickly. The need for maintaining strong female skeletons through multiple pregnancies may have been the ultimate evolutionary reason for the origin of differences in skin color between men and women.
While Jablonski and Chaplin (2000: 78) write:
We suggest that lighter pigmentation in human females began as a trait directly tied to increased fitness and was subsequently reinforced and enhanced in many human populations by sexual selection.
It is obvious that skin color in women represents a complex balancing act between giving the body the ability to synthesize ample vitamin D and protect from UVR. Skin coloration in humans is very clearly highly adaptive to UVR, and so, with differing average levels of UVR in certain geographic locales, skin color would have evolved to accommodate the human body to whichever climate it found itself in—because human physiology is perhaps the ultimate adaptation.
Sexual selection for skin color played a secondary, not primary role (Jablonski, 2004: 609) in the evolution of skin color differences between men and women. There is a delicate balancing act between skin color, vitamin D synthesis, and UVR protection. Women need to produce enough vitamin D in order to ensure enough calcium and its absorption to the baby and then ensure there are ample amounts to replace what the baby took while in the womb in order for future pregnancies to be successful. Sexual selection cannot explain the observed gradation in skin color between the races and ethnies of the human race. In my opinion, the only explanation for the observed explanation is the fact that skin color evolved due to climatic demands, while independent justification exists for the hypothesis as a whole (Jablonski and Chaplin, 2010).
I don’t see any way that sexual selection can explain the observed gradation in skin color around the world. Skin color is very clearly an adaptation to climate, though of course, cultural customs could widen the skin color differences between the sexes, and make women lighter over time. Nevertheless, what explains the observed skin gradation is adaptation to climate to ensure vitamin D synthesis among a slew of other factors (Jones et al, 2018). Sexual selection, while it may explain small differences between the sexes, cannot explain the differences noted between the native human races.
The relationship between vitamin D and the vitamin D receptor (VDR) has been found to be of recent importance in explaining the modulation of gene expression. The VDR helps us adapt to the climate, is epistatic with skin color genes, and so on. Due to the importance of the VDR, vitamin D, and another nutrient I’ve discussed in the past—folate—this drives the argument that the need to produce vitamin D was an important factor in the evolution of skin colors around the world as migrations out of Africa took place. It is also important to note that other competing hypotheses are not necessarily alternative hypotheses to the VDH (which is short for vitamin D-folate hypothesis), since there is significant overlap between them due to what we now know about the roles of vitamin D, folate (especially due to what we know now about how vitamin D, folate and the VDR regulate gene expression),the VDR, and skin color genes. Thus, the theories have been integrated and the updated hypothesis takes into account the other theories which has significant overlap with the VDH.
Jones et al (2018) is the most recent review of the VDH; in the review, they integrate new findings of folate, vitamin D, the VDR, and skin color genes with other supposedly competing hypotheses into a new and improved VDH model which will be discussed at the end of this article.
Vitamin D is an important hormone (since it is a steroid, not a vitamin), which is the only one that is produced exogenously (from UV rays). Vitamin D is responsible for many physiologic functions including: regulating calcium levels by increasing calcium absorption, stimulates intestinal absorption of phosphate, stimulates osteoblasts which then produce receptor activator nuclear factor (RANKL) which then stimulates osteoclastogenesis which then activates osteoclasts for bone reabsorption (DeLuca, 2004). It has been further noted that around 5 percent of the human genome is under the influence of vitamin D (Jones et al, 2018).
Folate is an important water-soluble B vitamin. Since vitamin D and folate are linked by their sensitivities to UVR, then we must look at them independently and see what they do. In the case of folate, UVR causes folate degradation through the absorption of UVRs or, on the other hand, when folate oxidizes through free radicals after UVR exposure (Jones et al, 2018). So the hypothesis proposes that skin color in high UV areas evolved due to the need for protection of folate levels due to UVR degradation. On the other hand, depigmentation occurred in order for the body to produce adequate vitamin D in low UV areas.
The potential impacts of a deficiency of these nutrients on natural selection is an ongoing debate and is a common argument raised against the vitamin D–folate hypothesis. However, these arguments often do not consider that the benefits of an adequate vitamin D and folate status on reproductive success extend far beyond their roles in maintaining reproductive health.
Vitamin D receptor
In recent years, it has been found that the VDR has had a profound influence on our adaptation to local climates our ancestors found themselves in after the trek out of Africa. Most cells and organs of the body have a vitamin D receptor (Wacker and Holick, 2013), so the importance of the VDR and certain genes involved in the production of skin color, vitamin D, and folate can be seen. Thus, evidence for the hypothesis would be differential expression of certain genes that are related to the VDR. Jones et al (2018) report on a few common VDR variants and ethnicity: FOK1 which has a lower frequency in African than European and East Asian populations, and Cdx2 which was highest in Africans and lowest in Europeans. Tiosano et al (2016) reported that multiple loci which are involved with the VDR gene display strong latitudinal clines, which is evidence for the hypothesis.
The VDR helps humans adapt to changes in UV radiation, it is “part of an evolutionary complex that adapts humans to changing UV radiation” (Hochberg and Templeton, 2010: 310). This is further corroborated by the fact that the VDR promoter and skin color genes are epistatic (Popsiech et al, 2014; Tiosano et al, 2016). Skin pigmentation levels, furthermore, determine plasma vitamin D levels and VDR autoregulation (Saccone, Asani, and Bornman, 2015).
The VDR works in concert with retinoic acid receptors (Schrader et al, 1993) which then bind to nucleotide base pairs called the vitamin D-responsive elements (VDRE) which then exert their effects on gene expression (Kato, 2000; Pike and Meyer, 2010; Janik et al, 2017).
Vitamin D elicits numerous functions on gene expression through the VDR, by binding elements of vitamin D to the target genes. Since the VDR works together with other receptors that bind to the VDRE, they can have strong effects on gene expression. Now, we know that vitamin D and folate are important for humans. We know that the VDR gene appears to be under strong selection, though only in the context of other genes (Tiosano et al, 2016). Thus, the VDR—along with folate and vitamin D—are extremely important for gene expression and the adaptation of the human body to differing climates.
Skin barrier hypothesis
The skin barrier hypothesis (SBH) proposes that dark skin color arose to protect against environmental damage. This hypothesis is based on the fact that darker-pigmented peoples posess an enchanced barrier function in comparison to ligher-pigmented people, which is mainly due to the role of melanin in the scattering of UVR across the skin (Jones et al, 2018). Jones et al state that this hypothesis is “proposed as a discrete theory to the vitamin D-folate hypothesis“, but since both vitamin D and folate both have other responsibilities in the human body such as the development of skin structure, and the development of defense mechanisms that protect against UV radiation including heat and microbial stressors.
Folate may also have another important role in the human body: regulating the production, and stabilizing tetrahydrobiopterin. Melanin supports folate from UVR degradation, which then supports folate’s influence on melanin. But, as Jones et al write, tetrahydrobiopterin also acts as a cofactor in the synthesis of nitric oxide which is important in regard to vasoconstriction (blood vessel constriction). Vasoconstriction is related to increased heat flow since blood vessels are constricted, along with an increase in heart rate. As I have noted in the past, shivering revs the body’s metabolism in cold clmates in order to produce ample heat. Jones et al (2018) write:
From an evolutionary perspective, our ability to maintain vasodilation/vasoconstriction mechanisms would have been important in surviving varying UVR environments. As these mechanisms may been seen as relatively short-term responses to temperature changes, they are likely to be of greater importance in temperate UVR environments rather than environments of high UVR. This is supported by nitric oxide dependent vasodilation shown to be reduced in darkly skinned populations . This suggests that vasodilation processes offer no advantage in extreme UVR environments but may be important in temperate UVR environments, where seasonal and daily temperature fluctuations are seen.
Thus, since there would be no advantage for this mechanism in equatorial climates, it must be for more colder, Arctic climates which further lends credence to the VDH. (Since vitamin D and folate play many roles in regard to human physiologic adaptation to climate, along with the VDR.)
Metabolic conservation hypothesis
This hypothesis proposes that our ancestors became depigmented after the migrations out of Africa since there was a need to draw energetic resources away from melanin production and move that energy that would have been for melanin production for other metabolic processes that a population would need in a colder environment. Thus, it is argued that the lighter skin of European and East Asian populations can be explained by the need energetic resources being moved away from pigmenting the skin to other, more important, metabolic processes that the ancestors of Europeans and East Asians experienced. But this hypothesis has numerous premises of the VDH, including the main premise: that human skin depigmented as we migrated into areas with fewer UV rays (Jones et al, 2018). Thus, vitamin D was extremely important in driving the effects of vasodilation/vasoconstriction.
Clearly, the role of vitamin D in the adipose tissue was important for human adaptation to colder climates. Since lighter skin can produce more vitamin D in low UV climates, this was another factor that helped when we left Africa: skin lightened for better vitamin D synthesis. Since vitamin D synthesis is related to gene expression and expression of about 5 percent of our genomes, the production of more vitamin D was beneficial. So depigmentation, while being primarily due to low UV radiation, can also be seen to allow for more efficient physiologic responses and adaptations to the newer, colder climates.
Skin mutagenesis hypothesis
The last competing theory is the skin mutagenesis hypothesis. This hypothesis proposes that skin pigmentation arose as a mechanism to protect against various skin cancers. The hypothesis is based on the fact that darker-pigmented individuals are at lower risk of developing skin cancers since their skin pigmentation can fight off UV radiation. Of course, knowing what we know about vitamin D and folate, these two agents would be involved regarding this hypothesis, since both agents have photoprotective effects. Vitamin D is extremely important to DNA repair (Graziano et al, 2016), as vitamin D reduces cell and DNA damage.
Though many authors dispute the claims of this hypothesis since the effects of skin cancer would occur after the reproductive years and would thusly not have an effect on natural selection for skin color. Though those who argue for the validity of the hypothesis propose that it would help in hunter-gatherer peoples whose old train their young their ways of life.
Since these interactions have between these variables have been verified at the molecular genetic level, this lends even more credence to the VDH. (The findings inclue the frequency of common VDR variants between different ethnic groups, to UVR and folate metabolism genes which were found to be significantly associated with the frequency of 16 common folate variants and skin pigmentation in a genomic analysis of 30,000 people which were novel relationships; Jones et al, 2018a). These findings discussed by Jones et al (2018b) “indicate the existence of interactions between UVR, skin type, and vitamin D and folate genes, and they provide supporting molecular evidence for the vitamin D–folate hypothesis.”
Madrigal and Kelly (2007a) tested a sexual selection hypothesis proposed by a few proponents of the sexual selection hypithesis. Madrigal and Kelly (2007a) tested the hypothesis that skin color reflectance should be positively correlated with distance from the equator. They, however, showed that the pattern in skin color dimorphism seen around the globe was not consistent with the sexual selection hypothesis, and thus their data did not lend credence to the sexual selection hypothesis. The hypothesis states that in areas with low UV radiation, environmental selection for skin color should be relaxed and there should be a higher rate of sexual dimorphism in peoples from northerly climates due to sexual selection for lighter-skinned women. Nevertheless, the data compiled by Madrigal and Kelly (2007a) do not lend credence to the hypothesis.
Frost (2007) responded that Madrigal and Kelly (2007a) presumed that sexual selection was equal in all areas, but was constrained by natural selection for dark skin. Frost (2007) also states that sexual dimorphism in human skin color may not be able to be expressed in lighter-skinned populations at higher latitudes. Frost’s objections stem from the fact that Madrigal and Kelly tested a specific hypothesis proposed by proponents of the sexual selection hypothesis, though Madrigal and Kelly hope that Frost can test his hypotheses. However, I think it’s a moot issue. Sexual selection for women occurred after selection for light skin due to vitamin D synthesis which ensured more calcium for pregnancy and lactation.
Thusly, sexual selection for lighter skin would continue to ensure ample vitamins for women and their pregnancies and lactation to feed their babies. This would further be butressed by the fact that vitamin D exerts effects on the adipocites which lends even more credence to the claim that light skin evolved first for vitamin D synthesis. Vitamin D then exerted effects on the adipocite since more vitamin D could be produced in the absence of high levels of UV, which then aided in human physiologic adaptations to climate.
Integration of current skin color theories
As can be seen from the competing theories, they are not necessarily explaining different things, and each supposed competing theory has an aspect from the VDH in it. Thusly, it is possible to integrate the so-called competing theories into a larger explanatory framework.
Jones et al (2018b) update the VDH by integrating the other theories into it, since they are similar and do not contradict the VDH (since aspects of each one can be used to explain different aspects of the VDH). The updated hypothesis is thus:
Vitamin D and folate have differing sensitivities to UVR. Vitamin D can be synthesized following UVR exposure, folate may be degraded. So the VDH proposes that the two differing skin colors (light and dark) evolved at differing latitudes as a “balancing mechanism” to maintain adequate levels of the two agents vitamin D and folate. Since adequate levels of vitamin D and folate were maintained, there would be no ill health effects after migrating into colder climates. Vitamin D and folate both act as photoprotectors of the skin and can decrease environmental stressors. Vitamin D also exerts important effects on adipocites—both types—which then further aid in human physiologic adaptations to the cold. Perhaps most importantly, the VDR and skin color genes are epistatic—the VDR is imperative in the human body’s adaptation to new climates.
The latest research (reviewed by Jones et al, 2018b) show strong support for the interaction between genes and folate/vitamin D processes with skin pigmentation and UVR.
Health disparities due to vitamin D deficiency are well-noted in the literature. Human migrations over the recent centuries and decades have caused environmental mismatches between a population’s adapted skin type and current UV level in the location the population migrated to. Many darkly-pigmented people now live in areas with low UVR, and thusly suffer from health consequences. This leads to them either not having an adequate vitamin D-folate balance along with the risk of not having the adequate skin protections for a given environment, since UV rays influence folate and vitamin D production and so, a mismatched skin color to UV environment would cause problems for skin protection since the environment is not ancestral to that certain skin color.
As I have previously noted, it has been argued that blacks are not vitamin D deficient, and thusly not vitamin D deficient. Though, these claims rest on a slew of false arguments that have since been rebutted. It has been argued that since blacks are deficient in vitamin D, which begins in the womb, and vitamin D deficiencies cause changes in large and small arteries and arterials, that vitamin D deficiency could be the cause of higher rates of hypertension in black Americans (Rostand, 2010).
The role of vitamin D, folate, the VDR, and certain genes is under further invesitgation. This group of agents exert powerful effects on human physiology which then help with the adaptation of humans to differing climates. Folate and the vitamin D receptor play a crucial role in protecting the skin from environmental and microbial stressors. Vitamin D and the VDR are expressed in the adipose tissue, while vitamin D regulates adipogenesis and adipocite apoptosis (Abbas, 2017). Further evidence shows that there are multiple loci that are involved in the VDR that show latitudinal clines (Tiosano et al, 2016). One of the most things that lends credence to the VDH is the fact that the VDR and skin color genes are epistatic and help humans adapt to climates.
The VDH is in great shape, contrary to popular belief (Elias, Williams, and Bikle, 2016). The VDH is one of the only games in town to explain the skin color gradient noticed around the world, with vitamin D being the only agent that accounts for skin color differences. The VDH explains how and why human skin color is vastly different, and the main reason is adaptation to UV rays—or lack thereof.
Grant (2018) concludes that:
The UVB–vitamin D–cancer hypothesis has considerable supporting scientific evidence from a variety of study types: geographical ecological, observational, and laboratory studies of mechanisms, as well as several clinical trials.
Clearly, the VDH explains the incidence of the observed skin gradiation around the world the best out of the so-called competing hypotheses (which are similar enough to the VDH to where they can be absorbed into the VDH). Most importantly, the VDH predicted a novel fact—that molecular genetic evidence would show that light skin evolved independently numerous times in our lineage (Jablonksi and Chaplin, 2009).
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.
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.
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 Differences in Penis Size Revisited: Is Rushton’s r/K Theory of Race Differences in Penis Length Confirmed?
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.
The first Darwin Day I started writing just for this day, I wrote about (and defended Darwin’s words) how both Creationists and evolutionists who are themselves evolutionary progressionists twist Darwin’s words for their own gain. Darwin never wrote in The Descent of Man that the ‘higher races’ would take out ‘the lower races’, but that doesn’t stop Creationists and evolutionists—who I presume have not read one sentence in Darwin’s words from one of his books—from taking what Darwin meant out of context and attributing to him beliefs he does not hold. This year, though, I am going in a different direction. The Modern Synthesis (MS) has causation in biology wrong. The MS upholds the ‘gene’ as one of the highest seats in evolutionary biology, with a sort of ‘power’ to direct. Though, as I will show, genes do nothing unless transcribed by the system. Since the MS has causation in biology wrong, then we either need to extend or replace the MS.
To begin, Darwin, without knowledge of genes or other hypothesized units of inheritance, had a theory of inheritance in which things called ‘gemmules’ (what Darwin called heritable molecules) were transmitted to offspring (Choi and Mango, 2014). It’s ironic, because Darwin’s theory of inheritance was one of the more Lamarckian theories of inheritance in his day, and Darwin himself sympathized with the Lamarckian view of evolution—he most definitely did not discard it like modern-day Darwinists do. Darwin suggested that these gemmules circulated in the body and that some were used for the regeneration of some bodily tissues, but most aggregated in the reproductive organs (Jablonka and Lamb, 2015: 23). Further, according to Darwin, gemmules were not always immediately used but could reappear later in life or even be used in future generations. Darwin even said that “inheritance must be looked at as a form of growth” (Darwin, 1883, vol 2, p. 398; quoted by Jablonka and Lamb, 2015: 24).
The crux of the MS is the selfish gene theory of Dawkins (1976). Dawkins (1976, 2006) writing “They are in you and me; they created us, body and mind; and their preservation is the ultimate rationale for our existence.” “They”, of course, being genes. The gene has been given a sort of power that it does not have, but has been placed on it by overzealous people, quick to jump to conclusions while we still have yet to understand what ‘genes’ do. The MS—with the selfish gene theory—is at the forefront of the neo-Darwinist revolution, that evolution is gene-centered, with genes playing the starring role in the evolutionary story.
Though, numerous researchers are against such simplistic and reductionist viewpoints of evolution, mainly the gene-centered view of evolution pushed by the MS. There is no privileged level of causation in biology (though I will state later in this article that I think ATP comes close to it) (Noble, 2016).
Neo-Darwinists, like Richard Dawkins, overstate natural selection’s importance regarding evolution. They elevate the gene’s overall importance. In the quote from Dawkins above, where he stated that “they” (genes) “created us, body and mind”, he is implying that genes are a sort of ‘blueprint’, like a ‘plan’ or ‘recipe’ for the form of the organism. But this was taken care of by Susan Oyama in her 1985 book The Ontogeny of Information where she writes on pages 77:
“Though a plan implies action, it does not itself act, so if the genes are a blueprint, something else is the constructor-construction worker. Though blueprints are usually contrasted with building materials, the genes are quite easily conceptualized as templates for building tools and materials; once so utilized, of course, they enter the developmental process and influence its course. The point of the blueprint analogy, though, does not seem to be to illuminate developmental processes, but rather to assume them and, in celebrating their regularity, to impute cognitive functions to genes. How these functions are exercised is left unclear in this type of metaphor, except that the genetic plan is seen in some peculiar way to carry itself out, generating all the necessary steps in the necessary sequence. No light is shed on multiple developmental possibilities, species-typical or atypical.“
The genes-as-blueprints canard is one that is heavily used by proponents of the MS. Oyama also writes on page 53 “Just as traditional thought placed biological forms in the mind of God, so modern thought finds many ways of endowing the genes with ultimate formative power, a power bestowed by Nature over countless millennia.” This same sentiment from Oyama is also echoed by developmental systems theorist and psychologist David Moore in his book The Dependent Gene: The Fallacy of “Nature VS. nurture”, where he writes:
Such contextual dependence renders untenable the simplistic belief that there are coherent, long-lived entities called “genes” that dictate instructions to cellular machinery that merely constructs the body accordingly. The common belief that genes contain context-independent “information”—and so are analogous to “blueprints” or “recipes”—is simply false. (p. 81) (Quoted from Schneider, 2007)
Environmental factors are imperative in determining which protein-coding exons get read from a cistron, when and how often. So the very concept of a gene depends on the environment and environmental inputs, and thusly gene ABC does not code for trait T on its own.
When it comes to epigenetics (defined here as inherited changes in gene expression with no genetic change to the genome), this completely changes how we view evolution.
The underlying nucleotide sequence stays the same but differences are inherited due to environmental stressors. I’ve stated in the past that these inherited marks on the genome (through histone modification, DNA methylation, which then alter the chromatin structure of the DNA. Further, this would show up on heritability estimates as ‘genetic’ when the ’cause’ was ‘environmental’ in nature (which is also yet another reason that heritability estimates are inflated).
DNA methylation, histone modification and noncoding RNA all can affect the structure of chromatin. As of now, the mechanisms of mitotic inheritance aren’t too well known, but advances in the field are coming.
If you want to talk the P and F1 generations regarding transgenerational epigenetics, then you must realize that these changes do not occur on the genome, the genome remains the same, just certain genes are expressed differently (as I’m sure you know). Though mi-MRNA signals can change the DNA methylation patterns in the F2 sperm which then is replicated in meiotic and mitotic cycles (Trerotola et al, 2015).
For another similar process on how DNA methylation persists, this (semiconservative) replication of DNA methylation occurs on both strands of the DNA which then become hemimethylated DNA which can then become fully methylated by methylase maintenance. So chromatin structure affects the genetic expression of the eukaryotic genome which then becomes the basis for epigenetic effects. Xist RNA also mediates the X-chromosome deactivation. This doesn’t even get into how and why the microbiome can also affect gene expression (which has also been called ‘the second genome’ (Zhu, Wang, and Li, 2010) with other authors calling it an ‘organ’ (Clarke et al, 2014; Brown and Hazen, 2015) this can also affect gene expression and heritable variation that becomes the target of selection (along with the other modes of selection) (Maurice, Haiser, and Turnbaug, 2014; Byrd and Segre, 2015). This shows that gene expression in the F2 and F3 generations is not so simple, and that other factors such as our gut microbiota can also affect gene expression and stressors experienced by parents and grandparents can also be passed to future generations, and may have a chance of becoming part of heritable variation that natural selection then acts on (Jablonka and Lamb, 2015).
The point of the debate with neo-Darwinists is over causation: do genes hold this ‘ultimate formative power’ as people like Dawkins contest? Or are genes nothing but ‘slaves’, passive, not active, causes as Denis Noble writes in his 2016 book Dance to the Tune of Life. (Noble, 2008 discusses genes and causation, again showing that there is no true causation, but getting technical, ATP is up there in the ‘chain’, if you want to get literal. The point is that genes do not have the ‘power’ that the neo-Darwinists think they do, they’re just slaves for the intelligent physiological system.)
When discovering the structure of DNA, Francis Crick famously announced to his drinking companions in a Cambridge tavern that he had discovered ‘the secret of life’. The director of his Institute, Max Perutz, was rather more careful than Crick when he said that DNA was the ‘score of life’. That is more correct since a musical score does nothing until it is played, DNA does nothing until activated to do so.
Recent experimental work in biological science has deconstructed the idea of a gene, and an important message of this book is that it has thereby drthroned the gene as a uniquely privileged level of causation. As we will see, genes, defined as DNA sequences, are indeed essential, but not in the way in which they are often portrayed. (Noble, 2016: 53)
A 2017 paper titled Was the Watchmaker Blind? Or Was She One-Eyed?, Noble and Noble (2017) write that organisms and their interacting populations have evolved mechanisms so that they can harness blind stochasticity, thereby generating functional changes to the phenotype as to better respond to environmental challenges. They put forth a good argument, though it really makes me think because I’ve been such a staunch critic against evolution having a ‘direction’ and against the ‘teleological view’ of evolution: “If organisms have agency and, within obvious limits, can choose their lifestyles, and if these lifestyles result in inheritable epigenetic changes, then it follows that organisms can at least partially make choices that can have long-term evolutionary impact.”
Noble and Noble (2017) argue (using Dawkins’ analogy of the Blind Watchmaker) that humans are the only Watchmakers that we know of. Humans evolved from other organisms. The ability to become a Watchmaker has evolved. Ergo, there is no surprise that there is directed agency for other organisms that directs their evolution too. There are several processes, they conclude, that could account for directed evolutionary change which are “targeted mutation, gene transposition, epigenetics, cultural change, niche construction and adaptation” (Noble and Noble, 2017). Niche construction, for instance, is heavily pushed by Kevin Laland, author of the book Darwin’s Unfinished Symphony: How Culture Made the Human Mind who has a few papers and featured it heavily in his new book. Either way, these ways in which organisms can in a way direct their own evolution are not covered by the MS.
Though I couldn’t end this article without, of course, discussing Jerry Coyne who goes absolutely crazy at people pushing to either extend or replace the MS. His most recent article is about Kevin Laland and how he is “at it again” touting “a radically different view of evolution”. It seems as Coyne has made up his mind and that the MS is all there is—he believes it is no problem for our current understanding of evolutionary theory to absorb things such as niche construction, epigenetic inheritance, stochasticity, and even (way more controversially) directed mutations. Coyne has also criticized Noble’s attacks on the MS, though Noble came back and responded to Coyne during a video presentation.
Lastly, Portin and Wilkins (2017) review the history of the gene, and go through different definitions it has been given over the decades. They conclude in this paper that they “will propose a definition that we believe comes closer to doing justice to the idea of the “gene,”
in light of current knowledge. It makes no reference to “the unit of heredity”—the long-standing sense of the term—because we feel that it is now clear that no such generic universal unit exists.” Writing on page 1361-1362:
A gene is a DNA sequence (whose component segments do not necessarily need to be physically contiguous) that specifies one or more sequence-related RNAs/proteins that are both evoked by GRNs and participate as elements in GRNs, often with indirect effects, or as outputs of GRNs, the latter yielding more direct phenotypic effects. [GRNs are genetic regulatory networks]
This is similar to what Jablonka and Lamb (2015: 17) write:
Although many psychiatrists, biochemists, and other scientists who are not geneticists (yet express themselves with remarkable facility on genetic issues) still use the language of genes as simple causal agents, and promise their audience rapid solutions to all sorts of problems, they are no more than propagandists whose knowledge or motives must be suspect. The geneticists themselves now think and talk (most of the time) in terms of genetic networks composed of tens or hundreds of genes and gene products, which interact with each other and together affect the development of a particular trait. They recognize that whether or not a trait (a sexual preference, for example) develops does not depend, in the majority of cases, on a difference in a single gene. It involves interactions among many genes, many proteins and other types of molecule, and the environment in which an individual develops.
The gene as an active causal actor has been definitively refuted. Genes on their own do nothing at all, until they are transcribed by the intelligent physiological system. Noble likens genes as slaves that are used by the system to carry out processes by and for the system. So genes are caused to give their information by and to the system that activates them (Noble, 2011). Noble’s slave metaphor makes much more sense than Dawkins’ selfish metaphor, since genes are used like slaves by the system, the genes are then caused to give their information by and to the system that activates them, which shows how they are a passive, not active, cause, completely upending the MS and how it views causation in biology. Indeed, Jablonka and Lamb state that one of their problems with Dawkins is that “Dawkins assumes that the gene is the only biological (noncultural) hereditary unit. This simply is not true. There are additional biological inheritance systems, which he does not consider, and these have properties different from those we see in the genetic system. In these systems his distinction between replicator and vehicle is not valid.”
So, both Gould and Dawkins overlooked the inheritance of acquired characters, as Jablonka and Lamb write in their book. They argue that inherited variation had a large effect on the evolution of species, but admit that evidence for the view is scant. They write on page 145 “If you accept that heritable epigenetic variation is possible, self-evidently some of the variants will have an advantage relative to other variants. Even if all epigenetic variations were blind, this would happen, and it’s very much more likely if we accept that a lot of them are induced and directed.” Not everything that is inherited is genetic.
DNA is found in the cell, and what powers the cell? ATP (adenosine triphosphate). Cells use and store ATP to carry out their functions (Khakh and Burnstock, 2016). Cells produce ATP from ADP and Pi. Cells use exergonic reactions to provide the energy needed to synthesize ATP from ADP and Pi. The hydrolysis of ATP provides the energy needed to drive endergonic actions.So the cells continuously produced more ATP from ADP and Pi to then carry out diverse functionings across the body. So, in a way, you can argue that one of the ultimate causes is ATP since it has to power the cell, then you can look at all of the other reactions that occur before ATP is created and privilege that part of the chain, but there will never be some ultimate causation, since, as Noble argues in his book Dance to the Tune of Life, there is no privileged causation in biology.
In conclusion, evolution, development, and life, in general, is extremely complex. Paradigms like the selfish gene—a largely reductionist paradigm—do not account for numerous other factors that drive the evolution of species, such as targeted mutation, niche construction etc. An extended evolutionary synthesis that integrates these phenomena will better be able to describe what occurs to drive the evolution of species, and if the directed mutation idea has any weight, then it will be interesting to see how and why certain organisms have evolved this ability. It’s ironic how the MS is being defended as if it is infallible—like it can do no wrong and that it does not need to be added to/extended or replaced by something else that incorporates the phenomena brought up in this article.
Either way, a revolution in modern biology is coming, and Darwin would have it no other way. The Modern Synthesis has causation in biology wrong: the gene is not an active agent in evolution, it only does what it is told by the intelligent physiological system, and so we must look at whole organisms and not reduce organisms down to genes, but we must look at the whole organism—a holistic view of the organism, not one that is reduced down to just ‘the genes’, because there is no privileged level of causation in biology (Noble, 2016).
The microbiome is the number and types of different microorganisms and viruses in the human body. Racial differences are seen everywhere, most notably in the phenotype and morphology. Though, of course, there are unseen racial differences that then effect bodily processes of different races and ethnic groups. The microbiome is one such difference, which is highly heritable (Goodrich et al, 2014; Beaumont et al, 2016; Hall, Tolonen, and Xavier, 2017) (though they use the highly flawed twin method, so heritabilities are most likely substantially lower). They also show that certain genetic variants predispose individuals to microbial dysbiosis. However, diet, antibiotics and birth mode can also influence the diversity of microbiota in your biome (Conlon and Bird, 2015; Bokulich et al, 2017; Singh et al, 2017) and so while the heritability of the microbiome is important (which is probably inflated due to the twin method), diet can and does change the diversity of the biome.
It used to be thought that our bodies contained 90 percent bacteria and only 10 percent human cells (Collen, 2014), however that has been recently debunked and the ratio is 1.3 to 1, human to microbe (Sender, Fuchs, and Milo, 2016). (Collen’s book is still an outstanding introduction to this subject despite the title of her book being incorrect.) Though the 10:1 microbe/human cell dogma is debunked, in no way does that lessen the importance of the microbiome regarding health, disease and longevity.
Lloyd-Price, Abu-Ali, and Huttenhower (2016) review definitions for the ‘healthy human microbiome’ writing “several population-scale studies have documented the ranges and diversity of both taxonomic compositions and functional potentials normally observed in the microbiomes of healthy populations, along with possible driving factors such as geography, diet, and lifestyle.” Studies comparing the biomes of North and South America, Europe and Africa, Korea and Japan, and urban and rural communities in Russia and China have identified numerous different associations that are related to differences in the microbiome between continents that include (but are not limited to) diet, genetics, lifestyle, geography, and early life exposures though none of these factors have been shown to be directly causal regarding geographic microbiome diversity.
Gupta, Paul, and Dutta (2017) question the case of a universal definition of a ‘healthy microbiome’ since it varies by geographic ancestry. Of course, ancestry and geographic location influence culture which influences diet which influences microbiome diversity between populations. This, of course, makes sense. why have a universal healthy microbiome with a reference man that doesn’t reflect the diversity of both the individual and group differences in the microbiome? This will better help different populations with different microbiomes lose weight and better manage diseases in certain populations.
The microbiome of athletes also differs, too. Athletes had enhanced microbiome diversity when compared to non-athletes (Clarke et al, 2016). In a further follow-up study, it was found that microbial diversity correlated with both protein consumption and creatine kinase levels in the body (Clarke et al, 2017) are proxies for exercise, and since they’re all associations, causality remains to be untangled. Nevertheless, these papers are good evidence that both lifestyle and diet leads to changes in the microbiome.
Fortenberry (2013: 165) notes that American racial and ethnic classifications are “social and political in origin and represent little meaningful biologic basis of between-group racial/ ethnic diversity“. It is also known that eating habits, differing lifestyles and metabolic levels also influence the diversity of the microbiome in the three ‘races’* studied (Chen et al, 2016), while deep sequencing of oral microbiota has the ability to classify “African Americans with a 100% sensitivity and 74% specificity and Caucasians with a 50% sensitivity and 91% specificity” (Mason et al, 2014). The infant microbiome, furthermore, is influenced by maternal diet and breastfeeding as well as the infant’s diet (Stearns et al, 2017). This is why differences in race/ethnicity call into question the term of ‘healthy human microbiota’ (Gupta, Paul, and Dutta, 2017). These differences in the microbiome also lead to increased risk for colorectal cancer in black Americans (Goyal et al, 2016; Kinross, 2017).
Further, the healthy vagina “contains one of the most remarkably structured microbial ecosystems, with at least five reproducible community types, or “community state types” (Lloyd-Price, Abu-Ali, and Huttenhower 2016). The diversity of the microbiome in the vagina also varies by race. It was found that 80 percent of Asian women and 90 percent of white women harbored a microbiota species named Lactobacillus, whereas only about 60 percent of ‘Hispanics’ and blacks harbored this species. The pH level, too, varied by race with blacks and ‘Hispanics’ averaging 4.7 and 5.0 and Asians and whites averaging 4.4 and 4.2. So, clearly, since Asians and whites have similar vaginal pH levels, then it is no surprise that they have similar levels of vaginal Lactobacillus, whereas blacks and ‘Hispanics’, with similar pH levels have similar vaginal levels of Lactobacillus.
White subjects also have more diverse species of microbiota than non-white subjects while also having a different microbiota structure (Chen et al, 2015). Caucasian ethnicity/race was also shown to have a lower overall microbiome diversity, but higher Bacteroidetes scores, while white babes also had lower scores of Proteobacteria than black Americans (Sordillo et al, 2017). This comes down to both diet and genetic factors (though causation remains to be untangled).
Differences in the skin microbiome also exist between the US population and South Americans (Blaser et al, 2013). They showed that Venezuelan Indians had a significantly different skin biome when compared to US populations from Colorado and New York, having more Propionibacterium than US residents. Regarding the skin microbiota in the Chinese, Leung, Wilkins, and Lee (2015) write “skin microbiomes within an individual is more similar than that of different co-habiting individuals, which is in turn more similar than individuals living in different households.” Skin microbiota also becomes similar in cohabitating couples (Ross, Doxey, and Neufeld, 2017) and even cohabitating family members and their dogs (Song et al, 2013; Cusco et al, 2017; Torres et al, 2017).
Differences between the East and West exist regarding chronic liver disease, which may come down to diet which may influence the microbiota and along with it, chronic liver disease. (Nakamoto and Schabl, 2016). The interplay between diet, the microbiome and disease is critical if we want to understand racial/ethnic differentials in disease acquisition/mortality, because the microbiome influences so many diseases (Cho and Blaser, 2012; Guinane and Cotter, 2013; Bull and Plummer, 2014; Shoemark and Allen, 2015; Zhang et al, 2015; Shreiner, Kao, and Young, 2016; Young, 2017).
The human microbiome has been called our ‘second genome’ (Zhu, Wang, and Li, 2010; Grice and Seger, 2012) with others calling it an ‘organ’ (Baquero and Nombela, 2012; Clarke et al, 2014; Brown and Hazen, 2015). This ‘organ’, our ‘second genome’ can also influence gene expression (Masotti, 2012; Maurice, Haiser, and Turnbaugh, 2013; Byrd and Seger, 2015) which could also have implications for racial differences in disease acquisition and mortality. This is why the study of the microbiome is so important; since the microbiome can up- and down-regulate gene expression—effectively, turning genes ‘on’ and ‘off’—then understanding the intricacies that influence the microbiome diversity along with the diet that one consumes will help us better understand racial differences in disease acquisition. Diet is a huge factor not only regarding obesity and diabetes differences within and between populations, but a ‘healthy microbiome’ also staves off obesity. This is important. The fact that the diversity of microbiota in our gut can effectively up- and down-regulate genes shows that we can, in effect, influence some of this ourselves by changing our diets, which would then, theoretically, lower disease acquisition and mortality once certain microbiome/diet/disease associations are untangled and shown to be causative.
Finally, the Hadza have some of the best-studied microbiota, and since they still largely live a hunter-gatherer lifestyle, this is an important look at what the diversity of microbiota may have looked like in our hunter-gatherer ancestors (Samuel et al, 2017). The fact that they noticed such diverse changes in the microbiome—some species effectively disappearing during the dry season and reappearing during the wet season—is good proof that what drives these changes in the diversity of the microbiota in the Hadza are seasonal changes in diet which are driven by the wet and dry seasons.
Gut microbiota may also influence our mood and behavior, and it would be interesting to see which types of microbiota differ between populations and how they would be associated with certain behaviors. The microbes are a part of the unconscious system which regulates behavior, which may have causal effects regarding cognition, behavioral patterns, and social interaction and stress management; this too makes up our ‘collective unconscious’ (Dinan et al, 2015). It is clear that the microbes in our gut influence our behavior, and it even may be possible to ‘shape our second genome’ (Foster, 2013). Endocrine and neurocrine pathways may also be involved in gut-microbiota-to-brain-signaling, which can then alter the composition of the microbiome and along with it behavior (Mayer, Tillisch, and Gupta, 2015). Gut microbiota also plays a role in the acquisition of eating disorders, and identifying the specific microbiotal profiles linked to eating disorders, why it occurs and what happens while the microbiome is out of whack is important in understanding our behavior, because the gut microbiome also influences our behavior to a great degree.
The debate on whether or not racial/ethnic differences in microbiome diversity differs due to ‘nature’ or ‘nurture’ (a false dichotomy in the view of developmental systems theory) remains to be settled (Gupta, Paul, and Dutta, 2017). However, like with all traits/variations in traits, it is due to a complex interaction of the developmental system in question along with how it interacts with its environment. Understanding these complex disease/gene/environment/microbiotal pathways will be a challenge, as will untangling direct causation and what role diet plays regarding the disease/microbiota/dysbiosis factor. As we better understand our ‘second genome’, our ‘other organ’, and individual differences in the genome and how those genomic differences interact with different environments, we will then be able to give better care to both races/ethnies along with individuals. Just like with race and medicine—although there is good correlative data—we should not jump to quick conclusions based on these studies on disease, diet, and microbiotal diversity.
The study of ethnic/racial/geographic/cultural/SES differences in the diversity of the microbiome and how it influences disease, behaviors and gene expression will be interesting to follow in the next couple of years. I think that there will be considerable ‘genetic’ (i.e., differences out of the womb; I am aware that untangling ‘genetic’ and ‘environmental’ in utero factors is hard, next to impossible) differences between populations regarding newborn children, and I am sure that even the microbiota will be found to influence our food choices in the seas of our obesogenic environments. The fact that our microbiota is changeable with diet means that, in effect, we can have small control over certain parts of our gene expression which may then have consequences for future generations of our offspring. Nevertheless, things such as that remain to be uncovered but I bet more interesting things never dreamed of will be found as we look into the hows and whys of both individual and populational differences in the microbiome.
Most race deniers say that race isn’t real because, as Lewontin (1972) and Rosenberg (2002) state, the within-group variation is larger than the between-group variation. Though, you can circumvent this claim by not even looking at genes/allele frequencies between races, you can show that race is real by looking at morphology, phenotype and geographic ancestry. This is one of Michael Hardimon’s race categories, the minimalist concept of race. This concept does not entail anything that we cannot physically ‘see’ with our eyes (e.g., mental and psychological traits are off the table). Using these concepts laid out by Hardimon can and does prove that race is real and useful without even arguing about any potential mental and psychological differences between human races.
Morphology is one of the most simple tells for racial classification. Just by looking at average morphology between the races we can use attempt to use this data point as a premise in the argument that races exist.
East Asians are shorter with shorter limbs and have an endomorphic somatype. This is due to evolving in cold climate, as a smaller body and less surface area can be warmer much quicker than a larger body. This is a great example of Allen’s rule: that animals in colder climates will be smaller than animals in warmer climates. Using average morphology, of course, can show how the population in question evolved and where they evolved.
Regarding Europeans, they have an endomorphic somatype as well. This, again, is due to where they evolved. Morphology can tell us a lot about the evolution of a species. Though, East Asians and Europeans have similar morphologies due to evolving in similar climates. Like East Asians, Europeans have a wider pelvis in comparison to Africans, so this is yet another morphological variable we can use to show that race exists.
Finally, the largest group is ‘Africans’ who have the largest phenotypic and genetic diversity on earth. Generally, you can say that they’re tall, have long limbs and a short torso, which is due to evolving in the tropics. Furthermore, and perhaps most important, Africans have narrower pelves than East Asians and Europeans. This character is one of the most important regarding the reality of race because it’s one of the most noticeable, and we do notice in when it comes to sports competition because that certain type of morphology is conducive to athletic success. (Also read my recent article on strength and race and my article on somatype and race for more information on morphologic racial differences.)
Morphology is a part of the phenotype too, obviously, but there is a reason why it’s separated. As is true with morphology, different characters evolved due to cultural evolution (whether or not they adopted farming early) or evolution through natural selection, drift and mutation. Though, of course, favorable mutations in a certain environment will be passed on and eventually become a part of the characteristics of the population in question.
East Asians have the epicanthic fold, which probably evolved to protect the eye from the elements and UV rays on the Mongolian steppes. They also have softer features than Europeans and Africans, but this is not due to lower testosterone as is popularly stated. (Amusingly enough, there is a paper that stated that East Asians have Down Syndrome-like qualities due to their epicanthic folds to bring up one reason.) Even then, what some races find attractive or not can show how and why certain facial phenotypes evolved. To quote Gau et al (2018):
Compared with White women, East Asian women prefer a small, delicate and less robust face, lower position of double eyelid, more obtuse nasofrontal angle, rounder nose tip, smaller tip projection and slightly more protruded mandibular profile.
And they conclude:
The average faces are different from the attractive faces, while attractive faces differ according to race. In other words, the average facial and aesthetic criteria are different. We should use the attractive faces of a race to study that races aesthetic criteria.
We can use studies such as this to discern different facial phenotypes, which, again, proves that race exists.
The climate one’s ancestors evolved in dictates nose shape. In areas where it is extremely dry and also has a lot of heat, a larger mucous area is required to moisten inspired (inhaled) air, which is why a more flat and narrow nose is needed.
Zaidi et al (2017) write:
We find that width of the nares is correlated with temperature and absolute humidity, but not with relative humidity. We conclude that some aspects of nose shape may have indeed been driven by local adaptation to climate.
Though climate, of course, isn’t the only reason for differences in nose shape; sexual selection plays a part too, as seen in the above citation on facial preferences in East Asian and European women.
There are also differences in hirsutism between the races. Racial differences exist regarding upper lip hair, along with within-race differences (Javorsky et al, 2014). The self-reported races of African American, East Asian, Asian Indian, and ‘Hispanic’ predicted facial hair differences in women, but not how light their skin was. The women were from Los Angeles, USA; Rome, Italy; Akita, Japan; and London, England. Indian women had more hair than any other race, while European women had the least. Regarding within-race variation, Italian women had more hair on their upper lip than American and British women. Skin lightness was related to hair on the upper lip. (Also read my article The Evolution of Human Skin Variation for more information on racial differences in skin color.)
In 2012, an interesting study was carried out on hair greying on a sample population of a large number of the world’s ethnies titled Greying of the human hair: a worldwide survey, revisiting the ‘50’ rule of thumb. The objective of the study was to test the ’50-50-50′ rule; that at age 50, 50 percent of the population has at least 50 percent of their hair grey. Africans and Asians showed fewer grey hairs than whites who showed the most. The results imply that hair greyness varies by ethnicity/geographic origin, which is perfect for the argument laid out in this article. The global range for people over 50 with 50 percent or more of their hair grey was between 6 and 23 percent, far lower than what was originally hypothesized (Panhard, Lozano, and Loussouarn, 2012). They write on page 870:
With regard to the intensity of hair greying, the lowest values were found among African and Asian groups, especially Thai and Chinese, whereas the highest values were in subjects with the blondest hair (Polish, Scottish, Russian, Danish, CaucasianAustralian and French).
Altogether, these analyses clearly illustrate that the lowest incidences and intensities of grey hair are found in populations of the darkest hair whereas the highest intensities are found in populations with the lightest hair tones.
Actual hair diversity is much more concentrated in Europeans, however (Frost, 2005). (See Peter Frost’s article Why Do Europeans Have So Many Hair and Eye Colors?) It is largely due to sexual selection, with a few climatic factors thrown in. Dark hair, on the other hand, is a dominant trait, which is found all over the world.
Zhuang et al (2010) found significant differences in facial morphology between the races, writing:
African-Americans have statistically shorter, wider, and shallower noses than Caucasians. Hispanic workers have 14 facial features that are significantly larger than Caucasians, while their nose protrusion, height, and head length are significantly shorter. The other ethnic group was composed primarily of Asian subjects and has statistically different dimensions from Caucasians for 16 anthropometric values.
Statistically significant differences in facial anthropometric dimensions (P < 0.05) were noted between males and females, all racial/ethnic groups, and the subjects who were at least 45 years old when compared to workers between 18 and 29 years of age.
Blacks had statistically significant differences in lip and face length when compared to whites (whites had shorted lips than blacks who had longer lips than whites).
Brain size and cranial morphology, too, differs by geographic ancestry which is directly related to the climate where that population evolved (Beals, Smith, and Dodd, 1984). Most every trait that humans have—on average of course—differs by geographic location and the cause of this is evolution in these locations along with being a geographically isolated breeding population.
The final piece to this argument is using where one’s recent ancestors came from. There are five major populations from a few geographic locales: Oceania, the Americas (‘Native Americans), Europe, Africa and East Asia. These geographic locales have peoples that evolved there and underwent different selective pressures due to their environment and their bodies evolved to better suit their environment, and so racial differences in morphology and phenotype occurred so the peoples could survive better in that location. No one part of this argument is more important than any other, though geographic ancestry is the final piece of the puzzle that brings everything together. Because race is correlated with morphology and phenotype, the geographic ancestry dictates what these characteristics look like.
Thus, this is the basic argument:
P1: Differing populations have differing phenotypes, including (but not limited to) facial structure, hair type/color, lip structure, skull size, brain size etc.
P2: Differing populations have differing morphology which, along with this population’s phenotype, evolved in response to climatic demands along with sexual selection.
P3: This population must originate from a distinct geographic location.
C: If all three of the above premises are true, then race—in the minimalist sense—exists and is biologically real.
This argument is extremely simple, and along with the papers cited above in support of the three premises and the ultimate conclusion, it will be extremely hard for race deniers to counter. We can say that P1 is logically sound because geographically isolated populations differ in the above-mentioned criteria. We can say that P2 is logically sound since differing populations have differing morphology (as I have discussed numerous times which leads to racial differences in sporting competition) such as differing trunk lengths, leg lengths, arm lengths and heights which are largely due to evolution in differing climates. We can say that P3 is logically sound because the populations that would satisfy P1 and P2 do come from geographically distinct locations; that is, they have a peculiar ancestry that they only share.
This concept of minimalist race from Michael Hardimon is (his) the racialist concept of race “stripped down to its barest bones” (Hardimon, 2017: 3). The minimalist concept of race, then, does not discuss any differences between populations that cannot be directly discerned with the naked eye. (Note: You can also use the above arguments/data laid out for the populationist concept of race, which, according to Hardimon (2017: 3) is: “A nonracialist (nonessentialist, nonhierarchical) candidate scientific concept that characterizes races as groups of populations belonging to biological lines of descent, distinguished by patterns of phenotypic differences, that trace back to geographically separated and extrinsically reproductively isolated founder populations.)
Minimalist race is biologically sound, grounded in genetics (though I have argued here that you don’t need genetics to define race), and is grounded in biology. Minimalist race is defined as characteristics of the group, not of the individual. Minimalist race are biologically real. Minimalist races exist because, as shown with the data presented in this article, phenotypic and morphologic traits are unevenly distributed throughout the world which then correlates with geographic ancestry. It cannot get any more simpler than that: race exists because differences in phenotype and morphology exist which then corresponds with geographic ancestry.
From Hardimon (2017: 177)\
No sane or logical person would deny the existence of race based on the criteria laid out in this article. We can also make another leap in logic and state that since minimalist races exist and are biologically real then geographic ancestry should be a guide when dealing with medicine and different minimalist races.
It is clear that race exists in the minimal sense; you do not need genes to show that race is real, nor that race has any utility in a medical context. This is important for race deniers to understand: genes are irrelevant when talking about the reality of race; you only need to just use your eyes and you’ll see that certain morphologies and phenotypes are distributed across geographic locations. It is also very easy to get someone to admit that races exist in this minimalist-biological sense. No one denies the existence of Africans, Europeans, ‘Native’ Indians, East Asians and Pacific Islanders. These populations differ in morphology and other physical characters which are unevenly distributed by geographic ancestry, so, therefore: minimialist races exist and are a biological reality.
Last year I bought The Genius in All of Us: New Insights Into Genetics, Talent, and IQ (Shenk, 2010) and while the book is interesting and I agree with a few things he says, he gets it horribly wrong on athleticism and ethnicity. Some of it I may be able to forgive since the book was written in 2010, but he does make some glaring errors. Chapter 6—pages 100-111—is titled Can White Men Jump? Ethnicity, Genes, Culture, and Success.
In the beginning of the chapter, Shenk writes that after the 2008 Beijing Summer Olympics, many articles were written about the Jamaican women who took the top three spots in the 100 and 200m races, with the emergence of Usain Bolt and his record-setting performance. Shenk (2010: 101) writes:
The powerful protein [alpha-actinin-3] is produced by a special gene variant called ACTN3, at least one copy of which is found in 98 percent of Jamaicans—far higher than in many other ethnic populations.
An impressive fact, but no one stopped to do the math. Eighty percent of Americans also had at least one copy of ACTN3—that amounts to 240 million people. Eighty-two percent of Europeans have it as well—that tacks on another 597 million potential sprinters. “There’s simply no clear relationship between the frequency of this variant in a population and its capacity to produce sprinting superstars,” concluded geneticist Daniel MacArthur.
I have written about MacArthur’s thoughts on the ACTN3 variant—that he helped discover, no less—in an article on Jamaicans, Kenyans, and Ethiopians and the explanatory factors in regard to their success in running competitions. Though, the article from MacArthur was written in 2008 and Shenk’s book was written in 2010, considerable advances have been made in this field. It was found that “combined effects of morphological and contractile properties of individual fast muscle fibers attribute to the enhanced performance observed in RR genotypes during explosive contractions” (Broos et al, 2016). Of course when talking about sprinting and morphology, you must think of the somatype. The somatype that is conducive to running success is a tall, lanky body with long limbs, as longer limbs can cover more distance. So European runners don’t have the right somatype, nor are the XX genotype for the ACTN3 variant high in Jamaicans (this genotype is present in ~2 percent of the Jamaican population; Scott et al, 2010). This—among other reasons I have laid out in the past—are why Jamaicans excel in sprinting competitions compared to other ethnic groups.
Shenk (2014: 10) further writes that sports success seem to come in ‘geographic clusters’, and the field of sports geography has been developed to understand it. “What they’ve discovered is that there’s never a single cause for a single cluster,” Shenk writes. “Rather, the success comes from many contributions of climate, media, demographics, politics, training, spirituality, education, economics and folklore. In short, athletic clusters are not genetic, but systemic.” Shenk then discusses the fact that these explanations are not good enough and that some ‘sports geographers’ have transformed themselves into ‘sports geneticists’ and then cites Jon Entine’s 2002 book Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid to Talk About It where Shenk quotes Entine who quotes geneticist and physiologist Claude Bouchard who says that “these biological characteristics are not unique to West or East African blacks. These populations are seen in all populations, including whites” (Shenk, 2010: 102). Of course they’re not unique to one population and I don’t think that anyone has ever claimed that. Though the frequencies of these biological, morphological and physiological characteristics are not distributed evenly amongst populations and this explains how and why certain populations excel in certain sports when compared to others.
Shenk (2010: 102) also quotes Entine (2002), writing: “Entine also acknowledges that we haven’t actually found the actual genes he’s alluding to. “These genes will likely be identified early in the [twenty-first century],” he predicts.” We have ‘found some genes’ that aid in athletic performance, the ACTN3 genotype combined with type II fibers and the right morphology, as mentioned above for one. (Though a systems view—one of holism—makes much more sense here than a reducionist view. You must look at the whole system, not reduce things down, but that’s for another day.) That, in my opnion, is a large driver for ethnic differences in sports like this, because you need certain traits if you want to excel in these types of competitions.
He then discusses the success of the Kenyans in distance running—stating that 90 percent of Kenyan runners come from a small subset of Kenyans called the Kalenjin. He cites a few stories of some Kalenjin who talk about their experiences with no running water in their homes and that they had to “run to the river, to take your shower, run home, change, [run] to school . . . Everything is running” (Keino, a Kalenjin boy, quoted from Shenk, 2010: 104). Of course this is attributed to a multitude of factors, all of which have to work in concert to get the desired effect. For instance, sports psychologists have found that strong cultural achievement and the ability to work hard, compete, outdo others and seek new challenges drives their running dominance.
Shenk (2010: 106-107) then writes:
1.DESPITE APPEARANCES TO THE CONTRARY, RACIAL AND ETHNIC GROUPS ARE NOT GENETICALLY DISCRETE.
Skin color is a great deceiver; actual genetic differences between ethnic and geographic groups are very, very limited. All human beings are descended from the same African ancestors … [blah blah blah] … By no stretch of the imagination, then, does any ethnicity or region have an exclusive lock on a particular body type or secret high-performance gene. Body shapes, muscle fiber types, etc., are actually quite varied and scattered, and true athletic potential is widespread and plentiful.
Of course, I don’t think I have ever read anyone who denies this. However, as I’ve noted too many times to count, certain body types and muscle fiber distributions are more likely to be found in certain populations due to where their ancestors evolved recently, and so the fact that ‘actual genetic differences between ethnic and geographic groups are very, very, limited’ does not mean much when talking about dominance by a few populations in elite sporting competition. It just so happens to be the case that the somatypes and muscle fiber distributions that are conducive to running success are more likely to be found in populations of West and East African descent. This is an undeniable fact. (Also note how these ‘appearances to the contrary’ show how race is real.)
2.GENES DON’T DIRECTLY CAUSE TRAITS; THEY ONLY INFLUENCE THE SYSTEM.
Consistent with other lessons of GxE [Genes x Environment], the surprising finding of the $3 billion Human Genome Project is that only in rare instances do specific gene variants directly cause specific traits or diseases. …
As the search for athletic genes continues, therefore, the overwhelming evidence suggests that researchers will instead locate genes prone to certain types of interactions: gene variant A in combination with gene variant B, provoked into expression by X amount of training + Y altitude + Z will to win + a hundred other life variables (coaching, injuries, etc.), will produce some specific result R. What this means, of course, What this means, of course, is that we need to dispense rhetorically with thick firewall between biology (nature) and training (nurture). The reality of GxE assures that each persons genes interacts with his climate, altitude, culture, meals, language, customs and spirituality—everything—to produce unique lifestyle trajectories. Genes play a critical role, but as dynamic instruments, not a fixed blueprint. A seven- or fourteen- or twenty-eight-year-old is not that way merely because of genetic instruction. (Shenk, 2010: 107)
Nothing really wrong here. He is correct, which is why you need to look at the whole biological system, which also includes the culture, climate, environment and so on that the biological, developmental system finds itself in. However, Shenk then gets it wrong again writing that Jamaicans are a ‘quite heterogenous genetic group’ due to being a transport between North and South America. He states—correctly—that Jamaicans ancestry is about equal to that of African-Americans, but the individual variation in ancestry varies by “46.8 to 97.0 percent” (Shenk, 2010: 108).
Shenk gets a lot wrong here. For example. African-American and Jamaicans—despite both being descended from slave populations—have differing maternal ancestry which somehow influences athletic success. Deason (2017) found that 1) modern Jamaicans are descended from slaves and, who had considerable selective pressure on the population; 2) maternal ancestry could either influence sports success or be a false positive; 3) maternal lineages were different in Jamaicans and African-Americans, implying that the same maternal lineage is not distributed evenly between both sprinting populations; 4) some evidence exists that the genetic histories of Jamaicans and African-Americans are different based on their maternal haplotypes; 5) low SES and low access to healthcare—classic indicators of high African ancestry—were not directly linked to elite athletic success; 6) comparisons of the genomes of African-Americans and Jamaicans did not significantly differ since the estimated number of generations since admixture occurred, which implies that controls were not more likely to have more recent European ancestry than athletes; and 7) the regions of the genome that influence sprinting performance may be different in both populations. This is the best evidence to date against Shenk’s simplistic notions of the genetics between Jamaicans and African-Americans.
Differences in fast twitch fibers between Europeans and West Africans explain a large amount of the variance between Europeans and West African descendants in regard to sprinting success, while those with more symmetrical knees and ankles tend to run faster in the 100m dash (Trivers et al, 2014). This would also imply that Jamaicans have more symmetry in their knees and ankles than Europeans, though I am not aware of data that makes this comparison.
Shenk finally discusses the psycho-social-cultural aspects behind the phenomenon, stating that Roger Bannister, the first person to break the four minute mile, stated that while “biology sets limits to performance, it is the mind that plainly determines how close individuals come to those absolute limits” (Shenk, 2010: 110-111). Numerous psychological factors do, indeed, need to combine in order for the individual in question to excel in sports—along with the requisite anatomical/physiological/morphological traits too. Sasaki and Sekiya note that “changes in physiological arousal and movement velocuty induced by mild psychological pressure played a significant role in the sprint performance.” (See also Bali, 2015.)
Lippi, Favaloro, and Guidi, (2008) note how “An advantageous physical genotype is not enough to build a top-class athlete, a champion capable of breaking Olympic records, if endurance elite performances (maximal rate of oxygen uptake, economy of movement, lactate/ventilatory threshold and, potentially, oxygen uptake kinetics) (Williams & Folland, 2008) are not supported by a strong mental background.” I have argued this for months, even if the beneficial somatype is there in the athlete in question, if he/she does not have the will to win they will not succeed in their goals. Psychosocial factors, of course, matter just as much as the physical but all of these factors work in concert to get the outcomes that occur in these sports.
Attempting to pinpoint one or a few traits—while it may help us to understand better physilogic and anatomic processes—tells us nothing about the entire system. This is why, for instance, the whole athletes system needs to be looked at—call it the ‘systems view of the athlete’, where all of these aforementioned variables work in concert to express elite athletic performance, with no one variable being higher than another as an explanatory factor in sports success. Though Shenk gets a few things right (like his point on genes not causing traits on their own, they just influence the system, and I’d take it a step further to note that genes are passive in their relationship to the physiological system as a whole and are only activated by the system as needed, not being ’causes’ on their own; Noble, 2008), he’s largely misguided on how certain aspects of Jamaican ancestry and morphology help propel them to running success in comparison to other ethnies.
When explaining elite athletic performance in certain areas of sports, you must take a view of the whole system, with each known variable influencing the next in the chain, if you want to explain why certain ethnies or racial groups do better in a given sport than other groups. A systems view is the only view to take when comparing populations in different athletic competitions. So the influence of culture, psychology, social effects, morphology, ancestry, anatomy, physiology, muscle fibers, etc all work in concert to produce elite athletic phenotypes that then excel in these sports, and reducing this down to certain variables—while it may help us understand some of the inner mechanics—it does nothing to help advance the hows and whys of elite success in sports competition when comparing different populations.
I was alerted to a response to my article r/K Selection Theory Rebuttals on Twitter. I enjoy when people write responses to my pieces as I can better build my arguments. It’s also fun defending what I wrote.
This Pastebin is where the response is. He states that he disagrees with AC (Anonymous Conservative) on two things: calling them liberals when he would call then progressives and his clear conservative bias.
First it refers to a criticism of Ruston’s application of r/K to humans:
This article applies r/K selection to differences between races, I don’t see how this is relevant. AC never discusses race and I’m only interested in how r/K selection applies to individuals within a civilization too.
It is very apt when rebutting AC’s ‘theory’. Human races are not local populations therefore it doesn’t apply to human races. To then bring this wrong theory to individual differences is stupid. Hell, I agree more with Rushton’s application than AC’s application and that’s saying something. The point of bringing up Rushton’s r/K theory is that he was the one who repopularized the theory and you have to give credit where it is due (I’m certain he heard of r/K from Rushton; the fact that he doesn’t give him credit there is dishonest, but AC is a dishonest guy so this is no surprise to me).
r/K selection applies to almost all life forms, next to other selection mechanisms. So it goes much deeper than the specific situation a specific race may have lived in. Even if people in races now commonly express more r-selected or K-selected behavior, I’d expect that to change if their children grew up in a different environment.
You only say that because organisms have offspring and at different rates. I won’t even go through the different cites that show that r/K theory is bunk, but I will cite one that shows that it’s been dead for years. Reznick et al, (2002: 1518) write: “The distinguishing feature of the r- and K-selection paradigm was the focus on density-dependent selection as the important agent of selection on organisms’ life histories. This paradigm was challenged as it became clear that other factors, such as age-specific mortality, could provide a more mechanistic causative link between an environment and an optimal life history (Wilbur et al. 1974, Stearns 1976, 1977). The r- and K-selection paradigm was replaced by new paradigm that focused on age-specific mortality (Stearns 1976, Charlesworth 1980).” This is simple. Age-specific mortality replaced r/K theory. People like AC attempt to ‘show’ their ‘hypothesis’ is true. They notice something in this snapshot in time then say oh this this and that make sense therefore this! It doesn’t work like that.
On his point that ‘he’d expect that to change if their children grew up in a different environment’, to say that one race is ‘r’ or ‘K’ over another, you must study the population in question in the location where the adaptations were hypothesized to have occurred (Anderson, 1991).
RR: “It is erroneously assumed that living in colder temperatures is somehow ‘harder’ than it is in Africa”
Yes, there is much less biomass available in colder temperatures. Of course Africans would still compete with each other for resources. The idea is also that there’s more requirement to think ahead, in order to prepare for the winter. Requiring more deferral of gratification.
The idea is dumb. Africa is harsher than Eurasia (Dobzhansky, 1950: 221). Did people in Africa not have to plan ahead? This is the same old rebutted cold winter garbage in terms of ‘selection for higher IQ;.
The article generally asserts that r/K selection is a simple model:
RR: “One of the main reasons that Rushton’s r/K continuum gets pushed is because it’s a ‘simple model’ that so ‘parsimoniously’ explains racial differences … But ecological systems are never simple”:
Where was an implication that any ecological system is simple? I’d say the tropics are way more complicated than cold area’s. The relevant aspect here is that a cold area is more difficult to live in, has less resources and thus supports fewer individuals. Which is a K-selected pressure.
It is a simple model. “Simple models will be successful only if their simplifying assumptions either match reality or are unimportant” (Anderson, 1991: 57). This does neither. It is surely not easy to live in the tropics. This canard that those in Africa had an easy life in comparison to the people who migrated out of Africa doesn’t make any sense. It’s like people think that food just dropped on their laps from the trees, they didn’t have to deal with predators or heat, etc. It’s an extremely simple model which is why it doesn’t work. Africans are ‘K-selected’ if Rushton is to be believed, not r-selected (Anderson, 1991).
AC’s book is for the public, not to be the bleeding edge of science. Most people have no idea about these theories. I think it would greatly improve their understanding of reality if they knew about it, it did mine. This seems like the situation with Newton’s theory of gravity. It’s been proven wrong, but we still use it when useful.
I get that, but his premises are wrong which means his theory is false. What ‘reality’? It’s just stories, fables. Whatever sounds good to AC, whatever he thinks will buttress his theory he’ll write. Anything about the ‘rabbits’ or ‘wolves’ (so-called r- and K-selected organisms respectively). r/K has been proven wrong and it’s still not useful so we should not use it.
RR: ‘So “the actual adaptation they have” is to “wear thick clothing“? This is bullshit and you know it’
No it’s not. The clothing is far thicker and thus harder to make with a higher required investment. It requires more quality of the individuals. The writer assumes a binary difference here, where none was asserted. Of course these things are on a spectrum.
Yes it is. Sorry, you didn’t understand what I meant here. The actual adaptation is not ‘to wear thick clothing’. What is ‘more quality’, is that a scientific term? What does that even mean?
RR: “The preparation does work.” (Preparation of anti-malarial remedies as seen in Wilcox and Bodecker, 2004)
Maybe it helps, much of traditional remedy use is based in tradition and superstition. Europeans where slaughtered by all kinds of diseases. It probably depends on the situation. If you can find a cure for the disease, then maybe it is a K-selected pressure.
It’s irrelevant that ‘much of the traditional remedy use is based in tradition and superstition‘, because these remedies are proven to work (Wilcox and Bodecker, 2004). “If you can find a cure for disease, then maybe it is a K-selected pressure“, you’re clueless and don’t know what you’re talking about.
RR: “Here is what people like Samuel Skinner and AC don’t get: r/K selection theory WAS discarded; it is no longer in use. Age-specific mortality better explains these trends than r/K selection”
But age-specific mortality doesn’t apply to humans and doesn’t explain differences between individuals within a species or population.
Are you saying that we can’t apply this theory to humans at all?
Yes it does apply to humans. Why talk about something when you don’t know about it? Should I care that it doesn’t explain differences between individuals within a species or population? Not everything needs to be some grand, overarching theory to explain everything so perfectly.
RR: “We found that high K scores were related to earlier sexual debut and unrelated to either pubertal onset or number of sexual partners.”
In humans that correlation is broken because of advanced society. However, we can still find that correlation in progressive or conservative politics.
Yet Rushton et al assert that Africans are r, for instance, and have more children but as you can see from Copping, Campbell and Muncer, (2014), earlier sexual debuts were seen in the so-called K dimension, completely against Rushtonian r/K theory and against whatever theory AC cooked up in his head.
There are several links to scientific papers, several of which are no longer working, but fails to summarize how they support his position.
They don’t work because sci-hub is down. I need to fix the broken links and I did summarize how they support me which is why I did “claim then (citation)”.
RR: “Individuals WITHIN A SPECIES are not R OR K”
Since environments can change, why would species not be able to adapt to the new situation?
That’s not even what the original theory spoke about. If the liberals environment changed, would they become K (according to AC)? You’re completely missing the r/K dynamic.
A Jelly fish has several reproductive strategies available and chooses based on available resources.
Humans are much more complicated, but we could still have that ability.
This doesn’t mean that r/K selection has any utility.
RR: “Something AC doesn’t get is that using the discredited r/K continuum, conservatives would be r”
I don’t get that either.
Because the continuum comes from Pianka (1970) and Rushton adapted it to show that lower IQ peoples who had more children were r-selected. Therefore, if this did apply to individuals within the human species then conservatives would be r while liberals would be K (they have fewer children and higher IQs).
RR: “women who reported being religious stated that having children was more important to them”
And are in favor of investing in those children through their mother staying home to take care of them. Where progressives are more likely to be in favor of the mother working and putting the children in day-care. Progressives are also in favor of birth control and abortion. Allowing them to maintain the r-selected sexual life style, without having the burden of a child. r/K selection is about the underlying psychology, not surface level attributes like total number of children.
Liberals still have fewer children than conservatives who have more. What you’re saying is largely irrelevant. “r-selected sexual lifestyle”, this is dumb. r/K selection is predicated on number of children which conceived, supposedly, differs on the basis of differential psychology, supposedly, between two human groups. It doesn’t, it’s wrong.
“I’ve already covered that libs are more intelligent than cons (Kanazawa, 2010; Kanazawa, 2014), and that conservative countries have lower IQs”
I don’t think we should expect a correlation between IQ and r or K in modern human societies. What happens is that high IQ people raise their children in abundance, which makes them more likely to be r-selected. Availability of resources is a trigger for r-selected psychology.
Riiiiight. But you would expect a correlation between other so-called r/K measures in modern societies? You don’t even make sense.
“Conservatives are more likely to be religious”
Yes because religions like Christianity are viewed as tradition. And progressives oppose tradition where conservatives favor it.
Right, and they have more children than liberals, which is r-selected behavior (supposedly).
This guy tried, but clearly, this wasn’t good enough. r/K is dead when speaking about race and the differences between human individuals. For anyone who believes AC’s bullshit, where did liberals and conservatives evolve these different behaviors? Are they local populations? People like AC ignoring the continuum by Pianka, yet use that same hierarchy are dishonest. They’re using a discredited continuum and attempt to prove their political biases. “The other team has X, Y, and Z bad while we have A, B, and C good! The other side does X and Y while we do A and B, therefore, we are better!” AC has a huge bias; he will never admit he’s wrong because he has a book to sell that pushes this discredited garbage. (Don’t worry, I’ll review it and pick it apart soon enough.)
To conclude, people really need to stop letting their biases get in the way of rational thought. If they did, they’d be able to look at these dumb theories for what they are: pseudoscience, cherry-picking and pigeon-holing the other group, the “enemy” with all of the bad qualities while their side has all of the good ones. However, as I’ve shown countless times, real life is completely different from the fantasy world AC and his followers live in.