About
Community
Bad Ideas
Drugs
Booze - The Legal Drug
Legal Issues of Drug Use
Marijuana
Miscellaneous Drug Information
Nitrous
OTC Drugs and Household Items
Psychedelics
Rare and Exotic Drugs
Speedy Drugs
Ego
Erotica
Fringe
Society
Technology
register | bbs | search | rss | faq | about
meet up | add to del.icio.us | digg it

DEXTROMENTHORPHAN FAQ 2.2 (12/94)


NOTICE: TO ALL CONCERNED Certain text files and messages contained on this site deal with activities and devices which would be in violation of various Federal, State, and local laws if actually carried out or constructed. The webmasters of this site do not advocate the breaking of any law. Our text files and message bases are for informational purposes only. We recommend that you contact your local law enforcement officials before undertaking any project based upon any information obtained from this or any other web site. We do not guarantee that any of the information contained on this system is correct, workable, or factual. We are not responsible for, nor do we assume any liability for, damages resulting from the use of any information on this site.
Newsgroups: alt.drugs,alt.drugs.psychoactives
From: bwhite@oucsace.cs.ohiou.edu (William E. White )
Subject: FAQ-Dextromethorphan 2.2 (last modified 12/1/1994)
Message-ID: <D0D1z1.A4E@oucsace.cs.ohiou.edu>
Date: Mon, 5 Dec 1994 23:16:12 GMT


The Dextromethorphan FAQ

William White

Release 2.2, December 1994





This is a fairly comprehensive list of questions and answers relating
to the recreational and medical use of dextromethorphan, a cough
suppressant in common use in over-the-counter (non-prescription) cough
formulae. The contents of this file is copyright (C) 1994 by William
White. This is version 2.2, the second release version, first
revision, dated 12/1/1994.

This file may be freely reproduced, subject to the following
limitations:
1) Part 2 may not be distributed without Part 1. In physical
distribution, this means both parts must be distributed together.
In Internet, Usenet, BBS, or other electronic distribution, it
means both files must be distributed to the same audience within
1 day of each other.
2) Electronic distribution must be in either plaintext or
PostScript[TM] format. For information pertaining to other
formats, please contact me.
2) This file may be cited as:
White, William E. (1994) The Dextromethorphan FAQ. Usenet
alt.drugs, alt.psychoactives. Available via HTTP in HTML format
at http://oucsace.cs.ohiou.edu/personal/bwhite/DXM.html
3) As I do not wish my motives to be misrepresented, no citation or
quotation of this document may be used so as to explicitly or
implicitly suggest that I am in favor of the illegal use of any
drug (legal or not), or any other illegal activity, subject to
USA law.
4) No modified version of this document may be distributed. No prior
version may be distributed once a new current version has been
released.

Any questions or comments may be addressed to me:

Email: bwhite@oucsace.cs.ohiou.edu (finger for PGP2.2 block)
US Mail: William White / 44 Canterbury Dr. / Athens OH 45701 USA
Phone: (USA) 1-614-594-3434 (10:00 - 21:00 Eastern Standard Time)

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 recommendation, 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.

Any data sent PGP encoded will be decoded on my private system (MS-
DOS) which is offline. After decoding, all information regarding the
sender's identity is overwritten (200 pass random pattern). Thus I
cannot link testimonials or information to senders after this
operation. Note that my system is NOT TEMPEST SECURE (not that I've
noticed any strange vans near my house).

This is part 1/2. Part 2/2 contains: Personal Testimonials;
References.


FAQ OVERVIEW: Part 1/2

<0> Why a DXM FAQ?

<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
<1.10> Are there other non-narcotic cough suppressants?

<2> Psychological Effects of DXM use
<2.1> What is the general character of a DXM trip?
<2.2> What are the effects of a "first plateau" dose?
<2.3> What are the effects of a "second plateau" dose?
<2.4> What are the effects of a "third plateau" dose?
<2.5> Is there anything beyond the third plateau?
<2.6> What are the effects of chronic, high-level use?
<2.7> Why is there so much individual variance in response?

<3> Side Effects and Risks of DXM use
<3.1> What are the side effects and risks of occasional DXM use?
<3.2> What are the side effects and risks of chronic DXM use?
<3.3> How toxic is DXM? What is the LD50? Should I worry?
<3.4> Do you recommend DXM for recreation use?

<4> Physiological Effects of DXM
<4.1> How does DXM inhibit the cough reflex?
<4.2> How does DXM cause its psychoactive effects?
<4.3> Wow, that sure is complicated, isn't it?
<4.4> What happens to DXM after you take it? (Pharmacokinetics)

<5> Sigma, NMDA, and PCP2 receptors, and Ion Channels
<5.1> What is a receptor, anyway? (Basic Neuropharmacology)
<5.2> What are Sigma receptors?
<5.3> What are NMDA receptors?
<5.4> What are PCP2 receptors?
<5.5> What are N+ and Ca2+ channels?
<5.6> How does DXM compare to other drugs at these receptors?

<6> Extraction of DXM from cough formulae
<6.1> How does one ideally extract DXM from cough formulae?
<6.2> How does one extract DXM without access to lab equipment?
<6.3> How does one use the DXM thus extracted?
<6.4> Is this safe?

<7> Interaction of DXM with other recreational drugs
<7.1> Alcohol
<7.2> Barbiturates and benzodiazepines
<7.3> Amphetamines and other psychostimulants
<7.4> Cannabis
<7.5> LSD, psilocybin, and other 5HT hallucinogens
<7.6> Opiates
<7.7> PCP and ketamine
<7.8> Miscellaneous other drugs

<8> DXM Drug Culture
<8.1> Is there, or was there, a DXM drug culture?
<8.2> Why haven't I ever heard about it?
<8.3> Is there a "drug-slang" for DXM?

<0> Why a DXM FAQ?

There is the philosophy among some in the USA (and probably
the rest of the world) that the best way to prevent people from making
mistakes is to withhold information from them. For example, this is
particularly noticeable in the case of sex education, where some
assert that teaching children about sex is equivalent to giving them
permission to have copulate, and that, since no sex is perfectly safe,
and since teenagers especially have a tendency to take risks (e.g., no
birth control), we ought not to teach sex education in the schools.
One might just as easily say that teaching children about cars is
equivalent to giving them permission to drive, and that, since no
driving is perfectly safe, and since teenagers especially have a
tendency to take risks (e.g., racing down Main St.), we ought not to
teach driving education in schools.
This misguided philosophy of "ignorance is strength" is just
as often applied to information pertaining to drug use. In the case
of drug use, however, good information is immediately useful towards
preventing drug-related injuries. In the case of DXM, there are
several possible mistakes people can make, and the chance for making a
mistake is compounded by the fact that people hear "you can get high
off cough syrup" as advertisement for DXM use. At best they are
unprepared for the trip; at worst, they get hold of an acetaminophen-
containing preparation and end up in the hospital or dead.
Make no mistake; this information will probably encourage some
to try, and continue to use, DXM. That is not my intention. A few of
these people may end up addicted, or at least habituated to the point
of trouble. That is certainly not my intention. What is my intention
is to make sure that everyone out there knows what the risks and
effects of DXM use are, so that s/he can make intelligent choices for
herself or himself. An intelligent choice is not always right, but
you always learn from it.
This FAQ sprung out of the Internet newsgroups alt.drugs and
alt.psychoactives, where about 1 or 2 questions a week about DXM would
appear. After responding weekly, or in some cases daily, I decided to
put together all the questions (and a few questions I thought would
follow) and write a full explanation of DXM. Some of the material is
fairly technical, but I thought it better to give too much information
than not enough. It is distributed twice a month (more or less) on
the above-mentioned newsgroups; please distribute it beyond Internet
and Usenet (subject to the restrictions above).
It is my sincere hope that this type of information may help
the Internet fulfill its potential as an information source. Those of
us who have the time and ability to provide good information should
feel obligated to do so; if we set a standard of high signal and low
noise, perhaps others will follow.

<1> General Information

This section covers general information about Dextromethorphan, herein
referred to as DXM. Note the following abbreviations:
CNS Central Nervous System (brain and spinal cord)
CYA Cover Your Ass. Remember this one!
DXM Dextromethorphan
DXO Dextrorphan
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", "green", etc.)
PPA Phenylpropanolamine
3-PPP [3-(3-hydroxyphenyl)-N-(1-propyl)piperidine]

also note that square brackets denote IUPAC names.

PLEASE NOTE that the UK (and European?) name of acetaminophen is
paracetamol. They refer to the same substance.

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/paracetamol
(Tylenol[TM]). Large doses of acetaminophen/paracetamol 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]), OR ANY OTHER PRESCRIPTION, NON-
DROWSY ANTIHISTAMINES (e.g., Claritin[TM] or Hisminal[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 in the USA 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 (1-3).
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 (1-2). 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, acetamino-
phen, 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 brand-name only, and often
contain other active ingredients. Capsule/tablet formulations of DXM
are not usually available in the USA, but are available in Canada
(notably, Contac CoughCaps[TM]).
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 (3). 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 (3-7).
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.
Information is taken from packaging. Note that a 4oz bottle is
approximately 120ml, and an 8oz bottle approximately 240ml).

Preparations containing DXM only: (SAFEST)

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 some bottles.)

Preparations containing DXM and other products: These should be
avoided. There used to be a small list in Part 2/2, but I have
removed it for space reasons. Please see <1.5> below for information
about other ingredients.

<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], has the IUPAC
name [(+)alpha-(1-methylamino)benzyl alcohol]. Phenyleprine is [(-)-
3-hydroxy-alpha-(methylaminomethyl)benzyl alcohol] (1,2).
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 vasoconstriction and decreased nasal secretions (the good
side), and -- with larger doses -- insomnia, hypertension, heart
rhythm abnormalities, hemmorhaging, stroke, or death (the bad side)
(8). 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
(see <5.1> for an explanation of 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" in
the USA are really just antihistamines (although melatonin is making
inroads as an alternative). 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
(8). Note that high doses of prescription antihistamines are much
more dangerous.
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 (1,2).
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 (called paracetamol in the UK) 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/paracetamol 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 (2,8)
Furthermore, this doesn't happe n 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. This is
unlikely but possible. DO NOT UNDER ANY CIRCUMSTANCES USE
RECREATIONALLY ANY DXM PRODUCT WHICH ALSO CONTAINS ACETAMINOPHEN /
PARACETAMOL!
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 (9). It may become
prescription in other countries.

<1.8> Other (medical) uses for DXM

Dextromethorphan is commonly used to determine cytochrome
P450-2D6 activity (10,11). Cytochrome P450-2D6, or debrisoquine 4-
hydroxylase, is a liver enzyme which converts DXM into dextrorphan,
and is extensively involved in the metabolism of other drugs. About
5-10% of people seem to lack P450-2D6 entirely (12-15); in the
remaining individuals, its activity can vary significantly due to
minor genetic variance (15-18). By looking at the metabolites of DXM,
a physician can determine P450-2D6 efficiency, and adjust drug dosage
to match.
One area in which DXM (as well as other NMDA blockers; see
<5.3> below) shows great promise is in the prevention of brain damage
resulting from excitotoxicity (overstimulation of nerve cells to the
point of cell death) and other types of nerve cell damage (19). DXM
may reduce or eliminate the damage associated such wide conditions as
fever, hypoxia (lack of oxygen) (20), ischemia (cutoff of blood) (21-
22), physical injury (23), infection (such as poliomyelitis,
encephalitis, and meningitis), stroke, siezure, drug toxicity (24-25),
and withdrawal from long-term dependence upon certain drugs (notably
alcohol, barbiturates, and benzodiazepines such as Valium[TM]) (26-
29).
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) (30,31).
Quinolinic acid is a very potent agonist (activator) 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
factors, being involved), it still has potential.
DXM is currently being evaluated as an anticonvulsant (32,33).
The animal data are somewhat conflicting, but the most accurate model
of epileptic siezures (kindling) responds well to DXM. Preliminary
studies in humans indicates that even very low levels of DXM may help
prevent siezures. This effect is not, as was originally thought, due
to NMDA receptors; instead, it is probably due to sigma receptors (see
<5.2>) or voltage-gated ion channels (see <5.5>) (32). Interestingly,
DXM produces different side-effects in kindled (siezure-susceptible)
animals than in non-kindled animals (32). It is possible that humans
susceptible to siezure may experience different effects from
recreational DXM use.
Another new area where DXM has potential is in combating the
withdrawal symptoms of opiate addiction. DXM plus diazepam was more
effective at combating the symptoms of heroin withdrawal (goose flesh,
tremors, dilated pupils, joint ache, etc.) than DXM plus
chlorpromazine (34). This is most likely due to DXM's ability to
block NMDA receptors (see <5.3>).
DXM has shown some potential for treating some of the problems
associated with mental retardation (35). It may also be of use in
treating Parkinson's disease (36). DXM may be useful in conjunction
with opiates for alleviation of both acute and chronic pain (37). It
may even be useful in fighting lung cancer (38).

<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).
Prescription MAOIs are usually given for depression or Parkinson's
disease. Combining DXM and a MAOI has resulted in death (3).
Fluoxetine (Prozac[TM]) is a cytochrome P450-2D6 inhibitor
(39), and will change the characteristics of a DXM trip somewhat (see
<1.8>; see also the testimonials in Part 2/2). Other P450-2D6
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. The
potency of DXM may also be enhanced by fluoxetine (40).
DXM should not be taken with the prescription antihistamine
terfenadine (Seldane[TM]). This combination has resulted in death
(41). Terfenadine has been implicated in other drug interactions,
incidentally. The reason for this interaction might be that
terfenadine, which is normally metabolized by a P450 enzyme, induces
heart irregularities when it builds up. DXM may saturate the P450
enzymes that normally metabolize terfenadine. Incidentally, this
probably applies to Claritin[TM] and Hismanal[TM] as well; avoid
combining them with DXM.
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. Note that, based on anecdotal evidence, I believe that
sensitivity to other dyes may develop from chronic use.
The large amount of glycerine, glucose syrup, and sugars
present in cough syrups can give some people problems ranging from
stomach ache to sugar shock. Obviously anyone with diabetes or a
family history of sugar problems should avoid these formulae.
Recently I have been hearing more reports of chronic DXM users
who have had problems associated with the long-term use of cough syrup
formulae. This is evidently a problem associated with the "inactive"
ingredients, and can probably be alleviated by not taking cough syrups
on an empty stomach.

<1.10> Are there other non-narcotic cough suppressants?

Yes, there are. The only one of which I am aware is a drug
called noscapine (42). I have little information on it as of yet;
look for more in the January 1, 1995 release of this FAQ. (I intended
to get the data for the December 1 94 release but I've been busy).

<2> Psychological Effects of DXM Use

This section discusses some of the effects you might expect to
feel if you were to use DXM (which I again do not recommend).

<2.1> What is the general character of a DXM trip?

This is a difficult question to answer, because DXM's effects
tend to vary widely depending on the person, their set and setting,
other drugs, their physiology, and so on. DXM, probably more than
most drugs, tends to exert its (recreational) effects on plateaus,
rather than being linearly dose-dependent. Within a given plateau, a
given set of effects will occur (at a roughly dose-dependent
strength). On the other hand, once the next plateau is reached, the
feel may change entirely. A reasonable analogy is water -- it exists
in three states (solid, liquid, and gas) which all can exist at
varying temperatures, but which have different characteristics.
As to how many plateaus DXM exhibits, this is debatable.
Formerly I partitioned DXM's effects into two plateaus ("low dose" and
"high dose"), but after review and suggestion I have changed to a
three-plateau structure. Some people will undoubtedly disagree, but I
think this is the best way to represent DXM's effects.
The specific effects at each plateau will be listed according
to the following categories: Sensory, Motor, Cognitive, Memory, and
Emotion.

<2.2> What are the effects of a "first plateau" dose?

The first plateau generally occurs around 120 to 240 mg, but
this may vary enormously depending on weight, metabolism, etc. Please
keep in mind that these are general effects, and that individual
results may vary considerably.
A first plateau trip usually takes between 20 and 40 minutes
to start (on an empty stomach), peaks about 1.5 to 2 hours later, and
lasts between 4 and 6 hours. Hangovers are very rare from this
plateau, but if they do occur, they tend to consist mainly of
lethargy.
The primary effects of the first plateau are general euphoria,
euphoria specifically linked to music and motion, slight disturbances
in balance, and very slight intoxication. The intoxication and
balance disturbances are similar to that induced by alcohol, but
without the mental confusion. It is interesting to note that there is
little if any mental sluggishness or confusion with a first plateau
trip.

SENSORY EFFECTS
Most of the effects of the first plateau relate to the senses.
The best known, and probably the most responsible for DXM's popularity
as a recreational drug, is the effect upon hearing (specifically upon
music). Sounds may seem "richer" or "deeper", and music in particular
is affected (the difference between listening to music on DXM versus
sober has been compared to the difference between music in a concert
hall versus on a cheap radio). In addition to the change in the
nature of hearing itself, music can bring a sense of euphoria, often
quite intense. In comparison to the positive effects on music
reported by some users of cannabis, the DXM music effect is usually
characterized as much "speedier".
The type of music with which this effect most strongly occurs
will tend to vary from person to person. Rave music is one of the
most commonly affected, possibly due to the regular beat (at higher
plateaus especially, much of DXM's sensory effects seam beat or rhythm
related). Classical and Celtic/folk also seems to be popular.
Really, though, the strongest indicator of personal response to a
given piece of music seems to be 1) that the user enjoys it, and 2)
that it has an "intense" or thematic quality.
Visual effects are not particularly profound at this plateau.
If present, they usually consist of motion trails (as if afterimages
of each "frame" of vision were not clearing quickly enough). There
may be some deterioration of stereoscopic vision (and thus depth
perception). Colors may seem slightly more vivid.
Taste, smell, and touch do not seem to be appreciably
affected, although some users have reported that taste and smell are
enhanced and mildly euphoria-linked. Others have reported the same
effect for touch.
Balance and body position sense can be significantly affected,
ranging from a mild disturbance (some call it "sea legs") to a near
total loss of position and balance sense. The changes seem to relate
to an anaesthesia of this sense in particular. The effect (like the
other sensory DXM effects) can be euphoric; some users like to roll
around, do cartwheels, dance, march, whatever. Interestingly, I have
not heard any reports of motion sickness (as might be expected if
balance sense were blocked).

MOTOR EFFECTS
The other main characteristic of a first plateau DXM trip is
its effect upon motion and motor skills. Users tend to walk and move
in specific ways (varying somewhat from person to person)
characterized by large, fluid movements. In fact, it may be difficult
to perform small or abrupt motion. Motor tasks initiated may continue
beyond their targets (this can range from fun to distracting). To an
outside observer, this can seem quite strange, especially the changes
in gait. It is possible, however, to move normally.
These changes may be related to euphoria linking of body
kinetic sense (see Sensory Effects, above) which would make large and
sweeping motions more enjoyable. It is also possible that something
more directly involved in the planning and carrying out of complex
motor tasks may be at work.

COGNITIVE EFFECTS
Even though DXM has a slight "stoning" or intoxicating effect
on the first plateau, there are surprisingly few deficits of cognitive
function. Language is the most strongly affected, although these
effects are usually limited to occasional word and syllable repitition
(especially in already-repeated syllables such as "banana"),
spoonerism (e.g., "share boulders" instead of "bare shoulders"), and
difficulty coming up with a specific word.
Some users report that they feel more creative and capable of
non-linear thought on DXM, and this seems to be maximized on the first
and second plateaus. Whether this is, in fact, true, or just seems
true because of the drug, I have no idea; to my knowledge there are no
studies on this. Another cognitive characteristic that occasionally
occurs at the first plateau (but more commonly at the second) is that
things can seem much more interesting, or at least much less dull and
boring, than they usually are. There may be an overall increase in
approach-related behaviour.

MEMORY EFFECTS
The memory effects of a first plateau trip are slight but
usually noticeable. Most of the effects probably come from a general
deterioration of short-term memory. Working memory (the "train of
thought") can become stuck in repetitive thoughts; other times it can
be very easy to become distracted. Recall of events prior to the trip
does not seem to be degraded. Encoding (i.e., making new memories)
may be worsened, so that after the trip there is some difficulty in
recalling events during the trip. Also probably because of the
deterioration of short-term memory, it may be easy to lose track of
time.

EMOTIONAL EFFECTS
Mood enhancement is the most regular effect of the first
plateau; many people find themselves fairly bouncy and happy. Unlike
many drugs, there is not usually much "let-down" when the trip ends.
Fear is rare at the first plateau. There may be a sense of energy or
drive.
The effects upon libido evidently tend to vary from person to
person. Some people report an increase in sex drive; others find that
playing, physical contact, music, etc., seem much more interesting and
enjoyable than sex. The effects on sexual performance itself are not
very strong at the first plateau, though males may have some
difficulty in achieving orgasm.

<2.3> What are the effects of a "second plateau" dose?

With the second plateau (around 240-600mg), several new
effects become evident. The most profound is that DXM begins to take
on a heavier "stoning" characteristic, and senses and cognitive
function are affected accordingly. Hallucinations start for some
people on the second plateau. Some of the first plateau effects,
e.g., the music and motion linked euphoria, may diminish or stop
entirely.

SENSORY EFFECTS
The most general sensory effect of the second plateau is
"phlanging". Phlanging, also called flanging, phasing, stop-action,
framing, etc., is the sensation that continuous sensory input has been
chopped up into frames (as if you were watching a badly animated
cartoon), often with some echo effect of each frame. There does not
seem to be any loss of sensory content; instead, it is as if the
ability to keep sensory input time-continuous were disturbed. The
best analogy from other drugs may be the effects of nitrous oxide upon
sound. The best analogy from non-drug experiences is listening to a
voice through an echo/delay line (which is where the term "phlanging"
comes from).
An interesting and probably associated sensory phenomenon is
that it seems as if one is aware of several temporal stages of sensory
processing all at once. In other words, a sentence may be heard not
sound for sound or word for word, but all at once (this is difficult
to describe). Similarly, visual images may be jumbled together with
previous images. This may be due to an excessive persistence of
sensory buffering.
Vision in particular is changed on this plateau. Depth
perception is often lost, and the ability to keep both eyes focussed
on the same thing is diminished (leading to slight double vision).
This is most noticeable in people without a dominant eye.
Sound, as already mentioned, tends to be phlanged. With the
sense of touch, there is not necessarily phlanging so much as a
noticeable delay between the stimulus and recognition of it. Pain
especially tends to be somewhat dissociated. Taste and smell are
simply dulled. The sense of balance is severely disrupted, as is body
position and kinetic sense. Note that the dissociation of pain and
the disruption of body sense together make physical exertion somewhat
risky, as it is possible to over-exert and not notice.
Hallucinations tend to begin at the second plateau (and in
fact are the reason I distinguish this from the first plateau).
Usually these are not "true" hallucinations, but instead are
considerable enhancement of imagination, up to fully eidetic imagery
(i.e., you experience lucidly what you imagine). This is especially
powerful with memories; some users are able to re-experience past
events, or "simulate" future events, as if actually there, interacting
with the environment (I call this the "Holodeck effect"). Many users
report this to be quite useful for introspection.
Actual hallucinations, if they do exist, tend to be abstract
and cartoon-like. There seems to be an emphasis on linear structures
-- long, thin lines, or long queues of simple objects. There may also
be Lilliputian hallucinations (everything seems either way too big or
way too small, or both). Some people find considerable similarity
with fever hallucinations. Note that this can be disturbing to some
people.

MOTOR EFFECTS
The first-plateau effects on motor skills continue to exist,
and may be considerably stronger. Some users find themselves
contorting their limbs into rigid positions, others may extend and
stretch themselves. These effects are not always immediately
apparent; when they are, the user usually reports that it just "feels
right" to be in that position. It is still possible to override this.
Another accentuation of first-plateau motion effects that
sometimes occurs is that the large, sweeping motions, once initiated,
may continue for considerable time (looking somewhat like a cross
between modern dance and Huntington's disease). Again, it just "feels
right" to do.

COGNITIVE EFFECTS
Higher reason is still not appreciably affected at the second
plateau; in fact one of the more interesting aspects of DXM at the
first and second plateau may be its ability to disturb one aspect of
the mind while leaving another almost untouched.
Language becomes difficult, partly due to cognitive changes
(as in the first plateau) and partly due to difficulty in coordinating
the mouth and tongue motions. Similarly, interpreting spoken language
is difficult due to sensory phlanging. However, thinking in language
is still fairly easy.

MEMORY EFFECTS
Short-term memory and working memory may be severely
disturbed, although experience with DXM seems to help people
compensate. Possibly because of the changes in memory, it may be very
difficult to get bored, even with repetitive tasks. At this plateau,
a lot of time may get lost, and the more mundane aspects of the trip
are easily forgotten after it is over.

EMOTIONAL EFFECTS
The other primary characteristic of the second plateau
(hallucination being the first) is probably the motivational aspects.
Repetitive, mundane, boring tasks suddenly become doable, and (if one
can avoid distraction) may be easily accomplished, even if they take
hours. There is often a fairly considerable stimulant effect at the
second plateau. The euphoria from the first plateau continues,
although it may diminish as dosage across the second plateau
increases.

<2.4> What are the effects of a "third plateau" dose?

At the transition between the second and third plateau,
several unrelated effects may occur. These probably belong more to
the transitional stage than to a given plateau, and will be dealt with
here.
The first is a sensation that has been described as the
opening of nasal passages, being full of helium, losing one's body, or
having one's heart stop beating. The actual effect is most likely a
sudden cutoff of sensory input from within the body -- everything from
all the little aches and pains to the awareness of one's own heartbeat
go away. This can be very disturbing if a naive user interprets it as
heart failure!
The second transitional effect is a temporary loss of all
sensory input (this does not always occur), as if one were in an
isolation tank. This is often accompanied by severe Lilliputian
hallucinations, probably because there is no internal size reference
(since the rest of the universe has just gone away). One user
reported feeling as if he shrunk down to the size of a proton, and the
rest of the world were light-years away.

The effects at the third plateau itself tend to be very
intense, and often very different from earlier plateaus. It is much
less "recreational" and much more "shamanic". Keep in mind that a
third plateau trip can be fairly disturbing, especially to people who
are not psychologically comfortable and prepared.

SENSORY EFFECTS
The phlanging of visual effects, coupled with the loss of
stereoscopic vision, become so profound that the brain seems to give
up trying to process vision entirely, leading to a sort of "chaotic
blindness". Simple images (e.g., a candle flame) are still parseable,
although given the loss of stereoscopic vision one tends to see two of
everything. More complex images, especially images that are not
sharply defined, are difficult if not impossible to recognize.
Simple sounds are still recognizable, and one can usually
understand language, although it may be necessary for the speaker to
phrase it in a complex rhythm (see Cognitive Effects). Music euphoria
is rare. Touch, smell, and taste are subject to considerable
anaesthesia, and pain especially may be completely dissociated (it's
still there, it just doesn't seem to apply). Body position, kinetic,
and balance senses are similarly disrupted.
Hallucinations may continue, although they tend to be more
abstract and "pre-sensory" rather than being predominantly visual.
Oftentimes there is an overall sensation of being surrounded by
"grey", which increases to white light as the dosage increases.
It is worth noting that at the third plateau, the phlanging of
sensory input occurs both on a raw level (sounds, images) and on
higher levels (words, phrases, faces, etc.) This is, to my knowledge,
unique to DXM.

MOTOR EFFECTS
At the third plateau it may be impossible to perform
coordinated movements. The large, sweeping motions of the first and
second plateau are no longer present. Instead, many users lack both
the desire and ability to move at this plateau.

COGNITIVE EFFECTS
Cognitive function becomes severely disrupted at the third
plateau. Complex tasks, such as mathematics, are very difficult.
Reaction time is significantly delayed. Decision-making is somewhat
degraded, although conceptual thought is less affected than concrete
thought.
Language changes can be quite profound. Sentences may stretch
on and on, or alternately be very terse (I call this the "Hemingway
effect"). Words, syllables, and phrases are commonly repeated. This
may be related to problems with working and short-term memory. Speech
may occur in a very rigid (but not necessarily simple) rhythm, and the
user may not respond to speech unless it is in a similar rhythm.
On the other hand, some people report that higher reasoning and
other cognitive functions not dependent upon short-term memory are not
disturbed on the third plateau. Your mileage may vary.

MEMORY EFFECTS
Working and short-term memory are seriously impaired.
Thoughts may get stuck in a "loop". Encoding of the more mundane
experiences of the trip tends to be very bad; expect to forget a lot
after the trip is over. The sense of time can be quite distorted,
incidentally, both in terms of chronological placement of events and
in the sense of the passage of time.
The day after a third plateau DXM trip, some users feel as if
there were a break in the continuity of their memory, almost like the
close of one chapter and the beginning of another. Some find this a
very positive feeling, like a rebirth or rite of passage. It can be
disconcerting if experienced without adequate foreknowledge and
preparation.
One of the most significant memory effects that can occur at
the third plateau is the spontaneous recall of memories, often
memories which were hidden (consciously or not). This can be a
positive experience if one is prepared to review the darkest secrets
of one's past; otherwise it can be quite disturbing, to say the least.
The user may also feel compelled to tell her or his companions about
these memories (not always a good idea).

EMOTIONAL EFFECTS
Mood can range from absolute mania to panic. Many people have
independently reported feeling as if they were dying, with some sense
of fear, although some people do not seem to associate fear with this.
Some people report a great increase in approach behaviour, as if every
event and object were a new experience; others find irrational fears
occuring (possibly due to body load).
DXM on the third plateau has a very "shamanic" feel to it.
Part of this is due to the sense of rebirth, part from the recall of
suppressed and/or partially forgotten memories. Additionally, some
people feel that the third plateau gives them contact with the "spirit
world" in a way that no other drug does. Complete annihilation of
self can occasionally occur (up to the point of forgetting one's
identity) but does not seem to be especially dangerous.
In general I find the "spiritual" aspects of the third plateau
to be intriguing, although a healthy dose of skepticism is probably
warranted. If there is some truth to these phenomena, DXM may have
great promise as a shamanic journeying tool.
Note that, to sober observers, the effects of a third plateau
trip can seem very disturbing (often much more than to the person
tripping).

<2.5> Is there anything beyond the third plateau?

Possibly. One user reported that very high dosage levels led
to a "pure white light" across (or perhaps deeper than) the senses.
Another distinguished the third plateau, as I defined it, from the
level at which spiritual effects occur. At very high dosage levels,
the effects on voltage-gated ion channels (see <5.5>) undoubtedly
exert more and more influence. Still, though, few people have
experimented at the 2000mg level and above; in any case this is
dangerously close to the possibly lethal range (see <3.3>), and should
be approached with extreme caution if at all.

<2.6> What are the effects of chronic, high-level use?

Chronic, high-level use (e.g., 500-1000mg daily) tends to
result in several undesirable effects. Psychological dependence is
certainly possible and there are numerous examples of this occurring
(3-5; also personal communications). Physical dependence is
debatable, but if it does occur, it is probably with very high dose
levels (1000mg per day and up) as a result of chronic NMDA blockade
(see <5.3> below). Amotivational syndrome has been reported (usually
when the drug wears off). Memory problems seem to be fairly common
(but seems to resolve upon stopping DXM use).
At least one chronic user (1500-2000mg daily), with no history
of psychological problems, developed a strong dependence upon DXM and
severe depression, leading to a suicide attempt and several months in
drug rehabilitation. This is not at all common, but cannot be
ignored. Exactly why some individuals seem to have drug dependence
problems with DXM is unknown; it may be a function of chronic high-
level use, or it may be a function of individual physiology.
Some users report benificial effects of chronic high-level
use. The effects usually include some antidepressant activity
(entirely reasonable given the possible significance of PCP2
receptors; see <5.4>), stimulant activity, long-term motivational
effect, and cognitive and creative enhancement (this has not been
quantified and may be entirely subjective). It is arguable that
chronic DXM use may actually be self-medication for depression in some
people.

<2.7> Why is there so much individual variance in response?

Several reasons. First off, there is a liver enzyme known as
cytochrome P450-2D6 (also CYP2D6, or debrisoquine 4-hydroxylase),
which metabolizes DXM. Some people lack this enzyme, and of those who
have it, subtle genetic variations can result in different activity
(10-18). Thus, while one person may metabolize DXM quickly, another
may not (there are other pathways which are much slower). Certain
drugs -- such as fluoxetine (Prozac[TM]) can inhibit this enzyme (39).
Second, 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 (43). Some individuals may metabolize high
doses of dextromethorphan to dextrorphan. Incidentally, my opinion --
based on anecdotal evidence of recreational DXM use while on
fluoxetine -- is that DXM, and not dextrorphan, is responsible for the
psychoactive effects. More evidence is mounting to show that it is
DXM and not dextrorphan which is responsible for the psychoactive
effects (32).
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
(there are exceptions). It is possible that, due to this extensive
involvement, many different cortical and limbic circuits may be
affected. In fact, DXM affects at least four different binding sites
(see <5>), and each of these is subject to subtle variance from person
to person (44).
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.

<3> Side Effects and Risks of DXM use

Like all drugs, DXM has side effects and risks. While mild in
most people, they cannot be ignored. DXM is not a "safe drug" or a
"harmless drug" (two oxymorons if there ever were).

<3.1> What are the side effects and risks of occasional DXM use?

Physical side effects are usually fairly mild, although at
higher dosage levels, there can be a heavy "body feel". Heart rate
may be increased. Even though DXM has been successfully used to
prevent siezures, it may acutally induce them at high dosage levels
(45). You want to avoid this.
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.
Many cough syrup preparations can cause considerable amounts
of bloating and gas. Expect to pass gas for the next day. Gastric
disturbances, probably from the amount of sugars and glycerine, are
also common. Preparations with guaifenesin tend to induce vomiting at
recreational DXM levels. The cough syrups themselves can also cause
significant nausea in some people.
Many people report a transient period of severe itching. This
may be a result of an allergic reaction, or it may simply be a result
of decreased sensory input. It does tend to pass. On the other hand,
at least one user has reported an actual allergic reaction (with hives
and swelling), which responded favorably to a normal dose of an OTC
antihistamine. If you are not experienced in DXM use you might want
to keep an antihistamine on hand in case trouble occurs.
Some users who have taken very high dosages of DXM (above
1000mg) have lost motor function to the point of choking on their
tongues. Obviously, nobody should be experimenting at this level
without a (sober) assistant. If this happens, seek medical
assistance. While I cannot vouch for the efficacy or safety of this
procedure, I have been told that one can maintain the airway by
grabbing the person's tongue and holding it out of his or her mouth
until motor function is regained. Don't try to insert anything into
the person's mouth to keep the tongue in place; it could slip and
cause much worse choking.
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. One user
reported that very heavy exercise seemed to clear all residual and
hangover effects.
One user with a blind spot in one eye due to a stroke reported
hallucinations in the blind spot persisting for several days. This
eventually went away but was not particularly enjoyable. LSD,
cannabis, and alcohol all failed to induce this effect.
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.

<3.2> What are the side effects and risks of chronic DXM use?

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) (1-3). Some
research has linked sigma receptors to schizophrenia (46-49), and
chronic use of NMDA antagonists has been shown to upregulate
(increase) dopamine receptors (50). This could theoretically mean
that DXM could trigger schizophrenia in susceptible individuals,
although nobody knows for sure. DXM could also decrease immune
function due to sigma activity (51). One thing that is known is that
neither DXM nor PCP nor ketamine cause any change in PCP or sigma
receptors.
Another possible effect of long-term DXM use is neurotoxicity.
This has not been observed, but would be consistent with DXM's
hypothesized ability to induce 5HT and dopamine release (52). Such
neurotoxicity would probably be restricted to 5HT (serotonin) neurons,
and be similar to the neurotoxicity resulting from use of MDMA
(ecstasy). Note that no animal studies have ever demonstrated this.
Chronic use of NMDA antagonists seems to modify 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. A
recent paper supports the ability of DXM to affect alcohol tolerance
(53).

<3.3> 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, for a total dose of
3000mg). 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 (9).
On the other hand, a dosage of 42mg/kg/day has been used in
children (33), which would be 2500 to 3000mg for a reasonable-sized
adult (60-70kg). There is also a very low incidence of death
associated with DXM use. Since a 42mg/kg dose in an adult may be
stronger than the equivalent dose in a child (I have no reason to
believe this, but it is possible), caution is advisable in taking this
as an indication of safety.
It is reasonable to expect, given the 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 (54).

<3.4> Do you recommend DXM for recreational 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.

<4> Physiological Effects of DXM

<4.1> How does DXM inhibit the cough reflex?

This is a complex problem. 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 (42,49,55,56). This may be a
direct involvement -- sigma receptors may directly inhibit the cough
reflex signals -- or it may be an indirect one. What is known is that
the cough suppressant effect of opiates (such as codeine) is not
related to the same effect of non-opiate morphinans like DXM (49).
The cough suppressant effect of opiates seems to be governed by
traditional opiate receptors (mu, kappa, or delta).
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 (57). This could
explain some of DXM's mood-altering activity. 5HT1A receptors are
involved in anxiety states and in resilience to aversive events.

<4.2> How does DXM cause its psychoactive effects?

DXM binds to at least four sites in the brain (58), which can
be arbitrarily labelled DM1, DM2, DM3, and DM4. There may be a fifth
binding site (DM5). The following table lists the binding affinity of
DXM, DTG, and 3-PPP (58), (+)-pentazocine sensitivity (60), and
haloperidol displacement ability (58) (binding values in nM unless
otherwise specified). "Low" means micromolar binding affinity.

DRUG DM1 DM2 DM3 DM4
DXM 50-83 8-19 low low
(+)-3-PPP 24-36 low 210-320 low
DTG 22-24 ---- 13-16 ---
pentaz. sensitive? Yes No
hal. displaced? Yes Yes

What this table demonstrates is that DXM binds to four
separate places, two with high affinity. The first binding site is
almost certainly the sigma1 receptor (see <5.2>). The second site is
probably the PCP2 receptor (see <5.4>), and the third site is probably
the sigma2 receptor. The identity of the fourth site is still up for
grabs but is probably the NMDA channel PCP1 site (see <5.3>). Because
DXM has been found to bind with Na+ and Ca2+ channels at low affinity
(59), (see <5.5>), there may be a fifth binding site.
Most of the "stoning" or intoxicating effects of DXM are
likely due to NMDA receptor blockade. Alcohol's intoxicant effect
seems to be mediated in part by NMDA receptor blockade (its depressant
effect is due to GABA activity; DXM has no activity at GABA receptors)
(28,61,62). The dissociative anaesthesia of high DXM doses is also
likely due to NMDA receptor blockade (63).
The disruption of sensory processing is probably a combination
of NMDA blockade and sigma activation (63-65). Both NMDA and sigma
receptors have been found to be involved in sensory processing, and
some of the auditory effects of DXM in particular seem to be sigma
mediated (65). I have a hunch that the phlanging effects come from a
disruption of sensory input persistence.
The effects on memory are almost certainly due to NMDA
blockade. NMDA receptors are intimately involved in long-term
potentiation (64,66-68), a part of (probably short-term) memory. By
blocking NMDA receptors, long-term potentiation, and thus short-term
memory, is disrupted.
The psychotomimetic (literally "psychosis-like") effects of
DXM may be a result of sigma activity (sigma receptors may be involved
in schizophrenia) (46-49). As for what is due to sigma1 and what is
due to sigma2 receptors, this is anyone's guess. There is very little
data on the subjective effects of sigma agents, in part because only
recently have selective ligands become available, and in part because
most researchers aren't very willing to dose themselves to find out.
The effects on motor skills may be a result specifically of
sigma2 receptors (69). Expect to see more data on this subject as
sigma2 receptors are investigated more fully. There may also be a
contribution from NMDA receptors, of course.
Finally, if (as some researchers believe) PCP2 "receptors" are
in fact a biogenic amine reuptake site (70), 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 active at these receptors (sigma, PCP) (71,74,75); it is
possible that the PCP2 site may be a target of some antidepressants.
If the site is a dopamine reuptake site, it may be similar to, or the
same, as the reuptake site where cocaine binds (73). 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 has a fairly strong ability to increase dopamine activity (both
from activating sigma receptors, and from preventing dopamine reuptake
at PCP2 sites) (72,76).
The overall disruptive effects of high-dosage DXM, and its
ability to suppress respiration at toxic levels, is most likely due to
NMDA receptor blockade or ion channel blockade.
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 <4.4>). Recent research
casts considerable doubt upon this.
I am currently working on a hypothesis concerning the effect of
DXM (and other "stoning" drugs) on the hippocampus, the area of the
brain where short-term memories are stored (for about a day; after
that, modifications of the cerebral cortex itself seem to occur). The
hippocampus is dense in NMDA receptors, and in fact these receptors
are probably the mechanism by which short-term memories are encoded.
Since all "stoning" drugs seem to share the ability to inhibit long-
term potentiation (either directly or indirectly), I have a feeling
that the disruption of hippocampal long-term potentiation may be the
cause of DXM's effects on memory and perception. It is interesting to
note that high-doses of DXM do not always seem to disrupt cognitive
activities (which are presumably dependent upon the cerebral cortex).

<4.3> 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
four and probably five neuroreceptors, one of which (the NMDA
receptor) is involved in learning and in higher reasoning, and two of
which (the sigma1 and sigma2 receptors) may be involved in
schizophrenia and in psychotomimetic effects. The fourth 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.

<4.4> What happens to DXM after you take it? (Pharmacokinetics)

DXM is absorbed quickly from the GI tract; within 30 minutes,
all of it may have entered the bloodstream (2,3). The polistirex
compound will obviously change the absorption time.
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 (10). The
enzymes responsible for the N-demethylation are cytochrome P450-3A4
and P450-3A5 (77).
The product of O-demethylation of DXM is dextrorphan, a
chemical which is also psychoactive and may be responsible for some
DXM's psychoactive effects. N-demethylation 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 cytochrome 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 metabolyte such as dextrorphan.

<5> Sigma, NMDA, and PCP2 receptors, and Ion Channels

<5.1> What is a receptor, anyway? (Basic Neuropharmacology)

A neuroreceptor (or receptor) is a location on the surface of
a nerve cell (neuron) where a neurotransmitter reacts to cause some
change in the nerve cell's activity. This change can either be on the
neuron's potential, thus contributing to (or detracting from) its
activity directly, or it can be regulatory.
The directly contributing neuroreceptors typically operate
very quickly, and act (and look) somewhat like an iris shutter in a
camera. The neurotransmitter (for example, acetylcholine) binds to a
specific area on the receptor, which (due to electrostatic forces)
causes the receptor to snap open. Ions then leak into and out of the
nerve cell, changing its electrical potential. The receptor then
snaps shut, having done its work. These are the receptors involved in
fast signal transmission.
The slower domain receptors have a modulatory role. Some of
them increase or decrease the number of other types of receptors.
Some cause changes in genetic expression in the cell. Some (called
autoreceptors) inhibit the release of their own matching
neurotransmitter, a process called negative feedback. A thermostat is
an example of a negative feedback system -- the hotter it gets, the
less the furnace is on.
It is important to notice that any given neurotransmitter will
probably be associated with several different receptors. For example,
serotonin (5HT) activates at least ten receptor subtypes (5HT1A,
5HT1B, 5HT1C, 5HT1D, 5HT1E, 5HT1F, 5HT2, 5HT3, and 5HT4)! The reason
there are several subtypes, instead of just one, is that each receptor
subtype is involved in a different process on a different type of
neuron.
Importantly, drugs which mimic, block, or otherwise affect
activity of a given neurotransmitter will not affect all receptor
subtypes equally. For example, LSD operates at 5HT1C and 5HT2
receptors; buspirone operates at 5HT1A receptors.

The biogenic amine neurotransmitters include acetylcholine,
noradrenaline, dopamine, serotonin (5HT), and histamine. They are
derived from amino acids (choline, tyrosine, tyrosine, tryptophan, and
histidine respectively), generally have a modulatory role, and are the
common targets of recreational drugs. For example: LSD, DMT, and
psilocybin target 5HT receptors; amphetamine causes a release of
dopamine and noradrenaline; cocaine blocks the reuptake of dopamine
(thus keeping it active longer); MDMA causes a release of 5HT and
dopamine; etc.
The neuropeptide neurotransmitters include a whole slew of
peptides (chains of amino acids), such as neuropeptide Y, angiotensin,
endorphins, substance P, and so on. The only recreational drugs
targeting neuropeptide receptors are the opiates, which target the mu,
kappa, and delta opioid receptors. Opioid receptors are (obviously)
involved in pain and addiction.
The amino acid neurotransmitters include GABA (gamma-
aminobutyric acid), glutamate, and aspartate. Receptors for these
neurotransmitters include the GABA receptors (which come in two main
flavors) for GABA, and the NMDA, quisqualate or AMPA, and kainate
receptors (all of which respond to glutamate and aspartate). The GABA
receptor is the target of benzodiazepines like Valium[TM],
barbiturates, and alcohol; the NMDA receptor is targeted by PCP,
ketamine, alcohol, and DXM.
And then there are those receptors that don't really fit in
anywhere else. The anandamine receptor is the recently-identified
target for the THC in marijuana. The adenosine receptor, which tends
to inhibit nerve activity, is blocked by caffeine (by which it exerts
its stimulant effect). The sigma receptor was originally classified
as an opioid receptor, but is now thought to be separate. Gamma-
hydroxybutyrate, GHB, seems to target a specific receptor as well.
Each receptor can have more than one binding site. For
example, the NMDA receptor has at least three. Excitatory amino acids
(glutamate and aspartate) bind at one site and activate the receptor.
PCP binds at another site within the channel and "clogs it up" (note
that it must be open for this to work; thus PCP acts as an open
channel blocker). Glycine binds at a third site and is necessary for
the normal functioning of the channel.
Voltage Dependent Ion Channels are similar to the fast-domain,
shutter-like receptors, except that they are opened by voltage
potentials across the cell membrane. They function to transmit
signals along nerve fibers. Sodium, potassium, and calcium ions (Na+,
K+, and Ca2+) are the ions in question. Tetrodotoxin, the active
ingredient in "zombie powder", is a sodium channel blocker.

<5.2> What are Sigma receptors?

Sigma receptors were originally thought of as opioid
receptors, since many morphine derivatives bind there. However, this
classification is probably false, and endogenous opioid peptides show
little sigma activity; furthermore, the usual characteristics of
opiates are mediated by the mu, kappa, and delta receptors. The exact
nature for sigma receptors is unknown, and the neurotransmitter for
sigma receptors has not been found, although there are speculations
and evidence (82-86). The neurotransmitter for sigma2 receptors may
be zinc ions (78); in fact, sigma2 receptors seem related to potassium
ion channels (79). One paper speculates that sigma receptors are not
receptors at all, but are simply enzymes (84).
There are at least two types of sigma receptors (sigma1 and
sigma2). The sigma1 receptor is one of the two main targets for DXM;
the sigma2 receptor is less affected by DXM (58). Sigma receptors
seem to be involved in psychotomimetic (literally "psychosis-like")
effects from schizophrenia and drugs (46-49). In addition to DXM,
PCP, cocaine, and opiates all show activity at sigma receptors (72).
Chronic amphetamine use increases the number of sigma receptors (80),
while chronic antidepressant and antipsychotic treatments decrease the
number of sigma receptors (47,74). Sigma receptors are involved in
the limbic areas of the brain (81), and thus may be involved in
emotion. They are also involved in the cough reflex.

<5.3> What are NMDA receptors?

NMDA is one type of excitatory amino acid receptor
(quisqualate and kainate are the others) (66,67). NMDA receptors are
unique in that, in addition to the normal chemical signal, they also
require glycine and 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. Learning
capacity may in fact be directly related to the number of NMDA
receptors in the hippocampus (where memory is thought to be regulated)
(88).
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) (87).
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 (19). 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 (30-31).

<5.4> 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 <5.3>). 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 or recycled. 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 of DXM. To my knowledge, there are no studies
indicating cocaine's binding to PCP2 sites; I'd be very interested to
find out.

<5.5> What are N+ and Ca2+ channels?

Sodium and calcium ion channels are two types of voltage
dependent ion channels. DXM has recently been found to block their
activity, although it is not particularly potent in this capacity.
Because of their extensive presence, blockade of these ion channels
could have overall depressant effect upon brain function, and might
explain DXM's toxic effects at very high dosages.

<5.6> How does DXM compare to other drugs at these receptors?

PCP and ketamine both bind more strongly to NMDA, and less
strongly to the PCP2 and sigma sites, than DXM. In fact, some users
report that DXM, at higher dosages, begins to resemble ketamine and
PCP. The resemblance is still fairly limited. DXM's unique
characteristics are most likely due to the PCP2 and sigma sites.

<6> Extraction of DXM from cough formulae

Recently several individuals have reported successful
extraction of DXM from cough formulae. This section explains their
procedures and results. Please remember to always wear safety goggles
when working with chemicals, and be generally careful with these
procedures. My thanks to all who did research on this subject.
Unfortunately, I do not have your names handy, although I will place
them in the next release (December). Also, if anyone has a better
procedure, please mail me.

<6.1> How does one ideally extract DXM from cough formulae?

Add cough syrup to an equal volume of distilled water. (If a
considerable amount of alcohol is present in the cough formula, heat
to 95 C for 10 minutes to drive off the alcohol). With stirring, add
1.0N NaOH (or other convenient strength; it really isn't that
important) dropwise until the pH rises above 11 (do not increase above
13). Centrifuge, decant, and filter with slow-speed filter paper
(optionally under mild vacuum). Wash the precipitate in several
volumes of distilled water until the wash is no longer alkaline. The
precipitate should be white to pink (depending on dyes) and fluffy or
powdery.
To purify, dissolve in methanol and filter, discarding any
solids. Evaporate the methanol. The result should be a white to off-
white solid.
Expect a yield of 60-90%. If, after centrifuging, added NaOH
causes further precipitation, you didn't add enough beforehand. Avoid
raising the pH too high; this is a major cause of failure.

<6.2> How does one extract DXM without access to lab equipment?

For this process, you will need: distilled water, a glass
flask or mason jar, fine filter paper (coffee filters are much too
coarse; you might get by with thin construction paper if you're
willing to wait a long time), and NaOH (sodium hydroxide). Although I
don't advise it, one can probably use Red Devil Lye for NaOH (add
about 1tsp to 16oz of distilled water, stir until dissolved, let sit
for 1 day, and discard any precipitate). Note that you must use
distilled water in this procedure; tap water can cause problems.
Add the cough syrup to an equal volume of distilled water in a
flask or jar, and stir until well mixed. Now, while stirring, add
NaOH solution with a dropper. As you add it, you will notice the
solution becoming cloudy. Keep adding until it no longer gets any
cloudier. Multi-range pH paper is a good investment, but not really
necessary. If in doubt, stop adding NaOH; you can always recycle the
liquid part and try again.
If you have access to a centrifuge, great. If not, let it sit
for a day. The precipitate (solid part) should have settled to the
bottom (if not, well, keep waiting. If nothing happens after 3 days,
try another brand). Note that you can use the spin cycle of a clothes
washer as a centrifuge provided it spins down slowly enough; some jerk
to a stop. If you really want to use your washer as a centrifuge, you
can mount a bicycle sprocket to the top so that when the spin cycle
stops, the "centrifuge" can spin down freely. Be sure to balance your
home-made centrifuge by mounting two evenly full flasks on opposite
sides of the sprocket or central mount.
Decant (i.e., remove the top 3/4 or 4/5 of liquid) using an
eyedropper, pipette, straw (using your thumb, not your mouth), or
whatever works. Keep the liquid for later use. Avoid decanting with
turkey basters, since they tend to cause splash-back (which stirs up
the precipitate). Filter the rest, adding the liquid to the liquid
you decanted.
Now, add more NaOH to the liquid part. If any more
precipitate forms, you can repeat this extraction process; otherwise,
you've probably gotten most of the DXM out.
After filtering, the precipitate still has NaOH, so pour
distilled water over the precipitate in the filter until the filter
funnel is full, and let it drain out. Repeat this four or five times
(don't skip this step!).
If you want to, you can purify by adding the precipitate to
methanol, stirring, and discarding any solid junk. Let the methanol
evaporate, and the solid is DXM.

<6.3> How does one use the DXM thus extracted?

The DXM you extracted is in free base form, so it is
theoretically possible to smoke it using a vaporization pipe. I don't
know of anyone who has done this, and I can't make any claim as to its
safety (for all I know, it could eat your lungs out; I doubt it but it
could). You can also load it into a capsule and take the capsule. I
would advise eating with this to avoid stomach pain (probably due to
the alkalinity of the DXM). Or, you can neutralize with dilute HCl
and drink the resulting liquid (which, from what I hear, is pretty
yucky).

<6.4> Is this safe?

Maybe. A lot depends on the quality of your reagents, but
even in a worst-case scenario (lye, alcohol burner fuel, and a washing
machine for a centrifuge) you can still achieve a fair degree of
purity by recrystalizing several times. Still, nothing is completely
safe. The DXM may be changed by the process, or other ingredients may
precipitate out and adversely affect the results.
Note that several people report that the DXM thus extracted is
considerably stronger than the equivalent amount in cough syrup.
Whether this is due to a chemical reaction, the method of dosing
(which I tend to think it is), or some other factor, I don't know.

<7> Interaction of DXM with other recreational drugs

This section is fairly sparse. I am looking for anyone with
experiences to add here.

<7.1> Alcohol

Some users report that a small amount of alcohol (a beer or
two) before the DXM can both enhance the trip and prevent some nausea.
Alcohol following the DXM trip seems to be reduced in some, but not
all, of its effects. Note that large doses of alcohol combined with
DXM are probably a bad idea.

<7.2> Barbiturates and benzodiazepines

<7.3> Amphetamines and other psychostimulants

<7.4> Cannabis (Marijuana)

One user reported that 360mg DXM followed 3.5h later by "a
bowl or two" produced a very profound, and unique, intoxication.
Severe phlanging of all sensory input was present, and there was an
overall "vibration" feeling present in the muscles. With eyes closed,
he could think fairly clearly, and solve simple and complex tasks much
easier than on DXM or cannabis alone; however, with eyes open (or
other sensory distraction) cognitive abilities deteriorated rapidly.
Motor skills were possible only when performed automatically; any
attempt to focus on them led to difficulties.
Several users have reported that cannabis and DXM generally
"go well" together.

<7.5> LSD, psilocybin, and other 5HT hallucinogens
<7.6> Opiates
<7.7> PCP and ketamine

<7.8> Miscellaneous other drugs

One user reported that after taking DMAE (dimethylaminoethanol)
for three weeks, some of the effects of a high-dose (second or third
plateau) DXM trip had changed. Specifically, although the "stoning"
effect was still present, cognitive abilities were almost completely
unimpaired.

<8> DXM Drug Culture

<8.1> Is there, or was there, a DXM drug culture?

The answer is an overwhelming yes, although DXM use has always
been deeply underground. For example, in the late 1980's, DXM was
widely popular with the hardcore/punk movement, and in the 1970's,
there seemed to be other groups of users. DXM users in the late
1980's had a sort of "network" that stretched across the USA and into
parts of Europe. The total number of users was probably less than
10,000. An interesting characterstic of their DXM use was that it was
a group activity, whereas many DXM users today regard it as a solitary
experience.
Some cities seemed to have considerable DXM use activity,
notably with youth; in one town, there were empty bottles of cough
syrup littering the street, and sale of cough syrups were restricted
to people 18 and up. However, these incidents seem to be few and far
between.

<8.2> Why haven't I ever heard about it?

I don't know; in fact, I'm researching DXM's use culture right
now and hope to write a more extended paper on it (please submit any
material to me). There have been occasional newspaper articles about
DXM's recreational use; however, it has mostly been kept in the dark.
My hunch is that medical authorities are, in general, aware of DXM's
(ab)use potential, and have chosen to keep it silent to prevent
further growth. In fact, until fairly recently, many physicians were
not even aware that DXM was psychoactive at high dosages.

<8.3> Is there a "drug-slang" for DXM?

Not really, because DXM users have not, in general, been well
connected with each other. However, here is what I have gathered
(there is some redundancy due to the fact that this is taken from
several different users).

heebie-jeebies (n) The hangover effect of higher or chronic DXM
use, characterized by amotivational syndrome and avoidance.
"I don't want to go to class; I still have the heebie-
jeebies."

robo (n) Any DXM-containing preparation. "Hand me that bottle
of robo". (v.i.) To dose with DXM. "I roboed last night".
From Robitussin[TM], a cough syrup brand.
Occasionally, tuss (v.i.) and tussin (n), or DM (pronounced
"dee emm") replace robo. "I tussed last night". "Hand me
the DM".

robo-cop (n) Any store employee who keeps track of DXM purchases
and/or requests proof of age for DXM purchases. "You go
buy; the robo-cop there recognizes me". A pun on the movie
of the same name.

roly-polies (n) The desire to roll around, do cartwheels, spin,
or otherwise engage in rolling motions.

sea legs (n) Disturbance in gait and balance somewhat like
walking on land when accustomed to ocean balance (or vice
versa).

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

1. Fleeger CA (ed.). USAN and the USP Dictionary of Drug Names.
USP Convention Inc. 1993 (Rockville).

2. McEnvoy GK (ed.). AHFS Drug Information. ASHP Inc. 1993
(Bethesda).

3. Bem JL, Peck R. Dextromethorphan. An overview of safety
issues. Drug Saf. 1992;7:190-199.

4. Murray S, Brewerton T. Abuse of over-the-counter
dextromethorphan by teenagers. South. Med. J. 1993;86:1151-1153.

5. Schadel M, Romach MK, Sellers EM. Mania and cough syrup
[letter]. J. Clin. Psychiatry 1993;54:200.

6. Craig DF. Psychosis with Vicks Formula 44-D abuse. Can. Med.
Assoc. J. 1992;146:1199-1200.

7. Jacobs MR, Fehr KO. Drugs and Drug Abuse. 1987 (Toronto).

8. Dukes, MNG (ed.). Meyler's Side Effects of Drugs. Elsevier
1992 (Amsterdam).

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

10. Jacqz-Aigrain E, Cresteil T. Cytochrome P450-dependent
metabolism of dextromethorphan: fetal and adult studies. Dev.
Pharmacol. & Therapeutics 1992;18:161-168.

11. Kerry NL, Somogyi AA, et al. Primary and secondary oxidative
metabolism of dextromethorphan. In vitro studies with female
Sprague-Dawley and Dark agouti rat liver microsomes. Biochem.
Pharmacol. 1993;45:833-839.

12. Duche JC, Querol-Ferrer V, et al. Dextromethorphan O-
demethylation and dextrorphan glucuronidation in a French
population. Int. J. Clin. Pharmacol., Therapy, & Toxicology
1993;31:392-398.

13. Irshaid YM, al-Hadidi HF, Raweshdeh NM. Dextromethorphan O-
demethylation polymorphism in Jordanians. Eur. J. Clin.
Pharmacol. 1993;45:271-273.

14. Freche JP, Dragacci S, et al. Development of an ELISA to
study the polymorphism of dextromethorphan oxidation in a French
population. Eur. J. Clin. Pharmacol 1990;39:481-485.

15. Funck-Brentano C, Thomas G, et al. Polymorphism of
dextromethorphan metabolism: relationships between phenotype,
genotype, and response to the administration of encainide in
humans. J. Pharmacol. & Exp. Therapeutics 1992;263:780-786.

16. Mura C, Panserat S, et al. DNA haplotype dependency of
debrisoquine 4-hydroxylase (CYP2D6) expression among extensive
metabolisers. Human Gen. 1993;92:367-372.

17. Jacqz-Aigrain E, Funck-Brentano C, Cresteil T. CYP2D6- and
CYP3A-dependent metabolism of dextromethorphan in humans.
Pharmacogenetics 1993;3:197-204.

18. Evans WE, Relling MV. Concordance of P450 2D6 (debrisoquine
hydroxylase) phenotype and genotype: inability of
dextromethorphan metabolic ratio to discriminate reliably
heterozygous and homozygous extensive metabolizers.
Pharmacogenetics 1991;1:143-148.

19. Meldrum BS. Excitatory amino acid receptors and disease.
Opin. Neurol. Neurosurg. 1992;5:508-513.

20. Radek RJ, Giardina WJ. The neuroprotective effects of
dextromethorphan on guinea pig oxygen-derived hippocampal slices
during hypoxia. Neurosci. Lett. 1992;139:191-193.

21. Steinberg GK, Lo EH, et al. Dextromethorphan alters cerebral
blood flow and protects against cerebral injury following focal
ischemia. Neurosci. Lett. 1991;133:225-228.

22. Steinberg GK, Kunis D, et al. Neuroprotection following focal
cerebral ischaemia with the NMDA antagonist dextromethorphan, has
a favourable dose response profile. Neurological Res.
1993;15:174-180.

23. Panter SS, Faden AI. Pretreatment with NMDA antagonists
limits release of excitatory amino acids following traumatic
brain injury. Neurosci. Lett. 1992;136:165-168.

24. Finnegan KT, Kerr JT, et al. Dextromethorphan protects
against the neurotoxic effects of p-chloroamphetamine in rats.
Brain Res. 1991;558:109-111.

25. Henderson MG, Fuller RW. Dextromethorphan antagonizes the
acute depletion of brain serotonin by p-chloroamphetamine and
H75/12 in rats. Brain Res. 1992;594:323-326.

26. Lancaster FE. Alcohol, nitric oxide, and neurotoxicity: is
there a connection? -- a review. Alcohol Clin. Exp. Res.
1992;16:539-541.

27. Morgan PF. Is quinolinic acid an endogenous excitotoxin in
alcohol withdrawal? Med. Hypotheses 1991;36:118-121.

28. Danysz W, Dyr W, et al. The involvement of NMDA receptors in
acute and chronic effects of ethanol. Alcohol Clin. Exp. Res.
1992;16:499-504.

29. Morgan PF, Nadi NS, et al. Mapping rat brain structures
activated during ethanol withdrawal: role of glutamate and NMDA
receptors. Eur. J. Pharmacol. 1992;225:217-223.

30. Heyes MP, Saito K, Markey SP. Human macrophages convert L-
tryptophan into the neurotoxin quinolinic acid. Biochem. J.
1992;283(pt 3):633-635.

31. Heyes MP, Satio K, et al. Poliovirus induces indolamine-2,3-
dioxygenase and quinolinic acid synthesis in macaque brain.
FASEB-J. 1992;6:2977-2989.

32. Loscher W, Honack D. Differences in anticonvulsant potency
and adverse effects between dextromethorphan and dextrorphan in
amygdala-kindled and non-kindled rats. Eur. J. Pharmacol.
1993;238:191-200.

33. Schmitt B, Netzer R, et al. Drug refractory epilepsy in brain
damage: effect of dextromethorphan on EEG in four patients. J.
Neurol., Neurosurg. & Psychiatry 1994;57:333-339.

34. Koyuncuoglu H, Saydam B. The treatment of heroin addicts with
dextromethorphan: a double-blind comparison of dextromethorphan
with chlorpromazine. Int. J. Clin. Pharmacol., Therapy, &
Toxicol. 1990;28:147-152.

35. Welch L, Sovner R. The treatment of a chronic organic mental
disorder with dextromethorphan in a man with severe mental
retardation. Br. J. Psychiatry 1992;161:118-120.

36. Bonuccelli U, Del Dotto P, et al. Dextromethorphan and
parkinsonism [letter]. Lancet. 1992;340:53.

37. Chapman V, Dickenson AH. The combination of NMDA antagonism
and morphine produces profound antinociception in the rat dorsal
horn. Brain Res. 1992;573:321-323.

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

39. Otton SV, Wu D, et al. Inhibition by fluoxetine of cytochrome
P450 2D6 activity. Clin. Pharmacol. & Therapeutics 1993;53:401-
409.

40. Achamallah NS. Visual hallucinations after combining
fluoxetine and dextromethorphan [letter]. Am. J. Psychiatry
1992;149:1406.

41. Kintz P, Mangin P. Toxicological findings in a death
involving dextromethorphan and terfenadine. Am. J. Forensic Med.
Pathol. 1992;13:351-352.

42. Kamei J, Iwamoto Y, Misawa M, Kasuya Y. Effects of rimcazole,
a specific antagonist of sigma sites, on the antitussive effects
of non-narcotic antitussive drugs. Eur. J. Pharmacol.
1993;242:209-211.

43. Szekely JI, Sharpe LG, Jaffe JH. Induction of phencyclidine-
like behavior in rats by dextrorphan but not dextromethorphan.
Pharmacol. Biochem. Behav. 1991;40:381-386.

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

45. Thompson KW, Westerlain CG. Dextromethorphan and its
combination with phenytoin facilitate kindling. Neurology
1993;43:992-994.

46. Simpson MD, Slater P, et al. Alterations in phencyclidine and
sigma binding sites in schizophrenic brains. Effects of disease
process and neuroleptic medication. Schizophr. Res. 1991;6:41-
48.

47. Lang A, Vasar E, et al. The involvement of sigma and
phencyclidine receptors in the action of antipsychotic drugs.
Pharmacol. Toxicol. 1992;71:132-138.

48. Shibuya H, Mori H, Toru M. Sigma receptors in schizophrenic
cerebral cortices. Neurochem. Res. 1992;17:983-990.

49. Debonnel G. Current hypotheses on sigma receptors and their
physiological role: possible implications in psychiatry.
[Review]. J. Psychiatry & Neurosci. 1993;18:157-172.

50. Micheletti G, Lannes B, et al. Chronic administration of NMDA
antagonists induces D2 receptor synthesis in rat striatum.
Brain. Res. Mol. Brain Res. 1992;14:362-368.

51. Wolfe SA Jr, De Souza EB. Sigma and phencyclidine receptors
in the brain-endocrine-immune axis. [Review]. NIDA Res.
Monograph Ser. 1993;133:95-123.

52. Huang X, Nichols DE. 5-HT2 receptor-mediated potentiation of
dopamine synthesis and central serotonergic deficits. Eur. J.
Pharmacol. 1993;238:291-296.

53. Khanna JM, Shah G, Weiner J, et al. Effect of NMDA receptor
antagonists on rapid tolerance to ethanol. Eur. J. Pharmacol.
1993;230:23-31.

54. Schneider SM, Michelson EA, et al. Dextromethorphan poisoning
reversed by naloxone. [Review]. Am. J. Emerg. Med. 1991;9:237-
238.

55. Kamei J, Iwamoto Y, et al. Involvement of haloperidol-
sensitive sigma-sites in antitussive effects. Eur. J. Pharmacol.
1992;224:39-43.

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

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

58. Zhou GZ, Musacchio JM. Computer-assisted modeling of multiple
dextromethorphan and sigma binding sites in guinea pig brain.
Eur. J. Pharmacol. 1991;206:261-269.

59. Netzer R, Pflimlin P, Trube G. Dextromethorphan blocks N-
methyl-D-aspartate-induced currents and voltage-operated inward
currents in cultured cortical neurons. Eur. J. Pharmacol.
1993;238:209-216.

60. Canoll PD, Smith PR, Musacchio JM. Ropizine concurrently
enhances and inhibits [3H]dextromethorphan binding to different
structures of the guinea pig brain: autoradiographic evidence for
multiple binding sites. Life Sci. 1990;46:PL9-16.

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

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

63. Bubser M, Keseberg U, Notz PK, Schmidt WJ. Differential
behavioural and neurochemical effects of competitive and non-
competitive NMDA receptor antagonists in rats. Eur. J.
Pharmacol. 1992;229:75-82.

64. Oye I, Paulsen O, et al. Effects of ketamine on sensory
perception: evidence for a role of N-methyl-D-aspartate
receptors. Pharmacol. Exp. Ther. 1992;260:1209-1213.

65. Miller CL, Bickford PC, et al. Phencyclidine and auditory
sensory gating in the hippocampus of the rat. Neuropharmacology
1992;31:1041-1048.

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

67. Gasic GP, Heinemann S. Receptors coupled to ionic channels:
the glutamate receptor family. Curr. Opin. Neurobiol. 1991;1:20-
26.

68. Bortolotto ZA, Collingridge GL. Activation of glutamate
metabotropic receptors induces long-term potentiation. Eur. J.
Pharmacol. 1992;214:297-298.

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

70. Akunne HC, Johannessen JN, et al. 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
reuptake complex. Neurochem. Res. 1992;17:261-264.

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

72. Izenwasser S, Newman AH, Katz JL. Cocaine and several sigma
receptor ligands inhibit dopamine uptake in rat caudate-putamen.
Eur. J. Pharmacol. 1993;243:201-205.

73. Witkin JM, Terry P, et al. Effects of the selective sigma
receptor ligand, 6-[6-(4-hydroxypiperidinyl)hexyloxyl-3-
methylflavone (NPC 16377), on behavioral and toxic effects of
cocaine. J. Pharmacol. & Exp. Therapeutics 1993;266:473-482.

74. Shirayama Y, Nishikawa T, Umino A, Takahashi K. p-
Chlorophenylalanine-reversible reduction of sigma binding sites
by chronic imipramine treatment in rat brain. Eur. J. Pharmacol.
1993;237:117-126.

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

76. Rao TS, Cler JA, et al. Neurochemical characterization of
dopaminergic effects of opipramol, a potent sigma receptor
ligand, in vivo. Neuropharmacology 1991;4:95-102.

77. Gorski JC, Jones DR, et al. Characterization of
dextromethorphan N-demethylation by human liver microsomes.
Contribution of the cytochrome P450 3A (CYP3A) subfamily.
Biochem. Pharmacol. 1994;48:173-182.

78. Conner MA, Chavkin C. Ionic zinc may function as an
endogenous ligand for the haloperidol-sensitive sigma 2 receptor
in rat brain. Mol. Pharmacol. 1992;42:471-479.

79. Jeanjean AP, Mestre M, Maloteaux JM, et al. Is the sigma-2
receptor in rat brain related to the K+ channel of class III
antiarrhythmic drugs? Eur J. Pharmacol. 1993;241:111-116.

80. Itzhak Y. Repeated methamphetamine-treatment alters brain
sigma receptors. Eur. J. Pharmacol. 1993;230:243-244.

81. Mash DC, Zabetian CF. Sigma receptors are associated with
cortical limbic areas in the primate brain. Synapse 1992;12:195-
205.

82. Roman FJ, Martin B, Junien JL. In vivo interaction of
neuropeptide Y and peptide YY with sigma receptor sites in the
mouse brain. Eur. J. Pharmacol. 1993;242:305-307.

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

84. Klein M, Canoll PD, Musacchio JM. SKF 525-A and cytochrome P-
450 ligands inhibit with high affinity the binding of
[3H]dextromethorphan and sigma ligands to guinea pig brain. Life
Sci. 1991;48:543-550.

85. Larson AA, Sun X. Regulation of sigma activity by amine-
terminus of substance P in the mouse spinal cord: involvement of
phencyclidine (PCP) sites not linked to N-methyl-D-aspartate
(NMDA) activity. Neuropharmacology 1993;32:909-917.

86. Su TP. Deliniating biochemical and functional properties of
sigma receptors: emerging concepts. [Review]. Crit. Rev. in
Neurobiol. 1993;7:187-203.

87. Beaton JA, Stemsrud K, Monaghan DT. Identification of a novel
N-methyl-D-aspartate receptor population in the rat medial
thalamus. J. Neurochem. 1992;59:754-757.

88. Keller EA, Borghese CM, et al. The learning capacity of high
or low performance rats is related to the hippocampus NMDA
receptors. Brain Res. 1992;576:162-164.

(General references used for the FAQ, but not specifically cited)

89. Loscher W, Annies R, Honack D. Comparison of competitive and
uncompetitive NMDA receptor antagonists with regard to
monoaminergic neuronal activity and behavioural effects in rats.
Eur. J. Pharmacol. 1993;242:263-274.

90. Loscher W, Honack D. Effects of the novel 5-HT1A
receptor antagonist, (+)-WAY 100135, on the stereotyped
behaviour induced by NMDA receptor antagonist dizocilpine in
rats. Eur. J. Pharmacol. 1993;242:99-104.

91. Brent PJ, Chahl LA, Cantarella PA, Kavanagh C. The kappa-
opioid receptor agonist UH50,488H induces acute physical
dependence in guinea-pigs. Eur. J. Pharmacol. 1993;241:149-156.

92. Grynne BH, Holmen AT, Maurset A. Evidence for distinct
phencyclidine and SKF10047 receptors following detergent
treatment of rat brain membranes. Pharmacol. Toxicol.
1992;70:25-30.

93. Muraki A, Komaya T, et al. MK-801, a non-competative
antagonist of NMDA receptor, prevents methamphetamine-induced
decrease of striatal dopamine uptake sites in the rat striatum.
Neurosci. Lett. 1992;136:39-42.

94. Koyuncuoglu H, Aricioglu F. Previous chronic blockade of NMDA
receptors intensifies morphine dependence in rats.

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

96. Shinn AF (ed.). Evaluations of Drug Interactions. Macmillan,
1988 (NY).
--
| Bill White +1-614-594-3434 | bwhite@oucsace.cs.ohiou.edu |
| 44 Canterbury, Athens OH 45701 | finger for PGP2.2 block |
| http://oucsace.cs.ohiou.edu/personal/bwhite.html (check it out!) |
 
To the best of our knowledge, the text on this page may be freely reproduced and distributed.
If you have any questions about this, please check out our Copyright Policy.

 

totse.com certificate signatures
 
 
About | Advertise | Bad Ideas | Community | Contact Us | Copyright Policy | Drugs | Ego | Erotica
FAQ | Fringe | Link to totse.com | Search | Society | Submissions | Technology
Hot Topics
Pesticide synth
the raid thread
thermite
Where to Start?
Fishtea's E-Book Collection
Insering Drugs onto blotter paper ?
a meth synth is basically...
Concrete Question
 
Sponsored Links
 
Ads presented by the
AdBrite Ad Network

 

TSHIRT HELL T-SHIRTS