Stuart Glennan, and the team of Peter Machamer, Lindley Darden, and Carl Craver have recently provided two accounts of the concept of a mechanism. The main difference between these two versions rests on how the behavior of the parts of the mechanism is conceptualized. Glennan considers mechanisms to be an interaction of parts, where the interaction between parts can be characterized by direct, invariant, change-relating generalizations. Machamer, Darden, and Craver criticize traditional conceptualizations of mechanisms which are based solely on parts (...) interacting and introduce a new conceptactivity. This essay is an attempt at carving out a relationship between these two philosophical interpretations of a mechanism. I will claim that, rather than being in conflict, Glennan's concept of interaction and Machamer, Darden, and Craver's notion of activity actually complement one another, each emphasizing a missing element of the other. (shrink)
This essay examines the origin of genotype-environment interaction, or G×E. "Origin" and not "the origin" because the thesis is that there were actually two distinct concepts of G×E at this beginning: a biometric concept, or \[G \times E_B\], and a developmental concept, or \[G \times E_D \]. R. A. Fisher, one of the founders of population genetics and the creator of the statistical analysis of variance, introduced the biometric concept as he attempted to resolve one of the main problems in (...) the biometric tradition of biology - partitioning the relative contributions of nature and nurture responsible for variation in a population. Lancelot Hogben, an experimental embryologist and also a statistician, introduced the developmental concept as he attempted to resolve one of the main problems in the developmental tradition of biology - determining the role that developmental relationships between genotype and environment played in the generation of variation. To argue for this thesis, I outline Fisher and Hogben's separate routes to their respective concepts of G × E; then these separate interpretations of G × E are drawn on to explicate a debate between Fisher and Hogben over the importance of G × E, the first installment of a persistent controversy. Finally, Fisher's \[G \times E_B\] and Hogben's \[G \times E_D \] are traced beyond their own work into mid-2Oth century population and developmental genetics, and then into the infamous IQ Controversy of the 1970s. (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)
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)
Traditional, quantitative behavioral geneticists and developmental psychobiologists such as Gilbert Gottlieb have long debated what it would take to create a truly developmental behavioral genetics. These disputes have proven so intractable that disputants have repeatedly suggested that the problem rests on their opponents' conceptual confusion; whilst others have argued that the intractability results from the non-scientific, political motivations of their opponents. The authors provide a different explanation of the intractability of these debates. They show that the disputants have competing interpretations (...) of the concepts of reaction norm, genotype-environment interaction, and gene. The common thread that underlies each of these disagreements, the authors argue, is the relevance of potential variation that is not manifest in any actual population to the understanding of development. (shrink)
I provide a history of research on G×E in this article, showing that there have actually been two distinct concepts of G×E since the very origins of this research. R. A. Fisher introduced what I call the biometric concept of G×E, or G×EB, while Lancelot Hogben introduced what I call the developmental concept of G×E, or G×ED. Much of the subsequent history of research on G×E has largely consisted in the separate legacies of these separate concepts, along with the (sometimes (...) acrimonious) disputes that have arisen time and again when employers of each have argued over the appropriate way to conceptualize the phenomenon. With this history in place, I then consider more recent attempts to distinguish between different concepts of G×E, paying particular attention to the commonly made distinction between “statistical interaction” and “interactionism,” and also Michael Rutter’s distinction between “statistical interaction” and “the biological concept of interaction.” I argue that the history of the separate legacies of G×EB and G×ED better supports Rutter’s analysis of the situation, and that this analysis best paves the way for an integrative relationship between the various scientists investigating the place of G×E in the etiology of complex traits. (shrink)
This article discusses the work of George Udny Yule in relation to the evolutionary synthesis and the biometric-Mendelian debate. It has generally been claimed that (i.) in 1902, Yule put forth the first account showing that the competing biometric and Mendelian programs could be synthesized. Furthermore, (ii.) the scientific figures who should have been most interested in this thesis (the biometricians W. F. Raphael Weldon and Karl Pearson, and the Mendelian William Bateson) were too blinded by personal animosity towards each (...) other to appreciate Yule's proposal. This essay provides a detailed account of (i.), maintaining that Yule's 1902 proposal is better understood as a reduction, not a synthesis of the two programs. The results of this analysis are then used to evaluate (ii.), where I will instead argue that Bateson and the biometricians had good reasons to avoid endorsing Yule's account. (shrink)
Variability of aggression: human aggressive behavior varies on a number of dimensions. We argue that this variability is best understood through an interdisciplinary evolutionary approach.
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: tabery@philosophy.utah.edu. (shrink)
The prospect of a severe influenza pandemic poses a daunting public health threat to hospitals and the public they serve. The event of a severe influenza pandemic will put hospitals under extreme stress; only so many beds, ventilators, nurses, and physicians will be available, and so it is likely that more patients will require medical attention than can be completely treated. Triage is the process of sorting patients in a time of crisis to determine who receives what level of medical (...) attention. How will hospitals sort patients to determine priority for treatment? What criteria will be used? Who will develop these criteria? This article formulates an answer to these questions by constructing a conceptual framework for anticipating and responding to the ethical issues raised by triage in the event of a severe influenza pandemic. (shrink)
James Tabery Helen Longino’s Studying Human Behavior is an overdue effort at a nonpartisan evaluation of the many scientific disciplines that study the nature and nurture of human behavior, arguing for the acceptance of the strengths and weaknesses of all approaches. After years of conflict, Longino makes the pluralist case for peaceful coexistence. Her analysis of the approaches raises the following question: how are we to understand the pluralistic relationship among the peacefully coexisting approaches? Longino is ironically rather unpluralistic about (...) her pluralism, forcing a choice between integrative pluralism and her preferred ineliminative pluralism. I hope to show that the analysis of approaches she offers actually accommodates a pluralism that is both integrative and ineliminative.Approaches to studying human behaviorPhilosophy of biology took shape as a discipline in the 1970s. This disciplinary formation over. (shrink)
In recent years, philosophers of science have found a renewed interest in mechanisms. The motivation is the thought that the elucidation of a mechanism generates a causal explanation for the phenomenon under investigation. For example, a question such as, How do rats form spatial memories of their environments?, is answered by elucidating the regular causal mechanisms responsible for the individual development of spatial memory in rats. But consider a slightly different question: How do some rats come to have better spatial (...) memory than other rats? This is a question about the causes of variation responsible for variation in spatial memory. The first question demands an answer about regularity; the second question demands an answer about variation. The account of causal-mechanical explanation on offer by philosophers of science captures regularity, but it neglects variation. In this essay, I attempt to modify the mechanical program so as to incorporate both regularity and variation. The task is to explicate the relationship between the regular causal mechanisms responsible for individual development and the causes of variation responsible for variation in populations. As it turns out, this is precisely the relationship that has divided the biometric research tradition and the developmental research tradition in the long-standing debates over genotype-environment interaction, or G×E. Ultimately, the product will be an account of causal-mechanical explanation that captures both regularity and variation, and which may be utilized to resolve an aspect of the debates over G×E. (shrink)
