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)

One way in which bioethicists can benefit the medical community is by clarifying the concept of disorder. Since insurance companies refer to the DSM for whether a patient should receive assistance, one must consider the consequences of one’s concept of disorder for who should be provided with care. I offer a refinement of Jerome Wakefield’s hybrid concept of disorder, the harmful dysfunction analysis. I criticize both the factual component and the value component of Wakefield’s account and suggest how they might (...) be improved. I propose that the factual component should be statistical variation analyzed in multilevel and chronological compilations of physiological data. I propose that the value component should prioritize the individual’s authority regarding the experience of suffering from a physiological condition. My account preserves the insight of using a factual and a value component while avoiding the problems that Wakefield’s original account faces. (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)

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)

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.

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)