There are two competing views regarding the role of mechanistic knowledge in inferences about the effectiveness of interventions. One view holds that inferences about the effectiveness of interventions should be based only on data from population-level studies (often statistical evidence from randomised trials). The other view holds that such inferences must be based in part on mechanistic evidence. The competing views are local principles of inference, the plausibility of which can be assessed by a more general normative principle of inference. (...) Bayesianism tells us to base inferences on both the ‘likelihood’ and the ‘prior’. The likelihood represents statistical evidence. One influence on the prior probability of a hypothesis like ‘d causes x’ is mechanistic knowledge of how d causes x. Thus, reasoning about such inferences by appealing to both statistical and mechanistic evidence is vindicated by our best general theory of inference. The primary contribution of this paper is to assess the merits and weaknesses of the arguments on both sides of the debate, using the Bayesian framework. This analysis lends support to those who argue that we should base our causal inferences about interventions in part on mechanistic evidence. (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)

This chapter addresses the problem of ranking available drugs in guideline development to support clinicians in their work. Based on a pragmatic approach to the notion of evidence and a hierarchical view on different kinds of evidence this chapter introduces a decision aid, HiDAD, which draws on the multi criteria decision making literature. This decision aid implements the wide-spread intuition that there are different kinds of evidence with varying degrees of importance by relying on a strict ordinal ordering of kinds (...) of evidence. In order to construct a ranking every pair of drugs is first compared separately on all kinds of evidence. Next, these quantitative comparisons are then aggregated into an overall comparison between drugs based on all the available evidence in a way which avoids that evidence of less importance is trumped by evidence of the higher levels. Finally, these overall comparisons are used to determine the final ranking of drugs which then informs the process of guideline writing. Properties, modifications and applicability of the decision aid HiDAD are discussed and assessed. (shrink)

This book aims to show that recent developments in neuroscience permit a defense of free will. Through language, human beings can escape strict biological determinism.

In order to support health interventions, biomedical and population health researchers need to collect solid evidence. This article asks what type of evidence this should be and expands on previous work that focused on etiological explanations, or causal-mechanical explanations of why and how illness occurs. The article proposes adding predictive evidence to the explanatory evidence, in order to form a joint evidence set, or JES = [A,B,C,D], which consists of four different types of evidence: association [A], biology [B], confirmation [C], (...) and difference-making [D]. The article discusses explanatory coherence as a backbone for this proposal, suggests criteria for each type of evidence, and offers a rubric for multi-evidence mapping. (shrink)

Thinking about illness causation has a long and rich history in medicine. After a hiatus in the 1990s, the last one-and-a-half decades have seen a surge of publications on causality in the biomedical sciences. Interestingly, this surge is visible not only in the medical, epidemiological, bioinformatics, and public health literatures, but also among philosophical publications. In this essay, I review and discuss one most recent addition to the literature, "Causality: Philosophical Theory Meets Scientific Practice" written by philosophers Phyllis Illari and (...) Federica Russo about causality in the sciences, and particularly about the health sciences. (shrink)

This article examines two theses formulated by Russo and Williamson in their study of causal inference in the health sciences. The two theses are assessed against evidence from a specific case in the social sciences, i.e., research on the institutional determinants of the aggregate unemployment rate. The first Russo–Williamson Thesis is that a causal claim can only be established when it is jointly supported by difference-making and mechanistic evidence. This thesis is shown not to hold. While researchers in my case (...) study draw extensively on both types of evidence, one causal claim out of the three analyzed is established even though it is exclusively supported by mechanistic evidence. The second Russo–Williamson Thesis is that standard accounts of causality fail to handle the dualist epistemology highlighted in the first Thesis. I argue that a counterfactual-manipulationist account of causality—which is endorsed by many philosophers as well as many social scientists—can perfectly make sense of the typical strategy in my case study to draw on both difference-making and mechanistic evidence; it is just an instance of the common strategy of increasing evidential variety. (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)

Economists reason causally. Like many other scientists, they aim at formulating justified causal claims about their object of study. This thesis contributes to our understanding of how causal reasoning proceeds in economics. By using the research on the causes of unemployment as a case study, three questions are adressed. What are the meanings of causal claims? How can a causal claim be adequately supported by evidence? How are causal beliefs affected by incoming facts? In the process of answering these semantic, (...) epistemic and dynamical questions, the richness of causal reasoning in economics is brought to the foreground. In the part on semantics, it is argued that the meaning of causal generalizations in policy-oriented economics is best captured by using the concept of ‘inferential relation’ rather than the one of ‘referential relation’. This part contributes to develop an inferentialist semantics by distinguishing among types of inferential relations. In the part on epistemology, it is argued that justification in sciences like economics often relies, and ought to rely, on evidential variety―i.e. the combination of evidence from multiple sources. An interpretation of independence among evidential sources is offered: two evidential sources are fully independent if and only if the reasons why they would be unreliable do not overlap. It is then shown that the variety-of-evidence thesis does not hold under extreme circumstances. The part on dynamics focuses on deviant-case study. A storyline is provided for what deviant-case study aims at and how it proceeds in what is characterized as an ‘eclectic science’. (shrink)

Philosophers of science and medicine now aspire to provide useful, socially relevant accounts of mechanism. Existing accounts have forged the path by attending to mechanisms in historical context, scientific practice, the special sciences, and policy. Yet, their primary focus has been on more proximate issues related to therapeutic effectiveness. To take the next step toward social relevance, we must investigate the challenges facing researchers, clinicians, and policy makers involving values and social context. Accordingly, we learn valuable lessons about the connections (...) between mechanistic processes and more fundamental reasons for medical interventions, particularly moral, ethical, religious, and political concerns about health, agency, and power. This paper uses debates over the controversial morning-after pill to gain insight into the deeper reasons for the production and use of mechanistic knowledge throughout biomedical research, clinical practice, and governmental regulation. To practice socially relevant philosophy of science, I argue that we need to account for mechanistic knowledge beyond immediate effectiveness, such as how it can also provide moral guidance, aid ethical categorization in the clinic, and function as a political instrument. Such insights have implications for medical epistemology, including the value-laden dimensions of mechanistic reasoning and the “epistemic friction” of values. Furthermore, there are broader impacts for teaching research ethics and understanding the role of science advisors as political advocates. (shrink)

Glennan appeals to interventions to solve the ontological and explanatory regresses that threaten his mechanistic account of causality . I argue that Glennan’s manoeuvre fails. The appeal to interventions is not able to address the ontological regress, and it blocks the explanatory regress only at the cost of making the account inapplicable to non-modular mechanisms. I offer a solution to the explanatory regress that makes use of dynamic Bayesian networks. My argument is illustrated by a case study from systems biology, (...) namely, the mechanism for the irreversibility of apoptosis. I conclude by pointing out the implications of my argument for Glennan’s mechanistic account of causality and, more generally, for accounts of mechanistic explanation based on interventions. 1 Introduction2 Glennan’s Account of Causality3 Objections to Glennan’s Account4 Glennan’s Replies5 Ontological Symmetry?6 Explanatory Symmetry?7 A Solution to the Explanatory Regress8 The Prospects of Glennan’s Account. (shrink)

How many notions of cause are there? The causality literature is witnessing a flourishing of pluralist positions. Here I focus on a recent debate on whether interpreting causality in terms of inferential relations commits one to semantic pluralism (Reiss 2011) or not (Williamson 2006). I argue that inferentialism is compatible with a ‘weak’ form of monism, where causality is envisaged as one, vague cluster concept. I offer two arguments for this, one for vagueness, one for uniqueness. Finally, I qualify in (...) what sense the resulting form of monism is ‘weak’.¿Cuántas nociones de causa hay? Hay un resurgir de posiciones pluralistas en la bibliografía sobre causalidad. Me ocuparé aquí de un debate reciente sobre si la interpretación de la causalidad en términos de relaciones inferenciales nos compromete con el pluralismo semántico (Reiss 2011) o no (Williamson 2006). Defiendo que el inferencialismo es compatible con una forma ’debil’ de monismo, donde la causalidad se presenta como un único concepto vago y de agrupación (cluster). Ofrezco para ello dos argumentos, uno sobre vaguedad y otro sobre unicidad. Finalmente, matizaré en qué sentido esta forma demonismo es ’débil’. (shrink)

This paper defends the need for evidential diversity and the mix of methods that that can in train require. The focus is on causal claims, especially ‘singular’ claims about the effects of causes in a specific setting—either what will happen or what has happened. I do so by offering a template that categorises kinds of evidence that can support these claims. The catalogue is generated by considering what needs to happen for a causal process to carry through from putative cause (...) at the start to the targeted effect at the end. The usual call for mixed methods focusses on a single overall claim and argues that we increase certainty by the use of different methods with compensating strengths and weaknesses. My proposals instead focus on the evidence that supports the great many subsidiary claims that must hold if the overall one is to be true. As is typical for singular causal claims, the mix of methods that will generally be required to collect the kinds of evidence I urge will usually have little claim to the kind of rigour that is now widely demanded in evidencing causal claims, especially those for policy/treatment effectiveness. So I begin with an exploration of what seems to be intended by ‘rigour’ in such discussions, since it is seldom made clear just what makes the favoured methods especially rigorous. I then argue that the emphasis on rigour can be counterproductive. Rigour is often the enemy of evidential diversity, and evidential diversity—lots of it—can make for big improvements in the reliability of singular causal predictions and post hoc evaluations. I illustrate with the paragon of rigour for causal claims, randomised controlled trials (RCTs), rehearsing at some length what they can and cannot do to make it easier to assess the importance of rigour in warranting singular causal claims. (shrink)

In current philosophical discussions on evidence in the medical sciences, epidemiology has been used to exemplify a specific version of evidential pluralism. According to this view, known as the Russo–Williamson Thesis, evidence of both difference-making and mechanisms is produced to make causal claims in the health sciences. In this paper, I present an analysis of data and evidence in epidemiological practice, with a special focus on research on the exposome, and I cast doubt on the extent to which evidential pluralism (...) holds in this case. I start by focusing on the claim that molecular data allows for the production of mechanistic evidence. On the basis of a close look at the ways in which molecular data is used in exposome research, I caution against interpretations in terms of mechanistic evidence. Secondly, I expand my critical remarks on the thesis by addressing the conditions under which data is categorised as evidence in exposome research. I argue that these show that the classification of a dataset as a type of evidence is dependent on the ways in which the data is used. This is in contrast with the approach of evidential pluralism, where evidence is classified in different types on the basis of its intrinsic properties. Finally, I come back to what I consider the core of the thesis and suggest that the epidemiological research analysed in the paper indicates different interpretations of evidential pluralism and its applicability in the health sciences. (shrink)

This article focuses on the assessment of mechanistic relations with specific attention to medicine, where mechanistic models are widely employed. I first survey recent contributions in the philosophical literature on mechanistic causation, and then take issue with Federica Russo and Jon Williamson’s thesis that two types of evidence, probabilistic and mechanistic, are at stake in the health sciences. I argue instead that a distinction should be drawn between previously acquired knowledge of mechanisms and yet-to-be-discovered knowledge of mechanisms and that both (...) probabilistic evidence and manipulation are essential with respect to newly discovered mechanisms. (shrink)

This contribution claims that the two fundamental notions of causation at work in the health sciences are manipulative and mechanistic, and investigates what kinds of evidence matter for the assessment of causal relations. This article is a development of our 2007 article, ‘Plurality of Causality’, where we argue for a pluralistic account of causation with an eye to econometrics and a single medical example. The present contribution has a wider focus, and considers the notion of evidence within a whole range (...) of disciplines belonging to the health sciences. Section 1 addresses the relations between kinds of evidence and causal accounts, and it is shown how different notions of causation can be employed in various medical cases. Section 2 calls attention to issues crucial for any adequate epistemological theory of causation, such as the distinctions between types and tokens, observational and experimental regimes, explanation and prediction. Lastly, the notion of context is articulated, highlighted in its role in the assessment of causal links. All these issues are tackled in the framework of what we label a ‘bottom–up’ epistemology. (shrink)

Nearly 400 million adults have been vaccinated against COVID-19. Children have been excluded from the vaccination programmes owing to their lower vulnerability to COVID-19 and to the special protections that apply to children’s exposure to new biological products. WHO guidelines and national laws focus on medical safety in the process of vaccine approval, and on national security in the process of emergency authorisation. Because children suffer much from social distancing, it is argued that the harms from containment measures should be (...) factored in a broader perspective on the good of the child. Considering the available knowledge on the disease, vaccine, and coping strategies, the decision about vaccine access to children is a public responsibility. The ultimate choice is a matter of paediatric informed consent. Moreover, jurisdictions that permit non-participation in established childhood vaccination programmes should also permit choice of vaccines outside of the approved programmes. Even if vaccine supply is too short to cover the paediatric population, the a priori exclusion of children is unjust. It may also exacerbate local and global inequalities. The second part of the paper delineates a prudent and ethical scheme for gradual incorporation of minors in vaccination programmes that includes a rigorous postvaccination monitoring. This is a theoretical paper in ethics that uses the Pfizer vaccine as a stock example, without discussing possible differences among existing vaccines. The key purpose is reflection on the good of the child in emergencies and vaccine policymaking. All data relevant to the study are included in the article and in its refernces. (shrink)

Not only has the philosophical debate on causation been gaining ground in the last few decades, but it has also increasingly addressed the sciences. The biomedical sciences are among the most prominent fields that have been considered, with a number of works tackling the understanding of the notion of cause, the assessment of genuinely causal relations and the use of causal knowledge in applied contexts. Far from denying the merits of the debate on causation and the major theories it comprises, (...) this paper is meant as a stimulus for theorists of causation in the philosophy of biomedicine, with a focus on clinical matters. Without aiming at putting forward an original theory of causation and starting from the narration of two actual but paradigmatic cases at the joints between biomedical research and clinical practice, we want to point out that some pathological situations addressed by molecular medicine actually prove resistant to some of our major epistemological accounts of causal explanation. Given this scenario, which is very frequent in our hospitals, our analysis aims to provide a stimulus for the debate among theorists of causation in biomedicine interested in real cases in science in practice. We believe that this might in turn encourage some more general rethinking of the complex intertwinement of science, philosophy of science and ethics, as well as of the role of philosophy of science for clinical medicine itself. (shrink)

The epidemiologist Bradford Hill famously argued that in epidemiology, specificity of association (roughly, the fact that an environmental or behavioral risk factor is associated with just one or at most a few medical outcomes) is strong evidence of causation. Prominent epidemiologists have dismissed Hill’s claim on the ground that it relies on a dubious `one-cause one effect’ model of disease causation. The paper examines this methodological controversy, and argues that specificity considerations do have a useful role to play in causal (...) inference in epidemiology. More precisely, I argue that specificity considerations help solve a pervasive inferential problem in contemporary epidemiology: the problem of determining whether an exposure-outcome correlation might be due to confounding by a social factor. This examination of specificity has interesting consequences for our understanding of the methodology of epidemiology. It highlights how the methodology of epidemiology relies on local tools designed to address specific inference problems peculiar to the discipline, and shows that observational causal inference in epidemiology can proceed with little prior knowledge of the causal structure of the phenomenon investigated. I also argue that specificity of association cannot (despite claims to the contrary) be entirely explained in terms of Woodward’s well-known concept of “one-to-one” causal specificity. This is because specificity as understood by epidemiologists depends on whether an exposure (or outcome) is associated with a `heterogeneous’ set of variables. This dimension of heterogeneity is not captured in Woodward’s notion, but is crucial for understanding the evidential import of specificity of association. (shrink)

Is evidential pluralism possible when we move to the social sciences, and if so, to what degree? What are the analytical benefits? The answer put forward in this article is that there is a tradeoff between how serious social science methodologies take the study of mechanisms and the analytical benefits that flow from evidential pluralism. In the social sciences, there are a range of different approaches to studying mechanisms, differentiated by the degree to which the ‘process’ is unpacked theoretically, and (...) whether the approach takes seriously the particular nature of social phenomena and the epistemological consequences that flow from this, as in realist approaches to the study of mechanisms, or whether more neopositivist-based foundational assumptions are adopted. Depending on which approach to study mechanisms is used, evidential pluralism is either: easy but superficial, very productive but challenging, or almost impossible because of the fundamental differences between the types of claims being made and the forms of evidence used. (shrink)

Despite the consensus promoted by the evidence-based medicine framework, many authors continue to express doubts about the superiority of randomized controlled trials. This paper evaluates four objections targeting the legitimacy, feasibility, and extrapolation problems linked to the experimental practice of random allocation. I argue that random allocation is a methodologically sound and feasible practice contributing to the internal validity of controlled experiments dealing with heterogeneous populations. I emphasize, however, that random allocation is solely designed to ensure the validity of causal (...) inferences at the level of groups. By itself, random allocation cannot enhance test precision, doesn’t contribute to external validity, and limits the applicability of causal claims to individuals. (shrink)

Causal pluralism can be defended not only in respect to causal concepts and methodological guidelines, but also at the finer-grained level of causal inference from a particular source of evidence for causation. An argument for this last variety of pluralism is made based on an analysis of causal inference from randomized experiments (RCTs). Here, the causal interpretation of a statistically significant association can be established via multiple paths of reasoning, each relying on different assumptions and providing distinct elements of information (...) in favour of a causal interpretation. (shrink)

This paper proposes an extended version of the interventionist account for causal inference in the practical context of biological mechanism research. This paper studies the details of biological mechanism researchers’ practices of assessing the evidential legitimacy of experimental data, arguing why quantity and variety are two important criteria for this assessment. Because of the nature of biological mechanism research, the epistemic values of these two criteria result from the independence both between the causation of data generation and the causation in (...) question and between different interventions, not techniques. The former independence ensures that the interventions in the causation in question are not affected by the causation that is responsible for data generation. The latter independence ensures the reliability of the final mechanisms not only in the empirical but also the formal aspects. This paper first explores how the researchers use quantity to check the effectiveness of interventions, where they at the same time determine the validity of the difference-making revealed by the results of interventions. Then, this paper draws a distinction between experimental interventions and experimental techniques, so that the reliability of mechanisms, as supported by the variety of evidence, can be safely ensured in the probabilistic sense. The latter process is where the researchers establish evidence of the mechanisms connecting the events of interest. By using case studies, this paper proposes to use ‘intervention’ as the fruitful connecting point of literature between evidence and mechanisms. (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)

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)

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)

In his book “Medical Philosophy: Conceptual issues in Medicine”, Mario Bunge provides a unique account of medical philosophy that is deeply rooted in a realist ontology he calls “systemism”. According to systemism, the world consists of systems and their parts, and systems possess emergent properties that their parts lack. Events within systems may form causes and effects that are constantly conjoined via particular mechanisms. Bunge supports the views of the evidence-based medicine movement that randomized controlled trials (RCTs) provide the best (...) evidence to establish the truth of causal hypothesis; in fact, he argues that _only_ RCTs have this ability. Here, we argue that Bunge neglects the important feature of patients being open systems which are in steady interaction with their environment. We show that accepting this feature leads to counter-intuitive consequences for his account of medical hypothesis testing. In particular, we point out that (i) the confirmation of hypotheses is inherently stochastic and affords a probabilistic account of both confirmation and evidence which we provide here; (ii) RCTs are neither necessary nor sufficient to establish the truth of a causal claim; (iii) testing of causal hypotheses requires taking into account background knowledge and the context within which an intervention is applied. We conclude that there is no “best” research methodology in medicine, but that different methodologies should coexist in a complementary fashion. (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)

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)

Theory of illness causation is an important issue in all biomedical sciences, and solid etiological explanations are needed in order to develop therapeutic approaches in medicine and preventive interventions in public health. Until now, the literature about the theoretical underpinnings of illness causation research has been scarce and fragmented, and lacking a convenient summary. This interdisciplinary book provides a convenient and accessible distillation of the current status of research into this developing field, and adds a personal flavor to the discussion (...) by proposing the etiological stance as a comprehensive approach to identify modifiable causes of illness. (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 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.

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)

The history of economic thought witnessed several prominent economists who took seriously models and concepts in physics for the elucidation and prediction of economic phenomena. Econophysics is an emerging discipline at the intersection of heterodox economics and the physics of complex systems, with practitioners typically engaged in two overlapping but distinct methodological programs. The first is to export mathematical methods used in physics for the purposes of studying economic phenomena. The second is to export mechanisms in physics into economics. A (...) conclusion is drawn that physics transfer is often justified at the level of mathematical transfer but unjustified at the level of mechanistic transfer. (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)

That one person's modus ponens is another's modus tollens is the bane of philosophy because it strips many philosophical arguments of their persuasive force. The problem is that philosophical arguments become mere pantomemes: arguments that are reasonable to resist simply by denying the conclusion. Appeals to proof, intuition, evidence, and truth fail to alleviate the problem. Two broad strategies, however, do help in certain circumstances: an appeal to normal informal standards of what is reasonable (nisowir) and argument by interpretation. The (...) method of explication features prominently in both strategies, and the paper extends this method to apply to nisowir, introducing the concept of canonical explication. The paper illustrates the two strategies with examples of arguments from formal epistemology and suggests that an appeal to nisowir might help to defend against philosophical scepticism by shifting the burden of proof to the sceptic. (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.

At least historically, it was common for medical practitioners to believe causal hypotheses on the basis of standalone mechanistic reasoning. However, it is now widely acknowledged that standalone mechanistic reasoning is insufficient for appropriately believing a causal hypothesis in medicine, thanks in part to the so-called problem of masking. But standalone mechanistic reasoning is not the only type of mechanistic reasoning. When exactly then is it appropriate to believe a causal hypothesis on the basis of mechanistic reasoning? In this paper, (...) I argue that it has proved difficult to provide a satisfying answer to this question. I also argue that this difficulty is predicted by recent work in knowledge-first epistemology. I think this shows that recent work in epistemology has important implications for practice in the philosophy of science. It is therefore worth paying closer attention in the philosophy of science to this recent work in knowledge-first epistemology. (shrink)

Systems medicine is a promising new paradigm for discovering associations, causal relationships and mechanisms in medicine. But it faces some tough challenges that arise from the use of big data: in particular, the problem of how to integrate evidence and the problem of how to structure the development of models. I argue that objective Bayesian models offer one way of tackling the evidence integration problem. I also offer a general methodology for structuring the development of models, within which the objective (...) Bayesian approach fits rather naturally. (shrink)

Russo and Williamson (Int Stud Philos Sci 21(2):157–170, 2007) put forward the thesis that, at least in the health sciences, to establish the claim that C is a cause of E, one normally needs evidence of an underlying mechanism linking C and E as well as evidence that C makes a difference to E. This epistemological thesis poses a problem for most current analyses of causality which, in virtue of analysing causality in terms of just one of mechanisms or difference (...) making, cannot account for the need for the other kind of evidence. Weber (Int Stud Philos Sci 23(2):277–295, 2009) has suggested to the contrary that Giere’s probabilistic analysis of causality survives this criticism. In this paper, we look in detail at the case of medical imaging technology, which, we argue, supports the thesis of Russo and Williamson, and we respond to Weber’s suggestion, arguing that Giere’s account does not survive the criticism. (shrink)