In their paper "How Fundamental Physics represents Causality", Andreas Bartels and Daniel Wohlfarth maintain that there is place for causality in General Relativity. Their argument contains two steps: First they show that there are time-asymmetric models in General Relativity, then they claim to derive that two events are causally connected if and only if there is a time-asymmetric energy flow from one event to the other. In our comment we first give a short summary of their paper followed by a (...) section introducing and pondering different conceptions of causation since Bartels and Wohlfarth don’t explicitly declare which notion of causation they build on in the paper. In order to analyze their argument in detail we formalize their crucial step in logical terms. This helps to pose the question whether their proposed derivation is not just a definition in a more precise way. (shrink)

In the years spanning the first half of the 20th century Bertrand Russell wavered between two incompatible accounts of physical reality. On one account, physical objects were taken to be logical constructs of phenomenal entities, the immediate data of sense experience. Such a view roughly fits the familiar characterization of being a combination of “Hume plus mathematical logic.” This type of phenomenalism, in the empiricist tradition, contrasted starkly with a variant of scientific realism, including a realistic account of causal (...) connections as relations between universals, that Russell developed between 1912 and 1927, and which was derived from Kant’s distinction between a noumenal and a phenomenal world. My concern in this paper is with the viability of the unique form of scientific realism Russell developed, the role of universals and causal explanation in it, and criticisms that have been directed at it. I will argue that an early refutation of Russell’s realism by the mathematician M. Newman and a recent revival of that refutation by W. Demopoulos and M. Friedman ignore the critical role universals play in Russell’s scientific realism and hence fail to refute his view. I will also briefly consider a recent “anti-realist” argument that repeats Newman’s mistake: interpreting predicates in terms of extensions and not as referring to universal properties and relations. (shrink)

Numerous studies of the beliefs of people with anorexia nervosa (AN) suggest that a subset of such individuals may experience delusions. We first describe what makes a belief delusional and conclude that such characteristics can be appropriately applied to some beliefs of people with AN. Next, we outline how delusional beliefs may relate to the broader psychopathological process in AN, including: (1) they may be epiphenomenal; (2) they may be an initial partial cause of AN; (3) they may be caused (...) by aspects of AN; or (4) they may be sustaining causes, possibly involved in reciprocal causal relations with aspects of AN. We argue that there is good reason to believe that delusional beliefs of people with AN are not merely epiphenomenal, but rather that they’re causally connected to AN. Because of this, empirical studies can be designed to test for the presence of causal relations. We describe how these studies should be designed. The results of such studies have important implications for understanding the experience of individuals with AN and for the treatment of AN. We outline these implications. (shrink)

In this paper, I consider Sterba’s recent criticism of skeptical theism in context of his argument from evil. I show that Sterba’s criticism of skeptical theism shares an undesirable trait with all past criticisms of skeptical theism: it fails. This is largely due to his focus on causal connections and his neglect of logical connections. Because of this, his argument remains vulnerable to skeptical theism.

In the years spanning the first half of the 20th century Bertrand Russell wavered between two incompatible accounts of physical reality. On one account, physical objects were taken to be logical constructs of phenomenal entities, the immediate data of sense experience. Such a view roughly fits the familiar characterization of being a combination of “Hume plus mathematical logic.” This type of phenomenalism, in the empiricist tradition, contrasted starkly with a variant of scientific realism, including a realistic account of causal (...) connections as relations between universals, that Russell developed between 1912 and 1927, and which was derived from Kant’s distinction between a noumenal and a phenomenal world. My concern in this paper is with the viability of the unique form of scientific realism Russell developed, the role of universals and causal explanation in it, and criticisms that have been directed at it. I will argue that an early refutation of Russell’s realism by the mathematician M. Newman and a recent revival of that refutation by W. Demopoulos and M. Friedman ignore the critical role universals play in Russell’s scientific realism and hence fail to refute his view. I will also briefly consider a recent “anti-realist” argument that repeats Newman’s mistake: interpreting predicates in terms of extensions and not as referring to universal properties and relations. (shrink)

Assumptions of stochastic independence are crucial to statistical models in science. Under what circumstances is it reasonable to suppose that two events are independent? When they are not causally or logically connected, so the standard story goes. But scientific models frequently treat causally dependent events as stochastically independent, raising the question whether there are kinds of causal connection that do not undermine stochastic independence. This paper provides one piece of an answer to this question, treating the simple case (...) of two tossed coins with and without a midair collision. (shrink)

Davidson’s account of singular causal statements as expressing relations between events together with his views on event identity lead to inferences involving causal statements which many of his critics find counterintuitive. These are sometimes said to be avoided on Kim’s view of events, in terms of which this line of criticism is often formulated. It is argued that neither Davidson nor Kim offer a satisfactory account of events - an essential prerequisit for the relational theory - and an (...) account of singular causal statements in terms of a modal sentential connective is advocated in place of the relational view. Such an account suffices to block the counter-intuitive inferences without needing to resort to a theory of events. It is suggested that a theory of events might be built upon a connective account of singular causal statements, but no such theory is presented here. (shrink)

In this article, I weigh in on the debate between "Humeans" and "New Humeans" concerning David Hume's stance on the existence of causal connections in "the objects." According to New Humeans, Hume believes in causal connections; according to Humeans, he does not. -/- My argument against New Humeans is that it is too difficult to reconcile Hume's repeated claims that causal connections are inconceivable with any belief that they these inconceivable somethings still exist. Specifically, Hume either assumes (...) or does not assume that causal connections do or must exist. If he does not, then the New Hume is false. If he does, then it is only reasonable to expect him to do one of two things: (1) provide explicit and unambiguous statements to the effect that he still believes that causal connections do or must exist despite his belief that we cannot even conceive of them and/or (2) provide textual evidence that he subscribes to a reason for believing that causal connections do or must exist in the objects despite his belief that we cannot even conceive of them. I then argue that Hume never satisfies either (1) or (2). -/- My ultimate conclusion is not that the New Hume is false. On the contrary, in section IX, I will argue that the New Hume is still a viable possibility if we attribute a certain other position to Hume – what I will refer to as "Newtonian Empiricism." But I will also argue that this rather plausible interpretation of Hume is equally consistent with Hume's being an agnostic about causal connections and Hume's being a Humean about causal connections. Therefore while we have no good reason to subscribe to the New Hume (rather than Hume's being an agnostic or a Humean), we cannot conclusively rule out this interpretation. (shrink)

According to David Hume our idea of a necessary connection between what we call cause and effect is produced when repeated observation of the conjunction of two events determines the mind to consider one upon the appearance of the other. No matter how we interpret Hume's theory of causation this explanation of the genesis of the idea of necessity is fraught with difficulty. I hope to show, looking at the three major interpretations of Hume's causal theory, that his (...) account is contradictory, plainly wrong, or inherently impossible to verify. (shrink)

While the role of discourse connectives has long been acknowledged in argumentative frameworks, these approaches often take a coarse-grained approach to connectives, treating them as a unified group having similar effects on argumentation. Based on an empirical study of the straw man fallacy, we argue that a more fine-grained approach is needed to explain the role of each connective and illustrate their specificities. We first present an original corpus study detailing the main features of four causal connectives in French (...) that speakers routinely use to attribute meaning to another speaker, which is a key element of straw man fallacies. We then assess the influence of each of these connectives in a series of controlled experiments. Our results indicate each connective has different effects for the persuasiveness of straw man fallacies, and that these effects can be explained by differences in their semantic profile, as evidenced in our corpus study. Taken together, our results demonstrate that connectives are important for argumentation but should be analyzed individually, and that the study of fallacies should include a fine-grained analysis of the linguistic elements typically used in their formulation. (shrink)

A central issue confronting both philosophers and practitioners in formulating an analysis of causation is the question of what constitutes evidence for a causal association. From the 1950s onward, the biostatistician Jerome Cornfield put himself at the center of a controversial debate over whether cigarette smoking was a causative factor in the incidence of lung cancer. Despite criticisms from distinguished statisticians such as Fisher, Berkson and Neyman, Cornfield argued that a review of the scientific evidence supported the conclusion of (...) a causal association. Cornfield's odds ratio in case‐control studies — as a good estimate of relative risk — together with his argument of ''explanatory common cause'' became important tools to use in confronting the skeptics. In this paper, I revisit this important historical episode as recorded in the Journal of National Cancer Institute and the Journal of the American Statistical Association. More specifically, I examine Cornfield's necessary condition on the minimum magnitudes of relative risk in light of confounders. This episode yields important insight into the nature of causal inference by showing the sorts of evidence appealed to by practitioners in supporting claims of causal association. I discuss this event in light of the manipulationist account of causation. (shrink)

Leading philosophers & psychologists offer an assessment of the commonsense view that perceptual experience is an immediate awareness of mind-independent objects. They examine the nature of perception, its role in the acquisition of knowledge, the role of causation in perception, & how perceptual understanding develops in humans.

This paper, like its companion explores some ways in which, on the one hand, normative theorizing about causation and causal reasoning and, on the other, empirical psychological investigations into causal cognition can be mutually illuminating. The paper carries out this exploration in connection with a variety of topics—the role of information about the presence of a “physical connection” between cause and effect in causal judgment, the role of “proportionality” in choosing the appropriate “level” of explanation, (...) and the role of mechanism information in causal judgment. (shrink)

Ethics failure in academia is not new, yet its prevalence, causes, and methods to prevent it remain a matter of debate. The author’s premise is that value dissonance underlies most of the reasons ethics failure occurs. Vignettes are used to illustrate value dissonance at the individual and institutional levels. Suggestions are offered for ways academic institutions can assume greater responsibility as a moral agency to prevent the occurrence of ethics failure.

In "A Modal Argument for Narrow Content" ("Journal of Philosophy", LXXXVIII, 1991, pp 5-26), Jerry Fodor proposes a necessary condition for the distinctness of causal powers. He uses this condition to support psychological individualism. I show that Fodor's argument relies on inconsistent interpretations of his condition on distinct causal powers. Moreover, on no consistent interpretation does Fodor's condition yield the results claimed for it.

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships (...) to disease. When Koch’s postulates are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

This paper analyses the similarities and connections between philosophy of science and causal layered analysis. The paper points out that philosophy of science can be understood as a kind of causal layered analysis of science. These similarities and connections mean that the insights in philosophy of science can be used to investigate the important but neglected topic of possible futures of science. The connections make it possible (i) to open up the present and past to create alternative futures (...) of science, and (ii) to reveal deep worldview commitments behind surface phenomena in science-related discourses. (shrink)

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

Understanding the neural basis of schizophrenia (SZ) is important for shedding light on the neurobiological mechanisms underlying this mental disorder. Structural and functional alterations in the anterior cingulate cortex (ACC), dorsolateral prefrontal cortex (DLPFC), hippocampus, and medial prefrontal cortex (MPFC) have been implicated in the neurobiology of SZ. However, the effective connectivity among them in SZ remains unclear. The current study investigated how neuronal pathways involving these regions were affected in first-episode SZ using functional magnetic resonance imaging (fMRI). Forty-nine patients (...) with a first-episode of psychosis and diagnosis of SZ—according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision—were studied. Fifty healthy controls (HCs) were included for comparison. All subjects underwent resting state fMRI. We used spectral dynamic causal modeling (DCM) to estimate directed connections among the bilateral ACC, DLPFC, hippocampus, and MPFC. We characterized the differences using Bayesian parameter averaging (BPA) in addition to classical inference (t-test). In addition to common effective connectivity in these two groups, HCs displayed widespread significant connections predominantly involved in ACC not detected in SZ patients, but SZ showed few connections. Based on BPA results, SZ patients exhibited anterior cingulate cortico-prefrontal-hippocampal hyperconnectivity, as well as ACC-related and hippocampal-dorsolateral prefrontal-medial prefrontal hypoconnectivity. In summary, spectral DCM revealed the pattern of effective connectivity involving ACC in patients with first-episode SZ. This study provides a potential link between SZ and dysfunction of ACC, creating an ideal situation to associate mechanisms behind SZ with aberrant connectivity among these cognition and emotion-related regions. (shrink)

Evidential decision theory (EDT) says that the choiceworthiness of an option depends on its evidential connections to possible outcomes. Causal decision theory (CDT) holds that it depends on your beliefs about its causal connections. While Newcomb cases support CDT, Arif Ahmed has described examples that support EDT. A new account is needed to get all cases right. I argue that an option A's choiceworthiness is determined by the probability that a good outcome ensues at possible A‐worlds that match (...) actuality in the facts causally unaffected by your decision (the “unaffected facts”). Moreover, you should evaluate A on the assumption that A is compossible with the unaffected facts. This view entails that you should use EDT when evaluating A on the assumption that the unaffected facts determine your action, but use CDT when assessing A on the opposite assumption. A's choiceworthiness equals a weighted average of these conditional assessments. The weights are determined by your beliefs about whether the unaffected fact determine your action. This account gets both Newcomb and Ahmed cases right. According to an influential view, whether you take the unaffected facts to determine your action can make a difference to whether you can regard yourself as free and the action as being under your control. While my account is neutral on this issue, it entails that whether you take the unaffected facts to determine your action is important in a different way: it matters to whether you should follow EDT or CDT. (shrink)

Written by one of the preeminent researchers in the field, this book provides a comprehensive exposition of modern analysis of causation. It shows how causality has grown from a nebulous concept into a mathematical theory with significant applications in the fields of statistics, artificial intelligence, economics, philosophy, cognitive science, and the health and social sciences. Judea Pearl presents and unifies the probabilistic, manipulative, counterfactual, and structural approaches to causation and devises simple mathematical tools for studying the relationships between causal (...) connections and statistical associations. Cited in more than 2,100 scientific publications, it continues to liberate scientists from the traditional molds of statistical thinking. In this revised edition, Judea Pearl elucidates thorny issues, answers readers' questions, and offers a panoramic view of recent advances in this field of research. Causality will be of interest to students and professionals in a wide variety of fields. Dr Judea Pearl has received the 2011 Rumelhart Prize for his leading research in Artificial Intelligence and systems from The Cognitive Science Society. (shrink)

Supplements the statistical‐relevance model of scientific explanation with causal components. Some S‐R relationships can be explained by reference to spatiotemporally continuous causal connections. In this context, it is crucial to distinguish genuine causal processes – those with the ability to transmit marks – from pseudoprocesses. Other S‐R relationships are explained terms of common causes. It introduces causal processes and the common cause principle, and it presents the strategy for incorporating causal considerations into the theory of (...) scientific explanation, while making it seem natural to appeal to unobserved or unobservable entities. (shrink)

Argues that indeterministic causality cannot be explicated adequately by means of statistical‐relevance relations alone. Physical considerations are also required. The same point applies to deterministic causality. This essay sets the author's view of causality apart from standard treatments in terms of abstract relations such as necessary condition, sufficient condition, and statistical relevance. These relationships, in and of themselves, do not provide physical – or causal – connections.

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships (...) to disease. When Koch’s postulates are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships (...) to disease. When Koch’s postulates are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

Not all scientific explanations work by describing causal connections between events or the world's overall causal structure. In addition, mathematicians regard some proofs as explaining why the theorems being proved do in fact hold. This book proposes new philosophical accounts of many kinds of non-causal explanations in science and mathematics.

This article looks at the way people determine the antecedent of a pronoun in sentence pairs, such as: Albert invited Ron to dinner. He spent hours cleaning the house. The experiment reported here is motivated by the idea that such judgments depend on reasoning about identity . Because the identity of an individual over time depends on the causal-historical path connecting the stages of the individual, the correct antecedent will also depend on causal connections. The experiment varied how (...) likely it is that the event of the first sentence would cause the event of the second for each of the two individuals . Decisions about the antecedent followed causal likelihood. A mathematical model of causal identity accounted for most of the key aspects of the data from the individual sentence pairs. (shrink)

Knowledge of mechanisms is critical for causal reasoning. We contrasted two possible organizations of causal knowledge—an interconnected causal network, where events are causally connected without any boundaries delineating discrete mechanisms; or a set of disparate mechanisms—causal islands—such that events in different mechanisms are not thought to be related even when they belong to the same causal chain. To distinguish these possibilities, we tested whether people make transitive judgments about causal chains by inferring, given A (...) causes B and B causes C, that A causes C. Specifically, causal chains schematized as one chunk or mechanism in semantic memory led to transitive causal judgments. On the other hand, chains schematized as multiple chunks led to intransitive judgments despite strong intermediate links. Normative accounts of causal intransitivity could not explain these intransitive judgments. (shrink)