The ‘no-difference problem’ challenges us to explain in which way the occurrence of an aggregate effect gives us reason to act in a specific way, although our individual actions make no difference to the effect’s occurrence. When discussing this problem, philosophers usually distinguish between so-called ‘triggering cases’, where the aggregate effect in question is brought about upon reaching a precise threshold, and ‘non-triggering cases’, in which no such precise threshold exists. However, despite their relevant differences, it is widely assumed not (...) only that both categories of cases confront us with the same moral problem, but also that this problem should be solved in the same way no matter which category we are considering. In this paper, I argue that this assumption is mistaken by showing that non-triggering cases pose very different moral problems than triggering cases unless very specific and, arguably, unlikely assumptions in neighbouring debates about causation and decision-making under indeterminacy hold. (shrink)

Cancer biology features the ascription of normal functions to parts of cancers. At least some ascriptions of function in cancer biology track local normality of parts within the global abnormality of the aberration to which those parts belong. That is, cancer biologists identify as functions activities that, in some sense, parts of cancers are supposed to perform, despite cancers themselves having no purpose. The present paper provides a theory to accommodate these normal function ascriptions—I call it the Modeling Account of (...) Normal Function (MA). MA comprises two claims. First, normal functions are activities whose performance by the function-bearing part contributes to the self-maintenance of the whole system and, thereby, results in the continued presence of that part. Second, MA holds that models of system-level activities that are (partly) constitutive of self-maintenance are improved by including a representation of the relevant function-bearing part and by making reference to the activity/activities that part performs which contribute(s) to those system-level activities. I contrast MA with two other accounts that seek to explicate the ascription of normal functions in biology, namely, the organizational account and the selected effects account. Both struggle to extend to cancer biology. However, I offer ecumenical readings which allow them to recover some ascriptions of normal function to parts of cancers. So, though I contend that MA excels in this respect, the purpose of this paper is served if it provides materials for bridging the gap between cancer biology, philosophy of cancer, and the literature on function. (shrink)

In this dissertation, I develop and defend a model of causation that allows for dualist mental causation in worlds where the physical domain is physically complete. In Part I, I present the dualist ontology that will be assumed throughout the thesis and identify two challenges for models of mental causation within such an ontology: the exclusion worry and the common cause worry. I also argue that a proper response to these challenges requires a thoroughly lightweight account of causation, i.e. an (...) account that allows for causes to be metaphysically distinct from the phenomena that produce or physically necessitate their effects. In Part II, I critically evaluate contemporary responses to these challenges from the philosophical literature. In particular, I discuss List and Stoljar’s criticism of exclusion worries, Kroedel’s alternative dualist ontology, concerns about the notion of causal sufficiency, and Lowe’s models of dualist mental causation. I argue that none of these proposals provide independent motivation for a thoroughly lightweight account of causation and therefore leave room for improvement. In the first four chapters of Part III, I develop a thoroughly lightweight model of causation, which builds on interventionist approaches to causation. First, I explain how so-called ‘holding fixed’-requirements in standard interventionist accounts stand in the way of dualist mental causation. I then argue that interventionist accounts should impose a robustness condition on causal correlations and that, with this condition in place, the ‘holding fixed’-requirements can be weakened such that they do allow for dualist mental causation. I dub the interventionist model with such weakened ‘holding fixed’-requirements ‘insensitive interventionism’, argue that it can counter the exclusion worry as well as the common cause worry, and explain under which circumstances it would predict there to be dualist mental causation. Importantly, these circumstances might, for all we know, hold in the actual world. In the final three chapters of Part III, I defend insensitive interventionism against some objections. I consider the objection that causation must be productive, the objection that causes must physically necessitate their effects, and the objection that insensitive interventionism is too permissive. I respond by drawing from the literature on causation by absences and on the relation between causation and fundamental physics. Overall, insensitive interventionism performs as well as standard interventionist accounts. I conclude that insensitive interventionism is a credible model of causation. (shrink)