An influential tradition in the philosophy of causation has it that all token causal facts are, or are reducible to, facts about difference-making. Challenges to this tradition have typically focused on pre-emption cases, in which a cause apparently fails to make a difference to its effect. However, a novel challenge to the difference-making approach has recently been issued by Alyssa Ney. Ney defends causal foundationalism, which she characterizes as the thesis that facts about (...) class='Hi'>difference-making depend upon facts about physical causation. She takes this to imply that causation is not fundamentally a matter of difference-making. In this paper, I defend the difference-making approach against Ney’s argument. I also offer some positive reasons for thinking, pace Ney, that causation is fundamentally a matter of difference-making. (shrink)

Consider the following causal exclusion principle: For all distinct properties F and F* such that F* supervenes on F, F and F* do not both cause a property G. Peter Menzies and Christian List have proven that it follows from a natural conception of causation as difference-making that this exclusion principle is not generally true. Rather, it turns out that whether the principle is true is a contingent matter. In addition, they have shown that in a wide (...) range of empirically ordinary cases, it follows that F* causes G and F does not. These cases plausibly include instances where F* is a mental property and F and G are physical properties. If this is the right conception of causation, it therefore turns out that the physical world is not causally closed. In this paper I show that there is an alternative conception of causation as difference-making that does not have the same consequences. Whether the physical world is causally closed therefore turns out to depend, inter alia, on which conception of difference-making is correct. I give a number of arguments for the alternative conception of difference-making. (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)

It is natural to think of causes as difference-makers. What exact difference causes make, however, is an open question. In this paper, I argue that the right way of understanding difference-making is in terms of causal processes: causes make a difference to a causal process that leads to the effect. I will show that this way of understanding difference-making nicely captures the distinction between causing an outcome and helping determine how the outcome happens (...) and, thus, explains why causation is not transitive. Moreover, the theory handles tricky cases that are problematic for competing accounts of difference-making. (shrink)

It is often argued that higher-level special-science properties cannot be causally efficacious since the lower-level physical properties on which they supervene are doing all the causal work. This claim is usually derived from an exclusion principle stating that if a higher-level property F supervenes on a physical property F* that is causally sufficient for a property G, then F cannot cause G. We employ an account of causation as difference-making to show that the truth or falsity of (...) this principle is a contingent matter and derive necessary and sufficient conditions under which a version of it holds. We argue that one important instance of the principle, far from undermining non-reductive physicalism, actually supports the causal autonomy of certain higher-level properties. (shrink)

There are at least two different concepts that philosophers might target when analyzing causation: a pre-selective notion and a selective notion. This paper argues that these two distinct conceptions have been conflated to date, citing the puzzles of overdetermination, extensionality, and transitivity as evidence. The primary aim of the paper is to help reset the methodological scene concerning analyses of causation.

According to the new mechanistic approach, an acting entity is at a lower mechanistic level than another acting entity if and only if the former is a component in the mechanism for the latter. Craver and Bechtel :547–563, 2007. doi:10.1007/s10539-006-9028-8) argue that a consequence of this view is that there cannot be causal interactions between acting entities at different mechanistic levels. Their main reason seems to be what I will call the Metaphysical Argument: things at different levels of a mechanism (...) are related as part and whole; wholes and their parts cannot be related as cause and effect; hence, interlevel causation in mechanisms is impossible. I will analyze this argument in more detail and show under which conditions it is valid. This analysis will reveal that interlevel causation in mechanisms is indeed possible, if we take seriously the idea that the relata of the mechanistic level relation are acting entities and accept a slightly modified notion of a mechanistic level that is highly plausible in the light of the first clarification. (shrink)

In his influential book 'Making Things Happen' and in other places, Jim Woodward has noted some affinities between his own account of causation and that of Menzies and Price, but argued that the latter view is implausibly ‘subjective’. In this piece I discuss Woodward’s criticisms. I argue that the Menzies and Price view is not as different from Woodward’s own account as he believes, and that in so far as it is different, it has some advantages whose importance (...) Woodward misses; but also that the Menzies and Price view lacks some elements whose importance Woodward rightly stresses. When properly characterized, however, the ‘subjectivity’ survives unscathed. (shrink)

We offer a critical assessment of the “exclusion argument” against free will, which may be summarized by the slogan: “My brain made me do it, therefore I couldn't have been free”. While the exclusion argument has received much attention in debates about mental causation (“could my mental states ever cause my actions?”), it is seldom discussed in relation to free will. However, the argument informally underlies many neuroscientific discussions of free will, especially the claim that advances in neuroscience seriously (...) challenge our belief in free will. We introduce two distinct versions of the argument, discuss several unsuccessful responses to it, and then present our preferred response. This involves showing that a key premise – the “exclusion principle” – is false under what we take to be the most natural account of causation in the context of agency: the difference-making account. We finally revisit the debate about neuroscience and free will. (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)

Andreas & Günther have recently proposed a difference-making definition of actual causation. In this paper I show that there exist conclusive counterexamples to their definition, by which I mean examples that are unacceptable to everyone, including AG. Concretely, I show that their definition allows c to cause e even when c is not a causal ancestor of e. I then proceed to identify their non-standard definition of causal models as the source of the problem, and argue that (...) there is no viable strategy open to AG to fixing it. I conclude that their definition of causation is damaged beyond repair. (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)

In this thesis, I give a metascientific account of causality in medicine. I begin with two historical cases of causal discovery. These are the discovery of the causation of Burkitt’s lymphoma by the Epstein-Barr virus, and of the various viral causes suggested for cervical cancer. These historical cases then support a philosophical discussion of causality in medicine. This begins with an introduction to the Russo- Williamson thesis (RWT), and discussion of a range of counter-arguments against it. Despite these, I (...) argue that the RWT is historically workable, given a small number of modifications. I then expand Russo and Williamson’s account. I first develop their suggestion that causal relationships in medicine require some kind of evidence of mechanism. I begin with a number of accounts of mechanisms and produce a range of consensus features of them. I then develop this consensus position by reference to the two historical case studies with an eye to their operational competence. In particular, I suggest that it is mechanistic models and their representations which we are concerned with in medicine, rather than the mechanism as it exists in the world. -/- I then employ these mechanistic models to give an account of the sorts of evidence used in formulating and evaluating causal claims. Again, I use the two human viral oncogenesis cases to give this account. I characterise and distinguish evidence of mechanism from evidence of difference-making, and relate this to mechanistic models. I then suggest the relationship between types of evidence presents us with a means of tackling the reference-class problem. This sets the scene for the final chapter. Here, I suggest the manner in which these two different classes of evidence become integrated is also reflected in the way that developing research programmes change as their associated causal claims develop. (shrink)

In this paper we defend the view that mechanisms are underpinned by networks of difference-making relations. First, we distinguish and criticise two different kinds of arguments in favour of an activity-based understanding of mechanism: Glennan’s metaphysics- first approach and Illari and Williamson’s science-first approach. Second, we present an alternative difference-making view of mechanism and illustrate it by looking at the history of the case of scurvy prevention. We use the case of scurvy to argue that evidence (...) for a mechanism just is evidence for difference-making relations. (shrink)

Proponents of grounding often describe the notion as "metaphysical causation" involving determination and production relations similar to causation. This paper argues that the similarities between grounding and causation are merely superficial. I show that there are several sorts of causation that have no analogue in grounding; that the type of "bringing into existence" that both involve is extremely different; and that the synchronicity of ground and the diachronicity of causation make them too different to be (...) explanatorily intertwined. (shrink)

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

Coherentism maintains that coherent beliefs are more likely to be true than incoherent beliefs, and that coherent evidence provides more confirmation of a hypothesis when the evidence is made coherent by the explanation provided by that hypothesis. Although probabilistic models of credence ought to be well-suited to justifying such claims, negative results from Bayesian epistemology have suggested otherwise. In this essay we argue that the connection between coherence and confirmation should be understood as a relation mediated by the causal relationships (...) among the evidence and a hypothesis, and we offer a framework for doing so by fitting together probabilistic models of coherence, confirmation, and causation. We show that the causal structure among the evidence and hypothesis is sometimes enough to determine whether the coherence of the evidence boosts confirmation of the hypothesis, makes no difference to it, or even reduces it. We also show that, ceteris paribus, it is not the coherence of the evidence that boosts confirmation, but rather the ratio of the coherence of the evidence to the coherence of the evidence conditional on a hypothesis. (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)

In his early metaphysics, Leibniz interprets the results of Santorio’s quantitative methods as supporting the possibility of the natural immortality of human beings. A closer look into Santorio’s more theoretically oriented medical writings reveals that he vehemently rejected the idea of natural immortality. Still, it may be interesting to ask what the theoretical differences between the natural philosophies of Santorio and the early Leibniz are that could explain their diverging attitudes toward the possibility of natural immortality. I will argue for (...) two claims: (1) Santorio but not the early Leibniz, makes use of emergentist ideas along lines developed by Alexander of Aphrodisias and Galen. (2) The early Leibniz, but not Santorio, uses the concept of emanative causation to characterize the relation between the soul and its potencies. (shrink)

Climate change appears to be a classic aggregation problem, in which billions of individuals perform actions none of which seem to be morally wrong taken in isolation, and yet which combine to drive the global concentration of greenhouse gases (GHGs) ever higher toward environmental (and humanitarian) catastrophe. When an individual can choose between actions that will emit differing amounts of GHGs―such as to choose a vegan rather than carnivorous meal, to ride a bike to work rather than drive a car, (...) or to take a reusable bag to the supermarket rather than send another plastic bag to landfill―does she have any reason to choose the lower-emitting actions? In this chapter I'll reject the claim that individuals don't make a difference when it comes to climate change. I first discuss making a difference with every action, as a way of getting clearer about how individuals' actions impact causally on the harms resulting from climate change, making a distinction so far overlooked in the climate ethics discussion between 'macro' thresholds like ice-cap melt, and 'micro' thresholds like severe weather events. I set aside making a difference with every action as implausible, and then move on to discuss both low probability of major difference, and high probability of minor difference. I argue that both of these are plausible characterizations of individuals' causal contributions to climate change. I conclude by noting some policy implications of having (probabilistic) individual difference-making back in play. (shrink)

This dissertation shows how initial conditions play a special role in the explanation of contingent and irregular outcomes, including, in the form of geographic context, the special case of uneven development in the social sciences. The dissertation develops a general theory of this role, recognizes its empirical limitations in the social sciences, and considers how it might be applied to the question of uneven development. The primary purpose of the dissertation is to identify and correct theoretical problems in the study (...) of uneven development; it is not intended to be an empirical study. Chapter 1 introduces the basic problem, and discusses why it has become especially salient in debates concerning uneven development. Chapter 2 develops an argument for the importance of initial conditions in the philosophy of science, developed specifically in the context of the Bhaskar/Cartwright ‘open systems’ (and by extension, ‘exogenous factor’) emphasis on the ubiquity of contingency in the universe and rejection of explanation based on laws of nature (regularity accounts) of causation. Chapter 3 makes three claims concerning the concept of contingency, especially as related to the study of society: 1) that there are eight distinct uses of the word contingency, and its many meanings are detrimental to clarity of discussion and thought in history and the social sciences; 2) that it is possible to impose some order on these different uses through developing a classification of contingency into three types based on assumptions concerning possible worlds and determinism; 3) that one of the classes is a special use of the word without relevance to the social sciences, while the two remaining classes are nothing more than a variety of the ‘no hidden factors’ argument in the debate on indeterminism and determinism (and thus related to the concept of spacetime trajectories caused by initial conditions and the interference of these in the form of ‘exogenous factors’ with ‘open systems’). Chapter 4 The concept of explanation based on initial conditions together with laws of nature is widely associated with determinism. In the social sciences determinism has frequently been rejected due to the moral dilemmas it is perceived as presenting. Chapter 4 considers problems with this view. Chapter 5 considers attitudes among geographers, economists, and historians towards using geographic factors as initial conditions in explanation and how they might acceptably be used, in particular their role in ‘anchoring’ aspatial theories of social processes to real-world distributions. Chapter 6 considers the relationship of the statistical methods common in development studies with the trend towards integrating geographical factors into econometric development studies. It introduces the statistical argument on ‘apparent populations’ that arrives at conclusions concerning determinism consistent with Chapters 2 and 3 of the dissertation. The need for the visual interpretation of data with descriptive statistics and maps and their utility in the study of uneven development is discussed with a number of examples. Chapter 7 applies these concepts to the ‘institutions versus geography’ debate in development studies, using Acemoglu, Johnson and Robinson’s 2002 ‘reversal of fortune’ argument as a primary example. Chapter 8 considers possible directions for future work, both theoretical and empirical. Chapter 9 concludes with a discussion of additional possible objections to the use of initial conditions as exogenous factors in explanation. (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.

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)

Many approaches to quantum gravity -the theory that should account for quantum and gravitational phenomena under the same theoretical umbrella- seem to point at some form of spacetime emergence, i.e., the fact that spacetime is not a fundamental entity of our physical world. This tenet has sparked many philosophical discussions: from the so-called empirical incoherence problem to different accounts of emergence and mechanisms thereof. In this contribution, I focus on the partial order relation of causal set theory and argue that (...) causation can be characterized as an a-temporal constraint over the kinematic space defined by the theory. The relation constrains the growth of a new element/event with respect to the other elements/events of a given set. Therefrom, the flow of time emerges from the collection of the possible growths of the given set, where each possibility is characterized by a classical probability assigned by the dynamics of the theory. (shrink)

Reconstructs the original Greek version of the confatalia-argument that Cicero attributes to Chrysippus in De fato and misrepresent in crucial ways. Compares this argument with Seneca's discussion of determinism in the Naturales quaestiones. Clarifies that Seneca makes a different distinction from that attested in Cicero's De fato. Argues that problems with interpreting both accounts derive from disregarding terminological distinctions harder to spot in the Latin versions and, related to this, insufficient attention to the ontological distinction between bodies (such as Fate) (...) and predicates (e.g. "what is fated"), which unfortunately does not square well with the modern ontological category "event." Contains some corrections to the author's earlier discussion of the topic in Seneca und die Stoa: Der Platz des Menschen in der Welt, De Gruyter 2006, ch. 3.3.4. (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)

When is a cause of a cause of an effect also a cause of that effect? The right answer is either Sometimes or Always . In favour of Always , transitivity is considered by some to be necessary for distinguishing causes from redundant non-causal events. Moreover transitivity may be motivated by an interest in an unselective notion of causation, untroubled by principles of invidious discrimination. And causal relations appear to add up like transitive relations, so that the obtaining of (...) the overarching relation is not independent of the obtaining of the intermediaries. On the other hand, in favour of Sometimes , often we seem not to treat events that are very spatiotemporally remote from an effect as its causes, even when connected to the effect in question by a chain of counterfactual or chance-raising dependence. Moreover cases of double prevention provide counterexamples to causal transitivity even over short chains. According to the argument of this paper, causation is non-transitive. Transitizing causation provides no viable account of causal redundancy. An unselective approach to causation may motivate resisting the distance counterexamples to transitivity, but it does not help with double prevention, and even makes it more intractable. The strongest point in favour of transitivity is the adding up of causal relations, and this is the point that extant non-transitizing analyses have not adequately addressed. I propose a necessary condition on causation that explains the adding up phenomenon. In doing so it also provides a unifying explanation of distance and double prevention counterexamples to transitivity. (shrink)

In the evolution of the vertebrates and probably a few other animals (Metazoa), biological values have been translated (subjectivized) into affective experience that necessarily involves the consciousness of external objects/events (as different from one’s body), which is tantamount to the origins of subjectivity. Mammals, birds and other vertebrates are experiencing subjects even though their negative and positive experience greatly vary in scope. Some mammals are capable of vicarious experience and may act as empathic agents, and some of them, at least (...) the great apes, use true reflective self-consciousness and thus perceive themselves as agents, which generates attributive feelings. The balance of positive and negative experience determines the intrinsic value of (an individual) life. Every subjective life is autotelic in striving to maximize this balance. A subjective life may also have a social value that is measured in terms of the impact on intrinsic values of other lives. The social value of life is contingent upon an agency, that is, conscious intentional actions that impact intrinsic value of other lives. The difference between the social value of a subjective life and an instrumental value of an individual comes down to the difference between agent causation and event causation. The moral agency refers to a subcategory of agent causation that involves the awareness of impact on another subject’s wellbeing (interests). The moral agency is at present known only in the hominids (including the chimpanzees) which understand causality and use reflective self-consciousness, which in turn enables them to perceive themselves as agents and attribute to themselves responsibility. The moral agency originated as a motivational mechanism of reciprocity execution , and thus as an adaptation for group life, which is why it favors ingroup members and often promotes norms that harm other groups. The human moral agency is frequently used by third parties to implement group norms that are based on ideologies (religious or secular) and may actually harm both group members and the entire groups. Any received, bioculturally evolved morality is unlikely to be good in either absolute or universal sense. Therefore, the moral capacity alone does not make a human life categorically more valuable, even if human motivation were dominated by moral agency (which is true only of some people). The life of a vertebrate has, therefore, two values, intrinsic and social. Each can be negative or positive, and may vary to a large extent independently of the other, whereby a joint value of a subjective life cannot be sensibly assessed and compared without prior assessments of the intrinsic and social component separately. In the absence of objective reasons to rate the intrinsic value of a human life as categorically higher than that of other mentally advanced mammals, and in consideration of the observed range of social values of human lives, some of which approach zero and some are highly negative (lower than any thinkable negative values of non-human lives), the doctrine of extraordinary and inalienable (innate) human „dignity” is groundless and unethical, as it leads to a depreciation of the lives of non-human subjects, and often preempts the need to impart a real social value to one’s own life. (shrink)

Those of us who enjoy certain products of the global industrial economy but also believe it is wrong to consume them are often so demoralized by the apparent inefficacy of our individual, private choices that we are unable to resist. Although he was a deontologist, Kant was clearly aware of this ‘consequent-dependent’ side of our moral psychology. One version of his ‘moral proof’ is designed to respond to the threat of such demoralization in pursuit of the Highest Good. That version (...) of the argument says that the capacity that faith and trust in God has to sustain our moral resolve licenses that faith and trust, from a practical point of view. My goal here is to argue that Kant’s proof has a contemporary, secular analogue in modern industrial contexts where the apparent “inefficacy” of an individual consumer’s choices in the face of massive insensitive supply-chains is a threat to her moral resolve. I conclude by suggesting that the Kantian approach may license us in adopting (as an item of defeasible moral faith) an evidential decision-theoretic principle regarding what it is to ‘make a difference.’ This in turn licenses trust -- if not in God then in other right-minded people. (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)

Taking seriously the social dimensions of knowledge puts pressure on the assumption that epistemic agents can usefully be thought of as autonomous, interchangeable individuals, capable, insofar as they are rational and objective, of transcending the specificities of personal history, experience, and context. If this idealization is abandoned as the point of departure for epistemic inquiry, then differences among situated knowers come sharply into focus. These include differences in cognitive capacity, experience, and expertise; in access to information and the heuristics that (...) make it intelligible; and in motivating interests and orienting standpoint. Dissent takes on rather different significance, as a potentially productive feature of epistemic life rather than evidence of a failure of aperspectivality or an indication of error. The central questions are, then, what forms of diversity are epistemically consequential, and how can they best be deployed to ensure that the beliefs we warrant as knowledge are as well grounded and truth-tracking as possible. (shrink)

As a way to make medical decisions, Evidence-Based Medicine (EBM) has failed. EBM's failure arises from not being founded on real-world decision-making. EBM aspires to a scientific standard for the best way to treat a disease and determine its cause, but it fails to recognise that the scientific method is inapplicable to medical and other real-world decision-making. EBM also wrongly assumes that evidence can be marshaled and applied according to an hierarchy that is determined in an argument by (...) authority to the method by which it has been obtained. If EBM had valid theoretical, practical or empirical foundations, there would be no hierarchy of evidence. In all real-world decision-making, evidence stands or falls on its inherent reliability. This has to be and can only be assessed on a case-by-case basis applying understanding and wisdom against the background of all available facts—the "factual matrix." EBM's failure is structural and was inevitable from its inception. EBM confuses the inherent reliability and probative value of evidence with the means by which it is obtained. -/- EBM is therefore an ad hoc construct and is not a valid basis for medical decision-making. This is further demonstrated by its exclusion of relevant scientific and probative real-world decision-making evidence and processes. It draws upon a narrow evidence base that is itself inherently unreliable. It fails to take adequate account of the nature of causation, the full range of evidence relevant to its determination, and differing approaches to determining cause and effect in real-world decision-making. EBM also makes a muddled attempt to emulate the scientific method and it does not acknowledge the role of experience, understanding and wisdom in making medical decisions. (shrink)

1. Introduction: a look back at the reasons vs. causes debate. 2. The interventionist account of causation. 3. Four objections to interventionism. 4. The counterfactual analysis of event causation. 5. The role of free agency. 6. Causality in the human sciences. -- The reasons vs. causes debate reached its peak about 40 years ago. Hempel and Dray had debated the nature of historical explanation and the broader issue of whether explanations that cite an agent’s reasons are causal or (...) not. Melden, Peters, Winch, Kenny and Anscombe had contributed their anticausal conceptions. The neo-Wittgensteinians seemed to be winning the day when in 1963 Donald Davidson published his seminal paper “Actions, Reasons, and Causes”. Davidson’s paper devastated the Wittgensteinian camp. It contained, among other things, a powerful attack on the logical connection argument. Davidson argued that the existence of a logical or conceptual connection between descriptions can never eliminate a causal relation, which holds between events simpliciter, not between events under certain descriptions. Davidson maintained that in a way, reasons can be causes. When somebody acts for a certain reason, his intentional attitudes, or rather changes in his attitudes, cause his bodily movements. Davidson also argued that rationalization is a species of causal explanation. For the definition of action, he argued that intentional actions are bodily movements caused in the right way by beliefs and desires that rationalize them. Davidson’s paper paved the way for causal theories of action, which superseded neo-Wittgensteinian analyses in the following decades. The causal theory was rapidly adopted by Alvin Goldman, David Armstrong, Paul Churchland, Myles Brand and many others, entering the mainstream and dominating the philosophy of action to this very day. In 1971 Georg Henrik von Wright published his book "Explanation and Understanding". The second chapter did not deal with agency, but with causation. It developed a new account of causation, the interventionist or experimentalist account. Focusing on causation, von Wright remedied a major shortcoming of the reasons vs. causes debate. The concept of causality, and the nature of the causal relation, received little attention in this debate, a fact that holds true for both camps. Mostly it was simply taken for granted that, as Hempel had declared, “causal explanation is a special type of deductive-nomological explanation”. One camp then aligned intentional explanations with D-N explanations, while the other camp insisted on their disparity. So strictly speaking, the label “reasons/causes debate” was a misnomer. The controversy dealt primarily with the question as to whether intentional explanations can take the form of D-N explanations, while the notion of causation, and the metaphysics of the causal relation, were left obscured. With von Wright’s new approach, the situation changed. Von Wright was primarily concerned with causation, but his approach contained an implicit attack on the causal theory of action as well. His core idea was that the notion of causality is intimately linked with, or even derived from, the notion of intentionally making something happen. Other philosophers, even Hume, had considered such a connection before, but often just to reject this view, regarding it as a kind of myth belonging to the infancy of the human mind. Von Wright took the idea seriously. He submitted the analysis that p is the cause of q if and only if by doing p we could bring about q. The causal theory of action was also concerned with the relation between causation and agency, to which its name bears witness. The causal theory of action holds that actions are bodily movements with a certain causal history. This is why von Wright’s account constituted a momentous challenge to the causal theory: it reversed the direction of conceptual dependency between both notions. Davidson and his followers tried to define what an intentional action is by using the notion of causation. The causal condition which the causal theory sets is part of the definition of “doing something intentionally”. Von Wright claimed that the conceptual dependency is the other way round. He used the notions of doing, and bringing about, to explain what causal relations are. So, instead of a causal theory of action, he advocated an agency theory of causation, as it may be dubbed. It is remarkable how seldom this clash of opinions about conceptual primacy is reflected in the literature. There are few exceptions: Fred Stoutland noticed the conflict, and he published a number of papers in which he compared Davidson’s and von Wright’s views. Von Wright’s book "Explanation and Understanding" was widely read and discussed in the seventies, especially in Europe. But it strikes me that especially in North America, where the causal theory of action became the orthodoxy of the day, von Wright’s challenge went largely unnoticed. Even Davidson did not seem to take it seriously. He nowhere takes notice of the interventionist theory of causation, while he does discuss von Wright’s earlier book "Norm and Action". As is well-known, Davidson favoured an alternative account of causation, based on “the principle of the nomological character of causality”, as he somewhat clumsily called it, or, later and less clumsily, “the cause-law thesis”. Davidson’s firm adherence to a nomological theory of causality may explain why he did not take much interest in alternative accounts. [...] -/- . 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In this paper I argue that the extent to which a human trait is genetically caused can causally depend upon whether the trait is categorized within human genetics as genetically caused. This makes the kindgenetically caused traitan interactive kind. I demonstrate that this thesis is both conceptually coherent and empirically plausible. I outline the core rationale of this thesis and demonstrate its conceptual coherence by drawing upon Waters’ (2007) analysis of genetic causation. I add empirical plausibility to the thesis (...) by describing a hypothetical but empirically plausible mechanism by which the fact that obesity is categorized as genetically caused within human genetics increases the extent to which obesity is in fact genetically caused. (shrink)

What makes a valid argument valid? Generally speaking, in a valid argument, if the premisses are true, then the conclusion must necessarily also be true. But on its own, this doesn’t tell us all that much. What is truth? And what is necessity? In what follows, I consider answers to these questions proposed by the fourteenth century logician John Buridan († ca. 1358). My central claim is that Buridan’s logic is downstream from his metaphysics. Accordingly, I treat his metaphysical discussions (...) as the key to his logic. As has been often noted, Buridan’s metaphysics are radically anti-realist about universals, though I think the depth and scope of his anti-realism has at times been papered over. Buridan constructs his logic on an amazingly spartan ontology, and this accomplishment is overdue for reconsideration. To the foregoing questions: truth is a feature of propositions, and of propositions only—not of proposition-like states of affairs, or anything like that. It is a function of the reference or supposition (suppositio) of their terms, which depends on predication in a propositional context. And necessary truth is grounded in causation: a predication is necessary if it cannot be falsified by any power, natural or supernatural, without ii annihilating what its terms stand for. “Socrates is a human”, for instance, can only be falsified by annihilating Socrates, and so it is a necessary truth. -/- These considerations provide an ample theoretical basis for a thorough examination of Buridan’s modal logic. This is what the thesis culminates with. In the final chapter, I set forth some novel and surprising findings, chief of which is this: Buridan’s modal syntax and semantics are nothing like Kripke’s—and indeed are incompatible with them. This has significant implications not only for modal logic and metaphysics, but for how we think about medieval logic and philosophy more generally. -/- Throughout the thesis, I advocate a methodology of emphasising the differences, rather than the similarities, between past and present thought. Buridan is wildly unlike what we’re used to, and we should let him speak for himself. (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)

Positions taken in the current debate over free will can be seen as responses to the following conditional: -/- If every action is caused solely by another event and a cause necessitates its effect, then there is no action to which there is an alternative (C). -/- The Libertarian, who believes that alternatives are a requirement of free will, responds by denying the right conjunct of C’s antecedent, maintaining that some actions are caused, either mediately or immediately, by events whose (...) effects could be different, even if they were to recur under identical circumstances. We have here a denial of Laplacian Determinism (LD), according to which the condition of the world at any instant makes only one state possible at any other instant. One prominent defender of this view, Robert Kane, holds that unless an agent’s neural mechanisms operated indeterministicly in forming her character she is not responsible for its manifestations. This requirement is entailed by the principle of “ultimate responsibility” (UR) according to which an act is freely willed only if (a) its agent is personally responsible for its performance in the sense of having caused it to occur by voluntarily doing something that was avoidable and (b) there is no sufficient condition for its performance for which its agent is not personally responsible. The orthodox Compatibilist, adducing counterexamples to UR, argues that even if C and its antecedent are true, free will is possible. Ned Markosian has provided the Compatibilist with yet another response to UR-based objections to her view, wedding it to the notion of agent causation: here the deterministic causing of an act by its agent is necessary and sufficient for its being “morally free.” I criticize this view as inconsistent with the agent causalist's belief that moral responsibility precludes causation of a choice by any power other than the maker thereof: he being its efficient cause. (shrink)

Work on causation in psychopathology often emphasizes variation in the causes but variation in what is to be explained further complicates matters. Focusing on the protean nature of psychopathology, this chapter explores different ways that classificatory variation is generated. For example, choices about what features of disorders to foreground and background can produce variation. The chapter also examines, from the perspective of scientific conventionalism, how classificatory decisions made at choice points partly constitute what is classified, but not in the (...) sense of making it up. In contrast to the view that conventions are neither true nor false and thus isolated from the domain of facts, the chapter argues that scientific conventions are implemented to promote the discovery of facts. Scientific conventions must also answer to conceptual and factual constraints. The chapter concludes by looking at how classificatory choices can produce different versions of a psychiatric which may also result in variations in causal models across those versions. In agreement with ideas articulated by Putnam, the chapter argues that we cannot divide the language of psychopathology into a part that describes disorders as they are in themselves and a part that contains our conceptual contributions to what we know about disorders. (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.

Analyses of factual causation face perennial problems, including preemption, overdetermination, and omissions. Arguably, the thorniest, are cases of omissive overdetermination, involving two independent omissions, each sufficient for the harm, and neither, independently, making a difference. A famous example is Saunders, where pedestrian was hit by a driver of a rental car who never pressed on the (unbeknownst to the driver) defective (and, negligently, never inspected) brakes. Causal intuitions in such cases are messy, reflected in disagreement about which (...) omission mattered. What these analyses mistakenly take for granted, is that at issue is the 'efficacy' of each omission. I argue, on the contrary, the puzzle of omissive overdetermination favors taking the act/omission distinction seriously. Factual causation, properly understood precludes omissions (i.e. omissions are not causal). Of course, the law also attaches liability to omissions, but this works differently from liability for real causes (e.g. omissions have a duty requirement, they also respond differentially to difference-making considerations). The manner in which liability attaches for omissions differs from that of straightforward causal liability, and is entirely dependent on the underlying causal structure. Attention to that structure (e.g. that the driver's hitting the pedestrian with his car is what actually caused the injury) sheds light on which omissions matter (e.g. driver's failure to press on the brakes) and why (because that failure removes a defense the driver would have to liability for the accident he caused). Other cases, where the parties' connection is entirely omissive (e.g. two physicians fail to detect independently lethal conditions), come out differently (tracking moralized elements). The analysis offered makes better sense of both why omissive determination cases are puzzling and how to resolve them. (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)

In this paper, we analyse actual causation in terms of production. The latter concept is made precise by a strengthened Ramsey Test semantics of conditionals: \ iff, after suspending judgement about A and C, C is believed in the course of assuming A. This test allows us to verify or falsify that an event brings about another event. Complementing the concept of production by a weak condition of difference-making gives rise to a full-fledged analysis of causation.

Philosophical analyses of causation have been centred on the question of what causation is. More precisely speaking, philosophers tend to address four different issues: metaphysical (what is causation out there?), epistemological (how can a causal claim be established and assessed?), conceptual (what does the word ‘cause’ mean?), and methodological (what methods ought one to use in order to establish and assess causal claims?). This chapter argues that the practical issue of causation (what is a causal claim (...) for in practice?) is highly relevant to the metaphysical, epistemological, conceptual, and methodological issues of causation. Any philosophical enquiry into causation without an examination of this practical issue is incomplete. In other words, a promising approach to causation ought to take all of the metaphysical, epistemological, conceptual, methodological, and practical issues into account. (shrink)

In this paper I argue that many scholars involved in the contemporary free will debates have underappreciated the philosophical appeal of agent causation because the resources of contemporary emergentism have not been adequately introduced into the discussion. Whereas I agree that agent causation’s main problem has to do with its intelligibility, particularly with respect to the issue of how substances can be causally relevant, I argue that the notion of substance causation can be clearly articulated from an (...) emergentist framework. According to my proposal, a free agent is _a causally powerful substance that emerges in an anomic way from her constitutive mental events_, downwardly constraining, selecting and, in this way, having control on them. As we shall see, this particular concept of agent causation not only makes sense of the deep insight behind agent libertarianism, but it also provides us with the resources to solve some of the main objections that have been raised against it. It is true that here I cannot develop a complete defense of the evidential credentials of emergentism. Still, even if the considerations that follow do not serve to convince detractors of agent causal libertarian accounts of free will, they do suggest that libertarian agent causation is more promising than is typically acknowledged. (shrink)

The striking difference between the orthodox nomological necessitation view of laws and the claims made recently by Scientific Essentialism is that on the latter interpretation laws are metaphysically necessary while they are contingent on the basis of the former. This shift is usually perceived as an upgrading: essentialism makes the laws as robust as possible. The aim of my paper—in which I contrast Brian Ellis’s Scientific Essentialism and David Armstrong’s theory of nomological necessity—is threefold. (1) I first underline the (...) familiar fact that metaphysical necessity (of Kripkean “water is necessarily H2O” kind) is not a stronger kind of necessity than nomological necessity but an entirely different kind of thing: nomological, but not metaphysical necessity, is an intra-world necessitation which Armstrong (almost) identifies with causation; metaphysical, but not nomological necessitation, has a canonical link to possible world considerations and counterfactual reasoning. Hence, the change from one necessity to the other is not an upgrading but a substantial shift. (2) I will explain how the essentialists, who promote this shift, are nonetheless able to retain the features of nomological necessity. (3) I also explore, for both the essentialist and the Armstrongian, whether they could extract a modal force from intra-world nomological necessity which it does not have per se. I argue that such a modal force is, indeed, obtainable for them. I will close the paper with some remarks and questions about the relation between Kripkean metaphysical necessity and the modal version of nomological necessity as defined in (3). (shrink)

Rudolf Haag’s Local Quantum Physics (LQP) is an alternative framework to conventional relativistic quantum field theory for combining special relativity and quantum theory based on first principles, making it of great interest for the purposes of conceptual analysis despite currently being relatively limited as a tool for making experimental predictions. In LQP, the elementary particles are defined as species of causal link between interaction events, together with which they comprise its most fundamental entities. This notion of particle has (...) yet to be independently assessed as such. Here, it is captured via a set of propositions specifying particle characteristics and then compared to previous particle notions. Haag’s particle differs decisively with respect to mechanical intuitions about particles by lacking, among other things, even an approximate independent space–time location. This notion is thus found to differ greatly even from those of relativistic quantum mechanics and quantum field theory, which have been applied to the known elementary particles. (shrink)

The enduring problem of free will has defied resolution across centuries. There is reason to believe that novel factors must be integrated into the analysis to make progress. Within the current physicalist framework, these factors encompass emergence and information theory, in the context of constraints imposed by physical limits on the representation of information. Furthermore the common, but vague, characterization of free will as 'being able to act differently' is rephrased into an explicatum more suitable for formal analysis. It is (...) argued that the mind is an ontologically open system; a causal high-level system, the dynamics of which cannot be reduced to the states of its associated low-level neural systems, not even if it is rendered physically closed. A positive answer to the question of free will for conscious agents is subsequently outlined. (shrink)

Eyal Shahar’s essay review [1] of James Penston’s remarkable book [2] seems more inspired playful academic provocation than review or essay, expressing dramatic views of impossible validity. The account given of modern biostatistical causation reveals the slide from science into the intellectual confusion and non-science RCTs have created: “…. the purpose of medical research is to estimate the magnitude of the effect of a causal contrast, for example the probability ratio of a binary outcome …” But Shahar’s world is (...) simultaneously not probabilistic, but of absolute uncertainty: “We should have no confidence in any type of evidence ….. We should have no confidence at all”. Shahar’s "Causal contrast" is attractive. It seems to make sense, but bypasses in two words the means of establishing causation by the scientific method. This phrase assumes a numeric statistically significant “contrast” is causal rather than a potential correlation requiring further investigation. The concept of “causal contrast” is a slippery slope from sense into biostatistical non-science. This can be illustrated with an hypothetical RCT where 100% of interventions exhibit a posited treatment effect and 0% of placebo controls. Internal validity is seemingly quite reasonably assumed satisfied (common-sense dictating the likelihood of an awesome magnificent fraud, bias or plain error of the magnitude required is infinitesimal). Scientific method appears satisfied. The RCT demonstrates: (1) strict regularity of outcome in the presence of posited cause; (2) the absence of outcome in its absence and (3) an intervention (experiment) showing the direction of causation is from posited cause to posited effect. Now travel further down the slope from science. Assume 50% of interventions and 0% of controls are positive. We compromise scientific method, but justify this by assuming a large subgroup which we say surely must on these figures be exhibiting the posited treatment effect. But what of 10% of interventions and 9% of placebo controls exhibiting the posited treatment effect? Our biostatistician says the 1% “causal contrast” is statistically significant. But we have: (1) minimal evidence of regularity; (2) the posited outcome irrespective of presence of posited cause and (3) our intervention is at the highest equivocal in demonstrating any form of causation. This is not science. It is, however, where biostatistics has unthinkingly taken us, as Penston has shown comprehensively [2]. We, the audience of published medical research, are now for the 10% / 9% example well down the slope from science. An unattractive hypothesis results requiring numerous assumptions similar to these:- "There is a 'contrast' which is ‘causal’, albeit the method employed is not scientific. An effect of the intervention has been observed in a very small subgroup. This subgroup is susceptible to treatment. The similar number of placebo controls exhibiting the outcome sought is irrelevant, because the 1% difference between intervention and controls is statistically significant. The statistical analysis is valid and reliable. The RCT’s internal validity is sufficiently satisfied. No funding or bias or fraud has affected the results or their analysis.” As Penston notes: “Confirming and refuting the results of research is crucial to science …. But … there’s no way of testing the results of any particular large-scale RCT or epidemiological study. Each study … is left hanging in the air, unsupported.” It gets worse. To identify a rare serious adverse reaction of a frequency of 1:10,000 can require a trial of 200,000 or larger split between controls and interventions. This is not done. But for every 100 who prospectively benefit from the intervention, 9,900 also receive it. And for every 100 benefiting one person (who likely gains no benefit) will suffer a serious unidentified adverse reaction. This is also without taking account of more common adverse reactions whether serious or otherwise. References [1] Shahar, E. (2011) Research and medicine: human conjectures at every turn. International Journal of Person Centered Medicine 1 (2), 250-253. [2] Penston, J. (2010). stats.con: How we’ve been fooled by statistics-based research in medicine. London: The London Press, UK. (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)

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)