Psychological measurement has received strong criticism throughout the history of psychological science. Nevertheless, measurements of attributes such as emotions or intelligence continue to be widely used in research and society. I address this puzzle by presenting a new causal perspective to psychological measurement. I start with assumptions that both critics and proponents of psychological measurement are likely to accept: a minimal causal condition and the observation that most psychological concepts are ill-defined or ambiguous. Based on this, I argue that psychological (...) measurement is fundamentally different from measurement in the physical sciences but can nevertheless be useful. (shrink)

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. (shrink)

Behavior genetics is a controversial science. For decades, scholars have sought to understand the role of heredity in human behavior and life-course outcomes. Recently, technological advances and the rapid expansion of genomic databases have facilitated the discovery of genes associated with human phenotypes such as educational attainment and substance use disorders. To maximize the potential of this flourishing science, and to minimize potential harms, careful analysis of what it would mean for genes to be causes of human behavior is needed. (...) In this paper, we advance a framework for identifying instances of genetic causes, interpreting those causal relationships, and applying them to advance causal knowledge more generally in the social sciences. Central to thinking about genes as causes is counterfactual reasoning, the cornerstone of causal thinking in statistics, medicine, and philosophy. We argue that within-family genetic effects represent the product of a counterfactual comparison in the same way as average treatment effects (ATEs) from randomized controlled trials (RCTs). Both ATEs from RCTs and within-family genetic effects are shallow causes: They operate within intricate causal systems (non-unitary), produce heterogeneous effects across individuals (non-uniform), and are not mechanistically informative (non-explanatory). Despite these limitations, shallow causal knowledge can be used to improve understanding of the etiology of human behavior and to explore sources of heterogeneity and fade-out in treatment effects. (shrink)

The environmental elbow room model of free will posits the unshared proportion of environmental variance in twins is a measure of the degree to which free will may be exercised with respect to one’s life outcomes for a trait. This model attempts to unify the behavioral genetic study of socially important psychological characteristics such as intelligence and academic achievement with Dennett’s broadly compatibilist elbow room notion of free will. We demonstrate that the philosophy and genetics underlying the environmental elbow room (...) model are both fundamentally flawed. Philosophically the degree to which an outcome might be predicted in a given situation does not give any sense of whether the course of action to achieve an outcome was free or unfree. With respect to genetics, quantities such as heritability and its environmental complement, even when they do reflect the actions of independently identifiable causes are not indicative of the chain of decisions one would have to evaluate to judge if an action was freely chosen. We show the contemporary human behavioral genetics focus on heritability is wholly misplaced for purposes of making decisions about policy and free will alike. Variance components sample a single instance of the distribution of variation arising from different sources and do not constrain outcomes in other contexts. The claim that the high heritability of a trait, life outcomes included, makes us less free to change it is similar in key ways to Jensenism’s contention that high heritability makes social change impossible. (shrink)

The literatures on bounded and ecological rationality are built on adaptationism—and its associated modular, cognitivist and computational paradigm—that does not address or explain the evolutionary origins of rationality. We argue that the adaptive mechanisms of evolution are not sufficient for explaining human rationality, and we posit that human rationality presents exaptive origins, where exaptations are traits evolved for other functions or no function at all, and later co-opted for new uses. We propose an embodied reconceptualization of rationality—embodied rationality—based on the (...) reuse of the perception-action system, where many neural processes involved in the control of the sensory-motor system, salient in ancestral environments have been later co-opted to create—by tinkering—high-level reasoning processes, employed in civilized niches. (shrink)