In this paper I argue that the extent to which a human trait is genetically caused can causally depend upon whether the trait is categorized within human genetics as genetically caused. This makes the kind genetically caused trait an interactive kind. I demonstrate that this thesis is both conceptually coherent and empirically plausible. I outline the core rationale of this thesis and demonstrate its conceptual coherence by drawing upon Waters’ (2007) analysis of genetic causation. I add empirical plausibility to the (...) thesis by describing a hypothetical but empirically plausible mechanism by which the fact that obesity is categorized as genetically caused within human genetics increases the extent to which obesity is in fact genetically caused. (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)

Genome-wide association studies of human complex traits have provided us with new estimates of heritability. These estimates foreground the question of genetic causation. After having presen...

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.

We often hear how scientists have discovered that a certain human trait – or a trait of another type of organism – is innate, genetic, heritable, inherited, naturally selected etc. All these claims have something in common: they all declare a trait to have significant organism internal (for instance genetic) causes that are present in the organism at its birth. I call claims like these “nativist claims”. Nativist claims are important. They shape our overall understanding of what we are, what (...) we can do and what is good for us. They also impact our practical decision making. For instance, we know that certain types of genes increase the risk of certain diseases, and increasingly this has an effect on healthcare practices. Many people believe that in the matter of children’s education we should consider the fact that many cognitive abilities are highly heritable. Associations between genetics and aggressive behavior have been taken to be alleviating circumstances in criminal sentencing. It is therefore important to correctly understand the content and implications of nativist claims. In this doctoral thesis I analyze, by philosophical means, the content of different kinds of nativist claim. What does it mean that some psychological tendency is innate? What does it mean that intelligence is 50% heritable? How (if at all) do genes come to carry information about the traits of an organism – they are nothing like the information carriers familiar to us, such as newspapers, e-mails, secret codes, and audio files. This thesis emphasizes two things. Firstly, I demonstrate, that in different scientific contexts these words ('innate', 'genetically caused' etc.) can mean very different things. Therefore, the implications of a given nativist claim in one scientific context can be remarkably different from another nativist claim’s implications in some other scientific context. Secondly, I explain how the development of innate, heritable and genetically caused traits can be determined in different and often unexpected ways by our environment and experiences. I demonstrate that the content of a concept that is considered innate by cognitive scientists can be determined by what the organism that possesses the concept has experienced. I also show that even a trait which is 100% heritable can at the same time be a socially constructed trait. (shrink)

This paper explores the interpretation and use of polygenic risk scores (PRSs). We argue that PRSs generally do not directly embody causal information. Nonetheless, they can assist us in tracking other causal relationships concerning genetic effects. Although their purely predictive/correlational use is important, it is this tracking feature that contributes to their potential usefulness in other applications, such as genetic dissection, and their use as controls, which allow us, indirectly, to "see" more clearly the role of environmental variables.

This paper analyzes recent attempts to reject reproduction with lineage formation as a necessary condition for evolution by means of natural selection :560–570, 2008; Stud Hist Philos Sci Part C Stud Hist Philos Biol Biomed Sci 42:106–114, 2011; Bourrat in Biol Philos 29:517–538, 2014; Br J Philos Sci 66:883–903, 2015; Charbonneau in Philos Sci 81:727–740, 2014; Doolittle and Inkpen in Proc Natl Acad Sci 115:4006–4014, 2018). Building on the strengths of these attempts and avoiding their pitfalls, it is argued that (...) a robust formulation of evolution by natural selection without reproduction can be established. The main contribution of this paper is a reformulation of Lewontin’s three principles stating that minimal evolution by natural selection occurs when two conditions are met in a population: fitness-related variation and memory. Paradigmatic evolution by natural selection, which can generate adaptations, takes place when an additional condition is present, namely regeneration. (shrink)

The question of whether cultural transmission is faithful has attracted significant debate over the last 30 years. The degree of fidelity with which an object is transmitted depends on 1) the features chosen to be relevant, and 2) the quantity of details given about those features. Once these choices have been made, an object is described at a particular grain. In the absence of conventions between different researchers and across different fields about which grain to use, transmission fidelity cannot be (...) evaluated because it is relative to the choice of grain. In biology, because a genotype-to-phenotype mapping exists and transmission occurs from genotype to genotype, a privileged grain of description exists that circumvents this ‘grain problem.’ In contrast, in cultural evolution, the genotype–phenotype distinction cannot be drawn, rendering claims about fidelity dependent upon researchers’ choices. Thus, due to a lack of unified conventions, claims about fidelity transmission are difficult to evaluate. (shrink)

I extend work from Krakauer et al. (2020), who propose a conception of individuality as the capacity to propagate information through time. From this conception, they develop information-theoretic measures. I identify several shortcomings with these measures—in particular, that they are associative rather than causal. I rectify this shortcoming by deriving a causal information-theoretic measure of individuality. I then illustrate how this measure can be implemented and extended in the context of evolutionary transitions in individuality.