The first part of this paper argues that if Craver’s ([2007a], [2007b]) popular mutual manipulability account (MM) of mechanistic constitution is embedded within Woodward’s ([2003]) interventionist theory of causation--for which it is explicitly designed--it either undermines the mechanistic research paradigm by entailing that there do not exist relationships of constitutive relevance or it gives rise to the unwanted consequence that constitution is a form of causation. The second part shows how Woodward’s theory can be adapted in such a way that (...) (MM) neither undermines the mechanistic paradigm nor reduces constitution to causation. However, it turns out that this modified theoretical embedding of (MM) makes it impossible to produce empirical evidence for constitutive relations. The paper ends by suggesting an additional criterion, the fat-handedness criterion, which, when combined with (MM), generates indirect empirical evidence for constitutive relevance. (shrink)

Examples from the sciences showing that mechanisms do not always succeed in producing the phenomena for which they are responsible have led some authors to conclude that the regularity requirement can be eliminated from characterizations of mechanisms. In this article, I challenge this conclusion and argue that a minimal form of regularity is inextricably embedded in examples of elucidated mechanisms that have been shown to be causally responsible for phenomena. Examples of mechanistic explanations from the sciences involve mechanisms that have (...) been shown to produce phenomena with a reproducible rate of success. By contrast, if phenomena are infrequent to the point that they amount to irreproducible observations and experimental results, they are indistinguishable from the background noise of accidental happenings. The inability to detect or measure the phenomenon of interest against the background noise of accidental correlations makes it impossible to elucidate a mechanism by experimental means, to demonstrate that a proposed mechanism actually produces the phenomenon, and ultimately to justify why a hypothetical scenario involving an irregular mechanism should be preferred over attributing irreproducible happenings to chance. (shrink)

This paper discusses the important paper by Paul Thagard on the pathway version of mechanistic explanation that is currently used in chemical explanation. The author claims that this method of explanation has a respectable pedigree and can be traced back to the Chemical Revolution in the arguments used by the Lavoisier School in their theoretical duels with Richard Kirwan, the proponent of a revised phlogistonian theory. Kirwan believed that complex chemical reactions could be explained by recourse to affinity tables that (...) catalogued the attraction that various simple bodies possessed towards each other. To explain was in effect to make a delayed prediction, it is not enough just to show how a phenomenon fits into the discernible patterns of the world. Lavoisier, Fourcroy and their colleagues used pathway reasoning, although disguising this fact by suggesting that affinities varied when subjected to n-body situations. (shrink)

The goal of this paper is to present and defend an empiricist, neo-Hempelian account of scientific explanation as ampliative, specialized embedding. The proposal aims to preserve what I take to be the core of Hempel’s empiricist account, by weakening it in some respects and strengthening it in others, introducing two new conditions that solve most of Hempel’s problems without abandoning his empiricist strictures. According to this proposal, to explain a phenomenon is to make it expectable by introducing new conceptual/ontological machinery (...) and using special, and non-ad hoc, non-accidental regularities. The new conditions are elaborated making essential use of two central structuralist ideas, namely T-theoreticity and specialization. I first introduce and qualify the project, then present the new account in detail and assess it vis-à-vis its rivals, and finally discuss some possible objections, concluding that the account fares better than its monistic rivals and well enough to qualify as a promising neo-Hempelian account. Even for those unpersuaded by its monistic goals, it has the merit of calling attention to two new necessary conditions not explicitly emphasized thus far and showing how they serve to answer many of the criticisms addressed against Hempel’s account. (shrink)

A critical review of Frans de Waal's book on evolution of morality (Frans de Waal, Primates and Philosophers: How Morality Evolved, Princeton, NJ: Princeton University Press, 2006).

Although “theory” has been the prevalent unit of analysis in the meta-study of science throughout most of the twentieth century, the concept remains elusive. I further explore the leitmotiv of several authors in this issue: that we should deal with theorizing (rather than theory) in biology as a cognitive activity that is to be investigated naturalistically. I first contrast how philosophers and biologists have tended to think about theory in the last century or so, and consider recent calls to upgrade (...) the role of theory in the life sciences against the background of the recent “data deluge” in molecular biology, systems biology, etc. I then review thinking about theory in biology in relation to physical theory as a positive or negative exemplar. I conclude by discussing various aspects of a positive program for “naturalizing theorizing.”. (shrink)

Mechanistic philosophy of science views a large part of scientific activity as engaged in modelling mechanisms. While science textbooks tend to offer qualitative models of mechanisms, there is increasing demand for models from which one can draw quantitative predictions and explanations. Casini et al. (Theoria 26(1):5–33, 2011) put forward the Recursive Bayesian Networks (RBN) formalism as well suited to this end. The RBN formalism is an extension of the standard Bayesian net formalism, an extension that allows for modelling the hierarchical (...) nature of mechanisms. Like the standard Bayesian net formalism, it models causal relationships using directed acyclic graphs. Given this appeal to acyclicity, causal cycles pose a prima facie problem for the RBN approach. This paper argues that the problem is a significant one given the ubiquity of causal cycles in mechanisms, but that the problem can be solved by combining two sorts of solution strategy in a judicious way. (shrink)

The current antireductionist consensus rests in part on the indefensibility of the deductive-nomological model of explanation, on which classical reductionism depends. I argue that the DN model is inessential to the reductionist program and that mechanism provides a better framework for thinking about reductionism. This runs counter to the contemporary mechanists’ claim that mechanism is an alternative to reductionism. I demonstrate that mechanists are committed to reductionism, as evidenced by the historical roots of the contemporary mechanist program. This view shares (...) certain core commitments with reductionism. It is these shared commitments that constitute the essential elements of the reductionist program. (shrink)

This chapter provides an introduction to the study of the philosophical notions of mechanisms and causality in biology and economics. This chapter sets the stage for this volume, Mechanism and Causality in Biology and Economics, in three ways. First, it gives a broad review of the recent changes and current state of the study of mechanisms and causality in the philosophy of science. Second, consistent with a recent trend in the philosophy of science to focus on scientific practices, it in (...) turn implies the importance of studying the scientific methods employed by researchers. Finally, by way of providing an overview of each chapter in the volume, this chapter demonstrates that biology and economics are two fertile fields for the philosophy of science and shows how biological and economic mechanisms and causality can be synthesized. (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)

The mechanistic and causal accounts of explanation are often conflated to yield a ‘causal-mechanical’ account. This paper prizes them apart and asks: if the mechanistic account is correct, how can causal explanations be explanatory? The answer to this question varies according to how causality itself is understood. It is argued that difference-making, mechanistic, dualist and inferentialist accounts of causality all struggle to yield explanatory causal explanations, but that an epistemic account of causality is more promising in this regard.

Proponents of evidence-based medicine and some philosophers of science seem to agree that knowledge of mechanisms can help solve the problem of applying results of controlled studies to target populations (‘the problem of extrapolation’). We describe the problem of extrapolation, characterize mechanisms, and outline how mechanistic knowledge might be used to solve the problem. Our main thesis is that there are four often overlooked problems with using mechanistic knowledge to solve the problem of extrapolation. First, our understanding of mechanisms is (...) often (and arguably, likely to remain) incomplete. Secondly, knowledge of mechanisms is not always applicable outside the tightly controlled laboratory conditions in which it is gained. Thirdly, mechanisms can behave paradoxically. Fourthly, as Daniel Steel points out, using mechanistic knowledge faces the problem of the ‘extrapolator’s circle’. At the same time, when the problems with mechanistic knowledge have been addressed, such knowledge can and should be used to mitigate (nothing can entirely solve) the problem of extrapolation. (shrink)

En este trabajo me propongo desarrollar un estudio crítico de la concepción mecanicista de la explicación científica. En primer lugar, argumento que la caracterización mecanicista de los modelos fenoménicos (no explicativos) es inadecuada, pues no ofrece un análisis aceptable de los conceptos de modelo científico y similitud, que son fundamentales para la propuesta. En segundo lugar, sostengo que la caracterización de los modelos mecanicistas (explicativos) es igualmente inadecuada, pues los análisis disponibles de la relación explicativa de relevancia constitutiva implican una (...) tesis metafísica que es rechazada por los mismos mecanicistas. Concluyo que el mecanicismo no ofrece todavía una elucidación aceptable de la explicación científica. In this paper, I offer a critical assessment of the mechanicist approach to scientific explanation. Firstly, I argue that the mechanicist characterization of (non explanatory) phenomenological models is inadequate, since it does not develop an explication of the concepts of scientific model and similarity, which are indispensable to the approach. Secondly, I claim that the mechanicist conception of (explanatory) mechanicist models is inadequate as well, since all the available analices of the explanatory relation of constitutive relevance imply a metaphysical thesis that is rejected by the mechanicists themselves. I conclude that mechanicism needs to be emended if it aims to be considered as a genuinely illuminating approach to scientific explanation. (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 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.

I argue that examining the explanatory power of the hypothesis of extended cognition (HEC) offers a fruitful approach to the problem of cognitive system demarcation. Although in the discussions on HEC it has become common to refer to considerations of explanatory power as a means for assessing the plausibility of the extended cognition approach, to date no satisfying account of explanatory power has been presented in the literature. I suggest that the currently most prominent theory of explanation in the special (...) sciences, James Woodward’s contrastive-counterfactual theory, and an account of explanatory virtues building on that theory can be used to develop a systematic picture of cognitive system demarcation in the psychological sciences. A major difference between my differential influence (DI) account and most other theories of cognitive extension is the cognitive systems pluralism implied by my approach. By examining the explanatory power of competing traditions in psychological memory research, I conclude that internalist and externalist classificatory strategies are characterized by different profiles of explanatory virtues and should often be considered as complementary rather than competing approaches. This suggests a deflationary interpretation of HEC. (shrink)

Mechanisms are often characterized as causal structures and the interventionist account of causation is then used to characterize what it is to be a causal structure. The associated modularity constraint on causal structures has evoked criticism against using the theory as an account of mechanisms, since many mechanisms seem to violate modularity. This paper answers to this criticism by making a distinction between a causal system and a causal structure. It makes sense to ask what the modularity properties of a (...) given causal structure are, but not whether a causal system is modular tout court. The counter-examples to the interventionist account are systems in which a particular structure is modular in variables, but not in parameters. A failure of parameter-modularity does not by itself threaten the interventionist interpretation of the structure and the possibility of causally explaining with that structure, but it does mean that knowledge of the structure is not sufficient to constitutively explain system-level properties of the embedding system. (shrink)

Part I of this paper introduces a range of mechanistic theories of causality, including process theories and the complex-systems theories, and some of the problems they face. Part II argues that while there is a decisive case against a purely mechanistic analysis, a viable theory of causality must incorporate mechanisms as an ingredient, and describes one way of providing an analysis of causality which reaps the rewards of the mechanistic approach without succumbing to its pitfalls.

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 essay is concerned with concentrations of entities, which play an important—albeit often overlooked—role in scientific explanation. First, I discuss an example from molecular biology to show that concentrations can play an irreducible causal role. Second, I provide a preliminary philosophical analysis of this causal role, suggesting some implications for extant theories of causation. I conclude by introducing the concept of causation by concentration, a form of statistical causation whose widespread presence throughout the sciences has been unduly neglected and which (...) deserves to be studied in more depth. 1 Introduction2 Solving Lillie's Paradox: Lysogenic Induction in Phage λ3 Repressor Concentration and the Tuning of the Switch4 Concentration and Causality5 Preemption in Concentrations: Analysis and Implications6 Causation by Concentration: General Definition, Refinements, and Further Applications. (shrink)

In this paper we argue that in recent literature on mechanistic explanations, authors tend to conflate two distinct features that mechanistic models can have or fail to have: plausibility and richness. By plausibility, we mean the probability that a model is correct in the assertions it makes regarding the parts and operations of the mechanism, i.e., that the model is correct as a description of the actual mechanism. By richness, we mean the amount of detail the model gives about the (...) actual mechanism. First, we argue that there is at least a conceptual reason to keep these two features distinct, since they can vary independently from each other: models can be highly plausible while providing almost no details, while they can also be highly detailed but plainly wrong. Next, focusing on Craver's continuum of ?how-possibly,? to ?how-plausibly,? to ?how-actually? models, we argue that the conflation of plausibility and richness is harmful to the discussion because it leads to the view that both are necessary for a model to have explanatory power, while in fact, richness is only so with respect to a mechanism's activities, not its entities. This point is illustrated with two examples of functional models. (shrink)

This paper provides an account of the experimental conditions required for establishing whether correlating or causally relevant factors are constitutive components of a mechanism connecting input (start) and output (finish) conditions. I argue that two-variable experiments, where both the initial conditions and a component postulated by the mechanism are simultaneously manipulated on an independent basis, are usually required in order to differentiate between correlating or causally relevant factors and constitutively relevant ones. Based on a typical research project molecular biology, a (...) flowchart model detailing typical stages in the formulation and testing of hypotheses about mechanistic components is also developed. (shrink)

This article addresses the question of whether we should conceive of mechanisms as productive of change in a regular way. I argue that, if mechanisms are characterized as fully regular, on the one hand, then not enough processes will count as mechanisms for them to be interesting or useful. If no appeal to regularity is made at all in their characterization, on the other hand, then mechanisms can no longer be useful for grounding prediction and supporting intervention strategies. I conclude (...) that, if the New Mechanistic Philosophy is to be successful, a stochastic characterization of mechanisms must be adopted. (shrink)

Instances of negative causation—preventions, omissions, and the like—have long created philosophical worries. In this paper, I argue that concerns about negative causation can be addressed in the context of causal explanation generally, and mechanistic explanation specifically. The gravest concern about negative causation is that it exacerbates the problem of causal promiscuity—that is, the problem that arises when a particular account of causation identifies too many causes for a particular effect. In the explanatory context, the problem of promiscuity can be solved (...) by characterizing the phenomenon to be explained as a contrast between two or more events or non-events. This contrastive strategy also can solve other problems that negative causation presents for the leading accounts of mechanistic explanation. Along the way, I argue that to be effective, accounts of causal explanation must incorporate negative causation. I also develop a taxonomy of negative causation and incorporate each variety of negative causation into the leading accounts of mechanistic explanation. (shrink)

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)

This paper is about mechanisms and models, and how they interact. In part, it is a response to recent discussion in philosophy of biology regarding whether natural selection is a mechanism. We suggest that this debate is indicative of a more general problem that occurs when scientists produce mechanistic models of populations and their behaviour. We can make sense of claims that there are mechanisms that drive population-level phenomena such as macroeconomics, natural selection, ecology, and epidemiology. But talk of mechanisms (...) and mechanistic explanation evokes objects with well-defined and localisable parts which interact in discrete ways, while models of populations include parts and interactions that are neither local nor discrete in any actual populations. This apparent tension can be resolved by carefully distinguishing between the properties of a model and those of the system it represents. To this end, we provide an analysis that recognises the flexible relationship between a mechanistic model and its target system. In turn, this reveals a surprising feature of mechanistic representation and explanation: it can occur even when there is a mismatch between the mechanism of the model and that of its target. Our analysis reframes the debate, providing an alternative way to interpret scientists’ mechanism-talk , which initially motivated the issue. We suggest that the relevant question is not whether any population-level phenomenon such as natural selection is a mechanism, but whether it can be usefully modelled as though it were a particular type of mechanism. (shrink)

We contrast reactive and endogenously active perspectives on brain activity. Both have been pursued continuously in neurophysiology laboratories since the early 20thcentury, but the endogenous perspective has received relatively little attention until recently. One of the many successes of the reactive perspective was the identification, in the second half of the 20th century, of the distinctive contributions of different brain regions involved in visual processing. The recent prominence of the endogenous perspective is due to new findings of ongoing oscillatory activity (...) in the brain at a wide range of time scales, exploiting such techniques as single-cell recording, EEG, and fMRI. We recount some of the evidence pointing to ways in which this endogenous activity is relevant to cognition and behavior. Our major objective is to consider certain implications of the contrast between the reactive and endogenous perspectives. In particular, we relate these perspectives to two different characterizations of explanation in the new mechanistic philosophy of science. In a basic mechanistic explanation, the operations of a mechanism are characterized qualitatively and as functioning sequentially until a terminating condition is realized. In contrast, a dynamic mechanistic explanation allows for non-sequential organization and emphasizes quantitative modeling of the mechanisms's behavior. For example, with appropriate parameter values a set of differential equations can be used to demonstrate ongoing oscillations in a system organized with feedback loops. We conclude that the basic conception of mechanistic explanation is adequate for reactive accounts of brain activity, but dynamical accounts are required to explain sustained, endogenous activity. (shrink)

The concept of technical function is a key concept to describe technical artifacts and artifacts-to-be-designed. Engineers often give such descriptions in terms of functional decomposition models, which represent relationships between functions and sets of other functions. Despite the importance of the concept of function there is no consensus among engineers about its meaning. Models of functional decomposition are likewise conceptually divergent. Although this conceptual diversity hampers information exchange between engineers, they accept and maintain it. Engineers do not, by and large, (...) engage in a focused debate to establish commonly shared functional conceptualizations. This contrasts with science where both debates on the adequacy of key conceptualizations and convergence toward shared conceptualizations are common. This book investigates the side-by-side usage of different functional decomposition models in engineering. It explains this phenomenon by applying and extending the analysis of theory choice in terms of methodological incommensurability to engineering functional decomposition, rather than to science. This analysis shows that engineers’ usage of competing functional decomposition models is rational from a practical point of view. This book furthermore investigates the communication problems that the side-by-side usage of different models engenders and presents a strategy that supports the exchange and re-use of functional information between engineers. (shrink)

My topic is the confluence of two recently active philosophical research programs. One research program concerns the metaphysics of realization. The other research program concerns scientific explanation in terms of mechanisms. In this paper I introduce a distinction between descriptive and explanatory approaches to realization. I then use this distinction to argue that a well-known account of realization, due to Carl Gillett, is incompatible with a well-known account of mechanistic explanation, due to Peter Machamer, Lindley Darden, and Carl Craver (MDC, (...) Philos Sci 57: 1-25, 2000). This is surprising, not least of which because Gillett has cited MDC's work as evidence that his account of realization is the right way to think about realization in the sciences. (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)

James Woodward offers a conception of explanation and mechanism in terms of interventionist counterfactuals. Based on a case from ecology, I show that ecologists’ approach to that case satisfies Woodward’s conditions for explanation and mechanism, but his conception does not fully capture what ecologists view as explanatory. The new mechanistic philosophy likewise aims to describe central aspects of mechanisms, but I show that it is not sufficient to account for ecological mechanisms. I argue that in ecology explanation involves identification of (...) invariant and insensitive causal relationships and descriptions of the mechanistic characteristics that make these relations possible. †To contact the author, please write to: Department of Philosophy, University of Dayton, 300 College Park, Dayton, OH 45469‐1546; e‐mail: [email protected]. (shrink)

Laws in the special sciences are usually regarded to be non-universal. A theory of laws in the special sciences faces two challenges. (I) According to Lange's dilemma, laws in the special sciences are either false or trivially true. (II) They have to meet the ?requirement of relevance?, which is a way to require the non-accidentality of special science laws. I argue that both challenges can be met if one distinguishes four dimensions of (non-) universality. The upshot is that I argue (...) for the following explication of special science laws: L is a special science law just if (1) L is a system law, (2) L is quasi-Newtonian, and (3) L is minimally invariant. (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)

Philosophers of science have developed an account of causal-mechanical explanation that captures regularity, but this account neglects variation. In this article I amend the philosophy of mechanisms to capture variation. The task is to explicate the relationship between regular causal mechanisms responsible for individual development and causes of variation responsible for variation in populations. As it turns out, disputes over this relationship have rested at the heart of the nature–nurture debate. Thus, an explication of the relationship between regular causal mechanisms (...) and causes of variation and between individual development and variation offers both the necessary amendment to the philosophy of mechanisms and the resources to mediate the dispute. (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)

Scientists of many disciplines use theoretical models to explain and predict the dynamics of the world. They often have to rely on digital computer simulations to draw predictions fromthe model. But to deliver phenomenologically adequate results, simulations deviate from the assumptions of the theoretical model. Therefore the role of simulations in scientific explanation demands itself an explanation. This paper analyzes the relation between real-world system, theoretical model, and simulation. It is argued that simulations do not explain processes in the real (...) world directly. The way in which simulations help explaining real-world processes is conceived as indirect, mediated by the theoretical model. Simulacra are characterized further, and turn out to be a priori measurable. This gives a clue to a better understanding of the epistemic role of computer simulations in scientific research. (shrink)

In 1747, James Lind carried out an experiment which proved the usefulness of citrus fruit as a cure for scurvy. Nonetheless, he rejected the earlier hypothesis of Bachstrom that the absence of fresh fruit and vegetables was the only cause of the disease. I explain why it was rational for James Lind not to accept Bachstrom’s explanation. I argue that it was the urge for scientific understanding that guided Lind in his rejection and in the development of his alternative theory (...) that humidity was the primary cause of the disease. Central in this process was the search for causal mechanisms which could provide understanding of how the disease developed and which fitted in with the knowledge of the time. Given that the relevant background knowledge and statistical methods were not yet available to Lind, he was right to prefer his own explanation to that of Bachstrom. Although his explanation turned out to be wrong, and Bachstrom’s right, from a historical point of view it offered deeper causal understanding of both the development of the disease and the preventive and curative effects of fresh vegetable food. This case study illustrates how the search for causal mechanisms can not only be enlightening, but also very misleading. (shrink)

Abell, Felin and Foss argue that "macro-explanations" in strategic management, explanations in which organizational routines figure prominently and in which both the explanandum and explanans are at the macro-level, are necessarily incomplete. They take a diagram (which has the form of a trapezoid) from Coleman, Foundations of Social Theory, The Belknap Press of Harvard University Press, Cambridge (Mass.)/London, (1990) to task to show that causal chains connecting two macro-phenomena always involve "macro-to-micro" and "micro-tomacro" links, links that macro-explanations allegedly fail to (...) recognize. Their plea for micro-foundations in strategic management is meant to shed light on these "missing links". The paper argues that while there are good reasons for providing micro-foundations, Abell, Felin and Foss's causal incompleteness argument is not one of them. Their argument does not sufficiently distinguish between causal and constitutive relations. Once these relations are carefully distinguished, it follows that Coleman's diagram has to be squared. This in turn allows us to see that macroexplanations need not be incomplete. (shrink)

Cybernetics promoted machine-supported investigations of adaptive sensorimotor behaviours observed in biological systems. This methodological approach receives renewed attention in contemporary robotics, cognitive ethology, and the cognitive neurosciences. Its distinctive features concern machine experiments, and their role in testing behavioural models and explanations flowing from them. Cybernetic explanations of behavioural events, regularities, and capacities rely on multiply realizable mechanism schemata, and strike a sensible balance between causal and unifying constraints. The multiple realizability of cybernetic mechanism schemata paves the way to principled (...) comparisons between biological systems and machines. Various methodological issues involved in the transition from mechanism schemata to their machine instantiations are addressed here, by reference to a simple sensorimotor coordination task. These concern the proper treatment of ceteris paribus clauses in experimental settings, the significance of running experiments with correct but incomplete machine instantiations of mechanism schemata, and the advantage of operating with real machines ??? as opposed to simulated ones ??? immersed in real environments. (shrink)

In the increasing body of metatheoretical literature on "causal mechanisms," definitions of "mechanism" proliferate, and these increasingly divergent definitions reproduce older theoretical and methodological oppositions. The reason for this proliferation is the incompatibility of the various metatheoretical expectations directed to them: (1) to serve as an alternative to the scientific theory of individual behavior (for some social theorists, most notably Jon Elster); (2) to provide solutions for causal inference problems in the quantitative social sciences, in social history, and in the (...) (3) qualitative research context; and (4) to serve as an alternative for narratives (Charles Tilly). Mechanisms can do (1) only as under-specified law-like regularities, deliver (2) as robust generative processes represented by models, and accomplish (3) as fragile generative processes (stories), but these are not all compatible. (edited). (shrink)