Phyllis Illari

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

In this opening chapter, we review the literature on information quality. Our major aim is to introduce the issues, and trace some of the history of the debates, with a view to situating the chapters in this volume – whose authors come from different disciplines – to help make them accessible to readers with different backgrounds and expertise. We begin in this section by tracing some influential analyses of IQ in computer science. This is a useful basis for examining some examples of developing work on IQ in section two. We look at some cases for applying IQ in section three, and conclude with some discussion points in section four

In this paper, we compare the mechanisms of protein synthesis and natural selection. We identify three core elements of mechanistic explanation: functional individuation, hierarchical nestedness or decomposition, and organization. These are now well understood elements of mechanistic explanation in fields such as protein synthesis, and widely accepted in the mechanisms literature. But Skipper and Millstein have argued that natural selection is neither decomposable nor organized. This would mean that much of the current mechanisms literature does not apply to the mechanism of natural selection.We take each element of mechanistic explanation in turn. Having appreciated the importance of functional individuation, we show how decomposition and organization should be better understood in these terms. We thereby show that mechanistic explanation by protein synthesis and natural selection are more closely analogous than they appear—both possess all three of these core elements of a mechanism widely recognized in the mechanisms literature

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

Craver claims that mechanistic explanation is ontic, while Bechtel claims that it is epistemic. While this distinction between ontic and epistemic explanation originates with Salmon, the ideas have changed in the modern debate on mechanistic explanation, where the frame of the debate is changing. I will explore what Bechtel and Craver’s claims mean, and argue that good mechanistic explanations must satisfy both ontic and epistemic normative constraints on what is a good explanation. I will argue for ontic constraints by drawing on Craver’s work in Sect. 2.1, and argue for epistemic constraints by drawing on Bechtel’s work in Sect. 2.2. Along the way, I will argue that Bechtel and Craver actually agree with this claim. I argue that we should not take either kind of constraints to be fundamental, in Sect. 3, and close in Sect. 4 by considering what remains at stake in making a distinction between ontic and epistemic constraints on mechanistic explanation. I suggest that we should not concentrate on either kind of constraint, to the neglect of the other, arguing for the importance of seeing the relationship as one of integration

Russo and Williamson claim that establishing causal claims requires mechanistic and difference-making evidence. In this article, I will argue that Russo and Williamson's formulation of their thesis is multiply ambiguous. I will make three distinctions: mechanistic evidence as type vs object of evidence; what mechanism or mechanisms we want evidence of; and how much evidence of a mechanism we require. I will feed these more precise meanings back into the Russo–Williamson thesis and argue that it is both true and false: two weaker versions of the thesis are worth supporting, while the stronger versions are not. Further, my distinctions are of wider concern because they allow us to make more precise claims about what kinds of evidence are required in particular cases.

In this paper, we examine what is to be said in defence of Machamer, Darden and Craver’s (MDC) controversial dualism about activities and entities (Machamer, Darden and Craver’s in Philos Sci 67:1–25, 2000). We explain why we believe the notion of an activity to be a novel, valuable one, and set about clearing away some initial objections that can lead to its being brushed aside unexamined. We argue that substantive debate about ontology can only be effective when desiderata for an ontology are explicitly articulated. We distinguish three such desiderata. The first is a more permissive descriptive ontology of science, the second a more reductive ontology prioritising understanding, and the third a more reductive ontology prioritising minimalism. We compare MDC’s entities-activities ontology to its closest rival, the entities-capacities ontology, and argue that the entities-activities ontology does better on all three desiderata

According to current hierarchies of evidence for EBM, evidence of correlation 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. 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.

The use of evidence in medicine is something we should continuously seek to improve. This book seeks to develop our understanding of evidence of mechanism in evaluating evidence in medicine, public health, and social care; and also offers tools to help implement improved assessment of evidence of mechanism in practice. In this way, the book offers a bridge between more theoretical and conceptual insights and worries about evidence of mechanism and practical means to fit the results into evidence assessment procedures.

In this paper, I examine the comparatively neglected intuition of production regarding causality. I begin by examining the weaknesses of current production accounts of causality. I then distinguish between giving a good production account of causality and a good account of production. I argue that an account of production is needed to make sense of vital practices in causal inference. Finally, I offer an information transmission account of production based on John Collier’s work that solves the primary weaknesses of current production accounts: applicability and absences

Current research in molecular epidemiology uses biomarkers to model the different disease phases from environmental exposure, to early clinical changes, to development of disease. The hope is to get a better understanding of the causal impact of a number of pollutants and chemicals on several diseases, including cancer and allergies. In a recent paper Russo and Williamson address the question of what evidential elements enter the conceptualisation and modelling stages of this type of biomarkers research. Recent research in causality has examined Ned Hall’s distinction between two concepts of causality: production and dependence. In another recent paper, Illari examined the relatively under-explored production approach to causality, arguing that at least one job of an account of causal production is to illuminate our inferential practices concerning causal linking. Illari argued that an informational account solves existing problems with traditional accounts. This paper follows up this previous work by investigating the nature of the causal links established in biomarkers research. We argue that traditional accounts of productive causality are unable to provide a sensible account of the nature of the causal link in biomarkers research, while an informational account is very promising

Evidence and CausalityCausality is a vibrant and thriving topic in philosophy of science. It is closely related to many other challenging scientific concepts, such as probability and mechanisms, which arise in many different scientific contexts, in different fields. For example, probability and mechanisms are relevant to both causal inference (finding out what causes what) and causal explanation (explaining how a cause produces its effect). They are also of interest to fields as diverse as astrophysics, biochemistry, biomedical and social sciences. At the same time, there has been an explosion of interest in evidence, most obviously in biomedical contexts with the rise of ‘evidence-based medicine’, but also elsewhere, such as in social science. What is evidence? How do we decide what our best sources of evidence are?This topos examines the relation between causality and evidence in different scientific areas. This involves questions about the foundations of the sciences, e.g. what is e ..

This book serves as the main reference for an undergraduate course on Philosophy of Information. The book is written to be accessible to the typical undergraduate student of Philosophy and does not require propaedeutic courses in Logic, Epistemology or Ethics. Each chapter includes a rich collection of references for the student interested in furthering her understanding of the topics reviewed in the book. The book covers all the main topics of the Philosophy of Information and it should be considered an overview and not a comprehensive, in-depth analysis of a philosophical area. As a consequence, 'The Philosophy of Information: a Simple Introduction' does not contain research material as it is not aimed at graduate students or researchers.

We show how more general knowledge can be built in information security, by the building of knowledge of mechanism clusters, some of which are multifield. By doing this, we address in a novel way the longstanding philosophical problem of how, if at all, we come to have knowledge that is in any way general, when we seem to be confined to particular experiences. We also address the issue of building knowledge of mechanisms by studying an area that is new to the mechanisms literature: the methods of what we shall call mechanism discovery in information security. This domain offers a fascinating novel constellation of challenges for building more general knowledge. Specifically, the building of stable communicable mechanistic knowledge is impeded by the inherent changeability of software, which is deployed by malicious actors constantly changing how their software attacks, and also by an ineliminable secrecy concerning the details of attacks not just by attackers, but also by information security defenders as they protect their methods from both attackers and commercial competitors. We draw out ideas from the work of the mechanists Darden, Craver, and Glennan to yield an approach to how general knowledge of mechanisms can be painstakingly built. We then use three related examples of active research problems from information security to develop philosophical thinking about building general knowledge using mechanisms, and also apply this to develop insights for information security. We show that further study would be instructive both for practitioners and for philosophers.

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

The Recursive Bayesian Net formalism was originally developed for modelling nested causal relationships. In this paper we argue that the formalism can also be applied to modelling the hierarchical structure of mechanisms. The resulting network contains quantitative information about probabilities, as well as qualitative information about mechanistic structure and causal relations. Since information about probabilities, mechanisms and causal relations is vital for prediction, explanation and control respectively, an RBN can be applied to all these tasks. We show in particular how a simple two-level RBN can be used to model a mechanism in cancer science. The higher level of our model contains variables at the clinical level, while the lower level maps the structure of the cell's mechanism for apoptosis.

In the last decades, Systems Biology (including cancer research) has been driven by technology, statistical modelling and bioinformatics. In this paper we try to bring biological and philosophical thinking back. We thus aim at making diferent traditions of thought compatible: (a) causality in epidemiology and in philosophical theorizing—notably, the “sufcient-component-cause framework” and the “mark transmission” approach; (b) new acquisitions about disease pathogenesis, e.g. the “branched model” in cancer, and the role of biomarkers in this process; (c) the burgeoning of omics research, with a large number of “signals” and of associations that need to be interpreted. In the paper we summarize frst the current views on carcinogenesis, and then explore the relevance of current philosophical interpretations of “cancer causes”. We try to ofer a unifying framework to incorporate biomarkers and omic data into causal models, referring to a position called “evidential pluralism”. According to this view, causal reasoning is based on both “evidence of diference-making” (e.g. associations) and on “evidence of underlying biological mechanisms”. We conceptualize the way scientists detect and trace signals in terms of information transmission, which is a generalization of the mark transmission theory developed by philosopher Wesley Salmon. Our approach is capable of helping us conceptualize how heterogeneous factors such as micro and macro-biological and psycho-social—are causally linked. This is important not only to understand cancer etiology, but also to design public health policies that target the right causal factors at the macro-level.

As the usual regulatory framework did not fit well during the last Ebola outbreak, innovative thinking still needed. In the absence of an outbreak, randomised controlled trials of clinical efficacy in humans cannot be done, while during an outbreak such trials will continue to face significant practical, philosophical, and ethical challenges. This article argues that researchers should also test the safety and effectiveness of novel vaccines in wild apes by employing a pluralistic approach to evidence. There are three reasons to test vaccines in wild populations of apes: i) protect apes; ii) reduce Ebola transmission from wild animals to humans; and iii) accelerate vaccine development and licensing for humans. Data obtained from studies of vaccines among wild apes and chimpanzees may even be considered sufficient for licensing new vaccines for humans. This strategy will serve to benefit both wild apes and humans.

There has been a burst of work in the last couple of decades on mechanistic explanation, as an alternative to the traditional covering-law model of scientific explanation. That work makes some interesting claims about mechanistic explanations rendering phenomena ‘intelligible’, but does not develop this idea in great depth. There has also been a growth of interest in giving an account of scientific understanding, as a complement to an account of explanation, specifically addressing a three-place relationship between explanation, world, and the scientific community. The aim of this paper is to use the contextual theory of scientific understanding to build an account of understanding phenomena using mechanistic explanations. This account will be developed and illustrated by examining the mechanisms of supernovae, which will allow synthesis of treatment of the life sciences and social sciences on the one hand, where many accounts of mechanisms were originally developed, and treatment of physics on the other hand, where the contextual theory drew its original inspiration.

From the operation of the universe to DNA, the brain and the economy, natural and social frequently describe their activity as being concerned with discovering mechanisms. Despite this fact, for much of the twentieth century philosophical discussions of the nature of mechanisms remained outside philosophy of science. The Routledge Handbook of Mechanisms and Mechanical Philosophy is an outstanding reference source to the key topics, problems and debates in this exciting subject and is the first collection of its kind. Comprising over thirty chapters by a team of international contributors the _Handbook_ is divided into four parts: Historical Perspectives on Mechanisms The Nature of Mechanisms Mechanisms and the Philosophy of Science Disciplinary Perspectives. Within these sections central topics and problems are examined, including the rise of mechanical philosophy in the seventeenth century; mechanisms as parts and wholes and their interactive powers; mechanisms and laws and regularities; how mechanisms are discovered and explained; dynamical systems theory; and disciplinary perspectives from physics, chemistry, biology, biomedicine, ecology, neuroscience and the social and political sciences. Essential reading for students and researchers in philosophy of science and philosophy the _Handbook _will also be of interest to those in related fields, such as metaphysics, philosophy of psychology and history of science.