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)

McCaffrey and Danks have posed the challenge of discovering causal relations in data drawn from a mixture of distributions as an impossibility result in functional magnetic resonance. We give an algorithm that addresses this problem for the distributions commonly assumed in fMRI studies and find that in testing, it can accurately separate data from mixed distributions. As with other obstacles to automated search, the problem of mixed distributions is not an impossible one, but rather a challenge. 1Introduction2Background3Addressing the Problem4Discussion.

In psychology, measurement instruments are constructed from scales, which are obtained on the grounds of exploratory and confirmatory factor analysis. Looking at the literature, one can find various recommendations regarding how these techniques should be used during the scale construction process. Some authors suggest to use exploratory factor analysis on the entire data set while others advice to perform an internal cross-validation by randomly splitting the data set in two and then either perform exploratory factor analysis on both parts or (...) exploratory factor analysis on the first part and confirmatory factor analysis on the other. In spite of all these divergent recommendations, there is no consensus on which method yields the best result. In this paper, we analyze this issue in light of the prediction versus accommodation debate and argue that the answer to this question depends on one’s conception of the criteria that should be used to achieve the goals of the scientific enterprise. (shrink)

:Statisticians have proposed formal techniques for evaluation of treatments, often in the context of models that do not explicitly specify how treatments are generated. Under such procedures they run the risk of attributing causation in settings where the implementation neutrality condition required for causal interpretation of parameter estimates is not satisfied. When treatment assignments are explicitly modelled, as economists recommend, these issues can be formally analysed, and the existence of implementation neutrality, and therefore quantifiable causation, can be determined. Examples are (...) given. (shrink)

Many approaches to evidence amalgamation focus on relatively static information or evidence: the data to be amalgamated involve different variables, contexts, or experiments, but not measurements over extended periods of time. However, much of scientific inquiry focuses on dynamical systems; the system’s behavior over time is critical. Moreover, novel problems of evidence amalgamation arise in these contexts. First, data can be collected at different measurement timescales, where potentially none of them correspond to the underlying system’s causal timescale. Second, missing variables (...) have a significantly different impact on time series measurements than they do in the traditional static setting; in particular, they make causal and structural inference much more difficult. In this paper, we argue that amalgamation should proceed by integrating causal knowledge, rather than at the level of “raw” evidence. We defend this claim by first outlining both of these problems, and then showing that they can be solved only if we operate on causal structures. We therefore must use causal discovery methods that are reliable given these problems. Such methods do exist, but their successful application requires careful consideration of the problems that we highlight. (shrink)

ABSTRACT Darwin claims in the Origin that similarity is evidence for common ancestry, but that adaptive similarities are ‘almost valueless’ as evidence. This second claim seems reasonable for some adaptive similarities but not for others. Here we clarify and evaluate these and related matters by using the law of likelihood as an analytic tool and by considering mathematical models of three evolutionary processes: directional selection, stabilizing selection, and drift. Our results apply both to Darwin’s theory of evolution and to modern (...) evolutionary biology. _1_ Introduction _2_ The Likelihood Framework _3_ A Sufficient Condition for a Similarity to Favour Common Ancestry over Separate Ancestry _4_ The 1/p Criterion and Its Limitations _5_ Directional Selection versus Drift _6_ Stabilizing Selection versus Drift _7_ Going beyond Two Taxa _8_ Conclusions Appendix. (shrink)

Non-reductive interventionist theories of causation and methodologies of causal reasoning embedded in that theoretical framework have become increasingly popular in recent years. This paper argues that one variant of an interventionist account of causation, viz. the one presented, for example, in Woodward (2003), is unsuited as a theoretical fundament of interventionist methodologies of causal reasoning, because it renders corresponding methodologies incapable of uncovering a causal structure in a finite number of steps. This finding runs counter to Woodward's own assessment and (...) to other recent studies which presume that Woodward's version of interventionism is effectively applicable to uncover causal structures, e.g. Campbell (2007) or Shapiro and Sober (2007). (shrink)

Complex organisms thwart the simple rectilinear causality paradigm of “necessary and sufficient,” with its experimental strategy of “knock down and overexpress.” This Essay organizes the eccentricities of biology into four categories that call for new mathematical approaches; recaps for the biologist the philosopher's recent refinements to the causation concept and the mathematician's computational tools that handle some but not all of the biological eccentricities; and describes overlooked insights that make causal properties of physical hierarchies such as emergence and downward causation (...) straightforward. Reviewing and extrapolating from similar situations in physics, it is suggested that new mathematical tools for causation analysis incorporating feedback, signal cancellation, nonlinear dependencies, physical hierarchies, and fixed constraints rather than instigative changes will reveal unconventional biological behaviors. These include “eigenisms,” organisms that are limited to quantized states; trajectories that steer a system such as an evolving species toward optimal states; and medical control via distributed “sheets” rather than single control points. (shrink)

Complex organisms thwart the simple rectilinear causality paradigm of “necessary and sufficient,” with its experimental strategy of “knock down and overexpress.” This Essay organizes the eccentricities of biology into four categories that call for new mathematical approaches; recaps for the biologist the philosopher's recent refinements to the causation concept and the mathematician's computational tools that handle some but not all of the biological eccentricities; and describes overlooked insights that make causal properties of physical hierarchies such as emergence and downward causation (...) straightforward. Reviewing and extrapolating from similar situations in physics, it is suggested that new mathematical tools for causation analysis incorporating feedback, signal cancellation, nonlinear dependencies, physical hierarchies, and fixed constraints rather than instigative changes will reveal unconventional biological behaviors. These include “eigenisms,” organisms that are limited to quantized states; trajectories that steer a system such as an evolving species toward optimal states; and medical control via distributed “sheets” rather than single control points. (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)

This thesis studies Judea Pearl’s logic of counterfactuals derived from the causal modeling framework, in comparison to the influential Stanlnaker-Lewis counterfactual logics. My study focuses on a characteristic principle in Pearl’s logic, named reversibility. The principle, as Pearl pointed out, goes beyond Lewis’s logic. Indeed, it also goes beyond the stronger logic of Stanlnaker, which is more analogous to Pearl’s logic. The first result of this thesis is an extension of Stanlnaker’s logic incorporating reversibility. It will be observed that the (...) translation of reversibility from Pearl’s language to the standard language for conditional logic deserves some attention. In particular, a straightforward translation following Pearl’s suggestion would render reversibility incompatible with Stanlnaker’s logic. A new translation of reversibility will be proposed, and an extension of Stanlnaker’s logic with the inclusion of the translated reversibility will be investigated. More importantly, it will be shown that the extended Stanlnaker’s logic is sound and complete with respect to a modified Stanlnaker’s semantics. The extension of Stanlnaker’s logic has an interesting implication. Zhang, Lam, and de Clercq have shown that special case of reversibility, despite its name, actually states an important kind of irreversibility: counterfactual dependence between distinct events is irreversible. In other words, reversibility entails that there is no cycle of counterfactual dependence altogether generalizations of reversibility. However, as shown in Zhang et al., Pearls’ logic does not rule out cycles of counterfactual dependence altogether. It in fact allows cycles that involve three or more distinct events. This is peculiar because the status of cyclic counterfactual dependence seems no more metaphysically secure than that of mutual counterfactual dependence. This consideration leads to an exploration of logics that rule out all cycles of counterfactual dependence. A surprising result is that the extension of Stanlnaker’s logic is precisely a logic of this sort. (shrink)

Using a variety of different results from the literature, I show how causal discovery with experiments is limited unless substantive assumptions about the underlying causal structure are made. These results undermine the view that experiments, such as randomized controlled trials, can independently provide a gold standard for causal discovery. Moreover, I present a concrete example in which causal underdetermination persists despite exhaustive experimentation and argue that such cases undermine the appeal of an interventionist account of causation as its dependence on (...) other assumptions is not spelled out. (shrink)

Although for many years a sharp distinction has been made in language research between rules and words—with primary interest on rules—this distinction is now blurred in many theories. If anything, the focus of attention has shifted in recent years in favor of words. Results from many different areas of language research suggest that the lexicon is representationally rich, that it is the source of much productive behavior, and that lexically specific information plays a critical and early role in the interpretation (...) of grammatical structure. But how much information can or should be placed in the lexicon? This is the question I address here. I review a set of studies whose results indicate that event knowledge plays a significant role in early stages of sentence processing and structural analysis. This poses a conundrum for traditional views of the lexicon. Either the lexicon must be expanded to include factors that do not plausibly seem to belong there; or else virtually all information about word meaning is removed, leaving the lexicon impoverished. I suggest a third alternative, which provides a way to account for lexical knowledge without a mental lexicon. (shrink)

The pivotal problem of comorbidity research lies in the psychometric foundation it rests on, that is, latent variable theory, in which a mental disorder is viewed as a latent variable that causes a constellation of symptoms. From this perspective, comorbidity is a (bi)directional relationship between multiple latent variables. We argue that such a latent variable perspective encounters serious problems in the study of comorbidity, and offer a radically different conceptualization in terms of a network approach, where comorbidity is hypothesized to (...) arise from direct relations between symptoms of multiple disorders. We propose a method to visualize comorbidity networks and, based on an empirical network for major depression and generalized anxiety, we argue that this approach generates realistic hypotheses about pathways to comorbidity, overlapping symptoms, and diagnostic boundaries, that are not naturally accommodated by latent variable models: Some pathways to comorbidity through the symptom space are more likely than others; those pathways generally have the same direction (i.e., from symptoms of one disorder to symptoms of the other); overlapping symptoms play an important role in comorbidity; and boundaries between diagnostic categories are necessarily fuzzy. (shrink)

Explanations in psychiatry often integrate various factors relevant to psychopathology. Identifying genuine causes among them is theoretically and clinically important, but epistemically challenging. Woodward’s interventionism appears to provide a promising tool to achieve this. However, Woodward’s interventionism is too demanding to be applied to psychiatry. I thus introduce difference-making interventionism, which detects relevance in general rather than causation, to make interventionist reasoning viable in clinical practice. DMI mirrors the empirical reality of psychiatry even more closely than interventionism, but it needs (...) to be supplied with additional heuristics to disambiguate between causes and other difference-makers. To achieve this, I suggest employing heuristics based on multiple experiments, temporal order and scientific domain. (shrink)

The first part of this paper reveals a conflict between the core principles of deterministic causation and the standard method of difference, which is widely seen as a correct method of causally analyzing deterministic structures. We show that applying the method of difference to deterministic structures can give rise to causal inferences that contradict the principles of deterministic causation. The second part then locates the source of this conflict in an inference rule implemented in the method of difference according to (...) which factors that can make a difference to investigated effects relative to one particular test setup are to be identified as causes, provided the causal background of the corresponding setup is homogeneous. The paper ends by modifying the method of difference in a way that renders it compatible with the principles of deterministic causation. (shrink)

ABSTRACT Joseph Halpern and Judea Pearl draw upon structural equation models to develop an attractive analysis of ‘actual cause’. Their analysis is designed for the case of deterministic causation. I show that their account can be naturally extended to provide an elegant treatment of probabilistic causation. 1Introduction 2Preemption 3Structural Equation Models 4The Halpern and Pearl Definition of ‘Actual Cause’ 5Preemption Again 6The Probabilistic Case 7Probabilistic Causal Models 8A Proposed Probabilistic Extension of Halpern and Pearl’s Definition 9Twardy and Korb’s Account 10Probabilistic (...) Fizzling 11Conclusion. (shrink)

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)

Two key ideas of scientific explanation−explanation as causal information and explanation as unification-have frequently been set into mutual opposition. This paper proposes a “dialectical solution” to this conflict, by arguing that causal explanations are preferable to non-causal ones, because they lead to a higherdegree of unification at the level of explaining statistical regularities. The core axioms of the theory of causal nets (TC) are justified because they offer the best if not the only unifying explanation of two statistical phenomena: screening (...) off and linking up. Alternative explanations of the two phenomena are discussed and it isshown why they don’t work. It is demonstrated that although the core axioms of TC are empirically vacuous, extended versions of TC have empirical content by means of which they can generate independently testable predictions.Con frecuencia se han planteado como contrapuestas dos ideas clave en la explicacion cientifica (explicacion como informacion causal y explicacion como unificacion). El presente articulo propone una “solucion dialectica” argumentando que las explicaciones causales son preferibles a las no-causales porque aquellas comportan un mayor grado de unificacion en la explicacion de regularidades estadisticas. Los axiomas centrales de la teoria de redes causales (TC) estan justificados porque ofrecen la mejor, si no la unica, explicacion unificada de dos fenomenos estadisticos: neutralizacion (screening off) y vinculacion (linking up). Se discuten las explicaciones alternativas de estos dos fenomenos y se razona por que no funcionan. Se demuestra ademas que aunque los axiomas centrales de TC son empiricamente vacuos, las versiones extendidas de TC tienen un contenido empirico gracias al cual pueden generar predicciones independientemente contrastables. (shrink)

This paper examines Patrick Suppes’ probabilistic theory of causality understood as a theory of causal inference, and draws some lessons for empirical economics and contemporary debates in the foundations of econometrics. It argues that a standard method of empirical economics, multiple regression, is inadequate for most but the simplest applications, that the Bayes’ nets approach, which can be understood as a generalisation of Suppes’ theory, constitutes a considerable improvement but is still subject to important limitations, and that the currently fashionable (...) ‘design-based approach’ suffers from the same flaws Suppes anticipated a long time ago. It then sketches an alternative in response, one that differs drastically from the formalisms Suppes endorsed but is consistent with his pragmatic general take on science. (shrink)

The aim of the paper is to relate Bell’s notion of local causality to the Causal Markov Condition. To this end, first a framework, called local physical theory, will be introduced integrating spatiotemporal and probabilistic entities and the notions of local causality and Markovity will be defined. Then, illustrated in a simple stochastic model, it will be shown how a discrete local physical theory transforms into a Bayesian network and how the Causal Markov Condition arises as a special case of (...) Bell’s local causality and Markovity. (shrink)

What are scientific theories and how should they be represented? In this article, I propose a causal–structural account, according to which scientific theories are to be represented as sets of interrelated causal and credal nets. In contrast with other accounts of scientific theories (such as Sneedian structuralism, Kitcher’s unificationist view, and Darden’s theory of theoretical components), this leaves room for causality to play a substantial role. As a result, an interesting account of explanation is provided, which sheds light on explanatory (...) unification within a causalist framework. The theory of classical genetics is used as a case study. 1 Introduction2 The Theory of Classical Genetics3 Three Philosophical Accounts of the Theory of Classical Genetics3.1 The structuralist account3.2 Kitcher’s unificationism3.3 Darden and theory change in science4 A Common Lacuna: Where is Causality?5 Woodward’s Interventionist Account of Causation6 Causal Bayes Nets and Their Interrelations6.1 Causal Bayes nets6.2 Relations among causal nets6.3 Credal nets and their interrelations7 The Theory of the Gene and its Causal Graph8 A First Exemplar: Stem Length in Pea Plants8.1 Three crosses on stem length in pea plants8.2 The causal graph for stem length in pea plants8.3 Morgan’s explanatory principles and the credal net for stem length in pea plants9 Explaining Mendel’s Crosses: A Causal–Structural Account10 Monohybrid Crosses with Complete Dominance11 Exemplars,Explanatory Patterns, Generic Credal Nets, and Mechanism Schemas12 Incomplete Dominance13 Anomalies14 Multi-hybrid Crosses with Independent Assortment15 Multi-hybrid Crosses with Linkage and Crossing-Over16 Double Crossing-Over and the Linear Order of the Gene17 Causal–Structural Explanation18 Explanatory Unification19 Concluding Remarks. (shrink)

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

The paper pleads for compatibilism by distinguishing the first-person’s normative and the observer’s empirical perspective. In the normative perspective one’s own actions are uncaused and free, in the empirical perspective they are caused and may be predetermined. Still, there is only one notion of causation that is able to account for the relation between the causal conceptions within the two perspectives. The other main idea for explicating free will by explaining free actions or intentions as appropriately caused in a specified (...) way is acknowledged, but not discussed. The paper finally argues that the normative and the empirical perspective are on a par; none is prior; even from within the empirical perspective the normative perspective is ineliminable. (shrink)

There is a tension between, on the one hand, the view that natural selection refers to individual-level causes, and on the other hand, the view that it refers to a population-level cause. In this article, I make the case for the individual-level cause view. I respond to recent claims made by McLoone that the individual-level cause view is inconsistent. I show that if one were to follow his arguments, any causal claim in any context would have to be regarded as (...) vindicating a form of population-level cause view. I show why this is implausible and how a consistent individual-level cause position can be held within the interventionist account of causation. Finally, I argue that there is one sense in which natural selection might be said to refer to population-level causes of evolutionary change. The upshot is that, as noted by others, natural selection can be regarded as referring to a population-level cause in the context of frequency-dependent selection and other situations of fitness-altering interactions between the individuals of a population. But whether this statement is true will depend on the empirical case investigated, not some a priori conceptual distinction. Thus, even though situations of frequency dependence might be ubiquitous, it is orthogonal to the conceptual question of whether frequency-independent natural selection—McLoone’s target—refers to individual- or population-level causes. (shrink)

Back in 1987 the physicist/theoretical biologist Walter Elsasser reviewed a range of philosophical issues at the foundation of organismal biology above the molecular level. Two of these are particularly relevant to quantifications of form: the concept of ordered heterogeneity and the principle of nonstructural memory, the truism that typically the forms of organisms substantially resemble the forms of their ancestors. This essay attempts to weave Elsasser’s principles together with morphometrics for one prominent data type, the representation of animal forms by (...) positions of landmark points. I introduce a new spectrum of pattern descriptors of the shape variation of landmark configurations, ranging from the most homogeneous through growth gradients and focal features to a model of totally disordered heterogeneity incompatible with the rhetoric of functional explanation. An investigation may end up reporting its findings by one of these descriptors or by several. These descriptors all derive from one shared diagrammatic device: a log–log plot of sample variance against one standard formalism of today’s geometric morphometrics, the bending energies of the principal warps that represent all the scales of variability around the sample average shape. The new descriptors, which I demonstrate over a variety of contemporary morphometric examples, may help build the bridge we urgently need between the arithmetic of today’s burgeoning image-based data resources and the rhetoric of biological explanations aligned with the principles of Elsasser along with an even earlier philosopher of biology, the Viennese visionary Hans Przibram. (shrink)

Identifying causal relations from correlational data is a fundamental challenge in personality psychology. In most cases, random assignment is not feasible, leaving observational studies as the primary methodological tool. Here, we document several techniques from behavior genetics that attempt to demonstrate causality. Although no one method is conclusive at ruling out all possible confounds, combining techniques can triangulate on causal relations. Behavior genetic tools leverage information gained by sampling pairs of individuals with assumed genetic and environmental relatedness or by measuring (...) genetic variants in unrelated individuals. These designs can find evidence consistent with causality, while simultaneously providing strong controls against common confounds. We conclude by discussing several potential problems that may limit the utility of these techniques when applied to personality. Ultimately, genetically informative designs can aid in drawing causal conclusions from correlational studies. (shrink)

Hitchcock demonstrated that the validity of causal exclusion arguments as well as the plausibility of several of their premises hinges on the specific theory of causation endorsed. In this paper I show that the validity of causal exclusion arguments—if represented within the theory of causal Bayes nets the way Gebharter suggests—actually requires much weaker premises than the ones which are typically assumed. In particular, neither completeness of the physical domain nor the no overdetermination assumption are required.

:The most basic question one can ask of a model is ‘What is the effect on variable y2 of variable y1?’ Causation is ‘implementation neutral’ when all interventions on external variables that lead to a given change in y1 have the same effect on y2, so that the effect of y1 on y2 is defined unambiguously. Familiar ideas of causal analysis do not apply when causation is implementation neutral. For example, a cause variable cannot be linked to an effect variable (...) by both a direct path and a distinct indirect path. Discussion of empirical aspects of implementation neutrality leads to further unexpected results, such as that if one variable causes another the coefficient representing that causal link is always identified. (shrink)

The ability to learn the direction of causal relations is critical for understanding and acting in the world. We investigated how children learn causal directionality in situations in which the states of variables are temporally dependent (i.e., autocorrelated). In Experiment 1, children learned about causal direction by comparing the states of one variable before versus after an intervention on another variable. In Experiment 2, children reliably inferred causal directionality merely from observing how two variables change over time; they interpreted Y (...) changing without a change in X as evidence that Y does not influence X. Both of these strategies make sense if one believes the variables to be temporally dependent. We discuss the implications of these results for interpreting previous findings. More broadly, given that many real-world environments are characterized by temporal dependency, these results suggest strategies that children may use to learn the causal structure of their environments. (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)

Several authors have claimed that mechanisms play a vital role in distinguishing between causation and mere correlation in the social sciences. Such claims are sometimes interpreted to mean that without mechanisms, causal inference in social science is impossible. The author agrees with critics of this proposition but explains how the account of how mechanisms aid causal inference can be interpreted in a way that does not depend on it. Nevertheless, he shows that this more charitable version of the account is (...) still unsuccessful as it stands. Consequently, he advances a proposal for shoring up the account, which is founded on the possibility of acquiring knowledge of social mechanisms by linking together norms or practices found in a society. Key Words: causality • social mechanisms • interpretation • anthropology. (shrink)

Scientific conflicts often stem from differences in the conceptual framework through which scientists view and understand their own field. In this chapter, I analyze the ontological and methodological assumptions of three traditions in evolutionary biology, namely, Ernst Mayr’s population thinking, the gene-centered view of the Modern Syn thesis, and the Extended Evolutionary Synthesis. Each of these frameworks presupposes a different account of "evolutionary causes," and this discrepancy prevents mutual understanding and objective evaluation in the recent contention surrounding the EES. From (...) this perspective, the chapter characterizes the EES research program as an attempt to introduce causal structures beyond genes as additional units of evolution, and compares its research methodology and objectives with those of the traditional MS framework. (shrink)

These preprints were automatically compiled into a PDF from the collection of papers deposited in PhilSci-Archive in conjunction with the PSA 2012.

In "The Comparative Method" Ragin (1987) has outlined a procedure of Boolean causal reasoning operating on pure coincidence data that has meanwhile become widely known as QCA (Qualitative Comparative Analysis) among social scientists. QCA -- also in its recent form as presented in Ragin (2000) -- is designed to analyze causal structures featuring one effect and a possibly complex configuration of mutually independent direct causes of that effect. The paper at hand presents a procedure of causal reasoning that operates on (...) the same type of empirical data as QCA and that implements Boolean techniques related to the ones resorted to by QCA, yet, in contrast to QCA, the procedure introduced here successfully identifies causal structures involving both mutually dependent causes, i.e. causal chains, and multiple effects, i.e. epiphenomena. In this sense, the paper at hand generalizes QCA. (shrink)

Hans Reichenbach is well known for his limiting frequency view of probability, with his most thorough account given in The Theory of Probability in 1935/1949. Perhaps less known are Reichenbach's early views on probability and its epistemology. In his doctoral thesis from 1915, Reichenbach espouses a Kantian view of probability, where the convergence limit of an empirical frequency distribution is guaranteed to exist thanks to the synthetic a priori principle of lawful distribution. Reichenbach claims to have given a purely objective (...) account of probability, while integrating the concept into a more general philosophical and epistemological framework. A brief synopsis of Reichenbach's thesis and a critical analysis of the problematic steps of his argument will show that the roots of many of his most influential insights on probability and causality can be found in this early work. (shrink)

Though common sense says that causes must temporally precede their effects, the hugely influential interventionist account of causation makes no reference to temporal precedence. Does common sense lead us astray? In this paper, I evaluate the power of the commonsense assumption from within the interventionist approach to causal modeling. I first argue that if causes temporally precede their effects, then one need not consider the outcomes of interventions in order to infer causal relevance, and that one can instead use temporal (...) and probabilistic information to infer exactly when X is causally relevant to Y in each of the senses captured by Woodward’s interventionist treatment. Then, I consider the upshot of these findings for causal decision theory, and argue that the commonsense assumption is especially powerful when an agent seeks to determine whether so-called “dominance reasoning” is applicable. (shrink)

This paper addresses a problem that arises when it comes to inferring deterministic causal chains from pertinent empirical data. It will be shown that to every deterministic chain there exists an empirically equivalent common cause structure. Thus, our overall conviction that deterministic chains are one of the most ubiquitous (macroscopic) causal structures is underdetermined by empirical data. It will be argued that even though the chain and its associated common cause model are empirically equivalent there exists an important asymmetry between (...) the two models with respect to model expansions. This asymmetry might constitute a basis on which to disambiguate corresponding causal inferences on non-empirical grounds. (shrink)

These preprints were automatically compiled into a PDF from the collection of papers deposited in PhilSci-Archive in conjunction with the PSA 2018.

Humans excel in categorization. Yet from a computational standpoint, learning a novel probabilistic classification task involves severe computational challenges. The present paper investigates one way to address these challenges: assuming class-conditional independence of features. This feature independence assumption simplifies the inference problem, allows for informed inferences about novel feature combinations, and performs robustly across different statistical environments. We designed a new Bayesian classification learning model that incorporates varying degrees of prior belief in class-conditional independence, learns whether or not independence holds, (...) and adapts its behavior accordingly. Theoretical results from two simulation studies demonstrate that classification behavior can appear to start simple, yet adapt effectively to unexpected task structures. Two experiments—designed using optimal experimental design principles—were conducted with human learners. Classification decisions of the majority of participants were best accounted for by a version of the model with very high initial prior belief in class-conditional independence, before adapting to the true environmental structure. Class-conditional independence may be a strong and useful default assumption in category learning tasks. (shrink)

The authors challenge the reigning “causal power framework” as an explanation for whether a particular outcome was actually caused by a specific potential cause. They test a new measure of causal attribution in two experiments by embedding the measure within the Structure Induction model of Singular Causation (SISC, Stephan & Waldmann, 2016).