Racial constructionists, anti-naturalists, and anti-realists have challenged users of the biological race concept to provide and defend, from the perspective of biology, biological philosophy, and ethics, a biologically informed concept of race. In this paper, an ontoepistemology of biology is developed. What it is, by this, to be "biological real" and "biologically meaningful" and to represent a "biological natural division" is explained. Early 18th century race concepts are discussed in detail and are shown to be both sensible and not greatly (...) dissimilar to modern concepts. A general biological race concept (GBRC) is developed. It is explained what the GBRC does and does not entail and how this concept unifies the plethora of specific ones, past and present. Other race concepts as developed in the philosophical literature are discussed in relation to the GBRC. The sense in which races are both real and natural is explained. Racial essentialism of the relational sort is shown to be coherent. Next, the GBRC is discussed in relation to anthropological discourse. Traditional human racial classifications are defended from common criticisms: historical incoherence, arbitrariness, cluster discordance, etc. Whether or not these traditional human races could qualify as taxa subspecies – or even species – is considered. It is argued that they could qualify as taxa subspecies by liberal readings of conventional standards. Further, it is pointed out that some species concepts potentially allow certain human populations to be designated as species. It is explained why, by conventional population genetic and statistical standards, genetic differences between major human racial groups are at least moderate. Behavioral genetic differences associated with human races are discussed in general and in specific. The matter of race differences in cognitive ability is briefly considered. Finally, the race concept is defended from various criticisms. First, logical and empirical critiques are dissected. These include: biological scientific, sociological, ontological, onto-epistemological, semantic, and teleological arguments. None are found to have any merit. Second, moral-based arguments are investigated in context to a general ethical frame and are counter-critiqued. Racial inequality, racial nepotism, and the “Racial Worldview" are discussed. What is dubbed the Anti-Racial Worldview is rejected on both empirical and moral grounds. Finally, an area of future investigation – the politics of the destruction of the race concept – is pointed to. (shrink)

The presence of gene–environment statistical interaction and correlation in biological development has led both practitioners and philosophers of science to question the legitimacy of heritability estimates. The paper offers a novel approach to assess the impact of GxE and rGE on the way genetic and environmental causation can be partitioned. A probabilistic framework is developed, based on a quantitative genetic model that incorporates GxE and rGE, offering a rigorous way of interpreting heritability estimates. Specifically, given an estimate of heritability and (...) the variance components associated with estimates of GxE and rGE, I arrive at a probabilistic account of the relative effect of genes and environment. (shrink)

Lucas Matthews and I substantially revised my SEP entry on Heritability. This version includes discussion of the missing heritability problem and other issues that arise from the use of Genome Wide Association Studies by Behavioral Geneticists.

Heritability is routinely interpreted causally. Yet, what such an interpretation amounts to is often unclear. Here, I provide a causal interpretation of this concept in terms of range of causal influence, one of several causal dimensions proposed within the interventionist account of causation. An information-theoretic measure of range of causal influence has recently been put forward in the literature. Starting from this formalization and relying upon Woodward’s analysis, I show that an important problem associated with interpreting heritability causally, namely the (...) locality problem, amounts, at least partly, to a low invariance and low stability between the genotype/environment and the phenotype of individuals. In light of this, I plead for a causal interpretation of heritability that takes the notions of Woodward’s invariance and stability into consideration. In doing so, I defuse naive causal interpretations of heritability. (shrink)

Despite the long history of scientific, philosophical, and political debate around heritability studies, certain fundamental conceptual issues have not been recognized or well appreciated. The starting point is that heritability does not measure the degree of influence that genes have on a trait or provide a reliable basis for choosing which traits to investigate further with molecular genetic research. The short argument on this point revolves around two issues: the disconnect between analyzing measurements of a trait and exposing the measurable (...) genetic and environmental factors underlying the trait’s development; and the possibility of heterogeneity in these underlying factors, that is, different factors may lead to the same trait value. The idea of underlying heterogeneity is elaborated through schematic diagrams and distinguished from other senses of heterogeneity. Five conceptually distinct approaches for addressing underlying heterogeneity are identified, corresponding to distinct ways of managing the reciprocal relationship between the degree of knowledge of the dynamics through which the trait develops and the actions that can be reliably be based on what is known . This framework, which extends the interventionist notion of causality, allows the scope and limitations of heritability studies to be clarified in greater detail. It can also inform critical appreciation of newer methods of analysis of genetic and environmental factors. The issues discussed in this article do not centre on empirical data or technical detail and should be accessible to non-specialists as well as challenging active researchers. (shrink)

Can heritability estimates provide causal information? This paper argues for an affirmative answer: since a non-nil heritability estimate satisfies certain characteristic properties of causation (i.e., association, manipulability, and counterfactual dependence), it increases the probability that the relation between genotypic variance and phenotypic variance is (at least partly) causal. Contrary to earlier proposals in the literature, the argument does not assume the correctness of any particular conception of the nature of causation, rather focusing on properties that are characteristic of causal relationships. (...) The argument is defended against Lewontin's (1974) locality objection and Kaplan and Turkheimer's (2021) recent critique of Genome-Wide Association Studies (GWAS). (shrink)