How reliable are causal inferences in complex empirical scenarios? For example, a physician prescribes a drug to a patient, and then the patient undergoes various changes to their symptoms. They then increase their confidence that it is the drug that causes such changes. Are such inferences reliable guides to the causal relation in question, particularly when the physician can gain a large volume of such clinical experience by treating many patients? The evidence-based medicine movement says no, while (...) some physicians and philosophers support such appeals to first-person experience. We develop a formal model and simulate causal inference based on clinical experience. We conclude that in very particular clinical scenarios such inference can be reliable, while in many other routine clinical scenarios such inferences are not reliable. (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)

ABSTRACT: Abstract Most modern knowledge is not science. The physical sciences have successfully validated theories to infer they can be used universally to predict in previously unexperienced circumstances. According to the conventional conception of science such inferences are falsified by a single irregular outcome. And verification is by the scientific method which requires strict regularity of outcome and establishes cause and effect. -/- Medicine, medical research and many “soft” sciences are concerned with individual people in complex heterogeneous populations. These populations (...) cannot be tested to demonstrate strict regularity of outcome in every individual. Neither randomised controlled trials nor observational studies in medicine are science in the conventional conception. Establishing and using medical and other “soft science” theories cannot be scientific. It requires conceptually different means: requiring expert judgement applying all available evidence in the relevant available factual matrix. -/- The practice of medicine is observational. Prediction of outcomes for the individual requires professional expertise applying available medical knowledge and evidence. Expertise in any profession can only be acquired through experience. Prior cases are the fundament of knowledge and expertise in medicine. Case histories, studies and series can provide knowledge of extremely high reliability applicable to establishing reliable general theories and falsifying others. Their collation, study and analysis should be a priority in medicine. Their devaluation as evidence, the failure to apply their lessons, the devaluation of expert professional judgement and the attempt to emulate the scientific method are all historic errors in the theory and practice of modern medicine. (shrink)

There are two competing views regarding the role of mechanistic knowledge in inferences about the effectiveness of interventions. One view holds that inferences about the effectiveness of interventions should be based only on data from population-level studies (often statistical evidence from randomised trials). The other view holds that such inferences must be based in part on mechanistic evidence. The competing views are local principles of inference, the plausibility of which can be assessed by a more general normative principle (...) of inference. Bayesianism tells us to base inferences on both the ‘likelihood’ and the ‘prior’. The likelihood represents statistical evidence. One influence on the prior probability of a hypothesis like ‘d causes x’ is mechanistic knowledge of how d causes x. Thus, reasoning about such inferences by appealing to both statistical and mechanistic evidence is vindicated by our best general theory of inference. The primary contribution of this paper is to assess the merits and weaknesses of the arguments on both sides of the debate, using the Bayesian framework. This analysis lends support to those who argue that we should base our causal inferences about interventions in part on mechanistic evidence. (shrink)

Current debates surrounding the virtues and shortcomings of randomization are symptomatic of a lack of appreciation of the fact that causation can be inferred by two distinct inference methods, each requiring its own, specific experimental design. There is a non-statistical type of inference associated with controlled experiments in basic biomedical research; and a statistical variety associated with randomized controlled trials in clinical research. I argue that the main difference between the two hinges on the satisfaction of the comparability requirement, which (...) is in turn dictated by the nature of the objects of study, namely homogeneous or heterogeneous populations of biological systems. Among other things, this entails that the objection according to which randomized experiments fail to provide better evidence for causation because randomization cannot guarantee comparability is mistaken. (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)

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)

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)

Since its introduction just over two decades ago, evidence-based medicine (EBM) has come to dominate medical practice, teaching, and policy. There are a growing number of textbooks, journals, and websites dedicated to EBM research, teaching, and evidence dissemination. EBM was most recently defined as a method that integrates best research evidence with clinical expertise and patient values and circumstances in the treatment of patients. There have been debates throughout the early 21st century about what counts as (...) good research evidence between EBM proponents and philosophical critics and even within the EBM community itself. Similar controversy arises about the relative worth of patient values and clinical expertise (and how these can be integrated). EBM has also evolved in ways that have come under scrutiny. Specifically, policymakers have used EBM research methodology to increase the relative importance of clinical guidelines that some clinicians have argued are tyrannical. Philosophers have addressed all of these controversies, and with very few exceptions have been critical of EBM. In addition most philosophical attention has been on the epistemic role of Randomization and evidence hierarchies, with relatively little attention being paid to the role of Diagnosis, expertise, patient values, and Systematic Reviews within EBM. (shrink)

Evidence-based medicine is a clinical decision-making framework which makes claims about what physicians ought to do. Though heralded as the cutting edge of medical science, evidence-based medicine is a value-laden normative theory which implicitly depends on substantive views regarding what is morally good or right. In this paper, I provide an ethical analysis of evidence-based medicine. I consider its normative underpinnings in three ethical theories: utilitarianism, Kantian deontology, and virtue ethics. In the face of uncertainty, evidence-based (...) medicine endorses expected utility theory using the best available evidence in order to avoid doing more harm than good. In accordance with the Kantian respect for individuals as ends in themselves, evidence-based medicine calls for integrating the values and preferences of the patient. De-emphasizing intuition, clinical expertise, and pathophysiologic rationale emphasizes the need for the intellectual virtues of curiosity, critical thinking, and courage. Evidence-based medicine is a successful clinical practice that can be morally justified by all three major ethical theories. Although its focus on maximizing good health outcomes and integrating respect for individual patients has been emphasized, the role of the intellectual virtues in evidence-based medicine remains highly under-explored. (shrink)

Evidence-based medicine is a clinical decision making framework which makes claims about what physicians ought to do. Though heralded as the cutting edge of medical science evidence-based medicine is a value laden normative theory which implicitly depends on substantive views regarding what is morally good or right. In this paper, I provide an ethical analysis of evidence-based medicine. I consider its normative underpinnings in three ethical theories: utilitarianism, Kantian deontology, and virtue ethics. In the face of uncertainty, (...) evidence-based medicine endorses expected utility theory using the best available evidence in order to avoid doing more harm than good. In accordance with the Kantian respect for individuals as ends in themselves, evidence-based medicine calls for integrating the values and preferences of the patient. De-emphasizing intuition, clinical expertise, and pathophysiologic rationale emphasizes the need for the intellectual virtues of curiosity, critical thinking, and courage. Evidence-based medicine is a successful clinical practice that can be morally justified by all three major ethical theories. Although its focus on maximizing good health outcomes and integrating respect for individual patients has been emphasized, the role of the intellectual virtues in evidence- based medicine remains highly under-explored. (shrink)

This chapter presents a typology of the different kinds of inductive inferences we can draw from our evidence, based on the explanatory relationship between evidence and conclusion. Drawing on the literature on graphical models of explanation, I divide inductive inferences into (a) downwards inferences, which proceed from cause to effect, (b) upwards inferences, which proceed from effect to cause, and (c) sideways inferences, which proceed first from effect to cause and then from that cause to an additional effect. (...) I further distinguish between direct and indirect forms of downwards and upwards inferences. I then show how we can subsume canonical forms of inductive inference mentioned in the literature, such as inference to the best explanation, enumerative induction, and analogical inference, under this typology. Along the way, I explore connections with probability and confirmation, epistemic defeat, the relation between abduction and enumerative induction, the compatibility of IBE and Bayesianism, and theories of epistemic justification. (shrink)

In this article, I offer a methodological analysis of the empirical research on the causal effects of trade liberalisation, and assess whether such studies can be of any use for guiding policy prescriptions in real-world economies. The analysis focuses on the mainstream economic research that has been used to support arguments in favour of trade liberalisation during the last decades. Even though there are empirical results that could be taken as valid evidence for a causal connection between (...) free trade and economic gains, none of the existing evidence licences trustworthy inferences about the policy effectiveness of trade liberalisation reforms in real-world cases. There are three aspects of the empirical literature that make it highly problematic for making reliable policy inferences: (a) the criteria used to define the notion of ‘free trade’, (b) the background assumptions embedded in the econometric techniques used for estimating causal effects, and (c) the widespread desire among academic economists to attain scientific results in terms of universally valid generalisations. The analysis exposes a worrisome mismatch between, on the one hand, the research aims and outcomes of scientific economics and, on the other, the kind of evidence that would be useful for guiding actual policy deliberations. (shrink)

Configurational Comparative Methods (CCMs) aim to learn causal structures from datasets by exploiting Boolean sufficiency and necessity relationships. One important challenge for these methods is that such Boolean relationships are often not satisfied in real-life datasets, as these datasets usually contain noise. Hence, CCMs infer models that only approximately fit the data, introducing a risk of inferring incorrect or incomplete models, especially when data are also fragmented (have limited empirical diversity). To minimize this risk, evaluation measures for sufficiency and (...) necessity should be sensitive to all relevant evidence. This article points out that the standard evaluation measures in CCMs, consistency and coverage, neglect certain evidence for these Boolean relationships. Correspondingly, two new measures, contrapositive consistency and contrapositive coverage, which are equivalent to the binary classification measures specificity and negative predictive value, respectively, are introduced to the CCM context as additions to consistency and coverage. A simulation experiment demonstrates that the introduced contrapositive measures indeed help to identify correct CCM models. (shrink)

What are the roles of scientific causal knowledge in relation to the evidential requirements of policy making? In this chapter, I review the existing approaches in philosophy of science to the policy relevance of causal knowledge. I assess the specific concerns and questions on which these philosophical accounts have focused and show how they only offer a partial perspective of the relation between causal knowledge and policy making. Most existing views are top-down approaches: they start from philosophical (...) concerns about causation and evidence, and then make general claims about (potential) policy implications, but leave the notion of “policy” unanalyzed. As an alternative, I put forward some ideas toward a bottom-up approach: one that understands policy making as a dynamic process with several stages, and that starts from concrete policy problems, to then examine how causal notions and methods can contribute in various ways to the specifics of the process of policy making. (shrink)

Evidence based medicine (EBM) is under critical debate, and person centered healthcare (PCH) has been proposed as an improvement. But is PCH offered as a supplement or as a replacement of EBM? Prima facie PCH only concerns the practice of medicine, while the contended features of EBM also include methods and medical model. I here argue that there are good philosophical reasons to see PCH as a radical alternative to the existing medical paradigm of EBM, since the two seem (...) committed to conflicting ontologies. This paper aims to make explicit some of the most fundamental assumptions that motivate EBM and PCH, respectively, in order to show that the choice between them ultimately comes down to ontological preference. While EBM has a solid foundation in positivism, or what I here call Humeanism, PCH is more consistent with causal dispositionalism. I conclude that if there is a paradigmatic revolution on the way in medicine, it is first of all one of ontology. (shrink)

Mental simulation refers to the imagination of alternative, counterfactual realities. This chapter provides an overview of research on simulations of the past— retrospective simulation—and simulations of the future— prospective simulation. Two major themes run throughout. The first is that both retrospective and prospective thinking are inextricably linked, relying on a mixture of episodic and semantic memories that share common neural substrates. The second is that retrospective and prospective simulation present trade-offs for the individual. On the one hand, they are functional, (...) identifying causal inferences and potential obstacles that prepare us to try harder and perform better in the future. On the other hand, they sometimes produce bias—retrospective thinking can enhance hindsight bias, whereas prospective thinking can evoke biased predictions about the likelihood of certain events as well as how one is going to feel about those events in the future. Fortunately, however, these biases can be diminished with debiasing techniques. (shrink)

In this paper, I examine Cicero’s oft-neglected De Divinatione, a dialogue investigating the legitimacy of the practice of divination. First, I offer a novel analysis of the main arguments for divination given by Quintus, highlighting the fact that he employs two logically distinct argument forms. Next, I turn to the first of the main arguments against divination given by Marcus. Here I show, with the help of modern probabilistic tools, that Marcus’ skeptical response is far from the decisive, proto-naturalistic assault (...) on superstition that it is sometimes portrayed to be. Then, I offer an extended analysis of the second of the main arguments against divination given by Marcus. Inspired by Marcus’ second main argument, I formulate, explicate, and defend a substantive principle of scientific methodology that I call the “Ciceronian Causal-Nomological Requirement” (CCR). Roughly, this principle states that causal knowledge is essential for relying on correlations in predictive inference. Although I go on to argue that Marcus’ application of the CCR in his debate with Quintus is dialectically inadequate, I conclude that De Divinatione deserves its place in Cicero’s philosophical corpus, and that ultimately, its significance for the history and philosophy of science ought to be recognized. (shrink)

There is a middle ground of imperfect knowledge in fields like medicine and the social sciences. It stands between our day-to-day relatively certain knowledge obtained from ordinary basic observation of regularities in our world and our knowledge from well-validated theories in the physical sciences. -/- The latter enable reliable prediction a great deal of the time of the happening of events never before experienced. The former enable prediction only of what has happened before and beyond that of educated guesses which (...) may sometimes prove right and others not when we test them. -/- The imperfection of our knowledge between those limits is a consequence of complexity. -/- Reductionist empiricism fails when faced with complexity but we all still have to live in a complex world where reductionist science cannot help us devise reliable theories from which we can predict the behaviour of the world around us. We cannot predict reliably. We can only monitor actively and manage actively the world around us if we want to try to control our environment. We have a limited prediction horizon. -/- Science and empiricism work well if we want to send Voyager I and II over 3 billion miles away but not for most other things. -/- In medicine how and when to apply probabilistic, conjectural, incomplete medical theories and explanations requires professional expertise, intuition and judgement (non scientific knowledge) which is essential. Medical diagnosis is a skill of predicting from knowledge of what has happened before that the past will recur in the current patient applying expertise and intuition from knowledge and experience of prior cases and probabilistic medical research and theory. The physician is left to an educated guess as to how the future will develop for the particular individual patient the focus of his or her current attention. (shrink)

In clinical medicine, a diagnosis can offer an explanation of a patient's symptoms by specifying the pathology that is causing them. Diagnoses in psychiatry are also sometimes presented in clinical texts as if they pick out pathological processes that cause sets of symptoms. However, current evidence suggests the possibility that many diagnostic categories in psychiatry are highly causally heterogeneous. For example, major depressive disorder may not be associated with a single type of underlying pathological process, but with a range (...) of different causal pathways, each involving complex interactions of various biological, psychological, and social factors. This paper explores the implications of causal heterogeneity for whether psychiatric diagnoses can be said to serve causal explanatory roles in clinical practice. I argue that while they may fall short of picking out a specific cause of the patient's symptoms, they can nonetheless supply different sorts of clinically relevant causal information. In particular, I suggest that some psychiatric diagnoses provide negative information that rules out certain causes, some provide approximate or disjunctive information about the range of possible causal processes, and some provide causal information about the relations between the symptoms themselves. (shrink)

Translating risk estimates derived from epidemiologic study into evidence of causality for a particular patient is problematic. The difficulty of this process is not unique to the medical context; rather, courts are also challenged with the task of using risk estimates to infer evidence of cause in particular cases. Thus, an examination of how this is done in a legal context might provide insight into when and how it is appropriate to use risk information as evidence of (...) cause in a medical context. A careful study of the case of Goodman v. Viljoen, a medical malpractice suit litigated in the Ontario Superior Court of Justice in 2011, reveals different approaches to how risk information is used as or might be considered a substitute for evidence of causation, and the pitfalls associated with these approaches. Achieving statistical thresholds, specifically minimizing the probability of falsely rejecting the null hypothesis, and exceeding a relative risk of 2, plays a significant role in establishing causality of the particular in the legal setting. However, providing a reasonable explanation or establishing “biological plausibility” of the causal association also seems important, and (to some) may even take precedent over statistical thresholds for a given context. (shrink)

To study climate change, scientists employ computer models, which approximate target systems with various levels of skill. Given the imperfection of climate models, how do scientists use simulations to generate knowledge about the causes of observed climate change? Addressing a similar question in the context of biological modelling, Levins (1966) proposed an account grounded in robustness analysis. Recent philosophical discussions dispute the confirmatory power of robustness, raising the question of how the results of computer modelling studies contribute to the body (...) of evidence supporting hypotheses about climate change. Expanding on Staley’s (2004) distinction between evidential strength and security, and Lloyd’s (2015) argument connecting variety-of-evidence inferences and robustness analysis, I address this question with respect to recent challenges to the epistemology robustness analysis. Applying this epistemology to case studies of climate change, I argue that, despite imperfections in climate models, and epistemic constraints on variety-of-evidence reasoning and robustness analysis, this framework accounts for the strength and security of evidence supporting climatological inferences, including the finding that global warming is occurring and its primary causes are anthropogenic. (shrink)

Public policymakers and institutional decision-makers routinely face questions about whether interventions “work”: does universal basic income improve people’s welfare and stimulate entrepreneurial activity? Do gated alleyways reduce burglaries or merely shift the crime burden to neighbouring communities? What is the most cost-effective way to improve students’ reading abilities? These are empirical questions that seem best answered by looking at the world, rather than trusting speculations about what will be effective. Evidence-based policy (EBP) is a movement that concretizes this intuition. (...) It maintains that policy should be based on evidence of “what works.” Not any evidence will do, however. Following on the heels of its intellectual progenitor, evidence-based medicine (EBM), EBP insists on the use of high-quality evidence produced in accordance with rigorous methodological standards. Though intuitively compelling, EBP has attracted significant criticism from methodologists, political scientists, and philosophers. This chapter provides a critical overview of EBP through a philosophical lens, reviewing and discussing some of the most pressing challenges that EBP faces and outlining some proposals for improving it. I first provide a brief overview of EBP and distinguish a broader and narrower understanding of it. I then review existing lines of criticism of EBP, two of which are considered in detail. The first elaborates how EBP struggles with extrapolation, that is, the use of evidence from study populations to make inferences about the effects of policies on novel target populations. The second maintains that EBP’s methodological tenets are deeply entwined with moral and political values, which can threaten EBP’s promise to promote objectivity in policymaking. Finally, I make some proposals for how EBP could be improved going forward. (shrink)

We simulate trial data to test speculative claims about research methods, such as the impact of publication bias.

In Lehrer’s case of the superstitious lawyer, a lawyer possesses conclusive evidence for his client’s innocence, and he appreciates that the evidence is conclusive, but the evidence is causally inert with respect to his belief in his client’s innocence. This case has divided epistemologists ever since Lehrer originally proposed it in his argument against causal analyses of knowledge. Some have taken the claim that the lawyer bases his belief on the evidence as a data point (...) for our theories to accommodate, while others have denied that the lawyer has knowledge, or that he bases his belief on the evidence. In this paper, we move the dialectic forward by way of arguing that the superstitious lawyer genuinely infers his client’s innocence from the evidence. To show that the lawyer’s inference is genuine, we argue in defense of a version of a doxastic construal of the ‘taking’ condition on inference. We also provide a pared-down superstitious lawyer-style case, which displays the key features of the original case without including its complicated and distracting features. But interestingly, although we argue that the lawyer’s belief is based on his good evidence, and is also plausibly doxastically justified, we do not argue that the lawyer knows that his client is innocent. (shrink)

“Excited Delirium Syndrome” (ExDS) is a controversial diagnosis. The supposed syndrome is sometimes considered to be a potential cause of death. However, it has been argued that its sole purpose is to cover up excessive police violence because it is mainly used to explain deaths of individuals in custody. In this paper, we examine the epistemic conditions giving rise to the controversial diagnosis by discussing the relation between causal hypotheses, evidence, and data in forensic medicine. We argue that (...) the practitioners’ social context affects causal inquiry through background assumptions that enter inquiry at multiple stages. This analysis serves to better understand the wide usage of the controversial diagnosis of ExDS. (shrink)

Archaeological data are shadowy in a number of senses. Not only are they notoriously fragmentary but the conceptual and technical scaffolding on which archaeologists rely to constitute these data as evidence can be as constraining as it is enabling. A recurrent theme in internal archaeological debate is that reliance on sedimented layers of interpretative scaffolding carries the risk that “preunderstandings” configure what archaeologists recognize and record as primary data, and how they interpret it as evidence. The selective and (...) destructive nature of data capture in archeology further suggests that there may be little scope for putting “legacy” data to work in new ways. And yet archaeologists have been strikingly successful in mining old datasets for new insights. I situate these concerns in the broader context of debate about the epistemic standing of the historical sciences, and then consider three strategies by which archaeologists address the challenges posed by legacy data. The first two – secondary retrieval and recontextualization – are a matter of reconfiguring the scaffolding that underpins evidential reasoning. The third turns on redeploying old data in the context of computational models that support the experimental simulation of the cultural systems and contexts under study. (shrink)

Philosophers of science have insisted that evidence of underlying mechanisms is required to support claims about the effects of medical interventions. Yet evidence about mechanisms does not feature on dominant evidence-based medicine “hierarchies.” After arguing that only inferences from mechanisms (“mechanistic reasoning”)—not mechanisms themselves—count as evidence, I argue for a middle ground. Mechanistic reasoning is not required to establish causation when we have high-quality controlled studies; moreover, mechanistic reasoning is more problematic than has been assumed. Yet (...) where the problems can be overcome, mechanistic reasoning can and should be used as evidence. (shrink)

This article provides a conceptual account of causal understanding by connecting current psychological research on time and causality with philosophical debates on the causal asymmetry. I argue that causal relations are viewed as asymmetric because they are understood in temporal terms. I investigate evidence from causal learning and reasoning in both children and adults: causal perception, the temporal priority principle, and the use of temporal cues for causal inference. While this account does not (...) suffice for correct inferences of causal structure, I show it to serve as a preliminary understanding of causal concepts as asymmetric, that later incorporates other types of evidence. This approach supplies causal models with an asymmetric concept of causation that underlies hypotheses about causal structure, as I will illustrate from the framework of the knowledge-based causal induction model. I further argue for an integrating perspective, showing how the understanding of causes as preceding their effects underlies both psychological models and philosophical debates over time and the causal asymmetry, particularly regarding problem cases such as simultaneous causation or backwards causation, and the conceptual connection between causation and action. (shrink)

Evidence-Based Medicine has little consideration for mechanisms and philosophers of science and medicine have recently made pleas to increase the place of mechanisms in the medical evidence hierarchy. However, in this debate the notions of mechanisms seem to be limited to 'mechanistic processes' and 'complex-systems mechanisms,' understood as 'componential causal systems'. I believe that this will not do full justice to how mechanisms are used in biological, psychological and social sciences and, consequently, in a more biopsychosocial approach (...) to medicine. Here, I propose, following (Kuorikoski, 2009), to pay more attention to 'abstract forms of interaction' mechanisms. The present work scrutinized review articles on depression and medically unexplained pain, which are considered to be of multifactorial pathogenesis, for their use of mechanisms. In review articles on these disorders there seemed to be a range of uses between more 'abstract forms of interaction' and 'componential causal system' mechanisms. I therefore propose to expand the notions of mechanisms considered in medicine to include that of more 'abstract forms of interaction' to better explain and manage biopsychosocial disorders. (shrink)

The epidemiologist Bradford Hill famously argued that in epidemiology, specificity of association (roughly, the fact that an environmental or behavioral risk factor is associated with just one or at most a few medical outcomes) is strong evidence of causation. Prominent epidemiologists have dismissed Hill’s claim on the ground that it relies on a dubious `one-cause one effect’ model of disease causation. The paper examines this methodological controversy, and argues that specificity considerations do have a useful role to play in (...) causal inference in epidemiology. More precisely, I argue that specificity considerations help solve a pervasive inferential problem in contemporary epidemiology: the problem of determining whether an exposure-outcome correlation might be due to confounding by a social factor. This examination of specificity has interesting consequences for our understanding of the methodology of epidemiology. It highlights how the methodology of epidemiology relies on local tools designed to address specific inference problems peculiar to the discipline, and shows that observational causal inference in epidemiology can proceed with little prior knowledge of the causal structure of the phenomenon investigated. I also argue that specificity of association cannot (despite claims to the contrary) be entirely explained in terms of Woodward’s well-known concept of “one-to-one” causal specificity. This is because specificity as understood by epidemiologists depends on whether an exposure (or outcome) is associated with a `heterogeneous’ set of variables. This dimension of heterogeneity is not captured in Woodward’s notion, but is crucial for understanding the evidential import of specificity of association. (shrink)

Alienation has been recently revived as a central theme in critical theory. Current debates, however, tend to focus on normative rather than on explanatory issues. In this paper, I confront the latter and advance an account of alienation that bears on the mechanisms that bring it about in order to locate alienation as a distinctive social and psychological fact. In particular, I argue that alienation can be explained as a disruption induced by social factors in the sense of mental ownership (...) that comes with the first personal awareness of being a subject of attitudes, emotions, and actions, and outline how social factors can play a structuring causal role in the process that brings it about. In the first section, I introduce the theme and explain why it is important to focus on the mechanisms that underlie alienation. In the second section, I maintain that understanding how alienation works is crucial to make sense of false consciousness. In the third section, I consider the relevance of mental ownership to explaining alienation and discuss existing evidence about whether and how it can fail. In the final section, I argue that disturbances in the simulation routines that support social cognition might underpin alienation, and outline how social factors might play a structuring causal role in this connection. (shrink)

Transcranial magnetic stimulation is used to make inferences about relationships between brain areas and their functions because, in contrast to neuroimaging tools, it modulates neuronal activity. The central aim of this article is to critically evaluate to what extent it is possible to draw causal inferences from repetitive TMS data. To that end, we describe the logical limitations of inferences based on rTMS experiments. The presented analysis suggests that rTMS alone does not provide the sort of premises that are (...) sufficient to warrant strong inferences about the direct causal properties of targeted brain structures. Overcoming these limitations demands a close look at the designs of rTMS studies, especially the methodological and theoretical conditions which are necessary for the functional decomposition of the relations between brain areas and cognitive functions. The main points of this article are that TMS-based inferences are limited in that stimulation-related causal effects are not equivalent to structure-related causal effects due to TMS side effects, the electric field distribution, and the sensitivity of neuroimaging and behavioral methods in detecting structure-related effects and disentangling them from confounds. Moreover, the postulated causal effects can be based on indirect effects. A few suggestions on how to manage some of these limitations are presented. We discuss the benefits of combining rTMS with neuroimaging in experimental reasoning and we address the restrictions and requirements of rTMS control conditions. The use of neuroimaging and control conditions allows stronger inferences to be gained, but the strength of the inferences that can be drawn depends on the individual experiment’s designs. Moreover, in some cases, TMS might not be an appropriate method of answering causality-related questions or the hypotheses have to account for the limitations of this technique. We hope this summary and formalization of the reasoning behind rTMS research can be of use not only for scientists and clinicians who intend to interpret rTMS results causally but also for philosophers interested in causal inferences based on brain stimulation research. (shrink)

Despite being a milestone in the history of statistical causal inference, Sewall Wright’s 1918 invention of path analysis did not receive much immediate attention from the statistical and scientific community. Through a careful historical analysis, this paper reveals some previously overlooked philosophical issues concerning the history of causal inference. Placing the invention of path analysis in a broader historical and intellectual context, I portray the scientific community’s initial lack of interest in the method as a natural consequence of (...) relevant scientific and philosophical conditions. In addition to Karl Pearson’s positivist refutation of causation, I contend that the acceptance of path analysis faced several other challenges, including the introduction of a new formalism, conceptual barriers to causal inference, and the lack of model-based statistical thinking. The presence of these challenges shows that the delayed progress in causal inference in the early twentieth century was inevitable. (shrink)

"Correlation is not causation" is one of the mantras of the sciences—a cautionary warning especially to fields like epidemiology and pharmacology where the seduction of compelling correlations naturally leads to causal hypotheses. The standard view from the epistemology of causation is that to tell whether one correlated variable is causing the other, one needs to intervene on the system—the best sort of intervention being a trial that is both randomized and controlled. In this paper, we argue that some purely (...) correlational data contains information that allows us to draw causal inferences: statistical noise. Methods for extracting causal knowledge from noise provide us with an alternative to randomized controlled trials that allows us to reach causal conclusions from purely correlational data. (shrink)

Eyal Shahar’s essay review [1] of James Penston’s remarkable book [2] seems more inspired playful academic provocation than review or essay, expressing dramatic views of impossible validity. The account given of modern biostatistical causation reveals the slide from science into the intellectual confusion and non-science RCTs have created: “…. the purpose of medical research is to estimate the magnitude of the effect of a causal contrast, for example the probability ratio of a binary outcome …” But Shahar’s world is (...) simultaneously not probabilistic, but of absolute uncertainty: “We should have no confidence in any type of evidence ….. We should have no confidence at all”. Shahar’s "Causal contrast" is attractive. It seems to make sense, but bypasses in two words the means of establishing causation by the scientific method. This phrase assumes a numeric statistically significant “contrast” is causal rather than a potential correlation requiring further investigation. The concept of “causal contrast” is a slippery slope from sense into biostatistical non-science. This can be illustrated with an hypothetical RCT where 100% of interventions exhibit a posited treatment effect and 0% of placebo controls. Internal validity is seemingly quite reasonably assumed satisfied (common-sense dictating the likelihood of an awesome magnificent fraud, bias or plain error of the magnitude required is infinitesimal). Scientific method appears satisfied. The RCT demonstrates: (1) strict regularity of outcome in the presence of posited cause; (2) the absence of outcome in its absence and (3) an intervention (experiment) showing the direction of causation is from posited cause to posited effect. Now travel further down the slope from science. Assume 50% of interventions and 0% of controls are positive. We compromise scientific method, but justify this by assuming a large subgroup which we say surely must on these figures be exhibiting the posited treatment effect. But what of 10% of interventions and 9% of placebo controls exhibiting the posited treatment effect? Our biostatistician says the 1% “causal contrast” is statistically significant. But we have: (1) minimal evidence of regularity; (2) the posited outcome irrespective of presence of posited cause and (3) our intervention is at the highest equivocal in demonstrating any form of causation. This is not science. It is, however, where biostatistics has unthinkingly taken us, as Penston has shown comprehensively [2]. We, the audience of published medical research, are now for the 10% / 9% example well down the slope from science. An unattractive hypothesis results requiring numerous assumptions similar to these:- "There is a 'contrast' which is ‘causal’, albeit the method employed is not scientific. An effect of the intervention has been observed in a very small subgroup. This subgroup is susceptible to treatment. The similar number of placebo controls exhibiting the outcome sought is irrelevant, because the 1% difference between intervention and controls is statistically significant. The statistical analysis is valid and reliable. The RCT’s internal validity is sufficiently satisfied. No funding or bias or fraud has affected the results or their analysis.” As Penston notes: “Confirming and refuting the results of research is crucial to science …. But … there’s no way of testing the results of any particular large-scale RCT or epidemiological study. Each study … is left hanging in the air, unsupported.” It gets worse. To identify a rare serious adverse reaction of a frequency of 1:10,000 can require a trial of 200,000 or larger split between controls and interventions. This is not done. But for every 100 who prospectively benefit from the intervention, 9,900 also receive it. And for every 100 benefiting one person (who likely gains no benefit) will suffer a serious unidentified adverse reaction. This is also without taking account of more common adverse reactions whether serious or otherwise. References [1] Shahar, E. (2011) Research and medicine: human conjectures at every turn. International Journal of Person Centered Medicine 1 (2), 250-253. [2] Penston, J. (2010). stats.con: How we’ve been fooled by statistics-based research in medicine. London: The London Press, UK. (shrink)

I defend the view, hardly original with me, that there is no evidence, deductive or non-deductive, for any of our causal beliefs, that does not already assume that there are some causal connections, and hence that there is no way in which experience on its own, or with causalität-free principles, can support the structure of out causal knowledge. The deductive case is perhaps obvious. In the case of non-deductive arguments, I consider how experience of constant conjunctions, (...) together with the employment of an inference to the best explanation, might lead to a causal conclusion. But I argue that such an inference would need as a premiss that the causal explanation of the constant conjunction is the best explanation of that evidence, and ‘best’ in this context requires the thought that the causal hypothesis best fits with our existing causal beliefs. (shrink)

In the biomedical context, policy makers face a large amount of potentially discordant evidence from different sources. This prompts the question of how this evidence should be aggregated in the interests of best-informed policy recommendations. The starting point of our discussion is Hunter and Williams’ recent work on an automated aggregation method for medical evidence. Our negative claim is that it is far from clear what the relevant criteria for evaluating an evidence aggregator of this sort (...) are. What is the appropriate balance between explicitly coded algorithms and implicit reasoning involved, for instance, in the packaging of input evidence? In short: What is the optimal degree of ‘automation’? On the positive side: We propose the ability to perform an adequate robustness analysis as the focal criterion, primarily because it directs efforts to what is most important, namely, the structure of the algorithm and the appropriate extent of automation. Moreover, where there are resource constraints on the aggregation process, one must also consider what balance between volume of evidence and accuracy in the treatment of individual evidence best facilitates inference. There is no prerogative to aggregate the total evidence available if this would in fact reduce overall accuracy. (shrink)

Recent attempts to resolve the Paradox of the Gatecrasher rest on a now familiar distinction between individual and bare statistical evidence. This paper investigates two such approaches, the causal approach to individual evidence and a recently influential (and award-winning) modal account that explicates individual evidence in terms of Nozick's notion of sensitivity. This paper offers counterexamples to both approaches, explicates a problem concerning necessary truths for the sensitivity account, and argues that either view is implausibly committed (...) to the impossibility of no-fault wrongful convictions. The paper finally concludes that the distinction between individual and bare statistical evidence cannot be maintained in terms of causation or sensitivity. We have to look elsewhere for a solution of the Paradox of the Gatecrasher. (shrink)

In their 2013 study of traumatic flashback formation, Bourne, Mackay and Holmes raise the question of whether the propensity of a traumatic experience to produce flashbacks is determined by the emotions that are felt at the time of that experience. They suggest that it is not, but the grounds on which they make this suggestion are flawed. Further research is required. That research will need to overcome a significant methodological difficulty — one which is hard to avoid when fMRI data (...) and introspective reports are combined in a single causal inference. (shrink)

In order to support health interventions, biomedical and population health researchers need to collect solid evidence. This article asks what type of evidence this should be and expands on previous work that focused on etiological explanations, or causal-mechanical explanations of why and how illness occurs. The article proposes adding predictive evidence to the explanatory evidence, in order to form a joint evidence set, or JES = [A,B,C,D], which consists of four different types of (...) class='Hi'>evidence: association [A], biology [B], confirmation [C], and difference-making [D]. The article discusses explanatory coherence as a backbone for this proposal, suggests criteria for each type of evidence, and offers a rubric for multi-evidence mapping. (shrink)

Thirty years after the rise of the evidence-based medicine (EBM) movement, formal training in philosophy remains poorly represented among medical students and their educators. In this paper, I argue that EBM’s reception in this context has resulted in a privileging of empiricism over rationalism in clinical reasoning with unintended consequences for medical practice. After a limited review of the history of medical epistemology, I argue that a solution to this problem can be found in the method of the 2nd-century (...) Roman physician Galen, who brought empiricism and rationalism together in a synthesis anticipating the scientific method. Next, I review several of the problems that have been identified as resulting from a staunch commitment to empiricism in medical practice. Finally, I conclude that greater epistemological awareness in the medical community would precipitate a Galenic shift toward a more epistemically balanced, scientific approach to clinical research. (shrink)

Abstract -/- Rationale, aims and objectives: Irregularity limits human ability to know, understand and predict. A better understanding of irregularity may improve the reliability of knowledge. -/- Method: Irregularity and its consequences for knowledge are considered. -/- Results: Reliable predictive empirical knowledge of the physical world has always been obtained by observation of regularities, without needing science or theory. Prediction from observational knowledge can remain reliable despite some theories based on it proving false. A naïve theory of irregularity is outlined. (...) Reducing irregularity and/or increasing regularity can increase the reliability of knowledge. Beyond long experience and specialization, improvements include implementing supporting knowledge systems of libraries of appropriately classified prior cases and clinical histories and education about expertise, intuition and professional judgement. -/- Conclusions: A consequence of irregularity and complexity is that classical reductionist science cannot provide reliable predictions of the behaviour of complex systems found in nature, including of the human body. Expertise, expert judgement and their exercise appear overarching. Diagnosis involves predicting the past will recur in the current patient applying expertise and intuition from knowledge and experience of previous cases and probabilistic medical theory. Treatment decisions are an educated guess about the future (prognosis). Benefits of the improvements suggested here are likely in fields where paucity of feedback for practitioners limits development of reliable expert diagnostic intuition. Further analysis, definition and classification of irregularity is appropriate. Observing and recording irregularities are initial steps in developing irregularity theory to improve the reliability and extent of knowledge, albeit some forms of irregularity present inherent difficulties. (shrink)

Social scientists often draw on a variety of evidence for their causal inferences. There is also a call to use a greater variety of evidence in social science research. This topical collection examines the philosophical foundations and implications of evidential diversity in the social sciences. It assesses the application of Evidential Pluralism in the context of the social sciences, especially its application to economics and political science. It also discusses the concept of causation in cognitive science and (...) the implications of evidential diversity for the social sciences. (shrink)

This chapter explores the idea that the need to establish common knowledge is one feature that makes social cognition stand apart in important ways from cognition in general. We develop this idea on the background of the claim that social cognition is nothing but a type of causal inference. We focus on autism as our test-case, and propose that a specific type of problem with common knowledge processing is implicated in challenges to social cognition in autism spectrum disorder (ASD). (...) This problem has to do with the individual’s assessment of the reliability of messages that are passed between people as common knowledge emerges. The proposal is developed on the background of our own empirical studies and outlines different ways common knowledge might be comprised. We discuss what these issues may tell us about ASD, about the relation between social and non-social cognition, about social objects, and about the dynamics of social networks. (shrink)

In this BA dissertation, I deploy examples of non-causal explanations of physical phenomena as evidence against the view that causal models of explanation can fully account for explanatory practices in science. I begin by discussing the problems faced by Hempel’s models and the causal models built to replace them. I then offer three everyday examples of non-causal explanation, citing sticks, pilots and apples. I suggest a general form for such explanations, under which they can be (...) phrased as inductive-statistical arguments incorporating plausible assumptions. I then show the applicability of this form to explanatory practices in thermal physics. I explore the possibility that population genetics provides a similar form of explanation, and offer a novel defence of the statistical interpretation of population genetics proposed by Matthen and Ariew (2002). I close with remarks concerning how, when faced with competing causal and non-causal explanations of the same phenomenon, we can perform an Inference to the Best Explanation. (shrink)

As the opening line of Dickens' classic novel suggests, it is very often the case that people can imagine both better and worse alternatives to their present reality. Although Dickens was writing about events that occurred over two centuries ago, it remains just as true today that we clearly live in neither the best nor the worst of possible worlds. For instance, we can wish for the amelioration of present difficulties in the Middle East yet still take comfort in the (...) fact that the threat of nuclear war has been greatly reduced since the end of the Cold War. On a more mundane level, it is easy for us to imagine how various aspects of our lives, such as our jobs, marriages, or physical fitness, could be both better and worse. Undoubtedly due to the pervasiveness and intrinsically fascinating qualities of this phenomenon of imagining alternatives to reality, there has been a veritable explosion of research in recent years on what have been termed mental simulation and counterfactual thinking processes. This chapter speculates upon and provides evidence for the antecedents and consequences of two types of counterfactuals: upward (it could have been better) and downward (it could have been worse). The importance of studying the antecedents and consequences of counterfactual direction lie in the differential structures, emotions, intentions, inferences, and behavioral consequences of upward versus downward counterfactual thinking. (shrink)

Medical scientists employ ‘quality assessment tools’ (QATs) to measure the quality of evidence from clinical studies, especially randomized controlled trials (RCTs). These tools are designed to take into account various methodological details of clinical studies, including randomization, blinding, and other features of studies deemed relevant to minimizing bias and error. There are now dozens available. The various QATs on offer differ widely from each other, and second-order empirical studies show that QATs have low inter-rater reliability and low inter-tool reliability. (...) This is an instance of a more general problem I call the underdetermination of evidential significance. Disagreements about the strength of a particular piece of evidence can be due to different—but in principle equally good—weightings of the fine-grained methodological features which constitute QATs. (shrink)

To justify inductive inference and vanquish classical skepticisms about human memory, external world realism, etc., Richard Fumerton proposes his “inferential internalism,” an epistemology whereby humans ‘see’ by Russellian acquaintance Keynesian probable relations (PRs) between propositions. PRs are a priori necessary relations of logical probability, akin to but not reducible to logical entailments, such that perceiving a PR between one’s evidence E and proposition P of unknown truth value justifies rational belief in P to an objective degree. A recent critic (...) of inferential internalism is Alan Rhoda, who questions its psychological plausibility. Rhoda argues that in order to see necessary relations between propositions E and P, one would need acquaintance with too many propositions at once, since our evidence E is often complex. In this paper, I criticize Rhoda’s implausibility objection as too quick. Referencing the causal status effect (CSE) from psychology, I argue that some of the complex features of evidence E contribute to our type-categorizing it as E-type, and thus we do not need to ‘see’ all of the complex features when we see the PR between E and P. My argument leaves unchanged Fumerton’s justificatory role for the PR, but enhances its psychological plausibility. (shrink)