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)

Limitations of antiarrhythmic drugs on cardiac sudden death prevention appeared since the early 80's. The "Cardiac Arrhythmia Suppression Trial"(CAST) showed more recently that mortality was significantly higher inpatients treated with some particular antiarrhythmic drugs than in non-treated patients. In this field, our group recently demonstrated that a bolus of a Class 1B antiarrhythmic drug was able to trigger a ventricular fibrillation due to transient blocks induction. The aim of the present work was to systematically study, by use of the van (...) Capelle and Durrer (VCD) model which allows to simulate ventricular activation wave propagation, the link between arrhythmogenic effects and the ability of transient blocks to possibly degenerate in severe arrhythmias. A fragment of the ventricular wall is represented by an array of 16384elements electrically coupled. Effects of induction of one or several transient blocks, as the effects of their size and duration on possible induction of reentries have been studied. Results obtained show that various combinations between these different parameters may trigger reentries, ventricular tachycardia and/or more complex patterns assimilable to ventricular fibrillation. These results clearly evidence the fact that possible induction of transient blocks may directly be related to risk factor associated to arrhythmogenic effects of antiarrhythmic drugs. (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)

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

This article provides the foundation for a new predictive theory of animal learning that is based upon a simple logical model. The knowledge of experimental subjects at a given time is described using logical equations. These logical equations are then used to predict a subject’s response when presented with a known or a previously unknown situation. This new theory suc- cessfully anticipates phenomena that existing theories predict, as well as phenomena that they cannot. It provides a theoretical account for phenomena (...) that are beyond the domain of existing models, such as extinction and the detection of novelty, from which “external inhibition” can be explained. Examples of the methods applied to make predictions are given using previously published results. The present theory proposes a new way to envision the minimal functions of the nervous system, and provides possible new insights into the way that brains ultimately create and use knowledge about the world. (shrink)

In this paper, using a multilevel approach, we defend the positive role of natural selection in the generation of organismal form. Despite the currently widespread opinion that natural selection only plays a negative role in the evolution of form, we argue, in contrast, that the Darwinian factor is a crucial (but not exclusive) factor in morphological organization. Analyzing some classic arguments, we propose incorporating the notion of ‘downward causation’ into the concept of ‘natural selection.’ In our opinion, this kind of (...) causation is fundamental to the operation of selection as a creative evolutionary process. (shrink)

We have argued elsewhere that: (A) Natural selection is not a cause of evolution. (B) A resolution-of-forces (or vector addition) model does not provide us with a proper understanding of how natural selection combines with other evolutionary influences. These propositions have come in for criticism recently, and here we clarify and defend them. We do so within the broad framework of our own “hierarchical realization model” of how evolutionary influences combine.

We have argued elsewhere that: (A) Natural selection is not a cause of evolution. (B) A resolution-of-forces (or vector addition) model does not provide us with a proper understanding of how natural selection combines with other evolutionary influences. These propositions have come in for criticism recently, and here we clarify and defend them. We do so within the broad framework of our own “hierarchical realization model” of how evolutionary influences combine.

How do fitness and natural selection relate to other evolutionary factors like architectural constraint, mode of reproduction, and drift? In one way of thinking, drawn from Newtonian dynamics, fitness is one force driving evolutionary change and added to other factors. In another, drawn from statistical thermodynamics, it is a statistical trend that manifests itself in natural selection histories. It is argued that the first model is incoherent, the second appropriate; a hierarchical realization model is proposed as a basis for a (...) statistical treatment. It emerges that natural selection does not cause evolution; it just is evolution. The theory incorporates relations of statistical correlation, but not the kind of causation found in fundamental physical processes. (shrink)

The authors attempt to show that certain forms of behavior of the human immune system are illuminatingly regarded as errors in that system's operation. Since error-ascription can occur only within the context of an intentional/teleological characterization of the system, it follows that such a characterization is illuminating. It is argued that error-ascription is objective, non-anthropomorphic, irreducible to any purely causal form of explanation of the same behavior, and further that it is wrong to regard all errors of the immune system (...) as due to malfunction or maladaptation. <br>. (shrink)

Advancing the reductionist conviction that biology must be in agreement with the assumptions of reductive physicalism (the upward hierarchy of causal powers, the upward fixing of facts concerning biological levels) A. Rosenberg argues that downward causation is ontologically incoherent and that it comes into play only when we are ignorant of the details of biological phenomena. Moreover, in his view, a careful look at relevant details of biological explanations will reveal the basic molecular level that characterizes biological systems, defined by (...) wholly physical properties, e.g., geometrical structures of molecular aggregates (cells). In response, we argue that contrary to his expectations one cannot infer reductionist assumptions even from detailed biological explanations that invoke the molecular level, as interlevel causal reciprocity is essential to these explanations. Recent very detailed explanations that concern the structure and function of chromatin—the intricacies of supposedly basic molecular level—demonstrate this. They show that what seem to be basic physical parameters extend into a more general biological context, thus rendering elusive the concepts of the basic level and causal hierarchy postulated by the reductionists. In fact, relevant phenomena are defined across levels by entangled, extended parameters. Nor can the biological context be explained away by basic physical parameters defining molecular level shaped by evolution as a physical process. Reductionists claim otherwise only because they overlook the evolutionary significance of initial conditions best defined in terms of extended biological parameters. Perhaps the reductionist assumptions (as well as assumptions that postulate any particular levels as causally fundamental) cannot be inferred from biological explanations because biology aims at manipulating organisms rather than producing explanations that meet the coherence requirements of general ontological models. Or possibly the assumptions of an ontology not based on the concept of causal powers stratified across levels can be inferred from biological explanations. The incoherence of downward causation is inevitable, given reductionist assumptions, but an ontological alternative might avoid this. We outline desiderata for the treatment of levels and properties that realize interlevel causation in such an ontology. (shrink)

One of the fundamental questions of life sciences is one of whether there are genuinely random biological processes. An affirmative or negative answer to this question may have important methodological consequences. It appears that a number of biological processes are explicitly classified as random. One of them is the so-called somatic hypermutation. However, closer analysis of somatic hypermutation reveals that it is not a genuinely random process. Somatic hypermutation is called random because the exact outcome of this process is difficult (...) to predict in practice. The case of somatic hypermutation suggests that there may be no scientific evidence of a single case of ontologically random process in the biological world. (shrink)

Coordination of immune responses in the gut is a complex task. In order to fight pathogens and maintain a defined population of commensal microbes, the mucosal immune system has to coordinate information from the external (luminal) and internal (abluminal) environment and respond accordingly. Dendritic cells (DCs) are crucial cell types involved in this process as they integrate these signals and direct immunogenic or tolerogenic responses. Here, we review how various functions of DCs depend on microbial stimuli and how these stimuli (...) influence the course of immune activation. (shrink)

There are two competing interpretations of the modern synthesis theory of evolution: the dynamical (also know as ‘traditional’) and the statistical. The dynamical interpretation maintains that explanations offered under the auspices of the modern synthesis theory articulate the causes of evolution. It interprets selection and drift as causes of population change. The statistical interpretation holds that modern synthesis explanations merely cite the statistical structure of populations. This paper offers a defense of statisticalism. It argues that a change in trait frequencies (...) in a population can be attributed only to selection or drift against the background of a particular statistical description of the population. The traditionalist supposition that selection and drift are description‐independent causes of population change leads the dynamical interpretation into a dilemma: it must face a contradiction or accept the loss of explanatory power. (shrink)

This paper attempts to elucidate three characteristics of causal relationships that are important in biological contexts. Stability has to do with whether a causal relationship continues to hold under changes in background conditions. Proportionality has to do with whether changes in the state of the cause “line up” in the right way with changes in the state of the effect and with whether the cause and effect are characterized in a way that contains irrelevant detail. Specificity is connected both to (...) David Lewis’ notion of “influence” and also with the extent to which a causal relation approximates to the ideal of one cause–one effect. Interrelations among these notions and their possible biological significance are also discussed. (shrink)