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

In this article we set out to understand the significance of the process matrix formalism and the quantum causal modelling programme for ongoing disputes about the role of causation in fundamental physics. We argue that the process matrix programme has correctly identified a notion of ‘causal order’ which plays an important role in fundamental physics, but this notion is weaker than the common-sense conception of causation because it does not involve asymmetry. We argue that causal order plays (...) an important role in grounding more familiar causal phenomena. Then we apply these conclusions to the causal modelling programme within quantum foundations, arguing that since no-signalling quantum correlations cannot exhibit causal order, they should not be analysed using classical causal models. This resolves an open question about how to interpret fine-tuning in classical causal models of no-signalling correlations. Finally we observe that a quantum generalization of causal modelling can play a similar functional role to standard causal reasoning, but we emphasize that this functional characterisation does not entail that quantum causal models offer novel explanations of quantum processes. (shrink)

This paper brings together Thompson's naive action explanation with interventionist modeling of causal structure to show how they work together to produce causal models that go beyond current modeling capabilities, when applied to specifically selected systems. By deploying well-justified assumptions about rationalization, we can strengthen existing causal modeling techniques' inferential power in cases where we take ourselves to be modeling causal systems that also involve actions. The internal connection between means and end (...) exhibited in naive action explanation has a modal strength like that of distinctively mathematical explanation, rather than that of causal explanation. Because it is stronger than causation, it can be treated as if it were merely causal in a causal model without thereby overextending the justification it can provide for inferences. This chapter introduces and demonstrate the usage of the Rationalization condition in causal modeling, where it is apt for the system(s) being modeled, and to provide the basics for incorporating R variables into systems of variables and R arrows into DAGs. Use of the Rationalization condition supplements causal analysis with action analysis where it is apt. (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)

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)

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

Causal models provide a framework for precisely representing complex causal structures, where specific models can be used to efficiently predict, infer, and explain the world. At the same time, we often do not know the full causal structure a priori and so must learn it from data using a causal model search algorithm. This chapter provides a general overview of causal models and their uses, with a particular focus on causal graphical models (the most (...) commonly used causal modeling framework) and methods for learning such models from observational and experimental data. The chapter concludes with two examples of productive causal search and modeling in experimental philosophy. (shrink)

Causal Modeling Semantics (CMS, e.g., Galles and Pearl 1998; Pearl 2000; Halpern 2000) is a powerful framework for evaluating counterfactuals whose antecedent is a conjunction of atomic formulas. We extend CMS to an evaluation of the probability of counterfactuals with disjunctive antecedents, and more generally, to counterfactuals whose antecedent is an arbitrary Boolean combination of atomic formulas. Our main idea is to assign a probability to a counterfactual (A ∨ B) € C at a causal model M (...) as a weighted average of the probability of C in those submodels that truthmake A ∨ B (Briggs 2012; Fine 2016, 2017). The weights of the submodels are given by the inverse distance to the original model M, based on a distance metric proposed by Eva, Stern, and Hartmann (2019). Apart from solving a major problem in the epistemology of counterfactuals, our paper shows how work in semantics, causal inference and formal epistemology can be fruitfully combined. (shrink)

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

An important question for the causal modeling approach is how to integrate non‐causal dependence relations such as asymmetric supervenience into the approach. The most prominent proposal to that effect (due to Gebharter) is to treat those dependence relationships as formally analogous to causal relationships. We argue that this proposal neglects some crucial differences between causal and non‐causal dependencies, and that in the context of causal modeling non‐causal dependence relationships should be represented (...) as mutual dependence relationships. We develop a new kind of model – “hybrid models” ‐ based on this suggestion, and formulate a set of axioms for those models. Our formalism has important implications for Kim's exclusion problem: whereas Gebharter's framework vindicates Kim's causal exclusion objection against nonreductive physicalism, our framework has no such implication, and can help non‐reductive physicalists vindicate the efficacy of high‐level properties. A further benefit of our formalism is that it yields a natural and plausible way of thinking about interventions in multi‐level contexts. (shrink)

Brandon claims that to explain adaptation one must specify fitnesses in each selective environment and specify the distribution of individuals across selective environments. Glymour claims, using an example of the adaptive evolution of costly plasticity in a symmetric environment, that there are some predictive or explanatory tasks for which Brandon’s claim is limited. In this paper, I provide necessary conditions for carrying out Brandon’s task, produce a new version of the argument for his claim, and show that Glymour’s reasons for (...) making his claim are problematic. I provide a few interpretations of Glymour’s argument but ultimately raise worries for what I take to be the key premises. (shrink)

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

Some cases show that counterfactual conditionals (‘counterfactuals’ for short) are inherently ambiguous, equivocating between forward-tracking and backtracking counterfactu- als. Elsewhere, I have proposed a causal modeling semantics, which takes this phenomenon to be generated by two kinds of causal manipulations. (Lee 2015; Lee 2016) In an important paper (Hiddleston 2005), Eric Hiddleston offers a different causal modeling semantics, which he claims to be able to explain away the inherent ambiguity of counterfactuals. In this paper, I (...) discuss these two semantic treatments and argue that my (bifurcated) semantics is theoretically more promising than Hiddleston’s (unified) semantics. (shrink)

Philosophers have long analyzed the truth-condition of counterfactual conditionals in terms of the possible-worlds semantics advanced by Lewis [13] and Stalnaker [23]. In this paper, I argue that, from the perspective of philosophical semantics, the causal modeling semantics proposed by Pearl [17] and others (e.g., Briggs [3]) is more plausible than the Lewis-Stalnaker possible-worlds semantics. I offer two reasons. First, the possible-worlds semantics has suffered from a specific type of counterexamples. While the causal modeling semantics can (...) handle such examples with ease, the only way for the possible-worlds semantics to do so seems to cost it its distinctive status as a philosophical semantics. Second, the causal modeling semantics, but not the possible-worlds semantics, has the resources enough for accounting for both forward-tracking and backtracking counterfactual conditionals. (shrink)

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)

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

Mechanist philosophers have examined several strategies scientists use for discovering causal mechanisms in neuroscience. Findings about the anatomical organization of the brain play a central role in several such strategies. Little attention has been paid, however, to the use of network analysis and causal modeling techniques for mechanism discovery. In particular, mechanist philosophers have not explored whether and how these strategies incorporate information about the anatomical organization of the brain. This paper clarifies these issues in the light (...) of the distinction between structural, functional and effective connectivity. Specifically, we examine two quantitative strategies currently used for causal discovery from functional neuroimaging data: dynamic causal modeling and probabilistic graphical modeling. We show that dynamic causal modeling uses findings about the brain’s anatomical organization to improve the statistical estimation of parameters in an already specified causal model of the target brain mechanism. Probabilistic graphical modeling, in contrast, makes no appeal to the brain’s anatomical organization, but lays bare the conditions under which correlational data suffice to license reliable inferences about the causal organization of a target brain mechanism. The question of whether findings about the anatomical organization of the brain can and should constrain the inference of causal networks remains open, but we show how the tools supplied by graphical modeling methods help to address it. (shrink)

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

We construct a causal-modeling semantics for both indicative and counterfactual conditionals. As regards counterfactuals, we adopt the orthodox view that a counterfactual conditional is true in a causal model M just in case its consequent is true in the submodel M∗, generated by intervening in M, in which its antecedent is true. We supplement the orthodox semantics by introducing a new manipulation called extrapolation. We argue that an indicative conditional is true in a causal model M (...) just in case its con- sequent is true in certain submodels M∗, generated by extrapolating M, in which its antecedent is true. We show that the proposed semantics can account for some important minimal pairs nicely and naturally. We also prove a theorem showing under what conditions intervention and extrapolation will yield the same result, and thus explain how counterfactual and indicative conditionals would behave in a causal-modeling semantics. (shrink)

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

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)

Charles Peirce, Mikhail Bakhtin and Thomas Sebeok all develop original research itineraries around the sign and, despite terminological differences, canbe related with reference to the concept of dialogism and modelling. Jakob von Uexküll’s biosemiosic “functional cycle”, a model for semiosic processes, is alsoimplied in the relation between dialogue and communication.Biological models which describe communication as a self-referential, autopoietic and semiotically closed system (e.g., the models proposed by Maturana,Varela, and Thure von Uexküll) contrast with both the linear (Shannon and Weaver) and (...) the circular (Saussure) paradigms. The theory of autopoietic systems is only incompatible with dialogism if reference is to a linear causal model which describes communication as developing from source to destination, or to the conversation model governed by the turning around together rule. Dialogism understood in biosemiotic terms overlaps with the concepts of interconnectivity,interrelation, intercorporeity and presupposes the otherness relation.As Uexküll says, the relation with the umwelt in nonhuman living beings is stable and concerns the species; on the contrary, in human beings it is, changeableand concerns the single individual, which is at once an advantage and a disadvantage. Thanks to “syntactics”, human beings can construct, deconstruct and reconstruct an infinite number of worlds from a finite number of elements. This distinguishes human beings from other animals and determines their capacity for posing problems and asking questions. The human being not only produces his or her own world, but can also endanger it, and even destroy it to the point of causing the extinction of all other life forms on Earth. The unique capacity for reflection on signs makes human beings responsible for life across the planet, both human and nonhuman. Such reflections shift semiotic research in the direction of semioethics. (shrink)

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

I argue against counterfactual theories of causation , develop a pragmatic version of the Covering Law view, and offer a causal theory of counterfactuals. ;The initial idea of CTCs is that event a causes event b if b would not have occurred, if a had not occurred. David Lewis proposes this view as a solution to problems of "effects" and "epiphenomena". I argue that CTCs cannot solve these problems. Covering Law theories can, but only by rejecting traditional Humean accounts (...) of laws. ;Following Nancy Cartwright , I argue that there is no a priori route from probabilistic association to causal relevance, and that distinguishing causal relevance from mere association requires further causal knowledge. Some recent literature on causal modelling is also examined. ;Much causal knowledge concerns rough, approximate ceteris paribus laws and generalizations. I examine these and argue that they involve important pragmatic components. ;Many aspects of intuitive causal judgment and reasoning are explained by ceteris paribus causes. For example, many causes are preventable, and only ceteris paribus causes could be prevented. Ceteris paribus causes are capacities, which make similar contributions to different circumstances, and interact with each other . The pragmatic features of ceteris paribus laws hold equally of ceteris paribus causes. ;Singular and generic causes are unified by appeal to the a posteriori impossibility of "action at a distance". The locality of causal relations requires that causes act by continuous intervening processes. Singular causes and effects are instances of generic causal process types. ;Numerous cases of unclear and conflicting intuitions about causes and effects are explained by contextual factors . ;I explain away the attraction of CTCs by offering a causal account of counterfactuals. It is natural to express causal facts using counterfactuals because the truth conditions of counterfactuals are direct consequences of causal facts. (shrink)

A shared problem across the sciences is to make sense of correlational data coming from observations and/or from experiments. Arguably, this means establishing when correlations are causal and when they are not. This is an old problem in philosophy. This paper, narrowing down the scope to quantitative causal analysis in social science, reformulates the problem in terms of the validity of statistical models. Two strategies to make sense of correlational data are presented: first, a 'structural strategy', the goal (...) of which is to model and test causal structures that explain correlational data; second, a 'manipulationist or interventionist strategy', that hinges upon the notion of invariance under intervention. It is argued that while the former can offer a solution the latter cannot. (shrink)

ABSTRACT Contrastive and deviant/default accounts of causation are becoming increasingly common. However, discussions of these accounts have neglected important questions, including how the context determines the contrasts, and what shared knowledge is necessary for this to be possible. I address these questions, using organic chemistry as a case study. Focusing on one example—nucleophilic substitution—I show that the kinds of causal claims that can be made about an organic reaction depend on how the reaction is modelled, and argue that paying (...) attention to the various ways that reactions are modelled has important implications for our understanding of causation. _1_ Introduction _2_ General Contrastive Causal Claims in Organic Chemistry _3_ Deviant Causal Claims in Organic Chemistry _4_ Nucleophilic Substitution Reactions _5_ The Causal Modelling Tradition _5.1_ The type/token distinction _6_ Competing Reactions _6.1_ Type- and token-causal claims, variables, and values of variables _7_ Disambiguation of ‘Reaction’ _8_ Reaction Kinds _9_ Specific Reactions _9.1_ Specific reactions and token-causal claims _9.2_ Specific reactions and type-causal claims _10_ Implications _10.1_ Kinds of causal claim _10.2_ Contrastive and deviant causal claims _10.3_ Model relativity. (shrink)

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

This paper deals with causal analysis in the social sciences. We first present a conceptual framework according to which causal analysis is based on a rationale of variation and invariance, and not only on regularity. We then develop a formal framework for causal analysis by means of structural modelling. Within this framework we approach causality in terms of exogeneity in a structural conditional model based which is based on (i) congruence with background knowledge, (ii) invariance under a (...) large variety of environmental changes, and (iii) model fit. We also tackle the issue of confounding and show how latent confounders can play havoc with exogeneity. This framework avoids making untestable metaphysical claims about causal relations and yet remains useful for cognitive and action-oriented goals. (shrink)

Aging is accompanied by stereotyped changes in functional brain activations, for example a cortical shift in activity patterns from posterior to anterior regions is one hallmark revealed by functional magnetic resonance imaging (fMRI) of aging cognition. Whether these neuronal effects of aging could potentially contribute to an amelioration of or resistance to the cognitive symptoms associated with psychopathology remains to be explored. We used a visual illusion paradigm to address whether aging affects the cortical control of perceptual beliefs and biases. (...) Our aim was to understand the effective connectivity associated with volitional control of ambiguous visual stimuli and to test whether greater top-down control of early visual networks emerged with advancing age. Using a bias training paradigm for ambiguous images we found that older participants (n = 16) resisted experimenter-induced visual bias compared to a younger cohort (n = 14) and that this resistance was associated with greater activity in prefrontal and temporal cortices. By applying Dynamic Causal Models for fMRI we uncovered a selective recruitment of top-down connections from the middle temporal to Lingual gyrus (LIN) by the older cohort during the perceptual switch decision following bias training. In contrast, our younger cohort did not exhibit any consistent connectivity effects but instead showed a loss of driving inputs to orbitofrontal sources following training. These findings suggest that perceptual beliefs are more readily controlled by top-down strategies in older adults and introduce age-dependent neural mechanisms that may be important for understanding aberrant belief states associated with psychopathology. (shrink)

Recently, there has been a large amount of support for the idea that causal claims can be sensitive to normative considerations. Previous work has focused on the concept of actual causation, defending the claim that whether or not some token event c is a cause of another token event e is influenced by both statistical and prescriptive norms. I focus on the policy debate surrounding alternative energies, and use the causal modelling framework to show that in this context, (...) people’s normative commitments don’t just affect the causal claims they are willing to endorse, but also their understanding of the causal structure. In the context of the alternative energy debate, normative considerations affect our understanding of the causal structure by influencing our judgements about which variables should be held fixed, and therefore which variables should be relegated to the background of a causal model. In cases of extreme disagreement, normative commitments can also affect which causal structure we think should be instantiated. Thus, focusing on a new context has revealed a previously unexplored sense in which normative factors are incorporated into causal reasoning. (shrink)

The Lotka–Volterra predator-prey-model is a widely known example of model-based science. Here we reexamine Vito Volterra’s and Umberto D’Ancona’s original publications on the model, and in particular their methodological reflections. On this basis we develop several ideas pertaining to the philosophical debate on the scientific practice of modeling. First, we show that Volterra and D’Ancona chose modeling because the problem in hand could not be approached by more direct methods such as causal inference. This suggests a philosophically (...) insightful motivation for choosing the strategy of modeling. Second, we show that the development of the model follows a trajectory from a “how possibly” to a “how actually” model. We discuss how and to what extent Volterra and D’Ancona were able to advance their model along that trajectory. It turns out they were unable to establish that their model was fully applicable to any system. Third, we consider another instance of model-based science: Darwin’s model of the origin and distribution of coral atolls in the Pacific Ocean. Darwin argued more successfully that his model faithfully represents the causal structure of the target system, and hence that it is a “how actually” model. (shrink)

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

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

Causal Bayes nets (CBNs) provide one of the most powerful tools for modelling coarse-grained type-level causal structure. As in other fields (e.g., thermodynamics) the question arises how such coarse-grained characterisations are related to the characterisation of their underlying structure (in this case: token-level causal relations). Answering this question meets what is called a “coherence-requirement” in the reduction debate: How are different accounts of one and the same system (or kind of system) related to each other. We argue (...) that CBNs as tools for type-level causal inference are abstract enough to roughly fit any current token-level theory of causation as long as certain modelling assumptions are satisfied, but accounts of actual causation, i.e. accounts that attempt to infer token-causation based on CBNs, for the very same reason, face certain limitations. (shrink)

In recent decades, economists have developed methods for measuring the country-wide level of inequality of opportunity. The most popular method, called the ex-ante method, uses data on the distribution of outcomes stratified by groups of individuals with the same circumstances, in order to estimate the part of outcome inequality that is due to these circumstances. I argue that these methods are potentially biased, both upwards and downwards, and that the unknown size of this bias could be large. To argue that (...) the methods are biased, I show that they ought to measure causal or counterfactual quantities, while the methods are only capable of identifying correlational information. To argue that the bias is potentially large, I illustrate how the causal complexity of the real world leads to numerous non-causal correlations between circumstances and outcomes and respond to objections claiming that such correlations are nonetheless indicators of unfair disadvantage, that is, inequality of opportunity. (shrink)

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

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

Psychiatric researchers typically assume that the modelling of psychiatric symptoms is not influenced by psychiatric categories; symptoms are modelled and then grouped into a psychiatric category. I highlight this primarily through analysing research domain criteria. RDoC’s importance makes it worth scrutinizing, and this assessment also serves as a case study with relevance for other areas of psychiatry. RDoC takes inadequacies of existing psychiatric categories as holding back causal investigation. Consequently, RDoC aims to circumnavigate existing psychiatric categories by directly investigating (...) the causal basis of symptoms. The unique methodological approach of RDoC exploits the supposed lack of influence of psychiatric categories on symptom modelling, taking psychiatric symptoms as the same regardless of which psychiatric category is employed or if no psychiatric category is employed. But this supposition is not always true. I will show how psychiatric categories can influence symptom modelling, whereby identical behaviours can be considered as different symptoms based on an individual’s psychiatric diagnosis. If the modelling of symptoms is influenced by psychiatric categories, then psychiatric categories will still play a role, a situation which RDoC researchers explicitly aim to avoid. I discuss four ways RDoC could address this issue. This issue also has important implications for factor analysis, cluster analysis, modifying psychiatric categories, and symptom based approaches. (shrink)