It is illegitimate to read any ontology about "race" off of biological theory or data. Indeed, the technical meaning of "genetic variation" is fluid, and there is no single theoretical agreed-upon criterion for defining and distinguishing populations (or groups or clusters) given a particular set of genetic variation data. Thus, by analyzing three formal senses of "genetic variation"—diversity, differentiation, and heterozygosity—we argue that the use of biological theory for making epistemic claims about "race" can only seem plausible when it relies (...) on the user’s own assumptions about race; the move from biological measures to claims about “race” inevitably amounts to a pernicious reification. We also excavate assumptions in the history of the technical discourse over the concept of "race" (e.g., Livingstone's and Dobzhansky's 1962 exchange, Edwards' 2003 response to Lewontin 1972, as well as contemporary discussions of cladistic "race", and "races" as clusters). We show that claims about the existence (or non-existence) of "race" are underdetermined by biological facts, methods, and theories. Biological theory does not force the concept of "race" upon us; our social discourse, social ontology, and social expectations do. We become prisoners of our abstractions at our own hands, and at our own expense. (shrink)

This paper distinguishes three concepts of "race": bio-genomic cluster/race, biological race, and social race. We map out realism, antirealism, and conventionalism about each of these, in three important historical episodes: Frank Livingstone and Theodosius Dobzhansky in 1962, A.W.F. Edwards' 2003 response to Lewontin (1972), and contemporary discourse. Semantics is especially crucial to the first episode, while normativity is central to the second. Upon inspection, each episode also reveals a variety of commitments to the metaphysics of race. We conclude by interrogating (...) the relevance of these scientific discussions for political positions and a post-racial future. (shrink)

All eyes are turned towards genomic data and models as the source of knowledge about whether human races exist or not. Will genomic science make the final decision about whether racial realism (e.g., racial population naturalism) or anti-realism (e.g., racial skepticism) is correct? We think not. We believe that the results of even our best and most impressive genomic technologies underdetermine whether bio-genomic races exist, or not. First, different sub-disciplines of biology interested in population structure employ distinct concepts, aims, measures, (...) and models, producing cross-cutting categorizations of population subdivisions rather than a single, universal bio-genomic concept of "race." Second, within each sub-discipline (e.g., conservation biology, phylogenetics), genomic results are consistent with, and map multiply to, racial realism and anti-realism. Indeed, racial ontologies are constructed conventionally, rather than discovered. We thus defend a /constructivist conventionalism/ about bio-genomic racial ontology. Choices and conventions must always be made in identifying particular kinds of groups. Political agendas, social programs, and moral questions premised on the existence of naturalistic race must accept that no scientifically grounded racial ontology is forthcoming, and adjust presumptions, practices, and projects accordingly. (shrink)

We attempt to improve the understanding of the notion of agene being `for a phenotypic trait or traits. Considering theimplicit functional ascription of one thing being `for another,we submit a more restrictive version of `gene for talk.Accordingly, genes are only to be thought of as being forphenotypic traits when good evidence is available that thepresence or prevalence of the gene in a population is the resultof natural selection on that particular trait, and that theassociation between that trait and the gene (...) in question isdemonstrably causal. It is therefore necessary to gatherstatistical, biochemical, historical, as well as ecologicalinformation before properly claiming that a gene is for aphenotypic trait. Instead of hampering practical use of the `genefor talk, our approach aims at stimulating much needed researchinto the functional ecology and comparative evolutionary biologyof gene action. (shrink)

Some authors defending the “hereditarian” hypothesis with respect to differences in average IQ scores between populations have argued that the sorts of environmental variation hypothesized by some researchers rejecting the hereditarian position should leave discoverable statistical traces, namely changes in the overall variance of scores or in variance–covariance matrices relating scores to other variables. In this paper, I argue that the claims regarding the discoverability of such statistical signals are broadly mistaken—there is no good reason to suspect that the hypothesized (...) environmental causes would leave detectable traces of the sorts suggested. As there remains no way to gather evidence that would permit the direct refutation of the environmental hypotheses, and no direct evidence for the hereditarian position, it remains the case, I argue, that the hereditarian position is unsupported by current evidence. (shrink)

This article is an introduction to the Synthese Special Issue, Philosophy of Epidemiology. The overall goals of the issue are to revisit the state of philosophy of epidemiology and to provide a forum for new voices, approaches, and perspectives in the philosophy of epidemiology literature. The introduction begins by drawing on Geoffrey Rose’s work on how to conceptualize and design interventions for populations, rather than individuals. It then goes on to highlight some themes that emerged in the articles that make (...) up the issue: philosophy of epidemiology and epidemiological theory—what they are and what they ought to be, pluralism in measurement and causal attribution, epistemic and non-epistemic values in disputes epidemiological practices, decentering philosophy of epidemiology’s Eurocentrism, letting pragmatism guide uses of big data in epidemiology, and revisiting the lessons of classic texts in epidemiological causal inference. The introduction concludes with comments on a philosophy of epidemiology debate we see on, regarding the politics of philosophy of epidemiology. (shrink)

Phylogenetic information is often necessary to distinguish between evolutionary scenarios. Recently, some prominent proponents of evolutionary psychology have acknowledged this, and have claimed that such evidence has in fact been brought to bear on adaptive hypotheses involving complex human psychological traits. Were this possible, it would be a valuable source of evidence regarding hypothesized adaptive traits in humans. However, the structure of the Hominidae family makes this difficult or impossible. For many traits of interest, the closest extant relatives to the (...) human species are too phenotypically different from humans for such methods to provide meaningful data. While phylogenetic information can be useful for testing adaptive hypotheses in humans, these generally involve traits that are not widely shared in the species or fairly widely shared in the Hominidae family, and hence likely of a lower order of complexity than the sorts of traits evolutionary psychology has so far been interested in. (shrink)

Madole & Harden argue that just as the results of randomized controlled trials (RCTs) represent gains in causal knowledge and are useful, despite their limitations, so too are the findings of human behavior genetics. We argue that this analogy is misleading. Unlike RCTs, the results of human behavior genetics research cannot suggest efficacious interventions, nor point toward future research.

Matthen (Philos Sci 76(4):464–487, 2009) argues that explanations of evolutionary change that appeal to natural selection are statistically abstractive explanations, explanations that ignore some possible explanatory partitions that in fact impact the outcome. This recognition highlights a difficulty with making selective analyses fully rigorous. Natural selection is not about the details of what happens to any particular organism, nor, by extension, to the details of what happens in any particular population. Since selective accounts focus on tendencies, those factors that impact (...) the actual outcomes but do not impact the tendencies must be excluded. So, in order to properly exclude the factors irrelevant to selection, the relevant factors must be identified, and physical processes, environments, and populations individuated on the basis of being relevantly similar for the purposes of selective accounts. Natural selection, on this view, becomes in part a measure of the robustness of particular kinds of outcomes given variations over some kinds of inputs. (shrink)

Lewis et al. (2011) attempted to restore the reputation of Samuel George Morton, a 19th century physician who reported on the skull sizes of different folk-races. Whereas Gould (1978) claimed that Morton's conclusions were invalid because they reflected unconscious bias, Lewis et al. alleged that Morton's findings were, in fact, supported, and Gould's analysis biased. We take strong exception to Lewis et al.’s thesis that Morton was “right.” We maintain that Gould was right to reject Morton's analysis as inappropriate and (...) misleading, but wrong to believe that a more appropriate analysis was available. Lewis et al. fail to recognize that there is, given the dataset available, no appropriate way to answer any of the plausibly interesting questions about the “populations” in question (which in many cases are not populations in any biologically meaningful sense). We challenge the premise shared by both Gould and Lewis et al. that Morton's confused data can be used to draw any meaningful conclusions. This, we argue, reveals the importance of properly focusing on the questions asked, rather than more narrowly on the data gathered. (shrink)

We argue that heritability estimates cannot be used to make informed judgments about the populations from which they are drawn. Furthermore, predicting changes in heritability from population changes is likely impossible, and of limited value. We add that the attempt to separate human environments into cultural and non-cultural components does not advance our understanding of the environmental multiplier effect.

Recently, Estes and Arnold claimed to have “solved” the paradox of evolutionary stasis; they claim that stabilizing selection, and only stabilizing selection, can explain the patterns of evolutionary divergence observed over “all timescales.” While Estes and Arnold clearly think that they have identified the processes that produce evolutionary stasis, they have not. Instead, Estes and Arnold identify a particular evolutionary pattern but not the processes that produce that pattern. This mistake is important; the slippage between pattern and process is common (...) in population and quantitative genetics and contributes to a persistent misunderstanding of the nature of explanations in evolutionary biology. †To contact the author, please write to: Philosophy Department, 208 Hovland Hall, Oregon State University, Corvallis, OR 97331‐3902; e‐mail: [email protected]. (shrink)

The dissertation explores the way that large-scale research projects in human genetics influence and are influenced by various social and political issues in contemporary U.S. society. In short, the dissertation argues that the same cultural assumptions which make research projects like the Human Genome Project and human behavioral genetics research seem like promising and worthwhile endeavors simultaneously lead to the results of these projects getting used to define the terms that various social issues are discussed in. In cases where the (...) issues involve conflicting agendas, those cultural assumptions that drive the research projects often point towards a specific form of resolution, a form that is often implicitly or explicitly supported by the results of the research projects themselves. ;There is, in other words, a complex relationship of mutual support between certain kinds of research projects in human genetics, the legal and social decisions made in various areas in political life, and the kinds of discourse that can exist around those same areas. This relationship is pernicious insofar as those assumptions that encourage the research and influence the way the research is used are assumptions that many people would question the wisdom of uncritically accepting. And indeed, they are assumptions that, I argue, have strong racist and sexist overtones, assumptions born out of a radically anti-egalitarian framework. Political decisions and social discourse that might otherwise seem radically racist, sexist, or classist can, once they are being made in the shadow of research undertaken under these same kinds of assumptions, be made to seem somehow natural, inevitable, or at the very least, scientifically well-motivated. (shrink)

This chapter contains sections titled: Introduction: Rational Decisions as an Ideal Rational Decision Making? Assumptions and Difficulties: Preferences, Outcome Spaces, and Probabilities in the World Reasons without Decisions What Kinds of Reasons? The Failure of RCT as a Unifying Principle The Failures of RCT and Rethinking Rationality.