Several authors have argued that causes differ in the degree to which they are ‘specific’ to their effects. Woodward has used this idea to enrich his influential interventionist theory of causal explanation. Here we propose a way to measure causal specificity using tools from information theory. We show that the specificity of a causal variable is not well-defined without a probability distribution over the states of that variable. We demonstrate the tractability and interest of our (...) proposed measure by measuring the specificity of coding DNA and other factors in a simple model of the production of mRNA. (shrink)

I use some recent formal work on measuring causation to explore a suggestion by James Woodward: that the notion of causal specificity can clarify the distinction in biology between permissive and instructive causes. This distinction arises when a complex developmental process, such as the formation of an entire body part, can be triggered by a simple switch, such as the presence of particular protein. In such cases, the protein is said to merely induce or "permit" the developmental process, (...) whilst the causal "instructions" for guiding that process are already prefigured within the cells. I construct a novel model that expresses in a simple and tractable way the relevant causal structure of biological development and then use a measure of causal specificity to analyse the model. I show that the permissive-instructive distinction cannot be captured by simply contrasting the specificity of two causes as Woodward proposes, and instead introduce an alternative, hierarchical approach to analysing the interaction between two causes. The resulting analysis highlights the importance of focusing on gene regulation, rather than just the coding regions, when analysing the distinctive causal power of genes. (shrink)

Griffiths et al. (2015) have proposed a quantitative measure of causal specificity and used it to assess various attempts to single out genetic causes as being causally more specific than other cellular mechanisms, for example, alternative splicing. Focusing in particular on developmental processes, they have identified a number of important challenges for this project. In this discussion note, I would like to show how these challenges can be met.

Philosophers of biology generally agree that causal specificity tracks biological importance: more specific causes are more important. I argue that this correlation does not hold in much research aimed at biomedical intervention. Applying James Woodward’s analysis of causal specificity to the development and design of HIV treatments, I show that drugs that are less causally specific produce better therapeutic outcomes and are more highly valued. Thus, I conclude that the importance of biological causes does not track (...) their specificity but instead varies depending on the biological practice we consider and the goals of that practice. (shrink)

Several authors have used the notion of causal specificity in order to defend non-parity about genetic causes (Waters 2007, Woodward 2010, Weber 2017, forthcoming). Non-parity in this context is the idea that DNA and some other biomolecules that are often described as information-bearers by biologists play a unique role in life processes, an idea that has been challenged by Developmental Systems Theory (e.g., Oyama 2000). Indeed, it has proven to be quite difficult to state clearly what the alleged (...) special role of genetic causes consists in. In this paper, I show that the set of biomolecules that are normally considered to be information-bearers (DNA, mRNA) can be shown to be the most specific causes of protein primary structure, provided that causal specificity is measured over a relevant space of biological possibilities, disregarding physical as well as logically possible states of the causal variables. (shrink)

The identification of memory engrams remains a methodological obstacle in neuroscience if they are to play the explanatory role ascribed to them by engram theory. I tackle the problem of specificity, namely the extent to which engrams can be identified, tracked, and distinguished from other engram and non-engram vehicles. I propose that adopting causal specificity from the interventionist framework of causation allows us to describe how engrams are specific to the memories and behaviors they generate. Drawing on (...) recent work using information-theoretic measures to describe causal specificity, I illustrate how this approach can be used to model the reduction of uncertainty about retrieved memories following optogenetic interventions on engram cells. (shrink)

The concept of causal specificity is drawing considerable attention from philosophers of biology. It became the rationale for rejecting (and occasionally, accepting) a thesis of causal parity of developmental factors. This literature assumes that attributing specificity to causal relations is at least in principle a straightforward (if not systematic) task. However, the parity debate in philosophy of biology seems to be stuck at a point where it is not the biological details that will help move (...) forward. In this paper, I take a step back to reexamine the very idea of causal specificity and its intended role in the parity dispute in philosophy of biology. I contend that the idea of causal specificity across variations as currently discussed in the literature is irreducibly twofold in nature: it is about two independent components that are not mutually entailed. I show this to be the source of prior complications with the notion of specificity itself that ultimately affect the purposes for which it is often invoked, notably to settle the parity dispute. (shrink)

I present a reconstruction of F.H.C. Crick's two 1957 hypotheses "Sequence Hypothesis" and "Central Dogma" in terms of a contemporary philosophical theory of causation. Analyzing in particular the experimental evidence that Crick cited, I argue that these hypotheses can be understood as claims about the actual difference-making cause in protein synthesis. As these hypotheses are only true if restricted to certain nucleic acids in certain organisms, I then examine the concept of causal specificity and its potential to counter (...) claims about causal parity of DNA and other cellular components. I first show that causal specificity is a special kind of invariance under interventions, namely invariance of generalizations that range over finite sets of discrete variables. Then, I show that this notion allows the articulation of a middle ground in the debate over causal parity. (shrink)

The interventionist account provides us with several notions permitting the qualification of causal relationships. In recent years, there has been a push toward formalizing these notions using information theory. In this paper, I discuss one of them, namely causal specificity. The notion of causal specificity is ambiguous as it can refer to at least two different concepts. After having presented these, I show that current attempts to formalize causal specificity in information theoretic terms (...) have mostly focused on one of these two concepts. I then propose and apply a new information-theoretic measure which captures the other concept. (shrink)

Griffiths et al. have proposed a quantitative measure of causal specificity and used it to assess various attempts to single out genetic causes as being causally more specific than other cellular mechanisms, for example, alternative splicing. Focusing in particular on developmental processes, they have identified a number of important challenges for this project. In this discussion note, I would like to show how these challenges can be met.

Purpose The purpose of this paper is to suggest a definition of genetic information by taking into account the debate surrounding it. Particularly, the objections raised by Developmental Systems Theory to Teleosemantic endorsements of the notion of genetic information as well as deflationist approaches which suggest to ascribe the notion of genetic information a heuristic value at most, and to reduce it to that of causality. Design/methodology/approach The paper presents the notion of genetic information through its historical evolution and analyses (...) it with the conceptual tools offered by philosophical theories of causation on one side and linguistics on the other. Findings The concept of genetic information is defined as a special kind of cause which causes something to be one way rather than another, by combining elementary units one way rather than another. Tested against the notion of “genetic error” this definition demonstrates to provide an exhaustive account of the common denominators associated with the notion of genetic information: causal specificity; combinatorial mechanism; arbitrariness. Originality/value The definition clarifies how the notion of information is understood when applied to genetic phenomena and also contributes to the debate on the notion of information, broadly meant, which is still affected by lack of consensus. (shrink)

Binding specificity is a centrally important concept in molecular biology, yet it has received little philosophical attention. Here I aim to remedy this by analyzing binding specificity as a causal property. I focus on the concept’s role in drug design, where it is highly prized and hence directly studied. From a causal perspective, understanding why binding specificity is a valuable property of drugs contributes to an understanding of causal selection—of how and why scientists distinguish (...) between causes, not just causes from noncauses. In particular, the specificity of drugs is precisely what underwrites their value as experimental interventions on biological processes. (shrink)

The epidemiologist Bradford Hill famously argued that in epidemiology, specificity of association (roughly, the fact that an environmental or behavioral risk factor is associated with just one or at most a few medical outcomes) is strong evidence of causation. Prominent epidemiologists have dismissed Hill’s claim on the ground that it relies on a dubious `one-cause one effect’ model of disease causation. The paper examines this methodological controversy, and argues that specificity considerations do have a useful role to play (...) in causal inference in epidemiology. More precisely, I argue that specificity considerations help solve a pervasive inferential problem in contemporary epidemiology: the problem of determining whether an exposure-outcome correlation might be due to confounding by a social factor. This examination of specificity has interesting consequences for our understanding of the methodology of epidemiology. It highlights how the methodology of epidemiology relies on local tools designed to address specific inference problems peculiar to the discipline, and shows that observational causal inference in epidemiology can proceed with little prior knowledge of the causal structure of the phenomenon investigated. I also argue that specificity of association cannot (despite claims to the contrary) be entirely explained in terms of Woodward’s well-known concept of “one-to-one” causal specificity. This is because specificity as understood by epidemiologists depends on whether an exposure (or outcome) is associated with a `heterogeneous’ set of variables. This dimension of heterogeneity is not captured in Woodward’s notion, but is crucial for understanding the evidential import of specificity of association. (shrink)

Lynch et al. (Biol Philos 34:62, 2019) employ stability, specificity, and proportionality as criteria for evaluating microbiome causal explanations. Although these causal characteristics signify relevant differences between causal roles, I suggest that they should not be used as general criteria for strong or good causal explanations.

In this paper I analyze the process by which modelers in systems biology arrive at an adequate representation of the biological structures thought to underlie data gathered from high-throughput experiments. Contrary to views that causal claims and explanations are rare in systems biology, I argue that in many studies of gene regulatory networks modelers aim at a representation of causal structure. In addressing modeling challenges, they draw on assumptions informed by theory and pragmatic considerations in a manner that (...) is guided by an interventionist conception of causal structure. While doubts have been raised about the applicability of this notion of causality to complex biological systems, it is here seen to be an adequate guide to inquiry. (shrink)

The paper argues against the central dogma and its interpretation by C. Kenneth Waters and Alex Rosenberg. I argue that certain phenomena in the regulation of gene expression provide a break with the central dogma, according to which sequence specificity for a gene product must be template derived. My thesis of 'molecular epigenesis' with its three classes of phenomena, sequence 'activation', 'selection', and 'creation', is exemplified by processes such as transcriptional activation, alternative cis- and trans-splicing, and RNA editing. It (...) argues that other molecular resources share the causal role of genes; the sequence specificity for the linear sequence of any gene product is distributed between the coding sequence, cis-acting sequences, trans-acting factors, environmental signals, and the contingent history of the cell (thesis of distributed causal specificity). I conclude that the central dogma has unnecessarily restricted genetic research to the sequencing of protein-coding genes, unilinear pathway analyses, and the focus on exclusive specificity. (shrink)

In recent years the notion of biological specificity has attracted significant philosophical attention. This paper focuses on host specificity, a kind of biological specificity that has not yet been discussed by philosophers, and which concerns the extent to which a species is selective in the range of other species it exploits for feeding and/or reproduction. Host specificity is an important notion in ecology, where it plays a variety of theoretical roles. Here I focus on the role (...) of host specificity in biological control, a field of applied ecology that deals with the suppression of pests through the use of living organisms. Examining host specificity and its role in biological control yields several valuable contributions to our understanding of biological specificity. In particular, I argue that host specificity cannot be fully understood in terms of Woodward’s well-known account of causal specificity. To adequately account for host specificity, we need a notion of causal specificity that takes into consideration the extent to which a variable’s effects are similar to one another – a dimension not captured in Woodward’s account. In addition, the literature on host specificity in biological control highlights certain aspects in which causally specific relationships can be practically valuable that have not yet been addressed in philosophical discussions of specificity. That literature also reveals that in certain contexts specificity can hinder rather than foster effective control, thus leading to a nuanced assessment of the practical value of specific causes. (shrink)

In this paper I present a metaphysically minimalist but theoretically strong version of fact causation, in which the causal relata constitute a full Boolean algebra, mirroring the entailment relation of the sentences that express them. I suggest a generalization of the notion of multiple realizability of causes in terms of specificity of facts, and employ this in an interpretation of what goes on in cases of apparently redundant causation.

From its first proposal, the Central Dogma had a graphical form, complete with arrows of different types, and this form quickly became its standard presentation. In different scientific contexts, arrows have different meanings and in this particular case the arrows indicated the flow of information among different macromolecules. A deeper analysis illustrates that the arrows also imply a causal statement, directly connected to the causal role of genetic information. The author suggests a distinction between two different kinds of (...) causal links, defined as 'physical causality' and 'biological determination', both implied in the production of biological specificity. (shrink)

A cause may influence its effect via multiple paths. Paradigmatically (Hesslow [1974]), taking birth control pills both decreases one’s risk of thrombosis by preventing pregnancy and increases it by producing a blood chemical. Building on Pearl ([2001]), I explicate the notion of a path-specific effect. Roughly, a path-specific effect of C on E via path P is the degree to which a change in C would change E were they to be transmitted only via P. Facts about such effects may (...) be gleaned from the structural equations commonly used to represent the causal relationships among variables. I contrast my analysis of the Hesslow case with those given by theorists of probabilistic causality, who mistakenly link it to issues of causal heterogeneity, token-causation and indeterminism. The reason probabilistic theories misdiagnose this case is that they pay inadequate attention to the structural relationships among variables. (shrink)

This paper argues that specific phobia is an ideal kind of psychiatric disorder because it bears the marks of a mature medical diagnosis and is amenable to causal explanation. A new and ambitious program of ‘causal revolution’ has recently emerged in psychiatry that hopes to refurnish our taxonomies by discovering the underlying biological and psychological causes that create and maintain mental illness. I show that the sort of causal story envisioned by the program is a mechanistic property (...) cluster (MPC) structure, which involves a causal mechanism that explains the co-occurrence of a disorder’s signs and symptoms (Kendler, Zachar & Craver, 2011). I then build a model of fear in humans and sketch a novel account of specific phobia as a configuration of the fear system in thrall to deregulated network dynamics such as hysteresis, tipping points, and feedback loops. Specific phobia has an MPC structure. I close by reflecting on whether we can reasonably expect other mental disorders to fit an MPC mold, and thus lend themselves to future causal validation. This paper shows that specific phobia holds a unique place in our picture of mental disorder that has so far been missed. It is an ideal kind of psychopathology. (shrink)

Causal selection is the task of picking out, from a field of known causally relevant factors, some factors as elements of an explanation. The Causal Parity Thesis in the philosophy of biology challenges the usual ways of making such selections among different causes operating in a developing organism. The main target of this thesis is usually gene centrism, the doctrine that genes play some special role in ontogeny, which is often described in terms of information-bearing or programming. This (...) paper is concerned with the attempt of confronting the challenge coming from the Causal Parity Thesis by offering principles of causal selection that are spelled out in terms of an explicit philosophical account of causation, namely an interventionist account. I show that two such accounts that have been developed, although they contain important insights about causation in biology, nonetheless fail to provide an adequate reply to the Causal Parity challenge: Ken Waters's account of actual-difference making and Jim Woodward's account of causal specificity. A combination of the two also doesn't do the trick, nor does Laura Franklin-Hall's account of explanation (in this volume). We need additional conceptual resources. I argue that the resources we need consist in a special class of counterfactual conditionals, namely counterfactuals the antecedents of which describe biologically normal interventions. (shrink)

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

A large number of molecular, physiological, and biochemical events accompany the mitogen‐induced transition from a quiescent, nonproliferating state to a cycling state. However, it is difficult to distinguish causal steps in the commitment to cell division from correlative events. To approach this problem we have isolated mitogen‐specific nonproliferative variants of 3T3 cells, namely cell lines that are unable to mount a mitogenic response to specific mitogens.

The concepts of hierarchical organization, genetic determinism and biological specificity have played a crucial role in biology as a modern experimental science since its beginnings in the nineteenth century. The idea of genetic information and genetic determination was at the basis of molecular biology that developed in the 1940s with macromolecules, viruses and prokaryotes as major objects of research often labelled “reductionist”. However, the concepts have been marginalized or rejected in some of the research that in the late 1960s (...) began to focus additionally on the molecularization of complex biological structures and functions using systems approaches. This paper challenges the view that ‘molecular reductionism’ has been successfully replaced by holism and a focus on the collective behaviour of cellular entities. It argues instead that there are more fertile replacements for molecular ‘reductionism’, in which genomics, embryology, biochemistry, and computer science intertwine and result in research that is as exact and causally predictive as earlier molecular biology. (shrink)

Following from my criticisms of Calcott’s analysis on the permissive/instructive distinction, I rebut his claims that 1) he clarifies my measure one-to-one specificity; 2) for all intents and purposes of his analysis his notion of precision is different from my measure of one- to-one specificity; 3) Waddington box is a better and different model than the extension of Woodward’s radio I propose.

Causal selection is the task of picking out, from a field of known causally relevant factors, some factors as elements of an explanation. The Causal Parity Thesis in the philosophy of biology challenges the usual ways of making such selections among different causes operating in a developing organism. The main target of this thesis is usually gene centrism, the doctrine that genes play some special role in ontogeny, which is often described in terms of information-bearing or programming. This (...) paper is concerned with the attempt of confronting the challenge coming from the Causal Parity Thesis by offering principles of causal selection that are spelled out in terms of an explicit philosophical account of causation, namely an interventionist account. I show that two such accounts that have been developed, although they contain important insights about causation in biology, nonetheless fail to provide an adequate reply to the Causal Parity challenge: Ken Waters's account of actual-difference making and Jim Woodward's account of causal specificity. A combination of the two also doesn't do the trick, nor does Laura Franklin-Hall's account of explanation (in this volume). We need additional conceptual resources. I argue that the resources we need consist in a special class of counterfactual conditionals, namely counterfactuals the antecedents of which describe biologically normal interventions. (shrink)

The recent literature on causality has seen the introduction of several distinctions within causality, which are thought to be important for understanding the widespread scientific practice of focusing causal explanations on a subset of the factors that are causally relevant for a phenomenon. Concepts used to draw such distinctions include, among others, stability, specificity, proportionality, or actual-difference making. In this contribution, I propose a new distinction that picks out an explanatorily salient class of causes in biological systems. Some (...) select causes in complex biological systems, I argue, have the property of enabling coherent causal control of these systems. Examples of such control variables include hormones and other signaling molecules, e.g., TOR (target of rapamycin), morphogens or the products of homeotic selector genes in embryonic pattern formation. I propose an analysis of this notion based on concepts borrowed from causal graph theory. (shrink)

Two experiments are reported in which nondysphoric participants, not prone to excessive levels of rumination in everyday life, were asked to retrieve autobiographical memories using the Williams and Broadbent (Citation1986) procedure (AMT). In the first experiment, two variants of a self‐related category fluency task were interleaved among sets of autobiographical memory cues. In one variant (blocked) a normal model of analytic rumination was induced by grouping prompts on a single superordinate theme together. In the other (intermixed) prompts from several different (...) themes were grouped together. It was predicted that the blocked variant would reduce the number of specific memories recollected and increase the number of categoric memories relative to the intermixed variant. This prediction was confirmed and provides the first demonstration of a bidirectional causal influence of analytic rumination on the balance between specific and categoric retrievals. A second experiment showed no alteration in this balance when the same fluency manipulation involved animal‐related categories rather than self‐related ones. The results support a two component model of autobiographical retrieval being driven in part by the extent to which an analytic mode of processing is adopted in the short term and in part by the level of differentiation in self‐related schematic models. (shrink)

The statistical community has brought logical rigor and mathematical precision to the problem of using data to make inferences about a model’s parameter values. The TETRAD project, and related work in computer science and statistics, aims to apply those standards to the problem of using data and background knowledge to make inferences about a model’s specification. We begin by drawing the analogy between parameter estimation and model specification search. We then describe how the specification of a structural equation model entails (...) familiar constraints on the covariance matrix for all admissible values of its parameters; we survey results on the equivalence of structural equation models, and we discuss search strategies for model specification. We end by presenting several algorithms that are implemented in the TETRAD II program. (shrink)

A comparative fMRI study by Peeters et al. (2009) provided evidence that a specific sector of left inferior parietal lobule is devoted to tool use in humans, but not in monkeys. We propose that this area represents the neural substrate of the human capacity to understand tool use by using causal reasoning.

We summarise and respond to the main points made by the commentators on our target article, which concern: whether structural similarity can play a causal role in normal object identification and in neuropsychological deficits for living things, the nature of our structural knowledge of the world, the relations between sensory and functional knowledge of objects, and the nature of our functional knowledge about living things, whether we need to posit a “core” semantic system, arguments that can be marshalled from (...) evidence on functional imaging, the causal mechanisms by which category differences can emerge in object representations, and the nature of our knowledge about categories other than living and nonliving things. We also highlight points raised in our article that seem to be accepted. (shrink)

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

Moritz Schlick’s interpretation of the causality principle is based on Schlick’s understanding of quantum mechanics and on his conviction that quantum mechanics strongly supports an empiricist reading of causation in his sense. The present paper compares the empiricist position held by Schlick with Bas van Fraassen’s more recent conception of constructive empiricism. It is pointed out that the development from Schlick’s understanding of logical empiricism to constructive empiricism reflects a difference between the understanding of quantum mechanics endorsed by Schlick and (...) the understanding that had been established at the time of van Fraassen’s writing. (shrink)

Synchronous oscillations are ubiquitous throughout the cortex, but the frequency of oscillations differs from area to area. To elucidate the mechanistic architectures underlying various rhythmic activities, we tested whether spontaneous neural oscillations in different local cortical areas and large-scale networks can be phase-entrained by direct perturbation with distinct frequencies of repetitive transcranial magnetic stimulation. While recording the electroencephalogram, we applied single-pulse TMS and rTMS at 5, 11, and 23 Hz over the motor or visual cortex. We assessed local and global (...) modulation of phase dynamics using the phase-locking factor. sp-TMS to the motor and the visual cortex triggered a transient increase in PLF in distinct frequencies that peaked at 21 and 8 Hz, respectively. rTMS at 23 Hz over the motor cortex and 11 Hz over the visual cortex induced a prominent and progressive increase in PLF that lasted for a few cycles after the termination of rTMS. Moreover, the local increase in PLF propagated to other cortical areas. These results suggest that distinct cortical areas have area-specific oscillatory frequencies, and the manipulation of oscillations in local areas impacts other areas through the large-scale oscillatory network with the corresponding frequency specificity. We speculate that rTMS that is close to area-specific frequencies enables direct manipulation of brain dynamics and is thus useful for investigating the causal roles of synchronous neural oscillations. Moreover, this technique could be used to treat clinical symptoms associated with impaired oscillations and synchrony. (shrink)

The concepts of hierarchical organization, genetic determinism and biological specificity have played a crucial role in biology as a modern experimental science since its beginnings in the nineteenth century. The idea of genetic information and genetic determination was at the basis of molecular biology that developed in the 1940s with macromolecules, viruses and prokaryotes as major objects of research often labelled “reductionist”. However, the concepts have been marginalized or rejected in some of the research that in the late 1960s (...) began to focus additionally on the molecularization of complex biological structures and functions using systems approaches. This paper challenges the view that ‘molecular reductionism’ has been successfully replaced by holism and a focus on the collective behaviour of cellular entities. It argues instead that there are more fertile replacements for molecular ‘reductionism’, in which genomics, embryology, biochemistry, and computer science intertwine and result in research that is as exact and causally predictive as earlier molecular biology. (shrink)

In earlier publications of the first author it was shown that intentional explanation of actions, functional explanation of biological traits and causal explanation of abnormal events share a common structure. They are called explanation by specification (of a goal, a biological function, an abnormal causal factor, respectively) as opposed to explanation by subsumption under a law. Explanation by specification is guided by a schematic train of thought, of which the argumentative steps not concerning questions were already shown to (...) be logically valid (elementary) arguments.Independently, the second author developed a new, inferential approach to erotetic logic, the logic of questions. In this approach arguments resulting in questions, with declarative sentences and/or other questions as premises, are analyzed, and validity of such arguments is defined. (shrink)

This paper seeks to determine the significance, if any, of epidemiological evidence to prove the specific causation element of liability in negligence or other relevant torts—in particular, what importance can be attached to a relative risk > 2, where that figure represents a sound causal inference at the general level. The paper discusses increased risk approaches to epidemiological evidence and concludes that they are a last resort. The paper also criticizes the proposal that the probability of causation can be (...) estimated with reference to the RR, such that RR > 2 is necessary and sufficient for causation. It is argued, following arguments by Sander Greenland and others, that RR > 2 is not necessary for proof of specific causation, except under restrictive biological assumptions that are not known to be satisfied for any important disease, and therefore must never be required. However, the paper argues that in some circumstances RR > 2 can be sufficient to prove causation at law. This position is defended against the widely held judicial and academic view that epidemiological evidence must be accompanied by something else, particular to the case at hand, if it is to have probative force for specific causation. It is argued that far from being epistemically irrelevant, to achieve correct and just outcomes it is in fact mandatory to take epidemiological evidence into account in deciding specific causation. Failing to consider such evidence when it is available leads to error and injustice. The conclusion is that in certain circumstances epidemiological evidence of RR > 2 is not necessary to prove specific causation but that it is sufficient. This “sufficiency” is confined to circumstances where there is no other evidence, as a way of getting clear on what the epidemiological evidence says. Once we have worked out what it says, this must be weighed against the other relevant evidence, if there is any. (shrink)

The qualitative division between domain-general and domain-specific cognition is unsubstantiated. The distinction is instead better viewed as opposites on a gradual scale, which has more explanatory power and fits current empirical evidence better. We also argue that causal cognition may be more general than social learning, which it often involves.