Causal Reasoning, Misc

There is, among some scientists and philosophers, the idea that any theory that would allow the time travel would introduce causal issues. These types of temporal paradoxes can be avoided by the Novikov self-consistency principle or by a variation in the interpretation of many worlds with interacting worlds. The world in which we live has, according to David Lewis, a Parmenidean ontology: "a manifold of events in four dimensions," and the occupants of the world are the 4-dimensional aggregates of the (...) stages - "temporal lines". The causal loops in backwards time travel involve events that appear to "come from nowhere," paradoxical "self-existent" objects or information, resulting in a bootstrap paradox. Many believe that causality loops are not impossible or unacceptable, but only inexplicable. DOI: 10.13140/RG.2.2.28792.70407. (shrink)

In this paper, I critically evaluate several related, provocative claims made by proponents of data-intensive science and “Big Data” which bear on scientific methodology, especially the claim that scientists will soon no longer have any use for familiar concepts like causation and explanation. After introducing the issue, in section 2, I elaborate on the alleged changes to scientific method that feature prominently in discussions of Big Data. In section 3, I argue that these methodological claims are in tension with a (...) prominent account of scientific method, often called “Inference to the Best Explanation” (IBE). Later on, in section 3, I consider an argument against IBE that will be congenial to proponents of Big Data, namely the argument due to Roche and Sober (2013) that “explanatoriness is evidentially irrelevant”. This argument is based on Bayesianism, one of the most prominent general accounts of theory-confirmation. In section 4, I consider some extant responses to this argument, especially that of Climenhaga (2017). In section 5, I argue that Roche and Sober’s argument does not show that explanatory reasoning is dispensable. In section 6, I argue that there is good reason to think explanatory reasoning will continue to prove indispensable in scientific practice. Drawing on Cicero’s oft-neglected De Divinatione, I formulate what I call the “Ciceronian Causal-nomological Requirement”, (CCR), which states roughly that causal-nomological knowledge is essential for relying on correlations in predictive inference. I defend a version of the CCR by appealing to the challenge of “spurious correlations”, chance correlations which we should not rely upon for predictive inference. In section 7, I offer some concluding remarks. (shrink)

A good definition of process tracing should highlight what is distinctive about process tracing as a methodology of causal inference. I look at eight criteria that are used to define process tracing in the methodological literature, and I dismiss all eight criteria as unhelpful (some because they are too restrictive, and others because they are vacuous). In place of these criteria, I propose four alternative criteria, and I draw a distinction between process tracing for the ultimate aim of testing a (...) start--end hypothesis versus process tracing as an ultimate end in itself. Although it is clear enough how the former method works, there is still much methodological work to be done in understanding the latter method as a distinctive method of causal inference, I argue. (shrink)

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

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)

Among the many causes of an event, how do we distinguish the important ones? Are there ways to distinguish among causes on principled grounds that integrate both practical aims and objective knowledge? Psychologist Tania Lombrozo has suggested that causal explanations “identify factors that are ‘exportable’ in the sense that they are likely to subserve future prediction and intervention” (Lombrozo 2010, 327). Hence portable causes are more important precisely because they provide objective information to prediction and intervention as practical aims. However, (...) I argue that this is only part of the epistemology of causal selection. Recent work on portable causes has implicitly assumed them to be portable within the same causal system at a later time. As a result, it has appeared that the objective content of causal selection includes only facts about the causal structure of that single system. In contrast, I present a case study from systems biology in which scientists are searching for causal factors that are portable across rather than within causal systems. By paying careful attention to how these biologists find portable causes, I show that the objective content of causal selection can extend beyond the immediate systems of interest. In particular, knowledge of the evolutionary history of gene networks is necessary for correctly identifying causal patterns in these networks that explain cellular behavior in a portable way. (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)

"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)

People more frequently select norm-violating factors, relative to norm- conforming ones, as the cause of some outcome. Until recently, this abnormal-selection effect has been studied using retrospective vignette-based paradigms. We use a novel set of video stimuli to investigate this effect for prospective causal judgments—i.e., judgments about the cause of some future outcome. Four experiments show that people more frequently select norm- violating factors, relative to norm-conforming ones, as the cause of some future outcome. We show that the abnormal-selection effects (...) are not primarily explained by the perception of agency (Experiment 4). We discuss these results in relation to recent efforts to model causal judgment. (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)

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)

During the first half of the twentieth century, many philosophers of memory opposed the postulation of memory traces based on the claim that a satisfactory account of remembering need not include references to causal processes involved in recollection. However, in 1966, an influential paper by Martin and Deutscher showed that causal claims are indeed necessary for a proper account of remembering. This, however, did not settle the issue, as in 1977 Malcolm argued that even if one were to buy Martin (...) and Deutscher’s argument for causal claims, we still don’t need to postulate the existence of memory traces. This paper reconstructs the dialectic between realists and anti-realists about memory traces, suggesting that ultimately realists’ arguments amount to inferences to the best explanation. I then argue that Malcolm’s anti-realist strategy consists in the suggestion that causal explanations that do not invoke memory traces are at least as good as those that do. But then, Malcolm, I argue that there are a large number of memory phenomena for which explanations that do not postulate the existence of memory traces are definitively worse than explanations that do postulate them. Next, I offer a causal model based on an interventionist framework to illustrate when memory traces can help to explain memory phenomena and proceed to substantiate the model with details coming from extant findings in the neuroscience of memory. (shrink)

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

In temporal binding, the temporal interval between one event and another, occurring some time later, is subjectively compressed. We discuss two ways in which temporal binding has been conceptualized. In studies showing temporal binding between a voluntary action and its causal consequences, such binding is typically interpreted as providing a measure of an implicit or pre-reflective “sense of agency”. However, temporal binding has also been observed in contexts not involving voluntary action, but only the passive observation of a cause-effect sequence. (...) In those contexts, it has been interpreted as a top-down effect on perception reflecting a belief in causality. These two views need not be in conflict with one another, if one thinks of them as concerning two separate mechanisms through which temporal binding can occur. In this paper, we explore an alternative possibility: that there is a unitary way of explaining temporal binding both within and outside the context of voluntary action as a top-down effect on perception reflecting a belief in causality. Any such explanation needs to account for ways in which agency, and factors connected with agency, have been shown to affect the strength of temporal binding. We show that principles of causal inference and causal selection already familiar from the literature on causal learning have the potential to explain why the strength of people’s causal beliefs can be affected by the extent to which they are themselves actively involved in bringing about events, thus in turn affecting binding. (shrink)

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

The COVID-19 pandemic has demonstrated how different (even conflicting) interventions on nature can be scientifically justified: interventions can be deemed "effective" only in relation to specific target variables - in relation to variables the values of which we seek to control. Choosing the "right" target variables, in turn, depends on our values and pragmatic aims. This essay is based on a presentation given at the symposium "Multidisciplinary Perspectives on the COVID-19 Pandemic", organised at the Helsinki Collegium for Advanced Studies on (...) 16 June 2020. (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)

It is sometimes thought that randomized study group allocation is uniquely proficient at producing comparison groups that are evenly balanced for all confounding causes. Philosophers have argued that in real randomized controlled trials this balance assumption typically fails. But is the balance assumption an important ideal? I run a thought experiment, the CONFOUND study, to answer this question. I then suggest a new account of causal inference in ideal and real comparative group studies that helps clarify the roles of confounding (...) variables and randomization. 1Confounders and Causes2The Balance Assumption3The CONFOUND Study 3.1CONFOUND 13.2CONFOUND 24Disjunction C and the Ideal Study 4.1The ultimate ‘other cause’: C4.2The ideal comparative group study4.3Required conditions for causal inference5Confounders as Causes, Confounders as Correlates6Summary. (shrink)

The purpose of this research is to articulate how a theory of causation might be serviceable to a theory of sport. This article makes conceptual links between Bernard Suits’ theory of game-playing, causation, and theories of causation. It justifies theories of causation while drawing on connections between sport and counterfactuals. It articulates the value of theories of causation while emphasizing possible limitations. A singularist theory of causation is found to be more broadly serviceable with particular regard to its analysis of (...) sports. (shrink)

Causation has always been a philosophically controversial subject matter. While David Hume’s empiricist account of causation has been the dominant influence in analytic philosophy and science during modern times, a minority view has instead connected causation essentially to agency and manipulation. A related approach has for the first time gained widespread popularity in recent years, due to new powerful theories of causal inference in science that are based in a technical notion of intervention, and James Woodward’s closely connected interventionist theory (...) of causation in philosophy. This monograph assesses five manipulationist or interventionist theories of causation, viewed as theories that purport to tell us what causation is by providing us with the meaning of causal claims. It is shown that they cannot do this, as the conditions on causation that they impose are too weak, mainly due to ineliminable circularities in their definitions of causal terms. It is then argued that a subset of Woodward’s theory can nevertheless contribute crucially to an explanation of the unique role that manipulation has in our acquisition of causal knowledge. This explanation differs from the common regularist explanation of the epistemic utility of manipulation and experiment, and it is taken to confirm several important manipulationist intuitions. However, the success of the explanation depends on interventionism not itself being understood as a theory of causation, but as a theory of intervention. (shrink)

A cause may influence its effect via multiple paths. Paradigmatically (Hesslow [1974]), taking birth control pills both decreases one’s risk of thrombosis by preventing pregnancy and increases it by producing a blood chemical. Building on Pearl ([2001]), I explicate the notion of a path-specific effect. Roughly, a path-specific effect of C on E via path P is the degree to which a change in C would change E were they to be transmitted only via P. Facts about such effects may (...) be gleaned from the structural equations commonly used to represent the causal relationships among variables. I contrast my analysis of the Hesslow case with those given by theorists of probabilistic causality, who mistakenly link it to issues of causal heterogeneity, token-causation and indeterminism. The reason probabilistic theories misdiagnose this case is that they pay inadequate attention to the structural relationships among variables. (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)

Newton’s Regulae philosophandi—the rules for reasoning in natural philosophy—are maxims of causal reasoning and induction. This essay reviews their significance for Newton’s method of inquiry, as well as their application to particular propositions within the Principia. Two main claims emerge. First, the rules are not only interrelated, they defend various facets of the same core idea: that nature is simple and orderly by divine decree, and that, consequently, human beings can be justified in inferring universal causes from limited phenomena, if (...) only fallibly. Second, the rules make substantive ontological assumptions on which Newton’s argument in the Principia relies. (shrink)

Many theories in philosophy, law, and psychology, make no distinction in meaning between causing and enabling conditions. Yet, psychologically people readily make such distinctions each day. In this paper we report three experiments, showing that individuals distinguish between causes and enabling conditions in brief descriptions of wrongful outcomes. Respondents rate actions that bring about outcomes as causes, and actions that make possible the causal relation as enablers. Likewise, causers (as opposed to enablers) are rated as more responsible for the outcome, (...) as liable to longer prison sentences, and as liable to pay higher fines. Moreover, the more actors involved, the more blame volume there is psychologically to be apportioned between them. The implication is that theories and the law in practice, both criminal and civil, may dangerously mismatch the intuitions of those to whom they are supposed to apply. The findings are discussed in light of contemporary psychological theories of how people reason about cause. -/- The paper presents the extended findings supplementary to the conference paper: Frosch, C. A., Johnson-Laird, P. N., Cowley, M. (2007). Don’t blame me your Honor, I’m only the enabler. Proceedings of the Twenty–Ninth Annual Conference of the Cognitive Science Society, p. 1755, Mahweh, N. J: Erlbaum. Nashville, USA. *Main findings now cited in the Oxford Handbook of Causal Reasoning. (shrink)

Simple regression (regression analysis with a single explanatory variable), and multiple regression (regression models with multiple explanatory variables), typically correspond to very different biological questions. The former use regression lines to describe univariate associations. The latter describe the partial, or direct, effects of multiple variables, conditioned on one another. We suspect that the superficial similarity of simple and multiple regression leads to confusion in their interpretation. A clear understanding of these methods is essential, as they underlie a large range of (...) procedures in common use in biology. Beyond simple and multiple regression in their most basic forms, understanding the key principles of these procedures is critical to understanding, and properly applying, many methods, such as mixed models, generalised models, and causal inference using graphs (including path analysis and its extensions). A simple, but careful, look at the distinction between these two analyses is valuable in its own right, and can also be used to clarify widely-held misconceptions about collinearity (correlations among explanatory variables). There is no general sense in which collinearity is a problem. We suspect that the perception of collinearity as a hindrance to analysis stems from misconceptions about interpretation of multiple regression models, and so we pursue discussions about these misconceptions in this light. In particular, collinearity causes multiple regression coefficients to be less precisely estimated than corresponding simple regression coefficients. This should not be interpreted as a problem, as it is perfectly natural that direct effects should be harder to characterise than univariate associations. Purported solutions to the perceived problems of collinearity are detrimental to most biological analyses. (shrink)

There is widespread recognition at universities that a proper understanding of science is needed for all undergraduates. Good jobs are increasingly found in fields related to Science, Technology, Engineering, and Medicine, and science now enters almost all aspects of our daily lives. For these reasons, scientific literacy and an understanding of scientific methodology are a foundational part of any undergraduate education. Recipes for Science provides an accessible introduction to the main concepts and methods of scientific reasoning. With the help of (...) an array of contemporary and historical examples, definitions, visual aids, and exercises for active learning, the textbook helps to increase students’ scientific literacy. The first part of the book covers the definitive features of science: naturalism, experimentation, modeling, and the merits and shortcomings of both activities. The second part covers the main forms of inference in science: deductive, inductive, abductive, probabilistic, statistical, and causal. The book concludes with a discussion of explanation, theorizing and theory-change, and the relationship between science and society. The textbook is designed to be adaptable to a wide variety of different kinds of courses. In any of these different uses, the book helps students better navigate our scientific, 21st-century world, and it lays the foundation for more advanced undergraduate coursework in a wide variety of liberal arts and science courses. Selling Points Helps students develop scientific literacy—an essential aspect of _any_ undergraduate education in the 21 st century, including a broad understanding of scientific reasoning, methods, and concepts Written for all beginning college students: preparing science majors for more focused work in particular science; introducing the humanities’ investigations of science; and helping non-science majors become more sophisticated consumers of scientific information Provides an abundance of both contemporary and historical examples Covers reasoning strategies and norms applicable in all fields of physical, life, and social sciences, _as well as_ strategies and norms distinctive of specific sciences Includes visual aids to clarify and illustrate ideas Provides text boxes with related topics and helpful definitions of key terms, and includes a final Glossary with all key terms Includes Exercises for Active Learning at the end of each chapter, which will ensure full student engagement and mastery of the information include earlier in the chapter Provides annotated ‘For Further Reading’ sections at the end of each chapter, guiding students to the best primary and secondary sources available Offers a Companion Website, with: For Students: direct links to many of the primary sources discussed in the text, student self-check assessments, a bank of exam questions, and ideas for extended out-of-class projects For Instructors: a password-protected Teacher’s Manual, which provides student exam questions with answers, extensive lecture notes, classroom-ready Power Point presentations, and sample syllabi Extensive Curricular Development materials, helping any instructor who needs to create a Scientific Reasoning Course, ex nihilo. (shrink)

Where E is the proposition that [If H and O were true, H would explain O], William Roche and Elliot Sober have argued that P(H|O&E) = P(H|O). In this paper I argue that not only is this equality not generally true, it is false in the very kinds of cases that Roche and Sober focus on, involving frequency data. In fact, in such cases O raises the probability of H only given that there is an explanatory connection between them.

How do mental states come to be about something other than their own operations, and thus to serve as ground for effective action? This papers argues that causation in the mental domain should be understood to function on principles of intelligibility (that is, on principles which make it perfectly intelligible for intentions to have a causal role in initiating behavior) rather than on principles of mechanism (that is, on principles which explain how causation works in the physical domain). The paper (...) considers Dharmakīrti’s kāryānumāna argument (that is, the argument that an inference is sound only when one infers from the effect to the cause and not vice versa), and proposes a naturalized account of reasons. On this account, careful scrutiny of the effect can provide a basis for ascertaining the unique causal totality that is its source, but only for reasoning that is context‐specific. (shrink)

In this chapter, we outline the range of argument forms involving causation that can be found in everyday discourse. We also survey empirical work concerned with the generation and evaluation of such arguments. This survey makes clear that there is presently no unified body of research concerned with causal argument. We highlight the benefits of a unified treatment both for those interested in causal cognition and those interested in argumentation, and identify the key challenges that must be met for a (...) full understanding of causal argumentation. (shrink)

People generally accept that there is causation by omission—that the omission of some events cause some related events. But this acceptance elicits the selection problem, or the difficulty of explaining the selection of a particular omissive cause or class of causes from the causal conditions. Some theorists contend that dependence theories of causation cannot resolve this problem. In this paper, we argue that the appeal to norms adequately resolves the selection problem for dependence theories, and we provide novel experimental evidence (...) for it. (shrink)

How do we determine whether some candidate causal factor is an actual cause of some particular outcome? Many philosophers have wanted a view of actual causation which fits with folk intuitions of actual causation and those who wish to depart from folk intuitions of actual causation are often charged with the task of providing a plausible account of just how and where the folk have gone wrong. In this paper, I provide a range of empirical evidence aimed at showing just (...) how and where the folk go wrong in determining whether an actual causal relation obtains. The evidence suggests that folk intuitions of actual causation are generated by two epistemically defective processes. I situate the empirical evidence within a background discussion of debunking, arguing for a two-pronged debunking explanation of folk intuitions of actual causation. I conclude that those who wish to depart from folk intuitions of actual causation should not be compelled to square their account of actual causation with the verdicts of the folk. In the dispute over actual causation, folk intuitions deserve to be rejected. (shrink)

This paper examines the adequacy of causal graph theory as a tool for modeling biological phenomena and formalizing biological explanations. I point out that the causal graph approach reaches it limits when it comes to modeling biological phenomena that involve complex spatial and structural relations. Using a case study from molecular biology, DNA-binding and -recognition of proteins, I argue that causal graph models fail to adequately represent and explain causal phenomena in this field. The inadequacy of these models is due (...) to their failure to include relevant spatial and structural information in a way that does not render the model non-explanatory, unmanageable, or inconsistent with basic assumptions of causal graph theory. (shrink)

Humans often attribute the things that happen to one or another actual cause. In this chapter, we survey some recent philosophical and psychological research on causal attribution. We pay special attention to the relation between graphical causal modeling and theories of causal attribution. We think that the study of causal attribution is one place where formal and experimental techniques nicely complement one another.

When agents violate norms, they are typically judged to be more of a cause of resulting outcomes. In this paper, we suggest that norm violations also affect the causality attributed to other agents, a phenomenon we refer to as "causal superseding." We propose and test a counterfactual reasoning model of this phenomenon in four experiments. Experiments 1 and 2 provide an initial demonstration of the causal superseding effect and distinguish it from previously studied effects. Experiment 3 shows that this causal (...) superseding effect is dependent on a particular event structure, following a prediction of our counterfactual model. Experiment 4 demonstrates that causal superseding can occur with violations of non-moral norms. We propose a model of the superseding effect based on the idea of counterfactual sufficiency. (shrink)

When people want to identify the causes of an event, assign credit or blame, or learn from their mistakes, they often reflect on how things could have gone differently. In this kind of reasoning, one considers a counterfactual world in which some events are different from their real-world counterparts and considers what else would have changed. Researchers have recently proposed several probabilistic models that aim to capture how people do (or should) reason about counterfactuals. We present a new model and (...) show that it accounts better for human inferences than several alternative models. Our model builds on the work of Pearl (2000), and extends his approach in a way that accommodates backtracking inferences and that acknowledges the difference between counterfactual interventions and counterfactual observations. We present six new experiments and analyze data from four experiments carried out by Rips (2010), and the results suggest that the new model provides an accurate account of both mean human judgments and the judgments of individuals. (shrink)

Decision-making typically requires judgments about causal relations: we need to know the causal effects of our actions and the causal relevance of various environmental factors. We investigate how several individuals' causal judgments can be aggregated into collective causal judgments. First, we consider the aggregation of causal judgments via the aggregation of probabilistic judgments, and identify the limitations of this approach. We then explore the possibility of aggregating causal judgments independently of probabilistic ones. Formally, we introduce the problem of causal-network aggregation. (...) Finally, we revisit the aggregation of probabilistic judgments when this is constrained by prior aggregation of qualitative causal judgments. (shrink)

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

A medical intervention is a medical procedure or application intended to relieve or prevent illness or injury. Examples of medical interventions include vaccination and drug administration. After a medical intervention, adverse events (AEs) may occur which lie outside the intended consequences of the intervention. The representation and analysis of AEs are critical to the improvement of public health. Description: The Ontology of Adverse Events (OAE), previously named Adverse Event Ontology (AEO), is a community-driven ontology developed to standardize and integrate data (...) relating to AEs arising subsequent to medical interventions, as well as to support computer-assisted reasoning. OAE has over 3,000 terms with unique identifiers, including terms imported from existing ontologies and more than 1,800 OAE-specific terms. In OAE, the term ‘adverse event’ denotes a pathological bodily process in a patient that occurs after a medical intervention. Causal adverse events are defined by OAE as those events that are causal consequences of a medical intervention. OAE represents various adverse events based on patient anatomic regions and clinical outcomes, including symptoms, signs, and abnormal processes. OAE has been used in the analysis of several different sorts of vaccine and drug adverse event data. (shrink)

This paper is on the problem of causal selection and comments on Collingwood's classic paper "The so-called idea of causation". It discusses the relevance of Collingwood’s control principle in contemporary life sciences and defends that it is not the ability to control, but the willingness to control that often biases us towards some rather than other causes of a phenomenon. Willingness to control is certainly only one principle that influences causal selection, but it is an important one. It shows how (...) norms make causes. (shrink)

The present studies investigate how the intentions of third parties influence judgments of moral responsibility for other agents who commit immoral acts. Using cases in which an agent acts under some situational constraint brought about by a third party, we ask whether the agent is blamed less for the immoral act when the third party intended for that act to occur. Study 1 demonstrates that third-party intentions do influence judgments of blame. Study 2 finds that third-party intentions only influence moral (...) judgments when the agent's actions precisely match the third party's intention. Study 3 shows that this effect arises from changes in participants' causal perception that the third party was controlling the agent. Studies 4 and 5, respectively, show that the effect cannot be explained by changes in the distribution of blame or perceived differences in situational constraint faced by the agent. (shrink)

Causal selection is the cognitive process through which one or more elements in a complex causal structure are singled out as actual causes of a certain effect. In this paper, we report on an experiment in which we investigated the role of moral and temporal factors in causal selection. Our results are as follows. First, when presented with a temporal chain in which two human agents perform the same action one after the other, subjects tend to judge the later agent (...) to be the actual cause. Second, the impact of temporal location on causal selection is almost canceled out if the later agent did not violate a norm while the former did. We argue that this is due to the impact that judgments of norm violation have on causal selection—even if the violated norm has nothing to do with the obtaining effect. Third, moral judgments about the effect influence causal selection even in the case in which agents could not have foreseen the effect and did not intend to bring it about. We discuss our findings in connection to recent theories of the role of moral judgment in causal reasoning, on the one hand, and to probabilistic models of temporal location, on the other. (shrink)

There have recently been a number of strong claims that normative considerations, broadly construed, influence many philosophically important folk concepts and perhaps are even a constitutive component of various cognitive processes. Many such claims have been made about the influence of such factors on our folk notion of causation. In this paper, we argue that the strong claims found in the recent literature on causal cognition are overstated, as they are based on one narrow type of data about a particular (...) type of causal cognition; the extant data do not warrant any wide-ranging conclusions about the pervasiveness of normative considerations in causal cognition. Of course, almost all empirical investigations involve some manner of ampliative inference, and so we provide novel empirical results demonstrating that there are types of causal cognition that do not seem to be influenced by moral considerations. (shrink)

The results from a number of recent studies suggest that ascriptions of intentionality are based on evaluative considerations: specifically, that the likelihood of viewing a person’s actions as intentional is greater when the outcome is bad than good (see Knobe, 2006, 2010). In this research we provide an alternative explanation for these findings, one based on the idea that ascriptions of intentionality depend on causal structure. As predicted by the causal structure view, we observed that actions leading to bad outcomes (...) are associated with negative social pressures (Experiment 1), that these negative pressures give rise to a specific kind of causal structure (Experiment 2), and that when these causal structures are pitted against the badness of the outcome, intentionality judgments track with causal structure and not badness (Experiment 3). While the badness of an outcome may have an indirect effect on judgments of intentionality, our results suggest that the factors that affect judgments of intentionality most directly are non-evaluative and objective. (shrink)

Empirical research has recently emerged as a key method for understanding the nature of causation, and our concept of causation. One thread of research aims to test intuitions about the nature of causation in a variety of classic cases. These experiments have principally been used to try to resolve certain debates within analytic philosophy, most notably that between proponents of transference and dependence views of causation. The other major thread of empirical research on our concept of causation has investigated the (...) role that normative considerations play in causal judgments. These experimental results suggest that philosophical accounts of our concept of causation should take a broader view of what might be relevant. For both lines of research, we describe some of the significant experiments and outline key philosophical morals that have been drawn, all while pointing out various limitations. We conclude by considering other kinds of empirical research that should be philosophically interesting for those studying the nature of causation and our concept of causation. In particular, we point towards the need for philosophical research about causal perception, causal reasoning, and causal learning, as well as ways in which this research could play a role in prescriptive metaphysics. (shrink)

Causal claims are context sensitive. According to the old orthodoxy (Mackie 1974, Lewis 1986, inter alia), the context sensitivity of causal claims is all due to conversational pragmatics. According to the new contextualists (Hitchcock 1996, Woodward 2003, Maslen 2004, Menzies 2004, Schaffer 2005, and Hall ms), at least some of the context sensitivity of causal claims is semantic in nature. I want to discuss the prospects for causal contextualism, by asking why causal claims are context sensitive, what they are sensitive (...) to, and where they are sensitive to it. (shrink)

In psychiatry, pharmacological drugs play an important experimental role in attempts to identify the neurobiological causes of mental disorders. Besides being developed in applied contexts as potential treatments for patients with mental disorders, pharmacological drugs play a crucial role in research contexts as experimental instruments that facilitate the formulation and revision of neurobiological theories of psychopathology. This paper examines the various epistemic functions that pharmacological drugs serve in the discovery, refinement, testing, and elaboration of neurobiological theories of mental disorders. I (...) articulate this thesis with reference to the history of antipsychotic drugs and the evolution of the dopamine hypothesis of schizophrenia in the second half of the twentieth century. I argue that interventions with psychiatric patients through the medium of antipsychotic drugs provide researchers with information and evidence about the neurobiological causes of schizophrenia. This analysis highlights the importance of pharmacological drugs as research tools in the generation of psychiatric knowledge and the dynamic relationship between practical and theoretical contexts in psychiatry. (shrink)

Causation is one of philosophy's most venerable and thoroughly-analyzed concepts. However, the study of how ordinary people make causal judgments is a much more recent addition to the philosophical arsenal. One of the most prominent views of causal explanation, especially in the realm of harmful or potentially harmful behavior, is that unusual or counternormative events are accorded privileged status in ordinary causal explanations. This is a fundamental assumption in psychological theories of counterfactual reasoning, and has been transported to philosophy by (...) Hitchcock and Knobe (2009). A different view--the basis of the culpable control model of blame (CCM)--is that primary causal status is accorded to behaviors that arouse negative evaluative reactions, including behaviors that stem from nefarious motives, negligence or recklessness, a faulty character, or behaviors that lead to harmful or potentially harmful consequences. This paper describes four empirical studies that show consistent support for the CCM. (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)

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)