Lorenzo Casini

I argue for an inferentialist account of the meaning of causal claims, which draws on the writings of Sellars and Brandom. The account is meant to be widely applicable. In this work, it is motivated and defended with reference to complex systems sciences, i.e., sciences that study the behaviour of systems with many components interacting at various levels of organisation (e.g. cells, brain, social groups). Here are three, seemingly-uncontroversial platitudes about causality. (1) Causal relations are objective, mind-independent relations and, as such, analysable in objective, mind-independent terms. (2) There is a tight connection between our practice of predicting, explaining and controlling phenomena, and the use of causal notions. (3) The second platitude should be explained in terms of the first. Contrary to this widely-held stance, I suggest that we reverse the order of analysis, by taking our activities of agents as the raw material in terms of which to account for the obtaining of causal relations. To this end, I propose and defend an inferentialist account of causality. Causality is a ‘category’ that the knowing subject employs to ‘mediate’ between himself and the world. In inferentialist terms, this mediation is the result of the concept of cause figuring in a network of inferences, used in our practice of gathering evidence and using it to explain, predict and intervene. Complexity only makes the mediation more difficult, thereby rendering the meaning of causality more evident.

What can we learn from “minimal” economic models? I argue that learning from such models is not limited to conceptual explorations—which show how something could be the case—but may extend to explanations of real economic phenomena—which show how something is the case. A model may be minimal qua certain world-linking properties, and yet “not-so-minimal” qua learning, provided it is externally valid. This, in turn, depends on using the right principles for model building and not necessarily “isolating” principles. My argument is buttressed by a case study from computational economics, namely, two agent-based models of asset pricing.

Gebharter has proposed using one of the best known Bayesian network causal discovery algorithms, PC, to identify the constitutive dependencies underwriting mechanistic explanations. His proposal assumes that mechanistic constitution behaves like deterministic direct causation, such that PC is directly applicable to mixed variable sets featuring both causal and constitutive dependencies. Gebharter claims that such mixed sets, under certain restrictions, comply with PC’s background assumptions. The aim of this article is to show that Gebharter’s proposal incurs severe problems, ultimately rooted in the widespread non-compliance of mechanistic systems with PC’s assumptions. This casts severe doubts on the attempt to implicitly define constitution as a form of deterministic direct causation complying with PC’s assumptions.

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.

The core idea of statistical accounts of biological functions is that to function normally is to provide a statistically typical contribution to some goal state of the organism. In this way, statistical accounts purport to naturalize the teleological notion of function in terms of statistical facts. Boorse’s, 542–573, 1977) original biostatistical account was criticized for failing to distinguish functions from malfunctions. Recently, many have attempted to circumvent the criticism, 519–541, 2012, Journal of Medicine and Philosophy, 39, 634–647, 2014). Here, I review such attempts and find them inadequate. The reason, ultimately, is that functional attribution depends on how traits would behave in relevant situations, a condition that resists statistical characterizations in terms of how they typically behave. This, I conclude, undermines the attempt to naturalize functions in statistical terms.

The Recursive Bayesian Net (RBN) 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

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.

Some authors claim that minimal models have limited epistemic value (Fumagalli, 2016; Grüne-Yanoff, 2009a). Others defend the epistemic benefits of modelling by invoking the role of robustness analysis for hypothesis confirmation (see, e.g., Levins, 1966; Kuorikoski et al., 2010) but such arguments find much resistance (see, e.g., Odenbaugh & Alexandrova, 2011). In this paper, we offer a Bayesian rationalization and defence of the view that robustness analysis can play a confirmatory role, and thereby shed light on the potential of minimal models for hypothesis confirmation. We illustrate our argument by reference to a case study from macroeconomics. At the same time, we also show that there are cases in which robustness analysis is detrimental to confirmation. We characterize these cases and link them to recent investigations on evidential variety (Landes, 2020b, 2021; Osimani and Landes, forthcoming). We conclude that robustness analysis over minimal models can confirm, but its confirmatory value depends on concrete circumstances.

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

How many notions of cause are there? The causality literature is witnessing a flourishing of pluralist positions. Here I focus on a recent debate on whether interpreting causality in terms of inferential relations commits one to semantic pluralism (Reiss 2011) or not (Williamson 2006). I argue that inferentialism is compatible with a ‘weak’ form of monism, where causality is envisaged as one, vague cluster concept. I offer two arguments for this, one for vagueness, one for uniqueness. Finally, I qualify in what sense the resulting form of monism is ‘weak’.¿Cuántas nociones de causa hay? Hay un resurgir de posiciones pluralistas en la bibliografía sobre causalidad. Me ocuparé aquí de un debate reciente sobre si la interpretación de la causalidad en términos de relaciones inferenciales nos compromete con el pluralismo semántico (Reiss 2011) o no (Williamson 2006). Defiendo que el inferencialismo es compatible con una forma ’debil’ de monismo, donde la causalidad se presenta como un único concepto vago y de agrupación (cluster). Ofrezco para ello dos argumentos, uno sobre vaguedad y otro sobre unicidad. Finalmente, matizaré en qué sentido esta forma demonismo es ’débil’.

How many notions of cause are there? The causality literature is witnessing a flourishing of pluralist positions. Here I focus on a recent debate on whether interpreting causality in terms of inferential relations commits one to _semantic_ pluralism or not. I argue that inferentialism is compatible with a `weak' form of monism, where causality is envisaged as _one_, _vague_ cluster concept. I offer two arguments for this, one for vagueness, one for uniqueness. Finally, I qualify in what sense the resulting form of monism is `weak'.

Alexander Gebharter has recently proposed to use Bayesian network causal discovery methods to identify the constitutive dependencies that underwrite mechanistic explanations. The proposal depends on using the assumptions of the causal Bayesian network framework to implicitly define mechanistic constitution as a kind of deterministic direct causal dependence. The aim of this paper is twofold. In the first half, we argue that Gebharter’s proposal incurs severe conceptual problems. In the second half, we present an alternative way to bring Bayesian network tools to bear on the issue of understanding mechanistic constitution. More precisely, our proposal interprets constitution as the relation explaining why a target phenomenon has its characteristic causal role in terms of the causal roles of some of its spatiotemporal parts---where the notion of causal role is probabilistically understood.

According to Woodward’s influential account of explanation, explanations have a counterfactual structure, and explanatory counterfactuals are analysed in terms of causal relations and interventions. In this paper, we provide a formal semantics of explanatory counterfactuals based on a Ramsey Test semantics of conditionals. Like Woodward’s account, our account is guided by causal considerations. Unlike Woodward’s account, it makes no reference to causal graphs and it also covers cases of explanation where interventions are impossible.

While ideal interventions are acknowledged by many as valuable tools for the analysis of causation, recent discussions have shown that, since there are no ideal interventions on upper-level phenomena that non-reductively supervene on their underlying mechanisms, interventions cannot—contrary to a popular opinion—ground an informative analysis of constitution. This has led some to abandon the project of analyzing constitution in interventionist terms. By contrast, this paper defines the notion of a horizontally surgical intervention, and argues that, when combined with some innocuous metaphysical principles about the relation between upper and lower levels of mechanisms, that notion delivers a sufficient condition for constitution. This, in turn, strengthens the case for an interventionist analysis of constitution.

While ideal interventions are acknowledged by many as valuable tools for the analysis of causation, recent discussions have shown that, since there are no ideal interventions on upper-level phenomena that non-reductively supervene on their underlying mechanisms, interventions cannot—contrary to a popular opinion—ground an informative analysis of constitution. This has led some to abandon the project of analyzing constitution in interventionist terms. By contrast, this paper defines the notion of a horizontally surgical intervention, and argues that, when combined with some innocuous metaphysical principles about the relation between upper and lower levels of mechanisms, that notion delivers a sufficient condition for constitution. This, in turn, strengthens the case for an interventionist analysis of constitution.

The first part of this paper finds Craver’s (2007) mutual manipulability theory (MM) of constitution inadequate, as it definitionally ties constitution to the feasibility of idealized experiments, which, however, are unrealizable in principle. As an alternative, the second part develops an abductive theory of constitution (NDC), which exploits the fact that phenomena and their constituents are unbreakably coupled via common causes. The best explanation for this common-cause coupling is the existence of an additional dependence relation, viz. constitution. Apart from adequately capturing the essential characteristics of constitution missed by MM, NDC has important ramifications for constitutional discovery—most notably, that there is no experimentum crucis for constitution, not even under ideal discovery circumstances.