This paper aims to provide Humean metaphysics for the interventionist theory of causation. This is done by appealing to the hierarchical picture of causal relations as being realized by mechanisms, which in turn are identified with lower-level causal structures. The modal content of invariances at the lowest level of this hierarchy, at which mechanisms are reduced to strict natural laws, is then explained in terms of projectivism based on the best-system view of laws.

This paper critiques the new mechanistic explanatory program on grounds that, even when applied to the kinds of examples that it was originally designed to treat, it does not distinguish correct explanations from those that blunder. First, I offer a systematization of the explanatory account, one according to which explanations are mechanistic models that satisfy three desiderata: they must 1) represent causal relations, 2) describe the proper parts, and 3) depict the system at the right ‘level.’ Second, I argue that (...) even the most developed attempts to fulfill these desiderata fall short by failing to appropriately constrain explanatorily apt mechanistic models. -/- *This paper used to be called "The Emperor's New Mechanisms". (shrink)

How regular do mechanisms need to be, in order to count as mechanisms? This paper addresses two arguments for dropping the requirement of regularity from the definition of a mechanism, one motivated by examples from the sciences and the other motivated by metaphysical considerations regarding causation. I defend a broadened regularity requirement on mechanisms that takes the form of a taxonomy of kinds of regularity that mechanisms may exhibit. This taxonomy allows precise explication of the degree and location of regular (...) operation within a mechanism, and highlights the role that various kinds of regularity play in scientific explanation. I defend this regularity requirement in terms of regularity’s role in individuating mechanisms against a background of other causal processes, and by prioritizing mechanisms’ ability to serve as a model of scientific explanation, rather than as a metaphysical account of causation. It is because mechanisms are regular, in the expanded sense described here, that they are capable of supporting the kinds of generalizations that figure prominently in scientific explanations. (shrink)

In this paper I develop five worries concerning Cartwright’s realism about entities and capacities. The first is that while she was right to insist on the ontic commitment that flows from causal explanation, she was wrong to tie these commitments solely to the entities that do the causal explaining. This move obscured the nature of causal explanation and its connection to laws. The second worry is that when she turned her attention to causal inference, by insisting on the motto of (...) ‘the most likely cause’, she underplayed her powerful argument for realism. For she focused her attention on an extrinsic feature of causal inference (or, indeed, of any ampliative inference), that is the demand of high probability, leaving behind the intrinsic qualities that causal explanation should have in order to provide the required understanding. The third worry is that her objections to Inference to the Best Explanation were unnecessarily tied to her objections about the falsity of fundamental laws. The fourth worry is that though her argument for positing capacities and being realist about them was supposed to take strength from its parallel with Sellars’s powerful argument for the indispensable explanatory role of positing unobservable entities, there are important disanalogies between the two arguments which cast doubt on the indispensability of capacities. The final (fifth) worry is that laws—perhaps brute regularities—might well have to come back from the front door, since they are still the most plausible candidates for explaining why objects have the capacities to do what they can do. (shrink)

Polygenic effects have more than one cause. They testify to the fact that several causal contributors are sometimes simultaneously involved in causation. The importance of polygenic causation was noticed early on by Mill (1893). It has since been shown to be a problem for causal-law approaches to causation and accounts of causation cast in terms of capacities. However, polygenic causation needs to be examined more thoroughly in the emerging literature on causal mechanisms. In this paper I examine whether an influential (...) theory of mechanisms proposed by Peter Machamer, Lindley Darden and Carl Craver can accommodate polygenic effects and other forms of causal interaction. This theory is problematic, I will argue, because it ascribes a central role to activities. In it, activities are needed not only to constitute mechanisms but also to perform the causal role of mechanisms. Any such mechanism-as-activity will be incompatible with causal situations where either no or merely another kind of activity occurs. But, as I will try to illustrate in this paper, both kinds of situation may be frequent. If I am right, the view that Machamer and colleagues suggest leads to an impoverished conception of mechanism. (shrink)

This article defends the use of interventionist counterfactuals to elucidate causal and explanatory claims against criticisms advanced by James Bogen and Peter Machamer. Against Bogen, I argue that counterfactual claims concerning what would happen under interventions are meaningful and have determinate truth values, even in a deterministic world. I also argue, against both Machamer and Bogen, that we need to appeal to counterfactuals to capture the notions like causal relevance and causal mechanism. Contrary to what both authors suppose, counterfactuals are (...) not "unscientific" - a substantial tradition within statistics and the causal modelling literature makes heavy use of them. (shrink)

Explanations in behavioural neuroscience are often said to be mechanistic in the sense that they explain an organism’s behaviour by describing the activities and organisation of the organism’s parts that are “constitutively relevant” to organism behaviour. Much has been said about the constitutive relevance of working parts (in debates about the so-called “mutual manipulability criterion”), but relatively little has been said about the constitutive relevance of the organising relations between working parts. Some New Mechanists seem to endorse a simple causal-linking (...) account: organising relations are constitutively relevant to organism behaviour if and only if (and because) they are causal relations that link the working parts that are constitutively relevant to organism behaviour. In this paper, I argue that the causal-linking account is inadequate because it neglects the constitutive relevance of anatomical relations that organise the working parts of a behaving organism. I demonstrate this by considering a case study where the anatomical organisation of the barn owl (Tyto alba) is constitutively relevant to their mechanism for sound localization. The anatomical organisation of this mechanism is best understood as the back-and-forth flow of task information across 7 “levels of anatomy” (a notion that I distinguish from levels of mechanism). A further implication, I conclude, is that at least some of the interlevel structure of neuroscientific explanation is accounted for by levels of anatomy, not levels of mechanism. (shrink)

Although the literature on the issue of pluralism within the philosophy of science is very extensive, this paper focuses on the metaphysical causal pluralism that emerges from the new mechanistic discussion on causality. The main aim is to situate the new mechanistic views on causation within the account of varieties of causal pluralism framed by Psillos ( 2009 ). Paying attention to his taxonomy of metaphysical views on causation (i.e., the straightjacket view, the functional view, the two-concept view, the agnostic (...) view and the atheist view) will help clarify differences in opinion and, at the same time, make it possible to elucidate the main metaphysical theses present within the new mechanistic debate. Special attention is given to S. Glennan’s theory of causation, since it is unique in offering an overall metaphysical view of the issue. It is also argued that mechanists are not “atheists” on causation: while all of them are causal realists, most mechanists are “agnostic” on causation, with a few exceptions such as S. Glennan, P. Machamer and J. Bogen. (shrink)

Powers are properties defined by what they do. The focus of the large majority of the powers literature has been mainly put on explicating the (multifaceted) results of the production of a power in certain (multifaceted) initial conditions: but all this causal complexity is bound to be—and, in fact, it has proved to be—quite difficult to handle. In this paper we take a different approach by focusing on the very activity of producing those multifaceted manifestations themselves. In this paper, we (...) propose an original account of what the essence of a power consists in which stems from a radical reconceptualisation of power-causation according to which counterfactuals are to be explained away by powers, and not vice-versa. We call this approach the dynamical operator account of powers. According to this account, the causal role of powers consists in their ensuring that the ontological transition from a stimulus S to a manifestation M happens. Powers thus have a dynamical essence which consists in the fundamental activity of generating the counterfactuals typically associated with them. We show that if one conceptualises this functional activity as the metaphysical fulcrum around which counterfactual-based causation revolves, one is granted not only an improved methodology to individuate powers but also a better understanding of their knowability, modality and directedness. (shrink)

This paper advances the thesis of methodological mechanism, the claim that to be committed to mechanism is to adopt a certain methodological postulate, i.e. to look for causal pathways for the phenomena of interest. We argue that methodological mechanism incorporates a minimal account of understanding mechanisms, according to which a mechanism just is a causal pathway described in the language of theory. In order to argue for this position we discuss a central example of a biological mechanism, the mechanism of (...) cell death, known as apoptosis. We argue that this example shows that our philosophically deflationary account is sufficient in order to have an illuminating account of mechanisms as the concept is used in biology. (shrink)

According to the new mechanistic approach, an acting entity is at a lower mechanistic level than another acting entity if and only if the former is a component in the mechanism for the latter. Craver and Bechtel :547–563, 2007. doi:10.1007/s10539-006-9028-8) argue that a consequence of this view is that there cannot be causal interactions between acting entities at different mechanistic levels. Their main reason seems to be what I will call the Metaphysical Argument: things at different levels of a mechanism (...) are related as part and whole; wholes and their parts cannot be related as cause and effect; hence, interlevel causation in mechanisms is impossible. I will analyze this argument in more detail and show under which conditions it is valid. This analysis will reveal that interlevel causation in mechanisms is indeed possible, if we take seriously the idea that the relata of the mechanistic level relation are acting entities and accept a slightly modified notion of a mechanistic level that is highly plausible in the light of the first clarification. (shrink)

Leuridan (2011) questions whether mechanisms can really replace laws at the heart of our thinking about science. In doing so, he enters a long-standing discussion about the relationship between the mech-anistic structures evident in the theories of contemporary biology and the laws of nature privileged especially in traditional empiricist traditions of the philosophy of science (see e.g. Wimsatt 1974; Bechtel and Abrahamsen 2005; Bogen 2005; Darden 2006; Glennan 1996; MDC 2000; Schaffner 1993; Tabery 2003; Weber 2005). In our view, Leuridan (...) misconstrues this discussion. His weak positive claim that mechanistic sciences appeal to generalizations is true but uninteresting. His stronger claim, that all causal claims require laws, is unsupported by his arguments. Though we proceed by criticizing Leuridan’s arguments, our greater purpose is to embellish his arguments in order to show how thinking about mechanisms enriches and transforms old philosophical debates about laws in biology and provides new insights into how generalizations afford prediction, explanation and control. (shrink)

The central aim of this article is to specify the ontological nature of constitutive mechanistic phenomena. After identifying three criteria of adequacy that any plausible approach to constitutive mechanistic phenomena must satisfy, we present four different suggestions, found in the mechanistic literature, of what mechanistic phenomena might be. We argue that none of these suggestions meets the criteria of adequacy. According to our analysis, constitutive mechanistic phenomena are best understood as what we will call ‘object-involving occurrents’. Furthermore, on the basis (...) of this notion, we will clarify what distinguishes constitutive mechanistic explanations from etiological ones. 1 Introduction 2 Criteria of Adequacy 2.1 Descriptive adequacy 2.2 Constitutive–etiological distinction 2.3 Constitution 3 The Ontological Nature of Constitutive Mechanistic Phenomena 3.1 Phenomena as input–output relations 3.2 Phenomena as end states 3.3 Phenomena as dispositions 3.4 Phenomena as behaviours 4 Phenomena as Object-Involving Occurrents 4.1 What object-involving occurrents are and why we need them 4.2 The object in the phenomenon 4.3 The adequacy of option 5 Conclusion. (shrink)

In a backlash against the prevalence of statistical methods, recently social scientists have focused more on studying causal mechanisms. They increasingly rely on a technique called process-tracing, which involves contrasting the observable implications of several alternative mechanisms. Problematically, process-tracers do not commit to a fundamental notion of causation, and therefore arguably they cannot discern between mere correlation between the links of their purported mechanisms and genuine causation. In this paper, I argue that committing to Woodward's interventionist notion of causation would (...) solve this problem: process-tracers should take into account evidence for possible interventions on the mechanisms they study. (shrink)

Manipulationism holds that information about the results of interventions is of utmost importance for scientific practices such as causal assessment or explanation. Specifically, manipulation provides information about the stability, or invariance, of the relationship between X and Y: were we to wiggle the cause X, the effect Y would accordingly wiggle and, additionally, the relation between the two will not be disrupted. This sort of relationship between variables are called 'invariant empirical generalisations'. The paper focuses on questions about causal assessment (...) and analyses the status of manipulation. It is argued that manipulationism is trapped in a dilemma. If manipulationism is read as providing a conceptual analysis of causation, then it fails to provide a story about the methods for causal assessment. If, instead, manipulationism is read as providing a method for causal assessment, then it is at an impasse concerning causal assessment in areas where manipulations are not performed. Empirical generalisations are then reassessed, in such a way that manipulation is not taken as methodologically fundamental. The paper concludes that manipulation is the appropriate tool for some scientific contexts, but not for all. (shrink)

Glennan appeals to interventions to solve the ontological and explanatory regresses that threaten his mechanistic account of causality . I argue that Glennan’s manoeuvre fails. The appeal to interventions is not able to address the ontological regress, and it blocks the explanatory regress only at the cost of making the account inapplicable to non-modular mechanisms. I offer a solution to the explanatory regress that makes use of dynamic Bayesian networks. My argument is illustrated by a case study from systems biology, (...) namely, the mechanism for the irreversibility of apoptosis. I conclude by pointing out the implications of my argument for Glennan’s mechanistic account of causality and, more generally, for accounts of mechanistic explanation based on interventions. 1 Introduction2 Glennan’s Account of Causality3 Objections to Glennan’s Account4 Glennan’s Replies5 Ontological Symmetry?6 Explanatory Symmetry?7 A Solution to the Explanatory Regress8 The Prospects of Glennan’s Account. (shrink)

The purpose of this article is to examine two important issues concerning the agency theory of causality: the charge of anthropomorphism and the relation of simultaneous causation. After a brief outline of the agency theory, sections 2–4 contain the refutation of the three main forms in which the charge of anthropomorphism is to be found in the literature. It will appear that it is necessary to distinguish between the subjective and the objective aspect of the concept of causation. This will (...) lead, in section 5, to contrast two kinds of anthropomorphism, one which has been rightly rejected by modern science and one which is fully compatible with the objective reality of the causal processes. Finally, section 6 will apply the preceding considerations to simultaneous causation. On the one hand, in a basic sense, there can be no simultaneous causal relations. On the other hand, simultaneous causation arises when we consider the natural change by abstracting from the agent and from her/his projects of interven.. (shrink)

My aim in this paper is to make a case for the singularist view from the perspective of a mechanical theory of causation, and to explain what, from this perspective, causal generalizations mean, and what role they play within the mechanical theory.

A shared problem across the sciences is to make sense of correlational data coming from observations and/or from experiments. Arguably, this means establishing when correlations are causal and when they are not. This is an old problem in philosophy. This paper, narrowing down the scope to quantitative causal analysis in social science, reformulates the problem in terms of the validity of statistical models. Two strategies to make sense of correlational data are presented: first, a 'structural strategy', the goal of which (...) is to model and test causal structures that explain correlational data; second, a 'manipulationist or interventionist strategy', that hinges upon the notion of invariance under intervention. It is argued that while the former can offer a solution the latter cannot. (shrink)

Today, mechanisms and mechanistic explanation are very popular in philosophy of science and are deemed a welcome alternative to laws of nature and deductive‐nomological explanation. Starting from Mitchell's pragmatic notion of laws, I cast doubt on their status as a genuine alternative. I argue that (1) all complex‐systems mechanisms ontologically must rely on stable regularities, while (2) the reverse need not hold. Analogously, (3) models of mechanisms must incorporate pragmatic laws, while (4) such laws themselves need not always refer to (...) underlying mechanisms. Finally, I show that Mitchell's account is more encompassing than the mechanistic account *Received August 2008; revised January 2010. †To contact the author, please write to: Centre for Logic and Philosophy of Science, Ghent University, Blandijnberg 2, B‐9000 Belgium; e‐mail: [email protected]. (shrink)

The anti-causal prophecies of last century have been disproved. Causality is neither a ‘relic of a bygone’ nor ‘another fetish of modern science’; it still occupies a large part of the current debate in philosophy and the sciences. This investigation into causal modelling presents the rationale of causality, i.e. the notion that guides causal reasoning in causal modelling. It is argued that causal models are regimented by a rationale of variation, nor of regularity neither invariance, thus breaking down the dominant (...) Human paradigm. The notion of variation is shown to be embedded in the scheme of reasoning behind various causal models: e.g. Rubin’s model, contingency tables, and multilevel analysis. It is also shown to be latent – yet fundamental – in many philosophical accounts. Moreover, it has significant consequences for methodological issues: the warranty of the causal interpretation of causal models, the levels of causation, the characterisation of mechanisms, and the interpretation of probability. This book offers a novel philosophical and methodological approach to causal reasoning in causal modelling and provides the reader with the tools to be up to date about various issues causality rises in social science. (shrink)

Most philosophical accounts of causation take causal relations to obtain between individuals and events in virtue of nomological relations between properties of these individuals and events. Such views fail to take into account the consequences of the fact that in general the properties of individuals and events will depend upon mechanisms that realize those properties. In this paper I attempt to rectify this failure, and in so doing to provide an account of the causal relevance of higher-level properties. I do (...) this by critiquing one prominent model of higher-level properties—Kim’s functional model of reduction—and contrasting it with a mechanistic approach to higher-level properties and causation. (shrink)

The topic of mechanistic explanation in neuroscience has been a subject of recent discussion. There is a lot of interest in understanding what these explanations involve. Furthermore, there is disagreement about whether neurological mechanisms themselves should be viewed as reductionist in nature. In this paper I will explain how these two issues are related. I will, first, describe how mechanisms support a form of antireductionism. This is because the mechanisms that exist should be seen as involving part-whole relations, where the (...) behavior of a whole is more than the sum of its parts. After this, I will consider mechanistic explanations and how they can be understood. While some people think the explanations concern existing entities in the world, I will argue that we can understand the explanations by viewing them in terms of arguments. Despite the fact that it is possible to understand mechanistic explanations in this manner, the antireductionist point remains. (shrink)

This paper defends an invariance-based account of laws of nature: Laws are generalizations that remain invariant under various sorts of changes. Alternatively, laws are generalizations that exhibit a certain kind of independence from background conditions.

This paper discusses von Wright's theory of causation from Explanation and Understanding and Causality and Determinism in contemporary context. I argue that there are two important common points that von Wright's view shares with the version of manipulability currently supported by Woodward: the analysis of causal relations in a system modelled on controlled experiments, and the explanation of manipulability through counterfactuals - with focus on the counterfactual account of unmanipulable causes. These points also mark von Wright's departure from previous action-based (...) theories of causation. Owing to these two features, I argue that, upon classifying different versions of manipulability theories, von Wright's view should be placed closer to the interventionist approach than to the agency theory, where it currently stands. Furthermore, given its relevance in contemporary context, which this paper aims to establish, I claim that von Wright's theory can be employed to solve present problems connected to manipulability approaches to causation. (shrink)

This volume argues for a new image of science that understands both natural and social phenomena to be the product of mechanisms, casting the work of science as an effort to understand those mechanisms. Glennan offers an account of the nature of mechanisms and of the models used to represent them in physical, life, and social sciences.

In this chapter we examine the relation between mechanisms and laws/counterfactuals by revisiting the main notions of mechanism found in the literature. We distinguish between two different conceptions of ‘mechanism’: mechanisms-of underlie or constitute a causal process; mechanisms-for are complex systems that function so as to produce a certain behavior. According to some mechanists, a mechanism fulfills both of these roles simultaneously. The main argument of the chapter is that there is an asymmetrical dependence between both kinds of mechanisms and (...) laws/counterfactuals: while some laws and counterfactuals must be taken as primitive (non-mechanistic) facts of the world, all mechanisms depend on laws/counterfactuals. (shrink)

Colombo’s (Phenomenology and the Cognitive Sciences, 2013) plea for neural representationalism is the focus of a recent contribution to Phenomenology and Cognitive Science by Daniel D. Hutto and Erik Myin. In that paper, Hutto and Myin have tried to show that my arguments fail badly. Here, I want to respond to their critique clarifying the type of neural representationalism put forward in my (Phenomenology and the Cognitive Sciences, 2013) piece, and to take the opportunity to make a few remarks of (...) general interest concerning what Hutto and Myin have dubbed “the Hard Problem of Content.”. (shrink)

In this paper, we examine what is to be said in defence of Machamer, Darden and Craver’s (MDC) controversial dualism about activities and entities (Machamer, Darden and Craver’s in Philos Sci 67:1–25, 2000). We explain why we believe the notion of an activity to be a novel, valuable one, and set about clearing away some initial objections that can lead to its being brushed aside unexamined. We argue that substantive debate about ontology can only be effective when desiderata for an (...) ontology are explicitly articulated. We distinguish three such desiderata. The first is a more permissive descriptive ontology of science, the second a more reductive ontology prioritising understanding, and the third a more reductive ontology prioritising minimalism. We compare MDC’s entities-activities ontology to its closest rival, the entities-capacities ontology, and argue that the entities-activities ontology does better on all three desiderata. (shrink)

This paper addresses questions about how the levels of causality (generic and single-case causality) are related. One question is epistemological: can relationships at one level be evidence for relationships at the other level? We present three kinds of answer to this question, categorised according to whether inference is top-down, bottom-up, or the levels are independent. A second question is metaphysical: can relationships at one level be reduced to relationships at the other level? We present three kinds of answer to this (...) second question, categorised according to whether single-case relations are reduced to generic, generic relations are reduced to single-case, or the levels are independent. We then explore causal inference in autopsy. This is an interesting case study, we argue, because it refutes all three epistemologies and all three metaphysics. We close by sketching an account of causality that survives autopsy—the epistemic theory. (shrink)

Causal pluralism can be defended not only in respect to causal concepts and methodological guidelines, but also at the finer-grained level of causal inference from a particular source of evidence for causation. An argument for this last variety of pluralism is made based on an analysis of causal inference from randomized experiments (RCTs). Here, the causal interpretation of a statistically significant association can be established via multiple paths of reasoning, each relying on different assumptions and providing distinct elements of information (...) in favour of a causal interpretation. (shrink)

Philosophers of social science have emphasized mechanistic approaches to causal inquiry for some time now, showing why focusing on the mechanisms behind correlations is preferable to focusing on correlations alone (cf. Johnson 2006, Little 1991, Reiss 2007, 2009, Steel 2004, see also King, Keohane, and Verba 1994 for an example of purely correlational research). In Process Tracing: from Metaphor to Analytic Tool, political scientists Andrew Bennett and Jeffrey Checkel present a concrete method for finding evidence of causal mechanisms, process tracing. (...) Process tracers give evidence for causal relations in terms of the observable implications of the underlying causal mechanisms through which a putative cause affects some effect of interest. Such observable implications often take the form of a chain of events, or process, which connects cause and effect. Though Process Tracing contains applications of mechanistic reasoning unfamiliar to philosophers, and as such will be of interest to those working in the mechanist tradition, Bennett and Checkel’s own discussion of the philosophical foundations of process tracing is limited. The reader will have to delve deep into the volume’s contributed chapters for links between the literature on causation and this new method. (shrink)

Thought experiments de facto play many different roles in biology: economical, ethical, technical and so forth. This paper, however, is interested in whether there are any distinctive features of biological TEs as such. The question may be settled in the affirmative because TEs in biology have a function that is intimately connected with the epistemological and methodological status of biology. Peculiar to TEs in biology is the fact that the reflexive, typically human concept of finality may be profitably employed to (...) discover mechanical-experimental causal relations in all living beings—with the obvious caveat that we do not hypostatise and interpret this concept as an ontological quality, since this would land one in an implicitly animistic, pre-Galilean view of nature. From a methodical point of view, the concept of finality is an essential assumption as well as a powerful heuristic tool in the practice of biology, that is, in the investigation of living beings in an intersubjectively testable and reproducible way. (shrink)

According to Woodward’s influential account of explanation, explanations have a counterfactual structure, and explanatory counterfactuals are analysed in terms of causal relations and interventions. In this paper, we provide a formal semantics of explanatory counterfactuals based on a Ramsey Test semantics of conditionals. Like Woodward’s account, our account is guided by causal considerations. Unlike Woodward’s account, it makes no reference to causal graphs and it also covers cases of explanation where interventions are impossible.

Resurgent interest in both mechanistic and counterfactual theories of explanation has led to a fair amount of discussion regarding the relative merits of these two approaches. James Woodward is currently the pre-eminent counterfactual theorist, and he criticizes the mechanists on the following grounds: Unless mechanists about explanation invoke counterfactuals, they cannot make sense of claims about causal interactions between mechanism parts or of causal explanations put forward absent knowledge of productive mechanisms. He claims that these shortfalls can be offset if (...) mechanists will just borrow key tenets of his counterfactual theory of causal claims. What mechanists must bear in mind, however, is that by pursuing this course they risk both the assimilation of the mechanistic theories of explanation into Woodward’s own favored counterfactual theory, and they risk the marginalization of mechanistic explanations to a proper subset of all explanations. An outcome more favorable to mechanists might be had by pursuing an actualist-mechanist theory of the contents of causal claims. While it may not seem obvious at first blush that such an approach is workable, even in principle, recent empirical research into causal perception, causal belief, and mechanical reasoning provides some grounds for optimism. (shrink)

In this paper I offer an anti-Humean critique to Williamson and Russo’s approach to medical mechanisms. I focus on one of the specific claims made by Williamson and Russo, namely the claim that micro-structural ‘mechanisms’ provide evidence for the stability across populations of causal relationships ascertained at the (macro-) level of (test) populations. This claim is grounded in the epistemic account of causality developed by Williamson, an account which—while not relying exclusively on mechanistic evidence for justifying causal judgements—appeals nevertheless to (...) mechanisms, and rejects their anti-Humean interpretation in terms of capacities, powers, potencies, etc. By using (and expanding on) Cartwright’s basic critique against Humean mechanisms, I suggest that, in order to move beyond the level of plausibility, Williamson and Russo’s position is in need of a clarification as to the occurent reading of the components, functioning and interferences of mechanisms. Relatedly, as concerns Williamson’s epistemic account of causation, I argue that this account is in need of a more straightforward answer as to what truth-makers its causal claims should have. (shrink)

Accounts of ontic explanation have often been devised so as to provide an understanding of mechanism and of causation. Ontic accounts differ quite radically in their ontologies, and one of the latest additions to this tradition proposed by Peter Machamer, Lindley Darden and Carl Craver reintroduces the concept of activity. In this paper I ask whether this influential and activity-based account of mechanisms is viable as an ontic account. I focus on polygenic scenarios—scenarios in which the causal truths depend on (...) more than one cause. The importance of polygenic causation was noticed early on by Mill (1893). It has since been shown to be a problem for both causal-law approaches to causation (Cartwright 1983) and accounts of causation cast in terms of capacities (Dupré 1993; Glennan 1997, pp. 605-626). However, whereas mechanistic accounts seem to be attractive precisely because they promise to handle complicated causal scenarios, polygenic causation needs to be examined more thoroughly in the emerging literature on activity-based mechanisms. The activity-based account proposed in Machamer et al. (2000, pp. 1-25) is problematic as an ontic account, I will argue. It seems necessary to ask, of any ontic account, how well it performs in causal situations where—at the explanandum level of mechanism—no activity occurs. In addition, it should be asked how well the activity-based account performs in situations where there are too few activities around to match the polygenic causal origin of the explanandum. The first situation presents an explanandum-problem and the second situation presents an explanans-problem—I will argue—both of which threaten activity-based frameworks. (shrink)

Here I consider the relative merits of two recent models of explanation, James Woodward's interventionist-counterfactual model and the model model. According to the former, explanations are largely constituted by information about the consequences of counterfactual interventions. Problems arise for this approach because countless relevant interventions are possible in most cases and because it overlooks other kinds of equally relevant information. According the model model, explanations are largely constituted by cognitive models of actual mechanisms. On this approach, explanations tend not to (...) represent any of the aforementioned information explicitly but can instead be used to produce it on demand. The model model thus offers the more plausible account of the information of which we are aware when we have an explanation and of the ratiocinative process through which we derive many kinds of information that are relevant to the evaluation of explanations. (shrink)

An important strategy in the discovery of biological mechanisms involves the piecing together of experimental results from interventions. However, if mechanisms are investigated by means of ideal interventions, as defined by James Woodward and others, then the kind of information revealed is insufficient to discriminate between modular and non-modular causal contributions. Ideal interventions suffice for constructing webs of causal dependencies that can be used to make some predictions about experimental outcomes, but tell us little about how causally relevant factors are (...) organized together and how they interact with each other in order to produce a phenomenon. I argue that lab research relies on more elaborated types of interventions targeting in a controlled fashion multiple variables at the same time in order to probe the temporal organization of causally-relevant factors along distinct causal pathways and to test for non-modular interaction effects, thus providing crucial spatial-temporal constraints guiding the formulation of more detailed mechanistic explanations. (shrink)

Ever since Wesley Salmon’s theory, the mechanical approach to causality has found an increasing number of supporters who have developed it in different directions. Mechanical views such as those advanced by Stuart Glennan, Jim Bogen and Peter Machamer, Lindley Darden and Carl Craver have met with broad consensus in recent years. This paper analyses the main features of these mechanical positions and some of the major problems they still face, referring to the latest debate on mechanisms, causal explanation and the (...) relationship between mechanisms and counterfactuals. I shall claim that the mechanical approach can be recognised as having a fundamental explanatory power, whereas the counterfactual approach, recently developed mainly by Jim Woodward and essentially linked to the notion of intervention, has an important heuristic role. Claiming that mechanisms are by no means to be seen as parasitic on counterfactuals or less fundamental than them – as it has been recently suggested –, and that yet counterfactuals can play a part in a conceptual analysis of causation, I shall look for hints in support of the peaceful coexistence of the two. (shrink)

Mechanism realists assert the existence of mechanisms as objective structures in the world, but their exact metaphysical commitments are unclear. We introduce Local Hierarchy Realism (LHR) as a substantive and plausible form of mechanism realism. The limits of LHR reveal a deep tension between two aspects of mechanists’ explanatory strategy. Functional decomposition identifies locally relevant entities and activities, while these same entities and activities are also embedded in a nested hierarchy of levels. In principle, a functional decomposition may identify entities (...) engaging in causal interactions that crosscut the hierarchical structure of composition relations, violating the mechanist’s injunction against interlevel causation. We argue that this possibility is realized in the example of ephaptic coupling, a subsidiary process of neural computation that crosscuts the hierarchy derived from synaptic transmission. These considerations undermine the plausibility of LHR as a general view, yet LHR has the advantages that (i) its metaphysical implications are precisely stateable; (ii) the structure it identifies is not reducible to mere aggregate causation; and (iii) it clearly satisfies intuitive and informal definitions of mechanism. We conclude by assessing the prospects for a form of mechanism realism weaker than LHR that nevertheless satisfies all three of these requirements. (shrink)

In this essay the authors explore the nature of efficient causal explanation in Newton’s "Principia and The Opticks". It is argued that: (1) In the dynamical explanations of the Principia, Newton treats the phenomena under study as cases of Hall’s second kind of atypical causation. The underlying concept of causation is therefore a purely interventionist one. (2) In the descriptions of his optical experiments, Newton treats the phenomena under study as cases of Hall’s typical causation. The underlying concept of causation (...) is therefore a mixed interventionist/mechanicist one. (shrink)

I argue that difference-making should be a crucial element for evaluating the quality of evidence for mechanisms, especially with respect to the robustness of mechanisms, and that it should take central stage when it comes to the general role played by mechanisms in establishing causal claims in medicine. The difference- making of mechanisms should provide additional compelling reasons to accept the gist of Russo-Williamson thesis and include mechanisms in the protocols for Evidence- Based Medicine (EBM), as the EBM+ research group (...) has been advocating. (shrink)

Mechanism is undoubtedly a causal concept, in the sense that ordinary definitions and philosophical analyses explicate the concept in terms of other causal concepts such as production and interaction. Given this fact, many philosophers have supposed that analyses of the concept of mechanism, while they might appeal to philosophical theories about the nature of causation, could do little to inform such theories. On the other hand, methods of causal inference and explanation appeal to mechanisms. Discovering a mechanism is the gold (...) standard for establishing and explaining causal connections. This fact suggests that it might be possible to provide an analysis of causation that appeals to mechanisms. (shrink)

Despite the miraculous progress of science—it’s practitioners continue to run into mistakes, either discrediting research unduly or making leaps of causal inference where none are warranted. In this we isolate two of the reasons for such behavior involving the misplaced understanding of the role of mechanisms and mechanistic knowledge in the establishment of cause-effect relationships. We differentiate causal knowledge into causes, effects, mechanisms, cause-effect relationships, and causal stories. Failing to understand the role of mechanisms in this picture, including their absence (...) of knowledge or incorrect specification, leads to errors of wrongly excluding cause-effect relationships or wrongly inferring their existence. We highlight the primary of causality over mechanistic knowledge and causal stories in scientific reasoning. (shrink)