Identifying the necessary and sufficient conditions for individuating and classifying diseases is a matter of great importance in the fields of law, ethics, epidemiology, and of course, medicine. In this paper, I first propose a means of achieving this goal, ensuring that no two distinct disease-types could correctly be ascribed to the same disease-token. I then posit a metaphysical ontology of diseases—that is, I give an account of what a disease is. This is essential to providing the most effective means (...) of interfering with disease processes. Following existing work in the philosophy of medicine and epidemiology (primarily Christopher Boorse; Caroline Whitbeck; Alexander Broadbent), philosophy of biology (Joseph LaPorte; D.L. Hull), conditional analyses of causation (J.L. Mackie; David Lewis), and recent literature on dispositional essentialism (Stephen Mumford and Rani Anjum; Alexander Bird), I endorse a dispositional conception of disease. Following discussion of various conceptions of disease-identity, their relations to the clinical and pathological effects of the diseases in question, and how diseases are treated, I conclude (i) that diseases should be individuated by their causes, and (ii) that diseases are causal processes best seen as simultaneously acting sequences of mutually manifesting dispositions. (shrink)

Assumptions about obesity—e.g., its connection to ill health, its causes, etc.—are still prevalent today, and they make up what I call the medical model of fatness. In this paper, I argue that the medical model was established on the basis of insufficient evidence and has nevertheless continued to be relied upon to justify methodological choices that further entrench the assumptions of the medical model. These choices are illegitimate in so far as they conflict with both the epistemic and social aims (...) of obesity research. I conclude the paper with a partial solution to these epistemic and social shortcomings. (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)

In The Biopsychosocial Model of Health and Disease, Derek Bolton and Grant Gillett argue that a defensible updated version of the biopsychosocial model requires a metaphysically adequate account of disease causation that can accommodate biological, psychological, and social factors. This present paper offers a philosophical critique of their account of biopsychosocial causation. I argue that their account relies on claims about the normativity and the semantic content of biological information that are metaphysically contentious. Moreover, I suggest that these claims are (...) unnecessary for a defence of biopsychosocial causation, as the roles of multiple and diverse factors in disease causation can be readily accommodated by a more widely accepted and less metaphysically contentious account of causation. I then raise the more general concern that they are misdiagnosing the problem with the traditional version of the biopsychosocial model. The challenge when developing an explanatorily valuable version of the biopsychosocial model, I argue, is not so much providing an adequate account of biopsychosocial causation, but providing an adequate account of causal selection. Finally, I consider how this problem may be solved to arrive at a more explanatorily valuable and clinically useful version of the biopsychosocial model. (shrink)

Modern medicine is often said to have originated with nineteenth century germ theory, which attributed diseases to bacterial contagions. The success of this theory is often associated with an underlying principle referred to as the “doctrine of specific etiology”. This doctrine refers to specificity at the level of disease causation or etiology. While the importance of this doctrine is frequently emphasized in the philosophical, historical, and medical literature, these sources lack a clear account of the types of specificity that it (...) involves and why exactly they matter. This paper argues that nineteenth century germ theory involves two types of specificity at the level of etiology. One type receives significant attention in the literature, but its influence on modern medicine has been misunderstood. A second type is present in this model, but it has been completely overlooked in the extant literature. My analysis clarifies how these types of specificity led to a novel conception of etiology that continues to figure in medicine today. (shrink)

In this article, I will reconstruct the monocausal model and argue that modern 'multifactorial diseases' are not monocausal by definition. 'Multifactorial diseases' are instead defined according to a constitutive disease model. On closer analysis, infectious diseases are also defined using the constitutive model rather than the monocausal model. As a result, our classification models alone cannot explain why infectious diseases have a universal etiology while chronic and noncommunicable diseases lack one. The explanation is instead provided by the nineteenth-century germ theorists.

An astonishing volume and diversity of evidence is available for many hypotheses in the biomedical and social sciences. Some of this evidence—usually from randomized controlled trials (RCTs)—is amalgamated by meta-analysis. Despite the ongoing debate regarding whether or not RCTs are the ‘gold-standard’ of evidence, it is usually meta-analysis which is considered the best source of evidence: meta-analysis is thought by many to be the platinum standard of evidence. However, I argue that meta-analysis falls far short of that standard. Different meta-analyses (...) of the same evidence can reach contradictory conclusions. Meta-analysis fails to provide objective grounds for intersubjective assessments of hypotheses because numerous decisions must be made when performing a meta-analysis which allow wide latitude for subjective idiosyncrasies to influence its outcome. I end by suggesting that an older tradition of evidence in medicine—the plurality of reasoning strategies appealed to by the epidemiologist Sir Bradford Hill—is a superior strategy for assessing a large volume and diversity of evidence. (shrink)

Evidence-Based Medicine has little consideration for mechanisms and philosophers of science and medicine have recently made pleas to increase the place of mechanisms in the medical evidence hierarchy. However, in this debate the notions of mechanisms seem to be limited to 'mechanistic processes' and 'complex-systems mechanisms,' understood as 'componential causal systems'. I believe that this will not do full justice to how mechanisms are used in biological, psychological and social sciences and, consequently, in a more biopsychosocial approach to medicine. Here, (...) I propose, following (Kuorikoski, 2009), to pay more attention to 'abstract forms of interaction' mechanisms. The present work scrutinized review articles on depression and medically unexplained pain, which are considered to be of multifactorial pathogenesis, for their use of mechanisms. In review articles on these disorders there seemed to be a range of uses between more 'abstract forms of interaction' and 'componential causal system' mechanisms. I therefore propose to expand the notions of mechanisms considered in medicine to include that of more 'abstract forms of interaction' to better explain and manage biopsychosocial disorders. (shrink)

Semmelweis’ discovery of the etiology of childbed fever has long attracted the attention of historians of medicine and biographers. In recent years it has also become of increasing interest to philosophers. In this paper I discuss the interpretation of Semmelweis’ methodology from the viewpoint of the inference to the best explanation and argue that Popperian methodology is better at capturing the dynamics of the growth of knowledge. Furthermore, I criticize the attempts to explain the failure of Semmelweis to have his (...) discovery accepted on the basis of the Kuhnian concept of paradigms, and warn that this view may endorse dogmatism as the norm The Kuhnian position also raises the problem of the authoritarian nature of scientific institutions which defend a paradigm against unorthodox, rebellious views, such as in the case of Semmelweis. Popperian philosophy is seen as a challenge to promote a link between an open society and open science with its main aim being to cherish a free critical spirit. (shrink)

This paper investigates the representation of authors with different linguistic backgrounds in academic publishing. We first review some common rebuttals of concerns about linguistic injustice. We then analyze 1039 authors of philosophy journals, primarily selected from the 2015 Leiter Report. While our data show that Anglophones dominate the output of philosophy papers, this unequal distribution cannot be solely attributed to language capacities. We also discover that ethics journals have more Anglophone authors than logic journals and that most authors are affiliated (...) with English-speaking universities, suggesting other factors may also play significant roles. Moreover, some interesting results are revealed when we combine the factor of sex with place of affiliation and linguistic background. It indicates that while certain linguistic injustice is inevitable in academic publishing, it may be more complex than thought. We next introduce Broadbent’s :457–476, 2012, Philosophy of epidemiology, Palgrave Macmillan, New York, 2013, Stud Hist Philos Biol Biomed Sci 48:250–257, 2014) contrastive account of causation to give a causal explanation of our findings. Broadbent’s account not only well characterizes the multifaceted causality in academic publishing but also provides a methodological guideline for further investigation. (shrink)

In this paper, I utilise the tools of analytic philosophy to amalgamate mono-causal and multi-causal theories of disease. My aim is to better integrate viral and socio-economic explanations of AIDS in particular, and to consider how the perceived divide between mono-causal and multi-causal theories played a role in the tragedy of AIDS denialism in South Africa in the early 2000s. Currently, there is conceptual ambiguity surrounding the relationship between mono-causal and multi-causal theories in biomedicine and epidemiology. Mono-causal theories focus on (...) single, typically microbial, sources of illness and are most concerned with infectious diseases. By contrast, multi-causal theories allow for multiple factors to underpin a disease’s aetiology, including socio-economic and behavioural factors, and they usually focus on chronic non-communicable diseases. However, if these theories are taken to be strictly distinct, this prevents the inclusion of both microbial and socio-economic factors in a single explanation of any particular disease. This strict distinction became a problem when trying to explain the disproportionate prevalence of AIDS in southern Africa and ultimately contributed to the tragedy of AIDS denialism in South Africa. In tandem with viewing how the perceived divide between multi-causal and mono-causal theories underpinned AIDS denialism, I examine Thabo Mbeki’s specific role, while acknowledging that AIDS is being deprioritised on a broader international level. Overall, I will demonstrate that any long-term plan to eliminate AIDS will require viral and socio-economic factors to be considered simultaneously and that such a theoretical approach requires a clearer understanding of the underlying concepts of disease aetiology. (shrink)

The case of Semmelweis has been well known since Hempel. More recently, it has been revived by Peter Lipton, Donald Gillies, Alexander Bird, Alex Broadbent, and Raphael Scholl. While these accounts differ on what exactly the case of Semmelweis shows, they all agree that Semmelweis was an excellent reasoner. This widespread agreement has also given rise to a puzzle: why Semmelweis’s views were rejected for so long. I aim to dissolve both this puzzle and the standard view of Semmelweis by (...) showing that, contrary to prevailing opinion, Semmelweis was not the excellent reasoner he has been assumed to be. (shrink)

Philosophy of epidemiology has recently emerged as a distinct branch of philosophy. The field will surely benefit from pluralism, reflected in the broad range of topics and perspectives in this special issue. Here, I argue that a healthy pluralistic field of philosophy of epidemiology has social responsibilities that require the field as a whole to engage actively with research on social determinants of health and health disparities. Practicing epidemiologists and the broader community of public health scientists have gradually acknowledged that (...) much of their attention ought to be paid to these, i.e. inequitable between-population health variations that largely reflect the world’s inequitable distribution of resources and social conditions. The paper illustrates how and why health disparities and social determinants of health, through no ill will, become de facto secondary concerns in Alex Broadbent’s field-defining Philosophy of Epidemiology, showing the ease with which these topics can be incidentally sidelined. As means for philosophy of epidemiology to meet its social responsibility obligations, I suggest philosophy of epidemiology expand its attention to two particular lines research. First, the paper discusses Geoffrey Rose’s concept of “causes of incidence”—causes of disparities between populations—and argues for the importance of engaging with these causes. Second, the paper argues for the value of engaging with Bruce Link and Jo Phelan’s “fundamental causes” model of how flexible social resources serve as buffers from harms, generating a plethora of shifting and locally-contingent health effects. (shrink)

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)

In the traditional philosophical debate over different conceptual analyses of “disease,” it is often presupposed that “disease” is univocally definable and that there are clear boundaries which distinguish this univocal category “disease” from the category of “nondisease.” In this paper, I will argue for a shift in the discussion on the concept of “disease” and propose an alternative, pragmatic approach that is based on the conviction that “disease” is not a theoretical concept but a practical term. I develop a view (...) on which our use of the term “disease” is determined by two interacting factors, namely, value-laden considerations about the desirabilty of certain states and discoveries of cause which is/are explanatorily relevant. I show how these factors interact with regard to a taxonomy of kinds of diseases. This pragmatic approach will not lead me to a final definition of “disease,” but will result in a more realistic description of the way we build, use, apply, and change our concept of “disease.” Meanwhile, it is useful as a basis for critical reflection on disease-labeling in medicine. (shrink)

Cancer—and scientific research on cancer—raises a variety of compelling philosophical questions. This entry will focus on four topics, which philosophers of science have begun to explore and debate. First, scientific classifications of cancer have as yet failed to yield a unified taxonomy. There is a diversity of classificatory schemes for cancer, and while some are hierarchical, others appear to be “cross-cutting,” or non-nested. This literature thus raises a variety of questions about the nature of the disease and disease classification. Second, (...) philosophers of science have historically taken the aim of science to be arriving at true theories. However, scientists studying cancer come from a variety of disciplines, with different scientific as well as practical aims. Perhaps it is not surprising, then, that historians and philosophers of science do not seem to agree on how best to characterize the aim and structure of cancer research; it is far from clear whether the appropriate characterization of the aim is arriving at true theories, or even whether the proper units of analysis are “theories”, or instead, “models”, “explanatory frameworks”, “research programs”, “paradigms”, or perhaps, “experimental traditions”. With the rise of “big data” science—such as the Cancer Genome Atlas Project (or TCGA)—and “systems” approaches to the study of disease, both philosophers and historians of science are rethinking how best to describe and explain these distinctive kinds of scientific inquiry. -/- Third, cancer is in part a byproduct of our developmental and life history, as well as our evolutionary history. Cancer progression can be compared to a reversion of development, or, to the evolution of multicellularity. Thus, cancer raises intriguing questions about how we conceive of “functions”, “development”, and the role of our evolutionary history and particularly, selective trade-offs, in vulnerability to disease. -/- Last but not least, cancer research provides a case study for consideration of the roles of values at the science-policy interface. Epidemiological and toxicological research on cancer’s causes informs toxics law and regulatory policy, which raises a variety of questions about the nature of evidence and inductive risk in such contexts. (shrink)

We argue that Koch’s postulates are best understood within an interventionist account of causation, in the sense described in Woodward. We show how this treatment helps to resolve interpretive puzzles associated with Koch’s work and how it clarifies the different roles the postulates play in providing useful, yet not universal criteria for disease causation. Our paper is an effort at rational reconstruction; we attempt to show how Koch’s postulates and reasoning make sense and are normatively justified within an interventionist framework (...) and more difficult to understand within alternative frameworks for thinking about causation. (shrink)

What kind of a thing are chronic diseases? Are they objects, bundles of signs and symptoms, properties, processes, or fictions? Rather than using concept analysis—the standard approach to disease in the philosophy of medicine—to answer this metaphysical question, I use a bottom-up, inductive approach. I argue that chronic diseases are bodily states or properties—often dispositional, but sometimes categorical. I also investigate the nature of related pathological entities: pathogenesis, etiology, and signs and symptoms. Finally, I defend my view against alternate accounts (...) of the nature of disease. (shrink)

Proponents of evidence-based medicine and some philosophers of science seem to agree that knowledge of mechanisms can help solve the problem of applying results of controlled studies to target populations (‘the problem of extrapolation’). We describe the problem of extrapolation, characterize mechanisms, and outline how mechanistic knowledge might be used to solve the problem. Our main thesis is that there are four often overlooked problems with using mechanistic knowledge to solve the problem of extrapolation. First, our understanding of mechanisms is (...) often (and arguably, likely to remain) incomplete. Secondly, knowledge of mechanisms is not always applicable outside the tightly controlled laboratory conditions in which it is gained. Thirdly, mechanisms can behave paradoxically. Fourthly, as Daniel Steel points out, using mechanistic knowledge faces the problem of the ‘extrapolator’s circle’. At the same time, when the problems with mechanistic knowledge have been addressed, such knowledge can and should be used to mitigate (nothing can entirely solve) the problem of extrapolation. (shrink)

Are the small and indolent cancers found in abundance in cancer screening normal variations, risk factors, or disease? Naturalists in philosophy of medicine turn to pathophysiological findings to decide such questions objectively. To understand the role of pathophysiological findings in disease definition, we must understand how they mislead in diagnostic reasoning. Participants on all sides of the definition of disease debate attempt to secure objectivity via reductionism. These reductivist routes to objectivity are inconsistent with the Bayesian nature of clinical reasoning; (...) when they appeal to the sciences, they are inconsistent with what philosophy of biology tells us about its natural kinds. Proposals that we narrow the scope of our claims in the disease definition debates are useful, but paradigms can still distort our reasoning in particular cases, even when we are self-conscious about their status. (shrink)

If there is any value in the idea that disease is something other than the mere absence of health then that value must lie in the way that diseases are classified. This paper offers further development of a view advanced previously, the 'contrastive model' of disease: it develops the account to handle asymptomatic disease ; and in doing so it relates the model to a broadly biostatistical view of health. The developments are prompted by considering cancers featuring viruses as prominent (...) causes, since these appear to amount to cases where the prescriptions of the contrastive model could be followed, but aren't. The resulting irrelevance objection claims that the contrastive model is irrelevant to medical science and practice. The paper seeks to rebut the irrelevance objection. (shrink)

This paper reassesses Robert Koch’s work on tropical infections of humans and cattle as being inspired by an underlying interest in epidemiology. Such an interest was developed from the early 1890s when it became clear that an exclusive focus on pathogens was insufficient as an approach to explain the genesis and dynamics of epidemics. Koch, who had failed to do so before, now highlighted differences between infection and disease and described the role of various sub-clinical states of disease in the (...) propagation and—consequently—in the control of epidemics. Studying pathologies of men and cattle in tropical countries eventually facilitated the application of such measures in Europe through the screening of healthy carriers of typhoid, which was carried out in 1902. The concept of the carrier state can be understood as a spin-off from tropical medicine into the study and control of infectious disease in Europe. With it travelled assumptions that were typical for colonial and veterinary medicine where the health of indigenous individuals or cattle would be a secondary objective compared to the control of diseases in populations. (shrink)

Concussions are a significant public health problem worldwide. This brain injury is problematic in the paediatric population for a variety of reasons; however, the enquiry into these problems has been mainly through the biomedical perspective. This approach has impacted nursing knowledge and practice of children and youth with a concussion, primarily since other perspectives are viewed as not being objective. In this manuscript, I draw on Thomas Kuhn's view of objectivity to evaluate the biomedical perspective of concussion. I utilize current (...) research and clinical examples to illustrate the advantages and drawbacks of this perspective for nursing. From this discussion, I propose an alternative perspective to capture the complexity of paediatric concussions for nursing, a systems perspective. Although I argue for an alternative perspective to approach paediatric concussions for nursing, I maintain that the biomedical perspective can be incorporated as one part of nursing knowledge and practice for paediatric concussion. (shrink)