Suicidality and COVID-19: Suicidal ideation, suicidal behaviors and completed suicides amidst the COVID-19 pandemic (Review)

Abstract

Since the outbreak of the coronavirus 2019 (COVID-19) pandemic, there has been widespread concern that social isolation, financial stress, depression, limited or variable access to health care services and other pandemic-related stressors may contribute to an increase in suicidal behaviors. In patients who have recovered from COVID-19, an increased risk of developing suicidal behaviors may be noted, while post-COVID syndrome comprises another potential risk factor contributing to increased suicidal behaviors. Despite the initial alarming predictions for an increase in suicide rates due to the COVID-19 pandemic, the majority of published studies to date suggest that experienced difficulties and distress do not inevitably translate into an increased number of suicide-related deaths, at least not in the short-term. Nevertheless, the long-term mental health effects of the COVID-19 pandemic have yet to be unfolded and are likely to remain for a long period of time. Suicide prevention and measures aiming at promoting well-being and mitigating the effects of COVID-19 on mental health, particularly among vulnerable groups, should thus be a priority for healthcare professionals and policymakers amidst the evolving COVID-19 pandemic.

Keywords: COVID-19; COVID-19 survivors; SARS-CoV-2; suicidal behavior; suicidality.

Figure 1

Risk factors for suicidality during COVID-19 pandemic and suicide prevention strategies.

Figure 2

Neurobiological correlates of COVID-19 suicidal behavior. (A) SARS-CoV-2 infection induces distinctive effects in the CNS, which are mediated by the retrograde axonal transport of the virus in the CNS in acute COVID-19, or immune responses, including the cytokine ‘storm’, that precipitate acute or chronic neuroinflammatory and neurodegenerative cascades. Additionally, SARS-CoV-2 may cause the dysregulation of neurotransmitters (i.e., serotonin, glutamate, GABA) and the dysfunction of large cortical networks and subcortical brain structures, which may be linked to an increased risk of suicidality in patients with COVID-19. Further pathways possibly involved in COVID-19-related suicidal behavior involve the hypothalamic-pituitary adrenal axis. In COVID-19, stress responses and cortisol hypersecretion have been shown to upregulate the hypothalamus-pituitary-adrenal axis (adrenal glands are depicted in orange), while further suggested mechanisms that may contribute to emergence or exacerbation of suicidal behavior involve dysregulation of the gut microbiota and the brain-gut axis. (B) All the aforementioned mechanisms may induce dysfunction in several brain regions, which have been implicated in the pathophysiology of suicidal behavior, and are mainly located in the ventral and dorsal prefrontal cortex, insula, mesial temporal, subcortical and posterior regions. Notably, neuroimaging and histopathological evidence of COVID-19-related suicidality is currently unavailable; thus, the depicted brain regions have been linked with suicidal behavior in previous neuroimaging studies in non-COVID-19 patients with suicidal ideation or behavior. Further brain structures implicated in suicidality include the DMPFC, the hippocampus and the basal ganglia (not shown). Notably, as previously demonstrated, autopsies of patients with COVID-19 have indicated neuronal loss and hypoxic changes in some of the aforementioned brain regions (64). CNS, central nervous system; GABA, glutamate and gamma-aminobutyric acid; RLPFC, rostrolateral prefrontal cortex; DMPFC, dorsomedial prefrontal cortex; dACC, dorsal anterior cingulate cortex; PCC, posterior cingulate cortex; Thal, thalamus; VS, ventral striatum; Amyg, amygdala; RF, reticular formation.