This monograph looks at causal nets from a philosophical point of view. The author shows that one can build a general philosophical theory of causation on the basis of the causal nets framework that can be fruitfully used to shed new light on philosophical issues. Coverage includes both a theoretical as well as application-oriented approach to the subject. The author first counters David Hume’s challenge about whether causation is something ontologically real. The idea behind this is that good metaphysical concepts (...) should behave analogously to good theoretical concepts in scientific theories. In the process, the author offers support for the theory of causal nets as indeed being a correct theory of causation. Next, the book offers an application-oriented approach to the subject. The author shows that causal nets can investigate philosophical issues related to causation. He does this by means of two exemplary applications. The first consists of an evaluation of Jim Woodward’s interventionist theory of causation. The second offers a contribution to the new mechanist debate. Introductory chapters outline all the formal basics required. This helps make the book useful for those who are not familiar with causal nets, but interested in causation or in tools for the investigation of philosophical issues related to causation. (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)

An overview of the German philosophy of science community is given for the years 1992–2012, based on a survey in which 159 philosophers of science in Germany participated. To this end, the institutional background of the German philosophy of science community is examined in terms of journals, centers, and associations. Furthermore, a qualitative description and a quantitative analysis of our survey results are presented. Quantitative estimates are given for: (a) academic positions, (b) research foci, (c) philosophers’ of science most important (...) publications, and (d) externally funded projects, where for (c) all survey participants had indicated their five most important publications in philosophy of science. In addition, the survey results for (a)–(c) are also qualitatively described, as they are interesting in their own right. With respect to (a), we estimated the gender distribution among academic positions. Concerning (c), we quantified philosophers’ of science preference for (i) journals and publishers, (ii) publication format, (iii) language, and (iv) coauthorship for their most important publications. With regard to research projects, we determined their (i) prevalence, (ii) length, and (iii) trend (an increase in number?) as well as their most frequent (iv) research foci and (v) funding organizations. We also distinguished between German-based and non-German-based journals, publishers, and funding institutions, making it thereby possible to evaluate the involvement of the German philosophy of science community in the international research landscape. Finally, we discuss some implications of our findings. (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)

Sociologists are increasingly attentive to the mechanisms responsible for cause-and-effect relationships in the social world. But an aspect of mechanistic causality has not been sufficiently considered. It is well recognized that most phenomena of interest to social science result from multiple mechanisms operating in sequence. However, causal chains—sequentially linked mechanisms and their enabling background conditions—vary not just substantively, by the kind of causal work they do, but also structurally, by their formal properties. In this article, the author examines the nature (...) of causal chains, identifies major structural dimensions along which they differ, and makes a case that a mechanism-based explanation would be enhanced if causal chains and their structures were brought to the analytical forefront. (shrink)

Causal Bayes nets (CBNs) can be used to model causal relationships up to whole mechanisms. Though modelling mechanisms with CBNs comes with many advantages, CBNs might fail to adequately represent some biological mechanisms because—as Kaiser (2016) pointed out—they have problems with capturing relevant spatial and structural information. In this paper we propose a hybrid approach for modelling mechanisms that combines CBNs and cellular automata. Our approach can incorporate spatial and structural information while, at the same time, it comes with all (...) the merits of a CBN representation of mechanisms. (shrink)

One of Stuart Glennan's most prominent contributions to the new mechanist debate consists in his reductive analysis of higher-level causation in terms of mechanisms (Glennan, 1996). In this paper I employ the causal Bayes net framework to reconstruct his analysis. This allows for specifying general assumptions which have to be satis ed to get Glennan's approach working. I show that once these assumptions are in place, they imply (against the background of the causal Bayes net machinery) that higher-level causation indeed (...) reduces to interactions between component parts of mechanisms. I also briefly discuss the plausibility of these assumptions and some consequences for the mechanism debate. (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.

I propose a dynamic causal approach to characterizing the notion of a mechanism. Levy and Bechtel, among others, have pointed out several critical limitations of the new mechanical philosophy, and pointed in a new direction to extend this philosophy. Nevertheless, they have not fully fleshed out what that extended philosophy would look like. Based on a closer look at neuroscientific practice, I propose that a mechanism is a dynamic causal system that involves various components interacting, typically nonlinearly, with one another (...) to produce a phenomenon of interest. (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)

According to one large family of views, scientific explanations explain a phenomenon (such as an event or a regularity) by subsuming it under a general representation, model, prototype, or schema (see Bechtel, W., & Abrahamsen, A. (2005). Explanation: A mechanist alternative. Studies in History and Philosophy of Biological and Biomedical Sciences, 36(2), 421–441; Churchland, P. M. (1989). A neurocomputational perspective: The nature of mind and the structure of science. Cambridge: MIT Press; Darden (2006); Hempel, C. G. (1965). Aspects of scientific (...) explanation. In C. G. Hempel (Ed.), Aspects of scientific explanation (pp. 331–496). New York: Free Press; Kitcher (1989); Machamer, P., Darden, L., & Craver, C. F. (2000). Thinking about mechanisms. Philosophy of Science, 67(1), 1–25). My concern is with the minimal suggestion that an adequate philosophical theory of scientific explanation can limit its attention to the format or structure with which theories are represented. The representational subsumption view is a plausible hypothesis about the psychology of understanding. It is also a plausible claim about how scientists present their knowledge to the world. However, one cannot address the central questions for a philosophical theory of scientific explanation without turning one’s attention from the structure of representations to the basic commitments about the worldly structures that plausibly count as explanatory. A philosophical theory of scientific explanation should achieve two goals. The first is explanatory demarcation. It should show how explanation relates with other scientific achievements, such as control, description, measurement, prediction, and taxonomy. The second is explanatory normativity. It should say when putative explanations succeed and fail. One cannot achieve these goals without undertaking commitments about the kinds of ontic structures that plausibly count as explanatory. Representations convey explanatory information about a phenomenon when and only when they describe the ontic explanations for those phenomena. (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)

In (Gebharter 2014) I suggested a framework for modeling the hierarchical organization of mechanisms. In this short addendum I want to highlight some connections of my approach to the statistics and machine learning literature and some of its limitations not mentioned in the paper.