Science Proves That Race Does Not Exist

[Abdul-Aziz]

Science teaches us that race does not exist

 

 

There are no genes for race

 

Numerous epistemological difficulties beset the formulation of a systematic taxonomic classification based on human differences. The nonexistence of universal racial essences, or their corresponding nominalist analogues, upon which conventional typological definitions of race are mapped poses a significant challenge to this gargantuan task. Even the usage of racialized labels are subject to numerous ideological constraints, such as the lack of sufficiently contingent, even homogeneous conditions by which they can be both consistently and thoroughly applied. However, the enormous philosophical problems that beset the epistemological substructure upon which the concept of biological race is founded, are dwarfed by a substantial body of scientific evidence which explicitly denies the existence of racial essences on a genetic level. Thus, no specific causal gene for race has ever been uncovered; no sophisticated gene-gene interactions have ever been implicated in the elaboration of ethno-racial differences amongst human beings. Hence, there is no direct connection between genetic substructure and the specifically racialized morphology of folk taxonomy. For example, in classical typological definitions of biological race, Australians, Tasmanians, and Melanesians are phenotypically Africoid; unfortunately, the genetic distance between these South Pacific populations and the classical “Negro” morphologies of sub-Saharan Africa is much greater than whatever gulf exists between Australians/Tasmanians/Melanesians and northeast Asians. In other words, not only is there no genetic substructure that can be identified as being specifically racial, but there is no structural isomorphism that characterizes the relationship between genomic DNA and human phenotypic variance.

 

In order to fully comprehend the implications of what is being said, let us contrast ethno-racial designation with sexual dimorphism amongst human beings. Unlike conventional ethno-racial designations, being male or female is largely determined by the presence of XY and XX chromosomes. Although whatever genomic boundary that exists between the sexes is disrupted by the presence of intersexuality, the genotypic information contained within both pairs of sex chromosomes are reliably correlated with both secondary and tertiary sex characteristics, regardless of the gender in which they are manifested. From a general nomological perspective, a statistical generalization constructed on the presence or absence of XX possesses greater predictive value than atomic propositions about the genotypic or phenotypic basis of either secondary or tertiary sex characters. Even the aetiology of a condition such as hermaphroditism can be traced back to chromosomal dysmorphologies, such as XXX, XXY, or XYY, or to certain individual-level endocrinological disorders, such as the lack of gonadal androgen synthesis during embryological development, which can be traced back to various genes on either XX or XY chromosomes.

 

Genes may be responsible for a human morphological structure which can be conceptually associated with certain features of biological race, such as cranio-facial features or hair texture. However, it must be remembered that there are no chromosomal markers that code for being “black” or “white”; neither are there genes that pre-determine ethno-racial identity. When it comes to the modern conceptualization of race, there is no ethno-racial equivalent of our XX and XY chromosomes that determine sex, neither is there any ethno-racial analogue for the various combinations of X and Y that form the aetiological basis for congenital hermaphroditism, as in the case of ethno-racial intermixture. Although genes for certain aspects of gross human morphology may exist, the lack of any identifiable genetic substructure means that there is no connection between genes and any of the traditional morphological features associated with the standard typological definitions of race. Hence, the biological basis of sexual dimorphism is much stronger than whatever exists for race. The ground work upon which sexual identification rests are both objective and scientifically real, whereas no such proposition could be stated in favour of the doctrine of race. Based on this, it seems more likely that race is a social construction that is super-imposed from without over the processes of biological differentiation amongst human beings. There may be genes for certain morphological features traditionally deemed racial, but there are no specifically “racial” genes.

 

Moreover, the fact that there is no identifiable allele that corresponds to our modern conceptualization of “race” strongly suggests that we are dealing with an arbitrary form of social categorization which consists of a highly diverse and variable membership. This tremendous variability and biodiversity within the concept of race, with genetically dissimilar individuals belonging to the same taxonomic category, makes ascribing a definite biological basis to race scientifically implausible. In fact, the elaboration of human phenotypic variance is so complex, that it is almost impossible to separate environmental-genotypic interactions from purely genetic variables by mathematically partitioning them into exact percentages.

 

The notion that there exists within nature a one-to-one correspondence between the gene itself and the phenotypic trait (“a gene for race”) is an ideological assertion that finds its origins in those pseudo-scientific, eugenic speculations that immediately surrounded the work of Gregor Mendel at the turn of the twentieth century. From the standpoint of classical Mendelian genetics, the enormous variation present throughout nature means that genes that code for universal, highly differentiated population-based traits are non-existent. Instead, genes are represented as factors that determine the expression of individual phenotypic differences through successive cross-fertilizations, such as the intergenerational transmission of specific pathologies. These traits are expressed on an individual phenotypic level, depending on the levels of dominance or recessiveness involved. Because the supposedly “ethno-racial” phenotype as such possesses no genetic basis whatsoever, it is never expressed in terms of allelic dominance or recessiveness (appearing amongst some descendents, but not others) clearly demonstrating that it functions as a social construct on all levels of conceptual analysis.

 

In fact, all genomic/phenotypic characteristics are geographically dispersed amongst world populations. All gene frequencies that are highly correlated with trait expression, such as cranio-facial features and melanin pigmentation (which seems to be correlated with melanocotin 1 receptor genes), are present within all populations, suggesting a level of both genetic and physiological continuity that gravely undermines any system of ethno-racial classification.

 

To sum up, this is why the modern social construct of race is one of the greatest biological fictions of all time.

 

The study of Barbujani and Belle (2006) contradicts the findings of Rosenberg et al. (2002, 2005): race is a social construct without objective basis in perceptual biological reality

 

There are no putative genomic boundaries that divide human populations unambiguously into genetically distinguishable, geographically defined, and discrete biological categories. In this sense the concept of subspecies is an entirely mythological construct without foundation in objective reality. All forms of phenotypic variance, representing all gene frequencies and genomic configurations, are universally present within all populations. To say that any race, without being clearly delineated by identifiable differentia, can exist along a continuum without being wholly indistinguishable from the continuum itself is positively absurd. Thus, classical typological definitions of subspecies quickly break down as a legitimate means of systematizing empirical data, because there are no differentia unique to any subspecies that can reliably facilitate its structural differentiation from other subspecies.

 

Standard phylogeographic criteria dictates that in order for one subspecies to be distinguished from another, one must possess a series of differentia that are unique only to that subspecies, and no other. However, given the continuous distribution of human phenotypic/genotypic variation, heavily modulated by the presence of randomly distributed and linear clinal gradients, all traits are found in varying degrees of frequency within all populations. Because geographic dispersion of allele frequencies transcend conventional typological-populational definitions of subspecies, it is virtually impossible to classify the human species into subspecies categories. Ethno-racial differentiation is dependent on the existence of unique characteristics that can be assigned to one group and no other, meaning that in order for “raciation” to take place there must be some discontinuity in terms of the distribution of human trait variance. However, because of the continuity of human biodiversity, such ethno-racial differentiation is rendered impossible.

 

According to a study conducted by Barbujani and Belle (2006), the existence of patterns of genetic continuity on a universal level gravely undermine any attempt at differentiating the human species along ethno-racial lines. Although the researchers observe a certain degree of clustering within the data set, these clusters tend to show a considerable amount of variation in terms of overall structural composition, and are certainly very different from those initially observed by Rosenberg et al (2002, 2005). In order for the research of Rosenberg et al to have any validity, his exact results should be easily replicated, regardless of the scientific methodological approach employed.

 

The main contention of Barbujani and Belle is that human biodiversity cannot be partitioned into gene clusters because regardless of which experimental methodological approach is employed, those clusters and the individual genotypes they group will vary from data set to data set. In other words, k-means Bayesian clustering around the various loci of geographical ancestry can only be validated if it can be replicated using other analytical/statistical techniques. Although, the authors of the study did manage to produce discrete clusters, they varied in number and structural configuration each time the data was falsified, demonstrating that the 2002 and 2005 study of Rosenberg et al cannot be accurately replicated and is therefore, scientifically obsolete. This means that biological distinctions between human populations do not permit the classification of individuals into discrete clusters because of constantly shifting boundaries which depend on which methodological approach is being used and what implicit assumptions are worked with. Barbujani and Belle write:

 

An analysis of 377 microsatellites of the CEPH human diversity panel was interpreted as evidence that most genotypes cluster into one of five distinct groups, approximately corresponding to continents, which were proposed by some authors as the major biological subdivisions of humankind. Here we analyse the same dataset by a specific numerical method, designed to detect genomic boundaries, i.e. zones of increased change in maps of genomic variation. We show that statistically significant boundaries can be described between groups of populations, but different clusters are identified, depending on the assumptions of the model. In addition, these clusters do not correspond to the clusters inferred from previous analyses of the same or of other polymorphisms. We conclude that it is indeed possible to cluster genotypes according to geography, but no study so far identified unambiguously anything that can be regarded as a major genetic subdivision of humankind, and hence discontinuous models of human diversity are unsupported by data.

 

Although some individuals claim that the Bayesian clustering of genetic data corresponds to conventional typological definitions of subspecies, it must be realized that this position can only be given credence by grossly distorting the available evidence. All major researchers who have familiarized themselves with the HGDP-CEPH Human Genome Diversity Panel are of the unanimous position that gene cluster formation is heavily dependent on the kind of software and statistical techniques used to analyze autosomal microsatellites and other polymorphisms. This means that there is virtually no correspondence between the gene clusters and the amorphous reality of human biogeographical ancestry. Those studies that have found a loose correlation between continental ancestry and the formation of discrete, STRUCTURE-mediated clusters within human genomic data, because of differing statistical methodologies and paradigmatic frameworks, do not conflate k-means clustering with ethno-racial differentiation. To assume, as numerous racialist authors have repeatedly done, that k clusters are adequate proxies for race is a gross distortion of the available evidence.

 

In the initial 2002 paper of Rosenberg et al, it was admitted that individual genotypes reflect the clinal nature of human phenotypic variance. They write:

 

In several populations, individuals had partial membership in multiple clusters, with similar membership coefficients for most individuals. These populations might reflect continuous gradations across regions or admixture of neighbouring groups.

 

Rosenberg et al. (2005) have repeatedly asserted that, because of the clinal distribution of allele frequencies along linear gradients and across geographical space, the concept of biological race is a tangential issue that is statistically independent of their research:

 

Our evidence for clustering should not be taken as evidence of our support of any particular concept of ‘‘biological race.’’ In general, representations of human genetic diversity are evaluated based on their ability to facilitate further research into such topics as human evolutionary history and the identification of medically important genotypes that vary in frequency across populations. Both clines and clusters are among the constructs that meet this standard of usefulness: for example, clines of allele frequency variation have proven important for inference about the genetic history of Europe, and clusters have been shown to be valuable for avoidance of the false positive associations that result from population structure in genetic association studies. The arguments about the existence or nonexistence of ‘‘biological races’’ in the absence of a specific context are largely orthogonal to the question of scientific utility, and they should not obscure the fact that, ultimately, the primary goals for studies of genetic variation in humans are to make inferences about human evolutionary history, human biology, and the genetic causes of disease.

 

Consistent with the research of Barbujani and Belle, using alternative technical equipment and statistical methodologies to analyze human genomic data helps produce relatively ambiguous gene clusters characterized by highly unstable boundaries, constantly shifting in structural composition from one data set to the next. This demonstrates the sheer impossibility of classifying human beings into discrete clusters. The fact that human genetic variation is continuous has tremendous ramifications for how we as a species view ourselves. It would ultimately mean that all systems of ethno-racial classification are arbitrary, primarily socio-cultural in origin, and do not map onto human genotypic/phenotypic variance. Notwithstanding the fact that, in the opinion of Rosenberg et al (2005), clusters cannot be confused with biological definitions of race, Barbujani and Belle dispute the results of both studies conducted by Rosenberg et al in 2002 and 2005. They have repeatedly emphasized that the STRUCTURE program employed by Rosenberg et al was seriously plagued by numerous methodological short-comings and limitations, easily overcome by Barrier version 2.2 and Arlequin version 2.0 software. In their 2006 paper, Barbujani and Belle write:

 

In fact, interpretation of these results is not straightforward. Structure estimates the likely genetic contributions of k parental populations to the current populations, but does not take geography into consideration, provides no information about the existence of boundaries of increased genetic change between populations, nor does it test for their statistical significance.

 

Through the Barrier version 2.2 software, researchers Barbujani and Belle assigned 377 autosomal microsatellite markers to corresponding population co-ordinates on a map. A Delauney triangulation was super-imposed over the co-ordinates in order to facilitate the statistical evaluation of the rate of genetic change between neighbouring and peripheral populations. Using the program Arlequin version 2.0, mean values quantifying both between-population genetic diversity (FST) and genetic differentiation between population-based allele frequencies on a molecular level (RST) were calculated. Through Monmonier’s maximum-difference algorithm, 10 putative genomic boundaries were identified in the Americas, Africa, and Asia. A number of randomization trials were used to evaluate the data in order to determine whether the populations allocated within these boundaries would be more homogeneous in genetic makeup than a series of randomly distributed populations. This was done using the program Analysis of Molecular Covariance (AMOVA) and MsatBootstrap software. Using AMOVA to analyze the data, it was found that the percentage of RST/FST variance across 7 out of ten genomic boundaries was much greater than that produced by randomly allocating individual genotypes within the putative genomic boundaries. For the MsatBootstrap software, values for all genomic boundaries, except the one in tenth ranking, exceeded 70%.

 

The results obtained by Barbujani and Belle are stunning, and in sharp contradistinction to those results produced by previous investigators. The clusters observed within the data set were very different in structural composition from those produced in the study conducted by Rosenberg et al in 2002 and 2005. Rosenberg et al had produced genetic clusters that roughly corresponded to 6 geographic regions, being that of Africa, Eurasia, East Asia, Oceania, and the Americas, whereas in the study of Barbujani and Belle, 9 major clusters were uncovered, with 4 of them located in the Americas and another 3 found in sub-Saharan Africa. One cluster stretched from the east African coast to Mexico.

 

Employing another model based on the estimation of RST variance, a total of 8 clusters were obtained. Belle and Barbujani write:

 

However, the main difference with respect to the previous model is not the number of clusters, but their scope. All populations from Subsaharan Africa form a single group, when analysed by RST. Western Eurasia is separated from East-Central Asia and Papua New Guinea by boundary 7 that closes on itself around the Kalash from Pakistan, thus defining a one-population cluster.

 

These results strongly confirm those uncovered by other groups of researchers, most notably Serre and Paabo (2004) and Ramachandran et al (2005), which strongly contradict, if not refute the initial study of Rosenberg et al (2002). Serre and Paabo used a different methodological approach, employing both a homogeneous sampling strategy and a model based on implicit assumptions about the noncorrelated distribution of allele frequencies on a global level. Their research clearly demonstrated the superiority of geography-based sampling of individual genotypes through the analysis of microsatellite loci, as opposed to the population-based sampling techniques used by Rosenberg et al. It was found that human diversity was continuous and distributed across gradients of noncorrelated allele frequencies, rather than being organized into discrete, homogeneous clusters. Populations blend imperceptibly into other populations and the geographical allocation of human phenotypic variance assumes an infinite variety of forms; phenotypes coexist with other, more variable phenotypes, regardless of so-called biogeographical ancestry. Serre and Paabo’s momentous discovery has ultimately lead researchers to the conclusion that human biodiversity is best explained by worldwide patterns of admixture across a global distribution of clines, not genetically distinguishable continental groups.

 

Moreover, Ramachandran et al, in a 2005 study, found that genetic differentiation between geographically distributed populations steadily increased as a function of genetic distance, suggesting the absence of genomic boundaries and the clinal variation of human phenotypic variance. As indicated by Ramachandran et al:

 

Equilibrium models of isolation by distance predict an increase in genetic differentiation with geographic distance. Here we find a linear relationship between genetic and geographic distance in a worldwide sample of human populations, with major deviations from the fitted line explicable by admixture or extreme isolation. A close relationship is shown to exist between the correlation of geographic distance and genetic differentiation (as measured by FST) and the geographic pattern of heterozygosity across populations. Considering a worldwide set of geographic locations as possible sources of the human expansion, we find that heterozygosities in the globally distributed populations of the data set are best explained by an expansion originating in Africa and that no geographic origin outside of Africa accounts as well for the observed patterns of genetic diversity. Although the relationship between FST and geographic distance has been interpreted in the past as the result of an equilibrium model of drift and dispersal, simulation shows that the geographic pattern of heterozygosities in this data set is consistent with a model of a serial founder effect starting at a single origin. Given this serial-founder scenario, the relationship between genetic and geographic distance allows us to derive bounds for the effects of drift and natural selection on human genetic variation.

 

In addition, Ramachandran et al provided tremendous evidence that human beings come from a single common ancestor, indicating the primordial existence of a Y-chromosomal Adam or a mitochondrial Eve. Through multiple regression analysis of expected population heterozygosities based on estimations of genetic distance, the initial expansion of human beings was traced to a serial founder effect originating in the heart of Africa. It was found that as the genetic distance from Africa was increased, the percentage of variance in heterozygosity (R2) explained by multiple regression analysis decreased. However, as the genetic distance from South America was increased, the regression coefficient increased correspondingly, suggesting that all mankind is descended from a single lineage located in the heart of Africa.

 

In the words of scholar A.R. Templeton:

 

The pattern of overall genetic differences instead tells us that genetic lineages rapidly spread out to all of humanity, indicating that human populations have always had a degree of genetic contact with one another, and thus historically don't show any distinct evolutionary lineages within humanity. Rather, all of humanity is a single long-term evolutionary lineage.

 

All men are of one lineage and one blood

 

 

The above diagrammatic representation is an individual and population ancestry dendrogram (A) and maximum likelihood tree (B) taken from the study of Jun Li et al (2008). It is based on the genetic analysis of the single nucleotide polymorphism loci of 938 individuals from 51 different populations. The fact that the individual ancestries actually cluster around regions of continental origin is one means by which discrete clusters are produced. However, depending on the implicit assumptions inherent within the model used or the methodological approach involved, either no discrete clusters are formed (Serre and Paabo, 2004) or multiple clusters are formed around alternative biogeographical loci (Barbujani and Belle, 2006). Looking at the dendrogram, one can see that the colour-coded individual ancestries of the 938 individuals examined frequently exceed, even transcend the vertical barriers used to denote individual populations, vividly illustrating the fact that allele frequencies are both continuously and randomly distributed along a clinal gradient. Instead, a wide range of both phenotypes and genotypes, ranging from the very “Negrid” to the very “Europid” and originating from all regions of the globe, coexist within a single genomic boundary. Nevertheless, this provides absolutely no support for the belief that human beings can be ethno-racially categorized.

 

The ancestries of Middle Eastern and Central Asian populations are so heavily compromised by a plethora of “racial” identities as to be virtually impossible to classify with any degree of exactitude, severely undermining conventional typological definitions of biological race. Even the relative homogeneity of African, East Asian, and European populations rests upon a seemingly deceptive illusion, because even these can be broken down into numerous genetic clusters (representing tribal, even family units) that have greater genetic distances between each other than the population ancestries used to subdivide the dendrogram. Concerning the maximum likelihood tree diagram, the researchers Li et al state:

 

The sub-Saharan African populations are located nearest to the root of the tree (Fig. 1B), outward from which are branches that correspond, sequentially, to populations from North Africa, the Middle East, Europe, South/Central Asia, Oceania, America, and East Asia. This population tree shows not only major splits between different continents but also sublineages within continents consistent with the ancestry analysis shown above as well as with results from microsatellite markers. The branching pattern largely agrees with the approximate order of human expansion and supports the “out of Africa” model of human origin.

 

Incidentally enough, this study also provides considerable evidentiary support for the single lineage hypothesis of human origins. Based on the data provided by Li et al, not only is the “Negrid” phenotype/genotype the ancestral phenotype/genotype from which all others are systematically derived, but all human beings spring from a single common ancestor in sub-Saharan Africa.

 

Given the tremendous amount of recent, converging lines of scientific evidence on this point, what more powerful confirmation of the single lineage hypothesis does one need, other than this?

 

Hence, the final conclusion is undeniable: all men are of one blood and one lineage.

Edited January 2, 2009 by Abdul-Aziz

[Mokele]

A few points:

 

First, and foremost is just stylistic, but is important: Succinctness. I have no doubt you're written a well-constructed essay here, it's rather long. It'd be fine for a book of essays or somesuch, but this particular medium of conversation (bulletin boards) is susceptible to the 'wall of text' phenomenon. I'll freely admit I didn't read all of this post - I just don't have time. I suspect most others won't either. IMHO, it'd be much better to have short, succinct posts either with links to segments of this essay stored elsewhere (a blog, perhaps), or simply explaining in more detail when asked.

 

Anyhow, onwards to two points:

 

Moreover, the fact that there is no identifiable allele that corresponds to our modern conceptualization of “race” strongly suggests that we are dealing with an arbitrary form of social categorization which consists of a highly diverse and variable membership.

 

While I do agree that genetics have shown races to be a lot less distinct and to have a lot more mixing than previously appreciated, I don't think you can draw the conclusion that 'race' is entirely fictional based on mere alleles.

 

Basically, there's more to an organism than just genes:

 

1) Each gene can be spliced multiple different ways to make different proteins, and which splicing is used at any given point in time is determined through mechanisms I'm not sure anyone really understands (I certainly don't).

 

2) What gene is present isn't as important as when and where it's used in development. We have the same arm genes as a spider monkey, but what makes our arms different is when, where, and how intensely various proteins are expressed.

 

3) Genes aren't the only heritable component - there are segments of DNA which function solely to regulate the expression of genes. These are what controls the when, where and how much aspect of gene expression. We also don't have a very good map of these at all.

 

Think of houses - some of your genes are like wood, steel, pipes, glass, etc, and work as structures, while others are like saws, rulers, levels, etc, and are used to assemble the parts, and finally there are gene and regulatory elements that are like the blueprints that show the way everything is used. As it stands, we have the parts list, and some of the tools, but we don't actually have the blueprints yet.

 

 

 

The point is that there *may* be differences between the races in the regulatory elements, splicing patterns, or other poorly understood portions of DNA, and declaring that lack of major allele differences invalidates the concept of race is premature.

 

 

Hence, the final conclusion is undeniable: all men are of one blood and one lineage.

 

Technically, this is true even if there *are* races, since all humans share a common ancestor. You could also say "Humans, chimps and gorillas are of one blood and one lineage" or even say "Humans, snakes, and fish are of one blood and one lineage".

 

All life shares a common ancestor, so the issue isn't relatedness, but how close the relationship is.