new evidence indicating that many uninterrupted or rarely

interrupted chunks of DNA (referred as haplotypes) appear

to be common across different populations socially classi-

ﬁed as belonging to different races (Wilson et al., 2001).

To appreciate the signiﬁcance of this ﬁnding, consider

the example of population variability in mutations in the

phenylalanine hydroxylase (PAH) gene, the gene whose

disrupted protein results in the manifestation of PKU (as

described earlier). It has been established that multiple

mutations in this gene result in PKU. The mutations differ

in terms of their speciﬁc location within the gene, and the

frequencies of individual mutations vary across popula-

tions. However, each of these mutations appears to arise on

one of a limited number of haplotypes and continues to be

associated with that haplotype. Most common haplotypes

are seen in all populations, and the greatest number of

haplotypes are seen in African populations (J. R. Kidd et

al., 2000).

Third, the essence of the race–intelligence– genetics

discussion has been an assumption that if race is somehow

a surrogate for unknown genetic mechanisms, then ob-

served racial differences in intelligence and achievement

can be explained by genetic differences. But can they be?

Although we have gained signiﬁcant understanding of

monogenetic (i.e., single-gene) conditions, there are still

enormous blank spots in our understanding of complex

human traits (i.e., traits controlled by many genes, often in

combination with many environments) such as blood pres-

sure, autism, reading disability, and intelligence. To illus-

trate, consider the observation that the majority of rare

single-gene disorders (e.g., Tay Sachs, sickle-cell anemia,

and thalassaemia) are caused by gene mutations that result

in the production of changed and, therefore, often faulty

proteins. In the literature, these deleterious mutations are

typically referred to as “coding single nucleotide polymor-

phisms” (cSNPs). Consider two facts about cSNPs. First,

they are rare; second, they are of recent origin, presumably

dating to the post-African diaspora (Tishkoff & Williams,

2002). Both assertions have implications for the discussion

here.

First, the rarity of cSNPs implies that they are unlikely

candidates for controlling quantitative traits such as blood

pressure, bone density, and intelligence. The more likely

candidates, as a result of their abundance, are so-called

nontranscribed regulatory elements of the genome (i.e., a

piece of DNA that does not contribute to the production of

proteins or noncoding sequences). The amount of variation

in these elements is remarkable. At present, the signiﬁcance

of this variation is unclear, because it has no obvious

impact on the proteins. However, information from re-

search involving organisms other than human ones is of

interest here. For example, in Drosophila , these noncoding

alleles have been closely associated with quantitative traits

(Mackay, 2001).

Second, the timing of the origin of cSNPs is linked to

the observation that their frequency varies among popula-

tions (Risch et al., 2002). The reasoning is simple. Because

cSNPs arose after the differentiation of the populations,

their distribution is a consequence of ethnic differentiation,

not a reason for it. It appears that common noncoding

variants, some of which are assumed to contribute to or

even to underlie susceptibility to common diseases or vari-

ation in quantitative traits, are observed worldwide and can

be referred to as “pan-ethnic” alleles (Cooper, 2003). In

other words, to the best of our knowledge today, there are

no explainable population differences in noncoding allele

frequencies that can be meaningfully linked to variation in

phenotypes. We simply do not see a clear pattern of ethnic

differences in allele frequencies that can be associated with

differences in speciﬁc phenotypes. Ethnic groups, of

course, are socially deﬁned. “Race” sounds like it is bio-

logically deﬁned. It is not. It, too, is socially deﬁned.

Social Versus Biological Definitions of Race

When biological and behavioral markers of socially deﬁned

races are investigated, studies primarily or even exclusively

rely on participants’ self-reporting of socially deﬁned ra-

cial, ethnic, and cultural groups. Many researchers use

social labels such as Asian American, African American,

Chinese, or Hispanic, implicitly ignoring the fact that these

labels generalize across substantial amounts of cultural,

linguistic, and biological diversity (Cooper et al., 2000).

For example, “Hispanic” includes diverse populations from

areas such as Cuba, Puerto Rico, the Dominican Republic,

Guatemala, Costa Rica, Argentina, and, of course, Spain.

The ancestry of individuals in these groups varies from

entirely African, entirely Native American, and entirely

European to any possible mixture of these three. Even

ignoring the substantial variation within each of these large

regions, there is no basis, except in the case of certain

social cultural traits, for grouping these individuals. Even

when a more speciﬁc populational reference such as

Yoruba (i.e., a West African population of about 10 million

people dispersed throughout different countries in the re-

gion) is made, this reference subsumes a great amount of

intra-Yoruba variability (Reich et al., 2001).

Moreover, self-naming of social labels might change

depending on the past and present social surroundings of

surveyed participants. For example, during the Soviet era,

many immigrating Soviet Jews referred to themselves as

Jewish by ethnicity, but upon their arrival to Israel or the

United States they referred to themselves as Russians

(Gozman, 1997). In the United States, indeed, Judaism is

viewed not as an ethnicity but as a religion. Similarly,

individuals who met the classiﬁcation of “colored” estab-

lished by the apartheid government of South Africa would

have probably identiﬁed themselves as Black in the United

States (Braun, 2002). Thus, because most medical and

psychological research on racial differences is based on

self-deﬁned racial or ethnic categories and there is substan-

tial evidence questioning the accuracy of these self-classi-

ﬁcations, the validity of racial and ethnic differences as

commonly investigated is questionable.

People will probably always label themselves and

others, regardless of what scientists ﬁnd. The problem is

not the use of social labeling per se, but rather the confu-

sion of it with biological labeling. And it is especially

problematic when scientists contribute to this confusion by

56 January 2005

●

American Psychologist