Genetic Essentialism, Neuroessentialism, and Stigma: Commentary on Dar-Nimrod and Heine (2011)
Department of Psychology, University of Melbourne, Parkville, Victoria 3010, Australia.Psychological Bulletin (Impact Factor: 14.76). 09/2011; 137(5):819-24. DOI: 10.1037/a0022386
Dar-Nimrod and Heine (2011) presented a masterfully broad review of the implications of genetic essentialism for understandings of human diversity. This commentary clarifies the reasons that essentialist thinking has problematic social consequences and links genetic forms of essentialism to those invoking neural essences. The mounting evidence that these forms of essentialist thinking contribute to the stigma of mental disorder is reviewed. Genetic and neuroessentialisms influence media portrayals of scientific research and distort how they are interpreted by laypeople. The common thread of these essentialisms is their tendency to deepen social divisions and promote forms of social segregation.
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- "This is important because anti-stigma interventions often attempt to reduce stigma through the provision of educational information (Corrigan, Morris, Michaels, Rafacz, & Rüsch, 2012), including biogenetic explanations of mental disorders. Biogenetic explanations appear to convey both stigmatizing and de-stigmatizing meanings (e.g., Easter, 2012; Haslam, 2011). Because of this ambiguity, people who receive a biogenetic explanation for a mental disorder may have considerable interpretive freedom, allowing motivational factors to operate on the inferences drawn about affected people. "
ABSTRACT: It has been hoped that disseminating biological and genetic (biogenetic) explanations for mental disorders would reduce the tendency to stigmatize affected people. However, biogenetic explanations convey both stigmatizing and destigmatizing meanings (reducing blame but inducing perceived dangerousness and pessimism). This ambiguity may allow motivational factors to influence how individuals make sense of biogenetic explanations. In this research, we aimed: (1) to shed light on the motives that underpin stigmatizing attitudes, and (2) to investigate if these motives also predict how people interpret biogenetic explanations. In Study 1 (N= 177), we found that motivations to compete for group dominance (Social Dominance Orientation; SDO) and to maintain security and social cohesion (Right Wing Authoritarianism; RWA) were associated with stigmatizing attitudes toward individuals suffering from depression and schizophrenia. Further, biogenetic explanations had different implications for stigma as a function of RWA, predicting high stigma in high-RWA people and low stigma in low-RWA people. In Study 2 (N= 93), we found that the motives indexed by SDO and RWA predicted how people responded to a biogenetic explanation of schizophrenia, tending to reinforce stigmatizing attitudes. We discuss the implications of these findings for efforts to reduce stigma.
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- "For instance, Weiner et al. (1988) , depicting conditions as having a controllable versus noncontrollable onset, found no effect on persons' perceptions of the condition's course as more or less reversible. In contrast, research investigating genetic or neurological " essentialism " has shown that attributing a condition to genetic causes results in higher beliefs that the condition will persist throughout a person's life (Phelan, 2005), and researchers have argued that attributing a condition to brain-based causes may have similar effects (e.g., Corrigan and Watson, 2004; Haslam, 2011). The present study reverses this approach. "
ABSTRACT: Background: The classification of Alzheimer's disease is undergoing a significant transformation. Researchers have created the category of "preclinical Alzheimer's," characterized by biomarker pathology rather than observable symptoms. Diagnosis and treatment at this stage could allow preventing Alzheimer's cognitive decline. While many commentators have worried that persons given a preclinical Alzheimer's label will be subject to stigma, little research exists to inform whether the stigma attached to the label of clinical Alzheimer's will extend to a preclinical disorder that has the label of "Alzheimer's" but lacks the symptoms or expected prognosis of the clinical form. Research questions: The present study sought to correct this gap by examining the foundations of stigma directed at Alzheimer's. It asked: do people form stigmatizing reactions to the label "Alzheimer's disease" itself or to the condition's observable impairments? How does the condition's prognosis modify these reactions? Methods: Data were collected through a web-based experiment with N = 789 adult members of the U.S. general population (median age = 49, interquartile range, 32-60, range = 18-90). Participants were randomized through a 3 × 3 design to read one of 9 vignettes depicting signs and symptoms of mild stage dementia that varied the disease label ("Alzheimer's" vs. "traumatic brain injury" vs. no label) and prognosis (improve vs. static vs. worsen symptoms). Four stigma outcomes were assessed: discrimination, negative cognitive attributions, negative emotions, and social distance. Results: The study found that the Alzheimer's disease label was generally not associated with more stigmatizing reactions. In contrast, expecting the symptoms to get worse, regardless of which disease label those symptoms received, resulted in higher levels of perceived structural discrimination, higher pity, and greater social distance. Conclusion: These findings suggest that stigma surrounding pre-clinical Alzheimer's categories will depend highly on the expected prognosis attached to the label. They also highlight the need for models of Alzheimer's-directed stigma that incorporate attributions about the condition's mutability.
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- "The evidence regarding how these attributions affect stigma is inconsistent, as some studies have suggested that biogenetic attributions lead to reduced stigmatising attitudes in comparison to personal responsibility attributions (Crandall, 1994; Hilbert, Rief, & Braehler, 2008; Rodin, Price, Sanchez, & McElligot, 1989), but another found that they had no impact on unconscious weight bias (Teachman et al., 2003). Furthermore, research on stigmatisation of other health conditions has suggested that biological attributions can increase stigma by exacerbating perceptions that affected individuals are fundamentally different from 'healthy' people and that their health problems are intrinsic to them (Haslam, 2011). Consequently, one might expect that this attribution could lead to greater internalised weight bias among overweight individuals by increasing the extent to which they view their weight as reflective of a deep-seated fundamental flaw, although no study to our knowledge has investigated this aspect of weight-stigmatising attitudes. "
ABSTRACT: Abstract 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, stigmatizing attitudes, and policy support. Design: In Study 1, an online sample of 95 U.S. adults rated the extent to which they believed various factors caused their own weight status. In Study 2, 125 U.S. 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-stigmatizing 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 internalized weight bias. "Food environment" attributions were not associated with any outcomes, while "personal responsibility" attributions were associated with high prejudice and blame. In Study 2, participants who received information about the food environment reported greater support for food-related policies and greater self-efficacy to lose weight. Conclusion: Emphasizing the role of the food environment in causing obesity may promote food-policy support and health behaviors without imposing the negative consequences associated with other attributions.
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