Asymmetric Causal Attributions to Environmental Influences for Prosocial Versus Antisocial Behavior.

Several recent studies have explored how people may favor different explanations for others' behavior depending on the moral or evaluative valence of the behavior in question. This research tested whether people would be less willing to believe that a person's environment played a role in causing her to exhibit antisocial (as compared to prosocial) behavior. In three experiments, participants read a description of a person engaging in either antisocial or prosocial behavior. Participants were less willing to endorse environmental causes of antisocial (versus prosocial) behavior when the environmental influence in question was witnessing others behaving similarly, either during childhood (Experiment 1) or recently (Experiment 2), or being directly encouraged by others to engage in the behavior described (Experiment 3). These results could be relevant to understanding why people resist attributing wrongdoing to causes outside of individual control in some cases.

Individualized interventions for rare genetic conditions and the research-treatment spectrum: Stakeholder perspectives.

PURPOSE: Advances in the study of ultrarare genetic conditions are leading to the development of targeted interventions developed for single or very small numbers of patients. Owing to the experimental but also highly individualized nature of these interventions, they are difficult to classify cleanly as either research or clinical care. Our goal was to understand how parents, institutional review board members, and clinical geneticists familiar with individualized genetic interventions conceptualize these activities and their implications for the relationship between research and clinical care. METHODS: We conducted qualitative, semi-structured interviews with 28 parents, institutional review board members, and clinical geneticists and derived themes from those interviews through content analysis. RESULTS: Individuals described individualized interventions as blurring the lines between research and clinical care and focused on hopes for therapeutic benefit and expectations for generalizability of knowledge and benefit to future patients. CONCLUSION: Individualized interventions aimed at one or few patients reveal the limitations of a binary framing of research and clinical care. As a hybrid set of activities, individualized interventions suggest the need for flexibility and new frameworks that acknowledge these activities across the spectrum of research and clinical care.

Asymmetrical genetic attributions for the presence and absence of health problems.

OBJECTIVE: Recent research has suggested that people more readily make genetic attributions for positively valenced or desirable traits than for negatively valenced or undesirable traits-an asymmetry that may be mediated by perceptions that positive characteristics are more 'natural' than negative ones. This research sought to examine whether a similar asymmetry in genetic attributions would emerge between positive and negative health outcomes. DESIGN: Across seven experiments, participants were randomly assigned to read a short vignette describing an individual experiencing a health problem (e.g. hypertension) or a corresponding healthy state (e.g. normal blood pressure). MAIN OUTCOME MEASURES: All participants provided ratings of naturalness and genetic attributions for the outcome described in their assigned vignette. RESULTS: For diagnoses other than addictive disorders, participants rated the presence of a diagnosis as less genetically caused than its absence; for addictive disorders, the presence of a diagnosis was rated as more genetically caused than its absence. Participants consistently rated the presence of a health problem as less natural than its absence. CONCLUSION: Even within a single domain of health, people ascribe differing degrees of 'naturalness' and genetic causation to positive versus negative health outcomes, which could impact their preferences for treatment and prevention strategies.

The Emergence of Psychiatry: 1650-1850.

Western psychiatry emerged as a medical specialty caring for the mentally ill over the course of the late 18th and early 19th centuries. This emergence was a contingent process, dependent on the co-occurrence of three historical developments that together shaped the young discipline. The first was the rise of the mind as an entity with numerous active faculties in the conceptual space between the body and the Christian soul. Only by the latter half of the 18th century was it common to conceptualize conditions like mania or melancholy as mental illnesses. The second advance critical to psychiatry's proto-specialty status, with its increasing focus on a mechanistic understanding of disease, was the rejection of humoral theories of insanity in favor of the brain and nerves as the seat of madness. The third development was the rise of the asylum. Only in dedicated institutions could mad-doctors be exposed to large numbers of the insane, permitting the development of a specialized clinical vocabulary grounded in faculties of mind, which led to new nosologic systems. The decline of humoral medicine, with its purges, bleeding, and emetics, and the urgent clinical need for care produced, in early asylums, the first novel treatment from the young specialty: moral therapy. We tell this story focusing mainly on the work of five philosophers and physicians: Descartes, Willis, Locke, Boerhaave, de Sauvages, and Cullen. Throughout its history, psychiatry has struggled with its sometimes disconjugate goals of understanding both mind and brain, with alternating efforts to expel one of these tasks from the profession. A historical perspective demonstrates that psychiatry is a profession inextricably linked to these two contrasting projects-and, indeed, jointly constituted by them.

Asymmetric genetic attributions for one's own prosocial versus antisocial behavior.

People tend to rate prosocial or positive behavior as more strongly influenced by the actor's genes than antisocial or negative behavior. The current study tested whether people would show a similar asymmetry when rating the role of genes in their own behavior, and if so, what variables might mediate this difference. Participants were prompted to think about an example of their own behavior from the past year that was either prosocial or antisocial. Those in the prosocial condition rated the role of genetics in causing the behavior as significantly greater than did those in the antisocial condition. A mediation analysis suggested that this asymmetry could be accounted for by a tendency to view prosocial behavior as more natural and more aligned with one's true self than antisocial behavior. These findings add to a growing body of evidence suggesting that people's reasoning about genetics may be influenced by evaluative judgments.

Genetic attributions and perceptions of naturalness are shaped by evaluative valence.

Genetic influences on human behavior are increasingly well understood, but laypeople may endorse genetic attributions selectively; e.g., they appear to make stronger genetic attributions for prosocial than for antisocial behavior. We explored whether this could be accounted for by the relationship of genetic attributions to perceptions of naturalness. Participants read about positively or negatively valenced traits or behaviors and rated naturalness and genetic causation. Positively valenced phenotypes were rated significantly more natural and significantly more genetically influenced than negatively valenced phenotypes, and the former asymmetry significantly mediated the latter (Experiments 1 and 2). Participants' interpretation of what "natural" meant was not synonymous with valence or genetic attributions (Experiment 3). People ascribe differing degrees of genetic influence to the same phenotype depending on whether it is expressed in socially favored or disfavored ways, potentially representing a significant threat to public understanding of genetics.

The prospects of precision psychiatry.

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.

Psychopathy as an Emergent Interpersonal Syndrome: Further Reflections and Future Directions.

In our article (Lilienfeld et al., 2019), we hypothesized that psychopathy and some other personality disorders are emergent interpersonal syndromes (EISs): interpersonally malignant configurations of distinct personality subdimensions. We respond to three commentaries by distinguished scholars who raise provocative challenges to our arguments and intriguing suggestions for future research. We clarify the role of folk concepts in our understanding of psychopathy, offer further suggestions for testing our interactional hypotheses, consider the role of boldness in motivational accounts of psychopathy, and discuss future directions for incorporating developmental considerations and the role of victims in our EIS account. We are optimistic that this account will prove to be of heuristic value, and should encourage researchers and theoreticians to explore alternative models of psychopathy and other personality disorders.

Personality Disorders as Emergent Interpersonal Syndromes: Psychopathic Personality as a Case Example.

Personality disorders have long been bedeviled by a host of conceptual and methodological quandaries. Starting from the assumption that personality disorders are inherently interpersonal conditions that reflect folk concepts of social impairment, the authors contend that a subset of personality disorders, rather than traditional syndromes, are emergent interpersonal syndromes (EISs): interpersonally malignant configurations (statistical interactions) of distinct personality dimensions that may be only modestly, weakly, or even negatively correlated. Preliminary support for this perspective derives from a surprising source, namely, largely forgotten research on the intercorrelations among the subscales of select MMPI/MMPI-2 clinical scales. Using psychopathic personality as a case example, the authors offer provisional evidence for the EIS hypothesis from four lines of research and delineate its implications for personality disorder theory, research, and classification. Conceptualizing some personality disorders as EISs elucidates long-standing quandaries and controversies in the psychopathology literature and affords fruitful avenues for future investigation.

Asymmetrical genetic attributions for prosocial versus antisocial behaviour.

Genetic explanations of human behaviour are increasingly common. While genetic attributions for behaviour are often considered relevant for assessing blameworthiness, it has not yet been established whether judgements about blameworthiness can themselves impact genetic attributions. Across six studies, participants read about individuals engaging in prosocial or antisocial behaviour, and rated the extent to which they believed that genetics played a role in causing the behaviour. Antisocial behaviour was consistently rated as less genetically influenced than prosocial behaviour. This was true regardless of whether genetic explanations were explicitly provided or refuted. Mediation analyses suggested that this asymmetry may stem from people's motivating desire to hold wrongdoers responsible for their actions. These findings suggest that those who seek to study or make use of genetic explanations' influence on evaluations of, for example, antisocial behaviour should consider whether such explanations are accepted in the first place, given the possibility of motivated causal reasoning.

Why not be pluralists about explanatory reduction?

Borsboom et al. convincingly argue that, from their symptom network perspective, mental disorders cannot be reduced to brain disorders. While granting that network structures exist, I respond that there is no reason to think they are the only psychiatric phenomena worth explaining. From a pluralist perspective, what is required is not a full-scale rejection of explanatory reductionism but a critical attention to the circumstances of its application.

Behavioral Genetics and Attributions of Moral Responsibility.

While considerable research has examined how genetic explanations for behavior impact assessments of moral responsibility, results across studies have been inconsistent. Some studies suggest that genetic accounts diminish ascriptions of responsibility, but others show no effect. Nonetheless, conclusions from behavior genetics are increasingly mobilized on behalf of defendants in court, suggesting a widespread intuition that this sort of information is relevant to assessments of blameworthiness. In this paper, we consider two sorts of reasons why this kind of intuition, if it exists, is not consistently revealed in empirical studies. On the one hand, people may have complex and internally conflicting intuitions about the relationship between behavior genetics and moral responsibility. On the other hand, it may be that people are motivated to think about the role of genetics in behavior differently depending on the moral valence of the actions in question.

Correction to: Behavioral Genetics and Attributions of Moral Responsibility.

The original version of this article unfortunately contained a few mistakes in the Introduction section.

Darwin at Orchis Bank: Selection after the Origin.

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.