Much has been learned and written about other neurobiological mechanisms that play a role in suicidal behavior and whether pharmacological agents that act on those systems can contribute to reducing the risk for suicide and suicide attempt. Antiepileptic drugs were also found by the FDA in a meta-analysis to be associated with greater risk for ideation [161] but others found the opposite [162]. Antiepileptic drugs act mostly to enhance GABAergic inhibitory function in the cortex and that raises a question about the impact of GABA on suicide risk as an area for future research. PUFA profile can predict suicide attempt risk and perhaps omega-3 supplements may help reduce risk. Ketamine is very rapidly acting antidepressant and is reported to also have a profound therapeutic benefit for suicidal ideation. It is an AMPA receptor antagonist and raises GABA levels and perhaps those properties contribute to its rapid and profound reduction in suicidal ideation. Other new agents targeting other neurobiological mechanisms related to suicidal behavior beyond the major neurotransmitters that are currently being examined, including the corticotrophin-releasing factor 1 receptor, neuropeptide Y, vasopressin V1b, N-methyl-daspartate, nicotinic acetylcholine, dopamine D1, glucocorticoid system, δ-opioid, cannabinoid and cytokine receptors, γ-amino butyric acid (GABA), intracellular messenger systems, transcription, and neuroprotective and neurogenic factors [163]. Moreover, emerging data from pharmacogenetic studies showing gene effects on treatment response will provide additional tools for developing more personalized pharmacotherapies for suicidal behavior [164].
© 2012 by Taylor & Francis Group, LLC.