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

Which way does causation proceed? The pattern in the material world seems to be upward: particles to molecules to organisms to brains to mental processes. In contrast, the principles of quantum mechanics allow us to see a pattern of downward causation. These new ideas describe sets of multiple levels in which each level influences the levels below it through generation and selection. Top-down causation makes exciting sense of the world: we can find analogies in psychology, in the formation of our (...) minds, in locating the source of consciousness, and even in the possible logic of belief in God. (shrink)

I examine to what extent accounts of mechanisms based on formal interventionist theories of causality can adequately represent biological mechanisms with complex dynamics. Using a differential equation model for a circadian clock mechanism as an example, I first show that there exists an iterative solution that can be interpreted as a structural causal model. Thus, in principle, it is possible to integrate causal difference-making information with dynamical information. However, the differential equation model itself lacks the right (...) modularity properties for a full integration. A formal mechanistic model will therefore have to leave out either noncausal or causal explanatory relations. (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)

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)

manuscript delves into the philosophical debate surrounding the Special Composition Question (SCQ), focusing on the causal relationships between objects and their constituent parts. By distinguishing between Weak and Strong Causal Composition, the article explores how causal mechanisms underpin the composition of objects. Theories from notable philosophers, including van Inwagen and Leibniz, are evaluated. This study seeks to bridge the gap between common sense perspectives and principled ontological theories by introducing the concepts of Weak and Strong (...) class='Hi'>Causal Composition. The analysis reveals how a causal approach can offer insightful resolutions to longstanding debates in mereology and ontology, emphasizing the role of causality in understanding the essence of material composition. The proposed causal perspective encourages further philosophical inquiry into the foundational principles governing the composition of objects. (shrink)

The chapter explores whether, or to what extent, recent work in experimental philosophy puts pressure on the idea that the concept of causation is ‘egalitarian’. Causal selection – where experimental subjects tend to rate the causal strength of (for example) a norm-violator more strongly than a non-norm-violator – is a well established phenomenon, and is in prima facie tension with an egalitarian conception of causation; it also, indirectly, puts prima facie pressure on the idea that causation is a (...) worldly phenomenon whose obtaining is independent of facts about norms. The chapter explores both the various psychological mechanisms and the broadly pragmatic approaches to explaining causal selection. It argues that the answer to the question whether or not the concept of causation is egalitarian is currently significantly empirically underdetermined, and suggests some avenues for further investigation. (shrink)

Leuridan (2011) questions whether mechanisms can really replace laws at the heart of our thinking about science. In doing so, he enters a long-standing discussion about the relationship between the mech-anistic structures evident in the theories of contemporary biology and the laws of nature privileged especially in traditional empiricist traditions of the philosophy of science (see e.g. Wimsatt 1974; Bechtel and Abrahamsen 2005; Bogen 2005; Darden 2006; Glennan 1996; MDC 2000; Schaffner 1993; Tabery 2003; Weber 2005). In our view, (...) Leuridan misconstrues this discussion. His weak positive claim that mechanistic sciences appeal to generalizations is true but uninteresting. His stronger claim, that all causal claims require laws, is unsupported by his arguments. Though we proceed by criticizing Leuridan’s arguments, our greater purpose is to embellish his arguments in order to show how thinking about mechanisms enriches and transforms old philosophical debates about laws in biology and provides new insights into how generalizations afford prediction, explanation and control. (shrink)

Some recent accounts of constitutive relevance have identified mechanism components with entities that are causal intermediaries between the input and output of a mechanism. I argue that on such accounts there is no distinctive inter-level form of mechanistic explanation and that this highlights an absence in the literature of a compelling argument that there are such explanations. Nevertheless, the entities that these accounts call ‘components’ do play an explanatory role. Studying causal intermediaries linking variables Xand Y provides knowledge (...) of the counterfactual conditions under which X will continue to bring about Y. This explanatory role does not depend on whether intermediate variables count as components. The question of whether there are distinctively mechanistic explanations remains open. (shrink)

In this chapter we examine the relation between mechanisms and laws/counterfactuals by revisiting the main notions of mechanism found in the literature. We distinguish between two different conceptions of ‘mechanism’: mechanisms-of underlie or constitute a causal process; mechanisms-for are complex systems that function so as to produce a certain behavior. According to some mechanists, a mechanism fulfills both of these roles simultaneously. The main argument of the chapter is that there is an asymmetrical dependence between both (...) kinds of mechanisms and laws/counterfactuals: while some laws and counterfactuals must be taken as primitive (non-mechanistic) facts of the world, all mechanisms depend on laws/counterfactuals. (shrink)

Griffiths et al. (2015) have proposed a quantitative measure of causal specificity and used it to assess various attempts to single out genetic causes as being causally more specific than other cellular mechanisms, for example, alternative splicing. Focusing in particular on developmental processes, they have identified a number of important challenges for this project. In this discussion note, I would like to show how these challenges can be met.

In this paper I address an important question in Aristotle’s biology, What are the causal mechanisms behind the transmission of biological form? Aristotle’s answer to this question, I argue, is found in Generation of Animals Book 4 in connection with his investigation into the phenomenon of inheritance. There we are told that an organism’s reproductive material contains a set of "movements" which are derived from the various "potentials" of its nature (the internal principle of change that initiates and (...) controls development). These movements, I suggest, function as specialized vehicles for communicating the parts of the parent’s heritable form during the act of reproduction. After exploring the details of this mechanism, I then take up Aristotle’s theory of inheritance proper. At the heart of the theory are three general principles (or 'laws') that govern the interactions between the maternal and paternal movements, the outcome of which determines the pattern of inheritance for the offspring. Although this paper is primarily aimed at providing a detailed analysis of Aristotle’s account of inheritance, the results of that analysis have implications for other areas of Aristotle’s biology. One of the most interesting of these is the question of whether Aristotle’s biology is anti-evolutionary (as traditionally assumed) or whether (as I argue) it leaves room for a theory of evolution by natural selection, even if Aristotle himself never took that step. (shrink)

This thesis examines philosophical controversies surrounding the evaluation of medical treatments, with a focus on the evidential roles of randomised trials and mechanisms in Evidence-Based Medicine. Current 'best practice' usually involves excluding non-randomised trial evidence from systematic reviews in cases where randomised trials are available for inclusion in the reviews. The first paper challenges this practice and evaluates whether adding of evidence from non-randomised trials might improve the quality and precision of some systematic reviews. The second paper compares the (...) alleged methodological benefits of randomised trials over observational studies for investigating treatment benefits. It suggests that claims about the superiority of well-conducted randomised controlled trials over well-conducted observational studies are justified, especially when results from the two methods are contradictory. The third paper argues that postulating the unpredictability paradox in systematic reviews when no detectable empirical differences can be found requires further justification. The fourth paper examines the problem of absence causation in the context of explaining causal mechanisms and argues that a recent solution is incomplete and requires further justification. Solving the problem by describing absences as causes of 'mechanism failure' fails to take into account the effects of absences that lead to vacillating levels of mechanism functionality. The fifth paper criticises literature that has emphasised functioning versus 'broken' or 'non-functioning' mechanisms emphasising that many diseases result from increased or decreased mechanism function, rather than complete loss of function. Mechanistic explanations must account for differences in the effectiveness of performed functions, yet current philosophical mechanistic explanations do not achieve this. The last paper argues that the standard of evidence embodied in the ICE theory of technological function is too permissive for evaluating whether the proposed functions of medical technologies have been adequately assessed and correctly ascribed. It argues that high-quality evidence from clinical studies is necessary to justify functional ascriptions to health care technologies. (shrink)

There are simple mechanical systems that elude causal representation. We describe one that cannot be represented in a single directed acyclic graph. Our case suggests limitations on the use of causal graphs for causal inference and makes salient the point that causal relations among variables depend upon details of causal setups, including values of variables.

For many old and new mechanists, Mechanism is both a metaphysical position and a thesis about scientific methodology. In this paper we discuss the relation between the metaphysics of mechanisms and the role of mechanical explanation in the practice of science, by presenting and comparing the key tenets of Old and New Mechanism. First, by focusing on the case of gravity, we show how the metaphysics of Old Mechanism constrained scientific explanation, and discuss Newton’s critique of Old Mechanism. Second, (...) we examine the current mechanistic metaphysics, arguing that it is not warranted by the use of the concept of mechanism in scientific practice, and motivate a thin conception of mechanism (the truly minimal view), according to which mechanisms are causal pathways for a certain effect or phenomenon. Finally, we draw analogies between Newton’s critique of Old Mechanism and our thesis that the metaphysical commitments of New Mechanism are not necessary in order to illuminate scientific practice. (shrink)

Quantum mechanics admits a “linguistic interpretation” if one equates preliminary any quantum state of some whether quantum entity or word, i.e. a wave function interpret-able as an element of the separable complex Hilbert space. All possible Feynman pathways can link to each other any two semantic units such as words or term in any theory. Then, the causal reasoning would correspond to the case of classical mechanics (a single trajectory, in which any next point is causally conditioned), and the (...) probabilistic reasoning, to the case of quantum mechanics (many Feynman trajectories). Frame semantics turns out to be the natural counterpart of that linguistic interpretation of quantum mechanics. (shrink)

Applied Evolutionary Epistemology is a scientific-philosophical theory that defines evolution as the set of phenomena whereby units evolve at levels of ontological hierarchies by mechanisms and processes. This theory also provides a methodology to study evolution, namely, studying evolution involves identifying the units that evolve, the levels at which they evolve, and the mechanisms and processes whereby they evolve. Identifying units and levels of evolution in turn requires the development of ontological hierarchy theories, and examining mechanisms and (...) processes necessitates theorizing about causality. Together, hierarchy and causality theories explain how biorealities form and diversify with time. This paper analyzes how Applied EE redefines both hierarchy and causality theories in the light of the recent explosion of network approaches to causal reasoning associated with studies on reticulate and macroevolution. Causality theories have often been framed from within a rigid, ladder-like hierarchy theory where the rungs of the ladder represent the different levels, and the elements on the rungs represent the evolving units. Causality then is either defined reductionistically as an upward movement along the strands of a singular hierarchy, or holistically as a downward movement along that same hierarchy. Upward causation theories thereby analyze causal processes in time, i.e. over the course of natural history or phylogenetically, as Darwin and the founders of the Modern Synthesis intended. Downward causation theories analyze causal processes in space, ontogenetically or ecologically, as the current eco-evo-devo schools are evidencing. This work demonstrates how macroevolution and reticulate evolution theories add to the complexity by examining reticulate causal processes in space–time, and the interactional hierarchies that such studies bring forth introduce a new form of causation that is here called reticulate causation. Reticulate causation occurs between units and levels belonging to different as well as to the same ontological hierarchies. This article concludes that beyond recognizing the existence of multiple units, levels, and mechanisms or processes of evolution, also the existence of multiple kinds of evolutionary causation as well as the existence of multiple evolutionary hierarchies needs to be acknowledged. This furthermore implies that evolution is a pluralistic process divisible into different kinds. (shrink)

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

The basic kinds of physical causality that are foundational for other kinds of causality involve objects and the causal relations between them. These interactions do not involve events. If events were ontologically significant entities for causality in general, then they would play a role in simple mechanical interactions. But arguments about simple collisions looked at from different frames of reference show that events cannot play a role in simple mechanical interactions, and neither can the entirely hypothetical causal relations (...) between events. These arguments show that physics, which should be authoritative when it comes to the metaphysics of causality, gives no reasons to believe that events are causal agents. Force relations and some cases of energy-momentum transfer are examples of causal relations, with forces being paradigmatic in the macroscopic world, though it is conceivable that there are other kinds of causal relation. A relation between two objects is a causal relation if and only if when it is instantiated by the two objects there is a possibility that the objects that are the terms of the relation could change. The basic metaphysics of causality is about objects, causal relations, changes in objects, and a causal primitive. The paper also includes a discussion of the metaphysics of forces and a discussion of the metaphysics of energy and momentum exchanges. (shrink)

I propose a dynamic causal approach to characterizing the notion of a mechanism. Levy and Bechtel, among others, have pointed out several critical limitations of the new mechanical philosophy, and pointed in a new direction to extend this philosophy. Nevertheless, they have not fully fleshed out what that extended philosophy would look like. Based on a closer look at neuroscientific practice, I propose that a mechanism is a dynamic causal system that involves various components interacting, typically nonlinearly, with (...) one another to produce a phenomenon of interest. (shrink)

There is a long tradition of logic, from Aristotle to Gödel, of understanding a proof from the concepts of necessity and causality. Gödel's attempts to define provability in terms of necessity led him to the distinction of formal and absolute (abstract) provability. Turing's definition of mechanical procedure by means of a Turing machine (TM) and Gödel's definition of a formal system as a mechanical procedure for producing formulas prompt us to understand formal provability as a mechanical causality. We propose a (...) formalism which makes explicit the mechanical causal nature of a TM's work. We claim that Gödel's axiomatised ontotheology and his ontological proof give a clue for the understanding of the concept of absolute provability and the pattern of the corresponding absolute completeness proof, respectively. (shrink)

Rival causal and interpretive approaches to explaining social phenomena have important ethical differences. While human actions can be explained as a result of causal mechanisms, as a meaningful choice based on reasons, or as some combination of the two, it is morally important that social scientists respect others by recognizing them as persons. Interpretive explanations directly respect their subjects in this way, while purely causal explanations do not. Yet although causal explanations are not themselves expressions (...) of respect, they can be used in respectful ways if they are incorporated into subjects’ self-directed projects. This can occur when subjects correctly understand and freely adopt researchers’ goals through a process of informed consent. It can also occur when researchers correctly understand and adopt their subject’s goals, using their research to empower those they study. (shrink)

Characterization of a form of explanation involving grounding on the model of mechanistic causal explanation.

Many political philosophers hold the Feasible Alternatives Principle (FAP): justice demands that we implement some reform of international institutions P only if P is feasible and P improves upon the status quo from the standpoint of justice. The FAP implies that any argument for a moral requirement to implement P must incorporate claims whose content pertains to the causal processes that explain the current state of affairs. Yet, philosophers routinely neglect the need to attend to actual causal processes. (...) This undermines their arguments concerning moral requirements to reform international institutions. The upshot is that philosophers’ arguments must engage in causal analysis to a greater extent than is typical. -/- [Supplement: Handout available at http://db.tt/fyuVW3Xv]. (shrink)

In most accounts of realization of computational processes by physical mechanisms, it is presupposed that there is one-to-one correspondence between the causally active states of the physical process and the states of the computation. Yet such proposals either stipulate that only one model of computation is implemented, or they do not reflect upon the variety of models that could be implemented physically. In this paper, I claim that mechanistic accounts of computation should allow for a broad variation of models (...) of computation. In particular, some non-standard models should not be excluded a priori. The relationship between mathematical models of computation and mechanistically adequate models is studied in more detail. (shrink)

In most accounts of realization of computational processes by physical mechanisms, it is presupposed that there is one-to-one correspondence between the causally active states of the physical process and the states of the computation. Yet such proposals either stipulate that only one model of computation is implemented, or they do not reflect upon the variety of models that could be implemented physically. -/- In this paper, I claim that mechanistic accounts of computation should allow for a broad variation of (...) models of computation. In particular, some non-standard models should not be excluded a priori. The relationship between mathematical models of computation and mechanistically adequate models is studied in more detail. (shrink)

The thesis explores and suggests a solution to a problem that I identify in John McDowell’s and Lynne Rudder Baker’s approaches to mental and intention-dependent (ID) causation in the physical world. I begin (chapter 1) with a brief discussion of McDowell’s non-reductive and anti-scientistic account of mind and world, which I believe offers, through its vision of the unbounded conceptual and the world as within the space of reasons, to liberate and renew philosophy. However, I find an inconsistency in McDowell’s (...) criticism of Davidson’s anomalous monism (chapter 2), stemming from a tension between McDowell’s naïve common sense view of mental causation and an understanding of ordinary physical causation which I think McDowell ought to embrace, which portrays it as both objective, in the sense of being recognition- independent, and as belonging within the space of reasons. The question of the relation between these two concepts of causation is an aspect of the more general question of the relation between the space of reasons and the realm of law. In chapter 3 I begin examining the possibility that Baker’s account of material and property constitution could form the basis of a bridge between the two spaces, and find it generally promising. However, I find that her defence of her version of non-reductive monism against Kim’s causal arguments also runs into problems, which I attribute to the fact that she holds a view of causation as secondary to causal explanation. 2 3 In chapter 4 I develop an account of what I call manifest physical causation – of objective causal relations in the world of Sellars’s manifest image. Based upon McDowell’s transcendental empiricism, which takes the existence of the ordinary perceived world as a condition of the possibility of our possession of conceptual capacities, I contend that it is this picture of reality, rather than that of fundamental physics, that should be the starting point of our theorizing. Causation in the manifest image, I argue, covers the behaviour of the familiar physical world as well as that of its well-understood extensions into the special sciences and engineering. Manifest physical causation, on my account, is productive, acts through mechanisms which are almost entirely mechanical, electromagnetic, and/ or chemical, and is causally closed. In my view, normative, semantic, contentful property-instances are not part of the manifest physical causal nexus. In my final chapter I suggest a modification of Baker’s constitution account, which I call Constituted Causation, whereby higher-level – mental and other ID – causal relations are constituted, in favourable circumstances, by lower-level ones. ID causal relations belong in their own causal nexus but are connected to the manifest physical world through constitution, a relation of unity without identity. Causation and constitution are, respectively, intra- and inter-level relations, and they are non-overlapping. The constituted network of rational and normative relations bears, I believe, striking parallels with McDowell’s view of reality. According to Baker’s view of constitution, the essential properties of constituted entities subsume those of their constituters; extending this to my account enables us to say that the real cause and explanation of someone’s action is that they consciously performed it 4 rather than that certain manifest causal processes occurred at the lower level. (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)

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)

The paper is concentrated on the special changes of the conception of causality from quantum mechanics to quantum information meaning as a background the revolution implemented by the former to classical physics and science after Max Born’s probabilistic reinterpretation of wave function. Those changes can be enumerated so: (1) quantum information describes the general case of the relation of two wave functions, and particularly, the causal amendment of a single one; (2) it keeps the physical description to be (...) class='Hi'>causal by the conservation of quantum information and in accordance with Born’s interpretation; (3) it introduces inverse causality, “backwards in time”, observable “forwards in time” as the fundamentally random probability density distribution of all possible measurements of any physical quantity in quantum mechanics; (4) it involves a kind of “bidirectional causality” unifying (4.1) the classical determinism of cause and effect, (4.2) the probabilistic causality of quantum mechanics, and (4.3) the reversibility of any coherent state; (5) it identifies determinism with the function successor in Peano arithmetic, and its proper generalized causality with the information function successor in Hilbert arithmetic. (shrink)

This chapter explores the idea that causal inference is warranted if and only if the mechanism underlying the inferred causal association is identified. This mechanistic stance is discernible in the epidemiological literature, and in the strategies adopted by epidemiologists seeking to establish causal hypotheses. But the exact opposite methodology is also discernible, the black box stance, which asserts that epidemiologists can and should make causal inferences on the basis of their evidence, without worrying about the (...) class='Hi'>mechanisms that might underlie their hypotheses. I argue that the mechanistic stance is indeed a bad methodology for causal inference. However, I detach and defend a mechanistic interpretation of causal generalisations in epidemiology as existence claims about underlying mechanisms. (shrink)

It is difficult to extract reliable criteria for causal locality from the limited ingredients found in textbook quantum theory. In the end, Bell humbly warned that his eponymous theorem was based on criteria that “should be viewed with the utmost suspicion.” Remarkably, by stepping outside the wave-function paradigm, one can reformulate quantum theory in terms of old-fashioned configuration spaces together with ‘unistochastic’ laws. These unistochastic laws take the form of directed conditional probabilities, which turn out to provide a hospitable (...) foundation for encoding microphysical causal relationships. This unistochastic reformulation provides quantum theory with a simpler and more transparent axiomatic foundation, plausibly resolves the measurement problem, and deflates various exotic claims about superposition, interference, and entanglement. Making use of this reformulation, this paper introduces a new principle of causal locality that is intended to improve on Bell's criteria, and shows directly that systems that remain at spacelike separation cannot exert causal influences on each other, according to that new principle. These results therefore lead to a general hidden-variables interpretation of quantum theory that is arguably compatible with causal locality. (shrink)

One of the goals of physiologists who study the detailed physical, chemical,and neurological mechanisms operating within the human body is to understand the intricate causal processes which underlie human abilities and activities. It is doubtless premature to predict that they will eventually be able to explain the behaviour of a particular human being as we might now explain the behaviour of a pendulum clock or even the invisible changes occurring within the hardware of a modern electronic computer. Nonetheless, (...) it seems fair to say that hovering in the background of investigations into human physiology is the promise or threat, depending upon how one looks at the matter that human beings are complete physical-chemical systems and that all events taking place within their bodies and all movements of their bodies could be accounted for by physical causes if we but knew enough. I am not concerned at the moment with whether or not this ’mechanistic’ hypothesis is true, assuming that it is clear enough to be intelligible, nor with whether or not we could ever know that it is true. I wish to consider the somewhat more accessible yet equally important question whether our coming to believe that the hypothesis is true would warrant our relinquishing our conception of ourselves as beings who are capable of acting for reasons to achieve ends of our own choosing. I use the word ’warrant’ to indicate that I will not be discussing the possibility that believing the mechanistic hypothesis might lead us, as a matter of psychological fact, to think of human beings as mere automata, as objects whose movements are to be explained only by causes rather than by reasons, as are the actions of a personal subject. I intend to consider only whether the acceptance of mechanism would in fact justify such a change in conception. (shrink)

The homeostatic property cluster theory is widely influential for its ability to account for many natural-kind terms in the life sciences. However, the notion of homeostatic mechanism has never been fully explicated. In 2009, Carl Craver interpreted the notion in the sense articulated in discussions on mechanistic explanation and pointed out that the HPC account equipped with such notion invites interest-relativity. In this paper, we analyze two recent refinements on HPC: one that avoids any reference to the causes of the (...) clustering of properties and one that replaces homeostatic mechanisms with causal networks represented by causal graphs. We argue that the former is too slender to account for some inductive inference in science and the latter, thicker account invites interest-relativity, as the original HPC does. This suggests that human interest will be an un-eliminative part of a satisfactory account of natural kindness. We conclude by discussing the implication of interest-relativity to the naturalness, reality, or objectivity of kinds and indicating an overlooked aspect of natural kinds that requires further studies. (shrink)

Causal finitism, the view that the causal history of any event must be finite, has garnered much philosophical interest recently—especially because of its applicability to the Kalām cosmological argument. The most prominent argument for causal finitism is the Grim Reaper argument, which attempts to show that, if infinite causal histories are possible, then other paradoxical states of affairs must also be possible. However, this style of argument has been criticized on the grounds of (i) relying on (...) controversial modal principles, and (ii) providing a false diagnosis of the paradoxes involved. In this paper, I develop a new kind of Grim Reaper argument immune to these criticisms. I show that, by using insights from the literature on time travel, causal finitists should instead argue that infinite causal histories are problematically inexplicable, as they entail the possibility of unexplained foiling mechanisms. The fruits of this paper are that (i) a novel supporting argument for the Kalām is developed, and (ii) along the way of building this argument, it is shown that the literatures on time travel and causal finitism are deeply and intimately connected. (shrink)

The received view in physicalist philosophy of mind assumes that causation can only take place at the physical domain and that the physical domain is causally closed. It is often thought that this leaves no room for mental states qua mental to have a causal influence upon the physical domain, leading to epiphenomenalism and the problem of mental causation. However, in recent philosophy of causation there has been growing interest in a line of thought that can be called (...) class='Hi'>causal antifundamentalism: causal notions cannot play a role in physics, because the fundamental laws of physics are radically different from causal laws. Causal anti-fundamentalism seems to challenge the received view in physicalist philosophy of mind and thus raises the possibility of there being genuine mental causation after all. This paper argues that while causal anti-fundamentalism provides a possible route to mental causation, we have reasons to think that it is incorrect. Does this mean that we have to accept the received view and give up the hope of genuine mental causation? I will suggest that the ontological interpretation of quantum theory provides us both with a view about the nature of causality in fundamental physics, as well as a view how genuine mental causation can be compatible with our fundamental (quantum) physical ontology. (shrink)

In the present paper I argue that the formalism of Newtonian mechanics stems directly from the general principle to be called the principle of microlevel reducibility which physical systems obey in the realm of classical physics. This principle assumes, first, that all the properties of physical systems must be determined by their states at the current moment of time, in a slogan form it is ``only the present matters to physics.'' Second, it postulates that any physical system is nothing but (...) an ensemble of structureless particles arranged in some whose interaction obeys the superposition principle. I substantiate this statement and demonstrate directly how the formalism of differential equations, the notion of forces in Newtonian mechanics, the concept of phase space and initial conditions, the principle of least actions, etc. result from the principle of microlevel reducibility. The philosophical concept of thick presentism and the introduction of two dimensional time-physical time and meta-time that are mutually independent on infinitesimal scales-are the the pivot points in these constructions. (shrink)

As the demand for explainable deep learning grows in the evaluation of language technologies, the value of a principled grounding for those explanations grows as well. Here we study the state-of-the-art in explanation for neural models for natural-language processing (NLP) tasks from the viewpoint of philosophy of science. We focus on recent evaluation work that finds brittleness in explanations obtained through attention mechanisms.We harness philosophical accounts of explanation to suggest broader conclusions from these studies. From this analysis, we assert (...) the impossibility of causal explanations from attention layers over text data. We then introduce NLP researchers to contemporary philosophy of science theories that allow robust yet non-causal reasoning in explanation, giving computer scientists a vocabulary for future research. (shrink)

The purpose of this paper is to present a general mechanistic framework for analyzing causal representational claims, and offer a way to distinguish genuinely representational explanations from those that invoke representations for honorific purposes. It is usually agreed that rats are capable of navigation because they maintain a cognitive map of their environment. Exactly how and why their neural states give rise to mental representations is a matter of an ongoing debate. I will show that anticipatory mechanisms involved (...) in rats’ evaluation of possible routes give rise to satisfaction conditions of contents, and this is why they are representationally relevant for explaining and predicting rats’ behavior. I argue that a naturalistic account of satisfaction conditions of contents answers the most important objections of antirepresentationalists. (shrink)

There is traditionally a division of labor between economics and economic history, the task of economic history being that of studying the evolving constraints of economic mechanisms. Recent theorizing on endogenous structural change challenges this view: if structural change is endogenous to economic mechanisms, any strict division of labor between causal analysis and structural analysis breaks down. Rather such views call for an integration of causal and structural analysis. This paper looks for such a methodology, noting (...) especially the contributions made by two Swedish economists, Johan Åkerman (1896-1982) and Erik Dahmén (1916-2005). With evolutionary, Marxian, Hayekian and critical realist contributions, the paper examines notions of endogenous structural change with the aim of expounding how the notion can be thought in terms of underlying mechanisms to aid such structural analysis. The findings of endogenous mechanisms underlying structural change are crystallized into a mathematical model and a simple methodological framework. (shrink)

I present three reasons why philosophers of science should be more concerned about violations of causal faithfulness (CF). In complex evolved systems, mechanisms for maintaining various equilibrium states are highly likely to violate CF. Even when such systems do not precisely violate CF, they may nevertheless generate precisely the same problems for inferring causal structure from probabilistic relationships in data as do genuine CF-violations. Thus, potential CF-violations are particularly germane to experimental science when we rely on probabilistic (...) information to uncover the DAG, rather than already knowing the DAG from which we could predict the right experiments to ‘catch out’ the hidden causal relationships. (shrink)

The principle of causality is one of the most fundamental principles that has been discovered in the history of philosophy and science. Several foundations revolve around this concept. The importance of this principle in classical physics lies in giving physicists the ability to predict phenomena. Furthermore, due to causality is recognized as a fundamental principle in classical physics. With the introduction of the principle of uncertainty, the principle of causality is empirically called into question. Because the claim of the principle (...) of uncertainty in quantum mechanics is that the relationships between fundamental particles are not causally related to each other, and even the behavior of an electron or a subatomic particle is not based on the principle of causality. If we want to identify the speed of particles, we will not be able to identify their state, and if we want to determine their state, we will not be able to identify their speed. The best way to resolve this conflict is to bring the discussion into philosophy, which is exactly what has been done in Islamic philosophy. The concept of causality in Western philosophy seems to be based on Newtonian concepts. But what has been stated in Islamic philosophy is based on metaphysical concepts, and therefore the principle of uncertainty cannot contradict the concept of causality in Islamic philosophy, especially what has been discussed in the philosophy of Avicenna and Allameh Tabataba'i. (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)

The revolution brought about by quantum mechanics in the early 20th century was nothing short of remarkable. It shattered the foundational principles of classical physics, giving rise to a plethora of controversial and intriguing conceptual questions. Questions that still perplex and confound the scientific community today. Is the quantum mechanical description of physical reality complete? Are the objects of nature truly inseparable? And most importantly, do objects not have a specific position before measurement, and are there non-causal quantum jumps? (...) These vital problems continue to garner more attention as time passes, particularly with the fading of positivism. If you're a student seeking to explore the fascinating philosophical foundations of quantum mechanics, this book might be just what you need. Written in Persian, brings you closer to the heart of quantum controversies and the fascinating world of quantum mechanics. (shrink)

Jacques Monod (1971) argued that certain molecular processes rely critically on the property of chemical arbitrariness, which he claimed allows those processes to “transcend the laws of chemistry”. It seems natural, as some philosophers have done, to interpret this in modal terms: a biological relationship is chemically arbitrary if it is possible, within the constraints of chemical “law”, for that relationship to have been otherwise than it is. But while modality is certainly important for understanding chemical arbitrariness, understanding its biological (...) role also requires an account of the concrete causal-functional features that distinguish arbitrary from non-arbitrary phenomena. In this paper I elaborate on this under-emphasised aspect by offering a general account of these features: arbitrary relations are instantiated by mechanisms that involve molecular adapters, which causally couple two properties or processes which would otherwise be uncorrelated. Additionally, adapters work by acting as intermediate rather than cooperating causes. (shrink)

According to a particular interpretation of quantum mechanics, the causal role of human consciousness in the measuring process is called upon to solve a foundational problem called the “measurement problem.” Traditionally, this interpretation is tied up with the metaphysics of substance dualism. As such, this interpretation of quantum mechanics inherits the dualist’s mind-body problem. Our working hypothesis is that a process-based approach to the consciousness causes collapse interpretation (CCCI) ---leaning on Whitehead’s solution to the mind-body problem--- offers a better (...) metaphysical understanding of consciousness and its role in interpreting quantum mechanics. This article is the kickoff for such a research program in the metaphysics of science. (shrink)

According to the new mechanistic approach, an acting entity is at a lower mechanistic level than another acting entity if and only if the former is a component in the mechanism for the latter. Craver and Bechtel :547–563, 2007. doi:10.1007/s10539-006-9028-8) argue that a consequence of this view is that there cannot be causal interactions between acting entities at different mechanistic levels. Their main reason seems to be what I will call the Metaphysical Argument: things at different levels of a (...) mechanism are related as part and whole; wholes and their parts cannot be related as cause and effect; hence, interlevel causation in mechanisms is impossible. I will analyze this argument in more detail and show under which conditions it is valid. This analysis will reveal that interlevel causation in mechanisms is indeed possible, if we take seriously the idea that the relata of the mechanistic level relation are acting entities and accept a slightly modified notion of a mechanistic level that is highly plausible in the light of the first clarification. (shrink)