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)

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)

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)

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)

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)

The explanatory role of natural selection is one of the long-term debates in evolutionary biology. Nevertheless, the consensus has been slippery because conceptual confusions and the absence of a unified, formal causal model that integrates different explanatory scopes of natural selection. In this study we attempt to examine two questions: (i) What can the theory of natural selection explain? and (ii) Is there a causal or explanatory model that integrates all natural selection explananda? For the first question, we argue (...) that five explananda have been assigned to the theory of natural selection and that four of them may be actually considered explananda of natural selection. For the second question, we claim that a probabilistic conception of causality and the statistical relevance concept of explanation are both good models for understanding the explanatory role of natural selection. We review the biological and philosophical disputes about the explanatory role of natural selection and formalize some explananda in probabilistic terms using classical results from population genetics. Most of these explananda have been discussed in philosophical terms but some of them have been mixed up and confused. We analyze and set the limits of these problems. (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)

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)

Functionalist theories have been proposed for just about everything: mental states, dispositions, moral properties, truth, causation, and much else. The time has come for a functionalist theory of nothing. Or, more accurately, a role functionalist theory of those absences that are causes and effects.

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)

Much contemporary debate on the nature of mechanisms centers on the issue of modulating negative causes. One type of negative causability, which I refer to as “causation by absence,” appears difficult to incorporate into modern accounts of mechanistic explanation. This paper argues that a recent attempt to resolve this problem, proposed by Benjamin Barros, requires improvement as it overlooks the fact that not all absences qualify as sources of mechanism failure. I suggest that there are a number of (...) additional types of effects caused by absences that need to be incorporated to account for the diversity of causal connections in the biological sciences. Furthermore, it is argued that recognizing natural variability in mechanisms, such as attenuation, leads to some interesting line-drawing issues for contemporary philosophy of mechanisms. (shrink)

The purpose of this research is to articulate how a theory of causation might be serviceable to a theory of sport. This article makes conceptual links between Bernard Suits’ theory of game-playing, causation, and theories of causation. It justifies theories of causation while drawing on connections between sport and counterfactuals. It articulates the value of theories of causation while emphasizing possible limitations. A singularist theory of causation is found to be more broadly serviceable with (...) particular regard to its analysis of sports. (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)

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)

“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)

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)

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)

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.

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)

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)

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)

Origin of a dissipative structure in a chemical dynamic system: occurs under the following constraints: 1) Affinity must be high. (The system must be far from equilibrium.); 2) There must be an auto-catalytic process; 3) A process that reduces the concentration of the auto-catalyst must operate; 4) The relevant parameters (rate constants, etc.) must lie in a range corresponding to a limit cycle trajectory. That is, there must be closure of the network of reaction such that a state sufficiently close (...) to the prior condition is achieved at the corresponding part of each oscillation. If these constraints continue to be met interactions of the system with the rest of the world are quite different in the presence of the dissipative structure than they would be in the absence of that self-organized coherence. Closure of a network of relationships which gives rise to a dissipative structure is a 'unit-determining' feature. The effects of the structure as a whole are the resultants of the effects of the components, but the concentrations of the components at any instant are effects of the closure of the limit cycle. This is an influence on components arising from what those components constitute --- downward causation. (shrink)

Some recent accounts of constitutive relevance have identified mechanism components with entities that are causal intermediaries between the input and output of a mechanism. I argue that on such accounts there is no distinctive inter-level form of mechanistic explanation and that this highlights an absence in the literature of a compelling argument that there are such explanations. Nevertheless, the entities that these accounts call ‘components’ do play an explanatory role. Studying causal intermediaries linking variables Xand Y provides knowledge of (...) the counterfactual conditions under which X will continue to bring about Y. This explanatory role does not depend on whether intermediate variables count as components. The question of whether there are distinctively mechanistic explanations remains open. (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 “Causality and Determination”, Anscombe stressed that, in her view, physical determinism and free action were incompatible. As the relevant passage suggests, her espousal of incompatibilism was not merely due to specific features of human ‘ethical’ freedom, but due to general features of agency, intentionality, and voluntariness. For Anscombe went on to tentatively suggest that lack of physical determination was required for the intentional conduct of animals we would not classify as ‚free‘, too. In this paper, I examine three different (...) lines of argument to establish Anscombe’s latter suggestion, which are based on general considerations about the causal efficacy of psychological-agential phenomena, the nature of agency, and the specific features of intentional agency. I start with Anscombe’s own claim from “The Causation of Action” that microphysical determinism would make psychological and personal phenomena epiphenomenal, before I turn to the view of ‘Agency Incompatibilism’, that genuine agency requires the absence of antecedent necessitation, and, lastly, to concerns about some crucial features of intentional agency which we find in both human and animal agents. (shrink)

The idea that time does not exist is, for many, unthinkable: time must exist. Almost every experience we have tells us so. There has been plenty of debate around what time is like, but not whether it exists. The goal of this book is to make the absence of time thinkable. Time might not exist. Beginning with an empirically flavoured examination of the 'folk' concept of time, the book explores the implications this has for our understanding of agency, and (...) the extent to which our best physics and best metaphysics are compatible with a timeless conception of reality. (shrink)

Davidson's anomalous monism, his argument for the identity between mental and physical event tokens, has been frequently attacked, usually demanding a higher degree of physicalist commitment. My objection runs in the opposite direction: the identities inferred by Davidson from mental causation, the nomological character of causality and the anomaly of the mental are philosophically problematic and, more dramatically, incompatible with his famous argument against the third dogma of empiricism, the separation of content from conceptual scheme. Given the anomaly of (...) the mental and the absence of psychophysical laws, there are no conceptual resources to relate mental and physical predicates. We fall in the third dogma if we claim that the very same token event is mental and physical. One of the premises must be rejected: I will claim that we do not need a law to subsume cause and effect to be entitled to speak of causation. Davidson has never offered an argument to back this premise. Against such a dogma I will sketch some ideas pointing towards a different conception of causality, singularist and undetachable from explanatory practices. (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)

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)

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)

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)

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)

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

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

This paper explores the prospects of employing a functional approach in order to improve our concept of actual causation. Claims of actual causation play an important role for a variety of purposes. In particular, they are relevant for identifying suitable targets for intervention, and they are relevant for our practices of ascribing responsibility. I argue that this gives rise to the challenge of purpose. The challenge of purpose arises when different goals demand adjustments of the concept that pull (...) in opposing directions. More specifically, I argue that a common distinction between certain kinds of preempted and preempting factors is difficult to motivate from an interventionist viewpoint. This indicates that an appropriately revised concept of actual causation would not distinguish between these two kinds of factors. From the viewpoint of retributivist responsibility, however, the distinction between preempted and preempting factors sometimes is important, which indicates that the distinction should be retained. (shrink)

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

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

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)

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

The 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)

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

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)

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

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

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)

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)

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)

Disputes about the causal structure of natural selection have implications for teleosemantics. Etiological, mainstream teleosemantics is based on a causalist view of natural selection. The core of its solution to Brentano’s Problem lies in the solution to Kant’s Puzzle provided by the Modern Synthesis concerning populational causation. In this paper, I suggest that if we adopt an alternative, statisticalist view on natural selection, the door is open for two reflections. First, it allows for setting different challenges to etiological teleosemantics (...) that arise if a statisticalist reading of natural selection is right. Second, by providing a different solution to Kant’s Puzzle based on individual causes of evolution, statisticalism promotes a different answer to Brentano’s Problem, what I label as Agential Teleosemantics. (shrink)

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

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