Neuroscience is a laboratory-based science that spans multiple levels of analysis from molecular genetics to behavior. At every level of analysis experiments are designed in order to answer empirical questions about phenomena of interest. Understanding the nature and structure of experimentation in neuroscience is fundamental for assessing the quality of the evidence produced by such experiments and the kinds of claims that are warranted by the data. This article provides a general conceptual framework for thinking about evidence and experimentation in (...) neuroscience with a particular focus on two research areas: cognitive neuroscience and cognitive neurobiology. (shrink)

The interventionist theory of causation has been advertised as an empirically informed and more nuanced approach to causality than the competing theories. However, previous literature has not yet analyzed the regression discontinuity (hereafter, RD) and the difference-in-differences (hereafter, DD) within an interventionist framework. In this paper, I point out several drawbacks of using the interventionist methodology for justifying the DD and RD designs. However, I argue that the first step towards enhancing our understanding of the DD and RD designs from (...) an interventionist perspective is to take advantage of the assumptions of common trend and continuity. (shrink)

At least historically, it was common for medical practitioners to believe causal hypotheses on the basis of standalone mechanistic reasoning. However, it is now widely acknowledged that standalone mechanistic reasoning is insufficient for appropriately believing a causal hypothesis in medicine, thanks in part to the so-called problem of masking. But standalone mechanistic reasoning is not the only type of mechanistic reasoning. When exactly then is it appropriate to believe a causal hypothesis on the basis of mechanistic reasoning? In this paper, (...) I argue that it has proved difficult to provide a satisfying answer to this question. I also argue that this difficulty is predicted by recent work in knowledge-first epistemology. I think this shows that recent work in epistemology has important implications for practice in the philosophy of science. It is therefore worth paying closer attention in the philosophy of science to this recent work in knowledge-first epistemology. (shrink)

Russo and Williamson put forward the following thesis: in order to establish a causal claim in medicine, one normally needs to establish both that the putative cause and putative effect are appropriately correlated and that there is some underlying mechanism that can account for this correlation. I argue that, although the Russo-Williamson thesis conflicts with the tenets of present-day evidence-based medicine, it offers a better causal epistemology than that provided by present-day EBM because it better explains two key aspects of (...) causal discovery. First, the thesis better explains the role of clinical studies in establishing causal claims. Second, it yields a better account of extrapolation. (shrink)

A particular tradition in medicine claims that a variety of evidence is helpful in determining whether an observed correlation is causal. In line with this tradition, it has been claimed that establishing a causal claim in medicine requires both probabilistic and mechanistic evidence. This claim has been put forward by Federica Russo and Jon Williamson. As a result, it is sometimes called the Russo–Williamson thesis. In support of this thesis, Russo and Williamson appeal to the practice of the International Agency (...) for Research on Cancer. However, this practice presents some problematic cases for the Russo–Williamson thesis. One response to such cases is to argue in favour of reforming these practices. In this paper, we propose an alternative response according to which such cases are in fact consistent with the Russo–Williamson thesis. This response requires maintaining that there is a role for mechanism-based extrapolation in the practice of the IARC. However, the response works only if this mechanism-based extrapolation is reliable, and some have argued against the reliability of mechanism-based extrapolation. Against this, we provide some reasons for believing that reliable mechanism-based extrapolation is going on in the practice of the IARC. The reasons are provided by appealing to the role of robustness analysis. (shrink)

Some recent accounts of constitutive relevance have identified mechanism components with entities that are causal intermediaries between the input and output of a mechanism. I argue that on such accounts there is no distinctive inter-level form of mechanistic explanation and that this highlights an absence in the literature of a compelling argument that there are such explanations. Nevertheless, the entities that these accounts call ‘components’ do play an explanatory role. Studying causal intermediaries linking variables Xand Y provides knowledge of the (...) counterfactual conditions under which X will continue to bring about Y. This explanatory role does not depend on whether intermediate variables count as components. The question of whether there are distinctively mechanistic explanations remains open. (shrink)

The scope of this paper can be clarified by means of a well-known phenomenon that is usually called ‘industrial melanism’: the fact that the melanic form of the peppered moth became dominant in industrial areas in England in the second half of the nineteenth century. Such changes in relative phenotype frequencies are important explananda for population biologists. Apart from trying to explain such changes over time, population biologists also often try to explain differences between populations, e.g. why yellow shell colour (...) is dominant in certain colonies of land snails and almost absent in other colonies. The causal explanations that are given to address such explananda are the objects of analysis in this paper. Our primary aim is to explicate their structure: we want to capture the typical ingredients of causal explanations in population biology, and their organisation. Based on this explication, we discuss how natural selection fits into recent mechanical philosophy of science, and engage in the debate on the nature of evolutionary theory. (shrink)

In a recent article in this journal, Federica Russo and Jon Williamson argue that an analysis of causality in terms of probabilistic relationships does not do justice to the use of mechanistic evidence to support causal claims. I will present Ronald Giere's theory of probabilistic causation, and show that it can account for the use of mechanistic evidence (both in the health sciences—on which Russo and Williamson focus—and elsewhere). I also review some other probabilistic theories of causation (of Suppes, Eells, (...) and Humphreys) and show that they cannot account for the use of mechanistic evidence. I argue that these theories are also inferior to Giere's theory in other respects. (shrink)

In this paper, we analyse the fruitfulness of Ronald Giere’s comparative model for causation in populations. While the original model was primarily developed to capture the meaning of causal claims in the biomedical and health sciences, we want to show that the model is not only useful in these domains, but can also fruitfully be applied to other scientific domains. Specifically, we demonstrate that the model is fruitful for characterizing the meaning of causal claims found in classical genetics, epidemiology and (...) electoral sociology. Additionally, we propose an adapted comparative model which is needed to get a grip on higher level causal claims. We show that such claims are present in population genetics, epidemiology and electoral systems research. We conclude with some reflections on the implications of our findings for the issue of causal pluralism. (shrink)

Comparative syllogism is a type of scientific reasoning widely used, explicitly or implicitly, for inferences from observations to conclusions about effectiveness, but its philosophical significance has not been fully elaborated or appreciated. In its simplest form, the comparative syllogism derives a conclusion about the effectiveness of a factor (e.g. a treatment or an exposure) on a certain property via an experiment design using a test (experimental) group and a comparison (control) group. Our objective is to show that the comparative syllogism (...) can be understood as encoding a simulation view of counterfactuals, in that counterfactual situations are conceptual constructs that can be correctly simulated by homogeneous comparison groups. In this simulation view, the empirical data from the comparison groups play an evidential role in the evaluation of counterfactuals and in obtaining counterfactual knowledge. We further indicate how successful experimental designs can help us to obtain correct simulations, and thus to bring us to scientifically-empirically based counterfactual knowledge. (shrink)

Scientists often respond to failures to replicate by citing differences between the experimental components of an original study and those of its attempted replication. In this paper, we investigate these purported mismatch explanations. We assess a body of failures to replicate in neuroscience studies on spinal cord injury. We argue that a defensible mismatch explanation is one where a mismatch of components is a difference maker for a mismatch of outcomes, and the components are relevantly different in the follow-up study, (...) given the scope of the original study. With this account, we argue that not all differences between studies are meaningful, even if they are difference makers. As our examples show, focusing only on these differences results in disregarding the representativeness of the original experiment’s components and the scope of its outcomes, undercutting other epistemic aims, such as translation, in the process. (shrink)

Ian Hacking uses the looping effect to describe how classificatory practices in the human sciences interact with the classified people. While arguably this interaction renders the affected human kinds unstable and hence different from natural kinds, realists argue that also some prototypical natural kinds are interactive and human kinds in general are stable enough to support explanations and predictions. I defend a more fine-grained realist interpretation of interactive human kinds by arguing for an explanatory domain account of the looping effect. (...) First, I argue that knowledge of the feedback mechanisms that mediate the looping effect can supplement, and help to identify, the applicability domain over which a kind and its property variations are stably explainable. Second, by applying this account to cross-cultural case studies of psychiatric disorders, I distinguish between congruent feedback mechanisms that explain matches between classifications and kinds, and incongruent feedback mechanisms that explain mismatches. For example, congruent mechanisms maintain Western auditory experiences in schizophrenia, whereas exporting diagnostic labels inflicts incongruence by influencing local experiences. Knowledge of the mechanisms can strengthen explanatory domains, and thereby facilitate classificatory adjustments and possible interventions on psychiatric disorders. (shrink)

In the human sciences, experimental research is used to establish causal relationships. However, the extrapolation of these results to the target population can be problematic. To facilitate extrapolation, we propose to use the statistical technique Latent Class Regression Analysis in combination with the analogical reasoning theory for extrapolation. This statistical technique can identify latent classes that differ in the effect of X on Y. In order to extrapolate by means of analogical reasoning, one can characterize the latent classes by a (...) combination of features, and then compare these features to features of the target. (shrink)

In this paper we argue that an existing theory of concepts called dynamic frame theory, although not developed with that purpose in mind, allows for the precise formulation of a number of problems associated with induction from a single instance. A key role is played by the distinction we introduce between complete and incomplete dynamic frames, for incomplete frames seem to be very elegant candidates for the format of the background knowledge used in induction from a single instance. Furthermore, we (...) show how dynamic frame theory provides the terminology to discuss the justification and the fallibility of incomplete frames. In the Appendix, we give a formal account of incomplete frames and the way these lead to induction from a single instance. (shrink)

While the importance of mechanisms in determining causality in medicine is currently the subject of active debate, the role of mechanistic reasoning in clinical practice has received far less attention. In this paper we look at this question in the context of the treatment of a particular individual, and argue that evidence of mechanisms is indeed key to various aspects of clinical practice, including assessing population-level research reports, diagnostic as well as therapeutic decision making, and the assessment of treatment effects. (...) We use the pulmonary condition bronchiectasis as a source of examples of the importance of mechanistic reasoning to clinical practice. (shrink)

Kerry et al. criticize our discussion of causal knowledge in evidence-based medicine (EBM) and our assessment of the relevance of their dispositionalist ontology for EBM. Three issues need to be addressed in response: (1) problems concerning transfer of causal knowledge across heterogeneous contexts; (2) how predictions about the effects of individual treatments based on population-level evidence from RCTs are fallible; and (3) the relevance of ontological theories like dispositionalism for EBM.

This article examines the relationship between the precautionary principle and the well-known Hill criteria of causation. Some have charged that the Hill criteria are anti-precautionary because the...

Measuring the effectiveness of medical interventions faces three epistemological challenges: the choice of good measuring instruments, the use of appropriate analytic measures, and the use of a reliable method of extrapolating measures from an experimental context to a more general context. In practice each of these challenges contributes to overestimating the effectiveness of medical interventions. These challenges suggest the need for corrective normative principles. The instruments employed in clinical research should measure patient-relevant and disease-specific parameters, and should not be sensitive (...) to parameters that are only indirectly relevant. Effectiveness always should be measured and reported in absolute terms (using measures such as 'absolute risk reduction'), and only sometimes should effectiveness also be measured and reported in relative terms (using measures such as 'relative risk reduction')-employment of relative measures promotes an informal fallacy akin to the base-rate fallacy, which can be exploited to exaggerate claims of effectiveness. Finally, extrapolating from research settings to clinical settings should more rigorously take into account possible ways in which the intervention in question can fail to be effective in a target population. (shrink)

In order to make scientific results relevant to practical decision making, it is often necessary to transfer a result obtained in one set of circumstances—an animal model, a computer simulation, an economic experiment—to another that may differ in relevant respects—for example, to humans, the global climate, or an auction. Such inferences, which we can call extrapolations, are a type of argument by analogy. This essay sketches a new approach to analogical inference that utilizes chain graphs, which resemble directed acyclic graphs (...) (DAGs) except in allowing that nodes may be connected by lines as well as arrows. This chain graph approach generalizes the account of extrapolation I provided in my (2008) book and leads to new insights that integrate the contributions of the other participants of this symposium. More specifically, this approach explicates the role of “fingerprints,” or distinctive markers, as a strategy for avoiding an underdetermination problem having to do with spurious analogies. Moreover, it shows how the extrapolator’s circle, one of the central challenges for extrapolation highlighted in my book, is closely tied to distinctive markers and the Markov condition as it applies to chain graphs. Finally, the approach suggests additional ways in which investigations of a model can provide information about a target that are illustrated by examples concerning nanomaterials in sunscreens and Wendy Parker’s discussion of fingerprints in climate science. (shrink)

We show how more general knowledge can be built in information security, by the building of knowledge of mechanism clusters, some of which are multifield. By doing this, we address in a novel way the longstanding philosophical problem of how, if at all, we come to have knowledge that is in any way general, when we seem to be confined to particular experiences. We also address the issue of building knowledge of mechanisms by studying an area that is new to (...) the mechanisms literature: the methods of what we shall call mechanism discovery in information security. This domain offers a fascinating novel constellation of challenges for building more general knowledge. Specifically, the building of stable communicable mechanistic knowledge is impeded by the inherent changeability of software, which is deployed by malicious actors constantly changing how their software attacks, and also by an ineliminable secrecy concerning the details of attacks not just by attackers, but also by information security defenders as they protect their methods from both attackers and commercial competitors. We draw out ideas from the work of the mechanists Darden, Craver, and Glennan to yield an approach to how general knowledge of mechanisms can be painstakingly built. We then use three related examples of active research problems from information security to develop philosophical thinking about building general knowledge using mechanisms, and also apply this to develop insights for information security. We show that further study would be instructive both for practitioners and for philosophers. (shrink)

Evidential Pluralism maintains that in order to establish a causal claim one normally needs to establish the existence of an appropriate conditional correlation and the existence of an appropriate mechanism complex, so when assessing a causal claim one ought to consider both association studies and mechanistic studies. Hitherto, Evidential Pluralism has been applied to medicine, leading to the EBM+ programme, which recommends that evidence-based medicine should systematically evaluate mechanistic studies alongside clinical studies. This paper argues that Evidential Pluralism can also (...) be fruitfully applied to the social sciences. In particular, Evidential Pluralism provides (i) a new approach to evidence-based policy; (ii) an account of the evidential relationships in more theoretical research; and (iii) new philosophical motivation for mixed methods research. The application of Evidential Pluralism to the social sciences is also defended against two objections. (shrink)

The claim that randomized controlled trials can improve policy-making in developing countries seemed to be severely challenged by the widespread belief that RCTs lack external validity. This belief led to the articulation of strategies to alleviate this problem which developed under the assumption that policy-making in developing countries can be best understood as a problem of prediction. The causal structures that characterize developing contexts, however, render this framing inadequate. I propose to understand policy-making in developing contexts as a planning process. (...) In this new framework, the relevance of several kinds of evidence is highlighted and the role of causal effects refocused. Interestingly, also the concern for the external validity of causal effects seems now less forceful than the critics of RCTs suggest. (shrink)

In the last decades philosophers of science and social scientists promoted the view that knowledge of mechanisms might help causal inference considerably in the social sciences. Mechanisms, however, can only assist causal inference effectively if scientists have a means to identify them correctly. Some scholars suggested that process-tracing might be a helpful strategy in this respect. Shared criteria to assess its performance, however, are not available yet; furthermore, the criteria proposed so far tie the validity of process-tracing findings to the (...) specific kind of evidence it uses. In this paper I shall propose a criterion to assess process-tracing performance in cases in which favorable epistemic circumstances do not occur and the existing criteria thus fail to apply. The criterion I propose does not double as a condition for validity. Rather, it aims to assess whether the mechanism process-tracing outlines constitutes admissible evidence for the hypothesis at hand. It will be argued that only if this requirement is fulfilled process-tracing can be used as an effective complement for causal inference. (shrink)

Causal assessment is the problem of establishing whether a relation between (variable) X and (variable) Y is causal. This problem, to be sure, is widespread across the sciences. According to accredited positions in the philosophy of causality and in social science methodology, invariance under intervention provides the most reliable test to decide whether X causes Y. This account of invariance (under intervention) has been criticised, among other reasons, because it makes manipulations on the putative causal factor fundamental for the causal (...) methodology; consequently, the argument goes, the account is ill-suited to those contexts where manipulations are not performed, for instance, the social sciences. The article aims to extend the account of invariance (under intervention), in a way that manipulations on the putative causal factors are not methodologically fundamental, and yet invariance remains key for causal assessment both in experimental and non-experimental contexts. (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.

According to Russo and Williamson (Int Stud Philos Sci 21(2):157–170, 2007, Hist Philos Life Sci 33:389–396, 2011a, Philos Sci 1(1):47–69, 2011b ), in order to establish a causal claim of the form, ‘_C_ is a cause of _E_’, one typically needs evidence that there is an underlying mechanism between _C_ and _E_ as well as evidence that _C_ makes a difference to _E_. This thesis has been used to argue that hierarchies of evidence, as championed by evidence-based movements, tend to (...) give primacy to evidence of difference making over evidence of mechanisms and are flawed because the two sorts of evidence are required and they should be treated on a par. An alternative approach gives primacy to evidence of mechanism over evidence of difference making. In this paper, we argue that this alternative approach is equally flawed, again because both sorts of evidence need to be treated on a par. As an illustration of this parity, we explain how scientists working in the ‘EnviroGenomarkers’ project constantly make use of the two evidential components in a dynamic and intertwined way. We argue that such an interplay is needed not only for causal assessment but also for policy purposes. (shrink)

A shared problem across the sciences is to make sense of correlational data coming from observations and/or from experiments. Arguably, this means establishing when correlations are causal and when they are not. This is an old problem in philosophy. This paper, narrowing down the scope to quantitative causal analysis in social science, reformulates the problem in terms of the validity of statistical models. Two strategies to make sense of correlational data are presented: first, a 'structural strategy', the goal of which (...) is to model and test causal structures that explain correlational data; second, a 'manipulationist or interventionist strategy', that hinges upon the notion of invariance under intervention. It is argued that while the former can offer a solution the latter cannot. (shrink)

Evidential pluralists, like Federica Russo and Jon Williamson, argue that causal claims should be corroborated by establishing both the existence of a suitable correlation and a suitable mechanism complex. At first glance, this fits well with mixed method research in the social sciences, which often involves a pluralist combination of statistical and mechanistic evidence. However, statistical evidence concerns a population of cases, while mechanistic evidence is found in individual case studies. How should researchers combine such general statistical evidence and specific (...) mechanistic evidence? This article discusses a very recent answer to this question, ‘multi-method large-N qualitative analysis’ or multi-method LNQA, popular in political science and international relations studies of rare events like democratic transitions and cease-fire agreements. Multi-method LNQA combines a comprehensive study of all relevant event cases with statistical analysis, in an attempt to solve the issues of generalization faced by other types of qualitative research, such as selection bias and lack of representativeness. I will argue that the kind of general causal claim that multi-method LNQA is after, however, is crucially different from the average treatment effect found in statistical analysis and can in fact only be supported with mechanistic evidence. I conclude from this that mixed method research, and thereby evidential pluralism, may be inappropriate in this context. (shrink)

The issue of causal comparability in the social sciences underlies matters of both generalization and extrapolation. After critiquing two existing interpretations of comparability, due to Hitchcock and Hausman, I propose a distinction between ontological and epistemic comparability. While the former refers to whether two cases are actually comparable, the latter respects that in cases of incomplete information, we need to rely on whatever evidence we have of comparability. I argue, using a political science case study, that in those cases of (...) imperfect information, an epistemic homogeneity criterion can be an adequate justification for generalization. (shrink)

Philosophers of social science have emphasized mechanistic approaches to causal inquiry for some time now, showing why focusing on the mechanisms behind correlations is preferable to focusing on correlations alone (cf. Johnson 2006, Little 1991, Reiss 2007, 2009, Steel 2004, see also King, Keohane, and Verba 1994 for an example of purely correlational research). In Process Tracing: from Metaphor to Analytic Tool, political scientists Andrew Bennett and Jeffrey Checkel present a concrete method for finding evidence of causal mechanisms, process tracing. (...) Process tracers give evidence for causal relations in terms of the observable implications of the underlying causal mechanisms through which a putative cause affects some effect of interest. Such observable implications often take the form of a chain of events, or process, which connects cause and effect. Though Process Tracing contains applications of mechanistic reasoning unfamiliar to philosophers, and as such will be of interest to those working in the mechanist tradition, Bennett and Checkel’s own discussion of the philosophical foundations of process tracing is limited. The reader will have to delve deep into the volume’s contributed chapters for links between the literature on causation and this new method. (shrink)

Explainable artificial intelligence (XAI) is an emerging, multidisciplinary field of research that seeks to develop methods and tools for making AI systems more explainable or interpretable. XAI researchers increasingly recognise explainability as a context-, audience- and purpose-sensitive phenomenon, rather than a single well-defined property that can be directly measured and optimised. However, since there is currently no overarching definition of explainability, this poses a risk of miscommunication between the many different researchers within this multidisciplinary space. This is the problem we (...) seek to address in this paper. We outline a framework, called Explanatory Pragmatism, which we argue has two attractive features. First, it allows us to conceptualise explainability in explicitly context-, audience- and purpose-relative terms, while retaining a unified underlying definition of explainability. Second, it makes visible any normative disagreements that may underpin conflicting claims about explainability regarding the purposes for which explanations are sought. Third, it allows us to distinguish several dimensions of AI explainability. We illustrate this framework by applying it to a case study involving a machine learning model for predicting whether patients suffering disorders of consciousness were likely to recover consciousness. (shrink)

Laws in the special sciences are usually regarded to be non-universal. A theory of laws in the special sciences faces two challenges. (I) According to Lange's dilemma, laws in the special sciences are either false or trivially true. (II) They have to meet the ?requirement of relevance?, which is a way to require the non-accidentality of special science laws. I argue that both challenges can be met if one distinguishes four dimensions of (non-) universality. The upshot is that I argue (...) for the following explication of special science laws: L is a special science law just if (1) L is a system law, (2) L is quasi-Newtonian, and (3) L is minimally invariant. (shrink)

This paper aims (a) to provide characterizations of realism and instrumentalism that are philosophically interesting and applicable to economics; and (b) to defend instrumentalism against realism as a methodological stance in economics. Starting point is the observation that ‘all models are false’, which, or so I argue, is difficult to square with the realist's aim of truth, even if the latter is understood as ‘partial’ or ‘approximate’. The three cheers in favour of instrumentalism are: (1) Once we have usefulness, truth (...) is redundant. (2) There is something disturbing about causal structure. (3) It's better to do what one can than to chase rainbows. (shrink)

Francesco Guala once wrote that ‘The problem of extrapolation is a minor scandal in the philosophy of science’. This paper agrees with the statement, but for reasons different from Guala’s. The scandal is not, or not any longer, that the problem has been ignored in the philosophy of science. The scandal is that framing the problem as one of external validity encourages poor evidential reasoning. The aim of this paper is to propose an alternative—an alternative which constitutes much better evidential (...) reasoning about target systems of interest, and which makes do without consideration of external validity. (shrink)

Amalgamating evidence from heterogeneous sources and across levels of inquiry is becoming increasingly important in many pure and applied sciences. This special issue provides a forum for researchers from diverse scientific and philosophical perspectives to discuss evidence amalgamation, its methodologies, its history, its pitfalls, and its potential. We situate the contributions therein within six themes from the broad literature on this subject: the variety-of-evidence thesis, the philosophy of meta-analysis, the role of robustness/sensitivity analysis for evidence amalgamation, its bearing on questions (...) of extrapolation and external validity of experiments, its connection with theory development, and its interface with causal inference, especially regarding causal theories of cancer. (shrink)

Extrapolation from a well-understood base population to a less-understood target population can fail if the base and target populations are not sufficiently similar. Differences between laboratory mice and humans, for example, can hinder extrapolation in medical research. Mice that carry a partial or complete human physiological system, known as humanized mice, are supposed to make extrapolation more reliable by simulating a variety of human diseases. But what justifies our belief that these mice are similar enough to their human counterparts to (...) simulate human disease? I argue that, unless three requirements are met in the process of humanizing mice, very little does. My requirements are not meant to provide necessary and sufficient conditions that guarantee a particular outcome. Instead, they serve as a heuristic for guiding scientific judgments involving extrapolation. In developing each requirement, I engage with philosophical issues concerning the nature of model-based science and the mechanistic approach (and its limits) to making generalizations in the life sciences. (shrink)

This paper defends the thesis of learning from non-causal models: viz. that the study of some model can prompt justified changes in one’s confidence in empirical hypotheses about a real-world target in the absence of any known or predicted similarity between model and target with regards to their causal features. Recognizing that we can learn from non-causal models matters not only to our understanding of past scientific achievements, but also to contemporary debates in the philosophy of science. At one end (...) of the philosophical spectrum, my thesis undermines the views of those who, like Cartwright (Erkenntnis 70:45–58, 2009), follow Hesse (Models and Analogies in Science, Notre Dame, University of Notre Dame Press, 1963) in restricting the possibility of learning from models to only those situations where a model identifies some causal factors present in the target. At the other end of the spectrum, my thesis also helps undermine some extremely permissive positions, e.g., Grüne-Yanoff’s (Erkenntnis 70(1):81–99, 2009, Philos Sci 80(5): 850–861, 2013) claim that learning from a model is possible even in the absence of any similarity at all between model and target. The thesis that we can learn from non-causal models offers a cautious middle ground between these two extremes. (shrink)

While the history and methodology of laboratory experiments in economics have been extensively studied by philosophers, those of field experiments have not attracted much attention until recently. What is the historical context in which field experiments have been advocated? And what are the methodological rationales for conducting experiments in the field as opposed to in the lab? This article addresses these questions by combining historical and methodological perspectives. In terms of history, we show that the movement toward field experiments in (...) economics has two distinct roots. One is the general orientation of medical and social sciences to evidence-based policy evaluation, which gave rise to randomized field experiments in economics. The other is an awareness of several methodological limitations of lab experiments in economics, which required practitioners to get out of the lab and into the field. In these senses, the movement is a consequence of influences from both outside and inside economics: the general evidence-based trend in policy science and an internal methodological development of experimental economics. In terms of methodology, we show that these two roots resulted in two somewhat different notions of “external validity” as methodological rationales of field experiment. Finally, we suggest that analysis of experiments as exhibits highlights a methodological strategy in which both strands complement each other. (shrink)

Daniel Steel’s new book on the precautionary principle illustrates the need to work ahead to fuse perspectives of epistemology and philosophy of science with those of ethics to accomplish progress in the debate on the proper role of precaution in a broad selection of bioethical areas. Steel advances the territory greatly with regard to conceptual clarity and epistemology, but from a bioethics standpoint he is mistaken in discounting the need for ethical underpinnings of a sound theory of the precautionary principle.

The aim of this paper is to reconstruct and critically assess the evidential relationship between neuroscience and educational practice. To do this, I reconstruct a standard way in which evidence from neuroscience is used to support recommendations about educational practice, that is, testing pedagogical interventions using neuroimaging methods, and discuss and critically assess the inference behind this approach. I argue that this inference rests on problematic assumptions, and, therefore, that neuroimaging intervention studies have no special evidential status for basing educational (...) practice. I conclude arguing that these limitations could be resolved by integrating evidence from neurocognitive and educational science. (shrink)

It has recently been argued that successful evidence-based policy should rely on two kinds of evidence: statistical and mechanistic. The former is held to be evidence that a policy brings about the desired outcome, and the latter concerns how it does so. Although agreeing with the spirit of this proposal, we argue that the underlying conception of mechanistic evidence as evidence that is different in kind from correlational, difference-making or statistical evidence, does not correctly capture the role that information about (...) mechanisms should play in evidence-based policy. We offer an alternative account of mechanistic evidence as information concerning the causal pathway connecting the policy intervention to its outcome. Not only can this be analyzed as evidence of difference-making, it is also to be found at any level and is obtainable by a broad range of methods, both experimental and observational. Using behavioral policy as an illustration, we draw the implications of this revised understanding of mechanistic evidence for debates concerning policy extrapolation, evidence hierarchies, and evidence integration. (shrink)

Recently, a research program has emerged that aims to show that animals have a memory capacity that is similar to the human episodic memory capacity. Researchers within this program argue that nonhuman animals have episodic-like memory of personally experienced past events. In this paper, I specify and evaluate the goals of this research program and the progress it has made in achieving them. I will examine some of the data that the research program has produced, as well as the operational (...) definitions and assumptions that have gone into producing that data, in order to call into question the ultimate value of the episodic-like memory research program. I argue that there is a gap between the claims that the research program makes and the data it uses to support these claims, and that bridging this gap is essential if we want to claim that human episodic memory has a meaningful analog in animals. I end with some suggestions of how to potentially fix these problems. (shrink)

James Woodward’s manipulationist counterfactual theory of explanation offers strong tools for an adequate approach to explanation endeavours. One of these tools is the notion of intervention, which serves as a guiding principle for identifying explanations as causal, thus preserving the unidirectionality of explanatory praxis. Nevertheless, in this paper, I argue that in some cases of explanation, this notion has a rather redundant role since it is either impossible to define or it can be replaced by other types of manipulations or (...) both. I shall show these shortcomings of intervention in two particularly detailed analyses of an economic example pertaining to Okun’s law and the pendulum explanation. In analysing the former example, I contend that given the complex causal situation of economic phenomena, the notion of intervention is inept at helping explain them. In the latter example, I show that the notion of intervention is readily replaceable by other types of variation—conceptual or mathematical. Finally, I shall end this article by examining the case of pendulum explanation in light of Woodward’s new approach to explanation direction. In the end, the conclusion is that the variables of the pendulum law are in a symmetrical relationship. (shrink)

I am grateful for Joshua Alexander and Jonathan Weinberg’s, Avner Baz’s and Max Deutsch’s insightful comments on Philosophy Within Its Proper Bounds. I have lea.

Model organisms are central to contemporary biology and studies of embryogenesis in particular. Biologists utilize only a small number of species to experimentally elucidate the phenomena and mechanisms of development. Critics have questioned whether these experimental models are good representatives of their targets because of the inherent biases involved in their selection (e.g., rapid development and short generation time). A standard response is that the manipulative molecular techniques available for experimental analysis mitigate, if not counterbalance, this concern. But the most (...) powerful investigative techniques and molecular methods are applicable to single-celled organisms (‘microbes’). Why not use unicellular rather than multicellular model organisms, which are the standard for developmental biology? To claim that microbes are not good representatives takes us back to the original criticism leveled against model organisms. Using empirical case studies of microbes modeling ontogeny, we break out of this circle of reasoning by showing: (a) that the criterion of representation is more complex than earlier discussions have emphasized; and, (b) that different aspects of manipulability are comparable in importance to representation when deciding if a model organism is a good model. These aspects of manipulability harbor the prospect of enhancing representation. The result is a better understanding of how developmental biologists conceptualize research using experimental models and suggestions for underappreciated avenues of inquiry using microbes. More generally, it demonstrates how the practical aspects of experimental biology must be scrutinized in order to understand the associated scientific reasoning. (shrink)

Many biological investigations are organized around a small group of species, often referred to as ‘model organisms’, such as the fruit fly Drosophila melanogaster. The terms ‘model’ and ‘modelling’ also occur in biology in association with mathematical and mechanistic theorizing, as in the Lotka–Volterra model of predator-prey dynamics. What is the relation between theoretical models and model organisms? Are these models in the same sense? We offer an account on which the two practices are shown to have different epistemic characters. (...) Theoretical modelling is grounded in explicit and known analogies between model and target. By contrast, inferences from model organisms are empirical extrapolations. Often such extrapolation is based on shared ancestry, sometimes in conjunction with other empirical information. One implication is that such inferences are unique to biology, whereas theoretical models are common across many disciplines. We close by discussing the diversity of uses to which model organisms are put, suggesting how these relate to our overall account. 1 Introduction2 Volterra and Theoretical Modelling3 Drosophila as a Model Organism4 Generalizing from Work on Model Organisms5 Phylogenetic Inference and Model Organisms6 Further Roles of Model Organisms6.1 Preparative experimentation6.2 Model organisms as paradigms6.3 Model organisms as theoretical models6.4 Inspiration for engineers6.5 Anchoring a research community7 Conclusion. (shrink)