Explanations in the life sciences frequently involve presenting a model of the mechanism taken to be responsible for a given phenomenon. Such explanations depart in numerous ways from nomological explanations commonly presented in philosophy of science. This paper focuses on three sorts of differences. First, scientists who develop mechanistic explanations are not limited to linguistic representations and logical inference; they frequently employ diagrams to characterize mechanisms and simulations to reason about them. Thus, the epistemic resources for presenting mechanistic explanations are (...) considerably richer than those suggested by a nomological framework. Second, the fact that mechanisms involve organized systems of component parts and operations provides direction to both the discovery and testing of mechanistic explanations. Finally, models of mechanisms are developed for specific exemplars and are not represented in terms of universally quantified statements. Generalization involves investigating both the similarity of new exemplars to those already studied and the variations between them. (shrink)

Even if one can experiment on relevant factors, learning the causal structure of a dynamical system can be quite difficult if the relevant measurement processes occur at a much slower sampling rate than the “true” underlying dynamics. This problem is exacerbated if the degree of mismatch is unknown. This paper gives a formal characterization of this learning problem, and then provides two sets of results. First, we prove a set of theorems characterizing how causal structures change under undersampling. Second, we (...) develop an algorithm for inferring aspects of the causal structure at the “true” timescale from the causal structure learned from the undersampled data. Research on causal learning in dynamical contexts has largely ignored the challenges of undersampling, but this paper provides a framework and foundation for learning causal structure from this type of complex time series data. (shrink)

Using Gebharter’s representation, we consider aspects of the problem of discovering the structure of unmeasured submechanisms when the variables in those submechanisms have not been measured. Exploiting an early insight of Sober’s, we provide a correct algorithm for identifying latent, endogenous structure—submechanisms—for a restricted class of structures. The algorithm can be merged with other methods for discovering causal relations among unmeasured variables, and feedback relations between measured variables and unobserved causes can sometimes be learned.

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)

We start this paper by arguing that causality should, in analogy with force in Newtonian physics, be understood as a theoretical concept that is not explicated by a single definition, but by the axioms of a theory. Such an understanding of causality implicitly underlies the well-known theory of causal nets and has been explicitly promoted by Glymour. In this paper we investigate the explanatory warrant and empirical content of TCN. We sketch how the assumption of directed cause–effect relations can be (...) philosophically justified by an inference to the best explanation. We then ask whether the explanations provided by TCN are merely post-facto or have independently testable empirical content. To answer this question we develop a fine-grained axiomatization of TCN, including a distinction of different kinds of faithfulness. A number of theorems show that although the core axioms of TCN are empirically empty, extended versions of TCN have successively increasing empirical content. (shrink)

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

The concept of mechanism is analyzed in terms of entities and activities, organized such that they are productive of regular changes. Examples show how mechanisms work in neurobiology and molecular biology. Thinking in terms of mechanisms provides a new framework for addressing many traditional philosophical issues: causality, laws, explanation, reduction, and scientific change.

In this paper I offer an analysis of causation based upon a theory of mechanisms-complex systems whose internal parts interact to produce a system's external behavior. I argue that all but the fundamental laws of physics can be explained by reference to mechanisms. Mechanisms provide an epistemologically unproblematic way to explain the necessity which is often taken to distinguish laws from other generalizations. This account of necessity leads to a theory of causation according to which events are causally related when (...) there is a mechanism that connects them. I present reasons why the lack of an account of fundamental physical causation does not undermine the mechanical account. (shrink)

In this article I tackle the question of how the hierarchical order of mechanisms can be represented within a causal graph framework. I illustrate an answer to this question proposed by Casini, Illari, Russo, and Williamson and provide an example that their formalism does not support two important features of nested mechanisms: (i) a mechanism’s submechanisms are typically causally interacting with other parts of said mechanism, and (ii) intervening in some of a mechanism’s parts should have some influence on the (...) phenomena the mechanism brings about. Finally, I sketch an alternative approach taking (i) and (ii) into account. (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)

The Recursive Bayesian Net formalism was originally developed for modelling nested causal relationships. In this paper we argue that the formalism can also be applied to modelling the hierarchical structure of mechanisms. The resulting network contains quantitative information about probabilities, as well as qualitative information about mechanistic structure and causal relations. Since information about probabilities, mechanisms and causal relations is vital for prediction, explanation and control respectively, an RBN can be applied to all these tasks. We show in particular how (...) a simple two-level RBN can be used to model a mechanism in cancer science. The higher level of our model contains variables at the clinical level, while the lower level maps the structure of the cell's mechanism for apoptosis. (shrink)

Mechanisms are usually viewed as inherently hierarchical, with lower levels of a mechanism influencing, and decomposing, its higher-level behaviour. In order to adequately draw quantitative predictions from a model of a mechanism, the model needs to capture this hierarchical aspect. The recursive Bayesian network formalism was put forward as a means to model mechanistic hierarchies by decomposing variables. The proposal was recently criticized by Gebharter and Gebharter and Kaiser, who instead propose to decompose arrows. In this paper, I defend the (...) RBN account from the criticism and argue that it offers a better representation of mechanistic hierarchies than the rival account. (shrink)

Casini, Illari, Russo, and Williamson (2011) suggest to model mechanisms by means of recursive Bayesian networks (RBNs) and Clarke, Leuridan, and Williamson (2014) extend their modelling approach to mechanisms featuring causal feedback. One of the main selling points of the RBN approach should be that it provides answers to questions concerning manipulation and control. In this paper I demonstrate that the method to compute the effects of interventions the authors mentioned endorse leads to absurd results under the additional assumption of (...) faithfulness, which can be expected to hold for many RBN models of mechanisms. (shrink)

Arguments for the autonomy of psychology or other higher-level sciences have often taken the form of denying the possibility of reduction. The form of reduction most proponents and critics of the autonomy of psychology have in mind is theory reduction. Mechanistic explanations provide a different perspective. Mechanistic explanations are reductionist insofar as they appeal to lower-level entities—the component parts of a mechanism and their operations— to explain a phenomenon. However, unlike theory reductions, mechanistic explanations also recognize the fundamental role of (...) organization in enabling mechanisms to engage their environments as units (as well as the role of yet higher-level structures in constraining such engagement). Especially when organization is non-linear, it can enable mechanisms to generate phenomena that are quite surprising given the operations of the components taken in isolation. Such organization must be discovered—it cannot simply be derived from knowledge of lower-level parts and their operations. Moreover, the organized environments in which mechanisms operate must also be discovered. It is typically the higher-level disciplines that have the tools for discovering the organization within and between mechanisms. Although these inquiries are constrained by the knowledge of the parts and operations constituting the mechanism, they make their own autonomous contribution to understanding how a mechanism actually behaves. Thus, mechanistic explanations provide a strong sense of autonomy for higher levels of organization and the inquiries addressing them even while recognizing the distinctive contributions of reductionistic research investigating the operations of the lower level components. (shrink)

Causal reasoning is primarily concerned with what would happen to a system under external interventions. In particular, we are often interested in predicting the probability distribution of some random variables that would result if some other variables were forced to take certain values. One prominent approach to tackling this problem is based on causal Bayesian networks, using directed acyclic graphs as causal diagrams to relate post-intervention probabilities to pre-intervention probabilities that are estimable from observational data. However, such causal diagrams are (...) seldom fully testable given observational data. In consequence, many causal discovery algorithms based on data-mining can only output an equivalence class of causal diagrams. This paper is concerned with causal reasoning given an equivalence class of causal diagrams, represented by a ancestral graph. We present two main results. The first result extends Pearl 's celebrated do-calculus to the context of ancestral graphs. In the second result, we focus on a key component of Pearl's calculus---the property of invariance under interventions, and give stronger graphical conditions for this property than those implied by the first result. The second result also improves the earlier, similar results due to Spirtes et al. (shrink)