Human brain evolution and the “Neuroevolutionary Time-depth Principle:” Implications for the Reclassification of fear-circuitry-related traits in DSM-V and for studying resilience to warzone-related posttraumatic stress disorder

Abstract

The DSM-III, DSM-IV, DSM-IV-TR and ICD-10 have judiciously minimized discussion of etiologies to distance clinical psychiatry from Freudian psychoanalysis. With this goal mostly achieved, discussion of etiological factors should be reintroduced into the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V). A research agenda for the DSM-V advocated the "development of a pathophysiologically based classification system". The author critically reviews the neuroevolutionary literature on stress-induced and fear circuitry disorders and related amygdala-driven, species-atypical fear behaviors of clinical severity in adult humans. Over 30 empirically testable/ falsifiable predictions are presented. It is noted that in DSM-IV-TR and ICD-10, the classification of stress and fear circuitry disorders is neither mode-of-acquisition-based nor brain-evolution-based. For example, snake phobia (innate) and dog phobia (overconsolidational) are clustered together. Similarly, research on blood-injection-injury-type-specific phobia clusters two fears different in their innateness: 1) an arguably ontogenetic memory-trace-overconsolidation-based fear (hospital phobia) and 2) a hardwired (innate) fear of the sight of one's blood or a sharp object penetrating one's skin. Genetic architecture-charting of fear-circuitry-related traits has been challenging. Various, non-phenotype-based architectures can serve as targets for research. In this article, the author will propose one such alternative genetic architecture. This article was inspired by the following: A) Nesse's "Smoke-Detector Principle", B) the increasing suspicion that the "smooth" rather than "lumpy" distribution of complex psychiatric phenotypes (including fear-circuitry disorders) may in some cases be accounted for by oligogenic (and not necessarily polygenic) transmission, and C) insights from the initial sequence of the chimpanzee genome and comparison with the human genome by the Chimpanzee Sequencing and Analysis Consortium published in late 2005. Neuroevolutionary insights relevant to fear circuitry symptoms that primarily emerge overconsolidationally (especially Combat related Posttraumatic Stress Disorder) are presented. Also introduced is a humanevolution-based principle for clustering innate fear traits. The "Neuroevolutionary Time-depth Principle" of innate fears proposed in this article may be useful in the development of a neuroevolution-based taxonomic re-clustering of stress-triggered and fear-circuitry disorders in DSM-V. Four broad clusters of evolved fear circuits are proposed based on their time-depths: 1) Mesozoic (mammalian-wide) circuits hardwired by wildtype alleles driven to fixation by Mesozoic selective sweeps; 2) Cenozoic (simian-wide) circuits relevant to many specific phobias; 3) mid Paleolithic and upper Paleolithic (Homo sapiens-specific) circuits (arguably resulting mostly from mate-choice-driven stabilizing selection); 4) Abbreviations: WR-PTSD, warzone-related posttraumatic stress disorder; FOXP2, forkhead box ...

Group climate, personality, and self-reported aggression in incarcerated male youth

“…al, 2006). Other research (Dye, 2010;Gover, Layton Mackenzie, Styve, & Armstrong, 2000) supports a 'situational' or 'deprivational' model in which inmates react to the 'pains of prison' (loss of autonomy, humiliation, fear; Sykes, 1958), causing increased anger, stress, depression and anxiety (White, Shi, Mun, Hirschfeld, & Loeber, 2010), mutual hostility and aggression towards staff (Bracha, 2006, Whittle, Allen, Lubman, Yu¨cel, 2006Toch & Kupers, 2008). Gover, Mackenzie and Amstrong (2000), in their study on adjustment to youth prison, found empirical evidence for both models.…”

Reflexiones sobre el miedo en el siglo XXI: filosofía, política, genética y evolución

“…Por ejemplo, según Bracha et al (2005) algunos genes responsables del miedo vendrían del Neolítico. Como era de suponer, cada uno de estos componentes del miedo tiene diferentes valores para su heredabilidad (Bracha, 2006), y por tanto cada uno de ellos dependerá en su manifestación fenotípica de diferentes combinaciones de factores genéticos y ambientales. Se han propuesto algunos modelos genéticos y algunos genes candidatos (genes que se supone que pueden tener un efecto sobre el carácter estudiado).…”

“…Por ejemplo, el miedo a las alturas está presente en todos los mamíferos y posiblemente se desarrolló en el mesozoico (Bracha et al, 2005;Bracha, 2006). En cambio el miedo a las serpientes se pudo desarrollar en los simios durante el cenozoico (Bracha et al, 2005;Bracha, 2006) y actualmente sabemos que estos animales reaccionan de manera muy rápida ante la visión de las serpientes, gracias a unas neuronas de la zona pulvinarmedial y dorsolateral (Van Le et al, 2013). El miedo a los a172 insectos o a las ratas posiblemente sea más tardío y debió desarrollarse durante el paleolítico y el neolíti-co cuando transmitían enfermedades y destrozaban las cosechas y los alimentos guardados celosamente en las cavernas (Bracha, 2006).…”

Topiramate diminishes fear memory consolidation and extinguishes conditioned fear in rats

“…3 Topiramate has been proposed for the treatment of some psychiatric disorders, such as alcohol abuse, 4 bulimia and bingeeating disorder 5 and, more recently, borderline personality disorder (BPD) 6 and posttraumatic stress disorder (PTSD). 7 Borderline personality disorder can be included in the new proposed category of overconsolidational spectrum disorders 8 since it is associated with child abuse and neglect. 9 Facilitation of memory extinction is one of the possible mechanisms by which topiramate is effective in the treatment of BPD and PTSD.…”