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)

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)

Two widely accepted assumptions within cognitive science are that (1) the goal is to understand the mechanisms responsible for cognitive performances and (2) computational modeling is a major tool for understanding these mechanisms. The particular approaches to computational modeling adopted in cognitive science, moreover, have significantly affected the way in which cognitive mechanisms are understood. Unable to employ some of the more common methods for conducting research on mechanisms, cognitive scientists’ guiding ideas about mechanism have developed in conjunction with their (...) styles of modeling. In particular, mental operations often are conceptualized as comparable to the processes employed in classical symbolic AI or neural network models. These models, in turn, have been interpreted by some as themselves intelligent systems since they employ the same type of operations as does the mind. For this paper, what is significant about these approaches to modeling is that they are constructed specifically to account for behavior and are evaluated by how well they do so—not by independent evidence that they describe actual operations in mental mechanisms. (shrink)

This paper explores the question of whether all or most explanations in biology are, or ideally should be, ‘mechanistic’. I begin by providing an account of mechanistic explanation, making use of the interventionist ideas about causation I have developed elsewhere. This account emphasizes the way in which mechanistic explanations, at least in the biological sciences, integrate difference‐making and spatio‐temporal information, and exhibit what I call fine‐tunedness of organization. I also emphasize the role played by modularity conditions in mechanistic explanation. I (...) will then argue, in agreement with John Dupré, that, given this account, it is plausible that many biological systems require explanations that are relatively non‐mechanical or depart from expectations one associates with the behaviour of machines. (shrink)

This article examines the role of experimental generalizations and physical laws in neuroscientific explanations, using Hodgkin and Huxley’s electrophysiological model from 1952 as a test case. I show that the fact that the model was partly fitted to experimental data did not affect its explanatory status, nor did the false mechanistic assumptions made by Hodgkin and Huxley. The model satisfies two important criteria of explanatory status: it contains invariant generalizations and it is modular (both in James Woodward’s sense). Further, I (...) argue that there is a sense in which the explanatory heteronomy thesis holds true for this case. †To contact the author, please write to: SNF‐Professorship for Philosophy of Science, University of Basel, Missionsstrasse 21, 4003 Basel, Switzerland; e‐mail: [email protected]. (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.

Mechanisms are often characterized as causal structures and the interventionist account of causation is then used to characterize what it is to be a causal structure. The associated modularity constraint on causal structures has evoked criticism against using the theory as an account of mechanisms, since many mechanisms seem to violate modularity. This paper answers to this criticism by making a distinction between a causal system and a causal structure. It makes sense to ask what the modularity properties of a (...) given causal structure are, but not whether a causal system is modular tout court. The counter-examples to the interventionist account are systems in which a particular structure is modular in variables, but not in parameters. A failure of parameter-modularity does not by itself threaten the interventionist interpretation of the structure and the possibility of causally explaining with that structure, but it does mean that knowledge of the structure is not sufficient to constitutively explain system-level properties of the embedding system. (shrink)

The key idea of the interventionist account of causation is that a variable A causes a variable B if and only if B would change if A were manipulated in the appropriate way. This paper raises two problems for Woodward's (2003) version of interventionism. The first is that the conditions it imposes are not sufficient for causation, because these conditions are also satisfied by non-causal relations of nomological dependence expressed in association laws. Such laws ground a relation of mutual manipulability (...) that is incompatible with the asymmetry of causation. Several ways of defending the interventionist account are examined and found unsatisfying. The second problem is that it often seems to be impossible, in a model that contains variables linked by an association law, to satisfy the conditions imposed on interventions on such variables. Various ways to solve this second problem, most importantly the analysis of manipulability in terms of difference making, are examined. Given that none solves the problem, I conclude that the interventionist conditions are neither sufficient nor necessary for causation. It is suggested that they provide an analysis of nomological dependence, which may be supplemented with the notion of a causal process to yield an analysis of causation. (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)

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)

Mechanisms play an important role in many sciences when it comes to questions concerning explanation, prediction, and control. Answering such questions in a quantitative way requires a formal represention of mechanisms. Gebharter (2014) suggests to represent mechanisms by means of one or more causal arrows of an acyclic causal net. In this paper we show how this approach can be extended in such a way that it can also be fruitfully applied to mechanisms featuring causal feedback.

Modeling mechanisms is central to the biological sciences – for purposes of explanation, prediction, extrapolation, and manipulation. A closer look at the philosophical literature reveals that mechanisms are predominantly modeled in a purely qualitative way. That is, mechanistic models are conceived of as representing how certain entities and activities are spatially and temporally organized so that they bring about the behavior of the mechanism in question. Although this adequately characterizes how mechanisms are represented in biology textbooks, contemporary biological research practice (...) shows the need for quantitative, probabilistic models of mechanisms, too. In this paper we argue that the formal framework of causal graph theory is well-suited to provide us with models of biological mechanisms that incorporate quantitative and probabilistic information. On the ba-sis of an example from contemporary biological practice, namely feedback regulation of fatty acid biosynthesis in Brassica napus, we show that causal graph theoretical models can account for feedback as well as for the multi-level character of mechanisms. However, we do not claim that causal graph theoretical representations of mechanisms are advantageous in all respects and should replace common qualitative models. Rather, we endorse the more balanced view that causal graph theoretical models of mechanisms are useful for some purposes, while being insufficient for others. (shrink)