Epigenetics, genetics and biochemistry of suicide

The development of molecular biology methods has made it possible to identify new, previously unknown mechanisms of the formation of the suicidal phenotype and suicidal behavior. This allowed specialists in the field of suicidology to regard the suicidal phenotype as an independent polygenic and multifactorial pathology that can accompany mental illness as a comorbid condition. The aim of the publication is to systematize the known literature data on persistent biochemical changes associated with the suicidal phenotype. Epigenetic, genetic and biochemical markers associated with suicidal behavior and suicides of persons without previous mental illnesses, as well as molecular biological analysis of suicide cases in patients with major depressive disorder are considered. Analysis of modern literature publications of direct studies of biological material obtained from individuals with suicidal behavior and suicide victims, as well as meta-analyses gives grounds to consider the main cause of the suicidal phenotype to be neuroinflammation and/or penetration into the cerebrospinal fluid through the genetically compromised blood-brain barrier of inflammatory cytokines formed in individuals with long-term debilitating chronic inflammatory diseases (latent Toxoplasma infection gondii, rheumatoid diseases, atopic dermatitis, bronchial asthma). Neuroinflammation, which forms the suicidal phenotype, is realized as a result of single nucleotide polymorphisms of genes associated with homeobox and immune response genes, such as interleukins -2, -4, 6, tumor necrosis factor. While interleukin-8 may have a protective effect. In addition, the suicidal phenotype is most likely associated with a genetically determined disorder of tryptophan metabolism caused by activation of the kynurenine pathway with concomitant depletion of the serotonin pool and induction neuroinflammation of the kynurenine type. Chronic neuroinflammation changes psychotype and behavior towards the formation of a suicidal phenotype. As a result, the individual creates a social environment around himself that contributes to the aggravation of neuroinflammation and suicide as the final outcome of the disease. It was concluded that the suicidal phenotype is formed by neuroinflammation.