The concept of causation is essential to ascribing moral and legal responsibility since the only way an agent can make a difference in the world is through her acts causing things to happen. Yet the extent and manner in which the complex features of causation bear on responsibility ascriptions remain unclear. I present an analysis of four aspects of causation which yields new insights into different properties of responsibility and offers increased plausibility to certain moral views. Chapter I examines the realist assumption that causation is an objective and mind-independent relation between space-time located relata – a postulate meant to provide moral assessment with a naturalistic basis and make moral properties continuous with a scientific view of the world. I argue that such a realist stance is problematic, and by extension so are the views seeking to tie responsibility attributions to an objective relation. Chapter II combines the context sensitivity of causal claims with the plausible idea that responsibility ascriptions rest on the assessment of causal sequences relating agents and consequences. I argue that taking context sensitivity seriously compels us to face a choice between moral contrastivism and a mild version of scepticism, viz. responsibility is not impossible, but ultimately difficult to identify with confidence. I show why the latter view is preferable. Chapter III explores the concern that group agents would causally (and morally) overdetermine the effects already caused by their constituent individuals. I argue that non-reductive views of agency and responsibility lack a coherent causal story about how group agents impact the world as relatively independent entities. I explain the practical importance of higher-order entities and suggest a fictionalist stance towards group agency talk. Chapter IV analyses the puzzle of effect selection – if causes have infinitely many effects, but only one or a few are mentioned in causal claims, what determines their selection from the complete set of consequents? I argue that the criteria governing the difference between effects and by-products lack clarity and stability. I use the concerns about appropriate effect selection to formulate an epistemic argument against consequentialism.

This dissertation treats of the problem of attributing the occurrence of an individual event or state to a single cause — a problem commonly understood either as a question of distinguishing the cause from the mere conditions or as a matter of singling out, from several causes, one cause, as the cause. The main purpose of the study is to clarify some basic concepts, and some criteria of ascertainment of the cause, that may be discerned in the literature on causal attribution. Special attention is devoted to how the adequacy of causal attributions depends on pragmatic factors. The study begins with an analysis of J. S. Mill’s distinction in A System of Logic between a scientific and a common-parlance approach to the problem of causal attribution. Mill’s assumption that causal attribution in science always requires a universal-law subsumption is then examined in the context of a general discussion of the range of applicability of the covering-law model of explanation. Mill’s scientific and common-parlance notions of cause are compared with R. G. Collingwood’s historical (sense-I) and scientific (sense-II and -III) notions of cause. It is argued that there are purposes of inquiry for which Mill’s common-parlance approach is more relevant to causal attribution in natural science than his scientific approach. And, more generally, it is argued that although law subsumptions are necessary for the ascertainment of the causes, more is often required for explaining the effect. Samuel Gorovitz’s differentiating-factor analysis is discussed, and limitations of the model are identified. The relevance of Morton White’s abnormalistic approach to historical research is also examined. Further, a number of objectivistic approaches are discussed, and it is argued that objectivity is not attainable in causal attributions in a sense in which it always implies an improvement of our ability to attribute the occurrence of an individual event or state to a single cause.

Alors qu’il n’existe pas de définition consensuelle du concept de maladie génétique, ce concept s’est progressivement élargi pour désigner des maladies communes, non héréditaires, non mendéliennes et polygéniques, aboutissant à une généticisation des maladies. Pour résoudre ce paradoxe de la génétique médicale contemporaine, les philosophes réfutent généralement cette généticisation comme une extension génocentriste abusive du concept de maladie génétique et cherchent à redéfinir un concept plus strict de maladie génétique. Nous montrons que cette stratégie échoue et proposons au contraire d’abandonner le concept de maladie génétique et de supposer que la généticisation révèle l’élaboration d’une explication du rôle commun des gènes dans toutes les maladies, que nous appelons une « théorie génétique de la maladie ». Nous définissons les conditions de possibilité et les critères nécessaires d’une théorie génétique a minima et aboutissons à un spectre des théories génétiques possibles. Nous proposons alors de tester si la généticisation des maladies révèle plutôt une théorie génétique des maladies, c’est-à-dire un ensemble de théories génétiques spécifiques à chaque classe de maladie, ou une théorie génétique de la maladie, reposant sur une définition générale de la maladie qui unifie le rôle commun des gènes dans toutes les maladies. Pour ce faire, nous analysons deux exemples de théories génétiques contemporaines : la théorie génétique des maladies infectieuses et la théorie génétique de la médecine des réseaux. Nous concluons à la coexistence nécessaire de plusieurs formes de théories génétiques dans la littérature biomédicale contemporaine. / While there is no consensual definition of the concept of genetic disease, this concept has gradually extended to designate common, non-hereditary, non-Mendelian, polygenic diseases, leading to the geneticization of diseases. In order to solve this paradox of the contemporary medical genetics, philosophers usually discard geneticization as an inappropriate genocentrist extension of the concept of genetic disease and attempt to define a stricter concept of genetic disease. We demonstrate the failure of this strategy and argue on the contrary that we should give up the concept of genetic disease and understand geneticization as the elaboration of an explanation of the common role of genes in diseases, what we call “a genetic theory of disease”. We define the conditions of possibility and the necessary criteria for a genetic theory a minima and end up with describing the spectrum of potential genetic theories. We then suggest to test whether geneticization of diseases reveals rather a genetic theory of diseases, that is, a set of genetic theories specific to each class of disease, or a genetic theory of disease, that is, a general definition of disease unifying the common role of genes in disease explanations. In order to do so, we analyse two examples of contemporary genetic theories: the genetic theory of infectious diseases and the genetic theory of network medicine. We conclude that several forms of genetic theories coexist in the contemporary biomedical literature and that this coexistence is necessary.