Many psychometricians and behavioral geneticists believe that high heritability of IQ test scores within racial groups coupled with environmental hypotheses failing to account for the differences between the mean scores for groups lends plausibility to explanations of mean differences in terms of genetic factors. This two-component argument cannot be sustained when viewed in the light of the conceptual and methodological themes introduced in Taylor . These themes concern the difficulties of moving from the statistical analysis of variance of observed traits (...) to investigation of measurable genetic factors and measurable environmental factors. One such theme is that quantities estimated by an AOV of observed traits cannot be equated with measurable genetic or environmental factors involved in the development of those traits. Once this distinction is clear, the argument that environmental factors have failed to explain the differences lacks weight because it does not consider whether genetic factors have been more successful. This article exposes additional flaws in the lines of thinking associated with the two-component argument, with the distinction between passive, reactive, and active associations between genetic and environmental factors, and with the reciprocal causation models Dickens and Flynn propose in order to reconcile high estimates of heritability and large IQ test score gains between generations. Human heritability estimates are irrelevant in developing explanations of differences across groups or across generations. My critique is directed at opening up more conceptual space for deriving empirically validated models of developmental pathways whose components are heterogeneous and differ among individuals at any one time and over generations. (shrink)

The method in human genetics of ascribing causal responsibility to genotype by the use of heritability estimates has been heavily criticized over the years. It has been argued that these estimates are rarely valid and do not serve the purpose of tracing genetic causes. Recent contributions strike back at this criticism. I present and discuss two opposing views on these matters represented by Richard Lewontin and Neven Sesardic, and I suggest that some of the disagreement is based on differing concepts (...) of genetic causation. I use the distinction of structuring and triggering causes to help clarifying the basis for the opposing views. (shrink)

Gene–environment covariance is the phenomenon whereby genetic differences bias variation in developmental environment, and is particularly problematic for assigning genetic and environmental causation in a heritability analysis. The interpretation of these cases has differed amongst biologists and philosophers, leading some to reject the utility of heritability estimates altogether. This paper examines the factors that influence causal reasoning when G–E covariance is present, leading to interpretive disagreement between scholars. It argues that the causal intuitions elicited are influenced by concepts of agency (...) and blame-worthiness, and are intimately tied with the conceptual understanding of the phenotype under investigation. By considering a phenotype-specific approach, I provide an account as to why causal ascriptions can differ depending on the interpreter. Phenotypes like intelligence, which have been the primary focus of this debate, are more likely to spark disagreement for the interpretation of G–E covariance cases because the concept and ideas about its ‘normal development’ relatively ill-defined and are a subject of debate. I contend that philosophical disagreement about causal attributions in G–E covariance cases are in essence disagreements regarding how a phenotype should be defined and understood. This moves the debate from one of an ontological flavour concerning objective causal claims, to one concerning the conceptual, normative and semantic dependencies. (shrink)