Efforts to bridge emotion theory with neurobiology can be facilitated by dynamic systems (DS) modeling. DS principles stipulate higher-order wholes emerging from lower-order constituents through bidirectional causal processes cognition relations. I then present a psychological model based on this reconceptualization, identifying trigger, self-amplification, and self-stabilization phases of emotion-appraisal states, leading to consolidating traits. The article goes on to describe neural structures and functions involved in appraisal and emotion, as well as DS mechanisms of integration by which they interact. These mechanisms (...) include nested feedback interactions, global effects of neuromodulation, vertical integration, action-monitoring, and synaptic plasticity, and they are modeled in terms of both functional integration and temporal synchronization. I end by elaborating the psychological model of emotion–appraisal states with reference to neural processes. (shrink)

Our model integrates the nativist assumption of prespecified neural structures underpinning basic emotions with the constructionist view that emotions are assembled from psychological constituents. From a dynamic systems perspective, the nervous system self-organizes in different ways at different time scales, in relation to functions served by emotions. At the evolutionary scale, brain parts and their connections are specified by selective pressures. At the scale of development, connectivity is revised through synaptic shaping. At the scale of real time, temporary networks of (...) synchronized activity mediate responses to situations. To the degree that humans share common emotional functions, neural structuration is similar across scales, giving rise to “basic” emotions. However, unique developmental and situational factors select for neural configurations mediating emotional variants. (shrink)

Ainslie’s contribution offers a useful refinement of his powerful model of intertemporal bargaining. However, he focuses mostly on the cognitive mechanisms of choice. I suggest that these interact with emotional, personality, and developmental dynamics that cannot be ignored, either psychologically or neurally.

Snoek, like other commentators, conflates some of my neural claims with those of the Brain Disease Model of Addiction. But she sees other details of my modeling with precision and depth. I welcome her emphasis on individual and developmental differences in addicts' capacity to recognize and deploy their personal agency. In fact we agree that belief in personal agency is a critical first step to cultivating it. Yet I wish to steer away from the disease nomenclature, to give that belief (...) its best chance to flourish. (shrink)

Intentions and emotions arise together, and emotions compel us to pursue goals. However, it is not clear when emotions become objects of awareness, how emotional awareness changes with goal pursuit, or how psychological and neural processes mediate such change. We first review a psychological model of emotional episodes and propose that goal obstruction extends the duration of these episodes while increasing cognitive complexity and emotional intensity. We suggest that attention is initially focused on action plans and their obstruction, and only (...) when this obstruction persists does focal attention come to include emotional states themselves. We then model the self-organization of neural activities that hypothetically underlie the evolution of an emotional episode. Phases of emotional awareness are argued to parallel phases of synchronization across neural systems. We suggest that prefrontal activities greatly extend intentional states while focal attention integrates emotional awareness and goal pursuit in a comprehensive sense of the self in the world. (shrink)

Flanagan asserts that my model of addiction would apply as well to sonnet writing. Yet his most interesting point is that “addiction” is an imprecise label for a cluster of distinct phenomena. I agree with him that we need to examine these distinctions, but that doesn’t negate their shared features. Neuroscience can play an important role in advancing our understanding of both commonalities and distinctions within the phenomena of addiction.

Although I reject neuronormativity -- an idea central to the Brain Disease Model of Addiction -- Henden and Gjelsvik argue that the disease definition might refer to normativity in nonneural domains. They profess that a cognitive dysfunction, or a mismatch of evolutionary intentions, could also qualify as norm violations, thus legitimizing the disease label. The need for dividing lines is questioned as well. I rebut these criticisms in turn, but I must admit they are thought provoking.

Wakefield doesn't mind my focus on parallels between addiction and love. But love can fall outside the bounds of what evolution intended. So, he claims, comparing addiction with love does not preclude a naturally defined "disorder." I counter with the argument that evolution handed us such highly general response systems, the bounds of normality cannot be defined.

Frank and Nagel are very interested in the causes and consequences of moralizing about addiction. If addiction is a disease, moralistic concerns are sidelined. If it's a choice, we'd better identify clear reasons to absolve addicts from blame. While these are interesting considerations, they don't have much to do with the model of addiction I put forward in the target article.

The authors and I agree on many features of addiction, such as its developmental nature. But because I rely on much of the same data as the Brain Disease Model of Addiction, they seem to conflate my work with that of my opponents. Indeed they are generally skeptical of the use of neuroscientific data to help understand addiction, calling it "immature." Thus my work is also suspect. Hall and colleagues believe that it is impossible to look at neural and social (...) processes at the same time, yet that is exactly what I do. I suggest that interdisciplinary approaches to addiction are crucial. (shrink)

Both Matthews and I see addiction as the outcome of developmental processes that arrive at diverse levels of dysfunction for different individuals at different stages. Matthews characterizes "late-stage" addiction in terms of lost control and extreme automaticity, a degree of dysfunction he calls a "disorder" and compares to another disorder -- depersonalization. I don't mind the label "disorder." Yet addiction is no more like depersonalization than it is like other conditions, most notably obsessive-compulsive disorder. Automaticity is never pure or total. (...) My dual focus on the phenomenology and neuroscience of addiction has helped me capture these critical details and differences. In fact, I think we've had enough of comparing, classifying, and defining addiction. It's time to recognize addiction as a thing in itself, unlike anything else. (shrink)

Szalavitz’s model and mine share a good many components. Foremost among them is the conviction that addiction is a developmental trajectory, not a disease. Szalavitz is correct that we should consider controlled substance use an acceptable outcome, though I would like her to shift her terminology away from the medical mainstream. Finally, I suggest that Szalavitz's important idea of a "reset" in brain development might best be addressed by the notion of kindling.

Some dynamic systems approaches posit discontinuous changes, even universal stages, in development. Conversely, Thelen and colleagues see development as gradual because it relies on real-time interactions among many components. Yet their new model hinges on one parameter, neural cooperativity, that should change discontinuously because it engenders new skills that catalyze neural connectivity. In fact, research on cortical connectivity finds development to be discontinuous, and possibly stage-like, based on experience-dependent and experience-independent factors.

I applaud Fenton and Wiers' attempt to find a demarcation point between cases of addiction that fall within the range of normal function and those that may count as disease. However, I argue that continua don't offer demarcation points, the mechanisms involved are not demonstrably different, and trying to pin down subjectivity doesn't help.

Pickard’s contribution reminds me that conceptualizing choice is no simple matter. Pickard sees choice as entirely voluntary, while I argue that choice is only partially voluntary. Choices are based on appraisals of situations, which fluctuate due to external circumstances and internal states such as emotion and mood. Habit itself competes with volition, and all these parameters vary with development. Psychological factors such as delay discounting and especially one's belief in one's agency are critical for volitional choice as well.

Berridge's nuanced approach to the conceptualization of addiction as a disease is easier for me to accept than most others. In fact, Berridge and I agree on many core features of addiction, but still not on how to label it. When competing definitions reach a standoff on intellectual grounds, we should look at the clinical utility of each. And here I think that Berridge misses a critical insight. Yet, we end by agreeing to keep listening to each other.

The target article developed a dynamic systems framework that viewed the causal basis of emotion as a self-organizing process giving rise to cognitive appraisal concurrently. Commentators on the article evaluated this framework and the principles and mechanisms it incorporated. They also suggested additional principles, mechanisms, modeling strategies, and phenomena related to emotion and appraisal, in place of or extending from those already proposed. There was general agreement that nonlinear causal processes are fundamental to the psychology and neurobiology of emotion.

Although these authors sometimes resort to medical terminology, we strongly agree that addiction is not a disease and that the Brain Disease Model of Addiction captures only one part of the story and distorts the big picture. Yet Satel and Lilienfeld continue to conflate a neurobiological model with a disease model. They also complain that my modeling of addiction reveals a hidden “neurocentric” bias, despite my integration of multiple levels of analysis, exactly as they recommend.

Despite its historical contribution, Heather sees the Brain Disease Model of Addiction as failing to relieve stigma, increasing fatalism, and fundamentally wrong. He also sees “choice” as partly volitional and partly unconscious, implying no moral violation. I agree on all counts. Heather then presents a disorder-of-choice model of addiction, highlighting the failure of self-regulation with respect to immediate goals. Not only do I endorse such modeling, but the neural mechanisms I describe may help to explicate it more thoroughly.

Rolls demonstrates how reward/punishment systems are key mediators of cognitive appraisal, and this suggests a fundamental, causal role for emotion in thought and behaviour. However, this causal role for emotion seems to drop out of Rolls's model of consciousness, to be replaced by the old idea that emotion is essentially epiphenomenal. We suggest a modification to Rolls's model in which cognition and emotion activate each other reciprocally, both in appraisal and consciousness, thus allowing emotion to maintain its causal status where (...) it matters most. (shrink)

I review the brain disease model of addiction promoted by medical, scientific, and clinical authorities in the US and elsewhere. I then show that the disease model is flawed because brain changes in addiction are similar to those generally observed when recurrent, highly motivated goal seeking results in the development of deep habits, Pavlovian learning, and prefrontal disengagement. This analysis relies on concepts of self-organization, neuroplasticity, personality development, and delay discounting. It also highlights neural and behavioral parallels between substance addictions, (...) behavioral addictions, normative compulsive behaviors, and falling in love. I note that the short duration of addictive rewards leads to negative emotions that accelerate the learning cycle, but cortical reconfiguration in recovery should also inform our understanding of addiction. I end by showing that the ethos of the disease model makes it difficult to reconcile with a developmental-learning orientation. (shrink)

It has often been argued that Humean accounts of natural law cannot account for the role played by laws in scientific explanations. Loewer (Philosophical Studies 2012) has offered a new reply to this argument on behalf of Humean accounts—a reply that distinguishes between grounding (which Loewer portrays as underwriting a kind of metaphysical explanation) and scientific explanation. I will argue that Loewer’s reply fails because it cannot accommodate the relation between metaphysical and scientific explanation. This relation also resolves a puzzle (...) about scientific explanation that Hempel and Oppenheim (Philosophy of Science 15:135–75, 1948) encountered. (shrink)

Suppose that unobtanium-346 is a rare radioactive isotope. Consider: (1) Every Un346 atom, at its creation, decays within 7 microseconds (µs). (50%) Every Un346 atom, at its creation, has a 50% chance of decaying within 7µs. (1) and (50%) can be true together, but (1) and (50%) cannot together be laws of nature. Indeed, (50%)'s mere (non-vacuous) truth logically precludes (1)'s lawhood. A satisfactory analysis of chance and lawhood should nicely account for this relation. I shall argue first that David (...) Lewis's Humean picture accounts for this relation only by inserting this relation ‘by hand’. Next, I shall argue that this relation between law and chance also threatens a radically non-Humean picture of laws and chances. Finally, I shall offer an account of natural law that nicely explains the relation between chancy facts and deterministic laws. This explanation is not ad hoc because it derives the relation from the very same features of lawhood that account for the laws' special relation to counterfactuals and explain how the laws (unlike the accidents) possess a variety of necessity. The reason that a chancy fact such as (50%) keeps (1) from being a law, without keeping (1) from being true, is ultimately that a chancy fact constrains the subjunctive facts and (1)'s lawhood, unlike (1)'s truth, depends upon the subjunctive facts. (shrink)

After reviewing several failed arguments that laws cannot change, I use the laws' special relation to counterfactuals to show how temporary laws would have to differ from eternal but time-dependent laws. Then I argue that temporary laws are impossible and that neither Lewis's nor Armstrong's analyses of law nicely accounts for the laws' immutability. *Received September 2006; revised September 2007. ‡Many thanks to John Roberts and John Carroll for valuable comments on earlier drafts, as well as to several anonymous (...) referees for their good suggestions. †To contact the author, please write to: Department of Philosophy, University of North Carolina, CB #3125, Caldwell Hall, Chapel Hill, NC 27599-3125; e-mail: [email protected]. (shrink)

We introduce the virtual special issue on content in signalling systems. The issue explores the uses and limits of ideas from evolutionary game theory and information theory for explaining the content of biological signals. We explain the basic idea of the Lewis-Skyrms sender-receiver framework, and we highlight three key themes of the issue: (i) the challenge of accounting for deception, misinformation and false content, (ii) the relevance of partial or total common interest to the evolution of meaningful signals, and (...) (iii) how the sender-receiver framework relates to teleosemantics. (shrink)

Parkinson's disease (PD) is generally sporadic but a number of genetic diseases have parkinsonism as a clinical feature. Two dominant genes, α‐synuclein (SNCA) and leucine‐rich repeat kinase 2 (LRRK2), are important for understanding inherited and sporadic PD. SNCA is a major component of pathologic inclusions termed Lewy bodies found in PD. LRRK2 is found in a significant proportion of PD cases. These two proteins may be linked as most LRRK2 PD cases have SNCA‐positive Lewy bodies. Mutations in both proteins are (...) associated with toxic effects in model systems although mechanisms are unclear. LRRK2 is an intracellular signaling protein possessing both GTPase and kinase activities that may contribute to pathogenicity. A third protein, tau, is implicated as a risk factor for PD. We discuss the potential relationship between these genes and suggest a model for PD pathogenesis where LRRK2 is upstream of pathogenic effects through SNCA, tau, or both proteins. (shrink)

These 17 essays covers all aspects of Bernard Stiegler's work, from poststructuralism, anthropology and psychoanalysis to his work on the politics of memory, 'libidinal economy', technoscience and aesthetics, keeping a focus on his key theory of technics throughout. Stiegler brings together key concepts from Plato, Freud, Derrida and Simondon to argue that the human is 'invented' through technics rather than a product of purely biological evolution. Stiegler is a thinker at the forefront of our contemporary concerns with consumerism, technology, inter-generational (...) division, political apathy and economic crisis. His ambitious project is to go beyond these sources of social distress to uncover and examine precisely 'what makes life worth living'. Contributors include: Stephen Barker, University of California Irvine and translator of Steigler; Richard Beardsworth, American University of Paris and translator of Stiegler; Miguel de Beistegui; University of Warwick; Marc Crepon, Ecole normale superieure and co-founder of Stiegler's think tank, Ars Industrialis and Daniel Ross, co-director of 'The Ister', the award-winning film on Heidegger, and translator of Stiegler. (shrink)

In this introduction we set out some salient themes that will help structure understanding of a complex set of intersecting issues discussed in this special issue on the work of Marc Lewis: conceptual foundations of the disease model, tolerating the disease model given socio-political environments, and A third wave: refining conceptualization of addiction in the light of Lewis’s model.

What is a law of nature? Traditionally, philosophical discussion of this question has been dominated by two prominent alternatives; David Lewis’s best-systems analysis, according to which a law is a regularity that serves as a theorem in our best axiomatization of the facts about the world, and the Dretske-Armstrong-Tooley analysis, which incorporates universals to distinguish laws from mere accidental generalizations. Marc Lange’s first book presents a provocative alternative to this tradition, providing a novel treatment of natural laws that (...) should be of interest to those philosophers concerned with the analysis of lawhood, physical necessity, causation, inductive confirmation, counterfactual analysis, and explanation. (shrink)

Marc Lewis argues that addiction is not a disease, it is instead a dysfunctional outcome of what plastic brains ordinarily do, given the adaptive processes of learning and development within environments where people are seeking happiness, or relief, or escape. They come to obsessively desire substances or activities that they believe will deliver happiness and so on, but this comes to corrupt the normal process of development when it escalates beyond a point of functionality. Such ‘deep learning’ emerges (...) from consumptive habits, or ‘motivated repetition’, and although addiction is bad, it ferments out of the ordinary stuff underpinning any neural habit. Lewis gives us a convincing story about the process that leads from ordinary controlled consumption through to quite heavy addictive consumption, but I claim that in some extreme cases the eventual state of deep learning tips over into clinically significant impairment and disorder. Addiction is an elastic concept, and although it develops through mild and moderate forms, the impairment we see in severe cases needs to be acknowledged. This impairment, I argue, consists in the chronic automatic consumption present in late stage addiction. In this condition, the desiring self largely drops out the picture, as the addicted individual begins to mindlessly consume. This impairment is clinically significant because the machinery of motivated rationality has become corrupted. To bolster this claim I compare what is going on in these extreme cases with what goes on in people who dissociate in cases of depersonalization disorder. (shrink)

This article uses Marc Lewis’ work as a springboard to discuss the socio-political context of the brain disease model of addiction (BDMA). The claim that promotion of the BDMA is the only way the general public can be persuaded to withhold blame and punishment from addicts is critically examined. After a discussion of public understandings of the disease concept of addiction, it is pointed out that it is possible to develop a scientific account of addiction which is neither (...) a disease nor a moral model but which the public could understand. Evidence is reviewed to suggest that public acceptance of the disease concept is largely lip-service and that the claim the BDMA removes stigma among the public and professionals is unsupported by evidence. Further, there is good evidence that biogenetic explanations of mental/behavioural disorders in general have been counterproductive in the attempt to ally stigma. A model of addiction as a disorder of choice may attract special problems in public-facing communications and risks being misunderstood. However, ways of presenting this model to the public are suggested that may avoid such risks. Lastly, the claim that the BDMA is the only way of ensuring access to treatment and of maintaining research funding for addiction is disputed and a way in which these benefits can be retained under a disorder-of-choice model proposed. The article concludes by enthusiastically endorsing Lewis’ call for a third stage in the governing image of addiction. (shrink)

Not all scientific explanations work by describing causal connections between events or the world's overall causal structure. In addition, mathematicians regard some proofs as explaining why the theorems being proved do in fact hold. This book proposes new philosophical accounts of many kinds of non-causal explanations in science and mathematics.

(Citation/Reference) Williams, S. H. Lewis Carroll handbook.

Many philosophers argue that explanatoriness plays no special role in confirmation – that “inference to the best explanation” (IBE) incorrectly demands giving hypotheses extra credit for their potential explanatory qualities beyond the credit they already deserve for their predictive successes. This paper argues against one common strategy for responding to this thought – that is, for trying to fit IBE within a Bayesian framework. That strategy argues that a hypothesis’ explanatory quality (its “loveliness”) contributes either to its prior probability or (...) to its likelihood. This paper argues that this strategy fails because it must give different treatments to two hypotheses that are unlovely for the very same reason. The strategy therefore loses the insight into scientific reasoning that its reconstruction in terms of IBE is supposed to provide. The paper then provides a Bayesian account of the confirmatory role of explanatoriness that represents explanatory quality as having an impact in the same place for two hypotheses that are unlovely for the very same reason. This approach works by “putting explanation back into IBE” – that is, by invoking hypotheses that refer explicitly to scientific explanation and by invoking the agent's background opinions regarding the kind of explanation that the evidence is liable to have. On this approach, there is no list of “explanatory virtues” the possession of which always helps to make an explanation better. Rather, for different facts, there are different characteristics that our background knowledge of other explanations gives us some reason to expect the given fact's explanation to possess. (shrink)

Several logical operators are defined as dual pairs, in different types of logics. Such dual pairs of operators also occur in other algebraic theories, such as mathematical morphology. Based on this observation, this paper proposes to define, at the abstract level of institutions, a pair of abstract dual and logical operators as morphological erosion and dilation. Standard quantifiers and modalities are then derived from these two abstract logical operators. These operators are studied both on sets of states and sets of (...) models. To cope with the lack of explicit set of states in institutions, the proposed abstract logical dual operators are defined in an extension of institutions, the stratified institutions, which take into account the notion of open sentences, whose satisfaction is parametrised by sets of states. A hint on the potential interest of the proposed framework for spatial reasoning is also provided. (shrink)

The intellectual history of the last quarter of this century has been marked by the growing influence of Africana thought--an area of philosophy that focuses on issues raised by the struggle over ideas in African cultures and their hybrid forms in Europe, the Americas, and the Caribbean. Existentia Africana is an engaging and highly readable introduction to the field of Africana philosophy and will help to define this rapidly growing field. Lewis R. Gordon clearly explains Africana existential thought to (...) a general audience, covering a wide range of both classic and contemporary thinkers--from Douglass and DuBois to Fanon, Davis and Zack. (shrink)

Philosophers who regard some mathematical proofs as explaining why theorems hold, and others as merely proving that they do hold, disagree sharply about the explanatory value of proofs by mathematical induction. I offer an argument that aims to resolve this conflict of intuitions without making any controversial presuppositions about what mathematical explanations would be.