A theoretical framework is provided to explore teleonomy as a problem of self-causation, distinct from upward, downward and reticulate causation. Causality theories in biology are often formulated within hierarchy theories, where causation is conceptualized as running up or down the rungs of a ladder-like hierarchy or, more recently, as moving between multiple hierarchies. Research on the genealogy of cosmologies demonstrates that in addition to hierarchy theories, causality theories also depend upon ideas of time. This paper explores (...) the roots and impact of both time and hierarchy thinking on causal reasoning in the evolutionary sciences. Within evolutionary biology, the Neodarwinian synthesis adheres to a linear notion of time associated with linear hierarchies that portray upward causation. Eco-evo-devo schools recognize the importance of downward causation and consequently receive resistance from the standard view because downward causation is sometimes understood as backward causation, considered impossible by adherents of a linear time model. In contrast, downward causation works with a spatial or presential time notion. Hybridization, lateral gene transfer, infective heredity, symbiosis and symbiogenesis require recognition of reticulate causation occurring in both space and time, or spacetime, between distinct and interacting ontological hierarchies. Teleonomy is distinct from these types of causation because it invokes the problem of self-causation. By asking how the focal level in a hierarchy can persist through time, self-causation raises philosophical concerns on the nature of duration, identity and individuality. (shrink)

Applied Evolutionary Epistemology is a scientific-philosophical theory that defines evolution as the set of phenomena whereby units evolve at levels of ontological hierarchies by mechanisms and processes. This theory also provides a methodology to study evolution, namely, studying evolution involves identifying the units that evolve, the levels at which they evolve, and the mechanisms and processes whereby they evolve. Identifying units and levels of evolution in turn requires the development of ontological hierarchy theories, and examining mechanisms and processes necessitates theorizing (...) about causality. Together, hierarchy and causality theories explain how biorealities form and diversify with time. This paper analyzes how Applied EE redefines both hierarchy and causality theories in the light of the recent explosion of network approaches to causal reasoning associated with studies on reticulate and macroevolution. Causality theories have often been framed from within a rigid, ladder-like hierarchy theory where the rungs of the ladder represent the different levels, and the elements on the rungs represent the evolving units. Causality then is either defined reductionistically as an upward movement along the strands of a singular hierarchy, or holistically as a downward movement along that same hierarchy. Upward causation theories thereby analyze causal processes in time, i.e. over the course of natural history or phylogenetically, as Darwin and the founders of the Modern Synthesis intended. Downward causation theories analyze causal processes in space, ontogenetically or ecologically, as the current eco-evo-devo schools are evidencing. This work demonstrates how macroevolution and reticulate evolution theories add to the complexity by examining reticulate causal processes in space–time, and the interactional hierarchies that such studies bring forth introduce a new form of causation that is here called reticulate causation. Reticulate causation occurs between units and levels belonging to different as well as to the same ontological hierarchies. This article concludes that beyond recognizing the existence of multiple units, levels, and mechanisms or processes of evolution, also the existence of multiple kinds of evolutionary causation as well as the existence of multiple evolutionary hierarchies needs to be acknowledged. This furthermore implies that evolution is a pluralistic process divisible into different kinds. (shrink)

The view that living beings as well as plant-based medicaments possess causal properties that are caused by the causal properties of their constituents, without being reducible to the combination of the causal properties of these constituents goes back to ancient thinkers such as Alexander of Aphrodisias and Johannes Philoponus. In the early modern period, this view was not only criticized by natural philosophers taking a reductionist stance; it was also criticized by Neo-Platonic thinkers such as Jean Fernel. One of the (...) relatively few early modern natural philosophers who adopted an emergentist position was Jacob Schegk. The present article discusses whether Schegk’s analysis of the structure of plants and medicaments offers the theoretical resources required to answer Fernel’s critique of the tradition going back to Alexander. In particular, it examines whether Schegk’s account of synchronic upward causation and diachronic downward causation could offer solutions to two interrelated problems identified by Fernel: the question of whether a mere aggregates of material particles could form a composite that possesses substantiality, not only accidental unity; and the question of whether multitudes of material particles could bring forth simple forms, whose existence seems to be presupposed by powers that cannot be ascribed to the constituents. (shrink)

The article proposes to further develop the ideas of the Extended Evolutionary Synthesis by including into evolutionary research an analysis of phenomena that occur above the organismal level. We demonstrate that the current Extended Synthesis is focused more on individual traits (genetically or non-genetically inherited) and less on community system traits (synergetic/organizational traits) that characterize transgenerational biological, ecological, social, and cultural systems. In this regard, we will consider various communities that are made up of interacting populations, and for which the (...) individual members can belong to the same or to different species. Examples of communities include biofilms, ant colonies, symbiotic associations resulting in holobiont formation, and human societies. The proposed model of evolution at the level of communities revises classic theorizing on the major transitions in evolution by analyzing the interplay between community/social traits and individual traits, and how this brings forth ideas of top-down regulations of bottom-up evolutionary processes (collaboration of downward and upward causation). The work demonstrates that such interplay also includes reticulate interactions and reticulate causation. In this regard, we exemplify how community systems provide various non-genetic ‘scaffoldings’, ‘constraints’, and ‘affordances’ for individual and sociocultural evolutionary development. Such research complements prevailing models that focus on the vertical transmission of heritable information, from parent to offspring, with research that instead focusses on horizontal, oblique and even reverse information transmission, going from offspring to parent. We call this reversed information transfer the ‘offspring effect’ to contrast it from the ‘parental effect’. We argue that the proposed approach to inheritance is effective for modelling cumulative and distributed developmental process and for explaining the biological origins and evolution of language. (shrink)

This paper aims to explain how the human Self can be said a cause of his/her free actions, especially when they are voluntary and physical. First it is analyzed the natural causation in the physical world, particularly in self-organized living beings and afterwards in animal intentional behaviour, which is guided by cognition and emotions. An important distinction between downward causation and bottom-up causation is useful to explain the complex causality in self-organized intentional beings. Downward causation, coming (...) from a higher level, has in influence over lower ontological levels. Bottom-up causation operates inversely. It is also drawn a distinction between the “natural Self” (nature enhanced by habits) and the “intentional Self” (a subject endowed with consciousness and the power of controlling operations). This framework is applied to man, whose higher downward causality comes from the person (intellect and free will) and, guiding the sensitive lower layer of his/her nature, reaches in a quite natural way the voluntary control of the body. (shrink)

Which way does causation proceed? The pattern in the material world seems to be upward: particles to molecules to organisms to brains to mental processes. In contrast, the principles of quantum mechanics allow us to see a pattern of downward causation. These new ideas describe sets of multiple levels in which each level influences the levels below it through generation and selection. Top-down causation makes exciting sense of the world: we can find analogies in psychology, in (...) the formation of our minds, in locating the source of consciousness, and even in the possible logic of belief in God. (shrink)

Plotinus holds an important position in the history of late ancient philosophy on the concept of human agency. On the one hand, he follows Plato in regarding a human agent as one who self-identifies with the rational soul, becomes one from many, and acts from reason (Republic, 443de). On the other hand, due to the view characteristic of the second century CE that destiny causally determines the sensible world and sophisticated debates concerning freedom and determinism up to, and during, the (...) second century CE, Plotinus develops Plato’s view further in an effort to meet the challenges posed by earlier determinists. The position he develops in the Enneads is a dynamic synthesis of Platonic, Peripatetic, Stoic, and Middle-Platonic theorizing on human causation that shows how one can be a self-determining agent even while living in a world governed by destiny. I argue that the key to understanding Plotinus’ theory of human agency is to understand the role that consciousness plays since he holds that in order to be the sole causal source of our actions, and therefore truly self-determining, we must derive our premises for action from Intellect. Important for my purposes is his peculiar view that Intellect is also “in ourselves” (V.1.10.5-8) and can be reached by turning inwards and ascending upwards which is possible through possessing a unique mode of consciousness, namely awareness (sunaisthēsis). (shrink)

Abstract: A common explanatory error concerns conflating epistemological roles between two domains. Here I deal with a special case: when explanations of development replace evolutionary explanations or vice versa. Ernst Mayr famously distinguished between proximate and ultimate causal explanations in biology. His view was central to keeping development outside the theory of evolution. Nevertheless, the explanatory role of developmental processes in evolution is a central theme in current theoretical biology, which has led to several revisions of Mayr’s distinction. In the (...) following, I will review these reviewers to determine whether the integration of development and evolution is based on an appropriate reinterpretation of Mayr’s distinction. The revisionists often propose an interactionist alternative in which proximate and ultimate causes interact to produce evolved traits. The most common interactionist account relies on the idea of reciprocal causation. I will argue that this perspective is still problematic and that the boundaries between explanatory domains are crossed. Instead, we should rethink Mayr’s distinction by adopting an alternative view of evolutionary causation, the so-called Statisticalist view on natural selection, which claims that the only level of causation is the proximate level. By excluding two different levels of causation, this framework is able to avoid fallacious explanations and fully consider reciprocal causation as a proximate phenomenon. I introduce the concept of “statistical reciprocity” to explain the statistical effects of (proximate) reciprocal causation in ultimate explanations and outline some ideas of “population ontogenetics” as a prominent framework for unifying development and evolution beyond interactionist positions. (shrink)

A phenome occurs through the many pathways of the complex net of interaction between the phenome and its environment; therefore researching and understanding how it arises requires investigation into many possible causes that are in constant interaction with each other. The most comprehensive investigations in biology are the ones in which many biologists from different sub-areas—evolutionary biology, developmental biology, molecular biology, physiology, genetics, epigenetics, ecology—have collaborated. Still, biologists do not always need to collaborate or look for the most comprehensive explanations. (...) A more standard investigation in biology occurs within a single subarea, and uses well-defined experiments with very specific conditions. This paper is about causation and related explanation in plant phenome research and its relevance to Aristotle’s Theory of Four Causes. I argue that there are causes which resemble Aristotle’s formal, material, and efficient causes in phenotype explanation and occurrence; but causes which resemble Aristotle’s final causes occur in phenotype explanation only, not in the occurrence. (shrink)

In many spheres, the law takes the legal concept of causation to correspond to the folk concept (the correspondence assumption). Courts, including the US Supreme Court, tend to insist on the "common understanding" and that which is "natural to say" (Burrage v. United States) when it comes to expressions relating to causation, and frequently refuse to clarify the expression to juries. As recent work in psychology and experimental philosophy has uncovered, lay attributions of causation are susceptible to (...) a great number of unexpected factors, some of which seem rather peripheral to causation. One of those is the norm effect (Knobe & Fraser, 2008): Agents who, in acting as they do, break a salient norm, are more likely to be considered as having caused a certain consequence than when they do not violate a norm. According to some (e.g., Alicke, 1992) this constitutes a bias. According to others (e.g., Sytsma, 2020), the folk concept of causation is sensitive to normative factors, and there’s nothing wrong with that. In this paper, we explore the question whether the norm effect should be considered a bias from the legal perspective on the one hand, and from the psychological perspective on the other. To do this, we test whether norms which are nonpertinent to the consequences or outright silly also impact causation judgements. The data from two preregistered experiments (total N=593) clearly show they do. This, we argue, makes the bias interpretation plausible from the psychological perspective, and both plausible and problematic from the legal perspective. It also shows that the law should abstain from unreflectively assuming conceptual correspondence between legal and ordinary language concepts. (shrink)

In most academic and non-academic circles throughout history, the world and its operation have been viewed in terms of cause and effect. The principles of causation have been applied, fruitfully, across the sciences, law, medicine, and in everyday life, despite the lack of any agreed-upon framework for understanding what causation ultimately amounts to. In this engaging and accessible introduction to the topic, Douglas Kutach explains and analyses the most prominent theories and examples in the philosophy of causation. (...) The book is organized so as to respect the various cross-cutting and interdisciplinary concerns about causation, such as the reducibility of causation, its application to scientific modeling, its connection to influence and laws of nature, and its role in causal explanation. Kutach begins by presenting the four recurring distinctions in the literature on causation, proceeding through an exploration of various accounts of causation including determination, difference making and probability-raising. He concludes by carefully considering their application to the mind-body problem. _Causation_ provides a straightforward and compact survey of contemporary approaches to causation and serves as a friendly and clear guide for anyone interested in exploring the complex jungle of ideas that surround this fundamental philosophical topic. (shrink)

The 'completeness of physics' is the key premise in the causal argument for physicalism. Standard formulations of it fail to rule out emergent downwards causation. I argue that it must do this if it is tare in a valid causal argument for physicalism. Drawing on the notion of conferring causal power, I formulate a suitable principle, 'strong completeness'. I investigate the metaphysical implications of distinguishing this principle from emergent downwards causation, and I argue that categoricalist accounts of properties (...) are better equipped to sustain the distinction than dispositional essentialist accounts. Finally, I argue that the additional evidence needed for strong completeness renders the causal argument otiose for any properties amenable to scientific reduction. (shrink)

I provide a comprehensive metaphysics of causation based on the idea that fundamentally things are governed by the laws of physics, and that derivatively difference-making can be assessed in terms of what fundamental laws of physics imply for hypothesized events. Highlights include a general philosophical methodology, the fundamental/derivative distinction, and my mature account of causal asymmetry.

Many philosophical theories of causation are egalitarian, rejecting a distinction between causes and mere causal conditions. We sought to determine the extent to which people's causal judgments discriminate, selecting as causes counternormal events—those that violate norms of some kind—while rejecting non-violators. We found significant selectivity of this sort. Moreover, priming that encouraged more egalitarian judgments had little effect on subjects. We also found that omissions are as likely as actions to be judged as causes, and that counternormative selectivity appears (...) to apply equally to actions and omissions. (shrink)

Our ordinary causal concept seems to fit poorly with how our best physics describes the world. We think of causation as a time-asymmetric dependence relation between relatively local events. Yet fundamental physics describes the world in terms of dynamical laws that are, possible small exceptions aside, time symmetric and that relate global time slices. My goal in this paper is to show why we are successful at using local, time-asymmetric models in causal explanations despite this apparent mismatch with fundamental (...) physics. In particular, I will argue that there is an important connection between time asymmetry and locality, namely: understanding the locality of our causal models is the key to understanding why the physical time asymmetries in our universe give rise to time asymmetry in causal explanation. My theory thus provides a unified account of why causation is local and time asymmetric and thereby enables a reply to Russell’s famous attack on causation. (shrink)

Which country, politician, or policy is more of a cause of the Covid-19 pandemic death toll? Which of the two factories causally contributed more to the pollution of the nearby river? A wide-ranging portion of our everyday thought and talk, and attitudes rely on a graded notion of causation. However, it is sometimes highlighted that on most contemporary accounts, causation is on-off. Some philosophers further question the legitimacy of talk of degrees of causation and suggest that we (...) avoid it. Some hold that the notion of degrees of causation is an illusion. In this paper, I’ll argue that causation does come in degrees. (shrink)

We propose that all actual causes are simultaneous with their direct effects, as illustrated by both everyday examples and the laws of physics. We contrast this view with the sequential conception of causation, according to which causes must occur prior to their effects. The key difference between the two views of causation lies in differing assumptions about the mathematical structure of time.

What would it be for a process to happen backwards in time? Would such a process involve different causal relations? It is common to understand the time-reversal invariance of a physical theory in causal terms, such that whatever can happen forwards in time can also happen backwards in time. This has led many to hold that time-reversal symmetry is incompatible with the asymmetry of cause and effect. This article critiques the causal reading of time reversal. First, I argue that the (...) causal reading requires time-reversal-related models to be understood as representing distinct possible worlds and, on such a reading, causal relations are compatible with time-reversal symmetry. Second, I argue that the former approach does, however, raise serious sceptical problems regarding the causal relations of paradigm causal processes and as a consequence there are overwhelming reasons to prefer a non-causal reading of time reversal, whereby time reversal leaves causal relations invariant. On the non-causal reading, time-reversal symmetry poses no significant conceptual nor epistemological problems for causation. _1_ Introduction _1.1_ The directionality argument _1.2_ Time reversal _2_ What Does Time Reversal Reverse? _2.1_ The B- and C-theory of time _2.2_ Time reversal on the C-theory _2.3_ Answers _3_ Does Time Reversal Reverse Causal Relations? _3.1_ Causation, billiards, and snooker _3.2_ The epistemology of causal direction _3.3_ Answers _4_ Is Time-Reversal Symmetry Compatible with Causation? _4.1_ Incompatibilism _4.2_ Compatibilism _4.3_ Answers _5_ Outlook. (shrink)

This paper presents a puzzle or antinomy about the role of properties in causation. In theories of properties, a distinction is often made between determinable properties, like red, and their determinates, like scarlet (see Armstrong 1978, volume II). Sometimes determinable properties are cited in causal explanations, as when we say that someone stopped at the traffic light because it was red. If we accept that properties can be among the relata of causation, then it can be argued that (...) there are good reasons for allowing that some of these are determinable properties. On the other hand, there are strong arguments in the metaphysics of properties to treat properties as sparse in David Lewis’s (1983) sense. But then it seems that we only need to believe in the most determinate properties: particular shades of colour, specific masses, lengths and so on. And if we also agree with Lewis that sparse properties are ‘the ones relevant to causal powers’ (1983: 13) it seems we must conclude that if properties are relevant to causation at all, then all of these are determinate properties. I call this ‘the antinomy of determinable causation’. On the one hand, we have a good argument for the claim that determinable properties can be causes, if any properties are. I call this the Thesis. But on the other hand, we have a good argument for the claim that only the most determinate properties can be causes, if any properties are. I call this the Antithesis. Clearly, we need to reject either the Thesis or the.. (shrink)

Russell famously argued that causation should be dispensed with. He gave two explicit arguments for this conclusion, both of which can be defused if we loosen the ties between causation and determinism. I show that we can define a concept of causation which meets Russell’s conditions but does not reduce to triviality. Unfortunately, a further serious problem is implicit beneath the details of Russell’s arguments, which I call the causal exclusion problem. Meeting this problem involves deploying a (...) minimalist pragmatic account of the nature and function of modal language. Russell’s scruples about causation can be accommodated, even as we partially legitimise the pervasive causal explanations in folk and scientific practice. (shrink)

The Problems of Mental Causation. Functionalism in the philosophy of mind identifies mental states with their dispositional connections with other mental states, perceptions and actions. Many theories of the mind have sailed under the Functionalist flag. But what I take to be essential to Functionalism is that mental states are individuated causally: the reality of mental states depends essentially on their causal efficacy.

The problem of downward causation is that an intuitive response to an intuitive picture leads to counterintuitive results. Suppose a mental event, m1, causes another mental event, m2. Unless the mental and the physical are completely independent, there will be a physical event in your brain or your body or the physical world as a whole that underlies this event. The mental event occurs at least partly in virtue of the physical event’s occurring. And the same goes for m2 (...) [2] and p2. Let’s not worry about what exactly “underlying” or “in virtue of” means here. Here’s the picture. m1 -----> m2 | | p1 -----> p2 The horizontal arrows represent causation, and the vertical lines represent underlying, whatever that may be. There’s some reason to think that the only way m1 can bring about m2 is by bringing about p2. You can’t convince someone of something through mental telepathy. You need to interact with the physical world, perhaps by saying something and so making some noise, or by pointing and getting them to turn their head and see. What goes for the case of two people goes for the case of one person as well. Superstition aside, there is no purely mental energy that floats free of the merely physical workings of the brain. If m1 brings about m2 by bringing about p2, then m1 brings about p2. This is downward causation. But wait. Doesn’t p1 bring about p2? Isn’t that what the bottom arrow represents? Maybe m1 and p1 work together to bring about p2. There are little holes in the physical causal structure that need to be filled by mental events. You don’t need a sweeping metaphysical thesis about the causal closure of the physical to find this implausible. Maybe p2 is overdetermined. (shrink)

In this paper, I argue that causal theories of memory are typically committed to two independent, non-mutually entailing theses. The first thesis pertains to the necessity of appropriate causation in memory, specifying a condition token memories need to satisfy. The second pertains to the explanation of memory reliability in causal terms and it concerns memory as a type of mental state. Post-causal theories of memory can reject only the first (weak post-causalism) or both (strong post-causalism) theses. Upon this backdrop, (...) I examine Werning’s (2020) causalist argument from probabilistic correlation. I argue that it doesn’t establish the necessity of appropriate causation and thus it can only target strong post-causalist theories. I end up by presenting some general considerations, suggesting that memories may not always be causally linked to past experiences. (shrink)

There have recently been a number of strong claims that normative considerations, broadly construed, influence many philosophically important folk concepts and perhaps are even a constitutive component of various cognitive processes. Many such claims have been made about the influence of such factors on our folk notion of causation. In this paper, we argue that the strong claims found in the recent literature on causal cognition are overstated, as they are based on one narrow type of data about a (...) particular type of causal cognition; the extant data do not warrant any wide-ranging conclusions about the pervasiveness of normative considerations in causal cognition. Of course, almost all empirical investigations involve some manner of ampliative inference, and so we provide novel empirical results demonstrating that there are types of causal cognition that do not seem to be influenced by moral considerations. (shrink)

Causation is one of philosophy's most venerable and thoroughly-analyzed concepts. However, the study of how ordinary people make causal judgments is a much more recent addition to the philosophical arsenal. One of the most prominent views of causal explanation, especially in the realm of harmful or potentially harmful behavior, is that unusual or counternormative events are accorded privileged status in ordinary causal explanations. This is a fundamental assumption in psychological theories of counterfactual reasoning, and has been transported to philosophy (...) by Hitchcock and Knobe (2009). A different view--the basis of the culpable control model of blame (CCM)--is that primary causal status is accorded to behaviors that arouse negative evaluative reactions, including behaviors that stem from nefarious motives, negligence or recklessness, a faulty character, or behaviors that lead to harmful or potentially harmful consequences. This paper describes four empirical studies that show consistent support for the CCM. (shrink)

The standard objection to dualist theories of mind is that they seemingly cannot account for the obvious fact that mental phenomena cause our behaviour. On the plausible assumption that all our behaviour is physically necessitated by entirely physical phenomena, there appears to be no room for dualist mental causation. Some argue that dualists can address this problem by making minimal adjustments in their ontology. I argue that no such adjustments are required. Given recent developments in philosophy of causation, (...) it is plausible that mental phenomena cause behaviour in standard dualist ontologies. (shrink)

The reduction of grounding to causation, or each to a more general relation of which they are species, has sometimes been justified by the impressive inferential capacity of structural equation modelling, causal Bayes nets, and interventionist causal modelling. Many criticisms of this assimilation focus on how causation is inadequate for grounding. Here, I examine the other direction: how treating grounding in the image of causation makes the resulting view worse for causation. The distinctive features of causal (...) modelling that make this connection appealing are distorted beyond use by forcing them to fit onto grounding. The very inferential strength that makes causation attractive is only possible because of a narrow construal of what counts as a causal relation; as soon as that broadens, the inferential capacity markedly diminishes. Making causation suitable for application to grounding spoils what was appealing about causation for this task in the first place. However, grounding need not appeal to causation: causal modelling does not have exclusive claim to structural equation modeling or other formal techniques of modelling structure. I offer a case in favour of a different kind of metaphysical frugality, which tend towards narrow, more restrictive construals of relations like causation or grounding, because then each relation behaves more homogenously. This more homogenous behavior delivers stronger inferential power per relation even though there may be more relations to which one is committed. (shrink)

Much of the modern philosophy of causation has been governed by two ideas: (i) causes make their effects inevitable; (ii) a cause is something that makes a difference to whether its effect occurs. I focus on explaining the origin of idea (ii) and its connection to (i). On my view, the frequent attempts to turn (ii) into an analysis of causation are wrongheaded. Patterns of difference-making aren't what makes causal claims true. They merely provide a useful test for (...) causal claims. Moreover, what justifies us in using them as a test is idea (i). That's how (i) and (ii) are connected. (shrink)

This paper examines a promising probabilistic theory of singular causation developed by David Lewis. I argue that Lewis' theory must be made more sophisticated to deal with certain counterexamples involving pre-emption. These counterexamples appear to show that in the usual case singular causation requires an unbroken causal process to link cause with effect. I propose a new probabilistic account of singular causation, within the framework developed by Lewis, which captures this intuition.

My primary aim is to defend a nonreductive solution to the problem of action. I argue that when you are performing an overt bodily action, you are playing an irreducible causal role in bringing about, sustaining, and controlling the movements of your body, a causal role best understood as an instance of agent causation. Thus, the solution that I defend employs a notion of agent causation, though emphatically not in defence of an account of free will, as most (...) theories of agent causation are. Rather, I argue that the notion of agent causation introduced here best explains how it is that you are making your body move during an action, thereby providing a satisfactory solution to the problem of action. (shrink)

Theories of graded causation attract growing attention in the philosophical debate on causation. An important field of application is the controversial relationship between causation and moral responsibility. However, it is still unclear how exactly the notion of graded causation should be understood in the context of moral responsibility. One question is whether we should endorse a proportionality principle, according to which the degree of an agent’s moral responsibility is proportionate to their degree of causal contribution. A (...) second question is whether a theory of graded causation should measure closeness to necessity or closeness to sufficiency. In this paper, we argue that we should indeed endorse a proportionality principle and that this principle supports a notion of graded causation relying on closeness to sufficiency rather than closeness to necessity. Furthermore, we argue that this insight helps to provide a plausible analysis of the so-called ‘Moral Difference Puzzle’ recently described by Bernstein. (shrink)

In a recent paper I argued that agent causation theorists should be compatibilists. In this paper, I argue that compatibilists should be agent causation theorists. I consider six of the main problems facing compatibilism: (i) the powerful intuition that one can't be responsible for actions that were somehow determined before one was born; (ii) Peter van Inwagen's modal argument, involving the inference rule (β); (iii) the objection to compatibilism that is based on claiming that the ability to do (...) otherwise is a necessary condition for freedom; (iv) "manipulation arguments," involving cases in which an agent is manipulated by some powerful being into doing something that he or she would not normally do, but in such a way that the compatibilist's favorite conditions for a free action are satisfied; (v) the problem of constitutive luck; and (vi) the claim that it is not fair to blame someone for an action if that person was determined by forces outside of his or her control to perform that action. And in the case of each of these problems, I argue that the compatibilist has a much more plausible response to that problem if she endorses the theory of agent causation than she does otherwise. (shrink)

The problem of mental causation in contemporary philosophy of mind concerns the possibility of holding two different views that are in apparent tension. The first is physicalism, the view that there is nothing more to the world than the physical. The second is that the mental has genuine causal efficacy in a way that does not reduce to pure physical particle-bumping. This article provides a historical background to this question, with focus on Davidson’s anomalous monism and Kim’s causal exclusion (...) problem. Responses to causal exclusion are categorized in terms of six different argumentative strategies. In conclusion, caution is advised regarding the inclination to reduce the mental to the physical and sketch a positive direction for substantively characterizing mental causation by recourse to well-confirmed accounts of causation coupled with empirical research. (shrink)

This essay proposes a new interpretation of Clauberg’s account of the mind-body problem, against both occasionalist and interactionist readings. It examines his treatment of the mind-body relation through the lens of his theories of substance and cause. It argues that, whereas Clauberg embraces Descartes’s substance dualism, he retains a broadly scholastic theory of causation as the action of essential powers. On this account, mind and body are distinct, power-bearing substances, and each is a genuine secondary cause of its own (...) modifications. Between mental and bodily modes, however, there is only a special, divinely instituted correlation, but no causation. Clauberg’s view has the consequence that the conjunction of mind and body cannot be understood causally but only as the covariation of sensations and brain states, which he treats as mutually referring signs. (shrink)

The problem of mental causation is discussed by taking into account some recent developments in the philosophy of science. The problem is viewed from the perspective of the new interventionist theory of causation developed by Woodward. The import of the idea that causal claims involve contrastive classes in mental causation is also discussed. It is argued that mental causation is much less a problem than it has appeared to be.

I propose a new formalist account of legal (/proximate) causation – one that holds legal causation to be a matter of amoral, descriptive fact. The account starts with a metaphysical relation, akin to but distinct from common-sense causation, and it argues that legal causation aligns exactly with that relation; it is unified and principled.

In this paper, I offer one example of conceptual change. Specifically, I contend that the discovery that viruses could cause cancer represents an excellent example of branch jumping, one of Thagard’s nine forms of conceptual change. Prior to about 1960, cancer was generally regarded as a degenerative, chronic, non-infectious disease. Cancer causation was therefore usually held to be a gradual process of accumulating cellular damage, caused by relatively non-specific component causes, acting over long periods of time. Viral infections, on (...) the other hand, were generally understood to be acute processes, whereby single, specific and necessary causal agents acted alone to produce disease. However, during the 1960s and 1970s, a number of cancers were discovered to have an infectious aetiology. Of particular note were two—Burkitt’s lymphoma and cervical cancer—which I will discuss in detail later in this piece. Together, these discoveries led, in the short term, to a tentative aetiological reclassification of some types of cancer as infectious diseases and, in the longer term, to a full-blown reclassification of cancer as an aetiological disease branch in its own right. This process of reclassification forms the empirical basis for my concluding remarks on the influence of classification upon causation in medicine. Through this, I aim to demonstrate that conceptual change, far from being a purely abstract concern of the philosopher of science, is of substantial import to scientific practitioners. (shrink)

I defend what may loosely be called an eliminativist account of causation by showing how several of the main features of causation, namely asymmetry, transitivity, and necessitation, arise from the combination of fundamental dynamical laws and a special constraint on the macroscopic structure of matter in the past. At the microscopic level, the causal features of necessitation and transitivity are grounded, but not the asymmetry. At the coarse-grained level of the macroscopic physics, the causal asymmetry is grounded, but (...) not the necessitation or transitivity. Thus, at no single level of description does the physics justify the conditions that are taken to be constitutive of causation. Nevertheless, if we mix our reasoning about the microscopic and macroscopic descriptions, the structure provided by the dynamics and special initial conditions can justify the folk concept of causation to a significant extent. I explain why our causal concept works so well even though at bottom it is comprised of a patchwork of principles that don't mesh well. (shrink)

Several philosophers claim that the phenomenology of one’s own agency conflicts with standard causal theories of action, couched in terms of causation by mental events or states. Others say that the phenomenology is prima facie incompatible with such a theory, even if in the end a reconciliation can be worked out. Here it is argued that the type of action theory in question is consistent with what can plausibly be said to be presented to us in our experience of (...) our agency. Several routes to a claim that there is nevertheless a prima facie incompatibility are examined, and all are found wanting. The phenomenology of agency, it is argued, is no threat to a standard causal theory of action. (shrink)

Suppose that, for every event, whether mental or physical, there is some physical event causally sufficient for it. Suppose, moreover, that physical reductionism in its various forms fails—that mental properties cannot be reduced to physical properties and mental events cannot be reduced to physical events. In this case, how could there be mental causation? More specifically, how could mental events cause other mental events, physical events, and intentional actions? The primary goal of this paper is to answer this question.

What is offered here is an interpretation of Hume’s views on causation. While it might not be literally Hume’s view, it is certainly consistent with Hume, and is probably what Hume should say on causation, in light of recent developments in science and logic. As a way in, it is argued that the considerations that Hume brings against rationalist theories of causation can be applied to counterfactual theories of causation. Since, counterfactuals, possible worlds and modality were (...) not ideas that would have been overly familiar to Hume, some supplementation of Hume’s arguments will be necessary. (shrink)

This chapter explores the idea that causal inference is warranted if and only if the mechanism underlying the inferred causal association is identified. This mechanistic stance is discernible in the epidemiological literature, and in the strategies adopted by epidemiologists seeking to establish causal hypotheses. But the exact opposite methodology is also discernible, the black box stance, which asserts that epidemiologists can and should make causal inferences on the basis of their evidence, without worrying about the mechanisms that might underlie their (...) hypotheses. I argue that the mechanistic stance is indeed a bad methodology for causal inference. However, I detach and defend a mechanistic interpretation of causal generalisations in epidemiology as existence claims about underlying mechanisms. (shrink)

Nonreductive physicalism states that actions have sufficient physical causes and distinct mental causes. Nonreductive physicalism has recently faced the exclusion problem, according to which the single sufficient physical cause excludes the mental causes from causal efficacy. Autonomists respond by stating that while mental-to-physical causation fails, mental-to-mental causation persists. Several recent philosophers establish this autonomy result via similar models of causation :1031–1049, 2016; Zhong, J Philos 111:341–360, 2014). In this paper I argue that both of these autonomist models (...) fail on account of the problem of Edwards’s Dictum. However, I appeal to foundational principles of action theory to resuscitate mental-to-mental causation in a manner that is consistent with the models of causation endorsed by these autonomists. (shrink)

The issue of downward causation (and mental causation in particular), and the exclusion problem is discussed by taking into account some recent advances in the philosophy of science. The problem is viewed from the perspective of the new interventionist theory of causation developed by Woodward. It is argued that from this viewpoint, a higher-level (e.g., mental) state can sometimes truly be causally relevant, and moreover, that the underlying physical state which realizes it may fail to be such.

In The Biopsychosocial Model of Health and Disease, Derek Bolton and Grant Gillett argue that a defensible updated version of the biopsychosocial model requires a metaphysically adequate account of disease causation that can accommodate biological, psychological, and social factors. This present paper offers a philosophical critique of their account of biopsychosocial causation. I argue that their account relies on claims about the normativity and the semantic content of biological information that are metaphysically contentious. Moreover, I suggest that these (...) claims are unnecessary for a defence of biopsychosocial causation, as the roles of multiple and diverse factors in disease causation can be readily accommodated by a more widely accepted and less metaphysically contentious account of causation. I then raise the more general concern that they are misdiagnosing the problem with the traditional version of the biopsychosocial model. The challenge when developing an explanatorily valuable version of the biopsychosocial model, I argue, is not so much providing an adequate account of biopsychosocial causation, but providing an adequate account of causal selection. Finally, I consider how this problem may be solved to arrive at a more explanatorily valuable and clinically useful version of the biopsychosocial model. (shrink)

This paper takes a critical stance on Tallis’s separation of causation and agency. While his critique of the causal theory of action and the assumptions about causation underlying different versions of determinism, including the one based on neuroscience is right, his rejection of causation (of all sorts) has implausible consequences. Denying the link between action and causation amounts to overlooking the role action plays in causal inference and in the origin of causal concepts. I suggest that (...) a weaker version of Tallis’ claim, compatible with causation understood as agency, would work better. (shrink)

Hume was correct in his critique of causation as understood by the New Science, a critique deadly to both causal and scientific realism. Getting beyond Hume's critique of causation requires that we call into question the New Science's understanding of causation and replace it with a Neo-Aristotelian account of causal processes. In this paper, I try to point the way to such an account.

Several theories of causation reject causation of or by absences. They thereby clash with much of what we think and say about what causes what. This paper examines a way in which one kind of theory, causal dispositionalism, can be modified so as to accept absence causation, while still retaining a fundamental commitment of dispositionalism. The proposal adopts parts of a strategy described by David Lewis. The paper concludes with a brief discussion of the problem of the (...) proliferation of causes. (shrink)

Downward causation is commonly held to create problems for ontologically emergent properties. In this paper I describe two novel examples of ontologically emergent properties and show how they avoid two main problems of downward causation, the causal exclusion problem and the causal closure problem. One example involves an object whose colour does not logically supervene on the colours of its atomic parts. The other example is inspired by quantum entanglement cases but avoids controversies regarding quantum mechanics. These examples (...) show that the causal exclusion problem can be avoided, in one case by showing how it is possible to interact with an object without interacting with its atomic parts. I accept that emergence cannot be reconciled with causal closure, but argue that violations of causal closure do not entail violations of the base-level laws. Only the latter would conflict with empirical science. (shrink)

This dissertation begins by addressing the question of when a causal model is apt for deciding questions of actual causation with respect to some target situation. I first provide relevant background about causal models, explain what makes them promising as a tool for analyzing actual causation, and motivate the need for a theory of aptness as part of such an analysis (Chapter 1). I then define what it is for a model on a given interpretation to be accurate (...) of, that is, say only true things about, some target situation. This involves a systematization of various representational principles mentioned and/or discussed throughout the literature into a method of interpretation, which I propose be taken as standard (Chapter 2). Next, I explain and address two reasons for which accuracy as I’ve defined it is insufficient for aptness. The first reason – already discussed in the literature – is the problem of structural isomorphs. In response, I propose the aptness condition of Explicit Partial Mediation (Chapter 3). The second reason – which has yet to be noticed – is the problem of the indeterminacy of accuracy. As I demonstrate, a model is accurate of a target situation only relative to a set of background possibilities – what I call a modal profile. It follows that a model represents a situation only relative to some modal profile or other. I go on to discuss the ramifications of this observation for a theory of actual causation in terms of models. I argue that the relativity be taken at face value and built into our metaphysical account of causation, resulting in a view that I call causal relativism (Chapter 4). I explore one advantage of this view in detail: that the resulting account can defend the principle of strong proportionality against several objections (Chapter 5). Finally, I apply the earlier discussion of aptness to attempts to provide a semantics of counterfactuals in terms of causal models – an interventionist semantics. I show how just as a similarity semantics relies on an opaque notion of similarity, an interventionist semantics relies on an analogous notion of aptness. The challenge of articulating aptness thus undermines the claim that an interventionist semantics avoids representational problems inherent in a similarity semantics (Chapter 6). I close with a recap and suggestions for future research (Chapter 7). -/- . (shrink)