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.

In this article, I present two conceptual problems for Craver's mutual manipulability account of constitutive relevance in mechanisms. First, constitutive relevance threatens to imply causal relevance despite Craver (and Bechtel)'s claim that they are strictly distinct. Second, if (as is intuitively appealing) parthood is defined in terms of spatio-temporal inclusion, then the mutual manipulability account is prone to counterexamples, as I show by a case of endosymbiosis. I also present a methodological problem (a case of experimental underdetermination) and formulate two (...) partial, but fallible solutions based on the notions of parthood and synchronicity. (shrink)

This article deals with mechanisms conceived as composed of entities and activities. In response to many perplexities about the nature of activities, a number of arguments are developed concerning their epistemic and ontological status. Some questions concerning the relations between cause and causal explanation and mechanisms are also addressed.

Mechanistic explanation has an impressive track record of advancing our understanding of complex, hierarchically organized physical systems, particularly biological and neural systems. But not every complex system can be understood mechanistically. Psychological capacities are often understood by providing cognitive models of the systems that underlie them. I argue that these models, while superficially similar to mechanistic models, in fact have a substantially more complex relation to the real underlying system. They are typically constructed using a range of techniques for abstracting (...) the functional properties of the system, which may not coincide with its mechanistic organization. I describe these techniques and show that despite being non-mechanistic, these cognitive models can satisfy the normative constraints on good explanations. (shrink)

The field of the philosophy of biology is flourishing in its aim to evaluate and rethink the view inherited from the previous century ---the Modern Synthesis. Different research areas and theories have come to the fore in the last decades in order to account for different biological phenomena that, in the first instance, fall beyond the explanatory scope of the Modern Synthesis. This thesis is anchored and motivated by this revolt in the philosophy of biology. -/- The central target in (...) this context is the possibility of naturalizing teleology, a classical nightmare for the history of biology itself. This requires, principally, understanding the causes of teleological explanations without assuming an unfashioned backward causation of sorts. As the riddles of teleological explanations are about their temporal dimension, I analyze different temporal scales of biological processes: evolutionary, developmental, and physiological. -/- The first one is the one defended in the context of the Modern Synthesis. As expected, one of the aims of this thesis is to evaluate the adequacy of an evolutionary account of teleological explanation. The scrutiny is negative. Evolutionary explanations in the context of the Modern Synthesis lack the necessary causal roots to naturalize teleology. Concerning the physiological scale, a long tradition pushed up by Kant and the organicist movement in the 20th century allows us to better understand how teleological explanations can be naturalized in physiological process. The key notions in this temporal scale are self-organization and the recursive, looped character of physiological process. While the physiological scale may be suitably accounted by contemporaries views, such as Autonomous Systems Theory, different central teleological phenomena remain unexplained from a purely physiological perspective. In particular, different issues concerning the (adaptive) construction of organism ---such as plasticity, robustness, variation, novelty, inheritance--- deserve an ontogenetic analysis. -/- The principal aim of this thesis is to provide a theory of teleological development that falls beyond the Modern Synthesis' framework and is prompted by different insights from the history of biology. I call it Agential Teleosemantics. It rests on two central pillars. First, that developmental processes, beyond any gene-centered stance, can be understood in informational terms; i.e. developmental processes are about the interaction of developmental resources conveying biological information. The second ingredient is agentivity, namely the idea that development is regulated by an agentive system according to the adaptiveness of the phenotypic outcomes produced. The role of agency in Agential Teleosemantic is equivalent to the role of genes in the Modern Synthesis: it is responsible for explaining the order and the adaptive complexity in the living realm. -/- The second target of this thesis regards the possibility of naturalizing intentional explanations in cognitive science. The central project involved in such an aim is known as teleosemantics. Classical teleosemantics however is etiological: it explains the teleofunctions of representational systems in terms of evolutionary processes. The different disputes in the contemporary philosophy of biology provide two insights to analyze teleosemantics in cognitive science. First, the challenges against the Modern Synthesis must be extended to the evolutionary approach of etiological teleosemantics. Second, as Agential Teleosemantics suggests an alternative source for teleofunctions ---ontogeny, I offer an attempt to integrate Agential Teleosemantics into cognitive science in order to provide an alternative teleosemantic project to understand intentional explanations in cognitive science. (shrink)

Relative to digital computation, analogue computation has been neglected in the philosophical literature. To the extent that attention has been paid to analogue computation, it has been misunderstood. The received view—that analogue computation has to do essentially with continuity—is simply wrong, as shown by careful attention to historical examples of discontinuous, discrete analogue computers. Instead of the received view, I develop an account of analogue computation in terms of a particular type of analogue representation that allows for discontinuity. This account (...) thus characterizes all types of analogue computation, whether continuous or discrete. Furthermore, the structure of this account can be generalized to other types of computation: analogue computation essentially involves analogue representation, whereas digital computation essentially involves digital representation. Besides being a necessary component of a complete philosophical understanding of computation in general, understanding analogue computation is important for computational explanation in contemporary neuroscience and cognitive science. (shrink)

In evolutionary biology changes in population structure are explained by citing trait fitness distribution. I distinguish three interpretations of fitness explanations—the Two‐Factor Model, the Single‐Factor Model, and the Statistical Interpretation—and argue for the last of these. These interpretations differ in their degrees of causal commitment. The first two hold that trait fitness distribution causes population change. Trait fitness explanations, according to these interpretations, are causal explanations. The last maintains that trait fitness distribution correlates with population change but does not cause (...) it. My defense of the Statistical Interpretation relies on a distinctive feature of causation. Causes conform to the Sure Thing Principle. Trait fitness distributions, I argue, do not. *Received July 2009; revised October 2009. †To contact the author, please write to: Department of Philosophy/Institute for the History, Philosophy of Science and Technology, University of Toronto, Victoria College, 91 Charles Street West, Toronto, ON M5S 1K7, Canada; e‐mail: [email protected]. (shrink)

The paper discusses how systems biology is working toward complex accounts that integrate explanation in terms of mechanisms and explanation by mathematical models—which some philosophers have viewed as rival models of explanation. Systems biology is an integrative approach, and it strongly relies on mathematical modeling. Philosophical accounts of mechanisms capture integrative in the sense of multilevel and multifield explanations, yet accounts of mechanistic explanation have failed to address how a mathematical model could contribute to such explanations. I discuss how mathematical (...) equations can be explanatorily relevant. Several cases from systems biology are discussed to illustrate the interplay between mechanistic research and mathematical modeling, and I point to questions about qualitative phenomena, where quantitative models are still indispensable to the explanation. Systems biology shows that a broader philosophical conception of mechanisms is needed, which takes into account functional-dynamical aspects, interaction in complex networks with feedback loops, system-wide functional properties such as distributed functionality and robustness, and a mechanism’s ability to respond to perturbations. I offer general conclusions for philosophical accounts of explanation. (shrink)

Machamer, Darden, and Craver argue that causal explanations explain effects by describing the operations of the mechanisms which produce them. One of this paper’s aims is to take advantage of neglected resources of Mechanism to rethink the traditional idea that actual or counterfactual natural regularities are essential to the distinction between causal and non-causal co-occurrences, and that generalizations describing natural regularities are essential components of causal explanations. I think that causal productivity and regularity are by no means the same thing, (...) and that the Regularists are mistaken about the roles generalizations play in causal explanation. Humean, logical empiricist, and other Regularist accounts of causal explanation have had the unfortunate effect of distracting philosophers’ from important non-explanatory scientific uses of laws and lesser generalizations which purport to describe natural regularities. My second aim is to characterize some of these uses, illustrating them with examples from neuroscientific research. (shrink)

This paper explores whether natural selection, a putative evolutionary mechanism, and a main one at that, can be characterized on either of the two dominant conceptions of mechanism, due to Glennan and the team of Machamer, Darden, and Craver, that constitute the “new mechanistic philosophy.” The results of the analysis are that neither of the dominant conceptions of mechanism adequately captures natural selection. Nevertheless, the new mechanistic philosophy possesses the resources for an understanding of natural selection under the rubric.

Behavior genetics is a controversial science. For decades, scholars have sought to understand the role of heredity in human behavior and life-course outcomes. Recently, technological advances and the rapid expansion of genomic databases have facilitated the discovery of genes associated with human phenotypes such as educational attainment and substance use disorders. To maximize the potential of this flourishing science, and to minimize potential harms, careful analysis of what it would mean for genes to be causes of human behavior is needed. (...) In this paper, we advance a framework for identifying instances of genetic causes, interpreting those causal relationships, and applying them to advance causal knowledge more generally in the social sciences. Central to thinking about genes as causes is counterfactual reasoning, the cornerstone of causal thinking in statistics, medicine, and philosophy. We argue that within-family genetic effects represent the product of a counterfactual comparison in the same way as average treatment effects (ATEs) from randomized controlled trials (RCTs). Both ATEs from RCTs and within-family genetic effects are shallow causes: They operate within intricate causal systems (non-unitary), produce heterogeneous effects across individuals (non-uniform), and are not mechanistically informative (non-explanatory). Despite these limitations, shallow causal knowledge can be used to improve understanding of the etiology of human behavior and to explore sources of heterogeneity and fade-out in treatment effects. (shrink)

This article compares causal and constitutive explanation. While scientific inquiry usually addresses both causal and constitutive questions, making the distinction is crucial for a detailed understanding of scientific questions and their interrelations. These explanations have different kinds of explananda and they track different sorts of dependencies. Constitutive explanations do not address events or behaviors, but causal capacities. While there are some interesting relations between building and causal manipulation, causation and constitution are not to be confused. Constitution is a synchronous and (...) asymmetric relation between relata that cannot be conceived as independent existences. However, despite their metaphysical differences, the same key ideas about explanation largely apply to both. Causal and constitutive explanations face similar challenges (such as the problems of relevance and explanatory regress) and both are in the business of mapping networks of counterfactual dependence—i.e. mechanisms—although the relevant counterfactuals are of a different sort. In the final section the issue of developmental explanation is discussed. It is argued that developmental explanations deserve their own place in taxonomy of explanations, although ultimately developmental dependencies can be analyzed as combinations of causal and constitutive dependencies. Hence, causal and constitutive explanation are distinct, but not always completely separate forms of explanation. (shrink)

This paper defends an interventionist treatment of mechanisms and contrasts this with Waskan (forthcoming). Interventionism embodies a difference-making conception of causation. I contrast such conceptions with geometrical/mechanical or “actualist” conceptions, associating Waskan’s proposals with the latter. It is argued that geometrical/mechanical conceptions of causation cannot replace difference-making conceptions in characterizing the behavior of mechanisms, but that some of the intuitions behind the geometrical/mechanical approach can be captured by thinking in terms of spatio-temporally organized difference-making information.

This essay advocates a “functional” approach to causation and causal reasoning: these are to be understood in terms of the goals and purposes of causal thinking. This approach is distinguished from accounts based on metaphysical considerations or on reconstruction of “intuitions.”.

Kaplan and Craver claim that all explanations in neuroscience appeal to mechanisms. They extend this view to the use of mathematical models in neuroscience and propose a constraint such models must meet in order to be explanatory. I analyze a mathematical model used to provide explanations in dynamical systems neuroscience and indicate how this explanation cannot be accommodated by the mechanist framework. I argue that this explanation is well characterized by Batterman’s account of minimal model explanations and that it demonstrates (...) how relationships between explanatory models in neuroscience and the systems they represent is more complex than has been appreciated. (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)

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 two distinct senses. The ‘new (...) mechanisms’ sense is the primary sense from which other senses will be distinguished. In part II of this field guide, I consider three further senses of the term that are ontologically ‘flat’ or at least not explicitly hierarchical in character: equations in structural equation models of causation, causal-physical processes, and information-theoretic constraints on states available to systems. After characterizing each sense, I clarify its ontological commitments, its methodological implications, how it figures in explanations, its implications for reduction, and the key manners in which it differs from other senses of mechanism. I conclude that there is no substantive core meaning shared by all senses, and that debates in contemporary philosophy of science can benefit from clarification regarding precisely which sense of mechanism is at stake. (shrink)

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.

As much as assumptions about mechanisms and mechanistic explanation have deeply affected psychology, they have received disproportionately little analysis in philosophy. After a historical survey of the influences of mechanistic approaches to explanation of psychological phenomena, we specify the nature of mechanisms and mechanistic explanation. Contrary to some treatments of mechanistic explanation, we maintain that explanation is an epistemic activity that involves representing and reasoning about mechanisms. We discuss the manner in which mechanistic approaches serve to bridge levels rather than (...) reduce them, as well as the different ways in which mechanisms are discovered. Finally, we offer a more detailed example of an important psychological phenomenon for which mechanistic explanation has provided the main source of scientific understanding. (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)

Most consciousness researchers, almost no matter what their views of the metaphysics of consciousness, can agree that the first step in a science of consciousness is the search for the neural correlate of consciousness (the NCC). The reason for this agreement is that the notion of ‘correlation’ doesn’t by itself commit one to any particular metaphysical view about the relation between (neural) matter and consciousness. For example, some might treat the correlates as causally related, while others might view the correlation (...) as evidence for identity between conscious states and brain states. The common ground therefore seems to be that the scientific search for the NCC is largely independent of the metaphysics of consciousness. (shrink)

Causation appears to present us with an interpretative difficulty. While arguably a redundant relation given fundamental physics, it is nevertheless apparently pragmatically indispensable. This chapter revisits certain arguments made previously by the author for these claims with the benefit of hindsight, starting with the role of causal models in the human sciences, and attempting to explain why it is not possible to straightforwardly ground such models in fundamental physics. This suggests that further constraints, going beyond physics, are needed to legitimate (...) such models. These supplementary constraints could be reified, but that would seem to conflict with the completeness of physics. A response is to emphasize the practical role of causal talk, and the author suggests that a fictionalist approach might be worth exploring. After clarifying fictionalism as a general approach, they carry out in some detail the project of clarifying what a fictionalist attitude to causation would involve. (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)

In what sense are the activities and properties of components in a mechanism explanatorily relevant to the behavior of a mechanism as a whole? I articulate this problem, the problem of constitutive relevance, and I show that it must be solved if we are to understand mechanisms and mechanistic explanation. I argue against some putative solutions to the problem of constitutive relevance, and I sketch a positive account according to which relevance is analyzed in terms ofrelationships of mutual manipulability between (...) the behavior of a mechanism as a whole and the properties and activities of its components. My account is a causal-mechanical account in the sense that it is a particular expression of the idea that constitutive explanation is a matter of showing how an explanandum phenomenon is situated within the causal structure of the world. It is thus offered as a rival to epistemic (argument-centered) and psychological accounts of interlevel explanation. (shrink)

Evolutionary developmental biology (evo-devo) is considered a ‘mechanistic science,’ in that it causally explains morphological evolution in terms of changes in developmental mechanisms. Evo-devo is also an interdisciplinary and integrative approach, as its explanations use contributions from many fields and pertain to different levels of organismal organization. Philosophical accounts of mechanistic explanation are currently highly prominent, and have been particularly able to capture the integrative nature of multifield and multilevel explanations. However, I argue that evo-devo demonstrates the need for a (...) broadened philosophical conception of mechanisms and mechanistic explanation. Mechanistic explanation (in terms of the qualitative interactions of the structural parts of a whole) has been developed as an alternative to the traditional idea of explanation as derivation from laws or quantitative principles. Against the picture promoted by Carl Craver, that mathematical models describe but usually do not explain, my discussion of cases from the strand of evo-devo which is concerned with developmental processes points to qualitative phenomena where quantitative mathematical models are an indispensable part of the explanation. While philosophical accounts have focused on the actual organization and operation of mechanisms, properties of developmental mechanisms that are about how a mechanism reacts to modifications are of major evolutionary significance, including robustness, phenotypic plasticity, and modularity. A philosophical conception of mechanisms is needed that takes into account quantitative changes, transient entities and the generation of novel types of entities, feedback loops and complex interaction networks, emergent properties, and, in particular, functional-dynamical aspects of mechanisms, including functional (as opposed to structural) organization and distributed, system-wide phenomena. I conclude with general remarks on philosophical accounts of explanation. (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)

Geologists, Paleontologists and other historical scientists are frequently concerned with narrative explanations targeting single cases. I show that two distinct explanatory strategies are employed in narratives, simple and complex. A simple narrative has minimal causal detail and is embedded in a regularity, whereas a complex narrative is more detailed and not embedded. The distinction is illustrated through two case studies: the ‘snowball earth’ explanation of Neoproterozoic glaciation and recent attempts to explain gigantism in Sauropods. This distinction is revelatory of historical (...) science. I argue that at least sometimes which strategy is appropriate is not a pragmatic issue, but turns on the nature of the target. Moreover, the distinction reveals a counterintuitive pattern of progress in some historical explanation: shifting from simple to complex. Sometimes, historical scientists rightly abandon simple, unified explanations in favour of disunified, complex narratives. Finally I compare narrative and mechanistic explanation, arguing that mechanistic approaches are inappropriate for complex narrative explanations. (shrink)

Among the current philosophical attempts to understand causation two seem to be the most prominent. The first is James Woodward’s counterfactual approach; the second is the mechanistic approach advocated by Peter Machamer, Lindley Darden, Carl Craver, Jim Bogen and Stuart Glennan. The counterfactual approach takes it that causes make a difference to their effects, where this difference-making is cashed out in terms of actual and counterfactual interventions. The mechanistic approach takes it that two events are causally related if and only (...) if there is a mechanism that connects them. On the face of it, the two approaches need not be in conflict. The mechanisms might satisfy (or depend on) certain interventionist counterfactuals and, conversely, the interventionist counterfactuals might be made true by the presence of certain mechanisms. But, overall, both approaches tend to be imperialistic. Advocates of each argue that their own approach fairs much better than their opponents’. The question then is this: are we forced to choose between the mechanistic approach and the counterfactual one? In this paper, I argue that, as they stand, both approaches face some important problems that need to be fixed. I shall also argue that there is a sense in which the counterfactual approach is more basic than the mechanistic, though the former will benefit from a better understanding of the mechanisms that are at work in causal connections. So both approaches can work together to offer a better understanding of causation. If they work in tandem, they can offer us a glimpse of what Hume famously called “the secret connexion”. But in so far as the ‘secret connexion’ is an intrinsic relation between the causal relata, neither of the above approaches tells us what this relation is. (shrink)

Genome-wide association studies of human complex traits have provided us with new estimates of heritability. These estimates foreground the question of genetic causation. After having presen...

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)

There have been recent disagreements in the philosophy of neuroscience regarding which sorts of scientific models provide mechanistic explanations, and which do not. These disagreements often hinge on two commonly adopted, but conflicting, ways of understanding mechanistic explanations: what I call the “representation-as” account, and the “representation-of” account. In this paper, I argue that neither account does justice to neuroscientific practice. In their place, I offer a new alternative that can defuse some of these disagreements. I argue that individual models (...) do not provide mechanistic explanations by themselves. Instead, individual models are always used to complement a huge body of background information and pre-existing models about the target system. With this in mind, I argue that mechanistic explanations are distributed across sets of different, and sometimes contradictory, scientific models. Each of these models contributes limited, but essential, information to the same mechanistic explanation, but none can be considered a mechanistic explanation in isolation of the others. (shrink)

Though the realm of biology has long been under the philosophical rule of the mechanistic magisterium, recent years have seen a surprisingly steady rise in the usurping prowess of process ontology. According to its proponents, theoretical advances in the contemporary science of evo-devo have afforded that ontology a particularly powerful claim to the throne: in that increasingly empirically confirmed discipline, emergently autonomous, higher-order entities are the reigning explanantia. If we are to accept the election of evo-devo as our best conceptualisation (...) of the biological realm with metaphysical rigour, must we depose our mechanistic ontology for failing to properly “carve at the joints” of organisms? In this paper, I challenge the legitimacy of that claim: not only can the theoretical benefits offered by a process ontology be had without it, they cannot be sufficiently grounded without the metaphysical underpinning of the very mechanisms which processes purport to replace. The biological realm, I argue, remains one best understood as under the governance of mechanistic principles. (shrink)

It has recently been argued that successful evidence-based policy should rely on two kinds of evidence: statistical and mechanistic. The former is held to be evidence that a policy brings about the desired outcome, and the latter concerns how it does so. Although agreeing with the spirit of this proposal, we argue that the underlying conception of mechanistic evidence as evidence that is different in kind from correlational, difference-making or statistical evidence, does not correctly capture the role that information about (...) mechanisms should play in evidence-based policy. We offer an alternative account of mechanistic evidence as information concerning the causal pathway connecting the policy intervention to its outcome. Not only can this be analyzed as evidence of difference-making, it is also to be found at any level and is obtainable by a broad range of methods, both experimental and observational. Using behavioral policy as an illustration, we draw the implications of this revised understanding of mechanistic evidence for debates concerning policy extrapolation, evidence hierarchies, and evidence integration. (shrink)

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

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

Recent papers by a number of philosophers have been concerned with the question of whether natural selection is a causal process, and if it is, whether the causes of selection are properties of individuals or properties of populations. I shall argue that much confusion in this debate arises because of a failure to distinguish between causal productivity and causal relevance. Causal productivity is a relation that holds between events connected via continuous causal processes, while causal relevance is a relationship that (...) can hold between a variety of different kinds of facts and the events that counterfactually depend upon them. I shall argue that the productive character of natural selection derives from the aggregation of individual processes in which organisms live, reproduce and die. At the same time, a causal explanation of the distribution of traits will necessarily appeal both to causally relevant properties of individuals and to causally relevant properties that exist only at the level of the population. (shrink)

The most compelling extant accounts of explanation casts all explanations as causal. Yet there are sciences, theoretical population biology in particular, that explain their phenomena by appeal to statistical, non-causal properties of ensembles. I develop a generalised account of explanation. An explanation serves two functions: metaphysical and cognitive. The metaphysical function is discharged by identifying a counterfactually robust invariance relation between explanans event and explanandum. The cognitive function is discharged by providing an appropriate description of this relation. I offer examples (...) of explanations from portfolio theory and population genetics that meet this characterisation. In each case the invariance relation holds between a statistical property of an ensemble and a change in structure of the ensemble. In neither case, however, does the statistical property cause the outcome it explains. There are genuine statistical, non-causal scientific explanations. (shrink)

In this paper we identify six theses that constitute core results of philosophical investigation into the nature of mechanisms, and of the role that the search for and identification of mechanisms play in the sciences. These theses represent the fruits of the body of research that is now often called New Mechanism. We concisely present the main arguments for these theses. In the literature, these arguments are scattered and often implicit. Our analysis can guide future research in many ways: it (...) provides critics of New Mechanism with clear targets, it can reduce misunderstandings, it can clarify differences of opinion among New Mechanists and it helps to define a research agenda for New Mechanists. (shrink)

One of Stuart Glennan's most prominent contributions to the new mechanist debate consists in his reductive analysis of higher-level causation in terms of mechanisms (Glennan, 1996). In this paper I employ the causal Bayes net framework to reconstruct his analysis. This allows for specifying general assumptions which have to be satis ed to get Glennan's approach working. I show that once these assumptions are in place, they imply (against the background of the causal Bayes net machinery) that higher-level causation indeed (...) reduces to interactions between component parts of mechanisms. I also briefly discuss the plausibility of these assumptions and some consequences for the mechanism debate. (shrink)

Mechanisms have become much-discussed, yet there is still no consensus on how to characterise them. In this paper, we start with something everyone is agreed on – that mechanisms explain – and investigate what constraints this imposes on our metaphysics of mechanisms. We examine two widely shared premises about how to understand mechanistic explanation: (1) that mechanistic explanation offers a welcome alternative to traditional laws-based explanation and (2) that there are two senses of mechanistic explanation that we call ‘epistemic explanation’ (...) and ‘physical explanation’. We argue that mechanistic explanation requires that mechanisms are both real and local. We then go on to argue that real, local mechanisms require a broadly active metaphysics for mechanisms, such as a capacities metaphysics. (shrink)

Like Laland et al., I think Mayr’s distinction is problematic, but I identify a further problem with it. I argue that Mayr’s distinction is a false dichotomy, and obscures an important question about evolutionary change. I show how this question, once revealed, sheds light on some debates in evo-devo that Laland et al.’s analysis cannot, and suggest that it provides a different view about how future integration between biological disciplines might proceed.

Both clinical research and basic science rely on the epistemic practice of extrapolation from surrogate models, to the point that explanatory accounts presented in review papers and biology textbooks are in fact composite pictures reconstituted from data gathered in a variety of distinct experimental setups. This raises two new challenges to previously proposed mechanistic-similarity solutions to the problem of extrapolation: one pertaining to the absence of mechanistic knowledge in the early stages of research and the second to the large number (...) of extrapolations underpinning explanatory accounts. An analysis of the strategies deployed in experimental research supports the conclusion that while results from validated surrogate models are treated as a legitimate line of evidence supporting claims about target systems, the overall structure of research projects also demonstrates that extrapolative inferences are not considered definitive or sufficient evidence, but only partially justified hypotheses subjected to further testing. 1 Introduction2 Surrogate Models2.1 What exactly is a surrogate model?2.2 Why use surrogate models?3 Prior Validation of Surrogate Models3.1 The validation and ranking of surrogate models in the early stages of basic research3.2 The validation of surrogate models in later stages of basic research and in clinical research4 ‘Big Picture’ Accounts and the Extrapolations Underpinning Them4.1 The mosaic nature of mechanistic descriptions in basic science4.2 Challenges for mechanistic-similarity-based validation protocols5 Retrospective Testing of Extrapolated Knowledge5.1 Holistic confirmation5.2 Fallback strategies6 Conclusions. (shrink)

In robustness analysis, hypotheses are supported to the extent that a result proves robust, and a result is robust to the extent that we detect it in diverse ways. But what precise sense of diversity is at work here? In this paper, I show that the formal explications of evidential diversity most often appealed to in work on robustness – which all draw in one way or another on probabilistic independence – fail to shed light on the notion of diversity (...) relevant to robustness analysis. I close by briefly outlining a promising alternative approach inspired by Horwich’s (1982) eliminative account of evidential diversity. (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)

The paper discusses methodological guidelines for evaluating mechanistic explanations. According to current accounts, a satisfactory mechanistic explanation should include all of the relevant features of the mechanism, its component entities and activities, and their properties and organization, as well as exhibit productive continuity. It is not specified, however, how this kind of mechanistic completeness can be demonstrated. I argue that parameter sufficiency inferences based on mathematical model simulations provide a way of determining whether a mechanism capable of producing the phenomenon (...) of interest can be constructed from mechanistic components organized, acting, and having the properties described in the mechanistic explanation. (shrink)

Mechanisms are a way of explaining how biological phenomena work rather than why single elements of biological systems are there. However, mechanisms are usually described as physiological entities, and little or no attention is paid to malfunction as an independent theoretical concept. On the other hand, malfunction is the main focus of interest of applied sciences such as medicine. In this paper I argue that malfunctions are parts of pathological mechanisms, which should be considered separate theoretical entities, conceptually having a (...) priority over physiological sequences. While pathological mechanisms can be described in terms of a Cummins-like mechanistic explanation, they show some unnoticed peculiarities when compared to physiological ones. Some features of pathological mechanisms are considered, such as outcome variability, ambivalence and dependence on a range. (shrink)

We argue that neuroeconomics should be a mechanistic science. We defend this view as preferable both to a revolutionary perspective, according to which classical economics is eliminated in favour of neuroeconomics, and to a classical economic perspective, according to which economics is insulated from facts about psychology and neuroscience. We argue that, like other mechanistic sciences, neuroeconomics will earn its keep to the extent that it either reconfigures how economists think about decision-making or how neuroscientists think about brain mechanisms underlying (...) behaviour. We discuss some ways that the search for mechanisms can bring about such top-down and bottom-up revision, and we consider some examples from the recent neuroeconomics literature of how varieties of progress of this sort might be achieved. (shrink)

Although contemporary metaphysics has recently undergone a neo-Aristotelian revival wherein dispositions, or capacities are now commonplace in empirically grounded ontologies, being routinely utilised in theories of causality and modality, a central Aristotelian concept has yet to be given serious attention – the doctrine of hylomorphism. The reason for this is clear: while the Aristotelian ontological distinction between actuality and potentiality has proven to be a fruitful conceptual framework with which to model the operation of the natural world, the distinction between (...) form and matter has yet to similarly earn its keep. In this chapter, I offer a first step toward showing that the hylomorphic framework is up to that task. To do so, I return to the birthplace of that doctrine - the biological realm. Utilising recent advances in developmental biology, I argue that the hylomorphic framework is an empirically adequate and conceptually rich explanatory schema with which to model the nature of organisms. (shrink)