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)

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)

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.

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.

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)