Abstract
Why some patients attempt or commit suicide and others do not has perplexed psychiatrists for years. We now have evidence for both clinical and biological correlates of suicidal behavior that can be understood as part of a clinical and neurobiologic explanatory model of suicidal behavior. Our lists of risk factors for suicidal behavior can be converted into an understandable pathogenic model that begins to explain the diathesis or predisposition to suicidal behavior that distinguishes high-risk patients. The association of suicidal behavior clinically with aggressive impulsive traits and pessimism or hopelessness, and biologically with deficits in serotonergic function related to behavioral inhibition and mood, and abnormalities in stress-response systems such as the hypotha-lamic-pituitary-adrenal axis have contributed to this stress-diathesis model. For the clinician, there is emerging evidence that biological testing can supplement clinical judgment in predicting the risk of suicidal behavior in the short-term and longer-term. Antecedents of suicidal behavior have been identified in more recent clinical and biologic studies that allow us to understand how genes and early childhood adversity interact to create the psychopathologic and neurobiologic underpinnings of the predisposition to suicidal behavior and suicide in adult life. These observations offer opportunities for new ways of detecting high-risk patients and new targets for therapeutic intervention to prevent the development of a predisposition for suicidal behavior and to prevent suicidal behavior when that predisposition is already present.