Psychopharmacological Agents and Suicide Risk Reduction: Ketamine and Other Approaches

This review (2015) examines the neurobiology of ketamine’s potential to treat suiciadility and proposes that its working mechanism functions via the suppression of pro-inflammatory cytokines and by restoring tryptophan/serotonin production via inhibition of the kynurenine pathway. It notes that this hypothesis requires further validation via replicated randomized control research with larger samples.


Review: Suicide is a major global public health problem and the leading cause of injury mortality in the USA. Suicide is a complex phenomenon involving several systems and neurobiological pathways, with interacting genetic and environmental mechanisms. The literature on the neurobiology and pharmacotherapy of suicide has been limited. To date, no medications have proven efficacious for treating acute suicidal crises. There is an emerging literature supporting a rapid anti-suicidal effect of ketamine, a non-competitive N-methyl-D-aspartate (NMDA) glutamate receptor antagonist, among depressed patients with suicidal ideation. Potential ketamine’s anti-suicidal effect mechanisms are linked to interruption of the kynurenine pathway and modulating pro-inflammatory cytokines exacerbation. However, available data are not sufficient for its routine integration in clinical practice, and larger and replicated randomized control studies are needed.

Authors: Rayan K. Al Jurdi, Alan Swann & Sanjay J. Mathew 

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Psychopharmacological Agents and Suicide Risk Reduction: Ketamine and Other Approaches

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Published in
Current Psychiatry Reports
August 27, 2015
25 citations

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Literature Review Bio/Neuro

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