Subject: FAQ-Dextromethorphan 2.2 (last modified 12/1/1994)

                            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
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
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
Any questions or comments may be addressed to me: (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
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;
    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
  GABAGamma-Aminobutyric Acid (a receptor type)
  NMDAN-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
- 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
  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 SuppressantRobins
 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.

	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
  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
  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
  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
  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
  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.
  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
  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-
  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,
  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
     <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
            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
            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).
            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.
            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.
            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
            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
            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
            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
            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.
            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.
            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.
            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
     <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
            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.
            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.
            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 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
            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.
            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
            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).
            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
     <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
     <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
     <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
            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
     <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
            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
            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)
            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
            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
     <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
     <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
            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
     <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-
          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
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