Finding causes is a central goal in psychological research. In this paper, I argue based on the interventionist approach to causal discovery that the search for psychological causes faces great obstacles. Psychological interventions are likely to be fat-handed: they change several variables simultaneously, and it is not known to what extent such interventions give leverage for causal inference. Moreover, due to problems of measurement, the degree to which an intervention was fat-handed, or more generally, what the intervention (...) in fact did, is difficult to reliably estimate. A further complication is that the causal findings in psychology are typically made at the population level, and such findings do not allow inferences to individual-level causal relationships. I also discuss the implications of these problems for research, as well as various ways of addressing them, such as focusing more on the discovery of robust but non-causal patterns. (shrink)

In this paper, I want to substantiate three related claims regarding causal discovery from non-experimental data. Firstly, in scientific practice, the problem of ignorance is ubiquitous, persistent, and far-reaching. Intuitively, the problem of ignorance bears upon the following situation. A set of random variables V is studied but only partly tested for (conditional) independencies; i.e. for some variables A and B it is not known whether they are (conditionally) independent. Secondly, Judea Pearl’s most meritorious and influential algorithm for (...) causal discovery (the IC algorithm) cannot be applied in cases of ignorance. It presupposes that a full list of (conditional) independence relations is on hand and it would lead to unsatisfactory results when applied to partial lists. Finally, the problem of ignorance is successfully treated by means of ALIC, the adaptive logic for causal discovery presented in this paper. (shrink)

It is commonplace to encounter nonstationary or heterogeneous data, of which the underlying generating process changes over time or across data sets. Such a distribution shift feature presents both challenges and opportunities for causal discovery. In this paper we develop a principled framework for causal discovery from such data, called Constraint-based causal Discovery from Nonstationary/heterogeneous Data, which addresses two important questions. First, we propose an enhanced constraint-based procedure to detect variables whose local mechanisms change (...) and recover the skeleton of the causal structure over observed variables. Second, we present a way to determine causal orientations by making use of independence changes in the data distribution implied by the underlying causal model, benefiting from information carried by changing distributions. Experimental results on various synthetic and real-world data sets are presented to demonstrate the efficacy of our methods. (shrink)

I would like to congratulate James Woodward for another landmark accomplishment, after publishing his Making things happen: A theory of causal explanation. Making things happen gives an elegant interventionist theory for understanding explanation and causation. The new contribution relies on that theory and further makes a big step towards empirical inference of causal relations from non-experimental data. In this paper, I will focus on some of the emerging computational methods for finding causal relations from non-experimental data and (...) attempt to complement Woodward's contribution with discussions on 1) how these methods are connected to the interventionist theory of causality, 2) how informative the output of the methods is, including whether they output directed causal graphs and how they deal with confounders, and 3) the assumptions underlying the asymptotic correctness of the output of the methods about causal relations. Different causal discovery methods may rely on different aspects of the joint distribution of the data, and this discussion aims to provide a technical account of the assumptions. (shrink)

Many investigations into the world, including philosophical ones, aim to discover causal knowledge, and many experimental methods have been developed to assist in causal discovery. More recently, algorithms have emerged that can also learn causal structure from purely or mostly observational data, as well as experimental data. These methods have started to be applied in various philosophical contexts, such as debates about our concepts of free will and determinism. This paper provides a “user's guide” to these (...) methods, though not in the sense of specifying exact button presses in a software package. Instead, we explain the larger “pipeline” within which these methods are used and discuss key steps in moving from initial research idea to validated causal structure. (shrink)

This thesis presents an alternative method for the detection of MIMIC models. Previous methods (such as factor analysis) suffer from a number of significant aws and limitations, which the new method (a causal search algorithm) doesn't suffer. A new algorithm is introduced, followed by a worked-through example of its application. Discussion focuses on some of the limiting assumptions the algorithm currently requires. Finally, recommendations for future work address improvements of the algorithm, as well as its applicability.

We examine the performance of some standard causal discovery algorithms, both constraint-based and score-based, from the perspective of how robust they are against failures of the Causal Faithfulness Assumption. For this purpose, we make only the so-called Triangle-Faithfulness assumption, which is a fairly weak consequence of the Faithfulness assumption, and otherwise allows unfaithful distributions. In particular, we allow violations of Adjacency-Faithfulness and Orientation-Faithfulness. We show that the PC algorithm, a representative constraint-based method, can be made more robust (...) against unfaithfulness by incorporating elements of the GES algorithm, a representative score-based method; similarly, the GES algorithm can be made less error-prone by incorporating elements of the conservative PC algorithm. As our simulations demonstrate, the increased robustness seems to matter even when faithfulness is not exactly violated, for with only finite sample, distributions that are not exactly unfaithful may be sufficiently close to being unfaithful to make trouble. (shrink)

Using the flexibility of recently developed methods for causal discovery based on Boolean satisfiability solvers, we encode a variety of assumptions that weaken the Faithfulness assumption. The encoding results in a number of SAT-based algorithms whose asymptotic correctness relies on weaker conditions than are standardly assumed. This implementation of a whole set of assumptions in the same platform enables us to systematically explore the effect of weakening the Faithfulness assumption on causal discovery. An important effect, suggested (...) by simulation results, is that adopting weaker assumptions greatly alleviates the problem of conflicting constraints and substantially shortens solving time. As a result, SAT-based causal discovery is potentially more scalable under weaker assumptions. (shrink)

Causal discovery becomes especially challenging when the possibility of latent confounding and/or selection bias is not assumed away. For this task, ancestral graph models are particularly useful in that they can represent the presence of latent confounding and selection effect, without explicitly invoking unobserved variables. Based on the machinery of ancestral graphs, there is a provably sound causal discovery algorithm, known as the FCI algorithm, that allows the possibility of latent confounders and selection bias. However, the (...) orientation rules used in the algorithm are not complete. In this paper, we provide additional orientation rules, augmented by which the FCI algorithm is shown to be complete, in the sense that it can, under standard assumptions, discover all aspects of the causal structure that are uniquely determined by facts of probabilistic dependence and independence. The result is useful for developing any causal discovery and reasoning system based on ancestral graph models. (shrink)

In “Flagpoles anyone? Causal and explanatory asymmetries”, James Woodward supplements his celebrated interventionist account of causation and explanation with a set of new ideas about causal and explanatory asymmetries, which he extracts from some cutting-edge methods for causal discovery from observational data. Among other things, Woodward draws interesting connections between observational causal discovery and interventionist themes that are inspired in the first place by experimental causal discovery, alluding to a sort of unity (...) between observational and experimental causal discovery. In this paper, I make explicit what I take to be the implicated unity. Like experimental causal discovery, observational causal discovery also relies on interventions, albeit interventions that are not carried out by investigators and hence need to be detected as part of the inference. The observational patterns appealed to in observational causal discovery are not only surrogates for would-be interventions, as Woodward sometimes puts it; they also serve to mark relevant interventions that actually happen in the data generating process. (shrink)

Integrative experiment design is a needed improvement over ad hoc experiments, but the specific proposed method has limitations. We urge a further break with tradition through the use of an enormous untapped resource: Decades of causal discovery artificial intelligence (AI) literature on optimizing the design of systematic experimentation.

In my field, animal developmental biology, and in what could be regarded as its “deep time derivative,” the evolutionary biology of the animal body plan, there exist two kinds of experimentally supported causal explanation. These can be described as “rooted” and “unrooted.” Rooted causal explanation provides logical links to and from the genomic regulatory code, extending right into the genomic sequences that control regulatory gene expression. The genomic regulatory code ultimately determines the developmental process in a direct way, (...) since subsequent developmental events all depend directly and specifically on what regulatory genes are being expressed and where in the developing organism they are being expressed.. (shrink)

In this paper, I review two related lines of computational research: discovery of scientific knowledge and causal models of scientific phenomena. I also report research on quantitative process models that falls at the intersection of these two themes. This framework represents models as a set of interacting processes, each with associated differential equations that express influences among variables. Simulating such a quantitative process model produces trajectories for variables over time that one can compare to observations. Background knowledge about (...) candidate processes enables search through the space of model structures and associated parameters to find explanations of time-series data. I discuss the representation of such process models, their use for prediction and explanation, and their discovery through heuristic search, along with their interpretation as causal accounts of dynamic behavior. (shrink)

We investigate the context of discovery of two significant achievements of twentieth century biochemistry: the chemiosmotic mechanism of oxidative phosphorylation and the dark reaction of photosynthesis. The pursuit of these problems involved discovery strategies such as the transfer, recombination and reversal of previous causal and mechanistic knowledge in biochemistry. We study the operation and scope of these strategies by careful historical analysis, reaching a number of systematic conclusions: even basic strategies can illuminate “hard cases” of scientific (...) class='Hi'>discovery that go far beyond simple extrapolation or analogy; the causal–mechanistic approach to discovery permits a middle course between the extremes of a completely substrate-neutral and a completely domain-specific view of scientific discovery; the existing literature on mechanism discovery underemphasizes the role of combinatorial approaches in defining and exploring search spaces of possible problem solutions; there is a subtle interplay between a fine-grained mechanistic and a more coarse-grained causal level of analysis, and both are needed to make discovery processes intelligible. (shrink)

We investigate the context of discovery of two significant achievements of twentieth century biochemistry: the chemiosmotic mechanism of oxidative phosphorylation and the dark reaction of photosynthesis. The pursuit of these problems involved discovery strategies such as the transfer, recombination and reversal of previous causal and mechanistic knowledge in biochemistry. We study the operation and scope of these strategies by careful historical analysis, reaching a number of systematic conclusions: even basic strategies can illuminate “hard cases” of scientific (...) class='Hi'>discovery that go far beyond simple extrapolation or analogy; the causal–mechanistic approach to discovery permits a middle course between the extremes of a completely substrate-neutral and a completely domain-specific view of scientific discovery; the existing literature on mechanism discovery underemphasizes the role of combinatorial approaches in defining and exploring search spaces of possible problem solutions; there is a subtle interplay between a fine-grained mechanistic and a more coarse-grained causal level of analysis, and both are needed to make discovery processes intelligible. (shrink)

I reconstruct the discovery of the Higgs boson by the ATLAS collaboration at CERN as the application of a series of inferences from effects to causes. I show to what extent such diagnostic causal inferences can be based on well established knowledge gained in previous experiments. To this extent, causal reasoning can be used to infer the existence of entities, rather than just causal relationships between them. The resulting account relies on the principle of causality, attributes (...) only a heuristic role to the theory’s predictions, and shows how, and to what extent, data selection can be used to exclude alternative causes, even “unconceived” ones. (shrink)

We present a logic, $$\mathbf {ELI^r}$$ ELI r, for the discovery of deterministic causal regularities starting from empirical data. Our approach is inspired by Mackie’s theory of causes as INUS-conditions, and implements a more recent adjustment to Mackie’s theory according to which the left-hand side of causal regularities is required to be a minimal disjunction of minimal conjunctions. To derive such regularities from a given set of data, we make use of the adaptive logics framework. Our knowledge (...) of deterministic causal regularities is, as Mackie noted, most often gappy or elliptical. The adaptive logics framework is well-suited to explicate both the internal and the external dynamics of the discovery of such gappy regularities. After presenting $$\mathbf {ELI^r}$$ ELI r, we first discuss these forms of dynamics in more detail. Next, we consider some criticisms of the INUS-account and show how our approach avoids them, and we compare $$\mathbf {ELI^r}$$ ELI r with the CNA algorithm that was recently proposed by Michael Baumgartner. (shrink)

We present a logic, \, for the discovery of deterministic causal regularities starting from empirical data. Our approach is inspired by Mackie’s theory of causes as INUS-conditions, and implements a more recent adjustment to Mackie’s theory according to which the left-hand side of causal regularities is required to be a minimal disjunction of minimal conjunctions. To derive such regularities from a given set of data, we make use of the adaptive logics framework. Our knowledge of deterministic (...) class='Hi'>causal regularities is, as Mackie noted, most often gappy or elliptical. The adaptive logics framework is well-suited to explicate both the internal and the external dynamics of the discovery of such gappy regularities. After presenting \, we first discuss these forms of dynamics in more detail. Next, we consider some criticisms of the INUS-account and show how our approach avoids them, and we compare \ with the CNA algorithm that was recently proposed by Michael Baumgartner. (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)

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)

Russo and Williamson put forward the following thesis: in order to establish a causal claim in medicine, one normally needs to establish both that the putative cause and putative effect are appropriately correlated and that there is some underlying mechanism that can account for this correlation. I argue that, although the Russo-Williamson thesis conflicts with the tenets of present-day evidence-based medicine, it offers a better causal epistemology than that provided by present-day EBM because it better explains two key (...) aspects of causal discovery. First, the thesis better explains the role of clinical studies in establishing causal claims. Second, it yields a better account of extrapolation. (shrink)

Perfect adaptation in a dynamical system is the phenomenon that one or more variables have an initial transient response to a persistent change in an external stimulus but revert to their original value as the system converges to equilibrium. With the help of the causal ordering algorithm, one can construct graphical representations of dynamical systems that represent the causal relations between the variables and the conditional independences in the equilibrium distribution. We apply these tools to formulate sufficient graphical (...) conditions for identifying perfect adaptation from a set of first-order differential equations. Furthermore, we give sufficient conditions to test for the presence of perfect adaptation in experimental equilibrium data. We apply this method to a simple model for a protein signalling pathway and test its predictions in both simulations and using real-world protein expression data. We demonstrate that perfect adaptation can lead to misleading orientation of edges in the output of causal discovery algorithms. (shrink)

Most causal discovery algorithms in the literature exploit an assumption usually referred to as the Causal Faithfulness or Stability Condition. In this paper, we highlight two components of the condition used in constraint-based algorithms, which we call “Adjacency-Faithfulness” and “Orientation- Faithfulness.” We point out that assuming Adjacency-Faithfulness is true, it is possible to test the validity of Orientation- Faithfulness. Motivated by this observation, we explore the consequence of making only the Adjacency-Faithfulness assumption. We show that the familiar (...) PC algorithm has to be modified to be correct under the weaker, Adjacency-Faithfulness assumption. The modified algorithm, called Conservative PC (CPC), checks whether Orientation- Faithfulness holds in the orientation phase, and if not, avoids drawing certain causal conclusions the PC algorithm would draw. Howtion: ever, if the stronger, standard causal Faith-. (shrink)

Behavior genetics is a controversial science. For decades, scholars have sought to understand the role of heredity in human behavior and life-course outcomes. Recently, technological advances and the rapid expansion of genomic databases have facilitated the discovery of genes associated with human phenotypes such as educational attainment and substance use disorders. To maximize the potential of this flourishing science, and to minimize potential harms, careful analysis of what it would mean for genes to be causes of human behavior is (...) needed. In this paper, we advance a framework for identifying instances of genetic causes, interpreting those causal relationships, and applying them to advance causal knowledge more generally in the social sciences. Central to thinking about genes as causes is counterfactual reasoning, the cornerstone of causal thinking in statistics, medicine, and philosophy. We argue that within-family genetic effects represent the product of a counterfactual comparison in the same way as average treatment effects (ATEs) from randomized controlled trials (RCTs). Both ATEs from RCTs and within-family genetic effects are shallow causes: They operate within intricate causal systems (non-unitary), produce heterogeneous effects across individuals (non-uniform), and are not mechanistically informative (non-explanatory). Despite these limitations, shallow causal knowledge can be used to improve understanding of the etiology of human behavior and to explore sources of heterogeneity and fade-out in treatment effects. (shrink)

Causal reasoning is primarily concerned with what would happen to a system under external interventions. In particular, we are often interested in predicting the probability distribution of some random variables that would result if some other variables were forced to take certain values. One prominent approach to tackling this problem is based on causal Bayesian networks, using directed acyclic graphs as causal diagrams to relate post-intervention probabilities to pre-intervention probabilities that are estimable from observational data. However, such (...) causal diagrams are seldom fully testable given observational data. In consequence, many causal discovery algorithms based on data-mining can only output an equivalence class of causal diagrams. This paper is concerned with causal reasoning given an equivalence class of causal diagrams, represented by a ancestral graph. We present two main results. The first result extends Pearl 's celebrated do-calculus to the context of ancestral graphs. In the second result, we focus on a key component of Pearl's calculus---the property of invariance under interventions, and give stronger graphical conditions for this property than those implied by the first result. The second result also improves the earlier, similar results due to Spirtes et al. (shrink)

In distinguishing justification from discovery, the logical empiricists hoped to avoid confusing causal matters with normative ones. Exaggerating the virtue of this distinction, however, has disguised from us important features of the concept of a reason as it functions in human practice. Surfacing those features gives some insight into reasoning and argument.

Over the past two decades, several consistent procedures have been designed to infer causal conclusions from observational data. We prove that if the true causal network might be an arbitrary, linear Gaussian network or a discrete Bayes network, then every unambiguous causal conclusion produced by a consistent method from non-experimental data is subject to reversal as the sample size increases any finite number of times. That result, called the causal flipping theorem, extends prior results to the (...) effect that causal discovery cannot be reliable on a given sample size. We argue that since repeated flipping of causal conclusions is unavoidable in principle for consistent methods, the best possible discovery methods are consistent methods that retract their earlier conclusions no more than necessary. A series of simulations of various methods across a wide range of sample sizes illustrates concretely both the theorem and the principle of comparing methods in terms of retractions. (shrink)

The literature on causal discovery has focused on interventions that involve randomly assigning values to a single variable. But such a randomized intervention is not the only possibility, nor is it always optimal. In some cases it is impossible or it would be unethical to perform such an intervention. We provide an account of ‘hard' and ‘soft' interventions and discuss what they can contribute to causal discovery. We also describe how the choice of the optimal intervention(s) (...) depends heavily on the particular experimental setup and the assumptions that can be made. ‡The first author is funded by the Causal Learning Collaborative Initiative supported by the James S. McDonnell Foundation. Many aspects of this paper were inspired by discussions with members of the collaborative. †To contact the authors, please write to: Department of Philosophy, Carnegie Mellon University, Pittsburgh, PA 15213; e-mail: [email protected] and [email protected]. (shrink)

This volume offers selected papers exploring issues arising from scientific discovery in the social sciences. It features a range of disciplines including behavioural sciences, computer science, finance, and statistics with an emphasis on philosophy. The first of the three parts examines methods of social scientific discovery. Chapters investigate the nature of causal analysis, philosophical issues around scale development in behavioural science research, imagination in social scientific practice, and relationships between paradigms of inquiry and scientific fraud. The next (...) part considers the practice of social science discovery. Chapters discuss the lack of genuine scientific discovery in finance where hypotheses concern the cheapness of securities, the logic of scientific discovery in macroeconomics, and the nature of that what discovery with the Solidarity movement as a case study. The final part covers formalising theories in social science. Chapters analyse the abstract model theory of institutions as a way of representing the structure of scientific theories, the semi-automatic generation of cognitive science theories, and computational process models in the social sciences. The volume offers a unique perspective on scientific discovery in the social sciences. It will engage scholars and students with a multidisciplinary interest in the philosophy of science and social science. (shrink)

Semmelweis’s discovery of the cause of puerperal fever around the middle of the 19th century counts among the paradigm cases of scientific discovery. For several decades, philosophers of science have used the episode to illustrate, appraise and compare views of proper scientific methodology.Here I argue that the episode can be profitably reexamined in light of two cognate notions: causal reasoning and mechanisms. Semmelweis used several causal reasoning strategies both to support his own and to reject competing (...) hypotheses. However, these strategies have gone unappreciated in the existing literature. I show that a causal reasoning approach makes sense of the multitude of tables in Semmelweis’s main text, which in later editions were often abridged because they appeared redundant.Moreover, the existing literature tends to focus on Semmelweis’s clinical intervention and on the extent to which it alone confirms his theoretical conclusions. This neglects Semmelweis’s efforts to show by animal experiments that his clinical results are in agreement with a demonstrable mechanism of puerperal fever pathogenesis. I argue that the full evidential force of Semmelweis’s argument can only be appreciated if both his clinical and his laboratory investigations are taken into account. (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)

In medicine and the social sciences, researchers often measure only a handful of variables simultaneously. The underlying assumption behind this methodology is that combining the results of dozens of smaller studies can, in principle, yield as much information as one large study, in which dozens of variables are measured simultaneously. Mayo-Wilson :864–874, 2011, Br J Philos Sci 65:213–249, 2013. https://doi.org/10.1093/bjps/axs030) shows that assumption is false when causal theories are inferred from observational data. This paper extends Mayo-Wilson’s results to cases (...) in which experimental data is available. I prove several new theorems that show that, as the number of variables under investigation grows, experiments do not improve, in the worst-case, one’s ability to identify the true causal model if one can measure only a few variables at a time. However, stronger statistical assumptions significantly aid causal discovery in piecemeal inquiry, even if such assumptions are unhelpful when all variables can be measured simultaneously. (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)

How ought we learn causal relationships? While Popper advocated a hypothetico-deductive logic of causal discovery, inductive accounts are currently in vogue. Many inductive approaches depend on the causal Markov condition as a fundamental assumption. This condition, I maintain, is not universally valid, though it is justifiable as a default assumption. In which case the results of the inductive causal learning procedure must be tested before they can be accepted. This yields a synthesis of the hypothetico-deductive (...) and inductive accounts, which forms the focus of this paper. I discuss the justification of this synthesis and draw an analogy between objective Bayesianism and the account of causal learning presented here. (shrink)

The causal Bayes net framework specifies a set of axioms for causal discovery. This article explores the set of causal variables that function as relata in these axioms. Spirtes showed how a causal system can be equivalently described by two different sets of variables that stand in a non-trivial translation-relation to each other, suggesting that there is no “correct” set of causal variables. I extend Spirtes’ result to the general framework of linear structural equation (...) models and then explore to what extent the possibility to intervene or a preference for simpler causal systems may help in selecting among sets of causal variables. (shrink)

The introduction of statistical models represented by directed acyclic graphs (DAGs) has proved fruitful in the construction of expert systems, in allowing efficient updating algorithms that take advantage of conditional independence relations (Pearl, 1988, Lauritzen et al. 1993), and in inferring causal structure from conditional independence relations (Spirtes and Glymour, 1991, Spirtes, Glymour and Scheines, 1993, Pearl and Verma, 1991, Cooper, 1992). As a framework for representing the combination of causal and statistical hypotheses, DAG models have shed light (...) on a number of issues in statistics ranging from Simpson’s Paradox to experimental design (Spirtes, Glymour and Scheines, 1993). The relations of DAGs with statistical constraints, and the equivalence and distinguishability properties of DAG models, are now well understood, and their characterization and computation involves three properties connecting graphical structure and probability distributions: (i) a local directed Markov property, (ii) a global directed Markov property, (iii) and factorizations of joint densities according to the structure of a graph (Lauritizen, et al., 1990). (shrink)

Why is understanding causation so important in philosophy and the sciences? Should causation be defined in terms of probability? Whilst causation plays a major role in theories and concepts of medicine, little attempt has been made to connect causation and probability with medicine itself. Causality, Probability, and Medicine is one of the first books to apply philosophical reasoning about causality to important topics and debates in medicine. Donald Gillies provides a thorough introduction to and assessment of competing theories of causality (...) in philosophy, including action-related theories, causality and mechanisms, and causality and probability. Throughout the book he applies them to important discoveries and theories within medicine, such as germ theory; tuberculosis and cholera; smoking and heart disease; the first ever randomized controlled trial designed to test the treatment of tuberculosis; the growing area of philosophy of evidence-based medicine; and philosophy of epidemiology. This book will be of great interest to students and researchers in philosophy of science and philosophy of medicine, as well as those working in medicine, nursing and related health disciplines where a working knowledge of causality and probability is required. (shrink)

How ought we learn causal relationships? While Popper advocated a hypothetico-deductive logic of causal discovery, inductive accounts are currently in vogue. Many inductive approaches depend on the causal Markov condition as a fundamental assumption. This condition, I maintain, is not universally valid, though it is justifiable as a default assumption. In which case the results of the inductive causal learning procedure must be tested before they can be accepted. This yields a synthesis of the hypothetico-deductive (...) and inductive accounts, which forms the focus of this paper. I discuss the justification of this synthesis and draw an analogy between objective Bayesianism and the account of causal learning presented here. (shrink)

In Norton(2003), it was urged that the world does not conform at a fundamental level to some robust principle of causality. To defend this view, I now argue that the causal notions and principles of modern physics do not express some universal causal principle, brought to light by discoveries in physics. Rather they merely assert that, according to relativity theory, spacetime has an invariant velocity, that of light; and that theories of matter admit no propagations faster than light.

Alexander Gebharter has recently proposed to use Bayesian network causal discovery methods to identify the constitutive dependencies that underwrite mechanistic explanations. The proposal depends on using the assumptions of the causal Bayesian network framework to implicitly define mechanistic constitution as a kind of deterministic direct causal dependence. The aim of this paper is twofold. In the first half, we argue that Gebharter’s proposal incurs severe conceptual problems. In the second half, we present an alternative way to (...) bring Bayesian network tools to bear on the issue of understanding mechanistic constitution. More precisely, our proposal interprets constitution as the relation explaining why a target phenomenon has its characteristic causal role in terms of the causal roles of some of its spatiotemporal parts---where the notion of causal role is probabilistically understood. (shrink)

According to the discovery model in the ontology of art, the facts concerning the ontological status of artworks are mind-independent and, hence, are facts about which the folk may be substantially ignorant or in error. In recent work Amie Thomasson has claimed that the most promising solution to the ‘ qua problem’—a problem concerning how the reference of a referring-expression is fixed—requires us to give up the discovery model. I argue that this claim is false. Thomasson's solution to (...) the qua problem—a hybrid descriptive/causal theory of reference-fixing—has a superior competitor, in the form of the account of reference-fixing suggested by Gareth Evans; and Evans's theory leaves the discovery model untouched. (shrink)

In medicine and the social sciences, researchers must frequently integrate the findings of many observational studies, which measure overlapping collections of variables. For instance, learning how to prevent obesity requires combining studies that investigate obesity and diet with others that investigate obesity and exercise. Recently developed causal discovery algorithms provide techniques for integrating many studies, but little is known about what can be learned from such algorithms. This article argues that there are causal facts that one could (...) learn by conducting a large study but which could not be learned by combining many smaller studies. Moreover, I characterize the frequency with which combining many studies increases underdetermination and exactly how much information is lost. 1 Introduction2 Causal Inference from Observational Data3 Piecemeal Causal Inference4 The Extent and Frequency of the Problem of Piecemeal Induction5 Conclusion. (shrink)

The discovery of conjunctive causes--factors that act in concert to produce or prevent an effect--has been explained by purely covariational theories. Such theories assume that concomitant variations in observable events directly license causal inferences, without postulating the existence of unobservable causal relations. This article discusses problems with these theories, proposes a causal-power theory that overcomes the problems, and reports empirical evidence favoring the new theory. Unlike earlier models, the new theory derives (a) the conditions under which (...) covariation implies conjunctive causation and (b) functions relating observable events to unobservable conjunctive causal strength. This psychological theory, which concerns simple cases involving 2 binary candidate causes and a binary effect, raises questions about normative statistics for testing causal hypotheses regarding categorical data resulting from discrete variables. (shrink)