After a decade of intense debate about mechanisms, there is still no consensus characterization. In this paper we argue for a characterization that applies widely to mechanisms across the sciences. We examine and defend our disagreements with the major current contenders for characterizations of mechanisms. Ultimately, we indicate that the major contenders can all sign up to our characterization.

According to one large family of views, scientific explanations explain a phenomenon (such as an event or a regularity) by subsuming it under a general representation, model, prototype, or schema (see Bechtel, W., & Abrahamsen, A. (2005). Explanation: A mechanist alternative. Studies in History and Philosophy of Biological and Biomedical Sciences, 36(2), 421–441; Churchland, P. M. (1989). A neurocomputational perspective: The nature of mind and the structure of science. Cambridge: MIT Press; Darden (2006); Hempel, C. G. (1965). Aspects of scientific (...) explanation. In C. G. Hempel (Ed.), Aspects of scientific explanation (pp. 331–496). New York: Free Press; Kitcher (1989); Machamer, P., Darden, L., & Craver, C. F. (2000). Thinking about mechanisms. Philosophy of Science, 67(1), 1–25). My concern is with the minimal suggestion that an adequate philosophical theory of scientific explanation can limit its attention to the format or structure with which theories are represented. The representational subsumption view is a plausible hypothesis about the psychology of understanding. It is also a plausible claim about how scientists present their knowledge to the world. However, one cannot address the central questions for a philosophical theory of scientific explanation without turning one’s attention from the structure of representations to the basic commitments about the worldly structures that plausibly count as explanatory. A philosophical theory of scientific explanation should achieve two goals. The first is explanatory demarcation. It should show how explanation relates with other scientific achievements, such as control, description, measurement, prediction, and taxonomy. The second is explanatory normativity. It should say when putative explanations succeed and fail. One cannot achieve these goals without undertaking commitments about the kinds of ontic structures that plausibly count as explanatory. Representations convey explanatory information about a phenomenon when and only when they describe the ontic explanations for those phenomena. (shrink)

An adequate understanding of the ubiquitous practice of mechanistic explanation requires an account of what Craver termed “constitutive relevance.” Entities or activities are constitutively relevant to a phenomenon when they are parts of the mechanism responsible for that phenomenon. Craver’s mutual manipulability account extended Woodward’s account of manipulationist counterfactuals to analyze how interlevel experiments establish constitutive relevance. Critics of MM argue that applying Woodward’s account to this philosophical problem conflates causation and constitution, thus rendering the account incoherent. These criticisms, we (...) argue, arise from failing to distinguish the semantic, epistemic, and metaphysical aspects of the problem of constitutive relevance. In distinguishing these aspects of the problem and responding to these critics accordingly, we amend MM into a refined epistemic criterion, the “matched interlevel experiments” account. Further, we explain how this epistemological thesis is grounded in the plausible metaphysical thesis that constitutive relevance is causal betweenness. (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)

This paper offers an account of what it is for a physical system to be a computing mechanism—a system that performs computations. A computing mechanism is a mechanism whose function is to generate output strings from input strings and (possibly) internal states, in accordance with a general rule that applies to all relevant strings and depends on the input strings and (possibly) internal states for its application. This account is motivated by reasons endogenous to the philosophy of computing, namely, doing (...) justice to the practices of computer scientists and computability theorists. It is also an application of recent literature on mechanisms, because it assimilates computational explanation to mechanistic explanation. The account can be used to individuate computing mechanisms and the functions they compute and to taxonomize computing mechanisms based on their computing power. (shrink)

Philosophers of neuroscience have traditionally described interfield integration using reduction models. Such models describe formal inferential relations between theories at different levels. I argue against reduction and for a mechanistic model of interfield integration. According to the mechanistic model, different fields integrate their research by adding constraints on a multilevel description of a mechanism. Mechanistic integration may occur at a given level or in the effort to build a theory that oscillates among several levels. I develop this alternative model using (...) a putative exemplar of reduction in contemporary neuroscience: the relationship between the psychological phenomena of learning and memory and the electrophysiological phenomenon known as Long-Term Potentiation. A new look at this historical episode reveals the relative virtues of the mechanistic model over reduction as an account of interfield integration. (shrink)

This paper describes a pattern of explanation prevalent in the biological sciences that I call a ‘lineage explanation’. The aim of these explanations is to make plausible certain trajectories of change through phenotypic space. They do this by laying out a series of stages, where each stage shows how some mechanism worked, and the differences between each adjacent stage demonstrates how one mechanism, through minor modifications, could be changed into another. These explanations are important, for though it is widely accepted (...) that there is an ‘incremental constraint’ on evolutionary change, in an important class of cases it is difficult to see how to satisfy this constraint. I show that lineage explanations answer important questions about evolutionary change, but do so by demonstrating differences between individuals rather than invoking population processes, such as natural selection.1. Introduction2. Turning a ‘Scale’ into a ‘Plume’3. Lineage Explanations in Biology3.1. The evolution of eyes3.2. The evolution of feathers4. The Two Dimensions of a Lineage Explanation4.1. The production dimension4.2. The continuity dimension4.3. The dual role of the parts5. Constraining the Explanations6. Operational and Generative Lineages7. Explaining Change Without Populations8. Conclusion. (shrink)

Defending or attacking either functionalism or computationalism requires clarity on what they amount to and what evidence counts for or against them. My goal here is not to evaluate their plausibility. My goal is to formulate them and their relationship clearly enough that we can determine which type of evidence is relevant to them. I aim to dispel some sources of confusion that surround functionalism and computationalism, recruit recent philosophical work on mechanisms and computation to shed light on them, and (...) clarify how functionalism and computationalism may or may not legitimately come together. (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)

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)

General Process Theory (GPT) is a new (non-Whiteheadian) process ontology. According to GPT the domains of scientific inquiry and everyday practice consist of configurations of ‘goings-on’ or ‘dynamics’ that can be technically defined as concrete, dynamic, non-particular individuals called general processes. The paper offers a brief introduction to GPT in order to provide ontological foundations for research programs such as interactivism that centrally rely on the notions of ‘process,’ ‘interaction,’ and ‘emergence.’ I begin with an analysis of our common sense (...) concept of activities, which plays a crucial heuristic role in the development of the notion of a general process. General processes are not individuated in terms of their location but in terms of ‘what they do,’ i.e., in terms of their dynamic relationships in the basic sense of one process being part of another. The formal framework of GPT is thus an extensional mereology, albeit a non-classical theory with a non-transitive part-relation. After a brief sketch of basic notions and strategies of the GPT-framework I show how the latter may be applied to distinguish between causal, mechanistic, functional, self-maintaining, and recursively self-maintaining interactions, all of which involve ‘emergent phenomena’ in various senses of the term. (shrink)

A scientific explanatory project, part-whole explanation, and a kind of science, part-whole science are premised on identifying, investigating, and using parts and wholes. In the biological sciences, mechanistic, structuralist, and historical explanations are part-whole explanations. Each expresses different norms, explananda, and aims. Each is associated with a distinct partitioning frame for abstracting kinds of parts. These three explanatory projects can be complemented in order to provide an integrative vision of the whole system, as is shown for a detailed case study: (...) the tetrapod limb. My diagnosis of part-whole explanation in the biological sciences as well as in other domains exploring evolved, complex, and integrated systems (e.g., psychology and cognitive science) cross-cuts standard philosophical categories of explanation: causal explanation and explanation as unification. Part-whole explanation is itself one essential aspect of part-whole science. (shrink)

Mechanisms are said to consist of two kinds of components, entities and activities. In the first half of this chapter, I examine what entities and activities are, how they relate to well-known ontological categories, such as processes or dispositions, and how entities and activities relate to each other (e.g., can one be reduced to the other or are they mutually dependent?). The second part of this chapter analyzes different criteria for individuating the components of mechanisms and discusses how real the (...) boundaries of mechanisms are. (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 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)

In this article, I argue that depression and suicide are natural kinds insofar as they are classes of abnormal behavior underwritten by sets of stable biological mechanisms. In particular, depression and suicide are neurobiological kinds characterized by disturbances in serotonin functioning that affect various brain areas (i.e., the amygdala, anterior cingulate, prefrontal cortex, and hippocampus). The significance of this argument is that the natural (biological) basis of depression and suicide allows for reliable projectable inferences (i.e., predictions) to be made about (...) individual members of a kind. In the context of assisted suicide, inferences about the decision-making capacity of depressed individuals seeking physician-assisted suicide are of special interest. I examine evidence that depression can hamper the decision-making capacity of individuals seeking assisted suicide and discuss some implications. (shrink)

Philosophers have proposed various kinds of relations between Mendelian genetics and molecular biology: reduction, replacement, explanatory extension. This paper argues that the two fields are best characterized as investigating different, serially integrated, hereditary mechanisms. The mechanisms operate at different times and contain different working entities. The working entities of the mechanisms of Mendelian heredity are chromosomes, whose movements serve to segregate alleles and independently assort genes in different linkage groups. The working entities of numerous mechanisms of molecular biology are larger (...) and smaller segments of DNA plus related molecules. Discovery of molecular DNA mechanisms filled black boxes that were noted, but unilluminated, by Mendelian genetics. (shrink)

“Functional homology” appears regularly in different areas of biological research and yet it is apparently a contradiction in terms—homology concerns identity of structure regardless of form and function. I argue that despite this conceptual tension there is a legitimate conception of ‘homology of function’, which can be recovered by utilizing a distinction from pre-Darwinian physiology (use versus activity) to identify an appropriate meaning of ‘function’. This account is directly applicable to molecular developmental biology and shares a connection to the theme (...) of hierarchy in homology. I situate ‘homology of function’ within existing definitions and criteria for structural assessments of homology, and introduce a criterion of ‘organization’ for judging function homologues, which focuses on hierarchically interconnected interdependencies (similar to relative position and connection for skeletal elements in structural homology). This analysis of biological concepts has at least three broad philosophical consequences: (1) it provides the grounds for the study of behavior and psychological categories as homologues; (2) it demonstrates that philosophers who take selected effect function as primary effectively ignore large portions of comparative, structural, and experimental research, thereby misconstruing biological reasoning and knowledge; and, (3) it underwrites causal generalizations, which illuminates inferences made from model organisms in experimental biology. (shrink)

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)

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

Skipper and Millstein (2005) argued that existing conceptions of mechanisms failed to "get at" natural selection, but left open the possibility that a refined conception of mechanisms could resolve the problems that they identified. I respond to Skipper and Millstein, and argue that while many of their points have merit, their objections can be overcome and that natural selection can be characterized as a mechanism. In making this argument, I discuss the role of regularity in mechanisms, and develop an account (...) of stochastic (i.e., probabilistic) mechanisms. Explaining the phenomenon of adaptation through the mechanism of natural selection illustrates the power and flexibility of using mechanistic strategies to explain natural phenomena. (shrink)

Leuridan (2010) argued that mechanisms cannot provide a genuine alternative to laws of nature as a model of explanation in the sciences, and advocates Mitchell’s (1997) pragmatic account of laws. I first demonstrate that Leuridan gets the order of priority wrong between mechanisms, regularity, and laws, and then make some clarifying remarks about how laws and mechanisms relate to regularities. Mechanisms are not an explanatory alternative to regularities; they are an alternative to laws. The existence of stable regularities in nature (...) is necessary for either model of explanation: regularities are what laws describe and what mechanisms explain. (shrink)

In this paper, I propose two theses, and then examine what the consequences of those theses are for discussions of reduction and emergence. The first thesis is that what have traditionally been seen as robust, reductions of one theory or one branch of science by another more fundamental one are a largely a myth. Although there are such reductions in the physical sciences, they are quite rare, and depend on special requirements. In the biological sciences, these prima facie sweeping reductions (...) fade away, like the body of the famous Cheshire cat, leaving only a smile.... The second thesis is that the "smiles" are fragmentary patchy explanations, and though patchy and fragmentary, they are very important, potentially Nobel-prize winning advances. To get the best grasp of these "smiles," I want to argue that, we need to return to the roots of discussions and analyses of scientific explanation more generally, and not focus mainly on reduction models, though three conditions based on earlier reduction models are retained in the present analysis. I briefly review the scientific explanation literature as it relates to reduction, and then offer my account of explanation. The account of scientific explanation I present is one I have discussed before, but in this paper I try to simplify it, and characterize it as involving field elements and a preferred causal model system abbreviated as FE and PCMS. In an important sense, this FE and PCMS analysis locates an "explanation" in a typical scientific research article. This FE and PCMS account is illustrated using a recent set of neurogenetic papers on two kinds of worm foraging behaviors: solitary and social feeding. One of the preferred model systems from a 2002 Nature article in this set is used to exemplify the FE and PCMS analysis, which is shown to have both reductive and nonreductive aspects. The paper closes with a brief discussion of how this FE and PCMS approach differs from and is congruent with Bickle's "ruthless reductionism" and the recently revived mechanistic philosophy of science of Machamer, Darden, and Craver. (shrink)

Modeling mechanisms is central to the biological sciences – for purposes of explanation, prediction, extrapolation, and manipulation. A closer look at the philosophical literature reveals that mechanisms are predominantly modeled in a purely qualitative way. That is, mechanistic models are conceived of as representing how certain entities and activities are spatially and temporally organized so that they bring about the behavior of the mechanism in question. Although this adequately characterizes how mechanisms are represented in biology textbooks, contemporary biological research practice (...) shows the need for quantitative, probabilistic models of mechanisms, too. In this paper we argue that the formal framework of causal graph theory is well-suited to provide us with models of biological mechanisms that incorporate quantitative and probabilistic information. On the ba-sis of an example from contemporary biological practice, namely feedback regulation of fatty acid biosynthesis in Brassica napus, we show that causal graph theoretical models can account for feedback as well as for the multi-level character of mechanisms. However, we do not claim that causal graph theoretical representations of mechanisms are advantageous in all respects and should replace common qualitative models. Rather, we endorse the more balanced view that causal graph theoretical models of mechanisms are useful for some purposes, while being insufficient for others. (shrink)

A large part of the controversy surrounding the publication of DSM-5 stems from the possibility of replacing the purely descriptive approach to classification favored by the DSM since 1980. This paper examines the question of how mental disorders should be classified, focusing on the issue of whether the DSM should adopt a purely descriptive or theoretical approach. I argue that the DSM should replace its purely descriptive approach with a theoretical approach that integrates causal information into the DSM’s descriptive diagnostic (...) categories. The paper proceeds in three sections. In the first section, I examine the goals (viz., guiding treatment, facilitating research, and improving communication) associated with the DSM’s purely descriptive approach. In the second section, I suggest that the DSM’s purely descriptive approach is best suited for improving communication among mental health professionals; however, theoretical approaches would be superior for purposes of treatment and research. In the third section, I outline steps required to move the DSM towards a hybrid system of classification that can accommodate the benefits of descriptive and theoretical approaches, and I discuss how the DSM’s descriptive categories could be revised to incorporate theoretical information regarding the causes of disorders. I argue that the DSM should reconceive of its goals more narrowly such that it functions primarily as an epistemic hub that mediates among various contexts of use in which definitions of mental disorders appear. My analysis emphasizes the importance of pluralism as a methodological means for avoiding theoretical dogmatism and ensuring that the DSM is a reflexive and self-correcting manual. (shrink)

In this paper, I critique two conceptions of mechanisms, namely those put forth by Stuart Glennan (Erkenntnis 44:49–71, 1996; Philosophy of Science 69:S342–S353, 2002) and Machamer et al. (Philosophy of Science 67:1–25, 2000). Glennan’s conception, I argue, cannot account for mechanisms involving negative causation because of its interactionist posture. MDC’s view encounters the same problem due to its reificatory conception of activities—this conception, I argue, entails an onerous commitment to ontological dualism. In the place of Glennan and MDC, I propose (...) a “modified conception” of mechanisms, which (a) obviates the problem of negative causation by reinterpreting MDC’s activities according to a “descriptivist” account, and (b) avoids MDC’s problem by postulating a monistic ontology of entities. Thus, by solving these problems, my modified conception offers a cogent, more adequate alternative to Glennan’s and MDC’s conceptions of mechanisms. (shrink)

Although molecular biology has meant different things at different times, the term is often associated with a tendency to view cellular causation as conforming to simple linear schemas in which macro-scale effects are specified by micro-scale structures. The early achievements of molecular biologists were important for the formation of such an outlook, one to which the discovery of recombinant DNA techniques, and a number of other findings, gave new life even after the complexity of genotype–phenotype
relations had become apparent. Against this (...) background we outline how a range of scientific developments and conceptual considerations can be regarded as enabling and perhaps necessitating contemporary systems approaches. We suggest that philosophical ideas have a valuable part to play in making sense of complex scientific and disciplinary issues. (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)

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)

Advocates of the New Mechanicism in philosophy of science argue that scientific explanation often consists in describing mechanisms responsible for natural phenomena. Despite its successes, one might think that this approach does not square with the ontological strictures of quantum mechanics. New Mechanists suppose that mechanisms are composed of objects with definite properties, which are interconnected via local causal interactions. Quantum mechanics calls these suppositions into question. Since mechanisms are hierarchical it appears that even macroscopic mechanisms must supervene on a (...) set of “objects” that behave non-classically. In this paper we argue, in part by appeal to the theory of quantum decoherence, that the universal validity of quantum mechanics does not undermine neo-mechanistic ontological and explanatory claims as they occur within in classical domains. Additionally, we argue that by relaxation of certain classical assumptions, mechanistic explanatory strategies can sometimes be carried over into the quantum domain. (shrink)

In this thesis, I give a metascientific account of causality in medicine. I begin with two historical cases of causal discovery. These are the discovery of the causation of Burkitt’s lymphoma by the Epstein-Barr virus, and of the various viral causes suggested for cervical cancer. These historical cases then support a philosophical discussion of causality in medicine. This begins with an introduction to the Russo- Williamson thesis (RWT), and discussion of a range of counter-arguments against it. Despite these, I argue (...) that the RWT is historically workable, given a small number of modifications. I then expand Russo and Williamson’s account. I first develop their suggestion that causal relationships in medicine require some kind of evidence of mechanism. I begin with a number of accounts of mechanisms and produce a range of consensus features of them. I then develop this consensus position by reference to the two historical case studies with an eye to their operational competence. In particular, I suggest that it is mechanistic models and their representations which we are concerned with in medicine, rather than the mechanism as it exists in the world. -/- I then employ these mechanistic models to give an account of the sorts of evidence used in formulating and evaluating causal claims. Again, I use the two human viral oncogenesis cases to give this account. I characterise and distinguish evidence of mechanism from evidence of difference-making, and relate this to mechanistic models. I then suggest the relationship between types of evidence presents us with a means of tackling the reference-class problem. This sets the scene for the final chapter. Here, I suggest the manner in which these two different classes of evidence become integrated is also reflected in the way that developing research programmes change as their associated causal claims develop. (shrink)

It is a widespread assumption in philosophy of science that data is what is explained by theory—that data itself is not explanatory. I draw on instances of representational and explanatory practice from mammalian chronobiology to suggest that this assumption is unsustainable. In many instances, biologists employ representations of data in explanatory ways that are not reducible to constraints on or evidence for representations of mechanisms. Data graphs are used to exemplify relationships between quantities in the mechanism, and often these representations (...) are necessary for explaining particular aspects of the phenomena under study. I argue that this kind of representation is distinct from representing laws or generalizations, and its primary purpose is to convey particular types or patterns of quantitative relationships. The benefit of the analysis is two-fold. First, it provides a more accurate account of explanatory practice in broadly mechanistic analysis in biology. Second, it suggests that there is not an explanatory “fundamental” type of representation in biology. Rather, the practice of explanation consists in the construction of different types of representations and their employment for distinct explanatory purposes. (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)

Robots are being extensively used for the purpose of discovering and testing empirical hypotheses about biological sensorimotor mechanisms. We examine here methodological problems that have to be addressed in order to design and perform “good” experiments with these machine models. These problems notably concern the mapping of biological mechanism descriptions into robotic mechanism descriptions; the distinction between theoretically unconstrained “implementation details” and robotic features that carry a modeling weight; the role of preliminary calibration experiments; the monitoring of experimental environments for (...) disturbing factors that affect both modeling features and theoretically unconstrained implementation details of robots. Various assumptions that are gradually introduced in the process of setting up and performing these robotic experiments become integral parts of the background hypotheses that are needed to bring experimental observations to bear on biological mechanism descriptions. (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)

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)

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)

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)

How are scientific explanations possible in ecology, given that there do not appear to be many—if any—ecological laws? To answer this question, I present and defend an account of scientific causal explanation in which ecological generalizations are explanatory if they are invariant rather than lawlike. An invariant generalization continues to hold or be valid under a special change—called an intervention—that changes the value of its variables. According to this account, causes are difference-makers that can be intervened upon to manipulate or (...) control their effects. I apply the account to ecological generalizations to show that invariance under interventions as a criterion of explanatory relevance provides interesting interpretations for the explanatory status of many ecological generalizations. Thus, I argue that there could be causal explanations in ecology by generalizations that are not, in a strict sense, laws. I also address the issue of mechanistic explanations in ecology by arguing that invariance and modularity constitute such explanations. (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)

Philosophy of psychiatry has boomed in the last few years. We are now seeing a growing literature on the nature of psychiatric explanation, including work that makes contact with longstanding disputes in the philosophy of science as well as more specific work on mental disorders. This paper looks at some recent work on both representing and explaining mental illness. An emerging picture sees explanation of mental disorder as first constructing causal-statistical networks that represent disease pathways as they unfold in time, (...) and then choosing strategies for causal explanation. The epistemic problems in psychiatry are huge, and they arise from the extreme variety in the causes and trajectories of mental disorders across patients. Existing concepts of levels of explanation and mechanism may seem like an obvious epistemic armoury, but they may not fit psychiatry very well, and philosophical theories of psychiatric explanation stress different ways of trying to understand robust patterns amid the individual variation. (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)

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)

In this essay I propose that what design principles in systems biology and systems neuroscience do is to present abstract characterizations of mechanisms, and thereby facilitate mechanistic explanation. To show this, one design principle in systems neuroscience, i.e., the multilayer perceptron, is examined. However, Braillard contends that design principles provide a sort of non-mechanistic explanation due to two related reasons: they are very general and describe non-causal dependence relationships. In response to this, I argue that, on the one hand, all (...) mechanisms are more or less general, and on the other, many design principles are causal systems. (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)

In discussion of mechanisms, philosophers often debate about whether quantitative descriptions of generalizations or qualitative descriptions of operations are explanatorily fundamental. I argue that these debates have erred by conflating the explanatory roles of generalizations and patterns. Patterns are types of variations within or between quantities in a mechanism over time or across conditions. While these patterns must often be represented in addition to descriptions of operations in order to explain a phenomenon, they are not equivalent to generalizations because their (...) explanatory role does not depend on any specific facts about their scope or domain of invariance. (shrink)

In the biological realm, a complete explanation of a trait seems to include an explanation in terms of function. It is natural to ask of some trait, "What is its function?" or "What purpose in the organism does the particular trait serve?" or "What is the goal of its activity?" There are several views concerning the appropriate definition of function for biological matters. Two popular views of function with respect to living things are Cummins' organizational account and the Griffiths/Godfrey-Smith modern (...) history account. Whereas Cummins argues that a trait functions so as to contribute to the general organization of some organism's present structure, Griffiths, and Godfrey-Smith argue that a trait functions because of its fitness with respect to the organism's recent evolutionary history. In this paper, I show how these accounts can be made compatible and compliment one another. Given that structure, organization, operational flexibility, function, and evolutionary history are all factors to be considered in an organism's makeup, we should expect that the traits of an organism function the way they do because such traits presently contribute to the overall organization of the organism (Cummins) as well as were selected for in the organism's species' recent ancestry (Griffiths/Godfrey-Smith). (shrink)