Back cover: This book develops a philosophical account that reveals the major characteristics that make an explanation in the life sciences reductive and distinguish them from non-reductive explanations. Understanding what reductive explanations are enables one to assess the conditions under which reductive explanations are adequate and thus enhances debates about explanatory reductionism. The account of reductive explanation presented in this book has three major characteristics. First, it emerges from a critical reconstruction of the explanatory practice of the life sciences itself. (...) Second, the account is monistic since it specifies one set of criteria that apply to explanations in the life sciences in general. Finally, the account is ontic in that it traces the reductivity of an explanation back to certain relations that exist between objects in the world (such as part-whole relations and level relations), rather than to the logical relations between sentences. Beginning with a disclosure of the meta-philosophical assumptions that underlie the author’s analysis of reductive explanation, the book leads into the debate about reduction(ism) in the philosophy of biology and continues with a discussion on the two perspectives on explanatory reduction that have been proposed in the philosophy of biology so far. The author scrutinizes how the issue of reduction becomes entangled with explanation and analyzes two concepts, the concept of a biological part and the concept of a level of organization. The results of these five chapters constitute the ground on which the author bases her final chapter, developing her ontic account of reductive explanation. (shrink)

This paper defends an interventionist treatment of mechanisms and contrasts this with Waskan (forthcoming). Interventionism embodies a difference-making conception of causation. I contrast such conceptions with geometrical/mechanical or “actualist” conceptions, associating Waskan’s proposals with the latter. It is argued that geometrical/mechanical conceptions of causation cannot replace difference-making conceptions in characterizing the behavior of mechanisms, but that some of the intuitions behind the geometrical/mechanical approach can be captured by thinking in terms of spatio-temporally organized difference-making information.

Woodward's long awaited book is an attempt to construct a comprehensive account of causation explanation that applies to a wide variety of causal and explanatory claims in different areas of science and everyday life. The book engages some of the relevant literature from other disciplines, as Woodward weaves together examples, counterexamples, criticisms, defenses, objections, and replies into a convincing defense of the core of his theory, which is that we can analyze causation by appeal to the notion of manipulation.

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)

A number of writers, myself included, have recently argued that an “interventionist” treatment of causation of the sort defended in Woodward, 2003 can be used to cast light on so-called “causal exclusion” arguments. This interventionist treatment of causal exclusion has in turn been criticized by other philosophers. This paper responds to these criticisms. It describes an interventionist framework for thinking about causal relationships when supervenience relations are present. I contend that this framework helps us to see that standard arguments for (...) causal exclusion involve mistaken assumptions about what it is appropriate to control for or hold fixed in assessing causal claims. The framework also provides a natural way of capturing the idea that properties that supervene on but that are not identical with realizing properties can be causally efficacious. (shrink)

I examine to what extent accounts of mechanisms based on formal interventionist theories of causality can adequately represent biological mechanisms with complex dynamics. Using a differential equation model for a circadian clock mechanism as an example, I first show that there exists an iterative solution that can be interpreted as a structural causal model. Thus, in principle, it is possible to integrate causal difference-making information with dynamical information. However, the differential equation model itself lacks the right modularity properties for a (...) full integration. A formal mechanistic model will therefore have to leave out either noncausal or causal explanatory relations. (shrink)

Various causal details of the genetic process of translation have been singled out to account for its privileged status as a ‘code'. We explicate the biological uses of coding talk by characterizing a class of special causal processes in which topological properties are the causally relevant ones. This class contains both the process of translation and communication theoretic coding processes as special cases. We propose a formalism in terms of graphs for expressing our theory of biological codes and discuss its (...) utility in understanding biological systems. *Received May 2007; revised May 2008. †To contact the authors, please write to: Department of Philosophy, Baker Hall 135, Carnegie Mellon University, Pittsburgh, PA 15213; e-mail: [email protected] or [email protected]. (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)

The first part of this paper argues that if Craver’s ([2007a], [2007b]) popular mutual manipulability account (MM) of mechanistic constitution is embedded within Woodward’s ([2003]) interventionist theory of causation--for which it is explicitly designed--it either undermines the mechanistic research paradigm by entailing that there do not exist relationships of constitutive relevance or it gives rise to the unwanted consequence that constitution is a form of causation. The second part shows how Woodward’s theory can be adapted in such a way that (...) (MM) neither undermines the mechanistic paradigm nor reduces constitution to causation. However, it turns out that this modified theoretical embedding of (MM) makes it impossible to produce empirical evidence for constitutive relations. The paper ends by suggesting an additional criterion, the fat-handedness criterion, which, when combined with (MM), generates indirect empirical evidence for constitutive relevance. (shrink)

Written by one of the preeminent researchers in the field, this book provides a comprehensive exposition of modern analysis of causation. It shows how causality has grown from a nebulous concept into a mathematical theory with significant applications in the fields of statistics, artificial intelligence, economics, philosophy, cognitive science, and the health and social sciences. Judea Pearl presents and unifies the probabilistic, manipulative, counterfactual, and structural approaches to causation and devises simple mathematical tools for studying the relationships between causal connections (...) and statistical associations. Cited in more than 2,100 scientific publications, it continues to liberate scientists from the traditional molds of statistical thinking. In this revised edition, Judea Pearl elucidates thorny issues, answers readers' questions, and offers a panoramic view of recent advances in this field of research. Causality will be of interest to students and professionals in a wide variety of fields. Dr Judea Pearl has received the 2011 Rumelhart Prize for his leading research in Artificial Intelligence and systems from The Cognitive Science Society. (shrink)

I examine the adequacy of the causal graph-structural equations approach to causation for modeling biological mechanisms. I focus in particular on mechanisms with complex dynamics such as the PER biological clock mechanism in Drosophila. I show that a quantitative model of this mechanism that uses coupled differential equations – the well-known Goldbeter model – cannot be adequately represented in the standard causal graph framework, even though this framework does permit causal cycles. The reason is that the model contains dynamical information (...) about the mechanism that concerns causal properties but that does not correspond to variables that could be subject to independent interventions. Thus, a representation of the mechanisms as a causal structural model necessarily suppresses causally relevant information. (shrink)

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)