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)

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.

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)

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)

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)

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)

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)

It is natural to think of remembering in terms of causation: I can recall a recent dinner with a friend because I experienced that dinner. Some fifty years ago, Martin and Deutscher (1966) turned this basic thought into a full-fledged theory of memory, a theory that came to dominate the landscape in the philosophy of memory. Remembering, Martin and Deutscher argue, requires the existence of a specific sort of causal connection between the rememberer's original experience of an event and (...) his later representation of that event: a causal connection sustained by a memory trace. In recent years, it has become apparent that this reference to memory traces may be out of step with memory science. Contemporary proponents of the causal theory are thus confronted with the question: is it possible to develop an empirically adequate version of the theory, or is it time to move beyond it? This chapter traces the recent history of the causal theory, showing how increased awareness of the theory’s problems has led to the development of modified version of the causal theory and ultimately to the emergence of postcausal theories. (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 article examines how specific realist and projectivist versions of manipulability theories of causation deal with the problem of objectivity. Does an agent-dependent concept of manipulability imply that conflicting causal claims made by agents with different capacities can come out as true? In defence of the projectivist stance taken by the agency view, I argue that if the agent’s perspective is shown to be uniform across different agents, then the truth-values of causal claims do not vary arbitrarily and, (...) thus, reach a satisfactory level of objectivity. My argument connects Price’s considerations on the situation of deliberation, whose structure, common to all agents, is the same with respect to both decision making and causal claims on a concept inspired by Douglas’s classification of objectivity of thought processes: the perspective of the detached agent. I further argue that, despite his agent-independent concept of intervention, Woodward’s claim of a stronger objectivity standard cannot be achieved, as the relativity of causal concepts to a variable set brings about the issue of the agent’s choice of variables. Consequently, a more permissive objectivity standard applies to both views. (shrink)

Jaegwon Kim’s influential exclusion argument attempts to demonstrate the inconsistency of nonreductive materialism in the philosophy of mind. Kim’s argument begins by showing that the three main theses of nonreductive materialism, plus two additional considerations, lead to a specific and familiar picture of mental causation. The exclusion argument can succeed only if, as Kim claims, this picture is not one of genuine causal overdetermination. Accordingly, one can resist Kim’s conclusion by denying this claim, maintaining instead that the effects of (...) the mental are always causally overdetermined. I call this strategy the ‘ overdetermination challenge’. One of the main aims of this paper is to show that the overdetermination challenge is the most appropriate response to Kim’s exclusion argument, at least in its latest form. I argue that Kim fails to adequately respond to the overdetermination challenge, thus failing to prevent his opponents from reasonably maintaining that the effects of the mental are always causally overdetermined. Interestingly, this discussion reveals a curious dialectical feature of Kim’s latest response to the overdetermination challenge: if it succeeds, then a new, simpler and more compact version of the exclusion argument is available. While I argue against the consequent of this conditional, thereby also rejecting the antecedent, this dialectical feature should be of interest to philosophers on either side of this debate. (shrink)

What are the roles of scientific causal knowledge in relation to the evidential requirements of policy making? In this chapter, I review the existing approaches in philosophy of science to the policy relevance of causal knowledge. I assess the specific concerns and questions on which these philosophical accounts have focused and show how they only offer a partial perspective of the relation between causal knowledge and policy making. Most existing views are top-down approaches: they start from philosophical (...) concerns about causation and evidence, and then make general claims about (potential) policy implications, but leave the notion of “policy” unanalyzed. As an alternative, I put forward some ideas toward a bottom-up approach: one that understands policy making as a dynamic process with several stages, and that starts from concrete policy problems, to then examine how causal notions and methods can contribute in various ways to the specifics of the process of policy making. (shrink)

This paper brings together Thompson's naive action explanation with interventionist modeling of causal structure to show how they work together to produce causal models that go beyond current modeling capabilities, when applied to specifically selected systems. By deploying well-justified assumptions about rationalization, we can strengthen existing causal modeling techniques' inferential power in cases where we take ourselves to be modeling causal systems that also involve actions. The internal connection between means and end exhibited in naive action (...) explanation has a modal strength like that of distinctively mathematical explanation, rather than that of causal explanation. Because it is stronger than causation, it can be treated as if it were merely causal in a causal model without thereby overextending the justification it can provide for inferences. This chapter introduces and demonstrate the usage of the Rationalization condition in causal modeling, where it is apt for the system(s) being modeled, and to provide the basics for incorporating R variables into systems of variables and R arrows into DAGs. Use of the Rationalization condition supplements causal analysis with action analysis where it is apt. (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 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.

Abstract In this paper I consider an easier-to-read and improved to a certain extent version of the causal chance-based analysis of counterfactuals that I proposed and argued for in my A Theory of Counterfactuals. Sections 2, 3 and 4 form Part I: In it, I survey the analysis of the core counterfactuals (in which, very roughly, the antecedent is compatible with history prior to it). In section 2 I go through the three main aspects of this analysis, which are (...) the following. First, it is a causal analysis, in that it requires that intermediate events to which the antecedent event is not a cause be preserved in the main truth-condition schema. Second, it highlights the central notion to the semantics of counterfactuals on the account presented here -- the notion of the counterfactual probability of a given counterfactual, which is the probability of the consequent given the following: the antecedent, the prior history, and the preserved intermediate events. Third, it considers the truth conditions for counterfactuals of this sort as consisting in this counterfactual probability being higher than a threshold. In section 3, I re-formulate the analysis of preservational counterfactuals in terms of the notion of being a cause, which ends up being quite compact. In section 4 I illustrate this analysis by showing how it handles two examples that have been considered puzzling – Morgenbesser's counterfactual and Edgington's counterfactual. Sections 5 and on constitute Part II: Its main initial thrust is provided in section 5, where I present the main lines of the extension of the theory from the core counterfactuals (analyzed in part I) to counterfactuals (roughly) whose antecedents are not compatible with their prior history. In this part II, I elaborate on counterfactuals that don't belong to the core, and more specifically on so-called reconstructional counterfactuals (as opposed to the preservational counterfactuals, which constitute the core counterfactual-type). The heart of the analysis is formulated in terms of processes leading to the antecedent (event/state), and more specifically in terms of processes likely to have led to the antecedent, a notion which is analyzed entirely in terms of chance. It covers so-called reconstructional counterfactuals as opposed to the core, so-called preservational counterfactuals, which are analyzed in sections 2 and 3 of part I. The counterfactual probability of such reconstructional counterfactuals is determined via the probability of possible processes leading to the antecedent weighed, primarily and roughly, by the conditional probability of the antecedent given such process: The counterfactual probability is thus, very roughly, a weighted sum for all processes most likely to have led to the antecedent, diverging at a fixed time. In section 6 I explain and elaborate further on the main points in section 5. In section 7 I illustrate the reconstructional analysis. I specify counterfactuals which are so-called process-pointers, since their consequent specifies stages in processes likely to have led to their antecedent. I argue that so-called backtracking counterfactuals are process-pointers counterfactuals, which fit into the reconstructional analysis, and do not call for a separate reading. I then illustrate cases where a speaker unwittingly employs a certain counterfactual while charitably construable as intending to assert (or ‘having in mind’) another. Here I also cover the issue of how to construe what one can take as back-tracking counterfactuals, or counterfactuals of the reconstructional sort, and more specifically, which divergence point they should be taken as alluding to (prior to which the history is held fixed). Some such cases also give rise to what one can take as a dual reading of a counterfactual between preservational and reconstructional readings. Such cases may yield an ambiguity, where in many cases one construal is dominant. In section 8 I illustrate the analysis by applying it to the famous Bizet-Verdi counterfactuals. This detailed analysis of counterfactuals (designed for the indeterministic case) has three main distinctive elements: its being chance-based, its causal aspect, and the use it makes of processes most likely to have led to the antecedent-event. This analysis is couched in a very different conceptual base from, and is an alternative account to, analyses in terms of the standard notion of closeness or distance of possible worlds, which is the main feature of the Stalnaker-Lewis-type analyses of counterfactuals. This notion of closeness or distance plays no role whatsoever in the analysis presented here. (This notion of closeness has been left open by Stalnaker, and to significant extent also by Lewis's second account.) . (shrink)

Causal theories of reference describe how terms acquire specific references (especially logical terms, proper names, and natural terms) based on evidence. In the case of names, a causal theory of reference assumes that 1) the referent of the name is fixed by an original designation (called by Saul Kripke "initial baptism"), after which the name becomes a rigid designator of that object; 2) the name is subsequently transmitted by communication through a causal chain. Saul Kripke and Hilary (...) Putnam proposed the extension of causal theory to natural terms. DOI: 10.13140/RG.2.2.35625.75364 . (shrink)

A finer-grained delineation of a given explanandum reveals a nexus of closely related causal and non- causal explanations, complementing one another in ways that yield further explanatory traction on the phenomenon in question. By taking a narrower construal of what counts as a causal explanation, a new class of distinctively mathematical explanations pops into focus; Lange’s characterization of distinctively mathematical explanations can be extended to cover these. This new class of distinctively mathematical explanations is illustrated with the (...) Lotka-Volterra equations. There are at least two distinct ways those equations might hold of a system, one of which yields straightforwardly causal explanations, but the other of which yields explanations that are distinctively mathematical in terms of nomological strength. In the first, one first picks out a system or class of systems, finds that the equations hold in a causal -explanatory way; in the second, one starts with the equations and explanations that must apply to any system of which the equations hold, and only then turns to the world to see of what, if any, systems it does in fact hold. Using this new way in which a model might hold of a system, I highlight four specific avenues by which causal and non- causal explanations can complement one another. (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.

For many causal endeavors, such as measuring, predicting, and explaining, individuating causal systems plays a crucial role. In this chapter, we focus on the individuation of a specific type of causal systems, what we call cross-cutting systems. These are systems that lack natural boundaries and that are not restricted to the spatiotemporal region of the individuals to which they belong. Based on examples taken from cognitive science and behavioral ecology, we explore how scientists individuate such cross-cutting (...) class='Hi'>causal systems. (shrink)

How do mental states come to be about something other than their own operations, and thus to serve as ground for effective action? This papers argues that causation in the mental domain should be understood to function on principles of intelligibility (that is, on principles which make it perfectly intelligible for intentions to have a causal role in initiating behavior) rather than on principles of mechanism (that is, on principles which explain how causation works in the physical domain). The (...) paper considers Dharmakīrti’s kāryānumāna argument (that is, the argument that an inference is sound only when one infers from the effect to the cause and not vice versa), and proposes a naturalized account of reasons. On this account, careful scrutiny of the effect can provide a basis for ascertaining the unique causal totality that is its source, but only for reasoning that is context‐specific. (shrink)

This paper provides a general introduction to the use of causal models in the metaphysics of causation, specifically structural equation models and directed acyclic graphs. It reviews the formal framework, lays out a method of interpretation capable of representing different underlying metaphysical relations, and describes the use of these models in analyzing causation.

A promising development in the philosophy of causation analyzes actual causation using structural equation models, i.e., “causal models”. This paper carefully considers what it means for an interpreted model to be accurate of its target situation. These considerations show, first, that our existing understanding of accuracy is inadequate. Further, and more controversially, they show that any causal model analysis is committed to a kind of relativism – a view whereby causation is a three-part relation holding between a cause, (...) an effect, and something else. In particular, insofar as a causal model analysis construes causation mind-and-language independently, it must treat causation as relative to a specification of background possibilities – i.e., a ‘modal profile.’ Or, so I argue. (shrink)

Contemporary philosophical debates about causation are dominated by two approaches, which are often referred to as difference-making and causal process approaches to causation, respectively. I provide a characterization of the dialectic between these two approaches, on which that dialectic turns crucially on the question as to whether our common sense concept of causation involves a commitment to locality – i.e., to the claim that causal relations are always subject to spatial constraints. I then argue that we can extract (...) from existing work on perceptual judgement (specifically work that invokes the notion of a simple theory of perception) materials for an argument in favour of a positive answer to that question, and that this work can also help to bring out a distinctive kind of role that a commitment to locality plays in our reasoning about causal relationships. (shrink)

My account of the causal role of consciousness in a physical world is modeled on Dretske’s celebrated explanation of the causal role of beliefs (something that Dretske himself never offered). First, behavior must be understood as a (broadly individuated) process that begins with some external stimulus causing some neurological event C, and ends with causing a bodily movement M (e.g., the Kennedy assassination is a process that begins with Oswald pulling the trigger at 12:30pm CST on November 23 (...) in 1963 in Dallas, Texas, but only ends half an hour later when Kennedy is pronounced dead at 1 pm CST). The internal neurological event C causes bodily movement M, but only by virtue of being recruited by natural selection to represent the instantiation of some external property F when properly stimulated under normal circumstances. But the reason why C causes M lies in the fact that C represents the instantiation of the external property F. I withdraw my hand from a hot surface because the activation of nociceptive specific neurons in my parietal lobe (together with the activation of neuronal patterns in my motor cortices) was recruited by natural selection to represent the tissue damage in my hand. The activation of nociceptive specific neurons causes my hand to withdraw but for the reason that it represents tissue data at the time that I felt pain in my hand. (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)

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)

This paper derives from a broader project dealing with the notion of causal order. I use this term to signify two kinds of parts-whole dependence: Orderly systems have rich, decomposable, internal structure; specifically, parts play differential roles, and interactions are primarily local. Disorderly systems, in contrast, have a homogeneous internal structure, such that differences among parts and organizational features are less important. Orderliness, I suggest, marks one key difference between individuals and collectives. My focus here will be the connection (...) between order and robustness, i.e. functional resilience in the face of internal or environmental perturbations. I distinguish three varieties of robustness. Ordered robustness is grounded in the system’s specific organizational pattern. In contrast, disorderly robustness stems from the aggregate outcome of many similar parts. In between, we find semi-ordered robustness, wherein a messy ensemble of elements is subjected to a selection or stabilization mechanism. I give brief characterizations of each category, discuss examples and remark on the connection between the order/disorder axis and the notions of individual versus collective. (shrink)

How feasible are conceptual engineering projects of social concepts that aim for the engineered concept to be widely adopted in ordinary everyday life? Predominant frameworks on the psychology of concepts that shape work on stereotyping, bias, and machine learning have grim implications for the prospects of conceptual engineers: conceptual engineering efforts are ineffective in promoting certain social-conceptual changes. Specifically, since conceptual components that give rise to problematic social stereotypes are sensitive to statistical structures of the environment, purely conceptual change won’t (...) be possible without corresponding world change. This tradition, however, tends to ignore that concepts don’t only encode statistical, but also causal information. Paying attention to this feature of concepts, I argue, shows that conceptual engineering is not only possible. There is an imperative to conceptually-engineer. (shrink)

Powers, capacities and dispositions (in what follows I will use these terms synonymously) have become prominent in recent debates in metaphysics, philosophy of science and other areas of philosophy. In this paper I will analyse in some detail a well-known argument from scientific practice to the existence of powers/capacities/dispositions. According to this argument the practice of extrapolating scientific knowledge from one kind of situation to a different kind of situation requires a specific interpretation of laws of nature, namely as attributing (...) dispositions to systems. My main interest will be to discuss what characteristics these dispositions need to have in order to account for the scientific practice in question. I will furthermore assess whether the introduction of dispositions in the context of the extrapolation argument can be described as a ‘revitalization’ or as a ‘return’ to those notions repudiated by early modern philosophers. More particularly I will argue for the following claims: I. In repudiating scholastic terminology, including substantial forms with their causal powers, post-cartesian philosophers focussed on a concept of causation that was much stronger than 21st century conceptions of causation. For this reason alone, whatever ‘causal’ is supposed to mean in today’s causal powers, embracing causal powers is not a simple return to a pre-cartesian notion. II. The dispositions presupposed in scientific practice need not (and should not) be construed in causal terms (whether strong or weak). III. While some early modern philosophers contrasted the characterisation of the natural world in terms of substantial forms (and their causal powers) on the one hand and a mathematical characterization on the other and suggested that these approaches are incompatible, the dispositions postulated by the extrapolation argument to account for scientific practice are themselves characterized in mathematical terms. More precisely: The behaviour the systems are disposed to display is – at least in physics – often characterized in mathematical terms. IV. The dispositions assumed in the law-statements in scientific practice are determinable rather than determinate properties. (shrink)

Recent studies indicate that indicative conditionals like "If people wear masks, the spread of Covid-19 will be diminished" require a probabilistic dependency between their antecedents and consequents to be acceptable (Skovgaard-Olsen et al., 2016). But it is easy to make the slip from this claim to the thesis that indicative conditionals are acceptable only if this probabilistic dependency results from a causal relation between antecedent and consequent. According to Pearl (2009), understanding a causal relation involves multiple, hierarchically organized (...) conceptual dimensions: prediction, intervention, and counterfactual dependence. In a series of experiments, we test the hypothesis that these conceptual dimensions are differentially encoded in indicative and counterfactual conditionals. If this hypothesis holds, then there are limits as to how much of a causal relation is captured by indicative conditionals alone. Our results show that the acceptance of indicative and counterfactual conditionals can become dissociated. Furthermore, it is found that the acceptance of both is needed for accepting a causal relation between two co-occurring events. The implications that these findings have for the hypothesis above, and for recent debates at the intersection of the psychology of reasoning and causal judgment, are critically discussed. Our findings are consistent with viewing indicative conditionals as answering predictive queries requiring evidential relevance (even in the absence of direct causal relations). Counterfactual conditionals in contrast target causal relevance, specifically. Finally, we discuss the implications our results have for the yet unsolved question of how reasoners succeed in constructing causal models from verbal descriptions. (shrink)

Frank Cabrera argues that informational explanatory virtues—specifically, mechanism, precision, and explanatory scope—cannot be confirmational virtues, since hypotheses that possess them must have a lower probability than less virtuous, entailed hypotheses. We argue against Cabrera’s characterization of confirmational virtue and for an alternative on which the informational virtues clearly are confirmational virtues. Our illustration of their confirmational virtuousness appeals to aspects of causal inference, suggesting that causal inference has a role for the explanatory virtues. We briefly explore this possibility, (...) delineating a path from Mill’s method of agreement to Inference to the Best Explanation (IBE). (shrink)

In clinical medicine, a diagnosis can offer an explanation of a patient's symptoms by specifying the pathology that is causing them. Diagnoses in psychiatry are also sometimes presented in clinical texts as if they pick out pathological processes that cause sets of symptoms. However, current evidence suggests the possibility that many diagnostic categories in psychiatry are highly causally heterogeneous. For example, major depressive disorder may not be associated with a single type of underlying pathological process, but with a range of (...) different causal pathways, each involving complex interactions of various biological, psychological, and social factors. This paper explores the implications of causal heterogeneity for whether psychiatric diagnoses can be said to serve causal explanatory roles in clinical practice. I argue that while they may fall short of picking out a specific cause of the patient's symptoms, they can nonetheless supply different sorts of clinically relevant causal information. In particular, I suggest that some psychiatric diagnoses provide negative information that rules out certain causes, some provide approximate or disjunctive information about the range of possible causal processes, and some provide causal information about the relations between the symptoms themselves. (shrink)

Presentism is the view that only present temporal entities (tenselessly) exist. A widely-discussed problem for presentism concerns causation and, more specifically, the supposed cross-temporally relational character of it. I think that the best reply to this problem can already be found in the literature on temporal ontology: it consists, roughly, in showing that (at least) some of the main approaches to causation can be rephrased so as to avoid commitment to any cross-temporal relation, including the causal relation itself. The (...) main purpose of this paper is to extend this reply to the process view, an approach to causation that has not been considered within this debate until now. I shall do this by taking into account Dowe’s conserved quantity theory—a recent and prominent theory of this sort— and employing it as a proxy for the other major process theories of causation. In dealing with Dowe’s process theory of causation, however, two additional problems must be faced: one concerns the four-dimensional spacetime framework on which its formulation relies; the other concerns the very notion of causal process (and the companion notion of causal interaction). While the presentistic account of Dowe’s theory (and, virtually, of the process view of causation in general) put forth in this paper is intended primarily as a contribution to the mentioned paraphrase- based enterprise of reconciliation between presentism and causation, I shall also offer some reasons for presentists to prefer the process view of causation to the other views of causation that have already been reconciled with presentism. (shrink)

We argue that many recent philosophical discussions about the reference of everyday concepts of intentional states have implicitly been predicated on descriptive theories of reference. To rectify this, we attempt to demonstrate how a causal theory can be applied to intentional concepts. Specifically, we argue that some phenomena in early social de- velopment ðe.g., mimicry, gaze following, and emotional contagionÞ can serve as refer- ence fixers that enable children to track others’ intentional states and, thus, to refer to those (...) states. This allows intentional concepts to be anchored to their referents, even if folk psy- chological descriptions turn out to be false. (shrink)

Eric Watkins has argued on philosophical, textual, and historical grounds that Kant’s account of causation in the first Critique should not be read as an attempt to refute Hume’s account of causation. In this paper, I challenge the arguments for Watkins’ claim. Specifically, I argue (1) that Kant’s philosophical commitments, even on Watkins’ reading, are not obvious obstacles to refuting Hume, (2) that textual evidence from the “Disciple of Pure Reason” suggests Kant conceived of his account of causation as such (...) a refutation, and (3) that none of Hume’s early German critics provided responses to this account that would have satisfied Kant. Watkins’ reading of Kant’s account of causation is thus more compatible with traditional views about Kant’s relationship to Hume than Watkins believes. (shrink)

This chapter explores the idea that the need to establish common knowledge is one feature that makes social cognition stand apart in important ways from cognition in general. We develop this idea on the background of the claim that social cognition is nothing but a type of causal inference. We focus on autism as our test-case, and propose that a specific type of problem with common knowledge processing is implicated in challenges to social cognition in autism spectrum disorder (ASD). (...) This problem has to do with the individual’s assessment of the reliability of messages that are passed between people as common knowledge emerges. The proposal is developed on the background of our own empirical studies and outlines different ways common knowledge might be comprised. We discuss what these issues may tell us about ASD, about the relation between social and non-social cognition, about social objects, and about the dynamics of social networks. (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)

The causal premise of the evolutionary debunking argument contends that human moral beliefs are explained by the process of natural selection. While it is universally acknowledged that such a premise is fundamental to the debunker’s case, the vast majority of philosophers focus instead on the epistemic premise that natural selection does not track moral truth and the resulting skeptical conclusion. Recently, however, some have begun to concentrate on the causal premise. So far, the upshot of this small but (...) growing literature has been that the causal premise is likely false due to the seemingly persuasive evidence that our moral beliefs are in fact not the result of natural selection. In this paper, I argue that this view is mistaken. Specifically, I advocate the Innate Biases Model, which contends that there is not only compelling evidence for an evolved cognitive capacity for acquiring norms but also for the existence of an evolutionarily instilled set of cognitive biases that make it either more or less likely that we adopt certain moral beliefs. (shrink)

In experimental settings, scientists often “make” new things, in which case the aim is to intervene in order to produce experimental objects and processes—characterized as ‘effects’. In this discussion, I illuminate an important performative function in measurement and experimentation in general: intervention-based experimental production. I argue that even though the goal of IEP is the production of new effects, it can be informative for causal details in scientific representations. Specifically, IEP can be informative about causal relations in: regularities (...) under study; ‘intervention systems’, which are measurement/experimental systems; and new technological systems. (shrink)

Does Aristotle offer a definition of the soul? In fact, he rejects the possibility of defining the soul univocally. Because “life” is a homonymous concept, so too is “soul”. Given the specific causal role that Aristotle envisages for form and essence, the soul requires multiple different definitions to capture how it functions as a cause in each form of life. Aristotle suggests demonstrations can be given which express these causal definitions; I reconstruct these demonstrations.

Volition and Allied Causal Concepts is a work of aetiology and metapsychology. Aetiology is the branch of philosophy and logic devoted to the study of causality (the cause-effect relation) in all its forms; and metapsychology is the study of the basic concepts common to all psychological discourse, most of which are causal. Volition (or free will) is to be distinguished from causation and natural spontaneity. The latter categories, i.e. deterministic causality and its negation, have been treated in a (...) separate work, The Logic of Causation. Volition may be characterized as personal causality, a relation between an agent (the self or soul) and his actions (acts of will). Unlike causation, this relation cannot be entirely defined using conditional (if–then) propositions. Although we can say that the agent is a sine qua non of his actions, we cannot say that the agent is invariably (in all or specific circumstances) followed by his actions. It appears that both an act of will and its negation remain possible to a soul in any given set of circumstances. This defines freedom of the will, and implies the responsibility of the agent for his actions. Introspection provides knowledge of particular acts of will. The existence of freewill implies a distinction between necessary causation (determinism independent of volition) and inertial causation (determinism, except when some contrary will interferes). An act of will occurs on a spiritual plane. It may have natural (mental or physical) consequences; those that inevitably follow it may be regarded as directly willed, whereas those that vary according to circumstances must be considered indirectly willed. Volition presupposes some degree of consciousness. So-called involuntary acts of will involve a minimum of attention, whereas mindful acts are fully conscious. Even pure whim involves intention. Most volitions moreover involve valuation, some sort of projection of goals, deliberation on means, choice and decision. To judge responsibility, various distinctions are called for, like that between intentional, incidental and accidental consequences. Volitional action can be affected through the terms and conditions of the world surrounding its agent, but also more intimately through the influence of concrete or abstract aspects of that world that the subject has cognized. The causal concept of influence, and its implication of cognition (of inner or outer information, including emotions), are crucial to measuring the effort involved in volition. Influences make willing easier or harder, yet do not curtail its essential freedom. All the causal concepts used in psychological explanation – affections, appetites, instincts, habits, obsessions, compulsions, urges and impulses – can be elucidated thanks to this important finding. Much of human (and animal) behavior can thus be both acknowledged as volitional and as variously influenced. Volition and Allied Causal Concepts is a work of ambitious scope, intent on finally resolving philosophical and logical issues that have always impeded progress in psychology. It clarifies the structure and workings of the psyche, facilitating hygienic and therapeutic endeavors. The relation between volition and physical laws is discussed, as is the place of volition in biology. Concepts used in biology, analogous to that of purpose, are incidentally analyzed. Theological issues are also dealt with, as are some topics in ethics and law. (shrink)

In Book I, III §9 of the Treatise, Hume makes the claim that “[all general] belief arises only from causation” (T 107). Following, he makes the even stronger claim that all general beliefs are to be thought of as beliefs in reality, and thus, all belief in reality is dependent on pre-established beliefs in both specific causal relations and the causal relation in general (T 108). In the first part of this paper, I explain Hume’s motivation behind both (...) claims, while in the second part, I argue that to some extent, Hume is correct; our belief in “reality”—a notion to be defined—is fundamentally dependent on a pre-established belief in the general notion of cause and effect and a cache of specific causal relations. Thus, epistemologically speaking, we must conclude that our notion of “reality” is intrinsically causal (note that this reading has been corrected/augmented in Rocknak 2013). (shrink)

It has been stated that the notion of cause and effect is one object of study that sciences and engineering revolve around. Lately, in software engineering, diagrammatic causal inference methods (e.g., Pearl’s model) have gained popularity (e.g., analyzing causes and effects of change in software requirement development). This paper concerns diagrammatical (graphic) models of causal relationships. Specifically, we experiment with using the conceptual language of thinging machines (TMs) as a tool in this context. This would benefit works on (...) causal relationships in requirements engineering, enhance our understanding of the TM modeling, and contribute to the study of the philosophical notion of causality. To specify the causality in a system’s description is to constrain the system’s behavior and thus exclude some possible chronologies of events. The notion of causality has been studied based on tools to express causal questions in diagrammatic and algebraic forms. Causal models deploy diagrammatic models, structural equations, and counterfactual and interventional logic. Diagrammatic models serve as a language for representing what we know about the world. The research methodology in the paper focuses on converting causal graphs into TM models and contrasts the two types of representation. The results show that the TM depiction of causality is more complete and therefore can provide a foundation for causal graphs. (shrink)

In biomedical measurement, biomarkers are used to achieve reliable prediction of, and useful causal information about patient outcomes while minimizing complexity of measurement, resources, and invasiveness. A biomarker is an assayable metric that discloses the status of a biological process of interest, be it normative, pathophysiological, or in response to intervention. The greatest utility from biomarkers comes from their ability to help clinicians (and researchers) make and evaluate clinical decisions. In this paper we discuss a specific methodological use of (...) clinical biomarkers in pharmacological measurement: Some biomarkers, called ‘surrogate markers’, are used to substitute for a clinically meaningful endpoint corresponding to events and their penultimate risk factors. We confront the reliability of clinical biomarkers that are used to gather information about clinically meaningful endpoints. Our aim is to present a systematic methodology for assessing the reliability of multiple surrogate markers (and biomarkers in general). To do this we draw upon the robustness analysis literature in the philosophy of science and the empirical use of clinical biomarkers. -/- After introducing robustness analysis we present two problems with biomarkers in relation to reliability. Next, we propose an intervention-based robustness methodology for organizing the reliability of biomarkers in general. We propose three relevant conditions for a robust methodology for biomarkers: (R1) Intervention-based demonstration of partial independence of modes: In biomarkers partial independence can be demonstrated through exogenous interventions that modify a process some number of “steps” removed from each of the markers. (R2) Comparison of diverging and converging results across biomarkers: By systematically comparing partially-independent biomarkers we can track under what conditions markers fail to converge in results, and under which conditions they successfully converge. (R3) Information within the context of theory: Through a systematic cross-comparison of the markers we can make causal conclusions as well as eliminate competing theories. We apply our robust methodology to currently developing Alzheimer’s research to show its usefulness for making causal conclusions. (shrink)

In this paper, I argue that looking at the concept of neural function through the lens of cognition alone risks cognitive myopia: it leads neuroscientists to focus only on mechanisms with cognitive functions that process behaviorally relevant information when conceptualizing “neural function”. Cognitive myopia tempts researchers to neglect neural mechanisms with noncognitive functions which do not process behaviorally relevant information but maintain and repair neural and other systems of the body. Cognitive myopia similarly affects philosophy of neuroscience because scholars overlook (...) noncognitive functions when analyzing issues surrounding e.g., functional decomposition or the multifunctionality of neural structures. I argue that we can overcome cognitive myopia by adopting a patchwork approach that articulates cognitive and noncognitive “patches” of the concept of neural function. Cognitive patches describe mechanisms with causally specific effects on cognition and behavior which are likely operative in transforming sensory or other inputs into motor outputs. Noncognitive patches describe mechanisms that lack such specific effects; these mechanisms are enabling conditions for cognitive functions to occur. I use these distinctions to characterize two noncognitive functions at the mesoscale of neural circuits: subsistence functions like breathing are implemented by central pattern generators and are necessary to maintain the life of the organism. Infrastructural functions like gain control are implemented by canonical microcircuits and prevent neural system damage while cognitive processing occurs. By adding conceptual patches that describe these functions, a patchwork approach can overcome cognitive myopia and help us explain how the brain’s capacities as an information processing device are constrained by its ability to maintain and repair itself as a physiological apparatus. (shrink)

The results from a number of recent studies suggest that ascriptions of intentionality are based on evaluative considerations: specifically, that the likelihood of viewing a person’s actions as intentional is greater when the outcome is bad than good (see Knobe, 2006, 2010). In this research we provide an alternative explanation for these findings, one based on the idea that ascriptions of intentionality depend on causal structure. As predicted by the causal structure view, we observed that actions leading to (...) bad outcomes are associated with negative social pressures (Experiment 1), that these negative pressures give rise to a specific kind of causal structure (Experiment 2), and that when these causal structures are pitted against the badness of the outcome, intentionality judgments track with causal structure and not badness (Experiment 3). While the badness of an outcome may have an indirect effect on judgments of intentionality, our results suggest that the factors that affect judgments of intentionality most directly are non-evaluative and objective. (shrink)

Mayr’s proximate–ultimate distinction has received renewed interest in recent years. Here we discuss its role in arguments about the relevance of developmental to evolutionary biology. We show that two recent critiques of the proximate–ultimate distinction fail to explain why developmental processes in particular should be of interest to evolutionary biologists. We trace these failures to a common problem: both critiques take the proximate–ultimate distinction to neglect specific causal interactions in nature. We argue that this is implausible, and that the (...) distinction should instead be understood in the context of explanatory abstractions in complete causal models of evolutionary change. Once the debate is reframed in this way, the proximate–ultimate distinction’s role in arguments against the theoretical significance of evo-devo is seen to rely on a generally implicit premise: that the variation produced by development is abundant, small and undirected. We show that a “lean version” of the proximate–ultimate distinction can be maintained even when this isotropy assumption does not hold. Finally, we connect these considerations to biological practice. We show that the investigation of developmental constraints in evolutionary transitions has long relied on a methodology which foregrounds the explanatory role of developmental processes. It is, however, entirely compatible with the lean version of the proximate–ultimate distinction. (shrink)

Existing research has shown that norm violations influence causal judgments, and a number of different models have been developed to explain these effects. One such model, the necessity/sufficiency model, predicts an interac- tion pattern in people’s judgments. Specifically, it predicts that when people are judging the degree to which a particular factor is a cause, there should be an interaction between (a) the degree to which that factor violates a norm and (b) the degree to which another factor in (...) the situation violates norms. A study of moral norms (N = 1000) and norms of proper functioning (N = 3000) revealed robust evidence for the predicted interaction effect. The implications of these patterns for existing theories of causal judgments is discussed. (shrink)