Kathryn Tabb

Locke added two new chapters to the fourth edition of his _Essay concerning Human Understanding_ (1700): ‘Of the Association of Ideas’, and ‘Of Enthusiasm’. When examined together, these chapters reveal that Locke was increasingly attentive to—and troubled by—the potential of mad ideas and pathological principles to thwart the reasonableness at the heart of his political and theological projects. While Locke saw religious zealotry as a vice, he attributed its ultimate causes not to a sinfulness of the will but to a disease of the understanding. Unlike later theorists who would treat the association of ideas as a general mechanism of cognition, Locke saw it as a pathological force that could explain the failures of otherwise rational people to respond to evidence. This technical account of madness is a linchpin not only for Locke’s theory of enthusiasm, but also for his mature views on toleration.

Until recently, medicine has had little to offer most of the millions of patients suffering from rare and ultrarare genetic conditions. But the development in 2019 of Milasen, the first genetic intervention developed for and administered to a single patient suffering from an ultrarare genetic disorder, has offered hope to patients and families. In addition, Milasen raised a series of conceptual and ethical questions about how individualised genetic interventions should be developed, assessed for safety and efficacy and financially supported. The answers to these questions depend in large part on whether individualised therapies are understood as human subjects research or clinical innovation, different domains of biomedicine that are regulated by different modes of oversight, funding and professional norms. In this article, with development and administration of the drug Milasen as our case study, we argue that at least some individualised genetic therapies are not, as some have argued, either research or treatment. Instead, they are research-treatment hybrids, a category that has both epistemological and pragmatic repercussions for funding, ethics oversight and regulation.

This chapter makes the case that John Locke was influenced by the Pyrrhonian medical tradition, both in his own methods and commitments as a physician, and in the philosophical strategies he employed. Following Sextus Empiricus and other Pyrrhonian physicians, Locke rejects metaphysical accounts of the causal processes underlying diseases and their cures in favor of practical guidelines based on observation and experience. This approach leads Locke to explain madness as an intellectual disorder based on phenomenology and self-report, instead of in terms of the neurological processes posited by his contemporaries. Locke ultimately mobilizes this original account of madness as part of his skeptical attack on innatism, in which, analogous to his employment of Pyrrhonian strategies from cultural diversity, he argues that the commitments of dogmatists might just as well be mad as inborn. The possibility of mad ideas aping certain ones, he suggests, should give the nativist pause.

Since the turn of the twenty-first century, biomedical psychiatry around the globe has embraced the so-called precision medicine paradigm, a model for medical research that uses innovative techniques for data collection and analysis to reevaluate traditional theories of disease. The goal of precision medicine is to improve diagnostics by restratifying the patient population on the basis of a deeper understanding of disease processes. This paper argues that precision is ill-fitting for psychiatry for two reasons. First, in psychiatry, unlike in fields like oncology, precision medicine has been understood as an attempt to improve medicine by casting out, rather than merely revising, traditional taxonomic tools. Second, in psychiatry the term “biomarker” is often used in reference to signs or symptoms that allow patients to be classified and then matched with treatments; however, in oncology “biomarker” usually refers to a disease mechanism that is useful not only for diagnostics, but also for discovering causal pathways that drug therapies can target. Given these differences between how the precision medicine paradigm operates in psychiatry and in other medical fields like oncology, while precision psychiatry may offer successful rhetoric, it is not a promising paradigm.

The biopsychosocial model, which was deeply influential on psychiatry following its introduction by George L. Engel in 1977, has recently made a comeback. Derek Bolton and Grant Gillett have argued that Engel’s original formulation offered a promising general framework for thinking about health and disease, but that this promise requires new empirical and philosophical tools in order to be realized. In particular, Bolton and Gillett offer an original analysis of the ontological relations between Engel’s biological, social, and psychological levels of analysis. I argue that Bolton and Gillett’s updated model, while providing an intriguing new metaphysical framework for medicine, cannot resolve some of the most vexing problems facing psychiatry, which have to do with how to prioritize different sorts of research. These problems are fundamentally ethical, rather than ontological. Without the right prudential motivation, in other words, the unification of psychiatry under a single conceptual framework seems doubtful, no matter how compelling the model. An updated biopsychosocial model should include explicit normative commitments about the aims of medicine that can give guidance about the sorts of causal connections to be prioritized as research and clinical targets.

Addicts are often portrayed as compelled by their addiction and thus as a paradigm of unfree action and mitigated blame. This chapter argues that our best scientific theories of addiction reveal that, psychologically, addicts are not categorically different from non-addicts. There is no pairing of contemporary accounts of addiction and of prominent theories of moral responsibility that can justify our intuitions about the mitigation of addicts but not non-addicts. Two conclusions are advanced. First, we should either treat addicts as we normally treat non-addicts (as fully culpable) or embrace the skeptical conclusion that everyone is less responsible than we thought—perhaps not responsible at all. Second, we should be doubtful that theorizing about responsibility will be advanced by focusing on particular kinds of psychopathologies.

A significant portion of the scholarship in analytic philosophy of psychiatry has been devoted to the problem of what kind of kind psychiatric disorders are. Efforts have included descriptive projects, which aim to identify what psychiatrists in fact refer to when they diagnose, and prescriptive ones, which argue over that to which diagnostic categories should refer. In other words, philosophers have occupied themselves with what I call “diagnostic kinds”. However, the pride of place traditionally given to diagnostic kinds in psychiatric research has recently come under attack, most notably by a recent initiative of the National Institute of Mental Health, the Research Domain Criteria Project, that seeks to exclude diagnostic categories from experimental designs and focus on other sorts of psychiatric kinds. I argue that philosophical accounts privileging diagnostic kinds must respond to this new line of criticism, and conclude that philosophers need to either counter psychiatrists’ growing suspicion about the hegemony of diagnostic categories in the clinic and the laboratory, or join in redirecting their efforts toward the development of robust accounts of other sorts of psychiatric objects and processes.

ABSTRACTJohn Locke is famous for popularizing the method of the philosophical thought experiment in discussions of personal identity; the cases introduced in the second edition of An Essay Concerning Understanding are still employed by contemporary philosophers. Here I argue that Locke’s method is nonetheless importantly different from later efforts in ways that can help us better appreciate his larger projects. Rather than pumping the reader’s intuitions in support of his preferred account, Locke’s thought experiments serve to illustrate common errors in assessments of identity that he sees as particularly prevalent and problematic. Locke defends his idea of ‘person’ otherwise, through what I call his ‘lived experiments’: observations about linguistic usage that serve to illustrate the term’s role in practical reasoning. I focus especially on Locke’s example of the forensic status of the madman. Examples like these do not, for Locke, demonstrate the intuitiveness of his analysis, but rather bolste...

The failure of psychiatry to validate its diagnostic constructs is often attributed to the prioritizing of reliability over validity in the structure and content of the Diagnostic and Statistical Manual of Mental Disorders. Here I argue that in fact what has retarded biomedical approaches to psychopathology is unwarranted optimism about diagnostic discrimination: the assumption that our diagnostic tests group patients together in ways that allow for relevant facts about mental disorder to be discovered. I consider the Research Domain Criteria framework as a new paradigm for classifying objects of psychiatric research that solves some of the challenges brought on by this assumption.

Darwin’s first publication after the Origin of Species was a volume on orchids that expanded on the theory of adaptation through natural selection introduced in his opus. Here I argue that On the Various Contrivances by which British and Foreign Orchids are Fertilised by Insects (1862) is not merely an empirical confirmation of his theory. In response to immediate criticisms of his metaphor of natural selection, Darwin uses Orchids to present adaptation as the result of innumerable natural laws, rather than discrete acts analogous to conscious choices. The means of selection among polliniferous plants cannot be neatly classed under the Origin’s categories of artificial, natural, or sexual selection. Along with Darwin’s exploration of sexual selection in his later works, Orchids serves to undo the restrictive metaphor so firmly established by the Origin and to win over those of Darwin’s contemporaries who were committed advocates of natural law but suspicious of evolution by natural selection.

This paper makes a case for the centrality of the passion of curiosity to Hobbes’s account of human nature. Hobbes describes curiosity as one of only a few capacities differentiating human beings from animals, and I argue that it is in fact the fundamen- tal cause of humanity’s uniqueness, generating other important difference-makers such as language, science and politics. I qualify Philip Pettit’s (2008) claim that Hobbes believes language to be the essence of human difference, contending that Pettit grants language too central a place in Hobbes’s psychology. Language is, for Hobbes, a tech- nology adopted on account of curiosity. Further, curiosity is necessary not only for linguistic but also for scientific activity. Only after what he calls original knowledge has been gathered are names employed to generate the conditional propositions that con- stitute science. Finally, curiosity can resolve another puzzle of Hobbesian psychology that Pettit leaves unanswered: our tendency towards strife. Hobbes believes that inso- far as human beings have an implacable hunger for knowledge of the future, we are unable to rest content with present gains and must always aspire to secure the best possible outcome for ourselves.