Causal claims in biomedical contexts are ubiquitous albeit they are not always made explicit. This paper addresses the question of what causal claims mean in the context of disease. It is argued that in medical contexts causality ought to be interpreted according to the epistemic theory. The epistemic theory offers an alternative to traditional accounts that cash out causation either in terms of “difference-making” relations or in terms of mechanisms. According to the epistemic approach, causal claims tell us about which (...) inferences (e.g., diagnoses and prognoses) are appropriate, rather than about the presence of some physical causal relation analogous to distance or gravitational attraction. It is shown that the epistemic theory has important consequences for medical practice, in particular with regard to evidence-based causal assessment. (shrink)

An overview of how mechanisms work in explanations.

This paper examines the explanatory distinctness of wiring optimization models in neuroscience. Wiring optimization models aim to represent the organizational features of neural and brain systems as optimal (or near-optimal) solutions to wiring optimization problems. My claim is that that wiring optimization models provide design explanations. In particular, they support ideal interventions on the decision variables of the relevant design problem and assess the impact of such interventions on the viability of the target system.

Many philosophers worry that cognitive scientists apply the concept REPRESENTATION too liberally. For example, William Ramsey argues that scientists often ascribe natural representations according to the “receptor notion,” a causal account with absurd consequences. I rehabilitate the receptor notion by augmenting it with a background condition: that natural representations are ascribed only to systems construed as organisms. This Organism-Receptor account rationalizes our existing conceptual practice, including the fact that scientists in fact reject Ramsey’s absurd consequences. The Organism-Receptor account raises some (...) worrying questions, but as a more faithful characterization of scientific practice it is a better guide to conceptual reform. (shrink)

A number of areas of biology raise questions about what is of value in the natural environment and how we ought to behave towards it: conservation biology, environmental science, and ecology, to name a few. Based on my experience teaching students from these and similar majors, I argue that the field of environmental ethics has much to teach these students. They come to me with pent-up questions and a feeling that more is needed to fully engage in their subjects, and (...) I believe some exposure to environmental ethics can help focus their interests and goals. I identify three primary areas in which environmental ethics can con- tribute to their education. The first is an examination of who (or what) should be considered to be part of our moral community (i.e., the community to whom we owe direct duties). Is it humans only? Or does it include all sentient life? Or all life? Or ecosystems considered holistically? Often, readings implicitly assume one or more of these answers; the goal is to make the student more sensitive to these implicit claims and to get them to think about the different reasons that support them. The second area, related to the first, is the application of the different answers concerning the extent of the ethical community to real environmental issues and problems. Students need to be aware of how the different answers concerning the moral community can imply conflicting answers for how we should act in certain cases and to think about ways to move toward conflict resolution. The third area in which environmental ethics can contribute is a more conceptual one, focusing on central concepts such as biodiversity, sustainability, species, and ecosystems. Exploring and evaluating various meanings of these terms will make students more reflective and thoughtful citizens and biologists, sensitive to the implications that different conceptual choices make. (shrink)

In this paper, we critically analyze the mechanicist approach to scientific explanation and propose to complement this view with a conception of level as interval of quasi-decompositionality. This conception allows us to metaphysically base the mechanicist proposals on characteristic systemic features. By means of concrete examples, we claim that this proposal is able to overcome some of the alleged limitations of predominant models of mechanistic explanation.

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 dissertation examines representationalism about sensory phenomenology—the claim that for a sensory experience to have a particular phenomenal character is a matter of it having a particular representational content. I focus on a particular issue that is central to representationalism: whether reductive versions of the theory should be internalist or externalist. My primary goals are to demonstrate that externalist representationalism fails to provide a reductive explanation for phenomenal qualities, and to present a reductive internalist version of representationalism that utilizes the (...) empirical framework of psychophysics and neuroscience to develop a philosophical theory of content. The bulk of the project is an attempt to provide the outlines of what such an empirically-based representationalist theory would look like. In chapter 2, I argue that reductive externalist representationalism fails because it is vulnerable to the problem of bad structural correlation: the mismatch between the structure of phenomenal qualities and the structure of physical properties “tracked” by our sensory systems with which phenomenal qualities are identified. In chapter 3, I develop the outlines of a reductive internalist version of representationalism that characterizes phenomenal qualities as modes of presentation of sensory representations that can be reductively characterized in terms of a location in a psychophysically-defined quality space, which can in turn be given a neurophysiological interpretation. In addition, I argue that the neural mechanisms responsible for the representation of spatial locations and visual objects serve a referential role in sensory psychosemantics that grounds the intentionality of sensory states. In chapter 5 I provide a detailed account of the representation of spatial locations in sensory experience, and in chapter 6 I examine the “binding problem”, demonstrating how object-based sensory representations function to demonstratively pick out sensory individuals without explicitly representing any of their features. I describe the resulting view as methodological representationalism: an attempt to demonstrate how a particular philosophical theory of sensory phenomenology can be integrated into the empirical framework of cognitive science, and thereby provide an explanatory psychosemantic framework for sensory phenomenology that is valuable to both philosophers and cognitive scientists. (shrink)

This paper focuses on the framework for the compositional relations of properties in the sciences, or "realization relations", offered by Ken Aizawa and Carl Gillett (A&G) in a series of papers, and in particular on the analysis of "multiple realizations" they build upon it. I argue that A&G's analysis of multiple realization requires an account of levels and I try to show, then, that the A&G framework is not successful under any of the extant accounts of levels. There is consequently (...) a real concern tha thte A&G framework for realization may not be viable. (shrink)

One of the central aims of science is explanation: scientists seek to uncover why things happen the way they do. This chapter addresses what kinds of explanations are formulated in biology, how explanatory aims influence other features of the field of biology, and the implications of all of this for biology education. Philosophical treatments of scientific explanation have been both complicated and enriched by attention to explanatory strategies in biology. Most basically, whereas traditional philosophy of science based explanation on derivation (...) from scientific laws, there are many biological explanations in which laws play little or no role. Instead, the field of biology is a natural place to turn for support for the idea that causal information is explanatory. Biology has also been used to motivate mechanistic accounts of explanation, as well as criticisms of that approach. Ultimately, the most pressing issue about explanation in biology may be how to account for the wide range of explanatory styles encountered in the field. This issue is crucial, for the aims of biological explanation influence a variety of other features of the field of biology. Explanatory aims account for the continued neglect of some central causal factors, a neglect that would otherwise be mysterious. This is linked to the persistent use of models like evolutionary game theory and population genetic models, models that are simplified to the point of unreality. These explanatory aims also offer a way to interpret many biologists’ total commitment to one or another methodological approach, and the intense disagreements that result. In my view, such debates are better understood as arising not from different theoretical commitments, but commitments to different explanatory projects. Biology education would thus be enriched by attending to approaches to biological explanation, as well as the unexpected ways that these explanatory aims influence other features of biology. I suggest five lessons for teaching about explanation in biology that follow from the considerations of this chapter. (shrink)

Philosophical theories of explanation characterize the difference between correct and incorrect explanations. While remaining neutral as to which of these ‘first-order’ theories is right, this paper asks the ‘meta-explanatory’ question: is the difference between correct and incorrect explanation real, i.e., objective or mind-independent? After offering a framework for distinguishing realist from anti-realist views, I sketch three distinct paths to explanatory anti-realism.

While the past century of neuroscientific research has brought considerable progress in defining the boundaries of the human cerebral cortex, there are cases in which the demarcation of one area from another remains fuzzy. Despite the existence of clearly demarcated areas, examples of gradual transitions between areas are known since early cytoarchitectonic studies. Since multi-modal anatomical approaches and functional connectivity studies brought renewed attention to the topic, a better understanding of the theoretical and methodological implications of fuzzy boundaries in brain (...) science can be conceptually useful. This article provides a preliminary conceptual framework to understand this problem by applying philosophical theories of vagueness to three levels of neuroanatomical research. For the first two levels (cytoarchitectonics and fMRI studies), vagueness will be distinguished from other forms of uncertainty, such as imprecise measurement or ambiguous causal sources of activation. The article proceeds to discuss the implications of these levels for the anatomical study of connectivity between cortical areas. There, vagueness gets imported into connectivity studies since the network structure is dependent on the parcellation scheme and thresholds have to be used to delineate functional boundaries. Functional connectivity may introduce an additional form of vagueness, as it is an organizational principle of the brain. The article concludes by discussing what steps are appropriate to define areal boundaries more precisely. (shrink)

I examine the adequacy of the causal graph-structural equations approach to causation for modeling biological mechanisms. I focus in particular on mechanisms with complex dynamics such as the PER biological clock mechanism in Drosophila. I show that a quantitative model of this mechanism that uses coupled differential equations – the well-known Goldbeter model – cannot be adequately represented in the standard causal graph framework, even though this framework does permit causal cycles. The reason is that the model contains dynamical information (...) about the mechanism that concerns causal properties but that does not correspond to variables that could be subject to independent interventions. Thus, a representation of the mechanisms as a causal structural model necessarily suppresses causally relevant information. (shrink)

The interventionist account of causation offers a criterion to distinguish causes from non-causes. It also aims at defining various desirable properties of causal relationships, such as specificity, proportionality and stability. Here we apply an information-theoretic approach to these properties. We show that the interventionist criterion of causation is formally equivalent to non-zero specificity, and that there are natural, information-theoretic ways to explicate the distinction between potential and actual causal influence. We explicate the idea that the description of causes should be (...) proportional to that of their effects. Then we draw a distinction between two ideas in the existing literature, the range of invariance of a causal relationship and its stability. The range of invariance is related to specificity and range of causal values. Stability concerns the effect of additional variables on the relationship between some focal pair of cause and effect variables. We show how to distinguish and measure the direct influence of background variables on the effect variable, and their influence on the relationship between the focal cause and the effect variable. Finally, we discuss the limitations of the information-theoretic approach, and offer prospects for complementary approaches. (shrink)

In this volume, leading philosophers of psychiatry examine psychiatric classification systems, including the Diagnostic and Statistical Manual of Mental Disorders, asking whether current systems are sufficient for effective diagnosis, treatment, and research. Doing so, they take up the question of whether mental disorders are natural kinds, grounded in something in the outside world. Psychiatric categories based on natural kinds should group phenomena in such a way that they are subject to the same type of causal explanations and respond similarly to (...) the same type of causal interventions. When these categories do not evince such groupings, there is reason to revise existing classifications. The contributors all question current psychiatric classifications systems and the assumptions on which they are based. They differ, however, as to why and to what extent the categories are inadequate and how to address the problem. Topics discussed include taxometric methods for identifying natural kinds, the error and bias inherent in DSM categories, and the complexities involved in classifying such specific mental disorders as "oppositional defiance disorder" and pathological gambling. -/- Contributors George Graham, Nick Haslam, Allan Horwitz, Harold Kincaid, Dominic Murphy, Jeffrey Poland, Nancy Nyquist Potter, Don Ross, Dan Stein, Jacqueline Sullivan, Serife Tekin, Peter Zachar. (shrink)

The psychiatric category of addiction has recently been broadened to include new behaviors. This has prompted critical discussion about the value of a concept that covers so many different substances and activities. Many of the debates surrounding the notion of addiction stem from different views concerning what kind of a thing addiction fundamentally is. In this essay, we put forward an account that conceptualizes different addictions as sharing a cluster of relevant properties (the syndrome) that is supported by a matrix (...) of causal mechanisms. According to this “addiction-as-a-kind” hypothesis, several different kinds of substance and behavioral addictions can be thought of as instantiations of the same thing – addiction. We show how a clearly articulated account of addiction can facilitate empirical research and the theoretical integration of different perspectives on addiction. The causal matrix approach provides a promising alternative to existing accounts of the nature of psychiatric disorders, the traditional disease model, and its competitors. It is a positive addition to discussions about diagnostic criteria, and sheds light on how psychiatric classification may be integrated with research done in other scientific fields. We argue that it also provides a plausible approach to understanding comorbidity. (shrink)

The study of psychological mechanisms is an interdisciplinary endeavour, requiring insights from many different domains. In this article, I argue that philosophy plays an essential role in this interdisciplinary project, and that effective scientific study of psychological mechanisms requires that working scientists be responsible metaphysicians. This means adopting deliberate metaphysical positions when studying mechanisms that go beyond what is empirically justified regarding the nature of the phenomenon being studied, the conditions of its occurrence, and its boundaries. Such metaphysical commitments are (...) necessary in order to set up experimental protocols, determine which variables to manipulate under experimental conditions, and which conclusions to draw from different scientific models and theories. It is important for scientists to be aware of the metaphysical commitments they adopt, since they can easily be led astray if invoked carelessly. (shrink)

Modeling mechanisms is central to the biological sciences – for purposes of explanation, prediction, extrapolation, and manipulation. A closer look at the philosophical literature reveals that mechanisms are predominantly modeled in a purely qualitative way. That is, mechanistic models are conceived of as representing how certain entities and activities are spatially and temporally organized so that they bring about the behavior of the mechanism in question. Although this adequately characterizes how mechanisms are represented in biology textbooks, contemporary biological research practice (...) shows the need for quantitative, probabilistic models of mechanisms, too. In this paper we argue that the formal framework of causal graph theory is well-suited to provide us with models of biological mechanisms that incorporate quantitative and probabilistic information. On the ba-sis of an example from contemporary biological practice, namely feedback regulation of fatty acid biosynthesis in Brassica napus, we show that causal graph theoretical models can account for feedback as well as for the multi-level character of mechanisms. However, we do not claim that causal graph theoretical representations of mechanisms are advantageous in all respects and should replace common qualitative models. Rather, we endorse the more balanced view that causal graph theoretical models of mechanisms are useful for some purposes, while being insufficient for others. (shrink)

We argue that mechanistic models elaborated by machine learning cannot be explanatory by discussing the relation between mechanistic models, explanation and the notion of intelligibility of models. We show that the ability of biologists to understand the model that they work with severely constrains their capacity of turning the model into an explanatory model. The more a mechanistic model is complex, the less explanatory it will be. Since machine learning increases its performances when more components are added, then it generates (...) models which are not intelligible, and hence not explanatory. (shrink)

The Extended Mind Thesis (EMT) is traditionally formulated against the bedrock of functionalism, and ongoing debates are typically bogged down with questions concerning the exact relationship between EMT and different versions of functionalism. In this paper, I offer a novel ally for EMT: the new mechanistic approach to explanation. I argue that the mechanistic framework provides useful resources not just to disambiguate EMT, and to show which objections fail to pose a serious challenge, but also to answer some of the (...) deeper problems that stem from the functionalist roots of EMT. (shrink)

In this paper I consider possible causation, specifically, would-cause counterfactuals of the form ‘had an event of kind A occurred, it would have caused an event of kind B’. I outline some difficulties for the Lewis program for understanding would-cause counterfactuals, and canvass an alternative. I then spell out a view on their significance, in relation to (i) absence causation, where claims such as ‘A’s not occurring caused B’s not occurring’ seem to make sense when understood in terms of the (...) would-cause counterfactual ‘had an event of kind A occurred, it would have caused an event of kind B’; (ii) contrastive causal explanation, where to explain why E rather than E* occurred we might appeal to the causal history of E and the counterfactual causal history of E*, an approach which appeals directly to would-cause counterfactuals ‘had an event of kind C* occurred, it would have caused an event of kind E*’; and (iii) dispositions, where the claim ‘the glass is fragile’ clearly has some connection or other with would-cause counterfactuals such as ‘were the glass to be struck, the striking would cause the glass to break’. (shrink)

In a recent article published in Ergo and entitled "Ontic explanation is either ontic or explanatory, but not both," Cory Wright and Dingmar van Eck have sought to undermine any ontic approach to explanation, providing three arguments to show that an epistemic approach is "the only game in town." I show that each of their arguments is straightforwardly question-begging. For brevity, I make my counter-arguments by showing how the claims of Sheredos (2016)-whom Wright & van Eck cite as an ally-undermine (...) each of their own arguments. The consumer update is: there is no new decisive argument against an ontic view, the epistemic view is not the only game in town, and reconciliation between the ontic and epistemic views remains possible. -/- . (shrink)

In recent years, a number of research projects have been proposed whose goal is to build large-scale simulations of brain mechanisms at unprecedented levels of biological accuracy. Here it is argued that the roles these simulations are expected to play in neuroscientific research go beyond the “synthetic method” extensively adopted in Artificial Intelligence and biorobotics. In addition we show that, over and above the common goal of simulating brain mechanisms, these projects pursue various modelling ambitions that can be sharply distinguished (...) from one another, and that correspond to conceptually different interpretations of the notion of “biological accuracy”. They include the ambition to reach extremely deep levels in the mechanistic decomposition hierarchy, to simulate networks composed of extremely large numbers of neural units, to build systems able to generate rich behavioural repertoires, to simulate “complex” neuron models, to implement the “best” theories available on brain structure and function. Some questions will be raised concerning the significance of each of these modelling ambitions with respect to the various roles played by simulations in the study of the brain. (shrink)

The paper argues that a functional reduction of ordinary psychology to neuropsychology is possible by means of constructing fine-grained functional, mental sub-types that are coextensive with neuropsychological types. We establish this claim by means of considering as examples the cases of the disconnection syndrome and schizophrenia. We point out that the result is a conservative reduction, vindicating the scientific quality of the mental types of ordinary psychology by systematically linking them with neuroscience. That procedure of conservative reduction by means of (...) functional sub-types is in principle repeatable down to molecular neuroscience. (shrink)