The following is an abstract of a presentation on the topic of ketamine and NDEs by Karl Jansen of the University of Auckland. The presentation itself was pretty much word for word what is included in the abstract.
Abstract: Ketamine is a dissociative anesthetic with powerful hallucinogenic and psychedelic properties, including out-of-body experiences, transcendence of time, an extension of awareness beyond consensus reality into other universes, and other effects. Ketamine can produce every feature of a near-death experience (NDE) (Jansen 2001), including the conviction that one has died, awareness leaving the body, ringing/buzzing/ whistling sounds followed by travel through a tunnel at high speed, emerging into light, communion with God, and a life review.
Because we know how ketamine acts in the brain, this provides us with an understanding of how NDE’s arise. Ketamine blocks ion channels attached to NMDA receptors, and causes a blockage so that salts cannot enter the cell. The neurotransmitter glutamate crosses the gap between cells and binds to NMDA receptors, turning the chemical key which should allow ions to enter the cell. However, while the tunnel is blocked by ketamine, this is not possible.
NDE’s also involve blockade of NMDA receptors. A sudden fall in O2 or blood sugar, a rise in CO2 (e.g. during a heart attack), and other factors cause a flood release of glutamate. This over-excites cells which die. This is called ‘excito-toxicity’. The glutamate flood also activates apoptotic genes which trigger the cell to commit suicide. Ketamine can prevent this brain damage via the same mechanism which is important to its psychedelic effects: blockade of channels so that ‘the ion sea’ cannot rush into the cells. This led to the prediction that the brain would have its own, natural protective mechanisms against the glutamate flood (Jansen 2001). There would be a huge evolutionary advantage in the development of a protective mechanism involving a counter-flood of natural NMDA receptor-complex blockers, producing ketamine-like NDE effects. While a person is having an NDE at the psychological level, the brain is thus protecting itself from excito-toxic damage. Natural blockers include NAAG (N-acetyl-aspartyl-glutamate), magnesium and kynurenic acid, all of which protect cells from excito-toxic damage.
People deprived of oxygen for long periods, e.g. after a heart attack, and who report NDE’s, sometimes survive with unimpaired brains. This lack of damage may result from an inherited mechanism for blocking over-excitation. Thus people who can have an NDE may be less likely to suffer brain damage. These may be the same group who report psychedelic experiences with ketamine. Dreams, ketamine ‘journeys’ and NDE’s are all states in which there is a dramatically reduced sensory input from the outside world. Those who do not recall dreams also do not recall ketamine ‘journeys’. The % who recall dreams is about the same as the % reporting ‘emergence phenomena’ after ketamine: about 40%, which is the % of the population who have had some kind of NDE. Genetic differences may be responsible, expressing themselves as different forms of NMDA receptors.
Ref: Jansen KLR (2001a) Ketamine: Dreams and Realities. Sarasota, Florida: Multidisciplinary Association for Psychedelic Studies (ISBN 0-9660019-3-1) (Available from
www.maps.org).
