Within the causal modeling literature, debates about the Causal Faithfulness Condition have concerned whether it is probable that the parameters in causal models will have values such that distinct causal paths will cancel. As the parameters in a model are fixed by the probability distribution over its variables, it is initially puzzling what it means to assign probabilities to these parameters. I propose that to assign a probability to a parameter in a model is to treat that parameter as a (...) function of a variable in an augmented model. By combining this proposal with widely adopted principles regarding which variables must be included in a model, I argue that the various proposed counterexamples to CFC involving coordinated parameters are not genuine counterexamples. I then consider the cases in which CFC fails due not to coordination, but by coincidence, and propose explanatory and predictive bases for ruling out such coincidences without presuming that they are improbable. The aim of the proposed defenses is not to show that CFC never fails, but rather to argue that its use in a particular context may be defended using general modeling assumptions rather than by relying on claims about how often it fails. (shrink)

A common strategy for simplifying complex systems involves partitioning them into subsystems whose behaviors are roughly independent of one another at shorter timescales. Dynamic causal models clarify how doing so reveals a system’s nonequilibrium causal relationships. Here I use these models to elucidate the idealizations and abstractions involved in representing a system at a timescale. The models reveal that key features of causal representations—such as which variables are exogenous—may vary with the timescale at which a system is considered. This has (...) implications for debates regarding which systems can be represented causally. (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)

In their 2010 book, Biology’s First Law, D. McShea and R. Brandon present a principle that they call ‘‘ZFEL,’’ the zero force evolutionary law. ZFEL says (roughly) that when there are no evolutionary forces acting on a population, the population’s complexity (i.e., how diverse its member organisms are) will increase. Here we develop criticisms of ZFEL and describe a different law of evolution; it says that diversity and complexity do not change when there are no evolutionary causes.

A cause may influence its effect via multiple paths. Paradigmatically (Hesslow [1974]), taking birth control pills both decreases one’s risk of thrombosis by preventing pregnancy and increases it by producing a blood chemical. Building on Pearl ([2001]), I explicate the notion of a path-specific effect. Roughly, a path-specific effect of C on E via path P is the degree to which a change in C would change E were they to be transmitted only via P. Facts about such effects may (...) be gleaned from the structural equations commonly used to represent the causal relationships among variables. I contrast my analysis of the Hesslow case with those given by theorists of probabilistic causality, who mistakenly link it to issues of causal heterogeneity, token-causation and indeterminism. The reason probabilistic theories misdiagnose this case is that they pay inadequate attention to the structural relationships among variables. (shrink)

Markus (2021) argues that the causal modelling frameworks of Pearl and Rubin are not ‘strongly equivalent’, in the sense of saying ‘the same thing in different ways’. Here I rebut Markus’ arguments against strong equivalence. The differences between the frameworks are best illuminated not by appeal to their causal semantics, but rather reflect pragmatic modelling choices.

Discussions of the causal status of race focus on the question of whether race itself can be experimentally manipulated. Yet many experiments testing for racial discrimination do not manipulate race, but rather a signal by which race influences an outcome. Such signal manipulations are easily formalized, though contexts of discrimination introduce significant philosophical complications. Whether a signal counts as a signal for race is not merely a causal question, but depends on sociological and normative issues regarding discrimination. The notion of (...) signal manipulation enables one to take these issues into account while still using causal counterfactual tests to detect discrimination. The analysis provided here is compatible with social constructivism and helps differentiate between cases in which it is more or less fruitful to model race causally. (shrink)

Some recent accounts of constitutive relevance have identified mechanism components with entities that are causal intermediaries between the input and output of a mechanism. I argue that on such accounts there is no distinctive inter-level form of mechanistic explanation and that this highlights an absence in the literature of a compelling argument that there are such explanations. Nevertheless, the entities that these accounts call ‘components’ do play an explanatory role. Studying causal intermediaries linking variables Xand Y provides knowledge of the (...) counterfactual conditions under which X will continue to bring about Y. This explanatory role does not depend on whether intermediate variables count as components. The question of whether there are distinctively mechanistic explanations remains open. (shrink)

Dynamical models of cognition have played a central role in recent cognitive science. In this paper, we consider a common strategy by which dynamical models describe their target systems neither as purely static nor as purely dynamic, but rather using a hybrid approach. This hybridity reveals how dynamical models involve representational choices that are important for understanding the relationship between dynamical and non-dynamical representations of a system.

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.

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)

In a recent paper, Brandon and Nijhout argue against genic selectionism—the thesis, roughly, that evolutionary processes are best understood from the gene’s-eye point of view—by presenting a case in which genic models of selection allegedly make predictions that conflict with the (correct) predictions of higher-level genotypic selection models. Their argument, if successful, would refute the widely held belief that genic models and higher-level models are predictively equivalent. Here, I argue that Brandon and Nijhout fail to demonstrate that the models make (...) incompatible predictions. (shrink)

Some recent accounts of constitutive relevance have identified mechanism components with entities that are causal intermediaries between the input and output of a mechanism. I argue that on such accounts there is no distinctive inter-level form of mechanistic explanation and that this highlights an absence in the literature of a compelling argument that there are such explanations. Nevertheless, the entities that these accounts call ‘components’ do play an explanatory role. Studying causal intermediaries linking variables Xand Y provides knowledge of the (...) counterfactual conditions under which X will continue to bring about Y. This explanatory role does not depend on whether intermediate variables count as components. The question of whether there are distinctively mechanistic explanations remains open. (shrink)

Causal representations are distinguished from non-causal ones by their ability to predict the results of interventions. This widely-accepted view suggests the following adequacy condition for causal models: a causal model is adequate only if it does not contain variables regarding which it makes systematically false predictions about the results of interventions. Here I argue that this condition should be rejected. For a class of equilibrium systems, there will be two incompatible causal models depending on whether one intervenes upon a certain (...) variable to fix its value, or ‘lets go’ of the variable and allows it to vary. The latter model will fail to predict the result of interventions on the let-go-of variable. I argue that there is no basis for preferring one of these models to the other, and thus that models failing to predict interventions on particular variables can be just as adequate as those making no such false predictions. This undermines a key argument (Dash in Caveats for causal reasoning with equilibrium models. University of Pittsburgh. PhD thesis, 2003) against relying upon causal models inferred from equilibrium data. (shrink)

Erratum to: Synthese 191:1925–1930 DOI:10.1007/s11229-013-0380-3 The authors were unaware that points in their article appeared in “Caveats for Causal Reasoning with Equilibrium Models,” by Denver Dash and Marek Druzdzel, published in S. Benferhat and P. Besnard : European Conferences on Symbolic and Quantitative Approaches to Reasoning with Uncertainty 2001, Lecture Notes in Artificial Intelligence 2143, pp. 192–203. The authors were unaware of this essay and would like to apologize to the authors for failing to cite their excellent work.

Causal representations are distinguished from non-causal ones by their ability to predict the results of interventions. This widely-accepted view suggests the following adequacy condition for causal models: a causal model is adequate only if it does not contain variables regarding which it makes systematically false predictions about the results of interventions. Here I argue that this condition should be rejected. For a class of equilibrium systems, there will be two incompatible causal models depending on whether one intervenes upon a certain (...) variable to fix its value, or ‘lets go’ of the variable and allows it to vary. The latter model will fail to predict the result of interventions on the let-go-of variable. I argue that there is no basis for preferring one of these models to the other, and thus that models failing to predict interventions on particular variables can be just as adequate as those making no such false predictions. This undermines a key argument against relying upon causal models inferred from equilibrium data. (shrink)