Abstract
According to the World Health Organization (WHO), more than 700,000 people die per year due to suicide. Suicide risk factors include a previous suicide attempt and psychiatric disorders. The highest mortality rate in suicide worldwide is due to depression. Current evidence suggests that suicide etiopathogenesis is associated with neuroinflammation that activates the kynurenine pathway and causes subsequent serotonin depletion and stimulation of glutamate neurotransmission. These changes are accompanied by decreased BDNF (brain-derived neurotrophic factor) levels in the brain, which is often linked to impaired neuroplasticity and cognitive deficits. Most suicidal patients have a hyperactive hypothalamus–pituitary–adrenal (HPA) axis. Epigenetic mechanisms control the above-mentioned neurobiological changes associated with suicidal behaviour. Suicide risk could be attenuated by appropriate psychological treatment, electroconvulsive treatment, and drugs: lithium, ketamine, esketamine, clozapine. In this review, we present the etiopathogenesis of suicide behaviour and explore the mechanisms of action of anti-suicidal treatments, pinpointing similarities among them.
Highlights
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Genome-wide association studies (GWAS) have indicated that polygenic risk and specific loci such as genes involved in circadian clock regulation, tyrosine metabolism, and risk factors for depressive disorder are associated with a higher risk of attempting suicide [20,21]
Suicidal behaviour is associated with multiple risk factors such as psychiatric disorders, personality traits, and stressful life events
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. Over 50% of suicides occur in patients with major depression or bipolar disorders, especially when they are treatment resistant [3,7,8]. Only 5% of psychiatric patients commit suicide This particular risk group includes patients requiring hospital treatment (10 times higher than in the general population) [13]. Genome-wide association studies (GWAS) have indicated that polygenic risk and specific loci such as genes involved in circadian clock regulation, tyrosine metabolism, and risk factors for depressive disorder are associated with a higher risk of attempting suicide [20,21]. Data suggest that early life adversity is especially harmful and increases the rate of impulsive and suicidal behaviour by two to five times [6,29,30]. Ketamine/esketamine (in depression, rapid effect), lithium (in depression and bipolar disorder, delayed effect), electroconvulsive therapy, psychotherapy, transcranial magnetic stimulation
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