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)

Glennan appeals to interventions to solve the ontological and explanatory regresses that threaten his mechanistic account of causality . I argue that Glennan’s manoeuvre fails. The appeal to interventions is not able to address the ontological regress, and it blocks the explanatory regress only at the cost of making the account inapplicable to non-modular mechanisms. I offer a solution to the explanatory regress that makes use of dynamic Bayesian networks. My argument is illustrated by a case study from systems biology, (...) namely, the mechanism for the irreversibility of apoptosis. I conclude by pointing out the implications of my argument for Glennan’s mechanistic account of causality and, more generally, for accounts of mechanistic explanation based on interventions. 1 Introduction2 Glennan’s Account of Causality3 Objections to Glennan’s Account4 Glennan’s Replies5 Ontological Symmetry?6 Explanatory Symmetry?7 A Solution to the Explanatory Regress8 The Prospects of Glennan’s Account. (shrink)

An important question for the causal modeling approach is how to integrate non‐causal dependence relations such as asymmetric supervenience into the approach. The most prominent proposal to that effect (due to Gebharter) is to treat those dependence relationships as formally analogous to causal relationships. We argue that this proposal neglects some crucial differences between causal and non‐causal dependencies, and that in the context of causal modeling non‐causal dependence relationships should be represented as mutual dependence relationships. We develop a new kind (...) of model – “hybrid models” ‐ based on this suggestion, and formulate a set of axioms for those models. Our formalism has important implications for Kim's exclusion problem: whereas Gebharter's framework vindicates Kim's causal exclusion objection against nonreductive physicalism, our framework has no such implication, and can help non‐reductive physicalists vindicate the efficacy of high‐level properties. A further benefit of our formalism is that it yields a natural and plausible way of thinking about interventions in multi‐level contexts. (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)

Systems medicine is a promising new paradigm for discovering associations, causal relationships and mechanisms in medicine. But it faces some tough challenges that arise from the use of big data: in particular, the problem of how to integrate evidence and the problem of how to structure the development of models. I argue that objective Bayesian models offer one way of tackling the evidence integration problem. I also offer a general methodology for structuring the development of models, within which the objective (...) Bayesian approach fits rather naturally. (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)

Some explanations appeal to facts about the causal structure of a system in order to shed light on a particular phenomenon; these are explanations which do more than cite the causes X and Y of some state-of-affairs Z, but rather appeal to “macro-level” causal features—for example the fact that A causes B as well as C, or perhaps that D is a strong inhibitor of E—in order to explain Z. Appeals to these kinds of “macro-level” causal features appear in a (...) wide variety of social scientific and biological research; statements about features such as “patriarchy,” “healthcare infrastructure,” and “functioning DNA repair mechanism,” for instance, can be understood as claims about what would be different in a system with a different causal structure. I suggest interpreting counterfactual questions involving structural features as questions about alternative parameter settings of causal models, and propose an extension of the usual interventionist framework for causal explanation which enables scientists to explore the consequences of interventions on “macro-level” structure. (shrink)

What are scientific theories and how should they be represented? In this article, I propose a causal–structural account, according to which scientific theories are to be represented as sets of interrelated causal and credal nets. In contrast with other accounts of scientific theories (such as Sneedian structuralism, Kitcher’s unificationist view, and Darden’s theory of theoretical components), this leaves room for causality to play a substantial role. As a result, an interesting account of explanation is provided, which sheds light on explanatory (...) unification within a causalist framework. The theory of classical genetics is used as a case study. 1 Introduction2 The Theory of Classical Genetics3 Three Philosophical Accounts of the Theory of Classical Genetics3.1 The structuralist account3.2 Kitcher’s unificationism3.3 Darden and theory change in science4 A Common Lacuna: Where is Causality?5 Woodward’s Interventionist Account of Causation6 Causal Bayes Nets and Their Interrelations6.1 Causal Bayes nets6.2 Relations among causal nets6.3 Credal nets and their interrelations7 The Theory of the Gene and its Causal Graph8 A First Exemplar: Stem Length in Pea Plants8.1 Three crosses on stem length in pea plants8.2 The causal graph for stem length in pea plants8.3 Morgan’s explanatory principles and the credal net for stem length in pea plants9 Explaining Mendel’s Crosses: A Causal–Structural Account10 Monohybrid Crosses with Complete Dominance11 Exemplars,Explanatory Patterns, Generic Credal Nets, and Mechanism Schemas12 Incomplete Dominance13 Anomalies14 Multi-hybrid Crosses with Independent Assortment15 Multi-hybrid Crosses with Linkage and Crossing-Over16 Double Crossing-Over and the Linear Order of the Gene17 Causal–Structural Explanation18 Explanatory Unification19 Concluding Remarks. (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)

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)

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.

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)

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)