物質使用障害における自殺リスクの増加：神経生物学的視点

Human actions are inherently driven to reduce unpleasant, aversive experiences through physiological and behavioral adaptations. Addictive substances can temporarily fulfil this need for avoidance when conditions are perceived as excessively aversive. However, long-term use can impair cognitive processes involved in self-preservation. Substance use directly and indirectly influences acute and chronic mental states characterized by dysphoria, negative emotions, altered cognition, an altered sense of reality, and diminished awareness of negative consequences, all of which have deleterious effects on the individual.

A narrative synthesis of the literature was conducted, focusing on neurochemical, neuroendocrine, neural pathway, immune, and genetic mechanisms implicated insuicide risk among individuals with SUD.

The complex mental state seen in individuals with problematic substance use is the result of altered neurobiology, which conveys a strong predisposition to suicidal behaviors. The etiology of suicide among individuals with substance use disorder (SUD) is multifactorial and mediated through several neurochemical modifications that eventually create a transient or long-lasting unique neurobiological state dependent on the pattern of use.

Multiple neuroendocrine and immune response pathways, along with underlying genetic sequences of interest, are a leading focus in identifying individuals at risk for suicide and in understanding disease heterogeneity and universality.