Lewontin’s other fallacy: 35% not 15%

Here’s a passage from Sarich and Miele’s Race: The Reality of Human Difference:

Yet the world had to wait until 2002 for someone to explain the basic problems with Lewontin’s famous 15 percent. It was Henry Harpending replying to a question from Frank Salter. Lewontin had noted that 85 percent of the genetic variability was among individuals within populations, and only an additional 15 percent was added when individuals in different populations were compared. However, this analysis omits a third level of variability—the within-individual one. The point is that we are diploid organisms, getting one set of chromosomes from one parent and a second from the other. To the extent that your mother and father are not especially closely related, then, those two sets of chromosomes will come close to being a random sample of the chromosomes in your population. And the sets present in some randomly chosen member of yours will also be about as different from your two sets as they are from one another. So how much of the variability will be distributed where?

First is the 15 percent that is interpopulational. The other 85 percent will then split half and half (42.5 percent) between the intra- and interindividual within-population comparisons. The increase in variability in between-population comparisons is thus 15 percent against the 42.5 percent that is between-individual within-population. Thus, 15/42.5 = 32.5 percent [This should be 35%], a much more impressive and, more important, more legitimate value than 15 percent.

Basically, Lewontin’s estimate concerns the average difference between populations, not the average genetic difference between individuals of different populations; for the later, you have to parse out the intraindividual difference. This isn’t an insignificant point since many still maintain that the “small amount of genetic variation between populations” makes a genetic basis for various differences implausible. For example, Brown and Armelago (2001) argue that:

the evidence against genetically mediated differences in behavior along racial lines is overwhelming (Table 1). First of all, a host of studies, beginning with those by Lewontin24 in 1972 and most recently by Barbujani and colleagues in 1997, have shown that the amount of human genetic diversity that is attributable to race is only about 5% to 10%. Following this, any particular “population” includes roughly 85% or more of the total human genetic diversity.

More importantly, this demolishes the second leg of Lewontin’s “race is a social construct (RISC)” concept. In 1972, Lewontin made the falsifiable claim that racial classifications are of “virtually no genetic or taxonomic significance.” A.W.F. Edwards pointed out the flaw with Lewontin’s taxonomic assertion; this establishes the flaw with his genetic one — not that establishing this should be needed.

Table 1 (variance between-individuals of different populations added: inter-betw)

Brown and Armelago, 2001. Apportionment of Racial Diversity: A Review

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One Response to Lewontin’s other fallacy: 35% not 15%

  1. bob sykes says:

    Most of these analyses are based on the important biochemical proteins (or their DNA code). These are so important to life that their structures (and code) are tightly controlled. In many cases, the structures are virtually the same across the entire spectrum of life from bacteria to man. This means that variation among them is minor and almost random and irrelevant to considerations of race.

    Moreover, the issue is not the variance within a given protein; the issue is the CORRELATION of variances between the proteins. Neither Lewontin nor the more recent studies consider this.

    Then there is the HOX Box business. These are the sequences of genetic code present in all animals that control the timing and amount of protein synthesis and so control the outcome of fetal development. If there is any place for racially relevant differences, it is there.

    Finally, the empirical differences among the races (20 to 50 or more of them) are so apparent at the phenotype level that any genotype level analyses that fail to reproduce them are ipso facto wrong.

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