In this paper we set out to examine thearguments for and against the claim thatEvidence-Based Medicine (EBM) will improve thequality of care. In particular, we examine thefollowing issues.

In the last decades, Systems Biology (including cancer research) has been driven by technology, statistical modelling and bioinformatics. In this paper we try to bring biological and philosophical thinking back. We thus aim at making diferent traditions of thought compatible: (a) causality in epidemiology and in philosophical theorizing—notably, the “sufcient-component-cause framework” and the “mark transmission” approach; (b) new acquisitions about disease pathogenesis, e.g. the “branched model” in cancer, and the role of biomarkers in this process; (c) the burgeoning of omics (...) research, with a large number of “signals” and of associations that need to be interpreted. In the paper we summarize frst the current views on carcinogenesis, and then explore the relevance of current philosophical interpretations of “cancer causes”. We try to ofer a unifying framework to incorporate biomarkers and omic data into causal models, referring to a position called “evidential pluralism”. According to this view, causal reasoning is based on both “evidence of diference-making” (e.g. associations) and on “evidence of underlying biological mechanisms”. We conceptualize the way scientists detect and trace signals in terms of information transmission, which is a generalization of the mark transmission theory developed by philosopher Wesley Salmon. Our approach is capable of helping us conceptualize how heterogeneous factors such as micro and macro-biological and psycho-social—are causally linked. This is important not only to understand cancer etiology, but also to design public health policies that target the right causal factors at the macro-level. (shrink)

The clinical decision is supposed to be based on evidence. In fact, what counts as evidence is far from being established. Some definition of "proof" is needed to distinguish between scientific medicine and charlatanism. My thesis is that unfortunately a clear-cut boundary between evidence and lack of evidence cannot be found, for several reasons that I summarise in the paper. Evidence in medicine very often has fuzzy boundaries, and dichotomising fuzziness and uncertainty can have serious consequences. Physicians and patients should (...) accept the irreducible fuzziness of many of the concepts they use when dealing with health and disease. (shrink)

Since the microbiological revolution, most infectious diseases have been defined and classified according to an etiologic criterion, i.e. the identification of single, external necessary causes (for example, Mycobacterium for tuberculosis). This is not the case with cancer. Not only external necessary causes of cancer have not been identified, but also the morphological classification cannot be based on univocal criteria. Although neoplasia and anaplasia appear to be universal attributes of cancer, these events are only quantitative. Neoplastic growth can be fast or (...) slow (development may take weeks or years), and tissue pathologies are difficult to detect from normal tissue in some cancers but are obvious in others. Common special properties of anaplasia appear to be concealed in the wide range of morphologies. In the absence of a coherent morphological definition, and of external necessary causes (such as bacteria for infectious diseases), a mechanistic definition could be adopted. However, unless molecular biology discovers specific mechanistic steps in carcinogenesis, which indicate the existence of necessary events in carcinogenesis, we cannot adopt a univocal (monothetic) definition of cancer. The alternative is to use a polythetic definition, according to Wittgenstein's model of a long rope twisted together out of many shorter fibres. (shrink)

The objective of the article is to examine the extensions of a clinical measure of efficacy, the Number Needed to Treat (NNT), in different settings including screening, scanning, genetic testing and primary prevention, and the associated ethical implications. We examine several situations in which the use of the NNT or NNS (Number Needed to Screen) has been suggested, such as Prostate-Specific Antigen for prostate cancer, Magnetic Resonance Imaging scans, genetic testing and banning of smoking. For each application, we explore the (...) ethical implications of the relevant measure. We have found that the different measures have different ethical implications. For example, the Number Needed to Prevent is the only measure that can be lower than one, indicating with a numerical example that prevention is better than cure. Conversely, we raise questions about the acceptability of genetic screening. In a realistic example, we show that primary prevention of the effects of arsenic in drinking water, targeted to the most susceptible, would require to genetically screen a large number of subjects, whereas giving rise to ethical concerns. We warn against the abuse of testing, in particular genetic testing, we show that different measures are associated with different ethical issues and that prevention tends to be better than cure. (shrink)

Epidemiology relies upon a broad interpretation of determinism. This paper discusses analogies with the evolution of the concept of cause in physics, and analyzes the classical nine criteria proposed by Sir Austin Bradford Hill for causal assessment. Such criteria fall into the categories of enumerative induction, eliminative induction, deduction and analogy. All of these four categories are necessary for causal assessment and there is no natural hierarchy among them, although a deductive analysis of the study design is preliminary to any (...) assessment. (shrink)

Using the example of air pollution, I criticize a restricted utilitarian view of environmental risks. It is likely that damage to health due to environmental pollution in Western countries is relatively modest in quantitative terms (especially when considering cancer and comparing such damage to the effects of some life-style exposures). However, a strictly quantitative approach, which ranks priorities according to the burden of disease attributable to single causes, is questionable because it does not consider such aspects as inequalities in the (...) distribution of risks. Secondly, the ability of epidemiological research to identify some health effects is limited. Third, the environment has symbolic and aesthetic components that overcome a strict evaluation of damage based on the impairment of human health. It is not acceptable that priorities be set just balancing the burden of disease caused by pollution in the environment against economic constraints. As an example of a computation that inherently includes economic analysis, I refer to the proposal of an estimator of mortality in coal mining, i.e., a rate which puts deaths in the numerator and tons of coal extracted in the denominator. According to this estimator, mortality due to accidents decreased from 1.15 to 0.42 in the period 1950–1970 in the United States, for each million tons of coal extracted. However, considering the steep decline in the workforce in the same period, the traditional mortality rate (deaths over persons-time) actually increased. The proposal of a measure of mortality based on the amount of coal extracted is just one example of the attempts to influence decisions by including an economic element (productivity) in risk assessment. This paper has three purposes: One, to describe empirical research concerning the health effects of environmental pollutants; two, to discuss the scientific principles and methods used in the identification of environmental hazards; and three, to critically discuss some of the ethical principles which are applied in medicine and in the assessment and management of risk. (shrink)