Starting with Lewontin (1972), studies have statistically apportioned variation in different genetic systems to different levels: among ‘races’ and within ‘races’ and smaller populations such as the Hopi, the Ainu, and the Irish. Lewontin collected data on blood group polymorphisms in different groups and races. He found that blood group variation between races statistically explains only about 6% of the total variation. These results show that if one is to adopt a racial paradigm, one must acknowledge that race will statistically explain only a small proportion of genetic variation. Moreover, this small variation is better explained by geographic distance (Templeton, 1998). Yu et al. (2002) more recently compared a large sequence of DNA, 25 000 letters or base pairs long, of ten individuals from each of the three main ‘races’ typically used in medical studies: Asian, European, and African. They counted out the number of differences between any two individuals and found that the average number of differences between any two individuals from Africa was greater than the average number of differences between an African and a European or an African and an Asian. These results support the understanding that there is greater genetic variation in Africa because of the increased evolutionary time humans have spent in Africa. Most startling perhaps is that Europeans and Asians, rather than being genetically separable, appear more accurately to be subsets of Africans. We truly are, it seems, all Africans.

Race: An Unrepeatable Explanatory Variable

Race is impossible to define in a stable and universal way because ‘race as biology’ varies with place and time, and the socially determined color line is even more dynamic. Other continuous variables such as head and foot size are classified into hat sizes and shoe sizes, and these systems work. A problem with race in practice is that there is no agreed-upon ‘race scale’ as there are hat and shoe size scales. Ideas about race are fluid and based on different phenotypic cues. The salient cues change over time, place, and circumstance and are subject always to social and cultural processes.

Race: Conflating Lived Experience And Genetics

Other key methods of classification such as social class may also differ widely. Although always imperfect, measures of social class begin to provide a glimpse at the underlying processes through which social and economic positions affect lived experience and health. Where race critically differs is in the breadth of potential interpretations of the underlying processes. As previously noted, some individuals view racial differences in disease as due to genes, while others view race differences as the consequence of the lived experience of race and racism. Obviously, this confusion has serious implications for theory and practice. One cannot do predictive science based on a changing and indefinable cause.

Conflating Human Genetic Variation And Race

Human genetic variation does exist: It is real and measurable. But it is also more dynamic than one might assume. For example, the genetics of Amherst, Massachusetts, in 1606 was very different from 1806 and 2006. And the road from genetic factors to complex diseases and behaviors is exceedingly interactive and less than fully determined. Where we end up – whether a behavior or disease becomes manifest – is undoubtedly related, though partly and incompletely, to genetics. But none of this has anything to do with race. A reasonable compromise position would be to accept the fact that racial inequalities in health are likely a result of both causal pathways: genetic and lived experience. In fact, this is precisely the position advocated by Francis Collins (2004), the powerfully placed head of the U.S. National Human Genome Institute. But Sankar and colleagues (2004) argue that such a position has the real consequence of overstating the importance of genetics, as well as continuing to conflate race with human genetic variation. In their analysis, such a position is likely to divert research funds from socioeconomic causes of health disparities.

Conclusions

No single reason noted above may be sufficient to throw race as genetics, or raciogenetics, onto the scrap heap of surpassed scientific ideas. But considered in combination, the critical discussion above clearly suggests that it is time to move beyond raciogenetic thinking in the health sciences. Such a move not only finally jettisons an outdated paradigm, it also provides the space to explore more fully the complex and critical connections between the experience of racism and health, and ultimately, the full range of causes of health inequities. Bibliography:

1. Collins FS (2004) What we do and don’t know about ‘race,’ ‘ethnicity,’ genetics, and health at the dawn of the genome era. Nature Genetics 36(supplement 111): S13–S15.
2. Goodman AH (1997) Bred in the bone? Sciences March/April: 20–25.
3. Goodman AH, Heath D, and Lindee SM (eds.) (2003) Genetic Nature/ Culture. Berkley, CA: University of California Press.