Abstract
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. (...)
(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. 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.”
by Scott O. Lilienfeld, Katheryn C. Sauvigné, Steven Jay Lynn, Robin L. Cautin, Robert D. Latzman, and Irwin D. Waldman, Frontiers in Psychology | Read more:
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. (...)
Inaccurate or Misleading Terms
(1) A gene for. The news media is awash in reports of identifying “genes for” a myriad of phenotypes, including personality traits, mental illnesses, homosexuality, and political attitudes (Sapolsky, 1997). For example, in 2010, The Telegraph (2010) trumpeted the headline, “‘Liberal gene’ discovered by scientists.” Nevertheless, because genes code for proteins, there are no “genes for” phenotypes per se, including behavioral phenotypes (Falk, 2014). Moreover, genome-wide association studies of major psychiatric disorders, such as schizophrenia and bipolar disorder, suggest that there are probably few or no genes of major effect (Kendler, 2005). In this respect, these disorders are unlike single-gene medical disorders, such as Huntington’s disease or cystic fibrosis. The same conclusion probably holds for all personality traits (De Moor et al., 2012).
Not surprisingly, early claims that the monoamine oxidase-A (MAO-A) gene is a “warrior gene” (McDermott et al., 2009) have not withstood scrutiny. This polymorphism appears to be only modestly associated with risk for aggression, and it has been reported to be associated with conditions that are not tied to a markedly heightened risk of aggression, such as major depression, panic disorder, and autism spectrum disorder (Buckholtz and Meyer-Lindenberg, 2013; Ficks and Waldman, 2014). The evidence for a “God gene,” which supposedly predisposes people to mystical or spiritual experiences, is arguably even less impressive (Shermer, 2015) and no more compelling than that for a “God spot” in the brain (see “God spot”). Incidentally, the term “gene” should not be confused with the term “allele”; genes are stretches of DNA that code for a given morphological or behavioral characteristic, whereas alleles are differing versions of a specific polymorphism in a gene (Pashley, 1994).
(2) Antidepressant medication. Medications such as tricyclics, selective serotonin reuptake inhibitors, and selective serotonin and norepinephrine reuptake inhibitors, are routinely called “antidepressants.” Yet there is little evidence that these medications are more efficacious for treating (or preventing relapse for) mood disorders than for several other conditions, such as anxiety-related disorders (e.g., panic disorder, obsessive-compulsive disorder; Donovan et al., 2010) or bulimia nervosa (Tortorella et al., 2014). Hence, their specificity to depression is doubtful, and their name derives more from historical precedence—the initial evidence for their efficacy stemmed from research on depression (France et al., 2007)—than from scientific evidence. Moreover, some authors argue that these medications are considerably less efficacious than commonly claimed, and are beneficial for only severe, but not mild or moderate, depression, rendering the label of “antidepressant” potentially misleading (Antonuccio and Healy, 2012; but see Kramer, 2011, for an alternative view).
(1) A gene for. The news media is awash in reports of identifying “genes for” a myriad of phenotypes, including personality traits, mental illnesses, homosexuality, and political attitudes (Sapolsky, 1997). For example, in 2010, The Telegraph (2010) trumpeted the headline, “‘Liberal gene’ discovered by scientists.” Nevertheless, because genes code for proteins, there are no “genes for” phenotypes per se, including behavioral phenotypes (Falk, 2014). Moreover, genome-wide association studies of major psychiatric disorders, such as schizophrenia and bipolar disorder, suggest that there are probably few or no genes of major effect (Kendler, 2005). In this respect, these disorders are unlike single-gene medical disorders, such as Huntington’s disease or cystic fibrosis. The same conclusion probably holds for all personality traits (De Moor et al., 2012).
Not surprisingly, early claims that the monoamine oxidase-A (MAO-A) gene is a “warrior gene” (McDermott et al., 2009) have not withstood scrutiny. This polymorphism appears to be only modestly associated with risk for aggression, and it has been reported to be associated with conditions that are not tied to a markedly heightened risk of aggression, such as major depression, panic disorder, and autism spectrum disorder (Buckholtz and Meyer-Lindenberg, 2013; Ficks and Waldman, 2014). The evidence for a “God gene,” which supposedly predisposes people to mystical or spiritual experiences, is arguably even less impressive (Shermer, 2015) and no more compelling than that for a “God spot” in the brain (see “God spot”). Incidentally, the term “gene” should not be confused with the term “allele”; genes are stretches of DNA that code for a given morphological or behavioral characteristic, whereas alleles are differing versions of a specific polymorphism in a gene (Pashley, 1994).
(2) Antidepressant medication. Medications such as tricyclics, selective serotonin reuptake inhibitors, and selective serotonin and norepinephrine reuptake inhibitors, are routinely called “antidepressants.” Yet there is little evidence that these medications are more efficacious for treating (or preventing relapse for) mood disorders than for several other conditions, such as anxiety-related disorders (e.g., panic disorder, obsessive-compulsive disorder; Donovan et al., 2010) or bulimia nervosa (Tortorella et al., 2014). Hence, their specificity to depression is doubtful, and their name derives more from historical precedence—the initial evidence for their efficacy stemmed from research on depression (France et al., 2007)—than from scientific evidence. Moreover, some authors argue that these medications are considerably less efficacious than commonly claimed, and are beneficial for only severe, but not mild or moderate, depression, rendering the label of “antidepressant” potentially misleading (Antonuccio and Healy, 2012; but see Kramer, 2011, for an alternative view).
(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. 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.”
(5) Brainwashing. This term, which originated during the Korean War (Hunter, 1951) but which is still invoked uncritically from time to time in the academic literature (e.g., Ventegodt et al., 2009; Kluft, 2011), implies that powerful individuals wishing to persuade others can capitalize on a unique armamentarium of coercive procedures to change their long-term attitudes. Nevertheless, the attitude-change techniques used by so-called “brainwashers” are no different than standard persuasive methods identified by social psychologists, such as encouraging commitment to goals, manufacturing source credibility, forging an illusion of group consensus, and vivid testimonials (Zimbardo, 1997). Furthermore, there are ample reasons to doubt whether “brainwashing” permanently alters beliefs (Melton, 1999). For example, during the Korean War, only a small minority of the 3500 American political prisoners subjected to intense indoctrination techniques by Chinese captors generated false confessions. Moreover, an even smaller number (probably under 1%) displayed any signs of adherence to Communist ideologies following their return to the US, and even these were individuals who returned to Communist subcultures (Spanos, 1996).
(6) Bystander apathy. The classic work of (e.g., Darley and Latane, 1968; Latane and Rodin, 1969) underscored the counterintuitive point that when it comes to emergencies, there is rarely “safety in numbers.” As this and subsequent research demonstrated, the more people present at an emergency, the lower the likelihood of receiving help. In early research, this phenomenon was called “bystander apathy” (Latane and Darley, 1969) a term that endures in many academic articles (e.g., Abbate et al., 2013). Nevertheless, research demonstrates that most bystanders are far from apathetic in emergencies (Glassman and Hadad, 2008). To the contrary, they are typically quite concerned about the victim, but are psychologically “frozen” by well-established psychological processes, such as pluralistic ignorance, diffusion of responsibility, and sheer fears of appearing foolish.
(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.
(6) Bystander apathy. The classic work of (e.g., Darley and Latane, 1968; Latane and Rodin, 1969) underscored the counterintuitive point that when it comes to emergencies, there is rarely “safety in numbers.” As this and subsequent research demonstrated, the more people present at an emergency, the lower the likelihood of receiving help. In early research, this phenomenon was called “bystander apathy” (Latane and Darley, 1969) a term that endures in many academic articles (e.g., Abbate et al., 2013). Nevertheless, research demonstrates that most bystanders are far from apathetic in emergencies (Glassman and Hadad, 2008). To the contrary, they are typically quite concerned about the victim, but are psychologically “frozen” by well-established psychological processes, such as pluralistic ignorance, diffusion of responsibility, and sheer fears of appearing foolish.
(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.
by Scott O. Lilienfeld, Katheryn C. Sauvigné, Steven Jay Lynn, Robin L. Cautin, Robert D. Latzman, and Irwin D. Waldman, Frontiers in Psychology | Read more:
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