Depression has been a vexing problem in Psychiatry. Our simplistic explanation of “too little serotonin” has hardly proven effective for most depression sufferers. In fact, some experts, such as Nassir Ghaemi, MD, noted expert on psychopharmacology recently wrote:
“Psychiatry… use(s) hundreds of made-up labels for professional purposes, without really getting at the reality of what is wrong with the patient…. (We have little understanding of) what the causes of those disease…We have a huge amount of neurobiology research now to conclude that the 20th century neurotransmitter theories of psychopharmacology basically are false.” (Nassir Ghaemi, MD, Psychiatry, Medscape Connect)
It seems that second messenger pathways actually are more important in treating depression. What an antidepressant does by raising serotonin or norepinephrine is hopefully activate one of these second messenger pathways. But the success of that medication depends upon genetics, enzymes, neurotrophic factors and many other variables. One of the key second messenger pathways is mediated by the chemical glutamate, acting on a particular receptor called the NMDA receptor. The NMDA receptor is involved in learning, memory, and plasticity of the brain. This glutamine receptor alters ion channels in brain cells and sets off a chain of secondary events, increasing brain growth factors and regenerative pathways. Ketamine, an anesthetic that has been in clinical use for many years, works very powerfully on the NMDA receptor. The result is a tremendous lifting of the depression in a great majority of cases. The relief of symptoms can begin almost immediately or over the next few hours.
Ketamine is a unique medication in the treatment for depression. It is not an SSRI, SNRI or a MAOI. Ketamine can be safely combined with most medications, so patients do not have to stop their current medications to begin ketamine.