Riin Kõiv

It is a common concern that broader audiences interpret scientific information about the genetic correlates and causes of complex human traits in an overly deterministic manner. A frequently proposed way to address this issue is to carefully select the linking expressions used to describe gene–trait relationships when communicating genetic information – for example, by replacing explicitly causal expressions with statistical ones, or by avoiding strong causal expressions in favor of weaker ones. Although such recommendations are widespread, the efficacy of linking‐expression substitutions in mitigating deterministic interpretations is rarely examined. This article argues that the context sensitivity of linguistic interpretation, together with the hypothesis of genetic essentialism, predicts that such substitutions have little effect on how deterministically broader audiences interpret genetic information.

Machery, E. (2021) argues to have identified a novel reason why deficient concepts of a certain kind are better eliminated than reformed. Namely, if the deficient concept is an attractor—a concept that we are psychologically drawn to think with—then eliminating this concept is a more feasible alternative than reforming it. Machery illustrates his argument with the example of the scientific concept of innateness, which he considers to be an attractor. I argue two things against Machery's thesis. First, there is little reason to believe that attempts to eliminate the scientific concept of innateness will be more feasible than attempts to reform it. Second, there is little reason to believe that attempts to eliminate a concept, whether it is an attractor or not, are more feasible than attempts to reform it. Moreover, a concept being an attractor even diminishes—instead of increasing—the chances that eliminating it is more feasible than reforming it.

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 kindgenetically caused traitan 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.

It is a widely accepted thesis in the cognitive sciences and in naturalistic philosophy of mind that the contents of at least some mental representations are innate. A question that has popped up in discussions concerning innate mental representations is this. Are externalist theories of mental content applicable to the content of innate representations? Views on the matter vary and sometimes conflict. To date, there has been no comprehensive assessment of the relationship between content externalism and content innateness. The aim of this paper is to provide such an assessment. I focus on the notions of innateness that are employed in innateness hypotheses within the cognitive sciences and adjacent fields of philosophy, and on causal externalist theories of content. I distinguish between three accounts of what being innate might amount to in innateness hypotheses within the cognitive sciences, and between three types of causal externalism. I explain what the possibility of innate externalistically individuated representations depends upon given all nine combinations. I explain why causal externalism can be true of innate mental representations, given but one of these combinations.

The teleosemantic theory of representational content is held by some philosophers to imply that genes carry semantic information about whole-organism phenotypes. In this paper, I argue that this position is not supported by empirical findings. I focus on one of the most elaborate defenses of this position: Shea’s view that genes represent whole-organism phenotypes. I distinguish between two ways of individuating genes in contemporary biological science as possible vehicles of representational content—as molecular genes and as difference-maker genes. I show that given either of these ways of individuating genes, genes fail to meet conditions which the teleosemantic theory requires an entity to meet if that entity is to qualify as a representational vehicle that represents a whole-organism phenotype. The considerations I present against Shea’s view generalize to other attempts to use the teleosemantic theory in support of the claim that genes represent whole-organism phenotypes.

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.