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)
We argue that the health sciences make causal claims on the basis of evidence both of physical mechanisms, and of probabilistic dependencies. Consequently, an analysis of causality solely in terms of physical mechanisms or solely in terms of probabilistic relationships, does not do justice to the causal claims of these sciences. Yet there seems to be a single relation of cause in these sciences - pluralism about causality will not do either. Instead, we maintain, the health sciences require a theory (...) of causality that unifies its mechanistic and probabilistic aspects. We argue that the epistemic theory of causality provides the required unification. (shrink)
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.
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.
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. (shrink)
The anti-causal prophecies of last century have been disproved. Causality is neither a ‘relic of a bygone’ nor ‘another fetish of modern science’; it still occupies a large part of the current debate in philosophy and the sciences. This investigation into causal modelling presents the rationale of causality, i.e. the notion that guides causal reasoning in causal modelling. It is argued that causal models are regimented by a rationale of variation, nor of regularity neither invariance, thus breaking down the dominant (...) Human paradigm. The notion of variation is shown to be embedded in the scheme of reasoning behind various causal models: e.g. Rubin’s model, contingency tables, and multilevel analysis. It is also shown to be latent – yet fundamental – in many philosophical accounts. Moreover, it has significant consequences for methodological issues: the warranty of the causal interpretation of causal models, the levels of causation, the characterisation of mechanisms, and the interpretation of probability. This book offers a novel philosophical and methodological approach to causal reasoning in causal modelling and provides the reader with the tools to be up to date about various issues causality rises in social science. "Dr. Federica... more on http://springer.com/978-1-4020-8816-2.. (shrink)
Causal claims in biomedical contexts are ubiquitous albeit they are not always made explicit. This paper addresses the question of what causal claims mean in the context of disease. It is argued that in medical contexts causality ought to be interpreted according to the epistemic theory. The epistemic theory offers an alternative to traditional accounts that cash out causation either in terms of “difference-making” relations or in terms of mechanisms. According to the epistemic approach, causal claims tell us about which (...) inferences (e.g., diagnoses and prognoses) are appropriate, rather than about the presence of some physical causal relation analogous to distance or gravitational attraction. It is shown that the epistemic theory has important consequences for medical practice, in particular with regard to evidence-based causal assessment. (shrink)
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. (shrink)
Epistemic diversity is the ability or possibility of producing diverse and rich epistemic apparati to make sense of the world around us. In this paper we discuss whether, and to what extent, different conceptions of knowledge—notably as ‘justified true belief’ and as ‘distributed and embodied cognition’—hinder or foster epistemic diversity. We then link this discussion to the widespread move in science and philosophy towards monolingual disciplinary environments. We argue that English, despite all appearance, is no Lingua Franca, and we give (...) reasons why epistemic diversity is also deeply hindered is monolingual contexts. Finally, we sketch a proposal for multilingual academia where epistemic diversity is thereby fostered. (shrink)
A shared problem across the sciences is to make sense of correlational data coming from observations and/or from experiments. Arguably, this means establishing when correlations are causal and when they are not. This is an old problem in philosophy. This paper, narrowing down the scope to quantitative causal analysis in social science, reformulates the problem in terms of the validity of statistical models. Two strategies to make sense of correlational data are presented: first, a 'structural strategy', the goal of which (...) is to model and test causal structures that explain correlational data; second, a 'manipulationist or interventionist strategy', that hinges upon the notion of invariance under intervention. It is argued that while the former can offer a solution the latter cannot. (shrink)
Why do ideas of how mechanisms relate to causality and probability differ so much across the sciences? Can progress in understanding the tools of causal inference in some sciences lead to progress in others? This book tackles these questions and others concerning the use of causality in the sciences.
Causal analysis in the social sciences takes advantage of a variety of methods and of a multi-fold source of information and evidence. This pluralistic methodology and source of information raises the question of whether we should accordingly have a pluralistic metaphysics and epistemology. This paper focuses on epistemology and argues that a pluralistic methodology and evidence dont entail a pluralistic epistemology. It will be shown that causal models employ a single rationale of testing, based on the notion of variation. Further, (...) I shall argue that this monistic epistemology is also involved in alternative philosophical theories of causation. (shrink)
This paper deals with causal analysis in the social sciences. We first present a conceptual framework according to which causal analysis is based on a rationale of variation and invariance, and not only on regularity. We then develop a formal framework for causal analysis by means of structural modelling. Within this framework we approach causality in terms of exogeneity in a structural conditional model based which is based on (i) congruence with background knowledge, (ii) invariance under a large variety of (...) environmental changes, and (iii) model fit. We also tackle the issue of confounding and show how latent confounders can play havoc with exogeneity. This framework avoids making untestable metaphysical claims about causal relations and yet remains useful for cognitive and action-oriented goals. (shrink)
According to Russo and Williamson :157–170, 2007, Hist Philos Life Sci 33:389–396, 2011a, Philos Sci 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)
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. (shrink)
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. (shrink)
Social research, from economics to demography and epidemiology, makes extensive use of statistical models in order to establish causal relations. The question arises as to what guarantees the causal interpretation of such models. In this paper we focus on econometrics and advance the view that causal models are ‘augmented’ statistical models that incorporate important causal information which contributes to their causal interpretation. The primary objective of this paper is to argue that causal claims are established on the basis of a (...) plurality of evidence. We discuss the consequences of ‘evidential pluralism’ in the context of econometric modelling. (shrink)
The paper examines definitions of ‘cause’ in the epidemiological literature. Those definitions all describe causes as factors that make a difference to the distribution of disease or to individual health status. In the philosophical jargon, causes in epidemiology are difference-makers. Two claims are defended. First, it is argued that those definitions underpin an epistemology and a methodology that hinge upon the notion of variation, contra the dominant Humean paradigm according to which we infer causality from regularity. Second, despite the fact (...) that causes be defined in terms of ‘difference-making’, this cannot fixes the causal metaphysics. Causality in epidemiology ought to be interpreted according to the epistemic theory. In this approach relations are deemed causal depending on the evidence and on the available methods. Indeed, evidence to establish causal claims requires difference-making considerations; furthermore, those definitions of cause reflect the ‘variational’ epistemology and methodology of epidemiology. (shrink)
Causal assessment is the problem of establishing whether a relation between (variable) X and (variable) Y is causal. This problem, to be sure, is widespread across the sciences. According to accredited positions in the philosophy of causality and in social science methodology, invariance under intervention provides the most reliable test to decide whether X causes Y. This account of invariance (under intervention) has been criticised, among other reasons, because it makes manipulations on the putative causal factor fundamental for the causal (...) methodology; consequently, the argument goes, the account is ill-suited to those contexts where manipulations are not performed, for instance, the social sciences. The article aims to extend the account of invariance (under intervention), in a way that manipulations on the putative causal factors are not methodologically fundamental, and yet invariance remains key for causal assessment both in experimental and non-experimental contexts. (shrink)
The notion of ‘causal web’ emerged in the epidemiological literature in the early Sixties and had to wait until the Nineties for a thorough critical appraisal. Famously, Nancy Krieger argued that such a notion isn’t helpful unless we specify what kind of spiders create the webs. This means, according to Krieger, (i) that the role of the spiders is to provide an explanation of the yarns of the web and (ii) that the sought spiders have to be biological and social. (...) This paper contributes to the development of the notion of causal web, elaborating on the two following points: (i) to catch the spiders we need multi-fold evidence—specifically, mechanistic and difference-making—and (ii) for the eco-social to be explanatory, the web has to be mechanistic in a sense to be specified. (shrink)
How should probabilities be interpreted in causal models in the social and health sciences? In this paper we take a step towards answering this question by investigating the case of cancer in epidemiology and arguing that the objective Bayesian interpretation is most appropriate in this domain.
The Agency and the Manipulability theory of causation, in spite of significant differences, share at least three claims. First, that manipulation – roughly, that by manipulating causes we bring about effects – is a central notion for causation; second, that such a notion of manipulation allows a reductive – i.e. general and comprehensive – account of causation; third, that this view has its forefathers in the works of Collingwood, Gasking and von Wright. This paper mainly challenges the third claim and (...) argues that the misreading of those authors leads to a more dangerous consequence: a confusion between epistemological, metaphysical and methodological issues about causation. (shrink)
The paper addresses the question of how different types of evidence ought to inform public health policy. By analysing case studies on obesity, the paper draws lessons about the different roles that different types of evidence play in setting up public health policies. More specifically, it is argued that evidence of difference-making supports considerations about ‘what works for whom in what circumstances’, and that evidence of mechanisms provides information about the ‘causal pathways’ to intervene upon.
In social science, one objection to causal analysis is that the assumption of the closure of the system makes the analysis too narrow in scope, that is, it considers only 'closed' and 'hermetic' systems thus neglecting many other external influences. On the contrary, system analysis deals with complex structures where every element is interrelated with everything else in the system. The question arises as to whether the two approaches can be compatible and whether causal analysis can be integrated into the (...) broader framework of system analysis. This article attempts a negative answer on the grounds of fundamental differences in their assumptions and suggests using system analysis as a post-hoc comparative tool. (shrink)
One of the guiding principles of modern medical and health sciences is the discovery and description of the modes of origin and the actions of pathogenic precursors of disease. This principle facilitates the design of interventions to reduce the burden of mortality and morbidity in individuals and populations. This enterprise is challenging because of the complexity of the pathogenic mechanisms involved. Although highly intricate descriptions of these mechanisms have been developed, they have mainly been at the biological level. In this (...) article, we focus on a relatively underexplored aspect of the complexity of pathogenic process: the integration of biological with social and behavioral causes in the same.. (shrink)
A careful analysis of Salmon’s Theoretical Realism and van Fraassen’s Constructive Empiricism shows that both share a common origin: the requirement of literal construal of theories inherited by the Standard View. However, despite this common starting point, Salmon and van Fraassen strongly disagree on the existence of unobservable entities. I argue that their different ontological commitment towards the existence of unobservables traces back to their different views on the interpretation of probability via different conceptions of induction. In fact, inferences to (...) statements claiming the existence of unobservable entities are inferences to probabilistic statements, whence the crucial importance of the interpretation of probability. (shrink)
It is widely agreed that social factors are related to health outcomes: much research served to establish correlations between classes of social factors on the one hand and classes of disease on the other hand. However, why and how social factors are an active part in the aetiology of disease development is something that is gaining attention only recently in the health sciences and in the medical humanities. In this paper, we advance the view that, just as bio-markers help trace (...) the causal continuum from exposure to disease development at the biological level, socio-markers ought to be introduced and studied in order to trace the social continuum from exposure to disease development. We explain how socio-markers differ from social indicators and how they can be used in combination with bio-markers in order to reconstruct the mixed mechanisms of health and disease, namely mechanisms in which both biological and social factors have an active causal role. (shrink)
Inconsistencies between scientific theories have been studied, by and large, from the perspective of paraconsistent logic. This approach considered the formal properties of theories and the structure of inferences one can legitimately draw from theories. However, inconsistencies can be also analysed from the perspective of modelling practices, in particular how modelling practices may lead scientists to form opinions and attitudes that are different, but not necessarily inconsistent. In such cases, it is preferable to talk about disagreement, rather than inconsistency. Disagreement (...) may originate in, or concern, a number of epistemic, socio-political or psychological factors. In this paper, we offer an account of the ‘loci and reasons’ for disagreement at different stages of the scientific process. We then present a controversial episode in the health sciences: the studies on hypercholesterolemia. The causes and effects of high levels of cholesterol in blood have been long and hotly debated, to the point of deserving the name of ‘cholesterol wars’; the debate, to be sure, isn’t settled yet. In this contribution, we focus on some selected loci and reasons for disagreement that occurred between 1920 and 1994 in the studies on hypercholesterolemia. We hope that our analysis of ‘loci and reasons’ for disagreement may shed light on the cholesterol wars, and possibly on other episodes of scientific disagreement. (shrink)
Manipulationism holds that information about the results of interventions is of utmost importance for scientific practices such as causal assessment or explanation. Specifically, manipulation provides information about the stability, or invariance, of the relationship between X and Y: were we to wiggle the cause X, the effect Y would accordingly wiggle and, additionally, the relation between the two will not be disrupted. This sort of relationship between variables are called 'invariant empirical generalisations'. The paper focuses on questions about causal assessment (...) and analyses the status of manipulation. It is argued that manipulationism is trapped in a dilemma. If manipulationism is read as providing a conceptual analysis of causation, then it fails to provide a story about the methods for causal assessment. If, instead, manipulationism is read as providing a method for causal assessment, then it is at an impasse concerning causal assessment in areas where manipulations are not performed. Empirical generalisations are then reassessed, in such a way that manipulation is not taken as methodologically fundamental. The paper concludes that manipulation is the appropriate tool for some scientific contexts, but not for all. (shrink)
Philosophy of medicine: between clinical trials and mechanisms Content Type Journal Article Category Book Review Pages 1-4 DOI 10.1007/s11016-011-9630-5 Authors Federica Russo, Philosophy-SECL, University of Kent, Canterbury, CT2 7NF UK Journal Metascience Online ISSN 1467-9981 Print ISSN 0815-0796.
Econometrics applies statistical methods to study economic phenomena. Roughly, by means of equations, econometricians typically account for the response variable in terms of a number of explanatory variables. The question arises under what conditions econometric models can be given a causal interpretation. By drawing the distinction between associational models and causal models, the paper argues that a proper use of background knowledge, three distinct types of assumptions (statistical, extra-statistical, and causal), and the hypothetico-deductive methodology provide sufficient conditions for a causal (...) interpretation of econometric models. (shrink)
Technologies have always been bearers of profound changes in science, society, and any other aspect of life. The latest technological revolution—the digital revolution—is no exception in this respect. This paper presents the revolution brought about by digital technologies through the lenses of a specific approach: the philosophy of information. It is argued that the adoption of an informational approach helps avoiding utopian or dystopian approaches to technology, both expressions of technological determinism. Such an approach provides a conceptual framework able to (...) address the ethical challenges that digital technologies pose, without getting stuck in the dichotomous thinking of technological determinism, and to bring together ethics, ontology, and epistemology into a coherent account. (shrink)
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 .. (shrink)
Large part of contemporary science is in fact technoscience, in the sense that it crucially depends on several technologies for the generation, collection, and analysis of data. This prompts a re-examination of the relations between science and technologies. In this essay, I advance the view that we’d better move beyond the ‘subordination view’ and the ‘instrumental’ view. The first aims to establish the primacy of science over technology, and the second uses technology instrumentally to support a realist position about theoretical (...) entities. I suggest that we should instead concentrate on how science and technology interact. This will reveal that technology has a poietic character, namely it actively partakes in the production of knowledge. But this poietic character can only be understood within the cognitive activity of scientific communities. Current research in molecular epidemiology, notably the projects funded within the ‘European exposome initiative’, serves as a motivation for such discussion and as an illustration of the claims made. (shrink)