Group 42-Sells Out! - The Information Archive/Group 42 Sells Out (Group 42) (1996).iso/drugs/psychade/faq_dext.txt

Text File | 1995-11-30 | 101KB | 1,820 lines

Newsgroups: alt.drugs,alt.psychoactives

Version 1.03

(NOTE: This FAQ will be posted roughly biweekly, on the 1st and 15th of
each month.  Part 2/2 will be posted on the 1st only).

This is a fairly comprehensive list of questions and answers relating to
the recreational and medical use of dextromethorphan, a sigma and NMDA
receptor ligand commonly used as a cough suppressant.  The contents of
these two files are copyright (C) 1994 by William White, and may be freely
reproduced by any means provided that both files are kept intact and are
kept together, and are not modified.  This is version 1.0, the first
release version.  Any questions or comments may be addressed to me at
[e-mail] (finger for PGP2.2 block), or William White,
44 Canterbury Dr., Athens OH  45701  USA.
Note that the use of any medicine in any way contrary to instructions may
be a violation of local, state, and/or federal laws.  I hereby instruct
all readers not to violate the law.  All factual data herein was obtained
from medical journals and references, and was accurate at the time I got
it.  None of it is guaranteed in any way, shape, or form.  This is for
informational purposes only; nothing herein is to be taken as a recommen-
dation, excepting the instructions in this paragraph.  Any actions taken
as a result of this text are the responsibility of the reader, and are
not the responsibility of me, Ohio University, or any subset of the
Usenet/Internet community.  Ohio University does not necessarily agree
with any views, expressed or implied, in this document.
Testimonials and personal data are presented anonymously.  I do NOT
maintain copies of the sender's name, address, or personal information,
either online or offline, and thus I cannot give information as to their
identities.  Any personal information, testimonials, or reports as to
DXM's effects that were or are sent to me will be considered anecdotal and
not specifically referring to the sender.  I encourage anyone with
applicable data to send it to me anonymously.

This is part 1/2.  Part 2/2 contains: List of Products containing DXM and
other active ingredients; Personal Testimonials; and References.

FAQ OVERVIEW: Part 1/2

<1>     General Information
<1.1>   What is Dextromethorphan Hydrobromide (DXM)?
<1.2>   What is Dextromethorphan Polistirex?
<1.3>   How does one obtain and use DXM?
<1.4>   What is the content of commonly available DXM preparations?
        (see also part 2/2)
<1.5>   What should I know about the other drug ingredients?
<1.6>   Why are so many of these in liquid form?
<1.7>   Is recreational DXM usage illegal?
<1.8>   Other (medical) uses for DXM
<1.9>   Drug Interactions

<2>     Subjective Effects and Side Effects of DXM
<2.1>   What are the effects of a low recreational dose?
        (see also part 2/2)
<2.2>   What are the effects of a high recreational dose?
        (see also part 2/2)
<2.3>   Why is there so much individual variance in response?
<2.4>   What are the side effects and risks of recreational DXM?
<2.5>   How toxic is DXM?  What is the LD50?  Should I worry?
<2.6>   Do you recommend DXM for recreation use?

<3>     Physiological Effects of DXM
<3.1>   How does DXM inhibit the cough reflex?
<3.2>   How does DXM cause its psychoactive effects?
<3.3>   Wow, that sure is complicated, isn't it?
<3.4>   Pharmacokinetics

<4>     Sigma, NMDA, and PCP2 receptors
<4.1>   What are NMDA receptors?
<4.2>   What are sigma receptors?
<4.3>   What are PCP2 receptors?
<4.4>   How does DXM compare to other NMDA/sigma ligands?

---------------------------------------------------------------------------

<1>     General Information

This section covers general information about Dextromethorphan, herein
referred to as DXM.  Note the following abbreviations:
    CYA     Cover Your Ass.  Remember this one!
    DXM     Dextromethorphan
    GABA    Gamma-Aminobutyric Acid (a receptor type)
    NMDA    N-Methyl-D-Aspartate (a receptor type)
    OTC     Over The Counter (as in, non-prescription)
    PCP     [1-(1-phenylcyclohexyl)piperidine] (phencyclidine, also
            known as "angel dust")
    PPA     Phenylpropanolamine
    3-PPP   [3-(3-hydroxyphenyl)-N-(1-propyl)piperidine]
also note that square brackets denote IUPAC names.

If you get nothing else out of this FAQ, let it be this: Remember that the
use of DXM is, in general, safe, but please remember the following basic
guidelines:
    - NEVER use a product containing acetaminophen (Tylenol [tm]); large
        doses of acetaminophen can cause liver damage or death.
    - NEVER take DXM if you are taking, or have taken within the past two
        weeks, a monoamine oxidase inhibitor (MAOI).
    - NEVER take DXM if you are taking the prescription antihistamine
        terfenadine (Seldane [tm]).
    - Avoid all products containing DXM and other active ingredients.
    - Always remember: recreational use of DXM is still a great unknown.
        The brain you are risking is your own.


<1.1>   What is Dextromethorphan Hydrobromide (DXM)?

    DXM is a synthetic morphine analog, similar to levorphanol.  DXM has
been in use for approximately 30 years, and has replaced codeine as an
OTC cough suppressant.  It has no traditional opiate-like activity, and
is not a substitute for codeine as an analgesic.  DXM is [(+)-cis-1,3,4,9,
10,10a-hexahydro-6-methoxy-11-methyl-2H-10,4a-iminoethanophenanthrene],
and is also known as 3-methoxy-17-methyl-(9alpha,13alpha,14alpha)-
morphinan.  CAS-125-71-3. [1]

   6-methyl group --->  CH3---N---CH2
                              :   |
                         _____:   |            Dextromethorphan
                        /     \   |
                  _____/   H...\__|__          (note : and .. are
                 //   \\       /  |  \          dotted lines).
                //     \\_____/...CH2 \
                \       /     \       /        The 6-methyl and the
           CH3O__\_____/       \_____/         3-methoxy group are
            ^     -----                        marked for later notes.
            |
3-methoxy group


<1.2>   What is Dextromethorphan Polistirex?

    Dextromethorphan Polistirex is a time-release formulation of DXM; the
"polistirex" refers to a sulfonated styrene-divinylbenzene copolymer
complex.  It is occasionally spelled polystirex or polystyrex.  Unlike the
HBr salt, which is absorbed fairly quickly, this compound is intended for
longer duration cough suppression.  Most, but not all, people who use DXM
recreationally tend to prefer the HBr form (which is also much more
readily available).


<1.3>   How does one obtain and use DXM?

    DXM is widely available in cough syrups, both brand-name (such as
Robitussin [tm] or Vicks Formula 44 [tm]) and store brands.  Most DXM
containing cough syrups also contain one or more of the following active
ingredients: nasal decongestants, antihistamines, acetaminophen, or
guaifenesin (see <1.5>).  As a rule, you want to avoid all of them.
    There are "gelcaps" (liquid or gel filled capsules) available that
contain DXM, but they tend to be fairly expensive and contain other active
ingredients.  Capsule/tablet formulations of DXM are not usually available
in the USA.  Drixoral Cough Caps [tm] are the notable exception (30mg
DXM per capsule).
    It is worth noting that some drugstores keep tabs on people who
frequently buy DXM-containing preparations, especially if they buy
multiple bottles at once or tend not to buy other things at the same time.
This is less common in larger supermarket/drug stores.

    DXM has been popular as an "underground" recreational drug for at
least 10 years, probably longer.  It is probably one of the few OTC
medicines with any serious recreational use potential (ephedrine might
also qualify).  It is both extremely safe and very effective as a cough
suppressant.
    The recreational use potential of DXM has not, in general, been well
known, either by drug users or by physicians.  Not too long ago, many
physicians denied that dextromethorphan was psychoactive at all; whether
this was out of ignorance or a desire to prevent recreational use, I do
not know.  At present, there is an increasing body of knowledge about
DXM's potential for recreational use (and abuse) available in medical
journals.
    DXM is unique among recreational drugs for several reasons.  First,
it is pharmacologically unlike most other recreational drugs (PCP and
ketamine being its nearest relatives).  Second, its effects can vary
considerably from individual to individual.  Finally, it can cause quite
different effects at low and at high dosage levels.


<1.4>   What is the content of commonly available DXM preparations?

NOTE: The following list is incomplete.  If you have information to add to
this list (esp. outside the USA), please email me.  Note also that I do NOT
recommend ANY of the following for recreational use.  Finally, note that
all expressions are metric.  1tsp is approx. 5ml.

Preparations containing DXM only: (SAFEST)

        Drixoral Cough Caps [tm]                                        ????
                Dextromethorphan HBr                                    30mg per capsule

    Vicks Pediatric Formula 44 [tm]             Richardson-Vicks
        Dextromethorphan HBr                    1mg/ml

    Robitussin [tm] Pediatric Cough Suppressant Robins
        Dextromethorphan HBr                    1.5mg/ml

    Benylin DM [tm] Cough Syrup                 Parke-Davis
        Dextromethorphan HBr                    2mg/ml

    Robitussin [tm] Maximum Strength            Robins
        Dextromethorphan HBr                    3mg/ml

    Vicks Formula 44 [tm]                       Richardson-Vicks
        Dextromethorphan HBr                    3mg/ml

    Kroger [tm] Cough Formula                   Kroger
        Dextromethorphan HBr                    3mg/ml
        Note: DXM is misspelled "dextromethrophan" on the bottle.


Preparations containing DXM and other products:
    This list is presented in Part 2/2 of the FAQ.


<1.5>   What should I know about other drug ingredients?

    There are five main classes of ingredients that are present in OTC
DXM-containing products: decongestants, antihistamines, guaifenesin,
analgesics, and alcohol.  Each will be discussed in turn.  With the
exception of alcohol, all should be avoided, although for differing
reasons.

    DECONGESTANTS: There are three nasal decongestants that are used in
OTC cough formulas in the USA: PPA, pseudoephedrine, and phenyleprine (the
latter is almost always found with antihistamines).  PPA is also known as
phenylpropanolamine (from which the acronym PPA is derived), norephedrine,
and the IUPAC name [alpha-(1-aminoethyl)benzyl alcohol].  Pseudoephedrine,
known by the brand name Sudafed [tm], is [(+)alpha-(1-methylamino)benzyl
alcohol].  Phenyleprine is [(-)-3-hydroxy-alpha-(methylaminomethyl)benzyl
alcohol].
    These decongestants belong to a class of chemicals known as the
phenethylamines; this class also includes amphetamine, methamphetamine,
MDMA, MDA, etc., and tend to be DEA scheduled.  The above three are not
scheduled by the DEA (this is USA laws) because they do not have
significant psychostimulant activity.  Ephedrine, which is similar to
pseudoephedrine, and is available throughout truck stops and mail-order
pharmaceutical companies in the USA, does have mild stimulant properties;
thus its popularity as a form of "legal speed".  All of these drugs
stimulate the sympathetic nervous system and are thus called
sympathomimetics.
    What nasal decongestants do share with the more potent amphetamines is
the peripheral activity common to sympathomimetics, such as vasoconstric-
tion and decreased nasal secretions (the good side), and -- with larger
doses -- insomnia, hypertension, heart rhythm abnormalities, hemmorhaging,
stroke, or death (the bad side).  Note that these are extreme reactions,
and that individual tolerance to sympathomimetics tends to vary
considerably.  Tolerance can build quickly, and a fatal dose for one
person may have only a mild effect on another person.
    Because of the potential danger of hypertension, exceeding the
recommended dose of DXM and decongestant containing preparations may be
asking for trouble.  Most people can probably handle it in smaller
recreational doses, but the peripheral "speediness" can be distinctly
unpleasant.  Anyone with high blood pressure or the like has no business
taking large quantities of decongestants.  TRY TO AVOID THESE DRUGS.

    ANTIHISTAMINES: The antihistamines operate by blocking histamine
receptors.  Peripherally, this has the effect of reducing the symptoms of
histaminergic activity (stuffy and runny nose, itchy eyes, hives, rashes,
etc.) associated with infections and allergies.  In the CNS, histamine is
partially responsible for wakefulness, and antihistamines that cross the
blood-brain barrier will cause sleepiness.  In fact, OTC "sleeping pills"
are really just antihistamines.  There are antihistamines that do not
cross the blood-brain barrier (Seldane [tm] is one) but these are
prescription drugs in the USA.
    High doses of antihistamines can result in dizziness, impairment of
concentration, extreme sedation (or, paradoxically, insomnia), headache,
heart palpitations, dry mouth, gastric discomfort, delusions, and
abnormally high blood pressure.  Doses of 30-60mg/kg have been fatal in
very young children; most adults, however, are very unlikely to overdose
on antihistamines.  Death, when it does occur, is from cardiovascular
collapse or respiratory arrest.
    The danger of an antihistamine overdose is very low when using a
DXM-containing product recreationally.  However, you will most likely
experience some unpleasant symptoms, such as sleepiness, dry mouth, heart
palpitations, etc.  For this reason, I RECOMMEND AGAINST PRODUCTS
CONTAINING ANTHISTAMINES.

    GUAIFENESIN: Guaifenesin [3-(2-methoxyphenoxy)-1,2-propanediol] is an
expectorant; it increases the production of respiratory tract fluids, thus
making phlegm less viscous and easier to cough up.  Guaifenesin has been
shown effective as an expectorant, but is of no use as a cough suppressant.
It is often combined with dextromethorphan.  Guaifenesin should not be
used for chronic coughs or coughs accompanied by excessive phlegm.
    High doses of guaifenesin tend to induce emesis (i.e., you puke).
Other effects from high guaifenesin doses are not well known, but probably
not serious.  However, as most people do not enjoy vomiting, I WOULD
RECOMMEND AVOIDING GUAIFENESIN-CONTAINING PRODUCTS.

    ANALGESICS: Acetaminophen is the most common analgesic present in
cough suppressant formulas.  It is closely related to the NSAIDs (non-
steroidal anti-inflammatory drugs) of which aspirin and ibuprofen are the
two most common examples.  Unlike the OTC NSAIDs, however, acetaminophen
does not tend to irritate the stomach, and thus its inclusion in cough
syrups.
    An acetaminophen overdose can be very dangerous.  Normally,
acetaminophen is metabolized in the body by two separate pathways, both of
which lead to harmless metabolites.  However, these two pathways can only
metabolize so much before saturating.  At that point, the remaining
acetaminophen is metabolized by a cytochrome P450 liver enzyme.  The
metabolite via the P450 pathway is toxic to the liver.
    Furthermore, this doesn't happen right away; it can take 16 hours
before any signs of liver damage show up.  This delayed toxic effect has
been responsible for the deaths of some people who (accidentally or not)
overdose on acetaminophen, and then think they are fine when no immediate
problems occur.  There is an antidote (acetylcystine), but it must be
administered within the first 12 to 16 hours.
    The toxic dose of acetaminophen can be as low as 50mg/kg; for a 60kg
person this is only six acetaminophen tablets.  DO NOT UNDER ANY
CIRCUMSTANCES USE RECREATIONALLY ANY DXM PRODUCT WHICH ALSO CONTAINS
ACETAMINOPHEN!
    As for aspirin and ibuprofen, the other two OTC painkillers, both tend
to irritate the stomach at high doses.  I recommend against them,
especially if you have an irritable stomach.  Never take large doses of
aspirin or ibuprofen if you have an ulcer.

    ALCOHOL: Most cough syrups contain some alcohol, to act as a carrier
and to numb the throat.  With a few exceptions (such as Nyquil [tm]), the
amount of alcohol is not usually very great.  While alcohol does not, in
general, mix well with DXM as a recreational drug, the amount in cough
syrups should not cause trouble unless you are specifically sensitive to,
or attempting to avoid, alcohol.  There are alcohol-free preparations
available.


<1.6>   Why are so many of these in liquid form?

    Cough preparations are in liquid form for one reason: most people have
the (mistaken) belief that in order for a cough suppressant formula to
work, it must coat the throat.  This is complete bunk.  If consumers were
a bit smarter, we wouldn't have to gag down cough syrup.  There are, in
fact, gel-capsule cough suppressants on the market, and I expect that
tablet or capsule dextromethorphan will eventually be common.  In the
mean time, we're all stuck with that lovely medicinal cherry taste.
    Note: there is some (reliable) evidence that tablet-form DXM
preparations have been kept from the market in an attempt to prevent their
recreational use.


<1.7>   Is recreational use of DXM illegal?

    Possibly.  There are laws making it a crime to use OTC medicines in
any way other than directed on the label.  Not that this stops people from
using ephedrine (a bronchodilator) as a stimulant.  Nor are you likely to
get caught and/or prosecuted; the authorities are much too busy infringing
upon our civil rights looking for the illegal drugs.  But, remember -- I
SPECIFICALLY instruct you NOT to use any medicine in a manner inconsistent
with its labelling.
    Furthermore, suggesting to someone that they use DXM as a recreational
drug could also be violating a law -- against prescribing drugs as a
layperson.  Again, it's not likely to happen, but it is possible.
    DXM is a prescription drug in Sweden.  It may become prescription in
other countries.


<1.8>   Other (medical) uses for DXM

    Dextromethorphan has been used to determine cytochrome P450-2D6
activity.  Cytochrome P450-2D6 is a liver enzyme which converts DXM into
dextrorphan, and is extensively involved in the metabolism of other drugs.
Some people lack P450-2D6 entirely; others have a highly efficient version
of it.  By looking for the metabolites of DXM, a physician can determine
whether a person has P450-2D6, and if so, how efficient it is.  This
information can then be used to titrate the dosage of drugs which are
metabolized by P450-2D6.
    One area in which DXM (as well as other NMDA blockers; see <4.1>
below) shows great promise is in the prevention of brain damage resulting
from excitotoxicity (overstimulation of nerve cells to the point of cell
death).  This excitotoxicity may be partially or wholly responsible for
the damage associated such wide conditions as fever, hypoxia (lack of
oxygen), infection (such as poliomyelitis, encephalitis, and meningitis),
stroke, siezure, physical injury, and withdrawal from long-term dependence
upon certain drugs (notably alcohol, barbiturates, and benzodiazepines).
    In the case of infection (and in particular poliomyelitis), it has
been demonstrated that the damage to the CNS often occurs not from the
infection, but from the body's own defenses, and notably from a chemical
called quinolinic acid (a metabolite of tryptophan).  Quinolinic acid is a
very potent agonist at excitatory amino acid receptors, of which NMDA is
one type; DXM prevents it from activating NMDA receptors.  (Incidentally,
the function of quinolinic acid -- if it has any -- is not currently
known; it may be involved in the immune response).
    As for physical trauma, hypoxia, siezure, stroke, etc., there are
several experiments which indicate that the majority of the damage again
comes from excitotoxicity at excitatory amino acid receptors.  While DXM
has shown somewhat less success there (possibly due to other receptors
being involved), it still has potential.
    DXM has also shown interesting potential in treating some of the
problems associated with mental retardation.  It may also be of use in
treating Parkinson's disease.  DXM may be useful in conjunction with
opiates for alleviation of both acute and chronic pain.  It may even be
useful in fighting lung cancer.


<1.9>   Drug Interactions and Contraindications

    DXM should not be used (either recreationally or at normal dosage
levels) by people who are taking a monoamine oxidase inhibitor (either
a prescription MAOI or a recreational one such as harmaline).  Combining
DXM and a MAOI has resulted in death.
    Fluoxetine (Prozac [tm]) is a cytochrome P450 inhibitor, and will
change the characteristics of a DXM trip somewhat (see <1.8>; see also the
testimonials in Part 2/2).  Other P450 inhibiting drugs will probably do
the same.  The duration of the trip may be greatly extended by P450-2D6
inhibitors; some users have reported effects lasting 12 to 24 hours past
the normal duration.
    Avoid DXM if taking the prescription antihistamine terfenadine
(Seldane [tm]).  This combination has resulted in death.  Terfenadine
has been implicated in other drug interactions, incidentally.
    Like other psychoactive drugs, DXM should not be used by people who
are mentally or emotionally unstable.  I tend to believe that NO
recreational drug (legal or not) should be used unless the user is in a
calm, rational mood, free from anxiety or negative emotions, and is in a
controlled setting where s/he will not have to drive.  Speaking of which,
as DXM is an intoxicating drug, don't drive under the influence.  Ever.
But I shouldn't have to tell you that, right?
    Some people are allergic to tartrazine (FD&C Yellow #5), which is
present in several cough syrups.  Sensitivity to tartrazine is rare, but
is frequent in people sensitive to aspirin.  Avoid tartrazine if you are,
or think you might be, allergic to it or to aspirin.


<2>     Subjective Effects and Side Effects of DXM

    This section discusses some of the effects you might expect to feel if
you were to use DXM (which I again do not recommend).  Note that people
with an abnormal P450-2D6 enzyme variant may experience no effects from
DXM, or may have a very long-duration (2-3 days), mild, irritating
intoxication.  Neither of these two possibilities occur frequently, but
they should be mentioned.


<2.1>   What are the effects of a low recreational dose?

@   Based on reports of users, there are at least two "levels" to a
@recreational DXM trip.  These will be dealt with separately, as they
@can be quite different.  Please note that the amounts given are
@averages, and there is a GREAT DEAL of individual variation, depending
@most likely on physical factors (such as cytochrome P450-2D6 activity,
@liver clearance, and the like).
@   The two "levels" of the DXM trip are plateaus in that, once a given
@level is reached, further increases (below the next level) will intensify
@the experience but will not necessarily change its character.  There may
@be other levels; however, the "low dose" and "high dose" effects tend to
@be the most consistent of any of them.

    Exactly what constitutes a low dose of DXM will vary from person to
person, but is usually in the range of 120mg to 360mg; this corresponds to
one third to one full 4oz bottle of "maximum strength" cough syrup.  The
effects of DXM can vary considerably depending on the person, their set
and setting, and probably numerous other factors.  There is no "typical"
DXM trip, although there are some common phenomena which do occur.  These
will be discussed separately, below.
    Low dose DXM trips usually take between 30 and 60 minutes to start,
peak about two hours later, and last between 5 and 6 hours.  Hangovers are
rare; if present, there is a general feeling of being lethargic and/or
slightly "off".  A low dose DXM trip has been compared with marijuana and
MDMA, although neither is really all that similar to DXM.

SENSORY CHANGES:
    Many of the initial effects of DXM relate to the senses.  The best
known, and probably responsible for a good deal of DXM's popularity, is
its effects upon hearing.  Sounds may seem to be "richer" or "deeper" in
content.  Music is particularly affected; music -- especially powerful,
intense (but not necessarily fast) music -- can become a euphoric
experience.  Music may develop a very rich "texture" to it, and some users
feel as if the music were lifting them up to great heights.  Some people
find this happens only with a certain type or tempo or structure of music.
Classical music seems to be popular, as is rave music (of course), and
Irish/Celtic/Folk (such as Enya and Lorenna McKennit).  Your mileage may
vary considerably.  Some people find the music euphoria only happens
within a narrow dosage range.
    Body position and kinetic senses are also greatly distorted.  Large,
fluid movements may also be euphoric, and DXM users may find it enjoyable
to move around a lot.  The sense of balance tends to be adversely
affected, and coordination may as well.  Taste and smell may be distorted.
Stimulation of the sense of touch often is pleasurable.  There is some
anaesthetic effect at low dosages; it has been likened to wearing a
body-suit of open-cell foam.
    Vision may be affected.  Colors may seem brighter or more "real".
There may be loss of ability to focus or track objects.  Double vision may
occur if the eyes lose their ability to track the same item, although this
tends to occur more at higher dosages.
    Overall, users may feel their senses have improved; certainly, sensory
input may be pleasurable or even euphoric.  The ability to process the
senses remains; objects are still identifiable, although it may take
longer than usual due to visual focussing problems.  There is a slight
"phasing" or "flanging" effect of hearing and vision (see <2.2>).  There
are few if any hallucinations, although imagination often becomes far more
powerful.  Eidetic imagery (the ability to see clearly what you imagine,
as if it were there) may occur.
    Some users have reported their skin feeling very hot or flushed,
especially in the face and hands.

INTELLECTUAL FUNCTION:
    Because DXM tends to have some "stoning" or intoxicating effect, there
is often some adverse effect upon higher mental function, especially at
larger doses.  Language is particularly affected.  Words, phrases, or
syllables may be repeated, especially when similar-sounding syllables are
next to each other (e.g., "animated it" becoming "animatedididit").  The
user may not be immediately aware of this.  Speech may develop a sense of
rhythm.
    Some users find they are more creative, more insightful, and more
capable of non-linear thought while under the influence.  I do not know if
this is in fact true.  I would like to see more research done on this
subject, as DXM tends to be an unusual drug.

MEMORY:
    Memory tends to be slightly affected at lower dosage levels.  Working
memory (the "train of thought") can become stuck in repetitive thoughts;
on the other hand, some users find that they are easily distracted.  Short
term memory tends to be degraded.  Recall of events prior to the trip is
usually not affected, but encoding of what happens during the trip (and
subsequent recall) may be diminished (again, this is not universal).  The
"break in continuity" feeling described in <2.2> (under MEMORY) may occur
at low to medium dosage levels.

EMOTION:
    Mood enhancement is typical; many users find themselves quite bouncy
and happy.  Unlike many other drugs, there is much less of a let-down in
mood when the drug wears off.  Accompanying the euphoria is often a sense
of energy or drive.  Users may find formerly boring, tedious tasks to be
far more tolerable, or even enjoyable, under the influence of DXM.  There
may be some sense of fear, although this is not common at lower dosages.


<2.2>   What are the effects of a high recreational dose?

    At the higher dosage level (around 720mg, or one 8oz bottle of the
same strength as in <2.1>), DXM takes on a very "heavy" character.  At
this level it is very "stoning" -- cognitive, sensory, and memory
functions are all strongly disrupted.  Some say it acts a bit like
ketamine at this level; others compare it to a heavy LSD trip.  Individual
response varies enormously at high dosage levels.  Some love it, some hate
it.  A high dose trip may last between 6 and 8 hours, peaking about three
hours in.

SENSORY CHANGES:
    Hearing, vision, and touch become subject to "flanging" effects --
sensory input seems to be chopped into regular, rhythmic bits, with some
echo or persistence effects.  This is similar, but more profound, to the
flanging from nitrous oxide intoxication.  The closest sober approximation
would be listening to the world through a delay-line flanger.  This
effect, and especially the echo/persistence effects, occur both on a "raw"
level (e.g., sounds, sights) and on a more complex level (shapes, faces,
words).  If extreme, it makes it impossible to process sensory input at
all.  Individual objects and sounds may still have meaning but the user
may find it impossible to connect them into a coherent whole.  Double
vision is common; the eyes tend to lose the ability to track objects.  At
very high doses, vision can become disrupted and confused to the point
where the user is effectively blind.  It may take a very long time to
process sensory input.
    Body position and kinetic sense are usually distorted to the point of
being useless.  It is often difficult if not impossible to walk.  Taste
and smell may be similarly affected.  Do not attempt to drive or operate
any complex machinery.  Some users find themselves wiggling or
alternatively tensing and relaxing their muscles, especially those in the
feet and toes; it may feel "wrong" to stop.
    Sensory distortions similar to that from fever may occur.  Objects may
seem both too big and too small, and both too far away and too close.
This may, or may not, be extremely disturbing.  Actual hallucinations also
occur at high dosage levels, and users have reported everything from
simple geometric patterns to full-blown, lifelike hallucinations.

INTELLECTUAL FUNCTION:
    The "stoning" effect is profound at this level.  Complex, tedious
functions (such as arithmetic) are very difficult.  Reaction time is
significantly delayed.  Decision-making is somewhat degraded, although
conceptual thinking is less affected than more concrete thinking.  Again,
the intellectual effects are sometimes unpleasant, and have been compared
to those deriving from a high fever.
    Language changes can be quite profound.  Sentences may stretch on for
quite a long time or be very terse (I call this the "Hemingway effect").
Words are very often repeated.  This may be related to problems with
working and short-term memory.  Speech may often occur in a very rigid
(but not necessarily simple) rhythm; the user may not respond to speech
unless it is in a similar rhythm.  Some users believe this state induces
rhythm-based creativity (music, poetry, etc).

MEMORY:
    Working and short-term memory are seriously impaired.  It is typical
for thoughts to get stuck in a "loop".  While some users report little or
no short-term memory loss, others find that they cannot remember what
happened even a few seconds ago.  Long-term memory recall is not
necessarily degraded, although encoding is usually bad.  Expect to forget
a lot of what happened during the trip.  The sense of time can be quite
distorted, incidentally, both in terms of chronological placement of
events and the sense of the passage of time.
    The day after the DXM trip, some users feel as if there has been a
break in the continuity of their memories, almost like the close of one
chapter and the beginning of another.  Some find this feeling a very
positive one, like a rebirth or transition.  It can be disconcerting if
you experience it without being prepared.

MOOD:
    Mood can range from mania to panic.  Irrational fears may occur,
especially in users naive of the bodily effects of this dosage range.
There may be a great increase in approach behaviour, as if every event and
object were a new experience.
    At this dosage level, DXM can have an almost "shamanic" feel to it;
the user may find himself or herself confronting aspects of the self for
which he/she is unprepared.  This can range from interesting to
terrifying.  At least one user has reported recall of repressed memories
(later verified to be true).  At very high levels, some users have
reported feeling that they have "lost" themselves for a time.  The amount
of control over this will tend to relate to experience with this drug and
hallucinogens in general.
    Several people have reported that high dosage DXM trips have a
definite "spiritual" component.  I cannot comment on the validity of
this type of observation, as I am not knowledgeable on the subject of
shamanic use of drugs.  However, enough people have mentioned it that
I have included it here.  Increased contact with the spirit world,
spiritual journeying, etc. are the usual fare.
    Many find this dosage level to be quite enjoyable.  A lot probably has
to do with familiarity with psychoactive drugs in general.  Some people
have reported mystical experiences on high dosage levels (e.g., connection
with the spirit world or with other beings).


<2.3>   Why is there so much individual variance in response?

    Several reasons.  First off, there is a liver enzyme known as
cytochrome P450IID6 (commonly P450) which metabolizes DXM.  Some people
have a different variant than others, or none at all (see above, question
<1.8>).  Thus, while one person may metabolize DXM quickly, another may
not.  Certain drugs -- such as fluoxetine (Prozac [tm]) -- can inhibit
P450 activity.
    Secondly, it is hypothesized that some of the effects of DXM,
especially at higher dosage levels, may actually be due to dextrorphan,
which is more similar to PCP and ketamine in its neuroreceptor activity.
Some individuals may metabolize high doses of dextromethorphan to
dextrorphan.  Incidentally, my opinion -- based on anecdotal evidence of
recreatioanl DXM use while on fluoxetine -- is that DXM, and not
dextrorphan, is responsible for the psychoactive effects.
    Third, NMDA receptors are intimately involved in most areas of the
brain, unlike the biogenic amine neurotransmitters (serotonin, dopamine,
noradrenaline, histamine, and acetylcholine); the biogenic amines are
usually secreted by small, distinct bundles of nerves.  It is possible
that, due to this extensive involvement, many different cortical and
limbic circuits may be affected.
    There are probably a gazillion other reasons why DXM has such a wide
range of effects.  The involvement of NMDA receptors in long-term
potentiation may be part of the reason.  Subtle differences in brain
chemistry, notably in terms of sigma receptors, may also be involved.  I
don't know; I doubt anyone does.


<2.4>   What are the side effects and risks of recreational DXM?

    Physical side effects are usually fairly mild, although at higher
dosage levels, there can be a heavy "body feel".  Heart rate may be
increased.  At very high dosages, siezures may occur -- you want to avoid
this.
@    Some users have reported getting a rash from use of DXM.  This
@tends to itch for awhile, and then go away.  This is most likely NOT
@due to the DXM itself, although there is some evidence that DXM may
@have some histaminergic activity (this is not the same thing as being
@an allergen).  Many people report that the syrup, rather than the DXM,
@is the culprit, and that they have had no reaction from capsules or
@gelcaps.  To be on the safe side, don't try too much at once, and
@always have antihistamines available.
    Hangovers are not common but do occur.  Don't plan on doing anything
too intensive or strenuous the next day.  Amotivation and lethargy are
common hangover effects.  There are occasionally memory problems the next
day, such as forgetting words or experiencing frequent deja vu.
    If a hangover continues for a long time, this may indicate that you
have difficulty metabolizing DXM.  Be patient; it may take several days
(this is very rare).  Take a multivitamin each day, and drink a lot of
water (the former helps with enzyme activity, the latter helps your body
get rid of things).  Exercise daily.
    Psychological side effects can be quite varied.  Bad trips are
certainly possible, as with any drug.  As with other psychoactive drugs,
especially hallucinogens, there is always the chance that a mental illness
may be triggered by the experience.  No drug, recreational or not, can
*cause* schizophrenia; most any drug can trigger it if it is latent.  DXM
is no exception.
    Prolonged, regular use of DXM has some definite risks.  The most
common is mania; this has been reported in people who used large amounts
of DXM (especially to self-medicate depression).  Some research has linked
sigma receptors to schizophrenia, and chronic use of NMDA antagonists has
been shown to upregulate (increase) dopamine receptors.  This could
theoretically mean that DXM could trigger schizophrenia in susceptible
individuals, although nobody knows for sure.  One thing that is known is
that neither DXM nor PCP nor ketamine cause any change in PCP or sigma
receptors.
    Chronic use of NMDA antagonists may also increase alcohol tolerance;
this is based mostly on anecdotal evidence and theory, but it appears to
be a very real phenomenon.  If true, then it is important to note that
the GABA receptor effects of alcohol may NOT be changed; in practical
terms, you might be a lot drunker than you feel, and this could possibly
lead to alcohol poisoning.  Be careful, and limit yourself to as little
alcohol as possible when using DXM.


<2.5>   How toxic is DXM?  What is the LD50?  Should I worry?

    The LD50 of DXM is not well known.  In searching medical literature, I
found only two cases of death associated with DXM use, both in Sweden.  In
one case, a girl was found dead in a public bathroom with two bottles of
30mg DXM tablets (the number of tablets is believed to be 50/bottle, but
may be 15 or 25).  She had previously tried to commit suicide using a
bottle of 50 tablets (this leads me to believe that she had, in fact,
taken 100 tablets).  The other case involved a 27 year old man, and few
details were specified.  In both cases, death was apparently due to
inhibition of respiration.  Plasma levels of DXM were 9.2 and 3.3
micrograms per gram (cases 1 and 2); plasma levels of dextrorphan were 2.9
and 1.5 micrograms per gram.  In both cases, the ratio of DXM to
dextrorphan was about 3.
    It is reasonable to expect, given this data, and the available data on
the effects of high DXM doses, that DXM starts becoming toxic around 2000
to 3000mg (for an adult).  This corresponds to between 5 and 8 4oz bottles
of 3mg/ml cough syrup, i.e., a fairly large amount, but still within the
realm of hardcore experimenters.  Keep this in mind before you consider
large doses.  IV naloxone is considered the antidote for DXM overdose.


<2.6>   Do you recommend DXM for recreation use?

    No.  Definitely not.  Use of medicine, OTC or not, contrary to
instructions may be a violation of local, state, and/or federal law.  I
hereby specifically tell you not to use any DXM-containing product (or any
other product) in a manner inconsistent with its labelling.
    Even if DXM *were* legal for recreational use, I still wouldn't
recommend it for frequent use, nor for high-dosage use.  Frequent use may
bring about undesirable changes (upregulation of dopamine receptors, for
example).  High-dosage use carries with it all the risks of any
hallucinogen, and can be distinctly unpleasant.  Very little is known
about sigma, PCP, or NMDA receptors.  You dork with them at your own risk,
and that risk may be considerable.
    Sound like a CYA answer?  It sure is.  Right now, in the country in
which I live, there are many people with nothing better to do than support
legal paternalism and legal moralism.  For whatever reason, some people
feel that they have the right to tell a legal adult what she or he can and
cannot do that involves only her/his body.  And as long as this goes on,
I'm going to make sure I'm not thrown into prison so they can free
murderers and rapists to make room for me.  So, I'm telling you -- don't
break the law.


<3>     Physiological Effects of DXM

    This section governs the effects of DXM on the body.  Unfortunately,
knowledge of NMDA/sigma ligands is far from complete.  Much of this
information will undoubtedly turn out to be wrong.


<3.1>   How does DXM inhibit the cough reflex?

    This is a complex question.  The cough reflex involves a series of
signals originating from the throat, lungs, and nasal passages, and ending
up in the muscles.  At any point in this pathway, signals are susceptible
to the effect of inhibitory transmission.  Sigma receptors are evidently
involved in this pathway.  This may be a direct involvement -- sigma
receptors may directly inhibit the cough reflex signals -- or it may be
an indirect one.
    There is some evidence that 5HT1a receptors (a type of serotonin
receptors) are involved somewhere in this pathway, and that cough
suppressants may increase 5HT1a activity.  This could explain some of
DXM's mood-altering activity.  5HT1a receptors are involved in anxiety
states and in resilience to aversive events.


<3.2>   How does DXM cause its psychoactive effects?

    Upon comparison with 3-PPP (similar to PCP), DXM has been found to
bind with at least three types of neuroreceptors; these have been labelled
DM1, DM2, and DM3 (remember, these are binding sites, not necessarily
receptors).  At the DM1 binding site, 3-PPP and DXM both have nanomolar
potency; at DM2, DXM is nanomolar while 3-PPP is micromolar (i.e. less
potent than DXM); and at the DM3 binding site, DXM is micromolar while
3-PPP is nanomolar.
    Given what is currently known about sigma and PCP receptors, the DM1
binding site is most likely the sigma receptors and the DM3 binding site
is most likely the NMDA/PCP1 receptor (see <4> below).  The DM2 binding
site is likely the PCP2 receptor, but some research has suggested another
site of DXM action separate from this receptor.
    Most of the "stoning" or intoxicant effects of DXM are likely the
result of NMDA receptor blockade.  Part of alcohol's intoxicant effect
seems to be mediated by NMDA receptor blockade; this may explain some of
the similarity.  Unlike alcohol, DXM does not affect GABA receptors.
    The severe disruption of sensory processing is also most likely due to
NMDA blockade.  Some analogy to auditory disturbances in schizophrenia
have been drawn, and potential mechanisms for "flanging" of sensory input
and for persistence/echo are being investiaged.  These, as well, are
likely due to NMDA activity.  Memory inhibition is almost certainly due to
NMDA blockade; NMDA receptors are involved in long-term potentiation (a
cellular component of memory).
    The psychotomimetic (literally "psychosis-like") effects of DXM may
be a result of sigma activity.  For better or for worse, little if any
data is available on the effects of sigma agonists without NMDA activity
on humans.  However, sigma agonism is likely much more "subtle" than NMDA
block.
    Finally, if (as some researchers believe) PCP2 "receptors" are in fact
a biogenic amine reuptake site, then many of DXM's euphoric, mood-
enhancing, and stimulant effects could result from occupancy (and thus
blockade) of this site.  Interestingly, DXM seems to be much more potent
at this site than other sigma/NMDA ligands (such as PCP or ketamine) in
comparison to activity at other sites.  Also interestingly, at least one
tricyclic antidepressant has been found to be a sigma ligand; it is
possible that this reuptake site is in the same category as those targeted
by antidepressants.  It is my belief that many of the effects felt at
lower dosages may be due to reuptake inhibition.
    Many of DXM's effects are undoubtedly due to indirect activity.  For
example, it may indirectly increase 5HT activity, especially at the 5HT1a
receptor.  This could explain some of its mood-altering properties.
Another example is dopaminergic activity; DXM seems to increase activity
at certain dopamine receptors.
    Note that DXM itself may not be responsible for the psychoactive
effects, especially at higher dosage levels.  DXM may be converted within
the body to dextrorphan (see <2.3>).


<3.3>   Wow, that sure is complicated, isn't it?

    Yes.  And unfortunately, it doesn't really say as much as you might
think.  What it means, basically, is that DXM works via at least three
neuroreceptors, one of which (the NMDA receptor) is involved in learning
and in higher reasoning, and one of which (the sigma receptor) may be
involved in schizophrenia and in psychotomimetic effects.  The third
receptor (PCP2) may be the same reuptake site (or a similar one) as that
targetted by antidepressants.  But, beyond that, nobody really knows why
or how DXM (or any other complex, psychoactive drug) works.


<3.4>   Pharmacokinetics

    DXM is absorbed quickly from the GI tract; within 30 minutes, all of
it may have entered the bloodstream.  The polistirex compound will
obviously take longer to be absorbed.
    DXM is subject to two first-pass metabolic changes: O-demethylation
(replacement of the 3-methoxy group with OH), and N-demethylation
(replacement of the 6-methyl group with H).  Refer to <1.1> and the
diagram of the DXM molecule.  The O-demethylation pathway can occur either
via cytochrome P450-2D6, or another (unidentified) enzyme which works at
about 70 times slower.  The enzyme responsible for the N-demethylation
pathway has not been identified.
    The product of O-demethylation of DXM is dextrorphan, a chemical which
many believe to be responsible for DXM's psychoactive effects.  N-demeth-
ylation of DXM produces 3-methoxymorphinan (3MM).  O-demethylation of 3MM
or N-demethylation of dextrorphan produces 3-hydroxymorphinan.  I could
not find any further information on DXM metabolism.  Incidentally, the
O-demethylation of 3MM is also performed by P450-2D6.
    Note that anecdotal evidence from recreational users of DXM who take
fluoxetine leads me to believe that dextrorphan is not, in fact,
responsible for DXM's psychoactive effects.  In fact, fluoxetine (which
inhibits P450-2D6) tends to extend the DXM trip.  This is consistent with
DXM's effects being due to the dextromethorphan itself and not a metabo-
lyte such as dextrorphan.


<4>     Sigma, NMDA, and PCP2 receptors

    This section covers some of the basics about the three receptor types
that DXM targets.  I apologize if this may get a bit complicated; I'm not
all that good at explaining this sort of thing.  I assume a basic
knowledge of neurotransmitters and neuroreceptors (consult any biological
psychology, psychophysiology, or psychopharmacology text).


<4.1>   What are NMDA receptors?

    When most people discuss neurotransmitters and neuroreceptors in the
context of drug activity, they usually refer to the biogenic amines:
acetylcholine, dopamine, noradrenaline, serotonin (5HT), and histamine.
From a psychopharmacological standpoint, these are probably the best
understood.  These neurotransmitters tend to have a regulatory function;
they modulate behaviour, mood, activity level, etc.  In general, the
receptors are slow and are not involved in the sort of high speed
information processing that takes place in the cortex.
    The bulk of neurotransmission takes place not with the biogenic amines
but with excitatory amino acids (glutamic acid and aspartic acid) and
inhibitory amino acids (GABA).  Unlike most biogenic amine receptors, many
receptors for excitatory and inhibitory amino acids are very fast, and
operate by directly polarizing or depolarizing the nerve membrane.
    NMDA is one type of excitatory amino acid receptor (quisqualate and
kainate are the others).  NMDA receptors are unique in that, in addition
to the normal chemical signal, they also require a Mg ion in order to
function.  NMDA receptors are involved in long-term potentiation, the
mechanism by which individual nerve cells "learn".  Long-term potentiation
is probably the basis of learning and memory, at least short-term.
    NMDA receptors operate, and look, a bit like an iris or camera
aperture.  There are five subunits, which normally fit together to close
the channel; each of the subunits has a spot where neurotransmitters
attatch.  When they do attatch, electrostatic forces snap the channel
open, and ions can flow in and out of the cell.  DXM, as well as PCP and
ketamine, are "open channel blockers"; they bind to a spot in the open
channel (blocking it), but have little or no effect upon a closed one.
Their activity is thus dependent upon the channel opening.  The "PCP1"
receptor is the name for this open channel attatchment site.
    There are at least three types of NMDA receptors (in the rat, at
least; this probably extends to humans as well).  One type is found in the
cerebellum, one in the thalamus, and one in the cortex.  These types
differ subtly, but it is possible that DXM may show a different spectrum
of effect on these types than other NMDA antagonists (such as ketamine or
PCP).
    NMDA receptors are also involved in excitotoxicity (nerve cell death
via overstimulation).  The chemicals which agonize (activate) NMDA
receptors can also kill the very same nerve cells they are activating.
Many substances, such as quinolinic acid (a metabolite of tryptophan) are
so potent that very small amounts can devastate great numbers nerve cells.
Others, like glutamic and aspartic acid, are less potent but still capable
of doing damage if present in sufficient amounts.  This excitotoxicity is
directly responsible for much of the damage attributed to various types of
trauma and insult to the CNS.  Polio is a good example; by blocking the
activity of quinolinic acid, all the damage resulting from poliomyelitis
can be prevented.


<4.2>   What are sigma receptors?

    Sigma receptors are a type of opioid receptor, the others being mu,
kappa, and delta.  This classification may, in fact, be false; there is
some evidence that, while many opioids show sigma activity, the sigma
receptor is not involved in the same domain as other opioid receptors
(reward mechanisms and painkilling).
    Sigma receptors are known to be involved in psychotic states and in
the cough reflex (I doubt the two are related).  Sigma receptors are
probably involved in schizophrenia.  Neither the actual "purpose" of sigma
receptors, nor the endogenous neurotransmitter that fits the sigma
receptor, has been identified.


<4.3>   What are PCP2 receptors?

    PCP2 receptors were, obviously, the second PCP receptor to be
positively identified (the first is the open channel site on the NMDA
receptor; see <4.1>).  Their use (if they have one) has not been
determined, nor has their significance.  PCP2 receptors could represent
the closed state of NMDA channels (or some other receptor).  They could be
an entirely new receptor.  One possibility which has received considerable
support is that PCP2 receptors are reuptake sites -- areas where "used"
neurotransmitters are taken back into the cells to be used again.
Reuptake sites are the target for antidepressants (except for monoamine
oxidase inhibitors), as well as the target for cocaine.  Reuptake
inhibition by DXM would result in some of the same effects as
antidepressants or cocaine, and could explain the euphoria.


<4.4>   How does DXM compare to other NMDA/sigma ligands?

    DXM, especially at higher dosages, begins to resemble ketamine and
PCP.  However, it still is very different (especially at lower dosages).
This is most likely due to the DM2 binding site (the PCP2 reuptake site),
where DXM is far stronger in effect than either PCP or ketamine, as well
as the DM3 binding site (the NMDA/PCP1 site) where PCP and ketamine are
far stronger in effect than DXM.  This is probably why DXM has a much
stronger mood-enhancing effect, and a much weaker dissociative anaesthetic
effect, than PCP or ketamine.


--
|  Bill White   [phone]     | [e-mail]             |
|  44 Canterbury, Athens OH  45701  | finger for PGP2.2 block                 |
|  SCA: Erasmus Marwick, Dernehealde Pursuivant, Dernehealde, Middle Kingdom  |

=============================================================================

Newsgroups: alt.drugs,alt.psychoactives
From: [e-mail] (William E. White )
Subject: Dextromethorphan FAQ (Part 2/2)
Message-ID: <[e-mail]>
Date: Fri, 6 May 1994 00:32:38 GMT

Version 1.02  Last modified 4/1/1994
(This FAQ will be posted more or less biweekly, on the 1st and 15th of
each month).
This is a fairly comprehensive list of questions and answers relating to
the recreational and medical use of dextromethorphan, a sigma and NMDA
receptor ligand commonly used as a cough suppressant.  The contents of
these two files are copyright (C) 1994 by William White, and may be freely
reproduced by any means provided that both files are kept intact and are
kept together, and are not modified.  This is version 1.0, the first
release version.  Any questions or comments may be addressed to me at
[e-mail] (finger for PGP2.2 block), or William White,
44 Canterbury Dr., Athens OH  45701  USA.
Note that the use of any medicine in any way contrary to instructions may
be a violation of local, state, and/or federal laws.  I hereby instruct
all readers not to violate the law.  All factual data herein was obtained
from medical journals and references, and was accurate at the time I got
it.  None of it is guaranteed in any way, shape, or form.  This is for
informational purposes only; nothing herein is to be taken as a recommen-
dation, excepting the instructions in this paragraph.  Any actions taken
as a result of this text are the responsibility of the reader, and are
not the responsibility of me, Ohio University, or any subset of the
Usenet/Internet community.  Ohio University does not necessarily agree
with any views, expressed or implied, in this document.
Testimonials and personal data are presented anonymously.  I do NOT
maintain copies of the sender's name, address, or personal information,
either online or offline, and thus I cannot give information as to their
identities.  Any personal information, testimonials, or reports as to
DXM's effects that were or are sent to me will be considered anecdotal and
not specifically referring to the sender.  I encourage anyone with
applicable data to send it to me anonymously.

This is part 2/2.

<5>     Preparations containing DXM and other ingredients
<6>     Personal testimonials and reports
<7>     References


<5>     Preparations containing DXM and other ingredients

    Remember, all these products should be AVOIDED.  Guaifenesin in large
doses will cause vomiting; antihistamines in large doses will put you to
sleep; decongestants in large doses might kill you; and acetaminophen in
large doses probably will kill you.

Preparations containing DXM and guaifenesin: (AVOID)

    Benylin [tm] Expectorant                    Parke-Davis
        Dextromethorphan HBR                    1mg/ml
        Guaifenesin                             20mg/ml

    Contac [tm] Cough Formula                   SmithKline Beecham
        Dextromethorphan HBR                    1.34mg/ml
        Guaifenesin                             13.34mg/ml

    Robitussin [tm] DM                          Robins
    Cheracol D [tm] Cough Formula               Roberts
    Mytussin [tm] DM                            Pharmaceutical Basics
        Dextromethorphan HBR                    2mg/ml
        Guaifenesin                             20mg/ml

    GuiaCough [tm] DM Expectorant Syrup         Schein
    Guiatuss DM [tm]                            Barre, Goldline
    Halotussin [tm] DM                          Halsey
        Dextromethorphan HBR                    3mg/ml
        Guaifenesin                             20mg/ml

    Naldecon [tm] Senior DX                     Apothecon
        Dextromethorphan HBR                    3mg/ml
        Guaifenesin                             40mg/ml

    Tuss-DM [tm] (tablets)                      Hyrex
        Dextromethorphan HBR                    10mg
        Guaifenesin                             200mg

    Queltuss [tm] (tablets)                     Forest
        Dextromethorphan HBR                    15mg
        Guaifenesin                             100mg

    Syracol-CF [tm] (tablets)                   Mallard
        Dextromethorphan HBR                    15mg
        Guaifenesin                             200mg

    Humibid [tm] DM (extended-release tabs)     Adams
        Dextromethorphan HBR                    30mg
        Guaifenesin                             600mg

    Delsym [tm] (time release)                  Fisons
        Dextromethorphan Polistirex             6mg/ml (HBr equiv.)

Preparations containing DXM and a decongestant: (NOT RECOMMENDED)

    Vicks Pediatric Formula 44 Cough & Congest. Richardson-Vicks
        Dextromethorphan HBR                    1mg/ml
        Pseudoephedrine HCl                     3mg/ml

    Triaminic-DM [tm] Syrup                     Sandoz
        Dextromethorphan HBR                    2mg/ml
        Phenylpropanolamine HCl                 2.5mg/ml

    Vicks Formula 44D [tm] Decongestant         Richardson-Vicks
        Dextromethorphan HBR                    2mg/ml
        Pseudoephedrine HCl                     4mg/ml

Preparations containing multiple ingredients: (AVOID)
    Products marked with a (#####) contain acetaminophen and should NEVER
    be taken in large doses.  If you, or someone you know, has taken a
    large amount of an acetaminophen-containing product, please take them
    to the hospital as soon as possible.

    Comtrex [tm] Multi-Symptom Liqui-Gel [tm]   Bristol-Myers       #####
        Dextromethorphan HBR                    10mg
        Acetaminophen                           325mg
        Chlorpheniramine Maleate                2mg
        PPA HCl                                 12.5mg

    Comtrex [tm] Multi-Symptom                  Bristol-Myers       #####
        Dextromethorphan HBR                    0.66mg/ml
        Acetaminophen                           21.66mg/ml
        Chlorpheniramine Maleate                0.133mg/ml
        Pseudoephedrine HCl                     2mg/ml

    Vicks Daycare [tm]                          Richardson-Vicks    #####
        Dextromethorphan HBR                    0.66mg/ml
        Acetaminophen                           21.66mg/ml
        Guaifenesin                             6.6mg/ml
        Pseudoephedrine HCl                     2mg/ml

    Tylenol [tm] Cold Night Time                McNeil              #####
        Dextromethorphan HBR                    1mg/ml
        Acetaminophen                           21.66mg/ml
        Diphenhydramine HCl                     1.66mg/ml
        Pseudoephedrine HCl                     2mg/ml

    Robitussin Night Relief [tm]
        Dextromethorphan HBR                    1mg/ml
        Acetaminophen                           21.66mg/ml
        Phenylephrine HCl                       0.33mg/ml
        Pyrilamine Maleate                      1.66mg/ml



Preparations containing multiple ingredients: (AVOID)

    Vicks [tm] Nyquil [tm]

    Vicks [tm] Nyquil LiquiCaps [tm]

    Vicks [tm] Dayquil [tm]

    Vicks [tm] Dayquil LiquiCaps [tm]



<6>     Personal testimonials and reports

---------------------------------------------------------------------------

At 8:18PM, I took 60ml of Kroger Cough Medicine Cough Formula (3mg/ml),
which works out to be 180mg of DXM HBr.  I was also taking Prozac, and
had been for several weeks; I was curious whether this would effect the
trip.  I'd also had several cups of coffee that day.
I first started feeling a buzz about 30 minutes into the trip.  My face
began to feel very hot.  At 60 minutes, I felt like I'd had five or six
drinks.  Music was quite incredible.  This was still much like the DXM
experiences I'd had prior to taking Prozac.  I was also having trouble
keeping my eyes focussed.  My head felt like it was full of helium and
my limbs like they were made out of lead.
At 75 minutes, I felt like I was in free-fall; like the feeling you get
when you've been sitting still meditating for a long time.  At 90 minutes
I was even more lightheaded, and my skin was numb -- this was the first
major change from prior DXM trips (not on Prozac).
At 120 minutes, I'd lost most of my sense of touch, and was having some
fairly hefty troubles keeping my thoughts straight.  At 140 minutes, I
sat and listened to music.  I was convinced that I was a cyclopropane
molecule, and then that I was a tetrahedron.  I was sitting Indian-style;
the three base points were my knees and my butt and the top of the tetra-
hedron was my head.  I felt incredibly small.  There was the same size-
distortion as during fevers, but I felt no unpleasantness -- another
difference from usual DXM trips.
At 180 minutes I started to come down.  It was weird -- one minute I was
swimming in a daze, the next I realized "hey, I'm coming down now" and it
was clear from then on out; I got more and more bursts of lucidity.
I woke up the next day, about 12 hours after dosing, and still had some
balance and memory problems.  These lasted throughout the day.  I felt
like my life had ended and started again, like there was a line drawn in
my memory, separating past from future.  It was disconcerting but not
unpleasant.  I was also extremely tired and lethargic; I just wanted to
sit around.  The next day I felt back to normal (save a lot of deja vu).
All of this was different from DXM trips prior to being on Prozac.

---------------------------------------------------------------------------

I had a very powerful -- and in some respects bad -- trip on 8oz of Robo
Maximum Strength.  After drinking the entire bottle, I started with the
usual Robo trip.  After about two hours, though, my vision continued to
get more and more dissociated, and eventually I found it easier to ignore
it than to try and figure out what I was seeing.  For the next two hours,
i.e., from 2 to 4 hours into the trip, I basically sat around a lot and
watched geometric, cartoon-like hallucinations.

About four hours in, though, I began to get an ever-increasing sense of
dread.  At first I felt maybe I was dying -- that my heart rate was too
high, or too low -- but then I realized that physically I was fine, I
was just scared.  And I started to feel really uncomfortable about myself,
and then I began to remember things which had previously been hidden
from my memory.  It was like all of my memories were in a box, and the
box was being shaken violently.  Everything was swirling about inside
my head.
For the next hour (hour 4 to hour 5) I began to lose myself, and got to
the point where I didn't know who I was or where I was.  The person who
was with me had to get me to recite my name, where I lived, that sort
of thing.  I wouldn't talk except in this drumbeat rhythm, and everything
I heard and saw fit that rhythm.
When I started to come down, I realized that all these things I'd forgot
about -- intentionally or not -- were now right in front of me -- I was
remembering them and seeing them as if they were happening.  It was not
a very fun experience, but I guess it was good for me.  It felt like I
was being shown bits and pieces of me I'd tried to hide away.  I finally
came down enough to sleep about 8 hours after dosing.
The whole next day I felt incredibly free, alive.  I felt like this big
heavy weight had been lifted off my shoulders.  I don't know if this
was because I'd remembered and confronted these painful memories, or if
it was because of the drug.

---------------------------------------------------------------------------

What it can do in very large doses for those who allow it, is A) reset a
person's psyche back to that of a baby's (or an animal's); and B) open up
a link with the spirit world (another dimension).
I'm up to 40 gels (30mg or 1200 per trip) per day (or every other day).
I've since passed the hallucination stage, and it's pretty much white
light proper, and no more of that endless infinity stuff.
I certainly don't tell people (other than a few on the net) about this
stuff, and I don't recommend it in the kind of doses I do. I've had maybe
5 out of 300 trips go slightly bad.  Usually these happened when I was in
need of sleep.  Essentially I lost my core identity and was basically fair
game for whatever entity wanted to possess my being.  This also bought
grand delusions of making me think a lot of stuff was happening that
really wasn't (even though I was sitting in a chair the whole time).
I used to meditate a lot, and I'm sure that is why I've had such great
success with this stuff -- it is really a drug that forces one to stay in
the moment if it is to be enjoyed properly.  Oh, and I used to take acid
alot, so that also did a good job of lubing my mind.
Anyways, I'd probably sum-up the effect by saying it causes unused brain
cells to be accessed by the conscious mind.  Cells which are strongly
linked to creativity and pure animal senses.  And what gets blocked out
is all the worry-type thinking stuff.
And far as damage goes ............... I have noticed that if I don't
take it for a couple days, I feel these sudden momentary spurts of being
pulled to an unconscious state.  It is as if all these new areas of my
brain that I've opened-up are now being closed down when the dxm
catalyst is removed.  Pretty scary.
I also find that it works best with a glass of wine or three and two beers
before starting.  Also a just barely empty stomach preceded by a meal with
lots of fresh vegtables (minerals) before hand.  And then ingesting the
1200 mg over a two hour span and drinking lots of water and eating a few
carbos along with them.  Then after eating the 40, a small meal is great,
with more carbos and a *little* protein.  Oh, and potassium supplements at
the start also makes the body willing to "tough-out" the trip.

---------------------------------------------------------------------------

As the result of a car accident, my friend had a freak stroke at the age of
18.  (The circumstances which casued the stroke are too long and complicated
to explain here.)  The stroke left him with minimal control of his left arm
and a permanent blind spot in a portion of his left eye.  One night, over
three years after his stroke, he decided to try dextromethorphan with a
group of friends.  He drank 5 ounces of generic "tussin" (300 mg of
dextromethorphan hydrobromide.)  Although he consumed less syrup than the
rest of us, the drug effected him more than anyone else in our group.  In
addition to experiencing extreme de-personalization, he reported active
hallucinations in his blind spot.  He could only describe these hallucina-
tions as "cartoon-like."  It was the first time images had appeared in this
spot since his stroke.  Although these "cartoons" diminished over time and
are now gone, they persisted for several days.
My friend did not like the experience and said that he would probably not
try DM again.  Despite his stroke, my friend is a normal, intelligent guy
who does not seem prone to "bad" trips.  He enjoys mushrooms and marijuana.
Neither of these drugs produce any activity in his blind spot, nor do they
have the de-personalizing effect of DM.

---------------------------------------------------------------------------

When I was in H.S., a bunch of friends of mine used to sit around in a
hotel room and drink 4oz bottles of Vicks Formula 44 -- they called it
"Robo-ing".  Actually, they had an entire language of words that they
only used when they were on dextromethorphan.  Like "pattern" for
dialing a phone -- because they couldn't remember the numbers, only the
pattern your finger made.  And getting the "telephones" -- the urge to
call all sorts of people -- or the "curiosities" -- the urge to go
around trying new things.  They also would have these group "dream
vacations" to places -- they all could talk about where they were
tripping to and see it as if they were really there.

---------------------------------------------------------------------------

    I first heard of the recreational properties of DXM (I will refer to
it by its slang name among my circle of users "Tussin", and its verb form,
to tuss) from a friend while I was in my first year of college, 1989.  I
tried it when I had no access to LSD and was antsy for such an experience.
I enjoyed mild dosages, and went on to Tuss about thirty more times over
the next three years.  I have not used Tussin in the last couple years.
Almost every time that I have tussed, I have taken the Robitussin DM or
its generic analog, because that was the type that was first recommended
to me {NOTE: AVOID THESE PRODUCTS AS THEY CONTAIN GUAIFENESIN, WHICH CAN
CAUSE VOMITING AT HIGH DOSAGES}.  I have used Comtrex tablets once in a
DXM dosage equivalent to 4oz of Tussin.
    Rather than bore you with anecdotes of actual times that I tussed,
I'll try to describe my overall experience with it.  Since my experience
has generally fallen into the areas that you described in your article,
with slight variations, I will describe what I feel to be a big
difference in side effects.  This probably is due to the fact that I
usually took other ingredients along with the DM.  I always noticed a
very strong and not pleasurable effect in my sense of touch. It begins
about fifteen minutes after the onset and continues after the peak of the
trip, but is usually gone and forgotten by about three hours into it.
The effect is that of hot flashes, localized to parts of my body.  Face
and hands are the main targets, especially the scalp for uncomfortable
feelings of heat.  My hands always feel swollen and hot and itchy during
this time.  luckily the euphoria allows one to successfully ignore this
irritation.
    Another interesting effect in conjunction with alcohol: I've noticed
that several different types of cough and cold medicine-- all that I've
tried have contained DXM, but I'm not sure if it is the causitive agent
here-- increase alcohol tolerance dramatically, about 2X.  I was visiting
my parents and had a cold, and was taking Comtrex with DM and Nyquil and
Vicks 44 at various times.  I hadn't been drinking en masse in a long
time, so I expected very low tolerance.  But while I was on the cold
medicine, I could really drink all of my sodden alcoholic friends from
high school under the table.  The effect of the drunk was very different
too.  I was extremely lucid.  When I get drunk, I often forget the finer
details of an evening: points of conversation, fights, arson, tattoos,
but that week, I was mentally alert, though euphoric and balance impaired
as normal heavy drinking would impart.  This is at about one to two times
the normal dosage, just what I was using to beat down the cold.
    After a few times trying to do things which one does on other
hallucinogens, walking around, finding adventure, ritual sacrifice, that
sort of thing, I tried to sleep right after a peak, and I came across what
I feel is the best method of tussing.  I have always taken 4-6 oz of the
syrup, and at that time, I was getting bored with the effects, which
weren't hallucinogenicly powerful enough to warrant trying to function,
because balance was so strongly affected.
    I discovered that the most pleasurable way to experience the drug was
to lie still and close your eyes and play music.  It reminds me quite a
bit of shamanic style meditation, except that tussin has the dual effect
of making physical relaxation and bodily detachment much easier, plus it
keeps you awake much longer.  Lights are kept low to off, perhaps candle,
incense, and tunes, preferably very loud.  There is really no guide to
which albums to play.  Generally it seems good to do it with a friend,
and you alternate picking albums. . . We once followed XTC Skylarking with
Black Sabbath's Heaven and Hell. . . I think anything striking and
thematic is acceptable.  None of this REM radioplay crap.
    The hallucinations were extremely vivid and not really dreamlike in
that there was not really participatory action, more like cartoons
presented very vividly.  It seems many of them appeared as if the
observer was going down a tunnel extremely fast and these vivid images
were flashing by.  Morphing of images, especially with a loss of
proportion, was very common, so that there seemed to be a connectivity
and constant motion to the visions.  Three to four hours of this was the
usual duration, I believe.  I have had a similar effect when smoking very
large amounts of pot before, but usually can't stay awake.  Attempts at
combining pot with tussin were foiled by lungs made sensitive by the
tussin.  I could remember most of the strong images, perhaps better than
a dream, but the memories faded with time.  The same images seemed to
recur throughout the tussin trip, and I believe those are the ones that
stuck in my memory the longest.
    The last thing which I would like to mention is one of the visual
hallucination properties.  I have noticed that with many hallucinogens,
there is the property of tracers and afterimages, especially with images
that move.  The end of a cigarette is a good example.  During the peak
time of the tussin trip, visuals are very odd.  For one, light is almost
intolerable.  The oddest part is "block tracers" when you look in the
same general direction for more than one minute or so, then shift your
vision, the block of vision that is centermost in your field of view is
transferred to the new field of view, and dissolves into the background.
On top of this, the peripheral part of your vision has fairly strong
tracers, which can be very confusing if you are trying to be mobile,
especially with the utter lack of balance involved.  This is noticed in
me at four to six ounces.

---------------------------------------------------------------------------

  I have in the past toyed around with 4-6oz of liquid Tussin, Robo, etc with
and without guaifenesin (sp?).  My experiences were interesting and fun, but
nothing as moving as taking two boxes of 10 Drixoral Cough Caps.  Last Friday,
I decided to go for broke and take 2 boxes.
  I started my journey about 8pm.  Finished the pills in a span of about 30
minutes.  About 30-45 minutes later, I started feeling the familiar effects of
drowsiness.  I decided that it would be best to get out and do something
before I fell asleep and wasted my time.  It was about 9:00, so I went to my
favorite alternative club where there was an awesome "mind candy" band called
Mindseye playing.  There weren't more than 20 people in the club including the
two bands that were playing.  I just kicked back in a booth, closed my eyes,
and went on an internal trip that lasted at least 45 minutes, although it felt
like hours.  I had a sensation of moving into a higher realm of thought.  I
was so focused on the music that it became a part of my consciousness and my
being.  Openeing my eyes just became a letdown because it reminded me that I
was in reality. :)  So I just closed them again and enjoyed the phosphenes
that were running rampant through my brain.  The only part I didn't like was
the feeling of being in a Doom game without the monsters.  I felt like I was
running through the corridors and riding the elevators.  Oh, well.  Nobody
promised that it would be COMPLETELY enjoyable.  Anyway, after the set, I went
to the bar to order a Miller Lite.  The barkeep said that they didn't have
Miller Lite.  I asked for Coors Light.  He said he didn't have Coors Light.
[blank stare with severely dilated pupils]  "What light beers do you have?"
"Lite."  "Lite?" "Lite."  "Lemme have that, then"  "$1.50" ("Hey, great
price", I thought)  It was Miller Lite.  Oh, well.  It felt like I was arguing
for 30 minutes.  Gawd, I hate interacting with people in that condition.  I
staggered back to my booth (at least it FELT like staggering ... it felt
REALLY weird to walk) and sipped my beer while watching the band take down
their equipment.  They looked like a bunch of worker bees from my perspective,
and is was really interesting to watch.  Drinking was an unusual experience,
too.  It was like the first time I had ever drunk anything.  All my movements
were very slow, methodical, and calculated.  After I finished my beer, I went
down to a techno club I had been meaning to visit.  It was about midnight.
I know that this is a big lapse in time.  I guess I wasted 2 1/2 hours in that
bar listeneing to the jukebox and watching the band.  It was only 4
blocks, but the way my legs were moving, it felt like I was walking
stiff-legged the whole way.  Fortunately, it was a slow night on my city's
version of Bourbon St., and I only passed about 5 people on the way.  The
doorman was the next big hurdle.  Actually, I managed to keep myself fairly
composed.  He warned me that it was kinda slow, and I went into a repeat of
the beer discussion.  "Slow?" "Slow." "Okay." (trying to avoid giving myself
away, even though my pupils filled my eyeballs)  I handed him the two bucks he
asked for and walked in.  I found an empty couch and plopped down.  It was
heavily padded and had a low back.  Perfect for slouching.  The DJ was playing
a fantastic mix of techno and classic rock.  As the night wore on, she was
playing almost constant techno.  They have a light show that is really
something to be seen.  The dance floor is surrounded by mirrors that reflect
the blue lights from the bar and make it look like a cityscape from the year
2020.  VERY impressive in my condition.  The only times I got up were to go to
the john twice and to the bar once for water.  Walking got stranger and
stranger.  I think I was having trouble keeping my balance, but I don't
remember staggering.  The worst part was the feeling that I was choking on my
uvula.  My mouth felt dry, and water wasn't helping.  It must have been the
anaesthetic effects of DXM.  I stayed there for two hours in the same spot
only moving the three times I mentioned.  I was still not bored, but I figured
that since it was 2am, it was about time to get home.  This may have been a
mistake.  The streetlights had started tracing, and the blinking lights were
playing hell on my perception.  In retrospect, I probably shouldn't have
driven home, but I was broke, so a cab was out of the question, and there was
no way I could have sobered up.  I didn't feel drunk.  It just felt like all
my surroundings were foreign.  I payed extra-close attention to my driving,
but still nearly jumped out of my skin at the sight of police.  I got home in
one piece and fell asleep to the mellow sounds of Pink Floyd's Ummagumma disc
2.  I woke up around 9:30am, fully alert.  Checked my eyes.  Fully dilated.
Made an excuse to get out of the house, wearing shades.  Went to see a movie
with a friend, which was pretty fun.  I was still feeling a bit weird.  The
dark theater helped me relax.  Got out of the movie and went home.  My eyes
were normal by this time, although I still felt a little strange.  That
feeling lasted until about 7pm.  So the brunt of the trip laster about 12
hours and the after-effects lasted another 11.  WOW!

------------------------------------------------------------------------------

took my 1st dosage of DM friday night, the gelcaps, 600 mg. took 'em
at 8:30 with a friend, walked around till about 11:00, neither of
us was feeling anything and i was *most* disappointed. i caught a
train back to my house, and in the station waiting to change trains
it started to hit *hard*. i was hanging out alone in the station,
hacky-sacking, and the walls started to bend to greet me. by the
time i got to my local station, things were getting pretty intense.
i *floated* home, as far as i could tell at the time. two hours
later i was hanging out with a bunch of friends, one of whom was
also on. i was warm, i was fuzzy, i loved everyone, and i was
directly aware of being a higher being making its temporary abode
in this body and this mind. oh; and i *itched* like nobody's
business. anyone else had this? i forgot a lot of things on my
way down, but based on what i did bring back i think that the
forgetting was because the normal ego-bound me couldn't have
understood too much of what was happening. i realize i'm raving
pretty thoroughly about it, but i haven't had this life-changing,
life-affirming of an experience since  my first couple of LSD
trips many many years ago. in short, i was *impressed*, and i want
to use it again just a couple of times, to open up the kind of
intense spiritual communication that it made possible with a couple
of the people in my life.

------------------------------------------------------------------------------

One of my favorite effects of Robo is its annihilation of short-term
memory, which has the excellent side-effect of destroying
self-identity.  You just sort of forget who you are.. This seems to
happen at the 700+mg level, not much lower than that.  It's more
pleasant than anything else, even though it sounds kinda scary at
first..

------------------------------------------------------------------------------

i went down to the lake one saturday morning and took a few boxes of
drixoral cough liqui-caps.  invited some friends along, but nobody
could come with me, so i took ALL the little motherfuckers.  i walked
along the side of the lake for a few miles, not feeling any major
effects yet.  then, suddenly, it hit.
i felt very dizzy, and very out of place.  i couldn't walk so i sat
down on a park bench.  it was foreign... here i was on a park bench in
some strange place, with everything spinning around me.  cars hissed
by on lake shore drive, seem like some kind of deadly monster, or
dangerous presence.  i was very confused & decided to walk back.  it
was hard to walk when everything was twisting in strange directions,
but i made it all the way down to where there was a tree in the sand.
(i'm not sure if there really WAS a tree there, but at the time there
seemed to be).  walked down to the tree and collapsed beneath it.
looking at the sky thru its branches, the cars seemed very far away.
it was somehow very comforting... sky & sand & tree & me, everything
else seemed distant & unimportant.  wanted to stay there, but after a
while (minutes or hours -- sense of time totally gone) i got up and
went on.  a mile or so further i sat down on a rock looking out on the
water.  the patterns of the light on the water were endlessly
fascinating, & when i closed my eyes i vividly saw a field of flame,
wild naked girls running thru it, somehow unharmed by the flame
because they were just a part of the flame, & i was a part of the
flame, & everything was unified in the flame.  when i opened my eyes,
all i saw was water... after a while of experiencing the fire world &
the water world i got up & decided to crawl home.  i was very paranoid
of getting hit by a car but somehow i made it.  realized i was getting
dehydrated (which might have been causing some of the delerium) so i
drank something.  then i sat down on the couch... & realized that
maybe i wasn't on the couch at all, i was still on the rock on the
beach & this whole thing had been a very strange hallucination.  for
the next few hours i was sure that's what was going on, & kept
expecting to open my eyes...
finally things returned more or less to normal.  later that night
there were some kind of weak residual visuals (fireworks)...
who knows? maybe i still AM on that rock...

------------------------------------------------------------------------------

    Robo is a much more mental trip. When your stoned you can say "Whoo
man I am fucked up..." With dex (dextromethorphan that is) you almost
can't tell that its a chemical making you feel good. Its very subtle but
strong at the same time. You just feel excellent. You feel free and
everyone around seems so nice. Music can become something more then just
music.  On one trip I was in a coffehouse and it felt like I was swimming
in a wild rushing torrent of musical notes. One of the most pleasurable
experiences of my life. I do not get that empty headed feeling I get with
pot. It also lasts much longer (for me, I know people that pot lasts
longer for them). Off 6 ozs or so I can get 6 to 8 eight hours of
incredible and intense tripping. For everyone who hasn't tried it, trust
me it is not a cheap buzz. Drinking 6 ozs can be one of the funnest things
you can do.

---------------------------------------------------------------------------

I ate 25 Vick's gel caps containing 30mg of DM each friday night at about
10:30pm. i was up until 11 the next morning, and fried until about 7am. it
didn't help that the gelcaps also had pseudoephedrine in them, of course.
but it was fantastic. i stayed up at a party with two other stoned guys
'till 6am. it's very comforting to just listen to someone talk when on
robo, and one guy talked for about 5 hours straight. it was fantastic. i
was in another world, and really uncoordinated. it's difficult to describe,
but sort of like mushrooms without the visuals or emotional surges. you're
out of it but you can still function, sort of. plus you can smoke like a
fiend and not feel a thing, so you can indulge your nervous habits. but
every physical movement was a labor. maybe kind of like being a bit
right-brain impaired. definitely recommended. you can steal packs of gel
caps easily from any large grocery store. just stay away from the
guafenisen, or however you spell it. it's hard to keep down and only gets
in the way. i've also eaten Delsym with polystirex - it's not as intense,
but then i only drank one bottle. might want to try two.

---------------------------------------------------------------------------

Let me provide my testimonial about roboing.  Yesterday I picked up an
8 oz. bottle of generic brand extra-strength cough syrup, containing
only Dextro as its active ingredient.  I immediately downed somewhere
under 4 oz. of the stuff. Taste wasn't as bad as I expected. Chugged a
good deal of water to wash it down anyway, and nibbled on some bread.
Nausea was not a problem at all.

About an hour later it started to hit. Motor skills were definitely
impaired. Pupils were very large. I felt like I was on shrooms, but
without mood-alterations or significant visuals. Television images
appeared to be moving in slow motion like when on acid. Unlike what
I've heard posted here, music did not sound very interesting. This was
a big disappointment since claims to the contrary were what convinced
me to give it a try.  I did not feel particularly euphoric or bad.  My
mood was essentially an unchanged neutral, which was wierd since in
other respects I was definitely "tripping". I kept saying to myself,
"OK, the good part of the trip should be coming soon..." but it never
did!

Walking was definitely difficult, although mental functioning seemed
to be OK. I carried on many conversations with little difficulty, in
contrast to my experiences with shrooms and 'cid. I was hoping the
amount I consumed would be a mild dose, but I must say I was
significantly affected. I can't imagine what would have happened if I
finished the bottle! It's now 16 hours after the initial consumption.
I slept fine last night, but I still feel the effects. My pupils are
still huge and I still feel like my motor skills are
impaired. (I'm typing much slower now than my usual 100 wpm.).
Is this usual for these effects to persist for so long? It's kinda
a pain because I have work to do! Wierd body chemistry I guess.
In short, I guess it was worth the experience but I can't see any
reason to try it again. It's lasting longer than any shroom or acid
trip I've ever had, and it just ain't nearly as much fun. I'll stick
with pot thank you.

---------------------------------------------------------------------------

There seems to be a line with ppl I have talked with at about 5 ozs, 4 for
smaller females.  After this line, you REALLY trip, before, youre just
fucked up, i.e. motor skills, mild hallucinations.
I generally recommend going for the big dose if you're gonna do it at all,
and if you can swing it (and want to) a little mj and some whippets add
wonderfully.
Now, for the day after, I always feel drugged for a day, but usually it
feels ok, i just can't do complicated mental thinking (i.e. coding).
One of my friends said she felt like a zombie for about 3 days, but
1 day recovery seems to be the norm for everyone else.

---------------------------------------------------------------------------

On Robo if you have a bad trip, it doesn't really do anything bad, it
just doesn't do anything. I find that how my trip is has alot to do with
where I am and most IMPORTANTLY who I am with. People you don't like can
cause your robo trip to go right down the drain.

---------------------------------------------------------------------------

Many of the descriptions of the actual effects were really on-target,
especially the reference to cognitive abilities as if in a febrile state
-- i've often thought of the sensation as a fever dream more than anything
else, especially with the depth perception distortion, which was uncannily
similar to several episodes of fever I had (When I was younger, the
thought of everything being larger and more ominous than it actually was
never even came CLOSE as a pleasurable sensation, in fact, it scared me
SHITLESS. :)

---------------------------------------------------------------------------

<7>     References

1   "Abuse of over-the-counter dextromethorphan by teenagers."  Murray-S,
    Brewerton-T.  South-Med-J.  1993 Oct; 86(10): 1151-1153.

2   "Alcohol, nitric oxide, and neurotoxicity: is there a connection?--a
    review."  Lancaster-FE.  Alcohol-Clin-Exp-Res. 1992 Jun; 16(3): 539-541

3   "Activation of glutamate metabotropic receptors induces long-term
    potentiation."  Bortolotto-ZA; Collingridge-GL.  Eur-J-Pharmacol.
    1992 Apr 22; 214(2-3): 297-298

4   "Alterations in phencyclidine and sigma binding sites in schizophrenic
    brains. Effects of disease process and neuroleptic medication."
    Simpson-MD; Slater-P; et al.  Schizophr-Res. 1991 Dec; 6(1): 41-48

5   "Biologically active MK-801 and SKF-10,047 binding sites distinct from
    "those in rat brain are expressed on human lung cancer cells."
    Maneckjee-R; Minna-JD.  Mol-Biol-Cell. 1992 Jun; 3(6): 613-619

6   "Characterization of [3H]desmethylimipramine binding in bovine adrenal
    medulla: interactions with sigma- and (or) phencyclidine-receptor
    ligands."  Rogers-C; Lemaire-S.  Can-J-Physiol-Pharmacol. 1992 Nov;
    70(11): 1508-1514

7   "Chronic administration of NMDA antagonists induces D2 receptor
    synthesis in rat striatum."  Micheletti-G; Lannes-B; et al.  Brain-
    Res-Mol-Brain-Res. 1992 Aug; 14(4): 363-368

8   "The combination of NMDA antagonism and morphine produces profound
    antinociception in the rat dorsal horn."  Chapman-V; Dickenson-AH.
    Brain-Res. 1992 Feb 28; 573(2): 321-323

9   "A comparison of (-)-deoxybenzomorphans devoid of opiate activity with
    their dextrorotatory phenolic counterparts suggests role of sigma 2
    receptors in motor function."  Walker-JM; Bowen-WD; et al.  Eur-J-
    Pharmacol. 1993 Jan 26; 231(1): 61-68

10  "Dextromethorphan alters cerebral blood flow and protects against
    cerebral injury following focal ischemia."  Steinberg-GK; Lo-EH; et
    al.  Neurosci-Lett. 1991 Dec 9; 133(2): 225-228

11  "Dextromethorphan. An overview of safety issues."  Bem-JL; Peck-R.
    Drug-Saf. 1992 May-Jun; 7(3): 190-199

12  "Dextromethorphan antagonizes the acute depletion of brain serotonin
    by p-chloroamphetamine and H75/12 in rats."  Henderson-MG; Fuller-RW.
    Brain-Res. 1992 Oct 30; 594(2): 323-326

13  "Dextromethorphan protects against the neurotoxic effects of p-chloro-
    amphetamine in rats."  Finnegan-KT; Kerr-JT; et al.  Brain-Res. 1991
    Aug 30; 558(1): 109-111

14  "Effects of 8-hydroxy-2-(di-n-propylamino)tetralin, a selective
    agonist of 5-HT1A receptors, on the cough reflex in rats."  Kamei-J;
    Mori-T; et al.  Eur-J-Pharmacol. 1991 Oct 15; 203(2): 253-258

15  "Effects of ketamine on sensory perception: evidence for a role of
    N-methyl-D-aspartate receptors."  Oye-I; Paulsen-O; et al.  J-
    Pharmacol-Exp-Ther. 1992 Mar; 260(3): 1209-1213

16  "Evidence for distinct phencyclidine and SKF10047 receptors following
    detergent treatment of rat brain membranes."  Grynne-BH; Holmen-AT;
    Maurset-A.  Pharmacol-Toxicol. 1992 Jan; 70(1): 25-30

17  "Excitatory amino acid receptors and disease."  Meldrum-BS.  Curr-
    Opin-Neurol-Neurosurg. 1992 Aug; 5(4): 508-513

18  "Fatal intoxication by dextromethorphan: a report on two cases."
    Rammer-L; Holmgren-P; Sandler-H.  Forensic-Sci-Int. 1988; 37: 233-236

19  "GABAA and NMDA receptor function during chronic administration of
    ethanol."  Sanna-E; Serra-M; et al.  Adv-Biochem-Psychopharmacol.
    1992; 47: 317-324

20  "GABA- and glutamate-gated ion channels as molecular sites of alcohol
    and anesthetic action."  Weight-FF; Aguayo-LG; et al.  Adv-Biochem-
    Psychopharmacol. 1992; 47: 335-347

21  "High-affinity dextromethorphan and (+)-3-(-3-hydroxyphenyl)-N-(1-
    propyl)piperidine binding sites in rat brain.  Allosteric effects of
    ropizine."   Klein-M; Musacchio-JM.  J-Pharmacol-Exp-Ther. 1992 Mar;
    260(3): 990-999

22  "Human macrophages convert L-tryptophan into the neurotoxin quinolinic
    acid."  Heyes-MP; Saito-K; Markey-SP.  Biochem-J. 1992 May 1: 283 (Pt.
    3): 633-635

23  "Identification of a novel N-methyl-D-aspartate receptor population in
    the rat medial thalamus."  Beaton-JA; Stemsrud-K; Monaghan-DT.  J-
    Neurochem. 1992 Aug; 59(2): 754-757

24  "Induction of phencyclidine-like behavior in rats by dextrorphan but
    not dextromethorphan."  Szekely-JI; Sharpe-LG; Jaffe-JH.  Pharmacol-
    Biochem-Behav. 1991 Oct; 40(2): 381-386

25  "The involvement of sigma and phencyclidine receptors in the action
    of antipsychotic drugs."  Lang-A; Vasar-E; et al.  Pharmacol-Toxicol.
    1992 Aug; 71(2): 132-138

26  "The neuroprotective effects of dextromethorphan on guinea pig-
    derived hippocampal slices during hypoxia."   Radek-RJ; Giardina-WJ.
    Neurosci-Lett. 1992 May 25; 139(2): 191-193

27  "Interactions of sigma and phencyclidine receptor ligands with the
    norepinephrine uptake carrier in both rat brain and rat tail artery."
    Massamiri-T; Duckles-SP.  J-Pharmacol-Exp-Ther. 1991 Feb; 256(2):
    519-524

28  "Involvement of haloperidol-sensitive sigma-sites in antitussive
    effects."  Kamei-J; Iwamoto-Y; et al.  Eur-J-Pharmacol. 1992 Nov 24;
    224(1): 39-43

29  "The involvement of NMDA receptors in acute and chronic effects of
    ethanol."  Danysz-W; Dyr-W; et al.  Alcohol-Clin-Exp-Res. 1992 Jun;
    16(3): 499-504

30  "Is quinolinic acid an endogenous excitotoxin in alcohol withdrawal?"
    Morgan-PF.  Med-Hypotheses. 1991 Oct; 36(2): 118-121

31  "The learning capacity of high or low performance rats is related to
    the hippocampus NMDA receptors."  Keller-EA; Borghese-CM; et al.
    Brain-Res. 1992 Mar 27; 576(1): 162-164

32  "Mania and Cough Syrup" [letter]  Schadel-M, Romach-MK, Sellers-EM.
    J Clin Psychiatry 1993 May 54(5): 200

33  "Mapping rat brain structures activated during ethanol withdrawal:
    role of glutamate and NMDA receptors."  Morgan-PF; Nadi-NS; et al.
    Eur-J-Pharmacol. 1992 Mar 12; 225(3): 217-223

34  "MK-801, a non-competitive antagonist of NMDA receptor, prevents
    methamphetamine-induced decrease of striatal dopamine uptake sites in
    the rat striatum."  Muraki-A; Koyama-T; et al.  Neurosci-Lett. 1992
    Feb 17; 136(1): 39-42

35  "MPTP lesions of the nigrostriatal dopaminergic projection decrease
    [3H]1-[1-(2-thienyl)cyclohexyl]piperidine binding to PCP site 2:
    further evidence that PCP site 2 is associated with the biogenic amine
    reputake complex."  Akunne-HC; Johannessen-JN; et al.  Neurochem-Res.
    1992 Mar; 17(3): 261-264

36  "Neurochemical characterization of dopaminergic effects of opipramol,
    a potent sigma receptor ligand, in vivo."  Rao-TS; Cler-JA; et al.
    Neuropharmacology. 1990 Dec; 29(12): 1191-1197

37  "NMDA receptors in sensory information processing." Nelson-SB; Sur-M.
    Curr-Opin-Neurobiol. 1992 Aug; 2(4): 484-488.

38  "PCP and sigma receptors in brain are not altered after repeated
    exposure to PCP in humans."  Weissman-AD; Casanova-MF; et al.
    Neuropsychopharmacology. 1991 Feb; 4(2): 95-102

39  "Pharmacological characterization of sigma binding sites in guinea pig
    brain membranes."  Karbon-EW; Enna-SJ.  Adv-Exp-Med-Biol. 1991; 287:
    51-59

40  "Pharmacologic properties of NMDA receptors."  Mayer-ML; Benveniste-M;
    et al.  Ann-N-Y-Acad-Sci. 1992 May 11; 648: 194-204

41  "Phencyclidine and auditory sensory gating in the hippocampus of the
    rat."  Miller-CL; Bickford-PC; et al.  Neuropharmacology. 1992 Oct;
    31(10): 1041-1048

42  "Poliovirus induces indoleamine-2,3-dioxygenase and quinolinic acid
    synthesis in macaque brain."  Heyes-MP; Satio-K; et al.  FASEB-J. 1992
    Aug; 6(11): 2977-2989

43  "Primary and secondary oxidative metabolism of dextromethorphan.  In
    vitro studies with female Sprague-Dawley and Dark Agouti rat liver
    microsomes."  Kerry-NL; Somogyi-AA; et al.  Biochem-Pharmacol. 1993
    Feb 24; 45(4): 833-839

44  "Pretreatment with NMDA antagonists limits release of excitatory
    amino acids following traumatic brain injury."  Panter-SS; Faden-AI.
    Neurosci-Lett. 1992 Mar 2; 136(2): 165-168

45  "Previous chronic blockade of NMDA receptors intensifies morphine
    dependence in rats."  Koyuncuoglu-H; Aricioglu-F.  Pharmacol-Biochem-
    Behav. 1991 Jul; 39(3): 575-579

46  "Psychosis with Vicks Formula 44-D abuse."  Craig-DF.  Can-Med-Assoc-J
    1992 Apr 1; 146(7): 1199-1200

47  "Receptors coupled to ionic channels: the glutamate receptor family."
    Gasic-GP; Heinemann-S.  Curr-Opin-Neurobiol. 1991 Jun; 1(1): 20-26

48  "Regionally selective deficits in uptake sites for glutamate and
    gamma-aminobutyric acid in the basal ganglia in schizophrenia."
    Simpson-MD; Slater-P; et al.  Psychiatry-Res. 1992 Jun; 42(3): 273-282

49  "Repeated methamphetamine-treatment alters brain sigma receptors."
    Itzhak-Y.  Eur-J-Pharmacol. 1993 Jan 12; 230(2): 243-244

50  "Serotonin release in nucleus of the solitary tract and its modulation
    by antitussive drugs."  Kamei-J; Mori-T; et al.  Res-Commun-Chem-
    Pathol-Pharmacol. 1992 Jun; 76(3): 371-374

51  "Sigma receptors are associated with cortical limbic areas in the
    primate brain."  Mash-DC; Zabetian-CP.  Synapse. 1992 Nov; 12(3):
    195-205

52  "Sigma receptors in schizophrenic cerebral cortices."  Shibuya-H;
    Mori-H; Toru-M.  Neurochem-Res. 1992 Oct; 17(10): 983-990

53  "The treatment of a chronic organic mental disorder with dextromethor-
    phan in a man with severe mental retardation."  Welch-L; Sovner-R.
    Br-J-Psychiatry. 1992 Jul; 161: 118-120

54  "Toxicological findings in a death involving dextromethorphan and
    terfenadine."  Kintz-P; Mangin-P.  Am-J-Forensic-Med-Pathol. 1992 Dec;
    13(4): 351-352


55  _AHFS Drug Information_.  McEnvoy, GK (editor).  ASHP Inc. 1993
    (Bethesda).

56  _Drugs and Drug Abuse_.  Jacobs, MR; Fehr, KO.  1987 (Toronto).

57  _Evaluations of Drug Interactions_.  Shinn, AF (editor).  Macmillan,
    1988 (NY).

58  _Meyler's Side Effects of Drugs_.  Dukes, MNG (editor).  Elsevier,
    1992 (Amsterdam).

59  _USAN and the USP Dictionary of Drug Names_.  Fleeger, CA (editor).
    USP Convention Inc. 1993 (Rockville).