Online research in philosophy

In this paper I offer an anti-Humean critique to Williamson and Russo’s approach to medical mechanisms. I focus on one of the specific claims made by Williamson and Russo, namely the claim that micro-structural ‘mechanisms’ provide evidence for the stability across populations of causal relationships ascertained at the (macro-) level of (test) populations. This claim is grounded in the epistemic account of causality developed by Williamson, an account which—while not relying exclusively on mechanistic evidence for justifying causal judgements—appeals nevertheless to mechanisms, and rejects their anti-Humean interpretation in terms of capacities, powers, potencies, etc. By using (and expanding on) Cartwright’s basic critique against Humean mechanisms, I suggest that, in order to move beyond the level of plausibility, Williamson and Russo’s position is in need of a clarification as to the occurent reading of the components, functioning and interferences of mechanisms. Relatedly, as concerns Williamson’s epistemic account of causation, I argue that this account is in need of a more straightforward answer as to what truth-makers its causal claims should have.

Mechanisms have become much-discussed, yet there is still no consensus on how to characterise them. In this paper, we start with something everyone is agreed on – that mechanisms explain – and investigate what constraints this imposes on our metaphysics of mechanisms. We examine two widely shared premises about how to understand mechanistic explanation: (1) that mechanistic explanation offers a welcome alternative to traditional laws-based explanation and (2) that there are two senses of mechanistic explanation that we call ‘epistemic explanation’ and ‘physical explanation’. We argue that mechanistic explanation requires that mechanisms are both real and local. We then go on to argue that real, local mechanisms require a broadly active metaphysics for mechanisms, such as a capacities metaphysics.

This reply to Erik Weber’s commentary agrees that mechanisms are important for causal inference in social science, but argues that Weber makes the mistake that was the main focus of my original essay: inferring that since a problem cannot be solved without mechanisms, it can be solved with them. As it stands, this inference is invalid since the problem might be unsolvable with or without mechanisms. Any claim about the usefulness of mechanisms for some purpose requires an adequate account of how mechanisms can actually fulfill that function, which Weber has not provided with regard to the issues he discusses.

Explanations of how psychological capacities are carried out often invoke functional brain areas. I argue that such explanations cannot succeed. Psychological capacities are carried out by identifiable entities and their activities in the brain, but functional brain areas are not the relevant entities. I proceed by assuming that if functional brain areas did carry out psychological capacities, then these brain areas could be included in descriptions of mechanisms. And if functional brain areas participate in mechanisms, then they must engage in activities. A number of ways in which we might understand the claim that functional brain areas engage in activities are examined. None are successful, and so one conclusion is that functional brain areas do not participate in mechanisms. Consequently, they are not the entities that carry out psychological capacities.

Fodor’s theory of concepts holds that the psychological capacities, beliefs or intentions which determine how we use concepts do not determine reference. Instead, causal relations of a specific kind between properties and our dispositions to token a concept are claimed to do so. Fodor does admit that there needs to be some psychological mechanisms mediating the property–concept tokening relations, but argues that they are purely accidental for reference. In contrast, I argue that the actual mechanisms that sustain the reference determining concept tokening relations are necessary for reference. Fodor’s atomism is thus undermined, since in order to refer with a concept it is necessary to possess some specific psychological capacities.

Inferences like these are known as extrapolations.

Any account of extrapolation from animal models to humans must confront two basic challenges: explain how extrapolation can be justified even when there are causally relevant differences between model and target, and explain how the suitability of a model can be established given only limited information about the target. We argue that existing approaches to extrapolation—either in terms of capacities or mechanisms—do not adequately address these challenges. However, we propose a further elaboration of the mechanisms approach that provides a better treatment of this issue. The central concept in our proposal is what we term comparative process tracing.

Several authors have claimed that mechanisms play a vital role in distinguishing between causation and mere correlation in the social sciences. Such claims are sometimes interpreted to mean that without mechanisms, causal inference in social science is impossible. The author agrees with critics of this proposition but explains how the account of how mechanisms aid causal inference can be interpreted in a way that does not depend on it. Nevertheless, he shows that this more charitable version of the account is still unsuccessful as it stands. Consequently, he advances a proposal for shoring up the account, which is founded on the possibility of acquiring knowledge of social mechanisms by linking together norms or practices found in a society. Key Words: causality • social mechanisms • interpretation • anthropology.