Virtual stressors with real impact: what virtual reality-based biobehavioral research can teach us about typical and atypical stress responsivity.

IF 5.8 1区 医学 Q1 PSYCHIATRY
Elizabeth A Shirtcliff, Tor T Finseth, Eliot H Winer, David C Glahn, Roselynn A Conrady, Stacy S Drury
{"title":"Virtual stressors with real impact: what virtual reality-based biobehavioral research can teach us about typical and atypical stress responsivity.","authors":"Elizabeth A Shirtcliff, Tor T Finseth, Eliot H Winer, David C Glahn, Roselynn A Conrady, Stacy S Drury","doi":"10.1038/s41398-024-03129-x","DOIUrl":null,"url":null,"abstract":"<p><p>Stress contributes to transdiagnostic morbidity and mortality across a wide range of physical and mental health problems. VR tasks have been validated as stressors with robust effect sizes for VR-based stressors to evoke stress across the most common autonomic and adrenocortical stress biomarkers. However, meta-analytic validation of VR stressors have resulted in inconsistent logic: why should something that isn't real evoke a very real suite of stress responses? This review posits that conceptually addressing this question requires differentiating a cause, \"stressor\", from effects, \"stress\". Stress comprises a series of well-delineated perturbations in biological systems, such as autonomic and adrenocortical biomarkers in response to stressors. Despite their ubiquity, decades of literature have back-calculated stressor intensity based on the magnitude of a stress response. This causal directionality is not logical, yet remains pervasive because seemingly objective stress indices have generated a wealth of findings showing how stress gets under the skin and skull. This has created challenges for providing clear guidance and strategies to measure acute stressor intensity. Binary thinking about whether something is (not) real has stifled advances in understanding how to measure the dosage of a stressful environment. As a function of being programmed, individualizable, and titrated, virtual reality (VR) based stressors offer the field a platform for quantifying the dose of a stressor and generating reliable dose-response curves. This also raises the possibility to safely and ethically integrate psychosocial stressor administration into clinical and therapeutic settings. For example, Social Evaluative Threat experiments effectively trigger a stress response both in a laboratory setting and in built environments, while also upholding hard-fought trust and rapport with care providers. By focusing attention on the measurement of the stressor, VR paradigms can advance tangible understanding of stressors themselves and the pathways to the stress response.</p>","PeriodicalId":23278,"journal":{"name":"Translational Psychiatry","volume":"14 1","pages":"441"},"PeriodicalIF":5.8000,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11487258/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Translational Psychiatry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1038/s41398-024-03129-x","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PSYCHIATRY","Score":null,"Total":0}
引用次数: 0

Abstract

Stress contributes to transdiagnostic morbidity and mortality across a wide range of physical and mental health problems. VR tasks have been validated as stressors with robust effect sizes for VR-based stressors to evoke stress across the most common autonomic and adrenocortical stress biomarkers. However, meta-analytic validation of VR stressors have resulted in inconsistent logic: why should something that isn't real evoke a very real suite of stress responses? This review posits that conceptually addressing this question requires differentiating a cause, "stressor", from effects, "stress". Stress comprises a series of well-delineated perturbations in biological systems, such as autonomic and adrenocortical biomarkers in response to stressors. Despite their ubiquity, decades of literature have back-calculated stressor intensity based on the magnitude of a stress response. This causal directionality is not logical, yet remains pervasive because seemingly objective stress indices have generated a wealth of findings showing how stress gets under the skin and skull. This has created challenges for providing clear guidance and strategies to measure acute stressor intensity. Binary thinking about whether something is (not) real has stifled advances in understanding how to measure the dosage of a stressful environment. As a function of being programmed, individualizable, and titrated, virtual reality (VR) based stressors offer the field a platform for quantifying the dose of a stressor and generating reliable dose-response curves. This also raises the possibility to safely and ethically integrate psychosocial stressor administration into clinical and therapeutic settings. For example, Social Evaluative Threat experiments effectively trigger a stress response both in a laboratory setting and in built environments, while also upholding hard-fought trust and rapport with care providers. By focusing attention on the measurement of the stressor, VR paradigms can advance tangible understanding of stressors themselves and the pathways to the stress response.

具有真实影响的虚拟压力源:基于虚拟现实的生物行为学研究能告诉我们什么是典型和非典型压力反应。
压力会导致各种身心健康问题的跨诊断发病率和死亡率。VR任务作为压力源已经得到验证,基于VR的压力源在最常见的自律神经和肾上腺皮质压力生物标志物中唤起压力的效应大小很强。然而,对 VR 压力源的元分析验证却产生了不一致的逻辑:为什么不真实的东西会唤起一系列非常真实的压力反应?本综述认为,要从概念上解决这个问题,就必须区分原因("压力源")和影响("压力")。压力包括生物系统中一系列明确界定的扰动,例如自律神经和肾上腺皮质生物标志物对压力源的反应。尽管压力无处不在,但几十年来的文献都是根据压力反应的大小来反向计算压力源的强度。这种因果方向性不符合逻辑,但仍然普遍存在,因为看似客观的压力指数已经产生了大量的研究结果,显示压力是如何侵入皮肤和头骨的。这就为提供明确的指导和策略来测量急性应激源强度带来了挑战。关于某件事情是否真实的二元思维阻碍了人们对如何测量压力环境剂量的理解。基于虚拟现实(VR)的应激源具有可编程、可个性化和可滴定的功能,为该领域提供了一个量化应激源剂量和生成可靠剂量-反应曲线的平台。这也为安全、合乎伦理地将社会心理应激源应用于临床和治疗提供了可能。例如,社会评价威胁实验在实验室环境和人造环境中都能有效触发应激反应,同时还能维护与护理提供者之间来之不易的信任和融洽关系。通过将注意力集中在应激源的测量上,虚拟现实范例可以促进对应激源本身和应激反应途径的切实了解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
11.50
自引率
2.90%
发文量
484
审稿时长
23 weeks
期刊介绍: Psychiatry has suffered tremendously by the limited translational pipeline. Nobel laureate Julius Axelrod''s discovery in 1961 of monoamine reuptake by pre-synaptic neurons still forms the basis of contemporary antidepressant treatment. There is a grievous gap between the explosion of knowledge in neuroscience and conceptually novel treatments for our patients. Translational Psychiatry bridges this gap by fostering and highlighting the pathway from discovery to clinical applications, healthcare and global health. We view translation broadly as the full spectrum of work that marks the pathway from discovery to global health, inclusive. The steps of translation that are within the scope of Translational Psychiatry include (i) fundamental discovery, (ii) bench to bedside, (iii) bedside to clinical applications (clinical trials), (iv) translation to policy and health care guidelines, (v) assessment of health policy and usage, and (vi) global health. All areas of medical research, including — but not restricted to — molecular biology, genetics, pharmacology, imaging and epidemiology are welcome as they contribute to enhance the field of translational psychiatry.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信