Body feedback is the proprioceptive feedback that denominates the afferent information from position and movement of the body to the central nervous system. It is crucial in experiencing emotions, in forming attitudes and in regulating emotions and behavior. This paper investigates effects of dynamic body feedback on affect and attitudes, focusing on the impact of movement rhythms with smooth vs. sharp reversals as one basic category of movement qualities. It relates those qualities to already explored effects of approach vs. avoidance (...) motor behavior as one basic category of movement shape. Studies 1 and 2 tested the effects of one of two basic movement qualities (smooth vs. sharp rhythms) on affect and cognition. The third study tested those movement qualities in combination with movement shape (approach vs. avoidance motor behavior) and the effects of those combinations on affect and attitudes toward initially valence-free stimuli. Results suggest that movement rhythms influence affect (studies 1 and 2), and attitudes (study 3), and moderate the impact of approach and avoidance motor behavior on attitudes (study 3). Extending static body feedback research with a dynamic account, findings indicate that movement qualities – next to movement shape – play an important role, when movement of the lived body is an independent variable. (shrink)

Volume 20, Issue 8, August 2020, Page 96-98.

Body Memory, Metaphor and Movement is an interdisciplinary volume with contributions from philosophers, cognitive scientists, and movement therapists. Part one provides the phenomenologically grounded definition of body memory with its different typologies. Part two follows the aim to integrate phenomenology, conceptual metaphor theory, and embodiment approaches from the cognitive sciences for the development of appropriate empirical methods to address body memory. Part three inquires into the forms and effects of therapeutic work with body memory, based on the integration of theory, (...) empirical findings, and clinical applications. It focuses on trauma treatment and the healing power of movement. The book also contributes to metaphor theory, application and research, and therefore addresses metaphor researchers and linguists interested in the embodied grounds of metaphor. Thus, it is of particular interest for researchers from the cognitive sciences, social sciences, and humanities as well as clinical practitioners. (shrink)

Pavarini et al. argue for the potential benefits of using games and other technologies to collect empirical data to enhance bioethics research. They propose a methodology called “design bioe...

Aftereffects induced by invisible stimuli constitute a powerful tool to investigate what type of neural information processing can occur in the absence of visual awareness. This approach has been successfully used to demonstrate that awareness of oriented gratings or translating stimuli is not necessary to obtain a robust orientation-specific or motion-specific aftereffect. We exploit motion-induced blindness to investigate the related question of the influence of visual awareness on the formation of negative afterimages. Our results show that MIB does not affect (...) the persistence and intensity of afterimages. Thus, there is no significant contribution to the formation of afterimages beyond the sites mediating MIB. (shrink)

People judge positive information to be more alike than negative information. This good-bad asymmetry in similarity was argued to constitute a true property of the information ecology (Alves, H., Koch, A., & Unkelbach, C. (2017). Why good is more alike than bad: Processing implications. Trends in Cognitive Sciences, 21, 69–79). Alternatively, the asymmetry may constitute a processing outcome itself, namely an influence of phasic affect on information processing. Because no research has yet tested whether phasic affect influences perceived similarity among (...) stimuli, we conducted 5 Experiments that also tested whether phasic affect can account for the higher judged similarity among positive compared to negative stimuli. In three experiments, we affectively charged pictures of different Pokemon by pairing them with monetary gains and losses (Exp. 1a, 1b) as well as positive and negative trait words (Exp. 2); yet, the evaluative charge did not differentially influence perceived similarity among the Pokemon. Experiment 3 replicated the basic similarity asymmetry among positive and negative words, and found that it was unaffected by externally induced phasic affect. Experiment 4 showed that phasic affect had no influence on perceived similarity of non-evaluative words either. We conclude that albeit a weak influence of phasic affect on perceived similarity of stimuli cannot be ruled out entirely, it can most likely not account for the typically medium to large sized asymmetry in similarity among positive and negative stimuli. (shrink)

In “Harmful Choices, the case of C, and decision making competence,” Pickering et al. offer a thought-provoking interpretation of the relationship between harm and capacity assessments by an...

How should pragmatists respond to and contribute to the resolution of one of America's greatest and most enduring problems? Given that the most important thinkers of the pragmatist movement—Charles S. Peirce, William James, John Dewey, and George Herbert Mead—said little about the problem of race, how does their distinctly American way of thinking confront the hardship and brutality that characterizes the experience of many African Americans in this country? In 12 thoughtful and provocative essays, contemporary American pragmatists connect ideas with (...) action and theory with practice to come to terms with this seemingly intractable problem. Exploring themes such as racism and social change, the value of the concept of race, the role of education in ameliorating racism, and the place of democracy in dealing with the tragedy of race, the voices gathered in this volume consider how pragmatism can focus new attention on the problem of race. Contributors are Michael Eldridge, Eddie S. Glaude, Jr., Judith M. Green, D. Micah Hester, Donald F. Koch, Bill E. Lawson, David E. McClean, Gregory F. Pappas, Scott L. Pratt, Alfred E. Prettyman, John R. Shook, Paul C. Taylor, and Cornel West. (shrink)

This article investigates the changing justifications of one of the hallmarks of orthodox psychoanalytic practice, the neutral and abstinent stance of the psychoanalyst, during the middle decades of the 20th century. To call attention to the shifting rationales behind a supposedly cold, detached style of treatment still today associated with psychoanalysis, explanations of the clinical utility of neutrality and abstinence by ‘classical’ psychoanalysts in the United States are contrasted with how intellectuals and cultural critics understood the significance of psychoanalytic abstinence. (...) As early as the 1930s, members of the Frankfurt School discussed the cultural and social implications of psychoanalytic practices. Only in the 1960s and 1970s, however, did psychoanalytic abstinence become a topic within broader intellectual debates about American social character and the burgeoning ‘therapy culture’ in the USA. The shift from professional and epistemological concerns to cultural and political ones is indicative of the changing appreciation of psychoanalysis as a clinical discipline: for psychoanalysts as well as cultural critics, I argue, changing social mores and the professional decline of psychoanalysis infused the image of the abstinent psychoanalyst with nostalgic longing, making it a symbol of resistance against a culture seen to be in decline. (shrink)

ArgumentThe article retraces the shifting conceptualizations of psychological trauma in experimental psychopathological research in the middle decades of the twentieth century in the United States. Among researchers studying so-called experimental neuroses in animal laboratories, trauma was an often-invoked category used to denote the clash of conflicting forces believed to lead to neurotic suffering. Experimental psychologists, however, soon grew skeptical of the traumatogenic model and ultimately came to reject neurosis as a disease entity. Both theoretical differences and practical circumstances, such as (...) the technical challenge of stabilizing neurotic symptoms in rats, led to this demise. Yet, despite their reservations, experimental psychologists continued to employ traumatic stimuli to produce psychopathological syndromes. In the 1960s, a new understanding of trauma evolved, which emphasized the loss of control experienced by traumatized animal subjects. These shifting ideas about trauma, I argue, reflect both varying experimental cultures, epistemic norms as well as changing societal concerns. (shrink)

L’interprétation de l’Antiquité gréco-latine que Michel Foucault développe dans ses derniers ouvrages publiés et ses derniers cours au Collège de France fait peu de place au néoplatonisme. L’Herméneutique du sujet, seul texte où il en soit question avec quelque attention, le présente comme un simple prolon­gement de la philosophie de Platon, relevant du « modèle platonicien » du souci de soi, que Foucault confronte aux modèles hellénistico-romain et chrétien. Pour­tant, c’est chez les commentateurs néoplatoniciens de l’Alcibiade que Foucault trouve certaines (...) distinctions, en particulier entre « politique » et « cathartique », qui fondent la construction de ces trois modèles et leur articulation. Ce rôle archi­tectonique des néoplatoniciens tardifs, par ailleurs, va de pair avec l’absence quasi totale d’un autre néoplatonisme, celui de Plotin, qui pourtant semblerait à pre­mière vue mieux trouver sa place dans une approche placée sous le signe des « exercices spirituels ». Le traitement du néoplatonisme est par là symptomatique de la lecture foucaldienne de l’histoire de la philosophie antique, qui se construit tout autant par ses exclusions que par ses focalisations. (shrink)

We need guidance in interpreting and evaluating C. S. Peirce. The scope, complexity, and ongoing development of his extensive body of philosophical work call for the location of central themes and arguments. This collection of essays, originally published or written between 1966 and 1995, sets forth those themes that dominate Potter’s thought.

Ce nouvel opus de la collection Les écrits de Plotin a été rédigé en italien par A. Linguiti, puis traduit en français par A.C. Peduzzi, la traduction française du texte grec de Plotin ayant naturellement été vérifiée par A. Linguiti. Les citations de Plotin extraites d’autres traités (dans l’Introduction et le Commentaire) sont données dans la traduction d’Émile Bréhier. Ce travail, en grande partie inédit, bénéficie de recherches déjà publiées par A. Linguiti dans un ouvrage plus volumineux...

It has been over a decade and half since Christof Koch and the late Francis Crick first advocated the now popular NCC project (Crick and Koch, 1990), in which one tries to find the neural correlate of consciousness (NCC) for perceptual processes. In his chapter in this book Chris Frith provides a splendid review of how neuroimaging has contributed greatly to this project. For the sake of contrast, this chapter takes a more critical stance on what we have actually learned. (...) Many authors have written on whether looking for the neural correlates would eventually lead to an explanatory theory of consciousness, while the proponents defend that focusing on correlates is a strategically sensible first step, given the complexity of the problem (Crick and Koch, 1998;Crick and Koch, 2003). My point here is not to argue whether studying the NCC is useful, but rather, to question whether we are really studying the NCC at all. I argue that in hoping to sidestep the difficult conceptual issues, we have sometimes also missed the phenomenon of perceptual consciousness itself. (shrink)

What exactly is a genetic disease? For a phrase one hears on a daily basis, there has been surprisingly little analysis of the underlying concept. Medical doctors seem perfectly willing to admit that the etiology of disease is typically complex, with a great many factors interacting to bring about a given condition. On such a view, descriptions of diseases like cancer as genetic seem at best highly simplistic, and at worst philosophically indefensible. On the other hand, there is clearly some (...) practical value to be had by classifying diseases according to their predominant cause when this can be accomplished in a theoretically satisfactory manner. The question therefore becomes exactly how one should go about selecting a single causal factor among many to explain the presence of disease. When an attempt to defend such causal selection is made at all, the standard accounts offered (Koch's postulates, Hill's epidemiological criteria, manipulability) are all clearly inadequate. I propose, however, an epidemiological account of disease causation which walks the fine line between practical applicability and theoretical considerations of causal complexity and attempts to compromise between patientcentered and population-centered concepts of disease. The epidemiological account is the most basic framework consistent with our strongly held intuitions about the causal classification of disease, yet it avoids the difficulties encountered by its competitors. (shrink)

This volume contains the contributions of philosophers and psychologists to one of the Rice University semicentennial symposia and includes the papers of Koch, MacLeod, Skinner, Rodgers, Malcolm and Scriven. Discussion from the audience and among the participants is recorded, and the general result of both is a blurring of distinctions between behaviorism and phenomenology. The peculiar logical character of first person utterances is duly considered and provides the backdrop for much of the rehash of the private-public problem in philosophy and (...) psychology.—C. V. (shrink)

What exactly is a genetic disease? For a phrase one hears on a daily basis, there has been surprisingly little analysis of the underlying concept. Medical doctors seem perfectly willing to admit that the etiology of disease is typically complex, with a great many factors interacting to bring about a given condition. On such a view, descriptions of diseases like cancer as geneticseem at best highly simplistic, and at worst philosophically indefensible. On the other hand, there is clearly some practical (...) value to be had by classifying diseases according to theirpredominant cause when this can be accomplished in a theoretically satisfactory manner. The question therefore becomes exactly how one should go about selecting a single causal factor among many to explain the presence of disease. When an attempt to defend such causal selection is made at all, the standard accounts offered (Koch's postulates, Hill's epidemiological criteria, manipulability) are all clearly inadequate. I propose, however, an epidemiological account of disease causation which walks the fine line between practical applicability and theoretical considerations of causal complexity and attempts to compromise between patient-centered and population-centered concepts of disease. The epidemiological account is the most basic framework consistent with our strongly held intuitions about the causal classification of disease, yet it avoids the difficulties encountered by its competitors. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s postulates (...) are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s postulates (...) are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

Human microbiome research makes causal connections between entire microbial communities and a wide array of traits that range from physiological diseases to psychological states. To evaluate these causal claims, we first examine a well-known single-microbe causal explanation: of Helicobacter pylori causing ulcers. This apparently straightforward causal explanation is not so simple, however. It does not achieve a key explanatory standard in microbiology, of Koch’s postulates, which rely on manipulations of single-microorganism cultures to infer causal relationships to disease. When Koch’s postulates (...) are framed by an interventionist causal framework, it is clearer what the H. pylori explanation achieves and where its explanatory strengths lie. After assessing this ‘simple’, single-microbe case, we apply the interventionist framework to two key areas of microbiome research, in which obesity and mental health states are purportedly explained by microbiomes. Despite the experimental data available, interventionist criteria for explanation show that many of the causal claims generated by microbiome research are weak or misleading. We focus on the stability, specificity and proportionality of proposed microbiome causal explanations, and evaluate how effectively these dimensions of causal explanation are achieved in some promising avenues of research. We suggest some conceptual and explanatory strategies to improve how causal claims about microbiomes are made. (shrink)

We argue that Koch’s postulates are best understood within an interventionist account of causation, in the sense described in Woodward. We show how this treatment helps to resolve interpretive puzzles associated with Koch’s work and how it clarifies the different roles the postulates play in providing useful, yet not universal criteria for disease causation. Our paper is an effort at rational reconstruction; we attempt to show how Koch’s postulates and reasoning make sense and are normatively justified within an interventionist framework (...) and more difficult to understand within alternative frameworks for thinking about causation. (shrink)

This paper reassesses Robert Koch’s work on tropical infections of humans and cattle as being inspired by an underlying interest in epidemiology. Such an interest was developed from the early 1890s when it became clear that an exclusive focus on pathogens was insufficient as an approach to explain the genesis and dynamics of epidemics. Koch, who had failed to do so before, now highlighted differences between infection and disease and described the role of various sub-clinical states of disease in the (...) propagation and—consequently—in the control of epidemics. Studying pathologies of men and cattle in tropical countries eventually facilitated the application of such measures in Europe through the screening of healthy carriers of typhoid, which was carried out in 1902. The concept of the carrier state can be understood as a spin-off from tropical medicine into the study and control of infectious disease in Europe. With it travelled assumptions that were typical for colonial and veterinary medicine where the health of indigenous individuals or cattle would be a secondary objective compared to the control of diseases in populations. (shrink)