A key assumption in the person-oriented approach is that a person must be understood as a complex, integrated system, represented by patterns of within-person variation rather than scores on separate variables. The term ‘system’ does, however, have multiple meanings, which are not clearly distinguished in the person-oriented literature. I try to disentangle causal interactionism, which describes the psychological consequences and functions of each component of the system as dependent upon its causal interaction with other system components, from content holism, which (...) describes the system components as in part constituted by their relations to each other and the system as a whole. Although the terms ‘interactionism’ and ‘holism’ are often treated as combinable and interchangeable, causal interactionism and content holism pertain to distinct kinds of research problems. Causal interactionism construes the person in terms of the hierarchically structured mechanistic systems that underpin his or her attributes and shape them over time, and can be exemplified in terms of Magnusson’s developmental approach, whereas content holism is integral to our understanding of the person as an intentional system, whose mental states and actions are interweaved through principles or logic and rationality rather than material causality, and can be exemplified in terms of Stephenson’s Q-methodological approach. (shrink)

The concept of mechanism in biology has three distinct meanings. It may refer to a philosophical thesis about the nature of life and biology (‘mechanicism’), to the internal workings of a machine-like structure (‘machine mechanism’), or to the causal explanation of a particular phenomenon (‘causal mechanism’). In this paper I trace the conceptual evolution of ‘mechanism’ in the history of biology, and I examine how the three meanings of this term have come to be featured in the philosophy of biology, (...) situating the new ‘mechanismic program’ in this context. I argue that the leading advocates of the mechanismic program (i.e., Craver, Darden, Bechtel, etc.) inadvertently conflate the different senses of ‘mechanism’. Specifically, they all inappropriately endow causal mechanisms with the ontic status of machine mechanisms, and this invariably results in problematic accounts of the role played by mechanism-talk in scientific practice. I suggest that for effective analyses of the concept of mechanism, causal mechanisms need to be distinguished from machine mechanisms, and the new mechanismic program in the philosophy of biology needs to be demarcated from the traditional concerns of mechanistic biology. (shrink)

Current psychological research on causal inference is dominated by two basic approaches: the covariation approach and the mechanism approach. This article reviews these two approaches, evaluates the contributions and limitations of each approach, and suggests how these approaches might be integrated into a more comprehensive framework. Covariation theorists assume that cognizers infer causal relations from conditional probabilities computed over samples of multiple events, but they do not provide an adequate account of how cognizers constrain their search for candidate causes and (...) relevant evidence. Mechanism theorists assume that cognizers use their knowledge of potential mechanisms to infer the causes of individual events, but they do not account for the origins of this kind of knowledge. Theorists might integrate these approaches into a framework that overcomes these limitations by (1) examining important relations between cognizers' beliefs about the nature of causality, the logic of causal inference, and the processes cognizers use to make causal inferences, and (2) providing a more complete account of cognizers' conceptions of causality and the origins of those conceptions. (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)

This chapter contains sections titled: Highlights of Past Literature Current Work Future Work.

In this study the notion of mechanistic entities is analyzed as it has been conceptualized by Hermann Lotze in his article Life. Vital Force (1842), the metaphysical foundation of which has recourse to his Metaphysik (1841) and Logik (1843). According to Lotze, explanations in the sciences are arguments which have a syntactic and a semantic structure—similar to that which became later known as the DN-model of explanation. The syntactic structure is delineated by ontological forms, the semantic by cosmological ones; the (...) latter comprise the preconditions for the construction of appearances in accord with the ontological forms. Mechanisms are embedded into this logical framework by representing the more complex spatio-temporal arrangements of cosmological entities. The coordinated model of a mechanism is a reductive type of explanation. This study also demonstrates how Lotze made use of his concept of mechanisms in order to explain law-like and probabilistic events in organic and inorganic nature, thereby establishing an original ‘oligomeric’ (i. e., a fraction of the parts of a system determines its development) variant of a preformative theory of ontogenesis which anticipates modern concepts of genetic determination. In this context, Lotze alludes to paradigms of dissipative structures. The relevance of these reflections for subsequent theories is shown by contrasting them with Schrödinger’s theory of organisms. Finally, a comparison of some aspects of Lotze’s concept of mechanisms with equivalent aspects of current normative approaches confirms that essential elements of the latter versions can be retrieved in the former one. Above that, Lotze employs the teleological aspect of ontological forms in order to determine the extent of the mechanistic system under consideration. He further differentiates three modal states of mechanisms and includes a concept to explain exceptions or irregularities. The concept of ‘activity’ is strictly excluded from his account and shown to be a metaphysical illusion. (shrink)

Although the analogy between macroscopic machines and biological molecular devices plays an important role in the conceptual framework of both neo-mechanistic accounts and nanotechnology, it has recently been claimed that certain complex molecular devices cannot be considered machines since they are subject to physicochemical forces that are different from those of macroscopic machines. However, the structural and physicochemical conditions that allow both macroscopic machines and microscopic devices to work and perform new functions, through a combination of elemental functional parts, have (...) not yet been examined. In order to fill this void, this paper has a threefold aim: first, to clarify the structural and organisational conditions of macroscopic machines and microscopic devices; second, to determine whether the machine-like analogy fits nanoscale devices; and third, to assess whether the machine-like analogy is appropriate for describing the behaviour of some biological macromolecules. Finally, the paper gives an account of ‘machine’ which, while acknowledging the physicochemical and organisational differences between man-made machines and biological microscopic devices, nevertheless identifies a common conceptual core that allows us to consider the latter ‘machines’. (shrink)

The claim defended in the paper is that the mechanistic account of explanation can easily embrace idealization in big-scale brain simulations, and that only causally relevant detail should be present in explanatory models. The claim is illustrated with two methodologically different models: Blue Brain, used for particular simulations of the cortical column in hybrid models, and Eliasmith’s SPAUN model that is both biologically realistic and able to explain eight different tasks. By drawing on the mechanistic theory of computational explanation, I (...) argue that large-scale simulations require that the explanandum phenomenon is identified; otherwise, the explanatory value of such explanations is difficult to establish, and testing the model empirically by comparing its behavior with the explanandum remains practically impossible. The completeness of the explanation, and hence of the explanatory value of the explanatory model, is to be assessed vis-à-vis the explanandum phenomenon, which is not to be conflated with raw observational data and may be idealized. I argue that idealizations, which include building models of a single phenomenon displayed by multi-functional mechanisms, lumping together multiple factors in a single causal variable, simplifying the causal structure of the mechanisms, and multi-model integration, are indispensable for complex systems such as brains; otherwise, the model may be as complex as the explanandum phenomenon, which would make it prone to so-called Bonini paradox. I conclude by enumerating dimensions of empirical validation of explanatory models according to new mechanism, which are given in a form of a “checklist” for a modeler. (shrink)

This article demonstrates that non-mechanistic, dynamical explanations are a viable approach to explanation in the special sciences. The claim that dynamical models can be explanatory without reference to mechanisms has previously been met with three lines of criticism from mechanists: the causal relevance concern, the genuine laws concern, and the charge of predictivism. I argue, however, that these mechanist criticisms fail to defeat non-mechanistic, dynamical explanation. Using the examples of Haken et al.’s model of bimanual coordination, and Thelen et al.’s (...) dynamical field model of infant perseverative reaching, I show how each mechanist criticism fails once the standards of Woodward’s interventionist framework are applied to dynamical models. An even-handed application of Woodwardian interventionism reveals that dynamical models are capable of producing genuine explanations without appealing to underlying mechanistic details. 1Introduction2Interventionism and Mechanistic Explanation 2.1Causal relevance and ideal interventions2.2Invariance2.3Explanation3Covering-Laws and Dynamical Explanation 3.1Dynamical models3.2Covering-law explanation3.3Prediction4Causal Relevance 4.1The causal relevance concern4.2Intervening on dynamical models4.3Test case I: The Haken–Kelso–Bunz model4.4Test case II: Dynamical field model5Genuine Laws 5.1The genuine laws concern5.2Using invariance in place of laws5.3Test case I: The Haken–Kelso–Bunz model5.4Test case II: Dynamical field model6Prediction 6.1Predictivism6.2Crude and invariant prediction7Interventionist Criticism of the Haken–Kelso–Bunz Model8Dynamical Explanation8Conclusion. (shrink)

Recently, a number of philosophers of science have claimed that much explanation in the sciences, especially in the biomedical and social sciences, is mechanistic explanation. I argue the account of mechanistic explanation provided in this tradition has not been entirely satisfactory, as it has neglected to describe in complete detail the crucial causal structure of mechanistic explanation. I show how the interventionist approach to causation, especially within a structural equations framework, provides a simple and elegant account of the causal structure (...) of mechanisms. This account explains the many useful insights of traditional accounts of mechanism, such as Carl Craver's account in his book Explaining the Brain , but also helps to correct the omissions of such accounts. One of these omissions is the failure to provide an explicit formulation of a modularity constraint that plays a significant role in mechanistic explanation. One virtue of the interventionist/structural equations framework is that it allows for a simple formulation of a modularity constraint on mechanistic explanation. I illustrate the role of this constraint in the last section of the paper, which describes the form that mechanistic explanation takes in the computational, information-processing paradigm of cognitive psychology. (shrink)

Much contemporary debate on the nature of mechanisms centers on the issue of modulating negative causes. One type of negative causability, which I refer to as "causation by absence," appears difficult to incorporate into modern accounts of mechanistic explanation. This paper argues that a recent attempt to resolve this problem, proposed by Benjamin Barros, requires improvement as it overlooks the fact that not all absences qualify as sources of mechanism failure. I suggest that there are a number of additional types (...) of effects caused by absences that need to be incorporated to account for the diversity of causal connections in the biological sciences. Furthermore, it is argued that recognizing natural variability in mechanisms, such as attenuation, leads to some interesting line-drawing issues for contemporary philosophy of mechanisms. (shrink)

Much contemporary debate on the nature of mechanisms centers on the issue of modulating negative causes. One type of negative causability, which I refer to as “causation by absence,” appears difficult to incorporate into modern accounts of mechanistic explanation. This paper argues that a recent attempt to resolve this problem, proposed by Benjamin Barros, requires improvement as it overlooks the fact that not all absences qualify as sources of mechanism failure. I suggest that there are a number of additional types (...) of effects caused by absences that need to be incorporated to account for the diversity of causal connections in the biological sciences. Furthermore, it is argued that recognizing natural variability in mechanisms, such as attenuation, leads to some interesting line-drawing issues for contemporary philosophy of mechanisms. (shrink)

mechanism" is frequently encountered in the social science literature, but there is considerable confusion about the exact meaning of the term. The article begins by addressing the main conceptual issues. Use of this term is the hallmark of an approach that is critical of the explanatory deficits of correlational analysis and of the covering-law model, advocating instead the causal reconstruction of the processes that account for given macro-phenomena. The term "social mechanisms" should be used to refer to recurrent processes generating (...) a specific kind of outcome. Explanation of social macro-phenomena by mechanisms typically involves causal regression to lower-level elements, as stipulated by methodological individualism. While there exist a good many mechanism models to explain emergent effects of collective behavior, we lack a similarly systematic treatment of generative mechanisms in which institutions and specific kinds of structural configurations play the decisive role. Key Words: causal regression • correlational analysis • emergent effects • micro-macro processes • social mechanisms • structural determinants. (shrink)

Diagnoses in medicine are often taken to serve as explanations of patients’ symptoms and signs. This article examines how they do so. I begin by arguing that although some instances of diagnostic explanation can be formulated as covering law arguments, they are explanatory neither in virtue of their argumentative structures nor in virtue of general regularities between diagnoses and clinical presentations. I then consider the theory that medical diagnoses explain symptoms and signs by identifying their actual causes in particular cases. (...) While I take this to be largely correct, I argue that for a diagnosis to function as a satisfactory causal explanation of a patient’s symptoms and signs, it also needs to be supplemented by understanding the mechanisms by which the identified cause produces the symptoms and signs. This mechanistic understanding comes not from the diagnosis itself, but rather from the theoretical framework within which the physician operates. (shrink)

In addition to theorizing about the role and value of mechanisms in scientific explanation or the causal structure of the world, there is a fundamental task of getting straight what a ‘mechanism’ is in the first place. Broadly, this paper is about the challenge of application: the challenge of aligning one's philosophical account of a scientific concept with the manner in which that concept is actually used in scientific practice. This paper considers a case study of the challenge of application (...) as it pertains to the concept of a mechanism: the debate about whether natural selection is a mechanism. By making clear what is and is not at stake in this debate, this paper considers various strategies for dealing with the challenge of application and makes a case for definitional pluralism about mechanism concepts. (shrink)

It is argued that once biological systems reach a certain level of complexity, mechanistic explanations provide an inadequate account of many relevant phenomena. In this article, I evaluate such claims with respect to a representative programme in systems biological research: the study of regulatory networks within single-celled organisms. I argue that these networks are amenable to mechanistic philosophy without need to appeal to some alternate form of explanation. In particular, I claim that we can understand the mathematical modelling techniques of (...) systems biologists as part of a broader practice of constructing and evaluating mechanism schemas. This argument is elaborated by considering the case of bacterial chemotactic networks, where some research has been interpreted as explaining phenomena by means of abstract design principles. (shrink)

Philosophers of the social sciences are increasingly convinced that macro-and micro-explanations are complementary. Whereas macro-explanations are broad, micro-explanations are deep. I distinguish between weak and strong complementarity: Strongly complementary explanations improve one another when integrated, weakly complementary explanations do not. To demonstrate the explanatory autonomy of different levels of explanation, explanatory pluralists mostly presuppose the weak form of complementarity. By scrutinizing the notions of explanatory depth and breadth, I argue that macro- and micro-accounts of the same phenomenon are more often (...) strongly complementary. This invites a revision of the pluralist position in which integration promotes explanatory progress. Key Words: explanatory pluralism • social science • explanatory depth • explanatory breadth • mechanism. (shrink)

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)

The concept of mechanism is analyzed in terms of entities and activities, organized such that they are productive of regular changes. Examples show how mechanisms work in neurobiology and molecular biology. Thinking in terms of mechanisms provides a new framework for addressing many traditional philosophical issues: causality, laws, explanation, reduction, and scientific change.

In natural kind debates, Boyd's famous Homeostatic Property Cluster theory (HPC) is often misconstrued in two ways: Not only is it thought to make for a normative standard for natural kinds, but also to require the homeostatic mechanisms underlying nomological property clusters to be uniform. My argument for the illegitimacy of both overgeneralizations, both on systematic as well as exegetical grounds, is based on the misconstrued view's failure to account for functional kinds in science. I illustrate the combination of these (...) two misconstruals with recent entries into the natural kind debate about emotions. Finally, I examine and reject Stich's "Kornblith-Devitt method" as a potential justification of these misconstruals. (shrink)

Science depends on judgments of the bearing of evidence on theory. Scientists must judge whether an observation or the result of an experiment supports, disconfirms, or is simply irrelevant to a given hypothesis. Similarly, scientists may judge that, given all the available evidence, a hypothesis ought to be accepted as correct or nearly so, rejected as false, or neither. Occasionally, these evidential judgments can be made on deductive grounds. If an experimental result strictly contradicts a hypothesis, then the truth of (...) the data deductively entails the falsity of the hypothesis. In the great majority of cases, however, the connection between evidence and hypothesis is non-demonstrative, or inductive. In particular, this is so whenever a general hypothesis is inferred to be correct on the basis of the available data, since the truth of the data will not deductively entail the truth of the hypothesis. It always remains possible that the hypothesis is false even though the data are correct. (shrink)

In 1958, Francis Crick distinguished the flow of information from the flow of matter and the flow of energy in the mechanism of protein synthesis. Crick’s claims about information flow and coding in molecular biology are viewed from the perspective of a new characterization of mechanisms and from the perspective of information as holding a key to distinguishing work in molecular biology from that of biochemistry in the 1950s–1970s . Flow of matter from beginning to end does not occur in (...) the protein synthesis mechanism; flow of information does. The flow of information and coding in molecular biological mechanisms are distinguished, on the one hand, from formal information theory, and, on the other, from information as used in cognitive neuroscience, where information and representation are often coupled. (shrink)

I distinguish three theses associated with the new mechanistic philosophy – concerning causation, explanation and scientific methodology. Advocates of each thesis are identified and relationships among them are outlined. I then look at some recent work on natural selection and mechanisms. There, attention to different kinds of New Mechanism significantly affects of what is at stake.

What are scientific theories and how should they be represented? In this article, I propose a causal–structural account, according to which scientific theories are to be represented as sets of interrelated causal and credal nets. In contrast with other accounts of scientific theories (such as Sneedian structuralism, Kitcher’s unificationist view, and Darden’s theory of theoretical components), this leaves room for causality to play a substantial role. As a result, an interesting account of explanation is provided, which sheds light on explanatory (...) unification within a causalist framework. The theory of classical genetics is used as a case study. 1 Introduction2 The Theory of Classical Genetics3 Three Philosophical Accounts of the Theory of Classical Genetics3.1 The structuralist account3.2 Kitcher’s unificationism3.3 Darden and theory change in science4 A Common Lacuna: Where is Causality?5 Woodward’s Interventionist Account of Causation6 Causal Bayes Nets and Their Interrelations6.1 Causal Bayes nets6.2 Relations among causal nets6.3 Credal nets and their interrelations7 The Theory of the Gene and its Causal Graph8 A First Exemplar: Stem Length in Pea Plants8.1 Three crosses on stem length in pea plants8.2 The causal graph for stem length in pea plants8.3 Morgan’s explanatory principles and the credal net for stem length in pea plants9 Explaining Mendel’s Crosses: A Causal–Structural Account10 Monohybrid Crosses with Complete Dominance11 Exemplars,Explanatory Patterns, Generic Credal Nets, and Mechanism Schemas12 Incomplete Dominance13 Anomalies14 Multi-hybrid Crosses with Independent Assortment15 Multi-hybrid Crosses with Linkage and Crossing-Over16 Double Crossing-Over and the Linear Order of the Gene17 Causal–Structural Explanation18 Explanatory Unification19 Concluding Remarks. (shrink)

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)

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)

Mechanistic approaches are very common in the causal interpretation of biological and neuroscientific experimental work in today’s philosophy of science. In the mechanistic literature a strict distinction is often made between causal relations and constitutive relations, where the latter cannot be causal. One of the typical reasons for this strict distinction is that constitutive relations are supposedly synchronic whereas most if not all causal relations are diachronic. This strict distinction gives rise to a number of problems, however. Our end goal (...) in this paper is to argue that it should be given up, at least in the context of the biological and the psychological sciences. To that effect, we argue that constitutive relations in this context are diachronic, thus undermining the aforementioned reason. We offer two cases from scientific practice in which constitutive relations are regarded as both diachronic and causally efficacious, review three existing ways of dealing with the apparent diachronic nature of interlevel relations in mechanisms and propose a new account of diachronic, causal constitutive relevance. (shrink)

Whole brain failure constitutes the diagnostic criterion for death determination in most clinical settings across the globe. Yet the conceptual foundation for its adoption was slow to emerge, has evoked extensive scientific debate since inception, underwent policy revision, and remains contentious in praxis even today. Complications result from the need to relate a unitary construal of the death event with an adequate account of organismal integration and that of the human organism in particular. Advances in the neuroscience of higher human (...) faculties, such as the self, personal identity, and consciousness, and dynamical philosophy of science accounts, however, are yielding a portrait of higher order global integration shared between body and brain. Such conceptual models of integration challenge a praxis relying exclusively on a neurological criterion for death. (shrink)

Proponents of Evidence-based medicine (EBM) do not provide a clear role for basic science in therapeutic decision making. Of what they do say about basic science, most of it is negative. Basic science resides on the lower tiers of EBM's hierarchy of evidence. Therapeutic decisions, according to proponents of EBM, should be informed by evidence from randomised studies (and systematic reviews of randomised studies) rather than basic science. A framework of models explicates the links between the mechanisms of basic science, (...) experimental inquiry, and observed data. Relying on the framework of models I show that basic science often plays a role not only in specifying experiments, but also analysing and interpreting the data that is provided. Further, and contradicting what is implied in EBM's hierarchy of evidence, appeals to basic science are often required to apply clinical research to therapeutic questions. © 2010 Springer Science+Business Media B.V. (shrink)

Although there has been much recent discussion on mechanisms in philosophy of science and social theory, no shared understanding of the crucial concept itself has emerged. In this paper, a distinction between two core concepts of mechanism is made on the basis that the concepts correspond to two different research strategies: the concept of mechanism as a componential causal system is associated with the heuristic of functional decomposition and spatial localization and the concept of mechanism as an abstract form of (...) interaction is associated with the strategy of abstraction and simple models. The causal facts assumed and the theoretical consequences entailed by an explanation with a given mechanism differ according to which concept of mechanism is in use. Research strategies associated with mechanism concepts also involve characteristic biases that should be taken into account when using them, especially in new areas of application. (shrink)

This paper aims to provide Humean metaphysics for the interventionist theory of causation. This is done by appealing to the hierarchical picture of causal relations as being realized by mechanisms, which in turn are identified with lower-level causal structures. The modal content of invariances at the lowest level of this hierarchy, at which mechanisms are reduced to strict natural laws, is then explained in terms of projectivism based on the best-system view of laws.

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

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

Volume 32, Issue 1, March 2019, Page 69-72.

In contemporary philosophy of science, the consensus view seems to be that scientific explanations describe mechanisms responsible for the phenomena to be explained. Two kinds of explanatory relevance figure in mechanistic accounts of explanation: causal and constitutive. Following prominent accounts, it seems natural to analyze both these relations in terms of systematic interventions into some factor X with respect to another factor Y. However, such interventions are tailored to uncover causal relations only. Construing the constitutive relationship between parts and wholes (...) in terms of interventions thus raises metaphysical, conceptual, and epistemological questions. We here review the barriers that intervention-based inquiry into mechanisms encounters and consider some solutions. (shrink)

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

Cartwright et al. in European Journal for Philosophy of Science, 10 and the new mechanists agree that regular behaviors described in cp laws are generated by mechanisms. However, there is disagreement with regard to the two questions that Cartwright at al. ask: the epistemological question and the ontological question. Most importantly, Cartwright et al. argue that the explanation involved is a CL-explanation, while the new mechanists insist that mechanistic explanation and CL-explanation are competitors. In this reply, I will highlight some (...) worries regarding Cartwright et al.’s analysis of the relationship between mechanisms and cp laws and I will provide alternative answers to the two questions in line with the new mechanistic approach. (shrink)

Most defenders of the new mechanistic approach accept ontic constraints for successful scientific explanation (Illari 2013; Craver 2014). The minimal claim is that scientific explanations have objective truthmakers, namely mechanisms that exist in the physical world independently of any observer and that cause or constitute the phenomena-to- be-explained. How can this idea be applied to type-level explanations? Many authors at least implicitly assume that in order for mechanisms to be the truthmakers of type-level explanation they need to be regular (Andersen (...) 2012; Sheredos 2015). One problem of this assumption is that most mechanisms are (highly) stochastic in the sense that they “fail more often than they succeed” (Bogen 2005; Andersen 2012). How can a mechanism type whose instances are more likely not to produce an instance of a particular phenomenon type be the truthmaker of the explanation of that particular phenomenon type? In this paper, I will give an answer to this question. I will analyze the notion of regularity and I will discuss Andersen's suggestion for how to cope with stochastic mechanisms. I will argue that her suggestion cannot account for all kinds of stochastic mechanisms and does not provide an answer as to why regularity grounds type-level explanation. According to my analysis, a mechanistic type- level explanation is true if and only if at least one of the following two conditions is satisfied: the mechanism brings about the phenomenon more often than any other phenomenon (comparative regularity) or the phenomenon is more often brought about by the mechanism than by any other mechanism/causal sequence (comparative reverse regularity). (shrink)

There are three main kinds of causal connections between two events: the transfer of energy, the transfer of information and the triggering of the transfer of one of them or both. There are also other kinds of causal connections.

We provide three innovations to recent debates about whether topological or “network” explanations are a species of mechanistic explanation. First, we more precisely characterize the requirement that all topological explanations are mechanistic explanations and show scientific practice to belie such a requirement. Second, we provide an account that unifies mechanistic and non-mechanistic topological explanations, thereby enriching both the mechanist and autonomist programs by highlighting when and where topological explanations are mechanistic. Third, we defend this view against some powerful mechanist objections. (...) We conclude from this that topological explanations are autonomous from their mechanistic counterparts. (shrink)

We argue that dynamical and mathematical models in systems and cognitive neuro- science explain (rather than redescribe) a phenomenon only if there is a plausible mapping between elements in the model and elements in the mechanism for the phe- nomenon. We demonstrate how this model-to-mechanism-mapping constraint, when satisfied, endows a model with explanatory force with respect to the phenomenon to be explained. Several paradigmatic models including the Haken-Kelso-Bunz model of bimanual coordination and the difference-of-Gaussians model of visual receptive fields are (...) explored. (shrink)

The central aim of this article is to specify the ontological nature of constitutive mechanistic phenomena. After identifying three criteria of adequacy that any plausible approach to constitutive mechanistic phenomena must satisfy, we present four different suggestions, found in the mechanistic literature, of what mechanistic phenomena might be. We argue that none of these suggestions meets the criteria of adequacy. According to our analysis, constitutive mechanistic phenomena are best understood as what we will call ‘object-involving occurrents’. Furthermore, on the basis (...) of this notion, we will clarify what distinguishes constitutive mechanistic explanations from etiological ones. 1 Introduction 2 Criteria of Adequacy 2.1 Descriptive adequacy 2.2 Constitutive–etiological distinction 2.3 Constitution 3 The Ontological Nature of Constitutive Mechanistic Phenomena 3.1 Phenomena as input–output relations 3.2 Phenomena as end states 3.3 Phenomena as dispositions 3.4 Phenomena as behaviours 4 Phenomena as Object-Involving Occurrents 4.1 What object-involving occurrents are and why we need them 4.2 The object in the phenomenon 4.3 The adequacy of option 5 Conclusion. (shrink)