Alexander Gebharter

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.

Certain hypotheses cannot be directly confirmed for theoretical, practical, or moral reasons. For some of these hypotheses, however, there might be a workaround: confirmation based on analogical reasoning. In this paper we take up Dardashti, Hartmann, Thébault, and Winsberg’s (in press) idea of analyzing confirmation based on analogical inference Baysian style. We identify three types of confirmation by analogy and show that Dardashti et al.’s approach can cover two of them. We then highlight possible problems with their model as a general approach to analogical inference and argue that these problems can be avoided by supplementing Bayesian update with Jeffrey conditionalization.

In the first part of this chapter I finish the axiomatization of the causal nets framework started in Chap. 3 I also argue that the causal Markov axiom provides the best explanation for two statistical phenomena. In the second part I present several results about the empirical content of different versions (i.e., combination of axioms) of the theory of causal nets. Both parts together show that causation satisfies the same modern standards as theoretical concepts of good empirical theories do. This can be seen as new empirical support for the theory of causal nets, but also as an answer to Hume’s skeptical challenge: Actually, it seems that we have good reasons to believe in causation as something ontologically real out there in the world.

In this chapter I enter the new mechanist debate within the philosophy of science. I discuss a proposal how to model mechanisms made by Casini, Illari, Russo, and Williamson and present three problems with their approach. I then present my alternative approach of how to represent mechanisms, compare it with Casini et al.’s approach, and discuss Casini’s recent objections to my approach. I also make a suggestion how constitutive relevance relations could be represented within my approach. In the rest of this chapter I extend the approach in such a way that it can also account for the diachronic character of mechanisms and the fact that many mechanisms feature causal cycles.

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.

Hitchcock demonstrated that the validity of causal exclusion arguments as well as the plausibility of several of their premises hinges on the specific theory of causation endorsed. In this paper I show that the validity of causal exclusion arguments—if represented within the theory of causal Bayes nets the way Gebharter suggests—actually requires much weaker premises than the ones which are typically assumed. In particular, neither completeness of the physical domain nor the no overdetermination assumption are required.

Chronic myeloid leukemia (CML) is a cancer of the hematopoietic system initiated by a single genetic mutation which results in the oncogenic fusion protein Bcr-Abl. Untreated, patients pass through different phases of the disease beginning with the rather asymptomatic chronic phase and ultimately culminating into blast crisis, an acute leukemia resembling phase with a very high mortality. Although many processes underlying the chronic phase are well understood, the exact mechanisms of disease progression to blast crisis are not yet revealed. In this paper we develop a mathematical model of CML based on causal Bayesian networks in order to study possible disease progression mechanisms. Our results indicate that an increase of Bcr-Abl levels alone is not sufficient to explain the phenotype of blast crisis and that secondary changes such as additional mutations are necessary to explain disease progression and the poor therapy response of patients in blast crisis.

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

In this paper I reconstruct and evaluate the validity of two versions of causal exclusion arguments within the theory of causal Bayes nets. I argue that supervenience relations formally behave like causal relations. If this is correct, then it turns out that both versions of the exclusion argument are valid when assuming the causal Markov condition and the causal minimality condition. I also investigate some consequences for the recent discussion of causal exclusion arguments in the light of an interventionist theory of causation such as Woodward's (2003) and discuss a possible objection to my causal Bayes net reconstruction.

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.

In this paper I argue that constitutive relevance relations in mechanisms behave like a special kind of causal relation in at least one important respect: Under suitable circumstances constitutive relevance relations produce the Markov factorization. Based on this observation one may wonder whether standard methods for causal discovery could be fruitfully applied to uncover constitutive relevance relations. This paper is intended as a first step into this new area of philosophical research. I investigate to what extent the PC algorithm, originally developed for causal search, can be used for constitutive relevance discovery. I also discuss possible objections and certain limitations of a constitutive relevance discovery procedure based on PC.

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.

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.

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.

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.

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.

Ever since it was discovered that hallucinations and illusions are not all that compatible with our natural view of the relation between the perceiving subject and the perceived object, according to which we always perceive the object itself (or, as most epistemologists prefer to say, we perceive it directly), the philosophical position of Direct (or Naïve) Realism which is meant to be the epistemological equivalent of this view, has begun to falter. To express these problems more explicitly, the argument from hallucination and the argument from illusion were created and brought direct realists in dire need of explaining how phenomenons such as hallucinations and illusions could possibly go together with their position. One of the main direct (or naïve) realists’ responses to these arguments is Disjunctivism, a position that, while being able to efficiently deal with both arguments, is subject to quite a few problems in its postulations as well. The intuitive plausibility of both arguments seems to have led many a philosopher to take their validity for granted. Because of this, it will be attempted to give an accurate and adequate reformulation of both arguments in this paper to find out whether their impact on the philosophy of perception is justified in the first place.