"All we have to fear is fear itself": Paradigms for reducing fear by preventing awareness of it.

IF 4 2区 医学 Q2 CHEMISTRY, MEDICINAL
ACS Infectious Diseases Pub Date : 2024-09-01 Epub Date: 2024-08-01 DOI:10.1037/bul0000437
Paul Siegel, Bradley S Peterson
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引用次数: 0

Abstract

Research on unconscious fear responses has recently been translated into experimental paradigms for reducing fear that bypass conscious awareness of the phobic stimulus and thus do not induce distress. These paradigms stand in contrast to exposure therapies for anxiety disorders, which require direct confrontation of feared situations and thus are distressing. We systematically review these unconscious exposure paradigms. A Preferred Reporting Items for Systematic Reviews and Meta-Analyses-based search yielded 39 controlled experiments based on 10 paradigms that tested whether exposure without awareness can reduce fear-related responses. In randomized controlled trials of phobic participants, unconscious exposure interventions: (a) reduced behavioral avoidance (weighted mean d = 0.77, N = 469) and self-reported fear (d = 0.78, N = 329) during in vivo exposure to feared situations; (b) reduced neurobiological indicators of fear and enhanced such indicators of fear regulation (d = 0.81, N = 205); (c) had significantly stronger effects on reducing symptomatic behaviors and enhancing neurobiological indicators of fear regulation than did conscious exposure (d = 0.78, N = 342); and (d) produced these effects without inducing subjective fear. In fear-conditioned participants, unconscious exposureinduced extinction learning (d = 0.80, N = 420), even during sleep, and yielded somewhat stronger extinction learning than conscious exposure did (d = 0.44, N = 438). We organize these findings within a neuroscientific framework and evaluate alternative mechanisms for unconscious exposure. The use of incommensurate outcome measures across exposure paradigms and nonreporting of relevant statistics limited meta-analyses. Despite steps taken to address publication bias, 25.6% of included studies came from a single laboratory. We propose potential clinical applications of these findings. Future research should clarify underlying mechanisms, use common outcome measures, and explore effects on other anxiety disorders. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

"我们所恐惧的只是恐惧本身":通过防止意识到恐惧来减少恐惧的范例。
关于无意识恐惧反应的研究最近被转化为减少恐惧的实验范例,这些范例绕过了对恐惧刺激的有意识意识,因此不会引起痛苦。这些范例与治疗焦虑症的暴露疗法形成了鲜明对比,后者需要直接面对恐惧情境,因此会让人感到痛苦。我们对这些无意识暴露疗法进行了系统回顾。通过基于系统综述和元分析首选报告项目的搜索,我们找到了基于 10 种范式的 39 项对照实验,这些实验测试了无意识暴露是否能减少与恐惧相关的反应。在对恐惧症参与者进行的随机对照试验中,无意识暴露干预:(a)减少了在体内暴露于恐惧情境时的行为回避(加权平均值 d = 0.77,N = 469)和自我报告的恐惧(d = 0.78,N = 329);(b)减少了恐惧的神经生物学指标,增强了恐惧调节指标(d = 0.81, N = 205);(c) 在减少症状行为和增强恐惧调节神经生物学指标方面的效果明显强于有意识暴露(d = 0.78, N = 342);(d) 在不诱发主观恐惧的情况下产生这些效果。在恐惧条件反射参与者中,无意识暴露诱导了消退学习(d = 0.80,N = 420),甚至在睡眠期间也是如此,并且产生的消退学习比有意识暴露更强(d = 0.44,N = 438)。我们在神经科学框架内整理了这些发现,并评估了无意识暴露的替代机制。在不同暴露范式中使用不一致的结果测量方法以及未报告相关统计数据限制了荟萃分析。尽管已采取措施解决发表偏倚问题,但25.6%的纳入研究来自单一实验室。我们提出了这些发现的潜在临床应用。未来的研究应阐明潜在的机制,使用通用的结果测量方法,并探讨对其他焦虑症的影响。(PsycInfo Database Record (c) 2024 APA,保留所有权利)。
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来源期刊
ACS Infectious Diseases
ACS Infectious Diseases CHEMISTRY, MEDICINALINFECTIOUS DISEASES&nb-INFECTIOUS DISEASES
CiteScore
9.70
自引率
3.80%
发文量
213
期刊介绍: ACS Infectious Diseases will be the first journal to highlight chemistry and its role in this multidisciplinary and collaborative research area. The journal will cover a diverse array of topics including, but not limited to: * Discovery and development of new antimicrobial agents — identified through target- or phenotypic-based approaches as well as compounds that induce synergy with antimicrobials. * Characterization and validation of drug target or pathways — use of single target and genome-wide knockdown and knockouts, biochemical studies, structural biology, new technologies to facilitate characterization and prioritization of potential drug targets. * Mechanism of drug resistance — fundamental research that advances our understanding of resistance; strategies to prevent resistance. * Mechanisms of action — use of genetic, metabolomic, and activity- and affinity-based protein profiling to elucidate the mechanism of action of clinical and experimental antimicrobial agents. * Host-pathogen interactions — tools for studying host-pathogen interactions, cellular biochemistry of hosts and pathogens, and molecular interactions of pathogens with host microbiota. * Small molecule vaccine adjuvants for infectious disease. * Viral and bacterial biochemistry and molecular biology.
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