| Ecstacy Pre-loading |
Ecstacy Info
Found this on the club planet board. Pretty
interesting post so I thought I'd show you guys.
Ecstasy is a generic name for pills and does not reflect their content. The
content of a pill varies not only from brand
to brand but also within brands [between batches]. So buying one E is no
guarantee that it will be the same as
another E you had. The contents could be completely different.
The prolonged duration of the pill, as well as the visuals you experienced,
would point to the content of the pill being
MDMA, as these are characteristic to the substance.
MDMA comparatively has a cleaner comedown, shorter duration of action, no
visuals, and feelings of empathy [love]
and euphoria [body buzzes].
MDEA is another variant molecule often found in "E". It has a
significant amphetamine effect but does not carry with it
the same emotional stimulation that the aforementioned types provide. It is
often the cause of the "e-tarded" feeling
people have - irritable yet speedy. "Heroin" is often blamed for
pills high in MDEA content, yet no tests have ever
found heroin - synthetic or otherwise - in ecstasy. Furthermore, pills are cut
with other substances mainly to drive
down costs - heroin is more expensive per gram than MDMA and hence it would not
make sense to cut a pill with it.
Furthermore the dose of heroin needed to provide an effect is greater than what
you could put into a tiny E pill that
already contains other substances. The same holds true for cocaine. Their
presence in ecstasy are simply myths.
Other myths regarding ecstasy include it draining spinal fluid [back pain is
more likely due to overuse of muscles in
that area because of the energy that ecstasy provides].
Obviously, MDMA is what most people are looking for. But because it is
relatively difficult to synthesize [and hence
more expensive] chemists often put in other less expensive substances.
MDMA produces its effects by increasing levels of dopamine and serotonin your
nervous system. Serotonin has many
functions in the body, including the regulation of sleep and dreaming, the
regulation of eating patterns, as well as
sensations of contentedness and satisfaction. Chronically low levels of
serotonin are related to depressive disorders.
Dopamine is a neurochemical that amongst other functions provides the body
buzz, speedy and euphoric feelings that
MDMA provides.
Pills can contain other substances [i.e. methamphetamine, caffeine, ephedrine,
etc.].
1] Timing is critical. Chemists often wait for a pill to earn a
reputation, then pump out copycat batches using garbage
ingredients? Why? Because garbage ingredients cost less. And knowing full well
that once a pill has earned a name for
itself, they can ride the reputation generated by the higher quality batch.
Case in point: Nothing after the first
generation of Mitsubishis came out last August even came close to the first
generation. Many of the ones circulating
now are total bullshit. But still they were bought up readily because people
actually thought they were getting their
hands on the real deal. Colors, stamps, etc. mean little after enough time has
passed.
Furthermore some pill types have been around since the beginnings of the rave
scene in England. Hearts, Diamonds,
E-stamps, Doves, Butterflies, etc. are not exactly unique or hard to find
stamps. So simply because you had a heart
two years ago does not mean the one you bought tonight will be any good.
Anyone with a 2nd year knowledge of organic chemistry can perform the reactions
necessary to synthesize MDMA.
Getting your hands on the equipment and chemical precursors is not easy but not
impossible. And it does involve the
use of toxic chemicals [mercury, etc.]. So don't think that all pills come from
one big factory somewhere and that
they're all the same. It could be overseas, in an abandoned building, a
suburban home or down your street. Anyone
with a pill press and a stamp can punch out copycats. If you get your hands on
pills within 3 weeks of it hitting the
streets then you are in good shape. Anything after that point and that it is
right when the copycats usually start
coming in for good pills.
2] Read, read, read. Don't go by your dealer's assurances or what your
friend heard or anything else removed from
facts. Read the facts and studies yourself, know the bottom line, don't let
someone else tell you what is right and
wrong [including myself. I openly urge everyone to read the research themselves
to verify what I'm writing]. "Don't
worry, it's good." is not a guarantee. Drug dealing does not obey the same
code of ethics real businesses have to
face. There are no penalties for lying, no penalties for putting out a shitty
product, no penalties for screwing people
over to make a buck.
Good places to get information are the reports page include :
http://www.bluelight.net/mdma
http://www.lycaeum.org/
http://www.erowid.org/
http://www.dropout.freeserve.co.uk/...es/preload.html
Read all of them.
..and for anyone interested in reading the actual studies
http://www.infotrieve.com/freemedline
You may need an introductory understanding of physiological psychology, in
which you should be able to turn up a
good used textbook at your local university. I suggest the Physiology of
Behaviour by Carlson.
Be forewarned that some spineless dealers post glowing reports from time to
time to sell their shitty products. So if
it's too good to be true, it probably is. Stick around, read everything that
you can. Wait a week or two before you try
digging up a certain pill to see if everyone's reactions are the same. Wait
until others have tried things out. Don't
trust everyone's reports, find people who judge hard and are intelligent about
their usage and ask them.
3] Know what you want ahead of time, how much you want to pay for it,
and don't settle for anything less. Your
dealer needs you more than you need them. Period. If you don't get what you
want from someone take your business
elsewhere. As long as people tolerate bullshit from dealers they'll keep trying
to pull it.
The whole reason why Mitsubishi's were pressed out was because over the past
few years the quality of pills had
decreased significantly. These days the average pill runs about 75mg of MDMA.
In 1994 the average pill contained 150
mg of MDMA. In other words you could buy a single pill and split it between
yourself and a friend and get the same
effect as a single pill today. People grew tired of this trend and the business
suffered accordingly. Mitsu's were
pumped out in the summer of last year from Amsterdam to restore faith in
E-trade in London. The first generation of
Mitsu's were tested at 140mg+ of MDMA. For more info check out the article that
Mixmag did this year on the
Mitsubishi phenomenon.
The point is, don't tolerate bullshit and people won't feed it to you.
4] Buy ahead of time and never at a party. You will pay 5-10 dollars
less and not have to deal with last minute mind
fucks and dealer tricks. If you buy more than $200 at a time you should be
entitled to a free tester from your dealer.
Good prices - 180-200 for 10, 20-25 dollars for any quantity less.
5] The taste of a pill is a good indication as to its content. MDMA has
a characteristic bitter taste - very bitter.
Scratch off a piece of the pill and put it on the tip of your tongue. If it
doesn't make your face wince it probably
doesn't have much good to it. It also has a characteristic
"sassafras" smell, because of the use of sassafrole in the
synthesis of MDMA. Pay close attention to the appearance of the pill - its
color, how hard it is, the stamp, how thick
it is, whether there is a score [line] down the back, whether there are
speckles etc. It will help you distinguish
between copycats.
6] Never depend on only one dealer. Dig for as many connections as you
can find. Don't tolerate mind fucks. If
someone plays mind games with you, walk away. Same as in normal business.
Accept only the best and that's what
you'll get.
7] Know your dealer, don't ever buy from someone you don't trust or
don't like.
8] Never dose more frequently than 1 - 1.5 hours apart. The amount
necessary to provide the desired effect varies
from individual to individual but in Alexander Shulgin's original studies it
was determined that 120 mg of MDMA is
enough to fuck up the majority of the population. Generally, unless someone has
acquired a tolerance from months of
excessive usage, 2 pills should be enough to fuck up the majority of people
[assuming that they're of relatively good
quality]. There is probably not a direct relationship with bodyweight and
number of pills needed for a potent dose and
more likely a greater relationship with brain mass and # of pills needed, but
it's generally true that the smaller you are,
the less you need, and that females can get away with less than males.
9] One can acquire a tolerance for MDMA from excessive usage,
necessitating more and more to produce the desired
effect while accumulating more and more side effects. The only thing that can
remedy the acquisition of a tolerance is
abstinence.
10] Do not combine E with monoamine oxidase inhibitor drugs. Monoamine
oxidase is the enzyme that helps to
eventually slow down the effects of MDMA, without it, your body is like a car
speeding without any breaks - it has no
way of controlling itself.
11] Handle your business yourself. Don't leave it to others.
12] Stay adequately hydrated. MDMA enhances serotonin secretion, high
levels of serotonin cause hyperthermia
[increase in body heat]. Not to mention the fact that dancing alone works up a
good sweat.
13] Take periodic sober breaks...you'll find out whether you're into the
scene because of the vibe/music or the drugs
rather quickly. Furthermore it will enhance the quality of your rolls when you
do.
14] Double stacks are sometimes a trick used by chemists to convince
people there is more MDMA in a pill than there
really is. Although some double stacked pills do contain significantly more
MDMA they are generally the exception
rather than the rule.
15] Information is regionally specific. Meaning that a pill that was
great in England may not be the same as ones
circulating around here, even if the stamps are the same.
16] Metaphorically, think of your brain as the engine of a car. Certain
substances floor the gas pedal and make the
car go faster than normal. This is fun. But in driving faster, you use up gas
[serotonin, in this specific situation] faster
as well.
When these substances wear off, you are obviously left with less gas than you would
have if you didn't do the
speed-racer thing.
With less gas, you can't drive as fast as you normally do. Therefore you
operate less efficiently. Low levels of
serotonin can be characterized by changes in eating patterns, sleeping
patterns, short term memory and the
appearance of depressive symptoms.
MDMA produces its loved up, empathic effect by increasing levels of serotonin.
If the body's "gas" [serotonin] is used
up faster than it is replaced, then one is left with less serotonin when it is all
said and done...
..unless you go to a gas station and refill the tank [supplement with 5-HTP,
eat foods rich in the amino acid
trytophan like bananas or turkey meat]...
..or put the car in economy mode to use the gas more efficiently [use of an SSRI
type anti-depressant]...
..or don't drive as fast, as often [use moderation in usage / frequency].
Because this is purely mathematical it applies to everyone regardless of their
prior condition.
It should however be noted that the lower levels of serotonin are not permanent
[i.e. the size of your gas tank has
not been reduced], but rather there is temporarily less gas in the tank than
normally.
Damage may even occur to the engine if driven hard with no gas in the tank.
Depletion of serotonin stores is one step
in a proposed mechanism for the neurotoxicity of MDMA. It can be theoretically
counteracted by using engine oil
[antioxidants such as Vitamin C]. I must however warn that studies correlating
MDMA with neurotoxicity have only
been performed in animals and only using ridiculously high dosages / frequency
of usage.
There are ways in which one can decrease the negative side effects of MDMA and
increase the positive ones.
Although no studies have been done on these techniques and MDMA specifically,
extrapolating biochemical facts and
observing the experiences of those who have done it support their practice.
These practices are called preloading and
postloading. The entire concept behind preloading and postloading is, extending
the above metaphor, adding gas to
the tank that MDMA is going to use up.
Serotonin as aforementioned is responsible for the empathic, loved-up feelings
from MDMA. Adding more serotonin to
your system enhances these effects. More importantly, it hypothetically counteracts
the mechanism MDMA is thought
to induce neurotoxicity with. 5-hydroxytrytophan is the direct precursor of
serotonin in the body. It is sold in health
food stores to help people with sleeping disorders [one of serotonin's roles is
in the regulation of sleep, as
aforementioned]. It is not a drug, it is an amino acid with a hydroxyl molecule
appended to it. Supplementation with
5-hydroxytrytophan enhances the loved-up, empathic feelings and cleans up the
comedown.
Hard come downs are usually generated by depletion of intraneuronal serotonin
stores. The result of lessed serotonin
stores, as mentioned above, are characterized by disruptions in normal sleeping
and eating patterns, difficulty in
verbal processing and committing facts to short term memory, as well as
irritatiblity. Most notably the impact of low
serotonin levels is characterized by depression. Supplementation with
5-hydroxtrytophan [5-HTP for short]
counteracts these negative side effects by putting more gas in the tank and
ensuring that you don't run out.
In animal studies, it is hypothesized that neurotoxicity from MDMA is due to
the following process. I'll put it in layman's
terms.
1] MDMA amps up serotonin and dopamine use.
2] Serotonin runs out
3] Dopamine goes where serotonin normally would
4] Altered dopamine molecules cause damage to nerves
Therefore by preventing the depletion of serotonin you minimize the amount of
oxidized dopamine radicals that feed
into pre-axonic serotonin terminals and cause axonic trimming.
One of magnesium's major roles in the body is in muscle relaxation. It is the
antagonist [opposite] of calcium, which
helps to induce muscle contraction. The jaw clenching observed on MDMA can be
minimized through magnesium
supplementation. Added magnesium can also minimizing cramping due to
dehydration.
Vitamin C is a potent antioxidant. As aforementioned it is thought that MDMA is
neurotoxic due to oxidized free
radicals. As such Vitamin C counteracts these free radicals and helps to
minimize damage incurred.
The aforementioned three elements are the most PROTECTIVE elements to a
preloading regimen. The following
elements are optional because they enhance the experience rather than protect
you from anything specific.
L-Tyrosine is to dopamine what 5-HTP is to serotonin. It is its precursor.
Dopamine provides the rushy, body buzz,
speedy effects...increasing L-tyrosine levels enhances these sensations.
DLPA amongst other functions, helps to prolong the duration of action of
pleasure inducing neurochemicals.
L-Glutamine is a precursor to neurotransmitters in the brain. It also imparts a
protective effect on the brain but not as
heavily as 5-HTP or Vitamin C.
Any substances that you are preloading with need to cross the blood brain
barrier to be effective. Amino acids
compete with each other to cross the blood brain barrier, hence eating foods
rich with protein lessen the effects of
the amino acids because so many are in competition. It's like having a race
with 2 people or 1000 people. Those one
of those two people are more likely to win when they're only racing against
themselves.
As such preloads are taken on a relatively empty stomach, 1-1.5 hours prior to
rolling. Preferably they are taken with
a sugary juice to help the amino acids cross the blood brain barrier.
Grapefruit juice inhibits one of the p450
cytochrome C digestive enzymes in the digestive tract that metabolizes MDMA and
hence can make the effects of the
drug somewhat more effective.
It should be noted that preloading can upset some people's stomachs or cause
diarrhea due to the acidity of the
stomach. In which case these symptoms are easily counteracted by the following
steps:
1] Mix the capped substances into juice, shake thoroughly, and sip the solution
slowly over the course of an hour prior
to a roll.
2] Immodium can counteract the diarrhea and does not interfere with a roll.
3] Tums or any calcium carbonate based antacid reduces the acidity of the
stomach and counteracts the feelings of
sickness one might encounter when coming up from a roll or after preloading. A
newbie I came across on the weekend
was doubled over from their pill hitting them too hard - two tums and ten
minutes later they were up on their feet
feeling fine. If necessary you can also eat a non-acidic carbohydrate based
food to buffer acidity, such as bread,
muffins, etc.
The practice of postloading is metaphorically to fill up the tank after a long,
fast ride. You restore the elements
depleted by MDMA, and in doing so, bypass negative side effects and clean up
your comedown while restoring normal
function.
The only elements required in a postloading regimen are the protective ones. It
is suggested that one employ 5-HTP,
Vitamin C, Magnesium for the aforementioned reasons. A multivitamin is
beneficial to help replace spent micronutrients.
Water is of course beneficial. L-Tyrosine, DLPA are not desired nor necessary.
You will know if you are bypassing the negative side effects of serotonin
depletion if you can sleep soundly after
rolling, and do not experience significant post-MDMA depression or disturbances
in verbal processing, short term
memory and eating patterns.
Natural sources of trytophan [the precursor to 5-hydroxtrytophan, two steps
away from serotonin] include bananas
and turkey meat. Turkey's high level of trytophan is the reason why most people
feel sleepy after thanksgiving /
christmas dinners - the high concentration of trytophan converts to serotonin
in the bloodstream. Because of
serotonin's relationship to the regulation of sleep, fatigue is induced.
In so far as exact dosages of these elements, it should be noted that it varies
from person to person and
experimentation is key. The following are guidelines that have been found to
work for many. It should also be noted
that changing the ratio's of elements can provide different effects. I.E.
Decreasing 5-HTP and increasing
L-Tyrosine/DLPA can enhance the speediness of a pill, but would not protect the
brain from neurotoxic effects as
much as more 5-HTP would. Excessive 5-HTP can mellow out a roll. Not make it
mashy, but reduce the speediness of
the pill.
Preloading:
1. 5-HTP - 200-400mg
2. L-Tyrosine - 500-1500mg
3. DLPA - 500-1500mg
4. Vitamin C - 1000+, since it is water soluble and so protective you really
can't go wrong going high. Remember that
orange juice and fruits are comparatively lower sources of vitamin C compared
to supplements.
5. L-Glutamine - 2-5 grams
6. Magnesium - 500-1000mg
Post load:
1. 5-HTP - 200-400mg
2. Vitamin C - 1000mg+
3. Magnesium - 500-1000mg
Remember to experiment and take these things slowly as the sheer volume of
pills ingested can upset the stomach. All
elements are legal and can be found readily in health food stores and at online
health food retailers.
It may seem expensive to buy all these things but to protect your brain against
neurotoxic effects and reduce other
negative side effects it is well worth it.
SSRI type antidepressants have been shown to impart a neuroprotective effect
after a roll as well. Specifically
fluoxetine [Prozac] has been shown to prevent neurotoxic effects in animals.
I have never met a person who has wanted to go back to rolling without
preloading / postloading once they tried it. I
don't benefit from any of this information directly nor do I have reason to
lie. I just hope that this helps makes things
safer for people out there.
You have to believe that you have control over what happens to you and that you
don't have to get screwed into
anything.
I hope that this information helps someone out there. I'm not normally a quote
person because people never practice
what they preach, but here are some maxims to roll by:
Knowledge is power
It is best to err on the side of caution
Moderation is key
Ecstasy Preloading
Ishkur's MDMA Preloading/postloading regimen
The Effects of Ecstacy
Think of your brain as the engine of a car. Ecstacy makes you floor the gas
pedal and make the car go faster than normal. This is fun. But in driving
faster, you use up gas faster as well. When the drug wears off, you obviously
have less gas. With less gas, you can't drive as fast as you normally do.
Therefore you operate less efficiently. This is what Ecstacy does--it uses up
all the gas (called serotonin) in your brain, which leaves your brain exhausted
and unable to carry out other functions that it uses serotonin for. Low levels
of serotonin often affect eating patterns, sleeping patterns, short term
memory, and induce symptoms of depression.
Preloading
The concept behind preloading is to add gas to the tank that MDMA is going
to use up, put the car in economy mode so it uses gas more efficiently, and to
prevent damage to the engine if its driven too hard, especially if there's no
gas in the tank. The following supplements safeguard against the drug's
negative side-effects while increasing the enjoyment of the positive ones. All
are perfectly legal, and can be found in just about any health food store.
Protection
The following three elements are the most protective to a preloading
regimen:
1] 5-HTP - 200-400mg
5-hydroxytrytophan is the direct precursor of serotonin in the body. It
enhances the loved-up, empathic feelings and cleans up the comedown. It
counteracts negative side effects like depression by putting more gas in the
tank and ensuring that you don't run out, and also reduces the chances of
oxidised dopamine radicals, which leads to neurotoxicity, which leads to brain
damage.
2] Vitamin C - 1000mg+
Vitamin C is a potent antioxidant. It is believed that MDMA is neurotoxic due
to oxidized free radicals. As such Vitamin C counteracts these free radicals
and helps to minimize damage incurred. It is also water soluble and so
protective you really can't go wrong going high.
3] Magnesium - 500-1000mg
One of Magnesium's major roles in the body is in muscle relaxation. It is the
antagonist [opposite] of calcium, which helps to induce muscle contraction. The
jaw clenching observed on MDMA can be minimized through magnesium
supplementation. Added magnesium can also minimize cramping due to dehydration.
Enhancement
The following elements are optional because they enhance the experience
rather than protect you from anything specific:
1] L-Tyrosine - 500-1500mg
Think of dopamine as engine oil. When the car runs out of gas (serotonin), it
starts using up engine oil in its place, which is very hard on the engine, and
can lead to permanent damage. L-Tyrosine is to dopamine what 5-HTP is to
serotonin. It is its precursor. Dopamine provides the rushy, body buzz, speedy
effects. Increasing L-tyrosine levels enhances these sensations.
2] DLPA - 500-1500mg
DLPA amongst other functions, helps to prolong the duration of action of
pleasure inducing neurochemicals.
3] L-Glutamine - 2-5 grams
L-Glutamine is a precursor to neurotransmitters in the brain. It also imparts a
protective effect on the brain but not as heavily as 5-HTP or Vitamin C.
Usage
It is preferable to preload on a relatively empty stomach, 1-1.5 hours
prior to rolling. Preferably take the supplements with a sugary juice to help
the amino acids cross the blood brain barrier. It should be noted that
preloading can upset some people's stomachs or cause diarrhea due to the
acidity of the stomach. In which case, some Immodium can counteract the
diarrhea and does not interfere with a roll, and Tums or any calcium carbonate
based antacid can reduce the acidity of the stomach and counteract the feelings
of sickness. Remember to experiment and take these things slowly as the sheer
volume of pills ingested can upset the stomach. It may seem expensive to buy
all these things but to protect your brain against neurotoxic effects and
reduce other negative side effects is well worth it.
Postloading
The concept behind postloading is to to fill up the tank after a long, fast
ride. You restore the elements depleted by MDMA, and in doing so, bypass
negative side effects and clean up your comedown while restoring normal
function. The only elements required in a postloading regimen are the
protective ones. The following supplements safeguard against the drug's
negative side-effects the best.
Protection
1] 5-HTP - 200-400mg
2] Vitamin C - 1000mg+
3] Magnesium - 500-1000mg
Usage
5-HTP, Vitamin C, Magnesium are used for reasons also explained in the
preloading regimen. A multivitamin is beneficial to help replace spent
micronutrients. Water is of course beneficial. You will know if you are
bypassing the negative side effects of serotonin depletion if you can sleep
soundly after rolling, and do not experience significant post-MDMA depression
or disturbances in verbal processing, short term memory and eating patterns.
Natural sources of trytophan (the precursor to 5-hydroxtrytophan, two steps
away from serotonin) include bananas and turkey meat. Turkey's high level of
trytophan is the reason why most people feel sleepy after
Thanksgiving/Christmas dinners--the high concentration of trytophan converts to
serotonin in the bloodstream. Because of serotonin's relationship to the
regulation of sleep, fatigue is induced.
This regimen is merely a guideline that has been found to work for many. It
should also be noted that changing the ratios of elements can provide different
effects. For instance, excessive 5-HTP can mellow out a roll. Not make it
mashy, but reduce the speediness of the pill.
Health
120mg of MDMA (about 1-2 caps) is generally all that is needed to
completely deplete all your serotonin. Taking more will not increase the
feelings, nor prolong them. Although the above supplements help, the best way
to restore your serotonin (fill up the tank) is abstinence. Your brain
typically takes about two weeks to recover from Ecstacy. And finally, do not
combine E with monoamine oxidase inhibitor drugs. Monoamine oxidase is the
enzyme that helps to eventually slow down the effects of MDMA, without it, your
body is a speeding car without any breaks--it has no way of controlling itself.
And remember to have fun, be safe, and drink lots of water.
Ketamine/Near Death Experience
Note: Author references were removed entirely,
they are in the full document, linked above (See Links)
Abstract
Near-death experiences (NDE's) can be reproduced
by ketamine via blockade of receptors in the brain (the N-methyl-D-aspartate,
NMDA receptors) for the neurotransmitter glutamate. Conditions which
precipitate NDE's (hypoxia, ischaemia, hypoglycaemia, temporal lobe epilepsy
etc.) have been shown to release a flood of glutamate, overactivating NMDA
receptors resulting in neuro ('excito') toxicity. Ketamine prevents this
neurotoxicity. There are substances in the brain which bind to the same
receptor site as ketamine. Conditions which trigger a glutamate flood may also
trigger a flood of neuroprotective agents which bind to NMDA receptors to
protect cells, leading to an altered state of consciousness like that produced
by ketamine. This article extends and updates the theory proposed in 1990.
Introduction
The near-death experience (NDE) is a phenomenon
of considerable importance to medicine, neuroscience, neurology, psychiatry,
philosophy and religion. Unfortunately, some scientists have been deterred from
conducting research upon the NDE by claims that NDE's are evidence for life
after death, and sensationalist media reports which impart the air of a
pseudoscience to NDE studies. Irrespective of religous beliefs, NDE's are not
evidence for life after death on simple logical grounds: death is defined as
the final, irreversible end. Anyone who 'returned' did not, by definition, die
- although their mind, brain and body may have been in a very unusual state.
There is overwhelming evidence that 'mind'
results from neuronal activity. The dramatic effects on the mind of adding
hallucinogenic drugs to the brain, and the religous experiences which sometimes
result, provide further evidence for this. One of the many contradictions which
'after-lifers' can not resolve is that "the spirit rises out of the body
leaving the brain behind, but somehow still incorporating neuronal functions
such as sight, hearing, and proprioception".
All features of a classic NDE can be reproduced
by the intravenous administration of 50 - 100 mg of ketamine. There is
increasing evidence which suggests that the reproduction of NDE's by ketamine
is unlikely to be a coincidence. This evidence includes the discovery of the
major neuronal binding site for ketamine, known as the phencyclidine (PCP)
binding site of the NMDA receptor, the importance of NMDA receptors in the
cerebral cortex, particularly in the temporal and frontal lobes, the key role
of these sites in cognitive processing, memory, and perception, their role in
epilepsy, psychoses, hypoxic/ischaemic and epileptic cell damage
(excitotoxicity), the prevention of this damage by ketamine, the discovery of
substances in the brain called 'endopsychosins' which bind to the same site as
ketamine, and the role of ions such as magnesium and zinc in regulating the
site.
Characteristic Features of the Near-Death
Experience
There is no internationally determined and agreed
set of criteria which define the NDE, no list of 'research diagnostic criteria'
similar to those provided by the American Psychiatric Association (APA) for
psychiatric disorders. This lack has allowed some critics of neurobiological
models to dismiss these models because some particular criterion which they
believe to be important may not have been fully accounted for by the model
being proposed, although it may well be that a consensus, statistical
definition of the key features of the NDE would not include those features -
just as, for example, the APA definition of schizophrenia (1980) represents an
international consensus and avoids the sectarian views of a few, or inclusion
of obscure cases which do not meet the general rule. For example, Gabbard and
Twemlow argued that Saavedra -Aguilar and Gomez-Jeria's neurobiological
hypothesis, which was based on temporal lobe electrical abnormalities, did not
have general validity because Gabbard and Twemlow had identified 5 cases in
which hypoxia and stress did not appear to be a triggering factor (temporal
lobe epilepsy, and many acute psychoses, can occur spontaneously without any
apparent triggering factors). These cases are certainly not adequate grounds
for the dismissal of neurobiological models.
Ketamine administered by intravenous injection,
in appropriate dosage, is capable of reproducing all of the features of the NDE
which have been commonly described in the most cited works in this field, and
the following account is based upon these. Important features of NDE's include
a sense that what is experienced is 'real' and that one is actually dead, a
sense of ineffability, timelessness, and feelings of calm and peace, although
some cases have been frightening. There may be analgesia, apparent clarity of
thought, a perception of separation from the body, and hallucinations of
landscapes, beings such as 'angels', people including partners, parents,
teachers and friends (who may be alive at the time), and religious and mythical
figures. Transcendent mystical states are commonly described. Memories may
emerge into consciousness, and are rarely organized into a 'life review'.
Hearing noises during the initial part of the NDE
has also been described. Ring classified NDE's on a 5 stage continuum:
1.feelings of peace and contentment; 2.a sense of detachment from the body; 3.
entering a transitional world of darkness (rapid movements through tunnels:
'the tunnel experience'); 4. emerging into bright light; and 5. 'entering the
light'. 60% experienced stage 1, but only 10% attained stage 5. As might be
expected in a mental state with a neurobiological origin, more mundane accounts
also occur, e.g. children who may 'see' their schoolfellows rather than God and
angels. It is clear that NDE's are not as homogeneous as some have claimed.
Ketamine and Phencyclidine
Ketamine is a short-acting, hallucinogenic,
dissociative anaesthetic 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, an uncontrolled drug in most
countries, and remains in use as an anaesthetic for children. Anaesthetists
attempt to prevent patients from having NDE's (emergence phenomena) by the
co-administration of benzodiazepines and other sedative substances which
produce 'true' unconsciousness rather than dissociation.
Ketamine produces an altered state of
consciousness which is very different from that of the 'psychedelic' drugs such
as LSD. It 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 and mystical states (see
ketamine references above). If given intravenously, it has a short action with
an abrupt end. Grinspoon and Bakalar wrote of: '...becoming a disembodied mind
or soul, dying and going to another world. Childhood events may also be
re-lived. 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.'
A psychologist with experience of LSD described
ketamine as 'experiments in voluntary death'. 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 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". 'Ketamine allows some patients to reason that
...the strange, unexpected intensity and unfamiliar dimension of their
experience means they must have died..'.
Attempts to explain NDE's as hallucinations are
sometimes rejected by spiritualists because many persons insist upon the
reality of their experiences. However, 30% of normal subjects given ketamine
were certain that they had not been dreaming or hallucinating, but that the
events had really happened. What is a hallucination ? " a hallucination
has the immediate sense of reality of a true perception .....transient
hallucinatory experiences are common in individuals without mental
disorder". 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 a
hallucination. It is thus important to note that hallucinations in
schizophrenia typically occur in clear consciousness and are believed to be
real. A personal conviction of the 'reality' of an NDE does not invalidate
scientific explanations. Some users of LSD have claimed that their minds are
clearer than usual, and that the LSD world is real while the 'normal' world is
a veil of illusion. Cardiac arrest survivors have been reported as describing
their resuscitation in detail. Ketamine can permit sufficient sensory input to
allow accounts of procedures during which the patient appeared wholly unconscious.
Glutamate, NMDA and Sigma Receptors, and the
Hippocampus
Most large neurones in the cerebral cortex use
glutamate as their neurotransmitter. Glutamate, an excitatory amino acid, is
central to the function of the hippocampus, temporal and frontal lobes and
plays a vital role in all cognitive processes involving the cerebral cortex,
including thinking, memory and perception.
The major neuronal binding site for ketamine is
called the PCP receptor, which is itself attached to the NMDA receptor. As they
are part of the same macromolecular complex, the two terms are sometimes used
interchangeably. It was formerly believed that the sigma and PCP sites were the
same entity, but it is now clear that sigma receptors are very different, have
a unique distribution in the CNS, and are not a form of opioid receptor.
There was initially some debate as to whether the
hallucinogenic properties of ketamine were due to NMDA or sigma receptors.
These effects are now largely attributed to NMDA receptor blockade. Sigma ligands
with a high degree of specificity (e.g. (+)pentazocine) do not produce NDE's at
doses where most of the binding is to sigma rather than NMDA and/or kappa
opioid receptors (sigma receptor ligands frequently have affinity for NMDA
and/or kappa opioid receptors at higher doses).
When glutamate is present in excess, neurones die
via a process called excitotoxicity. Conditions which have been proven to lead
to excessive release of glutamate include hypoxia/ischaemia, epilepsy and
hypoglycaemia. Blockade of PCP receptors prevents cell death from
excitotoxicity. The brain may thus have a protective mechanism against a
glutamate flood: release of a counter-flood of substances which block PCP
receptors, preventing neuronal death. Considering the sophistication of the
brain's many known defences, and the vulnerability of neurones to hypoxia, a
protective mechanism against excitotoxicity seems very likely. This is the only
speculation in the process outlined above: the other statements are strongly
supported by experimental evidence. A peptide called a-endopsychosin, which
binds to the PCP receptor, has been found in the brain (Quirion et al., 1984).
Certain ions such as magnesium and zinc also act as endogenous PCP channel
blockers, and it is possible that these ions are centrally involved in
producing NDE's.
Scientific Hypotheses and NDE's
Claims that NDE's must have a single explanation,
or that a scientific theory must explain all of the experiences ever given the
name of NDE are difficult to justify. It is well established that mental
phenomena have multiple causes and variable expressions. The NDE is more likely
to be the final common expression of several different causes. Even then, the
final 'common' expression contains sufficient variability to suggest different
types of NDE, for example in Ring's study, only 10% 'enter the light'. A
multi-levelled interpretation is thus the most useful. The glutamate hypothesis
of the NDE is not intended to apply to every NDE, and is not necessarily
incompatible with the theories described below.
Temporal Lobe Epilepsy
It has been claimed that there is some similarity
between the phenomena experienced in temporal lobe epilepsy (TLE) and NDE's.
Glutamate is the key neurotransmitter in the temporal lobe, particularly in the
hippocampus, and is implicated in epilepsy. The neuropathology of epilepsy is
believed to result from excito-toxic cell death.
A neuroprotective system might become active in
any excitotoxic situation including epilepsy. The degree of damage, and the
mental state, resulting from a glutamate flood may depend on the final balance
in each neuronal pathway between excito-toxic forces and neuroprotective
mechanisms. Persons who were oxygen deprived for prolonged periods and had a
profound NDE, sometimes survived the episode unimpaired. The lack of apparent
brain damage may result from a very effective mechanism for glutamatergic
blockade in those individuals.
It is also possible that ketamine has its effects
by mimicing some of the pathological processes seen in temporal lobe epilepsy.
Even though ketamine blocks glutamatergic transmission, and prevents
excitotoxic cell death, the effect of ketamine upon the human
electroencephalograph (the EEG) suggests that it can be epileptogenic - the
final result of ketamine acting in the brain is the result of a complex
interplay of forces. There is a reduction in a wave activity, but b, d and q
wave activity are increased. Ketamine acts both as an anticonvulsant and as a
pro-convulsant. Myslobodsky reported that ketamine could produce epileptiform
EEG patterns in human limbic and thalamic regions, but that there was no
evidence that this affected other cortical regions or that fits were likely to
occur. This is consistent with the NDE model presented by Saavedra-Aguilar and
Gomez-Jeria involving limited electrical abnormalites in the limbic system.
Thus production of NDE's by ketamine is not at odds with proposals that NDE's
may result from abnormal electrical activity. Reich and Silvay: " 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". Ketamine is probably anticonvulsant at NDE
producing doses suggesting that a PCP receptor blocker is released to produce
the NDE.
A Flood of Endorphins
Carr proposed that NDE's resulted from a flood
release of endogenous opioids (endorphins). It had been reported that survival
time was increased by giving opiate antagonists (e.g. naloxone) in fatal circumstances.
More recently, a sudden increment of b-endorphin has been reported in the brain
and body fluids of dogs who are 'conscious' at the moment of death. It is now
known that a glutamate flood results in excitotoxic cell death in
hypoxia/ischaemia and epilepsy (see above). However, glutamate is an amino
acid. Endorphins are unlikely to produce NDE's as they are not potent
dissociative hallucinogens. Injection of b-endorphin into the CSF has analgesic
effects lasting well over 22 hours. This does not match the time course of a
typical NDE which is relatively brief. Ketamine produces brief, deep analgesia
due to NMDA (PCP) receptor blockade. The limited psychotomimetic properties of
some opioids (e.g. (-) pentazocine) result from binding to k opioid receptors,
and to PCP receptors at higher doses. However, the effects of (-)pentazocine
binding to k receptors, at doses which are relatively selective, are described
as 'feelings of cheerfulness and strength' (Belville and Forrest, 1968), a
description bearing no resemblance to the dramatic effects of ketamine or
NDE's. With higher doses, more marked effects may appear as a result of binding
to PCP receptors - but pentazocine is not an endorphin. Claims that sigma-
selective (+)isomers of benzomorphan opiates have psychotomimetic effects are
not generally supported by human trials, carried out in the 1960's, which
demonstrated that it is the (-)isomers which have psychotomimetic properties -
and these may prefer PCP receptors rather than sigma sites. The naloxone-reversible
component is due to k opioid receptor binding, while the naloxone insensitive
component is due to PCP (i.e. NMDA) receptor binding, not sigma binding. The
role of opioid receptors in ketamine effects is contoversial. Naloxone could
not reverse the effects of ketamine in humans and dogs. However, ketamine is
supplied as a racemic mixture of (+)and (-) isomers. The controversy may be
resolved by studying the separate effects of the isomers, and the doses at
which these appear. As doses rise, drugs bind to a wider range of receptors.
Ketamine can induce NDE's at doses about four times less than those required
for anaesthesia. White et al. (1980) reported that it was (+)ketamine which has
some opioid binding properties and which produced the most anaesthesia, while
(-)ketamine produced more NDE's (described by anaesthetists as 'psychic
emergence reactions'). White went on to show that (+)ketamine is about four
times more potent as a hypnotic and analgesic, and has different effects upon
the EEG.
Saavedra-Aguilar and Gomez-Jeria cited animal
experiments showing b-endorphin to be epileptogenic to support an argument that
b-endorphins produce NDE's. While b-endorphin may have had these effects within
the rat paradigms used, opioids usually produce calming, inhibitory effects in
humans - not excitation or states resembling epilepsy. Released peptides
probably have protective functions rather than contributing further to
excito-toxicity. The finding of Su, London and Jaffe, that some steroids bind to
sigma receptors, was cited to suggest that steroids could play a role in NDE's.
However, the steroid was progesterone which is not a hallucinogen. Schwartz
reported that the affinity of progesterone for the sigma site is insufficient
to result in significant receptor occupancy, except in pregnancy.
Hypoxia and Hypercarbia
1. Hypoxia: Blacher suggested that hypoxia
induced NDE's. This has been criticised by some authors as studies involving a
slow fall in inspired oxygen produced mental clouding rather than NDE's.
However, these studies are not an accurate model of events in, for example,
cardiac arrest. Sudden hypoxia causes an excessive release of glutamate with
resulting excitotoxicity, which can be prevented by ketamine (see previous
references).
2. Hypercarbia: a CO2-enriched breathing mixture
can result in typical NDE phenomena such as bodily detachment and the
perception of being drawn towards a bright light. Diverse personality types
produced broadly similar reports, suggesting a shared neurological substrate.
Serotonin
Like endorphins, serotonergic effects may be
contributory but are unlikely to play a central role in the NDE. Psychedelic
drugs such as LSD are serotonergic in action and produce a mental state very
different from NDE's . There is frequently an overwhelming increase in sensory
input from the external environment, in contrast to the dissociation produced
by ketamine. Psychedelic visual phenomena bear little relationship to the
dream-like images of ketamine and the NDE. 'Ego dissolution' experienced on LSD
has a different quality from the conviction of having died which may arise with
ketamine. Loss of contact with the external environment leading rapidly to the
'tunnel experience' is not a typical psychedelic drug effect, although it may
occur.
Psychological
1. Depersonalisation: The NDE may be an adaptive
mechanism which alerts one to the threat of death while potentially
overwhelming emotion is held at bay. The reality can then be integrated without
panic. This model is applicable when death is psychologically near as when
falling from a cliff. While protecting nerve cells from excitotoxicity is then
irrelevant, glutamate and NMDA receptors would be involved in producing the
experience as they play a key role in cognition and perception.
2. Regression in the service of the ego:
confronting death cuts off the external world resulting in regression to a
pre-verbal level. This is experienced as mystical ineffability. Losing contact
with the external world is one of the most typical effects of ketamine. This is
partially due to blockade of NMDA receptors involved in sensory transmission.
NMDA receptors play a central role in the transmission of data from all sensory
modalities.
3. State dependant reactivation of birth
memories. Movement through tunnels towards light may be a memory of being born
: a 'near-birth experience'. NMDA receptor blockade could be the mechanism for
such a reactivation of primitive memories.
4. Sensory deprivation: memories may normally be
suppressed by a 'gate' which admits primarily external signals when we are
fully conscious and concentrating upon an external task. If this input is
dramatically reduced (e.g. by ketamine or a heart attack) in combination with
central stimulation (e.g. by excessive glutamate release during hypoxia,
epilepsy, or arising without external provocation), stored perceptions are
released and become 'organised' into a meaningful experience by psychodynamic
forces in the mind in question. The 'white light' may result from CNS stimulation
, and also a possible lowering of the phosphene perceptual threshold. Sensory
deprivation can produce profound alterations in consciousness.
The hippocampus is the anatomical location of the
'memory gate' described above. NMDA receptors form the molecular substrate of
the gate. NMDA receptors have their highest concentration in the hippocampus, a
part of the medial temporal lobe where data from the external world is
integrated with internal programs. The NMDA receptor plays an important role in
learning, and in the formation and retrieval of memories. The PCP receptor is
referred to as a 'gated channel'. Whether the gate is open or closed depends on
the degree of excitation - specifically, the position of a magnesium ion in the
channel. In simple terms, ketamine blocks this channel and closes the gate to
incoming data.
Drug-induced hallucinations ?
Administered drugs may explain some cases of
NDE's, but in most no drugs were given with effects of this nature.
Conclusions
NDE's can be safely induced by ketamine, and the
glutamate theory of the NDE can thus be investigated by experiment. Discoveries
in neuroscience suggest a common origin for ketamine experiences and the NDE in
events occuring at glutamatergic synapses, mediated by NMDA receptors via their
PCP channel component. This hypothesis links most of the neurobiological and
psychological theories (hypoxia, a peptide flood, temporal lobe electrical
abnormalities, regression in the service of the ego, reactivation of birth
memories, sensory deprivation etc.) rather than being an alternative to them.
Most of the tenets of the hypothesis are strongly supported by experimental
evidence which implicates glutamate and NMDA receptors in the processes which
precipitate NDE's. The postulate that anti-excitotoxic agents can flood the
brain remains to be clearly established.
Spiritualists have sometimes seen scientific explanations of NDE's as dull and reductionist. However, the exploration of the mind-brain interface is one of the most exciting adventures which humans have ever undertaken. The real reductionism lies in attempts to draw a mystical shroud over the NDE, and to belittle the substantial evidence in favour of an scientific explanation.
GHB Info
Doses should not be expressed in 'capfulls'. That
is ridiculous. Firstly...GHB doses need to be very accurately measured, usually
in grams. Understand the concentration that you have before taking any of it.
In the average sized adult male, a dose of .75-1.5 grams is enough to exert an
effect of mild relaxation. A dose of 1.5-2 grams can result in euphoria and a
deep sleep. Doses over 2 grams are generally considered to be excessive,
although the dose response is a very individual thing. Now then. You are
talking about GBL, which is NOT GHB, period. I know, you have heard all the
hype about the equivalency and so forth, and I myself have taken plenty of GBL.
Your best bet is to convert it into GHB. This is easy, and not only will it
teach you about dosing, it will also ensure that you research the subject
thoroughly and in the process become educated, which you NEED TO BE BEFORE
TRYING THIS STUFF OUT. So here's the basics: DO NOT MIX WITH ALCOHOL OR ANY
OTHER DEPRESSANT. You could die if you do. DO NOT ASSUME THAT MORE IS BETTER.
It isn't. Take it easy with this drug--it has a NASTY bite. Gradually adjust
the dose upwards. You wan to start with straight GBL? Okay. If you weigh between
165-200lbs, start with 3ml. measured in a syringe. Even at the most
concentrated solution available, this dose will not be lethal or even
problematic. About the release of GH...yes, it does cause this. It creates a
sixteen fold increase in GH release within the first four hours of ingestion,
peaking at around, I think, 90 minutes. The prolactin increase is only five
fold, so I cannot see how it would negate the benefits of the GH release. For
me, the BEST effect of GHB is the quality sleep it promotes at reasonable
doses. I use GHB, I have used it for years, I have overdosed on it twice, and I
am here to tell you that SO WILL YOU if you fuck around with it in a casual
way. Respect this drug and it will respect you. Disrespect it and you will wish
you never saw it, I guarantee it.
quote:
Originally posted by fatcrackhoe
why would the prolactine release have to be the same as the gh release to stop
the body from using the gh? how did you came up with that conclusion?
I think both gh and prolactine are made in the pancreas thus helping to achieve
a happy system balance, think of it like yin and yang. Icrease gh with ghb and
body compensates by making prolactine to counter gh's effects.
-------------
http://boards.elitefitness.com/foru...amine+and+bromo
Here's my post concerning...
L-Glutamine and Bromocriptine for sustained Growth Hormone release
It seems that if GHB and Bromocriptine can make sustained growth hormone in the
body and do away with the resulting prolactin increase problem thereby allowing
for benefits that HGH offers.
Then L-Glutamine and Bromocriptine may accomplish the same thing because oral
glutamine (2 grams) raises growth hormone over 400% above baseline and sustain
elevated amounts up to 90 minutes after ingestion.
For this to work, prolonged sustained growth releases would be required. that
would necessitate multiple 2 gram glutamine dosing throughout day.
If you are currently taking bromo for gyno or weight loss or post cycle
gainskeeper formula, then including a teaspoon of L-glutamine 4 to 6 times a
day couldn't hurt, and it may just help.
Sirwanksalot
Heres a few clips found about the L-glutamine study
There has been some discussion regarding glutamine's absorption and stability.
One of the most quoted studies regarding the effects of oral glutamine had the
subjects consume glutamine combined with soda pop, which acted as its vehicle
of transport. In this study the average increase in growth hormone was 400% for
a glutamine dosage of 2g dissolved in about 10 oz of a carbonated soft drink.
Plasma glutamine and growth hormone both increased and there was an increase in
the use of fat as an energy source. Glutamine + Club Soda for muscle
preservation and growth hormone anyone?
Am J Clin Nutr 1995 May;61(5):1058-61
Increased plasma bicarbonate and growth hormone after an oral glutamine
load.
An oral glutamine load was administered to nine healthy subjects to determine
the effect on plasma glutamine, bicarbonate, and circulating growth hormone
concentrations. Two grams glutamine were dissolved in a cola drink and ingested
over a 20-min period 45 min after a light breakfast. Forearm venous blood
samples were obtained at zero time and at 30-min intervals for 90 min and
compared with time controls obtained 1 wk earlier. Eight of nine subjects
responded to the oral glutamine load with an increase in plasma glutamine at 30
and 60 min before returning to the control value at 90 min. Ninety minutes
after the glutamine administration load both plasma bicarbonate concentration
and circulating plasma growth hormone concentration were elevated. These
findings demonstrate that a surprisingly small oral glutamine load is capable
of elevating alkaline reserves as well as plasma growth hormone.
http://www.lifeandsport.com/research/glutsoda.htm
http://www.ajcn.org/cgi/content/abs...ournalcode=ajcn