Recent philosophical studies of probabilistic causation and statistical explanation have opened up the possibility of unifying philosophical approaches with causal modeling as practiced in the social and biological sciences. This unification rests upon the statistical tools employed, the principle of common cause, the irreducibility of causation to statistics, and the idea of causal process as a suitable framework for understanding causal relationships. These four areas of contact are discussed with emphasis on the relevant aspects of causal (...) modeling. (shrink)

Causal modeling methods such as path analysis, used in the social and natural sciences, are also highly relevant to philosophical problems of probabilistic causation and statistical explanation. We show how these methods can be effectively used (1) to improve and extend Salmon's S-R basis for statistical explanation, and (2) to repair Cartwright's resolution of Simpson's paradox, clarifying the relationship between statistical and causal claims.

I highlight a metaphysical concern that stands in the way of more widespread adoption of causal modeling techniques such as causal Bayes nets. Researchers in some fields may resist adoption due to concerns that they don't 'really' understand what they are saying about a system when they apply such techniques. Students in these fields are repeated exhorted to be cautious about application of statistical techniques to their data without a clear understanding of the conditions required for those techniques (...) to yield genuine insight into the data. They are acutely aware that anyone can chuck some data into a software package and get what looks like an answer, even though these tests may not be well-defined for the data on which they can apparently be run. This is thus a healthy skepticism for uptake of causal modeling methods, which points directly to the need for a metaphysical understanding of causation in order to successfully use the modeling methods. Without a clear understanding of what the methods are committing to, including what it means to say that there exists a causal relationship, researchers have limited ability to identify potentially bad output, or to independently verify results. (shrink)

Recording of neural activity during grasping actions in macaques showed that grasp-related sensorimotor transformations are accomplished in a circuit constituted by the anterior part of the intraparietal sulcus (AIP), the ventral (F5) and the dorsal (F2) region of the premotor area. In humans, neuroimaging studies have revealed the existence of a similar circuit, involving the putative homolog of macaque areas AIP, F5, and F2. These studies have mainly considered grasping movements performed with the right dominant hand and only a few (...) studies have measured brain activity associated with a movement performed with the left non-dominant hand. As a consequence of this gap, how the brain controls for grasping movement performed with the dominant and the non-dominant hand still represents an open question. A functional magnetic resonance imaging (fMRI) experiment has been conducted, and effective connectivity (dynamic causal modeling, DCM) was used to assess how connectivity among grasping-related areas is modulated by hand (i.e., left and right) during the execution of grasping movements toward a small object requiring precision grasping. Results underlined boosted inter-hemispheric couplings between dorsal premotor cortices during the execution of movements performed with the left rather than the right dominant hand. More specifically, they suggest that the dorsal premotor cortices may play a fundamental role in monitoring the configuration of fingers when grasping movements are performed by either the right and the left hand. This role becomes particularly evident when the hand less-skilled (i.e., the left hand) to perform such action is utilized. The results are discussed in light of recent theories put forward to explain how parieto-frontal connectivity is modulated by the execution of prehensile movements. (shrink)

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)

This paper presents a formalism that combines useful properties of both logic and probabilities. Like logic, the formalism admits qualitative sentences and provides symbolic machinery for deriving deductively closed beliefs and, like probability, it permits us to express if-then rules with different levels of firmness and to retract beliefs in response to changing observations. Rules are interpreted as order-of-magnitude approximations of conditional probabilities which impose constraints over the rankings of worlds. Inferences are supported by a unique priority ordering on rules (...) which is syntactically derived from the knowledge base. This ordering accounts for rule interactions, respects specificity considerations and facilitates the construction of coherent states of beliefs. Practical algorithms are developed and analyzed for testing consistency, computing rule ordering, and answering queries. Imprecise observations are incorporated using qualitative versions of Jeffrey's rule and Bayesian updating, with the result that coherent belief revision is embodied naturally and tractably. Finally, causal rules are interpreted as imposing Markovian conditions that further constrain world rankings to reflect the modularity of causal organizations. These constraints are shown to facilitate reasoning about causal projections, explanations, actions and change. (shrink)

Throughout the Covid-19 pandemic, people have been eager to learn what factors, and especially what public health policies, cause infection rates to wax and wane. But figuring out conclusively what causes what is difficult in complex systems with nonlinear dynamics, such as pandemics. We review some of the challenges that scientists have faced in answering quantitative causal questions during the Covid-19 pandemic, and suggest that these challenges are a reason to augment the moral dimension of conversations about causal (...) inference. We take a lesson from Martha Nussbaum—who cautions us not to think we have just one question on our hands when we have at least two—and apply it to modeling for causal inference in the context of cost-benefit analysis. (shrink)

This book offers a discussion about how people think, talk, learn, and explain things in causal terms in terms of action and manipulation. Sloman also reviews the role of causality, causal models, and intervention in the basic human cognitive functions: decision making, reasoning, judgement, categorization, inductive inference, language, and learning.

I argue for the causal character of modeling in data-intensive science, contrary to widespread claims that big data is only concerned with the search for correlations. After discussing the concept of data-intensive science and introducing two examples as illustration, several algorithms are examined. It is shown how they are able to identify causal relevance on the basis of eliminative induction and a related difference-making account of causation. I then situate data-intensive modeling within a broader framework of an epistemology (...) of scientific knowledge. In particular, it is shown to lack a pronounced hierarchical, nested structure. The significance of the transition to such “horizontal” modeling is underlined by the concurrent emergence of novel inductive methodology in statistics such as non-parametric statistics. Data-intensive modeling is well equipped to deal with various aspects of causal complexity arising especially in the higher level and applied sciences. (shrink)

Social research, from economics to demography and epidemiology, makes extensive use of statistical models in order to establish causal relations. The question arises as to what guarantees the causal interpretation of such models. In this paper we focus on econometrics and advance the view that causal models are ‘augmented’ statistical models that incorporate important causal information which contributes to their causal interpretation. The primary objective of this paper is to argue that causal claims are (...) established on the basis of a plurality of evidence. We discuss the consequences of ‘evidential pluralism’ in the context of econometric modelling. (shrink)

Causal modelling provides a powerful set of tools for identifying causal structure from observed correlations. It is well known that such techniques fail for quantum systems, unless one introduces 'spooky' hidden mechanisms. Whether one can produce a genuinely quantum framework in order to discover causal structure remains an open question. Here we introduce a new framework for quantum causal modelling that allows for the discovery of causal structure. We define quantum analogues for core (...) features of classical causal modelling techniques, including the causal Markov condition and faithfulness. Based on the process matrix formalism, this framework naturally extends to generalised structures with indefinite causal order. (shrink)

Clark Glymour, Richard Scheines, Peter Spirtes and Kevin Kelly. Discovering Causal Structure: Artifical Intelligence, Philosophy of Science and Statistical Modeling.

The aim of this paper is to offer the first systematic exploration and definition of equivalent causal models in the context where both models are not made up of the same variables. The idea is that two models are equivalent when they agree on all "essential" causal information that can be expressed using their common variables. I do so by focussing on the two main features of causal models, namely their structural relations and their functional relations. In (...) particular, I define several relations of causal ancestry and several relations of causal sufficiency, and require that the most general of these relations are preserved across equivalent models. (shrink)

Causal models show promise as a foundation for the semantics of counterfactual sentences. However, current approaches face limitations compared to the alternative similarity theory: they only apply to a limited subset of counterfactuals and the connection to counterfactual logic is not straightforward. This paper addresses these difficulties using exogenous interventions, where causal interventions change the values of exogenous variables rather than structural equations. This model accommodates judgments about backtracking counterfactuals, extends to logically complex counterfactuals, and validates familiar principles (...) of counterfactual logic. This combines the interventionist intuitions of the causal approach with the logical advantages of the similarity approach. (shrink)

The verbs cause, enable, and prevent express beliefs about the way the world works. We offer a theory of their meaning in terms of the structure of those beliefs expressed using qualitative properties of causal models, a graphical framework for representing causal structure. We propose that these verbs refer to a causal model relevant to a discourse and that “A causes B” expresses the belief that the causal model includes a link from A to B. “A (...) enables/allows B” entails that the model includes a link from A to B, that A represents a category of events necessary for B, and that an alternative cause of B exists. “A prevents B” entails that the model includes a link from A to B and that A reduces the likelihood of B. This theory is able to account for the results of four experiments as well as a variety of existing data on human reasoning. (shrink)

Causal models have proven extremely useful in offering formal representations of causal relationships between a set of variables. Yet in many situations, there are non-causal relationships among variables. For example, we may want variables LDL, HDL, and TOT that represent the level of low-density lipoprotein cholesterol, the level of lipoprotein high-density lipoprotein cholesterol, and total cholesterol level, with the relation LDL+HDL=TOT. This cannot be done in standard causal models, because we can intervene simultaneously on all three (...) variables. The goal of this paper is to extend standard causal models to allow for constraints on settings of variables. Although the extension is relatively straightforward, to make it useful we have to define a new intervention operation that disconnects a variable from a causal equation. We give examples showing the usefulness of this extension, and provide a sound and complete axiomatization for causal models with constraints. (shrink)

Judea Pearl has been at the forefront of research in the burgeoning field of causal modeling, and Causality is the culmination of his work over the last dozen or so years. For philosophers of science with a serious interest in causal modeling, Causality is simply mandatory reading. Chapter 2, in particular, addresses many of the issues familiar from works such as Causation, Prediction and Search by Peter Spirtes, Clark Glymour, and Richard Scheines. But philosophers with a more general (...) interest in causation will also profit from reading Pearl’s book, especially the material in chapters 7, 9, and 10, which is self-contained and less technical than other parts of the book. The present review is aimed primarily at readers of the second type. (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.

The investigation of a method for postulating counterfactual histories of science has led to the development of a theory of science based on general units of knowledge, which are called “advances”. Advances are passed on from scientist to scientist, and may be seen as “causing” the appearance of other advances. This results in networks which may be analyzed in terms of probabilistic causal models, which are readily encodable in computer language. The probability for a set of advances to give (...) rise to another advance is taken to be invariant through history, but depends on a typical time span which is an inverse function of the degree of development of science. Examples are given from the early science of magnetism and from the 19th century physics. (shrink)

This paper explores some issues concerning how we should think about interventions (in the sense of unconfounded manipulations) of "upper-level" variables in contexts in which these supervene on but are not identical with lower-level realizers. It is argued that we should reject the demand that interventions on upper-level variables must leave their lower-level realizers unchanged– a requirement that within an interventionist framework would imply that upper-level variables are causally inert. Instead an intervention on an upper-level variable at the same time (...) changes its lower-level realizer in a way that is consistent with the change in the upper- level variable. The lower-level realizer should not be regarded as a potential "confounder" of upper-level causal relations, as in "exclusionist" arguments. Several proposals for making this precise are considered and several pro-exclusionist arguments are criticized. (shrink)

Counterfactuals are inherently ambiguous in the sense that the same counterfactual may be true under one mode of counterfactualization but false under the other. Many have regarded the ambiguity of counterfactuals as consisting in the distinction between forward-tracking and backtracking counterfactuals. This is incorrect since the ambiguity persists even in cases not involving backtracking counterfactualization. In this paper, I argue that causal modeling semantics has the resources enough for accounting for the ambiguity of counterfactuals. Specifically, we need to distinguish (...) two types of causal manipulation, which I call “intervention” and “extrapolation” respectively. To intervene in a causal model M is to change M’s structural equations in some specific ways, while to extrapolate M is to change the value assignment of M’s variables in some specific ways. I argue that intervention and extrapolation offer a natural explanation for the ambiguity of counterfactuals. (shrink)

Counterfactuals are inherently ambiguous in the sense that the same counterfactual may be true under one mode of counterfactualization but false under the other. Many have regarded the ambiguity of counterfactuals as consisting in the distinction between forward-tracking and backtracking counterfactuals. This is incorrect since the ambiguity persists even in cases not involving backtracking counterfactualization. In this paper, I argue that causal modeling semantics has the resources enough for accounting for the ambiguity of counterfactuals. Specifically, we need to distinguish (...) two types of causal manipulation, which I call “intervention” and “extrapolation” respectively. To intervene in a causal model M is to change M’s structural equations in some specific ways, while to extrapolate M is to change the value assignment of M’s variables in some specific ways. I argue that intervention and extrapolation offer a natural explanation for the ambiguity of counterfactuals. (shrink)

This paper provides a general introduction to the use of causal models in the metaphysics of causation, specifically structural equation models and directed acyclic graphs. It reviews the formal framework, lays out a method of interpretation capable of representing different underlying metaphysical relations, and describes the use of these models in analyzing causation.

In this paper we compare causal models with reason models in the construction of Bayesian networks for legal evidence. In causal models, arrows in the network are drawn from causes to effects. In a reason model, the arrows are instead drawn towards the evidence, from factum probandum to factum probans. We explore the differences between causal models and reason models and observe several distinct advantages with reason models. Reason models are better aligned with the philosophy of Bayesian (...) inference, as they model reasons for up-dating beliefs. Reason models are better suited for measuring the combined support of the evidence, and a prior probability of guilt that reflects the number of possible perpetrators is accommodated more easily with reason models. (shrink)

We consider a sequence of successively more restrictive definitions of abstraction for causal models, starting with a notion introduced by Rubenstein et al. (2017) called exact transformation that applies to probabilistic causal models, moving to a notion of uniform transformation that applies to deterministic causal models and does not allow differences to be hidden by the "right" choice of distribution, and then to abstraction, where the interventions of interest are determined by the map from low-level states to (...) high-level states, and strong abstraction, which takes more seriously all potential interventions in a model, not just the allowed interventions. We show that procedures for combining micro-variables into macro-variables are instances of our notion of strong abstraction, as are all the examples considered by Rubenstein et al. (shrink)

We propose a causal model theory to explain asymmetries in judgments of the intentionality of a foreseen side-effect that is either negative or positive (Knobe, 2003). The theory is implemented as a Bayesian network relating types of mental states, actions, and consequences that integrates previous hypotheses. It appeals to two inferential routes to judgment about the intentionality of someone else's action: bottom-up from action to desire and top-down from character and disposition. Support for the theory comes from three experiments (...) that test the prediction that bottom-up inference should occur only when the actor's primary objective is known. The model fits intentionality judgments reasonably well with no free parameters. (shrink)

Part of Allen et al.’s criticism of Hamilton’s rule makes sense only if we are interested in social adaptation rather than merely social selection. Under the assumption that we are interested in casually modeling social adaptation, I illustrate how graphical causal models of social adaptation can be useful for predicting evolution by adaptation. I then argue for two consequences of this approach given some of the recent philosophical literature. I argue Birch’s claim that the proper way to understand Hamilton’s (...) rule is as providing an organizational framework for causal models is incorrect. I provide an account of a causally adequate decomposition of evolutionary change due to social adaptation and show that my account is superior to Okasha’s. (shrink)

The construction of causal models for research in business ethics has become fashionable in recent years. This paper explores four recent proposals, comparing and contrasting their views. The primary purpose of this paper is to expose several confusions inherent in such models and to account for these errors in terms of a failure to distinguish between models as theories and models as representing a research tradition. We conclude with a brief set of recommendations for linking two major research traditions (...) in business ethics: empiricism and ethical theory. (shrink)

Ernst Mayr’s classical work on the nature of causation in biology has had a huge influence on biologists as well as philosophers. Although his distinction between proximate and ultimate causation recently came under criticism from those who emphasize the role of development in evolutionary processes, the formal relationship between these two notions remains elusive. Using causal graph theory, this paper offers a unified framework to systematically translate a given “proximate” causal structure into an “ultimate” evolutionary response, and illustrates (...) evolutionary implications of various kinds of causal mechanisms including epigenetic inheritance, maternal effects, and niche construction. These results not only reveal the essential interplay between proximate and ultimate causation in the study of evolution, but also provide a formal method to evaluate or discover non-standard or yet unknown evolutionary phenomena. (shrink)

Wood and Spekkens argue that any causal model explaining the EPRB correlations and satisfying the no-signalling constraint must also violate the assumption that the model faithfully reproduces the statistical dependences and independences—a so-called ‘fine-tuning’ of the causal parameters. This includes, in particular, retrocausal explanations of the EPRB correlations. I consider this analysis with a view to enumerating the possible responses an advocate of retrocausal explanations might propose. I focus on the response of Näger, who argues that the central (...) ideas of causal explanations can be saved if one accepts the possibility of a stable fine-tuning of the causal parameters. I argue that in light of this view, a violation of faithfulness does not necessarily rule out retrocausal explanations of the EPRB correlations. However, when we consider a plausible retrocausal picture in some detail, it becomes clear that the causal modelling framework is not a natural arena for representing such an account of retrocausality. _1_ Causal Models, Quantum Mechanics, and Faithfulness _2_ Fine-Tuning _2.1_ Fine-tuning in a retrocausal model _3_ Possible Responses _4_ Quantum Causal Models and Retrocausality _4.1_ A more detailed retrocausal account _4.2_ A model of the EPRB probabilities _4.3_ Mapping to a causal model _5_ Conclusion. (shrink)

Galles & Pearl (l998) claimed that s [possible-worlds] framework.s framework. Recursive models are shown to correspond precisely to a subclass of (possible-world) counterfactual structures. On the other hand, a slight generalization of recursive models, models where all equations have unique solutions, is shown to be incomparable in expressive power to counterfactual structures, despite the fact that the Galles and Pearl arguments should apply to them as well. The problem with the Galles and Pearl argument is identified: an axiom that they (...) viewed as irrelevant, because it involved disjunction (which was not in their language), is not irrelevant at all. (shrink)

Young children spend a large portion of their time pretending about non-real situations. Why? We answer this question by using the framework of Bayesian causal models to argue that pretending and counterfactual reasoning engage the same component cognitive abilities: disengaging with current reality, making inferences about an alternative representation of reality, and keeping this representation separate from reality. In turn, according to causal models accounts, counterfactual reasoning is a crucial tool that children need to plan for the future (...) and learn about the world. Both planning with causal models and learning about them require the ability to create false premises and generate conclusions from these premises. We argue that pretending allows children to practice these important cognitive skills. We also consider the prevalence of unrealistic scenarios in children's play and explain how they can be useful in learning, despite appearances to the contrary. (shrink)

Compared to constraint-based causal discovery, causal discovery based on functional causal models is able to identify the whole causal model under appropriate assumptions [Shimizu et al. 2006; Hoyer et al. 2009; Zhang and Hyvärinen 2009b]. Functional causal models represent the effect as a function of the direct causes together with an independent noise term. Examples include the linear non-Gaussian acyclic model, nonlinear additive noise model, and post-nonlinear model. Currently, there are two ways to estimate the (...) parameters in the models: dependence minimization and maximum likelihood. In this article, we show that for any acyclic functional causal model, minimizing the mutual information between the hypothetical cause and the noise term is equivalent to maximizing the data likelihood with a flexible model for the distribution of the noise term. We then focus on estimation of the PNL causal model and propose to estimate it with the warped Gaussian process with the noise modeled by the mixture of Gaussians. As a Bayesian nonparametric approach, it outperforms the previous one based on mutual information minimization with nonlinear functions represented by multilayer perceptrons; we also show that unlike the ordinary regression, estimation results of the PNL causal model are sensitive to the assumption on the noise distribution. Experimental results on both synthetic and real data support our theoretical claims. (shrink)

The development of causal modelling since the 1950s has been accompanied by a number of controversies, the most striking of which concerns the Markov condition. Reichenbach's conjunctive forks did satisfy the Markov condition, while Salmon's interactive forks did not. Subsequently some experts in the field have argued that adequate causal models should always satisfy the Markov condition, while others have claimed that non-Markovian causal models are needed in some cases. This paper argues for the second position (...) by considering the multi-causal forks, which are widespread in contemporary medicine (Section 2). A non-Markovian causal model for such forks is introduced and shown to be mathematically tractable (Sections 6, 7, and 8). The paper also gives a general discussion of the controversy about the Markov condition (Section 1), and of the related controversy about probabilistic causality (Sections 3, 4, and 5). (shrink)

This chapter explains the screening‐off rule in the psychological laboratory. The Markov assumption states that any variable in a set is independent in probability of all its ancestors in the set conditional on its own parents. The screening‐off rule is also critical to allow Bayes nets to make an inference of the state of an unknown variable in a causal structure from the states of other variables in that structure. The chapter examines which causal representations people use to (...) make predictions and whether people conform to the screening‐off rule with respect to a causal model they have in mind. It analyzes what leads them to modify their causal model and whether or not people are causally oriented when making predictions. Making probability judgments is hard and requires careful deliberation. People are capable of such deliberation although they avoid it until they cannot, until the facts require more careful thought. (shrink)

Recent attempts to fix the direction of causal priority without reference to the direction of temporal priority have begun with an analysis of the causal relation itself. I offer a method, based on causal modelling theory, designed to determine the direction of causal priority while remaining as agnostic as possible about the nature of the causal relation.

We aim to devise a Ramsey test analysis of actual causation. Our method is to define a strengthened Ramsey test for causal models. Unlike the accounts of Halpern and Pearl ([2005]) and Halpern ([2015]), the resulting analysis deals satisfactorily with both over- determination and conjunctive scenarios.