AT LAST! Honest talk about sloppy, self-serving and misleading claims. Of particular significance to anyone diagnosed with Autism or Asperger’s.
Frontiers in Psychology / 03 August 2015
The rest of the 50 terms can be read here: http://journal.frontiersin.org/article/10.3389/fpsyg.2015.01100/full/
Fifty psychological and psychiatric terms to avoid: a list of inaccurate, misleading, misused, ambiguous, and logically confused words and phrases
- 1Department of Psychology, Emory University, Atlanta, GA, USA
- 2Department of Psychology, Georgia State University, Atlanta, GA, USA
- 3Binghamton University – State University of New York, Binghamton, NY, USA
- 4Department of Psychology, Sacred Heart College, Fairfield, CT, USA
“The goal of this article is to promote clear thinking and clear writing among students and teachers of psychological science by curbing terminological misinformation and confusion. To this end, we present a provisional list of 50 commonly used terms in psychology, psychiatry, and allied fields that should be avoided, or at most used sparingly and with explicit caveats. We provide corrective information for students, instructors, and researchers regarding these terms, which we organize for expository purposes into five categories: inaccurate or misleading terms, frequently misused terms, ambiguous terms, oxymorons, and pleonasms. For each term, we (a) explain why it is problematic, (b) delineate one or more examples of its misuse, and (c) when pertinent, offer recommendations for preferable terms. By being more judicious in their use of terminology, psychologists and psychiatrists can foster clearer thinking in their students and the field at large regarding mental phenomena.”
“If names be not correct, language is not in accordance with the truth of things.” (Confucius, The Analects)
(3) Autism epidemic. Enormous effort has been expended to uncover the sources of the “autism epidemic” (e.g., King, 2011), the supposed massive increase in the incidence and prevalence of autism, now termed autism spectrum disorder, over the past 25 years. The causal factors posited to be implicated in this “epidemic” have included vaccines, television viewing, dietary allergies, antibiotics, and viruses.
Nevertheless, there is meager evidence that this purported epidemic reflects a genuine increase in the rates of autism per se as opposed to an increase in autism diagnoses stemming from several biases and artifacts, including heightened societal awareness of the features of autism (“detection bias”), growing incentives for school districts to report autism diagnoses, and a lowering of the diagnostic thresholds for autism across successive editions of the Diagnostic and Statistical Manual of Mental Disorders (Gernsbacher et al., 2005; Lilienfeld and Arkowitz, 2007). Indeed, data indicate when the diagnostic criteria for autism were held constant, the rates of this disorder remained essentially constant between 1990 and 2010 (Baxter et al., 2015). If the rates of autism are increasing, the increase would appear to be slight at best, hardly justifying the widespread claim of an “epidemic.”
(4) Brain region X lights up. Many authors in the popular and academic literatures use such phrases as “brain area X lit up following manipulation Y” (e.g., Morin, 2011). This phrase is unfortunate for several reasons. First, the bright red and orange colors seen on functional brain imaging scans are superimposed by researchers to reflect regions of higher brain activation.
They are NOT a product of the scan, but ADDED as graphic emphasis. (ie, technically “fake”)
Nevertheless, they may engender a perception of “illumination” in viewers. Second, the activations represented by these colors do not reflect neural activity per se; they reflect oxygen uptake by neurons and are at best indirect proxies of brain activity. Even then, this linkage may sometimes be unclear or perhaps absent (Ekstrom, 2010). Third, in almost all cases, the activations observed on brain scans are the products of subtraction of one experimental condition from another. Hence, they typically do not reflect the raw levels of neural activation in response to an experimental manipulation. For this reason, referring to a brain region that displays little or no activation in response to an experimental manipulation as a “dead zone” (e.g., Lamont, 2008) is similarly misleading. Fourth, depending on the neurotransmitters released and the brain areas in which they are released, the regions that are “activated” in a brain scan may actually be being inhibited rather than excited (Satel and Lilienfeld, 2013). Hence, from a functional perspective, these areas may be being “lit down” rather than “lit up.”
(7) Chemical imbalance. Thanks in part to the success of direct-to-consumer marketing campaigns by drug companies, the notion that major depression and allied disorders are caused by a “chemical imbalance” of neurotransmitters, such as serotonin and norepinephrine, has become a virtual truism in the eyes of the public (France et al., 2007; Deacon and Baird, 2009). This phrase even crops up in some academic sources; for example, one author wrote that one overarching framework for conceptualizing mental illness is a “biophysical model that posits a chemical imbalance” (Wheeler, 2011, p. 151). Nevertheless, the evidence for the chemical imbalance model is at best slim (Lacasse and Leo, 2005; Leo and Lacasse, 2008). One prominent psychiatrist even dubbed it an urban legend (Pies, 2011). There is no known “optimal” level of neurotransmitters in the brain, so it is unclear what would constitute an “imbalance.” Nor is there evidence for an optimal ratio among different neurotransmitter levels. Moreover, although serotonin reuptake inhibitors, such as fluoxetine (Prozac) and sertraline (Zoloft), appear to alleviate the symptoms of severe depression, there is evidence that at least one serotonin reuptake enhancer, namely tianepine (Stablon), is also efficacious for depression (Akiki, 2014). The fact that two efficacious classes of medications exert opposing effects on serotonin levels raises questions concerning a simplistic chemical imbalance model.
(23) Psychiatric control group. NOT a true control group! This phrase and similar phrases (e.g., “normal control group,” “psychopathological control group”) connote erroneously that (a) groups of ostensibly normal individuals or mixed psychiatric patients who are being compared with (b) groups of individuals with a disorder of interest (e.g., schizophrenia, major depression) are true “control” groups. They are not. They are “comparison groups” and should be referred to accordingly. The phrase “control group” in this context may leave readers with the unwarranted impression that the design of the study is experimental when it is actually quasi-experimental. Just as important, this term may imply that the only difference between the two groups (e.g., a group of patients with anxiety disorder and a group of ostensibly normal individuals) is the presence or absence of the disorder of interest. In fact, these two groups almost surely differ on any number of “nuisance” variables, such as personality traits, co-occurring disorders, and family background, rendering the interpretation of most group differences open to multiple interpretations (Meehl, 1969).