Anton de Bary is best known for his elucidation of the life cycle of Phytopthora infestans, the causal organism of late blight of potato and the crop losses that caused famine in nineteenth-century Europe. But while practitioner histories often claim this accomplishment as a founding moment of modern plant pathology, closer examination of de Bary’s experiments and his published work suggest that his primary motiviation for pursing this research was based in developmental biology, not agriculture. De Bary shied away from (...) making any recommendations for agricultural practice, and instead focused nearly exclusively on spontaneous generation and fungal development – both concepts promoted through prize questions posted by the Académie des Sciences in the 1850s and 1860s. De Bary’s submission to the Académie’s 1859 Alhumbert prize question illustrates his own contributions to debates about spontaneous generation and demonstrates the practical applications of seemingly philosophical questions – such as the origin of life. (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)

Anton de Bary is best known for his elucidation of the life cycle of Phytopthora infestans, the causal organism of late blight of potato and the crop losses that caused famine in nineteenth-century Europe. But while practitioner histories often claim this accomplishment as a founding moment of modern plant pathology, closer examination of de Bary's experiments and his published work suggest that his primary motiviation for pursing this research was based in developmental biology, not agriculture. De Bary shied away from (...) making any recommendations for agricultural practice, and instead focused nearly exclusively on spontaneous generation and fungal development – both concepts promoted through prize questions posted by the Académie des Sciences in the 1850s and 1860s. De Bary's submission to the Académie's 1859 Alhumbert prize question illustrates his own contributions to debates about spontaneous generation and demonstrates the practical applications of seemingly philosophical questions – such as the origin of life. (shrink)

Nineteenth-century medical advances were entwined with a conceptual innovation: the idea that many cases of disease which were previously thought to have diverse causes could be explained by the action of a single kind of cause, for example a certain bacterial or parasitic infestation. The focus of modern epidemiology, however, is on chronic non-communicable diseases, which frequently do not seem to be attributable to any single causal factor. This paper is an effort to resolve the resulting tension. The paper (...) criticises the monocausal model of disease, so successful in the nineteenth century. It also argues that a multifactorial model of disease can only be satisfactory if it amounts to more than a mere rejection of the monocausal model. A third alternative, the contrastive model, is proposed and defended on the grounds that it links the notions of disease and of general explanation, while avoiding the philosophical naiveties and practical difficulties of the monocausal model. (shrink)

The prevention, treatment and management of disease are closely linked to how the causes of a particular disease are explained. For multi-factorial conditions, the causal explanations are inevitably complex and competing models may exist to explain the same condition. Selecting one particular causal explanation over another will carry practical and ethical consequences that are acutely relevant for health policy. In this paper our focus is two-fold; the different models of causal explanation that are put forward within current scientific (...) literature for the high and rising prevalence of the common complex conditions of coronary artery disease and type 2 diabetes mellitus ; and how these explanations are taken up within national health policy guidelines. We examine the causal explanations for these two conditions through a systematic database search of current scientific literature. By identifying different causal explanations we propose a three-tier taxonomy of the most prominent models of explanations: evolutionary, lifecourse, and lifestyle and environment. We elaborate this taxonomy with a micro-level thematic analysis to illustrate how some explanations are semantically and rhetorically foregrounded over others. We then investigate the uptake of the scientific causal explanations in health policy documents with regard to the prevention and management recommendations of current National Service Frameworks for CAD and T2D. Our findings indicate a lack of congruence between the complexity and frequent overlap of causal explanations evident in the scientific literature and the predominant focus on lifestyle recommendations found in the mainstream health policy documents. (shrink)

This paper examines the way in which causal relations are understood in the dominant model in contemporary medicine. It argues that the causal relation is not definable in terms of the condition relation, but that in general for conditions of an occurrence to be among its causes they must answer instrumental interests in a certain way, and there are further criteria for distinguishing 'the' cause of a disease (i.e., its etiological agent) from other causal factors, which are based upon (...) instrumental interests peculiar to medicine. It also argues that diseases are complex processes of which both clinical and underlying patho-physiological manifestations are proper parts (as contrasted with effects). (shrink)

Causation is important when considering how an organism maintains health, why disease arises in a healthy person, and how one may intervene to change the course of a disease. This paper explores the form of causative relationships in health, disease and intervention, with particular regard to the pathological and biopsychosocial models. Consistent with the philosophical view of dispositionalism, we believe that objects are the fundamental relata of causation. By accepting the broad scope of the biopsychosocial (...) model, we argue that psychological and social constructs be considered objects. We think that this 'biopsychosocial dispositionalism' offers the flexibility required to describe causation throughout health, disease and intervention pathways. When constructing mechanistic chains to describe causative pathways, we argue that an object will causally connect with others through actions; transfers of energy from one object to another, initiated by the manifestation of one or more dispositional property. Finally, our analysis of causative interactions utilises the concept that a common form of interaction exists between disease and intervention pathways. This common form will always be an object, but the mode of interaction will vary with each disease. We describe how intervention may act through objects being shared between converging mechanistic chains, or through the removal and/or insertion of objects in such chains. We believe that this analysis provides novel insight to the forms of causative transactions that can occur. In addition, we hope that the findings of this analysis represent the first step towards developing a framework for appraising the composition of mechanistic theories. (shrink)

Causation is important when considering: how an organism maintains health; why disease arises in a healthy person; and, how one may intervene to change the course of a disease. This paper explores the form of causative relationships in health, disease and intervention, with particular regard to the pathological and biopsychosocial models. Consistent with the philosophical view of dispositionalism, we believe that objects are the fundamental relata of causation. By accepting the broad scope of the biopsychosocial (...) model, we argue that psychological and social constructs be considered objects. We think that this ‘biopsychosocial dispositionalism’ offers the flexibility required to describe causation throughout health, disease and intervention pathways. When constructing mechanistic chains to describe causative pathways, we argue that an object will causally connect with others through actions; transfers of energy from one object to another, initiated by the manifestation of one or more dispositional property. Finally, our analysis of causative interactions utilises the concept that a common form of interaction exists between disease and intervention pathways. This common form will always be an object, but the mode of interaction will vary with each disease. We describe how intervention may act through objects being shared between converging mechanistic chains, or through the removal and/or insertion of objects in such chains. We believe that this analysis provides novel insight to the forms of causative transactions that can occur. In addition, we hope that the findings of this analysis represent the first step towards developing a framework for appraising the composition of mechanistic theories. (shrink)

This paper summarizes the results from the first European Advanced Seminar in the Philosophy of the Life Sciences, which was held at the Brocher Foundation in Hermance (Switzerland) 6-10 September 2011. The Advanced Seminar brought together philosophers of the life sciences to discuss the topic of "Causation and Disease." The search for causes of disease in the biomedical sciences, we argue on the basis of the contributions to this conference, has not resulted in a simplification and unification (...) of biomedical knowledge, as once hoped for by philosophers of science, but rather in its "complexification.". (shrink)

This paper examines some criticisms that have been made of two standard genetic methodologies: heritability and path analysis. I conclude that the criticisms should be taken seriously, concerning both the accuracy of heritability measures and their significance. In light of the fact that such studies remain prominent in the literature, I consider what possible rationale they can retain consistent with these criticisms. In particular, I consider (1) a role in the identification of high-risk individuals and (2) a heuristic role in (...) the planning of research strategy. (shrink)

In this paper, I offer one example of conceptual change. Specifically, I contend that the discovery that viruses could cause cancer represents an excellent example of branch jumping, one of Thagard’s nine forms of conceptual change. Prior to about 1960, cancer was generally regarded as a degenerative, chronic, non-infectious disease. Cancer causation was therefore usually held to be a gradual process of accumulating cellular damage, caused by relatively non-specific component causes, acting over long periods of time. Viral infections, (...) on the other hand, were generally understood to be acute processes, whereby single, specific and necessary causal agents acted alone to produce disease. However, during the 1960s and 1970s, a number of cancers were discovered to have an infectious aetiology. Of particular note were two—Burkitt’s lymphoma and cervical cancer—which I will discuss in detail later in this piece. Together, these discoveries led, in the short term, to a tentative aetiological reclassification of some types of cancer as infectious diseases and, in the longer term, to a full-blown reclassification of cancer as an aetiological disease branch in its own right. This process of reclassification forms the empirical basis for my concluding remarks on the influence of classification upon causation in medicine. Through this, I aim to demonstrate that conceptual change, far from being a purely abstract concern of the philosopher of science, is of substantial import to scientific practitioners. (shrink)

Sir Austin Bradford Hill’s ‘aspects of causation’ represent some of the most influential thoughts on the subject of proximate causation in health and disease. Hill compiled a list of features that, when present and known, indicate an increasing likelihood that exposure to a factor causes—or contributes to the causation of—a disease. The items of Hill’s list were not labelled ‘criteria’, as this would have inferred every item being necessary for causation. Hence, criteria that are (...) necessary for causation in health, disease and intervention processes, whether known, knowable, or not, remain undetermined and deserve exploration. To move beyond this position, this paper aims to explore factors that are necessary in the constitution of causative relationships between health, disease processes, and intervention. To this end, disease is viewed as a causative pathway through the often overlapping stages of aetiology, pathology and patho-physiology. Intervention is viewed as a second, independent causative pathway, capable of causing changes in health for benefit or harm. For the natural course of a disease pathway to change, we argue that intervention must not only occupy the same time and space, but must also share a common form; the point at which the two pathways converge and interact. This improved conceptualisation may be used to facilitate the interpretation of clinical observations and inform future research, particularly enabling predictions of the mechanistic relationship between health, disease and intervention. (shrink)

Researchers, clinicians, and patients have good reasons for wanting answers to causal questions of disease and therapeutic intervention. This paper uses microbiologist Robert Koch’s pioneering work and famous postulates to extrapolate a logical sequence of evidence for confirming the causes of disease: association between individuals with and without a disease; isolation of causal agents; and the creation of a counterfactual. This paper formally introduces counter-counterfactuals, which appear to have been used, perhaps intuitively, since the time of Koch (...) and possibly earlier. An argument is presented that counter-counterfactuals are a useful tool for identifying necessary causes of disease, and sometimes must be used in place of isolation which is not always possible. In addition, a logical sequence of causal evidence for a therapeutic intervention is presented: creating a counterfactual, comparisons between subjects in receipt of treatment versus those who are not, and counter-counterfactuals. (shrink)

What exactly is a genetic disease? For a phrase one hears on a daily basis, there has been surprisingly little analysis of the underlying concept. Medical doctors seem perfectly willing to admit that the etiology of disease is typically complex, with a great many factors interacting to bring about a given condition. On such a view, descriptions of diseases like cancer as geneticseem at best highly simplistic, and at worst philosophically indefensible. On the other hand, there is clearly (...) some practical value to be had by classifying diseases according to theirpredominant cause when this can be accomplished in a theoretically satisfactory manner. The question therefore becomes exactly how one should go about selecting a single causal factor among many to explain the presence of disease. When an attempt to defend such causal selection is made at all, the standard accounts offered (Koch's postulates, Hill's epidemiological criteria, manipulability) are all clearly inadequate. I propose, however, an epidemiological account of disease causation which walks the fine line between practical applicability and theoretical considerations of causal complexity and attempts to compromise between patient-centered and population-centered concepts of disease. The epidemiological account is the most basic framework consistent with our strongly held intuitions about the causal classification of disease, yet it avoids the difficulties encountered by its competitors. (shrink)

Whipple disease is a rare, infectious, disease first described from a single case by Whipple in 1907. As well as characterising the clinical and pathological features of the condition, Whipple made two suggestions regarding its aetiology. These were either than the disease was caused by an infectious agent, or that it was of metabolic origin. As the disease is now thought to be caused by infection with the bacterium Tropheryma whipplei, historical reviews of the history of (...) the disease typically mention only the first of these suggestions. In this paper, we therefore revisit Whipple’s other theory. We argue that a diverse and often successful research programme was developed around this mechanism of disease causation which gave rise to many useful findings on the condition. In the later parts of this article, we then turn to discuss the surprising neglect of this period of Whipple disease research in the current literature, and conclude by offering a brief reconstruction of this early history suitable for use in a technical context. (shrink)

Epidemiologists’ discussions on causation are not always very enlightening with regard to the notion of ‘cause’ in epidemiology. Epidemiologists rightly work from a science-based approach to causation in epidemiology, but largely disagree about the matter. Disagreement may be partly due to confusion of the question of useful concepts for causal inference in epidemiological practice with the question of the metaphysical presuppositions of causal concepts used in epidemiology. In other words, epidemiologists seem to confuse the practical results of epidemiological (...) research at the population level with the metaphysical views about the reality of disease causation at the individual level in their writings on causation. (shrink)

Why do people get sick? I argue that a disease explanation is best thought of as causal network instantiation, where a causal network describes the interrelations among multiple factors, and instantiation consists of observational or hypothetical assignment of factors to the patient whose disease is being explained. This paper first discusses inference from correlation to causation, integrating recent psychological discussions of causal reasoning with epidemiological approaches to understanding disease causation, particularly concerning ulcers and lung cancer. (...) It then shows how causal mechanisms represented by causal networks can contribute to reasoning involving correlation and causation. The understanding of causation and causal mechanisms provides the basis for a presentation of the causal network instantiation model of medical explanation. (shrink)

In this paper, I focus on life-threatening medical conditions and argue that from the point of view of natural properties, induction(s), and participation in laws, at least some of the ill organisms dealt with in somatic medicine form natural kinds in the same sense in which the kinds in the exact sciences are thought of as natural. By way of comparing two ‘divisions of nature’, viz., a ‘classical’ exact science kind (gold) and a kind of disease (Graves disease), (...) I show that there is no justifiable ‘ontological gap’ between disease kinds and exact sciences kinds. We have instead a difference of degree. (shrink)

This open access book is a systematic update of the philosophical and scientific foundations of the biopsychosocial model of health, disease and healthcare. First proposed by George Engel 40 years ago, the Biopsychosocial Model is much cited in healthcare settings worldwide, but has been increasingly criticised for being vague, lacking in content, and in need of reworking in the light of recent developments. The book confronts the rapid changes to psychological science, neuroscience, healthcare, and philosophy that have occurred since (...) the model was first proposed and addresses key issues such as the model’s scientific basis, clinical utility, and philosophical coherence. The authors conceptualise biology and the psychosocial as in the same ontological space, interlinked by systems of communication-based regulatory control which constitute a new kind of causation. These are distinguished from physical and chemical laws, most clearly because they can break down, thus providing the basis for difference between health and disease. This work offers an urgent update to the model’s scientific and philosophical foundations, providing a new and coherent account of causal interactions between the biological, the psychological and social. (shrink)

By contrasting Hippocratic and nineteenth century theories of disease, this paper describes important conceptual changes that have taken place in the history of medicine. Disease concepts are presented as causal networks that represent the relations among the symptoms, causes, and treatment of a disease. The transition to the germ theory of disease produced dramatic conceptual changes as the result of a radically new view of disease causation. An analogy between disease and fermentation was (...) important for two of the main developers of the germ theory of disease, Pasteur and Lister. Attention to the development of germ concepts shows the need for a referential account of conceptual change to complement a representational account. (shrink)

Epidemiologists’ discussions on causation are not always very enlightening with regard to the notion of ‘cause’ in epidemiology. Epidemiologists rightly work from a science-based approach to causation in epidemiology, but largely disagree about the matter. Disagreement may be partly due to confusion of the question of useful concepts for causal inference in epidemiological practice with the question of the metaphysical presuppositions of causal concepts used in epidemiology. In other words, epidemiologists seem to confuse the practical results of epidemiological (...) research at the population level with the metaphysical views about the reality of disease causation at the individual level in their writings on causation. (shrink)

We propose that the onset and progressive destructive action of cancer within an individual bears a profound and striking similarity to the onset and progressive human-engendered destruction of global ecosystems and the extinction of entire species. Cancer in the human body and our human role in planetary, especially biotic, degradation are uncannily similar systems. For starters, they are the only two known complex systems where a discrete component changes its normal ecological role and function—turning on and potentially killing its host, (...) and in so doing, itself. Both are “hostile takeovers.” Clearly, humans are integral to both systems. With cancer we are the host and victims of the rogue behavior of what starts out as a normal, healthy, and functionally important part of our bodies. With the biodiversity crisis, we are the part of the system that has changed, expanded, and proven so destructive to the system in which we live. We argue that given that these threats to our bodies and Earth are both essentially ecological diseases, understanding the critical role of ecological interdependencies for avoiding both cancer’s and humankind’s destruction of their respective homes should hopefully promote better stewardship of both by the only animal capable of recognizing the problems—us. (shrink)

Major Depressive Disorder (MDD) is a serious condition with a large disease burden. It is often claimed that MDD is a “brain disease.” What would it mean for MDD to be a brain disease? I argue that the best interpretation of this claim is as offering a substantive empirical hypothesis about the causes of the syndrome of depression. This syndrome-causal conception of disease, combined with the idea that MDD is a disease of the brain, commits (...) the brain disease conception of MDD to the claim that brain dysfunction causes the symptoms of MDD. I argue that this consequence of the brain disease conception of MDD is false. It incorrectly rules out genuine instances of content-sensitive causation between adverse conditions in the world and the characteristic symptoms of MDD. Empirical evidence shows that the major causes of depression are genuinely psychological causes of the symptoms of MDD. This rules out, in many cases, the “brute” causation required by the brain disease conception. The existence of cases of MDD with non-brute causes supports the reinstatement of the old nosological distinction between endogenous and exogenous depression. (shrink)

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)

A standard platitude about the function of causal knowledge or theories is that they are valuable because they support prediction, explanation, and control. Knowledge of predator-prey relations enables us to predict future animal populations, as well as design policies or interventions that help influence those populations. If we understand the underlying biochemical mechanisms of some disease, then we can predict who is at risk for it, explain why it produces particular symptoms, and develop interventions to try to reduce its (...) prevalence or the symptom severity. Of course, there are many situations in which one has, for practical reasons, only some of these desiderata; for example, control might be infeasible for technical or ethical reasons. But these remain, for many researchers, the ideal for why causal knowledge is a valuable end of scientific inquiry, including biological inquiry. There are, however, certain types of systems—in particular, chaotic systems—in which it appears that these ends are unattainable, and these systems appear to be widespread in the biological domain, broadly construed. In this paper, we will show why it is natural to think that causal models of chaotic systems cannot satisfy any of the three functions. But we will also show why this natural thought is wrong: we can have usable causal knowledge about even chaotic systems. Moreover, the ways in which we can have such knowledge lead us naturally to rethink a standard understanding of how causal learning and modeling proceed. In particular, just as we often must find the appropriate variables for a causal system, we also must determine the proper level or granularity of description for the dynamics of that system. (shrink)

In this article I seek to say what it is for something to count as a neglected disease. I argue that neglect should be defined in terms of efforts at prevention, mitigation and cure, and not solely in terms of research dollars per disability-adjusted life-year. I further argue that the trend towards multifactorialism and risk factor thinking in modern epidemiology has lent credibility to the erroneous view that the primary problem with neglected diseases is a lack of research. A (...) more restrictive contrastive model of disease is endorsed as better suited to the definition of neglected disease. (shrink)

While it is well-established that poverty and disease are intimately connected, the nature of this connection and the role of poverty in disease causation remains contested in scientific and social studies of disease. Using the case of HIV/AIDS in South Africa and drawing on a theoretically grounded analysis, this paper reconceptualises disease and poverty as ontologically entangled. In the context of the South African HIV epidemic, this rethinking of the poverty-disease dynamic enables an account (...) of how social forces such as poverty become embodied in the very substance of disease to produce ontologies of HIV/AIDS unique to South Africa. (shrink)

This book is aimed at providing the reader with a systematic overview of the concepts of health and disease as utilized in various areas of the health sciences. It attempts to provide some historical background to modern models of health and disease. Special attention is given to controversial topics such as the notion of "mental health." the volume contains a number of new papers on health and disease by physicians, philosophers and others.

This original and lively book uses texts from ancient medicine, epic, lyric, tragedy, historiography, philosophy, and religion to explore the influence of Greek ideas on health and disease on Greek thought. Fundamental issues are deeply implicated: causation and responsibility, purification and pollution, the mind-body relationship and gender differences, authority and the expert, reality and appearances, good government, and good and evil themselves.

Philosophical discussions about health and disease often refer to a 'medical model' of bodily disease, in which diseases are regarded as causes of illness; diagnosis consists in identifying the disease affecting the patient, and this determines the appropriate treatment. This view is plausible only for diseases whose cause is known, though even in such instances the disease is the effect on the affected person, and must not be confused with its own cause. But in fact the (...) medical diagnostic process which progresses from recognition of patterns of symptoms and signs, through search for abnormalities of structure and/or function, towards knowledge of causation often stops short of this desirable end-point; and at whatever point it comes to a halt, its result is expressed in terms of 'diseases'. Thus in medical discourse the names of diseases are a convenient device by which the current conclusion of the diagnostic process can be stated briefly; and they have widely varying factual implications. This nominalist analysis of the medical usages of the names of diseases has consequences for definitions of health and disease, and for some problems in medical ethics. (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.

This original and lively book uses texts from ancient medicine, epic, lyric, tragedy, historiography, philosophy, and religion to explore the influence of Greek ideas on health and disease on Greek thought. Fundamental issues are deeply implicated: causation and responsibility, purification and pollution, the mind-body relationship and gender differences, authority and the expert, reality and appearances, good government, and good and evil themselves.

This paper focuses on the causation of diseases, particularly on the idea of a “genetic cause” taking Alzheimer’s Disease (AD) as an example. We (1) provide some historical information and a synopsis of the current knowledge on the etiology and pathogenesis of AD, (2) analyse some conceptual problems related to the notion of “genetic disease” (3) elaborate on the alleged (genetic) cause of AD, and (4) place the discussion on the cause of AD in a broader philosophical (...) context, paying attention to a constructivist perspective, the notions of causal connection and causal selection, and to some practical and normative consequences of our analysis. We conclude (a) that AD is not a specific disease entity with one specific cause, (b) that the idea of a single (sufficient) cause can still function as a heuristic tool in AD research and practice, and (c) that a “belief” in causation can go together with the notions of multicausality and probability. (shrink)

This article shows how funding research on Alzheimer's disease became a priority for the British Medical Research Council in the late 1970s and 1980s, thanks to work that isolated new pathological and biochemical markers, and showed that the disease affected a significant proportion of the elderly population. In contrast to histories that focus on the emergence of new and competing theories of disease causation in this period, I argue that concerns over the use of different assessment (...) methods ensured the MRC's immediate priority was standardising the ways in which researchers identified and recorded symptoms of Alzheimer's disease in potential research subjects. I detail how the rationale behind the development of standard assessment guidelines was less about arriving at a firm diagnosis and more about facilitating research by generating data that could be easily compared across the disciplines and sites that constitute modern biomedicine. Drawing on criticism of specific tests in the MRC's guidelines, which some psychiatrists argued were "middle class biased", I also show that debates over standardisation did not simply reflect concerns specific to the fields or areas of research that the MRC sought to govern. Questions about the validity of standard assessment guidelines for Alzheimer's disease embodied broader concerns about education and social class, which ensured that distinguishing normal from pathological in old age remained a contested and historically contingent process. (shrink)

This original and lively book explores Greek ideas about health and disease and their influence on Greek thought. Fundamental issues such as causation and responsibility, purification and pollution, mind-body relations and gender differences, authority and the expert and who can challenge them, reality and appearances, good government, happiness, and good and evil themselves are deeply implicated. Using the evidence not just from Greek medical theory and practice but also from epic, lyric, tragedy, historiography, philosophy, and religion, G. E. (...) R. Lloyd offers the first comprehensive account of the influence of Greek thought about health and disease on the Greek imagination. (shrink)

The problem of disease definition is related to theproblem of proving that a certain agent is thenecessary cause of a certain disease. Natural kindterms like ‘rheumatoid arthritis’ and ‘AIDS’ refer toessences which are discoverable rather thanpredeterminate. No statement about such diseases isa priori necessarily true. Because theories onnecessary causes involve natural kind semantics,Koch's postulates cannot be used to falsify or verifysuch theories. Instead of proving that agent A is thenecessary cause of disease D, we include A in (...) atheoretical definition of D, take this to representthe real meaning of ‘D’, and discard thepretheoretical definition. This is illustrated byKoch's own attempt to prove he had discovered thenecessary cause of tuberculosis. Methodologicalarguments about disease causation require a clear viewof our use of diagnostic terms. Medical lexicographersshould do more to provide such a view. (shrink)

Galen's treatises on the classification and causation of diseases and symptoms are an important component of his prodigious oeuvre, forming a bridge between his theoretical works and his practical, clinical writings. As such, they remained an integral component of the medical teaching curriculum well into the second millennium. This edition was originally published in 2006. In these four treatises, Galen not only provides a framework for the exhaustive classification of diseases and their symptoms as a prelude to his analysis (...) of their causation, but he also attempts to establish precise definitions of all the key terms involved. Unlike other of his works, these treatises are notably moderate in tone, taking into account different views on structure and causation in a relatively even-handed way. Nonetheless, they are a clear statement of the Dogmatic position on the theoretical foundations of medicine in his time. (shrink)

Conscious existence is the product of a neural brain mechanism, which is largely identical with Immanuel Kant's Oneness Function, a service performed by 200 million neurons in the prefrontal lobe, & makes possible our interior cosmos, the record of our interconnected, or general, experience. Essential for us humans is the well-being of our interior cosmos, or Saint Teresa of Avila's interior castle, in all interactions with each other \& the greater environment. Any disorders of our cosmos are liable to make (...) us fall ill, setting our existence on a path of psychosomatic etiology of a large class of mysterious undiagnosed diseases. (shrink)

I respond to the 4 commentaries by Awais Aftab & Kristopher Nielsen, Hane Htut Maung, Diane O’Leary and Kathryn Tabb under 3 main headings: “What is the BPSM really?” & Why update it?; “Is our approach foundationally compromised?”, and finally, “Antagonists or fellow travellers?”.

ABSTRACT:This article examines two medical journal research articles on tuberculosis, one published in 1938 and the other in 2014. The two articles, which use animal models to understand aspects of tuberculosis mycobacteria survival in the lungs, rely on markedly different research and biotechnological techniques, reach somewhat opposite conclusions, and reflect different paradigms of tuberculosis pathogenesis: the 1938 article (indirectly invoking Koch’s postulates) was written before the paradigm of so-called “latent” and “reactivation” tuberculosis became widely adopted, while the 2014 article (indirectly (...) invoking the molecular equivalents to Koch’s postulates) works within that paradigm but implicitly questions it. Despite this, both articles exhibit fascinating similarities in terms of how their authors tackled their research questions, formulated their results, and framed their research methodologies. These similarities reflect both the reliance on tenets of the scientific method but also the value of paradigms of disease causation. Using tuberculosis as an example, this article concludes with remarks about how disease paradigms evolve and can stimulate research that leads to advances in disease understanding. (shrink)

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, philosophy of biology, conditional analyses of causation, and recent literature on dispositional essentialism, I endorse a dispositional conception of disease whereby diseases are individuated by their causes, and diseases are causal processes best seen as simultaneously acting sequences of mutually manifesting dispositions - this, I claim, follows from the assumption that diseases should be classified by consideration of both their clinical and pathological effects, and importantly, events that can lead to the cessation of these symptoms. (shrink)

Near the end of his speech, Timaeus outlines a theory of bodily health and disease which has seemed to many commentators loosely unified or even inconsistent . But this section is better unified than it has appeared, and gives us at least one important insight into the workings of physical causality in the Timaeus. I argue first that the apparent disorder in Timaeus’s theory of disease is likely a deliberate effect planned by the author. Second, the taxonomy of (...) disease in the passage consists of one genus subsuming two species. Third, in Timaeus’s theory, health lies between perfect stability and a chaos of all possible motions; this indicates a conception of health as the activation of the body's powers in the right way. A power is a property directed towards bringing about some change. Fourth, the activation of these powers can change depending on the location of their possessors. This last point shows that causation among the physical items in the Timaeus involves structures as well as pushes. (shrink)

The aetio-pathogenetic sequences and the physio-pathological patterns of diabetes, emphysema, cholera, circulatory shock and thrombosis have been analysed with respect to an evolutionary interpretation. The diseases, although reflecting alterations of processes that can always be described in physico-chemical language, occur only at the level of biological systems which reflects the decodification of genomic project: the teleonomic projects that have been developed during evolution. The concepts of evolutionary emergence and of downward causation have been used to discuss the relationship between (...) the molecular events responsible for the initiation of the disease, and the subsequent events responsible for the aetio-pathogenesis, for the systemic disarrangement and for the additional alterations of tissues and cells independent of the initial molecular events. In diabetes the systemic disarrangement, glycosuria and hyperglycemia, reflect the evolutionary emergence of the processes regulating carbohydrate metabolism, whereas the cardiovascular and neurological alterations are effects of the systemic disarrangement by a mechanism of downward causation. The complexity of the aetio-pathogenesis and of the physio-pathological patterns of diseases is due to the generation of information during the evolution of multi-hierarchical entities. The evolutionary epistemology approach is useful to explain the behaviour of complex systems. (shrink)

The prelims comprise: Introduction Pre‐existing Conditions Case Model of Causation Case study of ‘Genetic Disease” The Future of Medical Insurance Conclusion Notes References Suggestions for Further Reading.