https://science.sciencemag.org/content/sci/5/110/206.full.pdf

The american psychological association.

1. Resolving Ethical Issues 1.01 Misuse of Psychologists’ Work 1.02 Conflicts Between Ethics and Law, Regulations, or Other Governing Legal Authority 1.03 Conflicts Between Ethics and Organizational Demands 1.04 Informal Resolution of Ethical Violations 1.05 Reporting Ethical Violations 1.06 Cooperating With Ethics Committees 1.07 Improper Complaints 1.08 Unfair Discrimination Against Complainants and Respondents

Ethical Principles of Psychologists and Code of Conduct

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Beck Depression Inventory-IIについての一考察

Crowdsourcing has had a dramatic impact on the speed and scale at which scientific research can be conducted. Clinical scientists have particularly benefited from readily available research study participants and streamlined recruiting and payment systems afforded by Amazon Mechanical Turk (MTurk), a popular labor market for crowdsourcing workers. MTurk has been used in this capacity for more than five years. The popularity and novelty of the platform have spurred numerous methodological investigations, making it the most studied nonprobability sample available to researchers. This article summarizes what is known about MTurk sample composition and data quality with an emphasis on findings relevant to clinical psychological research. It then addresses methodological issues with using MTurk--many of which are common to other nonprobability samples but unfamiliar to clinical science researchers--and suggests concrete steps to avoid these issues or minimize their impact.

https://www.annualreviews.org/doi/pdf/10.1146/annurev-clinpsy-021815-093623

Conducting Clinical Research Using Crowdsourced Convenience Samples

This article reviews scientific advances in the prevention and treatment of substance-use disorder and related developments in public policy. In the past two decades, research has increasingly supported the view that addiction is a disease of the brain. Although the brain disease model of addiction has yielded effective preventive measures, treatment interventions, and public health policies to address substance-use disorders, the underlying concept of substance abuse as a brain disease continues to be questioned, perhaps because the aberrant, impulsive, and compulsive behaviors that are characteristic of addiction have not been clearly tied to neurobiology. Here we review recent advances in the neurobiology of addiction to clarify the link between addiction and brain function and to broaden the understanding of addiction as a brain disease. We review findings on the desensitization of reward circuits, which dampens the ability to feel pleasure and the motivation to pursue everyday activities; the increasing strength of conditioned responses and stress reactivity, which results in increased cravings for alcohol and other drugs and negative emotions when these cravings are not sated; and the weakening of the brain regions involved in executive functions such as decision making, inhibitory control, and self-regulation that leads to repeated relapse. We also review the ways in which social environments, developmental stages, and genetics are intimately linked to and influence vulnerability and recovery. We conclude that neuroscience continues to support the brain disease model of addiction. Neuroscience research in this area not only offers new opportunities for the prevention and treatment of substance addictions and related behavioral addictions (e.g., to food, sex, and gambling) but may also improve our understanding of the fundamental biologic processes involved in voluntary behavioral control. In the United States, 8 to 10% of people 12 years of age or older, or 20 to 22 million people, are addicted to alcohol or other drugs. 1 The abuse of tobacco, alcohol, and illicit drugs in the United States exacts more than $700 billion annually in costs related to crime, lost work productivity, and health care. 2-4 After centuries of efforts to reduce addiction and its related costs by punishing addictive behaviors failed to produce adequate results, recent basic and clinical research has provided clear evidence that addiction might be better considered and treated as an acquired disease of the brain (see Box 1 for definitions of substance-use disorder and addiction). Research guided by the brain disease model of addiction has led to the development of more effective methods of prevention and treatment and to more informed public health policies. Notable examples include the Mental Health Parity and Addiction Equity Act of 2008, which requires medical insurance plans to provide the same coverage for substance-use disorders and other mental illnesses that is provided for other illnesses, 5 and the proposed bipartisan Senate legislation that From the National Institute on Drug Abuse (N.D.V.) and the National Institute of Alcohol Abuse and Alcoholism (G.F.K.) — both in Bethesda, MD; and the Treatment Research Institute, Philadelphia (A.T.M.). Address reprint requests to Dr. Volkow at the National Institute on Drug Abuse, 6001 Executive Bld., Rm. 5274, Bethesda, MD 20892, or at nvolkow@ nida . nih . gov.

Review Article: Neurobiologic Advances from the Brain Disease Model of Addiction

Mental disorders are increasingly understood in terms of biological mechanisms. We examined how such biological explanations of patients’ symptoms would affect mental health clinicians’ empathy—a crucial component of the relationship between treatment-providers and patients—as well as their clinical judgments and recommendations. In a series of studies, US clinicians read descriptions of potential patients whose symptoms were explained using either biological or psychosocial information. Biological explanations have been thought to make patients appear less accountable for their disorders, which could increase clinicians’ empathy. To the contrary, biological explanations evoked significantly less empathy. These results are consistent with other research and theory that has suggested that biological accounts of psychopathology can exacerbate perceptions of patients as abnormal, distinct from the rest of the population, meriting social exclusion, and even less than fully human. Although the ongoing shift toward biomedical conceptualizations has many benefits, our results reveal unintended negative consequences.

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Effects of biological explanations for mental disorders on clinicians’ empathy

Mental disorders are increasingly construed in terms of their biology, revolutionizing the conceptualization of psychopathology. Depression provides a compelling example of this conceptual shift: In 2006, 80% of Americans endorsed “a chemical imbalance in the brain,” as a cause of depression, while 64% endorsed “a genetic or inherited problem”—both figures representing double-digit increases from just ten years earlier (Pescosolido et al., 2010).

Unfortunately, studies have found that attributing mental disorders (e.g., depression) to such biological causes is associated with prognostic pessimism—a belief that mental health problems are relatively permanent and difficult to cure or treat effectively (Bennett, Thirlaway, & Murray, 2008; Deacon & Baird, 2009; Phelan, 2005; Phelan, Yang, & Cruz-Rojas, 2006). This association appears to stem from the belief that mental disorders have immutable essences (e.g., genes and neurobiology)—assumptions known as “genetic essentialism” and “neuroessentialism” (Dar-Nimrod & Heine, 2011; Haslam, 2011; Medin & Ortony, 1989). Popular media accounts of scientific advances often reinforce these essentialist biases by portraying genetic and neural influences as deterministic and immutable (Dar-Nimrod & Heine, 2011; Haslam, 2011).

Importantly, essentialist accounts contradict current understandings of genetics and neurochemistry. Neuroplasticity in the human brain persists throughout adulthood and is important for recovery from mental disorders, including depression (Brunoni, Lopes, & Fregni, 2008). Moreover, despite significant heritability, there is no “gene for” any psychiatric illness (Kendler, 2005), and epigenetics and gene-by-environment interactions show that experience can modulate genetic effects (Lau & Eley, 2010). The notion that biological explanations of mental disorders denote immutability is thus a misperception that should be corrected.

The present studies have two aims. First, they examine whether biochemical and genetic attributions for depression are associated with prognostic pessimism among individuals with depressive symptoms. Although considerable research has documented such an association in the general public (Haslam, 2011), the impact of biological attributions on people who actually have mental health problems has scarcely been examined. In one recent exception, genetic attributions for mental disorders were associated with implicit guilt among diagnosed individuals, but this research did not examine prognostic pessimism. Understanding how biological attributions relate to symptomatic individuals’ prognostic beliefs is clinically important, as depressed individuals’ prognostic expectancies can significantly affect their actual prognoses (Rutherford, Wager, & Roose, 2010).

The second goal is to examine whether psychoeducation about neuroplasticity and the malleability of gene effects can reduce prognostic pessimism among symptomatic individuals. Given the increasing prevalence of biological explanations for psychopathology, ways of presenting them without increasing prognostic pessimism are urgently needed, but research to date has not focused on this need. For this aim, we drew inspiration from previous research that has used educational interventions to dispel perceptions of immutability and promote the concept of malleability in domains like intelligence and social belonging (Aronson, Fried, & Good, 2002; Blackwell, Trzesniewski, & Dweck, 2007; Walton & Cohen, 2011).

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Fixable or fate? Perceptions of the biology of depression

Objective: The objective of this research was to compare the effects of different causal attributions for overweight and obesity, among individuals with overweight and obesity, on weight-related beliefs, stigmatising attitudes and policy support.Design: In Study 1, an online sample of 95 US adults rated the extent to which they believed various factors caused their own weight status. In Study 2, 125 US adults read one of three randomly assigned online passages attributing obesity to personal responsibility, biology, or the ‘food environment.’ All participants in both studies were overweight or obese.Main outcome measures: All participants reported beliefs about weight loss, weight-stigmatising attitudes, and support for obesity-related policies.Results: In Study 1, biological attributions were associated with low weight-malleability beliefs and blame, high policy support, but high internalised weight bias. ‘Food environment’ attributions were not associated with any outcomes, while ‘personal responsibilit...

Beyond personal responsibility: Effects of causal attributions for overweight and obesity on weight-related beliefs, stigma, and policy support

Objective: In recent years, the stigmatization faced by people with mental disorders has received considerable attention in the empirical literature. However, individuals with different disorders are subject to distinct types of negative attitudes, necessitating examinations of stigma that treat specific disorders individually. Method: This article reviews recent empirical literature concerning the stigmatization of ADHD. Further specificity is achieved by taking a developmental perspective, reviewing studies of stigmatizing attitudes as a function of the age of the target and perceiver. Results: Findings from nationally representative data sets, experimental investigations, surveys, and qualitative studies indicate that individuals of all ages who exhibit symptoms of ADHD are the recipients of substantial stigmatization. Conclusion: Although the stigmatizing attitudes of children and adolescents appear to differ in some ways from those of adults, negative perceptions toward people with ADHD appear to gen...

Stigmatization of ADHD A Developmental Review

Psychopathology is increasingly conceptualized as a biological phenomenon. The consequences of this conceptual shift for the general public's beliefs and attitudes regarding mental illness have been the subject of considerable study, but effects among individuals who suffer from mental disorders have received less attention. This review considers recent observational and experimental studies of the beliefs, attitudes, and behaviors associated with biological conceptions of psychopathology among affected individuals. Included in the review is research that has examined the implications of such conceptualizations for prognostic beliefs, internalization of stigmatizing attitudes, treatment usage and other behaviors and intentions, and perspectives on the use of biomedical technologies in mental health. Potential conclusions, limitations of the existing literature, and considerations for future studies are discussed.

Matthew S. Lebowitz

Papers

Effects of biological explanations for mental disorders on clinicians’ empathy

Fixable or fate? Perceptions of the biology of depression

Beyond personal responsibility: Effects of causal attributions for overweight and obesity on weight-related beliefs, stigma, and policy support

Stigmatization of ADHD A Developmental Review

Biological Conceptualizations of Mental Disorders Among Affected Individuals: A Review of Correlates and Consequences