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)

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)

Economists reason causally. Like many other scientists, they aim at formulating justified causal claims about their object of study. This thesis contributes to our understanding of how causal reasoning proceeds in economics. By using the research on the causes of unemployment as a case study, three questions are adressed. What are the meanings of causal claims? How can a causal claim be adequately supported by evidence? How are causal beliefs affected by incoming facts? In the process of answering these semantic, (...) epistemic and dynamical questions, the richness of causal reasoning in economics is brought to the foreground. In the part on semantics, it is argued that the meaning of causal generalizations in policy-oriented economics is best captured by using the concept of ‘inferential relation’ rather than the one of ‘referential relation’. This part contributes to develop an inferentialist semantics by distinguishing among types of inferential relations. In the part on epistemology, it is argued that justification in sciences like economics often relies, and ought to rely, on evidential variety―i.e. the combination of evidence from multiple sources. An interpretation of independence among evidential sources is offered: two evidential sources are fully independent if and only if the reasons why they would be unreliable do not overlap. It is then shown that the variety-of-evidence thesis does not hold under extreme circumstances. The part on dynamics focuses on deviant-case study. A storyline is provided for what deviant-case study aims at and how it proceeds in what is characterized as an ‘eclectic science’. (shrink)

Convincing disputes about explanatory reductionism in the philosophy of biology require a clear and precise understanding of what a reductive explanation in biology is. The central aim of this book is to provide such an account by revealing the features that determine the reductive character of a biological explanation. Chapters I-IV provide the ground, on which I can then, in Chapter V, develop my own account of explanatory reduction in biology: Chapter I reveals the meta-philosophical assumptions that underlie my analysis (...) of reduction, Chapter II introduces the previous debate about reduction in the philosophy of biology by pointing out the most crucial lessons one should learn from this debate, Chapter III critically discusses the two perspectives on explanatory reduction that have been proposed in the philosophy of biology so far, and Chapter IV clarifies in what ways the issue of reduction is entangled with the issue of explanation. In Chapter V I present my own account of explanatory reduction. My main claim is that reductive explanations in the biological sciences possess three main characteristics: they explain the behavior of a biological system S, first, exclusively in terms of factors that are located on a lower level of organization than S, second, by focusing on factors that are internal to S , and third, by describing the genuine parts of S only as “parts in isolation”. This account is ontic because it traces the reductivity of an explanation back to certain relations that exist in the world. (shrink)

This thesis examines philosophical controversies surrounding the evaluation of medical treatments, with a focus on the evidential roles of randomised trials and mechanisms in Evidence-Based Medicine. Current 'best practice' usually involves excluding non-randomised trial evidence from systematic reviews in cases where randomised trials are available for inclusion in the reviews. The first paper challenges this practice and evaluates whether adding of evidence from non-randomised trials might improve the quality and precision of some systematic reviews. The second paper compares the alleged (...) methodological benefits of randomised trials over observational studies for investigating treatment benefits. It suggests that claims about the superiority of well-conducted randomised controlled trials over well-conducted observational studies are justified, especially when results from the two methods are contradictory. The third paper argues that postulating the unpredictability paradox in systematic reviews when no detectable empirical differences can be found requires further justification. The fourth paper examines the problem of absence causation in the context of explaining causal mechanisms and argues that a recent solution is incomplete and requires further justification. Solving the problem by describing absences as causes of 'mechanism failure' fails to take into account the effects of absences that lead to vacillating levels of mechanism functionality. The fifth paper criticises literature that has emphasised functioning versus 'broken' or 'non-functioning' mechanisms emphasising that many diseases result from increased or decreased mechanism function, rather than complete loss of function. Mechanistic explanations must account for differences in the effectiveness of performed functions, yet current philosophical mechanistic explanations do not achieve this. The last paper argues that the standard of evidence embodied in the ICE theory of technological function is too permissive for evaluating whether the proposed functions of medical technologies have been adequately assessed and correctly ascribed. It argues that high-quality evidence from clinical studies is necessary to justify functional ascriptions to health care technologies. (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)

Evidence-based medicine (EBM) makes use of explicit procedures for grading evidence for causal claims. Normally, these procedures categorise evidence of correlation produced by statistical trials as better evidence for a causal claim than evidence of mechanisms produced by other methods. We argue, in contrast, that evidence of mechanisms needs to be viewed as complementary to, rather than inferior to, evidence of correlation. In this paper we first set out the case for treating evidence of mechanisms alongside evidence of correlation in (...) explicit protocols for evaluating evidence. Next we provide case studies which exemplify the ways in which evidence of mechanisms complements evidence of correlation in practice. Finally, we put forward some general considerations as to how the two sorts of evidence can be more closely integrated by EBM. (shrink)

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)

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)

Both the traditional Aristotelian and modern symbolic approaches to logic have seen logic in terms of discrete symbol processing. Yet there are several kinds of argument whose validity depends on some topological notion of continuous variation, which is not well captured by discrete symbols. Examples include extrapolation and slippery slope arguments, sorites, fuzzy logic, and those involving closeness of possible worlds. It is argued that the natural first attempts to analyze these notions and explain their relation to reasoning fail, so (...) that ignorance of their nature is profound. (shrink)

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)

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.

After a decade of intense debate about mechanisms, there is still no consensus characterization. In this paper we argue for a characterization that applies widely to mechanisms across the sciences. We examine and defend our disagreements with the major current contenders for characterizations of mechanisms. Ultimately, we indicate that the major contenders can all sign up to our characterization.

Laws of nature take center stage in philosophy of science. Laws are usually believed to stand in a tight conceptual relation to many important key concepts such as causation, explanation, confirmation, determinism, counterfactuals etc. Traditionally, philosophers of science have focused on physical laws, which were taken to be at least true, universal statements that support counterfactual claims. But, although this claim about laws might be true with respect to physics, laws in the special sciences (such as biology, psychology, economics etc.) (...) appear to have—maybe not surprisingly—different features than the laws of physics. Special science laws—for instance, the economic law “Under the condition of perfect competition, an increase of demand of a commodity leads to an increase of price, given that the quantity of the supplied commodity remains constant” and, in biology, Mendel's Laws—are usually taken to “have exceptions”, to be “non-universal” or “to be ceteris paribus laws”. How and whether the laws of physics and the laws of the special sciences differ is one of the crucial questions motivating the debate on ceteris paribus laws. Another major, controversial question concerns the determination of the precise meaning of “ceteris paribus”. Philosophers have attempted to explicate the meaning of ceteris paribus clauses in different ways. The question of meaning is connected to the problem of empirical content, i.e., the question whether ceteris paribus laws have non-trivial and empirically testable content. Since many philosophers have argued that ceteris paribus laws lack empirically testable content, this problem constitutes a major challenge to a theory of ceteris paribus laws. (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)

When a technique purports to provide information that is not available to the unaided senses, it is natural to think that the only way to validate that technique is by appealing to a theory of the processes that lead from the object of study to the raw data. In fact, scientists have a variety of strategies for validating their techniques. Those strategies can yield multiple independent arguments that support the validity of the technique. Thus, it is possible to produce a (...) robust body of data with a single technique. I illustrate and support these claims with a historical case study. *Received September 2009; revised October 2009. †To contact the author, please write to: Department of History and Philosophy of Science, 1017 Cathedral of Learning, University of Pittsburgh, Pittsburgh, PA 15260; e‐mail: [email protected]. (shrink)

Philosophers of science have recently focused on the scientific activity of modeling phenomena, and explicated several of its properties, as well as the activities embedded into it. A first approach to modeling has been elaborated in terms of representing a target system: yet other epistemic functions, such as producing data or detecting phenomena, are at least as relevant. Additional useful distinctions have emerged, such as the one between phenomenological and mechanistic models. In biological sciences, besides mathematical models, models now come (...) in three forms: in vivo, in vitro and in silico. Each has been investigated separately, and many specific problems they raised have been laid out. Another relevant distinction is disciplinary: do models differ in significant ways according to the discipline involved—medicine or biology, evolutionary biology or earth science? Focusing on either this threefold distinction or the disciplinary boundaries reveals that they might not be sufficient from a philosophical perspective. On the contrary, focusing on the interaction between these various kinds of models, some interesting forms of explanation come to the fore, as is exemplified by the papers included in this issue. On the other hand, a focus on the use of models, rather than on their content, shows that the distinction between biological and medical models is theoretically sound. (shrink)

Climate scientists often apply statistical tools to a set of different estimates generated by an “ensemble” of models. In this paper, I argue that the resulting inferences are justified in the same way as any other statistical inference: what must be demonstrated is that the statistical model that licenses the inferences accurately represents the probabilistic relationship between data and target. This view of statistical practice is appropriately termed “model-based,” and I examine the use of statistics in climate fingerprinting to show (...) how the difficulties that climate scientists encounter in applying statistics to ensemble-generated data are the practical difficulties of normal statistical practice. The upshot is that whether the application of statistics to ensemble-generated data yields trustworthy results should be expected to vary from case to case. (shrink)

Public policymakers and institutional decision-makers routinely face questions about whether interventions “work”: does universal basic income improve people’s welfare and stimulate entrepreneurial activity? Do gated alleyways reduce burglaries or merely shift the crime burden to neighbouring communities? What is the most cost-effective way to improve students’ reading abilities? These are empirical questions that seem best answered by looking at the world, rather than trusting speculations about what will be effective. Evidence-based policy (EBP) is a movement that concretizes this intuition. It (...) maintains that policy should be based on evidence of “what works.” Not any evidence will do, however. Following on the heels of its intellectual progenitor, evidence-based medicine (EBM), EBP insists on the use of high-quality evidence produced in accordance with rigorous methodological standards. Though intuitively compelling, EBP has attracted significant criticism from methodologists, political scientists, and philosophers. This chapter provides a critical overview of EBP through a philosophical lens, reviewing and discussing some of the most pressing challenges that EBP faces and outlining some proposals for improving it. I first provide a brief overview of EBP and distinguish a broader and narrower understanding of it. I then review existing lines of criticism of EBP, two of which are considered in detail. The first elaborates how EBP struggles with extrapolation, that is, the use of evidence from study populations to make inferences about the effects of policies on novel target populations. The second maintains that EBP’s methodological tenets are deeply entwined with moral and political values, which can threaten EBP’s promise to promote objectivity in policymaking. Finally, I make some proposals for how EBP could be improved going forward. (shrink)

This paper aims to clarify the nature of understanding in medicine. The first part describes in more detail what it means to understand something and links a type of understanding (i.e., objectual understanding) to explanations. The second part proceeds to investigate what objectual understanding of a disease (i.e., biomedical understanding) requires by considering the case of scurvy from the history of medi- cine. The main hypothesis is that grasping a mechanistic explanation of a condi- tion is necessary for a biomedical (...) understanding of that condition. The third part of the paper argues that biomedical understanding is necessary, but not sufficient for understanding in a clinical context (i.e., clinical understanding). The hypothe- sis is that clinical understanding combines biomedical understanding of a disease or pathological condition with understanding illness, which involves some degree of personal understanding of the patient. It is argued that, in many cases, clinical understanding necessitates adopting a particular second-personal stance and using cognitive resources in addition to those involved in biomedical understanding. (shrink)

Si bien en la filosofía de las ciencias ya se han explorado algunos ejemplos provenientes de la bioquímica como casos de estudio, la filosofía de la bioquímica es una subdisciplina naciente. En este artículo estudiaremos dos problemas filosóficos de relevancia contemporánea en esta ciencia. Por un lado, examinaremos las bases epistemológicas del problema del plegamiento de proteínas. En particular lo relacionado con la predicción de la estructura tridimensional de las proteínas a partir de su secuencia, asunto que ha dado mucho (...) que hablar debido a los nuevos avances utilizando deep learning. Por otro lado, exploraremos el problema in-vitro/in-vivo y, más generalmente, el problema de la extrapolación en las ciencias biológicas. Finalmente, a partir de las consecuencias de ambos temas consideraremos algunas reflexiones filosóficas generales acerca del reduccionismo, el pluralismo y el lugar de la bioquímica en las ciencias biológicas. Palabras clave: Bioquímica, Plegamiento de proteínas, In-vitro/in-vivo, Pluralismo, Reduccionismo. (shrink)

Mitchell & Gronenborn propose that we account for the presence of multiple models of protein structure, each produced in different contexts, through the framework of integrative pluralism. I argue that two interpretations of this framework are available, neither of which captures the relationship between a model and the protein structure it represents or between multiple models of protein structure. Further, it inclines us toward concluding prematurely that models of protein structure are right in their contexts and makes extrapolation of findings (...) from one context to another seem unwarranted. Instead, protein structure determination ought to be understood as modestly monistic. There is one model for every protein in each physicochemical context, and models of the same protein produced in different contexts are compatible with one another. ‘Integrating’ multiple models amounts to extrapolating from one context to another; this is possible because the effect of context on protein folding is relatively weak and predictable. Modest monism better describes the practice of protein structure determination than integrative pluralism and enables greater attention to how context affects protein folding. (shrink)

There are two competing views regarding the role of mechanistic knowledge in inferences about the effectiveness of interventions. One view holds that inferences about the effectiveness of interventions should be based only on data from population-level studies (often statistical evidence from randomised trials). The other view holds that such inferences must be based in part on mechanistic evidence. The competing views are local principles of inference, the plausibility of which can be assessed by a more general normative principle of inference. (...) Bayesianism tells us to base inferences on both the ‘likelihood’ and the ‘prior’. The likelihood represents statistical evidence. One influence on the prior probability of a hypothesis like ‘d causes x’ is mechanistic knowledge of how d causes x. Thus, reasoning about such inferences by appealing to both statistical and mechanistic evidence is vindicated by our best general theory of inference. The primary contribution of this paper is to assess the merits and weaknesses of the arguments on both sides of the debate, using the Bayesian framework. This analysis lends support to those who argue that we should base our causal inferences about interventions in part on mechanistic evidence. (shrink)

I argue that the appropriateness of an assertion is sensitive to context—or, really, the “common ground”—in a way that hasn’t previously been emphasized by philosophers. This kind of context-sensitivity explains why some scientific conclusions seem to be appropriately asserted even though they are not known, believed, or justified on the available evidence. I then consider other recent attempts to account for this phenomenon and argue that if they are to be successful, they need to recognize the kind of context-sensitivity that (...) I argue for. (shrink)

In this paper we identify six theses that constitute core results of philosophical investigation into the nature of mechanisms, and of the role that the search for and identification of mechanisms play in the sciences. These theses represent the fruits of the body of research that is now often called New Mechanism. We concisely present the main arguments for these theses. In the literature, these arguments are scattered and often implicit. Our analysis can guide future research in many ways: it (...) provides critics of New Mechanism with clear targets, it can reduce misunderstandings, it can clarify differences of opinion among New Mechanists and it helps to define a research agenda for New Mechanists. (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)

Winner of the 2020 Essay Competition of the International Social Ontology Society. -/- 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 mecha- nisms 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)

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)

To succeed, political science usually requires either prediction or contextual historical work. Both of these methods favor explanations that are narrow-scope, applying to only one or a few cases. Because of the difficulty of prediction, the main focus of political science should often be contextual historical work. These epistemological conclusions follow from the ubiquity of causal fragility, under-determination, and noise. They tell against several practices that are widespread in the discipline: wide-scope retrospective testing, such as much large-n statistical work; lack (...) of emphasis on prediction; and resources devoted to ‘pure theory’ divorced from frequent empirical application. I illustrate, via Donatella della Porta’s work on political violence, the important role that is still left for theory. I conclude by assessing the scope for political science to offer policy advice. (shrink)

Current debates surrounding the virtues and shortcomings of randomization are symptomatic of a lack of appreciation of the fact that causation can be inferred by two distinct inference methods, each requiring its own, specific experimental design. There is a non-statistical type of inference associated with controlled experiments in basic biomedical research; and a statistical variety associated with randomized controlled trials in clinical research. I argue that the main difference between the two hinges on the satisfaction of the comparability requirement, which (...) is in turn dictated by the nature of the objects of study, namely homogeneous or heterogeneous populations of biological systems. Among other things, this entails that the objection according to which randomized experiments fail to provide better evidence for causation because randomization cannot guarantee comparability is mistaken. (shrink)

Sustainability science seeks to extend scientific investigation into domains characterized by a distinct problem-solving agenda, physical and social complexity, and complex moral and ethical landscapes. In this endeavor it arguably pushes scientific investigation beyond its usual comfort zones, raising fundamental issues about how best to structure such investigation. Philosophers of science have long scrutinized the structure of science and scientific practices, and the conditions under which they operate effectively. We propose a critical engagement between sustainability scientists and philosophers of science (...) with respect to how to engage in scientific activity in these complex domains. We identify specific issues philosophers of science raise concerning current sustainability science and the contributions philosophers can make to resolving them. In conclusion we reflect on the steps philosophers of science could take to advance sustainability science. (shrink)

Conducting research on animals is supposed to be valuable because it provides information on how human mechanisms work. But for the use of animal models to be ethically justified, it must be epistemically justified. The inference from an observation about an animal model to a conclusion about humans must be warranted for the use of animals to be moral. When researchers infer from animals to humans, it’s an extrapolation. Often non-human primates are used as animal models in laboratory behavioral research. (...) The target populations are humans and other non-human primates. I argue that the epistemology of extrapolation renders the use of non-human primates in laboratory behavioral research unreliable. If the model is relevantly similar to the target, then the experimental conditions introduce confounding variables. If the model is not relevantly similar to the target, then the observations of the model cannot be extrapolated to the target. Since using non-human primates in as animal models in laboratory behavioral research is not epistemically justified, using them as animal models in laboratory behavioral research is not ethically justified. (shrink)

This paper looks at the question of what it means for a psychological test to have construct validity. I approach this topic by way of an analysis of recent debates about the measurement of implicit social cognition. After showing that there is little theoretical agreement about implicit social cognition, and that the predictive validity of implicit tests appears to be low, I turn to a debate about their construct validity. I show that there are two questions at stake: First, what (...) level of detail and precision does a construct have to possess such that a test can in principle be valid relative to it? And second, what kind of evidence needs to be in place such that a test can be regarded as validated relative to a given construct? I argue that construct validity is not an all-or-nothing affair. It can come in degrees, because both our constructs and our knowledge of the explanatory relation between constructs and data can vary in accuracy and level of detail, and a test can fail to measure all of the features associated with a construct. I conclude by arguing in favor of greater philosophical attention to processes of construct development. (shrink)

Multidisciplinary models aggregating ‘lower-level’ biological and ‘higher-level’ psychological and social determinants of a phenomenon raise a puzzle. How is the interaction between the physical, the psychological and the social conceptualized and explained? Using biopsychosocial models of pain as an illustration, I argue that these models are in fact level-neutral compilations of empirical findings about correlated and causally relevant factors, and as such they neither assume, nor entail a conceptual or ontological stratification into levels of description, explanation or reality. If inter-level (...) causation is deemed problematic or if debates about the superiority of a particular level of description or explanation arise, these issues are fueled by considerations other than empirical findings. (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)

I consider recent strategies proposed by econometricians for extrapolating causal effects from experimental to target populations. I argue that these strategies fall prey to the extrapolator’s circle: they require so much knowledge about the target population that the causal effects to be extrapolated can be identified from information about the target alone. I then consider comparative process tracing as a potential remedy. Although specifically designed to evade the extrapolator’s circle, I argue that CPT is unlikely to facilitate extrapolation in typical (...) econometrics and evidence-based policy applications. To argue this, I offer a distinction between two kinds of extrapolation, attributive and predictive, the latter being prevalent in econometrics and evidence-based policy. I argue that CPT is not helpful for predictive extrapolation when using the kinds of evidence that econometricians and evidence-based policy researchers prefer. I suggest that econometricians may need to consider qualitative evidence to overcome this problem. (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)

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)

The use of neuroscientific evidence in criminal trials has been steadily increasing. Despite progress made in recent decades in understanding the mechanisms of psychological and behavioral functioning, neuroscience is still in an early stage of development and its potential for influencing legal decision-making is highly contentious. Scholars disagree about whether or how neuroscientific evidence might impact prescriptions of criminal culpability, particularly in instances in which evidence of an accused’s history of mental illness or brain abnormality is offered to support a (...) plea of not criminally responsible. In the context of these debates, philosophers and legal scholars have identified numerous problems with admitting neuroscientific evidence in legal contexts. To date, however, less has been said about the challenges of evaluating the evidence upon which integrative mechanistic explanations that bring together evidence from different areas of neuroscience are based. As we explain, current criteria for evaluating such evidence to determine its admissibility in legal contexts are inadequate. Appealing to literature in the philosophy of scientific experimentation and theoretical work in the social, cognitive and behavioral sciences, we lay the groundwork for reforming these criteria and identify some of the implications of modifying them. (shrink)

The central aim of this article is to specify the ontological nature of constitutive mechanistic phenomena. After identifying three criteria of adequacy that any plausible approach to constitutive mechanistic phenomena must satisfy, we present four different suggestions, found in the mechanistic literature, of what mechanistic phenomena might be. We argue that none of these suggestions meets the criteria of adequacy. According to our analysis, constitutive mechanistic phenomena are best understood as what we will call ‘object-involving occurrents’. Furthermore, on the basis (...) of this notion, we will clarify what distinguishes constitutive mechanistic explanations from etiological ones. 1 Introduction 2 Criteria of Adequacy 2.1 Descriptive adequacy 2.2 Constitutive–etiological distinction 2.3 Constitution 3 The Ontological Nature of Constitutive Mechanistic Phenomena 3.1 Phenomena as input–output relations 3.2 Phenomena as end states 3.3 Phenomena as dispositions 3.4 Phenomena as behaviours 4 Phenomena as Object-Involving Occurrents 4.1 What object-involving occurrents are and why we need them 4.2 The object in the phenomenon 4.3 The adequacy of option 5 Conclusion. (shrink)

Economists and biologists have proposed a distinction between two mechanisms – “strong” and “weak” reciprocity – that may explain the evolution of human sociality. Weak reciprocity theorists emphasize the benefits of long-term cooperation and the use of low-cost strategies to deter free-riders. Strong reciprocity theorists, in contrast, claim that cooperation in social dilemma games can be sustained by costly punishment mechanisms, even in one-shot and finitely repeated games. To support this claim, they have generated a large body of evidence concerning (...) the willingness of experimental subjects to punish uncooperative free-riders at a cost to themselves. In this article, I distinguish between a “narrow” and a “wide” reading of the experimental evidence. Under the narrow reading, punishment experiments are just useful devices to measure psychological propensities in controlled laboratory conditions. Under the wide reading, they replicate a mechanism that supports cooperation also in “real-world” situations outside the laboratory. I argue that the wide interpretation must be tested using a combination of laboratory data and evidence about cooperation “in the wild.” In spite of some often-repeated claims, there is no evidence that cooperation in the small egalitarian societies studied by anthropologists is enforced by means of costly punishment. Moreover, studies by economic and social historians show that social dilemmas in the wild are typically solved by institutions that coordinate punishment, reduce its cost, and extend the horizon of cooperation. The lack of field evidence for costly punishment suggests important constraints about what forms of cooperation can or cannot be sustained by means of decentralised policing. (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.

The primary aim of biomedical research is to discover and develop new knowledge to advance human medicine. Frequently a ‘mouse model’ is taken to be a necessary step towards understanding a disease, biological mechanism or intervention. We argue for caution with respect to the mouse model: theoretical reasons, meta-analyses of empirical data, and viable alternatives all support a more restricted use of animals in laboratories than is current practice. On its own terms, a utilitarian scientific justification for using animals in (...) biomedical research converges more closely with welfarist claims than is usually recognised. (shrink)

Proponents of evidence-based medicine and some philosophers of science seem to agree that knowledge of mechanisms can help solve the problem of applying results of controlled studies to target populations (‘the problem of extrapolation’). We describe the problem of extrapolation, characterize mechanisms, and outline how mechanistic knowledge might be used to solve the problem. Our main thesis is that there are four often overlooked problems with using mechanistic knowledge to solve the problem of extrapolation. First, our understanding of mechanisms is (...) often (and arguably, likely to remain) incomplete. Secondly, knowledge of mechanisms is not always applicable outside the tightly controlled laboratory conditions in which it is gained. Thirdly, mechanisms can behave paradoxically. Fourthly, as Daniel Steel points out, using mechanistic knowledge faces the problem of the ‘extrapolator’s circle’. At the same time, when the problems with mechanistic knowledge have been addressed, such knowledge can and should be used to mitigate (nothing can entirely solve) the problem of extrapolation. (shrink)

Russo and Williamson claim that establishing causal claims requires mechanistic and difference-making evidence. In this article, I will argue that Russo and Williamson's formulation of their thesis is multiply ambiguous. I will make three distinctions: mechanistic evidence as type vs object of evidence; what mechanism or mechanisms we want evidence of; and how much evidence of a mechanism we require. I will feed these more precise meanings back into the Russo–Williamson thesis and argue that it is both true and false: (...) two weaker versions of the thesis are worth supporting, while the stronger versions are not. Further, my distinctions are of wider concern because they allow us to make more precise claims about what kinds of evidence are required in particular cases. (shrink)