Good explanations are not only true or probably true, but are also relevant to a causal question. Current models of causal explanation either only address the question of the truth of an explanation, or do not distinguish the probability of an explanation from its relevance. The tasks of scenario construction and conversational explanation are distinguished, which in turn shows how scenarios can interact with conversational principles to determine the truth and relevance of explanations. The proposed model distinguishes causal discounting from (...) causal backgrounding , and makes predictions concerning the differential effects of contextual information about alternative explanations on: (a) the kind of mental models constructed; (b) belief revision about probable cause; and (c) the perceived quality of a focal explanation. Four experiments are reported that test these predictions. The significance of the notion of explanatory relevance for research on causal explanation is then discussed. (shrink)

Recognizing that all traits are the result of an interaction between genes and environment, I offer a set of criteria for nevertheless making sense of our practice of singling out certain traits as genetic ones, in effect making a distinction between causes and mere conditions. The central criterion is that a trait is genetic if it is genetic differences that make the differences in that trait variable in a given population. A second criterion requires that genetic traits be individuated in (...) a way that matches what some genetic factors cause specifically. Clarifying our causal and classificatory language here can help us to avoid confusions of both theoretical and practical significance. (shrink)

The paper argues for a pragmatic account of genetic explanation. This is to say that when a disease or other trait is termed genetic, the reasons for singling out genes as causes over other, also necessary, genetic and nongenetic conditions are not wholly theoretical but include pragmatic dimensions. Whether the explanation is the presence of a trait in an individual or differences in a trait among individuals, genetic explanations are context-dependent in three ways: they are relative to a causal background (...) of genetic and nongenetic factors; they are relative to a population; and they are relative to the present state of knowledge. Criteria like causal priority, nonstandardness, and causal efficacy that purport to distinguish objectively between genetic causes and nongenetic conditions either incorporate pragmatic elements or fail for other reasons. When the pragmatic dimensions of genetic explanations are recognized, we come to understand the current phenomenon of geneticization to be a reflection of increased technological capacities to manipulate genes in the laboratory, and potentially the clinic, rather than theoretical progress in understanding how diseases and other traits arise. This calls into question the value of the search for theoretical definitions of designations like genetic disease or genetic susceptibility as directives for action. (shrink)

This paper focuses on the causation of diseases, particularly on the idea of a “genetic cause” taking Alzheimer’s Disease (AD) as an example. We (1) provide some historical information and a synopsis of the current knowledge on the etiology and pathogenesis of AD, (2) analyse some conceptual problems related to the notion of “genetic disease” (3) elaborate on the alleged (genetic) cause of AD, and (4) place the discussion on the cause of AD in a broader philosophical context, paying attention (...) to a constructivist perspective, the notions of causal connection and causal selection, and to some practical and normative consequences of our analysis. We conclude (a) that AD is not a specific disease entity with one specific cause, (b) that the idea of a single (sufficient) cause can still function as a heuristic tool in AD research and practice, and (c) that a “belief” in causation can go together with the notions of multicausality and probability. (shrink)

The pivotal problem of comorbidity research lies in the psychometric foundation it rests on, that is, latent variable theory, in which a mental disorder is viewed as a latent variable that causes a constellation of symptoms. From this perspective, comorbidity is a (bi)directional relationship between multiple latent variables. We argue that such a latent variable perspective encounters serious problems in the study of comorbidity, and offer a radically different conceptualization in terms of a network approach, where comorbidity is hypothesized to (...) arise from direct relations between symptoms of multiple disorders. We propose a method to visualize comorbidity networks and, based on an empirical network for major depression and generalized anxiety, we argue that this approach generates realistic hypotheses about pathways to comorbidity, overlapping symptoms, and diagnostic boundaries, that are not naturally accommodated by latent variable models: Some pathways to comorbidity through the symptom space are more likely than others; those pathways generally have the same direction (i.e., from symptoms of one disorder to symptoms of the other); overlapping symptoms play an important role in comorbidity; and boundaries between diagnostic categories are necessarily fuzzy. (shrink)

This paper is a response to Henk ten Have's Genetics and Culture: The Geneticization thesis . In it, I refute Ten Have's suggestion that geneticization is not the sort of process that can be measured and commented on in terms of empirical evidence,even if he is correct in suggesting that it should be seen as part of ‘philosophical discourse’. At the end, I relate this discussion to broader debates within bioethics between the social science and philosophy, and suggest the need (...) for philosophical approaches to take the social sciences seriously. (shrink)

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)