This dissertation focuses on teleology and functions in biology. More precisely, it focuses on the scientific legitimacy of teleofunctional attributions and explanations in biology. It belongs to a multi-faceted debate that can be traced back to at least the 1970s. One aspect of the debate concerns the naturalization of functions. Most authors try to reduce, translate or explain functions and teleology in terms of efficient causes so that they find their place in the framework of the natural sciences. Our approach (...) here is radically different, as we question the premise that teleological explanations are disguised causal explanations. On the contrary, we defend that they are acceptable in natural sciences and in biology in particular. We challenge the idea that teleological explanations are immature causal explanations, as well as the idea that teleology and functions are some sort of intentional explanations. We therefore reject the accusations of anthropomorphism, vitalism and finalism. On the contrary, we defend that teleology, causality and intentionality correspond to different, autonomous and complementary modes of representation of the outside world. -/- ———[FRANÇAIS]——— -/- Ce travail de thèse porte sur la téléologie et les fonctions en biologie. Plus précisément, il porte sur la légitimité scientifique des attributions et des explications téléofonctionnelles en biologie. Il s’inscrit dans le cadre d’un débat à plusieurs facettes que l’on peut faire remonter au moins jusqu’aux années 1970 et qui est encore très actif aujourd’hui. L’un des aspects du débat porte sur la naturalisation des fonctions, c’est-à-dire sur la manière de les réduire, de les traduire ou de les expliciter en termes de causes efficientes de sorte qu’elles trouvent leur place dans le cadre des sciences de la nature. Notre approche ici est radicalement différente, car nous remettons en question la prémisse selon laquelle les explications téléologiques seraient des explications causales déguisées. Nous défendons au contraire qu’elles sont acceptables en tant que telles aussi bien de façon générale que dans le domaine scientifique et en particulier en biologie. De façon générale, nous remettons en question l’idée selon laquelle la pensée téléologique serait une pensée causale immature, ainsi que sa dépendance présumée vis-à-vis de la psychologie, c’est-à-dire de l’intentionnalité. Nous rejetons donc les accusations d’anthropomorphisme, de vitalisme et de finalisme formulées contre elle. Nous défendons au contraire que la téléologie, la causalité et l’intentionnalité correspondent à des modes différents, autonomes et complémentaires de représentation du monde extérieur. (shrink)

Jaegwon Kim (1998a, 2005) claims that his exclusion problem follows a priori for the non-reductive physicalist given her commitment to five apparently inconsistent theses: mental causation, non-identity, supervenience, causal closure and non-overdetermination. For Kim, the combination of these theses entails that mental properties are a priori excluded as causes, forcing the non-reductive physicalist to accept either epiphenomenalism, or some form of reduction. In this thesis, I argue that Kim’s exclusion problem depends on a particular conception of causation, namely sufficient production, (...) and that when causation is understood in interventionist terms, the non-reductive physicalist can avoid the exclusion problem. I argue that Woodward’s (2003, 2008a, 2011a) version of interventionism not only provides an account of mental causation that avoids the exclusion problem, but argue that it also upholds all of the minimal commitments of non-reductive physicalism, thereby providing a successful non-reductive physicalist solution to the exclusion problem. In Chapter 2, I argue that all five theses are minimal commitments of non-reductive physicalism that cannot be rejected in order to avoid the exclusion problem. Chapter 3 identifies the assumptions that I take to underlie the exclusion problem. Chapter 4 introduces and outlines the central features of Woodward’s (2003) interventionism and Chapter 5 argues that Woodward’s interventionist account of mental causation provides a solution to the exclusion problem. I examine two alternative interventionist accounts of mental causation[1] that fail to provide satisfactory solutions to the exclusion problem and conclude that Woodward’s account therefore provides the only satisfactory account of mental causation and solution to the exclusion problem. Chapter 6 addresses some challenges proposed by Michael Baumgartner (2009, 2010) and argues that the interventionist is able to defend her position against these objections and uphold the interventionist solution to the exclusion problem outlined in this thesis. [1. Proposed by List and Menzies (2009) and Campbell (2007, 2008a, 2008b, 2010).]. (shrink)

A tension exists between those who do—e.g. Meyer (The British Journal for the Philosophy of Science 71:959–985, 2020 ) and Chemero ( 2011 )—and those who do not—e.g. Kaplan and Craver (Philosophy of Science 78:601–627, 2011 ) Piccinini and Craver (Synthese 183:283–311, 2011 )—afford nonmechanistic explanations a role in cognitive science. Here, I argue that one’s perspective on this matter will cohere with one’s interpretation of the tasks of cognitive science; that is, of the actions for which cognitive scientists are (...) specially fitted. To make this point concrete, I consider two tasks of cognitive science—establishing causal claims and unifying—and show how these tasks are interpreted differently by mechanists and nonmechanists respectively. I then argue that, as a result of these different interpretations, we cannot expect to resolve the tension between mechanists and nonmechanists by appeal to cognitive scientific practice. I conclude that we should give up on the debate between mechanists and nonmechanists, and search for progress elsewhere. (shrink)

Advancements in machine learning have fuelled the popularity of using AI decision algorithms in procedures such as bail hearings, medical diagnoses and recruitment. Academic articles, policy texts, and popularizing books alike warn that such algorithms tend to be opaque: they do not provide explanations for their outcomes. Building on a causal account of transparency and opacity as well as recent work on the value of causal explanation, I formulate a moral concern for opaque algorithms that is yet to receive a (...) systematic treatment in the literature: when such algorithms are used in life-changing decisions, they can obstruct us from effectively shaping our lives according to our goals and preferences, thus undermining our autonomy. I argue that this concern deserves closer attention as it furnishes the call for transparency in algorithmic decision-making with both new tools and new challenges. (shrink)

How do individuals guide their activities towards some goal? Harry Frankfurt once identified the task of explaining guidance as the central problem in action theory. An explanation has proved to be elusive, however. In this paper, I show how we can marshal empirical research to make explanatory progress. I contend that human agents have a primitive capacity to guide visual attention, and that this capacity is actually constituted by a sub-individual psychological control-system: the executive system. I thus illustrate how we (...) can explain exercises of individual-level guidance by appeal to its sub-individual constitution. This opens up a new avenue for explicating agency. (shrink)

According to the so-called 'proportionality principle', causes should be proportional to their effects: they should be both enough and not too much for the occurrence of their effects. This principle is the subject of an ongoing debate. On the one hand, many maintain that it is required to address the problem of causal exclusion and take it to capture a crucial aspect of causation. On the other hand, many object that it renders accounts of causation implausibly restrictive and often reject (...) the principle wholesale. I argue that there is exaggeration on both sides. While one half of the principle is overly demanding, the other half is unobjectionable. And while the unobjectionable half does not block exclusion arguments on its own, it provides a nuanced picture of higher-level causation, fits with recent developments in philosophy of causation, and motivates adjustments to standard difference-making accounts of causation. I conclude that at least half of the proportionality principle is worth taking seriously. (shrink)

In paradigm exercises of agency, individuals guide their activities toward some goal. A central challenge for action theory is to explain how individuals guide. This challenge is an instance of the more general problem of how to accommodate individuals and their actions in the natural world, as explained by natural science. Two dominant traditions–primitivism and the causal theory–fail to address the challenge in a satisfying way. Causal theorists appeal to causation by an intention, through a feedback mechanism, in explaining guidance. (...) Primitivists postulate primitive agential capacities in their explanations. The latter neglect to explain how primitive capacities integrate with findings from natural science. The former do not explain why some feedback mechanism’s activity amounts to the agent’s guidance. In this paper I argue that both traditions should acknowledge a capacity to guide, as actually constituted by the executive system. I argue that appeals to this empirically discovered psychological system explain how individuals guide in a way that integrates with explanations from cognitive science. Individuals’ capacity to guide is embedded in the natural world through the activity of its constituent (mechanistic) components. (shrink)

Dynamical systems play a central role in explanations in cognitive neuroscience. The grounds for these explanations are hotly debated and generally fall under two approaches: non-mechanistic and mechanistic. In this paper, I first outline a neurodynamical explanatory schema that highlights the role of dynamical systems in cognitive phenomena. I next explore the mechanistic status of such neurodynamical explanations. I argue that these explanations satisfy only some of the constraints on mechanistic explanation and should be considered pseudomechanistic explanations. I defend this (...) argument against three alternative interpretations of the neurodynamical explanatory schema. The independent interpretation holds that neurodynamical explanations and mechanisms are independent. The constitutive interpretation holds that neurodynamical explanations are constitutive but otherwise non-mechanistic. Both the independent and constitutive interpretations fail to account for all the features of neurodynamical explanations. The partial interpretation assumes that the targets of dynamical systems models are mechanisms and so holds that neurodynamical explanations are incomplete because they lack mechanistic details. I contend instead that the targets of those models are dynamical systems distinct from mechanisms and defend this claim against several objections. I conclude with a defense of the pseudomechanistic interpretation and a discussion of the source of their explanatory power in relation to a causal-mechanical description of the world. (shrink)

Neuroscience constrains psychology, but stating these constraints with precision is not simple. Here I consider whether mechanistic analysis provides a useful way to integrate models of cognitive and neural structure. Recent evidence suggests that cognitive systems map onto overlapping, distributed networks of brain regions. These highly entangled networks often depart from stereotypical mechanistic behaviors. While this casts doubt on the prospects for classical mechanistic integration of psychology and neuroscience, I argue that it does not impugn a realistic interpretation of either (...) type of model. Cognitive and neural models may depict different, but equally real, causal structures within the mind/brain. (shrink)

Both philosophers and psychologists have argued for the existence of distinct kinds of explanations, including teleological explanations that cite functions or goals, and mechanistic explanations that cite causal mechanisms. Theories of causation, in contrast, have generally been unitary, with dominant theories focusing either on counterfactual dependence or on physical connections. This paper argues that both approaches to causation are psychologically real, with different modes of explanation promoting judgments more or less consistent with each approach. Two sets of experiments isolate the (...) contributions of counterfactual dependence and physical connections in causal ascriptions involving events with people, artifacts, or biological traits, and manipulate whether the events are construed teleologically or mechanistically. The findings suggest that when events are construed teleologically, causal ascriptions are sensitive to counterfactual dependence and relatively insensitive to the presence of physical connections, but when events are construed mechanistically, causal ascriptions are sensitive to both counterfactual dependence and physical connections. The conclusion introduces an account of causation, an "exportable dependence theory," that provides a way to understand the contributions of physical connections and teleology in terms of the functions of causal ascriptions. (shrink)

According to several researchers, core affect lies at the foundation of our affective lives and may be characterized as a consciously accessible state combining arousal (activated-deactivated) and valence (pleasure-displeasure). The interaction between these two dimensions is still a matter of debate. In this paper we provide a novel hypothesis concerning their interaction, by arguing that subjective arousal levels modulate the experience of a stimulus’ affective quality. All things being equal, the higher the arousal, the more a given stimulus would be (...) experienced as pleasant (or unpleasant). While marshaling some preliminary evidence in favor of this hypothesis, we also show how it might be relevant in reframing our conception of depressive disorders (i.e., major and bipolar depression). (shrink)