The search for causes of perinatal brain damage needs a solid theoretical foundation. Current theory apparently does not offer a unanimously accepted view of what constitutes a cause, and how it can be identified. We discuss nine potential theoretical misconceptions: (1) too narrow a view of what is a cause (causal production vs. facilitation), (2) extrapolating from possibility to fact (potential vs. factual causation), (3) if X, then invariably Y (determinism vs. probabilism), (4) co-occurrence in individuals vs. association in populations, (...) (5) one cause is all that is needed (single cause attribution vs. multicausal constellations), (6) drawing causal inferences from very small numbers of observations (the tendency to generalize), (7) unstated causal inferences, (8) ignoring heterogeneity, and (9) failing to consider alternative explanations for what is observed. We hope that our critical discussion will contribute to fruitful research and help reduce the burden of perinatal brain damage. (shrink)

Understanding Scientific Reasoning, Fifth Edition, develops critical reasoning skills and guides students in the improvement of their scientific and technological literacy. The authors teach students how to understand and critically evaluate the scientific information they encounter in both textbooks and the popular media. With its focus on scientific pedagogy, Understanding Scientific Reasoning helps students learn how to examine scientific reports with a reasonable degree of sophistication. The book also explains how to reason through case studies using the same informal logic (...) skills employed by scientists and to analyse a complex series of propositions and hypotheses using sound scientific reasoning--Publisher's blurb. (shrink)

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

In a recent paper Wesley Salmon has replied to criticisms of his theory of causality, and has offered a revised theory which, he argues, is not open to those criticisms. The key change concerns the characterization of causal processes, where Salmon has traded “the capacity for mark transmission” for “the transmission of an invariant quantity.” Salmon argues against the view presented in Dowe, namely that the concept of “possession of a conserved quantity” is sufficient to account for the difference between (...) causal and pseudo processes. Here that view is defended, and important questions are raised about the notion of transmission and about gerrymandered aggregates. (shrink)

This article presents a distinct sense of ‘mechanism’, which I call the functional sense of mechanism. According to this sense, mechanisms serve functions, and this fact places substantive restrictions on the kinds of system activities ‘for which’ there can be a mechanism. On this view, there are no mechanisms for pathology; pathologies result from disrupting mechanisms for functions. Second, on this sense, natural selection is probably not a mechanism for evolution because it does not serve a function. After distinguishing this (...) sense fromsimilar explications of ‘mechanism’, I argue that it is ubiquitous in biology and has valuable epistemic benefits. (shrink)

This paper sets out to analyze how causation works by focusing on biology, as represented by epidemiology and by scientific information on how the body works (“physiology”). It starts by exploring the specificity of evolved physiological systems, in which evolutionary, developmental and proximal causes all fit together, and the concept of function is meaningful; in contrast, this structure does not apply in epidemiology (or outside biology). Using these two contrasting branches of biology, I examine the role both of mechanism and (...) of difference making in causation. I find that causation necessarily involves both mechanism and difference making, and that they play complementary roles. Both are seen as ontologically necessary, even if the evidence is not always available for both. Influential monist accounts that focus on one of these, at the expense of ignoring the other, are found to be inadequate on these and on other grounds. Recent attempts to combine them are reviewed, notably that of Russo and Williamson (Int Stud Philos Sci 21:157–170, 2007), and it is argued that their epistemic view requires there to be a source of the different types of evidence that a rational agent would consider, and that this source must be ontic. I then analyze how causal relationships work in evolved physiological systems and in those studied by epidemiology, with a particular focus on how mechanism interacts with input. Finally, I consider this concept of causation from the perspective of everyday language, and of its possible generalisability outside biology. (shrink)

According to Russo and Williamson (Int Stud Philos Sci 21(2):157–170, 2007, Hist Philos Life Sci 33:389–396, 2011a, Philos Sci 1(1):47–69, 2011b ), in order to establish a causal claim of the form, ‘_C_ is a cause of _E_’, one typically needs evidence that there is an underlying mechanism between _C_ and _E_ as well as evidence that _C_ makes a difference to _E_. This thesis has been used to argue that hierarchies of evidence, as championed by evidence-based movements, tend to (...) give primacy to evidence of difference making over evidence of mechanisms and are flawed because the two sorts of evidence are required and they should be treated on a par. An alternative approach gives primacy to evidence of mechanism over evidence of difference making. In this paper, we argue that this alternative approach is equally flawed, again because both sorts of evidence need to be treated on a par. As an illustration of this parity, we explain how scientists working in the ‘EnviroGenomarkers’ project constantly make use of the two evidential components in a dynamic and intertwined way. We argue that such an interplay is needed not only for causal assessment but also for policy purposes. (shrink)

Carl F. Craver investigates what we are doing when we use neuroscience to explain what's going on in the brain. When does an explanation succeed and when does it fail? Craver offers explicit standards for successful explanation of the workings of the brain, on the basis of a systematic view about what neuroscientific explanations are.

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

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

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)

How physicians approach patients and the problems they present is much influenced by the conceptual models around which their knowledge is organized. In this paper the implications of the biopsychosocial model for the study and care of a patient with an acute myocardial infarction are presented and contrasted with approaches used by adherents of the more traditional biomedical model. CiteULike Connotea Del.icio.us What's this?

Robustness is a common platitude: hypotheses are better supported with evidence generated by multiple techniques that rely on different background assumptions. Robustness has been put to numerous epistemic tasks, including the demarcation of artifacts from real entities, countering the “experimenter’s regress,” and resolving evidential discordance. Despite the frequency of appeals to robustness, the notion itself has received scant critique. Arguments based on robustness can give incorrect conclusions. More worrying is that although robustness may be valuable in ideal evidential circumstances (i.e., (...) when evidence is concordant), often when a variety of evidence is available from multiple techniques, the evidence is discordant. †To contact the author, please write to: Jacob Stegenga, Department of Philosophy, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093; e‐mail: [email protected]. (shrink)

In this book van Fraassen develops an alternative to scientific realism by constructing and evaluating three mutually reinforcing theories.

Causality offers the first comprehensive coverage of causal analysis in many sciences, including recent advances using graphical methods. Pearl presents a unified account of the probabilistic, manipulative, counterfactual and structural approaches to causation, and devises simple mathematical tools for analyzing the relationships between causal connections, statistical associations, actions and observations. The book will open the way for including causal analysis in the standard curriculum of statistics, artificial intelligence, business, epidemiology, social science and economics.

Knowledge and its Limits presents a systematic new conception of knowledge as a kind of mental stage sensitive to the knower's environment. It makes a major contribution to the debate between externalist and internalist philosophies of mind, and breaks radically with the epistemological tradition of analyzing knowledge in terms of true belief. The theory casts new light on such philosophical problems as scepticism, evidence, probability and assertion, realism and anti-realism, and the limits of what can be known. The arguments are (...) illustrated by rigorous models based on epistemic logic and probability theory. The result is a new way of doing epistemology and a notable contribution to the philosophy of mind. (shrink)

Wesley Salmon is renowned for his seminal contributions to the philosophy of science. He has powerfully and permanently shaped discussion of such issues as lawlike and probabilistic explanation and the interrelation of explanatory notions to causal notions. This unique volume brings together twenty-six of his essays on subjects related to causality and explanation, written over the period 1971-1995. Six of the essays have never been published before and many others have only appeared in obscure venues. The volume includes a section (...) of accessible introductory pieces, as well as more advanced and technical pieces, and will make essential work in the philosophy of science readily available to both scholars and students. (shrink)

Scientific reasoning is—and ought to be—conducted in accordance with the axioms of probability. This Bayesian view—so called because of the central role it accords to a theorem first proved by Thomas Bayes in the late eighteenth ...

Ever since David Hume, empiricists have barred powers and capacities from nature. In this book Cartwright argues that capacities are essential in our scientific world, and, contrary to empiricist orthodoxy, that they can meet sufficiently strict demands for testability. Econometrics is one discipline where probabilities are used to measure causal capacities, and the technology of modern physics provides several examples of testing capacities (such as lasers). Cartwright concludes by applying the lessons of the book about capacities and probabilities to the (...) explanation of the role of causality in quantum mechanics. (shrink)

Sometimes also called retro causation. A common feature of our world seems to be that in all cases of causation, the cause and the effect are placed in time so that the cause precedes its effect temporally. Our normal understanding of causation assumes this feature to such a degree that we intuitively have great difficulty imagining things differently. The notion of backward causation, however, stands for the idea that the temporal order of cause and effect is a mere contingent feature (...) and that there may be cases where the cause is causally prior to its effect but where the temporal order of the cause and effect is reversed with respect to normal causation, i.e. there may be cases where the effect temporally, but not causally, precedes its cause. (shrink)

This paper discusses several distinct process theories of causality offered in recent years by Phil Dowe and me. It addresses problems concerning the explication of causal process, causal interaction, and causal transmission, whether given in terms of transmission of marks, transmission of invariant or conserved quantities, or mere possession of conserved quantities. Renouncing the mark-transmission and invariant quantity criteria, I accept a conserved quantity theory similar to Dowe's--differing basically with respect to causal transmission. This paper also responds to several fundamental (...) constructive criticisms contained in Christopher Hitchcock's discussion of both the mark-transmission and the conserved quantity theories. (shrink)

The challenges posed by chronic illness have pointed out to epidemiologists the multifactorial complex nature of disease causality. This notion has been referred to as a web of causality. This web extends theoretically beyond risk markers. It includes determinants of emergence/non-emergence of disease. This web of determinants is a form of complex system. Due to its complexity, the determinants within such system are not linked to each others in a linear, predictable manner only. Predictability is possible only on a short-term (...) basis, and unpredictability sets in over the long run. Understanding such a system of determinants calls for articulation and testing of complex models which synthesize our knowledge of multiple determinants at many scales, both biological and otherwise. Given the complexity of this web and existing knowledge about the nonlinearity of such systems, the following question is posed: Can the challenge of studying causality be adequately addressed if emphasis continues to be placed on using tools and methods that are geared towards looking at such system from a linear paradigm? Or is it time to add to the epidemiologic research agenda the notion of nonlinearity and its relevant form of analytical approaches that are being tested in other disciplines? Furthermore, the question posed here applies as well to the study of determinants of health. Addressing determinants of heath adds further complexity to our task. (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.

Scientific and philosophical literature on causality has become highly specialised. It is hard to find suitable access points for students, young researchers, or professionals outside this domain. This book provides a guide to the complex literature, explains the scientific problems of causality and the philosophical tools needed to address them.

Bradford Hill (1965) highlighted nine aspects of the complex evidential situation a medical researcher faces when determining whether a causal relation exists between a disease and various conditions associated with it. These aspects are widely cited in the literature on epidemiological inference as justifying an inference to a causal claim, but the epistemological basis of the Hill aspects is not understood. We offer an explanatory coherentist interpretation, explicated by Thagard's ECHO model of explanatory coherence. The ECHO model captures the complexity (...) of epidemiological inference and provides a tractable model for inferring disease causation. We apply this model to three cases: the inference of a causal connection between the Zika virus and birth defects, the classic inference that smoking causes cancer, and John Snow’s inference about the cause of cholera. (shrink)

_Process Philosophy_ surveys the basic issues and controversies surrounding the philosophical approach known as “process philosophy.” Process philosophy views temporality, activity, and change as the cardinal factors for our understanding of the real—process has priority over product, both ontologically and epistemically. Rescher examines the movement’s historical origins, reflecting a major line of thought in the work of such philosophers as Heracleitus, Leibniz, Bergson, Peirce, William James, and especially A. N. Whitehead. Reacting against the tendency to associate process philosophy too closely (...) with this last-named thinker, Rescher writes, “Indeed, one cardinal task for the partisans of process at this particular juncture of philosophical history is to prevent the idea of ‘process philosophy’ from being marginalized through a limitation of its bearing to the work and influence of any one single individual or group.” This book will appeal to both students and professors of philosophy. Those teachers who have not been trained in process philosophy will welcome this new text by one one of North America’s foremost philosophers as a perspicuous and informative introduction. (shrink)

In this important new work, Haack develops an original theory of empirical evidence or justification, and argues its appropriateness to the goals of inquiry. In so doing, Haack provides detailed critical case studies of Lewis's foundationalism; Davidson's and Bonjour's coherentism; Popper's 'epistemology without a knowing subject'; Quine's naturalism; Goldman's reliabilism; and Rorty's, Stich's, and the Churchlands' recent obituaries of epistemology.

Evidence-based medicine (EBM) makes use of explicit procedures for grading evidence for causal claims. Normally, these procedures categorise evidence of correlation produced by statistical trials as better evidence for a causal claim than evidence of mechanisms produced by other methods. We argue, in contrast, that evidence of mechanisms needs to be viewed as complementary to, rather than inferior to, evidence of correlation. In this paper we first set out the case for treating evidence of mechanisms alongside evidence of correlation in (...) explicit protocols for evaluating evidence. Next we provide case studies which exemplify the ways in which evidence of mechanisms complements evidence of correlation in practice. Finally, we put forward some general considerations as to how the two sorts of evidence can be more closely integrated by EBM. (shrink)

According to current hierarchies of evidence for EBM, evidence of correlation (e.g., from RCTs) is always more important than evidence of mechanisms when evaluating and establishing causal claims. We argue that evidence of mechanisms needs to be treated alongside evidence of correlation. This is for three reasons. First, correlation is always a fallible indicator of causation, subject in particular to the problem of confounding; evidence of mechanisms can in some cases be more important than evidence of correlation when assessing a (...) causal claim. Second, evidence of mechanisms is often required in order to obtain evidence of correlation (for example, in order to set up and evaluate RCTs). Third, evidence of mechanisms is often required in order to generalise and apply causal claims. While the EBM movement has been enormously successful in making explicit and critically examining one aspect of our evidential practice, i.e., evidence of correlation, we wish to extend this line of work to make explicit and critically examine a second aspect of our evidential practices: evidence of mechanisms. (shrink)

Bayesian nets are widely used in artificial intelligence as a calculus for causal reasoning, enabling machines to make predictions, perform diagnoses, take decisions and even to discover causal relationships. This book, aimed at researchers and graduate students in computer science, mathematics and philosophy, brings together two important research topics: how to automate reasoning in artificial intelligence, and the nature of causality and probability in philosophy.

A theory of causality based upon physical processes is developed. Causal processes are distinguished from pseudo-processes by means of a criterion of mark transmission. Causal interactions are characterized as those intersections of processes in which the intersecting processes are mutually modified in ways which persist beyond the point of intersection. Causal forks of three kinds (conjunctive, interactive, and perfect) are introduced to explicate the principle of the common cause. Causal forks account for the production of order and modifications of order; (...) causal processes account for the propagation of causal influence. (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 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)