Suicidal behavior is a growing public health problem. Existing treatments have limited efficacy for people who have already attempted suicide, so new approaches are needed. Research on the neurobiology of social pain—a risk factor for suicide—has identified promising pharmacological targets. This paper reviews and critically evaluates evidence for these targets, examining how social pain relates to the anti-suicidal properties of recently approved treatments like ketamine and psilocybin. These strategies may reduce suicidal ideation and behavior in the short term, especially when social pain is a contributing factor, and may work regardless of psychiatric diagnosis, though careful evaluation is required.
Suicidal behavior is a growing public health problem. Existing treatments have limited effectiveness for people who have already attempted suicide, so new approaches are needed. Research on the neurobiology of social pain—the distress from social rejection or loss—identifies it as a key risk factor and suggests several promising drug targets. This paper reviews evidence on those targets and examines how recently approved treatments like ketamine and psilocybin may reduce suicidal ideation and behavior in the short term, especially when social pain is a contributing factor. These pharmacological strategies may work regardless of whether a person has a specific psychiatric diagnosis.
Complex PTSD (C-PTSD) is a chronic condition that includes both the classic PTSD triad of reexperiencing, avoidance, and hypervigilance, plus a second triad of disturbances in self-organization: mood dysregulation, interpersonal difficulties, and negative self-image. About 2-8% of the world's population is affected, with higher rates in refugees and childhood abuse survivors. Current treatments for PTSD symptoms show limited benefit for the disturbances in self-organization. Animal research suggests that alterations in oxytocin and vasopressin, linked to evolved appeasement and submission behaviors, may underlie these social and emotional symptoms. This model requires further verification in human studies.