Predictive genetic testing for susceptibility to psychiatric conditions is likely to become part of standard practice. Because the onset of most psychiatric diseases is in late adolescence or early adulthood, testing minors could lead to early identification that may prevent or delay the development of these disorders. However, due to their complex aetiology, psychiatric genetic testing does not provide the immediate medical benefits that current guidelines require for testing minors. While several authors have argued non-medical benefits may (...) play a crucial role in favour of predictive testing for other conditions, little research has explored such a role in psychiatric disorders. This paper outlines the potential non-medical benefits and harms of psychiatric genetic testing in minors in order to consider whether the non-medical benefits could ever make such testing appropriate. Five non-medical themes arise in the literature: psychological impacts, autonomy/self-determination, implications of the biomedical approach, use of financial and intellectual resources, and discrimination. Non-medical benefits were prominent in all of them, suggesting that psychiatric genetic testing in minors may be appropriate in some circumstances. Further research needs to empirically assess these potential non-medical benefits, incorporate minors in the debate, and include normative reflection to evaluate the very purposes and motivations of psychiatric genetic testing in minors. (shrink)

The article [Title], written by [AuthorNames], was originally published electronically on the publisher’s internet portal on [date of OnlineFirst publication] without open access.

The research program Spit For Science was launched at Virginia Commonwealth University (VCU) in 2011. Since then, more than 10,000 freshmen have been enrolled in the program, filling out extensive questionnaires about their drinking, general substance use, and related behaviors, and also contributing saliva for genotyping. The goals of the program, as initially stated by the investigators, were to find the genes underlying the heritability of alcohol use and related behaviors, and in addition to put genetic knowledge to work in (...) ways that might aid university administrators and mental health professionals in the prevention and treatment of substance abuse. We review every empirical paper involving genetic data that has emerged from the program, and reach a surprising conclusion: the study has never identified a single genetic effect of more than trivial magnitude. Although the quantitative results of the studies were reported transparently, the theoretical ramifications of the negligible results have never been acknowledged. To the contrary, most of the papers ignore the tiny effects, reaching optimistic conclusions about the prospects for future genetic explanations of alcohol use. We explore the implications of these results for the broader prospects of applied psychiatric genetics. (shrink)

Studies of the role of imprinted genes in psychological phenomena are long overdue. The target article is comprehensive, presenting a wealth of important and convergent evidence, and provides an excellent point of departure for further research. However, the authors' evidentiary grasp exceeds the explicatory capacity of the proposed model. Greater genotypic and phenotypic precision would significantly enhance its predictive power.

The research program Spit For Science was launched at Virginia Commonwealth University (VCU) in 2011. Since then, more than 10,000 freshmen have been enrolled in the program, filling out extensive questionnaires about their drinking, general substance use, and related behaviors, and also contributing saliva for genotyping. The goals of the program, as initially stated by the investigators, were to find the genes underlying the heritability of alcohol use and related behaviors, and in addition to put genetic knowledge to work in (...) ways that might aid university administrators and mental health professionals in the prevention and treatment of substance abuse. We review every empirical paper involving genetic data that has emerged from the program, and reach a surprising conclusion: the study has never identified a single genetic effect of more than trivial magnitude. Although the quantitative results of the studies were reported transparently, the theoretical ramifications of the negligible results have never been acknowledged. To the contrary, most of the papers ignore the tiny effects, reaching optimistic conclusions about the prospects for future genetic explanations of alcohol use. We explore the implications of these results for the broader prospects of applied psychiatric genetics. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Spit for Science and the Progress and Promise of Psychiatric GeneticsDanielle M. Dick, PhD (bio)In their paper “Spit for Science and the Limits of Applied Psychiatric Genetics,” Turkheimer and Rodock Greer use results from the Spit for Science (S4S) project to argue that the idea of psychiatric genetics1 yielding actionable results is a folly. Although there is much about which Turkheimer and I agree (I (...) took my first psychology class from him 30 years ago), we fundamentally disagree about the outlook of psychiatric genetics. His paper suggests that our differing conclusions arise from the authors misunderstanding the nature of the S4S project and a difference in our views on the broader purpose of psychiatric genetics.It is the characterization of S4S as a “program of research” that is the foundation for the conclusions Turkheimer and Rodock Greer draw about the unlikely potential for meaningful results from psychiatric genetics. But S4S was never intended to be a program of research. The dataset was established as a registry, owned and administered by Virginia Commonwealth University (VCU), and intended as a resource for the field. Accordingly, what is presented as a series of studies that bounce from one topic to another (which the paper mischaracterizes as resulting from “desultory progress”), actually reflects the use of the dataset by many scientific teams, including trainees and early career investigators, to explore various questions. The fact that the project attracted researchers from a diversity of fields (>140 faculty/trainees from 28 departments across VCU and 16 external collaborators) to study the many factors that impact college behavioral and emotional health is, to my mind, one of the strengths of the project.Within my own program of research, S4S is just one of many datasets with which I work; the papers included in their review account for only 3% of my more than 450 papers. Accordingly, my outlook on psychiatric genetics is not based solely, or even largely, upon S4S. As of 2021, I am no longer involved with the project, having ceded its stewardship to another VCU faculty member. Like with the other genetically informative datasets we analyze, the individual papers from S4S reflect the state of the science at the time they were initiated (often years before the eventual publication date). This fact is evident in the evolution of methods applied to S4S and would be true of a review of papers from Collaborative Study on the Genetics of Alcoholism, Avon Longitudinal Study of Parents [End Page 425] and Children, The National Longitudinal Study of Adolescent to Adult Health, the UK Biobank, or any other dataset made available as a resource for the field. Turkheimer’s paper abstract states “the negligible results have never been acknowledged,” but in fact, many papers have been devoted to discussing small effect sizes in psychiatric genetics (Gordon, 2021).The success of S4S was never intended to be evaluated based on the number of genetic loci identified. Turkheimer wrote, “S4S was not designed to investigate whether individual level genetic data might be useful at the scale of a mid-sized institution including about 10,000 students… it assumed as much.” In fact, they were correct only in the first part of that statement; studying whether individual level genetic data might be useful in a college setting (although a question I find interesting) was never the point of S4S. Turkheimer refers to the findings (of tiny effect sizes, few robust genetic loci identified) as “unexpected” and “surprising”; in fact, we find the results to be neither, as anyone following the progression of the field of psychiatric genetics would agree. The university administrators with whom we worked to launch the study never expected us to deliver actionable individual-level genetic findings. To use that as the benchmark for evaluating the success of S4S, and then to extrapolate to the larger field of psychiatric genetics, misses the point.The ways in which the S4S project made a significant contribution to the field can be found in other metrics. I am most proud of how we used a community-engaged approach (Dick, 2017) and were intentional about the recruitment of underrepresented populations (Dick et al., 2014), which were uncommon in... (shrink)

At this point in time, it is hard to say which consequences for the concept of mental illness result from modern genetics. Current research projects are trying to find significant statistical correlations between the diagnosis of a disease and a gene locus or an endophenotype. Up until now, there has not been any identification of alleles or mutations causing mental illness. In the meantime, the relations between the genetic basis and the disease are given the term genetic vulnerability as (...) a placeholder; this concept simplifies the complex relations between the DNA and even the simplest cell functions observed in modern genetics. According to complex gene models like the systemic theory of DNA, it will not be possible to identify the genetic factors without a precise knowledge of the factors which modulate the gene expression. The significance of genetics as part of the concept of mental illness will not be able to be defined without further progress in developmental biology and psychology. Currently, psychological theory fails to acknowledge the complexity of the relationship between the DNA and the environment. Some starting points from which to develop such an understanding can be received from developmental studies and studies of the psychophylogenesis . An interdisciplinary concept of the biological basis of the psyche is needed. (shrink)

A recent literature review of commentaries and ‘state of the art’ articles from researchers in psychiatric genetics (PMG) offers a consensus about progress in the science of genetics, disappointments in the discovery of new and effective treatments, and a general optimism about the future of the field. I argue that optimism for the field of psychiatric molecular genetics (PMG) is overwrought, and consider progress in the field in reference to a sample estimate of US National (...) Institute of Mental Health funding for this paradigm for the years 2008 and 2009. I conclude that the amounts of financial investment in PMG is questionable from an ethical perspective, given other research and clinical needs in the USA. (shrink)

Psychiatric genetic research investigates the genetic basis of psychiatric disorders with the aim of more effectively understanding, treating, or, ultimately, preventing such disorders. Given the challenges of recruiting research participants into such studies, the potential for long‐term benefits of such research, and seemingly minimal risk, a strong claim could be made that all non‐acute psychiatric inpatients, including forensic and involuntary patients, should be included in such research, provided they have capacity to consent. There are tensions, however, regarding (...) the ethics of recruiting psychiatric inpatients into such studies. In this paper our intention is to elucidate the source of these tensions from the perspective of research ethics committee interests and decision‐making. We begin by defining inpatient status and outline some of the assumptions surrounding the structures of inpatient care. We then introduce contemporary conceptions of vulnerability, including Florencia Luna’s account of vulnerability which we use as a framework for our analysis. While psychiatric inpatients could be subject to consent‐related vulnerabilities, we suggest that a particular kind of exploitation‐related vulnerability comes to the fore in the context of our case study. Moreover, a subset of these ethical concerns takes on particular weight in the context of genetic research in low‐ and middle‐income countries. At the same time, the automatic exclusion of inpatients from research elicits justice‐related vulnerabilities. (shrink)

Introduction The bioethics literature reflects significant interest in and concern with the use of genetic and genomic information in various settings. Because psychiatric treatment and research raises unique ethical, legal, and social issues, we conducted a scoping review of the biomedical, bioethics, and psychology literature regarding the application of genetic and genomic tools to psychiatric disorders (as listed in the DSM-5) and two associated behaviors or symptoms to provide a more detailed overview of the state of the field. (...) Objectives The primary objective was to examine the available bioethics, biomedical, and psychology literature on applying genetic and genomic tools to psychiatric disorders (other than neurodevelopmental disorders) and two behaviors or symptoms sometimes associated with them (aggression or violence and suicidality) to identify the disorders to which these tools have been applied, the contexts in or purposes for which they have been applied, the ethical, legal, or social concerns associated with those uses, and proposed recommendations for mitigating those concerns. Methods We used Arksey and O’Malley’s scoping review framework: (1) identify the research question; (2) identify relevant studies; (3) select studies; (4) chart the data; and (5) collate, summarize, and report results (2005). We relied on Levac et al. to inform our application of the framework (2010). The PRISMA extension for scoping reviews checklist informed our reporting (2018). We searched three electronic databases MEDLINE (PubMed), Embase, and PsycInfo (EbscoHost) for peer-reviewed journal articles in English to identify relevant literature. One author screened the initial results and additional screening was done in consultation with other authors. A data extraction form using DSM-5 diagnostic categories (excluding neurodevelopmental disorders) was developed and two authors independently each reviewed approximately half of the articles. Inter-rater reliability was ensured by double-coding approximately 10% of the papers. An additional author independently coded 10% of the articles to audit the data. Results In 365 coded publications, we identified 15 DSM-5 diagnostic categories in addition to the two pre-selected behaviors or symptoms (aggression or violence and suicidality) to which genetic or genomic tools have been applied. We identified 11 settings in or purposes for which these tools were applied. Twenty-two types of ethical, legal, or social concerns associated with the application of genetic or genomic tools to these disorders or behaviors/symptoms were identified along with 13 practices or policies that could mitigate these concerns. Conclusion Genetic and genomic tools have been applied to a wide range of psychiatric disorders. These raise a range of ethical, legal, and social concerns. Additional research is warranted to better understand the concerns and effective ways to address them. Advancing the literature to identify relevant ethical, legal, or social concerns and solutions to those problems likely requires greater attention to specific applications of genetic or genomic tools to particular psychiatric disorders and associated behaviors/symptoms as well as broad stakeholder engagement. (shrink)

Behaving presents an overview of the recent history and methodology of behavioral genetics and psychiatric genetics, informed by a philosophical perspective. Kenneth F. Schaffner addresses a wide range of issues, including genetic reductionism and determinism, "free will," and quantitative and molecular genetics. The latter covers newer genome-wide association studies that have produced a paradigm shift in the subject, and generated the problem of "missing heritability." Schaffner also presents cases involving pro and con arguments for genetic testing (...) for IQ and for Attention Deficit Hyperactivity Disorder. Schaffner examines the nature-nurture controversy and Developmental Systems Theory using C. elegans or "worm" studies as a test case, concluding that genes are special and provide powerful tools, including "deep homology," for investigating behavior. He offers a novel account of biological knowledge emphasizing the importance of models, mechanisms, pathways, and networks, which clarifies how partial reductions provide explanations of traits and disorders. The book also includes examinations of personality genetics and of schizophrenia and its etiology, alongside interviews with prominent researchers in the area, and discusses debates about psychosis that led to changes in the DSM-5 in 2013.Schaffner concludes by discussing additional philosophical implications of the genetic analyses in the book, some major worries about "free will," and arguments pro and con about why genes and DNA are so special. Though genes are special, newer perspectives presented in this book will be needed for progress in behavioral genetics- perspectives that situate genes in complex multilevel prototypic pathways and networks. With a mix of optimism and pessimism about the state of the field and the subject, Schaffner's book will be of interest to scholars in the history and philosophy of science, medicine, and psychiatry. (shrink)

Realizing the benefits of translating psychiatric genomics research into mental health care is not straightforward. The translation process gives rise to ethical challenges that are distinctive from challenges posed within psychiatric genomics research itself, or that form part of the delivery of clinical psychiatric genetics services. This article outlines and considers three distinct ethical concerns posed by the process of translating genomic research into frontline psychiatric practice and policy making. First, the genetic essentialism that is (...) commonly associated with the genomics revolution in health care might inadvertently exacerbate stigma towards people with mental disorders. Secondly, the promises of genomic medicine advance a narrative of individual empowerment. This narrative could promote a fatalism towards patients' biology in ways that function in practice to undermine patients' agency and autonomy, or, alternatively, a heightened sense of subjective genetic responsibility could become embedded within mental health services that leads to psychosocial therapeutic approaches and the clinician-patient therapeutic alliance being undermined. Finally, adopting a genomics-focused approach to public mental health risks shifting attention away from the complex causal relationships between inequitable socio-economic, political, and cultural structures and negative mental health outcomes. The article concludes by outlining a number of potential pathways for future ethics research that emphasizes the importance of examining appropriate translation mechanisms, the complementarity between genetic and psychosocial models of mental disorder, the implications of genomic information for the clinician-patient relationship, and funding priorities and resource allocation decision making in mental health. (shrink)

Consideration of ethics has established a firm place in the affairs of psychiatrists. An increased professional commitment to accountability, together with a growing "consumer" movement has paved the way for a creative engagement with the ethical movement. Psychiatric Ethics has carved out a niche for itself as a major comprehensive text and core reference covering the many complex ethical dilemmas which face clinicians and researchers in their everyday practice. This new edition takes a fresh look at recent trends and (...) developments at the interface between ethics and psychiatric practice.For this edition, Sydney Bloch and Paul Chodoff are joined by Stephen Green, a clinical professor in ethics and psychiatry at Georgetown University, in leading 29 of the finest scholars in the field from around the world. Eleven new contributors join the team of authors. They include Drs. Beauchamp, Gutheils, Sabin, McGuffin, Szmulter, Gabbard and Holmes. Since the second edition, the editors have observed several emerging aspects of psychiatric practice requiring coverage. As a result, six new chapters have been added covering the ethical aspects of community psychiatry, managed care, psychiatric genetics, resource allocation, codes of ethics and boundary violations. All others chapters have been fully revised and updated.The book will continue to be essential reading for psychiatrists and other mental health professionals, as well as of interest to ethicists, policy makers, managers and lawyers. (shrink)

Given that natural selection is so powerful at optimizing complex adaptations, why does it seem unable to eliminate genes (susceptibility alleles) that predispose to common, harmful, heritable mental disorders, such as schizophrenia or bipolar disorder? We assess three leading explanations for this apparent paradox from evolutionary genetic theory: (1) ancestral neutrality (susceptibility alleles were not harmful among ancestors), (2) balancing selection (susceptibility alleles sometimes increased fitness), and (3) polygenic mutation-selection balance (mental disorders reflect the inevitable mutational load on the thousands (...) of genes underlying human behavior). The first two explanations are commonly assumed in psychiatric genetics and Darwinian psychiatry, while mutation-selection has often been discounted. All three models can explain persistent genetic variance in some traits under some conditions, but the first two have serious problems in explaining human mental disorders. Ancestral neutrality fails to explain low mental disorder frequencies and requires implausibly small selection coefficients against mental disorders given the data on the reproductive costs and impairment of mental disorders. Balancing selection (including spatio-temporal variation in selection, heterozygote advantage, antagonistic pleiotropy, and frequency-dependent selection) tends to favor environmentally contingent adaptations (which would show no heritability) or high-frequency alleles (which psychiatric genetics would have already found). Only polygenic mutation-selection balance seems consistent with the data on mental disorder prevalence rates, fitness costs, the likely rarity of susceptibility alleles, and the increased risks of mental disorders with brain trauma, inbreeding, and paternal age. This evolutionary genetic framework for mental disorders has wide-ranging implications for psychology, psychiatry, behavior genetics, molecular genetics, and evolutionary approaches to studying human behavior. (Published Online November 9 2006) Key Words: adaptation; behavior genetics; Darwinian psychiatry; evolution; evolutionary genetics; evolutionary psychology; mental disorders; mutation-selection balance; psychiatric genetics; quantitative trait loci (QTL). (shrink)

How we ought to diagnose, categorise and respond to spectrum disabilities such as autism and Attention Deficit/Hyperactivity Disorder (ADHD) is a topic of lively debate. The heterogeneity associated with ADHD and autism is described as falling on various continua of behavioural, neural, and genetic difference. These continua are varyingly described either as extending into the general population, or as being continua within a given disorder demarcation. Moreover, the interrelationships of these continua are likewise often vague and subject to diverse interpretations. (...) -/- In this paper, I explore geneticists' and self-advocates’ perspectives concerning autism and ADHD as continua. These diagnoses are overwhelmingly analysed as falling on a continuum or continua of underlying traits, which supports the notion of “the neurodiversity spectrum”, i.e., a broader swath of human neural and behavioural diversity on which some concentrations of different functioning are diagnosed. I offer a taxonomy of conceptions of the genetic, phenotypic, and endophenotypic dimensionality within and beyond these diagnostic categories, and suggest that the spectrum of neurodiversity is characteristically endophenotypic. (shrink)

Background: Genetic research involving racial/ethnic populations has novel ethical implications for various stakeholders, but ethical acceptability among stakeholders regarding such research is not clear. Methods: As part of a multifaceted National Institute of Mental Health (NIMH)/National Human Genome Research Institute (NHGRI) funded survey, we used repeated-measures factorial multivariate analysis of variance (MANOVA) to compare the perspectives of institutional review board (IRB) chairs (n = 203), investigators (n = 183), and community members (n = 192) on the ethical acceptability of participating (...) in and reporting of psychiatric genetic research focused on racial/ethnic minority groups. Stakeholder views were assessed with two sets of three questions. Results: All stakeholder groups perceived participation in genetic studies focused on racial/ethnic groups as ethically acceptable and endorsed as ethical any decisions by racial/ethnic minorities to decline to participate in such studies if concerned about possible discrimination/stigmatization based on the study findings. Stakeholders disagreed considerably on the ethical acceptability of researchers or journal editors choosing not to publish genetic study results focused on racial/ethnic minority groups based on potential harm of the study findings. Conclusion: Findings show community and professional stakeholders support participation in genetic research focused on specific racial/ethnic groups but recognize that the results of such studies may contribute to discrimination or stigmatization. Stakeholders differed in their perspectives of investigators and editors in balancing ethical issues intrinsic to advancing science versus minimizing harm to potentially vulnerable populations. (shrink)

A large campaign has sought to destigmatize psychiatric disorders by disseminating the view that they are in fact brain disorders. But when psychiatric disorders are associated with neurobiological correlates, laypeople's attitudes toward patients are harsher, and the prognoses seem poorer. Here, we ask whether these misconceptions could result from the essentialist presumption that brain disorders are innate. To this end, we invited laypeople to reason about psychiatric disorders that are diagnosed by either a brain or a behavioral (...) test that were strictly matched for their informative value. Participants viewed disorders as more likely to be innate and immutable when the diagnosis was supported by a brain test as compared to a behavioral test. These results show for the first time that people spontaneously essentialize psychiatric conditions that are linked to the brain, even when the brain probe offers no additional diagnostic or genetic information. This bias suggests that people consider the biological essence of living things as materially embodied. (shrink)

Human genetics research appears to be approaching a period of re-examination due to the decades-long failure of molecular genetic research to uncover the genes presumed to underlie psychiatric disorders, psychological traits, and some common medical conditions. As currently dominant theories of genetic causation come more into question, we will see a renewed interest in reassessing the potential roles of genes and environment in these areas. To illustrate the potentially harmful and diversionary impact of emphasizing genetics over the (...) environment, the author tells a story in the form of a parable. In this parable, the citizens of a medium-size city are confronted with the task of dealing with a group of arsonists who are systematically burning down several houses each week. The Mayor argues that the best way to prevent arson is to analyze the types of wood used to build the city’s houses, with an accompanying lack of interest in arresting the arsonists. Her opponents argue that regardless of the type of wood used, the city and its citizens should prevent arson attacks by focusing attention on identifying and arresting the arsonists. The Mayor’s position prevails, and the arson attacks continue for years to come at the same time as researchers continue to study and analyze the wood used to construct the houses. Informed readers will recognize the analogous ideas, research strategies, interest groups, publications, and historical controversies related to “nature–nurture” issues, which encompass every aspect of the parable. (shrink)

Along with political, economic, ethical, rehabilitative and military dimensions, psychopathological sequelae of war and terrorism also deserve our attention. The terrorist attack on the World Trade Centre ( W.T.C.) in 2001 and the Gulf War of 1990-91 gave rise to a number of psychiatric disturbances in the population, both adult and children, mainly in the form of Post-traumatic Stress disorder (PTSD). Nearly 75,000 people suffered psychological problems in South Manhattan alone due to that one terrorist attack on the WTC (...) in New York and the Pentagon in Washington. In Gulf War I, more that 1,00,000 US veterans reported a number of health problems on returning from war, whose claims the concerned government has denied in more than 90% cases. Extensive and comprehensive neurological damage to the brain of Gulf War I veterans has been reported by one study, as has damage to the basal ganglia in another, and Amyotrophic Lateral Sclerosis (ALS) in a third, possibly due to genetic mutations induced by exposure to biological and chemical agents, fumes from burning oil wells, landfills, mustard or other nerve gases. The recent Gulf War will no doubt give rise its own crop of PTSD and related disorders. In a cost-benefit analysis of the post Gulf War II scenario, the psychopathological effects of war and terrorism should become part of the social audit any civilized society engages in. Enlightened public opinion must become aware of the wider ramifications of war and terrorism so that appropriate action plans can be worked out. (shrink)

This thesis investigates the nature of psychiatric disorders, and to what extent they can form a basis for classification, explanation, and treatment interventions. These questions are important in the light of the “crisis of validity” in psychiatry, according to which current diagnostic categories do not pick out real disorders. I address the questions by defending an account of psychiatric disorders that can better accommodate social aspects and non-epistemic values than the symptom-based model of the Diagnostic and Statistical Manual (...) of Mental Disorders (DSM) and the brain disease model of the biomedical approach, including the Research Domain Criteria (RDoC). I concentrate on three ways that psychiatric disorders can differ from prototypical natural kinds, such as biological species and chemical elements. First, the concept of psychiatric disorder or mental disorder is partly value-laden and cannot be defined based only on scientific facts. Second, the objects of psychiatric classifications are interactive human kinds because people with disorders respond to their classifications through looping effects. Third, sociocultural factors can shape disorders in complex ways, which is indicated by their cross-cultural variation. I argue that these challenges can be overcome with a pluralistic explanatory account that grants an explicit role to value-sensitive considerations and social scientific research. Based on this, I argue that particular disorders can in principle support inductive inferences. ------------------------------------------------------------------------------------------ My key argument is that although whether a condition is considered pathological is partly a value-laden question, this does not rule out a realist account of particular psychiatric disorders as homeostatic property cluster kinds (HPC). I assert that causal mechanisms responsible for psychiatric kinds can be understood non-metaphysically based on the contrastive-counterfactual and interventionist theories of explanation. An advantage of this account is that it can address the concern that psychiatric explanations require one to relate heterogeneous causal factors on different levels, such as genetic, neurological, psychological, and social. My novel argument is that mechanistic explanations of scientific kinds have applicability domains over which they account for specific aspects of kinds and warrant inductive inferences. That is, identifying the applicability domain of an explanation spells out the conditions under which the explanation is expected to be reliable and when it can break down. This helps to understand how different discipline approaches, including social and cultural ones, can be complementary and make an explanation of a psychiatric kind more reliable. On the other hand, the account also shows how the complex nature of psychiatric kinds can license re-classifications for different epistemic and non-epistemic purposes. Finally, in the light of the social implications of psychiatric classifications, I suggest a value-sensitive or ameliorative approach to engineering the concept of psychiatric disorder. In conclusion, my account shows that research on the social and cultural factors that shape psychiatric disorders, and weighing the non-epistemic values that influence classificatory practices, can and should inform classificatory choices as well as policy and treatment interventions. (shrink)

The study of mental illness by the methods of molecular genetics is still in its infancy, but the use of genetic markers in psychiatry may potentially lead to a Virchowian revolution in the conception of mental illness. Genetic markers may define novel clusters of patients having diverse clinical presentations but sharing a common genetic and mechanistic basis. Such clusters may differ radically from the conventional classification schemes of psychiatric illness. However, the reduction of even relatively simple Mendelian phenomena (...) to molecular genetics has been shown to be a surprisingly complex and problematic enterprise. Mental illnesses exist at many levels of including social, environmental, and developmental interactions. Reductionistic shifts in the classification of such a disease entity will have to address the interlevel dynamics that take place within the structure of theories of mental illness. The question of how molecular analysis of psychiatric disease will impact on the structure of existing theories and classification systems is the central topic of this paper. (shrink)

A Kuhnian reformulation of the recent debate in psychiatric nosography suggested that the current psychiatric classification system (the DSM) is in crisis and that a sort of paradigm shift is awaited (Aragona, 2009). Among possible revolutionary alternatives, the proposed fi ve-axes etiopathogenetic taxonomy (Charney et al., 2002) emphasizes the primacy of the genotype over the phenomenological level as the relevant basis for psychiatric nosography. Such a position is along the lines of the micro-reductionist perspective of E. Kandel (...) (1998, 1999), which sees mental disorders reducible to explanations at a fundamental epistemic level of genes and neurotransmitters. This form of micro-reductionism has been criticized as a form of genetic-molecular fundamentalism (e.g. Murphy, 2006) and a multi-level approach, in the form of the burgeoning Cognitive Neuropsychiatry, was proposed. This article focuses on multi-level mechanistic explanations, coming from Cognitive Science, as a possible alternative etiopathogenetic basis for psychiatric classification. The idea of a mechanistic approach to psychiatric taxonomy is here defended on the basis of a better conception of levels and causality. Nevertheless some critical remarks of Mechanism as a psychiatric general view are also offered. (shrink)

New genetic technologies promise to generate valuable insights into the aetiology of several psychiatric conditions, as well as a wider range of human and animal behaviours. Advances in the neurosciences and the application of new brain imaging techniques offer a way of integrating DNA analysis with studies that are looking at other biological markers of behaviour. While candidate 'genes for' certain conditions, including schizophrenia and bipolar disorders, are said to be 'un-discovered' at a faster rate than they are discovered, (...) many studies are being conducted on personality traits such as aggressiveness and anti-social traits. The clinical applicability and implications of these studies are often discussed within the scientific community. However, little attention has so far been paid to their possible policy implications in relation to criminality management and to Criminal Law itself. Similarly, the related ethical issues arising in the field of crime control, and the tensions between enhancing security for society and protecting civil liberties, are currently under-explored. This paper investigates these ethical issues by focusing on the views of those professionals – including judges, lawyers, probation officers and social workers – who work with individuals 'deemed at risk' of violent and aggressive behaviours. It also discusses and problematizes mainstream rhetoric and arguments around the notion of 'risky individuals'. (shrink)

There is a steadily growing literature on the role of the immune system in psychiatric disorders. So far, these advances have largely taken the form of correlations between specific aspects of inflammation (e.g. blood plasma levels of inflammatory markers, genetic mutations in immune pathways, viral or bacterial infection) with the development of neuropsychiatric conditions such as autism, bipolar disorder, schizophrenia and depression. A fundamental question remains open: why are psychiatric disorders and immune responses intertwined? To address this would (...) require a step back from a historical mind–body dualism that has created such a dichotomy. We propose three contributions of active inference when addressing this question: translation, unification, and simulation. To illustrate these contributions, we consider the following questions. Is there an immunological analogue of sensory attenuation? Is there a common generative model that the brain and immune system jointly optimise? Can the immune response and psychiatric illness both be explained in terms of self-organising systems responding to threatening stimuli in their external environment, whether those stimuli happen to be pathogens, predators, or people? Does false inference at an immunological level alter the message passing at a psychological level (or vice versa) through a principled exchange between the two systems? (shrink)

Given the rise of genetic etiological beliefs regarding psychiatric disorders, a growing body of research has focused on trying to elucidate the effects that such explanatory frameworks might be having on how mental disorders are perceived by patients, clinicians, and the general public. Genetic and other biomedical explanations of mental disorders have long been seen as a potential tool in the efforts to destigmatize mental disorders, given the harshness of the widespread negative attitudes about them and the important negative (...) clinical and social impacts of this stigma. The conventional wisdom has appeared to be that because the effects of genes are seen as falling outside individual control, conceiving of mental disorders as caused by genes casts patients as blameless, thereby reducing stigmatization. Indeed, the results of experimental and correlational research have now robustly linked genetic and other biomedical explanations for mental disorders with reductions in the extent to which people are blamed for their psychiatric symptoms. However, research examining the impact of genetic and other biomedical explanations of mental disorders has also suggested that they can have significant downsides. The most consistently observed negative effect of these kinds of explanations is that they can apparently lead to the assumption that mental disorders are unlikely to improve or abate. Genetic and other biomedical explanations of mental disorders can also increase people’s confidence in the effectiveness of biomedical treatments (such as pharmacotherapy) but decrease their confidence in the effectiveness of “nonbiomedical” treatments (such as psychotherapy). (shrink)

Attention-deficit/hyperactivity disorder is a neurodevelopmental disorder with a childhood prevalence of 5%. In about two-thirds of the cases, ADHD symptoms persist into adulthood and often cause significant functional impairment. Based on the results of family and twin studies, the estimated heritability of ADHD approximates 80%, suggests a significant genetic component in the etiological background of the disorder; however, the potential genetic effects on disease risk, symptom severity, and persistence are unclear. This article provides a brief review of the genome-wide and (...) candidate gene association studies with a focus on the clinical aspects, summarizing findings of ADHD disease risk, ADHD core symptoms as dimensional traits, and other traits frequently associated with ADHD, which may contribute to the susceptibility to other comorbid psychiatric disorders. Furthermore, neuropsychological impairment and measures from neuroimaging and electrophysiological paradigms, emerging as potential biomarkers, also provide a prominent target for molecular genetic studies, since they lie in the pathway from genes to behavior; therefore, they can contribute to the understanding of the underlying neurobiological mechanisms and the interindividual heterogeneity of clinical symptoms. Beyond the aforementioned aspects, throughout the review, we also give a brief summary of the genetic results, including polygenic risk scores that can potentially predict individual response to different treatment options and may offer a possibility for personalized treatment for the therapy of ADHD in the future. (shrink)

The exponential growth of genetic knowledge and precision medicine research raises hopes for improved prevention, diagnosis, and treatment options for children with behavioral and psychiatric conditions. Although well-intended, this prospect also raise the possibility — and concern — that behavioral, including psychiatric genetic data would be increasingly used — or misused — outside the clinical context, such as educational settings. Indeed, there are ongoing calls to endorse a “personalized education” model that would tailor educational interventions to children's behavioral (...) and psychiatric genetic makeup. This article explores the justifications for, and prospects and pitfalls of such endeavors. It considers the scientific challenges and highlights the ethical, legal, and social issues that will likely arise should behavioral genetic data become available and are routinely incorporated in student education records. These include: when to disclose students' behavioral and psychiatric genetic profile; whose genomic privacy is protected and by whom; and how students' genetic data may affect education-related decisions. I argue that the introduction of behavioral genetics in schools may overshadow the need to address underlying structural and environmental factors that increase the risk for psychiatric conditions of all students, and that the unregulated use of student behavioral genetic profiles may lead to unintended consequences that are detrimental for individuals, families and communities. Relevant stakeholders — from parents and students to health professionals, educators, and policy-makers — ought to consider these issues before we forge ahead with a genomically informed education system. (shrink)

Mitochondrial ATP synthesis, calcium buffering, and trafficking affect neuronal function and survival. Several genes implicated in mitochondrial functions map within the genomic region associated with 22q11.2 deletion syndrome (22q11DS), which is a key genetic cause of neuropsychiatric diseases. Although neuropsychiatric diseases impose a serious health and economic burden, their etiology and pathogenesis remain largely unknown because of the dearth of valid animal models and the challenges in investigating the pathophysiology in neuronal circuits. Mouse models of 22q11DS are becoming valid tools (...) for studying human psychiatric diseases, because they have hemizygous deletions of the genes that are deleted in patients and exhibit neuronal and behavioral abnormalities consistent with neuropsychiatric disease. The deletion of some 22q11DS genes implicated in mitochondrial function leads to abnormal neuronal and synaptic function. Herein, we summarize recent findings on mitochondrial dysfunction in 22q11DS and extend those findings to the larger context of schizophrenia and other neuropsychiatric diseases. (shrink)

Failings of a categorical systemFor decades, standardized classification systems have attempted to define psychiatric disorders in our mental health care system, with the Diagnostic and Statistical Manual of Mental Disorders (5th ed.; DSM-5; American Psychiatric Association (APA), 2013) and International Statistical Classification of Diseases and Related Health Problems 10th revision (ICD-10; World Health Organization, 2010) being internationally best-known. One of the major advantages of the DSM must be that it has seriously diminished the international linguistic confusion regarding (...) class='Hi'>psychiatric disorders. Since its introduction, it contributed extensively towards one common international language for defining and conceptualizing psychiatric disorders. Strikingly, within the field of psychological testing a similar step forward seems to have not yet been taken. At present, there exists no international standard for the use of psychological tests that takes the definition of a specific symptom as listed in DSM-5 as its starting point, and reliably and validly measures this symptom. Rather, the majority of tests are measuring constructs consisting of a multitude of symptoms. For example, the Beck’s Depression Inventory (Beck et al., 1996) measures core symptoms of depression summing up to a depression score. Accordingly, we believe it is time for a change. The diagnostics of psychiatric disorders, where disorders are defined as nosological units with a single cause, a single organic substrate, and a single time course, has been problematic for centuries. The field of psychiatry has always been ambivalent about its desire to follow a medical model (Blaney, 2015), but afflicted due to its definitions of pathology. The definition of a psychiatric disorder in DSM-5 offers little room for a clear cut pathogenesis and harsh demarcation of syndromes. This is reflected in the DSM-5, where it states: “A mental disorder is a syndrome characterized by clinically significant disturbance in an individual’s cognition, emotion regulation, or behavior that reflects a dysfunction in the psychological, biological, or developmental processes underlying mental functioning” (APA, 2013, p.20). An unfortunate and recognized consequence of this definition within the current system is that many symptoms overlap within categories of psychiatric disorders and patients end up diagnosed with many co-morbid disorders.Two fundamental problemsRegardless of new attempts to improve the diagnostics of psychiatric disorders, the DSM-5 represents the status quo. Consequently, the distinction between diagnosis and classification remains substantial and more than a discussion on semantics. We identify two fundamental problems within the current framework. Generally, a psychiatric diagnosis is considered to be descriptive (Hengeveld and Schudel, 2003). The clinician will describe a syndrome (its nature, timespan, and severity) within the framework of a disorder, and often include a differential diagnosis, predisposing protective or vulnerability factors, and provoking or maintaining factors. Within the DSM-5 framework, a similar ‘approach to clinical case formulation’ is taken (APA, 2013, p. 19). Evidently, a descriptive diagnosis has a hypothetical character. It consists of the clinician’s hypothesis and is based on his or hers professional considerations according to the abovementioned factors. Once the clinician has formulated a descriptive diagnosis, it is then complementary ‘translated’ into a DSM-5 classification. Herein lies the problem. For the layman, the existence of this distinction between diagnosis and classification is usually unknown. Preceding treatment, the clinician will give the client a classification of the existing psychiatric problems and the client may attribute more meaning to it than appropriate, thereby fostering the risk of reification. Second, the DSM-5 is a categorical system. Thus, individual disorders are regarded as discrete units – ‘you either have it, or you don’t’. DSM-5 states about this: “(…) scientific evidence places many, if not most, disorders on a spectrum with closely related disorders that have shared symptoms, shared genetic and environmental risk factors (…)”. And “(…) we have come to recognize that the boundaries between disorders are more porous than originally perceived.” (APA, 2013, p. 6). This leads to a fundamental problem. Because the overwhelming majority of psychiatric disorders examined thus far using taxometric methods appear to be dimensional in nature (Haslam, 2003; Widiger and Samuel, 2005), consequently all of their categorizations become artificial and debatable. Even though DSM-5 took a modest step towards a more dimensional approach, its core remains categorical. To illustrate, consider the Borderline Personality Disorder (BPD). This classification consists of nine diagnostic criteria of which a minimum of five need to be present for the diagnosis of BPD. A simple numerical combination algorithm leads to a staggering number of 256 distinct presentations of BPD (Albion et al., 2013). Due to this chameleon-like nature, the disorder’s diagnostic validity becomes questionable. Strikingly, this number is relatively small when compared to other conditions, e.g., there are 636,120 ways to have posttraumatic stress disorder (Galatzer-Levy and Bryant, 2013).DSM-5 does propose an alternative model for personality disorders based on personality functioning and traits (APA, 2013, p. 761), as a possible answer to the problem that most patients fit with multiple co-morbid personality disorders or to the category of personality disorder not otherwise specified. In November 2012, the chair committee of APA decided to move this alternative model to section III of DSM-5 and to sustain the categorical system in section II. A potential solutionDSM-5 and its predecessors have brought about an invaluable improvement regarding the formulation of a common international language for psychiatric disorders. However, the individual disorders fit poorly with its starting point of discrete units and strict boundaries. Van Os (2014) has argued for a better balance between the categorical and personalized aspects of psychiatric disorders. We argue for a two-step approach.Particularly due to the ‘weak boundaries’ between disorders, it might be beneficial to limit ourselves by merely categorizing clients into the main categories of the DSM-5 according to their most prominent symptoms (Van Os, 2014), i.e. their main complaint. In other words, clinicians could first ask themselves whether the symptomatology is concerning a neurodevelopmental disorder, or a bipolar and related disorder, or a depressive disorder, and so on. It will drastically reduce the over 400 classifications in DSM-5 down to 20 categories. Van Os (2014) even argues to combine some of the main categories, reducing this number even further to 15 categories. The advantages of reducing the over 400 classifications are fivefold: 1) a syndrome, being an aggregation of symptoms, creates a false relation between symptoms that are that are already heterogeneous themselves; 2) 15 broad categories are functional: it results into a very heterogeneous group of clients within a category and thus prevents stereotypes and invites further personalizing of complaints; and 3) a dimensional measure of a symptom rather than a syndrome will correspond better with the client regardless of it not providing the complete picture. Focusing on the main complaint will indicate where there is an immediate need for care (Van Os, 2014); 4) it will allow clinicians to recognise subthreshold conditions more easily (Magruder and Calderone, 2000); and 5) it might facilitate the development of clear demarcations between normal and abnormal functioning (Kessler, 2002; Widiger and Samuel, 2005). Please, see also Table 1.This also fits well within scientific advances, as thus far strongest evidence has been found for a distinction between internalizing and externalizing disorders, even superseding these 15 main categories (DSM-5; APA, 2013, p.13, but see Weiss et al., 1998). The second step would concern the personalized aspect, which we argue to define on a level of core symptoms of the specific main category, to be agreed upon later. To assess these core symptoms, the field of psychological testing could develop an internationally applicable instrument to reliably and validly measure each (core) symptom on a dimensional scale. Many of these instruments are readily available and have proven its psychometric properties within scientific research. Elements from these instruments could be easily transformed to work within the new system. Within the field of psychology, this approach could aid development of a common international language to define symptoms, analogous to the field of psychiatry. Importantly, current psychological testing mainly implies the use of self-report measures. This leads to an abundance of auto-amnestic information. To increase the reliability and validity of psychological tests to assess DSM-5 symptoms, it may be important to add two additional information resources. This would entail psychological tests where a next of kin answers questions about the symptom of the client, and psychological tests that include the clinicians’ judgment, such as structured clinician-based interviews. Conversely, we also need to acknowledge the well-known limitations of clinical judgment (e.g., Faust, 1986; Garb, 1998). Advantages of a new frameworkThe changes we suggest have big implications and are not easily implemented in the current framework. Clients may prefer the comfort of a single clear label, similar to what they are used to in other areas of medicine. Health insurance providers and policy makers may argue for single labels as well. Therefore, it would require a lot of explanation from our clinicians to promote a change. Our suggestions for broader categories may not disambiguate the current situation better than the existing approach, but it will promote personalisation of health care. Difficulties in diagnostic reliability will remain in disorders that fall on the boundaries of the taxons, e.g., schizoaffective disorder versus bipolar disorder with psychotic characteristics, which may benefit from further study. There are also some politically tinged questions to keep in mind: How will we finance our health care, and how will we ensure a gradual transition from the current financing system, including clients who already have their labels? What about visitations from insurers and health inspection? How can they control for a good standard of quality in health care when considering the increasing heterogeneity? Nevertheless, we argue that the benefits outweigh the disadvantages. We will see a shift from a categorical to a personalized approach, which will lead to less (self) stigmatizing, less estrangement, and it will challenge reification thinking. DSM-V states that “a reformulation of research goals should also keep DSM-5 central to the development of dimensional approaches to diagnosis that will likely supplement or supersede current categorical approaches to diagnosis in coming years” (APA, 2013, p. 13). Our proposition for psychological testing on symptom level could contribute to this development. Furthermore, this new approach will do more justice to the heterogeneity of symptoms within and outside of classification categories, see also Table 1. Moreover, in this new approach we join forces of expert knowledge from the fields of psychiatry and psychological science. Finally, it offers new and potentially better opportunities to map health care needs. This in turn will lead to a better interface for allocation of appropriate treatment. It will present a clearer picture of when preventative care is preferred over treatment and vice versa. Importantly, health care needs will be more closely attuned to the ‘own story’ of the client.We argue for the national and international psychological associations in Europe and the United States of America to support the idea of a collective approach to develop an internationally standardized psychological testing battery to reliably assess all the core symptoms of the main categories in DSM-5. (shrink)

In lieu of an abstract, here is a brief excerpt of the content:Dialectical Tension Between Gloomy and Rosy Prospects of Behavioral GeneticsAwais Aftab, MD (bio)Turkheimer and Greer’s article “Spit for Science and the Limits of Applied Psychiatric Genetics” (2024) offers a devastating critique of the state of psychiatric genetics, using Spit for Science (S4S) as a case study. I have read the paper many times in the process of writing this commentary, and each time I am (...) left inarticulate. Nonetheless, I hope that my comments, from the point of view of a practitioner who operates at the intersection of clinical psychiatry, psychiatric science, and philosophy of psychiatry, will be of some value to the discussion. I have no substantial disagreements with Turkheimer and Greer. The main point I wish to convey is that there is reason to hope that findings from genetic research will contribute to clinical progress in psychiatry in an incremental and iterative manner, but because psychiatric genetics has overpromised and underdelivered, we find ourselves vacillating between bullish and bearish moods.Some critics may say that the choice to selectively focus on S4S is unfair, or that it gives a misleading impression of the current state of psychiatric genetics. The launch and implementation of S4S captures a particular moment in the history of psychiatric genetics when it was known that individual associations will be small and that large samples will be needed for significant associations, but it was not appreciated exactly how small and how large respectively. Initial estimates of sample sizes needed for successful genetic associations turned out to be wildly inadequate. Progress occurred only with unprecedented international collaboration and extremely large sample sizes. For example, a 2022 genome-wide association study (GWAS) of schizophrenia included more than 76,000 people with schizophrenia and 240,000 controls (Trubetskoy et al., 2022)! S4S is one project from one institution. It is understandable in retrospect that a sample of 10,000 freshmen could only have delivered so much. It may be argued that whatever the promise of psychiatric genetics as a field, it is not constrained by the success or failure of S4S.On the one hand, it is true that S4S did not have the requisite sample size. On the other hand, the contemporary understanding of the genetics of alcohol use has not improved on insights from S4S by that much (Deak et al., 2019). SNP-based heritability estimate of problematic alcohol use [End Page 451] is close to 10% based on a GWAS of 435,000 individuals (Zhou et al., 2020), consistent with statistically non-significant estimates from S4S. The same GWAS has identified 29 risk variants, and genetic correlations with more than a hundred other phenotypes. Transcriptomic analysis has revealed that implicated genes are expressed in the brain but also in gastrointestinal, adipose, and liver tissue, pointing toward pathways of protection and vulnerability. A polygenic risk score (PRS) derived from associated variants is consistently and significantly associated with alcohol dependence, with variance explained ranging from 0.77% to 2.12% in different samples (Zhou et al., 2020).At present, PRS for problematic alcohol use has little predictive value at the individual level and is practically worthless from the standpoint of clinical practice. There are hints that genetic associations can point toward brain mechanisms involved in alcohol use disorder, but we have little to show for it yet. That PRS will achieve clinical utility is not guaranteed but neither is it impossible. A PRS for externalizing behavior explains approximately 10% of the variance, which is on par with factors such as socioeconomic status and neighborhood disadvantage (Karlsson Linnér et al., 2021). And even if PRS does not become a common part of clinical practice, it can still be a useful tool in clinical research. With regard to understanding mechanisms, the trivial effect size of the genetic association is by itself irrelevant. This point is made eloquently by Steven HymanWhen used as a tool to associate a trait with biology, the effect size of the allele on the ultimate phenotype does not matter… what makes a gene product a good drug target is not the effect size of the associated allele, but its overall role in biology… Once a pathway is shown to... (shrink)

Many of Rose's criticisms of determinism in biology have clear relevance to modern cognitive and psychiatric science; too narrow a focus on the brain as an information processing machine runs the risk of neglecting the context in which information processing takes place, and too narrow a focus on the neuroscience of psychopathology runs the risk of neglecting other levels of explanation for these phenomena. It should be emphasized, however, that animal and genetic studies of phenomena of interest to cognitive (...) and psychiatric science (e.g., Alzheimer's disorder, schizophrenia, attention deficit/hyperactivity disorder, and violence), while perhaps only providing a partial perspective, may be useful in understanding these phenomena and in leading to appropriate psychiatric interventions. (shrink)

The paper suggests an application of the precautionary principle to the use of genetics in psychiatry focusing on scientific uncertainty. Different levels of uncertainty are taken into consideration—from the acknowledgement that the genetic paradigm is only one of the possible ways to explain psychiatric disorders, via the difficulties related to the diagnostic path and genetic methods, to the value of the results of studies carried out in this field. Considering those uncertainties, some measures for the use of (...) class='Hi'>genetics in psychiatry are suggested. Some of those measures are related to the conceptual limits of the genetic paradigm; others are related to present knowledge and should be re-evaluated. (shrink)

In recent decades, attempts to explain autism have been frustrated by the heterogeneous nature of its behavioral symptoms and the underlying genetic, neural, and cognitive mechanisms that produce them. This has led some to propose eliminating the category altogether. The eliminativist inference relies on a conception of psychiatric categories as kinds defined by their underlying mechanistic structure. I review the evidence for eliminativism and propose an alternative model of the family of autisms. On this account, autism is a network (...) category defined by a set of idealized exemplars linked by multiple levels of theoretically significant properties. I argue that this network model better captures the empirical phenomena, the historical growth of the category, and the ways the category has been shaped by social norms and interests. Finally, I defend a realist interpretation of network categories against the challenge from eliminativists. (shrink)

In Two Minds is a practical casebook of problem solving in psychiatric ethics. Written in a lively and accessible style, it builds on a series of detailed case histories to illustrate the central place of ethical reasoning as a key competency for clinical work and research in psychiatry. Topics include risk, dangerousness and confidentiality; judgements of responsibility; involuntary treatment and mental health legislation; consent to genetic screening; dual role issues in child and adolescent psychiatry; needs assessment; cross-cultural and gender (...) issues; rational and irrational suicide; shared decision making in multi-agency teams, and the growing role of the user's voice in psychiatry. Key ethical concepts are carefully introduced and explained. The text is richly supported by detailed guides for further reading. There are separate chapters on teaching psychiatric ethics, including a sample seminar, and on writing a research ethics application. Each case history and discussion is followed by a critical commentary from a practitioner with relevant experience. Jim Birley adds a comparative international perspective on psychiatric ethics. Cartoons by Johnny Cowee provide punchy counterpoint! In Two Minds is the sister volume to the third edition of Sidney, Paul Chodoff and Steven Green's highly successful Psychiatric Ethics. In providing a bridge between theory and practice, it will be essential reading for everyone concerned with improving standards in mental health care. (shrink)

This paper will consider the right not to know in the context of psychiatric disorders. It will outline the arguments for and against acquiring knowledge about the results of genetic testing for conditions such as breast cancer and Huntington’s disease, and examine whether similar considerations apply to disclosing to clients the results of genetic testing for psychiatric disorders such as depression and Alzheimer’s disease. The right not to know will also be examined in the context of the diagnosis (...) of psychiatric disorders that are associated with stigma or for which there is no effective treatment. (shrink)

Mental disorders as defined by current classifications are not fully supported by scientific evidence. It is unclear whether main disorders should be broken down into separate categories or disposed along a continuous spectrum. In the near future, new classes of mental disorders could be defined through associations of so-called abnormalities observed at the genetic, molecular and neuronal circuitry levels.

Behavioral genetics has as its goal the discovery of genes that play a significant causal role in complex phenotypes that are socially relevant such a parenting, aggression, psychiatric disorders, intelligence, and even race. In this article, I present the stories of the discoveries of three such important phenotypes: maternal nurturing behavior and the c-fosB gene; intelligence and phenylketonuria ; and pair-bonding and monogamy and show that the reality is considerably more complex than often portrayed. These accounts also lay (...) bare some fundamental misconceptions of this field in which genes hold a privileged place and inherently subjective phenomena are mistakenly objectified. (shrink)

Currently, there is a growing interest in combining genetic information with physiological data measured by functional neuroimaging to investigate the underpinnings of psychiatric disorders. The first part of this paper describes this trend and provides some reflections on its chances and limitations. In the second part, a thought experiment using a commonsense definition of psychiatric disorders is invoked in order to show how information from this kind of research could be used and potentially abused to invent new mental (...) illnesses. It is then argued why an inference to the best explanation could provide an antidote to such attempts. The conclusion emphasises why normative criteria, such as those used to define disorders, cannot be derived from descriptive empirical results alone. While the etiology of some psychiatric diseases may be purely organic, there are many other cases where the psychiatric symptoms and the associated genotypes and phenotypes have an essentially and irreducibly external meaning that is derived from social and political factors. A limited perspective on the genes and brain of man carries the risk that psychiatry may increasingly treat the effects of other domains, although social and political solutions would be more appropriate. (shrink)

I begin by examining how genetics drivesschizophrenia research, and raise both familiar andrelatively novel criticisms of the evidence putativelysupporting the genetic basis of schizophrenia. Inparticular, I call attention to a set of concernsabout the effects of placentation on concordance ratesof schizophrenia in monozygotic twins, which furtherweakens the case for schizophrenia''s so-called stronggenetic component. I then underscore two criticalpoints. First, I emphasize the importance of takingseriously considerations about the complexity of bothontogenesis and the development of hereditarydiseases. The recognition of developmentalconstraints (...) and supports is crucial, for attention todevelopment exposes the naivete of too many models ofgene action in the aetiology of disease. Secondly, Iattend to those schizophreniologists who ignoremethodological criticisms and thus presume a geneticbasis for schizophrenia, and then seek the schizophrenic genotype lacking an adequatephenotype. In response I attempt to demonstrate thenecessity of a sustained effort at characterizing thephenotype of schizophrenia as an enabling conditionfor the whole enterprise of psychiatric genetics – andfor psychiatry itself. Without the organism-levelphenotype, research at the level of genes will remainunproductive – assuming of course that research at thegenetic level is appropriate at all. (shrink)

Contemporary psychiatry finds itself in the midst of a crisis of classification. The developments begun in the 1980s—with the third edition of the Diagnostic and Statistical Manual of Mental Disorders —successfully increased inter-rater reliability. However, these developments have done little to increase the predictive validity of our categories of disorder. A diagnosis based on DSM categories and criteria often fails to accurately anticipate course of illness or treatment response. In addition, there is little evidence that the DSM categories link up (...) with genetic findings, and even less evidence that they... (shrink)