Arguing for their evolutionary approach to self-deception, von Hippel & Trivers (VH&T) complain that “to the best of our knowledge no one has examined whether self-deception is more likely when people attempt to deceive others. Thus, the theoretical possibility of self-deception in service of other deception remains just that” (sect. 6, para. 2). Indeed, convincing evidence for their evolutionary hypothesis that self-deception evolved to facilitate interpersonal deception comes from clinical studies of psychiatric patients with somatoform disorders.
Current psychiatric classification includes several different conditions (somatoform disorders, factitious disorders, and malingering) in which the clinical picture is dominated by physical symptoms for which no organic cause can be found. These disorders have in common several features, including “illness as a way of life,” maladaptive use of medical care, refractoriness to palliative and symptomatic treatment, and the desire to seek those privileges afforded to the sick person by society (Krahn et al. Reference Krahn, Bostwick and Stonnington2008). This latter aspect points to the importance of deception of others in the psychological mechanisms underlying somatization and disease simulation. By simulating a disease and displaying care-eliciting behavior, the patient evokes predictable reactions from others (i.e., care of the sick) that are sanctioned in all human cultures and are probably related with invalid care behavior observed in several nonhuman species.
Even though these conditions share many common features, current diagnostic criteria separate somatoform disorders from factitious disorders and malingering. According to this diagnostic partitioning, the key difference is that patients with somatoform disorders actually believe they are ill, whereas patients with factitious disorders and malingerers feign illness and fake their physical symptoms. But the line between somatization (e.g., unconscious expression of emotional distress in physical terms) and deliberate simulation of physical symptoms is not easy to draw. Since the birth of modern psychiatry, clinical observations have repeatedly highlighted the difficulties in defining the patient's degree of voluntary control over symptom production.
In the nineteenth century, the French neurologist J.- M. Charcot was an international leader in the study of hysteria (a neurotic disorder currently classified under the rubric of somatoform disorders) (Goetz Reference Goetz2007). Speaking to his students on this topic, he provided a rare glimpse of his personal attitudes toward the creative spirit of hysterical simulators: “This leads me to say a word on simulation. You will meet with it at every point when dealing with the history of hysteria. One sometimes catches oneself admiring the amazing craft, sagacity, and perseverance which women, under the influence of this great névrose, will mobilize for the purpose of deception – especially when a physician is to be the victim.” (Charcot Reference Charcot1889, p. 230). More recently, Cameron noted that “the difference between hysteria and malingering must finally rest upon the criterion of self-deception…. there are many cases in which pretense and self-deception are so intermingled as to make clear distinction impossible.” (quoted in Ford Reference Ford1983, p. 130). In line with these classical descriptions, contemporary clinicians acknowledge the striking mixture of conscious and unconscious control over symptom production that characterizes not only the different diagnostic subtypes of somatoform disorders, but also the temporal course of individual cases with the same diagnosis (Rogers Reference Rogers1988).
A recent study has demonstrated how intentional faking may evolve into a less conscious form of symptom reporting (Merckelbach et al. Reference Merckelbach, Jelicic and Pieters2010). These authors conducted three experiments that addressed the residual effects of instructed feigning of symptoms. In experiment 1, undergraduates instructed to exaggerate symptoms on a malingering test continued to report more neurocognitive and psychiatric symptoms than did nonmalingering controls, when later asked to respond honestly to the same test. In experiment 2, students completed a symptom list of psychiatric complaints and then were asked to explain why they had endorsed two target symptoms that they did not, in actuality, endorse. A total of 57% of participants did not detect this mismatch between actual and manipulated symptom endorsement and even tended to adopt the manipulated symptoms when provided with an opportunity to do so. In experiment 3, it was found that self-deceptive enhancement is related to the tendency to continue to report neurocognitive and psychiatric symptoms that initially had been produced intentionally. Discussing the implications of their study for a better understanding of somatoform disorders, Merckelbach et al. concluded that “blindness” for the intentional aspect of symptom endorsement may explain the intrinsic overlap between feigning and somatoform complaints.
Twenty years ago, I collaborated on an article (Troisi & McGuire Reference Troisi, McGuire and Stefanis1990) focusing on somatoform disorders from an evolutionary perspective. The core argument of the article was that the evolution of self-deception as a means to improve deception of others could explain why patients with somatoform disorders distribute along a continuum of disease simulation that ranges from a sincere belief of having a serious disease to intentional presentation of false symptoms. We argued against a diagnostic partitioning based on the distinction between unconscious somatization and intentional faking and emphasized the importance of assessing the relative contribution of deception and self-deception in each single case presenting with physical symptoms for which no organic cause can be found. Using the deception/self-deception dimensional model, we explained several clinical features of somatoform disorders. For example, the degree of self-deception explains the heterogeneity of the clinical picture. Some patients present with objective and dramatic manifestations (e.g., pseudoseizures), whereas others just complain of subjective symptoms (e.g., nausea). We hypothesized that patients who do not believe in their diseases tend to exaggerate the conspicuousness of disease manifestations in an effort to prove their validity and to convince others. By contrast, patients with an extreme degree of self-deception (that, in some cases, can reach a delusional intensity) limit their symptom production to vague complaints.
Like the original article by Trivers (Reference Trivers and Dawkins1976/2006) on the evolution of self-deception, the Troisi & McGuire (Reference Troisi, McGuire and Stefanis1990) article on somatoform disorders has not been taken seriously in the psychiatric literature. I hope that VH&T's target article will convince researchers and clinicians that somatoform disorders are both a source of preliminary evidence for the interpersonal function of self-deception and a promising area to conduct experiments testing the evolutionary hypothesis.
Arguing for their evolutionary approach to self-deception, von Hippel & Trivers (VH&T) complain that “to the best of our knowledge no one has examined whether self-deception is more likely when people attempt to deceive others. Thus, the theoretical possibility of self-deception in service of other deception remains just that” (sect. 6, para. 2). Indeed, convincing evidence for their evolutionary hypothesis that self-deception evolved to facilitate interpersonal deception comes from clinical studies of psychiatric patients with somatoform disorders.
Current psychiatric classification includes several different conditions (somatoform disorders, factitious disorders, and malingering) in which the clinical picture is dominated by physical symptoms for which no organic cause can be found. These disorders have in common several features, including “illness as a way of life,” maladaptive use of medical care, refractoriness to palliative and symptomatic treatment, and the desire to seek those privileges afforded to the sick person by society (Krahn et al. Reference Krahn, Bostwick and Stonnington2008). This latter aspect points to the importance of deception of others in the psychological mechanisms underlying somatization and disease simulation. By simulating a disease and displaying care-eliciting behavior, the patient evokes predictable reactions from others (i.e., care of the sick) that are sanctioned in all human cultures and are probably related with invalid care behavior observed in several nonhuman species.
Even though these conditions share many common features, current diagnostic criteria separate somatoform disorders from factitious disorders and malingering. According to this diagnostic partitioning, the key difference is that patients with somatoform disorders actually believe they are ill, whereas patients with factitious disorders and malingerers feign illness and fake their physical symptoms. But the line between somatization (e.g., unconscious expression of emotional distress in physical terms) and deliberate simulation of physical symptoms is not easy to draw. Since the birth of modern psychiatry, clinical observations have repeatedly highlighted the difficulties in defining the patient's degree of voluntary control over symptom production.
In the nineteenth century, the French neurologist J.- M. Charcot was an international leader in the study of hysteria (a neurotic disorder currently classified under the rubric of somatoform disorders) (Goetz Reference Goetz2007). Speaking to his students on this topic, he provided a rare glimpse of his personal attitudes toward the creative spirit of hysterical simulators: “This leads me to say a word on simulation. You will meet with it at every point when dealing with the history of hysteria. One sometimes catches oneself admiring the amazing craft, sagacity, and perseverance which women, under the influence of this great névrose, will mobilize for the purpose of deception – especially when a physician is to be the victim.” (Charcot Reference Charcot1889, p. 230). More recently, Cameron noted that “the difference between hysteria and malingering must finally rest upon the criterion of self-deception…. there are many cases in which pretense and self-deception are so intermingled as to make clear distinction impossible.” (quoted in Ford Reference Ford1983, p. 130). In line with these classical descriptions, contemporary clinicians acknowledge the striking mixture of conscious and unconscious control over symptom production that characterizes not only the different diagnostic subtypes of somatoform disorders, but also the temporal course of individual cases with the same diagnosis (Rogers Reference Rogers1988).
A recent study has demonstrated how intentional faking may evolve into a less conscious form of symptom reporting (Merckelbach et al. Reference Merckelbach, Jelicic and Pieters2010). These authors conducted three experiments that addressed the residual effects of instructed feigning of symptoms. In experiment 1, undergraduates instructed to exaggerate symptoms on a malingering test continued to report more neurocognitive and psychiatric symptoms than did nonmalingering controls, when later asked to respond honestly to the same test. In experiment 2, students completed a symptom list of psychiatric complaints and then were asked to explain why they had endorsed two target symptoms that they did not, in actuality, endorse. A total of 57% of participants did not detect this mismatch between actual and manipulated symptom endorsement and even tended to adopt the manipulated symptoms when provided with an opportunity to do so. In experiment 3, it was found that self-deceptive enhancement is related to the tendency to continue to report neurocognitive and psychiatric symptoms that initially had been produced intentionally. Discussing the implications of their study for a better understanding of somatoform disorders, Merckelbach et al. concluded that “blindness” for the intentional aspect of symptom endorsement may explain the intrinsic overlap between feigning and somatoform complaints.
Twenty years ago, I collaborated on an article (Troisi & McGuire Reference Troisi, McGuire and Stefanis1990) focusing on somatoform disorders from an evolutionary perspective. The core argument of the article was that the evolution of self-deception as a means to improve deception of others could explain why patients with somatoform disorders distribute along a continuum of disease simulation that ranges from a sincere belief of having a serious disease to intentional presentation of false symptoms. We argued against a diagnostic partitioning based on the distinction between unconscious somatization and intentional faking and emphasized the importance of assessing the relative contribution of deception and self-deception in each single case presenting with physical symptoms for which no organic cause can be found. Using the deception/self-deception dimensional model, we explained several clinical features of somatoform disorders. For example, the degree of self-deception explains the heterogeneity of the clinical picture. Some patients present with objective and dramatic manifestations (e.g., pseudoseizures), whereas others just complain of subjective symptoms (e.g., nausea). We hypothesized that patients who do not believe in their diseases tend to exaggerate the conspicuousness of disease manifestations in an effort to prove their validity and to convince others. By contrast, patients with an extreme degree of self-deception (that, in some cases, can reach a delusional intensity) limit their symptom production to vague complaints.
Like the original article by Trivers (Reference Trivers and Dawkins1976/2006) on the evolution of self-deception, the Troisi & McGuire (Reference Troisi, McGuire and Stefanis1990) article on somatoform disorders has not been taken seriously in the psychiatric literature. I hope that VH&T's target article will convince researchers and clinicians that somatoform disorders are both a source of preliminary evidence for the interpersonal function of self-deception and a promising area to conduct experiments testing the evolutionary hypothesis.