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This dissertation is concerned with conceptual, epistemological, and by extension, ethical, issues in medicine. In Chapter 1, I start by exploring the concept of disease—a foundational and long-debated issue in the philosophy of medicine. Here I clarify important aspects of a well-developed naturalist account of disease—the biostatistical theory (BST)—and articulate an extension to the BST that shows how it is relevant to clinical medicine on a practical level. In Chapter 2, I further demonstrate the usefulness of the BST by showing how the way it conceives of disease can contribute to formation of a typology of clinical conditions, which I argue can help make sense of various conceptual issues in medicine. Chapter 3 addresses a major lacuna in the literature by presenting a novel account of medical treatment. Chapters 4 and 5 present an account of treatment effectiveness: Chapter 4 in the context of the generalizability of clinical trial results and the popular but problematic distinction between explanatory and pragmatic trials, and Chapter 5 regarding how treatment effectiveness is sensitive to non-epistemic considerations, and what this means for EBM+ and a reformulated set of Bradford Hill’s viewpoints that I apply specifically to helping to establish treatment effectiveness. The account of treatment effectiveness I develop in these two chapters sets the stage for Chapter 6, which presents a conceptual framework and clinically relevant model for collaborative, individualized treatment decision-making—a practical application borne from a philosophical approach. In Chapter 7, I further apply philosophy to practical matters in medicine by offering a comprehensive analysis of psychoneuroimmunology (PNI), and specifically that of a PNI-based therapeutic approach called mindfulness, which has been claimed to be effective for various ailments. I assert in this chapter that philosophy has much to offer PNI. Finally, in Chapter 8, I examine potential distorting effects on the evidence base for treatment effectiveness claims due to authors’ conflicts of interest. In what may seem a nonintuitive move (considering the prevailing sentiment among philosophers of medicine), I argue that these concerns may very well be misplaced. Overall, the chapters address fundamental issues in the philosophy of medicine, trying to advance the relevant philosophical debates, and highlighting potential practical implications for medicine and medical communications.

Interlevel causation, broadly defined as the causal infuence of an entity at one level on an entity at another level, is regularly rejected from a philosophical perspective. This rejection seems to conflict with both everyday experience and scientfic practice in the special sciences. Nowhere is this made clearer than in the context of mental causation, where the denial of downward causation has led to the proliferation of epiphenomenalist conclusions regarding the causal efficaciousness of the mental. In other words, mental events are said to have no causal influence on other mental events or on physical ones. It is my hypothesis in this thesis that the problem of mental causation, and other distinct but related problems, may be resolved by recasting the interlevel relations involved in these discussions as bidirectionally causal from an interventionist perspective. I focus on three such relations in this thesis: supervenience, emergence and constitutive relevance. This hypothesis was tested over the course of five central chapters. Chapter 2 provides a concise description of Woodward's interventionist theory. This does not just include the central principles underlying his account of causation, but also makes a case for its application to the problem of interlevel causation. The argument here is twofold. First, interventionism is already widely applied in the discussions surrounding these interlevel relations, most notably in the debate surrounding the interventionist exclusion argument with regards to mental causation and the mutual manipulability approach to constitutive relevance relations in mechanisms. Second, interventionism draws heavily from methodological considerations in social scientific and biomedical contexts, and as such, is uniquely situated to help overcome the apparent gap between philosophical theory and scientifc practice. Chapter 3 deals with a preliminary problem that arises from the bidirectionally causal approach suggested by my hypothesis. Such bidirectional causation is a form of cyclic causality. Even though such cyclic causality is typically assumed to be amenable to an interventionist reading, I illustrate how interventionist treatments of certain cyclic causal graphs run into acute problems. I subsequently show that through an appropriate modifcation of Woodward's conditions for an intervention variable this gap in interventionist theory may be remedied. Chapter 4 focuses on the supervenience relation. This relation often plays a crucial role in causal exclusion arguments. I zoom in on two prominent arguments of this kind, and the discussions in which they figure. The first of these is the oft-debated causal exclusion problem posited by Jaegwon Kim, which is commonly taken to lead to a rejection of mental causation. This conclusion has been criticized by those who conceive of causation in interventionist terms. I evaluate the specific arguments supporting this move, and show that they fail in at least one respect, namely countering the systematic overdetermination issue, an important component of Kim's exclusion problem. Moreover, this interventionist defense of mental causation has itself been determined to lead to its own version of the causal exclusion problem. This second exclusion argument, designated the interventionist causal exclusion problem, has led to an all new debate, and has resulted in Woodward proposing a modification of his interventionist account. I show that his modification again fails in one important respect, namely with regards to the so termed issue of fat-handedness. I subsequently introduce a novel approach to the supervenience relation, which casts it as a bidirectionally causal relation, supported by a further modification of the interventionist account, which does not fall prey to the issues of systematic overdetermination and fat-handedness, and safeguards mental properties from causal epiphenomenalism. The novel causal approach to supervenience shares many features with a parallel discussion in the emergence literature centered on diachronic emergence. Chapter 5 focuses on this new wave of diachronic emergence relations, which are similarly conceived of as causal to counter the supposed epiphenomenalism of mental phenomena. One common feature of these diachronic emergence accounts is that they explicitly dismiss the supervenience relation, even though the relation between emergents and their base is regularly expressed using supervenience. Different arguments for this dismissal are examined, the most notable of which concern the supposed inability of the supervenience relation to obtain in a diachronic context, the necessity of positing a causal interlevel relation, and the supposed need for a mereological conception of supervenience in conjunction with emergence. I argue that for the most part these reasons are resolved by the bidirectionally causal account of supervenience proposed in the preceding chapter, and that the remainder arise from a set of mistaken assumptions concerning supervenience. I subsequently introduce a new working definition for a diachronic emergence relation, which reformulates it as a distinct species of supervenient emergence within the context of the mind-body debate. The final application of the central hypothesis (chapter 6) revolves around the interlevel relation of constitutive relevance, as it is conceived of in the mechanistic literature. Constitutive relevance relations are explicitly demarcated from causal relations in this literature. However, such a non-causal conception seems to engender a tension with frequent claims of interlevel causation in the scientific literature on mechanisms. An additional issue concerns the fact that the constitutive relevance relation is modeled after Woodward's interventionist account of causation, even though a causal interpretation is excluded. I show that the three principal reasons for this exclusion: the logical independence of the relata, the supposed symmetry of the constitution relation, and its assumed synchronicity, are insufficient and may largely be resolved by the recognition of an inherently temporal dimension in the wet and messy psychological and (neuro)biological contexts in which the constitutive relevance relation in question figures. I consider two case studies, in this respect, to show that such a temporality is important to the scientific analysis of such cases. I subsequently show that this temporal dimension is increasingly recognized in the literature, but that the various proposed solutions seem to mainly add alternative causal interlevel relations instead of arguing on behalf of a causal constitutive relevance relation. I therefore propose a definition for such a bidirectionally causal relation that, I contend, emerges as the best fit in the psychological and (neuro)biological contexts in which the constitutive relevance relation figures. Having tested my hypothesis, I conclude that interlevel causation in these discussions is licensed by a modified interventionist treatment in the right contexts. Approaching these interlevel relations as causal then serves to resolve a number of issues, ranging from the safeguarding of mental causation to the easing of tensions between philosophy and science.

This dissertation explores current debates concerning the evidence used to establish causal claims, with a particular focus on claims made in medicine and the mental health sciences. It consists of three parts: First, I provide an analysis of the use of evidence hierarchies within evidence-based medicine (EBM). I focus on two kinds of systems for evaluating evidence – systematic ranking schemes like the OCEBM’s Levels of Evidence and GRADE, and Sir Austin Bradford Hill’s informal ‘characteristics’ for demonstrating causation – and weigh the relative merits of each. I also analyze the debate over EBM’s preference for randomized trials. I discuss the major arguments against the primacy of randomization, but ultimately, I argue that, while randomized trials are far from perfect, they nevertheless generally deserve their place at the top of evidence hierarchies. Finally, I move from the theoretical underpinnings of EBM to actual practice. I discuss one area of research in which the primacy of randomized trials – and the methodology of EBM in general – has been challenged, namely, psychotherapy. I dissect the arguments that have been made against using the EBM model in psychotherapy, demonstrating that they do not hold water. I end by proposing and advocating a piecemeal approach to measuring the effectiveness of psychotherapeutic interventions. Second, I explore the role of mechanistic evidence in establishing causal claims. I analyze the debate over the relative importance of statistical and mechanistic evidence, focusing on the arguments of Federica Russo and Jon Williamson on the one hand and Jeremy Howick on the other. Ultimately, I propose and defend the wRWT, a weakened version of the Russo-Williamson Thesis. Finally, I explore the implications of this debate within the context of psychiatry, using the monoamine hypothesis for depression as a case study to show the importance of mechanistic evidence. Returning to psychotherapy, I argue that the failure of the monoamine hypothesis demonstrates that biomedical explanations for depression should be deemphasized and that our focus should be directed toward furthering the pursuit of a psychosocial understanding of the disorder instead. Third, I move to evaluating the epistemic value of current approaches to evidence amalgamation. I look at two major organizations that perform evidence amalgamation: the Cochrane Collaboration and the International Agency for Research on Cancer (IARC). I ask whether evidence amalgamation in practice should try to satisfy Carnap’s principle of total evidence. Ultimately, I argue that we should not try to satisfy the PTE simpliciter since it is not a rational principle. However, more nuanced, local, and contextualized versions of the PTE can be rational and should be used.

Deze verhandeling betreft een onderzoek naar het epistemologische statuut van experimentele resultaten: hoe kunnen we de informatie die experimenten ons opleveren karakteriseren? Meer specifiek wordt er onderzocht of we kunnen stellen dat een experiment op zich tot feitelijke kennis kan leiden. De motivatie voor deze onderzoeksvraag komt voort uit het wetenschappelijk realisme-debat, dat de vraag betreft of we kunnen stellen dat een succesvolle wetenschappelijke theorie ons kennis oplevert over wat er zich afspeelt voorbij het observeerbare. Vanwege problemen met standaard wetenschappelijk realisme stelden Nancy Cartwright en Ian Hacking voor dat kennis over het onobserveerbare niet moet worden gezocht in wetenschappelijke theorie, maar eerder in succesvolle wetenschappelijke experimenten. Deze suggestie blijkt echter op haar beurt onderhevig aan problemen, wat leidt tot de onderzoeksvraag van deze verhandeling. Deze onderzoeksvraag wordt dan onderzocht aan de hand van een historisch-filosofische studie van twee reeksen van experimenten: experimenten betreffende de snelheidsafhankelijkheid van de massa van elektronen en experimenten betreffende de magnetische toestand van supergeleiders. Het vertrekpunt in beide reeksen is een experiment waarvan gedurende een bepaalde periode gedacht werd dat het specifieke kennis opleverde, maar waarvan het naderhand bleek dat deze kennis toch niet zo zeker was. Het bestuderen van zulke experimenten kan inzicht bieden in de onderzoeksvraag in die zin dat het toelaat om te onderzoeken welke factoren een rol speelden in de overtuiging dat deze experimenten specifieke kennis opleverden, en hoe deze overtuiging doorheen de tijd veranderde. Op basis van deze twee hoofdstukken wordt er dan beargumenteerd dat experimenten enkel informatie kunnen opleveren gegeven een theoretische interpretatie van het functioneren van het experiment, en dat deze informatie niet gezien mag worden als feitelijke kennis, maar eerder als kennis over de plausibiliteit van de theorie ten opzichte van andere theoretische interpretaties. Op basis hiervan wordt er dan een filosofisch kader uitgewerkt, een epistemologie van de exploratie, betreffende hoe deze plausibiliteit historisch-filosofisch begrepen moet worden. Meer specifiek wordt er beargumenteerd dat deze informatie over de plausibiliteit van een theoretische interpretatie kan veranderen doorheen de tijd, als een gevolg van de ontwikkeling van nieuwe experimenten en nieuwe theorieën, en dat dit er toe kan leiden dat eerdere experimentele resultaten anders geïnterpreteerd worden. Op basis van de hier ontwikkelde epistemologie van de exploratie wordt er dan beargumenteerd dat wat telt als een wetenschappelijk succes historisch variabel is, en bepaald wordt door wat gezien wordt als eerdere succesvolle theorieën en experimenten.