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

We examine possible causal structures of experiments with entangled quantum objects. Previously, these structures have been obscured by assuming a misleading probabilistic analysis of quantum non locality as 'Outcome Dependence or Parameter Dependence' and by directly associating these correlations with influences. Here we try to overcome these shortcomings: we proceed from a recent stronger Bell argument, which provides an appropriate probabilistic description, and apply the rigorous methods of causal graph theory. Against the standard view that there is only (...) an influence between the measurement outcomes, we show that there must be an influence from one setting to its distant outcome: EPR correlations can only come about if one of the outcomes is a common effect of both settings. Our discussion makes explicit under which assumptions similar conclusions from information theoretic considerations can be interpreted causally. (shrink)

Peter Spirtes. Building Causal Graphs from Statistical Data in the Presence of Latent Variables.

Kin selection and multilevel selection are alternative approaches for studying the evolution of social behaviour, the relation between which has long been a source of controversy. Many recent theorists regard the two approaches as ultimately equivalent, on the grounds that gene frequency change can be correctly expressed using either. However, this shows only that the two are formally equivalent, not that they offer equally good causal representations of the evolutionary process. This article articulates the notion of an ‘adequate (...) class='Hi'>causal representation’ using causal graphs, and then seeks to identify circumstances under which kin and multilevel selection do and do not satisfy the test of causal adequacy. 1 Introduction2 The KS and MLS Approaches2.1 The MLS decomposition2.2 The KS decomposition3 Equivalence and Causality4 Two Problem Cases4.1 The non-social trait case4.2 Genotypic selection with meiotic drive5 Casual Adequacy: A Graphical Approach5.1 The basic idea5.2 Graphs with individual and group variables5.3 Cases where KS is causally adequate5.4 Cases where MLS is causally adequate6 Discussion6.1 Relation to previous work. (shrink)

A general principle for good pedagogic strategy is this: other things equal, make the essential principles of the subject explicit rather than tacit. We think that this principle is routinely violated in conventional instruction in statistics. Even though most of the early history of probability theory has been driven by causal considerations, the terms “cause” and “causation” have practically disappeared from statistics textbooks. Statistics curricula guide students away from the concept of causality, into remembering perhaps the cliche disclaimer “correlation (...) does not mean causation,” but rarely thinking about what correlation does mean. The treatment of causality is a serious handicap to later studies of such topics as experimental design, where often the main goal is to establish (or disprove) causation. Much of the technical vocabulary of the language used in research design textbooks consists in euphemisms for specific causal relations, e.g, “latent variable,” “intervening variable,” “confounding factor,” etc. The multiplicity of terms used to refer to causation results in confusion and, in effect, may hinder understanding of the basic principles of research design. (shrink)

Curie’s Principle says that any symmetry property of a cause must be found in its effect. In this article, I consider Curie’s Principle from the point of view of graphical causal models, and demonstrate that, under one definition of a symmetry transformation, the causal modeling framework does not require anything like Curie’s Principle to be true. On another definition of a symmetry transformation, the graphical causal modeling formalism does imply a version of Curie’s Principle. These results yield (...) a better understanding of the logical landscape with respect to the relationship between Curie’s Principle and graphical causal modeling. (shrink)

I examine to what extent accounts of mechanisms based on formal interventionist theories of causality can adequately represent biological mechanisms with complex dynamics. Using a differential equation model for a circadian clock mechanism as an example, I first show that there exists an iterative solution that can be interpreted as a structural causal model. Thus, in principle, it is possible to integrate causal difference-making information with dynamical information. However, the differential equation model itself lacks the right modularity properties (...) for a full integration. A formal mechanistic model will therefore have to leave out either noncausal or causal explanatory relations. (shrink)

Previous asymptotically correct algorithms for recovering causal structure from sample probabilities have been limited even in sparse graphs to a few variables. We describe an asymptotically correct algorithm whose complexity for fixed graph connectivity increases polynomially in the number of vertices, and may in practice recover sparse graphs with several hundred variables. From..

I examine the adequacy of the causal graph-structural equations approach to causation for modeling biological mechanisms. I focus in particular on mechanisms with complex dynamics such as the PER biological clock mechanism in Drosophila. I show that a quantitative model of this mechanism that uses coupled differential equations – the well-known Goldbeter model – cannot be adequately represented in the standard causal graph framework, even though this framework does permit causal cycles. The reason is that the model (...) contains dynamical information about the mechanism that concerns causal properties but that does not correspond to variables that could be subject to independent interventions. Thus, a representation of the mechanisms as a causal structural model necessarily suppresses causally relevant information. (shrink)

I argue that one central aspect of the epistemology of causation, the use of causes as evidence for their effects, is largely independent of the metaphysics of causation. In particular, I use the formalism of Bayesian causal graphs to factor the incremental evidential impact of a cause for its effect into a direct cause-to-effect component and a backtracking component. While the “backtracking” evidence that causes provide about earlier events often obscures things, once we our restrict attention to the (...) cause-to-effect component it is true to say promoting (inhibiting) causes raise (lower) the probabilities of their effects. This factoring assumes the same form whether causation is given an interventionist, counterfactual or probabilistic interpretation. Whether we think about causation in terms of interventions and causal graphs, counterfactuals and imaging functions, or probability raising against the background of causally homogenous partitions, if we describe the essential features of a situation correctly then the incremental evidence that a cause provides for its effect in virtue of being its cause will be the same. (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)

The recent literature on causality has seen the introduction of several distinctions within causality, which are thought to be important for understanding the widespread scientific practice of focusing causal explanations on a subset of the factors that are causally relevant for a phenomenon. Concepts used to draw such distinctions include, among others, stability, specificity, proportionality, or actual-difference making. In this contribution, I propose a new distinction that picks out an explanatorily salient class of causes in biological systems. Some select (...) causes in complex biological systems, I argue, have the property of enabling coherent causal control of these systems. Examples of such control variables include hormones and other signaling molecules, e.g., TOR (target of rapamycin), morphogens or the products of homeotic selector genes in embryonic pattern formation. I propose an analysis of this notion based on concepts borrowed from causal graph theory. (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.

Independence of Conditionals (IC) has recently been proposed as a basic rule for causal structure learning. If a Bayesian network represents the causal structure, its Conditional Probability Distributions (CPDs) should be algorithmically independent. In this paper we compare IC with causal faithfulness (FF), stating that only those conditional independences that are implied by the causal Markov condition hold true. The latter is a basic postulate in common approaches to causal structure learning. The common spirit of (...) FF and IC is to reject causal graphs for which the joint distribution looks ‘non-generic’. The difference lies in the notion of genericity: FF sometimes rejects models just because one of the CPDs is simple, for instance if the CPD describes a deterministic relation. IC does not behave in this undesirable way. It only rejects a model when there is a non-generic relation between different CPDs although each CPD looks generic when considered separately. Moreover, it detects relations between CPDs that cannot be captured by conditional independences. IC therefore helps in distinguishing causal graphs that induce the same conditional independences (i.e., they belong to the same Markov equivalence class). The usual justification for FF implicitly assumes a prior that is a probability density on the parameter space. IC can be justified by Solomonoff’s universal prior, assigning non-zero probability to those points in parameter space that have a finite description. In this way, it favours simple CPDs, and therefore respects Occam’s razor. Since Kolmogorov complexity is uncomputable, IC is not directly applicable in practice. We argue that it is nevertheless helpful, since it has already served as inspiration and justification for novel causal inference algorithms. (shrink)

This paper has two main parts. In the first part, we motivate a kind of indeterminate, suppositional credences by discussing the prospect for a subjective interpretation of a causal Bayesian network, an important tool for causal reasoning in artificial intelligence. A CBN consists of a causal graph and a collection of interventional probabilities. The subjective interpretation in question would take the causal graph in a CBN to represent the causal structure that is believed by an (...) agent, and interventional probabilities in a CBN to represent suppositional credences. We review a difficulty noted in the literature with such an interpretation, and suggest that a natural way to address the challenge is to go for a generalization of CBN that allows indeterminate credences. In the second part, we develop a decision-theoretic foundation for such indeterminate suppositional credences, by generalizing a theory of coherent choice functions to accommodate some form of act-state dependence. The upshot is a decision-theoretic framework that is not only rich enough to, so to speak, ground the probabilities in a subjectively interpreted causal network, but also interesting in its own right, in that it accommodates both act-state dependence and imprecise probabilities. (shrink)

Recently developed theory using directed graphs permits simple and precise statements about the validity of causal inferences in most cases. Applying this while reading econometric papers can make it easy to understand assumptions that are vague in prose, and to isolate those assumptions that are crucial to support the main causal claims. The method is illustrated here alongside a close reading of the paper that introduced the use of settler mortality to instrument the impact of institutions on (...) economic development. Two causal pathways that invalidate the instrument are found not to be blocked by satisfactory strategies. The estimates in the original paper, and in many that have used the instrument since, should be considered highly suspect. (shrink)

I propose a new account of homology, according to which homology is a correspondence of developmental mechanisms due to common ancestry, formally defined as an isomorphism of causal graphs over lineages. The semiformal definition highlights the role of homology as a higher-order principle unifying evolutionary models and also provides definite meanings to concepts like constraints, evolvability, and novelty. The novel interpretation of homology suggests a broad perspective that accommodates evolutionary developmental biology and traditional population genetics as distinct but (...) complementary approaches to understand evolution, prompting further empirical and theoretical research. (shrink)

The rise of causality and the attendant graph-theoretic modeling tools in the study of counterfactual reasoning has had resounding effects in many areas of cognitive science, but it has thus far not permeated the mainstream in linguistic theory to a comparable degree. In this study I show that a version of the predominant framework for the formal semantic analysis of conditionals, Kratzer-style premise semantics, allows for a straightforward implementation of the crucial ideas and insights of Pearl-style causal networks. I (...) spell out the details of such an implementation, focusing especially on the notions of intervention on a network and backtracking interpretations of counterfactuals. (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)

Occam’s razor directs us to adopt the simplest hypothesis consistent with the evidence. Learning theory provides a precise definition of the inductive simplicity of a hypothesis for a given learning problem. This definition specifies a learning method that implements an inductive version of Occam’s razor. As a case study, we apply Occam’s inductive razor to causal learning. We consider two causal learning problems: learning a causal graph structure that presents global causal connections among a set of (...) domain variables, and learning context-sensitive causal relationships that hold not globally, but only relative to a context. For causal graph learning, Occam’s inductive razor directs us to adopt the model that explains the observed correlations with a minimum number of direct causal connections. For expanding a causal graph structure to include context-sensitive relationships, Occam’s inductive razor directs us to adopt the expansion that explains the observed correlations with a minimum number of free parameters. This is equivalent to explaining the correlations with a minimum number of probabilistic logical rules. The paper provides a gentle introduction to the learning-theoretic definition of inductive simplicity and the application of Occam’s razor for causal learning. (shrink)

We used a new method to assess how people can infer unobserved causal structure from patterns of observed events. Participants were taught to draw causal graphs, and then shown a pattern of associations and interventions on a novel causal system. Given minimal training and no feedback, participants in Experiment 1 used causal graph notation to spontaneously draw structures containing one observed cause, one unobserved common cause, and two unobserved independent causes, depending on the pattern of (...) associations and interventions they saw. We replicated these findings with less‐informative training (Experiments 2 and 3) and a new apparatus (Experiment 3) to show that the pattern of data leads to hidden causal inferences across a range of prior constraints on causal knowledge. (shrink)

Machine learning is used more and more in scientific contexts, from the recent breakthroughs with AlphaFold2 in protein fold prediction to the use of ML in parametrization for large climate/astronomy models. Yet it is unclear whether we can obtain scientific explanations from such models. I argue that when machine learning is used to conduct causal inference we can give a new positive answer to this question. However, these ML models are purpose-built models and there are technical results showing that (...) standard machine learning models cannot be used for the same type of causal inference. Instead, there is a pathway to causal explanations from predictive ML models through new explainability techniques; specifically, new methods to extract structural equation models from such ML models. The extracted models are likely to suffer from issues though: they will often fail to account for confounders and colliders, as well as deliver simply incorrect causal graphs due to ML models tendency to violate physical laws such as the conservation of energy. In this case, extracted graphs are a starting point for new explanations, but predictive accuracy is no guarantee for good explanations. (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)

This paper raises the question of the prominence and use of statistical graphs in science, and argues that their use in problem solving analysis can best be understood in an ‘interactionist’ frame of analysis, including bio-emotion, culture, social organization, and environment as elements. The frame contrasts both with philosophical realism and with social constructivism, which posit two variables and one way causal flows. We next posit basic differences between visual, verbal, and numerical media of perception and communication. (...) class='Hi'>Graphs are thus seen as key interactive sites where different media are transformed into more interpretable forms. Examples are taken from Limnology where numbers are transformed into graphs to find patterns in them, and thus, by implication in the environmental materials from which the numerical measurements were taken. Their revisualization by passes a human cognitive limitation, for the direct analysis — interpretation of lists and tables of numbers, visual imaging being a cognitive strength. Sense of problem, conceptual repertoire, and social relations are seen to direct this pattern search and interpretive process. (shrink)

There are simple mechanical systems that elude causal representation. We describe one that cannot be represented in a single directed acyclic graph. Our case suggests limitations on the use of causal graphs for causal inference and makes salient the point that causal relations among variables depend upon details of causal setups, including values of variables.

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

Does y obtain under the counterfactual supposition that x? The answer to this question is famously thought to depend on whether y obtains in the most similar world in which x obtains. What this notion of ‘similarity’ consists in is controversial, but in recent years, graphical causal models have proved incredibly useful in getting a handle on considerations of similarity between worlds. One limitation of the resulting conception of similarity is that it says nothing about what would obtain were (...) the causal structure to be different from what it actually is, or from what we believe it to be. In this paper, we explore the possibility of using graphical causal models to resolve counterfactual queries about causal structure by introducing a notion of similarity between causal graphs. Since there are multiple principled senses in which a graph G* can be more similar to a graph G than a graph G**, we introduce multiple similarity metrics, as well as multiple ways to prioritize the various metrics when settling counterfactual queries about causal structure. (shrink)

This article assesses how people reason with categories whose features are related in causal cycles. Whereas models based on causal graphical models have enjoyed success modeling category-based judgments as well as a number of other cognitive phenomena, CGMs are only able to represent causal structures that are acyclic. A number of new formalisms that allow cycles are introduced and evaluated. Dynamic Bayesian networks represent cycles by unfolding them over time. Chain graphs augment CGMs by allowing the (...) presence of undirected links that model feedback relations between variables. Unfolded chain graphs are chain graphs that unfold over time. An existing model of causal cycles is also evaluated. Four experiments in which subjects reason about categories with cyclically related features provided evidence against DBNs and alpha centrality and for the two types of chain graphs. Chain graphs—a mechanism for representing the equilibrium distribution of a dynamic system—may thus be good candidates for modeling how people reason causally with complex systems. Applications of chain graphs to areas of cognition other than category-based judgments are discussed. (shrink)

THE ART OF CAUSAL CONJECTURE Glenn Shafer Table of Contents Chapter 1. Introduction........................................................................................ ...........1 1.1. Probability Trees..........................................................................................3 1.2. Many Observers, Many Stances, Many Natures..........................................8 1.3. Causal Relations as Relations in Nature’s Tree...........................................9 1.4. Evidence............................................................................................ ...........13 1.5. Measuring the Average Effect of a Cause....................................................17 1.6. Causal Diagrams..........................................................................................20 1.7. Humean Events............................................................................................23 1.8. Three Levels of Causal Language................................................................27 1.9. An Outline of the Book................................................................................27 Chapter 2. Event Trees............................................................................................... .....31 2.1. Situations and Events...................................................................................32 2.2. The Ordering of Situations and Moivrean Events.......................................35 2.3. Cuts................................................................................................ ..............39 (...) 2.4. Humean Events............................................................................................43 2.5. Moivrean Variables......................................................................................49 2.6. Humean Variables........................................................................................53 2.7. Event Trees for Stochastic Processes...........................................................54 2.8. Timing in Event Trees.................................................................................56 2.9. Intersecting Event Trees...............................................................................60 2.10. Notes on the Literature...............................................................................61 Chapter 3. Probability Trees...........................................................................................63 3.1. Some Types of Probability Trees.................................................................64 ii 3.2. Axioms for the Probabilities of Moivrean Events.......................................68 3.3. Zero Probabilities....................................................................................... ..70 3.4. A Sample-Space Analysis of the Event-Tree Axioms.................................72 3.5. Probabilities and Expected Values for Variables.........................................74 3.6. Martingales......................................................................................... .........79 3.7. The Expectation of a Variable in a Cut........................................................83 3.8. Conditional Expected Value and Conditional Expectation.........................87 Chapter 4. The Meaning of Probability...........................................................................91 4.1. The Interpretation of Expected Value..........................................................92 4.2. The Interpretation of Expectation................................................................95 4.3. The Long Run..............................................................................................98 4.4. Changes in Belief.........................................................................................101 4.5. The Empirical Validation of Probability......................................................106 4.6. The Diversity of Uses of Probability...........................................................108 4.7. Notes on the Literature.................................................................................110 Chapter 5. Independent Events.......................................................................................113 5.1. Independence........................................................................................ .......114 5.2. Weak Independence.....................................................................................118 5.3. The Principle of the Common Cause...........................................................121 5.4. Conditional Independence............................................................................128 5.5. Notes on the Literature.................................................................................133 Chapter 6. Events Tracking Events.................................................................................135 6.1. Tracking............................................................................................ ...........137 6.2. Tracking and Conditional Independence.....................................................142 6.3. Stochastic Subsequence...............................................................................143 6.4. Singular Diagrams for Stochastic Subsequence...........................................147 6.5. Conjunctive and Interactive Forks...............................................................149 Chapter 7. Events as Signs of Events..............................................................................153 iii 7.1. Sign................................................................................................ ..............154 7.2. Weak Sign................................................................................................ ....159 7.3. The Ethics of Causal Talk............................................................................160 7.4. Screening Off...............................................................................................16 2 Chapter 8. Independent Variables...................................................................................167 8.1. Unconditional Independence........................................................................170 8.2. Conditional Independence............................................................................175 8.3. Independence for Partitions.........................................................................177 8.4. Independence for Families of Variables......................................................182 8.5. Individual Properties of the Independence Relations...................................186 Chapter 9. Variables Tracking Variables........................................................................189 9.1. Tracking and Conditional Independence: A Summary...............................190 9.2. Strong Tracking............................................................................................ 192 9.3. Strong Tracking and Conditional Independence..........................................198 9.4. Stochastic Subsequence...............................................................................201 9.5. Functional Dependence................................................................................203 9.6. Tracking in Mean.........................................................................................204 9.7. Linear Tracking............................................................................................ 207 9.8. Tracking by Partitions..................................................................................210 9.9. Tracking by Families of Variables...............................................................212 Chapter 10. Variables as Signs of Variables...................................................................215 10.1. Sign................................................................................................ ............219 10.2. Linear Sign................................................................................................ .222 10.3. Scored Sign................................................................................................ 225 10.4. Families of Variables.................................................................................227 Chapter 11. AnTheory of Event Trees.............................................................229 11.1. Event Trees as Sets of Sets........................................................................230 11.2. Event Trees as Partially Ordered Sets........................................................232 iv 11.3. Regular Event Trees...................................................................................240 11.4. The Resolution of Moivrean Variables......................................................244 11.5. Humean Events and Variables...................................................................246 Chapter 12. Martingale Trees..........................................................................................247 12.1. Examples of Decision Trees......................................................................249 12.2. The Meaning of Probability in a Decision Tree.........................................253 12.3. Martingales......................................................................................... .......257 12.4. The Structure of Martingale Trees.............................................................261 12.5. Probability and Causality...........................................................................265 12.6. Lower and Upper Probability.....................................................................269 12.7. The Law of Large Numbers.......................................................................272 12.8. Notes on the Literature...............................................................................274 Chapter 13. Refining............................................................................................ ...........275 13.1. Examples of Refinement............................................................................277 13.2. A Constructive Definition of Finite Refinement.......................................281 13.3. Axioms for Refinement..............................................................................282 13.4. Lifting Moivrean Events and Variables.....................................................288 13.5. Refining Martingale Trees.........................................................................288 13.6. Grounding........................................................................................... .......294 Chapter 14. Principles of Causal Conjecture..................................................................299 14.1. The Diversity of Causal Explanation.........................................................302 14.2. The Mean Effect of the Happening of a Moivrean Event..........................305 14.3. The Effect of a Humean Variable..............................................................311 14.4. Attribution and Generality.........................................................................316 14.5. The Statistical Measurement of the Effect of a Cause...............................319 14.6. Measurement by Experiment.....................................................................320 14.7. Using Our Knowledge of How Things Work............................................322 v 14.8. Sampling Error...........................................................................................329 14.9. The Sampling Frame..................................................................................329 14.10. Notes on the Literature.............................................................................330 Chapter 15. Causal Models.............................................................................................3 31 15.1. The Causal Interpretation of Statistical Prediction....................................333 15.2. Generalizing to a Family of Exogenous Variables....................................337 15.3 Some Joint Causal Diagrams......................................................................339 15.4. Causal Path Diagrams................................................................................342 15.5. Causal Relevance Diagrams.......................................................................346 15.6. The Meaning of Latent Variables..............................................................352 15.7. Notes on the Literature...............................................................................357 Chapter 16. Representing Probability Trees...................................................................359 16.1. Three Graphical Representations...............................................................361 16.2. Skeletal Simplifications.............................................................................368 16.3. Martingale Trees in Type Theory...............................................................371 Appendix A. Huygens’s Probability Trees.....................................................................379 Huygens’s Manuscript in Translation..................................................................380 Appendix B. Some Elements of Graph Theory..............................................................385 B1. Undirected Graphs........................................................................................385 B2. Directed Graphs............................................................................................386 Appendix C. Some Elements of Order Theory...............................................................393 C1. Partial and Quasi Orderings.........................................................................393 C2. Singular and Joint Diagrams for Binary Relations.......................................394 C3. Lattices............................................................................................ .............395 C4. The Lattice of Partitions of a Set..................................................................396 Appendix D. The Sample-Space Framework for Probability.........................................399 D1. Probability Measures....................................................................................399 D2. Variables........................................................................................... ...........400 vi D3. Families of Variables...................................................................................401 D4. Expected Value............................................................................................402 D5. The Law of Large Numbers.........................................................................405 D6. Conditional Probability................................................................................406 D7. Conditional Expected Value........................................................................407 Appendix E. Prediction in Probability Spaces................................................................409 E1. Conditional Distribution...............................................................................411 E2. Regression on a Single Variable...................................................................412 E3. Regression on a Partition or a Family of Variables......................................415 E4. Linear Regression on a Single Variable.......................................................418 E5. Linear Regression on a Family of Variables................................................422 Appendix F. Sample-Space Concepts of Independence.................................................425 F1. Overview............................................................................................ ...........426 F2. Independence Proper.....................................................................................432 F3. Unpredictability in Mean..............................................................................434 F4. Simple Uncorrelatedness..............................................................................437 F5. Mixed Uncorrelatedness...............................................................................438 F6. Partial Uncorrelatedness...............................................................................440 F7. Independence for Partitions..........................................................................442 F8. Independence for Families of Variables.......................................................445 F9. The Basic Role of Uncorrelatedness.............................................................448 F10. Dawid’s Axioms.........................................................................................449 Appendix G. Prediction Diagrams..................................................................................453 G1. Path Diagrams............................................................................................ ..454 G2. Generalized Path Diagrams..........................................................................462 G3. Relevance Diagrams.....................................................................................466 G4. Bubbled Relevance Diagrams......................................................................475 Appendix H. Abstract Stochastic Processes...................................................................479 vii H1. Probability Conditionals and Probability Distributions...............................477 H2. Abstract Stochastic Processes......................................................................479 H3. Embedding Variables and Processes in a Sample Space.............................480 References.......................................................................................... ..............................491. (shrink)

Mechanistic philosophy of science views a large part of scientific activity as engaged in modelling mechanisms. While science textbooks tend to offer qualitative models of mechanisms, there is increasing demand for models from which one can draw quantitative predictions and explanations. Casini et al. (Theoria 26(1):5–33, 2011) put forward the Recursive Bayesian Networks (RBN) formalism as well suited to this end. The RBN formalism is an extension of the standard Bayesian net formalism, an extension that allows for modelling the hierarchical (...) nature of mechanisms. Like the standard Bayesian net formalism, it models causal relationships using directed acyclic graphs. Given this appeal to acyclicity, causal cycles pose a prima facie problem for the RBN approach. This paper argues that the problem is a significant one given the ubiquity of causal cycles in mechanisms, but that the problem can be solved by combining two sorts of solution strategy in a judicious way. (shrink)

Recursive linear structural equation models can be represented by directed acyclic graphs. When represented in this way, they satisfy the Markov Condition. Hence it is possible to use the graphical d-separation to determine what conditional independence relations are entailed by a given linear structural equation model. I prove in this paper that it is also possible to use the graphical d-separation applied to a cyclic graph to determine what conditional independence relations are entailed to hold by a given non-recursive (...) linear structural equation model. I also give a causal intepretation to the linear coefficients in a non- recursive structural equation models, and explore the relationships between cyclic graphs and undirected graphs, directed acyclic graphs with latent variables, and chain independence graphs. (shrink)

The causal Markov condition (CMC) plays an important role in much recent work on the problem of causal inference from statistical data. It is commonly thought that the CMC is a more problematic assumption for genuinely indeterministic systems than for deterministic ones. In this essay, I critically examine this proposition. I show how the usual motivation for the CMC—that it is true of any acyclic, deterministic causal system in which the exogenous variables are independent—can be extended to (...) the indeterministic case. In light of this result, I consider several arguments for supposing indeterminism a particularly hostile environment for the CMC, but conclude that none are persuasive. Introduction Functional models and directed graphs The causal Markov theorem The causal Markov theorem and genuine indeterminism Are the exogenous variables independent? EPR Conclusion. (shrink)

The estimation of causal effects is fundamental in situations where the underlying system will be subject to active interventions. Part of building a causal inference engine is defining how variables relate to each other, that is, defining the functional relationship between variables entailed by the graph conditional dependencies. In this article, we deviate from the common assumption of linear relationships in causal models by making use of neural autoregressive density estimators and use them to estimate causal (...) effects within Pearl’s do-calculus framework. Using synthetic data, we show that the approach can retrieve causal effects from non-linear systems without explicitly modeling the interactions between the variables and include confidence bands using the non-parametric bootstrap. We also explore scenarios that deviate from the ideal causal effect estimation setting such as poor data support or unobserved confounders. (shrink)

Recent approaches to causal modelling rely upon the causal Markov condition, which specifies which probability distributions are compatible with a directed acyclic graph. Further principles are required in order to choose among the large number of DAGs compatible with a given probability distribution. Here we present a principle that we call frugality. This principle tells one to choose the DAG with the fewest causal arrows. We argue that frugality has several desirable properties compared to the other principles (...) that have been suggested, including the well-known causal faithfulness condition. _1_ Introduction _2_ The Causal Markov Condition _3_ Faithfulness _4_ Frugality _4.1_ Basic independences and frugality _4.2_ General properties of directed acyclic graphs satisfying frugality _4.3_ Connection to minimality assumptions _5_ Frugality as a Parsimony Principle _6_ Conclusion Appendix. (shrink)

Yarkoni argues that one solution is to abandon quantitative methods for qualitative ones. While we agree that qualitative methods are undervalued, we argue that both are necessary for thoroughgoing psychological research, complementing one another through the use of causal analysis. We illustrate how directed acyclic graphs can bridge qualitative and quantitative methods, thereby fostering understanding between different psychological methodologies.

Drawing substantive conclusions from linear causal models that perform acceptably on statistical tests is unreasonable if it is not known how alternatives fare on these same tests. We describe a computer program, TETRAD, that helps to search rapidly for plausible alternatives to a given causal structure. The program is based on principles from statistics, graph theory, philosophy of science, and artificial intelligence. We describe these principles, discuss how TETRAD employs them, and argue that these principles make TETRAD an (...) effective tool. Finally, we illustrate TETRAD's effectiveness by applying it to a multiple indicator model of Political and Industrial development. A pilot version of the TETRAD program is described in this paper. The current version is described in our forthcoming Discovering Causal Structure: Artificial Intelligence for Statistical Modeling. (shrink)

A graphical model is a graph that represents a set of conditional independence relations among the vertices (random variables). The graph is often given a causal interpretation as well. I describe how graphical causal models can be used in an algorithm for constructing partial information about causal graphs from observational data that is reliable in the large sample limit, even when some of the variables in the causal graph are unmeasured. I also describe an algorithm (...) for estimating from observational data (in some cases) the total effect of a given variable on a second variable, and theoretical insights into fundamental limitations on the possibility of certain causal inferences by any algorithm whatsoever, and regardless of sample size. (shrink)

This paper defends the view that the asymmetry of causation can be explained in terms of probabilistic relationships between event types. Papineau first explores three different versions of the "fork asymmetry", namely David Lewis' asymmetry of overdetermination, the screening-off property of common causes, and Spirtes', Glymour's and Scheines' analysis of probabilistic graphs. He then argues that this fork asymmetry is both a genuine phenomenon and a satisfactory metaphysical reduction of causal asymmetry. In his final section he shows how (...) this reduction can account for the relevance of causal direction to human agency, and in particular for the fact that we can manipulate causes to influence their effects, but not vice versa. (shrink)

The paper displays the similarity between the theory of probabilistic causation developed by Glymour et al. since 1983 and mine developed since 1976: the core of both is that causal graphs are Bayesian nets. The similarity extends to the treatment of actions or interventions in the two theories. But there is also a crucial difference. Glymour et al. take causal dependencies as primitive and argue them to behave like Bayesian nets under wide circumstances. By contrast, I argue (...) the behavior of Bayesian nets to be ultimately the defining characteristic of causal dependence. (shrink)

S There is a long tradition of representing causal relationships by directed acyclic graphs (Wright, 1934 ). Spirtes ( 1994), Spirtes et al. ( 1993) and Pearl & Verma ( 1991) describe procedures for inferring the presence or absence of causal arrows in the graph even if there might be unobserved confounding variables, and/or an unknown time order, and that under weak conditions, for certain combinations of directed acyclic graphs and probability distributions, are asymptotically, in sample (...) size, consistent. These results are surprising since they seem to contradict the standard statistical wisdom that consistent estimators of causal effects do not exist for nonrandomised studies if there are potentially unobserved confounding variables. We resolve the apparent incompatibility of these views by closely examining the asymptotic properties of these causal inference procedures. We show that the asymptotically consistent procedures are ‘pointwise consistent’, but ‘uniformly consistent’ tests do not exist. Thus, no finite sample size can ever be guaranteed to approximate the asymptotic results. We also show the nonexistence of valid, consistent confidence intervals for causal effects and the nonexistence of uniformly consistent point estimators. Our results make no assumption about the form of the tests or estimators. In particular, the tests could be classical independence tests, they could be Bayes tests or they could be tests based on scoring methods such as  or . The implications of our results for observational studies are controversial and are discussed briefly in the last section of the paper. The results hinge on the following fact: it is possible to find, for each sample size n, distributions P and Q such that P and Q are empirically indistinguishable and yet P and Q correspond to different causal effects. (shrink)

It is well known that there may be many causal explanations that are consistent with a given set of data. Recent work has been done to represent the common aspects of these explanations into one representation. In this paper, we address what is less well known: how do the relationships common to every causal explanation among the observed variables of some DAG process change in the presence of latent variables? Ancestral graphs provide a class of graphs (...) that can encode conditional independence relations that arise in DAG models with latent and selection variables. In this paper we present a set of orientation rules that construct the Markov equivalence class representative for ancestral graphs, given a member of the equivalence class. These rules are sound and complete. We also show that when the equivalence class includes a DAG, the equivalence class representative is the essential graph for the said DAG. (shrink)