After describing the disorder of psychopathy, I examine the theories and the evidence concerning the psychopaths’ deficient moral capacities. I first examine whether or not psychopaths can pass tests of moral knowledge. Most of the evidence suggests that they can. If there is a lack of moral understanding, then it has to be due to an incapacity that affects not their declarative knowledge of moral norms, but their deeper understanding of them. I then examine two suggestions: it is their deficient (...) practical reason or their stunted emotions that are at fault. The evidence supports both explanations. I conclude with an overview of the debate concerning whether they are morally or legally responsible for their actions. (shrink)

Genetics is in a postgenomic era, and this article illustrates this epistemological evolution using the debate between developmental criticism and traditional biometric genetics about gene × environment interaction. Quantitative geneticists are blamed for failing to respect the complexity of development; as a response, they claim a defensive position, called isolationist pluralism, which supports the idea that studying development is not their problem. But postgenomics seems to have accepted and integrated some developmental criticisms and the isolationist perspective has been challenged during (...) the last few years. The developmental and quantitative traditions actually represent two different levels of analysis, but biometrics has also a clear developmental explanatory potential as it suggests statistically the existence of mechanical causes. Both traditions work together to go ever further in the knowledge of the phenomena being studied. Postgenomic pluralism, instead of being isolationist, may be considered pragmatic. (shrink)

Keller explains the persistence of the nature/nurture debate by a chronic ambiguity in language derived from classical and behavioral genetics. She suggests that the more precise vocabulary of modern molecular genetics may be used to rephrase the underlying questions and hence provide a way out of this controversy. I show that her proposal fits into a long tradition in which other authors have wrestled with the same problem and come to similar conclusions. - Review of 'The mirage of a space (...) between nature and nurture' by Evelyn Fox Keller, Duke University Press, 2010, ISBN 9780822347316. (shrink)

Philosophers of science have developed an account of causal-mechanical explanation that captures regularity, but this account neglects variation. In this article I amend the philosophy of mechanisms to capture variation. The task is to explicate the relationship between regular causal mechanisms responsible for individual development and causes of variation responsible for variation in populations. As it turns out, disputes over this relationship have rested at the heart of the nature–nurture debate. Thus, an explication of the relationship between regular causal mechanisms (...) and causes of variation and between individual development and variation offers both the necessary amendment to the philosophy of mechanisms and the resources to mediate the dispute. (shrink)

Many cases of gene‐environment interaction, or , are misconstrued as evincing a genetic predisposition. I diagnose this misconstrual and then introduce a new concept— interactive predisposition —to correct for the mistake. I conclude by examining how recent debates over screening for individual predispositions are related to older debates about group differences between populations , drawing on the lessons of the latter to inform the former. †To contact the author, please write to: Department of Philosophy, University of Utah, Salt Lake City, (...) UT 84112; e‐mail: [email protected]. (shrink)

In a widely acclaimed study from 2002, researchers found a case of gene-environment interaction for a gene controlling neuroenzymatic activity (low vs. high), exposure to childhood maltreatment, and antisocial personality disorder (ASPD). Cases of gene-environment interaction are generally characterized as evincing a genetic predisposition; for example, individuals with low neuroenzymatic activity are generally characterized as having a genetic predisposition to ASPD. I first argue that the concept of a genetic predisposition fundamentally misconstrues these cases of gene-environment interaction. This misconstrual will (...) be diagnosed, and then a new concept—interactive predisposition—will be introduced. I then show how this conceptual shift reconfigures old questions and raises new questions for genetic screening. Attempts to screen embryos or fetuses for the gene associated with low neuroenzymatic activity with an eye towards selecting against the low-activity variant fall prey to the myth of pre-environmental prediction; attempts to screen newborns for the gene associated with low neuroenzymatic activity with an eye towards early intervention will have to face the interventionist’s dilemma. (shrink)