Mechanistic models in molecular systems biology are generally mathematical models of the action of networks of biochemical reactions, involving metabolism, signal transduction, and/or gene expression. They can be either simulated numerically or analyzed analytically. Systems biology integrates quantitative molecular data acquisition with mathematical models to design new experiments, discriminate between alternative mechanisms and explain the molecular basis of cellular properties. At the heart of this approach are mechanistic models of molecular networks. We focus on the articulation and development of mechanistic (...) models, identifying five constraints which guide the articulation of models in molecular systems biology. These constraints are not independent of one another, with the result that modeling becomes an iterative process. We illustrate the use of these constraints in the modeling of the mechanism for bistability in the lac operon. (shrink)

Many explanations in molecular biology, neuroscience, and other fields of experimental biology describe mechanisms underlying phenomena of interest. These mechanistic explanations account for higher-level phenomena in terms of causally active parts and their spatiotemporal organization. What makes such a mechanistic description explanatory? The best-developed answer, Craver's causal-mechanical account, has several weaknesses. It does not fully explicate the target of explanation, interlevel relation, or interactive nonmodular character of many biological mechanisms as we understand them. An alternative account of MEx, emphasizing interdependence (...) among a mechanism's components, remedies these difficulties. (shrink)

In this article, two issues regarding mechanisms are discussed. The first concerns the relationships between “mechanism description” and “mechanism explanation.” It is proposed that it is rather plausible to think of them as two distinct epistemic acts. The second deals with the different molecular biology explanatory contexts, and it is shown that some of them require physics and its laws.

Autoinhibition is a design principle realized in many molecular mechanisms in biology. After explicating the notion of a design principle and showing that autoinhibition is such a principle, we focus on how researchers discovered instances of autoinhibition, using research establishing the autoinhibition of the molecular motors kinesin and dynein as our case study. Research on kinesin and dynein began in the fashion described in accounts of mechanistic explanation but, once the mechanisms had been discovered, researchers discovered that they exhibited a (...) second phenomenon, autoinhibition. The discovery of autoinhibition not only reverses the pattern in terms of which philosophers have understood mechanism discovery but runs counter to the one phenomenon-one mechanism principle assumed to relate mechanisms and the phenomena they explain. The ubiquity of autoinhibition as a design principle, therefore, necessitates a philosophical understanding of mechanisms that recognizes how they can participate in more than one phenomenon. Since mechanisms with this design are released from autoinhibition only when they are acted on by control mechanisms, we advance a revised account of mechanisms that accommodates attribution of multiple phenomena to the same mechanism and distinguishes them from other processes that control them. (shrink)

Abstract Although noting the importance of organization in mechanisms, the new mechanistic philosophers of science have followed most biologists in focusing primarily on only the simplest mode of organization in which operations are envisaged as occurring sequentially. Increasingly, though, biologists are recognizing that the mechanisms they confront are non-sequential and the operations nonlinear. To understand how such mechanisms function through time, they are turning to computational models and tools of dynamical systems theory. Recent research on circadian rhythms addressing both intracellular (...) mechanisms and the intercellular networks in which these mechanisms are synchronized illuminates this point. This and other recent research in biology shows that the new mechanistic philosophers of science must expand their account of mechanistic explanation to incorporate computational modeling, yielding dynamical mechanistic explanations. Developing such explanations, however, is a challenge for both the scientists and the philosophers as there are serious tensions between mechanistic and dynamical approaches to science, and there are important opportunities for philosophers of science to contribute to surmounting these tensions. Content Type Journal Article Category Original paper in Philosophy of Science Pages 1-16 DOI 10.1007/s13194-012-0046-x Authors William Bechtel, Department of Philosophy, Center for Chronobiology, and Science Studies Program, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0119, USA Journal European Journal for Philosophy of Science Online ISSN 1879-4920 Print ISSN 1879-4912. (shrink)

La plupart des projets d’architectures cognitives dans les sciences cognitives et des explications des processus cérébraux dans les neurosciences interprètent l’esprit/cerveau comme réactif : le processus est déclenché par un stimulus et se termine par une réponse. Mais il y a de plus en plus de données laissant penser que le cerveau est endogéniquement actif : des oscillations de l’activité électrochimique à de multiples fréquences ont lieu dans le cerveau même en l’absence de stimuli et ceux-ci servent plutôt à moduler (...) ces oscillations qu’à déclencher l’activité. De plus, des données montrent que cette activité endogène est utilisée dans diverses activités de traitement de l’information. Je m’appuie sur les données issues des enregistrements cellulaires unitaires, de l’EEG et de l’IRMf en situation passive, afin de soutenir la thèse d’un comportement oscillatoire continu dans le cerveau et d’identifier plusieurs manières dont ce comportement peut contribuer à la cognition. Si les sciences cognitives ont pour but de comprendre comment nous effectuons des tâches cognitives, elles ont besoin de développer des architectures cognitives qui intègrent le type d’activité endogène dynamique présentée par le cerveau. (shrink)

La plupart des projets d’architectures cognitives dans les sciences cognitives et des explications des processus cérébraux dans les neurosciences interprètent l’esprit/cerveau comme réactif : le processus est déclenché par un stimulus et se termine par une réponse. Mais il y a de plus en plus de données laissant penser que le cerveau est endogéniquement actif : des oscillations de l’activité électrochimique à de multiples fréquences ont lieu dans le cerveau même en l’absence de stimuli et ceux-ci servent plutôt à moduler (...) ces oscillations qu’à déclencher l’activité. De plus, des données montrent que cette activité endogène est utilisée dans diverses activités de traitement de l’information. Je m’appuie sur les données issues des enregistrements cellulaires unitaires, de l’EEG et de l’IRMf en situation passive, afin de soutenir la thèse d’un comportement oscillatoire continu dans le cerveau et d’identifier plusieurs manières dont ce comportement peut contribuer à la cognition. Si les sciences cognitives ont pour but de comprendre comment nous effectuons des tâches cognitives, elles ont besoin de développer des architectures cognitives qui intègrent le type d’activité endogène dynamique présentée par le cerveau. (shrink)

According to new mechanists, mechanisms explain how specific biological phenomena are produced. New mechanists have had little to say about how mechanisms relate to the organism in which they reside. A key feature of organisms, emphasized by the autonomy tradition, is that organisms maintain themselves. To do this, they rely on mechanisms. But mechanisms must be controlled so that they produce the phenomena for which they are responsible when and in the manner needed by the organism. To account for how (...) they are controlled, we characterize mechanisms as sets of constraints on the flow of free energy. Some constraints are flexible and can be acted on by other mechanisms, control mechanisms, that utilize information procured from the organism and its environment to alter the flexible constraints in other mechanisms so that they produce phenomena appropriate to the circumstances. We further show that control mechanisms in living organisms are organized heterarchically—control is carried out primarily by local controllers that integrate information they acquire as well as that which they procure from other control mechanisms. The result is not a hierarchy of control but an integrated network of control mechanisms that has been crafted over the course of evolution. (shrink)

The neuron doctrine, according to which nerves consist of discontinuous neurons, presented investigators with the challenge of determining what activities occurred between them or between them and muscles. One group of researchers, dubbed the sparks, viewed the electrical current in one neuron as inducing a current in the next neuron or in muscles. For them there was no gap between the activities of neurons or neurons and muscles that required filling with a new type of activity. A competing group, the (...) soups, came to argue for chemicals, subsequently referred to neurotransmitters, as carrying out the activities between neurons or between neurons and muscles. But even for them the conclusion that chemicals performed this activity was only arrived over time. I examine the prolonged period in which proponents of chemical transmission developed their account and challenged the sparks. My goal is to illuminate the epistemic processes that led to the discovery of a new scientific phenomenon—chemical transmission between neurons. (shrink)

This article argues that the basic account of mechanism and mechanistic explanation, involving sequential execution of qualitatively characterized operations, is itself insufficient to explain biological phenomena such as the capacity of living organisms to maintain themselves as systems distinct from their environment. This capacity depends on cyclic organization, including positive and negative feedback loops, which can generate complex dynamics. Understanding cyclically organized mechanisms with complex dynamics requires coordinating research directed at decomposing mechanisms into parts and operations with research using computational (...) models to recompose mechanisms and determine their dynamic behavior. This coordinated endeavor yields dynamic mechanistic explanations. (shrink)

Accounts of mechanistic explanation have emphasized the importance of looking down—decomposing a mechanism into its parts and operations. Using research on visual processing as an exemplar, I illustrate how productive such research has been. But once multiple components of a mechanism have been identified, researchers also need to figure out how it is organized—they must look around and determine how to recompose the mechanism. Although researchers often begin by trying to recompose the mechanism in terms of sequential operations, they frequently (...) find that the components of a mechanism interact in complex ways involving positive and negative feedback and that the organization often exhibits highly interactive local networks linked by a few long-range connections (small-worlds organization) and power law distributions of connections. The mechanisms are themselves active systems that are perturbed by inputs but not set in motion by them. Researchers also need to look up —situate a mechanism in its context, which may be a larger mechanism that modulates its behavior. When looking down is combined with looking around and up, mechanistic research results in an integrated, multi-level perspective. (shrink)

Developing models of biological mechanisms, such as those involved in respiration in cells, often requires collaborative effort drawing upon techniques developed and information generated in different disciplines. Biochemists in the early decades of the 20th century uncovered all but the most elusive chemical operations involved in cellular respiration, but were unable to align the reaction pathways with particular structures in the cell. During the period 1940-1965 cell biology was emerging as a new discipline and made distinctive contributions to understanding the (...) role of the mitochondrion and its component parts in cellular respiration. In particular, by developing techniques for localizing enzymes or enzyme systems in specific cellular components, cell biologists provided crucial information about the organized structures in which the biochemical reactions occurred. Although the idea that biochemical operations are intimately related to and depend on cell structures was at odds with the then-dominant emphasis on systems of soluble enzymes in biochemistry, a reconceptualization of energetic processes in the 1960s and 1970s made it clear why cell structure was critical to the biochemical account. This paper examines how numerous excursions between biochemistry and cell biology contributed a new understanding of the mechanism of cellular respiration. (shrink)

Explanations in the life sciences frequently involve presenting a model of the mechanism taken to be responsible for a given phenomenon. Such explanations depart in numerous ways from nomological explanations commonly presented in philosophy of science. This paper focuses on three sorts of differences. First, scientists who develop mechanistic explanations are not limited to linguistic representations and logical inference; they frequently employ diagrams to characterize mechanisms and simulations to reason about them. Thus, the epistemic resources for presenting mechanistic explanations are (...) considerably richer than those suggested by a nomological framework. Second, the fact that mechanisms involve organized systems of component parts and operations provides direction to both the discovery and testing of mechanistic explanations. Finally, models of mechanisms are developed for specific exemplars and are not represented in terms of universally quantified statements. Generalization involves investigating both the similarity of new exemplars to those already studied and the variations between them. (shrink)

Two widely accepted assumptions within cognitive science are that (1) the goal is to understand the mechanisms responsible for cognitive performances and (2) computational modeling is a major tool for understanding these mechanisms. The particular approaches to computational modeling adopted in cognitive science, moreover, have significantly affected the way in which cognitive mechanisms are understood. Unable to employ some of the more common methods for conducting research on mechanisms, cognitive scientists’ guiding ideas about mechanism have developed in conjunction with their (...) styles of modeling. In particular, mental operations often are conceptualized as comparable to the processes employed in classical symbolic AI or neural network models. These models, in turn, have been interpreted by some as themselves intelligent systems since they employ the same type of operations as does the mind. For this paper, what is significant about these approaches to modeling is that they are constructed specifically to account for behavior and are evaluated by how well they do so—not by independent evidence that they describe actual operations in mental mechanisms. (shrink)

Various analytical tools originally developed for theories of mechanistic explanation have recently been imported into the ongoing debate on the hypothesis of extended cognition. One such tool that appears particularly relevant to that debate is Craver’s mutual manipulability account of constitution, most of all because it promises to settle the debate on experimental grounds. This paper investigates whether it is possible to deliver on that promise. We first find that, far from grounding an experimental evaluation of HEC, MM is conceptually (...) incompatible with both internalist and externalist accounts of cognition. Next, we propose a suitable modification of MM, MM*, but it turns out that MM* presupposes rather than produces clarity on the extension of cognition. Moreover, subject to MM* the inference to constitution is radically empirically underdetermined. Finally, we argue that our results can be generalized and conclude that, for principled reasons, it is impossible to experimentally determine whether cognitive processes have extracerebral constituents. Determining the extension of cognition is an inherently pragmatic matter. (shrink)

While ideal interventions are acknowledged by many as valuable tools for the analysis of causation, recent discussions have shown that, since there are no ideal interventions on upper-level phenomena that non-reductively supervene on their underlying mechanisms, interventions cannot—contrary to a popular opinion—ground an informative analysis of constitution. This has led some to abandon the project of analyzing constitution in interventionist terms. By contrast, this paper defines the notion of a horizontally surgical intervention, and argues that, when combined with some innocuous (...) metaphysical principles about the relation between upper and lower levels of mechanisms, that notion delivers a sufficient condition for constitution. This, in turn, strengthens the case for an interventionist analysis of constitution. (shrink)

While ideal interventions are acknowledged by many as valuable tools for the analysis of causation, recent discussions have shown that, since there are no ideal interventions on upper-level phenomena that non-reductively supervene on their underlying mechanisms, interventions cannot—contrary to a popular opinion—ground an informative analysis of constitution. This has led some to abandon the project of analyzing constitution in interventionist terms. By contrast, this paper defines the notion of a horizontally surgical intervention, and argues that, when combined with some innocuous (...) metaphysical principles about the relation between upper and lower levels of mechanisms, that notion delivers a sufficient condition for constitution. This, in turn, strengthens the case for an interventionist analysis of constitution. (shrink)

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)

The first part of this paper finds Craver’s (2007) mutual manipulability theory (MM) of constitution inadequate, as it definitionally ties constitution to the feasibility of idealized experiments, which, however, are unrealizable in principle. As an alternative, the second part develops an abductive theory of constitution (NDC), which exploits the fact that phenomena and their constituents are unbreakably coupled via common causes. The best explanation for this common-cause coupling is the existence of an additional dependence relation, viz. constitution. Apart from adequately (...) capturing the essential characteristics of constitution missed by MM, NDC has important ramifications for constitutional discovery—most notably, that there is no experimentum crucis for constitution, not even under ideal discovery circumstances. (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)

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)

Dynamical systems play a central role in explanations in cognitive neuroscience. The grounds for these explanations are hotly debated and generally fall under two approaches: non-mechanistic and mechanistic. In this paper, I first outline a neurodynamical explanatory schema that highlights the role of dynamical systems in cognitive phenomena. I next explore the mechanistic status of such neurodynamical explanations. I argue that these explanations satisfy only some of the constraints on mechanistic explanation and should be considered pseudomechanistic explanations. I defend this (...) argument against three alternative interpretations of the neurodynamical explanatory schema. The independent interpretation holds that neurodynamical explanations and mechanisms are independent. The constitutive interpretation holds that neurodynamical explanations are constitutive but otherwise non-mechanistic. Both the independent and constitutive interpretations fail to account for all the features of neurodynamical explanations. The partial interpretation assumes that the targets of dynamical systems models are mechanisms and so holds that neurodynamical explanations are incomplete because they lack mechanistic details. I contend instead that the targets of those models are dynamical systems distinct from mechanisms and defend this claim against several objections. I conclude with a defense of the pseudomechanistic interpretation and a discussion of the source of their explanatory power in relation to a causal-mechanical description of the world. (shrink)

Santiago Ramón y Cajal, the primary architect of the neuron doctrine and the law of dynamic polarization, is considered to be the founder of modern neuroscience. At the same time, many philosophers, historians, and neuroscientists agree that modern neuroscience embodies a mechanistic perspective on the explanation of the nervous system. In this paper, I review the extant mechanistic interpretation of Cajal’s contribution to modern neuroscience. Then, I argue that the extant mechanistic interpretation fails to capture the explanatory import of Cajal’s (...) law of dynamic polarization. My claim is that the definitive formulation of Cajal’s law of dynamic polarization, despite its mechanistic inaccuracies, embodies a non-mechanistic pattern of reasoning (i.e., design explanation) that is an integral component of modern neuroscience. (shrink)

Recent discussion of mechanism has suggested new approaches to several issues in the philosophy of science, including theory structure, causal explanation, and reductionism. Here, I apply what I take to be the fruits of the Ônew mechanical philosophyÕ to an analysis of a contemporary debate in evolutionary biology about the role of natural selection in speciation. Traditional accounts of that debate focus on the geographic context of genetic divergence— namely, whether divergence in the absence of geographic isolation is possible (or (...) significant). Those accounts are at best incomplete, I argue, because they ignore the mechanisms producing divergence and miss what is at stake in the biological debate. I argue that the biological debate instead concerns the scope of particular speciation mechanisms which assign different roles to natural selection at various stages of divergence. The upshot is a new interpretation of the crux of that debate—namely, whether divergence with gene flow is possible (or significant) and whether the isolating mechanisms producing it are adaptive. Ó 2005 Elsevier Ltd. All rights reserved. (shrink)

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

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

Understanding the role mechanistic constraints play in shaping evolution can relieve the tension between the generally accepted intuition that there are no strict laws in biology and empirical findings showing that evolutionary processes are biased toward preferred outcomes. Mechanistic constraints explain why some evolutionary outcomes are more probable than others and allow for predictions in specific lineages. At the same time, mechanistic constraints are neither necessary nor universal in the way laws are traditionally characterized: they remain contingent on the past (...) evolution of the biological mechanisms underpinning them and only constrain the future evolution of the organisms possessing them. (shrink)

In this article, I argue that genomic programs are not substitutes for multi-causal molecular mechanistic explanations of inheritance, but abstract representations of the same sort as mechanism schemas already described in the philosophical literature. On this account, the program analogy is not reductionistic and does not ignore or underestimate the active contribution of epigenetic elements to phenotypes and development. Rather, genomic program representations specifically highlight the genomic determinants of inheritance and their organizational features at work in the wider context of (...) the mechanisms of genome expression. (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)

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

Emergent antireductionism in biological sciences states that even though all living cells and organisms are composed of molecules, molecular wholes are characterized by emergent properties that can only be understood from the perspective of cellular and organismal levels of composition. Thus, an emergence claim (molecular wholes are characterized by emergent properties) is thought to support a form of antireductionism (properties of higher-level molecular wholes can only be understood by taking into account concepts, theories and explanations dealing with higher-level entities). I (...) argue that this argument is flawed: even if molecular wholes are characterized by emergent properties and even if many successful explanations in biology are not molecular, there is no entailment between the two claims. (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)

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

Theories of legal causation that identify the concept with probability‐raising generate false positives where the defendant's conduct raises the probability of harm but brings about that harm in the wrong kind of way. Moreover, what the law seeks to deter is not conduct that raises the probability of harm, but rather conduct that is dangerous. A legal or proximate cause is one that harms the plaintiff through the causal mechanism that sustains the lawful generalization that the defendant's conduct was dangerous.

The indeterminacy problem is one of the most prominent objections against naturalistic theories of content. In this essay I present this difficulty and argue that extant accounts are unable to solve it. Then, I develop a particular version of teleosemantics, which I call ’explanation-based teleosemantics’, and show how this outstanding problem can be addressed within the framework of a powerful naturalistic theory.

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)

The emphasis on the organization of entities and their activities and interactions has been labeled one of the most distinct contributions of mechanistic philosophy. In this paper I discuss the manner in which the organization of entities and their activities and interactions participates in bringing about phenomena. I present a well-known example from molecular biology—the functioning of the genetic switch in phage lambda—and discuss Marco J. Nathan’s notion of causation by concentration. Nathan introduces causation by concentration to account for the (...) irreducible causal role that the concentration ratio between two kinds of proteins possesses in the genetic switch mechanism in phage lambda. I discuss what the irreducibility of this causal role amounts to and provide a mechanistic interpretation of Nathan’s causation by concentration; that is, I explain this irreducible causal role as one organizational feature of this mechanism. The paper concludes that biological mechanisms need a causal pluralist framework [similar to Glennan’s account in, and but slightly modified] where organizational features such as the concentration ratio have a causally relevant role, yet all the causally productive relations occur at the level of entities or individuals. (shrink)

This paper addresses the methodological problem of analysing what it is to explain observed behaviours of engineered computing systems, focusing on the crucial role that abstraction and idealization play in explanations of both correct and incorrect BECS. First, it is argued that an understanding of explanatory requests about observed miscomputations crucially involves reference to the rich background afforded by hierarchies of functional specifications. Second, many explanations concerning incorrect BECS are found to abstract away from descriptions of physical components and processes (...) of computing systems that one finds below the logic circuit and gate layer of functional specification hierarchies. Third, model-based explanations of both correct and incorrect BECS that are provided in the framework of formal verification methods often involve idealizations. Moreover, a distinction between restrictive and permissive idealizations is introduced and their roles in BECS explanations are analysed. (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)

Even though the evidence‐based medicine movement (EBM) labels mechanisms a low quality form of evidence, consideration of the mechanisms on which medicine relies, and the distinct roles that mechanisms might play in clinical practice, offers a number of insights into EBM itself. In this paper, I examine the connections between EBM and mechanisms from several angles. I diagnose what went wrong in two examples where mechanistic reasoning failed to generate accurate predictions for how a dysfunctional mechanism would respond to intervention. (...) I then use these examples to explain why we should expect this kind of mechanistic reasoning to fail in systematic ways, by situating these failures in terms of evolved complexity of the causal system(s) in question. I argue that there is still a different role in which mechanisms continue to figure as evidence in EBM: namely, in guiding the application of population‐level recommendations to individual patients. Thus, even though the evidence‐based movement rejects one role in which mechanistic reasoning serves as evidence, there are other evidentiary roles for mechanistic reasoning. This renders plausible the claims of some critics of evidencebased medicine who point to the ineliminable role of clinical experience. Clearly specifying the ways in which mechanisms and mechanistic reasoning can be involved in clinical practice frames the discussion about EBM and clinical experience in more fruitful terms. (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 field guide, I distinguish five separate senses with which the term ‘mechanism’ is used in contemporary philosophy of science. Many of these senses have overlapping areas of application but involve distinct philosophical claims and characterize the target mechanisms in relevantly different ways. This field guide will clarify the key features of each sense and introduce some main debates, distinguishing those that transpire within a given sense from those that are best understood as concerning distinct senses. The ‘new mechanisms’ (...) sense is at the center of most of these contemporary debates and will be treated at greater length; subsequent senses of mechanism will be primarily distinguished from this one. In part I of this paper, I distinguish two senses of the term ‘mechanism’, both of which are explicitly hierarchical and nested in character, such that any given mechanism is comprised of smaller sub-mechanisms, in turn comprised of yet smaller sub-sub-mechanisms and so on. While both of the senses discussed here are anti-reductive, they differ in their focus on scientific practice versus metaphysics, in the degree of regularity they attribute to mechanisms, and in terms of their relationships to the discussions of mechanisms in the history of philosophy and science. (shrink)

In this paper, I describe grounds for dissatisfaction with certain aspects of the sciences of animal cognition and argue that a turn toward mathematical modeling of animal cognition is warranted. I consider some objections to this call and argue that the implications of such a turn are not as drastic for ordinary, commonsense understanding of animal minds as they might seem.

In the recent literature on causal and non-causal scientific explanations, there is an intuitive assumption according to which an explanation is non-causal by virtue of being abstract. In this context, to be ‘abstract’ means that the explanans in question leaves out many or almost all causal microphysical details of the target system. After motivating this assumption, we argue that the abstractness assumption, in placing the abstract and the causal character of an explanation in tension, is misguided in ways that are (...) independent of which view of causation or causal explanation one takes to be most accurate. On major accounts of causation, as well as on major accounts of causal explanation, the abstractness of an explanation is not sufficient for it being non-causal. That is, explanations are not non-causal by dint of being abstract. (shrink)

One might have thought that if something has two or more distinct realizations, then that thing is multiply realized. Nevertheless, some philosophers have claimed that two or more distinct realizations do not amount to multiple realization, unless those distinct realizations amount to multiple “ways” of realizing the thing. Corey Maley, Gualtiero Piccinini, Thomas Polger, and Lawrence Shapiro are among these philosophers. Unfortunately, they do not explain why multiple realization requires multiple “ways” of realizing. More significantly, their efforts to articulate multiple (...) “ways” of realizing turn out to be problematic. (shrink)

and was correct to conclude that the way a biological population is described should affect conclusions about whether natural selection occurs, but wrong to conclude that natural selection is therefore not a cause. After providing a new argument that ignored crucial biological details, I give a biological illustration that motivates a fairly extreme dependence on description. I argue that contrary to an implication of , biologists allow much flexibility in describing populations, as contemporary research on recent human evolution shows. Properly (...) understood, such description-dependence is consistent with descriptions capturing different causal relations involving the same population. I thus show that Walsh’s arguments fail for reasons that have not previously been understood; I argue that Walsh’s more recent “Sure Thing” argument fails for similar reasons. The resulting view provides a new perspective on causation in evolutionary processes. (shrink)

We contend that diagrams are tools not only for communication but also for supporting the reasoning of biologists. In the mechanistic research that is characteristic of biology, diagrams delineate the phenomenon to be explained, display explanatory relations, and show the organized parts and operations of the mechanism proposed as responsible for the phenomenon. Both phenomenon diagrams and explanatory relations diagrams, employing graphs or other formats, facilitate applying visual processing to the detection of relevant patterns. Mechanism diagrams guide reasoning about how (...) the parts and operations work together to produce the phenomenon and what experiments need to be done to improve on the existing account. We examine how these functions are served by diagrams in circadian rhythm research. (shrink)

Arguments for the autonomy of psychology or other higher-level sciences have often taken the form of denying the possibility of reduction. The form of reduction most proponents and critics of the autonomy of psychology have in mind is theory reduction. Mechanistic explanations provide a different perspective. Mechanistic explanations are reductionist insofar as they appeal to lower-level entities—the component parts of a mechanism and their operations— to explain a phenomenon. However, unlike theory reductions, mechanistic explanations also recognize the fundamental role of (...) organization in enabling mechanisms to engage their environments as units (as well as the role of yet higher-level structures in constraining such engagement). Especially when organization is non-linear, it can enable mechanisms to generate phenomena that are quite surprising given the operations of the components taken in isolation. Such organization must be discovered—it cannot simply be derived from knowledge of lower-level parts and their operations. Moreover, the organized environments in which mechanisms operate must also be discovered. It is typically the higher-level disciplines that have the tools for discovering the organization within and between mechanisms. Although these inquiries are constrained by the knowledge of the parts and operations constituting the mechanism, they make their own autonomous contribution to understanding how a mechanism actually behaves. Thus, mechanistic explanations provide a strong sense of autonomy for higher levels of organization and the inquiries addressing them even while recognizing the distinctive contributions of reductionistic research investigating the operations of the lower level components. (shrink)