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Ketamine and the Near Death Experience

Ketamine was a cult hit with doctors. Think Dead Ringers by David Cronenberg. Now the cat is out of the bag.

Perhaps the greatest appeal to a reader of cyberpunk fiction such as William Gibson or Neil Stephenson lies in its ability to simulate the experience of a brain consciousness roaming within a global neural network, untethered by a physical body.

It's medically relatively safe - but read below - on your body, and for 45 minutes you have an out of body experience a classic NDE (near-death experience.) Can induce glassoholia (speaking in tongues.) Induces schizophrenia, but you are conscious while on it. Creates an Out of Body Experience in users.

Ketamine is unique in that it causes dissociation rather than loss of consciousness. The ego field is conditioned and strongly associated with conscious process. Ketamine disperses the ego field, which is the basis for memory because personal memory always involves an ego and a world.

The experience results in very little lasting emotional and psychosomatic transformation. Its greatest value is in a profound and lasting change of one's world view and a radically new understanding of the process of death. In other words, it's a scientifically validated, religious sacrament.

Soon to come: Streaming video of the Near Death Experience Special on the Discovery Channel.

It appears yet again that Grace is achievable without divine intervention. And you can graph it. It also seems that this non-placebo sacramental drug can be used safely by crassly materialistic white people without the support of weird spiritualistic rituals. A “new age” or classical music CD helps with the setting but isn't essential.“Ketamine hydrochloride, a substance combining anesthetic and psychedelic properties, is extremely interesting from the heuristic point of view. It opens access to most extraordinary realms of experiences, offers remarkable philosophical and spiritual revelations, and mediates fascinating insights into the cosmic processes by which reality itself is created. Its disadvantage is that the subject feels strongly drugged, has poor coordination, and his or her capacity for verbal communication, as well as subsequent recall, are distinctly impaired.

The optimal dosage is about one-tenth to one-sixth of the anesthetic dose; it ranges between 100 and 150 milligrams intramuscularly. The music used for ketamine sessions should be slow, expansive, and “cosmic” in nature to reflect the quality of the experience. Some of the disadvantages of ketamine could be possibly overcome by separating its two optically-active components.

James Kent of resproject.com Ketamine and DMT)

I have a friend who has tried a DMT and Ketamine combo a couple of times. Sorry to report that the DMT + K experience did not resemble a classic NDE any more than your typical run-of-the-mill, surging, 5+ out-of-body peak experience you'd get on any heroic dose of a traditional psychedelic tryptamine.

The classic traits of the NDE (scenes of life flashing before you, tunnel of light, communing with departed loved ones, a feeling of emotional release and intense bliss…) did not accompany the DMT+K experience at all – it was MUCH weirder far more difficult to fit into stereotypical paranormal experiences like a classic NDE.

It was more like sending your consciousness into a light speed flipper-pinball frenzy around the center of a flickering-flourescent black-hole in the middle of hyperspace (surrounded by crazed, musical, subatomic giggling light-entities). No gentle reassuring tones. No fluffy clouds and strumming angels. No pearly gates. More like demented hilarity, mayhem, complex 3-D geometric imagery, complete sense of timelessness, chaos, and confusion….

Was it intense and weird? Yes. Fun? Yes. Out of body? Yes. Similar to a classic NDE ? Not at all. K all by itself more closely resembles the traits of a classic NDE than the K+DMT combo (IMFHO). I would also argue that DMT is generally more like a classic alien abduction experience than a classic NDE (and the two are VERY different).

James Kent of resproject.com A Note on Addiction

The rewarding aspects of Ketamine seem endless. Navigating these energy networks gives you access to a limitless area of deep knowledge. The most seductive power of Ketamine is that it is simply impossible to navigate through all of the networks presented in a single session, probably not even in a single lifetime of prolonged use. Since the imagination is infinite, Ketamine exploration could theoretically go on forever. This, more than anything else, is what makes Ketamine an extremely addictive substance. in order to combat it you must moderate your use and not let Ketamine take over your life. A few good rules of thumb to follow to avoid addiction are

i) Never do repeat doses in a single session. Always come down fully from each dose and wait a few days to a week before going in again;

2) Never take Ketamine impulsively, or just because you're bored. This can lead long-term binges and/or spree usage behavior;

3) Maintain a strict routine that lets you maximize the results of each session. There's no need to be in there all day when you know what you're going in for;

and 4) Never let your Ketamine use take priority over your real-world responsibilities. Trust me, you're always needed elsewhere. The emergent state should be your refuge, not your permanent address. If you moderate your use and keep your feet on the ground you'll be fine. If you become indulgent and careless, Ketamine will pull you down.

James Kent of resproject.com Ketamine and TheFuture?

Considering Ketamine's profound ability to reliable, and repeatedly induce hypnotic, lucid, and dreamlike states of deep relaxation, it is obviously an invaluable adjunct tool for therapies which deal with stress management, behavior modification, personality, programming, reprogramming, metaprogramming, memory regression, habit change, etc. To limit its sanctioned use to anaesthetic purposes seems repressive, and even now there are studies being done to test its therapeutic potential. In the UK, Dr. Karl Jansen is using Ketamine to study the neurochemical implications of near death experiences (NDEs), and in Russia Dr. Evgeny Krupitsky is studying the effects of Ketamine Psychedelic therapy (KPI) on treating alcohol abuse.

However, like all great secrets eventually do, 'Special K' has finally trickled down to the street level and has become a standard black market menu item among ravers, club kids, and psychonautic thrill seekers. It's no surprise that popular music bands like the Chemical Brothers, Kula Shakur, and Tool have started throwing around references to K in their work - some veiled, some not so veiled. Last season the X-Files used Ketamine as the convenient psychoactive plot device, of the week (even though they vetted a little with some of Ketamine I e' I s subjective psychoactive effects, like a single K session lasting 6 hours to 3 days. A little inaccurate, but hey, it's TV. We'll let them slide). Even Time Magazine couldn't resist the urge to jump on the bandwagon, and recently printed

A cautionary article entitled, 'is Your Kid on K?” ecently appeared in Time Magazine.

There's no doubt in my mind that Ketamine's popularity as a recreational drug will continue to grow, but this is a troubling trend. I predict that there are going to be more Ketamine-related accidents in the near future, and I would just like to emphasize again that Ketamine should not be used as a recreational drug in a party setting. It is simply too dangerous to be on K when you're walking around, dancing, etc. Unsafe use will wind up getting people hurt and killed, and it is only a matter of time before there is some K backlash in the hallowed halls of government.

Although laws vary from state to state, Ketamine is still fairly legal to possess. It is as high as Schedule III in some states, but unless you are trying to unload crates of it on the Mexican border, it is unlikely you would ever be prosecuted even if you were unfortunate enough to get caught in possession. However, it wouldn't surprise me if there was a federal ruling to place Ketamine into a more restrictive schedule within the year. That's usually what happens to any drug when parents find out that their kids are doing

Breathing and Energy Techniques with Ketamine

At about the fifteen minute mark of a Ketamine session, you will begin to feel all of the energy in your body unraveling. The threads of energy which keep you rigid and upright all day will begin to unwind, and each layer that peels off will feel like another layer of deep tension being evaporated from your body. As this happens, it is important to continue breathing and focus on activating and opening various chakras or energy centers in your body. As you energize the chakras in your head, your chest, and your stomach, you will be able to feel deep layers of buried stress unraveling and shooting out of your hands and body like beams of light.

At this point, it is helpful to visualize a bright bolt of energy about the diameter of a cardboard mailing tube running up through your tailbone, up your spine, and out the top of your head. This is your home axis, and it intersects with every primary chakra in your body. Practice moving energy up and down this axis by using breathing, visualization, posture, yoga, and/or stretching exercises.

When you pass your hands over various parts of your body, you will begin to feel how the lines of energy flowing through your body intersect and connect up with each other. These intersections are called nodal points, and by navigating through these points you can monitor the flow of CNS traffic through your body. If you find nodal points that are conversely weak or overflowing with backed-up energy, those are symptoms of some kind of stress that's trapped within the body. By locating these problem areas, you can diagnose specific areas of body tissue where stress packets are building up. Deleting these is easy, and can be accomplished through a combination of gentle massage, stretching, and yogic exercise. Hunting down knotted nodal points is a very invigorating practice, and a relaxing way to spend your postemergent recovery period.

The style of energy healing described here uses many of the same techniques and concepts found in acupuncture, rei-ki, jo-rei, chi-gong, pranayama, yoga, and many other spiritual medicines. It should also be emphasized that Ketamine is not a substitute for these techniques, but is instead a useful adjunct to these techniques. Ketamine by itself can be relaxing, but it can also be somewhat of a roller-coaster ride. First time users are often overwhelmed by the experience and can do little more than lay back and let the experience go. There is nothing wrong with this type of usage, but it doesn't have much practical application. In contrast, when Ketamine is used in concert with meditation and directed energy visualizations, it can be a very powerful and rewarding therapeutic and self-diagnostic tool.

When I first discovered this application of Ketamine I was amazed. I was able to learn volumes about the subtle internal process of my own body by simply immersing my awareness deep within them. It was so intimately revealing that I immediately thought a Ketamine induced guided tour of your own internal organs should be made an optional class for all first-year medical students. Imagine what a massive paradigm shift that would be.

In essence, all navigation within the Ketamine space can be done by focusing your consciousness into a single nodal point and moving up and down the various medians within your body. If you want to do some brainwork, simply slide the nodal point up into your head and traverse your neural networks until you find the routines you are looking for. They're all in there, as are all of your memories and internalized models of reality. While traversing through these networks you can relive memories as if you were an impartial observer; sort through lists of deeply ingrained personality constructs and behaviors without an emotional response; browse through all your autonomic controls and hormonal routines; and program future behavior through post-emergent suggestions.

The final and often most rewarding level of the Ketamine experience is the OBE, or out-of-body experience. This level is reached by successfully moving the nodal point outside of your body, and letting your consciousness slurp out along with it. Sometimes it is helpful to simply let the nodal point slide up the spine and slosh out the back of your head through the crown chakra. This is a slightly odd feeling, and will induce a sensation of floating above the body, giving you the strange perspective of looking down on yourself. You can move the nodal point up into the ceiling, down through the floor, through the sewers, up through the phone lines, across rivers, over mountains, around the world on the Internet, and out into space. You can even move through cellular stuff you don't even recognize, or through quantum worlds that are just flickering fields of energy transference. The key to finding your way around is setting landmarks - creating a hyperspatial trail of crumbs if you will. It is easier than it sounds because you'll find yourself in oddly familiar places that you know you've never been to before.

A single Ketamine session usually only lasts about 45 minutes to an hour, so before you know it your nodal point will begin to dissolve, and you'll be emerging back into a big tingling ball of white light. This is the true shape of your energy body, and this is the sensation of your body coming back online. If you happen to open your eyes during this period, there is a good chance you will actually be able to see your aura shimmering around you like a magnetic field in flux. At this point you should return to your home axis and let the nodal network map back onto your body. As you come back online, you will feel weak, but also cleansed, refreshed, and ready for a good stretch.

it.Ketamine Damage if you do it too often

James Kent of resproject.com

Nothing is a silver bullet. The allure of ketamine is its convenience and short acting effects. Many peoplel have lost their productivity and sense of community through excessive K use. Go into a K-hole more than once every couple weeks and you're risking the most important link to this 3D time/space that we call Planet Earth 1999.

Aaaaaaaahh!! K-Hole!!!! Where am I!?! You can get Olney's Lesions with excessive use: Dissociatives - Ketamine, PCP, dizocilpine and dextromethorphan - are all dissociatives, or NMDA antagonists. Research suggests that this class of drug leads to a kind of brain damage known as NMDA Antagonist Neurotoxicity (aka Olney's Lesions).

These are essentially tiny holes in various parts of the brain. They may or may not heal. Evidence suggests that they do after six months of abstinence.. Click here for more information on lifestyles of abuse.x

Using Ketamine to Induce the Near-Death Experience

Mechanism of Action and Therapeutic Potential

1996, Yearbook for Ethnomedicine and the Study of Consciousness (Jahrbuch furr Ethnomedizin und Bewubtseinsforschung) Issue 4, 1995 (Ed.s C. Ratsch; J. R. Baker); VWB, Berlin, pp55-81.

Dr. Karl L. R. Jansen , Psychiatrist 63 Denmark Hill London SE5 8AZ United Kingdom.

Abstract

Near-death experiences (NDE's) can be induced using the dissociative drug ketamine. Advances in neuroscience have recently provided us with new insights as to the mechanisms involved at the mind -brain interface. On the 'brain' side, it is now clear that these NDE's are due to blockade of brain receptors (drug binding sites) for the neurotransmitter glutamate. These binding sites are called the N-methyl-D-aspartate (NMDA) receptors. Conditions which precipitate NDE's (low oxygen, low blood flow, low blood sugar, temporal lobe epilepsy etc.) have been shown to release a flood of glutamate, over-activating NMDA receptors. This overactivation can kill brain cells ('excito' toxicity). Ketamine prevents excitotoxicity. Conditions which trigger a glutamate flood may also trigger a flood of ketamine-like brain chemicals which bind to NMDA receptors to protect cells, leading to an altered state of consciousness like that produced by ketamine. On the 'mind' side, induction of NDE's has psychotherapeutic value via several routes which will be explored in this article.

The near-death experience (NDE) is a phenomenon of wide general interest. Despite its association with sensationalist media reports, populist books of doubtful scientific value, and a series of dubious Hollywood films, the NDE is still of considerable importance to medicine, neuroscience, neurology, psychiatry, psychology and, more controversially, philosophy and theology

Recent advances in neuroscience are bringing us closer to a brain-based understanding of the NDE as an altered state of consciousness.

This discussion does not address the issue of whether there is life after death, but does argue that NDE's are not evidence for life after death. This would be appear to be self-evident on logical grounds: death is defined as the final, irreversible end. The Oxford English Dictionary (Sykes, 1982) defines death as the 'final cessation of vital functions. According to this definition, 'Returnees' did not die - although their minds, brains and bodies may have been in a highly unusual state for a period of time. If these definitions are not accepted, then we need a new terminology to describe these states.

There is now evidence from thousands of studies relating brain events to alterations in mental state that 'mind' results from neuronal activity. These studies range from observing the results of directly stimulating the brain with electrodes, for example the pioneering work of the neurosurgeon Wilder Penfield, to the most recent studies using magnetic resonance imaging to observe brain activity, for example to demonstrate activity in the temporal lobe while schizophrenics are experiencing auditory hallucinations (McGuire? et al., 1995). The dramatic effects on the mind which result from the action of hallucinogenic drugs in the brain, effects which can include profound religious experiences, provide further evidence for the dependence of mind upon neurochemical and neuroelectrical events (Grinspoon and Bakalar, 1981). However, the dimension in which mind itself exists remains a mystery.

Within a scientific paradigm, it is not possible that “the spirit rises out of the body leaving the brain behind, but somehow still incorporating neuronal functions such as sight, hearing, and proprioception” (Morse, 1989). To believe that this is possible, we must leave the realm of science and adopt a wholly different paradigm.

The Near-Death Experience: Typical Features

There is no internationally agreed set of criteria which define the NDE as exists, for example, for psychiatric disorders. Some critics of neurobiological models have dismissed them because a feature of the NDE which they believe to be important may not have been fully accounted for by the model being proposed, although it may well be that the statistically determined key features of the NDE (a consensus view) would not include those features. Just as with classification in psychiatry, it is important to reach an international consensus and avoid the sectarian views of a few. Neurobiological models should not be disregarded because of obscure and exceptional cases which cannot currently be explained.

The typical features of a 'classic' NDE include a sense that what is experienced is 'real' and that one is truly dead, ineffability (i.e. a sense that what is experienced cannot be described using language, 'beyond words'), timelessness, analgesia, apparent clarity of thought and feelings of calm and peace, although some NDE's have been disturbing and frightening. There may be a perception of separation from the body (out-of-body experiences).

Common hallucinations include landscapes, people including partners, parents, teachers and friends (who may be alive at the time), and religious and mythical figures including angels and a representation of 'God' as light.

Transcendent mystical states are common. Memories frequently emerge into consciousness, although the organisation of these into a 'life review' is a relatively rare phenomenon.

Hearing noises during the initial part of the NDE has been described - the significance of this feature will be discussed later (Noyes and Kletti, 1976a; Morse et al., 1985; Osis and Haraldsson, 1977; Greyson and Stevenson,

1.; Ring, 1980; Sabom, 1982; Greyson, 1983).

Ring (1980) classified NDE's on a 5 stage continuum:

1. feelings of peace and contentment;

2. a sense of detachment from the body;

1. entering a transitional world of darkness (rapid movements through tunnels: 'the tunnel experience');

4. emerging into bright light; and

1. 'entering the light'.

1. % experienced stage 1, but only 10% attained stage 5 (Ring, 1980).

As might be predicted in a mental state with a neurobiological origin, mundane accounts with less symbolic meaning also occur, e.g. children who may 'see' their school fellows rather than God and angels (Morse, 1985).

The intravenous administration of 50 - 100 mg of ketamine can reproduce all of the features which have commonly been associated with NDE's. Intramuscular administration also results in NDE's, but events evolve at a slower pace and are longer lasting (Domino et al., 1965; Rumpf ,1969; Collier, 1972; Siegel,1978, 1980,1981; Stafford, 1977; Lilly,

1. ; Grinspoon and Bakalar, 1981; White, 1982; Ghoniem et al., 1985; Sputz, 1989; Jansen, 1989a,b, 1990b, 1993,

2. , 1996).

Mounting evidence suggests that the reproduction/induction of NDE's by ketamine is not simply an interesting coincidence.

Exciting new discoveries include the major binding site for ketamine on brain cells, known as the phencyclidine (PCP) binding site of the NMDA receptor (Thomson et al., 1985), the importance of NMDA receptors in the cerebral cortex, particularly in the temporal and frontal lobes, and the key role of these sites in cognitive processing, memory, and perception. NMDA receptors play an important role in epilepsy, psychoses (Jansen and Faull, 1991), and in producing the cell death which results from a lack of oxygen, a lack of blood, and from epileptic fits (excitotoxicity). This form of brain cell damage can be prevented by administration of ketamine. Other key discoveries include that of chemicals in the brain called 'endopsychosins' which bind to the same site as ketamine, and the role of ions such as magnesium and zinc at this site

Ketamine administered by intravenous injection is capable of reproducing all of the features of the NDE which have been commonly described.

Unfortunately, the study in which persons who have had NDE's are given ketamine and asked to compare the two experiences has yet to be carried out, although the psychological effects of ketamine have been well documented in numerous clinical studies by anaesthetists (see Domino, 1992). Information in the area of ketamine and NDE's remains largely anecdotal, and some of these references are necessarily to secondary sources. The present author has experienced several NDE's and has also been administered ketamine as an anesthetic and within experimental paradigms.

The NDE's and ketamine experiences were clearly the same type of altered state of consciousness.

Ketamine repeatedly produced effects which were like the NDE's described by Moody (1975), Noyes and Kletti (1976a), Greyson and Stevenson (1980), Ring (1980), Sabom (1982) and Morse et al., (1985).

Ketamine reproduced travel through a tunnel (sometimes described as 'the plumbing of the world ', or in mundane terms such as 'like being on a subway train'), emergence into the light, and a 'telepathic' exchange with an entity which could be described as 'God'.

Neither the NDE's nor the ketamine experiences bore any resemblance to the effects of psychedelic drugs such as dimethyltryptamine (DMT ; also administered to the author in experimental paradigms) and lysergic acid diethylamide ( LSD).

Ketamine: Typical Features

Ketamine is a short-acting, hallucinogenic, 'dissociative' anaesthetic. The anaesthesia is the result of the patient being so 'dissociated' and 'removed from their body' that it is possible to carry out surgical procedures. This is wholly different from the 'unconsciousness' produced by conventional anesthetics, although ketamine is also an excellent analgesic (pain killer) by a different route (i.e. not due to dissociation). Ketamine is related to phencyclidine (PCP). Both drugs are arylcyclohexylamines - they are not opioids and are not related to LSD.

In contrast to PCP, ketamine is relatively safe, is much shorter acting, is an uncontrolled drug in most countries, and remains in use as an anaesthetic for children in industrialized countries and all ages in the third world as it is cheap and easy to use (White et al., 1982).

Anaesthetists prevent patients from having NDE's ('emergence phenomena') by the co-administration of sedatives which produce 'true' unconsciousness rather than dissociation (Reich and Silvay, 1989.)

The altered state of consciousness resulting from ketamine administration is very different from that produced by psychedelic drugs such as LSD and DMT (Grinspoon and Bakalar, 1981). As noted above,

ketamine can reproduce all features of the NDE, including travel through a dark tunnel into light, the conviction that one is dead, 'telepathic communion with God', hallucinations, out-of-body experiences, strange noises at the beginning of the experience etc. (see ketamine references above). A consideration of some of the accounts which have been given of the effects of ketamine makes this clear. For example, Grinspoon and Bakalar (1981, p34) described

'…becoming a disembodied mind or soul, dying and going to another world. Childhood events may also be relived. The loss of contact with ordinary reality and the sense of participation in another reality are more pronounced and less easily resisted than is usually the case with LSD. The dissociative experiences often seem so genuine that users are not sure that they have not actually left their bodies.'

Timothy Leary , who had very extensive personal experience of LSD, described his experiences with ketamine as 'experiments in voluntary death' (Leary, 1983, p375). One of the best accounts of the non-medical use of ketamine appeared in the popular magazine 'High Times' (Sputz, 1989, p65). Although not included in the Medline and Psychlit data bases, this account is recommended to those with an interest in the subject. Sputz noted: 'one infrequent ketamine user reported a classic near-death experience…

“I was convinced I was dead. I was floating above my body. I reviewed all of the events of my life and saw a lot of areas where I could have done better”.

The psychiatrist Stanislav Grof, who also had extensive experience of LSD, stated: “If you have a full-blown experience of ketamine, you can never believe there is death or that death can possibly influence who you are” (Stevens, 1989, p481-482).

An anaesthetist observed: 'Ketamine allows some to reason that …the strange, unexpected intensity and unfamiliar dimension of their experience means they have died..' (Collier, 1981, p552).

Attempts to explain NDE's as altered states of consciousness involving hallucinations are sometimes rejected by 'afterlifers' because many of those who have had NDE's insist upon the reality of their experiences (Osis and Haraldsson, 1977; Ring, 1980). However,

30% of subjects given ketamine were certain they had not been dreaming or hallucinating, but that the events had really happened (Rumpf et al., 1969; Siegel, 1978).

'Afterlifers' sometimes misunderstand the definition of a hallucination which is widely accepted to be as follows: “ a hallucination has the immediate sense of reality of a true perception …transient hallucinatory experiences are common in individuals without mental disorder” (APA, 1980).

If we are to consider that ketamine opens the door to alternative spaces which 'really exist', then what arguments shall we use to reassure a hallucinating, paranoid schizophrenic ?

The apparently clear sensorium of some persons who have had NDE's has also been used to argue that the NDE is 'real' and not an altered state of consciousness (Osis and Haraldsson, 1977; Ring, 1980), which argument presupposes that altered states and experiencing hallucinations necessarily involve a clouding of consciousness. This is certainly not the case, particularly where some drug induced states are concerned. It is important to note that hallucinations in schizophrenia typically occur in clear consciousness and are believed to be real. Indeed, this is one of the diagnostic criteria (APA, 1980). A personal conviction of the 'reality' of an NDE does not invalidate scientific explanations. It is not unusual for persons under the influence of hallucinogens to claim that their minds are clearer than usual.

Some users of hallucinogens adopt the view that the hallucinogenic world is real while the 'normal' world is a veil of illusion (Grinspoon and Bakalar, 1981).

John Lilly, perhaps the most experienced user of ketamine in the world today, maintained that ketamine could take the user beyond 'the social consensus reality' to deeper, 'meta' realities.

However, Lilly was also admitted three times to psychiatric hospitals with a paranoid psychosis linked to excessive ketamine use.

For example, on one of these occasions he was attempting to telephone the President of the United States to warn him concerning the machine plot to take over the universe, from which only dolphins could save us (Lilly, 1978).

It is nonsensical to argue that while this is a paranoid delusion, experiences with a religious flavor are 'real' and evidence for 'meta'-realities, because of the religious beliefs of ourselves and/or our culture.

Much has been made of the apparent mystery surrounding the occasional ability of cardiac arrest survivors to describe the resuscitation in detail (Sabom, 1982). It is worth noting that ketamine can permit sufficient sensory input to allow accounts of procedures during which the patient appeared wholly unconscious (Siegel, 1981; Hejja and Galloon, 1975).These reports are not regarded by anaesthetists as particularly mysterious.

Receptors, Neurotransmitters and Neuroanatomy

Over the last decade, it has become clear that that the overwhelming majority of large neurones in the cerebral cortex use glutamate as their neurotransmitter (chemical messenger between cells). These are the brain cells which connect different parts of the cerebral cortex, and which project out of the cerebral cortex to other areas.

It is the actions of glutamate, an excitatory amino acid, which make us human and unique, as this chemical is of central importance in the cerebral cortex - particularly in the frontal and temporal lobes and in the hippocampus. The hippocampus is a structure in the medial temporal lobe involved in memory, emotion and integrating inputs from many parts of the brain (White et al., 1977; Cotman et al., 1987; Fagg and Foster, 1983; Greenamyre et al., 1984; Monaghan, Bridges and Cotman, 1989; Jansen et al., 1989c, 1990a)

Glutamate plays a vital role in all cognitive processes involving the cerebral cortex, including thinking, memory and perception (Squire and Zola-Morgan, 1988; Monaghan, Bridges and Cotman, 1989; Oye et al., 1992).

The NMDA receptor is a large structure with several 'docking sites' for neurochemicals and a channel through which ions can enter the cell. One of these 'docking sites' is a binding site for ketamine and PCP, called the PCP receptor, attached to the binding site for NMDA (review: Monaghan, Bridges and Cotman, 1989). The term 'NMDA receptor' is often used to refer to the entire structure, although strictly speaking the NMDA binding site (which is also the binding site for glutamate) is only one part of the whole. This is largely for historical reasons.

Glutamate is excitatory. When glutamate is present in excess, neurones are overexcited and die via a process called 'excitotoxicity'. This involves the ion channel to which the NMDA receptor is attached remaining open for too long. Ions and water rush into the cell which bursts as a result. This is the mechanism of neuronal cell death in conditions of low oxygen, low blood sugar and epilepsy, conditions which have been proven to lead to excessive release of glutamate (e.g. Rothman, 1984; Rothman and Olney, 1986, 1987). Blockade of the PCP receptor prevents cell death from excitotoxicity (e.g. Meldrum, 1987; Rothman et al., 1987). This is because the PCP binding site is located within the ion channel. Ketamine binds to this site and thus prevents neuronal cell death in these conditions.

This suggests that the brain may have its own protective mechanism against the documented glutamate flood. This protective, 'anti-excitotoxic' mechanism is likely to take the form of a counter-flood of a substance which binds to the PCP receptor, preventing cell death.

The brain is a well-protected organ with many known defences: the skull, the meninges ('wrappings around the brain'), the protective hydraulics of the ventricular system and the cerebrospinal fluid, the blood-brain barrier and so on.

Considering the brain's exquisite vulnerability to excito-toxic damage, it is reasonable to propose the evolutionary development of protective mechanisms against excitotoxicity. In some individuals, this protective mechanism is probably more advanced than in others, just as individuals vary, for example, in the rates at which different drugs are metabolized.

The existence of a natural system to protect against excitotoxicity is the only speculation in the process outlined

above

the other statements are strongly supported by experimental data published in leading journals (Benveniste et al.,1984; Simon et al., 1984; Ben-Ari, 1985; King and Dingledine, 1986; Lobner and Lipton, 1990; Rothman et al.,

1.; Westerberg et al., 1987; Hoyer and Nitsch, 1989).

Endogenous substances have been found in the brain which bind to the PCP receptor, one of which is a peptide called 'alpha-endopsychosin' (Quirion et al., 1984). However, this is a controversial area of research. We do know that ions such as magnesium and zinc can block the channel, and it may be that a flood of ions occurs rather than large molecules such as peptides.

Psychological Explanations of the NDE

1. Depersonalisation

The depersonalisation theory proposes that the NDE is an adaptive mechanism of the personality which alerts one to the threat of death while potentially overwhelming emotion is held at bay, allowing the reality to be integrated without panic (Greyson, 1983; Noyes and Kletti, 1976a,b). While protecting nerve cells from ischaemic damage is largely irrelevant when one is falling from a cliff, the NDE-producing situation which first resulted in this hypothesis, NMDA receptors would certainly be involved in producing the experience of depersonalisation as they play a central role in cognition and perception.

1. Regression in the service of the ego

This theory maintains that confronting death leads to a cutting off the external world. The result is regression to a pre-verbal level which can be experienced as mystical ineffability (Greyson, 1983). Certainly a loss of contact with the external world is one of the most characteristic effects of ketamine.This is probably the result of blockade of NMDA receptors involved in sensory transmission. NMDA receptors play a key role in the transmission of incoming signals from all sensory modalities (Davies and Watkins, 1983; Greenamyre et al., 1984; Headley et al.,

1. ; Cotman et al., 1987; Cline et al.,1987; Monaghan, Bridges and Cotman, 1988; Kisvardy et al., 1989; Oye et al.,

2. ).

1. A state dependent reactivation of birth memories

This theory explains the movement through tunnels towards 'the light' as a memory of being born (Grof and Halifax,

1. ). The NDE is thus actually a 'near-birth experience' rather than a 'near-death experience'.

NMDA receptor blockade could certainly be the underlying mechanism for the release of extremely primitive memories not normally available to consciousness.

1. The NDE as a sensory deprivation phenomenon

This hypothesis maintains that memories may normally be suppressed by a mechanism which acts as a gate, admitting primarily external signals when we are fully conscious and concentrating upon an external task (Siegel,1980, 1981). If this input is dramatically reduced , for example when we are dreaming, have been given drugs such as ketamine, or have just had a heart attack, in combination with a high level of central stimulation (e.g. as would result from excessive glutamate release during hypoxia, ischaemia, epilepsy, or arising without external provocation), stored perceptions are released and become 'organised' by the mind into an experience with some symbolic meaning. According to Ron Siegel (1980), the 'white light' may result from CNS stimulation mimicing light on the retina, and a lowering of the phosphene perceptual threshold. Sensory deprivation itself produces a profound alteration in consciousness which is certainly mediated via NMDA receptors (see 'regression in the service of the ego' above (Lilly, 1961,1978).

There is substantial evidence implicating the hippocampus in memory formation and retrieval. It is highly likely that the hippocampus is the anatomical location of the 'gate' described above, and that NMDA receptors are the molecular substrate of this gate. In the human brain, I have demonstrated that NMDA receptors have their highest concentration in the hippocampus (Jansen et al., 1989c.)

NMDA receptors play a crucial role in learning, and in the formation and retrieval of memories.

The PCP binding site of the NMDA receptor is in fact referred to as a 'gated channel' (Foster and Fagg, 1987).

Whether the gate is open or closed will be determined by the degree of neuronal excitation: the amount of glutamate exciting the cell, which will determine the position of a magnesium ion in the channel -i.e. as the cell becomes increasingly excited, the magnesium ion is pushed out of the channel so that water and calcium ions can rush into the cell (Mayer, Westbrook and Guthrie, 1984).

Ketamine blocks this channel at the molecular level and, at a higher level, closes the 'gate' to incoming information (Monaghan, Bridges and Cotman, 1989; Morris et al., 1986; Collingridge, 1987; McNaughton? and Morris,

1. ; Cotman, Monaghan and Ganong, 1988).

The 'Drug-induced Hallucinations' Explanation of the NDE

The hypothesis presented in this paper is that much can be learnt about the mechanisms of the NDE by studying drug-induced hallucinations, specifically the state produced by ketamine. However, it is certainly not my argument that the NDE's reported by persons who have had heart attacks etc. are in any way due to drugs which they have been given. Administered drugs may explain a few cases of NDE's, but in most no drugs were given with effects which resemble the NDE (Sabom, 1982).

The Temporal Lobe Epilepsy Theory

It has been claimed that there is some similarity between the phenomena experienced in temporal lobe epilepsy and the NDE (Persinger and Makarec, 1987; Saavedra-Aguilar and Gomez-Jeria, 1989). There is considerable evidence that glutamate plays an important role in epilepsy. Glutamate is the key neurotransmitter in the temporal lobe, particularly in the hippocampus. The neuropathology of epilepsy (e.g. sclerotic cell damage in the hippocampus) is believed to result from excito-toxic cell death

The endogenous neuroprotective system proposed above may well become active in any excitotoxic situation - not just conditions of low oxygen and low blood flow. Temporal lobe epilepsy could lead to an activation of this system.

The degree of excitotoxic cell damage and the associated altered state of consciousness resulting from a glutamate flood, whatever the precipitating cause, may depend on the final balance in each neuronal pathway between excitotoxic forces and neuroprotective mechanisms.

It is of interest to consider reports of persons who underwent prolonged oxygen deprivation as the result of a medical emergency, had a profound NDE, and survived the incident without obvious cognitive impairment (Sabom, 1982).

The lack of apparent brain damage in these cases may be due to these individuals being possessed of a highly effective inbuilt mechanism for blockade of NMDA receptors in the face of a flood of glutamate. These individuals may have other characteristics such as increased tendency to report vivid dreams.

In this context, it is interesting to note that not all persons given ketamine report 'emergence phenomena'. Those who are not able to report experiences of this nature may be as high as 60% or more when the general population is sampled rather than illicit drug users who represent a biased and self-selecting group.

Interestingly, it has been claimed that 40% of adult Americans report an NDE at some point in their lives. Anaesthetists have shown that persons who report vivid dreams are in fact more likely to experience emergence phenomena.

It is also possible that there is no protective mechanism against excitotoxicity. Rather than mimicing a natural protective process, ketamine may have some of its psychological effects by mimicing some of the processes seen in temporal lobe epilepsy. Ketamine does block glutamatergic neuro-transmission and prevents excitotoxic cell death. However, the effect of ketamine upon human electrical brain waves (the electroencephalograph, EEG) suggests a complex interplay of forces. There is a reduction in alpha wave activity, while beta, delta and theta wave activity are increased (Schwartz et al. 1974; Pichlmayr et al., 1984). Ketamine has been reported to act both as an anticonvulsant (i.e. substance which prevents epilepsy) (e.g. McCarthy? et al., 1965; Celesia and Chen, 1974; Taberner,

1. ; Leccese et al., 1986; Mares et al., 1992) and as a pro-convulsant (epilepsy inducing substance) (Bennet et al., 1973; Gourie et al., 1983; Myslobodsky, 1981). Myslobodsky (1981) reported that ketamine could produce EEG patterns in human limbic and thalamic regions resembling epileptic patterns, but that there was no evidence that this affected other cortical regions or that clinical seizures were likely to occur. This is quite consistent with the NDE model presented by Saavedra-Aguilar and Gomez-Jeria (1989) which involved limited electrical abnormalities in the limbic system.

The hippocampus is one of the core structures in the limbic system. Thus the production of NDE's by ketamine is not inconsistent with the hypothesis that NDE's may result from abnormal electrical activity in the brain. Reich and Silvay (1989) concluded: “ it is hard to draw objective conclusions regarding the anti-convulsant properties of ketamine…animal data are particularly difficult to interpret because of interspecies variations”. Nevertheless, most of the available evidence favors the conclusion that ketamine is anticonvulsant at doses required to produce NDE's (Myslobodsky, 1981), supporting the hypothesis that NMDA receptor blockade results in NDE's.

Psychic Ketamine versus Anaesthetic Ketamine

“Ketamine is a racemic preparation, that is, a mixture of the dextro- and levorotatory fraction. Preliminary clinical research suggests that the anesthetic and psychedelic properties are selectively associated with the propensity of the two components to rotate polarized light to the right and to the left. Since these two can be separated, the psychedelic effects of ketamine can be studied in isolation from the anesthetic ones.” (inserted, from Stanislaus Grof)

Ketamine is supplied by the principal manufacturer (Parke-Davis, under the brand name 'Ketalar') as a mixture of (+)ketamine and (-)ketamine isomers. The controversy may be partially resolved by considering the separate effects of the isomers, and the dose levels at which these effects appear. As dose levels rise, drugs will bind to a wider range of receptors for which they have less affinity. In this context, it is important to note that ketamine induces NDE's at doses much lower than those required for anaesthesia - sometimes stated as being at least four times less (Stafford, 1977; Lilly, 1979; Grinspoon and Bakalar, 1981; Sputz, 1989).

White et al. (1980) demonstrated that (+)ketamine has some opioid binding properties and produces more 'conventional anaesthesia', while (-)ketamine produces psychic emergence reactions (NDE's).

(+)ketamine is about four times more potent as a hypnotic (sleep-inducing agent) and analgesic, and has different effects upon the EEG from (-)ketamine (White et al., 1985). This may explain some of the confusion concerning whether ketamine is an anticonvulsant or a proconvulsant (Myslobodsky et al.,1981), and suggests that future NDE research might be better done with (-)ketamine rather than the mixture currently supplied to anaesthetists.

The Abnormal Blood Gases Theory

1. Hypoxia (low oxygen):

The proposal that lack of oxygen might precipitate NDE's (Blacher, 1980) has been criticized (e.g. Sabom, 1982) because experiments in which the inspired oxygen was made to fall slowly resulted in mental clouding rather than states of consciousness resembling the NDE (Henderson et al., 1927). However, these experiments are clearly not a satifactory reproduction of events in, for example, cardiac arrest, a drug overdose or other types of medical emergency associated with NDE's. Hypoxia has been clearly shown to cause an excessive release of glutamate with resulting excitotoxicity and cell death, which can be prevented by ketamine (see previous references).

1. Hypercarbia (excessive CO2):

In experimental paradigms, CO2-enriched breathing mixtures can result in NDE phenomena such as bodily detachment, being drawn towards a bright light etc. As with NDE's, diverse personality types report similar experiences, suggesting that a shared neurological substrate is at work (Meduna, 1950). It is again likely that NMDA receptor blockade is involved in producing the effects.

Does Serotonin Play an Important Role ?

Serotonin was one of the first neurotransmitters to be identified, and the effect of LSD at serotonergic receptors was one of the first direct links to be established between a drug binding to a receptor and a potent change in the mental state. Unfortunately, however, because of its historical primacy attempts have been made to link serotonin with an absurdly wide range of mental phenomena, both normal and abnormal. The fact remains that the overwhelming majority of cortical neurones use glutamate as their neurotransmitter, and those small neurones which do not are likely to employ the other major amino acid in the brain, gamma-amino-butyric acid (GABA). These discoveries, however, are relatively recent and are only gradually having an impact upon the 'serotonin industry'. There are very few cells within the cerebral cortex itself which use serotonin as a neurotransmitter.

Like endorphins, serotonergic effects may be contributory but do not play a central role in producing NDE's. Psychedelic drugs such as LSD and DMT are serotonergic in action. The psychedelic mental state is very different from the NDE. One of the most important differences is that LSD frequently involves an overwhelming increase in sensory input from the environment (review: Grinspoon and Bakalar, 1981), in sharp contrast to the dramatic decrease in input, the cataleptic dissociation produced by ketamine. Psychedelic visual phenomena are largely based in the environment, and bear little relationship to the dream-like images of ketamine and the NDE. Ketamine removes the mind from the environment altogether. The 'ego dissolution' experienced on LSD has a very different quality from the conviction of having died which may arise with ketamine, and loss of contact with the environment leading rapidly to the 'tunnel experience' is not a typical psychedelic drug effect, although it may occur.

Ketamine: Therapeutic Potential

This section has been entitled 'therapeutic potential' rather than 'psychotherapeutic potential' as it is doubtful that ketamine could be used for psychotherapy within the conventional meaning of this term, which implies a 'talking' therapy. Ketamine interferes with cognitive function to such an extent that meaningful communication with another is largely out of the question, and the nature of the relationship between client and therapist is of limited relevance to the experience.

Ketamine removes the person from the environment to the extent that set and setting are greatly diminished in importance, although these factors do still have some impact upon the experience, and suitable music can influence the outcome.

The mild psychedelic drugs which act upon serotonin, such as MDMA ('Ecstasy') and MBDB ('Eden') are more suitable for 'talking therapies', and LSD can sometimes also be used to good effect depending upon the circumstances, although it is often too chaotic when used as the sole substance (the combination of MDMA followed by LSD at 90 minutes results in preservation of the ego and an anchoring in consensus reality which is particularly valuable for psychotherapeutic purposes, as a result of neurochemical changes and tolerance induced by the preceding MDMA).

However, the ketamine experience may nevertheless have therapeutic aspects via two routes: the effects of the resultant altered state of consciousness itself, and the neurochemical/neuroelectrical effects of the drug. With respect to the former, it has been reported that persons experience a number of positive benefits from an NDE. NDE's can have a favorable impact upon values (e.g. less concern with material goals), anxiety about death ( a reduction in death anxiety occurs), and have been linked to an increase in altruism (Noyes, 1980; Ring, 1980; Greyson, 1982; Sabom. 1982).

The event can be a pivotal turning point, encouraging significant and positive life changes. Suicide attempts which result in 'transcendental' NDE's may be followed by a reduced risk of subsequently committing suicide (Greyson,

1.).

In contrast, in those who attempt suicide considered as a complete group, the subsequent risk for completed suicide is 50 -100 times greater (Greyson, 1983). Of those who survived a jump from the Golden Gate bridge and had such an NDE, none went on to completed suicide, and all were united in their support for a barrier to prevent further attempts ( Rosen, 1975). This occurred despite an increased belief in an after-life. Psychodynamic explanations have centered around the idea of 'ego death' followed by 'rebirth' (Greyson, 1981).

It is evident from the above that psychotherapeutic benefits might follow from the artificial induction of NDE's by ketamine. This possibility hasd been pursued by Kungurtsev (1991), in the treatment of alcohol dependency, with good results.

The other possible avenue by which ketamine might benefit mental health lies in its effects upon the substance of the brain itself. As noted above, ketamine produces localized electrical abnormalities which bear some resemblance to temporal lobe epileptic phenomena. This suggests that treatment with ketamine may have some effects resembling electroshock treatment, one of the most effective means of combating severe depression. Electroshock treatment is still widely used in the United Kingdom. In this context, it is of interest to note that ketamine has some antidepressant properties (Khorramzedeh and Lofty, 1973; Shipelenia, 1984).

Conclusions

The NDE is an important phenomena which can be safely reproduced by ketamine, and the 'glutamate theory of the NDE' can thus be investigated by experiment. Recent advances in neuroscience strongly suggest a common origin for ketamine experiences and the NDE in events occurring at glutamatergic synapses, mediated by the NMDA (PCP) receptor.

This theory represents an extension of previous hypotheses, and incorporates most of the neurobiological and psychological theories which have been put forward. It links many of these ideas (hypoxia, peptide release, temporal lobe epilepsy, regression in the service of the ego, reactivation of birth memories, sensory deprivation etc.) rather than being an alternative to them. Most of the planks upon which the hypothesis is built are strongly supported by experimental evidence, which implicates glutamate and the NMDA receptor as unifying entities in the processes leading to an NDE . The main exception to this is the postulate that anti-excitotoxic agents can flood the brain, which remains to be clearly established.

It is unfortunate that those persons with an interest in the spiritual appear to view neurobiological explanations of the NDE as boring and reductionist. In fact,

The exploration of the mind-brain interface is one of the most exciting adventures which humans have ever undertaken

…and the real reductionism may lie in wrapping a mystical shroud around the NDE, through nothing new can ever be seen or tested by experiment.

About the Author

Dr. Karl Jansen was born in New Zealand and trained in medicine at the University of Otago. After registering as a medical practitioner, he proceeded to carry out brain research at the University of Auckland as a research fellow of the New Zealand Medical Research Council. At this time he became interested in ketamine and its effects and published his first observations in this area, and also in antipodean use, users and consequences of psilocybin-containing mushrooms. He then went to the United Kingdom, and attended the University of Oxford (New College) were he completed a Doctor of Philosophy in Clinical Pharmacology. He was the Glaxo Fellow at Green College. On completion of his studies at Oxford, he went to the Maudsley Hospital and London Institute of Psychiatry to complete his training as a psychiatrist. He is now a member of the Royal College of Psychiatrists. His current research interests are the ketamine model of the near-death experience and the consequences of long-term, high dose recreational use of Ecstasy (MDMA ).

He would be interested to receive correspondence concerning the subject of this paper. You can email him as: K@BTInternet.COM

Recent Criminalization... and Subsequent Potential for Popularization

(i.e. the “oh this is ILLEGAL? I should try this… what is it?” similar to the media popularization of date rape drugs)

The United States federal government declared ketamine to be a schedule 3 drug on August 12, changing its previous status as an uncontrolled drug. Dr. Karl Jansen, London based expert on the non-medical use, users and consequences of ketamine was strongly opposed to the move. He said today: 'there is no evidence that it is possible to reduce drug use by making drugs illegal and sending people to jail. The use of cocaine and heroin have gone through the roof in the United Kingdom in the last 10 years, despite these drugs having been class A drugs (United States schedule 1) for decades.

Those who think that we need 'to send young people a message' are sending them a message alright: that we are fools who can't learn a lesson from history no matter how many times we are given it. Regardless of where you stand on the morality of it, or the politics, or indeed anythingelse, the hard facts are that you can not reduce the use of drugs by making them illegal. We have known that since the failure of alcohol prohibition before the second world war. What will happen next is that the price of ketamine will rise, dealers will start to make more profits from it, more of them will sell it, and then the number of users will rise. The scheduling of every drug has been followed by a leap in its use.

There is also the fact that making a drug illegal does make it more attractive, rather than less attractive, to some types of users. The action taken by the Drug Enforcement Agency (DEA) in making ketamine a scheduled drug has changed its status forever from a 'cat tranquilliser' to a 'real drug' in the minds of many users. Let's remember what the actor Ewan McGregor? says in Irvine Welsh's film Train Spotting : 'we would have injected vitamin C if they had only made it illegal'.

Dr. Jansen was certain that the non-medical use of ketamine would suddenly increase, rather than decrease, in response to the scheduling of the drug -proving his point that this action was not taken to protect public health. 'It isn't Kosovo which is the new Vietnam. It's the War on Drugs. How many more people have to die before they pull out the troops?'

ketamine_and_near_death_experience.txt · Last modified: 2007/06/12 13:35 by nik