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)

The starting point in the development of probabilistic analyses of token causation has usually been the naïve intuition that, in some relevant sense, a cause raises the probability of its effect. But there are well-known examples both of non-probability-raising causation and of probability-raising non-causation. Sophisticated extant probabilistic analyses treat many such cases correctly, but only at the cost of excluding the possibilities of direct non-probability-raising causation, failures of causal transitivity, action-at-a-distance, prevention, and causation by (...) class='Hi'>absence and omission. I show that an examination of the structure of these problem cases suggests a different treatment, one which avoids the costs of extant probabilistic analyses. (shrink)

Hume thought that if you believed in powers, you believed in necessary connections in nature. He was then able to argue that there were none such because anything could follow anything else. But Hume wrong-footed his opponents. A power does not necessitate its manifestations: rather, it disposes towards them in a way that is less than necessary but more than purely contingent. -/- In this paper a dispositional theory of causation is offered. Causes dispose towards their effects and often (...) produce them. But a set of causes, even though they may succeed in producing an effect, cannot necessitate it since the effect could have been counteracted by some additional power. This would require a separation of our concepts of causal production and causal necessitation. The most conspicuous cases of causation are those where powers accumulate and pass a requisite threshold for an effect to occur. -/- We develop a model for representing powers as constituent vectors within an n-dimensional quality space, where composition of causes appears as vector addition. Even our resultant vector, however, has to be understood as having dispositional force only. This model throws new light on causal modality and cases of prevention, causation by absence and probabilistic causation. (shrink)

This is a brief philosophical introduction to, and an annotated translation of, the section on absence from Śālikanātha’s Pramāṇapārāyaṇa (Study of the Instruments of Knowledge), a foundational work of Prābhākara epistemology. In this section, which focuses on the epistemology of absence, Śālikanātha argues against the Bhāṭṭa view that there is a sui generis instrument of knowledge (pramāṇa) by which we learn of absence (abhāva). He does so by arguing for a subjective reductionist thesis about absence, according (...) to which the absence of a perceivable (dṛśya) object at a locus is identical with a positive state of awareness (buddhi) whose content includes the locus but not the perceivable object. If correct, Śālikanātha argues, we should therefore learn of absence in the same ways we acquire self-knowledge more generally. While developing his reductionism about absence, Śālikanātha responds to a range of concerns, including the objection that his view cannot explain causation by absence. (shrink)

Our approach aims at accounting for causal claims in terms of how the physical states of the underlying dynamical system evolve with time. Causal claims assert connections between two sets of physicals states—their truth depends on whether the two sets in question are genuinely connected by time evolution such that physical states from one set evolve with time into the states of the other set. We demonstrate the virtues of our approach by showing how it is able to account for (...) typical causes, causally relevant factors, being ‘the’ cause, and cases of overdetermination and causation by absences. (shrink)

I focus on token, deterministic causal claims as they feature in causal explanations. Adequately handling absences is difficult for most causal theories, including theories of causal explanation. Yet so is adequately handling cases of late preemption. The best account of absence-causal claims as they appear in causal explanations is Jonathan Schaffer's quaternary, contrastive account. Yet Schaffer's account cannot handle preemption. The account that best handles late preemption is James Woodward's interventionist account. Yet Woodward's account is inadequate when it comes (...) to absences. I propose an account that handles both absences and preemption by transposing Schaffer's account into an interventionist framework. (shrink)

In this article, I begin by giving a brief history of melanoma causation. I then discuss the current manner in which malignant melanoma is classified. In general, these systems of classification do not take account of the manner of tumour causation. Instead, they are based on phenomenological features of the tumour, such as size, spread, and morphology. I go on to suggest that misclassification of melanoma is a major problem in clinical practice. I therefore outline an alternative means (...) of classifying these tumours based on causal factors. By analogy with similar systems that have recently emerged for other cancers, I suggest that this causal classification is likely to be both workable and helpful, even in the absence of a full causal-mechanistic understanding of the aetiology of the tumour. (shrink)

Does A cause B simply if A prevents what would have prevented B? Such a case is known as double prevention: where we have the prevention of a prevention. One theory of causation is that A causes B when B counterfactually depends on A and, as there is such a dependence, proponents of the view must rule that double prevention is causation.<br><br>However, if double prevention is causation, it means that causation can be an extrinsic matter, that (...) the cause and effect need not be connected by a continuous chain of events, that there can be causation by absence, and that there can be causation at a distance. All of these implications jar with strong intuitions we have about the nature of causation. There is, on the other hand, a theory of causation based on an ontology of real dispositions, where causation involves the passing around of powers. This theory in contrast entails that double prevention is not causation and, on this issue, it can claim a victory over the counterfactual dependence account. (shrink)

This paper argues that several sorts of metaphysical and semantic indeterminacy afflict the causal relation. If, as it is plausible to hold, there is a relationship between causation and moral responsibility, then indeterminacy in the causal relation results in indeterminacy of moral responsibility more generally.

“Perception is controlled hallucination,” according to proponents of predictive processing accounts of vision. I say they are right that something like this is a consequence of their view but wrong in how they have pursued the idea. The focus of my counterproposal is the causal theory of perception, which I develop in terms of a productive concept of causation. Cases of what otherwise seem like successful perception are instead mere veridical hallucination if predictive processing accounts are correct, I argue, (...) because of the role played within such accounts by absences, which cannot enter into productive causal relations. -/- I offer two arguments in support of the productive theory of perception. The first is loosely Kantian, focusing on the role that receptivity and spontaneity play in perception. The second focuses on what perception and hallucination have in common. I conclude with a series of objections and replies. (shrink)

A standard way of representing causation is with neuron diagrams. This has become popular since the influential work of David Lewis. But it should not be assumed that such representations are metaphysically neutral and amenable to any theory of causation. On the contrary, this way of representing causation already makes several Humean assumptions about what causation is, and which suit Lewis’s programme of Humean Supervenience. An alternative of a vector diagram is better suited for a powers (...) ontology. Causation should be understood as connecting property types and tokens where there are dispositions towards some properties rather than others. Such a model illustrates how an effect is typically polygenous: caused by many powers acting with each other, and sometimes against each other. It models causation as a tendency towards an effect which can be counteracted. The model can represent cases of causal complexity, interference, over-determination and causation of absence (equilibrium). (shrink)

This paper aims at bringing a new philosophical perspective to the current debate on the death penalty through a discussion of peculiar kinds of uncertainties that surround the death penalty. I focus on laying out the philosophical argument, with the aim of stimulating and restructuring the death penalty debate. I will begin by describing views about punishment that argue in favour of either retaining the death penalty (‘retentionism’) or abolishing it (‘abolitionism’). I will then argue that we should not ignore (...) the so-called “whom-question”, i.e. “To whom should we justify the system of punishment?” I identify three distinct chronological stages to address this problem, namely, “the Harm Stage”, “the Blame Stage”, and “the Danger Stage”. I will also identify four problems arising from specific kinds of uncertainties present in current death penalty debates: (1) uncertainty in harm, (2) uncertainty in blame, (3) uncertainty in rights, and (4) uncertainty in causal consequences. In the course of examining these four problems, I will propose an ‘impossibilist’ position towards the death penalty, according to which the notion of the death penalty is inherently contradictory. Finally, I will suggest that it may be possible to apply this philosophical perspective to the justice system more broadly, in particular to the maximalist approach to restorative justice. (shrink)

The goal of this paper is to argue that there is indeterminacy in causation. I present three types of cases in which it is indeterminate whether an event c caused another event e: (1) cases of absence causation recently discussed by Bernstein and by Swanson, (2) cases leading to Sorites paradoxes for causation, and (3) cases where c and e occur in certain indeterministic causal structures and it is therefore indeterminate whether there is a causal relation (...) between them. These cases, I argue, provide strong evidence that indeterminacy is an important general feature of the causal relation and that philosophical theorizing about causation should take this observation into account. (shrink)

Many philosophers maintain that causation is to be explicated in terms of a kind of dependence between cause and effect. These “dependence” theories are opposed by “production” accounts which hold that there is some more fundamental causal “oomph”. A wide range of experimental research on everyday causal judgments seems to indicate that ordinary people operate primarily with a dependence-based notion of causation. For example, people tend to say that absences and double preventers are causes. We argue that the (...) impression that commonsense causal discourse is largely dependence-based is the result of focusing on a very narrow class of causal verbs. Almost all of the vignette-based experimental work on causal judgment has been prosecuted using the word “cause”. But much ordinary causal discourse involves special causal verbs, such as “burn” and “crack”. We find that these verbs display a quite different pattern from the verb “cause”. For instance, for absences and double preventers (Studies 1-3), we find that while people are inclined to say that X caused Y to burn, turn, crack or start, they are less inclined to think that X burned, turned, cracked or started Y. In Study 4, we find that for chains involving a distal and proximal event, people are inclined to say that the distal event is not a special cause of the outcome, though it is a “cause” of the outcome. Together, we find a surprising double dissociation between “cause” and a stock of special causal verbs. We conclude by suggesting that much commonsense causal judgment, which heavily trades in special causal verbs, might be better captured by production-based accounts of causation. (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)

The philosophy of superdeterminism is based on a single scientific fact about the universe, namely that cause and effect in physics are not real. In 2020, accomplished Swedish theoretical physicist, Dr. Johan Hansson published a physics proof using Albert Einstein’s Theory of Special Relativity that our universe is superdeterministic meaning a predetermined static block universe without cause and effect in physics. In the absence of cause and effect in physics, past, present and future events must all exist equally in (...) logical relationship. Our experience of time must be an illusion, because our experience of change in our world is not actually caused in time. Rather, the change we experience in our world is caused by the changing appearances in our static block universe in the static fourth dimension of time. We should think of time as a distance in the fourth dimension of time from our present position in the dimension of time to another position either towards or away from the beginning of the universe. Because physical reality is not actually caused to change in our static block universe, then static physical reality is actually timeless. But, because very good evidence supports the creation of timeless physical reality, then non-temporal causation of timeless physical reality outside of time is real. (shrink)

In this paper, I argue that absences pose a challenge to our understanding of physicalism that has not been properly appreciated. I do this by setting out a thought experiment involving a being in whom absence properties occupy the causal roles that functionalists take to define mental properties, in which case these absence properties realize the being’s mental properties. Such a being should be compatible with the truth of physicalism, I argue, even though its mental properties are neither (...) themselves physical properties nor are they realized/grounded in physical properties—instead, they are realized/grounded in (nonphysical) absence properties. I argue that the case serves as a counterexample to leading formulations of physicalism that appeal to realization or grounding, but not to standard supervenience-based formulations of physicalism, because the latter typically include negative truths in their supervenience base in addition to physical truths. I show how realization- and grounding-based formulations of physicalism might be revised to handle the problem, but also recommend that we rethink how we understand physicalism and the role that negative entities can play for physicalists. (shrink)

In order to defend mental explanations dualists may appeal to dispositions (powers). By accepting a powers theory of causation, a dualist can more plausibly defend mental explanations that are given independently of physical explanations. Accepting a power-based theory still comes with a price. Absences and double preventers are not causes in a powers theory, and solutions based on them can only defend their explanatory relevance in mental explanations. There is still a chance that such mental explanations can be causal (...) explanations, though they do not refer to real causes. (shrink)

This thesis examines philosophical controversies surrounding the evaluation of medical treatments, with a focus on the evidential roles of randomised trials and mechanisms in Evidence-Based Medicine. Current 'best practice' usually involves excluding non-randomised trial evidence from systematic reviews in cases where randomised trials are available for inclusion in the reviews. The first paper challenges this practice and evaluates whether adding of evidence from non-randomised trials might improve the quality and precision of some systematic reviews. The second paper compares the alleged (...) methodological benefits of randomised trials over observational studies for investigating treatment benefits. It suggests that claims about the superiority of well-conducted randomised controlled trials over well-conducted observational studies are justified, especially when results from the two methods are contradictory. The third paper argues that postulating the unpredictability paradox in systematic reviews when no detectable empirical differences can be found requires further justification. The fourth paper examines the problem of absence causation in the context of explaining causal mechanisms and argues that a recent solution is incomplete and requires further justification. Solving the problem by describing absences as causes of 'mechanism failure' fails to take into account the effects of absences that lead to vacillating levels of mechanism functionality. The fifth paper criticises literature that has emphasised functioning versus 'broken' or 'non-functioning' mechanisms emphasising that many diseases result from increased or decreased mechanism function, rather than complete loss of function. Mechanistic explanations must account for differences in the effectiveness of performed functions, yet current philosophical mechanistic explanations do not achieve this. The last paper argues that the standard of evidence embodied in the ICE theory of technological function is too permissive for evaluating whether the proposed functions of medical technologies have been adequately assessed and correctly ascribed. It argues that high-quality evidence from clinical studies is necessary to justify functional ascriptions to health care technologies. (shrink)

As Jaegwon Kim points out in his excellent new book, “reductionism” has become something of a pejorative term in philosophy and related disciplines. But originally (eg, as expressed in Ernest Nagel’s 1961 The Structure of Science) reduction was supposed to be a form of explanation, and one may wonder whether it is reasonable to reject in principle the advances in knowledge which such explanations may offer. Nagel’s own view, illustrated famously by the reduction of thermodynamics to statistical mechanics, was that (...) reduction is a relation between theories: theory A is reduced to theory B by formulating “bridge laws” which link the terminology of the theories, and using them to derive A from B. (An additional reductive claim is that Aphenomena are identical with certain B-phenomena—as when the temperature of a gas is identified with its mean molecular kinetic energy—but this kind of identity claim is, strictly speaking, independent of the claim about theories.) Applied to the case of mental states and brain states, a reduction would provide explanatory relations between psychology and neuroscience, normally supplemented with the claim that mental properties are identical with physical properties in the brain. (shrink)

Book review of 'Tropes: Properties, Objects, and Mental Causation' (2011, OUP). By DOUGLAS EHRING.

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)

A major criticism of David Lewis’ counterfactual theory of causation is that it allows too many things to count as causes, especially since Lewis allows, in addition to events, absences to be causes as well. Peter Menzies has advanced this concern under the title “the problem of profligate causation.” In this paper, I argue that the problem of profligate causation provides resources for exposing a tension between Lewis’ acceptance of absence causation and his modal realism. (...) The result is a different problem of profligate causation—one that attacks the internal consistency of Lewisian metaphysics rather than employing common sense judgments or intuitions that conflict with Lewis’ extensive list of causes. (shrink)

It could be argued that tort law is failing, and arguably an example of this failure is the recent public liability and insurance (‘PL&I’) crisis. A number of solutions have been proposed, but ultimately the chosen solution should address whatever we take to be the cause of this failure. On one account, the PL&I crisis is a result of an unwarranted expansion of the scope of tort law. Proponents of this position sometimes argue that the duty of care owed by (...) defendants to plaintiffs has expanded beyond reasonable levels, such that parties who were not really responsible for another’s misfortune are successfully sued, while those who really were to blame get away without taking any responsibility. However people should take responsibility for their actions, and the only likely consequence of allowing them to shirk it is that they and others will be less likely to exercise due care in the future, since the deterrents of liability and of no compensation for accidentally self-imposed losses will not be there. Others also argue that this expansion is not warranted because it is inappropriately fueled by ‘deep pocket’ considerations rather than by considerations of fault. They argue that the presence of liability insurance sways the judiciary to award damages against defendants since they know that insurers, and not the defendant personally, will pay for it in the end anyway. But although it may seem that no real person has to bear these burdens when they are imposed onto insurers, in reality all of society bears them collectively when insurers are forced to hike their premiums to cover these increasing damages payments. In any case, it seems unfair to force insurers to cover these costs simply because they can afford to do so. If such an expansion is indeed the cause of the PL&I crisis, then a contraction of the scope of tort liability, and a pious return to the fault principle, might remedy the situation. However it could also be argued that inadequate deterrence is the cause of this crisis. On this account the problem would lie not with the tort system’s continued unwarranted expansion, but in the fact that defendants really have been too careless. If prospective injurers were appropriately deterred from engaging in unnecessarily risky activities, then fewer accidents would ever occur in the first place, and this would reduce the need for litigation at its very source. If we take this to be the cause of tort law’s failure then our solution should aim to improve deterrence. Glen Robinson has argued that improved deterrence could be achieved if plaintiffs were allowed to sue defendants for wrongful exposure to ongoing risks of future harm, even in the absence of currently materialized losses. He argues that at least in toxic injury type cases the tortious creation of risk [should be seen as] an appropriate basis of liability, with damages being assessed according to the value of the risk, as an alternative to forcing risk victims to abide the outcome of the event and seek damages only if and when harm materializes. In a sense, Robinson wishes to treat newly-acquired wrongful risks as de-facto wrongful losses, and these are what would be compensated in liability for risk creation (‘LFRC’) cases. Robinson argues that if the extent of damages were fixed to the extent of risk exposure, all detected unreasonable risk creators would be forced to bear the costs of their activities, rather than only those who could be found responsible for another’s injuries ‘on the balance of probabilities’. The incidence of accidents should decrease as a result of improved deterrence, reduce the ‘suing fest’, and so resolve the PL&I crisis. So whilst the first solution involves contracting the scope of tort liability, Robinson’s solution involves an expansion of its scope. However Robinson acknowledges that LFRC seems prima facie incompatible with current tort principles which in the least require the presence of plaintiff losses, defendant fault, and causation to be established before making defendants liable for plaintiffs’ compensation. Since losses would be absent in LFRC cases by definition, the first evidentiary requirement would always be frustrated, and in its absence proof of defendant fault and causation would also seem scant. If such an expansion of tort liability were not supported by current tort principles then it would be no better than proposals to switch accident law across to no-fault, since both solutions would require comprehensive legal reform. However Robinson argues that the above three evidentiary requirements could be met in LFRC cases to the same extent that they are met in other currently accepted cases, and hence that his solution would therefore be preferable to no-fault solutions as it would only require incremental but not comprehensive legal reform. Although I believe that actual losses should be present before allowing plaintiffs to seek compensation, I will not present a positive argument for this conclusion. My aim in this paper is not to debate the relative merits of Robinson’s solution as compared to no-fault solutions, nor to determine which account of the cause of the PL&I crisis is closer to the truth, but rather to find out whether Robinson’s solution would indeed require less radical legal reform than, for example, proposed no-fault solutions. I will argue that Robinson fails to show that current tort principles would support his proposed solution, and hence that his solution is at best on an even footing with no-fault solutions since both would require comprehensive legal reform. (shrink)

When a group of processes achieves such closure that a set of states of affairs recurs continually, then the effect of that coherence on the world differs from what would occur in the absence of that closure. Such altered effectiveness is an attribute of the system as a whole, and would have consequences. This indicates that the network of processes, as a unit, has ontological significance. Whenever a network of processes generates continual return to a limited set of states (...) of affairs, the system may function as a “whole”— with respect to appropriate interaction partners. The balance achieved by the processes provides the form of definiteness of a unified agent. The causal powers of such coherent aggregates are indeed just the powers of the “constituents acting in concert”. However, the components act in concert in the specific way they do only because of their inclusion in the closed set of interactions that defines the coherence. This renders the causal powers of the coherence defined by that closure non-redundant, and hence the coherence, as a unit, is ontologically significant. The form of definiteness that provides internal coherence also grounds external efficacy of the societal aggregation. The closure is a structural feature of the coherence — possibly, but not necessarily, apparent in spatial structuring. This approach can provide a unified account that includes quantum microphysics, systems biology, and the philosophy of organism ─ without reducing any of these to another. (shrink)

Absences pose a dilemma for theories of causation. Allowing them to be causes seems to make theories too permissive (Lewis, 2000). Banning them from being causes seems to make theories too restrictive (Schaffer, 2000, 2004). An increasingly popular approach to this dilemma is to acknowledge that norms can affect which absences count as causes (e.g., Thomson, 2003; McGrath, 2005; Henne et al., 2017; Willemsen, 2018). In this article, I distinguish between two influential implementations of such ‘abnormality’ approaches and argue (...) that so-called ‘double-prevention mechanisms’ provide counterexamples against both. (shrink)

There is longstanding interpretive dispute between commentators over Spinoza’s commitment to necessitarianism, the doctrine that all things are metaphysically necessary and none are contingent. Those who affirm Spinoza’s commitment to the doctrine adhere to the necessitarian interpretation whereas those who deny it adhere to what I call the semi-necessitarian interpretation. As things stand, the disagreement between commentators appears to have reached an impasse. Notwithstanding, there seems to be no disagreement among commentators on the question of necessitarianism’s philosophical plausibility as a (...) metaphysical view: the doctrine is wildly untenable. This consensus view is more relevant to the interpretive debate than few have recognized, since leading semi-necessitarian commentators take the doctrine’s alleged absurdity to be one of the most compelling reasons (if not the most compelling reason) to prefer their reading over the necessitarian interpretation: for, as a matter of methodological principle, great philosophers like Spinoza should not be ascribed ridiculous views in the absence of better evidence. -/- This dissertation seeks to defend Spinoza’s commitment to necessitarianism on both the interpretive and philosophical fronts. I argue not only that the necessitarian interpretation of Spinoza is more plausible than the semi-necessitarian interpretation on textual grounds, but that Spinoza’s necessitarianism is a serviceable philosophical view whose tenability has been almost entirely overlooked and perfunctorily rejected. The principal basis upon which I build this defense is Spinoza’s rich and fascinating view of essences—what I simply refer to as his essentialism. Spinoza’s essentialism forms the bedrock of his metaphysics and is significant not least because it underlies and informs doctrines like his necessitarianism. Spinoza’s essentialism supplies resources to answer not just interpretive problems associated with necessitarianism, but philosophical challenges to the plausibility of the doctrine. My defense of Spinoza’s necessitarianism on philosophical grounds also offers a novel way of getting past much of the current interpretive impasse among commentators by effectively undercutting the methodological motivation for the semi-necessitarian reading. In addition to my defense on the interpretive front, then, my defense on the philosophical front provides supplementary reason to a fortiori favor the necessitarian reading of Spinoza. (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)

The paper addresses a question concerning George Ellis’s theory of top-down causation by considering a challenge to the “level-picture of nature” which he employs as a foundational element in his theory. According to the level-picture, nature is ordered by distinct and finitely many levels, each characterised by its own types of entities, relations, laws and principles of behavior, and causal relations to their respective neighbouring top- and bottom-level. The branching hierarchy that results from this picture enables Ellis to build (...) his model of modular hierarchical structure for complexity, his account of same-level, bottom-up and top-down causation, of emergence, equivalence-classes and multiple realisability. The three main arguments for the level-picture in Ellis’s works are reconstructed and shown to face serious problems. Finally, the paper presents a possible solution to this challenge by introducing a reformulation of certain fundamental points of Ellis’s theory that does without the level-picture of nature. This allows us to preserve all of his central claims about the model of complexity, the three types of causation, emergence, equivalence-classes and multiple realisability. Any problems pertaining to the level-picture can be remedied in the context of Ellis’s theory of top-down causation. (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)

A new series entitled Oxford Philosophical Concepts (OPC) made its debut in November 2014. As the series’ Editor Christia Mercer notes, this series is an attempt to respond to the call for and the tendency of many philosophers to invigorate the discipline. To that end each volume will rethink a central concept in the history of philosophy, e.g. efficient causation, health, evil, eternity, etc. “Each OPC volume is a history of its concept in that it tells a story about (...) changing solutions to specific philosophical problems” (xiii). The series presents itself as innovative along three main lines: its reexamination of the so-called “canon,” its reconsidering the value of interdisciplinary exchanges, and its encouraging philosophers to move beyond the current borders of philosophy. By engaging with non-Western traditions and carefully considering topics and materials which are not strictly philosophical, the collections from this series aim to render the history of philosophy accessible to a wide audience. -/- The first OPC volume to appear in print is “Efficient Causation – A History” edited by Tad Schmaltz. Using careful historical and philosophical analysis as well as interdisciplinary reflections this anthology proposes to tell the story of how efficient causation, equated nowadays with “causation” tout court, came to play its prominent role in our philosophical and scientific vocabulary. Eleven contributions cover the period from Ancient times (Aristotle and the Stoics), through the Middle Ages (both the Western and the Islamic traditions), passing through the Early Modern times (represented here by Descartes, Spinoza, Leibniz, Malebranche, Berkeley and Hume), all the way to Kant and finally contemporary philosophers (classified into two opposing camps: Humean and Neo-Aristotelian). There are also four reflections which explore the applications of the notion of efficient causation to areas different from philosophy, especially the arts (literature, music, painting, etc.). (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)

In this paper, I consider the implications of grief for philosophical theorising about absence experience. I argue that whilst some absence experiences that occur in grief might be explained by extant philosophical accounts of absence experience, others need different treatment. I propose that grieving subjects' descriptions of feeling as if the world seems empty or a part of them seems missing can be understood as referring to a distinctive type of absence experience. In these profound (...) class='Hi'>absence experiences, I will argue, the absence of a person as a condition on various possibilities is made manifest in the structure of experience over time. Thus, by paying close attention to grief, we can see that even accounts of absence experience that are presented as in competition with one another may not be so, and that to explain all kinds of absence experience we sometimes need to appeal to something overlooked in other accounts, and which is neither straightforwardly perceptual or cognitive. I also suggest that we would have good reason to take such experiences to be part of and not merely psychological effects of grief. (shrink)

It is widely thought that there is an important argument to be made that starts with premises taken from the science of physics and ends with the conclusion of physicalism. The standard view is that this argument takes the form of a causal argument for physicalism. Roughly: physics tells us that the physical realm is causally complete, and so minds (among other entities) must be physical if they are to interact with the world as we think they do. In what (...) follows, I raise problems for this view. After an initial review of the causal argument, I begin my case by showing that the totality of physical truths do not deductively entail the causal completeness of the physical realm, using a double-prevention scenario and causation by omission to show that nonphysical causes of physical effects would not need to violate physical conservation laws. I then move on to raise problems for an inductive argument for causal completeness by drawing on the neo-Russellian view that there is no causation in fundamental physics, and so causation must itself be a realized or derived entity. I conclude by suggesting that the underlying problem is that the causal argument has fallen out of touch with the sophisticated understanding that philosophers have developed of the role of causation within physics. (shrink)

A growing number of philosophers now hold that agent causation is required for agency, or free will, or moral responsibility. To clarify what is at issue, this paper begins with a distinction between agent causation that is ontologically fundamental and agent causation that is reducible to or realized in causation by events or states. It is widely accepted that agency presents us with the latter; the view in question claims a need for the former. The paper (...) then examines a “disappearing agent” argument from Derk Pereboom that is aimed at showing that free will requires agent causation that is ontologically fundamental. It is argued that the argument fails. Further, it is argued that, contrary to Pereboom’s claim, the issue raised by his disappearing agent argument is distinct from the problem of present luck that libertarian theories of free will face. The paper concludes with an assessment of the prospects for success of a disappearing agent argument showing that agent causation that is ontologically fundamental is required for agency tout court. (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)

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)

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.

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)

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)

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.

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)

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

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)

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)

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.

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)