This chapter focuses on one of the common fallacies in Western philosophy called 'proximate causation'. One commits this variety of causal fallacy when one mistakes the relevance of proximate causation. One mistakes the relevance of proximate causation when one thinks the fact that something is a proximate cause makes it irrelevant to the story of how the event in question happened. Mistaking the relevance of proximate causation can also “go the other (...) way”. That is, one can overinflate the importance of something being a proximate cause. This is often done by those looking to avoid responsibility for their actions. Matters of causation are never simple. And sometimes whether something is a proximate cause is relevant to the issue at hand. But we must be careful to make sure that we do not mistake its relevance. (shrink)

Many candidates have been tried out as proximate causes of actions: belief-desire pairs, volitions, motives, intentions, and other kinds of pro-attitudes. None of these mental states or events, however, seems to be able to do the trick, that is, to get things going. Each of them may occur without an appropriate action ensuing. After reviewing several attempts at closing the alleged “causal gap”, it is argued that on a correct analysis, there is no missing link waiting to be discovered. (...) On the counterfactual account of singular causation, the onset of belief or desire may perfectly well cause an action, although no kind of mental antecedent is ever a causally sufficient condition for a specific kind of action to occur. (shrink)

Direct Realists believe that perception involves direct awareness of an object not dependent for its existence on the perceiver. Howard Robinson rejects this doctrine in favour of a Sense-Datum theory of perception. His argument against Direct Realism invokes the principle ‘same proximate cause, same immediate effect’. Since there are cases in which direct awareness has the same proximate cerebral cause as awareness of a sense datum, the Direct Realist is, he thinks, obliged to deny this causal principle. I (...) suggest that although Direct Realism is in more than one respect implausible, it does not succumb to Robinson’s argument. The causal principle is true only if ‘proximate cause’ means ‘proximate sufficient cause’, and the Direct Realist need not concede that there is a sufficient cerebral cause for direct awareness of independent objects. (shrink)

Many candidates have been tried out as proximate causes of actions: belief-desire pairs, volitions, motives, intentions, and other kinds of pro-attitudes. None of these mental states or events, however, seems to be able to do the trick, that is, to get things going. Each of them may occur without an appropriate action ensuing. After reviewing several attempts at closing the alleged “causal gap”, it is argued that on a correct analysis, there is no missing link waiting to be discovered. (...) On the counterfactual account of singular causation, the onset of belief or desire may perfectly well cause an action, although no kind of mental antecedent is ever a causally sufficient condition for a specific kind of action to occur. [...]. (shrink)

Laland and colleagues have sought to challenge the proximate–ultimate distinction claiming that it imposes a unidirectional model of causation, is limited in its capacity to account for complex biological phenomena, and hinders progress in biology. In this article the core of their argument is critically analyzed. It is claimed that contrary to their claims Laland et al. rely upon the proximate–ultimate distinction to make their points and that their alternative conception of reciprocal causation refers to phenomena (...) that were already accounted for by standard theory. (shrink)

Made famous by Ernst Mayr (1961), the distinction between proximate and ultimate causation in biological explanation is widely seen as a key tenet of evolutionary theory and a central organizing principle for evolutionary research. The study of immediate, individual-level mechanistic causes of development or physiology (“proximate causation”) is distinguished from the study of historical, population-level statistical causes in evolutionary biology (“ultimate causation”). Since evolutionary developmental biology (evo-devo) is a field that explicitly uses so-called “proximate” (...) sciences such as developmental biology, morphology, and embryology in the study of evolution, it challenges the standard construal of the proximate-ultimate distinction and its associated account of causation. The exact nature of the challenge and its ramifications for the viability of the distinction more broadly are contested, but these conceptual questions are central to the status and significance of evo-devo in contemporary evolutionary biology. (shrink)

Ernst Mayr’s classical work on the nature of causation in biology has had a huge influence on biologists as well as philosophers. Although his distinction between proximate and ultimate causation recently came under criticism from those who emphasize the role of development in evolutionary processes, the formal relationship between these two notions remains elusive. Using causal graph theory, this paper offers a unified framework to systematically translate a given “proximate” causal structure into an “ultimate” evolutionary response, (...) and illustrates evolutionary implications of various kinds of causal mechanisms including epigenetic inheritance, maternal effects, and niche construction. These results not only reveal the essential interplay between proximate and ultimate causation in the study of evolution, but also provide a formal method to evaluate or discover non-standard or yet unknown evolutionary phenomena. (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.

In this article we argue that the classical—linear and bottom-up directed—models of causation in biology, and the ‘‘proximate/ultimate’’ dichotomy, are inappropriate to capture the complexity inherent to biological processes. We introduce a new notion of ‘‘multilevel causation’’ where old dichotomies such as proximate/ultimate and bottom-up/ top-down are reinterpreted within a multilevel, web-like, approach. In briefly reviewing some recent work on complexity, EvoDevo, carcinogenesis, autocatalysis, comparative genomics, animal regeneration, phenotypic plasticity, and niche construction, we will argue that (...) such reinterpretation is a necessary step for the advancement of the ‘‘Extended Synthesis.’’. (shrink)

The validity and utility of the proximate-ultimate distinction in biology have recently been under debate. Opponents of the distinction argue that it rules out individual-level organismic processes from evolutionary explanations, thereby leading to an unfounded separation between organismic causation and evolutionary causation. Proponents of the proximate-ultimate distinction, on the other hand, argue that it serves an important epistemological role in forming different kinds of explanation-seeking questions in biology. In this paper we offer an interpretation the (...) class='Hi'>proximate-ultimate distinction not only as a means of forming explanation-seeking questions, but also as a distinction that can help highlight the way in which individual-level organismic processes can be evolutionary causes. We do this by interpreting the distinction between proximate and ultimate causes as a distinction between structuring and triggering causes. (shrink)

Strong reciprocity has recently been subject to heated debate. In this debate, the “West camp” :231–262, 2011), which is critical of the case for SR, and the “Laland camp” :1512–1516, 2011, Biol Philos 28:719–745, 2013), which is sympathetic to the case of SR, seem to take diametrically opposed positions. The West camp criticizes advocates of SR for conflating proximate and ultimate causation. SR is said to be a proximate mechanism that is put forward by its advocates as (...) an ultimate explanation of human cooperation. The West camp thus accuses advocates of SR for not heeding Mayr’s original distinction between ultimate and proximate causation. The Laland camp praises advocates of SR for revising Mayr’s distinction. Advocates of SR are said to replace Mayr’s uni-directional view on the relation between ultimate and proximate causes by the bi-directional one of reciprocal causation. The paper argues that both the West camp and the Laland camp misrepresent what advocates of SR are up to. The West camp is right that SR is a proximate cause of human cooperation. But rather than putting forward SR as an ultimate explanation, as the West camp argues, advocates of SR believe that SR itself is in need of ultimate explanation. Advocates of SR tend to take gene-culture co-evolutionary theory as the correct meta-theoretical framework for advancing ultimate explanations of SR. Appearances notwithstanding, gene-culture coevolutionary theory does not imply Laland et al.’s notion of reciprocal causation. “Reciprocal causation” suggests that proximate and ultimate causes interact simultaneously, while advocates of SR assume that they interact sequentially. I end by arguing that the best way to understand the debate is by disambiguating Mayr’s ultimate-proximate distinction. I propose to reserve “ultimate” and “proximate” for different sorts of explanations, and to use other terms for distinguishing different kinds of causes and different parts of the total causal chain producing behavior. (shrink)

Extant research has shown that ordinary causal judgments are sensitive to normative factors. For instance, agents who violate a norm are standardly deemed more causal than norm-conforming agents in identical situations. In this paper, we explore two competing explanations for the Norm Effect: the Responsibility View and the Bias View. According to the former, the Norm Effect arises because ordinary causal judgment is intimately intertwined with moral responsibility. According to the alternative view, the Norm Effect is the result of a (...) blame-driven bias. In a series of five preregistered experiments (N = 2688), we present evidence that predominantly favours the Bias View. In particular, and against predictions made by the Responsibility View, we show that participants deem agents who violate nonpertinent or silly norms – norms that do not relate to the outcome at hand – as more causal, and that this effect cannot be explained in terms of plausible mediators such as the agent’s foreknowledge and desire, or the foreseeability of harm. We close with a discussion regarding the implications of these findings, in as regards the just assessment of proximate cause in the law. (shrink)

Deciding matters of legal liability, in torts and other civil actions, requires deciding causation. The injury suffered by a plaintiff must be caused by an event or condition due to the defendant. The courts distinguish between cause-in-fact and proximate causation, where cause-in-fact is determined by the “but-for” test: the effect would not have happened, “but for” the cause.1 Proximate causation is a set of legal limitations on cause-in-fact.

Conscious experience has been said to be outside of, or alien to, physics, and unexplained in a physical world. However, it is argued here that experience is entirely expected in a physical world that can only be defined by its power to determine patterns of experience. Something physical is something with the type of causal power that can contribute to determining the content of an experience if a subject is present at the right place and time. Physical powers also interact (...) with other physical powers, distant from any given subject, to form chains, and it is these interactions that physics handles mathematically. Nevertheless, actual causation is always defined by reference to determination of experience. The apparent puzzle of why there should be a link between experience and the physical may relate in part to the fact that experience is always immediately causally proximal, always 'here and now', at least as far as we can ascertain. Proximality, and with it the potential for mentality, cuts across existential/ ontological categories. Experience also requires a concept of an intrinsic individual, in order for there to be individual points of view. The practical problem for consciousness studies is to identify intrinsically individual causal units with event domains in human brains, that can have points of view and content that could fit with human experiences, in a way consistent with current physics. It is suggested that the 'causal diamond' concept of the here and now explored by Savitt (2015) and Arthur (2019), together with principles of field theory, may provide a useful starting point. (shrink)

Despite the productivity of basic cancer research, cancer continues to be a health burden to society because this research has not yielded corresponding clinical applications. Many proposed solutions to this dilemma have revolved around implementing organizational and policy changes related to cancer research. Here I argue for a different solution: a new conceptualization of causation in cancer. Neither the standard molecular biomarker approaches nor evolutionary biology approaches to cancer fully capture its complex causal dynamics, even when considered jointly. These (...) approaches map on to Ernst Mayr’s proximate–ultimate distinction, which is an inadequate conceptualization of causation in biological systems and makes it difficult to connect developmental and evolutionary viewpoints. I propose looking to evolutionary developmental biology to overcome the distinction and integrate the proximate and ultimate causal frameworks. I use the concepts of modularity and evolvability to show how an EvoDevo perspective can be manifested in cancer translational research. This perspective on causation in cancer is better suited for integrating the complexity of current empirical results and can facilitate novel developments in the investigation and clinical treatment of cancer. (shrink)

This paper sets out to analyze how causation works by focusing on biology, as represented by epidemiology and by scientific information on how the body works (“physiology”). It starts by exploring the specificity of evolved physiological systems, in which evolutionary, developmental and proximal causes all fit together, and the concept of function is meaningful; in contrast, this structure does not apply in epidemiology (or outside biology). Using these two contrasting branches of biology, I examine the role both of mechanism (...) and of difference making in causation. I find that causation necessarily involves both mechanism and difference making, and that they play complementary roles. Both are seen as ontologically necessary, even if the evidence is not always available for both. Influential monist accounts that focus on one of these, at the expense of ignoring the other, are found to be inadequate on these and on other grounds. Recent attempts to combine them are reviewed, notably that of Russo and Williamson (Int Stud Philos Sci 21:157–170, 2007), and it is argued that their epistemic view requires there to be a source of the different types of evidence that a rational agent would consider, and that this source must be ontic. I then analyze how causal relationships work in evolved physiological systems and in those studied by epidemiology, with a particular focus on how mechanism interacts with input. Finally, I consider this concept of causation from the perspective of everyday language, and of its possible generalisability outside biology. (shrink)

Like Laland et al., I think Mayr’s distinction is problematic, but I identify a further problem with it. I argue that Mayr’s distinction is a false dichotomy, and obscures an important question about evolutionary change. I show how this question, once revealed, sheds light on some debates in evo-devo that Laland et al.’s analysis cannot, and suggest that it provides a different view about how future integration between biological disciplines might proceed.

Not a day passes over society where the immediate expressions of violence are not widely propagated and subsequently witnessed through cultural or political mediums. Such depictions, accounts, scenes, have been uniquely framed as a lexis of ‘subjective violence’; reactions or evident illustrations of descent in physical form. Amidst their over-representation is a lapse of measured attention given to the pretext amounting to said outbursts. Seldom is the objective, if at all, contextualized as a catalytic toward the subjective. The following work (...) suggests that a violence exists amidst society that goes substantively under-analyzed thereby negating an ability to specifically address and, therefore, challenge its causality. While recognizing the importance of such research, a movement beyond affectual approaches of theorizing violence is needed through a complimentarily mapping of how distal relations of power influence, impact, and sustain enmity. What makes this discussion further dynamic is the ironic transparency of causation. Rather than a phenomenon of concealment, conventional dynamics of authority and influence exert control through, what could be argued to be, an invisibility of visibility. Supporting an addendum to theorizing violence may, then, enable a more holistic recognition that can assist an articulate response toward both subjective and objective expressions of violence. (shrink)

Sir Austin Bradford Hill’s ‘aspects of causation’ represent some of the most influential thoughts on the subject of proximate causation in health and disease. Hill compiled a list of features that, when present and known, indicate an increasing likelihood that exposure to a factor causes—or contributes to the causation of—a disease. The items of Hill’s list were not labelled ‘criteria’, as this would have inferred every item being necessary for causation. Hence, criteria that are necessary (...) for causation in health, disease and intervention processes, whether known, knowable, or not, remain undetermined and deserve exploration. To move beyond this position, this paper aims to explore factors that are necessary in the constitution of causative relationships between health, disease processes, and intervention. To this end, disease is viewed as a causative pathway through the often overlapping stages of aetiology, pathology and patho-physiology. Intervention is viewed as a second, independent causative pathway, capable of causing changes in health for benefit or harm. For the natural course of a disease pathway to change, we argue that intervention must not only occupy the same time and space, but must also share a common form; the point at which the two pathways converge and interact. This improved conceptualisation may be used to facilitate the interpretation of clinical observations and inform future research, particularly enabling predictions of the mechanistic relationship between health, disease and intervention. (shrink)

In “A Theory of Content, 11: The Theory,” Jerry Fodor presents two reasons why his asymmetric causal dependency theory does not lead to the conclusion that syntactic items “X” mean proximal sensory stimulations, rather than distal environmental objects. Here we challenge Fodor’s reasoning.

Theories of legal causation that identify the concept with probability‐raising generate false positives where the defendant's conduct raises the probability of harm but brings about that harm in the wrong kind of way. Moreover, what the law seeks to deter is not conduct that raises the probability of harm, but rather conduct that is dangerous. A legal or proximate cause is one that harms the plaintiff through the causal mechanism that sustains the lawful generalization that the defendant's conduct (...) was dangerous. (shrink)

We are grateful to the commentators for taking the time to respond to our article. Too many interesting and important points have been raised for us to tackle them all in this response, and so in the below we have sought to draw out the major themes. These include problems with both the term ‘ultimate causation’ and the proximate-ultimate causation dichotomy more generally, clarification of the meaning of reciprocal causation, discussion of issues related to the nature (...) of development and phenotypic plasticity and their roles in evolution, and consideration of the need for an extended evolutionary synthesis. (shrink)

Anorexia nervosa remains an enigma among Western cultures. Various causal explanations have been offered, encompassing biological, psychological, and sociocultural models. These explanations, however, focus on the immediate or proximal mechanisms of causation. A more thorough understanding of anorexia nervosa can be achieved by understanding the relationship between these factors and ultimate causation, the level of explanation which deals with individual reproductive fitness. This paper reviews the biological, psychological, sociocultural, and evolutionary models and indicates a necessary synthesis between (...) class='Hi'>proximate and ultimate levels of causation in examining the anorexia nervosa puzzle. (shrink)

In a laboratory experiment, we use a public goods game to examine the hypothesis that human subjects use an involuntary eye-detector mechanism for evaluating the level of privacy. Half of our subjects are “watched” by images of a robot presented on their computer screen. The robot—named Kismet and invented at MIT—is constructed from objects that are obviously not human with the exception of its eyes. In our experiment, Kismet produces a significant difference in behavior that is not consistent with existing (...) economic models of preferences, either self- or other-regarding. Subjects who are “watched” by Kismet contribute 29% more to the public good than do subjects in the same setting without Kismet. (shrink)

The Royal College of Physicians of London published the 2013 national clinical guidelines on prolonged disorders of consciousness in vegetative and minimally conscious states. The guidelines acknowledge the rapidly advancing neuroscientific research and evolving therapeutic modalities in PDOC. However, the guidelines state that end-of-life decisions should be made for patients who do not improve with neurorehabilitation within a finite period, and they recommend withdrawal of clinically assisted nutrition and hydration . This withdrawal is deemed necessary because patients in PDOC can (...) survive for years with continuation of CANH, even when a ceiling on medical care has been imposed, i.e., withholding new treatment such as cardiopulmonary resuscitation for acute life-threatening illness. The end-of-life care pathway is centered on a staged escalation of medications, including sedatives, opioids, barbiturates, and general anesthesia, concurrent with withdrawal of CANH. Agitation and distress may last from several days to weeks because of the slow dying process from starvation and dehydration. The potential problems of this end-of-life care pathway are similar to those of the Liverpool Care Pathway. After an independent review in 2013, the Department of Health discontinued the Liverpool Care pathway in England. The guidelines assert that clinicians, supported by court decisions, have become the final authority in nonconsensual withdrawal of CANH on the basis of “best interests” rationale. We posit that these guidelines lack high-quality evidence supporting: 1) treatment futility of CANH, 2) reliability of distress assessment from starvation and dehydration, 3) efficacy of pharmacologic control of this distress, and 4) proximate causation of death. Finally, we express concerns about the utilitarian-based assessment of what constitutes a person’s best interests. We are disturbed by the level and the role of medical authoritarianism institutionalized by these national guidelines when deciding on the worthiness of life in PDOC. We conclude that these guidelines are not only harmful to patients and families, but they represent the means of nonconsensual euthanasia. The latter would constitute a gross violation of the public’s trust in the integrity of the medical profession. (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)

A biological function is supposed to be performed adequately, and hence may fail to do so: this is dysfunction. This raises two questions. One is how to make explicit the way in which function can be discriminated from dysfunction without confusing dysfunction with non-function. The second question is how what is “right” and “wrong” can be legitimated by natural regulatory norms. A function can be viewed as a quality to which at least one variable with a definite set of values (...) is associated. Accordingly, function and dysfunction are the same quality of the same trait, but differ in the values associated to this variable. Dysfunction occurs when the associated set of values does not match this normal state. Biological systems have the epistemic singularity that their existence is the consequence of two distinct causal regimes, the so-called “proximate” and “ultimate” causes, whose convergence defines a system’s prescriptive normality. Each cause imposes restrictive rules that limit the possible ways these systems can putatively exist. When a system is insensitive to ultimate cause, it is determined by proximate causation alone, and hence escapes its own prescriptive norms. In conclusion: The normality of a biological system is defined by the convergence of proximate and ultimate causes. A function is a variable-associated quality whose values are defined relative to the norms of the system. Dysfunction occurs when the set of values of the same variable does not match the normality of the system, which can occur when the system is insensitive to ultimate causation. (shrink)

In the succession of states of consciousness that constitute James’s stream of consciousness, there occur, among others, states of consciousness that are themselves, or that include, perceptual mental acts. It is assumed some of the latter states of consciousness are purely perceptual, lacking both imaginal and signitive contents. According to Husserl, purely perceptual acts present to consciousness, uniquely, their environmental objects in themselves, in person. They do not present, as imaginal mental acts do, an image or other representation of their (...) object. Husserl’s theory resembles Gibson’s with respect to perception’s being direct. Both theorists hold perceptual awareness of the environment is not a "founded" act; its proximate causation does not involve any other mental act. Both theorists contend that perceptual acts keep the perceiver directly in touch with the surrounding environment. The present article considers Husserl’s account of this directness. Although this account has problems, and is largely phenomenological description, it may help psychologists to find their way to an adequate account of the objects of perceptual consciousness — perhaps if it is integrated with Gibson’s perception theory, as I will attempt in a sequel to which this article is introductory. Husserl seeks to provide the phenomenological side of the story, Gibson the stimulus-informational side. (shrink)

Perhaps more than any other scholar, Michael Moore has argued that there are deep and necessary connections between metaphysics, morality, and law. Moore has developed every contour of a theory of criminal law, from philosophy of action to a theory of causation. Indeed, not only is he the central figure in retributive punishment but his moral realist position places him at the center of many jurisprudential debates. Comprised of essays by leading scholars, this volume discusses and challenges the work (...) of Michael Moore from one or more of the areas where he has made a lasting contribution, namely, law, morality, metaphysics, psychiatry, and neuroscience. The volume begins with a riveting contribution by Heidi Hurd, wherein she takes an unadorned and unabashed look at the man behind this monumental body of work, full of both triumphs and sadness. A number of essays focus on Moore's view of the purpose and justification of the criminal law, specifically his endorsement of retributivism and legal moralism. The book then addresses Moore's work in the various aspects of the general part of the criminal law, including Moore's position on how to understand criminal acts for double jeopardy purposes, Moore's claim that accomplice liability is superfluous, and Moore's views about the culpability of negligence, as well as the relationship between that view and proximate causation. Furthermore, the subject of defenses in criminal law is addressed, including self-defense, and also the intersection of psychiatry, psychology, cognitive neuroscience, and the criminal law. Also discussed are features of morality, and Moore's work in general jurisprudence. Finally, Moore concludes the volume with an essay that defends and delineates the features of his views. (shrink)

To explain the menstrual cycle and menopause, human biologists during the past several decades have developed new models of the evolutionary origins and maintenance of female reproductive patterns that address both ultimate and proximate causation. Hypotheses proposed for these processes generally offer explanations for menstruation or for menopause, but not for both; ultimately, these explanations must be integrated. Reviewing current explanations, this paper offers an energetics-based evolutionary rationale compatible with past adaptations of Homo sapiens and with ecological patterns (...) in small-scale, preindustrial social systems in which food resources vary and sometimes are scarce. (shrink)

IntroductionE.J. LOWE: Event Causation and Agent CausationRalf STOECKER: Agents in ActionGeert KEIL: How Do We Ever Get Up? On the Proximate Causation of Actions and EventsMaria ALVAREZ: Letting Happen, Omissions, and CausationFrederick STOUTLAND: Responsive Action and the Belief-Desire ModelMarco IORIO: How Are Agents Related to Their Actions? The Existentialist ResponseJens KULENKAMPFF: What Oedipus Did When He Married Jocasta or What Ancient Tragedy Tells Us About Agents, Their Actions, and the WorldRüdiger BITTNER: Agents as RulersMonika BETZLER: How Can (...) an Agent Rationally Guide His Actions?Martina HERRMANN: Competence, Options, and RelationsWeitere Abhandlungen/Further ArticlesEduardo FERMANDOIS: Kommunikation ohne Sprache? Zu Davidsons später SprachphilosophieGuido IMAGUIRE: Die Form der Externalität in Russells An Essay on the Foundations of Geometry und die Ursprünge seiner RelationstheorieBuch-Symposium/Book-SymposiumJohn BICKLE: Precis of Psychoneural Reduction: The New WaveAnsgar BECKERMANN: Physicalism and New Wave ReductionismJ. Christopher MALONEY: Reservations about New Wave ReductionAchim STEPHAN: How to Lose the Mind-Body ProblemJohn BICKLE: New Wave Metascience. Replies to Beckermann, Maloney, and StephanBuchnotizen/Critical NotesEingesandte Bücher/Books Received. (shrink)

Evolution never stops. Stress is often a manifestation of competition which seems to drive human gene-culture coevolution. A popular, Dutch account on evolution in everyday life. People often claim that we are thoroughly cultural beings, but culture is based on a series of talents which are a product of directional and stabilizing selection. Culture also presupposes certain psychological characteristics. People adopt and change culture to fit their biopsychological needs.

L’objet de la présente recherche est d’interroger les mérites de la théorie utilitariste relative aux faillites personnelles, qui est dominante dans la littérature juridique depuis que le courant Law and Economics a gagné en importance. Nous démontrons que l’argumentation utilitariste, qui est assignée aux doctrines de l’acquittement des dettes personnelles par les spécialistes de Law and Economics travaillant dans le domaine du droit des faillites, soulève des questions normatives de taille et créée des tensions quand il s’agit de décrire le (...) phénomène. Ces deux problèmes invitent les théoriciens à proposer des modèles alternatifs pour décrire les conditions dans lesquelles nos systèmes juridiques soulagent les dettes des individus qui ne sont pas en mesure de les honorer. Dans notre ouvrage à paraître, The Virtue of Bankruptcy, nous embrassons ce projet. Ici, nous proposons une étape préliminaire à ce projet plus ambitieux en démontrant que les théories utilitaristes sur lesquelles s’appuient les contributions les plus importantes de la littérature sur la question à ce jour sont perfectibles lorsqu’il s’agit de comprendre les raisons et les circonstances dans lesquelles il est possible d’offrir un nouveau départ à ceux qui n’ont pas respecté leurs obligations financières. (shrink)

ABSTRACT: A systematic reconstruction of Chrysippus’ theory of causes, grounded on the Stoic tenets that causes are bodies, that they are relative, and that all causation can ultimately be traced back to the one ‘active principle’ which pervades all things. I argue that Chrysippus neither developed a finished taxonomy of causes, nor intended to do so, and that he did not have a set of technical terms for mutually exclusive classes of causes. Rather, the various adjectives which he used (...) for causes had the function of describing or explaining particular features of certain causes in particular philosophical contexts. I challenge the sometimes assumed close connection of Chrysippus’ notion of causation with explanation. I show that the standard view that the distinction between proximate and auxiliary causes and perfect and principal causes corresponds to the distinction between internal and external determining factors is not born out by the evidence, and argue that causes of the two types were not thought to co-operate, but rather conceived of as alternatives. (shrink)

This paper brings together the Sarvāstivāda (a major school of Abhidharma Buddhism) and Miller's (2019) moving spotlight theory to see how presentness is explained in terms of causation. The paper argues that a causal theory of presentness like Miller's encounters a dilemma: causation is either synchronic or diachronic, but neither is safe in the presence of the challenges. On the one hand, if causation is synchronic, how does a causal chain extend over time so that the wave (...) of causation (and hence the spotlight) can move at all? On the other, if causation is diachronic, then a present moment has a temporal extension enough to accommodate a cause and its proximate effect. The paper proposes a synchronic notion of causation that counters the first challenge. This can be done by bringing together the Sarvāstivādin grasp‐production model of causation, some Stoic ideas about causation, and some Armstrong's metaphysics. (shrink)

In 1990 Robert Lickliter and Thomas Berry identified the phylogeny fallacy, an empirically untenable dichotomy between proximate and evolutionary causation, which locates proximate causes in the decoding of ‘ genetic programs’, and evolutionary causes in the historical events that shaped these programs. More recently, Lickliter and Hunter Honeycutt argued that Evolutionary Psychologists commit this fallacy, and they proposed an alternative research program for evolutionary psychology. For these authors the phylogeny fallacy is the proximate/evolutionary distinction itself, which (...) they argue constitutes a misunderstanding of development, and its role in the evolutionary process. In this article I argue that the phylogeny fallacy should be relocated to an error of reasoning that this causal framework sustains: the conflation of proximate and evolutionary explanation. Having identified this empirically neutral form of the phylogeny fallacy, I identify its mirror image, the ontogeny fallacy. Through the lens of these fallacies I attempt to solve several outstanding problems in the debate that ensued from Lickliter and Honeycutt’s provocative article. (shrink)

I propose an Aristotelian approach to agent causation that is consistent with the hypothesis of strong emergence. This approach motivates a wider ontology than materialism by maintaining (1) that the agent is generated by the brain without being reducible to it on grounds of the unity of experience and (2) that the agent possesses (formal) causal power to affect (i.e., mold, sculpt, or organize) the brain on grounds of agent-directed neuroplasticity. After providing recent empirical evidence for the strong emergence (...) of the agent, I then articulate and analyze a dominant objection to agent causation discussed in neuroscience, which is based upon the observation of the readiness potential (or RP) in the brain. In this context, the RP refers to unconscious neuronal events (in the supplementary motor area) that precede the formation of a (proximal) conscious intention to act. So it appears as if the train of neuronal events has left the depot before the agent can act. In response to this objection, I argue (a) that even if one were to grant that the RP precedes the formation of a conscious intention, it would not follow (on both logical and empirical grounds) that there is no conscious agent causation; and (b) that the objection disappears when one takes into account distal versus proximal intentions. (shrink)

My understanding is that proximate explanations concern adaptive mechanism and that ultimate explanations concern adaptive rationale. Viewed in this light, the two kinds of explanation are quite distinct, but they interact in a complementary way to give a full understanding of biological adaptations. In contrast, Laland et al. (2013)—following a literal reading of Mayr (Science 134:1501–1506, 1961)—have characterized ultimate explanations as concerning any and all mechanisms that have operated over the course of an organism’s evolutionary history. This has unfortunate (...) consequences, such as allowing random drift to form the basis for ultimate explanations, and allowing proximate and ultimate explanations to bleed into each other until their distinction is meaningless. Here, I suggest Laland et al’s explanatory framework of “reciprocal causation” is not conducive to successful biological science, and that they have misunderstood key elements of the theory of Darwinian adaptation. (shrink)

Evolutionary psychology is a science in the making, working toward the goal of showing how psychological adaptation underlies much human behavior. The knee-jerk reaction that sociobiology is unscientific because it tells just-so stories has become a common charge against evolutionary psychology as well. My main positive thesis is that inference to the best explanation is a proper method for evolutionary analyses, and it supplies a new perspective on the issues raised in Schlinger's (1996) just-so story critique. My main negative thesis (...) is that, like many nonevolutionist critics, Schlinger's objections arise from misunderstandings of the evolutionary approach.Evolutionary psychology has progressed beyond telling just-so stories. It has found a host of ingenious special techniques to test hypotheses about the adaptive significance and proximate mechanisms of behavior. Naturalistic data using the comparative method combined with controlled tests using statistical analyses of data provide good evidence for a variety of hypotheses about behavioral control mechanisms — whether in nonhumans or in humans. For instance, the work of Gangestad and Thornhill on evolved mate preferences and fluctuating asymmetry of body type (FA) is a model of success. As the quantity and quality of evidence increase, we are entitled not just to regard such evolutionary hypotheses as preferable, but also as true. Such studies combine to show that the best explanation of the psychic unity of humankind — common patterns across societies, history, and cultures exposed by evolutionists — is the gendered, adapted, evolved species-typical design of the mind. (shrink)

Since the ENCODE project published its final results in a series of articles in 2012, there is no consensus on what its implications are. ENCODE’s central and most controversial claim was that there is essentially no junk DNA: most sections of the human genome believed to be «junk» are functional. This claim was met with many reservations. If researchers disagree about whether there is junk DNA, they have first to agree on a concept of function and how function, given a (...) particular definition, can be discovered. The ENCODE debate centered on a notion of function that assumes a strong dichotomy between evolutionary and non-evolutionary function and causes, prevalent in the Modern Evolutionary Synthesis. In contrast to how the debate is typically portrayed, both sides share a commitment to this distinction. This distinction is, however, much debated in alternative approaches to evolutionary theory, such as the EES. We show that because the ENCODE debate is grounded in a particular notion of function, it is unclear how it connects to broader debates about what is the correct evolutionary frame- work. Furthermore, we show how arguments brought forward in the controversy, particularly arguments from mathematical population genetics, are deeply embedded in their particular disciplinary contexts, and reflect substantive assumptions about the evolution of genomes. With this article, we aim to provide an anatomy of the ENCODE debate that offers a new perspective on the notions of function both sides employed, as well as to situate the ENCODE debate within wider debates regarding the forces operating in evolution. (shrink)

In 1961, Ernst Mayr published a highly influential article on the nature of causation in biology, in which he distinguished between proximate and ultimate causes. Mayr argued that proximate causes (e.g. physiological factors) and ultimate causes (e.g. natural selection) addressed distinct ‘how’ and ‘why’ questions and were not competing alternatives. That distinction retains explanatory value today. However, the adoption of Mayr’s heuristic led to the widespread belief that ontogenetic processes are irrelevant to evolutionary questions, a belief that (...) has (1) hindered progress within evolutionary biology, (2) forged divisions between evolutionary biology and adjacent disciplines and (3) obstructed several contemporary debates in biology. Here we expand on our earlier (Laland et al. in Science 334:1512–1516, 2011) argument that Mayr’s dichotomous formulation has now run its useful course, and that evolutionary biology would be better served by a concept of reciprocal causation, in which causation is perceived to cycle through biological systems recursively. We further suggest that a newer evolutionary synthesis is unlikely to emerge without this change in thinking about causation. (shrink)

According to the conventional view, causal and moral responsibility have a strict hierarchical relationship. Determining causal responsibility comes first; then we sort through the factors to which we have assigned causal responsibility and determine which, if any, should be assigned moral responsibility too. Moral inquiry accordingly stands not only apart but also above causal inquiry. But I am going to argue that this way of looking at causal and moral responsibility is a mistake. Rather than being separate and independent inquires (...) with different purposes and concerns, I am going to argue that finding causal responsibility actually entails finding moral responsibility even when there is no evidence of what we would call traditional fault. Indeed, I am going to argue we cannot find someone causally responsible without finding them morally responsible too. (shrink)

ABSTRACT The difference between perception and cognition seems introspectively obvious in many cases. Perceiving and thinking have also been assigned quite different roles, in epistemology, in theories of reference and of mental content, in philosophy of psychology, and elsewhere. Yet what is the nature of the distinction? In what way, or ways, do perception and cognition differ? The paper reviews recent work on these questions. Four main respects in which perception and cognition have been held to differ are discussed. First, (...) their phenomenal character, such as the often-remarked vivacity or immediacy of perception. Second, the way in which they represent the world, e.g. the non-propositional nature of the contents, or non-discursive character of the vehicles, that have been held to characterise perceptual representation. Third, their place in cognitive architecture, i.e., roughly, in the information-flow of the mind, such as their alleged (non-)modularity. Fourth, their mind-world relations, e.g. the way in which perceptions seem to be tightly causally linked with distal or proximal stimuli. Against this background, we distinguish some main options for an account of the perception/cognition distinction, in particular concerning whether there is one, several, or no interesting and principled distinction(s) to be drawn here. (shrink)

Eating disorders are evolutionarily novel conditions that lead to some of the highest mortality rates of all psychiatric disorders. Several evolutionary hypotheses have been proposed for eating disorders, but only the intrasexual competition hypothesis is extensively supported by evidence. We present the mismatch hypothesis as a necessary extension to the current theoretical framework of eating disorders. This hypothesis explains the evolutionarily novel adaptive metaproblem that has arisen when mating motives and readily available food rewards conflict with one another. This situation (...) is exacerbated in contemporary environments characterized by sedentary lifestyles, caloric surplus and the ubiquity of social comparisons that take place via social media. Our psychoneuroimmunological model connects ultimate-level causation with proximate mechanisms by showing how the adaptive metaproblem between mating motives and food rewards leads to chronic stress and, further, to disordered eating. Chronic stress causes neuroinflammation, which increases susceptibility to OCD-like behaviors that typically co-occur with eating disorders. Chronic stress upregulates the serotonergic system and causes dysphoric mood in patients with restricting-type anorexia nervosa. Dieting, however, reduces serotonin levels and dysphoric mood, leading to a vicious serotonergic-homeostatic stress/starvation cycle whereby cortisol and neuroinflammation increase through stringent dieting. Between-individual and within-individual variation in eating disorders partially arises from (co)variation in gut microbiota and stress responsivity, which influence neuroinflammation and the serotonergic system. In binge-related eating disorders, even a short period of fasting drops serotonin levels, a state alleviated by binge eating. Eating disorder treatments should aim to reduce the chronic stress, neuroinflammation, stress responsivity and gut dysbiosis that fuel the disorders. We review the advances that have been made in recent years in understanding how to best treat eating disorders, outlining directions for future clinical research. Connecting ultimate causes with proximate mechanisms and treating biopsychosocial causes rather than manifest symptoms will enable more effective and sophisticated long-term interventions for the millions of people who suffer from eating disorders. (shrink)