Department of Emergency Psychiatry and Acute Care, Lapeyronie Hospital, CHU Montpellier, Montpellier, France.
PSNREC, Univ Montpellier, INSERM, CHU de Montpellier, Montpellier, France.
Curr Psychiatry Rep. 2021 Mar 3;23(4):16. doi: 10.1007/s11920-021-01227-x.
The aim of this review was to analyze COVID-19 effect on the biological features of suicidal vulnerability and its interaction with suicide-related biological pathways. We carried out a narrative review of international publications on the interactions of COVID-19 with the biological bases of suicide.
We hypothesize that SARS-CoV-2 interacts with multiple biological processes that underlie suicidal behavior, such as the renin-angiotensin system, nicotinic receptors, and central and systemic inflammation. Social distancing measures may also worsen subjective or objective social disconnection, thus increasing the risk of suicide. Interestingly, the drugs used to prevent suicide could be promising options to counteract brain damage caused by this coronavirus. SARS-CoV-2 interacts with multiple biological pathways involved in suicide and opens a new window for understanding the suicidal process. The development of suicide prevention treatments in the context of a pandemic may benefit from knowledge on these interactions.
本综述旨在分析 COVID-19 对自杀脆弱性生物学特征的影响及其与自杀相关生物学途径的相互作用。我们对 COVID-19 与自杀生物学基础相互作用的国际出版物进行了叙述性综述。
我们假设 SARS-CoV-2 与多种生物学过程相互作用,这些过程是自杀行为的基础,如肾素-血管紧张素系统、烟碱受体以及中枢和全身炎症。社交隔离措施也可能恶化主观或客观的社会脱节,从而增加自杀的风险。有趣的是,用于预防自杀的药物可能是对抗这种冠状病毒引起的大脑损伤的有前途的选择。SARS-CoV-2 与参与自杀的多个生物学途径相互作用,为理解自杀过程开辟了新的窗口。在大流行背景下开发预防自杀的治疗方法可能受益于对这些相互作用的了解。