A high heritability estimate usually corresponds to a situation in which trait variation is largely caused by genetic variation. However, in some cases of gene-environment covariance, causal intuitions about the sources of trait difference can vary, leading experts to disagree as to how the heritability estimate should be interpreted. We argue that the source of contention for these cases is an inconsistency in the interpretation of the concepts ‘genotype’, ‘phenotype’, and ‘environment’. We propose an interpretation of these terms under which (...) trait variance initially caused by genetic variance is subsumed into a heritability for all cases of gene-environment covariance. (shrink)

Causation has multiple distinct meanings in genetics. One reason for this is meaning slippage between two concepts of the gene: Mendelian and molecular. Another reason is that a variety of genetic methods address different kinds of causal relationships. Some genetic studies address causes of traits in individuals, which can only be assessed when single genes follow predictable inheritance patterns that reliably cause a trait. A second sense concerns the causes of trait differences within a population. Whereas some single genes can (...) be said to cause population-level differences, most often these claims concern the effects of many genes. Polygenic traits can be understood using heritability estimates, which estimate the relative influences of genetic and environmental differences to trait differences within a population. Attempts to understand the molecular mechanisms underlying polygenic traits have been developed, although causal inference based on these results remains controversial. Genetic variation has also recently been leveraged as a randomizing factor to identify environmental causes of trait differences. This technique—Mendelian randomization—offers some solutions to traditional epidemiological challenges, although it is limited to the study of environments with known genetic influences. (shrink)

We are less optimistic than Madole & Harden that family-based genome-wide association studies (GWASs) will lead to significant second-generation causal knowledge. Despite bearing some similarities, family-based GWASs and randomised controlled trials (RCTs) are not identical. Most RCTs assess a relatively homogenous causal stimulus as a treatment, whereas GWASs assess highly heterogeneous causal stimuli. Thus, GWAS results will not translate so easily into second-generation causal knowledge.

The aim of this virtual special issue is to bring together philosophical and historical perspectives to address long-standing issues in the interpretation, utility, and impacts of quantitative genetics methods and findings. Methodological approaches and the underlying scientific understanding of genetics and heredity have transformed since the field's inception. These advances have brought with them new philosophical issues regarding the interpretation and understanding of quantitative genetic results. The contributions in this issue demonstrate that there is still work to be done integrating (...) old and new methodological and conceptual frameworks. In some cases, new results are interpreted using assumptions based on old concepts and methodologies that need to be explicitly recognised and updated. In other cases, new philosophical tools can be employed to synthesise historical quantitative genetics work with modern methodologies and findings. This introductory article surveys three general themes that have dominated philosophical discussion of quantitative genetics throughout history: (1) how methodologies have changed and transformed our knowledge and interpretations; (2) whether or not quantitative genetics can offer explanations relating to causation and prediction; and (3) the importance of defining the phenotypes under study. We situate the contributions in this virtual special issue within a historical framework addressing these three themes. (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)

Causal selection and priority are at the heart of discussions of the causal parity thesis, which says that all causes of a given effect are on a par, and that any justified priority assigned to a given cause results from causal explanatory interests. In theories of causation that provide necessary and sufficient conditions for the truth of causal claims, status as cause is an either/or issue: either a given cause satisfies the conditions or it does not. Consequently, assessments of causal (...) parity and priority require more resources, which can either be additional or part of the causal analysis itself. While adding resources in terms of a theory of causal explanation has been standard, here we develop a unified conceptual analysis that includes a range of different precise causal concepts that allows for assessments of causal priority in terms of different kinds of causal relevance. (shrink)

In the social constructionist literature, little has been said about what it means for social factors to cause X in such a way that X would count as causally socially constructed. In this paper, I argue that being caused by social factors – and thus being causally socially constructed – is best defined in terms of a contrastive counterfactual notion of causation. Unlike some plausible alternatives, this definition captures what is at stake in actual social constructionist debates. It makes transparent (...) which factors the truth of a causal constructionist claim may depend on. By doing so, it sheds light on what the disagreements over whether X is causally socially constructed may turn on. It also helps us to see under which condition the claim that X is socially causally constructed is compatible with the claim that X is caused by biological factors. (shrink)