The interventionist account of causal explanation, in the version presented by Jim Woodward, has been recently claimed capable of buttressing the widely felt—though poorly understood—hunch that high-level, relatively abstract explanations, of the sort provided by sciences like biology, psychology and economics, are in some cases explanatorily optimal. It is the aim of this paper to show that this is mistaken. Due to a lack of effective constraints on the causal variables at the heart of the interventionist causal-explanatory scheme, as presently (...) formulated it is either unable to prefer high-level explanations to low, or systematically overshoots, recommending explanations at so high of a level as to be virtually vacuous. (shrink)

In psychiatry, pharmacological drugs play an important experimental role in attempts to identify the neurobiological causes of mental disorders. Besides being developed in applied contexts as potential treatments for patients with mental disorders, pharmacological drugs play a crucial role in research contexts as experimental instruments that facilitate the formulation and revision of neurobiological theories of psychopathology. This paper examines the various epistemic functions that pharmacological drugs serve in the discovery, refinement, testing, and elaboration of neurobiological theories of mental disorders. I (...) articulate this thesis with reference to the history of antipsychotic drugs and the evolution of the dopamine hypothesis of schizophrenia in the second half of the twentieth century. I argue that interventions with psychiatric patients through the medium of antipsychotic drugs provide researchers with information and evidence about the neurobiological causes of schizophrenia. This analysis highlights the importance of pharmacological drugs as research tools in the generation of psychiatric knowledge and the dynamic relationship between practical and theoretical contexts in psychiatry. (shrink)

Causal mediation mechanisms are well supported by available experimental evidence and provide a practicable way to reductive physicalism. According to the causal mediation account of mechanistic explanation, descriptions as diverse as ‘black-box’ phenomena, mechanistic sketches and schemas mixing physically interpreted and operationalized biological, psychological and social variables, and detailed descriptions of mechanisms refer to the same causal structure circumscribed within the spatiotemporal boundaries of a replicable experimental setup. The coreference of coarser- and finer-grained descriptions of causal structures opens new possibilities (...) for testing the reductive physicalism conjecture. I discuss experimental designs supporting the causal mediation account and show how recent studies demonstrating the biological mediation of mind-mind causal processes can provide evidence for reductive physicalism. (shrink)

Winner of the 2020 Essay Competition of the International Social Ontology Society. -/- Ian Hacking uses the looping effect to describe how classificatory practices in the human sciences interact with the classified people. While arguably this interaction renders the affected human kinds unstable and hence different from natural kinds, realists argue that also some prototypical natural kinds are interactive and human kinds in general are stable enough to support explanations and predictions. I defend a more fine-grained realist interpretation of interactive (...) human kinds by arguing for an explanatory domain account of the looping effect. First, I argue that knowledge of the feedback mechanisms that mediate the looping effect can supplement, and help to identify, the applicability domain over which a kind and its property variations are stably explainable. Second, by applying this account to cross-cultural case studies of psychiatric disorders, I distinguish between congruent feedback mechanisms that explain matches between classifications and kinds, and incongruent feedback mecha- nisms that explain mismatches. For example, congruent mechanisms maintain Western auditory experiences in schizophrenia, whereas exporting diagnostic labels inflicts incongruence by influencing local experiences. Knowledge of the mechanisms can strengthen explanatory domains, and thereby facilitate classificatory adjustments and possible interventions on psychiatric disorders. (shrink)

It has been argued that supervenience generates unavoidable confounding problems for interventionist accounts of causation, to the point that we must choose between interventionism and supervenience. According to one solution, the dilemma can be defused by excluding non-causal determinants of an outcome as potential confounders. I argue that this solution undermines the methodological validity of causal tests. Moreover, we don’t have to choose between interventionism and supervenience in the first place. Some confounding problems are effectively circumvented by experimental designs routinely (...) employed in science. The remaining confounding issues concern the physical interpretation of variables and cannot be solved by choosing between interventionism and supervenience. (shrink)

Though the divide between reason-based and causal-explanatory approaches in psychiatry and psychopathology is old and deeply rooted, current trends involving multi-factorial explanatory models and evidence-based approaches to interpersonal psychotherapy, show that it has already been implicitly bridged. These trends require a philosophical reconsideration of how reasons can be causes. This paper contributes to that trajectory by arguing that Donald Davidson’s classic paradigm of 1963 is still a valid option.

We propose a formal framework for interpretable machine learning. Combining elements from statistical learning, causal interventionism, and decision theory, we design an idealised explanation game in which players collaborate to find the best explanation for a given algorithmic prediction. Through an iterative procedure of questions and answers, the players establish a three-dimensional Pareto frontier that describes the optimal trade-offs between explanatory accuracy, simplicity, and relevance. Multiple rounds are played at different levels of abstraction, allowing the players to explore overlapping causal (...) patterns of variable granularity and scope. We characterise the conditions under which such a game is almost surely guaranteed to converge on a optimal explanation surface in polynomial time, and highlight obstacles that will tend to prevent the players from advancing beyond certain explanatory thresholds. The game serves a descriptive and a normative function, establishing a conceptual space in which to analyse and compare existing proposals, as well as design new and improved solutions. (shrink)

Multidisciplinary models aggregating ‘lower-level’ biological and ‘higher-level’ psychological and social determinants of a phenomenon raise a puzzle. How is the interaction between the physical, the psychological and the social conceptualized and explained? Using biopsychosocial models of pain as an illustration, I argue that these models are in fact level-neutral compilations of empirical findings about correlated and causally relevant factors, and as such they neither assume, nor entail a conceptual or ontological stratification into levels of description, explanation or reality. If inter-level (...) causation is deemed problematic or if debates about the superiority of a particular level of description or explanation arise, these issues are fueled by considerations other than empirical findings. (shrink)

In psychiatry, pharmacological research has played a crucial role in the formulation, revision, and refinement of neurobiological theories of psychopathology. Besides being utilized as potential treatments for various mental disorders, pharmacological drugs play an important epistemic role as experimental instruments that help scientists uncover the neurobiological underpinnings of mental disorders (Tsou, 2012). Interventions with psychiatric patients using pharmacological drugs provide researchers with information about the neurobiological causes of mental disorders that cannot be obtained in other ways. This important source of (...) evidence for the biological causes of mental disorder is often overlooked in philosophical analyses of psychiatry, especially in skeptical analyses that debase the biological aspects of psychopathology (e.g., Szasz, 1960; Scheff, 1963; Laing, 1967). In discussing pharmacological interventions as a form of evidence for the physical basis of mental disorders, this paper aims to clarify the nature, reliability, and limitations of this evidence. In addition, it illustrates the central role that pharmacological findings in applied clinical contexts play in the acquisition of neurobiological knowledge in research contexts. (shrink)

James Woodward’s Making Things Happen presents the most fully developed version of a manipulability theory of causation. Although the ‘interventionist’account of causation that Woodward defends in Making Things Happen has many admirable qualities, Michael Strevens argues that it has a fatal flaw. Strevens maintains that Woodward’s interventionist account of causation renders facts about causation relative to an individual’s perspective. In response to this charge, Woodward claims that although on his account X might be a relativized cause of Y relative to (...) some perspective, this does not lead to the problematic relativity that Strevens claims. Roughly, Woodward argues this is so because if X is a relativized cause of Y with respect to some perspective, then X is a cause of Y simpliciter. So, the truth of whether X is a cause of Y is not relative to one’s perspective. Strevens counters by arguing that Woodward’s response fails because relativized causation is not monotonic. In this paper I argue that Strevens’ argument that relativized causation is not monotonic is unsound. (shrink)

The systems studied in the special sciences are often said to be causally autonomous, in the sense that their higher-level properties have causal powers that are independent of the causal powers of their more basic physical properties. This view was espoused by the British emergentists, who claimed that systems achieving a certain level of organizational complexity have distinctive causal powers that emerge from their constituent elements but do not derive from them. More recently, non-reductive physicalists have espoused a similar view (...) about the causal autonomy of special-science properties. They argue that since these properties can typically have multiple physical realizations, they are not identical to physical properties, and further they possess causal powers that differ from those of their physical realisers. Despite the orthodoxy of this view, it is hard to find a clear exposition of its meaning or a defence of it in terms of a well-motivated account of causation. In this paper, we aim to address this gap in the literature by clarifying what is implied by the doctrine of the causal autonomy of special-science properties and by defending the doctrine using a prominent theory of causation from the philosophy of science. (shrink)

Some recent arguments defending the genuine causal efficacy of the mental have been relying on empirical research on neuroprosthetics. This essay presents a critical analysis of these arguments. The problem of mental causation, and the basic idea and results of neuroprosthetics are reviewed. It is shown how appealing to the research on neuroprosthetics can be interpreted to give support to the idea of mental causation. However, it does so only in a rather deflationary sense: by holding the mental identical with (...) the neural. So contrary to what the arguments have been assuming, neuroprosthetics cannot be used to argue for nonreductive physicalism. It can rather be taken to illustrate just the opposite: how the mental and the physical are identical. (shrink)

Critics who are concerned over the epistemological status of psychiatric diagnoses often describe them as being constructed. In contrast, those critics usually see symptoms as relatively epistemologically unproblematic. In this paper I show that symptoms are also constructed. To do this I draw upon the demarcation between data and phenomena. I relate this distinction to psychiatry by portraying behaviour of individuals as data and symptoms as phenomena. I then draw upon philosophers who consider phenomena to be constructed to argue that (...) symptoms are also constructed. Rather than being ready made in the world I show how symptoms are constructs we apply to the world. I highlight this with a historical example and describe methodological constraints on symptom construction. I show the epistemic problems with psychiatric diagnoses are also applicable to symptoms. Following this, I suggest that critics of psychiatric diagnoses should extend their criticism to symptoms or, if they still believe symptoms are relatively epistemologically unproblematic, should rethink their concerns over psychiatric diagnoses. (shrink)

Interventionism is a theory of causal explanation developed by Woodward and Hitchcock. I defend an interventionist perspective on the causal explanations offered within scientific psychology. The basic idea is that psychology causally explains mental and behavioral outcomes by specifying how those outcomes would have been different had an intervention altered various factors, including relevant psychological states. I elaborate this viewpoint with examples drawn from cognitive science practice, especially Bayesian perceptual psychology. I favorably compare my interventionist approach with well-known nomological and (...) mechanistic theories of psychological explanation. (shrink)

In trying to establish the view that there are no non-living macrophysical objects, Trenton Merricks has produced an influential argument—the Overdetermination Argument—against the causal efficacy of composite objects. A serious problem for the Overdetermination Argument is the ambiguity in the notion of overdetermination that is being employed, which is due to the fact that Merricks does not provide any theory of causation to support his claims. Once we adopt a plausible theory of causation, viz. interventionism, problems with the Overdetermination will (...) become evident. After laying out the Overdetermination Argument and examining one extant objection to it, I will explicate the relevant aspects of an interventionist theory of causation and provide a characterization of overdetermination that follows from such an account. From this, I will argue that the Causal Principle that undergirds the Overdetermination Argument is false and hence the argument is invalid; and I claim that the only other available characterization of overdetermination would render a key premise in the argument false. Thus, the Overdetermination Argument fails to provide us with any reason to deny the causal efficacy of macrophysical objects, and therefore provides no reason to doubt their existence. (shrink)

Multidisciplinary models aggregating ‘lower-level’ biological and ‘higher-level’ psychological and social determinants of a phenomenon raise a puzzle. How is the interaction between the physical, the psychological and the social conceptualized and explained? Using biopsychosocial models of pain as an illustration, I argue that these models are in fact level-neutral compilations of empirical findings about correlated and causally relevant factors, and as such they neither assume, nor entail a conceptual or ontological stratification into levels of description, explanation or reality. If inter-level (...) causation is deemed problematic or if debates about the superiority of a particular level of description or explanation arise, these issues are fueled by considerations other than empirical findings. (shrink)

In this contribution, I comment on Raffaella Campaner’s defense of explanatory pluralism in psychiatry (in this volume). In her paper, Campaner focuses primarily on explanatory pluralism in contrast to explanatory reductionism. Furthermore, she distinguishes between pluralists who consider pluralism to be a temporary state on the one hand and pluralists who consider it to be a persisting state on the other hand. I suggest that it would be helpful to distinguish more than those two versions of pluralism – different understandings (...) of explanatory pluralism both within philosophy of science and psychiatry – namely moderate/temporary pluralism, anything goes pluralism, isolationist pluralism, integrative pluralism and interactive pluralism. Next, I discuss the pros and cons of these different understandings of explanatory pluralism. Finally, I raise the question of how to implement or operationalize explanatory pluralism in scientific practice; how to structure the “genuine dialogue” or shape “the pluralistic attitude” Campaner is referring to. As tentative answers, I explore a question-based framework for explanatory pluralism as well as social-epistemological procedures for interaction among competing approaches and explanations. (shrink)

This contribution claims that the two fundamental notions of causation at work in the health sciences are manipulative and mechanistic, and investigates what kinds of evidence matter for the assessment of causal relations. This article is a development of our 2007 article, ‘Plurality of Causality’, where we argue for a pluralistic account of causation with an eye to econometrics and a single medical example. The present contribution has a wider focus, and considers the notion of evidence within a whole range (...) of disciplines belonging to the health sciences. Section 1 addresses the relations between kinds of evidence and causal accounts, and it is shown how different notions of causation can be employed in various medical cases. Section 2 calls attention to issues crucial for any adequate epistemological theory of causation, such as the distinctions between types and tokens, observational and experimental regimes, explanation and prediction. Lastly, the notion of context is articulated, highlighted in its role in the assessment of causal links. All these issues are tackled in the framework of what we label a ‘bottom–up’ epistemology. (shrink)

This paper is concerned with the content of the causal proportionality constraint. It investigates two general versions of the constraint, namely “horizontal” and “vertical” proportionality. Moreover, it discusses whether proportionality is considered an ontic or an epistemic, i.e. explanatory, constraint on causation in the context of some of the most prominent theories of causation. The following main claims are defended: (1) The horizontal (HP) and the vertical version (VP) of the proportionality constraint are logically independent. (2) HP is implied by (...) some prominent theories of causation, not by others. (3) None of the discussed popular theories of causation contradicts either HP or VP. (4) HP and VP are not ontic or epistemic principles as such; rather, whether they are ontic or epistemic depends on the theories chosen plus background assumptions about the existence of higher-level causes and their non-identity to lower-level ones. (shrink)

Ian Hacking uses the looping effect to describe how classificatory practices in the human sciences interact with the classified people. While arguably this interaction renders the affected human kinds unstable and hence different from natural kinds, realists argue that also some prototypical natural kinds are interactive and human kinds in general are stable enough to support explanations and predictions. I defend a more fine-grained realist interpretation of interactive human kinds by arguing for an explanatory domain account of the looping effect. (...) First, I argue that knowledge of the feedback mechanisms that mediate the looping effect can supplement, and help to identify, the applicability domain over which a kind and its property variations are stably explainable. Second, by applying this account to cross-cultural case studies of psychiatric disorders, I distinguish between congruent feedback mechanisms that explain matches between classifications and kinds, and incongruent feedback mechanisms that explain mismatches. For example, congruent mechanisms maintain Western auditory experiences in schizophrenia, whereas exporting diagnostic labels inflicts incongruence by influencing local experiences. Knowledge of the mechanisms can strengthen explanatory domains, and thereby facilitate classificatory adjustments and possible interventions on psychiatric disorders. (shrink)

It is commonplace to distinguish between propositional justification (having good reasons for believing p) and doxastic justification (believing p on the basis of those good reasons).One necessary requirement for bridging the gap between S’s merely having propositional justification that p and S’s having doxastic justification that p is that S base her belief that p on her reasons (propositional justification).A plausible suggestion for what it takes for S’s belief to be based on her reasons is that her reasons must contribute (...) causally to S’s having that belief. Though this suggestion is plausible, causal accounts of the basing relation that have been proposed have not fared well. In particular, cases involving causal deviancy and cases involving over-determination have posed serious problems for causal accounts of the basing relation. Although previous causal accounts of the basing relation seem to fall before these problems, it is possible to construct an acceptable causal account of the basing relation. That is, it is possible to construct a causal account of the basing relation that not only fits our intuitions about doxastic justification in general, but also is not susceptible to the problems posed by causal deviancy and causal over-determination. The interventionist account of causation provides the tools for constructing such an account. My aim is to make use of the insights of the interventionist account of causation to develop and defend an adequate causal account of the basing relation. (shrink)

I examine the adequacy of the causal graph-structural equations approach to causation for modeling biological mechanisms. I focus in particular on mechanisms with complex dynamics such as the PER biological clock mechanism in Drosophila. I show that a quantitative model of this mechanism that uses coupled differential equations – the well-known Goldbeter model – cannot be adequately represented in the standard causal graph framework, even though this framework does permit causal cycles. The reason is that the model contains dynamical information (...) about the mechanism that concerns causal properties but that does not correspond to variables that could be subject to independent interventions. Thus, a representation of the mechanisms as a causal structural model necessarily suppresses causally relevant information. (shrink)

Network theory is applied across the sciences to study phenomena as diverse as the spread of SARS, the topology of the cell, the structure of the Internet and job search behaviour. Underlying the study of networks is graph theory. Whether the graph represents a network of neurons, cells, friends or firms, it displays features that exclusively depend on the mathematical properties of the graph itself. However, the way in which graph theory is implemented to the modelling of networks differs significantly (...) across scientific fields. This article compares the economics variant of network theory with those of other fields. It shows how the methodology employed by economists to model networks is shaped by two explanatory desiderata: that the explanandum phenomenon is based on micro-economic foundations and that the explanation is general. (shrink)