Background: Evidence suggesting adverse drug reactions often emerges unsystematically and unpredictably in form of anecdotal reports, case series and survey data. Safety trials and observational studies also provide crucial information regarding the (un-)safety of drugs. Hence, integrating multiple types of pharmacovigilance evidence is key to minimising the risks of harm. Methods: In previous work, we began the development of a Bayesian framework for aggregating multiple types of evidence to assess the probability of a putative causal link between drugs and side (...) effects. This framework arose out of a philosophical analysis of the Bradford Hill Guidelines. In this article, we expand the Bayesian framework and add “evidential modulators,” which bear on the assessment of the reliability of incoming study results. The overall framework for evidence synthesis, “E-Synthesis”, is then applied to a case study. Results: Theoretically and computationally, E-Synthesis exploits coherence of partly or fully independent evidence converging towards the hypothesis of interest (or of conflicting evidence with respect to it), in order to update its posterior probability. With respect to other frameworks for evidence synthesis, our Bayesian model has the unique feature of grounding its inferential machinery on a consolidated theory of hypothesis confirmation (Bayesian epistemology), and in allowing any data from heterogeneous sources (cell-data, clinical trials, epidemiological studies), and methods (e.g., frequentist hypothesis testing, Bayesian adaptive trials, etc.) to be quantitatively integrated into the same inferential framework. Conclusions: E-Synthesis is highly flexible concerning the allowed input, while at the same time relying on a consistent computational system, that is philosophically and statistically grounded. Furthermore, by introducing evidential modulators, and thereby breaking up the different dimensions of evidence (strength, relevance, reliability), E-Synthesis allows them to be explicitly tracked in updating causal hypotheses. (shrink)

I argue that manipulationist theories of causation fail as accounts of causal structure, and thereby as theories of “actual causation” and causal explanation. I focus on two kinds of problem cases, which I call “Perceived Abnormality Cases” and “Ontological Dependence Cases.” The cases illustrate that basic facts about social systems—that individuals are sensitive to perceived abnormal conditions and that certain actions metaphysically depend on institutional rules—pose a challenge for manipulationist theories and for counterfactual theories more generally. I then show how (...) law-based accounts of causal structure can answer such challenges. The moral of the story is that the basic manipulationist idea that our interest in causal structure is driven by our interest in manipulating our environment faces decisive problems in a central domain of application, the social sciences. (shrink)

In the court of law, a person can be punished for attempting to commit a crime. An open issue in the study of Artificial Intelligence and Law is whether the law of attempts could be formally modelled. There are distinct legal rules for determining attempted crime whereas the last-act rule (also called proximity rule) represents the strictest approach. In this paper, we provide a formal model of the last-act rule using structured argumentation.

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)

Introduction to a special issue of Erkenntnis.

It is argued that in deterministic contexts evidence for causal relations states whether a boundary condition makes a difference or not to a phenomenon. In order to substantiate the analysis, I show that this difference/indifference making is the basic type of evidence required for eliminative induction in the tradition of Francis Bacon and John Stuart Mill. To this purpose, an account of eliminative induction is proposed with two distinguishing features: it includes a method to establish the causal irrelevance of boundary (...) conditions by means of indifference making, which is called strict method of agreement, and it introduces the notion of a background against which causal statements are evaluated. Causal statements thus become three-place-relations postulating the relevance or irrelevance of a circumstance C to the examined phenomenon P with respect to a background B of further conditions. To underline the importance of evidence in terms of difference/indifference making, I sketch two areas, in which eliminative induction is extensively used in natural and engineering sciences. One concerns exploratory experiments, the other engineering design methods. Given that a method is discussed that has been used for centuries, I make no claims to novelty in this paper, but hope that the combined discussion of several topics that are still somewhat underrepresented in the philosophy of science literature is of some merit. (shrink)

I argue for the causal character of modeling in data-intensive science, contrary to widespread claims that big data is only concerned with the search for correlations. After discussing the concept of data-intensive science and introducing two examples as illustration, several algorithms are examined. It is shown how they are able to identify causal relevance on the basis of eliminative induction and a related difference-making account of causation. I then situate data-intensive modeling within a broader framework of an epistemology of scientific (...) knowledge. In particular, it is shown to lack a pronounced hierarchical, nested structure. The significance of the transition to such “horizontal” modeling is underlined by the concurrent emergence of novel inductive methodology in statistics such as non-parametric statistics. Data-intensive modeling is well equipped to deal with various aspects of causal complexity arising especially in the higher level and applied sciences. (shrink)

Analogical reasoning addresses the question how evidence from various phenomena can be combined and made relevant for theory development and prediction. In the first part of my contribution, I review some influential accounts of analogical reasoning, both historical and contemporary, focusing in particular on Keynes, Carnap, Hesse, and more recently Bartha. In the second part, I sketch a general framework. To this purpose, a distinction between a predictive and a conceptual type of analogical reasoning is introduced. I then take up (...) a common intuition according to which analogical inferences hold if the differences between source and target concern only irrelevant circumstances. I attempt to make this idea more precise by addressing possible objections and in particular by specifying a notion of causal irrelevance based on difference making in homogeneous contexts. (shrink)

A series of recent studies have explored the impact of people's judgments regarding physical law, morality, and probability. Surprisingly, such studies indicate that these three apparently unrelated types of judgments often have precisely the same impact. We argue that these findings provide evidence for a more general hypothesis about the kind of cognition people use to think about possibilities. Specifically, we suggest that this aspect of people's cognition is best understood using an idea developed within work in the formal semantics (...) tradition, namely the notion of modality. On the view we propose, people may have separate representations for physical, moral and probabilistic considerations, but they also integrate these various considerations into a unified representation of modality. (shrink)

Many psychometricians and behavioral geneticists believe that high heritability of IQ test scores within racial groups coupled with environmental hypotheses failing to account for the differences between the mean scores for groups lends plausibility to explanations of mean differences in terms of genetic factors. I show that heritability estimates and the statistical analysis of variance on which they are based have limited relevance in exposing genetic and environmental factors operating within any single group or population. I begin with agricultural investigations, (...) where replication of genetic types and control over environmental factors are possible, and highlight the difficulties of moving from AOV of observed traits to investigation of measurable genetic factors. The difficulties can only be exacerbated for human data sets, which are equivalent to a crop trial in which each variety is replicated in only one or two of the locations. (shrink)

The debate between the dynamical and the statistical interpretations of natural selection is centred on the question of whether all explanations that employ the concepts of natural selection and drift are reducible to causal explanations. The proponents of the statistical interpretation answer negatively, but insist on the fact that selection/drift arguments are explanatory. However, they remain unclear on where the explanatory power comes from. The proponents of the dynamical interpretation answer positively and try to reduce selection/drift arguments to some of (...) the most prominent accounts of causal explanation. In turn, they face the criticism raised by statisticalists that current accounts of causation have to be violated in some of their core conditions or otherwise used in a very loose manner in order to account for selection/drift explanations. We propose a reconciliation of both interpretations by conveying evolutionary explanations within the unificationist model of scientific explanation. Therefore, we argue that the explanatory power in natural selection arguments is a result of successful unification of individual- and population-level facts. A short case study based on research on sympatric speciation will be presented as an example of how population- and individual-level facts are unified to explain the morphological mosaic of bill shape in island scrub jays. (shrink)

Philosophers of science have often favoured reductive approaches to how-possibly explanation. This article identifies three alternative conceptions making how-possibly explanation an interesting phenomenon in its own right. The first variety approaches “how possibly X?” by showing that X is not epistemically impossible. This can sometimes be achieved by removing misunderstandings concerning the implications of one’s current belief system but involves characteristically a modification of this belief system so that acceptance of X does not result in contradiction. The second variety offers (...) a potential how-explanation of X. It is usually followed by a range of further potential how-explanations of the same phenomenon. In recent literature the factual claims implied by the second variety have been downplayed whereas the heuristic role of mapping the space of conceptual possibilities has been emphasized. I will focus especially on this truth-bracketing sense of potentiality when looking closer at the second variety in the paper. The third variety has attracted less interest. It presents a partial how-explanation of X. Typically it aims to establish the existence of a mechanism by which X could be and was generated. The third conception stands out as the natural alternative for the advocate of ontic how-possibly explanations. This article transfers Salmon’s view that explanation-concepts can be broadly divided into epistemic, modal, and ontic to the context of how-possibly explanations. Moreover, it is argued that each of the three above-mentioned varieties of how-possibly explanation occurs in science. To recognize this may be especially relevant for philosophers. We are often misled by the promises of various why-explanation accounts, and seem to have forgotten nearly everything about the diversity of how-possibly explanations. (shrink)

The estimation of causal effects is fundamental in situations where the underlying system will be subject to active interventions. Part of building a causal inference engine is defining how variables relate to each other, that is, defining the functional relationship between variables entailed by the graph conditional dependencies. In this article, we deviate from the common assumption of linear relationships in causal models by making use of neural autoregressive density estimators and use them to estimate causal effects within Pearl’s do-calculus (...) framework. Using synthetic data, we show that the approach can retrieve causal effects from non-linear systems without explicitly modeling the interactions between the variables and include confidence bands using the non-parametric bootstrap. We also explore scenarios that deviate from the ideal causal effect estimation setting such as poor data support or unobserved confounders. (shrink)

The import of Hodgkin and Huxley’s classic model of the action potential has been hotly debated in recent years, with particular controversy surrounding claims by prominent proponents of mechanistic explanation. For these authors, the Hodgkin-Huxley model is an excellent predictive tool but ultimately lacks causal/explanatory import. What is more, they claim that this is how Hodgkin and Huxley themselves saw the model. I argue that these claims rest on a problematic reading of the work. Hodgkin and Huxley’s model is both (...) causal and, in an important sense, explanatory. (shrink)

Default reasoning occurs whenever the truth of the evidence available to the reasoner does not guarantee the truth of the conclusion being drawn. Despite this, one is entitled to draw the conclusion “by default” on the grounds that we have no information which would make us doubt that the inference should be drawn. It is the type of conclusion we draw in the ordinary world and ordinary situations in which we find ourselves. Formally speaking, ‘nonmonotonic reasoning’ refers to argumentation in (...) which one uses certain information to reach a conclusion, but where it is possible that adding some further information to those very same premises could make one want to retract the original conclusion. It is easily seen that the informal notion of default reasoning manifests a type of nonmonotonic reasoning. Generally speaking, default statements are said to be true about the class of objects they describe, despite the acknowledged existence of “exceptional instances” of the class. In the absence of explicit information that an object is one of the exceptions we are enjoined to apply the default statement to the object. But further information may later tell us that the object is in fact one of the exceptions. So this is one of the points where nonmonotonicity resides in default reasoning. (shrink)

An intervention may have an effect on units other than those to which it was administered. This phenomenon is called interference and it usually goes unmodeled. In this paper, we propose to combine Lauritzen-Wermuth-Frydenberg and Andersson-Madigan-Perlman chain graphs to create a new class of causal models that can represent both interference and non-interference relationships for Gaussian distributions. Specifically, we define the new class of models, introduce global and local and pairwise Markov properties for them, and prove their equivalence. We also (...) propose an algorithm for maximum likelihood parameter estimation for the new models, and report experimental results. Finally, we show how to compute the effects of interventions in the new models. (shrink)

Recent advances in causal reasoning have given rise to a computational model that emulates the process by which humans generate, evaluate, and distinguish counterfactual sentences. Contrasted with the “possible worlds” account of counterfactuals, this “structural” model enjoys the advantages of representational economy, algorithmic simplicity, and conceptual clarity. This introduction traces the emergence of the structural model and gives a panoramic view of several applications where counterfactual reasoning has benefited problem areas in the empirical sciences.

Suppose that we are interested in the average causal effect of a binary treatment on an outcome when this relationship is confounded by a binary confounder. Suppose that the confounder is unobserved but a nondifferential proxy of it is observed. We show that, under certain monotonicity assumption that is empirically verifiable, adjusting for the proxy produces a measure of the effect that is between the unadjusted and the true measures.

This paper provides empirical interpretation of the do(x)do(x) operator when applied to non-manipulable variables such as race, obesity, or cholesterol level. We view do(x)do(x) as an ideal intervention that provides valuable information on the effects of manipulable variables and is thus empirically testable. We draw parallels between this interpretation and ways of enabling machines to learn effects of untried actions from those tried. We end with the conclusion that researchers need not distinguish manipulable from non-manipulable variables; both types are equally (...) eligible to receive the do(x)do(x) operator and to produce useful information for decision makers. (shrink)

Contemporary social-scientific research seeks to identify specific causal mechanisms for outcomes of theoretical interest. Experiments that randomize populations to treatment and control conditions are the “gold standard” for causal inference. We identify, describe, and analyze the problem posed by transformative treatments. Such treatments radically change treated individuals in a way that creates a mismatch in populations, but this mismatch is not empirically detectable at the level of counterfactual dependence. In such cases, the identification of causal pathways is underdetermined in a (...) previously unrecognized way. Moreover, if the treatment is indeed transformative it breaks the inferential structure of the experimental design. Transformative treatments are not curiosities or “corner cases,” but are plausible mechanisms in a large class of events of theoretical interest, particularly ones where deliberate randomization is impractical and quasi-experimental designs are sought instead. They cast long-running debates about treatment and selection effects in a new light, and raise new methodological challenges. (shrink)

By definition, metacognitive processes may monitor or regulate various stages of first-order processing. By combining causal analysis with hypotheses expressed by other authors we derive the theoretical and methodological consequences of this special relation between metacognition and the underlying processes. In particular, we prove that because multiple processing stages may be monitored or regulated and because metacognition may form latent feedback loops, 1) without strong additional causal assumptions, typical measures of metacognitive monitoring or regulation are confounded; 2) without strong additional (...) causal assumptions, typical methods of controlling for first-order task performance (i.e., calibration, staircase, including first-order task performance in a regression analysis, or analyzing correct and incorrect trials separately) not only do not deconfound measures of metacognition but may even introduce bias; 3) that the first two problems cannot be solved by using simple models of decision-making derived from Signal Detection Theory. We conclude the paper by advocating robust methods of discovering properties of latent mechanisms. (shrink)

Interventionism is a theory of causation with a pragmatic goal: to define causal concepts that are useful for reasoning about how things could, in principle, be purposely manipulated. In its original presentation, Woodward’s interventionist definition of causation is relativized to an analyzed variable set. In Woodward, Woodward changes the definition of the most general interventionist notion of cause, contributing cause, so that it is no longer relativized to a variable set. This derelativization of interventionism has not gathered much attention, presumably (...) because it is seen as an unproblematic way to save the intuition that causal relations are objective features of the world. This paper first argues that this move has problematic consequences. Derelativization entails two concepts of unmediated causal relation that are not coextensional, but which nonetheless do not entail different conclusions about manipulability relations within any given variable set. This is in conflict with the pragmatic orientation at the core of interventionism. The paper then considers various approaches for resolving this tension but finds them all wanting. It is concluded that interventionist causation should not be derelativized in the first place. Various considerations are offered rendering that conclusion acceptable. (shrink)

Psychoneural reduction has been debated extensively in the philosophy of neuroscience. In this article I will evaluate metascientific approaches that claim direct molecular and cellular explanations of cognitive functions. I will initially consider the issues involved in linking cellular properties to behaviour from the general perspective of neural circuits. These circuits that integrate the molecular and cellular components underlying cognition and behaviour, making consideration of circuit properties relevant to reductionist debates. I will then apply this general perspective to specific systems (...) where psychoneural reduction has been claimed, namely hippocampal long-term potentiation and the Aplysia gill-withdrawal reflex. (shrink)

Causation is a macroscopic phenomenon. The temporal asymmetry displayed by causation must somehow emerge along with other asymmetric macroscopic phenomena like entropy increase and the arrow of radiation. I shall approach this issue by considering ‘causal inference’ techniques that allow causal relations to be inferred from sets of observed correlations. I shall show that these techniques are best explained by a reduction of causation to structures of equations with probabilistically independent exogenous terms. This exogenous probabilistic independence imposes a recursive order (...) on these equations and a consequent distinction between dependent and independent variables that lines up with the temporal asymmetry of causation. (shrink)

Ernst Mayr’s classical work on the nature of causation in biology has had a huge influence on biologists as well as philosophers. Although his distinction between proximate and ultimate causation recently came under criticism from those who emphasize the role of development in evolutionary processes, the formal relationship between these two notions remains elusive. Using causal graph theory, this paper offers a unified framework to systematically translate a given “proximate” causal structure into an “ultimate” evolutionary response, and illustrates evolutionary implications (...) of various kinds of causal mechanisms including epigenetic inheritance, maternal effects, and niche construction. These results not only reveal the essential interplay between proximate and ultimate causation in the study of evolution, but also provide a formal method to evaluate or discover non-standard or yet unknown evolutionary phenomena. (shrink)

We critically examine Denis Walsh’s latest attack on the causalist view of fitness. Relying on Judea Pearl’s Sure-Thing Principle and geneticist John Gillespie’s model for fitness, Walsh has argued that the causal interpretation of fitness results in a reductio. We show that his conclusion only follows from misuse of the models, that is, (1) the disregard of the real biological bearing of the population-size parameter in Gillespie’s model and (2) the confusion of the distinction between ordinary probability and Pearl’s causal (...) probability. Properly understood, the models used by Walsh do not threaten the causalist view of fitness. (shrink)

The causal nature of evolution is one of the central topics in the philosophy of biology. The issue concerns whether equations used in evolutionary genetics point to some causal processes or purely phenomenological patterns. To address this question the present article builds well-defined causal models that underlie standard equations in evolutionary genetics. These models are based on minimal and biologically plausible hypotheses about selection and reproduction, and generate statistics to predict evolutionary changes. The causal reconstruction of the evolutionary principles shows (...) adaptive evolution as a genuine causal process, where fitness and selection are both causes of evolution. 1 Introduction2 The Philosophical Puzzle3 Causal Models4 Causal Foundations of Evolutionary Genetics4.1 Univariate quantitative genetics model4.1.1 The causal graph4.1.2 Structural equations4.1.3 Deriving evolutionary transition functions4.2 One-locus population genetics model5 Evolution as a Causal Process5.1 Selection as a causal process5.2 Causes of evolutionary change6 Conclusion. (shrink)

The causal nature of evolution is one of the central topics in the philosophy of biology. The issue concerns whether equations used in evolutionary genetics point to some causal processes or purely phenomenological patterns. To address this question the present article builds well-defined causal models that underlie standard equations in evolutionary genetics. These models are based on minimal and biologically plausible hypotheses about selection and reproduction, and generate statistics to predict evolutionary changes. The causal reconstruction of the evolutionary principles shows (...) adaptive evolution as a genuine causal process, where fitness and selection are both causes of evolution. 1 Introduction2 The Philosophical Puzzle3 Causal Models4 Causal Foundations of Evolutionary Genetics4.1 Univariate quantitative genetics model4.1.1 The causal graph4.1.2 Structural equations4.1.3 Deriving evolutionary transition functions4.2 One-locus population genetics model5 Evolution as a Causal Process5.1 Selection as a causal process5.2 Causes of evolutionary change6 Conclusion. (shrink)

Over the past decade philosophers of biology have discussed whether evolutionary theory is a causal theory or a phenomenological study of evolution based solely on the statistical features of a population. This article reviews this controversy from three aspects, respectively concerning the assumptions, applications, and explanations of evolutionary theory, with a view to arriving at a definite conclusion in each contention. In so doing I also argue that an implicit methodological assumption shared by both sides of the debate, namely the (...) overconfidence in conceptual analysis as a tool to understand the scientific theory, is the real culprit that has both generated the problem and precluded its solution for such a long time. (shrink)

If well-designed, the results of a Randomised Clinical Trial can justify a causal claim between treatment and effect in the study population; however, additional information might be needed to carry over this result to another population. RCTs have been criticized exactly on grounds of failing to provide this sort of information Evidence, inference and enquiry. Oxford University Press, New York, 2011), as well as to black-box important details regarding the mechanisms underpinning the causal law instantiated by the RCT result. On (...) the other side, so-called In Silico Clinical Trials face the same criticisms addressed against standard modelling and simulation techniques, and cannot be equated to experiments Philosophy of molecular medicine: foundational issues in research and practice, Routledge, New York, 2017; Parker in Synthese 169:483–496, 2009; Parke in Philos Sci 81:516–536, 2014; Diez Roux in Am J Epidemiol 181:100–102, 2015 and related discussions in Frigg and Reiss in Synthese 169:593–613, 2009; Winsberg in Synthese 169:575–592, 2009; Beisbart and Norton in Int Stud Philos Sci 26:403–422, 2012). We undertake a formal analysis of both methods in order to identify their distinct contribution to causal inference in the clinical setting. Britton et al.’s study :E2098–E2105, 2013) on the impact of ion current variability on cardiac electrophysiology is used for illustrative purposes. We deduce that, by predicting variability through interpolation, ISCTs aid with problems regarding extrapolation of RCTs results, and therefore in assessing their external validity. Furthermore, ISCTs can be said to encode “thick” causal knowledge —as opposed to “thin” difference-making information inferred from RCTs. Hence, ISCTs and RCTs cannot replace one another but rather, they are complementary in that the former provide information about the determinants of variability of causal effects, while the latter can, under certain conditions, establish causality in the first place. (shrink)

The problem of collecting, analyzing and evaluating evidence on adverse drug reactions (ADRs) is an example of the more general class of epistemological problems related to scientific inference and prediction, as well as a central problem of the health-care practice. Philosophical discussions have critically analysed the methodological pitfalls and epistemological implications of evidence assessment in medicine, however they have mainly focused on evidence of treatment efficacy. Most of this work is devoted to statistical methods of causal inference with a special (...) attention to the privileged role assigned to randomized controlled trials in Evidence Based Medicine. Regardless of whether the RCT’s privilege holds for efficacy assessment, it is nevertheless important to make a distinction between causal inference of intended and unintended effects, in that the unknowns at stake are heterogonous in the two contexts. This point has been emphasized by epidemiologists in the last decade. Their main focus is methodological, and regards the fact that bias and confounding do not affect studies on intended and unintended effects in the same way. However, deeper concerns ground the intuition for such a distinction; these are related to the constraints which we impose on evidence and their epistemological justification. My thesis is that such constraints ought to be understood to be different in the case of evidence for risk vs. benefit assessment. I present the recent debate on the causal association between acetaminophen and asthma in order to illustrate the point at issue. (shrink)

Decision theorists disagree about how instrumentally rational agents, i.e., agents trying to achieve some goal, should behave in so-called Newcomb-like problems, with the main contenders being causal and evidential decision theory. Since the main goal of artificial intelligence research is to create machines that make instrumentally rational decisions, the disagreement pertains to this field. In addition to the more philosophical question of what the right decision theory is, the goal of AI poses the question of how to implement any given (...) decision theory in an AI. For example, how would one go about building an AI whose behavior matches evidential decision theory’s recommendations? Conversely, we can ask which decision theories describe the behavior of any existing AI design. In this paper, we study what decision theory an approval-directed agent, i.e., an agent whose goal it is to maximize the score it receives from an overseer, implements. If we assume that the overseer rewards the agent based on the expected value of some von Neumann–Morgenstern utility function, then such an approval-directed agent is guided by two decision theories: the one used by the agent to decide which action to choose in order to maximize the reward and the one used by the overseer to compute the expected utility of a chosen action. We show which of these two decision theories describes the agent’s behavior in which situations. (shrink)

A prominent Thomistic cosmological argument maintains that an infinite regress of causes, which exhibits a certain pattern of ontological dependence among its members, would be vicious and so must terminate in a first member. Interestingly, Jonathan Schaffer offers a similar argument in the contemporary grounding literature for the view called metaphysical foundationalism. I consider the striking similarities between both arguments and conclude that both are unsuccessful for the same reason. I argue this negative result gives us indirect reason to consider (...) metaphysical infinitism as a genuine possibility, the view that chains of ontological dependence or ground can descend indefinitely. (shrink)

The paper sets out the challenges facing the Police in respect of the detection and prevention of the volume crime of burglary. A discussion of data mining and decision support technologies that have the potential to address these issues is undertaken and illustrated with reference the authors’ work with three Police Services. The focus is upon the use of “soft” forensic evidence which refers to modus operandi and the temporal and geographical features of the crime, rather than “hard” evidence such (...) as DNA or fingerprint evidence. Three objectives underpin this paper. First, given the continuing expansion of forensic computing and its role in the emergent discipline of Crime Science, it is timely to present a review of existing methodologies and research. Second, it is important to extract some practical lessons concerning the application of computer science within this forensic domain. Finally, from the lessons to date, a set of conclusions will be advanced, including the need for multidisciplinary input to guide further developments in the design of such systems. The objectives are achieved by first considering the task performed by the intended systems users. The discussion proceeds by identifying the portions of these tasks for which automation would be both beneficial and feasible. The knowledge discovery from databases process is then described, starting with an examination of the data that police collect and the reasons for storing it. The discussion progresses to the development of crime matching and predictive knowledge which are operationalised in decision support software. The paper concludes by arguing that computer science technologies which can support criminal investigations are wide ranging and include geographical information systems displays, clustering and link analysis algorithms and the more complex use of data mining technology for profiling crimes or offenders and matching and predicting crimes. We also argue that knowledge from disciplines such as forensic psychology, criminology and statistics are essential to the efficient design of operationally valid systems. (shrink)

Human cognition requires coping with a complex and uncertain world. This suggests that dealing with uncertainty may be the central challenge for human reasoning. In Bayesian Rationality we argue that probability theory, the calculus of uncertainty, is the right framework in which to understand everyday reasoning. We also argue that probability theory explains behavior, even on experimental tasks that have been designed to probe people's logical reasoning abilities. Most commentators agree on the centrality of uncertainty; some suggest that there is (...) a residual role for logic in understanding reasoning; and others put forward alternative formalisms for uncertain reasoning, or raise specific technical, methodological, or empirical challenges. In responding to these points, we aim to clarify the scope and limits of probability and logic in cognitive science; explore the meaning of the explanation of cognition; and re-evaluate the empirical case for Bayesian rationality. (shrink)

According to Aristotle, humans are the rational animal. The borderline between rationality and irrationality is fundamental to many aspects of human life including the law, mental health, and language interpretation. But what is it to be rational? One answer, deeply embedded in the Western intellectual tradition since ancient Greece, is that rationality concerns reasoning according to the rules of logic – the formal theory that specifies the inferential connections that hold with certainty between propositions. Piaget viewed logical reasoning as defining (...) the end-point of cognitive development; and contemporary psychology of reasoning has focussed on comparing human reasoning against logical standards. (shrink)

The discovery of conjunctive causes--factors that act in concert to produce or prevent an effect--has been explained by purely covariational theories. Such theories assume that concomitant variations in observable events directly license causal inferences, without postulating the existence of unobservable causal relations. This article discusses problems with these theories, proposes a causal-power theory that overcomes the problems, and reports empirical evidence favoring the new theory. Unlike earlier models, the new theory derives (a) the conditions under which covariation implies conjunctive causation (...) and (b) functions relating observable events to unobservable conjunctive causal strength. This psychological theory, which concerns simple cases involving 2 binary candidate causes and a binary effect, raises questions about normative statistics for testing causal hypotheses regarding categorical data resulting from discrete variables. (shrink)

Denis Walsh has written a striking new defense in this journal of the statisticalist (i.e., noncausalist) position regarding the forces of evolution. I defend the causalist view against his new objections. I argue that the heart of the issue lies in the nature of nonadditive causation. Detailed consideration of that turns out to defuse Walsh’s ‘description‐dependence’ critique of causalism. Nevertheless, the critique does suggest a basis for reconciliation between the two competing views. *Received December 2009; revised December 2009. †To contact (...) the author, please write to: Department of Philosophy, 599 Lucas Hall, One University Boulevard, University of Missouri, St. Louis, MO 63121; e‐mail: [email protected]. (shrink)

, whereby some causes are deemed more important than others, are ubiquitous in historical studies. Drawing from influential recent work on causation, I develop a definition of causal-explanatory strength. This makes clear exactly which aspects of explanatory weighting are subjective and which objective. It also sheds new light on several traditional issues, showing for instance that: underlying causes need not be more important than proximate ones; several different causes can each be responsible for most of an effect; small causes need (...) not be less important than big ones; and non-additive interactive effects between causes present no particular difficulty. Key Words: causation • explanation • history • interaction • proximate • underlying. (shrink)

I present a new definition of verisimilitude, framed in terms of causes. Roughly speaking, according to it a scientific model is approximately true if it captures accurately the strengths of the causes present in any given situation. Against much of the literature, I argue that any satisfactory account of verisimilitude must inevitably restrict its judgments to context-specific models rather than general theories. We may still endorse—and only need—a relativized notion of scientific progress, understood now not as global advance but rather (...) as the mastering of particular problems. This also sheds new light on longstanding difficulties surrounding language-dependence and models committed to false ontologies. (shrink)

Standard statistical measures of strength of association, although pioneered by Pearson deliberately to be acausal, nowadays are routinely used to measure causal efficacy. But their acausal origins have left them ill suited to this latter purpose. I distinguish between two different conceptions of causal efficacy, and argue that: 1) Both conceptions can be useful 2) The statistical measures only attempt to capture the first of them 3) They are not fully successful even at this 4) An alternative definition more squarely (...) based on causal thinking not only captures the second conception, it can also capture the first one better too. (shrink)

Jonathan Schaffer (2004 ) proposes an ingenious amendment to David Lewis's semantics for counterfactuals. This amendment explicitly invokes the notion of causal independence, thus giving up Lewis's ambitions for a reductive counterfactual account of causation. But in return, it rescues Lewis's semantics from extant counterexamples. I present a new counterexample that defeats even Schaffer's amendment. Further, I argue that a better approach would be to follow the causal modelling literature and evaluate counterfactuals via an explicit postulated causal structure. This alternative (...) approach easily resolves the new counterexample, as well as all the previous ones. Up to now, its perceived drawback relative to Lewis's scheme has been its non-reductiveness. But since the same drawback applies equally to Schaffer's amended scheme, this becomes no longer a point of comparative disadvantage. (shrink)