Gegenstand dieses Beitrags ist eine Auseinandersetzung mit der Wissenschaftlichkeit der Medizin. Den Leitfaden der Analyse bildet dabei ein jüngerer Ansatz in der analytischen Wissenschaftstheorie, wonach Systematizität als zentrales Kriterium von Wissenschaft anzusehen ist (Hoyningen-Huene 2013). Ich werde im Detail zeigen, dass die Medizin dieses mehrdimensionale Kriterium insgesamt erfüllt, dass aus der Wissenschaftlichkeit der Medizin aber gleichwohl normative Konsequenzen folgen, die beispielsweise zur Abgrenzung von der Homöopathie und einer kritischen Bewertung des biopsychosozialen Modells führen. Zudem resultieren der Anwendungscharakter der Medizin und (...) die zentrale Bedeutung des Arzt-Patienten-Verhältnisses nicht in einer Schwächung des Anspruchs der Medizin als Wissenschaft. (shrink)

My doctoral project is a study of epistemological and ethical issues in Evidence-Based Medicine, a movement in medicine which emphasizes the use of randomized controlled trials. Much of the research on EBM suggests that, for a large part of the movement's history, EBM considered expertise, mechanisms, and values to be forces contrary to its goals and has sought to remove them, both from medical research and from the clinical encounter. I argue, however, that expertise, mechanisms and values have important epistemological (...) and ethical roles to play and can be incorporated into the current EBM movement. (shrink)

Russo and Williamson put forward the following thesis: in order to establish a causal claim in medicine, one normally needs to establish both that the putative cause and putative effect are appropriately correlated and that there is some underlying mechanism that can account for this correlation. I argue that, although the Russo-Williamson thesis conflicts with the tenets of present-day evidence-based medicine, it offers a better causal epistemology than that provided by present-day EBM because it better explains two key aspects of (...) causal discovery. First, the thesis better explains the role of clinical studies in establishing causal claims. Second, it yields a better account of extrapolation. (shrink)

In the biomedical context, policy makers face a large amount of potentially discordant evidence from different sources. This prompts the question of how this evidence should be aggregated in the interests of best-informed policy recommendations. The starting point of our discussion is Hunter and Williams’ recent work on an automated aggregation method for medical evidence. Our negative claim is that it is far from clear what the relevant criteria for evaluating an evidence aggregator of this sort are. What is the (...) appropriate balance between explicitly coded algorithms and implicit reasoning involved, for instance, in the packaging of input evidence? In short: What is the optimal degree of ‘automation’? On the positive side: We propose the ability to perform an adequate robustness analysis as the focal criterion, primarily because it directs efforts to what is most important, namely, the structure of the algorithm and the appropriate extent of automation. Moreover, where there are resource constraints on the aggregation process, one must also consider what balance between volume of evidence and accuracy in the treatment of individual evidence best facilitates inference. There is no prerogative to aggregate the total evidence available if this would in fact reduce overall accuracy. (shrink)

After describing the disorder of psychopathy, I examine the theories and the evidence concerning the psychopaths’ deficient moral capacities. I first examine whether or not psychopaths can pass tests of moral knowledge. Most of the evidence suggests that they can. If there is a lack of moral understanding, then it has to be due to an incapacity that affects not their declarative knowledge of moral norms, but their deeper understanding of them. I then examine two suggestions: it is their deficient (...) practical reason or their stunted emotions that are at fault. The evidence supports both explanations. I conclude with an overview of the debate concerning whether they are morally or legally responsible for their actions. (shrink)

This volume argues for a new image of science that understands both natural and social phenomena to be the product of mechanisms, casting the work of science as an effort to understand those mechanisms. Glennan offers an account of the nature of mechanisms and of the models used to represent them in physical, life, and social sciences.

Diagnoses in medicine are often taken to serve as explanations of patients’ symptoms and signs. This article examines how they do so. I begin by arguing that although some instances of diagnostic explanation can be formulated as covering law arguments, they are explanatory neither in virtue of their argumentative structures nor in virtue of general regularities between diagnoses and clinical presentations. I then consider the theory that medical diagnoses explain symptoms and signs by identifying their actual causes in particular cases. (...) While I take this to be largely correct, I argue that for a diagnosis to function as a satisfactory causal explanation of a patient’s symptoms and signs, it also needs to be supplemented by understanding the mechanisms by which the identified cause produces the symptoms and signs. This mechanistic understanding comes not from the diagnosis itself, but rather from the theoretical framework within which the physician operates. (shrink)

Evidence based medicine (EBM) is under critical debate, and person centered healthcare (PCH) has been proposed as an improvement. But is PCH offered as a supplement or as a replacement of EBM? Prima facie PCH only concerns the practice of medicine, while the contended features of EBM also include methods and medical model. I here argue that there are good philosophical reasons to see PCH as a radical alternative to the existing medical paradigm of EBM, since the two seem committed (...) to conflicting ontologies. This paper aims to make explicit some of the most fundamental assumptions that motivate EBM and PCH, respectively, in order to show that the choice between them ultimately comes down to ontological preference. While EBM has a solid foundation in positivism, or what I here call Humeanism, PCH is more consistent with causal dispositionalism. I conclude that if there is a paradigmatic revolution on the way in medicine, it is first of all one of ontology. (shrink)

The purpose of this chapter is to describe what we see as several important new directions for philosophy of medicine. This recent work (i) takes existing discussions in important and promising new directions, (ii) identifies areas that have not received sufficient and deserved attention to date, and/or (iii) brings together philosophy of medicine with other areas of philosophy (including bioethics, philosophy of psychiatry, and social epistemology). To this end, the next part focuses on what we call the “epistemological turn” in (...) recent work in the philosophy of medicine; the third part addresses new developments in medical research that raise interesting questions for philosophy of medicine; the fourth part is a discussion of philosophical issues within the practice of diagnosis; the fifth part focuses on the recent developments in psychiatric classification and scientific and ethical issues therein, and the final part focuses on the objectivity of medical research. (shrink)

This paper considers the applicability of standard accounts of causation to living systems. In particular it examines critically the increasing tendency to equate causal explanation with the identification of a mechanism. A range of differences between living systems and paradigm mechanisms are identified and discussed. While in principle it might be possible to accommodate an account of mechanism to these features, the attempt to do so risks reducing the idea of a mechanism to vacuity. It is proposed that the solution (...) to this problem requires the development of a philosophical account of process adequate to apply to living systems. (shrink)

Hierarchies of evidence are an important and influential tool for appraising evidence in medicine. In recent years, hierarchies have been formally adopted by organizations including the Cochrane Collaboration [1], NICE [2,3], the WHO [4], the US Preventive Services Task Force [5], and the Australian NHMRC [6,7]. The development of such hierarchies has been regarded as a central part of Evidence-Based Medicine, a movement within healthcare which prioritises the use of epidemiological evidence such as that provided by Randomised Controlled Trials. Philosophical (...) work on the methodology of medicine has so far mostly focused on claims about the superiority of RCTs, and hence has largely neglected the questions of what hierarchies are, what assumptions they require, and how they affect clinical practice. This thesis shows that there is great variation in the hierarchies defended and in the interpretations they are, and can be, given. The interpretative assumptions made in using hierarchies are crucial to the content and defensibility of the underlying philosophical commitments concerning evidence and medical practice. Once this variation is been identified, it becomes clear that the little philosophical work that has been done so far affects only some hierarchies, under some interpretations. Modest interpretations offered by La Caze [11], conditional hierarchies like GRADE [12-14], and heuristic approaches such as that defended by Howick et al. [15,16] all survive previous philosophical criticism. This thesis extends previous criticisms by arguing that modest interpretations are so weak as to be unhelpful for clinical practice; that GRADE and similar conditional models omit clinically relevant information, such as information about variation in treatments’ effects and the causes of different responses to therapy; and that heuristic approaches lack the necessary empirical support. The conclusion is that hierarchies in general embed untenable philosophical assumptions: principally that information about average treatment effects backed by high-quality evidence can justify strong recommendations, and that the impact of evidence from individual studies can and should be appraised in isolation. Hierarchies are a poor basis for the application of evidence in clinical practice. The Evidence-Based Medicine movement should move beyond them and explore alternative tools for appraising the overall evidence for therapeutic claims. (shrink)

Measuring the effectiveness of medical interventions faces three epistemological challenges: the choice of good measuring instruments, the use of appropriate analytic measures, and the use of a reliable method of extrapolating measures from an experimental context to a more general context. In practice each of these challenges contributes to overestimating the effectiveness of medical interventions. These challenges suggest the need for corrective normative principles. The instruments employed in clinical research should measure patient-relevant and disease-specific parameters, and should not be sensitive (...) to parameters that are only indirectly relevant. Effectiveness always should be measured and reported in absolute terms (using measures such as 'absolute risk reduction'), and only sometimes should effectiveness also be measured and reported in relative terms (using measures such as 'relative risk reduction')-employment of relative measures promotes an informal fallacy akin to the base-rate fallacy, which can be exploited to exaggerate claims of effectiveness. Finally, extrapolating from research settings to clinical settings should more rigorously take into account possible ways in which the intervention in question can fail to be effective in a target population. (shrink)

Mechanistic information is used in the field of risk assessment in order to clarify two controversial methodological issues, the selection of inference guides and the definition of standards of evidence. In this paper we present an analysis of the concept of mechanistic information in risk assessment by recurring to previous philosophical analyses of mechanistic explanation. Our conclusion is that the conceptual analysis of mechanistic explanation facilitates a better characterization of the concept of mechanistic information. However, it also shows that the (...) use of this kind of information in risk assessment is heavily influenced by pragmatic factors, which have not been sufficiently taken into account in philosophical analysis. Mechanistic models are like hypothesis that have to be validated empirically. Due to their dependence on the standards of evidence, they are subject to the same pragmatic factors. Therefore, recurring to mechanistic information does not lead to closure of the methodological controversies in risk assessment. (shrink)

Since its introduction just over two decades ago, evidence-based medicine (EBM) has come to dominate medical practice, teaching, and policy. There are a growing number of textbooks, journals, and websites dedicated to EBM research, teaching, and evidence dissemination. EBM was most recently defined as a method that integrates best research evidence with clinical expertise and patient values and circumstances in the treatment of patients. There have been debates throughout the early 21st century about what counts as good research evidence between (...) EBM proponents and philosophical critics and even within the EBM community itself. Similar controversy arises about the relative worth of patient values and clinical expertise (and how these can be integrated). EBM has also evolved in ways that have come under scrutiny. Specifically, policymakers have used EBM research methodology to increase the relative importance of clinical guidelines that some clinicians have argued are tyrannical. Philosophers have addressed all of these controversies, and with very few exceptions have been critical of EBM. In addition most philosophical attention has been on the epistemic role of Randomization and evidence hierarchies, with relatively little attention being paid to the role of Diagnosis, expertise, patient values, and Systematic Reviews within EBM. (shrink)

Proponents of evidence-based medicine have argued convincingly for applying this scientific method to medicine. However, the current methodological framework of the EBM movement has recently been called into question, especially in epidemiology and the philosophy of science. The debate has focused on whether the methodology of randomized controlled trials provides the best evidence available. This paper attempts to shift the focus of the debate by arguing that clinical reasoning involves a patchwork of evidential approaches and that the emphasis on evidence (...) hierarchies of methodology fails to lend credence to the common practice of corroboration in medicine. I argue that the strength of evidence lies in the evidence itself, and not the methodology used to obtain that evidence. Ultimately, when it comes to evaluating the effectiveness of medical interventions, it is the evidence obtained from the methodology rather than the methodology that should establish the strength of the evidence. (shrink)

Current research in molecular epidemiology uses biomarkers to model the different disease phases from environmental exposure, to early clinical changes, to development of disease. The hope is to get a better understanding of the causal impact of a number of pollutants and chemicals on several diseases, including cancer and allergies. In a recent paper Russo and Williamson address the question of what evidential elements enter the conceptualisation and modelling stages of this type of biomarkers research. Recent research in causality has (...) examined Ned Hall’s distinction between two concepts of causality: production and dependence. In another recent paper, Illari examined the relatively under-explored production approach to causality, arguing that at least one job of an account of causal production is to illuminate our inferential practices concerning causal linking. Illari argued that an informational account solves existing problems with traditional accounts. This paper follows up this previous work by investigating the nature of the causal links established in biomarkers research. We argue that traditional accounts of productive causality are unable to provide a sensible account of the nature of the causal link in biomarkers research, while an informational account is very promising. (shrink)

Evidence-based medicine (EBM) makes use of explicit procedures for grading evidence for causal claims. Normally, these procedures categorise evidence of correlation produced by statistical trials as better evidence for a causal claim than evidence of mechanisms produced by other methods. We argue, in contrast, that evidence of mechanisms needs to be viewed as complementary to, rather than inferior to, evidence of correlation. In this paper we first set out the case for treating evidence of mechanisms alongside evidence of correlation in (...) explicit protocols for evaluating evidence. Next we provide case studies which exemplify the ways in which evidence of mechanisms complements evidence of correlation in practice. Finally, we put forward some general considerations as to how the two sorts of evidence can be more closely integrated by EBM. (shrink)

Nancy Cartwright begins her recent book, Hunting Causes and Using Them, by noting that while a few years ago real causal claims were in dispute, nowadays “causality is back, and with a vengeance.” In the case of the social sciences, Keith Morrison writes that “Social science asks ‘why?’. Detecting causality or its corollary—prediction—is the jewel in the crown of social science research.” With respect to the health sciences, Judea Pearl writes that the “research questions that motivate most studies in the (...) health sciences are causal in nature.” However, not all data used by people interested in making causal claims come from experiments that use random assignment to control and treatment groups. Indeed, much research in the social and health science depends on non-experimental, observational data. Thus, one of the most important problems in the social and health sciences concerns making warranted causal claims using non-experimental, observational data; viz., “Can observational data be used to make etiological inferences leading to warranted causal claims?” This paper examines one method of warranting causal claims that is especially widespread in epidemiology and the health sciences generally—the use of causal criteria. It is argued that cases of complex causation generally, and redundant causation—both causal overdetermination and causal preemption—specifically, undermine the use of such criteria to warrant causal claims. (shrink)

Evidence hierarchies are widely used to assess evidence in systematic reviews of medical studies. I give several arguments against the use of evidence hierarchies. The problems with evidence hierarchies are numerous, and include methodological shortcomings, philosophical problems, and formal constraints. I argue that medical science should not employ evidence hierarchies, including even the latest and most-sophisticated of such hierarchies.

This paper sets out to analyze how causation works by focusing on biology, as represented by epidemiology and by scientific information on how the body works (“physiology”). It starts by exploring the specificity of evolved physiological systems, in which evolutionary, developmental and proximal causes all fit together, and the concept of function is meaningful; in contrast, this structure does not apply in epidemiology (or outside biology). Using these two contrasting branches of biology, I examine the role both of mechanism and (...) of difference making in causation. I find that causation necessarily involves both mechanism and difference making, and that they play complementary roles. Both are seen as ontologically necessary, even if the evidence is not always available for both. Influential monist accounts that focus on one of these, at the expense of ignoring the other, are found to be inadequate on these and on other grounds. Recent attempts to combine them are reviewed, notably that of Russo and Williamson (Int Stud Philos Sci 21:157–170, 2007), and it is argued that their epistemic view requires there to be a source of the different types of evidence that a rational agent would consider, and that this source must be ontic. I then analyze how causal relationships work in evolved physiological systems and in those studied by epidemiology, with a particular focus on how mechanism interacts with input. Finally, I consider this concept of causation from the perspective of everyday language, and of its possible generalisability outside biology. (shrink)

The mechanistic and causal accounts of explanation are often conflated to yield a ‘causal-mechanical’ account. This paper prizes them apart and asks: if the mechanistic account is correct, how can causal explanations be explanatory? The answer to this question varies according to how causality itself is understood. It is argued that difference-making, mechanistic, dualist and inferentialist accounts of causality all struggle to yield explanatory causal explanations, but that an epistemic account of causality is more promising in this regard.

Semmelweis’s discovery of the cause of puerperal fever around the middle of the 19th century counts among the paradigm cases of scientific discovery. For several decades, philosophers of science have used the episode to illustrate, appraise and compare views of proper scientific methodology.Here I argue that the episode can be profitably reexamined in light of two cognate notions: causal reasoning and mechanisms. Semmelweis used several causal reasoning strategies both to support his own and to reject competing hypotheses. However, these strategies (...) have gone unappreciated in the existing literature. I show that a causal reasoning approach makes sense of the multitude of tables in Semmelweis’s main text, which in later editions were often abridged because they appeared redundant.Moreover, the existing literature tends to focus on Semmelweis’s clinical intervention and on the extent to which it alone confirms his theoretical conclusions. This neglects Semmelweis’s efforts to show by animal experiments that his clinical results are in agreement with a demonstrable mechanism of puerperal fever pathogenesis. I argue that the full evidential force of Semmelweis’s argument can only be appreciated if both his clinical and his laboratory investigations are taken into account. (shrink)

In this thesis, I give a metascientific account of causality in medicine. I begin with two historical cases of causal discovery. These are the discovery of the causation of Burkitt’s lymphoma by the Epstein-Barr virus, and of the various viral causes suggested for cervical cancer. These historical cases then support a philosophical discussion of causality in medicine. This begins with an introduction to the Russo- Williamson thesis (RWT), and discussion of a range of counter-arguments against it. Despite these, I argue (...) that the RWT is historically workable, given a small number of modifications. I then expand Russo and Williamson’s account. I first develop their suggestion that causal relationships in medicine require some kind of evidence of mechanism. I begin with a number of accounts of mechanisms and produce a range of consensus features of them. I then develop this consensus position by reference to the two historical case studies with an eye to their operational competence. In particular, I suggest that it is mechanistic models and their representations which we are concerned with in medicine, rather than the mechanism as it exists in the world. -/- I then employ these mechanistic models to give an account of the sorts of evidence used in formulating and evaluating causal claims. Again, I use the two human viral oncogenesis cases to give this account. I characterise and distinguish evidence of mechanism from evidence of difference-making, and relate this to mechanistic models. I then suggest the relationship between types of evidence presents us with a means of tackling the reference-class problem. This sets the scene for the final chapter. Here, I suggest the manner in which these two different classes of evidence become integrated is also reflected in the way that developing research programmes change as their associated causal claims develop. (shrink)

Part I of this paper introduced a range of mechanistic theories of causality, including process theories and the complex-systems theories, and some of the problems they face. Part II argues that while there is a decisive case against a purely mechanistic analysis, a viable theory of causality must incorporate mechanisms as an ingredient, and describes one way of providing an analysis of causality which reaps the rewards of the mechanistic approach without succumbing to its pitfalls.

Part I of this paper introduces a range of mechanistic theories of causality, including process theories and the complex-systems theories, and some of the problems they face. Part II argues that while there is a decisive case against a purely mechanistic analysis, a viable theory of causality must incorporate mechanisms as an ingredient, and describes one way of providing an analysis of causality which reaps the rewards of the mechanistic approach without succumbing to its pitfalls.

The development of causal modelling since the 1950s has been accompanied by a number of controversies, the most striking of which concerns the Markov condition. Reichenbach's conjunctive forks did satisfy the Markov condition, while Salmon's interactive forks did not. Subsequently some experts in the field have argued that adequate causal models should always satisfy the Markov condition, while others have claimed that non-Markovian causal models are needed in some cases. This paper argues for the second position by considering the multi-causal (...) forks, which are widespread in contemporary medicine (Section 2). A non-Markovian causal model for such forks is introduced and shown to be mathematically tractable (Sections 6, 7, and 8). The paper also gives a general discussion of the controversy about the Markov condition (Section 1), and of the related controversy about probabilistic causality (Sections 3, 4, and 5). (shrink)

Even though the evidence‐based medicine movement (EBM) labels mechanisms a low quality form of evidence, consideration of the mechanisms on which medicine relies, and the distinct roles that mechanisms might play in clinical practice, offers a number of insights into EBM itself. In this paper, I examine the connections between EBM and mechanisms from several angles. I diagnose what went wrong in two examples where mechanistic reasoning failed to generate accurate predictions for how a dysfunctional mechanism would respond to intervention. (...) I then use these examples to explain why we should expect this kind of mechanistic reasoning to fail in systematic ways, by situating these failures in terms of evolved complexity of the causal system(s) in question. I argue that there is still a different role in which mechanisms continue to figure as evidence in EBM: namely, in guiding the application of population‐level recommendations to individual patients. Thus, even though the evidence‐based movement rejects one role in which mechanistic reasoning serves as evidence, there are other evidentiary roles for mechanistic reasoning. This renders plausible the claims of some critics of evidencebased medicine who point to the ineliminable role of clinical experience. Clearly specifying the ways in which mechanisms and mechanistic reasoning can be involved in clinical practice frames the discussion about EBM and clinical experience in more fruitful terms. (shrink)

I present three reasons why philosophers of science should be more concerned about violations of causal faithfulness (CF). In complex evolved systems, mechanisms for maintaining various equilibrium states are highly likely to violate CF. Even when such systems do not precisely violate CF, they may nevertheless generate precisely the same problems for inferring causal structure from probabilistic relationships in data as do genuine CF-violations. Thus, potential CF-violations are particularly germane to experimental science when we rely on probabilistic information to uncover (...) the DAG, rather than already knowing the DAG from which we could predict the right experiments to ‘catch out’ the hidden causal relationships. (shrink)

The paper addresses the question of how different types of evidence ought to inform public health policy. By analysing case studies on obesity, the paper draws lessons about the different roles that different types of evidence play in setting up public health policies. More specifically, it is argued that evidence of difference-making supports considerations about ‘what works for whom in what circumstances’, and that evidence of mechanisms provides information about the ‘causal pathways’ to intervene upon.

Philosophers of science have insisted that evidence of underlying mechanisms is required to support claims about the effects of medical interventions. Yet evidence about mechanisms does not feature on dominant evidence-based medicine “hierarchies.” After arguing that only inferences from mechanisms (“mechanistic reasoning”)—not mechanisms themselves—count as evidence, I argue for a middle ground. Mechanistic reasoning is not required to establish causation when we have high-quality controlled studies; moreover, mechanistic reasoning is more problematic than has been assumed. Yet where the problems can (...) be overcome, mechanistic reasoning can and should be used as evidence. (shrink)

The paper considers the legal tools that have been developed in German pharmaceutical regulation as a result of the precautionary attitude inaugurated by the Contergan decision. These tools are the notion of “well-founded suspicion”, which attenuates the requirements for safety intervention by relaxing the requirement of a proved causal connection between danger and source, and the introduction of the reversal of proof burden in liability norms. The paper focuses on the first and proposes seeing the precautionary principle as an instance (...) of the requirement that one should maximise expected utility. In order to maximise expected utility certain probabilities are required and it is argued that objective Bayesianism offers the most plausible means to determine the optimal decision in cases where evidence supports diverging choices. (shrink)

In this paper, I examine the comparatively neglected intuition of production regarding causality. I begin by examining the weaknesses of current production accounts of causality. I then distinguish between giving a good production account of causality and a good account of production. I argue that an account of production is needed to make sense of vital practices in causal inference. Finally, I offer an information transmission account of production based on John Collier’s work that solves the primary weaknesses of current (...) production accounts: applicability and absences. (shrink)

Public health involves the application of a wide variety of scientific and non-scientific disciplines to the very practical problems of improving population health and preventing disease. Public health has received surprisingly little attention from philosophers of science. In this chapter we consider some neglected but important philosophical aspects of the science of public health.

The notion of ‘causal web’ emerged in the epidemiological literature in the early Sixties and had to wait until the Nineties for a thorough critical appraisal. Famously, Nancy Krieger argued that such a notion isn’t helpful unless we specify what kind of spiders create the webs. This means, according to Krieger, (i) that the role of the spiders is to provide an explanation of the yarns of the web and (ii) that the sought spiders have to be biological and social. (...) This paper contributes to the development of the notion of causal web, elaborating on the two following points: (i) to catch the spiders we need multi-fold evidence—specifically, mechanistic and difference-making—and (ii) for the eco-social to be explanatory, the web has to be mechanistic in a sense to be specified. (shrink)

Jenner (1749–1826) is known as the father of the smallpox vaccine. Through an inferential analysis of Jenner’s report of inquiry, in which medical practice and medical research are intrinsically intertwined, we highlight his use of abductive hypotheses. Our understanding of abduction is based on the Gabbay and Woods (2005, The Reach of Abduction Insight and Trial, 2, 39) model, in which hypotheses can be activated even when they have not been confirmed, as well as Magnani’s Select and Test model (1992, (...) 2017). We discuss the fundamental role of abductive hypotheses in experimental medicine and understood in the sense of Bernard (1865, Introduction à l’étude la médecine expérimentale). We conclude with remarks about mechanistic hypotheses discussed by Jenner, in relation to the thesis advocated by Russo and Williamson (2007, Int. Stud. Philos. Sci., 21, 157–170). (shrink)

The literature on pluralism in economics has focused on the benefits expected from the plurality of theories, methods, and frameworks. This overlooks half of the picture: the costs. Neither have the multifarious costs been systematically analyzed in philosophy of science. We begin rectifying this neglect. We discuss how the benefits of plurality and diversity in science presuppose distinct types of plurality and how various benefit and plurality types are associated with different types of costs. Finally, we ponder how the general (...) mechanisms that give rise to the costs of plurality and diversity are aggravated by various disciplinary characteristics of economics. (shrink)

This chapter focuses on the experimental practices and reasoning strategies employed in nineteenth century investigations on the causal origin of the phenomenon of Brownian movement. It argues that there was an extensive and sophisticated experimental work done on the phenomenon throughout the nineteenth century. Investigators followed as rigorously as possible the methodological standards of their time to make causal claims and advance causal explanations of Brownian movement. Two major methodological strategies were employed. The first was the experimental strategy of varying (...) the circumstances. Suspected causal factors were varied and the resulting effect on Brownian movement was studied. The main goal of this strategy was the identification of difference-making factors, i.e., factors having a causal influence on the phenomenon. The second was the so-called method of hypothesis. Rather than relying exclusively on the ability of experiments to identify difference-making factors, its proponents tried to show how the independently developed tenets of the new kinetic-molecular conception of matter provided a plausible causal explanation of Brownian movement. Each one of these methodological strategies had its distinctive practices and notions of control. None of these strategies could, on its own, establish molecular motion as the cause of Brownian movement. It was only the fruitful combination of the two strategies and of their accompanying practices and notions of control that led, at the end of the nineteenth century, to the recognition of molecular motion as the most probable cause of Brownian movement. (shrink)

We often hear how scientists have discovered that a certain human trait – or a trait of another type of organism – is innate, genetic, heritable, inherited, naturally selected etc. All these claims have something in common: they all declare a trait to have significant organism internal (for instance genetic) causes that are present in the organism at its birth. I call claims like these “nativist claims”. Nativist claims are important. They shape our overall understanding of what we are, what (...) we can do and what is good for us. They also impact our practical decision making. For instance, we know that certain types of genes increase the risk of certain diseases, and increasingly this has an effect on healthcare practices. Many people believe that in the matter of children’s education we should consider the fact that many cognitive abilities are highly heritable. Associations between genetics and aggressive behavior have been taken to be alleviating circumstances in criminal sentencing. It is therefore important to correctly understand the content and implications of nativist claims. In this doctoral thesis I analyze, by philosophical means, the content of different kinds of nativist claim. What does it mean that some psychological tendency is innate? What does it mean that intelligence is 50% heritable? How (if at all) do genes come to carry information about the traits of an organism – they are nothing like the information carriers familiar to us, such as newspapers, e-mails, secret codes, and audio files. This thesis emphasizes two things. Firstly, I demonstrate, that in different scientific contexts these words ('innate', 'genetically caused' etc.) can mean very different things. Therefore, the implications of a given nativist claim in one scientific context can be remarkably different from another nativist claim’s implications in some other scientific context. Secondly, I explain how the development of innate, heritable and genetically caused traits can be determined in different and often unexpected ways by our environment and experiences. I demonstrate that the content of a concept that is considered innate by cognitive scientists can be determined by what the organism that possesses the concept has experienced. I also show that even a trait which is 100% heritable can at the same time be a socially constructed trait. (shrink)

This paper develops an account of how the implementation of ML models into healthcare settings requires revising the methodological apparatus of philosophical bioethics. On this account, ML models are cognitive interventions that provide decision-support to physicians and patients. Due to reliability issues, opaque reasoning processes, and information asymmetries, ML models pose inferential problems for them. These inferential problems lay the grounds for many ethical problems that currently claim centre-stage in the bioethical debate. Accordingly, this paper argues that the best way (...) to make progress in remedying these ethical problems is to distil their epistemic core and to identify appropriate epistemic norms as guardrails. The viability of this approach will be highlighted based on four key issues: trust, responsibility, paternalism, and fairness. In that respect, the paper also contributes to a more pronounced view of the specific methodological challenges for ethical theorizing, when the point of reference are complex statistical models that make predictions, rather than individual agents, acting for reasons. (shrink)

Gender affirming hormone treatment is an important part of the care of trans adolescents which enables them to develop the secondary sexual characteristics congruent with their identified genders. There is an increasing amount of empirical evidence showing the benefits of gender affirming hormone treatment for psychological health and social well-being in this population. However, in several countries, access to gender affirming hormone treatment for trans adolescents has recently been severely restricted. While much of the opposition to gender affirming hormone treatment (...) for trans adolescents has in part been ideologically motivated, it also reflects a debate about whether there are harms that outweigh the benefits of the treatment. Accordingly, a systematic and comprehensive philosophical analysis of the ethics of gender affirming hormone treatment for trans adolescents is needed. Herein, I offer such an analysis that draws on the four principles of biomedical ethics by Tom Beauchamp and James Childress. Based on the considerations of beneficence, nonmaleficence, autonomy, and justice, I argue that the provision of access to gender affirming hormone treatment for consenting trans adolescents is ethically required and that the current restrictions to such treatment are ethically wrong. (shrink)

Philosophical analyses of causation have been centred on the question of what causation is. More precisely speaking, philosophers tend to address four different issues: metaphysical (what is causation out there?), epistemological (how can a causal claim be established and assessed?), conceptual (what does the word ‘cause’ mean?), and methodological (what methods ought one to use in order to establish and assess causal claims?). This chapter argues that the practical issue of causation (what is a causal claim for in practice?) is (...) highly relevant to the metaphysical, epistemological, conceptual, and methodological issues of causation. Any philosophical enquiry into causation without an examination of this practical issue is incomplete. In other words, a promising approach to causation ought to take all of the metaphysical, epistemological, conceptual, methodological, and practical issues into account. (shrink)

There have recently been novel applications of medical systematic review guidelines to economic policy interventions which contain controversial methodological assumptions that require further scrutiny. A landmark 2017 Cochrane review of unconditional cash transfer (UCT) studies, based on the Grading of Recommendations Assessment, Development and Evaluation (GRADE), exemplifies both the possibilities and limitations of applying medical systematic review guidelines to UCT and universal basic income (UBI) studies. Recognizing the need to upgrade GRADE to incorporate the differences between medical and policy interventions, (...) the GRADE Public Health Project Group (PHPG) was convened to enumerate and address these methodological challenges. However, in light of our analysis of additional methodological challenges that arise for UCT and UBI studies, we argue that the adaptation of medical systematic review guidelines to economic methodology is far from straightforward and is in fact more challenging than claimed by the PHPG. (shrink)

While loneliness has been linked to various mental and physical health problems, the sense in which loneliness is a cause of these conditions has so far attracted little philosophical attention. This paper aims to fill this gap by analyzing research on health effects of loneliness and therapeutic interventions through current approaches to causality. To deal with the problem of causality between psychological, social, and biological variables, the paper endorses a biopsychosocial model of health and disease. I will investigate how three (...) main approaches to causality used in psychiatry and public health apply to loneliness: interventionism, mechanisms, and dispositional theories. Interventionism can specify whether loneliness causes specific effects, or whether a treatment works, incorporating results from randomized controlled trials. Mechanisms help explain how loneliness brings about negative health effects, spelling out psychological processes involved in lonely social cognition. Dispositional approaches help stress particular features of loneliness connected to negative social interactions, such as defensiveness. I will conclude by showing that previous research alongside emerging approaches to health effects of loneliness lend themselves to analysis in terms of the causal models under discussion. (shrink)

The Covid-19 pandemic has challenged both medicine and governments as they have strived to confront the pandemic and its consequences. One major challenge is that evidence-based medicine has struggled to provide timely and necessary evidence to guide medical practice and public policy formulation. We propose an extension of evidence-based corona medicine to an organismic systems corona medicine as a multilevel conceptual framework to develop a robust concept-oriented medical system. The proposed organismic systems corona medicine could help to prevent or mitigate (...) future pandemics by transitioning to a bifocal medicine that extends an empirical evidence-based medicine to a theory-oriented organismic systems medicine. (shrink)

Evidence-based medicine (EBM) has long deemphasized mechanistic reasoning and pathophysiological rationale in assessing the effectiveness of interventions. The EBM+ movement has challenged this stance, arguing that evidence of mechanisms and comparative studies should both be seen as necessary and complementary. Advocates of EBM+ provide a combination of theoretical arguments and examples of mechanistic reasoning in medical research. However, EBM+ proponents have not provided recent examples of how downplaying mechanistic reasoning resulted in worse medical results than would have occurred otherwise. Such (...) examples are necessary to make the case that EBM+ responds to a problem in clinical practice that urgently demands a solution. In light of this, we examine the failed rollout of efavirenz as a first-line HIV treatment in Zimbabwe as evidence of the importance of mechanistic reasoning in improving clinical practice and public health policy decisions. We suggest that this case is analogous to examples commonly given to support EBM. (shrink)

This paper aims to clarify the nature of understanding in medicine. The first part describes in more detail what it means to understand something and links a type of understanding (i.e., objectual understanding) to explanations. The second part proceeds to investigate what objectual understanding of a disease (i.e., biomedical understanding) requires by considering the case of scurvy from the history of medicine. The main hypothesis is that grasping a mechanistic explanation of a condition is necessary for a biomedical understanding of (...) that condition. The third part of the paper argues that biomedical understanding is necessary, but not sufficient for understanding in a clinical context (i.e., clinical understanding). The hypothesis is that clinical understanding combines biomedical understanding of a _disease_ or pathological condition with understanding _illness,_ which involves some degree of personal understanding of the patient. It is argued that, in many cases, clinical understanding necessitates adopting a particular second-personal stance and using cognitive resources _in addition_ to those involved in biomedical understanding. (shrink)

This paper aims to clarify the nature of understanding in medicine. The first part describes in more detail what it means to understand something and links a type of understanding (i.e., objectual understanding) to explanations. The second part proceeds to investigate what objectual understanding of a disease (i.e., biomedical understanding) requires by considering the case of scurvy from the history of medi- cine. The main hypothesis is that grasping a mechanistic explanation of a condi- tion is necessary for a biomedical (...) understanding of that condition. The third part of the paper argues that biomedical understanding is necessary, but not sufficient for understanding in a clinical context (i.e., clinical understanding). The hypothe- sis is that clinical understanding combines biomedical understanding of a disease or pathological condition with understanding illness, which involves some degree of personal understanding of the patient. It is argued that, in many cases, clinical understanding necessitates adopting a particular second-personal stance and using cognitive resources in addition to those involved in biomedical understanding. (shrink)