Humans are extremely “plastic”. “Plastic” meaning that our development can be shaped by what goes on (or does not go in) in our developmental environment along with the environment outside of the womb. Many factors drive development, and if one factor changes then part of the developmental course for the organism changes as well. Thus, environment can and does drive development, with the addition (or subtraction) of different factors. In this article, I will discuss some of the factors that drive development and physical plasticity and what can change them.
Subsistence provides food while food provides nutrition. Nutrients, then, supply our bodies with energy and promote tissue growth—among other things. However, nutrient requirements vary across and between species, while all mammals need a mixture of macronutrients (carbs, fat, protein, water, and fiber) and micronutrients (vitamins and minerals). Biological variability in nutrient requirements and “the eventual degree of metabolic function that an individual can achieve for a particular intake level is determined to a greater or lesser extent by genetic variants in enzymes controlling the absorption, uptake, distribution, retention or utilization of the nutrient” (Molloy, 2004: 156). Thus, individuals who consume the same amount of micro and macronutrients—who also have different polymorphisms in genes coding for the metabolism of any nutrient (through hormones and enzymes)—can, and do, have differing physiological responses to same vitamin intake. Thus, differences in genetic polymorphisms between individuals can—and do—lead to different disease.
Next we have phenotypic plasticity. Phenotypic plasticity, simply put, is the ability for a genome to express a different phenotype in variable environments. For instance, people born in hotter environments—no matter their race or ethnicity—develop larger pores in order to sweat more, since sweating is needed for cooling the body (Lieberman, 2015). Phenotypic plasticity can be a problem, though, in environments with numerous environmental stressors that will stress the mother and, in turn, affect the baby’s development in the womb as well affecting post-birth events. An example of this is when food availability is low and exposure to infection is high (in-utero and post-birth), and when these stressors are removed, the organism in question shows “catch-up growth”, implying that these stressors impeded the development of the organism in question.
Maternal nutritional imbalance has been found—both in animal studies and epidemiological studies—and metabolic disturbances, during critical windows of development for the organism, have both a persistent effect on the health of the organism and can be transmitted epigenetically to future generations (Gallou-Kabani and Junien, 2005). Gallou-Kabani and Junien (2005) write:
Epigenetic chromatin marks may be propagated mitotically and, in some cases, meiotically, resulting in the stable inheritance of regulatory states. Transient nutritional stimuli occurring at critical ontogenic stages may have lasting influences on the expression of various genes by interacting with epigenetic mechanisms and altering chromatin conformation and transcription factor accessibility (11).
Thus, metabolic syndrome can show transgenerational effects by way of incomplete erasure of the epigenetic factors carried by grandparents and parents. (See also Treretola et al, 2005.) Epigenetic regulation was extremely important during our evolution and especially during the development of the human organism, and is how and why we are so phenotypically plastic.
Epigenetic regulation during fetal reprogramming of the individual in preparation for the environment they expect to enter is likely to be a response to seasonal energy imbalance; changes that favour the metabolic efficiency are likely to be adaptive in such circumstances. Removal of seasonal energy stress, as has taken place in contemporary industrialized societies, may turn efficiency toward pathology. Humans thus have evolved an animal model that can respond genetically (through natural selection), phenotypically (through developmental plasticity) and epigenetically (by a balance of both). (Ulijaszek, Mann, and Elton, 2013: 19)
This seems to be a fundamental response to the human organism in-utero, responding to the lack of food in its environment and growing accordingly (low birth weight, susceptibilities to differing disease), which are still a problem for much of the developed world. Though this can be maladaptive in the developed, industrialized world, since poor early-life environments can lead to epigenetic changes which then spell out bad consequences for the low-birth-weight baby who was exposed to a slew of negative nutritional factors during conception (and post-birth).
It has already been established that nutrition can alter the genome and epigenome (Niculescu and Lupu, 2011; Niculescu, 2012; Anderson, Sant, and Dolinoy, 2012). So if differing nutritional effects can alter the genome and epigenome and these effects are transgenerationally inherited by future generations, then famines change the expression of the genome and epigenome which can then inherited by future generations if the epigenetic factors carried by the grandparents and parents are not erased (and there is mounting evidence for this claim, see Yang, Liu, and Sun, 2017).
There is evidence of phenotypic plasticity regarding the lack of nutrition when it comes to humans, in-utero, and the evidence comes from the Dutch Family Studies (see Lumey et al, 2007 for an overview of the project). Individuals who were prenatally exposed to the Dutch winter famine of 1944-45, six decades later, had less DNA methylation of the IGF2 (insulin-like growth factor 2) gene than same-sex siblings who were not exposed to the winter famine (Heijmns et al, 2008). The IGF2 gene plays an essential role of the development of the fetus before birth. The gene is highly active during fetal development, but much less so after birth. (It should be noted that the loss of imprinting on the IGF2 gene can promote prostate cancer; Fenner, 2017 and loss of imprinting on IGF2 can also promote other types of cancer as well; Livingstone, 2013).
Stein et al (2009) concluded that “famine exposure prior to conception is associated with poorer self-reported mental health and a higher level of depressive symptoms.” Tobi et al (2009) write that their data “support the hypothesis that associations between early developmental conditions and health outcomes later in life may be mediated by changes in the epigenetic information layer.” Tobi et al (2014) also show that the “Epigenetic modulation of pathways by prenatal malnutrition may promote an adverse metabolic phenotype in later life.” The prenatal—and neonatal—periods of development are of utmost importance in order for the organism to develop normally, any deviation outside of these measures can—and does—affect the genome and epigenome (Hajj et al, 2014).
Another strong example that these responses are adaptive to the organism in question is the fact that people who were exposed to nutritional imbalances in the womb showed a higher chance of becoming obese later in life (Roseboom, de Rooji, and Painter, 2006). Their study has implications for babies born in developing countries (since famines mirror, in a way, developing countries). Roseboom, de Rooji, and Painter (2006: 489) write:
This may imply that adaptations that enable the fetus to continue to grow may nevertheless have adverse consequences for health in later life.
Roseboom, de Rooji, and Painter (2006: 490) also write:
The nutritional experience of babies who were exposed to famine in early gestation may resemble that of babies in developing countries whose mothers are undernourished in early pregnancy and receive supplementation later on, but also of babies in developed countries whose mothers suffer from severe morning sickness.
So on-going studies, such as the Dutch Famine Study, have the chance to elucidate the mechanisms of low birth weight, and it can also show us how and why those exposed to adverse conditions in the womb show so many negative symptoms which are not present in kin who were not exposed to such malnutrition in the womb. These findings also suggest that nutrition before—and after—pregnancy can play a role in disease acquisition later in life. The fact that those exposed to famines have a higher chance of becoming obese later in life (Abeleen et al, 2012; Meng et al, 2017) shows that this adaptive response of the organism in the womb was very important in our evolution; the babe exposed to low maternal nutrition in the womb can, after birth, consume enough energy to become overweight, which would have been an adaptive evolutionary response to low maternal caloric energy.
Babies who are exposed to maternal under-nutrition in the womb—when exposed to an environment with ample foodstuffs—are at heightened risk of becoming type II diabetics and acquiring metabolic syndromes (Robinson, Buchholz, and Mazurak, 2007). This seems to be an adaptive, plastic response of the organism: since nutrients/energy were in low quantity in the womb, low nutrients/energy in the womb changed the epigenome of the organism, and so when (if) the organism is exposed to an environment with ample amounts of food energy, they will then have a higher susceptibility to metabolic syndromes and weight gains, due to their uterine environment. (Diet also has an effect on brain plasticity in both animals and humans, in the womb and out of it; see Murphy, Dias, and Thuret, 2014.)
In sum, phenotypic plasticity, which is driven in part by epigenetics, was extremely important in our evolution. This epigenetic regulation that occurs in the womb prepared the individual in question to be able to respond to the energy imbalance of the environment the organism was born in. The plasticity of humans, and animals, in regard to what occurs (or does not occur) in the environment, is how we were able to survive in new environments (not ancestral to our species). Epigenetic changes that occur in the grandparental and parental generations, when not completely erased during the meiotic division of cells, can affect future generations of progeny in a negative way.
The implications of the data are clear: under-nutrition (and malnutrition) affect the genome and epigenome in ways that are inherited through the generations, which is due to the physical plasticity of the human in-utero as well as post-birth when the baby developing. These epigenetic changes then lead to the one who experienced the adverse uterine environment to have a higher chance of becoming obese later in life, which suggests that this is an adaptive response to low amounts of nutrients/caloric energy in the uterine environment.
Michael Hardimon has some of the best defenses of the reality of race that I am aware of. His 4 concepts are: the racialist concept (he says racialist races do not exist, which I will cover in the future), the minimalist race concept, the socialrace concept (which also will be covered more in depth in the future) and the populationist race concept. Racialist races do not exist, according to Hardimon. However, that does not mean that race does not exist nor does it mean that race isn’t real. On the contrary, race exists and is a biological reality. Simple arguments for the existence of race do indeed exist and see where mixed-race individuals, ‘Latinos’, and Brazilians fall. (Author of the book A Theory of Race Joshua Glasgow also reviewed Hardimon’s book (Glasgow, 2018), and I also left my thoughts on his review.)
Now, minimalist races exist and are biologically real. The concept, though, is vague. It doesn’t state which populations are races, but the populationist race concept, however, does. Hardimon (2017: 99) defines populationist races:
“A race is a subdivision of Homo sapiens—a group of populations that exhibits a distinctive pattern of genetically transmitted phenotypic characters that corresponds to the group’s geographic ancestry and belongs to a biological line of descent initiated by a geographically separated and reproductively isolated founding population.”
Are there groups that exhibit patterns of a distinctive pattern of visible physical features which are genetically transmitted and correspond to the group’s geographic ancestry? Are there groups that belong to a biological line of descent which was initiated by geographically and reproductively isolated founding populations? The answer is, obviously, yes. Which groups satisfy the definition of populationist races? I will discuss this below.
An important question to answer is: are races subspecies? The two terms are similar. Merriam Webster defines subspecies as: “a category in biological classification that ranks immediately below a species and designates a population of a particular geographic region genetically distinguishable from other such populations of the same species and capable of interbreeding successfully with them where its range overlaps theirs.” While “race” is similarly defined. So, are races subspecies?
The fixation index (Fst) is a measure of population differentiation due to genetic structure which is estimated from SNPs or microsattelites. Generally, the accepted criterion for subspeciation is between .25 and .30. Human groups have an Fst between .05 and .15, so human groups fall way short of subspeciation. Fst estimates for humans fall between .05 and .15, which is far and away what the consensus is on the delineation of subspecies within a group of like kinds. Further, Fst does not support the existence of distinct clusters in humans (Maglo, Mersha, and Martin, 2016; it should be noted that they believe that for human races to exist, human races must be subspecies—similar views are held by philosopher of science Adam Hochman—but their contentions were addressed by Spencer, 2015). Human populations are not subspecies, and the fact that they are not subspecies does not rail against the existence of populationist races.
Hochman (2013) makes the case that in order to claim that clusters represent subspecies, four conditions have to be met: “(i) the range of allele frequency differences between genetic Fstclusters corresponding to race must be relatively uniform, (ii) there must be a determinate number of such clusters, (iii) the allelic frequencies within such clusters must be relatively homogeneous, and (iv) there must be a large jump in genetic differences between such clusters” (Hardimon, 2017: 108).
Thus, the human species does not contain subspecies in the technical sense of the word, as humans Fst estimates range between .05 to .15. This further attests to the fact that the clusters—identified by Rosenberg et al (2002)—are not subspecies. “There is no need for US racial groups to be subspecies or clades, have high genetic variation among them, or be fundamental categories in human population genetics just in order to be biologically real races. Rather, in order for US racial groups to be biologically real races, they just need to be races and biologically real (Spencer, 2015: 6).
The populationist race concept, however, does not require that a division in a species be represented by a particular Fst estimated. It further doesn’t say that Hochman’s (2013) conditions must be met in order for the clusters to be races. Therefore the populationist race concept is not a subspecies concept; there are no subspecies in our genus. Though, if we were forced to accept Hochman’s (2013) conditions (which we do not have to), human races do not exist.
Next is the concept of phylogeny. If phylogenetic is taken to in the normal biological terminology, then the question is whether or not racial lines of descent capture evolutionary significant relationships. And if “evolutionary significant relationships” are taken in the normal biological context then the answer to the question is “no.” This is because the term “evolutionary significance”, taken in the general biological terminology, is understood in a way that for a relationship between populations to be “evolutionarily significant”, then the differences between these populations must be blocked by extensive gene flow.
However, regarding the populations that we take to be populationist races, if the features of these races have adaptive significance, such as skin color for differing climates, then the populationist race concept is of interest to evolutionary biologists since biological raciation makes it possible for divisions of Homo sapiens to survive in different climates. Thus, when discussing how and why divisions of our species adapted to different climates—physically speaking—then this concept is of use to evolutionary biologists since it can explain the adaptive physical features of divisions of Homo sapiens. We then have two choices. We can then further take the idea that to be “phylogenetic”, populations must block extensive gene flow, though we can grant that populationist races may well be of interest to evolutionary biologists (due to their adaptive features that arose due to climatic adaption), despite the fact that populationist races are nonphylogenetic (Hardimon, 2017: 111).
The populationist race concept is a candidate scientific concept. This is because the concept uses biological terminology such as “reproductive isolation”, “transmitted phenotypic characteristics”, “founding population”, and “geographic ancestry.” Hardimon then discusses how and why the concept can form a scientific concept:
“… concept C has the “form” of a scientific concept in biology if
(i) it is formulated in a “biological vocabulary”,
(ii) it is framed in terms of an accepted biological outlook,
(iii) it is suitable for deployment in an accepted branch of biological inquiry, and
(iv) it presents the scientific ground of the phenomenon it represents” (Hardimon, 2017: 112).
This concept satisfies all four conditions. It satisfies (i) since it uses biological vocabulary (e.g., phenotype, reproductive isolation). It satisfies (ii) since it’s framed in what Mayr terms “population thinking” (which is the rejection of essentialism—“the view that some properties of objects are essential to them.”. It satisfies (iii) since it is suitable for deployment in ecology, ethology and evolutionary biology. Areas of study, for example, can focus on how and why differing populationist races have differing patterns of visible physical features (i.e., how and why phenotypes changed as migration occurred out of Africa into Eurasia, the Pacific Islands and the Americas). And it satisfies (iv) in that representing populationist races as having arisen from reproducively isolated founding populations.
Now which groups are candidates for populationist races? There are two conditions: (1) they exhibit distinctive patterns of phenotypic characters which correspond to that population’s geographic ancestry and (2) belong to biological lines of descent which then trace back to geographically separated and reproductively isolated founding populations.
There are populations which exhibit distinctive patterns of visible physical features which correspond to geographic ancestry, and they are Sub-Saharan Africans, Caucasians, East Asians, Native Americans and Pacific Islanders. The distinctive patterns of visible physical features are genetically transmitted, and they correspond to geographic ancestry. These populations belong to biological lines of descent which can then be traced back to geographically separated and reproductively isolated founding populations. Thus, conditions (1) and (2) are satisfied, therefore populationist races exist.
Further support for (iii) (that the populationist race concept can be deployed in the biological sciences) can be found in my article You Don’t Need Genes to Delineate Race. I discussed differences in gross morphology between the races; I discussed differences in physiognomy between the races; and, of course, the differences in geographic ancestry that caused the differences in morphology and physiognomy (see here for discussions on skin color). Differences in climate that Homo sapiens encountered after trekking out of Africa then caused the distinctive differences in visible physical features which correspond with geographic ancestry which then make up populationist races. Thus, the study of populationist races will elucidate the caused of phenotypic differences between populationist races since they exist and are a biological reality.
There is a relationship between populationist and minimalist races, though they’re defined by different concepts. However if minimalist races are populationist races, then the kind minimalist race=populationist race. “The claim that minimalist race=populationist race is analogous to the claim that water=H2O. The latter claim, since true, provides scientific insight into the nature of minimalist race” (Hardimon, 2017: 120).
Furthermore, we can assume that the populations identified by Lewontin (1972) as races can be interpreted as lending support to the biological reality of populationist races exist. We can also assume that African, Caucasians, East Asians, Oceanians, and Native Americans constitute populationist races, then Rosenberg et al (2002) show support for the biological reality of populationist races, even though the fraction of diversity separating the clusters is between 3-5 percent, this still shows that populationist races capture a portion of biological human variation, no matter how small it is.
“If it is assumed that Africans, Eurasians, East Asians, Oceanians, and Americans constitute continental-level populationist races, Rosenberg and colleagues’ 2002 study can be interpreted as providing support for the biological reality of populationist race inasmuch as it shows that a very small fraction (3-5 percent) of human genetic variation is due to difference among continental-level populationist races. Modulo our assumption, the study results indicate that populationist race is a minor principle of human genetic structure and that populationist race is a minor principle of human variation.” (Hardimon, 2017: 124)
The same points made that minimalist races are human population partitions, that races can be distinguished at the level of the gene, and that the continental-level minimalist races differ in a small number of coding genes, also carry over to the populationist race concept since minimalist race=populationist race, so the biological reality of minimalist race carry over to populationist race. So if the five populations are populationist races, then populationist race correspond to a partition of genetic variation found between the races in the human species, which is then evidence for the existence of populationist races.
The five populations that make up populationist races are Native Americans, Caucasians, East Asians, Pacific Islanders, and Sub-Saharan Africans. These populations are biologically real, and they exist. They generically transmit phenotypic characteristics across the generations; these phenotypic characteristics differ due to geographic ancestry. These populations are identified in numerous K = 5 runs. So if we assume that the five populations are populationist races then K = 5 shows the real, but small, human genetic variation found within continental-level populationist races which is how the visible patterns of visible physical features which correspond to geographic ancestry are genetically transmitted.
The populationist race concept is a candidate scientific concept. This is a way to study the small genetic variation between the continental-level clusters. Human phenotypic (and physiologic) differences arose due to adaption to different climates. Thus, since populationist race is a biological reality then studying populationist races will better elucidate how and why differences in phenotype arose.
Both the populationist and minimalist race concepts are vague, I admit. However, they’re not so vague that one could argue that villages, countrys, social classes etc are populationist races. It should be noted, though, that it is implicitly stated in the definition for populationist race, that a morphological component exists. Therefore, groups like the Amish, social classes etc. Thus, the populationist race concept gaurentees that races will be races in the ordinary sense of the word (see Hardimon, 2003). So we can take two groups—G1 and G2—and if G1 does not have any pattern of visible physical features which distinguish it from another group, G2, then G1 is not a race. These visible physical differences that distinguish races from one another are biological in nature—hair color/type, skin color, eye type, morphology etc. This gaurentees that different villages, countries, economic classes and ethnies within a race are not counted as “races”, so defined.
The thing about the populationist race concept is that it directly relates to the minimalist race concept. Once we acknowledge that races exist and are real (since minimalist races exist and are real), then we start thinking “Which populations sastisfy the conditions of populationist races?” The populationist race concept—in tandem with the minimalist race concept—shows us that the patterns in visible physical features are genetically transmitted characters which which correspond to the population’s geoprahic ancestry who belong to biological lines of descent which were initiated by geographically separated and genetically isolated founding populations. The populationist race concept supports the claim that the minimalist race concept is a biological concept and secures the existence of minimalist races since minimalist race=populationist race.
P1) The five populations demarcated by Rosenberg et al (2002) are populationist races; K = 5 demarcates populationist races.
P2) Populationist race=minimalist race.
P3) If populationist race=minimalist race, then everything from showing that minimalist races are a biological reality carrys over to populationist races.
P4) Populationist races capture differences in genetic variation between continents and this genetic variation is responsible for the distinctive patterns of visible physical features which correspond to geographic ancestry who belong to biological lines of descent which were initiated by geographically isolated founding populations.
C) Therefore, since populationist races=minmalist races, and visible physical features which correspond to geographic ancestry are genetically transmitted by populations who belong to biological lines of descent, initiated by reproductively isolated founding populations, then populationist races exist and are biologically real.
Biology is one of the most interesting sciences since, at its core, it is the study of life and living systems. The biological organization of living systems and the ecosystems these living systems find themselves in are interesting to learn about, since we can then discern different species and learn how and when to delineate separate species based on a set of pre-conceived measures. The classification of human races in these systems will be discussed, along with why human races are not different species.
The organization of living systems
Living systems show hierarchical organization, each system—from the physiological to the physical—interacting with each other. However, a key factor in the organization of these interactions is the degree of the complexity of the interactions in question. We can look at the organization of the biological world as hierarchical—that is, each level builds on the preceding level, so we get from atoms to the biosphere and everything in between is what we call “life” and also show how these complex, living biological systems live and exist due to the hierarchical organization of living systems. The point is, life does not have a simple definition, but all living systems share similar characteristics that can describe life. Biologists organize living systems hierarchically, from the subcellular level to the entire biosphere, and then study the interactions that occur which cannot be predicted from just studying the sum of its parts. This is why a holistic—and not reductionistic—approach needs to be taken when studying and describing living systems.
The hierarchy is:
The cellular level, which includes: atoms, molecules, macromolecules, and organelles; the organismal level which include: tissue, organs, the organ system, and the organism; the populational level which includes: the population, species, and the community; and finally the highest level, the ecosystem level which includes the ecosystem and the biosphere.
At the cellular level, we have atoms which are the fundamental elements of matter and are joined together by chemical bonds called molecules. large and complex molecules are called macromolecules, DNA—which stores hereditary information—is a type of macromolecule. Complex biological molecules are then assembled into organelles, where cellular activities are organized. A mitochondrion is, for example, an organelle with a cell that extracted energy from consumed food molecules. And finally, we have cells, which are the basic unit of life.
Next, we have the organismal level, and cells of multicellular organisms make up three levels of organization. Tissues, which are groups of similar cells which function together as a unit. Tissues then are grouped into organs which are structures of the body which are composed of many different kinds of tissues which act in a structural manner and as a unit. Then we have organ systems, such as the nervous system which is the sensory organs, brain and spinal cord, and the network of neurons that convey signals to different parts of the body.
Then we have the populational level. This includes the individual organisms which occupy various hierarchical levels in the biological world. A population is a group of organisms all living in the same place. Together, all populations of a particular kind form a species—members of a species must look similar and be able to interbreed. Then finally, we have the biological community which consists of all of the populations coexisting together in one place.
Lastly, we have the ecosystem level. This is the highest tier of biological organization (the lowest being the cellular level). A biological community and its physical habitat (such as soil composition, available water etc) in which it finds itself in and lives and competes with other organisms constitute an ecosystem while the entire planet is the highest of all levels of biological organization—the biosphere. All of these systems together can be seen as the hierarchical organization of living systems.
(See Mason et al, 2018 for more discussion of the above points.)
Now, in these differing biological hierarchies, we find differing Eukarya, Prokarya, and Bacteria. The in-use classification system is the Linnean hierarchy. Differences exist between organisms, this is obvious. But it is a bit more tricky to classify these organisms and place them into like groups. Then, in the 1750s, Carolus Linnaeus came along and instituted a binomial classification system for organisms—the most commonly-known binomial being Homo sapiens—which was much simpler than the polynomial names
The hierarchy is as follows:
7. Kingdom; and
8. Domain. Domains can then be split into Archaea, Bacteria, and Eukarya. Domains are the largest taxons, being that they comprise every organism that we know of.
For example, our species is sapiens, our genus is Homo, our family is Hominidae, our order is primates, our class is Mammalia, our phylum is Chordata (with a subphylum Craniata), our kingdom is Animalia and our domain is Eukarya. This is our species’ taxonomic classification.
The traditional classification system—the Linnean system—groups species into genera, families, orders, classes, phyla, and kingdoms. Thus, these systems classify different organisms on the basis of similar traits, and since they consist of a mix of derived and ancestral traits, they do not necessarily take into account different evolutionary relationships.
There are of course limitations to the Linnean hierarchy:
1) Many “higher” taxonomic ranks are not monophyletic and so do not represent real groups (like Reptilia). For something to be a “natural group”, a common ancestor and its descendants must all derive from descent from a common ancestor, so any other type of taxonomic ranks are created by taxonomists, such as paraphyletic and polyphyletic.
2) Linnean ranks are not equivalent. Two families may not represent clades that arose at the same time, because one family may have diverged millions of years before the other family and so the two families had differing amounts of time to diverge and acquire new traits. So comparisons in the Linnean sense may be misleading and we should then use hypotheses of phylogenetic relationships.
What is a species?
It should first be noted that species are, indeed, real. New species arise when isolated organisms of one population become genetically/geographically isolated for a period of time. Over time, as the split population spends time geographically and genetically isolated, they cannot interbreed with the parent population and thusly attain separate species status. This is the received view, the biological species concept.
There are a wide range of species concepts and they all capture the differences that different theorists believe we should emphasize in our classification of organisms.
The phenetic species which appeal to the intrinsic similarities of organisms. The biological species concept which appeals to reproductive isolation (one version of the biological species concept is the recognition concept, which defines species as a system of mating recognition. The cohesion species concept which generalizes the biological species concept and it recognizes that gene flow isn’t the only factor that holds a population together and makes it different from other populations. The ecological species concept which defines species by appealing to the fact that members of a species are in competition with one another because of the need the same resources. And the phylogenetic and evolutionary species concept which define species as segments on the tree of life (the phylogenetic species concept, for instance, holds the term ‘species’ should be reserved for groups of populations that have been evolving independently of other populations.
Sterelny and Griffiths (1999) tackled this in their book Sex and Death: An Introduction to Philosophy of Biology:
While we think cladism presents the best view of systematics, biological classification nevertheless poses an unsolved problem. If we were to accept either evolutionary taxonomy, which builds disparity into its classification system, or phenetic taxonomy, which is based on the idea of nested levels of similarity, traditonal taxonomic levels would be quite defensible. Within those taxonomic pictures, the idea of genus, family, order, and so on makes quite good sense. If cladism is the only defensible picture of systematics, the situation is more troubling. From that perspective, these taxonomic ranks make little sense. Cladists do not think there is a well-defined objective notion of the amount of evolutionary divergence. That, in part, is why they are cladists. Hence, they do not think there will be any robust answer to the questions, when should we call a monophyletic group of species a genus? a family? an order? Only monophyletic groups should be called anything, for they are well-defined chucnks of the tree. But only science greets the question, are the chimps plus humans a genus? It has long been receieved wisdom in taxonomy that there is something arbitrary about taxonomic classification above species. These decisions are judgement calls. So cladists only show a somewhat more extreme version of a skepticism that has long existed. The problem of high taxonomic ranks would not matter except for the importance of the information expressed using them. Hence cladism reinforces the worry that when, for example, we consider divergent extinction and survival patterns, our data may not be tobust, for our units may not be commensurable. Unfortunately, it does this without suggesting much of a cure.
Where does race fit in?
Racehood is simple: A race is a group of humans that: Condition 1; is distinguished from other groups of humans by patterns of visible physical features; Condition 2: is linked by common geographic ancestry which is peculiar to members of this group; and Condition 3: originates from a distinctive geographic location.
So now all we need to do is go through four steps: 1) recognize that there are patterns of visible physical features which correspond to geographic ancestry; 2) observe that these patterns of visible physical features which correspond to geographic ancestry are exhibited between real, existing groups; 3) note that these real existing groups that exhibit these patterns by geographic ancestry satisfy C1-C3; and 4) infer that race exists.
Some may argue that the races are different species, citing the same patterns of visible physical features discussed above. However, if we are referring to the biological species concept, then the human races are not different species at all since all human races can produce fertile offspring with one another. Our genus, of course, is Homo, all of the human races are the same genus; though some may attempt to use the previously-discussed conditions for racehood as conditions for specieshood for humans, the most preferred method for delineating species currently is the biological species concept, and since all of the human races can produce fertile offspring then the human races are not different species.
In keeping with the classification system that is currently used today (see above), where would human races fit into our taxonomy? Falling within our species sapiens seems like a good start, and since the races can interbreed and have fertile offspring, then they are not different species but are the same species, despite phenotypic differences. Thus, human races would be within species but under subspecies. Using this line of logic, human races cannot be different species, despite claims to the contrary that human races are different species based on patterns of visible physical features which correspond to geographic ancestry. That’s enough to denote racehood, not specieshood.
The study of life—in all of its forms and in all of its environments—is one of the most important things we, as humans, can do. From it, we can learn where we came from and even—possibly—where we may be going. Once we understood the biological hierarchy and how upper levels are built from lower levels working together, then we were better able to understand how living systems act on the inside—cellularly and physiologically—to the outside—organismal and environmental interaction. From organismal and environmental interaction, speciation may occur. The highest level of the organization of living systems is the biosphere—and it is so because the living systems that are driven by the smallest cellular interactions interact with other species, the ecosystem and the biosphere.
Species do exist, but there are numerous species concepts—over twenty. One of the more popular species concepts in use is the cladistic species concept. In this species concept, a species is a lineage of populations between two specific branch points. The cladistic concept thusly recognizes differing species by differing branch points and how much change occurs between them (see Ridley, 1989).
The classification of different organisms into different species is pretty straightforward, though it falls prey to oversimplification since it only focuses on similar traits. Species exist, this is established. But races are not species, contrary to some beliefs. Different races can interbreed and, I would argue, that for there to be separate species, human races would not be able to interbreed. Yes, there are physical and morphological differences between races, but, as argued, this is not enough to denote speciation, but it is enough to denote raciation.
Everyone wants to know the keys to athletic success, however, as I have argued in the past, to understand elite athletic performance, we must understand how the system works in concert with everything—especially in the environments the biological system finds itself in. To reduce factors down to genes, or training, or X or Y does not make sense; to look at what makes an elite athlete, the method of reductionism, while it does allow us to identify certain differences between athletes, it does not allow us to appreciate the full-range of how and why elite athletes differ in their sport of choice. One large meta-analysis has been done on the effects of a few genotypes on elite athletic performance, and it shows us what we already know (blacks are more likely to have the genotype associated with power performance—so why are there no black Strongmen or any competitors in the World’s Strongest Man?). A few studies and one meta-analysis exist, attempting to get to the bottom of the genetics of elite athletic performance and, while it of course plays a factor, as I have argued in the past, we must take a systems view of the matter.
One 2013 study found that a functional polymorphism in the angiotensinogen (ATG) region was 2 to 3 times more common in elite power athletes than in (non-athlete) controls and elite endurance athletes (Zarebska et al, 2013). This sample tested was Polish, n = 223, 156 males, 67 females, and then they further broke down their athletic sample into tiers. They tested 100 power athletes (29 100-400 m runners; 22 powerlifters; 20 weightlifters; 14 throwers and 15 jumpers) and 123 endurance athletes (4 tri-athletes; 6 race walkers; 14 road cyclists; 6 15 to 50 m cross-country skiers; 12 marathon runners; 53 rowers; 17 3 to 10 km runners; and 11 800 to 1500 m swimmers).
Zarebska et al (2013) attempted to replicate previous associations found in other studies (Buxens et al, 2009) most notably the association with the M235T polymorphism in the AGT (angiotensinogen) gene. Zarebska et al’s (2013) main finding was that there was a higher representation of elite power athletes with the CC and C alleles of the M235T polymorphism compared with endurance athletes and controls, which suggests that the C allele of the M235T gene “may be associated with a predisposition to power-oriented
events” (Zarebska et al, 2013: 2901).
Elite power athletes were more likely to possess the CC genotype; 40 percent of power athletes had the genotype whereas 13 percent of endurance had it and 18 percent of non-athletes had it. So power athletes were more than three times as likely to have the CC genotype, compared to endurance athletes and twice as likely to have it compared to non-athletes. On the other hand, one copy of the C allele was found in 55 percent of the power athletes whereas, for the endurance athletes and non-athletes, the C allele was found in about 40 percent of individuals. (Further, in the elite anaerobic athlete, explosive power was consistently found to be a difference maker in predicting elite sporting performance; Lorenz et al, 2013.)
Now we come to the more interesting parts: ethnic differences in the M235T polymorphism. Zarebska et al (2013: 2901-2902) write:
The M235T allele distribution varies widely according to the subject’s ethnic origin: the T235 allele is by far the most frequent in Africans (;0.90) and in African-Americans (;0.80). It is also high in the Japanese population (0.65–0.75). The T235 (C4027) allele distribution of the control participants in our study was lower (0.40) but was similar to that reported among Spanish Caucasians (0.41), as were the sports specialties of both the power athletes (throwers, sprinters, and jumpers) and endurance athletes (marathon runners, 3- to 10-km runners, and road cyclists), thus mirroring the aforementioned studies.
Zarebska et al (2013: 2902) conclude that their study—along with the study they replicated—supports the hypothesis that the C allele of the M235T polymorphism in the AGT gene may confer a competitive advantage in power-oriented sports, which is partly mediated through ANGII production in the skeletal muscles. Mechanisms can explain the mediation of ANGII production in skeletal muscles, such as a direct skeletal muscle hypertrophic effect, along with the redistribution of between muscle blood flow between type I (slow twitch) and II fibers (fast twitch), which would then augment power and speed. However, it is interesting to note that Zarebska et al (2013) did not find any differences between “top-elite” level athletes who had won medals in international competitions compared to elite-level athletes who were not medalists.
The big deal about this gene is that the AGT gene is part of the renin-angiotensin system which is partly responsible for blood pressure and body salt regulation (Hall, 1991; Schweda, 2014). There seems to be an ethnic difference in this polymorphism, and, according to Zarebska et al (2013), African Americans and Africans are more likely to have the polymorphisms that are associated with elite power performance.
There is also a meta-analysis on genotyping and elite power athlete performance (Weyerstrab et al, 2017). Weyerstrab et al (2017) meta-analyzed 36 studies which attempted to find associations between genotype and athletic ability. One of the polymorphisms studied was the famous ACTN3. It has been noted that, when conditions are right (i.e., the right morphology), the combined effects of morphology along with the contractile properties of the individual muscle fibers contribute to the enhanced performance of those with the RR ACTN3 genotype (Broos et al, 2016), while Ma et al (2013) also lend credence to the idea that genetics influences sporting performance. This is, in fact, the most-replicated association in regard to elite sporting performance: we know the mechanism behind how muscle fibers contract; we know how the fibers contract and the morphology needed to maximize the effectiveness of said fast twitch fibers (type II fibers). (Blacks have a higher proportion of type II fibers [see Caeser and Henry, 2015 for a review].)
Weyerstrab et al (2017) meta-analyzed 35 articles, finding significant associations with genotype and elite power performance. They found that ten polymorphisms were significantly associated with power athlete states. Their most interesting findings, though, were on race. Weyerstrab et al (2017: 6) write:
Results of this meta-analysis show that US African American carriers of the ACE AG genotype (rs4363) were more than two times more likely to become a power athlete compared to carriers of the ACE preferential genotype for power athlete status (AA) in this population.
“Power athlete” does not necessarily have to mean “strength athlete” as in powerlifters or weightlifters (more on weightlifters below).
Lastly, the AGT M235T polymorphism, while associated with other power movements, was not associated with elite weightlifting performance (Ben-Zaken et al, 2018). As noted above, this polymorphism was observed in other power athletes, and since these movements are largely similar (short, explosive movements), one would rightly reason that this association should hold for weightlifters, too. However, this is not what we find.
Weightlifting, compared to other explosive, power sports, is different. The beginning of the lifts take explosive power, but during the ascent of the lift, the lifter moves the weight slower, which is due to biomechanics and a heavy load. Ben-Zaken et al (2018) studied 47 weightlifters (38 male, 9 female) and 86 controls. Every athlete that was studied competed in national and international meets on a regular basis. Thirty of the weightlifters were also classified as “elite”, which entails participating in and winning national and international competitions such as the Olympics and the European and World Championships).
Ben-Zaken et al (2018) did find that weightlifters had a higher prevalence of the AGT 235T polymorphism when compared to controls, though there was no difference in the prevalence of this polymorphism when elite and national-level competitors were compared, which “[suggests] that this polymorphism cannot determine or predict elite competitive weightlifting performance” (Ben-Zaken et al, 2018: 38). Of course, a favorable genetic profile is important for sporting success, though, despite the higher prevalence of AGT in weightlifters compared to controls, this could not explain the difference between national and elite-level competitors. Other polymorphisms could, of course, contribute to weightlifting success, variables “such as training experience, superior equipment and facilities, adequate nutrition, greater familial support, and motivational factors, are crucial for top-level sports development as well” (Ben-Zaken et al, 2018: 39).
I should also comment on Anatoly Karlin’s new article The (Physical) Strength of Nations. I don’t disagree with his main overall point; I only disagree that grip strength is a good measure of overall strength—even though it does follow the expected patterns. Racial differences in grip strength exist, as I have covered in the past. Furthermore, there are associations between muscle strength and longevity, with stronger men being more likely to live longer, fuller lives (Ruiz et al, 2008; Volkalis, Haille, and Meisinger, 2015; Garcia-Hermosa, et al, 2018) so, of course, strength training can only be seen as a net positive, especially in regard to living a longer and fuller life. Hand grip strength does have a high correlation with overall strength (Wind et al, 2010; Trosclair et al, 2011). While handgrip strength can tell you a whole lot about your overall health (Lee et al, 2016), of course, there is no better proxy than actually doing the lifts/exercises to ascertain one’s level of strength.
There are replicated genetic associations between explosive, powerful athletic performance, along with even the understanding of the causal mechanisms behind the polymorphisms and their carry-over to power sports. We know that if morphology is right and the individual has the RR ACTN3 genotype, that they will exceed in explosive sports. We know the causal pathways of ACTN3 and how it leads to differences in sprinting competitions. It should be worth noting that, while we do know a lot more about the genomics of sports than we did 20, even 10 years ago, current genetic testing has zero predictive power in regard to talent identification (Pitsladis et al, 2013).
So, of course, for parents and coaches who wonder about the athletic potential of their children and students, the best way to gauge whether or not they will excel in athletics is…to have them compete and compare them to other kids. Even if the genetics aspect of elite power performance is fully unlocked one day (which I doubt it will be), the best way to ascertain whether or not one will excel in a sport is to put them to the test and see what happens. We are in our infancy in understanding the genomics of sporting performance, but when we do understand which genotypes are more prevalent in regard to certain sports (and of course the interactions of the genotype with the environment and genes), then we can better understand how and why others are better in certain sports.
The genomics of elite sporting performance is very interesting; however, the answer that reductionists want to see will not appear: genes are difference makers (Sterelny and Griffith, 1999), not causes, and along with a whole slew of other environmental and mental factors (Lippi, Favaloro, and Guidi 2008), along with a favorable genetic profile with sufficient training (and everything else that comes along with it) are needed for the athlete to reach their maximum athletic potential (see Guth and Roth, 2013). Genetic and environmental differences between individuals and groups most definitely explain differences in elite sporting performance, though elucidating what causes what and the mechanisms that cause the studied trait in question will be tough.
Just because group A has gene or gene networks G and they compete in competition C does not mean that gene or gene networks G contribute in full—or in part—to sporting success. The correlations could be coincidental and non-functional in regard to the sport in question. Athletes should be studied in isolation, meaning just studying a specific athlete in a specific discipline to ascertain how, what, and why works for the specific athlete along with taking anthropomorphic measures, seeing how bad they want “it”, and other environmental factors such as nutrition and training. Looking at the body as a system will take us away from privileging one part over another—while we also do understand that they do play a role but not the role that reductionists believe.
These studies, while they attempt to show us how genetic factors cause differences at the elite level in power sports, they will not tell the whole story, because we must look at the whole system, not reduce it down to the sum of its parts (Shenk, 2011: chapter 5). While blacks are more likely to have these polymorphisms that are associated with elite power athlete performance, this does not obviously carry over to strongman and powerlifting competition.
In the 1940s, psychologist William Sheldon created a system of body measures known as “somatotyping”, then took his somatotypes and attempted to classify each soma (endomorph, ectomorph, or mesomorph) to differing personality types. It was even said that “constitutional psychology can guide a eugenics program and save the modern world from itself.”
Sheldon attempted to correlate different personality dimensions to different somas. But his somas fell out of favor before being revived by two of his disciples—without the “we-can-guess-your-personality-from-your-body-type” canard that Sheldon used. Somatotyping, while of course being put to use in a different way today compared to what it was originally created for, it gives us reliable dimensions for human appendages and from there we can ascertain what a given individual would excel at in regard to sporting events (obviously this is just on the basis of physical measures and does not measure the mind one needs to excel in sports).
The somatotyping system is straightforward: You have three values, say at 1-1-7; the first refers to endomorphy, the second refers to mesomorphy and the third refers to ectomorphy, therefore a 1-1-7 would be an extreme ectomorph. However, few people are at the extreme end of each soma, and most people have a combination of two or even all three of the somas.
According to Carter (2002): “The somatotype is defined as the quantification of the present shape and composition of the human body.” So, obviously, somas can change over time. However, it should be noted that the somatotype is, largely, based on one’s musculoskeletal system. This is where the appendages come in, along with body fat, wide and narrow clavicles and chest etc. This is why the typing system, although it began as a now-discredited method, should still be used today since we do not use the pseudoscientific personality measures with somatotyping.
Ectomorphs are long and lean, lanky, you could say. They have a smaller, narrower chest and shoulders, along with longer arms and legs, and have a hard time gaining weight, and a short upper body (I’d say they have a harder time gaining weight due to a slightly faster metabolism, in the variation of the normal range of metabolism, of course). Put simply, ectomorphs are just skinny and lanky with less body fat than mesos and endos. Human races that fit this soma are East Africans and South Asians (see Dutton and Lynn, 2015; one of my favorite papers from Lynn for obvious reasons).
Endomorphs are stockier, shorter and have wider hips, along with short limbs, a wider trunk, more body fat and can gain muscular strength easier than the other somas. Thus, endos, being shorter than ectos and mesos, have a lower center of gravity, along with shorter arms. Thus, we should see that these somas dominate strongman competitions and this is what we see. Pure strength competitions are perfect for this type, such as Strongman competitions and powerlifting. Races that generally conform to this type are East Asians, Europeans, and Pacific Islanders (see Dutton and Lynn, 2015).
Finally, we have mesomorphs (the “king” of all of the types). Mesos are more muscular on average than the two others, they have less body fat than endos but more body fat than ectos; they have wider shoulders, chest and hips, a short trunk and long limbs. The most mesomorphic races are West Africans (Malina, 1969), and due to their somatotype they can dominate sprinting competitions; they also have thinner skin folds (Vickery, Cureton, and Collins, 1988; Wagner and Heyward, 2000), and so they would have an easier time excelling at running competitions but not at weightlifting, powerlifting, or Strongman (see Dutton and Lynn, 2015).
These anatomic differences between the races of man are due to climatic adaptations. The somatypic differences Neanderthals and Homo sapiens mirror the somatotype difference between blacks and whites; since Neanderthals were cold-adapted, they were shorter, had wider pelves and could thusly generate more power than the heat-adapted Homo sapiens who had long limbs and narrow pelvis to better dissipate heat. Either way, we can look at the differences in somatotype between races that evolved in Europe and Africa to ascertain the somatotype of Neanderthals—and we also have fossil evidence for these claims, too (see e.g., Weaver and Hublin, 2009; Gruss and Schmitt, 2016)
Now, just because somatotyping, during its conception, was mixed with pseudoscientific views about differing somas having differing psychological types, does not mean that these differences in body type do not have any bearing on sporting performance. We can chuck the “constitutional psychology” aspect of somatotyping and just keep the anthropometric measures, and, along with the knowledge of human biomechanics, we can then discuss, in a scientific manner, why one soma would excel in sport X or why one soma would not excel in sport X. Attempting to argue that since somatotyping began as some crank psuedoscience does not mean that it is not useful today, since we do not ascribe inherent psychological differences to these somas (I’d claim that saying that this soma has a harder time gaining weight compared to that soma is not ascribing a psychological difference to the soma; it is taking physiologically and on average we can see that different somas have different propensities for weight gain).
In her book Straightening the Bell Curve: How Stereotypes about Black Masculinity Drive Research about Race and Intelligence, Hilliard (2012: 21) discusses the pitfalls of somatotyping and how Sheldon attempted to correlate personality measures with his newfound somatotypes:
As a young graduate student, he [Richard Herrnstein] had fallen under the spell of Harvard professor S. S. Stevens, who had coauthored with William Sheldon a book called The Varieties of Temperament: A Psychology of Constitutional Differences, which popularized the concept of “somatotyping,” first articulated by William Sheldon. This theory sought, through the precise measurement and analysis of human body types, to establish correlations comparing intelligence, temperament, sexual proclivities, and the moral worth of individuals. Thus, criminals were perceived to be shorter and heavier and more muscular than morally upstanding citizens. Black males were reported to rank higher on the “masculine component” scale than white males did, but lower in intelligence. Somatotyping lured the impressionable young Herrnstein into a world promising precision and human predictability based on the measuring of body parts.
Though constitutional psychology is now discredited, there may have been something to some of Sheldon’s theories. Ikeda et al (2018: 3) conclude in their paper, Re-evaluating classical body type theories: genetic correlation between psychiatric disorders and body mass index, that “a trans-ancestry meta-analysis of the genetic correlation between psychiatric disorders and BMI indicated that the negative correlation with SCZ supported classical body type theories proposed in the last century, but found a negative correlation between BD and BMI, opposite to what would have been predicted.” (Though it should be noted that SCZ is a, largely if not fully, environmentally-induced disorder, see Joseph, 2017.)
These different types (i.e., the differing limb lengths/body proportions) have implications for sporting performance. Asfaw and A (2018) found that Ethiopian women high jumpers had the highest ectomorph values whereas long and triple jumpers were found to be more mesomorphic. Sports good for ectos are distance running due to their light frame, tennis etc—anything that the individual can use their light frame as an advantage. Since they have longer limbs and a lighter frame, they can gain more speed in the run up to the jump, compared to endos and mesos (who are heavier). This shows why ectos have a biomechanical advantage when it comes to high jumping.
As for mesomorphs, the sports they excel at are weightlifting, powerlifting, strongman, football, rugby etc. Any sport where the individual can use their power and heavier bone mass will they excel in. Gutnik et al (2017) even concluded that “These results suggest with high probability that there is a developmental tendency of change in different aspects of morphometric phenotypes of selected kinds of sport athletes. These phenomena may be explained by the effects of continuous intensive training and achievement of highly sport-defined shapes.” While also writing that mesomorphy could be used to predict sporting ability.
Finally, for endomorphs, they too would excel in weightlifting, powerlifting, and strongman, but do on average better since they have different levers (i.e., shorter appendages so they can more weight and a shorter amount of time in comparison to those with longer limbs like ectos).
Thus, different somatotypes excel in different sports. Different races and ethnies have differing somatotypes (Dutton and Lynn, 2015), so these different bodies that the races have, on average, is part of the cause for differences in sporting ability. That somatotyping began as a pseudoscientific endeavor 70 years ago does not mean that it does not have a use in today’s world—because it clearly does due to the sheer amount of papers on the usefulness of somatotyping and relating differences in sporting performance due to somatotyping. For example, blacks have thinner skin folds (Vickery, Cureton, and Collins, 1988; Wagner and Heyward, 2000) which is due to their somatotype, which is then due to the climate their ancestors evolved in.
Somatotyping can show us the anthropometric reasons for how and why certain individuals, ethnies, and races far-and-away dominate certain sporting events. It is completely irrelevant that somatotyping began as a psychological pseudoscience (what isn’t in psychology, am I right?). Understanding anthropometric differences between individuals and groups will help us better understand the evolution of these somas along with how and why these somas lead to increased sporting performance in certain domains. Somatotyping has absolutely nothing to do with “intelligence” nor how morally upstanding one is. I would claim that somatotyping does have an effect on one’s perception of masculinity, and thus more masculine people/races would tend to be more mesomorphic, which would explain what Hilliard (2012) discussed when talking about somatotyping and the attempts to correlate differing psychological tendencies to each type.
Michael Hardimon published Rethinking Race: The Case for Deflationary Realism last year (Hardimon, 2017). I was awaiting some critical assessment of the book, and it seems that at the end of March, some criticism finally came. The criticism came from another philosopher, Joshua Glasgow, in the journal Mind (Glasgow, 2018). The article is pretty much just arguing against his minimalist race concept and one thing he brings up in his book, the case of a twin earth and what we would call out-and-out clones of ourselves on this twin earth. Glasgow makes some good points, but I think he is largely misguided on Hardimon’s view of race.
Hardimon (2017) is the latest defense for the existence of race—all the while denying the existence of “racialist races”—that there are differences in mores, “intelligence” etc—and taking the racialist view and “stripping it down to its barebones” and shows that race exists, in a minimal way. This is what Hardimon calls “social constructivism” in the pernicious sense—racialist races, in Hardimon’s eyes, are socially constructed in a pernicious sense, arguing that racialist races do not represent any “facts of the matter” and “supports and legalizes domination” (pg 62). The minimalist concept, on the other hand, does not “support and legalize domination”, nor does it assume that there are differences in “intelligence”, mores and other mental characters; it’s only on the basis of superficial physical features. These superficial physical features are distributed across the globe geographically and these groups are real and exist who show these superficial physical features across the globe. Thus, race, in a minimal sense, exists. However, people like Glasgow have a few things to say about that.
Glasgow (2018) begins by praising Hardimon (2017) for “dispatching racialism” in his first chapter, also claiming that “academic writings have decisively shown why racialism is a bad theory” (pg 2). Hardimon argues that to believe in race, on not need believe what the racialist concept pushes; one must only acknowledge and accept that there are:
1) differences in visible physical features which correspond to geographic ancestry; 2) these differences in visible features which correspond to geographic ancestry are exhibited between real groups; 3) these real groups that exhibit these differences in physical features which correspond to geographic ancestry satisfy the conditions of minimalist race; C) therefore race exists.
This is a simple enough argument, but Glasgow disagrees. As a counter, Glasgow brings up the “twin earth” argument. Imagine a twin earth was created. On Twin Earth, everything is exactly the same; there are copies of you, me, copies of companies, animals, history mirrored down to exact minutiae, etc. The main contention here is that Hardimon claims that ancestry is important for our conception of race. But with the twin earth argument, since everything, down to everything, is the same, then the people who live on twin earth look just like us but! do not share ancestry with us, they look like us (share patterns of visible physical features), so what race would we call them? Glasgow thusly states that “sharing ancestry is not necessary for a group to count as a race” (pg 3). But, clearly, sharing ancestry is important for our conception of race. While the thought experiment is a good one it fails since ancestry is very clearly necessary for a group to count as a race, as Hardimon has argued.
Hardimon (2017: 52) addresses this, writing:
Racial Twin Americans might share our concept of race and deny that races have different geographical origins. This is because they might fail to understand that this is a component of their race concept. If, however, their belief that races do not have different geographical origins did not reflect a misunderstanding of their “race concept,” then their “race concept” would not be the same concept as the concept that is the ordinary race concept in our world. Their use of ‘race’ would pick out a different subject matter entirely from ours.
and on page 45 writes:
Glasgow envisages Racial Twin Earth in such a way that, from an empirical (that is, human) point of view, these groups would have distinctive ancestries, even if they did not have distinctive ancestries an sich. But if this is so, the groups [Racial Twin Earthings] do not provide a good example of races that lack distinctive ancestries and so do not constitute a clear counterexample to C(2) [that members of a race are “linked by a common ancestry peculiar to members of that group”].
C(2) (P2 in the simple argument for the existence of race) is fine, and the objections from Glasgow do not show that P(C)2 is false at all. The Racial Twin Earth argument is a good one, it is sound. However, as Hardimon had already noted in his book, Glasgow’s objection to C(2) does not rebut the fact that races share peculiar ancestry unique to them.
Next, Glasgow criticizes Hardimon’s viewpoints on “Hispanics” and Brazilians. These two groups, says Glasgow, shows that two siblings with the same ancestry, though they have different skin colors, would be different races in Brazil. He uses this example to state that “This suggests that race and ancestry can be disconnected” (pg 4). He criticizes Hardimon’s solution to the problem of race and Brazilians, stating that our term “race” and the term in Brazil do not track the same things. “This is jarring. All that anthropological and sociological work done to compare Brazil with the rest of the world (including the USA) would be premised on a translation error” (pg 4). Since Americans and Brazilians, in Glasgow’s eyes, can have a serious conversation about race, this suggests to Glasgow that “our concept of race must not require that races have distinct ancestral groups” (pg 5).
I did cover Brazilians and “Hispanics” as regards the minimalist race concept. Some argue that the “color system” in Brazil is actually a “racial system” (Guimaraes 2012: 1160). While they do denote race as ‘COR’ (Brazilian for ‘color), one can argue that the term used for ‘color’ is ‘race’ and that we would have no problem discussing ‘race’ with Brazilians, since Brazilians and Americans have similar views on what ‘race’ really is. Hardimon (2017: 49) writes:
On the other hand, it is not clear that the Brazilian concept of COR is altogether independent of the phenomenon we Americans designate using ‘race.’ The color that ‘COR’ picks out is racial skin color. The well-known, widespread preference for lighter (whiter) skin in Brazil is at least arguably a racial preference. It seems likely that white skin color is preferred because of its association with the white race. This provides a reason for thinking that the minimalist concept of race may be lurking in the background of Brazilian thinking about race.
Since ‘COR’ picks out racial skin color, it can be safely argued that Brazilians and Americans at least are generally speaking about the same things. Since the color system in Brazil pretty much mirrors what we know as racial systems, demarcating races on the basis of physical features, we are, it can be argued, talking about the same (or similar) things.
Further, the fact that “Latinos” do not fit into Hardimon’s minimalist race concepts is not a problem with Hardimon’s arguments about race, but is a problem with how “Latinos” see themselves and racialize themselves as a group. “Latinos” can count as a socialrace, but they do not—can not—count as a minimalist race (such as the Caucasian minimalist race; the African minimalist race; the Asian minimalist race etc), since they do not share visible physical patterns which correspond to differences in geographic ancestry. Since they do not exhibit characters that demarcate minimalist races, they are not minimalist races. Looking at Cubans compared to, say, Mexicans (on average) is enough to buttress this point.
Glasgow then argues that there are similar problems when you make the claim “that having a distinct geographical origin is required for a group to be a race” (pg 5). He says that we can create “Twin Trump” and “Twin Clinton” might be created from “whole cloth” on two different continents, but we would still call them both “white.” Glasgow then claims that “I worry that visible trait groups are not biological objects because the lines between them are biologically arbitrary” (pg 5). He argues that we need a “dividing line”, for example, to show that skin color is an arbitrary trait to divide races. But if we look at skin color as an adaptation to the climate of the people in question (Jones et al, 2018), then this trait is not “arbitrary”, and the trait is then linked to geographic ancestry.
Glasgow then goes down the old and tired route that “There is no biological reason to mark out one line as dividing the races rather than another, simply based on visible traits” (pg 5). He then goes on to discuss the fact that Hardimon invokes Rosenberg et al (2002) who show that our genes cluster in specific geographic ancestries and that this is biological evidence for the existence of race. Glasgow brings up two objections to the demarcation of races on both physical appearance and genetic analyses: picture the color spectrum, “Now thicken the orange part, and thin out the light red and yellow parts on either side of orange. You’ve just created an orange ‘cluster’” (pg 6), while asking the question:
Does the fact that there are more bits in the orange part mean that drawing a line somewhere to create the categories orange and yellow now marks a scientifically principled line, whereas it didn’t when all three zones on the spectrum were equally sized?
I admit this is a good question, and that this objection would indeed go with the visible trait of skin color in regard to race; but as I said above, since skin color can be conceptualized as a physical adaptation to climate, then that is a good proxy for geographic ancestry, whether or not there is a “smooth variation” of skin colors as you move away from the equator or not, it is evidence that “races” have biological differences and these differences start on the biggest organ in the human body. This is just the classic continuum fallacy in action: that X and Y are two different parts of an extreme; there is no definable point where X becomes Y, therefore there is no difference between X and Y.
As for Glasgow’s other objection, he writes (pg 6):
if we find a large number of individuals in the band below 62.3 inches, and another large grouping in the band above 68.7 inches, with a thinner population in between, does that mean that we have a biological reason for adopting the categories ‘short’ and ‘tall’?
It really depends on what the average height is in regard to “adopting the categories ‘short’ and ‘tall’” (pg 6). The first question was better than the second, alas, they do not do a good job of objecting to Hardimon’s race concept.
In sum, Glasgow’s (2018) review of Hardimon’s (2017) book Rethinking Race: The Case for Deflationary Realism is an alright review; though Glasgow leaves a lot to be desired and I do think that his critique could have been more strongly argued. Minimalist races do exist and are biologically real.
I am of the opinion that what matters regarding the existence of race is not biological science, i.e., testing to see which populations have which differing allele frequencies etc; what matters is the philosophical aspects to race. The debates in the philosophical literature regarding race are extremely interesting (which I will cover in the future), and are based on racial naturalism and racial eliminativism.
(Racial naturalism “signifies the old, biological conception of race“; racial eliminativism “recommends discarding the concept of race entirely“; racial constructivism “races have come into existence and continue to exist through “human culture and human decisions” (Mallon 2007, 94)“; thin constructivism “depicts race as a grouping of humans according to ancestry and genetically insignificant, “superficial properties that are prototypically linked with race,” such as skin tone, hair color and hair texture (Mallon 2006, 534); and racial skepticism “holds that because racial naturalism is false, races of any type do not exist“.) (Also note that Spencer (2018) critiques Hardimon’s viewpoints in his book as well, which will also be covered in the future, along with the back-and-forth debate in the philosophical literature between Quayshawn Spencer (e.g., 2015) and Adam Hochman (e.g., 2014).)
Due to evolving in different climates, the different races of Man have differing anatomy and physiology. This, then, leads to differences in sports performance—certain races do better than others in certain bouts of athletic prowess, and this is due to, in large part, heritable biological/physical differences between blacks and whites. Some of these differences are differences in somatotype, which bring a considerable advantage for, say, runners (an ecto-meso, for instance, would do very well in sprinting or distance running depending on fiber typing). This article will discuss differences in racial anatomy and physiology (again) and how it leads to disparities in certain sports performance.
Kerr (2010) argues that racial superiority in sport is a myth. (Read my rebuttal here.) In his article, Kerr (2010) attempts to rebut Entine’s (2000) book Taboo: Why Black Athletes Dominate Sports and Why We’re Afraid to Talk About It. In a nutshell, Kerr (2010) argues that race is not a valid category; that other, nongenetic factors play a role other than genetics (I don’t know if anyone has ever argued if it was just genetics). Race is a legitimate biological category, contrary to Kerr’s assertions. Kerr, in my view, strawman’s Entine (2002) by saying he’s a “genetic determinist”, but while he does discuss biological/genetic factors more than environmental ones, Entine is in no way a genetic determinist (at least that’s what I get from my reading of his book, other opinions may differ). Average physical differences between races are enough to delineate racial categories and then it’s only logical to infer that these average physical/physiological differences between the races (that will be reviewed below) would infer an advantage in certain sports over others, while the ultimate cause was the environment that said race’s ancestors evolved in (causing differences in somatotype and physiology).
Black athletic superiority has been discussed for decades. The reasons are numerous and of course, this has even been noticed by the general public. In 1991, half of the respondents of a poll on black vs. whites in sports “agreed with the idea that “blacks have more natural physical ability,“” (Hoberman, 1997: 207). Hoberman (1997) of course denies that there is any evidence that blacks have an advantage over whites in certain sports that come down to heritable biological factors (which he spends the whole book arguing). However, many blacks and whites do, in fact, believe in black athletic superiority and that physiologic and anatomic differences between the races do indeed cause racial differences in sporting performance (Wiggins, 1989). Though Wiggins (1989: 184) writes:
The anthropometric differences found between racial groups are usually nothing more than central tendencies and, in addition, do not take into account wide variations within these groups or the overlap among members of different races. This fact not only negates any reliable physiological comparisons of athletes along racial lines, but makes the whole notion of racially distinctive physiological abilities a moot point.
This is horribly wrong, as will be seen throughout this article.
|Data from Malina, (1969: 438)||n||Mesomorph||Ectomorph||Endomorph|
|Data from Malina (1969: 438)||Blacks||Whites|
|Thin-build body type||8.93||5.90|
|Submedium fatty development||48.31||29.39|
|Fat and very fat categories||9.09||21.06|
This was in blacks and whites aged 6 to 11. Even at these young ages, it is clear that there are considerable anatomic differences between blacks and whites which then lead to differences in sports performance, contra Wiggins (1989). A basic understanding of anatomy and how the human body works is needed in order to understand how and why blacks dominate certain sports over whites (and vice versa). Somatotype is, of course, predicated on lean mass, fat mass, bone density, stature, etc, which are heritable biological traits, thus, contrary to popular belief that somatotyping holds no explanatory power in sports today (see Hilliard, 2012).
One variable that makes up somatotype is fat-free body mass. There are, of course, racial differences in fat mass, too (Vickery, Cureton, and Collins, 1988; Wagner and Heyward, 2000). Lower fat mass would, of course, impede black excellence in swimming, and this is what we see (Rushton, 1997; Entine, 2000). Wagner and Heyward (2000) write:
Our review unequivocally shows that the FFB of blacks and whites differs significantly. It has been shown from cadaver and in vivo analyses that blacks have a greater BMC and BMD than do whites. These racial differences could substantially affect measures of body density and %BF. According to Lohman (63), a 2% change in the BMC of the body at a given body density could, theoretically, result in an 8% error in the estimation of %BF. Thus, the BMC and BMD of blacks must be considered when %BF is estimated.
While Vickery, Cureton, and Collins (1988) found that blacks had thinner skin folds than whites, however, in this sample, somatotype did not explain racial differences in bone density, like other studies (Malina, 1969), Vickery, Cureton, and Collins (1988) found that blacks were also more likely to be mesomorphic (which would then express itself in racial differences in sports).
Hallinan (1994) surveyed 32 sports science, exercise physiology, biomechanics, motor development, motor learning, and measurement evaluation textbooks to see what they said racial differences in sporting performance and how they explained them. Out of these 32 textbooks, according to Wikipedia, these “textbooks found that seven [textbooks] suggested that there are biophysical differences due to race that might explain differences in sports performance, one [textbook] expressed caution with the idea, and the other 24 [textbooks] did not mention the issue.” Furthermore, Strklaj and Solyali (2010), in their paper “Human Biological Variation in Anatomy Textbooks: The Role of Ancestry” write that their “results suggest that this type of human variation is either not accounted for or approached only superficially and in an outdated manner.”
It’s patently ridiculous that most textbooks on the anatomy and physiology of the human body do not talk about the anatomic and physiologic differences between racial and ethnic groups. Hoberman (1997) also argues the same, that there is no evidence to confirm the existence of black athletic superiority. Of course, many hypotheses have been proposed to explain how and why blacks are at an inherent advantage in sport. Hoberman (1997: 269) discusses one, writing (quoting world record Olympian in the 400-meter dash, Lee Evans):
“We were bred for it [athletic dominance] … Certainly the black people who survived in the slave ships must have contained the highest proportion of the strongest. Then, on the plantations, a strong black man was mated with a strong black woman. We were simply bred for physical qualities.”
While Hoberman (1997: 270-1) also notes:
Finally, by arguing for a cultural rather than a biological interpretation of “race,” Edwards proposed that black athletic superiority results from “a complex of societal conditions” that channels a disproporitionate number of talented blacks into athletic careers.
The fact that blacks were “bred for” athletic dominance is something that gets brought up often but has little (if any) empirical support (aside from just-so stories about white slavemasters breeding their best, biggest and strongest black slaves). The notion that “a complex of societal conditions” (Edwards, 1971: 39) explains black dominance in sports, while it has some explanatory power in regard to how well blacks do in sporting competition, it, of course, does not tell the whole story. Edwards (1978: 39) argues that these complex societal conditions “instill a heightened motivation among black male youths to achieve success in sports; thus, they channel a proportionately greater number of talented black people than whites into sports participation.” While this may, in fact, be true, this does nothing to rebut the point that differences in anatomic and physiologic factors are a driving force in racial differences in sporting performance. However, while these types of environmental/sociological arguments do show us why blacks are over-represented in some sports (because of course motivation to do well in the sport of choice does matter), they do not even discuss differences in anatomy or physiology which would also be affecting the relationship.
For example, one can have all of the athletic gifts in the world, one can be endowed with the best body type and physiology to do well in any type of sport you can imagine. However, if he does not have a strong mind, he will not succeed in the sport. Lippi, Favaloro, and Guidi (2008) write:
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.
Any athlete—no matter their race—needs a strong mental background, for if they don’t, they can have all of the physical gifts in the world, they will not become top-tier athletes in the sport of their choice; advantageous physical factors are imperative for success in differing sports, though myriad variables work in concert to produce the desired effect so you cannot have one without the other. On the other side, one can have a strong mental background and not have the requisite anatomy or physiology needed to succeed in the sport in question, but if he has a stronger mind than the individual with the requisite morphology, then he probably will win in a head-to-head competition. Either way, a strong mind is needed for strong performance in anything we do in life, and sport is no different.
Echoing what Hoberman (1997) writes, that “racist” thoughts of black superiority in part cause their success in sport, Sheldon, Jayaratne, and Petty (2007) predicted that white Americans’ beliefs in black athletic superiority would coincide with prejudice and negative stereotyping of black’s “intelligence” and work ethic. They studied 600 white men and women to ascertain their beliefs on black athletic superiority and the causes for it. Sheldon, Jayaratne, and Petty (2007: 45) discuss how it was believed by many, that there is a “ perceived inverse relationship between athleticism and intelligence (and hard work).” (JP Rushton was a big proponent of this hypothesis; see Rushton, 1997. It should also be noted that both Rushton, 1997 and Entine, 2000 believe that blacks’ higher rate of testosterone—3 to 15 percent— [Ross et al, 1986; Ellis and Nyborg, 1992; see rebuttal of both papers] causes their superior athletic performance, I have convincingly shown that they do not have higher levels of testosterone than other races, and if they do the difference is negligible.) However, in his book The Sports Gene: Inside the Science of Extraordinary Athletic Performance, Epstein (2014) writes:
With that stigma in mind [that there is an inverse relationship between “intelligence” and athletic performance], perhaps the most important writing Cooper did in Black Superman was his methodological evisceration of any supposed inverse link between physical and mental prowess. “The concept that physical superiority could somehow be a symptom of intellectual superiority became associated with African Americans … That association did not begin until about 1936.”
What Cooper (2004) implied is that there was no “inverse relationship” with intelligence and athletic ability until Jesse Owens blew away the competition at the 1936 Olympics in Berlin, Germany. In fact, the relationship between “intelligence” and athletic ability is positive (Heppe et al, 2016). Cooper is also a co-author of a paper Some Bio-Medical Mechanisms in Athletic Prowess with Morrison (Morrison and Cooper, 2006) where they argue—convincingly—that the “mutation appears to have triggered a series of physiological adjustments, which have had favourable athletic consequences.”
Thus, the hypothesis claims that differences in glucose conversion rates between West African blacks and her descendants began, but did not end with the sickling of the hemoglobin molecule, where valine is substituted for glutamic acid, which is the sixth amino acid of the beta chain of the hemoglobin molecule. Marlin et al (2007: 624) showed that male athletes who were inflicted with the sickle cell trait (SCT) “are able to perform sprints and brief exercises at the highest levels.” This is more evidence for Morrison and Cooper’s (2006) hypothesis on the evolution of muscle fiber typing in West African blacks.
Bejan, Jones, and Charles (2010) explain that the phenomenon of whites being faster swimmers in comparison to blacks being faster runners can be accounted for by physics. Since locomotion is a “falling-forward cycle“, body mass falls forward and then rises again, so mass that falls from a higher altitude falls faster and forward. The altitude is set by the position of center of mass above the ground for running, while for swimming it is set by the body rising out of the water. Blacks have a center of gravity that is about 3 percent higher than whites, which implies that blacks have a 1.5 percent speed advantage in running whereas whites have a 1.5 percent speed advantage in swimming. In the case of Asians, when all races were matched for height, Asians fared even better, than whites in swimming, but they do not set world records because they are not as tall as whites (Bejan, Jones, and Charles, 2010).
It has been proposed that stereotype threat is part of the reasons for East African running success (Baker and Horton, 2003). They state that many theories have been proposed to explain black African running success—from genetic theories to environmental determinism (the notion that physiologic adaptations to climate, too, drive differences in sporting competition). Baker and Horton (2003) note that “that young athletes have internalised these stereotypes and are choosing sport participation accordingly. He speculates that this is the reason why white running times in certain events have actually decreased over the past few years; whites are opting out of some sports based on perceived genetic inferiority.” While this may be true, this wouldn’t matter, as people gravitate toward what they are naturally good at—and what dictates that is their mind, anatomy, and physiology. They pretty much argue that stereotype threat is a cause of East African running performance on the basis of two assertions: (1) that East African runners are so good that it’s pointless to attempt to win if you are not East African and (2) since East Africans are so good, fewer people will try out and will continue the illusion that East Africans would dominate in middle- and long-distance running. However, while this view is plausible, there is little data to back the arguments.
To explain African running success, we must do it through a systems view—not one of reductionism (i.e., gene-finding). We need to see how the systems in question interact with every part. So while Jamaicans, Kenyans, and Ethiopians (and American blacks) do dominate in running competitions, attempting to “find genes” that account for success n these sports seems like a moot point—since the whole system is what matters, not what we can reduce the system in question to.
However, there are some competitions that blacks do not do so well in, and it is hardly discussed—if at all—by any author that I have read on this matter. Blacks are highly under-represented in strength sports and strongman competitions. Why? My explanation is simple: the causes for their superiority in sprinting and distance running (along with what makes them successful at baseball, football, and basketball) impedes them from doing well in strength and strongman competitions. It’s worth noting that no black man has ever won the World’s Strongest Man competition (indeed the only African country to even place—Rhodesia—was won by a white man) and the causes for these disparities come down to racial differences in anatomy and physiology.
I discussed racial differences in the big four lifts and how racial differences in anatomy and physiology would contribute to how well said race performed on the lift in question. I concluded that Europeans and Asians had more of an advantage over blacks in these lifts, and the reasons were due to inherent differences in anatomy and physiology. One major cause is also the differing muscle fiber typing distribution between the races (Alma et al, 1986; Tanner et al, 2002; Caesar and Henry, 2015 while blacks’ fiber typing helps them in short-distance sprinting (Zierath and Hawley, 2003). Muscle fiber typing is a huge cause of black athletic dominance (and non-dominance). Blacks are not stronger than whites, contrary to popular belief.
I also argued that Neanderthals were stronger than Homo sapiens, which then had implications for racial differences in strength (and sports). Neanderthals had a wider pelvis than our species since they evolved in colder climes (at the time) (Gruss and Schmidt, 2016). With a wider pelvis and shorter body than Homo sapiens, they were able to generate more power. I then implied that the current differences in strength and running we see between blacks and whites can be used for Neanderthals and Homo sapiens, thusly, evolution in differing climates lead to differences in somatotype, which eventually then lead to differences in sporting competition (what Baker and Horton, 2003 term “environmental determinism” which I will discuss in the context of racial differences in sports in the future).
Finally, blacks dominate the sport of bodybuilding, with Phil Heath dominating the competition for the past 7 years. Blacks dominate bodybuilding because, as noted above, blacks have thinner skin folds than whites, so their striations in their muscles would be more prevalent, on average, at the same exact %BF. Bodybuilders and weightlifters were similar in mesomorphy, but the bodybuilders showed more musculature than the bodybuilders whereas the weightlifters showed higher levels of body fat with a significant difference observed between bodybuilders and weightlifters in regard to endomorphy and ectomorphy (weightlifters skewing endo, bodybuilders skewing ecto, as I have argued in the past; Imran et al, 2011).
To conclude, blacks do dominate American sporting competition, and while much ink has been spilled arguing that cultural and social—not genetic or biologic—factors can explain black athletic superiority, they clearly work in concert with a strong mind to produce the athletic phenotype, no one factor has prominence over the other; though, above all, if one does not have the right mindset for the sport in question, they will not succeed. A complex array of factors is the cause of black athletic dominance, including muscle fibers, the type of mindset, anatomy, overall physiology and fat mass (among other variables) explain the hows and whys of black athletic superiority. Cultural and social explanations—on their own—do not tell the whole story, just as genetic/biologic explanations on their own would not either. Every aspect—including the historical—needs to be looked at when discussing the dominance (or lack thereof) in certain sports along with genetic and nongenetic factors to see how and why certain races and ethnies excel in certain sports.