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)

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)

This paper sets out to analyze how causation works by focusing on biology, as represented by epidemiology and by scientific information on how the body works (“physiology”). It starts by exploring the specificity of evolved physiological systems, in which evolutionary, developmental and proximal causes all fit together, and the concept of function is meaningful; in contrast, this structure does not apply in epidemiology (or outside biology). Using these two contrasting branches of biology, I examine the role both of mechanism and (...) of difference making in causation. I find that causation necessarily involves both mechanism and difference making, and that they play complementary roles. Both are seen as ontologically necessary, even if the evidence is not always available for both. Influential monist accounts that focus on one of these, at the expense of ignoring the other, are found to be inadequate on these and on other grounds. Recent attempts to combine them are reviewed, notably that of Russo and Williamson (Int Stud Philos Sci 21:157–170, 2007), and it is argued that their epistemic view requires there to be a source of the different types of evidence that a rational agent would consider, and that this source must be ontic. I then analyze how causal relationships work in evolved physiological systems and in those studied by epidemiology, with a particular focus on how mechanism interacts with input. Finally, I consider this concept of causation from the perspective of everyday language, and of its possible generalisability outside biology. (shrink)

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.

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)

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)

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)

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)

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)

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)

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 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)

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)

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)

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)

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)

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)

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)

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)

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)