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THE DEXTROMETHORPHAN FAQ
ANSWERS TO FREQUENTLY ASKED QUESTIONS
ABOUT DEXTROMETHORPHAN (DXM)
William E. White
ASCII Text Version 3.0
Copyright (c) 1995
All Rights Reserved
Originally Written for Usenet alt.drugs
=============================================================================
NOTES on ASCII TEXT VERSION
This version is available from my website as an ASCII document, in two
parts (as a single part it is too big for my DOS version of vi).
My website, incidentally, is located at:
http://oucsace.cs.ohiou.edu/personal/bwhite/start.html
The Table of Contents is structured so that you can search for a given
section by looking for the bracketed number or letter set, e.g., [1.2]
for Section 1.2; [A.2] for Appendix 2; etc. Obviously, the index is
omitted from the ASCII text version, as there are no page numbers.
Chapters are separated by double (====) lines; sections by single (----)
lines. Subsections are separated by dotted (....) lines, and in some
cases (e.g., Chapter 10), I use half-dotted (. . . ) lines.
I've done my best to transfer the diagrams and drawings to ASCII, but
it's still not much more than adequate. If you wish you may download
and print the PostScript[TM] version from my website, or you may
purchase bound, printed copies from me. See below for further info
on purchasing and on license fees.
Part 01/02: Beginning through Chapter 9, inclusive
Part 02/02: Chapter 10 (personal reports), Appendices, References, and
Glossary.
Acknowledgements, Section 1
=============================================================================
This document is a FAQ ("fack"), i.e., a series of questions and answers.
The term comes from Usenet, and stands for Frequently Asked Questions.
These are the sorts of questions that people new to Usenet tend to ask
frequently. When these questions become frequent enough, the question and
its answer may be placed into the FAQ for the newsgroup (or for a topic
within the newsgroup). A few people use the term AFAQ (Answers to
Frequently Asked Questions), but most use FAQ to refer both to a frequent
question and to the document written to answer such questions.
This FAQ covers dextromethorphan (decks-tro-meth-OR-fan), the cough
suppressant commonly found in cough medicines available over-the-counter in
the USA and other parts of the world. Of course, dextromethorphan (DXM)
does more than suppress coughs; otherwise, there wouldn't be so much
discussion about it on alt.drugs (the Usenet newsgroup from which this FAQ
originated). The bizarre truth about DXM is that it is a very potent
psychoactive drug when taken in sufficient quantities. So if you've ever
heard about people drinking cough syrup for fun, well, now you know why.
The trouble, however, is that most cough medicines have other ingredients
which can make you uncomfortable, sick, or dead, depending on the
ingredient and how much you take. This document is primarily intended to
combat potentially dangerous misinformation about the recreational use of
DXM.
My own interest in DXM came quite by accident; once, while sick with the
flu, I misread the instructions on a bottle of cough syrup and drank two
shots from the included shotglass instead of two teaspoons. Soon after I
noticed that music and motion had become very satisfying experiences. This
left me puzzled, and my reaction was to go to the library and research DXM
through Medline, medical journals, and books.
Of course at that point I was hooked - not on DXM, but on neuropharma-
cology. I decided to learn as much as I could about DXM, and found it to
be one of the most unique and interesting of all recreational drugs in
terms of how it works on the brain.
About this time I noticed a number of incorrect and potentially dangerous
posts (articles) about DXM appearing on alt.drugs. So, I decided to gather
the information I had and write a FAQ. It eventually became much more than
a FAQ, giving explanations and information in addition to answers, but by
then the name had stuck. The FAQ took me over 150 hours to complete - I
figured if I'm going to do it, I'd better do it right.
After publishing the DXM FAQ, the reports of DXM use started coming in.
People who had been using DXM but were uncomfortable talking about "getting
high off cough syrup" shared their stories with me. Some were good, some
were bad, some indifferent. I've been trying my best to get all of these
personal reports together into a coherent whole, but this FAQ is written in
my free time and I don't get paid for it (although donations are
acceptable. :-)
Please note that it is not my intention to get a bunch of people hooked on
cough syrup (actually addiction is very rare, but you get my point). It is
my intention for people to know the truth so they don't make bad decisions
for lack of knowledge. DXM is not safe and harmless; nothing is. Nor is
it universally enjoyable; in fact, some find high-dose DXM experiences
terrifying. But I believe that people can only make good decisions, or
learn from bad decisions, if information is available. So please, use your
head!
William White
May 10, 1995
=============================================================================
IMPORTANT INFORMATION REGARDING
DRIXORAL COUGH LIQUID CAPS[tm]
Since this document was completed, Drixoral Cough Liquid Caps[tm], one of
the most popular forms of DXM for recreational use, have disappeared from
the market. The official stance of Schering-Plough (the manufacturer) is
that they were simply not popular. I strongly suspect, however, that
recreational use was a major factor, if not the only factor, in their
decision to pull the product from the market.
Replacing this product is a similar product (Drixoral Cough and Fever, if I
remember correctly), which contains acetaminophen. Recreational use of any
product containing acetaminophen could easily kill you.
As of this update, the Drixoral Cough Liquid Caps[tm] are still available
in a few stores which have not sold or destroyed their stock. Another
brand may come out with a similar product (or it may not; I don't know).
If you wish to continue using DXM, I strongly suggest you switch to the
extraction processes listed in Section 7.1 and 7.2. These processes will
allow you to remove the DXM from cough syrups, using easily available
materials, and yielding a pure product. Furthermore, since the DXM formed
is the free base, rather than the hydrobromide salt, you can avoid
excessive bromide intake (a potential problem with regular use of DXM -
see Section 2.7).
If you choose to switch to, or continue using, cough syrups (e.g.,
Robitussin Maximum Strength Cough[tm] or Vicks Formula 44[tm]), please be
aware that the large amount of glucose, thickeners, etc., may be hard on
your kidneys and pancreas. Precipitated DXM is probably safer.
I anticipate that DXM-only products will continue to disappear from the
market, as more and more people learn of DXM's psychoactive potential. In
response to this I am currently researching methods to extract DXM from
DXM+guafenesin and DXM+acetaminophen products, giving high yield of pure
DXM, and using easily available materials. I hope to complete these
experiments by the end of the year (1995).
=============================================================================
THE DEXTROMETHORPHAN FAQ
ANSWERS TO FREQUENTLY ASKED QUESTIONS
ABOUT DEXTROMETHORPHAN (DXM)
TABLE OF CONTENTS
[ACK] ACKNOWLEDGEMENTS
[1] PRELIMINARY
[1.1] Restrictions and Disclaimer (Read This First!)
Distribution Restrictions
General Disclaimer
How to Reach the Author
[1.2] Why a DXM FAQ?
[1.3] Keeping DXM Legal
[1.4] How to Use This Document
[2] GENERAL INFORMATION ABOUT DXM
[2.1] DXM Quick Reference Page
[2.2] What is Dextromethorphan (DXM) Hydrobromide?
[2.3] What is Dextromethorphan Polistirex?
[2.4] What is Dextrorphan (DXO)?
[2.5] How does one obtain and use DXM?
Drinking Cough Syrup
Gelcaps and Capsules
Pharmaceutical and Chemical Suppliers
Extracted DXM Ingestion
Injection and Other Routes
[2.6] What are some typical DXM-containing commercial preparations?
1mg/ml DXM (120mg per 4oz bottle)
1.5mg/ml DXM (180mg per 4oz bottle)
2mg/ml DXM (240mg per 4oz bottle)
3mg/ml DXM (360mg per 4oz bottle)
15mg/capsule or tablet
30mg/capsule or tablet
[2.7] What should I know about other drug ingredients?
Decongestants
Antihistamines
Guaifenesin
Analgesics
Alcohol
Food Coloring / Dyes
Bromide Ions
Other "Inactive" Ingredients
[2.8] Why are so many DXM preparations in liquid form?
[2.9] Is recreational use of DXM illegal?
[2.10] Other (medical) uses for DXM
[2.11] Drug Interactions
[2.12] What about other cough suppressants?
[2.13] Can DXM be detected on drug tests?
[3] THE DXM DRUG EXPERIENCE
[3.1] What is the general character of a DXM experience?
[3.2] The First Plateau
Sensory Effects
Cognitive Effects
Motor Effects
Memory Effects
Emotional Effects
[3.3] The Second Plateau
Sensory Effects
Cognitive Effects
Motor Effects
Memory Effects
Emotional Effects
[3.4] The Third Plateau
Sensory Effects
Cognitive Effects
Motor Effects
Memory Effects
Emotional Effects
[3.5] The Fourth Plateau
[3.6] Is there anything beyond the fourth plateau?
[3.7] What happens with long-term or regular use?
[3.8] What are some fun or interesting things to do on DXM?
Listen to Music
Dance
Go Swimming (low dose only!)
Group Tripping
Have Sex
Shamanic Journeying (see also Section 3.12)
Hang out in a Sensory Deprivation Tank
[3.9] What are some things to avoid on DXM?
Heavy Exercise
Driving
Going to Class or School
Dose "Boosting" and Redosing
[3.10] Why does DXM affect different people so differently?
[3.11] How does DXM compare with other dissociatives?
[3.12] Is there any connection between DXM and out-of-body or shamanic
experiences?
[3.13] Why can't I hallucinate on DXM?
[4] DXM SIDE EFFECTS AND OTHER THINGS TO AVOID
[4.1] What are the potential side effects and risks of
occasional use?
Nausea and other gastric disturbances
Itching and allergic reactions
Hangovers
Pupil dilation
Tachycardia (Increased heart rate)
Hot and cold flashes
Hyperthermia
Panic attacks
Overexertion
Psychotic episodes
Hypertension (high blood pressure)
Miscellaneous
[4.2] What are the potential side effects and risks of regular use?
Mania
Cognitive impairment
Memory impairment
Habituation and Psychological Addiction
Tolerance and Physical Addiction
Neurotoxicity
Excitotoxic Rebound
Psychosis
Kidney damage
Bromide poisoning
Miscellaneous
[4.3] Is DXM addictive?
[4.4] Is DXM withdrawal dangerous?
[4.5] DXM hangovers - avoiding and alleviating
[4.6] How toxic is DXM? What is the LD50? Should I worry?
[4.7] Do you recommend DXM for recreational use?
[4.8] Help! What do I do if...
Itching (the "Robo Itch")
Fast Heartbeat and Panic Attacks
Irregular Heartbeat, or "Skipped Beats"
Nausea, vomiting, gas, and diarrhea
Unconsciousness
High body temperature / fever
Shortness of breath
Sensation of choking one's tongue
Nosebleeds
Feeling "dead" / losing one's body
Hangovers (lethargy and feeling "not all there")
Prolonged dissociation from the real world
[5] PHYSIOLOGICAL EFFECTS OF DXM
[5.1] How does DXM inhibit the cough reflex?
[5.2] How does DXM cause its psychoactive effects?
General Information
Contribution of the PCP2 Binding Site
Contribution of the Sigma Binding Sites
Contribution of the NMDA Receptor
Contributions of Indirect Activity
Flanging
Hyper-Abstraction
Delusions and Memory Problems
[5.3] Why does DXM exhibit plateaus?
Plateaus 1-3: Multiple Receptors
The Fourth Plateau
[5.4] Why is this so complicated?
[5.5] How does DXM get metabolized? (Pharmacokinetics)
Factors Affecting DXM's Metabolism
[6] NEUROPHARMACOLOGY OF DXM
[6.1] What is a receptor, anyway? (Basic Neuropharmacology)
[6.2] What are Sigma Receptors?
Sigma 1 Receptors and General Sigma Information
Sigma 2 Receptors
Sigma 3 Receptors
[6.3] What are NMDA Receptors?
NMDA and Other Glutamate Receptors
NMDA Receptor Function and Structure
NMDA and Excitotoxicity
[6.4] What are PCP2 Receptors?
[6.5] What are Na+ and Ca2+ channels?
[6.6] How does DXM compare to other drugs at these receptors?
[6.7] Endopsychosin and the Big Picture
[7] DXM CHEMISTRY AND EXTRACTION
[7.1] How can I extract DXM from cough formulae?
[7.2] How can I get rid of other drug ingredients?
[7.3] How do I use free base DXM?
[7.4] How can I synthesize DXM?
[7.5] What can I synthesize from DXM?
Dextrorphan
Levorphanol / Levomethorphan
3-substituted Analogs [NOT IN POSTED VERSION]
[8] MIXING DXM WITH OTHER RECREATIONAL DRUGS
[8.1] Alcohol
[8.2] Barbiturates and Benzodiazepines
[8.3] Amphetamines and Other Psychostimulants
[8.4] Cannabis (Marijuana)
[8.5] LSD, psilocybin, and other 5HT hallucinogens
[8.6] Opiates
[8.7] PCP and ketamine
[8.8] Nicotine
[8.9] Nootropics (Smart Drugs)
[8.10] Miscellaneous Other Drugs
[9] DXM DRUG CULTURE
[9.1] Is there, or was there, a DXM drug culture?
[9.2] Why haven't I ever heard about it?
[9.3] Is there a "drug slang" for DXM?
[9.4] Are there any street names for DXM?
[9.5] How do I explain to my friends that I'm getting high off
cough syrup?
[10] DXM EXPERIENCES AND PERSONAL REPORTS [NOT IN POSTED VERSION]
[10.1] First and Second Plateau Experiences
Positive Experiences
Negative Experiences
[10.2] Third and Fourth Plateau Experiences
Positive Experiences
Negative Experiences
[10.3] Long-term Use Experiences
Positive Experiences
Negative Experiences
[10.4] Multiple Drug Experiences
DXM + Cannabis + Alcohol + Opium
DXM + Cyclizine
DXM + Psilocybe mushrooms + LSD + Cannabis + Nitrous Oxide
[A] APPENDICES
[A.1] Appendix 1: P450 Inhibiting Drugs
[A.2] Appendix 2: Receptor Binding of Recreational Drugs
[A.3] Appendix 3: Other Sigma and NMDA Ligands
[R] REFERENCES
[G] GLOSSARY
[I] INDEX
=============================================================================
Figure 1: DXM Molecule
Figure 2: Possible Basis of Plateaus
Figure 3: Fourth Plateau Pruning Hypothesis
Figure 4: DXM Metabolism
Figure 5: DXM Metabolism, normal and abnormal P450-2D6
Figure 6: Effects of doubled and repeated dosing
Figure 7: Ion Channel
Figure 8: NMDA Channel
Figure 9: Partially Open NMDA Channel
Figure 10: Fully Open NMDA Channel
Table 1: DXM Plateaus and Dosages
Table 2: DXM Binding Sites
Table 3: Differential Solubility Data
Table 4: 3-Substituted DXM Analogs
=============================================================================
[ACK] ACKNOWLEDGEMENTS
First and foremost I would like to thank my wife, Nicole, for providing me
with a seemingly endless supply of love and support, and for putting up
with my idiosyncrasies. I doubt anyone else could have coped with being
married to someone whose idea of fun is spending hours in a library
researching tripping off of cough syrup.
I would also like to thank Barbara Adeanna and Peter Zachariah Kramer who
helped me proofread the FAQ and who took the time to tell me when I was
confusing, unclear, or simply full of it. Additionally I would like to
thank them for their support and encouragement throughout the writing
process.
I would like to acknowledge Schering-Plough, Richardson-Vicks, and other
OTC pharmaceutical companies, for giving me something to write about. How
about bringing back DXM-only pills, folks?
The evolution of this document also owes a great deal to the participants
of Usenet alt.drugs, alt.psychoactives, and rec.drugs.psychedelic, notably
including P. L. and all the people who made hyperreal.com what it is today.
And to the hundred or so people who contributed their experiences to the
FAQ, thank you; my understanding of DXM came about because of your
assistance.
Finally, thanks to my friend H., who taught me about DXM in the first
place.
==============================================================================
[1] PRELIMINARY
[1.1] Restrictions and Disclaimer (Read This First!)
This text covers the recreational and medical uses of dextromethorphan, a
cough suppressant in common use in over-the-counter (non-prescription)
cough medicines. This is version 3.0-T (ASCII Text).
Distribution Restrictions
Distribution in electronic form is permitted, free of charge, except as
otherwise specified below.
o When distributed electronically, this document may be broken up into
sections, provided all sections receive the same distribution and all
are distributed within 1 day. (The exception is the Quick Reference
Page, which may be distributed by itself).
o When distributed by the author via Usenet, some sections may be
omitted at the author's discretion. Automatic redistribution (i.e.,
Usenet news) may legally duplicate this pattern of omissions.
o You are permitted to make a printed copy of the electronic document
for personal use, and encouraged to pay the US$10.00 license fee when
convenient. Any additional printed copies may be made at a license
fee of US$10.00 per copy, sent to my address (see below). You may also
purchase bound, printed copies of this text for US$20.00 plus shipping
and handling; email, mail, or telephone me for information.
o Sale of this document in any form (electronic or printed) by anyone
other than the author is expressly forbidden.
o When distribution in electronic form, this document must remain in the
same format as received (e.g., ASCII, PostScript[tm], etc.). For
information regarding specific formats, please contact me.
o The HTML format hypertext files on my website may not be distributed
without my approval; please use my site for them. You may, however,
provide links to them.
o Once a given version number has been released, no prior versions may
be distributed without written permission. Please stick to this rule
if you can; I try and keep the information in this document as up-to-
date as possible.
o This document may be cited as:
White, William E. (1995) The Dextromethorphan FAQ: Answers to
Frequently Asked Questions about Dextromethorphan (DXM), (v. 3.0-T).
Usenet newsgroup rec.drugs.psychedelic. Available in HTML at:
http://oucsace.cs.ohiou.edu/personal/bwhite/DXM.html.
o 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.
(This restriction is also present in the general copyright notice).
o No modified version of this document may be distributed in any form.
(This restriction is also present in the general copyright notice).
..............................................................................
General Disclaimer
This text discusses some rather controversial topics. Currently, there are
laws in most places of the world that make it illegal to use certain drugs
for recreational purposes. It doesn't take a genius to figure out that the
medical nature of the drugs in question has nothing to do with their legal
status (otherwise, alcohol would be illegal and we'd all be smoking
dope(1)).
In particular, a lot of people are making a lot of money from the illegal
drug trade. The distributors, manufacturers, and sellers of illegal drugs
are among them, of course. So are the law enforcement agencies and
politicians, and the manufacturers and distributors of legal drugs like
nicotine and alcohol. In the past few years, many scientists, physicians,
journalists, and others have suggested legalization as a way to reduce the
harm associated with the drug trade.
It is not my desire to address this topic in depth here. What is important
is that, in response to these suggestions, the proponents of the War on
Drugs (and its equivalents elsewhere) have become increasingly aggressive.
One of their goals is to prevent the dissemination of information about
recreational drugs (unless it's their own propaganda). As such, anyone
even discussing drug use is walking on thin ice, and once you go about
telling people how to do it, the ice becomes a lot thinner.
I have no intention of being thrown into prison so that they are forced to
release rapists, murderers, and child molesters in order to make room for
me. I'm not planning to become a martyr any time soon; I'd much prefer for
the Drug Peace to come without violence (legal or physical). However, I
feel it is important to provide true information about drugs. J. S. Mill
argued very eloquently that if an idea is true, then it can only become
stronger when it is confronted with falsehood; to prevent debate in the
hope of protecting the "truth" only leads to lies. I agree entirely, and
quite frankly I think anyone even thinking of getting into politics should
be familiar with (and hopefully agree with) Mill and his arguments. Honest
and open discussion of drugs can only lead to better policy and less harm.
In any case, like so many others, I am walking on somewhat thin ice here,
and must take certain steps to protect myself. Thus the following rather
verbose disclaimer, which may or may not be worth anything in an actual
court of law:
It is not my intention to influence anyone to commit an illegal act. I
explicitly instruct all readers not to violate any international, national,
state, regional, city, or other applicable laws governing any of the
information presented in any document authored by me or made available by
me through electronic or other publishing methods, including this document.
Specifically, I hereby advise everyone not to ingest, inject, smoke,
snort, shove up your ass, or otherwise administer any legal or illegal drug
(except for legal drugs under order of a physician), or to engage in the
manufacture, distribution, synthesis, analysis, or other processing of any
legal or illegal drug, regardless of anything you may see in the
aforementioned documents. I advise everyone not to follow any procedures
listed. All information is presented for EDUCATIONAL PURPOSES ONLY!
None of the information in this document is guaranteed to be accurate or
valid in any way. Anyone attempting any such action or process takes full
responsibility for any outcome resulting from such, and neither I, nor my
access provider, nor any other subset of the Usenet/Internet or world
community (except for the person or persons attempting the action) may be
held responsible.
By proceeding past this Disclaimer, you agree to assume all responsibility
for any actions, legal or not, that you may take. If any part of this
disclaimer is found to be invalid, then all rights to access and distribute
this information are revoked.
..............................................................................
How to Reach the Author
Any questions or comments may be addressed to me:
Email: bwhite@oucsace.cs.ohiou.edu
PGP 2.6.2 block available by finger
Encrypted mail preferred.
US Mail: William White
PO Box 536
Athens, OH 45701 USA
Telephone: 1-614-594-3434 (USA)
10:00 - 21:00 Eastern Standard Time
A number of people have reported difficulties obtaining my PGP key via
finger. If you experience problems, you can compare it against the
following (assuming, of course, someone hasn't dorked with this document).
If you're really paranoid, call me up and I can read it to you.
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Version: 2.6.2
mQCNAi1lhpkAAAEEALzR0vS+W7qdMjQJz0Lc+TQm86HMpHu1ZEGDtGHcZShBy/tB
xoDueEe7vy0nPJpvrfoEUjp8KhR55/Eb1i27CCTP47+5IvJNlV+1D0xrnaX6gSWr
OVPjz/rLOvi8BHQxu7XNQ1BfUaaV0CPs8McPSUyeEqzNNadKouCp8NBoN4HlAAUR
tC5XaWxsaWFtIEUuIFdoaXRlIDxid2hpdGVAb3Vjc2FjZS5jcy5vaGlvdS5lZHU+
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Please don't call me up, telling me I'm going to Hell or somesuch nonsense.
I don't believe in it and I don't have the time or inclination to listen
to that sort of drivel. Thus far I've gotten only good responses, and I
thank everyone who has taken the time to email me, call me, or otherwise
contact me.
Testimonials and personal data are presented anonymously. I do not
maintain copies of the sender's name, address, or personal information,
either online or offline, and thus I cannot give information as to their
identities. Any personal information, testimonials, or reports as to DXM's
effects that were or are sent to me will be considered anecdotal and not
specifically referring to the sender. I encourage anyone with applicable
data to send it to me anonymously. Any data sent PGP encoded will be
decoded on my private system (MS-DOS) which is offline. After decoding,
all information regarding the sender's identity is overwritten (200 pass
random pattern). Thus I cannot link testimonials or information to senders
after this operation. Note that my system is NOT TEMPEST(2) SECURE (not
that I've noticed any strange vans near my house).
------------------------------------------------------------------------------
[1.2] 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 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. 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 it is fair, and you always learn from it.
This text sprung out of the Usenet newsgroups alt.drugs and
alt.psychoactives(3), 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 once a month (more or less) on the Usenet newsgroups
rec.drugs.psychedelic and alt.drugs (until the latter disappears); 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.
------------------------------------------------------------------------------
[1.3] Keeping DXM Legal
Right now, DXM is legal for over-the-counter use in most places. This
seems to be for two reasons primarily. First, there is no substitute for
DXM that does not also have abuse potential. Nor is there likely to ever
be one; everywhere the cough reflex can be blocked involves some type of
receptor associated with recreational drug effects. Second, pharmaceutical
companies don't want to lose a major chunk of their income. DXM works as a
cough suppressant, and it works well. Besides, nobody wants to have to go
to the doctor to get a prescription every time they get a cold.
However, it is possible that DXM-only preparations might disappear from the
market. This would be unfortunate, both for recreational users and for the
general public; the most likely additive - guaifenesin - makes some people
vomit even at low doses. Another possibility would be the addition of
something which would be harmless at regular doses but induce nausea (or
other unpleasant effects) at recreational doses.
The best answer is probably prevention, which unfortunately involves two
conflicting goals. On the one hand, it is essential that DXM related
deaths do not occur - this was my primary motivation in making this FAQ in
the first place. Several DXM cough medicines can be dangerous if consumed
recreationally, due to the presence of other ingredients. There is also
the problem of drug interactions, e.g., DXM + Seldane[tm], which can be
fatal.
On the other hand, the spread of information to keep people from hurting
themselves is also likely to inform people who didn't know about DXM, and
will want to try it. DXM is still an unknown to many people (although not
as big an unknown as most think - pockets of recreational DXM use have
existed as long as DXM has). I've come to the conclusion that I'd rather
have a bunch of people doing it safely than a few doing it dangerously -
but then again, I'm also in favor of sex education.
Thus, I encourage anyone who may want to try DXM or tell her or his friends
to try it (which I again explicitly tell you not to do) to make sure and
emphasize all the risks and dangers involved. Don't rush into high
dosages. Don't trip alone, or without a designated sober person. Don't
encourage people who are not psychologically mature to experiment with DXM.
And please use common sense and be safe.
In the event that DXM-only preparations do get pulled, the best answer is
probably to have an isolation method that will separate the DXM from other
ingredients. In my opinion, the most likely additive is guaifenesin
(although people were using Robitussin DM[tm] long ago, and just toughing
out the inevitable extreme nausea). I've been working on a way to separate
the DXM from guaifenesin, using commonly available substances, and
producing a pure, safe product. We don't want another "cat" (methcath-
inone) media-scare on our hands(4). Currently I offer a method for
evaluation only; this method is not proven. I'm posting it with the FAQ
so that other people can give it their consideration.
In conclusion I'd like to remind everyone that we may be walking on thin
ice here. I've tried my absolute hardest to make this FAQ as accurate
and scholarly as possible, so that if anyone who matters ever does get a
look at it, they'll get bored somewhere around the explanation of P450-2D6
polymorphism :-). Still, please use common sense.
------------------------------------------------------------------------------
[1.4] How to Use This Document
I have tried to make this document useful for a variety of audiences, and
as such it can sometimes get fairly technical. If confused, consult the
glossary; if still confused, check with a basic neuropharmacology text. I
unfortunately do not have the time to answer general questions about
neuropharmacology; I'm employed full time, attempting to start a business,
entering graduate school, and married.
This document is broken up into chapters and sections by subject, with
appendices, references, glossary, and index. At present, figures and
diagrams are fairly minimal; I'm trying to improve that aspect. Also,
sometimes I simplify things a bit. If you take exception to anything,
email me with references and I'll consider modifying it.
If you're lucky enough to be reading this via the World Wide Web,
congratulations. I originally maintained the WWW copy as the primary one,
and derived a text copy; in recent months I've had to reverse this
tradition. I've also tried using several HTML editors before coming to the
conclusion that they all suck, and gone back to the trusty UNIX[tm] vi
editor. One Gen-Yoo-Wine Drixoral? Dollar to the first person who can
prove me wrong - and it had better be able to convert from MS Word[tm]. So
in any case, I've had to go to maintaining the WWW copy concurrently, and
thus it might not always look exactly the same as the printed copy.
From the WWW, on my site, you can also download the text version in the
following formats: Microsoft Word[tm] text source (changes locked out),
PostScript[tm] printouts, and plaintext. Email me for requests for any
other format. Requests for oddball printer formats will be redirected to
the bit bucket. Again, apologies; I just don't have much time anymore.
If this is coming to you via Usenet, please note that the Usenet version is
subdivided into sections; some news machines choke on very long files. I
do not post the section on what you can synthesize from DXM, since it's
mostly specialized information. Email me if you want it. Otherwise,
posting is once a month, with the DXM Quick Reference being posted weekly.
If I'm eating up your bandwidth, I'm sorry; recently a lot of DXM use has
been going on and I want to make sure everyone has the facts available.
---------------------
1 Even moderate quantities of alcohol are toxic to the brain and the
liver; while the liver can sometimes recover, the brain cannot.
Withdrawal from alcohol addiction is physically dangerous, kills large
number of brain cells,and can cause brain damage, coma, and death.
The difference between a recreational dose of alcohol and a toxic dose
is very small (about one order of magnitude). Contrast this with
marijuana, which does not damage brain cells, doesn't harm the liver,
isn't physically addictive, and is so non-toxic that nobody has ever
died of a marijuana overdose.
2 Transient ElectroMagnetic Pulse Electronic Surveillance Technology.
Computers give out a lot of electromagnetic noise, which can be
monitored from up to a mile away. Typically, signals from the
keyboard and monitor are detected. This is actually amazingly easy
(and inexpensive) to do, unless your computer is specifically TEMPEST
shielded.
3 The Usenet newsgroups rec.drugs.misc and rec.drugs,psychedelic (note
the singular form) have since been created. Discussion of DXM is
appropriate in the newsgroup rec.drugs.psychedelic. alt.psycho-
actives is geared more towards nootropics and non-recreational
psychoactive drugs.
4 Methcathinone, or "cat", is an amphetamine-like substance which can
be made using commonly available materials and ingredients.
Unfortunately, most people don't bother to purify it, leading to all
sorts of health problems.
==============================================================================
[2] GENERAL INFORMATION ABOUT DXM
This section covers general information about dextromethorphan, herein
referred to as DXM. IUPAC chemical names are in a sans serif font, in
square brackets. Note the following abbreviations:
CNS Central Nervous System (brain and spinal cord)
CYA Cover Your Ass. Remember this one!
DXM Dextromethorphan
DXO Dextrorphan
OTC Over The Counter (i.e., non-prescription)
PCP [1-(1-phenylcyclohexyl)piperidine] (phencyclidine, "angel dust",
etc.)
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:
o Do not use DXM on a constant or frequent basis! Like alcohol,
constant or frequent (more than once or twice a week) use may be
dangerous.
o Do not use DXM if you have a history of: mental illness, seizures,
epilepsy, liver or kidney disorders, or hypertension.
o Do not use DXM if you are pregnant or nursing. Dissociatives affect
fetal development.
o Never use a product containing acetaminophen/paracetamol (Tylenol[tm]).
Large doses of acetaminophen/paracetamol can cause liver damage or
death.
o Never take DXM if you are taking, will take, or have taken within the
past two weeks, a monoamine oxidase inhibitor (MAOI). MAOIs include
harmine, harmaline, and some prescription drugs for depression and
Parkinson's disease.
o Never take DXM if you are taking, will take, or have taken within six
weeks, the prescription antihistamine terfenadine (Seldane[tm]), or
any other prescription, non-drowsy antihistamine (e.g., Claritin[tm]
or Hisminal[tm]).
o Don't start out with a high dose, or rush in to higher dosage levels.
Instead, gradually increase from your last experiences. DXM can be
very different at different dosage levels.
o Never experiment with hallucinogens without a sober person around to
help you in case you get into trouble.
o NEVER, EVER, EVER drive under the influence of any intoxicating drug
including DXM!
o Avoid all products containing DXM and other active ingredients.
o Avoid the following DXM-only products, which when taken at recreational
doses cause unpleasant effects: Benylin DM
o Remember that DXM can sometimes trigger panic attacks in susceptible
individuals, especially those inexperienced with DXM. This is a major
cause (if not the major cause) of tachycardia (high heart rate) from
DXM. All the more reason not to rush in to anything.
o Always remember: recreational use of DXM is still a great unknown. The
brain you are risking is your own.
------------------------------------------------------------------------------
[2.1] DXM Quick Reference Page
[the following can be printed out on one page (66 lines)]
o----------------------------------------------------------------------------o
| Dextromethorphan (decks-tro-meth-OR-fan), or DXM, is a cough suppressant |
| found in over-the-counter medications. It has also been used recrea- |
| tionally for at least 30 years, without much harm or publicity. |
| Although chemically related to opiates, its effects are closest to |
| ketamine's. In addition to suppressing coughs, DXM is used medically |
| for diagnostic purposes, and may be useful for a variety of conditions |
| from seizures to heroin addiction. In the brain, DXM blocks the |
| dopamine reuptake site, activates the sigma receptor, and blocks the |
| open NMDA channel. (None of these effects are permanent). |
| Occasional recreational use of DXM is probably safe, though side effects |
| and risks have been noted (I hereby tell you not to use any recreational |
| drug including DXM). Many cough medicines contain ingredients other |
| than DXM; some, like acetaminophen (paracetamol) can be fatal when an |
| overdose is taken. The commercial preparations which can be used recre- |
| ationally are those containing DXM only. In the USA this includes |
| mostly Vicks Formula 44 [tm], Robitussin Maximum Strength Cough [tm], |
| Drixoral Cough Liquid Caps [tm], and generic equivalents. All should |
| list ONLY dextromethorphan hydrobromide under active ingredients. Avoid |
| Benylin DM[tm]. The above cough syrups have 3mg/ml (15mg per teaspoon), |
| for 360mg per 4oz bottle and 720mg per 8oz bottle; the cough gelcaps |
| have 30mg each. Preparations like Robitussin DM [tm] which contain guai- |
| fenesin may cause vomiting. |
| Never take DXM with, or up to two weeks before or six weeks after, the |
| prescription "non-drowsy" antihistamines (allergy medications) |
| Seldane[tm], Claritin[tm], or Hisminal[tm]. Never take DXM with, or up |
| to two weeks before or three weeks after, a MAOI (Monoamine Oxidase |
| Inhibitor) - certain drugs for depression; you will probably be told by |
| your doctor if your drug is a MAOI (Prozac[tm] isn't). Never drive under |
| the influence of DXM. Don't take DXM more than once or twice a week. |
| Don't take DXM if you have a history of mental illness, panic attacks, |
| seizures, liver or kidney disease. Some people react very badly to DXM; |
| others don't experience anything at all, partly from inherited lack of |
| an enzyme. Prozac[tm] blocks this enzyme and may lengthen or change the |
| DXM trip. Recreational DXM use may be illegal. DXM may cause false |
| positives on drug tests. |
| DXM trips vary depending on dosage, and can be lumped into four very |
| different plateaus, or types of trips, depending on the amount taken. |
| Dosages are given in milligrams per kilogram, so multiply the figure by |
| your mass in kg (or pounds divided by 2.2). The first plateau, 1.5 to |
| 2.5 mg/kg, is like a slightly intoxicating stimulant; music and movement |
| are often pleasurable. The second plateau, 2.5 to 7.5 mg/kg, is intoxi- |
| cating, with a "stoning" a bit like that of nitrous oxide or marijuana; |
| sounds and sights seem to be on strobe-effect ("flanging"), short-term |
| memory is somewhat disrupted, and there are occasional mild hallucina- |
| tions. The third plateau, at 7.5 to 15mg/kg, consists of strong intoxi- |
| cation, hallucinations, and overall disturbances in thinking, senses, |
| and memory; third plateau trips can be unpleasant. The fourth plateau, |
| above 15mg/kg, is similar to a sub-anesthetic dose of ketamine, with |
| dissociation of the mind from the body, and may be dangerous physically |
| and psychologically. Most recreational use of DXM happens at the first |
| and second plateau. DXM starts to become toxic around 20 to 30mg/kg. |
| While occasional recreational use of DXM is probably safe, some people |
| react very badly to dissociatives, especially at high doses, and may |
| panic. Frequent DXM use, like frequent alcohol use, may be dangerous and |
| should be avoided. Please be safe, be sensible, and use your brain; |
| it's the only one you'll ever have. |
|----------------------------------------------------------------------------|
| From The Dextromethorphan FAQ: Answers to Frequently Asked Questions about |
| DXM, v3.0T, by William White (bwhite@oucsace.cs.ohiou.edu). Available on |
| Usenet rec.drugs.psychedelic and on the World Wide Web via |
| http://oucsace.cs.ohiou.edu/personal/bwhite/start.html. This section may |
| be freely printed or photocopied separately provided it is kept intact, on |
| one page. |
o----------------------------------------------------------------------------o
------------------------------------------------------------------------------
[2.2] What is Dextromethorphan (DXM) Hydrobromide?
o----------------------------------------o Dextromethorphan hydrobromide
| 6-methyl group ---> CH3 | is the water-soluble salt of
| | | dextromethorphan (DXM) and
| N-----CH2 | hydrobromic acid. DXM is a
| H : | | synthetic morphine analog,
| ___\: | | similar to levorphanol. DXM
| / \ | | has been in use in the USA for
| ____ / H...\ _|__ | approximately 30 years, and has
| / ---- \ / | \ | replaced codeine as an OTC
| / \ ____ /....CH2 \ | cough suppressant. It has no
| \\ // \ / | traditional opiate-like
| \\____// \ ____ / | activity, and is not a substi-
| / | tute for codeine as an anal-
| CH3O <--- 3-methoxy group | gesic (1-3).
| |
| Figure 1: DXM Molecule | DXM has been popular as an
o----------------------------------------o "underground" recreational drug
for at least 30 years (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.
DXM's IUPAC name is [(+)-cis-1,3,4,9,10,10a-hexahydro-6-methoxy-11-methyl-
2H-10,4a-iminoethanophenanthrene], and is also (and more commonly) known
as 3-methoxy-17-methyl-(9alpha,13alpha,14alpha)-morphinan; CAS-125-71-3
(1). Note: the 3-methoxy and 6-methyl groups are pointed out for later
notes.
(Oh, just as a side note, I'm proud to say that for once I actually got
the IUPAC name right all by myself - the Merck Index lists the same thing).
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
(probably the latter). At present, there is an increasing body of
knowledge about DXM's potential for recreational use (and abuse) available
in medical journals (3-7,133,137,142-144).
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 different dosage levels, ranging from mild euphoria to full
dissociation.
------------------------------------------------------------------------------
[2.3] 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). The polistirex preparation will probably increase the
ratio of DXM to DXO (see next section).
Dextromethorphan polistirex may be more toxic than the hydrobromide
version, possibly due to buildup of DXM in the bloodstream (146).
------------------------------------------------------------------------------
[2.4] What is Dextrorphan (DXO)?
Dextrorphan is a metabolite of DXM (i.e., the body converts DXM to
dextrorphan). The conversion from DXM to DXO occurs via removal of the
methyl group at position 6, a process called "O-demethylation". DXO is
very similar chemically to DXM, and reacts with the same receptors in the
body, but with a very different spectrum. Whereas DXM is strongest at the
PCP2 and sigma receptors, DXO primarily targets the NMDA receptor (see
chapter 6). The practical upshot is that the dissociative and intoxicating
or "stoning" effects are stronger with DXO, whereas the stimulation,
cognitive alterations, and psychotomimetic (literally, "psychosis-like")
effects are stronger with DXM. Most DXM users find some balance between
the two to be the most pleasurable. Too much sigma activity is usually
regarded as unpleasantly dysphoric and disturbing, and if prolonged, may be
dangerous (102,136).
Fortunately, you don't have to worry about converting DXM to DXO; the body
does it for you via an enzyme called P450-2D6 (debrisoquine 4-hydroxylase).
However, between 5 to 10% of the Caucasian population lacks this enzyme
(12-15), and in the rest of us it can vary. Many drugs can temporarily
block P450-2D6 from working (10-11) and thus alter the balance between DXM
and DXO. For a list of these drugs, see Appendix 1.
One of DXM's metabolites, 3-methoxymorphinan, can itself block P450-2D6.
As a consequence, taking a second dose some time after the first dose of
DXM will probably increase the ratio of DXM to DXO in the bloodstream.
Taking the dose all at once, on the other hand, will probably increase the
relative amount of DXO. Generally, then, the quicker the dosing, the more
DXO and less DXM, and the more NMDA blockade (like ketamine) and the less
sigma and PCP2 activity. Subcutaneous injection leads to very little
conversion from DXM to DXO.
When discussing effects, this text often uses "DXM" to refer to both
dextromethorphan and its metabolite, DXO.
------------------------------------------------------------------------------
[2.5] How does one obtain and use DXM?
DXM is available at drugstores throughout the world; generally it is not
available on the street (I wouldn't trust anyone saying he or she had
street DXM; it's probably ketamine, PCP, or something totally unrelated).
It is most commonly available in cough syrups, though some syrups contain
other ingredients which can make you sick (or dead) if you take too much of
them. It is also available in gelcaps and in some places in capsules.
DXM can also be extracted from cough medicines, and the extract can be
taken orally, injected subcutaneously, intraperitoneally, intramuscuarly,
or intravenously. It can probably also be snorted or used rectally (though
why one would want to I don't know). Smoking doesn't seem very effective.
Some drugstores keep track of people who frequently buy DXM-containing
cough 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. In some cities where DXM use has become popular
(and come to public attention), sales have been restricted to adults. In
Utah in the 1980's, DXM was placed behind the counter due to recreational
use.
..............................................................................
Drinking Cough Syrup
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 other
active ingredients: nasal decongestants, antihistamines, acetaminophen,
or guaifenesin (see Section 2.7). As a rule, you want to avoid all of
them.
Generally speaking, DXM cough syrups all taste nasty. This is for two
reasons: to cover up the (even nastier) taste of DXM itself, and to
prevent recreational use. The generics tend to be less thick, and thus
more drinkable, than the brand names. Some people prefer to mix the DXM
with sodas; others find this only makes an already unpleasant task even
more unpleasant. Your Mileage May Vary.
Most people who have used DXM cough syrups recreationally seem to prefer
to take it on a mostly empty stomach, possibly with crackers or some
other source of carbohydrates. I generally feel that you should avoid
slamming your kidneys and pancreas with a lot of glucose at once; thus
I think some crackers or chips beforehand would be advisable. Greasy
food should be avoided both before and after taking DXM. Most people
report that if carbonated drinks are ingested, they should be clear
(e.g., 7-Up[tm]).
..............................................................................
Gelcaps and Capsules
There are "gelcaps" (liquid or gel filled capsules) available that
contain DXM, but they tend to be brand-name only. One brand containing
only DXM is Drixoral Cough Liquid Caps[tm]. They come in boxes of 10
or 20 gel capsules, each containing 30mg of DXM. The gel capsule
itself is red colored; the liquid inside is actually clear (and tastes
very, very bad). The capsules are somewhat large, and difficult if not
impossible to take without liquid to wash them down. This brand also
comes with a $0.50 or $1.00 manufacturer's coupon inside, which some
have taken to calling Drixoral[tm] Dollars (after Camel Bucks[tm], a
fake currency coupon in Camel[tm] cigarettes which could be collected
and "spent" on various stuff). Note that Drixoral also makes several
other liquid and capsule products, all of which contain undesirable
active ingredients besides DXM.
Absorption from the gelcaps takes some time, and can be sped up by
cracking open each gelcap in your mouth before it is swallowed. Note,
however, that the liquid inside is apt to spurt out, and it tastes bad.
Really, really bad - sour and bitter and cloying all at once with a
stickiness that won't go away. However, if you can stand it, you can
become used to it after the first few gelcaps. You can also crack
open the gelcaps and try to collect the liquid, but it tends to go
everywhere.
Contac CoughCaps[tm] are available in Canada, and are capsule formula-
tions of DXM. I have not personally seen them. In several countries,
there are over-the-counter tablet or capsule DXM pills containing 30mg
per tablet/capsule; one example is Romilar[tm]. Thus far I know they
are available in some areas of southeast Asia and in Saudi Arabia.
..............................................................................
Pharmaceutical and Chemical Suppliers
DXM is not scheduled in the USA (or most other parts of the world),
and consequently should be available via pharmaceutical chemical
suppliers. For example, Sigma Chemical Company (1-800-325-3010)
lists DXM hydrobromide (product D2531) for US $18.20 for 5 grams, US
$128.45 for 50 grams. Note that I have no affiliation with Sigma in
any way; I just happened to have a copy of their catalog handy when
writing this.
In theory, it would be fantastically cheap and easy to order DXM this
way; in practice, it's possibly difficult, and probably a Very Bad
Idea. First off, most chemical companies are wary about selling to
individuals (and if you're not a legal adult, forget it). Secondly,
there's a significant chance that your order will be reported to the
DEA, and although it's not technically illegal, if enough people do
this, that may change very quickly.
Still, though, if you have the courage or stupidity to try, there's
no reason why this shouldn't be a reasonable source. Just use your
head. And don't mention the FAQ.
..............................................................................
Extracted DXM Ingestion
DXM can be extracted (see Section 7.1 and 7.2) and the extracted DXM
can be taken orally, either as free base or as salt (the free base
should convert to the hydrochloride salt in your stomach). The salt
usually available is hydrobromide, but I see no reason why hydro-
chloride, or even acetate or citrate, cannot be used. The free base
tends to be somewhat alkaline and should be avoided unless combined
with food and/or juice (or other acidic beverage). When taken on a
mostly empty stomach, the extract is generally absorbed faster than
cough syrups, gelcaps, or capsules. Some extraction processes may
convert some or all of the DXM into dextrorphan (DXO). Extracted
DXM, unlike cough syrups and gelcaps, has no bromide toxicity (see
Section 2.7).
..............................................................................
Injection and Other Routes
DXM hydrobromide is soluble in saline, and I see no reason why other
acid salts shouldn't be - though their long-term stability may be
doubtful. However, injection is a very dangerous route, especially if
the substance in question is not prepared specifically to be injected.
Some of the potential risks include: sterile abscesses, torn or
collapsed veins, bruising, muscle fiber damage, histamine release,
infection (hepatitis B, HIV, etc.), embolism (and possible resulting
stroke or cardiac arrest), increased chance of addiction, overdose,
and people mistaking you for a junky. True, most of these are
unlikely, and if done correctly injection is generally very safe.
However, the key word is correctly. If you're still interested,
consult a medical text; I'm not going to teach you how to shoot up.
A few notes for those brave or stupid enough to still be interested.
Intravenous (IV) and intramuscular (IM) injection both seem to produce
similar results in animals, and IM injection is almost always safer.
DXM can also be injected intraperitoneally (IP), but that evidently
requires some skill. Subcutaneous (SC) injection ("skin popping")
leads to slower absorption and a great increase in the amount of DXM
relative to DXO. All injected drugs should be completely pure,
dissolved in the appropriate physiological saline. In the case of SC
(and possibly IM) injection, injecting too large a volume of material
can lead to a sterile abscess.
DXM can also theoretically be snorted, although I don't generally
think this is a very smart route; the nasal lining is very tender.
DXM free base is probably too alkaline to try this with. It can also
probably be used rectally, but somehow the thought of a cough syrup
enema doesn't thrill me.
Smoking DXM free base has been attempted several times by various
people without success. It seems that some of the DXM is destroyed by
the heat, and the remaining DXM is extremely harsh on the lungs. Too
bad, really, since self-titration is usually easiest with smoking.
------------------------------------------------------------------------------
[2.6] What are some typical DXM-containing commercial preparations?
Rather than listing the content of commercial DXM preparations (I gave up
since there are so many!), I have decided to list brands and generic
equivalents which contain only DXM. All expressions are in metric. 1tsp
is approx. 5ml; a 4oz bottle is approx. 120ml, and an 8oz bottle approx.
240ml. All preparations listed contain no other active ingredients besides
DXM.
1mg/ml DXM (120mg per 4oz bottle)
Vicks Pediatric Formula 44[tm] (Richardson-Vicks).
I am not aware of any generic equivalents. Very low DXM content.
1.5mg/ml DXM (180mg per 4oz bottle)
Robitussin Pediatric Cough[tm].
Some generic / store-brand equivalents. Most pediatric DXM-only cough
preparations run in this range; again a very low DXM content.
2mg/ml DXM (240mg per 4oz bottle)
Benylin Cough Syrup[tm]. Note: Benylin DM[tm] should be avoided due to
inactive ingredients which cause severe diarrhea.
Some generic / store-brand equivalents. Not terribly common in comparison
to 3mg/ml brands.
Several DXM plus guaifenesin products (e.g., Robitussin DM[tm]) are
2mg/ml. Guaifenesin in high doses tends to induce vomiting.
3mg/ml DXM (360mg per 4oz bottle)
Vicks Formula 44[tm], and generic equivalents. Make sure to avoid
other formulae, such as Vicks Formula 44D[tm].
Robitussin Maximum Strength Cough[tm], and generics. Avoid Robitussin
Maximum Strength Cough and Cold[tm] which has other ingredients.
15mg/capsule or tablet
Evidently, Romilar[tm] is available in 15mg tablets or capsules. I
have not personally seen them.
30mg/capsule or tablet
Drixoral Cough Liquid Caps[tm] and generics (there aren't many).
These are available in packages of 10 or 20 capsules (300mg or
600mg total DXM content per package).
Contac CoughCaps[tm], available in Canada.
Romilar[tm], available in some areas of the world (and possibly by
prescription elsewhere). Also available in 15mg/tablet.
------------------------------------------------------------------------------
[2.7] What should I know about other drug ingredients?
There are five main classes of active ingredients that are present in OTC
DXM-containing products: decongestants, antihistamines, guaifenesin,
analgesics, and alcohol. Each will be discussed in turn, followed by
"inactive" ingredients. With the exception of alcohol, all should be
avoided, although for differing reasons. Additionally, some of the dyes
and other "inactive" ingredients may cause some people trouble.
..............................................................................
Decongestants
There are three nasal decongestants that are used in OTC cough
formulas in the USA: PPA, pseudoephedrine, and phenyleprine (the latter
is almost always found with antihistamines). PPA is also known as
phenylpropanolamine (from which the acronym PPA is derived),
norephedrine, and the IUPAC name [alpha-(1-aminoethyl)benzyl alcohol].
Pseudoephedrine, known as 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 methamphetamine, MDMA
(ecstasy), MDA, etc., and tend to be DEA scheduled. Decongestants 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 (or was, depending on your state) 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 (the "fight or flight" 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 vaso-
constriction (constriction of blood vessels) and decreased nasal
secretions (the good side), and - with larger doses - insomnia,
hypertension, heart rhythm abnormalities, hemorrhaging, stroke, or
death (the bad side) (8). Note that these are extreme reactions, and
that individual tolerance to sympathomimetics tends to vary
considerably. Tolerance can build quickly, and a fatal dose for one
person may have only a mild effect on another person.
Because of the potential danger of hypertension, exceeding the
recommended dose of DXM and decongestant containing preparations may
be asking for trouble. Most people can probably handle it in smaller
recreational doses, but the peripheral "speediness" can be distinctly
unpleasant. Anyone with high blood pressure or the like has no
business taking large quantities of decongestants. Try to avoid these
drugs.
..............................................................................
Antihistamines
The antihistamines operate by blocking histamine receptors (see Section
6 for an explanation of receptors). Peripherally, this has the effect
of reducing the symptoms of histamine 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, most 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 (e.g., Seldane[tm]) but these are prescription 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). High doses of
prescription antihistamines are much more dangerous; do not mix DXM
with prescription antihistamines!
The danger of an antihistamine overdose is very low when using a
DXM-containing product recreationally. However, you will most likely
experience some unpleasant symptoms, such as sleepiness, dry mouth,
heart palpitations, etc. For this reason, I recommend against
products containing antihistamines.
..............................................................................
Guaifenesin
Guaifenesin (gwye-FEN-a-sin) [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 dextrometh-
orphan. Guaifenesin should not be used for chronic coughs or coughs
accompanied by excessive phlegm (1-2).
High doses of guaifenesin tend to induce emesis (i.e., you puke).
Other effects from high guaifenesin doses are not well known, but
probably not serious. However, as most people do not enjoy vomiting,
I would recommend avoiding guaifenesin-containing products.
..............................................................................
Analgesics
Acetaminophen (called paracetamol in the UK) is the most common
analgesic (painkiller) 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 is VERY DANGEROUS. Normally, acetaminophen
is metabolized (broken down) 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 happen right away; it can take 16 hours
before any signs of liver damage show up. This delayed toxic effect
has been responsible for the rather painful deaths of some people who
(accidentally or not) overdose on acetaminophen, and then think they
are fine when no immediate problems occur. There is an antidote
(acetylcystine), but it must be administered within the first 12 to 16
hours.
The toxic dose of acetaminophen can be as low as 50mg/kg; for a 60kg
person this is only six acetaminophen tablets. This is unlikely but
possible. DO NOT UNDER ANY CIRCUMSTANCES USE RECREATIONALLY ANY DXM
PRODUCT WHICH ALSO CONTAINS ACETAMINOPHEN / PARACETAMOL!
As for aspirin and ibuprofen, the other two most common OTC pain-
killers, both tend to irritate the stomach at high doses. I recommend
against them, especially if you have an irritable stomach. Never take
large doses of aspirin or ibuprofen if you have an ulcer.
..............................................................................
Alcohol
Most cough syrups contain some alcohol, to act as a carrier and to
numb the throat. With a few exceptions (such as Nyquil[tm]), the
amount of alcohol is not usually very great. While alcohol does not,
in general, mix well with DXM as a recreational drug, the amount in
cough syrups should not cause trouble unless you are specifically
sensitive to, or attempting to avoid, alcohol. There are alcohol-
free preparations available; many gelcaps are alcohol-free.
..............................................................................
Food Coloring / Dyes
Some of the dyes used in cough formulas may give some people allergic
reactions. Most notable among these is tartrazine (FD&C Yellow #5).
Generally, these dyes are not a problem unless you take a lot of them
(which recreational DXM use may involve). If you think you may be
allergic to a dye, switch to a different brand (or more accurately, a
different color). It is also a good idea to keep an antihistamine (not
a prescription or non-drowsy one!) nearby in case an allergic reaction
does occur.
..............................................................................
Bromide Ions
DXM is usually ingested as a hydrobromide salt. Large amounts of
bromide ions can cause sedation and eventually lead to bromism (bromide
poisoning), which affects (among other things) the skin and nervous
system. I don't think this is terribly relevant for users of DXM
(recreational or not); however it is one more reason to avoid prolonged
high-dose use. You can avoid bromide ions by converting the DXM to
free base and/or hydrochloride salt (see Section 7.6). Some physicians
do believe that prolonged heavy use of DXM may lead to bromism (147).
..............................................................................
Other "Inactive" Ingredients
Cough syrups tend to contain several thickening and sweetening agents.
Glucose, sucrose, invert sugar, and fructose are all commonly used as
sweetening agents. Obviously, a person with blood sugar problems
(diabetes or hypoglycemia) should not take large amounts of these
syrups. Thickening agents are not usually a problem. Occasionally
people will look on cough syrup labels and see propylene glycol or
polyethylene glycol, and (thinking about ethylene glycol, i.e.,
antifreeze) worry about toxicity. Propylene glycol (a thickening and
emulsifying agent) is not toxic, even though ethylene glycol is. The
same goes for polyethylene glycol (PEG) - it's also nontoxic. About
the worst you will get from any of these is an upset stomach.
One general note - keep in mind that your body does eventually have to
use or excrete whatever you eat and drink. Drinking huge amounts of
sugars and thickening agents can put a fair amount of load on the
kidneys, and should definitely be avoided if you have kidney problems
already. There is anecdotal evidence that regular high-dose use of
DXM cough syrups (without eating much) has led to kidney damage due
to the glucose load. I cannot confirm this but I can't disprove it
either.
------------------------------------------------------------------------------
[2.8] Why are so many DXM preparations in liquid form?
Cough preparations are in liquid form for two reasons. First and foremost,
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. Second, tablet-form DXM preparations have been kept from the
market in an attempt to prevent their recreational use.
------------------------------------------------------------------------------
[2.9] Is recreational use of DXM illegal?
Possibly. There may be 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 labeling.
Furthermore, suggesting to someone that they use DXM as a recreational drug
could also be violating a law - against prescribing drugs as a layperson.
Again, it's not likely to happen, but it is possible.
DXM is a prescription drug in Sweden (9). It is prescription and scheduled
in western Australia unless combined with other active ingredients. It may
become prescription in other countries. In drug stores in some areas it is
kept behind the counter, and must be requested.
------------------------------------------------------------------------------
[2.10] 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 Caucasians 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 - NMDA
Receptors) shows great promise is in the prevention of brain damage
resulting from excitotoxicity (over-stimulation of nerve cells to the point
of cell death) and other types of nerve cell damage (19). DXM may reduce
or eliminate the brain damage resulting from conditions such as fever,
hypoxia (lack of oxygen) (20), ischemia (cutoff of blood to brain cells)
(21-22), physical injury (23), infection (such as poliomyelitis,
encephalitis, and meningitis), stroke, seizure, drug toxicity (24-25), and
withdrawal from long-term dependence upon certain drugs (notably alcohol,
barbiturates, and benzodiazepines such as Valium[tm]) (26-29).
In the case of infection (and in particular poliomyelitis), it has been
demonstrated that the damage to the CNS often occurs not from the
infection, but from the body's own defenses, and notably from a chemical
called quinolinic acid (a metabolite of tryptophan) (30,31). Quinolinic
acid is a very potent agonist (activator) at excitatory amino acid
receptors, of which NMDA is one type; DXM prevents quinolinic acid 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, seizure, 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
seizures (called kindling) responds well to DXM. Preliminary studies in
humans indicates that even very low levels of DXM may help prevent
seizures. This effect is not, as was originally thought, due to NMDA
receptors; instead, it is probably due to sigma receptors or voltage-gated
ion channels (32). Interestingly, DXM produces different side-effects in
kindled (seizure-susceptible) animals than in non-kindled animals (this may
be due to uncoupling of NMDA receptors). It is possible that humans
susceptible to seizure 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 (Valium[tm]) was more
effective at combating the symptoms of heroin withdrawal (goose flesh,
tremors, dilated pupils, joint ache, etc.) than chlorpromazine (Thorazine[tm])
plus diazepam (34). This is most likely due to DXM's ability to block NMDA
receptors. A further study (134) verified this, and found that adding
tizanidine (an alpha-2 adrenergic agonist) to DXM was better yet.
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).
------------------------------------------------------------------------------
[2.11] Drug Interactions
DXM should not be used (either recreationally or at normal dosage levels)
by people who are taking a monoamine oxidase inhibitor (MAOI, rhymes with
"wowee") - either a prescription MAOI or a recreational one such as
harmaline. Note that there is considerable confusion among drug users
about what is and isn't a MAOI. MAOIs include a few drugs prescribed for
depression and Parkinson's disease, and a few rare recreational drugs
derived from exotic plant sources (harmine and harmaline, from Syrian Rue
and Yag?, for example). Prozac?, MDMA, cheese, beer, Seldane[tm], etc., are
not MAOIs - they are things to avoid when taking a MAOI. If you are taking
a prescription MAOI you will almost certainly know, as your physician will
have (hopefully!) told you to avoid eating aged cheeses. Combining DXM and
a MAOI has been fatal (3).
Fluoxetine (Prozac[tm]) is a cytochrome P450-2D6 inhibitor (39), and will
change the characteristics of a DXM trip somewhat (increasing the ratio of
DXM to DXO). Other P450-2D6 inhibiting drugs will probably do the same;
see Appendix 1. 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
via other mechanisms by fluoxetine (40).
DXM should not be taken (recreationally or at normal dosage levels) with
the prescription antihistamine terfenadine (Seldane[tm]). This combination
has been fatal (41). Terfenadine has been implicated in other drug
interactions, incidentally. The reason for this interaction seems to be
that terfenadine, which is normally metabolized by a P450 enzyme, induces
heart irregularities when it builds up. DXM may saturate the P450 enzymes
that normally metabolize terfenadine. Incidentally, this probably applies
to Claritin[tm] and Hismanal[tm] as well; avoid combining them with DXM.
Like other psychoactive drugs, DXM should not be used by people who are
mentally or emotionally unstable. I tend to believe that NO recreational
drug (legal or not) should be used unless the user is in a calm, rational
mood, free from anxiety or negative emotions, and is in a controlled
setting where s/he will not have to drive. Speaking of which, as DXM is an
intoxicating drug, don't drive under the influence. Ever. But I shouldn't
have to tell you that, right?
High doses of DXM can be very dissociative. While this is not necessarily
bad, you should know what you are getting into first. A high-dose DXM trip
is not like an LSD trip; it more closely resembles ketamine. You will most
likely encounter experiences that you didn't expect, and possibly didn't
want. While this is OK for the more committed psychonaut, casual users of
hallucinogens might want to think twice before taking a high dose.
Prolonged use of DXM, or extended doses of DXM (including the polistirex
formulation), may cause problems due to the buildup of DXM (as opposed to
DXO), and the resulting activity at sigma receptors (see Section 6). Sigma
receptors seem to have a potent modulatory role on neurons, possibly
inducing permanent or semi-permanent changes when they are activated for
long periods of time (most studies so far indicate over 3 days of high DXM
concentrations are required before such changes occur). Furthermore, sigma
activity seems to be correlated with delusional thinking, which should
probably be avoided, especially in the inexperienced.
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 blood sugar
problems should avoid cough syrups.
------------------------------------------------------------------------------
[2.12] What about other cough suppressants?
The only other non-narcotic cough suppressant of which I am aware is a drug
called noscapine (42). I have little information on it as of yet; look for
more soon. Narcotic cough suppressants include primarily codeine, although
any opiate can be used for that purpose (in fact, heroin was originally
marketed as a cough suppressant). Opiates have an entirely different set
of recreational effects than DXM, however, and are not covered here.
------------------------------------------------------------------------------
[2.13] Can DXM be detected on drug tests?
As DXM itself, probably not; nobody bothers to look for it. On the other
hand, anecdotal evidence indicates that some people will test positive for
opiate use after using recreational DXM(1). Keep this in mind before using
DXM if you have to take a drug test. If worse comes to worse, you can
always claim you had a bad cold, and ask them to do a test which will
discriminate between opiates and DXM. Good luck!
------------
(1) Drug tests aren't particularly good at discriminating between legal and
illegal drugs. Nasal decongestants can cause you to test positive for
amphetamine use, for example.
==============================================================================
[3] THE DXM DRUG EXPERIENCE
This section discusses some of the effects you might expect to feel if you
were to use DXM recreationally (which, for legal reasons, I recommend
against).
------------------------------------------------------------------------------
[3.1] What is the general character of a DXM experience?
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 feeling may change entirely. A reasonable analogy
is water - it exists in three states (solid, liquid, and gas) which all can
exist at varying temperatures (e.g., hot water and cold water), but which
have different and characteristics.
Importantly, DXM and its metabolite, dextrorphan (DXO), produce different
sets of effects. Normally, DXM is converted mostly or entirely into DXO,
but with recreational doses, the conversion enzyme (P450-2D6) can saturate,
leaving a mixture of DXM and DXO. Furthermore, another of DXM's
metabolites - 3-methoxymorphinan - can also block this enzyme, so that
taking divided doses leads to more DXM and less DXO than taking a combined
dose of the same amount.
DXM's effects are in some ways much more subtle than DXO's. Whereas DXO
produces a heavy "stoning" or intoxicating effect, DXM is only lightly
intoxicating. DXM, however, can alter the thought processes, leading to
highly abnormal, psychosis-like mental states. It is possible that DXM,
via sigma activation, may induce a mental state similar to that of
schizophrenia. Whether or not this is fun to you is, of course, up to you.
As to how many plateaus DXM exhibits, this is debatable. I previously
listed three; however, some daring (or foolish) individuals have pushed
into a qualitatively different level which I call the fourth plateau. Some
people will undoubtedly disagree with this classification method, but I
think this is the best way to represent DXM's effects. Note that both the
third and fourth plateaus have significant dissociative characteristics,
much like ketamine.
Keep in mind that the effects in different plateaus can be very different.
For example, on the first plateau, DXM tends to have a stimulant effect,
often quite potent. Upon reaching the second plateau, however, the
stimulant effect may no longer be present.
The beginning of the end of a DXM trip can come abruptly. Often, the user
will know when it's starting to end by noticing the return of normal
sensory processing. Coming down from there may take a significant amount
of time.
The following table can be used as a general guideline for the plateaus.
For convenience I give example dosages in gelcaps and 3mg/ml syrup for 75kg
and 150lb adults; adjust up or down by the amounts indicated per 10kg or
25lb. Calculating with the mg/kg is more accurate, but it's easy to make
mistakes when using non-metric measures.
Dosage will vary considerably from person to person, by as much as 5 times!
Also, these mg/kg figures should evidently be adjusted down for higher
mass (e.g., maybe 6mg/kg to 13mg/kg third plateau for a 150kg adult). Note
that kg = pounds * 0.45.
o------------------------------------------------------------------------o
| Plateau --> | First | Second | Third | Fourth |
|================+=============+=============+=============+=============|
| Dosage Range | 1.5-2.5 | 2.5-7.5 | 7.5-15 | >15 mg/kg |
| (mg/kg) | mg/kg | mg/kg | mg/kg | |
|================+=============+=============+=============+=============|
| Gelcaps (30mg) | 4 to 6 | 6 to 18 | 18 to 37 | >37 gelcaps |
| for 75kg adult | gelcaps | gelcaps | gelcaps | |
|----------------+-------------+-------------+-------------+-------------|
| Adjust per | 1/2 to 1 | 1 to 2.5 | 2.5 to 5 | 5 gelcaps |
| 10 kg | gelcap | gelcaps | gelcaps | |
|================+=============+=============+=============+=============|
| Gelcaps (30mg) | 3 to 5 | 5 to 17 | 17 to 34 | >34 gelcaps |
| for 150lb adult| gelcaps | gelcaps | gelcaps | |
|----------------+-------------+-------------+-------------+-------------|
| Adjust per | 1/2 to 1 | 1 to 2.5 | 2.5 to 5.5 | 5.5 gelcaps |
| 25 lb | gelcap | gelcaps | gelcaps | |
|================+=============+=============+=============+=============|
| Syrup (3mg/ml) | 37 to 62 ml | 62 to 187 | 187 to 375 | >375 ml |
| for 75kg adult | | ml | ml | |
|----------------+-------------+-------------+-------------+-------------|
| Adjust per | 5 to 8 ml | 8 to 25 ml | 25 to 50 ml | 50 ml |
| 10 kg | | | | |
|================+=============+=============+=============+=============|
| Syrup (3mg/ml) | 2 tbsp to 2 | 2 oz to 5.5 | 5.5oz to 11 | >11oz |
| for 150lb adult| oz (.25cup) | oz (2/3cup) | oz (1+1/3c) | |
|----------------+-------------+-------------+-------------+-------------|
| Adjust per | 1 tsp to | 2 tsp to 1 | 2tbsp to 2 | 2oz |
| 25 lb | 2 tsp | oz (1/8cup) | oz (1/4cup) | |
o------------------------------------------------------------------------o
Table 1: DXM Plateaus and Dosages
The specific effects at each plateau will be listed according to the
following categories: Sensory, Cognitive, Motor, Memory, and Emotion.
------------------------------------------------------------------------------
[3.2] The First Plateau
The first plateau generally occurs around 1.5 to 2.5 mg/kg, but this may
vary enormously depending on metabolism and other factors. The first
plateau is probably the hardest to hit; many people "overshoot" it. Please
keep in mind that these effects listed 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. Gel capsules take up to 1 hour additional to dissolve.
Hangovers are very rare from this plateau, but if they do occur, they tend
to consist mainly of lethargy.
The primary effects of the first plateau are general euphoria, euphoria
specifically linked to music and motion, slight disturbances in balance,
moderate stimulation, and very slight intoxication. The intoxication and
balance disturbances are similar to that induced by alcohol, but much
weaker and without the mental confusion; there is little if any mental
sluggishness or confusion with a first plateau trip.
Some people have difficulty hitting the first plateau. It can take several
trials; as a general guideline, if you notice double vision, you've gone
way too far. A lot of the more pleasurable first plateau effects, in
particular the music euphoria, are set and setting dependent. Being in
good physical condition, avoiding excessive caffeine, and being in a good
mood are all important factors in achieving a good first plateau dose.
..............................................................................
Sensory Effects
Most of the effects of the first plateau relate to the senses. The best
known, and probably the most responsible for first plateau use of DXM, 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 seem 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 strong 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 (generally this only happens on upper plateaus).
The changes seem to relate to an anesthesia of the body senses 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).
..............................................................................
Cognitive Effects
Even though DXM has a slight "stoning" or intoxicating effect on the first
plateau, there are surprisingly few deficits of cognitive function.
Language is the most strongly affected, although these effects are usually
limited to occasional word and syllable repetition (especially in
already-repeated syllables, e.g., "banana" to "banananana"), spoonerism
(e.g., "share boulders" instead of "bare shoulders"), and difficulty coming
up with specific words.
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 behavior.
Many DXM users report a moderate to strong stimulant effect at the first
plateau, which disappears at higher dosages. This seems to be enhanced by
caffeine. One user reported being able to stay up for 48 hours by
maintaining a first plateau level. (Note that I don't recommend this).
Another characteristic of first (and second) plateau trips is a lowering of
inhibitions related to conversation. Many people find they can discuss
painful or embarrassing topics without difficulty. This is usually
described as a very positive effect, and those who have experienced it
often state that they feel more comfortable with themselves after the trip.
Some have reported a strengthening of friendships due to this effect.
It's interesting that as the third plateau is approached, recall and
discussion of such topics seems to become more and more "mandatory".
..............................................................................
Motor Effects
The other main characteristic of a first plateau DXM trip is its effect
upon motion and motor skills. Users tend to walk and move in specific ways
(varying somewhat from person to person) characterized by large, fluid
movements. In fact, it may be difficult to perform small or abrupt motion.
Motor tasks initiated may continue beyond their targets (this can range
from fun to distracting). To an outside observer, this can seem quite
strange, especially the changes in gait. It is possible, however, to move
normally.
These changes may be related to euphoria linking of body kinetic sense (see
Sensory Effects, above) which would make large and sweeping motions more
enjoyable. It is also possible that something more directly involved in
the planning and carrying out of complex motor tasks may be at work.
..............................................................................
Memory Effects
The memory effects of a first plateau trip are slight but usually
noticeable. Most of the effects probably come from a general deterioration
of short-term memory. Working memory (the "train of thought") can become
stuck in repetitive thoughts; other times it can be very easy to become
distracted. Recall of events prior to the trip does not seem to be
degraded. Encoding (i.e., making new memories) may be worsened, so that
after the trip there is some difficulty in recalling events during the
trip. Also probably because of the deterioration of short-term memory, it
may be easy to lose track of time.
..............................................................................
Emotional Effects
Mood enhancement is the most regular emotional effect of the first plateau;
many people find themselves fairly bouncy and happy, occasionally euphoric.
Unlike many drugs, there is not usually much "let-down" when the trip
ends. Fear is rare at the first plateau. There may be a sense of energy
or drive.
The effects upon libido evidently tend to vary from person to person. Some
people report an increase in sex drive; others find that playing, physical
contact, music, etc., seem much more interesting and enjoyable than sex.
The effects on sexual performance itself are not very strong at the first
plateau, though males may have some difficulty in achieving orgasm. When
orgasm does occur, it is often accompanied by extreme muscle tension and
profuse sweating.
------------------------------------------------------------------------------
[3.3] The Second Plateau
With the second plateau (around 2.5-7.5mg/kg), several new effects become
evident. The most profound is that DXM begins to take on a heavier
"stoning" characteristic, and senses and cognitive function are affected
accordingly. Hallucinations start for some people on the second plateau.
Some of the first plateau effects, e.g., the music and motion linked
euphoria, may diminish or stop entirely.
Second plateau trips usually take between 30 and 60 minutes to start (on an
empty stomach), peak about 2 to 3 hours later, and last about 6 hours.
Again, gel capsules take up to 1 hour additional to dissolve. Hangovers
are not common with lower second plateau trips, but some people experience
them.
..............................................................................
Sensory Effects
The most general sensory effect of the second plateau is "flanging".
Flanging, also called phlanging, phasing, stop-action, framing, strobing,
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 effects box
(which is where the term "flanging" 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 focused 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 flanged. With the sense of touch,
there is not necessarily flanging so much as a noticeable delay between the
stimulus and recognition of it. Pain especially tends to be somewhat
dissociated. Taste and smell are usually simply dulled, though a few
people report a vastly improved sense of smell. The sense of balance is
severely disrupted, as is body position and kinetic sense. Keep in mind
that 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. This can be unpleasant to some people.
Your experiences throughout the day will influence the hallucinations you
see and the imagery you can create. For example, if you have spent the day
playing DOOM[tm], your hallucinations are likely to involve scenes and
elements from the game. Eidetic imagery works a little different - you can
conjure up images, but they are likely to have a "DOOM[tm]-esque" feel to
them (bitmapped textures, ugly walls, etc.). This is an interesting effect,
and my hunch is that DXM hallucinations and imagery may be very dependent
upon what's already stored in short term memory. So it might be worth
planning the events of the day with your trip objectives in mind. This may
also be possible to some extent during the trip itself; e.g., if you want
to imagine yourself in space, go to a planetarium.
..............................................................................
Cognitive Effects
Higher reasoning 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 function of the mind while
leaving another almost untouched.
An interesting cognitive effect that is pronounced at the upper second
through the third plateau is a change in self-referential thinking.
Self-referential thoughts or ideas (e.g., "this statement is false") may
seem much more easily understandable, both in the abstract and on a "gut
level". Thoughts can, in fact, get quite abstract, sometimes to the point
of seeming meaningless to other observers. Quite a few people have
reported some sort of self-referential or abstracting aspect to thoughts,
such as a "self-creating and self-invoking meme" that consists of the
concept of itself. Another example is abstracting the concept of
abstraction (and abstracting that, and so on and so on).
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 flanging. However, thinking in language is still fairly easy.
The curious detachment from painful or embarrassing topics of conversation
that occurs at the first plateau continues and is much stronger at this
plateau. Again, this is generally viewed as a positive event, although if
you're not prepared to encounter and possibly discuss your deepest, darkest
secrets, you might want to avoid higher doses until you're comfortable with
DXM.
..............................................................................
Motor Effects
The first-plateau effects on motor skills continue to exist, and may be
considerably stronger. Some users find themselves contorting their limbs
into rigid positions, others may extend and stretch themselves. These
effects are not always immediately apparent; when they are, the user
usually reports that it just "feels right" to be in that position. It is
still possible to override this.
Another accentuation of first-plateau motion effects that sometimes occurs
is that the large, sweeping motions, once initiated, may continue for
considerable time (looking somewhat like a cross between modern dance and
Huntington's disease). Again, it just "feels right" to do.
..............................................................................
Memory Effects
Short-term memory and working memory may be severely disturbed, although
experience with DXM seems to help people compensate. Possibly because of
the changes in memory, it may be very difficult to get bored, even with
repetitive tasks. At this plateau, a lot of time may get lost, and the
more mundane aspects of the trip are easily forgotten after it is over.
..............................................................................
Emotional Effects
The other primary characteristic of the second plateau (hallucination being
the first) is probably the motivational aspects. Repetitive, mundane,
boring tasks suddenly become doable, and (if one can avoid distraction) may
be easily accomplished, even if they take hours. There may be a
considerable stimulant effect remaining at the second plateau. The
euphoria from the first plateau continues but diminishes as dosage across
the second plateau increases.
------------------------------------------------------------------------------
[3.4] The Third Plateau
At the transition between the second and third plateau, (roughly 7.5 to
15mg/kg), several unrelated effects may occur. These probably belong more
to the transitional stage than to a given plateau, and will be dealt with
here.
The first is a sensation that has been described as the opening of nasal
passages, being full of helium, losing one's body, or having one's heart
stop beating. The actual effect is most likely a sudden cutoff of sensory
input from within the body - everything from all the little aches and pains
to the awareness of one's own heartbeat go away. This can be very
disturbing if a naive user interprets it as heart failure!
The second transitional effect is a temporary loss of all sensory input
(this does not always occur), as if one were in a sensory deprivation 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.
It is my opinion that these transitional effects occur because a critical
level of NMDA receptor antagonism (blocking) has been reached, which
profoundly changes the nature of the applicable neural networks (e.g., the
hippocampus). DXM seems to show two of these major transitions, once at
the beginning of the third plateau and once at the beginning of the fourth.
Other NMDA blocking drugs (dissociative anesthetics) tend to have only one
such transition.
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
terrifying to people who are not psychologically comfortable and prepared.
..............................................................................
Sensory Effects
The flanging of visual effects, coupled with the loss of stereoscopic
vision, becomes so strong that the brain seems to completely give up trying
to process vision, leading to a sort of "chaotic blindness". Simple images
(e.g., a candle flame) are still recognizable, 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. Vision, when possible, has a very dream-like
quality to it.
Simple sounds are still understandable, and one can usually comprehend
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 anesthesia, 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. Some people continue to report an enhanced sense of smell on
the third plateau.
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-ness", which brightens to
white light as the dosage increases.
At the third plateau, the flanging 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. Flanging may slow down and speed
up, leading to periods of lucidity alternating with periods of
semi-consciousness.
..............................................................................
Cognitive Effects
Cognitive function becomes severely disrupted at the third plateau.
Complex tasks, such as mathematics, may be very difficult (though some
report little or no difficulty with such skills). Reaction time is
significantly delayed. Decision-making is somewhat degraded, although
conceptual thought is less affected than concrete thought.
Language changes can be quite profound. Sentences may stretch on and on,
or alternately be very terse (I call this the "Hemingway Effect"). Words,
syllables, and phrases are commonly repeated. This may be related to
problems with working and short-term memory. Speech may occur in a very
rigid (but not necessarily simple) rhythm, and the user may not respond to
speech unless it is in a similar rhythm.
The normal "chatter" that goes on inside everyone's brain tends to slow
down or stop at this plateau, leaving a feeling of mental peace and quiet.
One person reported this as "it felt like the top of my skull was opened
into a clear blue sky".
..............................................................................
Motor Effects
At the third plateau it may be impossible to perform coordinated movements.
The large, sweeping motions of the first and second plateau are no longer
present. Instead, many users lack both the desire and ability to move at
this plateau.
Well-learned motor tasks (e.g., speaking and typing) are still possible at
this plateau, provided the user doesn't attempt to think about them. In
particular, some users have reported that they were able to express their
thoughts via typing, without even thinking about it or realizing they were
doing so; however, when they looked at the screen or keyboard, they were no
longer able to type. This is evidently a phenomenon unique to dissociative
anesthetics.
..............................................................................
Memory Effects
Short-term memory is seriously impaired; working memory is less impaired.
Thoughts may get stuck in a loop. Memory encoding of the more mundane
experiences of the trip tends to be very bad; expect to forget a lot of the
trip itself (a few people report that they begin to recall events from the
trip a few days after it has ended; I know of no mechanism for this). The
sense of time can be quite distorted, both in terms of chronological
placement of events and in the sense of the passage of time.
The day after a third plateau DXM trip, some users feel as if there were a
break in the continuity of their memory, almost like the close of one
chapter and the beginning of another. Some find this a very positive
feeling, like a rebirth or rite of passage. It can be disconcerting if
experienced without adequate foreknowledge and preparation.
One of the most significant memory effects that can occur at the third
plateau is the spontaneous recall of memories, often memories which were
hidden (consciously or not). This can be a positive experience if one is
prepared to review the darkest secrets of one's past; otherwise it range
from somewhat embarrassing to very unpleasant and disturbing. The user may
also feel compelled to tell her or his companions about these memories (not
always a good idea).
..............................................................................
Emotional Effects
Mood can range from absolute mania to panic. Many people have
independently reported feeling as if they were dying, with some sense of
fear, although some people do not seem to associate fear with this. Some
people report a great increase in approach behavior, as if every event and
object were a new experience; others find irrational fears occurring
(possibly due to body load).
Panic attacks have occurred at the third plateau. This can be a scary
experience, especially if one finds one's heart rate skyrocketing due to
the panic attack and doesn't know why. The best way to cope with this is
to try and calm down, much the same as one would with a bad trip on any
other hallucinogen.
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 (some similar effects which I formerly placed
on the third plateau (e.g., feelings of contact with other beings) I now
place on the fourth plateau as they tend to occur at substantially
different dosage levels). Complete annihilation of self can occasionally
occur (up to the point of forgetting one's identity) but does not seem to
be especially dangerous.
Note that, to sober observers, the effects of a third plateau trip can seem
very unusual and unpleasant (often much more than to the person tripping).
------------------------------------------------------------------------------
[3.5] The Fourth Plateau
Information pertaining to the fourth plateau (roughly, above 15mg/kg) is
limited, and what I have gathered will be presented as a general overview.
Please note that dosages in these ranges are approaching the danger zone,
and under no circumstances should anyone take this much DXM without a
sober assistant who can take you to the hospital if the need arises!
Fourth plateau doses are similar to fully dissociative doses of ketamine.
Generally, people entering the fourth plateau report that they lose all
contact with their bodies, often suddenly. This can be somewhat
frightening. In particular, the sense of breathing is one of those
missing, and people have occasionally interpreted this as evidence that
they were dead. The surrounding environment may be evenly colored (usually
grey or white), or it may appear vividly realistic, or cartoon-like, or
anywhere in between these.
Many users have reported experiences very similar to "out of body" and
"near death" experiences. In such cases, many report that they have
contacted other beings, whose reaction to the user is usually somewhere
between curiosity and amusement. Contact with "superior being(s)" has also
been reported, sometimes as a raw force, sometimes personified in some way.
In the reports given to me, the "superior being" image is more often
female than male.
Delusions can become fairly involved at this plateau; the crucial factor
seems to be whether or not the individual realizes that the belief or
thought is drug-induced. Some people, especially those more experienced at
this level, have reported that although they were aware that their thoughts
were delusional, they didn't really care at the time. In general these
delusions are fairly harmless (e.g., "I am a flower in the middle of a
field").
Generally an individual in this plateau won't be moving at all, which can
be frightening to observers. In many ways this state resembles dreaming.
If someone in this plateau does attempt to move, his or her attendants
should be very sure that he or she is conscious of these actions, and not
responding to a delusional environment.
Somewhat surprisingly, many cognitive abilities are still intact. Basic
computational skills and long-term memory recall do not seem to be
particularly affected. It is also possible for the "body" (actually body
and some parts of the mind) to undergo fairly complex tasks while the
conscious mind is dissociated.
One individual wrote the following of the fourth plateau trip, and I think
it is a good explanation both of the trip and of its possible origins:
I've come to the conclusion that DXM is almost unique in it's
ability to create a truly "alien" experience - one in which major
aspects of one's humanity can become entirely irrelevant. Most
obviously, one's body can be left behind; even forgotten. The
experience of becoming or encountering bizarre life-forms seems
at least somewhat common, as are weird, horizonless landscapes or
space-scapes. I think alot of this "alieness" comes from having
so many of one's ties to the familiar severed. When your body is
gone, your mind loses its sense of how "big" or how "small" you
are in relation to your surroundings. Hence hallucinations of huge
things like galaxies, or of being as large as a mountain, as small
as an atom, etc. I think the brain also misses subtle clues like
the sensation of breathing, blood flowing through the veins, etc. -
things which help remind you that you're human. And at some point,
even your memories of the familiar may be suppressed.
------------------------------------------------------------------------------
[3.6] Is there anything beyond the fourth plateau?
There may be yet another plateau beyond the fourth. One individual took
3000mg (I don't know his weight) and survived, although he regained
consciousness in a strange location and remembered nothing of the trip.
Given the toxicity of DXM at doses much higher than this, I don't think
anyone should try and go there. You might not be able to come back.
------------------------------------------------------------------------------
[3.7] What happens with long-term or regular use?
Long-term or regular use, especially in amounts above 6mg/kg daily, tends
to produce several undesirable effects, some of which may be dangerous.
These are discussed in detail in Section 4.2. Briefly, tolerance to DXM
can build, and as tolerance builds, most of the positive aspects of the
drug go away, leaving only the dysphoria and overall "weirdness". There is
evidence that NMDA receptors may upregulate with long-term use of DXM
(110,134); the practical upshot is that quitting DXM "cold turkey" after
weeks of constant use could produce withdrawal symptoms similar to that of
morphine withdrawal (though not as intense).
Psychological dependence is certainly possible and there are numerous
examples of this occurring (3-5; also personal communications).
Amotivational syndrome has been reported (usually when the drug wears off).
Memory problems seem to be fairly common (and resolve shortly after
quitting DXM).
I have one report on a DXM addiction which may be cause for concern
(related to me personally). The individual was roughly 60kg, and took a
dose of 480mg, three or four times a day. The total dosage was thus 1440mg
to 1920mg, i.e., 24 to 32mg/kg. This individual took the dosage regularly
to maintain a constant state of profound intoxication with a great deal of
opiate-like effects; neglecting the dose led to withdrawal symptoms
consistent with opiate withdrawal, and possibly also withdrawal from a
depressant. The individual had no history of psychological problems. The
individual developed severe depression, leading to a suicide attempt and
several months in drug rehabilitation.
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. PLEASE NOTE that this user built up to
this dose over a considerable time; a similar dose in a drug-naive
individual could well be fatal.
Over the past year I have given this incident some further thought, and I
have come to the conclusion that regular high-level use of DXM is probably
a very, very bad thing. I have encountered other reports of DXM addiction,
as well as studies implicating the NMDA receptor in tolerance and rebound
symptoms (110,134). Some of these reports show that chronic DXM use can
contribute to depression (4,6,142-144), and at least one study found
serious mental deterioration from long-term DXM use (137). To make matters
even worse, long-term sigma activity may cause permanent changes in neurons
(102), although evidently this is predominantly a problem with other sigma
ligands like haloperidol (it took 3 days for DXM to produce the changes
haloperidol produced in a few hours).
Some users report beneficial effects of chronic high-level use. The
effects usually include some antidepressant activity (entirely reasonable
given the possible significance of PCP2 receptors), stimulant activity,
long-term motivational effect, and cognitive and creative enhancement (this
has not been quantified and may be entirely subjective). It is arguable
that chronic DXM use may actually be self-medication for depression in some
people.
Overall, however, most people report that DXM loses its interesting
characteristics when used regularly, leaving the more mundane and
unpleasant aspects. One former user summed it up well by stating that
"being addicted to DXM was like being addicted to heroin. Except not as
fun." So please be careful and avoid regular use.
------------------------------------------------------------------------------
[3.8] What are some fun or interesting things to do on DXM?
This section lists some things that various people have done on DXM that
they have enjoyed. Note that not everyone will agree, and some of these
activities may be unpleasant to some. Activities that are pleasant at one
dosage may not be so at another.
..............................................................................
Listen to Music
Probably the most common fun thing to do on DXM, especially at lower doses,
is listen to music. Even at higher doses, music can be quite enjoyable,
and will often induce fantastic hallucinations. Many people have in fact
reported they were unable to hallucinate without music. Some use music to
help create an imaginary setting for their hallucinatory experiences. Why
music enhances the DXM experience so much, I don't know; other
dissociatives don't seem to go nearly as well with music.
As for what music is best, that's a matter of personal opinion. Some
prefer classical music, saying it brings a transcendent feeling and visions
of flight. Rave and techno music are also popular, possibly because of
the strong, regular beat. Ambient seems popular, especially towards the
end of DXM trips, where it has a soothing effect. Really, though, a lot
has to do with what you like.
..............................................................................
Dance
Many people enjoy dancing on DXM, usually at the first plateau and somewhat
less commonly on the second. Third and fourth plateau doses of DXM are
almost certainly not compatible with dancing (or most other motor skills).
Raves are the most common DXM dancing event, although I see no reason why
any other type of dance couldn't be enjoyable as well.
Please note that, as with any dissociative anesthetic, DXM can make you
less aware of overexertion, leaving you with a generally sore body the next
day. Also, as with any stimulant, take care not to overheat or become
dehydrated.
..............................................................................
Go Swimming (low dose only!)
A few users have reported that swimming on a first plateau DXM trip is an
ecstatic experience. Evidently, the regular, rhythmic motions of lap
swimming go well with DXM's rhythmic nature, and the feeling of the water
supporting the body provides a deep sense of calm. There should be little
danger with swimming on a first plateau DXM dose, although higher doses
could become quite dangerous. Overexertion is always a possibility, but
fortunately swimming's low-impact nature may minimize some potential
injuries. In any case, if you do decide to try swimming on DXM, never swim
alone.
..............................................................................
Group Tripping
One of the characteristics of the NMDA/sigma class of psychedelics is the
ability of people tripping together to synchronize their experiences as
they discuss them. This is not unique to DXM; ketamine users have noted
the same effect, and although I have no reports I'm certain PCP would act
similarly.
Group use of DXM was fairly common among some members of the hardcore
warehouse subculture in the 1980's in the USA. People would decide on a
"destination" or goal for their trips (which some called "vacations"), and
choose music, decorations, and other stimuli to match the destination.
Destinations ranged from the specific to the mythological (e.g., Hell).
Talking during the trip helped maintain synchronization. Most of the time,
the environment (sights, sounds, smells, etc.) was carefully crafted to fit
the destination.
It is interesting to compare this with the use of certain plants, notably
Salvia divinorum, among native peoples of Mexico and Central and South
America. The "trippers" were advised beforehand on what visions to expect
and how they would come, and were told to talk about their experiences as
they occurred. I have strong suspicions that NMDA/sigma agents are not
unknown among ethnobotanicals.
In any case, if you are planning a group DXM trip, it might be a good idea
to make sure that everyone is experienced with DXM beforehand, so that they
know what to expect. Try to adjust dosage for everyone to place everyone
at roughly the same place in the same plateau (group tripping seems most
effective at the upper second plateau). If desired, pick a destination
beforehand, and adjust your setting to match. Be wary of intense or
potentially unpleasant destinations (the "vacation to Hell" mentioned above
was undertaken by very experienced DXM users). Try to make sure everyone
stays together; many people have reported that having someone leave can
ruin the experience. And above all, make sure someone sober is available
to watch over you and make sure nothing goes wrong.
..............................................................................
Have Sex
Sex on DXM is certainly possible, and although many people don't
particularly enjoy it, others are enthusiastic about it. DXM can make it
difficult for males to achieve orgasm; I have no data on its effects on
females. Very large doses of DXM can cause (temporary) impotence, but
lower doses usually do not impair, and sometimes enhance, erectile ability.
As a consequence of this (enhanced erectile capability and delayed orgasm),
at least one DXM user reported that his partner really enjoyed the sex
even if he didn't.
..............................................................................
Shamanic Journeying (see also Section 3.12)
A few users have successfully attempted shamanic journeying and other
out-of-body or "psychonaut" work. From a skeptical viewpoint, these
experiences are nothing more than hallucinations, although I'd like to
point out there's a lot more we don't know about the mind and brain than we
do know.
In any case, success seems to depend on several factors. Prior experience,
both with DXM and with journeying or other out-of-body work, are strongly
encouraged if not necessary. The day should also be spent in preparation
of the experience, preferably in a natural environment, as the imagery of
the journey may be composed of bits and pieces of your daily experience.
Simple, regular drumming is, of course, always useful and may be very
beneficial for DXM-induced journeying (drumming tapes are available from
New Age and occult suppliers).
..............................................................................
Hang out in a Sensory Deprivation Tank
Call "Tools for Exploration" at 1-800-456-9887 and order their catalog.
Yes, you can buy them, they're about $4000; you can also make one yourself.
Basically, you float in darkness in a foot of water saturated with half a
ton of Epsom salts (I have no idea exactly where one gets half a ton of
Epsom salts, but that's another problem). You can also pipe in music. I
have no affiliation with this company, by the way.
Anyway, the end result is that you manage to cut off sensory input. This
sounds somewhat redundant, but can actually be quite useful for
dissociatives from what I understand. Hey, if you do it often enough,
maybe they'll make a movie about you. (Just don't turn into a monkey).
------------------------------------------------------------------------------
[3.9] What are some things to avoid on DXM?
This is a small list of some of the things which people have reported were
particularly unpleasant, boring, or otherwise unenjoyable.
..............................................................................
Heavy Exercise
Most individuals who have exercised under the influence of DXM have
reported negative effects such as nausea, vomiting, cramping, and a general
loss of the more enjoyable aspects of the trip. This seems to become more
and more significant with higher doses of DXM. The one exception seems to
be swimming, which if done on a first plateau DXM dose can be enjoyable.
..............................................................................
Driving
DXM is an intoxicating drug, and no intoxicating drug should be used when
you are driving. Ever. If you're pulled over, the cops will know you are
on something, as DXM strongly interferes with normal eye movements at
recreational levels. They may not know what you're on, but they can still
bust you, and even if you never get formally charged, this is definitely
not a fun tripping experience.
Not to mention, by driving (or operating heavy machinery) on DXM you are
placing yourself and potentially a lot of other people at risk. The
highways are full of enough carnage as it is, and there's no excuse for
adding to it. Quite frankly I think that anyone who drives while
intoxicated (on anything) is committing an act of attempted manslaughter
(if not murder) and repeat offenders should be charged and tried as such.
That's probably an extreme position, but I think far too many people are
willing to blame the alcohol (or drug) for the user's arrogance and
stupidity.
..............................................................................
Going to Class or School
Many people have had the experience of going to classes drunk, stoned, or
otherwise intoxicated. Going to class on a low dose of DXM should be
fairly similar. Once probably won't hurt you, although it certainly isn't
going to help you either. Doing this regularly is definitely bad news, as
DXM will interfere with memory when used regularly, and may cause cognitive
impairment with long-term use. High doses of DXM are even worse, since the
dissociative effects can lead to highly inappropriate behavior. To top it
off, as it becomes more difficult to judge the appropriateness of behavior,
the fear at doing something that will get you laughed at (or worse) can
make a trip turn unpleasant.
A special note for people still in high school (or younger): don't do DXM,
or any other drug, in school. Yes, school can really suck. The classes
are boring, repetitive, unchallenging, and full of potentially useless
information. The teachers are often (but not always!) more interested in
hearing you regurgitate facts than have an original thought. The
administrators generally aren't interested in you as a person, they're
interested in making sure the school runs smoothly and that they get paid.
And your peers usually don't give a rat's ass about your feelings; they're
too busy coping with newly found hormones and playing Cooler Than Thou.
And so, I might add, are you, in all likelihood.
During this time, many students with half a brain in their heads end up
going through the usual sort of teenage existential angst (you'll know it
when you get there). This is, I think, one of the rites of passage of
today's youth, which has the potential to liberate one from being
completely under the control of what one's peers think of as cool. It also
has the potential to get you into a lot of trouble, especially with drugs,
and DXM is no exception.
Don't get me wrong; I don't think drug use is inherently any more or less
wrong for teenagers than for adults. In practicality, however, one needs a
certain level of emotional and intellectual (and possibly physical)
maturity before responsible drug use becomes likely. And responsible
people know there are times and places not to use intoxicating or otherwise
mind-altering substances.
So in the mean time, avoid using drugs in school. Many of your teachers
and administrators will know (they may seem dumb as a post. Don't believe
it). Your grades will probably suffer, and for all their seeming
irrelevancy, good grades are really one of the better tickets out of a life
of boredom. You may also develop a stubborn habit, as the use of a drug
becomes associated with the everyday activity of going to school. Finally,
the bad trip potential shouldn't be ignored.
As for what to do instead, well, there's no easy answers there. Some
people find fulfillment in reading Sartre and Thoreau, others in reading
X-Men and romance novels. Regular exercise really does help, as with so
many other problems in life, and it helps one to cope with boredom and
mundanity. Don't neglect your mind either, even if your teachers do; you
can be your own teacher (and a damned good one at that). Question everyone
and everything; it's the only way to learn. And above all else, try to
keep a sense of humor; things that seem vastly important now will seem a
lot less serious in a few years.
..............................................................................
Dose "Boosting" and Redosing
Simply put, dose boosting (i.e., taking a second dose as the first one
wears off) doesn't work. By the time you take the second dose, the NMDA
receptors have already started to compensate, and saturation of P450-2D6 by
3-methoxymorphinan means that most of the DXM you take won't be nearly as
effective. Sigma agonist activity will increase, bringing an overall sense
of dysphoria and (temporary) disturbances in thought. Sorry, but there
doesn't seem to be an easy way around this; even if you used DXO, the brain
still responds quickly to NMDA blockade, as users of ketamine or PCP will
attest. Just wait a few days to a week and try again.
The one exception to this seems to be a first plateau dose, which (with
practice) can be maintained for some time, leading to a prolonged stimulant
effect. This is probably due to the dopamine reuptake inhibiting effect of
DXM (absent with DXO), similar to that of bupropion (Wellbutrin?) or
cocaine. Prolonging this will, however, intensify the "crash" and is
probably not a good idea.
------------------------------------------------------------------------------
[3.10] Why does DXM affect different people so differently?
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?) can inhibit
this enzyme (39). A list of P450-2D6 inhibiting drugs is given in Appendix
1.
Second, some of the effects of DXM are due to the DXM itself, and some are
due to its metabolite dextrorphan (DXO), which is more similar to PCP and
ketamine in its neuroreceptor activity (43). Some individuals may
metabolize high doses of dextromethorphan to dextrorphan more quickly than
others. Incidentally, my opinion - based on anecdotal evidence of
recreational DXM use while on fluoxetine - is that both DXM and dextorphan
are responsible for the psychoactive effects (yes, I changed my mind).
There is evidence to show that DXM is definitely involved, and may be
responsible for most of the lower plateau effects (32).
Third, NMDA receptors are intimately involved in many areas of the brain
where a great deal of processing takes place, such as the hippocampus and
the cerebellum. In contrast to the biogenic amine neurotransmitters
(serotonin, dopamine, noradrenaline, histamine, and acetylcholine) which
seem to play a modulatory role, excitatory amino acids and NMDA receptors
are involved in the "nitty gritty" of brain processes. 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 Section
5.2), 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. Subtle differences in brain chemistry, notably in terms of
sigma receptors, may also be involved. Psychological set, as well as
setting, are undoubtedly also part of the problem.
------------------------------------------------------------------------------
[3.11] How does DXM compare with other dissociatives?
Third and especially fourth plateau DXM experiences seem to resemble
ketamine experiences, and based on reports of people who have done both,
the similarity is considerable. This is not surprising, since both DXM and
ketamine block NMDA receptors. Although I have yet to receive any reports
comparing DXM to PCP, I would imagine that, since PCP and ketamine are
similar, upper DXM plateaus should resemble PCP as well.
Lower DXM plateaus, however, seem to show a number of differences from
other dissociatives. This is most likely due to DXM's unique potency at
the dopamine reuptake site (the PCP2 receptor) and the sigma receptor.
DXM's ability to block dopamine reuptake is probably the biggest factor in
its popularity at lower plateaus; neither ketamine nor PCP have substantial
ability to do this.
When DXM is taken in divided doses, or when it is taken with an inhibitor
of the P450-2D6 enzyme (e.g., fluoxetine), its sigma agonist activity
becomes much stronger in comparison to its effect at the NMDA receptor. As
expected, DXM taken under these conditions differs from other
dissociatives, and is sometimes reported to induce schizophrenic-like
thought processes and other unpleasant effects.
------------------------------------------------------------------------------
[3.12] Is there any connection between DXM and out-of-body or shamanic
experiences?
Maybe. It is somewhat established that many aspects of DXM trips,
especially higher plateaus (3rd and 4th), have shamanic or out-of-body
characteristics. Some users have reported experiences which are very
similar to published out-of-body and/or near-death experiences (many of the
users who reported these are fairly skeptical about that sort of thing).
One note though - DXM hallucinations and imagery tend to derive to a great
extent from what you've encountered throughout the day. If you've played
DOOM[tm] all day, you're going to have a difficult time coming up with any
images other than muck-walls and demons.
I can think of two explanations for the shamanic character of higher DXM
plateaus.. The first one, which I prefer, is less fun but probably a lot
more useful. Basically, it is possible that many of the aspects of
out-of-body or shamanic journeying experiences derive from neural network
states which DXM can approximate. To start with, unlike most drugs which
target very specific, limited clusters of neurons, DXM tends to affect
entire neural nets (via the NMDA receptor). A general "shutdown" or
interference with some of these neural nets may produce many of the
experiences associated with near-death, and could possibly be mimicked by
DXM. Some (very simple) models have demonstrated "spontaneous memory
recall" effects when the network is severely disrupted or disconnected;
again, DXM may mimic this. The only problem here is that the NMDA
receptor, although extensive, is involved in learning more than "ordinary"
neural network signals.
There is also a somewhat different, and possibly more compelling, neural
network model. It is possible that, in addition to encoding short-term
memory, NMDA receptors are involved in "synchronizing" or "interfacing" the
conscious mind to the rest of the brain and body. After all, we experience
things in terms of our previous experiences, so raw sensory data must be
translated into the "language" of memory before it can be consciously
experienced.
When enough NMDA receptors are blocked, the mind and body/brain lose the
ability to communicate. Each is still capable of "doing its thing",
however; in particular this might explain why it is possible to undertake
fairly complex tasks under partial or full dissociative anesthesia, but
attempting to consciously control these tasks fails. I'm also of the
opinion that hypnosis and trance states may involve the same processes.
Although the exact reason is unknown, several techniques for inducing
shamanic journeying involve the use of regular, even drumming. Several
high-dose DXM users have reported flanging of sound in a very similar
pattern and frequency to this drumming. If the flanging is the result of
the "uncovering" of a regular neural network "sweep" wave, it is possible
that drumming may induce network states similar to those caused by DXM.
At higher levels especially, there is considerable saturation of sigma
receptors. These receptors may be involved in psychotic states and
schizophrenia. While I don't believe that people who have out-of-body
experiences are psychotic, it is possible that these states may be
temporarily inducible in anyone.
The other explanation, which is considerably further out on a limb than I
want to go, is that DXM, by disconnecting the senses from the mind, allows
the mind to wander freely in the spiritual universe. Some users have
reported feeling like this at the time, in particular feeling that the
physical world wasn't real, that they weren't a part of it anymore. I
wouldn't advise testing this out.
In any case, and regardless of what you choose to believe, there are some
general guidelines that seem to be fairly universal to most systems of
shamanic journeying. Accept or reject them as you see fit (remember,
though, better safe than sorry).
o If you go somewhere, always return by the same path.
o Treat any entity you encounter with respect. They can't physically
hurt you, but they can make your trip (and possibly your life)
distinctly unpleasant. You can't really hurt them, either, but your
chances of being able to make their lives unpleasant are probably a
lot slimmer.
o Remember, if you leave your body behind, another entity may want to
use it. Although some cultures encourage this, most people find it
disturbing. It may be possible to prevent or control this by leaving
"guards" or defenses. This is beyond the subject of this text, but
serious psychonauts may wish to investigate this aspect of magick.
o Unpleasant entities generally feed off fear and anger; avoid getting
stuck in a vicious cycle.
o If an entity gives you its name, consider it your secret, and don't
tell anyone else.
------------------------------------------------------------------------------
[3.13] Why can't I hallucinate on DXM?
Some people have trouble achieving hallucinations on DXM. Here are some
suggestions that may be helpful, based on reports I have received (note:
none of this should be taken as advice in any way; I'm just passing this
along):
o Place yourself in partial or complete darkness. Most NMDA/sigma agents
seem to give the best hallucinations when there is little or no visual
input.
o Close your eyes. It is almost always easier to get closed-eye visuals
(CEVs) than open-eye visuals (OEVs), and DXM is no exception.
o Listen to music. Music often brings about intense visuals, sometimes
even open-eye visuals.
o Mentally focus on your phosphenes - those little blips and squiggly
patterns that appear in your field of vision in darkness (yes, everyone
has them; not everyone notices). For whatever reason, this seems to
help start hallucinations.
o Imagine things. This seems to help start the process in some people.
o Dose with other people and synchronize your trips.
o Increase the dosage the next time you trip.
o Decrease the absorption time the next time you trip. If you are taking
gelcaps, break them open. If you are drinking syrup, drink it on an
empty stomach.
o Increase the absorption time the next time you trip. Some people have
reported this to be useful. For example, if taking gelcaps, take one
every 5 minutes until all are taken.
o Combine with cannabis (marijuana). (Note: this is, of course, illegal,
and I advise you not to do this).
o Inhale a balloon of nitrous oxide (again, this is probably illegal, and
I'm advising you against it).
==============================================================================
[4] DXM SIDE EFFECTS AND OTHER THINGS TO AVOID
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).
------------------------------------------------------------------------------
[4.1] What are the potential side effects and risks of occasional use?
Although generally very safe, you should be aware of some of the possible
adverse effects that can occur with occasional use of DXM. These are
ordered roughly by frequency of reporting, but I don't have any hard
figures yet.
..............................................................................
Nausea and other gastric disturbances
Probably the most commonly reported side effect is nausea, most likely a
simple result of gagging down a bottle or two of cough syrup. People who
use the gelcap or capsule preparations do not, in general, experience
nausea, although DXM itself can occasionally cause nausea (this is
uncommon).
Many cough syrup preparations can cause considerable amounts of bloating
and gas. Expect to pass gas for the next day. Stomach cramps and other
gastric disturbances, probably from the amount of sugars and glycerine, are
also common. Preparations with guaifenesin tend to induce vomiting at
recreational DXM levels. Mixing DXM with large amounts of alcohol can have
the same effect; one poor individual who mixed DXM with a large quantity of
alcohol vomited for over two hours.
..............................................................................
Itching and allergic reactions
Ah, the "Robo Itch" . Some people get it and some don't. There's evidence
that at least some of the cases of "Robo Itch" are a psychological reaction
to mild anesthesia, but some are probably a result of histamine release -
not necessarily an allergic reaction per se, but a possible consequence of
DXM's pharmacology. The itching tends to go away, and although scratching
is pleasurable (and a loofah is wonderful), take care not to overdo it.
Actual allergic reactions have occurred, and often these are a result of
the "inert" ingredients, usually one of the dyes (e.g., tartrazine). A
topical antihistamine spray might be a good idea. You should probably
always keep an oral antihistamine on-hand, at least during your first few
DXM experiences (or when trying out new preparations). Just remember not
to use any prescription, non-drowsy antihistamine with DXM. Diphenhydr-
amine (Benadryl[tm]) is a good OTC antihistamine that is regarded as
safe to combine with DXM.
Note that some people find the itching to be extremely unpleasant.
..............................................................................
Hangovers
Yes, hangovers can happen. See Section 4.5.
..............................................................................
Pupil dilation
Although it doesn't happen to everyone, many report substantial pupil
dilation on DXM, similar to the pupil dilating effect of LSD. This is
probably a dead giveaway that you're "on something", so you might want to
know if it happens to you before trying to get away with being on DXM in
public. And may your eyes dilate to the size of saucers and attract cops
for miles around if you ever drive on DXM!
..............................................................................
Tachycardia (Increased heart rate)
This seems to be fairly common but not particularly serious; generally, a
heart rate in the range of 90 to 120 can occur. This is probably a side
effect of the stimulant qualities of DXM. Substantially higher heart rate
may indicate a panic attack.
..............................................................................
Hot and cold flashes
Hot and cold flashes during the trip are to be expected, and are not
generally serious. One user reported frequent extreme hot flashes, which
eventually got bad enough that he sought medical assistance. A few people
have reported hot flashes several days after the DXM trip is over.
..............................................................................
Hyperthermia
One user reported a case of hyperthermia (increased body temperature) which
could have been dangerous. See Section 4.8.
..............................................................................
Panic attacks
Several users have reported panic attacks, and I am beginning to think some
people may be susceptible to this from DXM. This seems to be worse when the
DXM is combined with other drugs, including marijuana (cannabis). The
trouble with a panic attack is, once you realize you're having one, it can
make you feel out of control of the drug experience, which makes the panic
attack even worse. This is a difficult vicious circle for some people to
break. Fortunately this mostly seems to happen with high doses (around
10mg/kg and up).
..............................................................................
Overexertion
As DXM is a dissociative anesthetic, it will make you less aware of the
normal body senses, including muscle fatigue and pain. As a result you can
easily over-exert or over-stretch yourself, especially if you are out
dancing or engaging in other physical activity. Pay close attention to
your body if you plan on moving a lot.
On a somewhat related note, many people report that heavy exercise under
the influence of DXM can cause nausea. This seems to occur mainly at the
second plateau and above; in contrast, one user reported swimming on a
first plateau dose to be a very pleasant experience.
..............................................................................
Psychotic episodes
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. Keep in mind that DXM is related (although
distantly) to PCP, and some people really don't get along well with
dissociative anesthetics. The chance of experiencing a psychotic episode
probably increases with dosage.
Many of the cases of DXM "abuse" in literature have concerned psychotic
episodes (the same is true for LSD). This probably seems more disturbing
than it really is; after all, these are cases compiled from hospital
visits. The vast majority of DXM users do not experience psychotic
episodes.
..............................................................................
Hypertension (high blood pressure)
I have heard of this happening exactly once, when DXM was used in
combination with pseudoephedrine. DXM itself may be capable of inducing
hypertension, since it is a dopamine reuptake inhibitor; however, at doses
high enough to do this, DXM's NMDA blocking activity seems to counteract
this problem. In any case, be careful when mixing DXM with other
stimulants (caffeine is probably OK), and don't use DXM if you have high
blood pressure.
..............................................................................
Miscellaneous
Even though DXM has been successfully used to prevent seizures, it may
actually induce them at high dosage levels (45), especially in epileptics
(145). You want to avoid this.
Some users who have taken very high dosages of DXM (above 15mg/kg) have
lost motor function to the point of choking on their tongues (or at least
feeling like it; I've been told that this is technically impossible).
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; it could slip and make the problem worse.
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. Ketamine did, however.
------------------------------------------------------------------------------
[4.2] What are the potential side effects and risks of regular use?
Mania
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) (1-3,133,137,142-144). This is
probably a result of dopamine reuptake inhibition, but sigma receptors may
be involved as well (see Section 6). On the other hand, one user who had
formerly used the antidepressant bupropion (Wellbutrin[tm]) reported a
similar but somewhat stronger antidepressant effect from DXM, though with
greater adverse side effects.
..............................................................................
Cognitive impairment
Recently, an article in Journal of Psychiatry and Neuroscience presented a
case of significant cognitive impairment associated with long-term DXM use.
The individual consumed 1500mg DXM, plus 5000mg guaifenesin, at least once
per week for at least a year. From the article it seems that he was
probably a slow metabolizer, lacking the normal P450-2D6 enzyme. It also
mentions that he abstained for "several weeks" without improvement,
possibly indicating permanent brain damage. The authors hypothesize that
this unfortunate individual may have had a temporal lobe seizure disorder
(137).
The reports I have received from several long-term (1-2 years) high-dosage
users do not show lasting cognitive impairment, and this case seems to be
the exception rather than the rule. Personal susceptibility may have a lot
to do with it. Still, please be careful about regular use.
..............................................................................
Memory impairment
DXM, like any other NMDA blocking agent (including alcohol), will impair
short-term and possibly long-term memory. This should go away after the
user has stopped taking DXM, although it may take some time for things to
return to normal.
..............................................................................
Habituation and Psychological Addiction
Addiction is certainly possible but not common; see Sections 4.3 and 4.4.
..............................................................................
Tolerance and Physical Addiction
Again, possible but not common. See Sections 4.3 and 4.4.
..............................................................................
Neurotoxicity
Another possible effect of long-term DXM use is neurotoxicity, specifically
toxicity to 5HT (serotonin) secreting neurons. This has not been observed,
but would be consistent with DXM's hypothesized ability to induce 5HT and
dopamine release (52). Such neurotoxicity would be similar to the
neurotoxicity resulting from use of MDMA (ecstasy). On the other hand,
MDMA's neurotoxicity in humans is itself doubtful.
Recently, animal studies have shown that PCP can cause damage to specific
types of brain cells, probably as a result of neurotransmitter release
triggered by NMDA blockade (101,136). This effect is known as NMDA
Receptor Hypofunction (NRH), and currently it is not known just how much of
a problem it is. It is possible that NRH may be partly responsible for
alcohol's neurotoxicity. However, nobody knows if NRH is relevant in
humans, nor is it known whether DXM would induce the same effect as PCP.
..............................................................................
Excitotoxic Rebound
Excitotoxic rebound is a process by which brain cells, accustomed to a
lower level of activity, essentially "burn themselves out" when a
depressant drug is removed. Alcohol, benzodiazepines (tranquilizers, e.g.,
Valium?), and barbiturates (sedative-hypnotics or "downers") are well known
for causing severe excitotoxic rebound. It is possible that regular use of
DXM could lead to an upregulation (i.e., increase in number) of NMDA
receptors as the body tries to compensate for the blocking effect of DXM.
Sudden cessation of DXM could leave the brain cells with too many NMDA
receptors, leading to excitotoxicity. This is certainly just speculation,
and although probably nothing to worry about, it might be another good
reason to avoid regular DXM use.
..............................................................................
Psychosis
Some research has linked sigma receptors to schizophrenia (46-49), and
chronic use of NMDA antagonists has been shown to upregulate (increase the
number or activity of) dopamine receptors (50). This could theoretically
mean that DXM could trigger schizophrenia in susceptible individuals,
although nobody knows for sure. PCP has been known to trigger psychosis in
susceptible individuals, and DXM may have the same capacity.
Along a similar line, people using dissociative anesthetics on a regular
basis sometimes develop a temporary psychosis a bit like mild
schizophrenia. Usually the users don't notice until people tell them they
are beginning to act inappropriately or weird. DXM may cause this problem
if used regularly. Some researchers have suggested that chronic NMDA
blockade and/or sigma activity may be responsible for schizophrenia or
Alzheimer's disease (101).
..............................................................................
Kidney damage
I have found no evidence of liver or kidney toxicity from DXM itself. This
doesn't mean that there isn't any, just that I haven't found any references
indicating this. DXM tends to be metabolized fairly well, and neither it
nor its metabolites seem to be toxic to the body.
On the other hand, the large amounts of "inert" ingredients may be
dangerous to the kidneys and/or pancreas, especially if taken on an empty
stomach. At least one chronic (9 month) user became unable to take any type
of cough syrup (containing DXM or not) without severe kidney pain and
bloody urine. Gel-caps failed to induce this adverse effect. Another two
former users have reported similar effects, so this may be something to
worry about.
..............................................................................
Bromide poisoning
Although some authors have suggested the possibility of DXM-induced bromism
(147), actual blood tests have revealed little danger to occasional users,
even with large doses of DXM (137). Daily use might lead to a dangerous
buildup. Notable symptoms of bromide poisoning include headache,
irritation, slurred speech, psychosis, weight loss, hallucinations, and an
acne-like rash.
..............................................................................
Miscellaneous
DXM may decrease immune function due to sigma activity (51).
Chronic use of NMDA antagonists seems to modify alcohol tolerance; this is
based mostly on anecdotal evidence and theory, but it appears to be a very
real phenomenon. If true, then it is important to note that the GABA
receptor effects of alcohol may NOT be changed; in practical terms, you
might be a lot drunker than you feel, and this could possibly lead to
alcohol poisoning. Be careful, and limit yourself to as little alcohol as
possible when using DXM. A recent paper supports the ability of DXM to
affect alcohol tolerance (53), although this paper was concerned with a
different effect, i.e., prevention of learned tolerance by NMDA
antagonists.
At least one user has reported that very long-term regular use of DXM
(recreationally) can lead to a constant hacking dry cough. I have not been
able either to confirm or to disprove this.
------------------------------------------------------------------------------
[4.3] Is DXM addictive?
From one viewpoint, of course, anything can be addictive - television,
chocolate, masturbation, self-mutilation, etc. So in that sense, yes, DXM
can be addictive. Somewhat more relevant are the degree to which DXM is
addictive, and how such addiction manifests itself. The quick answer is,
DXM can be addictive if you use too much, too often.
The traditional distinction made with respect to addiction is between
physical addiction and psychological addiction. As examples, alcohol is
physically addictive, whereas marijuana is psychologically addictive.
Unfortunately this distinction has its problems - not the least of which is
that since the brain is a physical construct, any addiction is in some
sense "physical."
As physical addiction is a somewhat nebulous concept at best, I prefer to
use the concrete ideas of tolerance and serious withdrawal symptoms.
Tolerance is a process by which the body and brain adjust to a drug so that
the dosage must be increased to achieve the same effect (some drugs, such
as nitrous oxide, exhibit reverse tolerance). "Serious" withdrawal
symptoms is somewhat less clear, unfortunately. Note that it is possible
to become tolerant to a drug without being psychologically addicted; in
fact, some people lose the desire to use a drug when tolerance takes away
its more interesting effects.
There is considerable evidence based on personal reports that tolerance to
DXM's more interesting dissociative effects builds quickly. This is a
result of upregulation or sensitization of NMDA receptors, as well as
possible changes in other receptors and systems indirectly affected by DXM.
Cross-tolerance exists between DXM, PCP and ketamine, naturally. Some
people seem to be immune to tolerance to dissociatives including DXM (lucky
them).
Usually it takes several doses before tolerance is noticeable, although a
few people have noted tolerance after just one dose. Larger doses will
lead to quicker tolerance. Once tolerance has built, it takes at least
three weeks before receptors will reregulate to normal levels. To avoid
this problem, it is probably best to dose only once a week at most. Also,
some people believe that receptors which are upregulated (or downregulated)
for long periods of time may tend to stay that way. The practical upshot
is you should take a month off every now and then (a good idea with any
drug, incidentally).
Interestingly, the first plateau music euphoria effect also seems to
disappear with repeated use of DXM. It's also one of the last effects to
come back. This may be due to downregulation of dopamine receptors rather
than upregulation of NMDA receptors. The practical upshot is, don't do DXM
all the time. Again, some people are luckily immune to this tolerance
effect.
For information on withdrawal and withdrawal symptoms, see the next
section.
Psychological addiction to DXM has been noted a few times, and can
theoretically lead to physical addiction. Generally, though, dissociatives
aren't considered particularly habit-forming, since they tend to have such
"heavy" effects. Low-dose DXM might be an exception due to its moderate to
strong stimulant effect; in practicality, it's probably too hard to
consistently hit the first plateau.
There are exceptions, some of them notable. One case report (133) involved
a 23-year old male who maintained an incredible daily dose of 30mg/kg to
40mg/kg DXM (plus a six-pack of beer)! Needless to say, after maintaining
this dose long enough, he had become addicted, although the authors
consider it a "psychological" addiction, with withdrawal symptoms such as
dysphoria, depression, and anxiety.
Most people who use DXM have noticed little or no addiction, and only mild
tolerance (don't let that scare you; remember that coffee produces both
tolerance and withdrawal symptoms). A few unfortunate people have
developed problems with DXM. Prolonged, heavy use of DXM seems to induce
dysphoria, anxiety, and/or depression in some people; as the dosage is
increased, the problem gets worse. Unfortunately, at this point, there may
be withdrawal problems (see the next section). If this happens to you,
seek medical assistance.
------------------------------------------------------------------------------
[4.4] Is DXM withdrawal dangerous?
Withdrawal from occasional DXM use is almost certainly not dangerous, and
in fact any "symptoms" felt are probably just "jonesing" - the same sort of
withdrawal "symptoms" felt with marijuana, television, sex, etc. At this
point it's a matter of willpower more than anything else.
Once tolerance has built, withdrawal has the potential to cause more
serious problems. Mild tolerance to DXM is probably no more dangerous than
mild tolerance to alcohol (tolerance at the level of "being able to hold
your liquor"). Withdrawal may produce boredom and mild anxiety, but rarely
anything more troubling than that.
Beyond the mild tolerance level, things get rapidly worse. There is
evidence that significant NMDA upregulation can lead to excitotoxic rebound
(101), and many of the symptoms of opiate withdrawal may occur via a
similar mechanism (110,134). The good news is, studies generally haven't
found any significant evidence of brain damage from heroin withdrawal, so
withdrawal from DXM probably wouldn't be much trouble. The bad news is,
heroin withdrawal isn't particularly enjoyable.
Interestingly, one person who developed addiction and tolerance to DXM also
compared the withdrawal symptoms to those of heroin (although DXM never
produced any of the positive effects of opiates in this individual). These
symptoms included watery eyes, stuffy nose, gooseflesh, muscle spasms,
increased pain sensitivity, nausea, anxiety, and depression. Furthermore,
the individual eventually began to develop some of these symptoms even
while using DXM. This is definitely something to avoid.
If you happen to develop a significant degree of tolerance to DXM, it might
be a good idea not to quit "cold turkey" (all at once). Build down slowly
over a few weeks, and avoid all other drugs in the mean time. One person
who had been using DXM twice daily reported no withdrawal symptoms after
decreasing the dosage 10% per day, and stopping at 180mg. This should
prevent any excitotoxic rebound.
------------------------------------------------------------------------------
[4.5] DXM hangovers - avoiding and alleviating
Hangovers from DXM trips are not common at lower dosage ranges (first and
second plateau). Instead, many people report feeling energetic and
refreshed the next day, although it seems that getting enough sleep is
important here.
At higher dosage levels (third and fourth plateau), hangovers are more
frequent. Hangover effects reported consist of lethargy, sleepiness,
amotivation, mild sensory dissociation, muscle rigidity, muscle tics
(especially in the jaw and hands), dizziness, loss of balance, headache,
photophobia, and sharply diminished sense of taste. Some people say that
everything tastes like slightly salty tepid water, or like MSG (monosodium
glutamate, the flavor enhancer). Note that you're very unlikely to get
all, or even most, of these symptoms.
Some of the hangover effect from high dosage trips is almost certainly due
to residual DXM or dextrorphan, especially in individuals who lack
P450-2D6, or in whom it is inhibited (e.g., by fluoxetine). To my
knowledge there doesn't seem to be any way to speed up the metabolism; the
best I can suggest is to exercise, drink plenty of water, take a
multivitamin every day (don't overdo it, one is plenty) and possibly a
small iron supplement (which just might increase cytochrome turnover), get
enough sleep, and eat right. Don't take too much iron; iron is very toxic.
Other hangover effects may be due to neurotransmitter depletion (due to
induction of 5HT and dopamine release), temporary inactivation of NMDA
receptors (I doubt it, but there's been speculation), or just plain lack of
sleep. Again, treating your body well is probably the best you can do.
Preventing hangovers may be possible to some degree. Certainly, make sure
you are in good physical condition to start with, and don't try to stay up
too late during your trip. Drink plenty of fluids (it is possible to get
dehydrated; this can slow down the kidneys), and don't mix DXM with
anything that could further deplete neurotransmitters (e.g., amphetamines,
MDMA, etc.). Try to avoid going to sleep while still tripping hard - it
seems to reduce the quality of sleep. Eat something before you go to
sleep; usually DXM kills the appetite.
Another possibility is the use of nootropics ("Smart Drugs") to help
prevent and alleviate hangovers. A good place to start for information is
alt.psychoactives; another good place is Dean and Morganthaler's text on
the subject. A healthy dose of skepticism is probably a good idea here;
some of it might be placebo effect. There's evidence for and against;
check Medline if you're interested. Note that unless otherwise specified,
everything I mention should be available at health-food or mail-order
vitamin suppliers (this is USA; I don't know about other countries).
Several people have reported beneficial effects from cholinergics,
specifically choline (the precursor to acetylcholine), and DMAE (also a
precursor, and a choline oxidase inhibitor). In both cases the bitartrate
salt seems to be the usual (there is a liquid DMAE para-aminobenzoic acid
formulation that tastes nasty and evidently doesn't work). Note that some
people with depression, primarily endogenous, react very poorly to
cholinergics. Also note that they can make you really, really irritable if
you're susceptible. Regular use of DMAE seems to be the most effective,
although that's something that you have to build up for a couple of weeks
(Dean and Morganthaler suggest around 800mg per day in divided doses;
please consult alt.psychoactives for nootropic information).
One-time use of DMAE or choline immediately before, during, or after the
trip has also been reported to work, (in that order of preference),
although not as well. Recommendations given to me have been 800mg DMAE, or
1500mg choline; in either case with 350mg vitamin B-5 (pantothenic acid)
which acts as the relevant cofactor here. Don't go much above that.
There is some preliminary evidence (still haven't found the reference) that
supplementary tyrosine may actually be useful in the case of dopamine
depletion. Normally, the rate-limiting enzyme in the process is nearly
saturated, so boosting tyrosine doesn't work. It's hypothesized that more
enzyme may be produced in response to dopamine depletion. Furthermore,
sigma activity may enhance synthesis of dopamine (115), so taking
supplemental tyrosine is even more likely to be a good idea.
Vasopressin might also be useful; it seems to have a fair amount of success
in combating intoxicants, possibly by affecting long-term potentiation (how
I don't know). It's prescription in the USA, and it does have side
effects.
One final note - do not take tryptophan! Although this isn't established,
it's possible that NMDA receptors may be upregulated after a DXM trip
(especially in chronic users). Tryptophan, in addition to leading to 5HT,
also leads (along a much more efficient pathway) to a substance called
quinolinic acid, which is very toxic to neurons, and acts via NMDA
receptors.
------------------------------------------------------------------------------
[4.6] 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. Liver levels of DXM were about an
order of magnitude higher. 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 60-70kg adult. 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.
The highest daily dose of DXM I've come across is from a case study of a
23-year old male (133). His daily dose was 3 to 4 12oz bottles of
Robitussin DM?, for a total of 2160mg (31mg/kg) to 2880mg (41mg/kg). He
was, of course, considerably addicted to DXM, and had built up this dose
over a long period of time.
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 25 to 30
mg/kg (about 2000g for adult of 150lb). 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).
------------------------------------------------------------------------------
[4.7] 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 labeling.
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 as mentioned above. 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 USA, 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.
------------------------------------------------------------------------------
[4.8] Help! What do I do if...
This section covers suggestions for undesirable, unexpected, and emergency
situations. Always remember, though, if you feel there is an emergency,
get to a hospital. While DXM-related deaths are very, very rare, they have
occurred. Nobody wants to see any more happen. None of this is intended
to be medical advice or replace the judgment of a physician, nor should it
be taken as such. These are general guidelines only, compiled from reports
of DXM users. Neither I nor anyone else take responsibility for any
injury, death, or other misfortune, resulting from this advice. There,
have I covered my ass well enough? Probably not. Just remember, please
use common sense and be careful!
..............................................................................
Itching (the "Robo Itch")
Some people get the itch, some don't. Unfortunately, I still haven't been
able to correlate it with anything, so I still can't figure out whether it
comes from the DXM itself, or from a dye or other additive. It very well
may be a reaction to dissociative anesthesia.
In any case, from all reports the best thing seems to be to wait for it to
go away, and try to think about something else. Scratching is OK, so long
as you don't injure yourself in the process (remember, you many not be
feeling pain as you normally would). A loofah can be quite enjoyable,
actually, should you feel the urge to take a bath (which evidently can
itself be enjoyable on DXM. Just be careful!) You can try a topical
antihistamine spray, but I doubt it will do any good.
If the itch is accompanied by a rash, swelling, or other symptoms of an
allergic reaction, you should definitely take an oral antihistamine (not a
prescription one), and make sure there is someone with you. If the
allergic reaction continues, or you feel you may be going into shock, get
to a hospital. To my knowledge this type of allergic reaction has never
occurred.
..............................................................................
Fast Heartbeat and Panic Attacks
Many times this is more a problem of perception than anything else. Still,
it does happen. As far as I have been able to determine, DXM itself can
raise the heart rate somewhat, about as much as a mild to moderate
stimulant (e.g. a few cups of coffee to a "coffee virgin"). Reports have
indicated a range of 90 to 120 beats per minute as the relevant range.
Panic attacks also can occur on DXM, especially in naive users or users
rushing in to higher doses. A panic attack can increase the heart rate
significantly, sometimes as much as 200 beats per minute! Unfortunately,
panic attacks can be hard to control; the best thing to do seems to be to
try to relax, go somewhere you feel comfortable, and focus on your
environment. A panic attack is a positive feedback situation; once you
start having one, the symptoms themselves can feed the fear. Breaking this
vicious cycle can be difficult. If you are predisposed to panic attacks
you should probably avoid DXM in the first place.
Prolonged very fast heartbeat, or fast heartbeat accompanied by chest pain
or tightness, should be taken seriously and may be cause for medical
attention (note that a panic attack can also cause a feeling of chest
tightness). If in doubt, go to the hospital. Note also that people with
existing heart problems should avoid recreational DXM use. Incidentally,
neither of the recorded deaths due to DXM overdose were attributed to heart
attack (respiratory failure was considered the cause).
..............................................................................
Irregular Heartbeat, or "Skipped Beats"
An irregular heartbeat, like a fast heartbeat, may be a problem of
perception more than anything else. Remember that, especially at higher
doses, there can be a "sensory echo" effect which may influence your
measurements.
An occasional feeling that your heart "skipped a beat" is usually not cause
for worry. Sometimes it is due to spasms of the esophagus, stomach, or
bronchial tubes and has nothing to do with the heart; it's hard to
distinguish sensations among internal organs. More frequent heart
irregularity, or irregularity with chest pain, may require medical
attention. Go to the hospital if in doubt.
..............................................................................
Nausea, vomiting, gas, and diarrhea
Ah, the joys of ingesting large amounts of thickening agents. Nausea is to
be expected, especially with cough syrups. It usually goes away. Do not
take anti-nausea medication. Some antiemetics are anticholinergics and/or
CNS depressants, neither one of which you want to mix with DXM (meclizine
would probably be okay, although I don't advise it). The best response
seems to be to tough it out, or switch to gel-caps. Incidentally, avoid
taking DXM with greasy or heavy foods.
Vomiting occasionally occurs, usually for the same reason as nausea.
Again, not much to worry about. If you do vomit, just make sure to drink
lots of water to replace what you just lost. Both guaifenesin and large
amounts of alcohol tend to contribute to the tendency to vomit.
Gas and diarrhea, especially after the trip, are also fairly common with
syrups. Not much to do, unfortunately; just tough it out and drink water.
..............................................................................
Unconsciousness
This is mostly advice for the designated sober person; obviously it won't
do you much good if you're unconscious. Unconsciousness with DXM is to my
knowledge extremely rare (I've heard of it happening once).
Generally if someone passes out, the first thing to do is make sure they
don't fall and hit their head. Yes, DXM may protect brain cells somewhat
from the effects of head trauma, but let's not try out that theory
ourselves. Make sure the unconscious person is lying down with their feet
elevated, and that someone (sober) is with them. If you feel there is any
danger of vomiting, roll the person onto his or her side.
At this point, if the individual is breathing well, and seems OK (other
than being unconscious), you can wait it out if you feel comfortable doing
so. The unconscious person may be flying around in a mental dreamscape,
oblivious to you and the rest of the world. If there is any indication of
irregular breathing, slow or weak heartbeat, or other problems (e.g., his
face is blue), get to a hospital immediately. You may wish to indicate that
IV naloxone is considered antidotal for DXM (naloxone is also used for
opiate overdose, incidentally). I suppose it would be possible to have a
syringe of naloxone on hand (it's actually fairly safe, being an opiate
antagonist; to my knowledge it's not possible to overdose on it). However,
it's not exactly something you can get at your local drugstore, and in any
case other measures may be necessary which would require hospitalization.
Remember, if there is any indication or suspicion of an overdose, get
medical assistance immediately!
..............................................................................
High body temperature / fever
First, make sure you actually have a fever. DXM can mess with your sense
of temperature. On the other hand, I have received one report of
DXM-induced hyperthermia that could have been dangerous. A temperature at
or above 102 F (39 C) is entering the danger zone. If this happens to you
(or someone you are with), the best way to cool down is by taking a cool
bath or shower (make sure it feels cool to a normal person!), and drinking
cold water. Incidentally, speaking from personal experience (with the flu,
not DXM), the "cool" water will feel damn cold.
In the case of a fever at or above 105 F (40.5 C) you've got a real
emergency on your hands. Immediately contact a doctor or hospital, and try
to reduce the body temperature as quickly as possible. Ice-water baths are
acceptable providing there is someone (sober) there to make sure the person
doesn't pass out and drown. Expect to hear a lot of screaming; this is a
significantly unpleasant experience even without a fever.
..............................................................................
Shortness of breath
Again this is usually a perceptional problem, and sometimes is related to
panic attacks. There is also evidence that dissociative anesthetics in
general cause a transient phase of shortness of breath, possibly because
the body is beginning to "take over" breathing from conscious control.
Take deep, even, and slow breaths; hyperventilating won't help, and can
make you feel even worse. It should clear up by itself. In the case of
hyperventilation, the "breathing into a paper bag" trick really does work,
by increasing blood CO2 levels.
..............................................................................
Sensation of choking one's tongue
If you start feeling like you are choking on your tongue, make sure someone
can assist you, or call a doctor if you believe you really are choking.
There is actually very little danger of choking on your tongue; it's pretty
much physically impossible. Nonetheless it can seem frightening.
If you are in the position of trying to assist someone in this situation,
open the person's mouth, tilt their head back slightly, and grasp and hold
their tongue out of the way of their airway until they feel better. Avoid
putting anything in their mouth; this could easily fall and cause much
worse choking.
..............................................................................
Nosebleeds
If you are prone to nosebleeds this probably isn't a problem and may be due
to nasal irritation. If possible, check your blood pressure. If the
nosebleed is prolonged, your blood pressure is high, you notice any burst
capillaries in your eyes, or you experience sharp pains in your head or
lungs, go to the hospital. I'm not familiar with any cases of DXM-induced
hypertension, although it might be possible, especially when mixed with
stimulants or MAOIs.
..............................................................................
Feeling "dead" / losing one's body
Remember, DXM at high levels can be very dissociative. You're not dead,
you just can't feel your body right now. This state can have a lot in
common with certain lucid dream states. A feeling of "being dead" is
common with third and fourth plateau DXM doses. The best thing seems to be
to try to make contact with some part of your body (this can take a lot of
effort), to reassure you that you're still there. Then, relax and enjoy
your trip.
This is another reason why you should a sober person with you. If you are
in any real danger, he or she should take care of you.
Note: see also the guidelines on shamanic journeying in Section 3.12.
..............................................................................
Hangovers (lethargy and feeling "not all there")
Hangovers can occur from higher doses. Usually you can expect to feel very
relaxed if not lethargic for the next day after a heavy trip. You may also
might experience dizziness, muscle rigidity, loss of balance, slight
double-vision, and a general feeling of being "not all there". Again, it
goes away. Sleep seems to improve things a great deal. Make sure to drink
a lot of liquids, get plenty of rest, take a multivitamin, and exercise.
As DXM is metabolized differently in different people, some may experience
hangovers (and trips) a lot longer than others. For more details, see
Section 4.5.
..............................................................................
Prolonged dissociation from the real world
Very rarely, someone will come out of a DXM trip and seem to be very
dissociated from the real world, behaving a little like a robot. Whenever
this has been reported to me, the person in question had always taken a
high (third to fourth plateau) dose, and in most cases had tried to achieve
an out-of-body state (draw your own conclusions). Make sure the person is
relaxed, and try to engage him or her in a familiar activity. Familiar
environmental cues should go a long way towards bringing him or her back to
the "real world". Also keep in mind that the person may be slow to
metabolize DXM and thus still be tripping.
If, after a couple of days, the person still hasn't returned to normal,
it's time to get worried. Contact your nearest psychologist, priest,
shaman, or other equivalent. Note that I don't think there's any biological
reason for this to happen.
==============================================================================
[5] PHYSIOLOGICAL EFFECTS OF DXM
This section explains some of what is currently known about DXM and its
physiological effects. As the recreational use of DXM is not well studied,
most of that information is speculation, some of it on my part.
------------------------------------------------------------------------------
[5.1] 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 can be blocked. Sigma
receptors are evidently involved in this pathway (42,49,55,56). This may
be a direct involvement - sigma activation may directly inhibit the cough
reflex signals - or it may be an indirect one. The cough suppressant
effect of opiates (such as codeine) is not related to the same effect of
non-opiate morphinans like DXM (49); instead, it seems to be governed by
traditional opiate receptors (mu, kappa, or delta).
There is some evidence that 5HT1A receptors (a serotonin receptor type) are
involved somewhere in this pathway, and that cough suppressants may
increase 5HT1A activity (57), possibly via NMDA antagonism (90). This
could explain some of DXM's mood-altering activity. 5HT1A receptors are
involved in anxiety states and in resilience to aversive events.
Buspirone, a 5HT1A receptor partial agonist, is an anti-anxiety drug less
potent (but considerably safer) than the benzodiazepines such as diazepam
(Valium[tm]).
------------------------------------------------------------------------------
[5.2] How does DXM cause its psychoactive effects?
General Information
DXM binds to at least four sites in the brain (58), which can be
arbitrarily labeled DM1, DM2, DM3, and DM4; there is probably also a fifth
binding site (DM5). Some of these sites are sensitive to pentazocine, a
known sigma ligand; some are sensitive to haloperidol, another sigma
ligand. On the following table, information from several sources has been
gathered and combined. The binding affinity of DXM, DTG, and 3-PPP are
listed (58), along with (+)-pentazocine sensitivity (60), and haloperidol
displacement ability (58), (binding values in nM unless otherwise
specified). "Low" means micromolar binding affinity.
o-------------------------------------------------------------------o
| DXM Site | DM1 | DM2 | DM3 | DM4 |
|-----------------------+----------+----------+----------+----------|
| Probable Binding Site | Sigma1 | PCP2 | Sigma2 | NMDA |
|===================================================================|
| DXM | 50-83 | 8-19 | low | low |
|-----------------------+----------+----------+----------+----------|
| (+)-3-PPP | 24-36 | low | 210-320 | low |
|-----------------------+----------+----------+----------+----------|
| DTG | 22-24 | ??? | 13-16 | ??? |
|-----------------------+----------+----------+----------+----------|
| Pentazocine Sensitive | Yes | No | ??? | ??? |
|-----------------------+----------+----------+----------+----------|
| Haloperidol Displaced | Yes | ??? | Yes | ??? |
o-------------------------------------------------------------------o
Table 2: DXM Binding Sites
What this table demonstrates is that DXM binds to four separate places, two
with high affinity. The first receptor is accepted to be the sigma1
receptor based on the binding to pentazocine and haloperidol, and the
potency of (+)-3-PPP. The second receptor is almost certainly the PCP2
receptor, given the insensitivity to pentazocine, and the very high
affinity for DXM. The third site is probably sigma2 (based on the potency
of DTG) but it is possible that "DM1" in this table represents both sigma1
and sigma2 and that the third site is something else. The fourth site is
probably the NMDA receptor's open channel site, although it might be the
ion channel binding site (59).
I don't have information on the binding of DXO (dextrorphan),
unfortunately. It would probably show strongest binding at DM4 (NMDA open
channel site), followed by DM1 (sigma1), and then by DM3 (sigma2) and/or
DM2 (PCP2), or both. I'm looking for this information currently.
..............................................................................
Contribution of the PCP2 Binding Site
The PCP2 binding site is probably the dopamine reuptake complex, so
blocking it would prevent the uptake of dopamine in much the same way that
the antidepressant bupropion (Wellbutrin[tm]) or cocaine does (73). Of
course, DXM is considerably weaker than cocaine (and stronger than
bupropion, incidentally) at this site. This probably accounts for the
euphoric effects of a low recreational dose, and almost certainly explains
the stimulant effects of a low dose. Interestingly, the stimulant effect
seems qualitatively different from amphetamines to most people (I have no
comparison information on cocaine). One user compared DXM and bupropion
favorably in stimulant effect.
The music euphoria and motion euphoria are probably partly due to PCP2
activity, and partly due to other activity. As NMDA blockade and sigma
activity can both lead to dopaminergic activity (see below), reuptake
inhibition would potentiate these effects.
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 related receptors (sigma, PCP) (71,74,75); it is
possible that the PCP2 site may be a target of some antidepressants.
..............................................................................
Contribution of the Sigma Binding Sites
As the sigma2 site is a fairly recent discovery, it is not known what
sigma-related effects and behaviors are attributable to which receptor
(sigma1 or sigma2). There is very little data on the subjective effects of
sigma ligands, 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. DXM binds to the sigma1 receptor and is generally
considered to be an agonist at this receptor. DXM is probably also an
agonist (as opposed to an antagonist) at sigma2, though it is much weaker
there.
The disruption of sensory processing is probably partly due to sigma
activation (and partly due to NMDA blockade) (63-65). Sigma receptors may
be specifically involved in the auditory effects of DXM (65), and these
effects may relate to a disruption of sensory input persistence.
The psychotomimetic (literally "psychosis-like") effects of DXM may be a
result of sigma activity (sigma receptors may be involved in schizophrenia)
(46-49). People who have used both DXM and ketamine have remarked that DXM
is much more likely to induce delusional and hyper-abstract thought
patterns. Interestingly, sigma receptors seem to temporarily modulate
cholinergic receptors (98), so sigma activity may produce temporary effects
somewhat like the delusional anticholinergics.
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.
..............................................................................
Contribution of the NMDA Receptor
Most of the effects on the NMDA receptor are due to DXO (dextrorphan),
DXM's main metabolite. DXO, and to a lesser extent DXM, block the NMDA
receptor once it opens, essentially by "plugging it up".
Most of the "stoning" or intoxicating effects of DXM are probably due to
NMDA receptor blockade. Alcohol's intoxicating 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 anesthesia of high DXM doses is also likely due to NMDA
receptor blockade (63).
As stated before, sensory processing disruption, especially at higher
doses, is probably due in part to NMDA receptors and partly to sigma
(63-65). Flanging, in particular visual flanging, probably derives from
NMDA blockade.
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.
DXM's ability to suppress respiration at toxic levels, is most likely due
to NMDA receptor blockade or (in my opinion) ion channel blockade. Some of
the effects from very high dosage levels may be due to overall disruption
of neural networks. There is some preliminary evidence that both the
"spontaneous memory" effect and the sensations similar to near-death
experiences may occur as general neural networks are disrupted. Most drugs
target specific clusters of neurons, whereas NMDA receptors tend to be more
evenly distributed within certain areas of the brain, so blockade of NMDA
receptors may be responsible for disruption of some of the brain's neural
networks.
..............................................................................
Contributions of Indirect Activity
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). NMDA receptor
blockade also has been shown to increase dopaminergic activity, as well as
activity of other neurotransmitter systems (101).
..............................................................................
Flanging
One of DXM's most prominent effects if the flanging of sensory input. This
happens to some extent with many drugs, and I have a hypothesis on this.
Note in particular the relation of flanging to "stoning" and "buzzing" - in
some ways, flanging is a more profound degree of stoning. Some people have
noticed a flanging or strobing effect after smoking a great deal of
cannabis, and nitrous oxide users are also familiar with flanging of
sounds. Even alcohol can produce it.
What it seems many of these drugs have in common is the ability to inhibit
short-term memory, almost certainly via blocking long-term potentiation (in
the case of nitrous oxide, of course, the inhibition lasts for such a short
period that it is generally not noticeable). Other drugs, such as the
benzodiazepines, block short-term memory as well, but this is more likely
due to an overall depressant effect on the brain.
Current theories point towards the hippocampus as the main location for
short-term memory, and although other parts of the brain are probably
involved, I will refer to it exclusively. The hippocampus is one of the
most regular neural networks in the brain, and seems ideally suited for
storing temporary associations. It also is to some extent "self-feeding"
(although not necessarily directly); as such it is capable of very complex,
nonlinear associations in much the same way that "self-feeding" functions
can give rise to fractals.
Simulations of self-feeding neural nets often show that information is
processed in a finite number of "cycles" before the output state settles
down (this sophisticated behavior may derive from some very simple rules,
and has even been observed in bulk optical material (138). Interestingly,
the hippocampus has a "sweep frequency" of unknown nature which may be
related to this cycling.
The activity of NMDA receptors certainly helps to maintain the normal
functioning of the hippocampus. As NMDA receptors become increasingly
blocked, individual neurons in the associative network of the hippocampus
lose part of their positive input. Although they may compensate by
reducing negative input (at GABA receptors, perhaps), the plastic or
"learnable" component of neural input will diminish in comparison to the
ordinary input (via AMPA and kainate glutamate receptors). Thus it may
take more cycles to reach a stable output state.
In cortex, NMDA receptors could be much less important, and some aspects of
"consciousness" may function mostly via "ordinary" glutamate receptors. If
this is the case, then cortical networks would still be operating at normal
(or near normal) speed, while the hippocampus slowed down. It is also
likely that unstable output from the hippocampus is ignored, or at least
dealt with differently than stable, final associative output. Finally,
note that raw sensory input probably needs some associative processing
before it can reach consciousness, since what we perceive is to some extent
"written" in the mental language of our past experiences.
Thus, as the hippocampal output slows down and becomes increasingly less
stable, one becomes conscious of increasingly less frequent sensory input.
Eventually, this becomes infrequent enough that flanging occurs. Finally,
with sufficient loss of NMDA function, the hippocampus may never reach a
stable state, leading only to chaotic output, totally unconnected to
sensory input. But more on that later.
This is all just a SWAG (scientific wild-assed guess), of course. But I
think this hypothesis has some merit, and in the next several years I hope
to further elaborate on it in my studies on hippocampal neurons.
..............................................................................
Hyper-Abstraction
Another interesting effect of DXM is its ability to induce peculiar
cognitive disturbances, which I lump together under the term of
"hyper-abstraction". Two examples:
o A meme is a "particle" or "virus" of thought - an idea which is in
some ways self-contained, and which spreads like a virus. For
example, the idea of civil liberties is a meme, which at some point
sprang into existence, spread rapidly, and has now become an integral
part of our consciousness.
One user during a DXM trip suddenly became aware of (or thought up)
"The self-invoking, self-creating meme", which was the concept of a
meme whose identification creates and invokes it. It seemed that
this meme was timeless in the sense that it must have always existed,
or it could not have come to mind.
o Another user wrote of thinking about convergent infinite sums (e.g.,
1/2 + 1/4 + 1/8 + etc., which sums up to 1). Although one can add
these terms up forever, it's easier to abstract the process and get
the answer that way. This user imagined an infinite series of
abstractions, and then imagined abstracting that infinite series to
get a new level or plane of abstraction.
Many DXM thought patterns involve what some have called "Strange Loops" in
logic (139). Like the self-contradicting statement "this statement is
false", some of them cannot be embodied in logical form; others can be, but
cannot be derived without presenting them as hypothesis. Thinking at this
degree of abstraction is very difficult (unless you are fortunate enough to
be Kurt G?del).
Several people who have written first-person accounts of psychosis and
schizophrenia have mentioned increasingly abstract thought patterns (Zen
and the Art of Motorcycle Maintenance springs to mind). This may of course
be complete bunk, and it may be that the increasingly "abstract" thoughts
are just increasingly loony (and thus difficult to relate to concrete
ideas). On the other hand, it may be that something about schizophrenia
and psychotic states is related to a blurring between levels of
abstraction. Once blurred sufficiently, a thought which cannot be
represented at a concrete degree of abstraction could be representable in
the mind.
Thus, DXM may induce a sort of temporary blurring of these levels of
abstraction. Whether this is due to NMDA or sigma activity, I don't know,
although I suspect the latter, since other NMDA antagonists don't tend to
induce such changes in thought patterns.
..............................................................................
Delusions and Memory Problems
As stated above, sigma activity may modulate cholinergic receptors in the
brain (98), leading to a temporary decrease in cholinergic function similar
to (but considerably safer than) that caused by anticholinergics like
atropine, scopolamine, cyclizine (Marezine), etc. It is known that
cholinergic activity is important in memory, and many nootropics ("Smart
Drugs") enhance cholinergic function. Sigma activity may very well cause
temporarily lowered effectiveness in some cholinergic receptors, thus
distorting memory and thought processes. Some people have in fact said
that DXM makes them feel temporarily stupid ("Dumb Drugs", anyone?)
although this by no means happens to everyone.
Many of the biogenic amine systems seem to have a modulatory role, and some
researchers think these modulating systems operate much like "control
knobs". For example, one theory on LSD is that it upsets the "gain
control" on sensory recognition networks, so that the random noise input
(necessary for any pattern matching network) becomes much stronger than the
sensory input. As a consequence, sensory recognition becomes increasingly
less and less precise - ergo, hallucinations.
LSD's effects are almost certainly more complex than this, but there may be
some truth to the "control knob" idea of the biogenic amine systems. If
so, then the cholinergic systems may be the "control knobs" for cognitive
networks in much the same way that 5HT2A/5HT2C systems are for sensory
recognition networks. Delusions may simply be the cognitive equivalent of
hallucinations. Or to put it another way, the difference between thinking
you look like a flower and thinking you are a flower may be a question of
which network is disrupted.
Memory problems derive to some extent from NMDA blockade, although some
users of ketamine have remarked that DXM can have a stronger effect on
memory than ketamine. It is possible that, in addition to inducing
delusional thoughts, a decrease in cholinergic function could be
responsible for some of the memory problems. This is certainly consistent
with the effects of the delusional anticholinergics.
Incidentally, the anticholinergics also affect acetylcholine receptors that
govern the functioning of the heart and respiration (these receptors do not
seem to be modulated by sigma activity). Recreational use of
anticholinergics can be extremely dangerous, leading to collapse of
respiration or heart failure.
------------------------------------------------------------------------------
[5.3] Why does DXM exhibit plateaus?
Plateaus 1-3: Multiple Receptors
This graph illustrates a potential effect of multiple receptors. Note that
it is a qualitative drawing, not a quantitative one; the actual degree of
saturation on different receptors for a given strength of DXM is still
mostly unknown. The lines represent saturation levels at the PCP2, sigma1,
and NMDA open channel sites, with full saturation at a given receptor
indicated by the "flattening out" of the curve.
o------------------------------------------------o
| |
| S | Pla | Plateau 2 | Plateau 3 _ |
| a | tea | | __-- |
| t | 1 | | __-- |
| u | | | __--.......... |
| r | | ..._.-.... |
| a | ......__-- |
| t | ***.*.*.**_*-********************** |
| i | ** .. __-- |
| o |* .. __-- ** = PCP2 .. = sigma |
| n |*._-- -- = NMDA |
| |______________________________________ |
| DXM Dose |
| |
| Figure 2: Possible Basis of Plateaus |
o------------------------------------------------o
[Note on text version: This graph didn't make it into ASCII very well.
Basically, you've got three curves; the first -- PCP2 -- reaches a
maximum value very quickly; the second -- sigma -- reaches a higher
maximum but takes somewhat longer; the third -- NMDA -- reaches the
highest maximum but takes the longest time. In "plateau 1", the PCP2
curve is the highest; in "plateau 2", it is the sigma curve that is
highest; and in "plateau 3" the NMDA curve is highest.]
Due to its increasing affinity for PCP2, sigma1, and NMDA receptors
respectively (sigma2 is not represented), a low dose will tend to have
proportionally more effect on PCP2 receptors, whereas as the dosage
increases, these receptors will saturate. Taking more DXM won't change
PCP2 levels much, but will still have a fair effect on other receptors.
Furthermore, the more subtle effects on the PCP2 receptors may be all but
obliterated by the effects on sigma1 and NMDA receptors (the differing
vertical maxima of the three curves represent this effect). This is
entirely reasonable, since sigma1 and NMDA activity seem to both produce
fairly profound behavioral effects, the latter more so than the former.
Thus, the first plateau probably corresponds to predominantly PCP2 activity
with some sigma activity and a little NMDA blocking effect; the second
plateau to sigma and some NMDA effects; and the third to profound NMDA
blockade.
This is, of course, a simplification, and it certainly doesn't take into
account individual variations in receptors. Some people probably have
receptors for which DXM has a stronger (or weaker) affinity. A person with
PCP2 receptors strongly bound by DXM may enjoy its stimulant effects a
great deal more than someone whose PCP2 receptors are only weakly affected.
Additionally, both ion channels and sigma2 receptors are omitted from this
graph. They undoubtedly contribute, and some people have asserted that
there are plateaus in between the first three. Some of these may be so
subtle as to be unnoticeable by most users.
..............................................................................
The Fourth Plateau
o-------------------------------------------------------------------o
| |
| o-------o-------o o-------o o o-------o o |
| | \ / | \ / | | / | \ | / | | |
| | X | X | | / | \ | / | | |
| | / \ | / \ | | / | \ | / | | |
| o-------o-------o o o o o o o |
| |
| 100% intact 50% intact 20% intact |
| |
| Figure 3: Fourth Plateau Pruning Hypothesis |
o-------------------------------------------------------------------o
[Another bad ASCII drawing. The original showed three "nets" or "meshes",
the first with all links in place, the second with 50% removed, and the
third with 80% removed. The first and second were both fully connected,
i.e., you could get from any node to any other. In the third, there
were isolated nodes and groups of nodes.]
What about the fourth plateau? Well, once again, here's another little
drawing that will hopefully clear up everything (yeah, right). This
drawing represents a neural network; the dots are the neurons and the
lines are their connections. Like most of the brain, this network is
highly interconnected. The percentage numbers show the number of
functional links remaining.
As enough NMDA receptors are blocked, one neuron may lose enough input from
another that the connection is effectively severed. Initially this isn't
such a problem, since both neurons and connections are dense enough so that
others can take over the job (although the end result will probably be a
slower and less accurate network). At some point, enough connectivity is
lost that the network no longer functions.
Compare this to the dissociation of the fourth plateau. At some level,
some part of the brain (possibly the hippocampus) loses enough
functionality that it can no longer operate as a cohesive unit. Sensory
processing halts, and raw sensory input cannot be converted to an
appropriately parsed output. The consciousness is then left without any
real sensory input; instead, the chaotic, unstable patterns are provided.
Ergo, dissociative anesthesia.
------------------------------------------------------------------------------
[5.4] Why is this so complicated?
DXM itself is a very complex drug; most drugs only bind to one or two
receptors (or at least one class of receptors). Its recreational abuse
potential, although known for years, has not been well studied, and it can
affect different people very differently. The receptors and binding sites
it affects - sigma, NMDA, and PCP2 - are all new discoveries. All this
adds up to a complicated and poorly understood drug.
Furthermore, the brain itself is a complicated system, and we're still
mostly ignorant of its function. The basics of neurotransmission seem to
be understood, but many questions remain. Nobody knows why there are so
many different neurotransmitters, nor why there are so many receptor
subtypes. The second messenger systems of most receptors are not well
understood either. A lot of what happens inside neurons occurs via changes
in genetic expression, and that's yet another topic about which little is
known.
To repeat a commonly quoted (and true) sentiment, if our brains were simple
enough for us to easily understand, we would be so simple that we couldn't
understand them. I do believe that eventually we will have a good idea of
how the brain works, but it may not be in my lifetime.
------------------------------------------------------------------------------
[5.5] How does DXM get metabolized? (Pharmacokinetics)
DXM, as the hydrobromide salt, is absorbed quickly from the GI tract;
within 30 minutes, all of it may have entered the bloodstream (2,3). The
polistirex compound is intended for continuous absorption, and may take 6
to 8 hours to fully enter the bloodstream.
o-------------------------------o
| | [Note: metabolism proceeds in the "down"
| DXM | direction on this graph; the lines from
| (P450-2D6) / \ (P450-3A) | DXM to DXO and 3MM, and from DXO to 3HM
| / \ | and from 3MM to 3HM, are supposed to
| DXO 3MM | have arrowheads on them. Sorry, more
| \ / | bad ASCII art. Buy the printed FAQ
| (P450-3A) \ / (P450-2D6) | and you get *real* diagrams. ;) ]
| 3HM |
| |
| Figure 4: DXM Metabolism |
o-------------------------------o
DXM is metabolized via two pathways, both of which lead to the same thing
(3-hydroxymorphinan, or 3HM). The first pathway goes from DXM to DXO
(dextrorphan) and then to 3HM; the second goes from DXO to 3MM (3-methoxy-
morphinan) and then to 3HM. By far most of the DXM (up to 90%) gets
metabolized via DXO in normal individuals.
DXM is converted to DXO by a liver enzyme called cytochrome P450-2D6
(debrisoquine 4-hydroxylase). Up to 10% of the population has a highly
inefficient (70 times slower) version of this enzyme, and cannot metabolize
DXM to DXO effectively (10). After being converted to DXO, the enzymes
P450-3A4 and P450-3A5 convert DXO to 3-hydroxymorphinan (77).
The other pathway goes to 3-methoxymorphinan first (via P450-3A4 and
P450-3A5), and then to 3-hydroxymorphinan. Most people do not metabolize
much DXM this way, although people who lack the normal P450-2D6 will
convert a substantial amount to 3MM. As 3MM is probably not psychoactive,
this means that the 5-10% who lack the normal 2D6 enzyme will experience
less effect from DXM (or more specifically, won't experience the effects of
DXO).
P450-2D6 functions by removing the 3-methoxy group and replacing it with a
hydroxyl (OH) (or more accurately, pruning the methyl off the oxygen); this
step is known as O-demethylation. P450-3A4 and 3A5 replace the 6-methyl
group with a hydrogen (H) ; this is the N-demethylation step. Refer to the
diagram of the DXM molecule in Section 2.2 for the location of the methyl
and methoxy groups.
..............................................................................
Factors Affecting DXM's Metabolism
As stated above, some people lack the normal P450-2D6 enzyme. In the rest
of the population, this enzyme can be inhibited by several factors. Many
drugs inhibit P450-2D6, notably including fluoxetine (Prozac[tm]). A
partial list of P450-2D6 inhibiting drugs is given in Appendix 1.
DXM itself naturally will compete with other drugs for P450-2D6, and
importantly, so will 3-methoxymorphinan (3MM) (17,140). In fact, 3MM may
have more affinity for the P450-2D6 enzyme than DXM itself does. This may
account for the fact that a second "boost" dose of DXM generally produces
different effects than the first dose; the competition for P450-2D6 will
reduce the amount of DXM converted to DXO in the second dose.
The following graphs come from computer simulations of DXM metabolism:
[Note: I'm not even going to *try* and put these into ASCII. There were
two figures, each consisting of two graphs. In each graph are shown the
plasma levels of DXM, DXO, and 3MM.
In figure 5, the first graph shows normal DXM metabolism. DXM drops
quickly, DXO rises as DXM drops and then slowly drops, and 3MM stays pretty
much at zero.
The second graph shows abnormal metabolism (no high-efficiency P450-2D6).
DXM drops *much* more slowly, DXO rises slowly and only to about 1/2 the
maximum in the first graph, and 3MM rises much as DXO does.
In figure 6, there are two graphs showing the effect of repeated dosing
with DXM. The first graph shows how the second dose of DXM takes much
longer to convert to DXO, and therefore less ends up as DXO and more as
3MM. The second graph shows numerous, repeated dosings; DXM eventually
rises above DXO.]
The first pair represent the metabolism of DXM in a normal individual (on
the left) and an individual without the normal P450-2D6 enzyme (on the
right). Note the rapid and almost complete conversion of DXM to DXO in
the normal individual, as opposed to the less efficient and slower
conversion in the P450-2D6 lacking individual.
The next pair demonstrate the probable results of taking additional doses
(dose boosting). Both graphs correspond to individuals with the normal
P450-2D6 variant. Note how the second dose of DXM is not converted to DXO
as quickly (thus the shallower slope). The right hand graph shows numerous
doses, and the "flattening out" of the metabolism curve for DXM is
increasingly evident with each dose.
Incidentally, that these are qualitative simulations, not quantitative
ones. I have tried to adhere to known KM and VMAX values for the
applicable reactions, but the simulation was just a discrete process (to be
honest, my differential equation skills are rusty enough that if you
stepped on them you'd need a tetanus shot). I did compare my results with
what little data I could find, and the comparison seemed reasonable, but
then again I could be completely off base. The purpose of these graphs is
to demonstrate the relative effects of changes in enzyme activity (via
genetic variance and competitive inhibition by 3MM), and hopefully this is
good enough for that purpose.
I have no information on what happens to 3-hydroxymorphinan itself. It may
be excreted directly by the kidneys, or it may undergo further metabolism.
==============================================================================
[6] NEUROPHARMACOLOGY OF DXM
------------------------------------------------------------------------------
[6.1] What is a receptor, anyway? (Basic Neuropharmacology)
A neuroreceptor (sometimes just called a receptor) is a location on the
surface of a nerve cell (neuron) or other type of cell (e.g., a muscle
cell) 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.
o-------------------------------------------------------o
| Closed Open |
| |
| /| |\ /| |\ |
| Receptor-> # | | | N.T. -> OO | | | |
| | | | | | | | | |
| ===========| >< |============| | | |=========== |
| ^ | | | | | | | | |
| | \| |/ \| |/ |
| Cell Wall |
| |
| Figure 7: Ion Channel before and after binding |
| with a neurotransmitter (N.T.) |
o-------------------------------------------------------o
The directly contributing neuroreceptors typically operate very quickly,
and act (and look) somewhat like an iris shutter in a camera. The neuro-
transmitter (for example, acetylcholine) binds to a specific area on the
channel, which (due to electrostatic forces) causes the channel to snap
open. Specific ions then leak into and out of the nerve cell, changing its
electrical potential. Different channels allow different ions to pass;
some ions (like potassium) excite the nerve cell, others (like sodium)
inhibit it. Once the neurotransmitter leaves the receptor, the channel
snaps shut, having done its work. These are the receptors involved in fast
signal transmission, and in conveying skeletal muscle impulses.
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. Generally, these slower domain
receptors operate by second messengers such as G-proteins.
Any given neurotransmitter will probably be associated with several
different receptors. For example, serotonin (5HT) activates at least
twelve receptor subtypes (5HT1A, 5HT1B, 5HT1D, 5HT1E, 5HT1F, 5HT2A, 5HT2C,
5HT3, 5HT4, 5HT5, 5HT6, and 5HT7)! There are several subtypes (instead of
just one) because each receptor subtype is involved in a different process
on a different type of neuron.
Drugs which mimic, block, or otherwise affect activity of a given
neurotransmitter will not affect all receptor subtypes equally. For
example, LSD operates at 5HT2A and 5HT2C receptors; buspirone operates at
5HT1A receptors. Consequently, they have very different effects; LSD is
psychedelic, whereas buspirone is an anti-anxiety drug.
Different substances may bind to the same receptor but affect it
differently. An agonist is a substance which binds to the receptor and
activates it. A partial agonist is an agonist which does not activate the
receptor fully. An antagonist binds to the receptor and prevents it from
operating.
One interesting property of partial agonists is that they tend to
"normalize" receptor activity levels. In the presence of a low amount of
neurotransmitter, the partial agonist will increase receptor function. In
the presence of a high amount of neurotransmitter, however, the partial
agonist will limit receptor activity; in fact, many antagonists may really
be partial agonists. It is still being debated as to whether LSD is a
5HT2C antagonist or a partial agonist.
Antagonists may bind to the same place where the neurotransmitter binds,
thus "competing" with the neurotransmitter - these are called competitive
antagonists. Or they may bind to a separate place on the receptor complex,
so that even if the neurotransmitter reaches its binding site, the receptor
won't activate. These are called noncompetitive antagonists. Note that in
either case, the binding of the drug is only temporary; if it were
permanent (thus effectively destroying the receptor) it would be
irreversible antagonism.
A rather whimsical analogy can be made between neurotransmitter functioning
and toilets. In this case, the toilet is the receptor, you are the
neurotransmitter, activating it by pushing the flush handle. If your
little brother comes up and flushes the toilet for you, he's is an agonist.
If he temporarily sticks the handle halfway down, he's a partial agonist.
If he holds the handle up so it won't flush, he's a competitive antagonist.
If he plugs up the toilet with toilet paper, he's a noncompetitive
antagonist. If he breaks the toilet handle off completely, he's an
irreversible antagonist.
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. A mostly complete list of
recreational drugs and their neuroreceptor activity is given in Appendix 2.
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.
Vasopressin, a nootropic ("Smart Drug") is also a peptide neurotransmitter.
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,
AMPA (formerly quisqualate), kainate, and metabotropic receptors (all of
which respond to glutamate and aspartate). The GABA receptor is the target
of benzodiazepines like diazepam (Valium?), 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
channel/receptor complex has seven (glutamate, glycine, magnesium ion, zinc
ion, PCP open channel site, polyamine site, and phosphorylation site).
Most have fewer than this; the NMDA channel is an extremely complicated
receptor.
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 usually transmit signals along nerve fibers, or to
cause the end of an axon to release its neurotransmitter. Sodium,
potassium, calcium, and chloride (Na+, K+, Ca2+, and Cl-) are the usual
ions in question. Tetrodotoxin, the active ingredient in "zombie powder",
is a sodium channel blocker. The NMDA receptor has some features of a
voltage dependent ion channel (see below).
------------------------------------------------------------------------------
[6.2] What are Sigma Receptors?
Sigma receptors (sigma is often written in Greek) are probably one of the
most elusive entities in neuropharmacology. Our knowledge of sigma
receptors pales in comparison to our ignorance; in fact, what we absolutely
know (or at least think we absolutely know) can be summed up very briefly
in the following paragraph:
Scattered throughout the brain and body there are places (sigma binding
sites) where a bunch of chemicals (sigma ligands) happen to stick. We
don't know if they're on the outside or inside of cells. We don't know if
sticking a chemical to them does anything or not, except in the vas
deferens. We don't really know what they do, if they do anything. We
don't know what they're for, why they're there, or whether the body uses
them. They may be neuroreceptors, steroid receptors, intracellular
messenger receptors, growth regulators, enzymes, or something else
entirely.
In other words, prepare to be confused. Don't worry, everyone else is as
well.
Sigma receptors were originally thought of as opioid receptors, since many
morphine derivatives bind there. However, this classification is probably
false, and the endogenous opioid peptides show little sigma activity. The
usual characteristics of opiates are mediated by the mu, kappa, and delta
receptors. There are at least two sigma receptors, and a third one
(sigma3, appropriately enough) has been discovered recently (115).
Some researchers have speculated that sigma receptors aren't really
receptors at all, but just enzyme binding sites (84). On the other hand,
sigma ligands affect the guinea pig vas deferens muscles, which probably
wouldn't happen unless sigma receptors really were receptors (98). Sigma
receptors may be intended for hormones or intracellular messengers rather
than neurotransmitters, as they are present on microsomes rather than on
the cell surface (130).
.............................................................................
Sigma 1 Receptors and General Sigma Information
Much of what is known about sigma receptors seems to apply more to sigma1
than sigma2 (though this is by no means universal). I grouped the
following information with sigma1 receptors, but don't take this as gospel.
I expect that a lot will turn out to be wrong. Fortunately, we may not
have to wait long; research in sigma receptors is proceeding rapidly.
Endogenous Ligands
The neurotransmitter for sigma1 receptors has not been found, although
there are speculations and evidence (82-86;99-100). The usual term for the
(unidentified) sigma1 neurotransmitter is "endopsychosin" (100), formerly
known as "angeldustin". Progesterone targets sigma1 receptors in the
placenta, and it and other steroid hormones may be natural ligands for
sigma1 receptors (98,103,104). If this is true, it is possible that some
of the effects of sex hormones on the brain may be mediated by the sigma1
receptor (98). Substance P (a peptide neurotransmitter) was considered but
rejected as an endogenous sigma1 ligand (112).
Location and Function in the Brain
Sigma receptors are densest in the cerebellar cortex, accumbens nucleus,
and cortex, and also present at lower density in the limbic areas and
extrapyramidal motor system. This is interesting because some of the
bizarre effects of DXM on motion may be related to sigma activity in the
cerebellar cortex and extrapyramidal motor system.
Sigma1 receptors (and possibly sigma2) appear to be functionally coupled to
some other receptors, notably nicotinic acetylcholine receptors (98,117)
and NMDA receptors (107-110). The nicotinic receptor coupling may be
direct, with sigma activation causing a change in the function of nicotinic
receptors. Whether modulation of nicotinic receptors would alter the
effects of nicotine on the brain, I don't know; some people have indicated
that tobacco induces strong responses during DXM use.
Sigma agonists (and/or possibly antagonists) seem to affect memory
function, reversing the impairment in memory caused by drugs such as
p-chloroamphetamine and MK-801 (a drug similar to ketamine) (131,132).
DTG, (+)-pentazocine, and SKF-10047 all improved memory impairment due to
MK-801. On the other hand, NE-100, which is considered a sigma antagonist,
seems to help with NMDA antagonist induced memory impairment as well
(107-108). DTG, a sigma agonist, reversed the memory impairment caused by
carbon monoxide (118).
Many drugs now considered sigma antagonists or agonists may in fact be
partial agonists. Another possibility is that the optimal level of sigma
activity may be a healthy medium; one study found a bell-curve dose
response on sigma agonists (118). This is similar to the effect of many
nootropics (smart drugs), specifically the cholinergics - taking too much
can be worse than taking none at all. This similarity may be further
evidence for the link between sigma receptors and acetylcholine receptors.
Both sigma1 agonists and antagonists may protect NMDA receptors from
glutamate toxicity (109). One study found that sigma antagonists protected
hippocampal cells from hypoxia and hypoglycemia (105), and this may be
related to NMDA receptors as well. Morphine has indirect effect on NMDA
receptors that seems to be mediated via sigma receptors, probably sigma1
(110). It is possible that all these effects are mediated via the
nicotinic receptor, i.e., sigma1 may not directly control NMDA functioning.
Behavioral Effects
The behavioral effects of sigma1 receptors have not been fully established.
However, sigma1 (and sigma2) receptors seem to have effects on motor
function, producing an increase in locomotion (113,114,121). Part of this
effect may occur at the cerebellum (113); the release of dopamine may also
be involved (114,129). This is probably the origin of DXM's curious
effects on motions and gait, including "sea legs" and the "Robo Shuffle".
Sigma1 activation may counteract some of the analgesic effects of opioids
(119). Pentazocine (Talwin), a synthetic opiate, is a potent sigma1
agonist which tends to be self-limiting; when too much is taken, the sigma
activity reverses the opiate activity. It is possible that the gradual
loss of euphoric effects experienced by morphine and heroin users may be
related to changes caused by sigma activity.
Sigma receptors seem to be involved in psychotomimetic (literally
"psychosis-like") effects from schizophrenia and drugs (46-49).
Amphetamine psychosis, a temporary condition resulting from heavy use of
psychostimulants, may be due to sigma1 activity (80,126). Sigma, and in
particular sigma1, receptors may be altered by schizophrenia. An
alternative possibility which is being studied is that some sort of
chemical - produced by the body itself, or by a virus or other foreign
agent - causes prolonged activation of sigma receptors, and this is one of
the causes for schizophrenia (47,49). Many neuroleptics, including some of
the atypical ones, are sigma antagonists (47).
In addition to DXM, other recreational drugs such as 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, and probably involved in seizures (or at least their
prevention).
Location and Function in the Body
Sigma1 receptors are also present throughout the body. Most tumor cells
express both sigma1 and sigma2 receptors (38,106). Liver and kidney cells
also contain sigma receptors (124), as do heart cells (125). As stated
above, the placenta contains sigma1 receptors. Sigma receptors are also
present in the immune system and endocrine glands, and may be responsible
for modulating these systems. There is some evidence that sigma agonists
may inhibit the immune system. The widespread presence of sigma receptors
may indicate some involvement in development, cellular regulation, or other
basic biological process.
..............................................................................
Sigma 2 Receptors
Much of what was stated about sigma1 receptors may apply to sigma2
receptors as well. There hasn't been much time to differentiate between
the two receptor types. The neurotransmitter for sigma2 receptors may be
zinc ions (78), and sigma2 receptors seem related to potassium ion channels
(79). The sigma2 receptor is less affected by DXM than the sigma1 receptor
(58). Some of the sigma-induced potentiation of NMDA function may be due
to sigma2 receptors (117).
One study found that chronic exposure to sigma ligands, both agonists and
antagonists, caused brain cells to degenerate and die (102). The
deterioration occurred as a gradual loss of cellular shape; cells
eventually became spherical (and died soon after). Interestingly, some
drugs, including DXM, seemed to be very weak in this effect. While
haloperidol induced significant changes and cell death in a few hours, it
took DXM 3 days to produce any changes at all, which reversed when the DXM
was removed. The potency of different sigma ligands seems to point towards
sigma2 receptors as the culprit in this effect.
By the way, I wouldn't worry too much about this. The concentration of DXM
required to induce any change at all was extremely high, and it took 3 days
of constant exposure. All changes were reversible, even after the cells
had assumed a spherical shape. Haloperidol and other sigma ligands, which
seem to be up to 100 times as potent as DXM at producing brain cell
degeneration, are used medically used without substantial evidence of brain
damage. Finally, steroid hormones may very well cause the same sort of
effects if present at sufficient levels (another reason not to use anabolic
steroids, I guess).
..............................................................................
Sigma 3 Receptors
Sigma3 receptors are a new discovery (115). They seem to be linked to the
conversion of tyrosine to dopamine, and sigma3 agonists may increase the
rate of dopamine synthesis. DXM's potency at the sigma3 receptor is
unknown, but if it binds strongly there, then increased dopamine synthesis
may be partially responsible for DXM's stimulant effects.
------------------------------------------------------------------------------
[6.3] What are NMDA Receptors?
NMDA and Other Glutamate Receptors
Most of the better known neurotransmitter systems - dopamine,
noradrenaline, serotonin (5HT), and acetylcholine in particular - have
modulatory roles. They are produced by a few neurons located in specific
clusters, and drugs affecting them often have specific effects
(recreational or medical, or both). Receptors for these neurotransmitters
tend to operate fairly slowly, taking milliseconds or longer to
communicate. Rather than directly changing the potential of the neuron,
they often trigger second-messenger responses.
On the other hand, most of the brain's regular function operates quickly,
and involves the excitatory and inhibitory amino acids (EAAs and IAAs,
respectively). The receptors for amino acids are generally ion channels;
when the receptor is activated, ions enter or exit the cell which change
its potential. EAA and IAA receptors generally correspond to the positive
and negative synaptic connections in electronic and computer neural
networks.
The excitatory amino acid neurotransmitters include glutamate and
aspartate. GABA is the only established inhibitory amino acid
neurotransmitter in the brain; the spinal column also uses glycine.
Generally, glutamate is more prominent (or at least better understood) than
aspartate, although they have similar effects at EAA receptors. Thus, the
receptors for EAAs are called glutamate receptors.
There are currently four identified type of glutamate receptors. Two of
them, the AMPA (formerly quisqualate) and kainate receptors, are ion
channel receptors which increase neuron activity in response to EAAs. A
third, the metabotropic glutamate receptor, is a newer discovery, and seems
to involve second messenger systems and produce metabolic effects. The
fourth is the NMDA receptor.
..............................................................................
NMDA Receptor Function and Structure
o-----------------------------------------------------------o
| Mg++ Zn++ |
| ____ __ Asterisks (*) |
| | \* _*| | indicate location |
| | |_ | | of binding sites |
| EAA --> * > => _> | | on the NMDA channel |
| | | _| _| |
| | | <_ <= \* <-- Gly |
| | | | | |
| OOOOOOOOOOO | | | | OOOOOOOOOOO |
| ||||||||||| | / | | ||||||||||| |
| ||||||||||| | <* | | ||||||||||| <-- Cell Wall |
| OOOOOOOOOOO | PCP\ | | OOOOOOOOOOO |
| | | | | |
| | | | | |
| | _ | | | <-- NMDA Channel Complex |
| \/*\/ *\___/ |
| |
| Polyamine Mg++ |
| |
| Figure 8: NMDA Channel |
o-----------------------------------------------------------o
This drawing represents the structure of the NMDA receptor, according to
current knowledge. The NMDA receptor has seven distinct binding sites.
Three of these are located on the exterior surface of the cell, two are
located on the cell interior, one on the inside of the channel, and one
(the magnesium ion site) is present both on the inside and outside
surfaces.
There are two agonist sites on the exterior are the cell, denoted EAA and
Gly; they correspond to the excitatory amino acids (glutamate and
aspartate) and glycine. Both sites must be occupied before the channel can
open enough for any ions to pass through. A third site is the target of
zinc ions (Zn2+), which block the channel when present.
The exterior of the channel contains a magnesium ion site. This site is
also present on the inside of the cell (alternatively, it may be located
within the channel itself). A magnesium ion normally occupies the exterior
site; the interior site is probably empty under biological conditions.
The interior of the cell contains two binding sites. One binds to
polyamines (spermine and spermidine), and its function is unknown. The
other, not shown in this diagram, is a phosphorylation site. Enzymes can
bind to this site and enhance or reduce the activity of the receptor.
o---------------------------------o o---------------------------------o
| /:\ | | /::\ |
| ____ : __ | | ____ :: __ |
| | Mg : __| | | | | | :: __| | |
| | | : | | | | | | ::| | |
| EAA | : | | | | EAA | ::| | |
| | | : | | | | | | ::| | |
| | | : | Gly | | | | ::| Gly |
| | | : | | | | | | ::| | |
| OOOOO | | : | | OOOOO | | OOOOO | | ::| | OOOOO |
| ||||| | / : | | ||||| | | ||||| | / ::| | ||||| |
| ||||| | < : | | ||||| | | ||||| | < ::| | ||||| |
| OOOOO | \ : | | OOOOO | | OOOOO | \ ::| | OOOOO |
| | | : | | | | | | ::| | |
| | | : | | | | | | ::| | |
| | _ | : | | | | | _ | ::| | |
| \/ \/ : \___/ | | \/ \/ :: \___/ |
| : | | :: |
| \:/ | | \::/ |
| Na+, K+ ions | | Na+, K+, Ca++ ions |
| | | |
| Figure 9: Partially Open | | Figure 10: Fully Open |
| NMDA Channel | | NMDA Channel |
o---------------------------------o o---------------------------------o
Finally, inside the channel itself is the PCP1 site, where PCP, ketamine,
MK-801 (dizocilpine), DXM, and dextrorphan all bind. The channel must be
fully open for these drugs to enter; once in place they "clog up" the
channel.
NMDA receptors are unique for several reasons. Unlike most receptors, they
require two agonists (glutamate or aspartate, plus glycine) before the
channel opens. These two agonists (Glu and Gly in the diagram) bind to two
different locations on the NMDA receptor. After both agonists have bound to
the channel, it opens enough for potassium to enter, and the receptor
operates much like AMPA and kainate receptors. This is shown in Figure 9.
The most important and unique characteristic of NMDA receptors, though, is
what happens next (Figure 10). Normally, a magnesium ion is bound to a
specific location at the opening of the channel; this ion allows potassium
to pass through but prevents calcium, possibly due to its size. This
binding is due to electrostatic forces; the same electrostatic attraction
that causes potassium ions to enter the cell makes the magnesium ion cling
to the channel.
Once the cell becomes activated enough, however, the cell potential rises
enough that the magnesium ion is no longer stuck to the cell. Calcium can
enter (and exit, although this doesn't happen) the cell through the fully
open NMDA channel. Once inside, calcium sets into motion a series of
responses which enhance the strength of the synapse.
So what's the point? Well, if the neuron is only slightly active, the NMDA
channel may open partially, but the magnesium ion won't get a chance to
leave its binding site. However, if the neuron should be rapidly or
substantially activated, the magnesium ion will be released, and calcium
can enter the cell, enhancing synaptic strength. This process, called
Long-Term Potentiation (LTP), is one of the mechanisms by which neurons can
change their functioning and "learn". LTP in the hippocampus is probably
responsible for short-term memory. Learning capacity may in fact be
directly related to the number of NMDA receptors in the hippocampus (where
short-term memory is thought to be stored) (88). LTP is reversible, and
long-term memory seems to be stored via more permanent changes in genetic
expression and synaptic shape.
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).
There is also some speculation that the NMDA receptor's ion channel may
(for reasons unknown) become "uncoupled" from the receptor itself (63).
Noncompetitive antagonism of NMDA receptors by the open channel blockers is
known to induce changes throughout the brain. NMDA blockade causes an
increase in dopamine release in the midbrain and prefrontal cortex (63).
NMDA blockade also causes activation of 5HT systems specifically targeting
the 5HT1A receptor (90).
..............................................................................
NMDA and Excitotoxicity
NMDA receptors are involved in excitotoxicity (nerve cell death via
over-stimulation). 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). DXM is not a particularly effective NMDA open
channel blocker, but DXO, PCP, ketamine, and MK-801 (dizocilpine) are all
very effective blockers.
Unfortunately, nothing in life is ever free. Lowered NMDA activity, called
NMDA Receptor Hypofunction (NRH), seems to be itself responsible for
excitotoxicity to other neurons. The theory is that normal NMDA activity
keeps other neurotransmitters (glutamate and acetylcholine, and possibly
dopamine) from being over-secreted. NRH releases this inhibition, and can
therefore lead to hyperactivity at some neurons. It is possible that
chronic NRH may be a cause for, or at least a factor in, schizophrenia and
Alzheimer's disease (101).
Acute, strong NRH of the type produced by the dissociative anesthetics has
not been studied. My hunch is that it probably isn't nearly as traumatic
to the brain as long-term NRH; otherwise, John Lilly would be a lot dumber
than he is. DXM in particular may be safer due to counteracting effects of
sigma activity. On the other hand, PCP has been shown to be toxic to
neurons in the posterior cingulate, retrosplenial cortex, and cerebellum
(136). This is probably a result of NRH, although sigma receptors may be
involved. Infants may be particularly susceptible to this effect, so use
of any NMDA antagonist during pregnancy or nursing is probably a bad idea
(113).
------------------------------------------------------------------------------
[6.4] 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).
Their use by the body (if they have one) has not been determined. Most
research indicates that the PCP2 receptor is the dopamine reuptake complex,
the very same one targeted by cocaine and the antidepressant bupropion
(Wellbutrin[tm]) (70,127).
A reuptake complex (or reuptake site), incidentally, is a structure on a
cell which takes used neurotransmitter back into the cell for recycling or
breakdown. By blocking reuptake of a neurotransmitter, its activity can be
increased. The tricyclic antidepressants block the reuptake of
noradrenaline, dopamine, and/or serotonin (5HT). Fluoxetine (Prozac[tm])
is a serotonin-specific reuptake inhibitor (SSRI), as are several other
newer antidepressants. The dopamine reuptake site seems to be the only
reuptake site targeted by recreational drugs (primarily cocaine).
Curiously, bupropion, a dopamine reuptake inhibitor, seems to have little
recreational use potential; then again, it isn't a particularly strong
dopamine reuptake inhibitor.
------------------------------------------------------------------------------
[6.5] What are Na+ and Ca2+ channels?
Sodium and calcium ion channels are two types of voltage dependent ion
channels. These channels open or close not due to neurotransmitters, but
instead due to voltage differences between the inside and outside of the
cell.
Voltage dependent sodium channels are typically involved in the action
potential - a domino-effect propagation of nerve impulses along the axon.
The sodium channel opens when the voltage reaches a certain activation
threshold; the resulting influx of sodium then further activates the neuron
(leading to more sodium channels opening). Eventually a second part of the
sodium channel closes (otherwise they would keep themselves open forever).
Incidentally, voltage dependent potassium channels are involved in bringing
the neuron back to its resting state.
Voltage dependent calcium channels are similar to voltage dependent sodium
channels, and typically open on activation voltages. Their effect,
however, is to cause calcium to enter the cell; the calcium then acts as a
messenger to intracellular mechanisms. The most common example is at the
end of the axon, where calcium influx causes neurotransmitters to be
released. NMDA receptors may be structurally related to voltage dependent
calcium channels.
DXM has recently been found to block sodium and calcium channels, 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.
------------------------------------------------------------------------------
[6.6] 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.
------------------------------------------------------------------------------
[6.7] Endopsychosin and the Big Picture
For whatever reason, some people involved in biological sciences like to
talk about the "big picture." I'm one of them. I think the reason why the
"big picture" seems so important is that science, especially biological
science, has become so specialized and compartmentalized that it's
difficult to keep one's perspective, especially when considering the
possible relevance of things.
Endopsychosin (en-doe-sy-KOE-sin) is the name given to an endogenous ligand
for the NMDA open channel site (PCP1) and/or sigma receptors. The search
for endopsychosins started several years ago in an attempt to find the
endogenous ligand for PCP; at the time, the term was "angeldustin".
Recently, the search for endopsychosins has resumed as NMDA and sigma
receptors have become increasingly understood. As I write this, nobody has
managed to positively identify an endopsychosin, although there are several
candidates. The most promising candidates for the NMDA PCP1 site seem to
be series of peptides (99-100). The endogenous ligand for the sigma1 site
may be an unknown aromatic chemical (98,100).
The original idea behind endopsychosin (or angeldustin, if you prefer) was
that the body was capable of secreting a substance which would mimic the
effects of PCP on the brain. It may be secreted in times of extreme
stress, leading to a sort of detached, dreamy feeling. Endopsychosin may
be responsible for such altered states of consciousness as religious
ecstasy, speaking in tongues, possession, astral projection, and other
paranormal experiences. Spontaneous releases of endopsychosin may account
for experiences such as alien abductions, encounters with ghosts, and that
sort of thing.
Note the similarity of these experiences with aspects of DXM, ketamine, and
PCP drug trips. In particular, the "emergence phenomenon" identified with
ketamine (and present also with PCP and DXM) often consists of experiences
with spiritual or alien beings.
What's going on here? Why the hell would the human brain secrete a
chemical that makes us think we've been talking to Elvis and Jim Morrison
on the far side of Mars? What's the big picture?
Well, to be honest, nobody knows. One potential clue is that the perforant
path of the hippocampus (a neural circuit) seems to release endopsychosin
when stimulated (141). Perhaps endopsychosin is a part of the memory
process; or perhaps it is involved in dreaming and the conversion of
short-term to long-term memories.
Another possibility is that endopsychosin is one of the brain's natural
defenses against injury. I find it interesting that sigma/NMDA agents
often mimic fever hallucinations; common characteristics include
Lilliputian hallucinations (feeling too big and/or too small), geometrical
and linear hallucinations, and psychosis-like effects. Perhaps the brain
secretes endopsychosins during high fever in an attempt to prevent
neurotoxicity.
In addition to potential neuroprotective roles, these substances may have
significant roles in regulating cognition and (in the body) the immune and
endocrine systems. A dysfunction of an endopsychosin, or of the sigma
receptors (or both) may be one of the causes of schizophrenia. And if some
steroids (e.g., progesterone and testosterone) turn out to be
endopsychosins, this could explain a lot about the long-term behavioral
effects of steroid use.
Or, it may simply be that altered states of consciousness are a natural
part of animal life, and that our culture's fear of such states is
abnormal. Certainly one doesn't need drugs to achieve altered states; even
profoundly dissociative states can be achieved with a certain amount of
ritual and faith. Most "primitive" cultures have some experience with
dissociative states such as astral projection, shamanic journeying,
possession, and that sort of thing. They may very well know something that
we don't.
So it is entirely possible that the similarity between NMDA PCP1 and sigma
receptors has a purpose. In any case, data about the effects of
sigma-specific agonists (or antagonists for that matter) are limited, but
our understanding of these receptors should improve in the next few years
as research continues. Not to mention the possibility of some brave and/or
stupid psychonaut deciding to experiment with sigma-specific agonists.
(+)-3-PPP and SKF-10,047 are good sigma-specific ligands; more sigma1
specific ligands include 1-phenylcycloalkanecarboxylic acid derivatives
(123,128). Anyone feeling brave? Maybe you can become the next Shulgin
("Endopsychosins I Have Known And Loved" anyone?). Then again, maybe you'd
better not; I don't need to be sued if you develop a stubborn case of
insanity.
==============================================================================
[7] DXM CHEMISTRY AND EXTRACTION
This section has been completely rewritten, as new information has been
received about acid-base extraction and about extraction of DXM+guai-
fenesin preparations. 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.
-----------------------------------------------------------------------------
[7.1] How can I extract DXM from cough formulae?
I'm going to present this as "kitchen chemistry" as I feel most people
with adequate chemistry knowledge (and equipment) will be able to do it
correctly anyway. The older procedure for extracting DXM was to basify
it with NaOH (sodium hydroxide), and filter out the precipitated DXM using
a coffee filter. This tended to fail for several reasons. First, the DXM
precipitate was often so fine that it went through the filter paper.
Second, many syrups contain propylene glycol, and DXM free base seems to
be moderately soluble in propylene glycol. You can, of course, still use
the precipitation procedure; I just don't recommend it. If you do choose
to precipitate DXM, try to get actual filter paper rather than a coffee
filter -- it will help.
.............................................................................
Acid-Base Extractions
The acid-base extraction process is a common method for isolating a
desired chemical from undesirable "gunk". The theory is that certain
chemicals (generally, alkaloids) occur in two forms: a water-soluble
complex with an acid, and an oil-soluble free base form. For example,
pseudoephedrine (Sudafed[tm]), a decongestant, is usually supplied as the
hydrochloride salt (pseudoephedrine HCl). It can also exist as a base,
without an acid molecule (thus the term "free base"). You can convert an
alkaloid from acid salt to free base (or vice versa) using a base (or acid).
The practical upshot is you take your chemical and "gunk", and lower the pH
until the chemical converts to free base form and precipitates out (since
it's no longer soluble in water). Now you add a nonpolar solvent (an
"oily" layer) for the chemical to dissolve in, shake for a long time, and
all the chemical you want is in the nonpolar layer. Discard the polar
(i.e., water) layer, and you're left with a nonpolar layer full of your
chemical .....
Plus anything else that might be oil-soluble. So you reverse the process,
by adding an acid until the free base turns into an acid salt, and
precipitates out of the nonpolar layer. Add water, shake, and you can
discard your nonpolar layer. This is the acid-base extraction, and it's
very frequently used to extract the active ingredients from plants (free
clue: the THC in marijuana is not an alkaloid and thus won't extract this
way).
.............................................................................
Acid-Base Extraction of DXM
So how do we apply this to DXM? Well, it turns out that DXM is an
alkaloid, and you can extract DXM from cough syrups using the same
process. Furthermore, this procedure even works for DXM plus guaifenesin
syrups, e.g., Robitussin DM[tm], and generic equivalents (invariably called
Tussin DM). The "DM" syrups usually only contain 10mg/ml of DXM, so you
won't get as much yield, but they're usually cheaper (and more commonly
available).
Do NOT try this extraction procedure with cough syrups or formulations
containing acetaminophen/paracetamol, pseudoephedrine, other
decongestants, or antihistamines. (I'm working on it)
For this procedure you will need:
o Cough syrup (obviously) or some other DXM-containing preparation.
The only active ingredients that should be listed are dextrometh-
orphan and guaifenesin. Avoid alcohol (check the inactive
ingredients). If you can get DXM-only preparations, do so; the DXM+
guaifenesin preparations tend to contain less DXM than the DXM-only
ones.
o A mason (canning) jar with a complete lid, big enough to contain
twice the volume of cough syrup/formula you have.
o A glass container to make your sodium hydroxide solution in (a mason
jar works; you can also use a drinking glass).
o Two plastic freezer bags with lock closures (e.g., Ziploc[tm] freezer
bags) -- the larger the better.
o A nonpolar solvent. The easiest to get is Zippo[tm] lighter fluid (or
an equivalent) -- note that this is cigarette lighter fluid, not
charcoal lighter fluid. You want your solvent to evaporate quickly,
leaving no residue. The easiest way to test it is by placing a drop
or two onto a pocket mirror, and letting it evaporate; if it leaves no
residue or smell, you can use it.
o Sodium hydroxide (NaOH). Photography supply stores carry this. In a
pinch, some people have been known to use Red Devil[tm] Lye. I do not
advise this! Lye is likely to be impure. If you must use lye, make
sure you let your sodium hydroxide solution settle (see below). Note
that sodium hydroxide is caustic and severely damaging to the eyes,
so wear your safety goggles!
o A heat-resistant glass baking dish (smaller is better).
o Distilled water (tap water won?t work very well due to the chlorine
ions)
o A pair of scissors
o Access to the outdoors.
To speed up the process (from overnight to about 30 minutes), you will
have to evaporate the solvent with heating. For this you will require:
o An electric wok or skillet, or a hot plate with a pot of water on it.
Basically, you want a flameless (electric) source of heat that will
heat up a volume of water, which you can put your baking dish in (the
hot water will heat the baking dish).
o A hair dryer
o An OSHA-certified organic vapor mask.
A brief word about organic vapors. The solvents you will in all likeli-
hood be dealing with (hexane, heptane, petroleum ether, whatever) are bad
for you. Really bad for you. You do NOT want to breathe the fumes. Get
it? So, if you want to speed up the process, pony up US$30.00 or so for
an OSHA organic vapor gas mask (tell `em you'll be painting with oil-
based paint). Sure, it's uncomfortable and looks dorky. But it sure
beats brain damage! Additionally, you must do the evaporation outdoors
(unless you happen to have a fume cabinet handy. And NO, the stove
or bathroom fan does NOT count as a fume cabinet).
Okay, here we go:
1. Form a solution of sodium hydroxide (NaOH) by placing one tablespoon
(15ml) of solid sodium hydroxide in one cup (about 236ml) of
distilled water in the sodium hydroxide solution container. Stir until
dissolved. If you are using lye (I don't recommend it), wait awhile to
let any impurities settle out to the bottom. Note that dissolving the
NaOH will generate some heat.
2. Empty your cough syrup or formula into the mason jar, rinsing the
bottle out with distilled water. If using gelcaps, break them open and
rinse out the inside of the capsules.
3. Add one tablespoon (15ml) of sodium hydroxide solution to the mason
jar. You should see a rapid formation of a milky precipitate. Swirl
the mason jar gently to mix the syrup evenly, and the precipitate
should redissolve (because there's not enough base yet).
4. Repeat step 3, until the precipitate doesn't redissolve with swirling.
The entire solution should be cloudy (stir well to make sure the base
is evenly distributed).
5. Add one more tablespoon (15ml) of sodium hydroxide solution to the
mason jar.
6. Add a small volume of nonpolar solvent (e.g., Zippo[tm] lighter fluid)
to the mason jar. How much? Well, as a suggestion, start with 1/4
cup (60ml); you want a layer roughly 3/8" (1cm) thick in the jar. It
will float on top of the water layer. (You may have to pry open the
pour spout to get a good flow rate on the lighter fluid container).
7. Cut one of the plastic bags along the seam so that you end up with a
quare of plastic. Place that over the mason jar, and then place the
lid on top of that. Close the lid tightly. The plastic protects the
rubber seal, which would otherwise dissolve in the lighter fluid.
8. Shake the mason jar for about 5 minutes, or until you feel like your
arms are going to fall off.
9. Place the mason jar on a flat surface and wait for the layers to
separate (this may take awhile). If they don't seem to separate
easily, try salting it (really).
10. Carefully pour the contents of the mason jar into the intact sealable
plastic bag, and close it shut ("yellow and blue make green--it's
sealed!"). Hold the bag up so that one of the bottom corners (not a
corner with the seal) points down.
11. Let the two layers separate again (this should only take a few seconds).
12. Cut off the tip of the bottom corner and allow the water layer (the
bottom layer) to drain out of the bag. When the water layer has
drained out, pinch the bag shut.
13. Hold the bag over the baking dish, and allow the nonpolar solvent
layer to drain out into the baking dish.
14. Take the baking dish outdoors. At this point, if you don't have a gas
mask and a way to heat the baking dish, you?ll have to let the
solvent evaporate (which may take a day or so), so go on to step 19.
15. Put on your gas mask
16. Place the baking dish into the container of water (electric wok,
electric skillet, hot plate with pan of water, whatever), and set it
to simmer. If you can't set the temperature low enough, you'll have to
turn the heater on and off manually to maintain a near-boiling
temperature.
17. Plug in the hair dryer and gently blow hot air into the baking dish.
Take care not to splash solvent over the sides of the dish.
Incidentally, make sure you don't overload your circuit; it might be a
good idea to alternate heating with the hot plate/wok/skillet and
heating with the hair dryer.
18. Continue heating until all the solvent evaporates. At this point you
may see a thin layer of crystalline material; you might see a shiny
layer of goo that looks a lot like the glass itself (which can be
confusing); or you might see a layer of brown gunk. Whatever. Anyway,
make sure all the solvent has evaporated.
19. If your baking dish is covered with an oily substance (goo, gunk,
whatever), you in all likelihood managed to extract some propylene
glycol (or something else) along with the DXM. Blow hot air from the
hair dryer onto the surface of the dish until the material dries
completely (this may take 5 to 10 minutes). This should evaporate the
propylene glycol, leaving behind only DXM.
20. Scrape the DXM off the baking dish with a razor blade or other
convenient sharp edge. You now have DXM free base.
A few comments. First, guaifenesin seems to itself convert to an oily
free base layer if you add too much sodium hydroxide, so don?t overdo it.
Second, if you happen to have lab equipment you can of course use a
separatory funnel (which is what the plastic baggie is for). Third, if
you don?t think you got anything, make sure the baking dish is completely
dry; sometimes the DXM free base plus propylene glycol can look a lot like
the glass itself.
Precipitation Method
If you want to use the precipitation method, all you have to do is add
sodium hydroxide to the cough formula as described above, until the DXM
precipitates out. Let it stand (or centrifuge it), and filter. The (very
fine) powder that hopefully was caught by the filter paper is the DXM free
base. I don't know if the precipitation method works with DXM +
guaifenesin preparations.
-----------------------------------------------------------------------------
[7.2] How can I get rid of other drug ingredients?
First I'd like to emphasize that this is still preliminary. Testing is not
complete, and in particular if the method fails to remove all the
acetaminophen you could be in a lot of trouble. So consider this as a
starting point for further research only.
The basic principle here is differential solubility - different ingredients
are soluble in different solvents. The relevant solvents here (with
solubility listed if I could find it) are:
o---------------------------------------------------------------o
| Substance | Cold H2O | Hot H2O | Ethanol | Ether |
|===============+===========+===========+===========+===========|
| DXM HBr | Soluble | Soluble | Soluble | Insoluble |
| | (<1.5%) | (25%) | (25%) | |
|---------------+-----------+-----------+-----------+-----------|
| DXM Freebase | Insoluble | Insoluble | Soluble | Insol.? |
| | | | | |
|---------------+-----------+-----------+-----------+-----------|
| Guaifenesin | Slightly | Soluble | Soluble | Soluble |
| | (1g/20ml) | | | |
|---------------+-----------+-----------+-----------+-----------|
| Pseudoephed- | Soluble | Soluble | Soluble | Soluble? |
| rine HCl | | | | |
|---------------+-----------+-----------+-----------+-----------|
| Pseudoephed- | Slightly | Slightly | Soluble | Soluble |
| rine Freebase | | | | |
|---------------+-----------+-----------+-----------+-----------|
| Acetaminophen | Insoluble | Soluble | Soluble | Slightly |
| (Paracetamol) | | | | |
|---------------+-----------+-----------+-----------+-----------|
| Propylene | Miscible | Miscible | ? | Soluble |
| Glycol | | | | |
|---------------+-----------+-----------+-----------+-----------|
| Polyethylene | Soluble | Soluble | Soluble? | ? |
| Glycol | | | | |
o---------------------------------------------------------------o
Table 3: Differential Solubility Data
This information is from the Merck Index; I'm trying to fill in the
unknowns from other sources. In particular, I'm fairly certain that DXM
free base is insoluble in ether, and that d-pseudoephedrine HCl is soluble
in ether. Three steps should take care of pretty much everything:
extraction with ether (to remove propylene glycol, guaifenesin, and
possibly d-pseudoephedrine HCl), precipitation of acetaminophen by cooling,
and precipitation of DXM by NaOH. It is possible that the removal of
acetaminophen in a separate step can be avoided if NaOH doesn't cause
precipitation of acetaminophen (I'm working on it).
As propylene glycol and guaifenesin are soluble in water as well as ether,
the extraction with ether should probably be repeated. In particular,
chilling the water would probably help by reducing the solubility of the
guaifenesin.
The removal of acetaminophen is fairly straightforward; just cool the water
and remove any precipitate. You want to make sure all the alcohol has been
removed before this step, though. Unfortunately DXM itself becomes less
soluble in cold water, so you might lose a little bit.
The final step (precipitation of free base) is the same as usual; the only
caveat is that if the original preparation contained d-pseudoephedrine,
some of it might have made it this far and precipitate as well. Again, I'm
working on it.
I'll include procedural steps when I finish research and testing. Please
remember that this is an untried procedure and may not be safe! I
encourage anyone with comments to let me know what you think.
-----------------------------------------------------------------------------
[7.3] How do I use free base DXM?
The DXM you extracted is in free base form, so it is theoretically possible
to smoke it using a vaporization pipe. I have received two reports on this
subject; the results were somewhat disappointing. Evidently, the DXM was
very rough on the throat, and smelled like burning plastic. It looks like
DXM may not be smokable. On the other hand, it may well have been
overheated. It is important to make sure that the DXM is heated just to
sublimation, and that it is very pure before this is attempted. I still
make no claims as to the safety of this procedure. Again, if you have
smoked free base DXM, please contact me for inclusion in the next FAQ.
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 (or orange juice, for
that matter) and drink the resulting liquid (which, from what I hear, is
pretty yucky in the case of HCl - evidently orange juice wins here).
Please note that using excess HCl may convert the DXM to dextrorphan. You
can also dissolve the free base DXM in alcohol (e.g., EverClear[tm] or
vodka) and shoot it (nasty tasting, but it works).
Or, you can use the free base DXM for further syntheses - see Section 7.6.
-----------------------------------------------------------------------------
[7.4] How can I synthesize DXM?
Still nothing yet. The patent hasn't come in, and the only articles I have
are in German. If anyone out there speaks German and can translate a bunch
of chemistry articles for me, I'll be happy to include this in version 3.1.
-----------------------------------------------------------------------------
[7.5] What can I synthesize from DXM?
All chemical processes in this section require pure DXM. If you do not
have pure DXM, you must extract from cough formulae as above (and purify it
really well). Most of these processes require significant skill, and access
to lab equipment and chemicals. To my knowledge none of this is illegal
(but don't take my word on it). Don't fret if your yields aren't as good
as specified. Most of the procedures are from the same source (97).
Dextrorphan
This is probably the easiest by far. In fact, it's often accidental in
the isolation of pure DXM. Any excess of acid (HCl or HBr) should
produce dextrorphan. The primary reference for this section (97) used
48% HBr. It is possible that this occurs accidentally in some
extraction procedures where HCl is used to convert DXM free base to
water-soluble form. This may account for people indicating that
extracted DXM is stronger than DXM in cough formulae.
Levorphanol / Levomethorphan
These compounds would most likely have opiate activity. Unfortunately,
as someone (wish I remembered who!) once put it, the isomer fairy isn't
going to descend from heaven and wave her magic wand. You'd basically
have to get the cross bridge to flip around (if you could do this, the
hydrogens would probably conform as desired). Good luck! Personally,
I don't think it can be done, at least not easily. By the time you got
the lab and chemicals to do it, it'd probably be easier just to make
methylfentanyl from scratch.
If you do figure out a way to do it, please don't tell anyone; nothing
would bring the DEA into this faster than someone making an opiate out
of DXM. You don't need to tell me either, since I don't consider
opiates to be much fun. Oh, and if the isomer fairy does show up, you
might as well ask her to make you some methamphetamine from Vicks Nasal
Inhalers[tm].
3-substituted Analogs
Several 3-substituted DXM analogs have been synthesized. A few of
these actually show interesting binding and anticonvulsant activity.
Table 4, on the following page, lists the analogs, their binding, and
their anticonvulsant activity in rats. All data on 3-substituted
analogs comes from (97). Incidentally, this article is marked as "not
subject to US Copyright"; therefore I've quoted large sections from it.
Curiously enough, the research was sponsored by NIDA (the National
Institute on Drug Abuse). ED50 Rats refers to the effective dose for
anticonvulsant activity; % Rats refers to the percentage of rats
protected. Sample size was 10 rats.
Some comments on the table. Both dextromethorphan and the N(CH3)2
derivative lost anticonvulsant activity at higher doses. The NH2, OEt,
and O2-Pr derivatives all showed no indication of psychotomimetic
activity at anticonvulsant doses. Most showed little ability to
displace [3H]TCP. Generally speaking, I think it's safe to say that
the [3H]TCP binding site is the NMDA open channel PCP1 site, and that
the [3H]DXM binding is occurring to DXM's high affinity sites (sigma1
and PCP2). The authors do not address the PCP2 site.
My guess is that the discrepancies between [3H]DXM binding affinity
and anticonvulsant activity relate to different binding at sigma1 and
PCP2, and that the anticonvulsant activity comes from the sigma1
activity. As far as any recreational use of these derivatives goes,
I have no idea. Potentially, the NH2 derivative might show effects
limited to sigma1 activity, and the OEt and O2-Pr derivatives might
show sigma1 and PCP2 activity. It doubt any of the above are specific
for PCP2; the closest would be the H "derivative". This is all
scientific wild-assed guessing; there's not much data on PCP2 (or the
sigma receptors for that matter).
o--------------------------------------------------------------------o
| 3-Position | IC50 [3H]DXM | IC50 [3H]TCP | ED50 Rats | % Rats |
| Substitution | | | | Rats |
|===============+===============+===============+===========+========|
| OCH3 (DXM) | 0.59uM +-0.12 | 2.0uM +-0.6 | 38 mg/kg | 70 |
|---------------+---------------+---------------+-----------+--------|
| OH (DXO) | 7.7uM +-0.9 | 1.2uM +-0.7 | 5 mg/kg | 90 |
|---------------+---------------+---------------+-----------+--------|
| NH2 | 45% at 10uM | 7.8uM +-1.4 | 25 mg/kg | 100 |
|---------------+---------------+---------------+-----------+--------|
| NHCH3 | 3.6uM +-1.4 | 43% at 10uM | | 0 |
|---------------+---------------+---------------+-----------+--------|
| N(CH3)2 | 4.4uM +-0.9 | 45% at 10uM | 40 mg/kg | 40 |
|---------------+---------------+---------------+-----------+--------|
| Cl | 1.1uM +-0.4 | 5.5uM +-1.5 | | 10 |
|---------------+---------------+---------------+-----------+--------|
| NCS | 1.5uM +-0.3 | 60% at 10uM | | 0 |
|---------------+---------------+---------------+-----------+--------|
| H (i.e. none) | 1.3uM +-0.3 | 53% at 10uM | | 0 |
|---------------+---------------+---------------+-----------+--------|
| O-Et (ethyl) | 0.42uM +-0.06 | 75% at 10uM | 5.6 mg/kg | 90 |
|---------------+---------------+---------------+-----------+--------|
| O-2-Pr | 0.88uM +-0.18 | 59% at 10uM | 3.9 mg/kg | 90 |
|---------------+---------------+---------------+-----------+--------|
| 0-n-Bu | 1.5uM +-0.4 | 58% at 10uM | | 40 |
|---------------+---------------+---------------+-----------+--------|
| 0-Bz (benzyl) | 3.1uM +-0.6 | 39% at 10uM | | 30 |
o--------------------------------------------------------------------o
Table 4: 3-Substituted DXM Analogs
So if you want to go about synthesizing any of these, I don't believe
it would be illegal (I could be wrong). I wouldn't advise taking any
of them, of course; in particular, there's been no LD50 determination.
The authors doubt that the NCS derivative even gets to the brain. If
it did get to the brain, it would likely bind irreversibly. You don't
want that (imagine tripping for three months).
I haven't had time to check these extensively for typos, so you might
want to check out the original article. Note that the authors made
some typos of their own (nothing in the chemistry though). If you're
reading this as a hypertext document, I put in plenty of cross-
reference links; if you get confused about a referred intermediate, you
can jump to it.
(+)-3-[(2-Phenyl-4-quinazolinyl)oxy]-17-methylmorphinan (intermediate)
Dextrorphan was obtained in quantitative yield by a general method of
O-demethylation of dextromethorphan HBr [obtained from Sigma/Aldrich]
with 48% HBr, and was found to be identical by TLC, mp, and 1H NMR to
an authentic sample. By using a modification of the procedure by
Conrow and Bernstein [Steroids 1968, 11, 151-164], [dextrorphan]
(16.10g, 62.3 mmol) was dissolved in hot acetone (500mL); Am-ex-OL
(15.51g, 64.4mmol, Aldrich Chemical Co.) and K2CO3 (17.13g, 123.9mmol)
were added. The reaction mixture was allowed to stir at reflux, under
an atmosphere of argon, overnight. After cooling, the reaction mixture
was extracted from H2O (500mL) with benzene (1x500 and 2x250mL) and
removing the solvent in vacuo, to give 27.51g (96%) of [this
intermediate] as a white glass which was homogeneous by TLC.
Recrystallization in EtOAc gave pure [this intermediate] as white
crystals: mp 138-139 C; EIMS m/z 461; [alpha]D +59.5 (c 1.03, acetone).
Anal. (C31H31N3O) C,H,N.
(+)-3-[4-Oxo-2-phenyl-3(4H)-quinazolinyl]-17-methylmorphinan (intermediate)
[The above intermediate] (10.0g, 21.7mmol) was placed in mineral oil
(100mL, light white oil, Sigma Chemical Co.) under a stream of argon,
and the vigorously stirring reaction mixture was carefully heated in a
sand bath to 330-350 C. Complete conversion of [the above
intermediate] to one major product spot occurred in 8-10 h. (Note:
This reaction proceeds significantly slower at lower temperatures and
will rapidly decompose at temperatures that exceed 360 C). The yellow
reaction mixture was allowed to cool to room temperature and suction
filtered through a pad of silica gel. The mixture was eluted with
700mL of ether (to remove all mineral oil). Then, the receiving flask
was changed, and the product was eluted with CHCl3/MeOH/NH4OH (800mL,
90:10:1) to give 5.95g of (60%) yellow foamy product that was
homogeneous by TLC. This intermediate was not crystalline. It was
characterized spectrally and taken to the next step without further
purification: IR 1690 (C=O) cm-1; EIMS m/z 461.
(+)-3-Amino-17-methylmorphinan Dihydrochloride (NH3 derivative)
Sodium hydroxide (4N, 30mL) was added to a solution of [the above,
second intermediate] (4.89g, 10.7mmol) in absolute EtOH (100mL), and
the reaction mixture was allowed to stir at reflux, under an
atmosphere of argon. After 18h, TLC showed a complete loss of [the
second intermediate]. The reaction mixture was cooled in an ice bath
and carefully acidified to pH 2 with concentrated HCl. Additional 1N
HCl (100mL) was added and the reaction mixture was allowed to stir at
reflux, under an atmosphere of argon for 1.5h. After cooling in an
ice bath, the aqueous reaction mixture was extracted with ether (1x200
and 2x100mL). The ether fraction was washed with 1N HCl (1x200mL) and
the combined aqueous fraction was neutralized to pH 9 with NH4OH.
Extraction with CHCl3 (1x200mL and 1x100mL) followed by CHCl3/MeOH
(4:1, 1x100mL) and removal of solvent in vacuo resulted in 2.53g (93%)
crude [NH3 derivative] as a white foamy free base. The free base was
dissolved in a minimal volume of hot MeOH and acidified with a
saturated solution of HCl in 2-PrOH. Addition of ether resulted in an
oily product, but removal of solvent followed by recrystallization in
MeOH/ether resulted in 1.0g (34%) of [NH3 derivative] as white
crystals, 280 C dec. The mother liquor was neutralized and purified
by flash column chromatography (CHCl3/MeOH/NH4OH, 95:5:1) to give
0.84g (31%) pure base as a white foam: IR (free base, CHCl3) 3400 cm-1
(two sharp bands, NH2); 1H NMR (CDCl3) delta 6.90 (d, J=8.4Hz, 1H),
6.60 (d, J=2.4Hz, 1H), 6.50 (dd, J=8.4,2.4Hz,
1H), 3.55 (brs, 2H), 2.60 (s, 3H); CIMS m/z 257 (M+1); [alpha]D +21.7 (c
0.53; MeOH). Anal. (C17H24N2*2HCl) C,H,N.
(+)-3-(Methylamino)-17-methylmorphinan Dioxalate (NHCH3 derivative)
Formaldehyde (37%, 0.30 mL) and succinimide (0.45g, 4.5mmol) were added
to a solution of [NH3 derivative] (0.76g, 3mmol, free base) in absolute
EtOH (8mL). The reaction mixture was allowed to stir at reflux, under
an atmosphere of argon, for 2h. The volatiles were evaporated, the
residue was redissolved in DMSO (3mL), and NaBH4 (0.18g, 4.7mmol) was
added, at room temperature. The reaction mixture was warmed to 100 C,
allowed to stir for 15 min, and cooled. Quenching with H2O (25mL) and
extraction with CH2Cl2 (3x25mL) was followed by washing the combined
organics with H2O (3x20mL), drying (Na2SO4), and evaporating to give
0.50g (63%) of an off white foam that was nearly homogeneous by TLC.
The foamy free base was dissolved in a minimal volume of hot MeOH, and
oxalic acid (0.33g, 3.7mmol, 2 equiv) was added (pH 4). The
crystalline product was isolated and recrystallized in MeOH to give
0.51g (61%) of [NHCH3 derivative]: mp 187-193 C; IR (salt, KBr) 2400
cm-1 (broad NH+); 1H NMR (CDCl3) delta 6.92 (d, J=8.4Hz, 1H), 6.50
(d, J=1Hz, 2.4H), 6.43 (dd, J=8.4,2.4Hz, 1H), 6.50 (d, J=1Hz, 2.4H),
6.43 (dd, J=8.4,2.4Hz, 1H), 2.78 (s, 3H), 2.35 (s, 3H); EIMS m/z 270;
[alpha]D +22.0 (c 1.08, MeOH). Anal. (C18H26N2*C4H4O8*1/4H2O) C,H,N.
(+)-3-(Dimethylamino)-17-methylmorphinan Sesquitartrate (N(CH3)2 derivate)
Formaldehyde (37%, 2.4mL) and NaBH3CN (0.60g, 13mmol) were added at
0 C to a solution of [NH3 derivative] (0.52g, 2mmol, free base) in
MeCN (10mL). The reaction mixture (pH 12) was allowed to stir at 0 C
for 5 min and then allowed to warm to room temperature. After a
reaction time of 30 min, glacial HOAc (0.3mL) was added and the
reaction mixture (pH 6) was allowed to stir at room temperature for
another 45 min. The volatiles were removed in vacuo, and the residue
was extracted with 2N KOH (1x20mL) and ether (4x10mL). The combined
organic fraction was washed with H2O (1x10mL), dried (Na2SO4), and
evaporated to 0.53g of a pale yellow oil (93%) which was nearly
homogeneous by TLC. The crude free base was dissolved in hot 2-PrOH
and added to a solution of D-(l)-tartaric acid (0.57g, 4mmol) in hot
2-PrOH. The crystalline [N(CH3)2 derivative] was carefully isolated
under an atmosphere of argon (hygroscopic): mp 96-99 C; 1H NMR (CDCl3)
delta 3.15 (s, 6H); EIMS m/z 284; [alpha]D +5.73 (c 0.96, MeOH). Anal.
(C19H28N2*C6H9O9*1/4 H2O) C,H,N.
(+)-3-Chloro-17-methylmorphinan Fumarate (Cl derivative)
Acetonitrile (16.0mL), tert-butyl nitrite (0.8mL, 90%, 5.4mmol), and
dried CuCl2 (0.68g, 5.0mmol) were combined and warmed to 60 C, in an
argon-purged round-bottom flask. A solution of [NH3 derivative] (1.0g,
4mmol, free base) in MeCN (8.0mL) was added dropwise, via addition
funnel, over 10 min, and the reaction mixture was allowed to stir at
this temperature for 2h. The reaction mixture was cooled and poured
into a separatory funnel into which 10% Na2CO3 (50mL, w/v) was added.
The aqueous layer was removed and the organic layer was saved. The
aqueous layer was then washed with EtOAc (3x30mL), and the combined
organic fraction was washed with H2O (1x25mL), dried (Na2SO4), and
evaporated to 0.98g (89%) of crude [Cl derivative] as a dark oil.
Purification by gradient flash column chromatography
(CHCl3/MeOH/NH4OH, 95:5:1/90:10:1) yielded 0.59g (55%) of pure [Cl
derivative] as the free base. The free base (0.48g, 1.7mmol) was
dissolved in a minimal volume of 2-PrOH and was added to a solution of
0.21g fumaric acid (1.8mmol) in 2-PrOH. Addition of anhydrous ether
resulted in crystalline [Cl derivative]. Recrystallization in 2-PrOH
gave 0.41g (56%) of pure [Cl derivative], mp 136-141C. (Note: if
crystallization was difficult and the crude salt was dark, boiling
in 2-PrOH with charcoal followed by filtration over Celite facilitated
isolation of pure product.) IR (KBr, salt) 650 cm-1 (C-Cl); 1H NMR
(CDCL3) delta 7.25 (d, J=1.9Hz, 1H), 7.14 (dd, J=6.3,1.9Hz, 1H),
7.08 (d, J=6.3Hz, 1H), 2.62 (s, 3H); EIMS m/z 275,277 (M+2);
[alpha]D +19.6 (c 0.53, MeOH). Anal. (C17H22NCl*C4H4O4*2H2O) C,H,N.
(+)-Isothiocyanato-17-methylmorphinan Hydrochloride (NCS derivative)
A solution of [NH3 derivative] (0.52g, 2.0mmol, free base) in
pentene-stabilized CHCl3 (45mL) was added to a solution of NaHCO3
(0.64g, 2.8mmol) in H2O (20mL) at 0 C. The biphasic reaction mixture
was allowed to stir under an atmosphere of argon, at 0 C for 10 min.
Freshly distilled thiophosgene (200 microL, 2.2mmol) was added and the
reaction mixture was allowed to stir at 0 C for 10 min and room
temperature for 30 min. The organic layer was removed, and the
aqueous layer was extracted with CHCl3 (2x20mL). The combined organic
fraction was washed with H2O (1x20mL), dried (Na2SO4), and evaporated
to 0.60g (98%) to an orange foam. The crude free base was dissolved
in a minimal volume of 2-PrOH and acidified with a saturated solution
of HCl in 2-PrOH (pH 4). Careful addition of anhydrous ether resulted
in 0.59g (88%) of crystalline [NCS derivative], mp 260 C dec; IR
(CHCl3) 2160 cm-1 (br, NCS); CIMS m/z 299 (M+1); HRMS (M+) calcd
for C18H22N2S 298.1504, found 298.1476; [alpha]D +19.1 (c 0.68, MeOH).
Anal. (C18H22N2S*HCl*3/4 H2O) C,H,N.
(+)-(1-Phenyl-1H-5-tetrazolyl)-17-methylmorphinan (intermediate)
A modification of the procedure described by Reden et al. [J. Med.
Chem 1979, 22, 256-259] was used beginning with the addition of
5-chloro-1-phenyl-1H-tetrazole (1.08g, 6.0mmol) and anhydrous K2CO3
(1.35g, 9.8mmol) to a solution of [DXM - note, not dextrorphan] (1.29g,
5.0mmol) in dry DMF (25mL). The reaction mixture was allowed to stir
at room temperature, under an atmosphere of argon, for 18 h.
Extraction from H2O (20mL) with ether (3x20mL) was followed by washing
the combined ether fractions with 15% NaOH (1x15mL) and then extracting
the organic phase with 1N HCl (3x20mL). The ether layer was discarded,
and the aqueous layer was neutralized with concentrated NH4OH to pH 9,
extracted with ether (3x20mL), dried (Na2SO4), and evaporated to 1.65g
of a white glass (100%) that was homogeneous by TLC and was taken to
the next step without further purification: IR (CHCl3) 1660 (C=N),
1600 (Ar) cm-1; 1H NMR delta 7.50 (d, J=8Hz, 1H), 7.47 (m, 2H), 7.14
(m, 6H), 2.37 (s, 3H); CIMS m/z 402 (M+1).
(+)-17-Methylmorphinan Fumarate (H "derivative")
A modification of the procedure described by Reden et al was used to
convert [above intermediate] to [H derivative]. A mixture of [above
intermediate] (1.55g, 4.7mmol) in glacial HoAC (40mL) and 10% Pd/C
(1.55g) was hydrogenated (40psig, 40 C) for 96 h, when the reaction
was determined to be complete by TLC (THF/hexane/NH4OH 1:1:0.1). The
reaction mixture was filtered over Celite and evaporated to 1.16g
(100% crude) of a clear oil. Purification by flash column
chromatography (THF/hexanes/NH4OH, 1:1:0.1 to THF/NH4OH, 9:1) afforded
0.60g (53%) pure [H derivative], as the free base. The oily free base
(0.30g, 1.24mmol) was dissolved in MeOH and added to a solution of
fumaric acid (0.15g, 1.24mmol) in MeOU. The volatiles were removed in
vacuo, and the salt was recrystallized in 2-PrOH/ether to give 0.30g
(68%) of [H derivative]: HRMS (M+) calcd for C17H23N 241.1830, found
241.1825; [alpha]D +14.9 (c 1.15, MeOH).
(+)-3-Methoxymorphinan Hydrochloride (intermediate)
[DXM - note not dextrorphan] was converted to the free base by
extraction from aqueous NH4OH (20% v/v, 25mL) into CHCl3, followed by
drying in vacuo. The crystalline free base was dissolved in freshly
distilled (from P2O5) dichloroethane (65mL); K2CO3 (11.0g, 80mmol) and
ACE-Cl (11.4g, 80mmol) were added at 0 C, under an atmosphere of argon.
The reaction mixture was warmed and allowed to stir at reflux for 6h.
Cooling was followed by filtration and removal of solvent in vacuo.
The residue was dissolved in MeOH (60mL) and allowed to stir at reflux
for 1h. Evaporation and recrystallization from EtOAc gave 5.29g (90%)
of pure [intermediate]: mp 250 C (lit. mp 249-250.5 C [J. Pharm. Sci.
1980, 69, 1447-1448]).
(+)-3-Hydroxy-17-formylmorphinan (intermediate)
[The above intermediate] (15.3g, 52.2mmol) was converted to the free
base by extraction from aqueous NH4OH (20% v/v, 100mL) into CHCl3,
followed by drying in vacuo. The free base was dissolved in ethyl
formate (200mL) and formic acid (100%, 150 microL) was added. The
reaction mixture was allowed to stir at reflux overnight. Evaporation
gave the crude N-formyl-3-methoxymorphinan as a clear gum; TLC showed
one major product spot, CIMS m/z 286 (M+1). The intermediate gum was
dissolved in CH2Cl2 (100mL), and a solution of BBr3 (20mL, 209mmol) in
CH2Cl2 was added via addition funnel, over 10 min, at 0 C under an
atmosphere of argon. Five minutes after the addition of BBr3, the
reaction was complete by TLC. The reaction mixture was poured onto a
slurry of NH4OH (100mL, 400g of ice) and stirred for 20 min. The
reaction mixture was then poured into a separatory funnel, the organic
phase was removed, and the aqueous phase was extracted with CHCl3/MeOH
(4:1, 3x100mL). The combined organic phase was washed with H2O
(1x250mL), dried (Na2SO4), and evaporated to 12.58g (89%) of [this
intermediate] as a white foam: IR (CHCl3) 3260 (OH), 1650 (NCHO) cm-1;
1H NMR (showed rotamers) delta 8.15 (s, 1H); 7.99 (s, 1H); 6.94 (t,
J=6.2Hz, 2H); 6.81 (s, 1H); 6.80 (s, 1H); 6.69 (dd, J=4.2,8.4Hz, 2H);
6.26 (brs, 1H); 6.24 (brs, 1H); CIMS m/z 272 (M+1).
Representative Procedure for O-Alkylation and Reduction.
(+)-3-(2-Propoxy)-17-methylmorphinan Fumarate (2-Pr derivative)
A reaction mixture of [above intermediate] (3.0g, 11mmol), K2CO3
(7.7g, 110mmol), and 2-bromopropane (7.0mL, 75mmol) in dry DMF (15mL)
was allowed to stir at 60 C overnight. The reaction mixture was
cooled, filtered, diluted with H2O (25mL), and extracted with ether
(3x25mL). The ether layer was washed with H2O (3x10mL) and evaporated
to a clear oil which was homogeneous by TLC and taken to the next step
without further purification, CIMS m/z 314 (M+1). A slurry of LiAlH4
(1.60g, 40mmol) in dry THF (20mL) was prepared in an argon-purged
three-necked round-bottom flask, at 0 C. The oily intermediate
described above [in this paragraph] was dissolved in THF (10mL) and
added dropwise to the reaction mixture, under an atmosphere of argon.
The ice bath was removed and the reaction was complete in 30 min. The
reaction mixture was cooled to 0 C and carefully quenched with H2O
(1.6mL), aqueous NaOH (1.6mL, 15% w/v), and H2O (4.8mL). The lithium
salts were filtered and washed with ether. Evaporation of the filtrate
and drying in vacuo gave 25.9g (87%) of the free base of [2-Pr
derivative] as a clear oil. The free base was dissolved in MeOH and
acidified with a solution of fumaric acid (1.0g, 10mmol) in MeOU,
addition of ether resulted in 3.29g (91%) of crystalline [2-Pr
derivative]: mp 181-185 C; 1H NMR (CDCl3) delta 6.83 (m, 3H), 4.56
(m, 1H), 2.90 (s, 3H), 1.28 (d, J=3.1Hz, 6H); CIMS m/z 300 (M+1);
[alpha]D +22.75 (c 1.09, MeOH). Anal. (C20H29NO*C4H4O4) C,H,N.
==============================================================================
[8] MIXING DXM WITH OTHER RECREATIONAL DRUGS
In addition to the sections below, you may wish to consult Section 10 to
see what people have written about their experiences with DXM and other
drugs.
------------------------------------------------------------------------------
[8.1] 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 often cause prolonged
(up to 2 hours!) vomiting. Alcohol after the end of a high dosage DXM trip
has been reported to temporarily bring back many of the dissociative
effects (cannabis and nitrous oxide also do this). This seems possible up
to five days after the DXM trip, depending on your metabolism and brain
chemistry.
------------------------------------------------------------------------------
[8.2] Barbiturates and Benzodiazepines
I have no data on this combination. I strongly suggest you avoid this;
both barbiturates and benzodiazepines tend to be dangerous enough by
themselves.
------------------------------------------------------------------------------
[8.3] Amphetamines and Other Psychostimulants
Some people enjoy this combination, others find it unpleasantly speedy.
Most who've tried it reported that DXM will potentiate other stimulants.
Since DXM inhibits dopamine reuptake, combining it with a dopamine
releasing agent (amphetamine or methamphetamine) will naturally produce a
combined, synergistic effect. Consequently, you should be careful to avoid
a hypertensive crisis.
Combining DXM, a psychostimulant, and a monoamine oxidase inhibitor is a
sure way to make your blood pressure skyrocket and will probably kill you
(if you're lucky) or leave you with severe brain damage (if you aren't
lucky).
------------------------------------------------------------------------------
[8.4] Cannabis (Marijuana)
DXM plus cannabis is a frequent combination, which most people seem to
enjoy, at least at lower doses of DXM. High doses of DXM (third plateau
and up) mixed with cannabis can be very, very dissociative and sometimes
unpleasant.
One user reported that 360mg DXM followed 3.5h later by "a bowl or two"
produced a very profound, and unique, intoxication. Severe flanging 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. Note that cannabis after the DXM trip is over seems to bring back
some of the dissociative effects, much like alcohol and nitrous oxide.
------------------------------------------------------------------------------
[8.5] LSD, psilocybin, and other 5HT hallucinogens
I have limited data on this combination. One person simply said that DXM
and LSD was "not recommended". Another person disagreed, and said that DXM
helped him avoid unpleasant cognitive effects and "bad trips" he might
otherwise get from LSD alone. LSD may help you remember the experiences of
higher plateau DXM trips.
------------------------------------------------------------------------------
[8.6] Opiates
One person says that small amounts of opiates tend to "mellow out" the DXM
trip, and reduce the possibility for panic attacks or anxiety. Another
user said opiates should only be taken after the peak of the DXM trip,
because otherwise they would cancel each other out to some degree.
On the other hand, this may be a dangerous combination, and I'd recommend
against it. Both DXM and opiates can depress respiration and high enough
doses, and there might be a synergistic effect.
------------------------------------------------------------------------------
[8.7] PCP and ketamine
The only report I have indicated that ketamine plus DXM was not much
different from ketamine. I expect that most of DXM's particular effects on
sigma receptors are overshadowed by ketamine's NMDA antagonism. Ketamine
is a much more potent NMDA antagonist than DXM, and since they both compete
for the same site, DXM isn't going to affect this much.
------------------------------------------------------------------------------
[8.9] Nicotine
This is a combination I hadn't considered before, but which evidently is
fairly interesting. Nicotine seems to vastly potentiate DXM's effects for
some people, enough so that one user reported that one cigarette could
floor him on a second plateau trip. Another user reported that nicotine
helped him overcome some of the memory problems with higher doses of DXM,
but tended to induce nausea.
------------------------------------------------------------------------------
[8.9] Nootropics (Smart Drugs)
A few regular users of dimethylaminoethanol (DMAE), around 800mg per day,
have reported that the regular use of DMAE prevents a lot of the memory and
cognitive problems associated with DXM use, while still leaving the rest of
its interesting effects.
A similar effect has been reported for piracetam. See also information on
use of nootropics to limit hangover in Section 4.5.
------------------------------------------------------------------------------
[8.10] Miscellaneous Other Drugs
Several people have reported to me that nitrous oxide goes well with DXM,
especially towards the end of the trip. This seems to be consistent with
nitrous oxide's effects in combination with other hallucinogens.
Specifically, nitrous oxide seems to intensely multiply the flanging,
"stoning", and dissociative effects without added adverse side effects.
It might be a good idea to avoid tetrodotoxin, given DXM's sodium channel
blocking ability. (This is a joke! No, don't go out and try zombie
potion)
==============================================================================
[9] DXM DRUG CULTURE
This section describes some of the current and past DXM culture. Most of
this is one big unknown, and I'm attempting to write the definitive text on
the history of DXM's recreational use (this will probably take me several
years). If you have information on this topic, especially related to the
use of DXM in the form of Romilar? prior to 1975, please contact me.
------------------------------------------------------------------------------
[9.1] 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 characteristic of their
DXM use was that it was a group activity, whereas many DXM users today
regard it as a solitary experience.
There seem to be (rare) medical references indicating DXM recreational
abuse dating back to the 1960's. I'm trying to get more on this. I have
talked to a few people who have said that recreational use of DXM in the
form of Romilar? tablets was extremely common. If so, then DXM's
recreational potential may be the best-kept secret in the recreational drug
world.
Some cities seemed to have considerable DXM use activity, notably with
youth; in one town, there were empty bottles of cough syrup littering the
street, and sale of cough syrups were restricted to people 18 and up.
However, these incidents seem to be few and far between.
------------------------------------------------------------------------------
[9.2] Why haven't I ever heard about it?
Damned good question. 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 (or if they were, they
denied it).
My hunch is that at some point, the medical authorities and manufacturers
of DXM-based preparations realized that they had two choices: take DXM off
the market, or convince people they couldn't get high off of it. They took
the latter approach, getting rid of DXM-only pills and leaving cough
medicines in which DXM was combined with other ingredients. The majority
of users decided it wasn't worth the effort of gulping down cough syrup
(and possibly vomiting due to guaifenesin), and the next generation grew up
ignorant.
------------------------------------------------------------------------------
[9.3] 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 high-dose or chronic DXM use,
characterized by amotivational syndrome and avoidance. "I
don't want to go to class; I still have the heebie-jeebies."
jolly (v) To take DXM-containing cough syrups and ride up and down
elevators. This term evidently dates to the late 1960's; to
my knowledge it hasn't been used in the past couple of decades.
robo (n) Any DXM-containing preparation. "Hand me that bottle of
robo". Occasionally tussin, DM ("dee emm"). "Hand me the DM".
(v.i.) To dose with DXM. "I roboed last night". From
Robitussin[tm], a cough syrup brand; possibly also influenced
by "robot-like" behavior caused by DXM. Occasionally tuss
(v.i.), and DM (v.i.). "I tussed last night".
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.
Robo Itch (n) A transient phase of intense itching that some people feel
at the beginning of a DXM trip. Occasionally "The Itch".
Robo Shuffle (n) Disturbance in gait consisting of rigidity and
"robot-like" motion, often accompanied by a slow, shuffling
movement. Typical with high doses of DXM. Occasionally just
"The Shuffle".
roly-polies (n) The desire to roll around, do cartwheels, spin, or
otherwise engage in rolling motions. Occurs to some during
and/or after a DXM trip.
sea legs (n) Disturbance in gait and balance somewhat like walking on
land when accustomed to ocean balance (or vice versa). Differs
from the "Robo Shuffle" in that this disturbance usually
involves large, fluid, sweeping motions. Typical with low doses
of DXM.
------------------------------------------------------------------------------
[9.4] Are there any street names for DXM?
Not really, at least not yet. Several people have been making suggestions,
though. Currently the ones I've heard of are:
DM I try to discourage this in favor of DXM, since most "DM" cough
syrups have other ingredients besides DXM. Also, most of the
literature I've come across uses DXM instead of DM to refer to
dextromethorphan.
DXM The most accepted but the least interesting.
Robo The old standby, although it is somewhat dated since a lot of
people use Drixoral Cough Caps[tm].
Rojo Meaning "red", this term refers to the usual color of cough
syrups and gelcaps. Interestingly similar to "Robo".
Euphoria Possibly too many syllables for a street term; besides, it's
already taken (methaminorex)
Nexus Already taken, unfortunately (2C-B); DXM's higher-dose effects
are reminiscent of Star Trek: Generations ("This is the nexus.
Time has no meaning here.")
Drix More up-to-date than Robo, but it too dates itself. What will
we use when Drixoral[tm] becomes less popular?
Sky An interesting one; not quite sure of the derivation.
Lucifer Somewhat appropriate, as DXM can be very illuminating, and you
may not like what you see. Unfortunately there are some rather
negative connotations (added by Christianity) to this particular
deity.
Rise Someone suggested this based on "rush" induced by DXM as it begins
to peak.
Gel Suggested to me by someone who observed that DXM is available in
gel-capsules (Drixoral[tm]), and that it tends to make some people
feel like they are swimming in Jell-O[tm].
Let me know if you come up with anything. I doubt DXM will ever be a true
"street drug", but you never know. Besides, "Dee Ecks Emm" takes too long
to say in casual conversation.
------------------------------------------------------------------------------
[9.5] How do I explain to my friends that I'm getting high off cough syrup?
Good question. Lots of people consider DXM to be a "second-class" drug,
good only for people who can't get the real thing. Here's some things to
try and point out:
o Heroin was originally marketed as a cough suppressant. Nobody's
calling it a kiddie drug now!
o DXM is in the same drug class as PCP and ketamine ("Vitamin K" or
"Special-K"), with an added stimulant effect functioning like that
of cocaine.
o DXM's recreational use potential has probably been purposefully hidden
by the medical community. So not only do you get a drug, you also get
conspiracy theory material as well!
o DXM has been used as a psychedelic longer than LSD has.
o DXM targets five different receptor sites _ that's five times the
complexity of marijuana!
o So what if you puke from drinking cough syrup? Peyote can make you
puke, too!
o DXM is a three-letter acronym just like PCP, LSD, DOB, DOI, and THC
(not to mention FBI, CIA, NSA, FEMA - oops, sorry, that's four
letters).
o It must be interesting, because some neuropharmacology geek (yours
truly) spent over 500 hours researching and writing a 200 page book
about it.
==============================================================================
[10] DXM EXPERIENCES AND PERSONAL REPORTS
This section covers various people's reports about their DXM use. All are
given anonymously, sometimes with a pseudonym. Because I have literally
hundreds of pages of data, I have chosen to present what I believe to be a
representative sample. I fully admit there may be bias here, although I
have tried to keep it to a minimum.
Note that I had a bit of a problem deciding how to sort this section. On
the one hand, I wanted to sort by mg/kg; on the other hand, only about 20%
of my reports list the subject's weight. So I settled on dosage, with
mg/kg listed as well. If you see your experience listed here and I don't
have your weight, feel free to tell me - just identify which one is yours,
since I no longer have any original names or addresses.
Also, I divided the single experiences into first/second and third/fourth
plateau trips based on certain elements which were present (or absent) in
the descriptions. Sometimes this led to higher dosages in the first
section than in the second, and sometimes the decision was difficult.
------------------------------------------------------------------------------
[10.1] First and Second Plateau Experiences
Positive Experiences
W. A. (male, age 19, 110kg), 75mg (0.68mg/kg) + pseudoephedrine
The entire bottle of children's DM, containing a total of 75mg of DXM, as
well as pseudoephedrine (don't remember the amount), was drank over the
course of about 45 minutes. The initial effect was a lightheaded,
disassociated feeling. Thought patterns remained completely lucid and clear
as ever. Very unusual perception of motion was also noticeable; it felt as
if I was "gliding" around the room, rather than walking. Falling onto the
floor into a pile of cushions was very very entertaining. No visual, or
audio hallucinations or distortions were noticed. The effects set in
around 1 hour after starting to drink the preparation (15 minutes after
finishing the bottle). The effects were mainly emotional and physical, as
previously stated. I'd heard that musical perception was altered, and I
did notice that when listening to music, I really "got into it" (as with
pot, but different), and I couldn't get the beat out of my head after
turning it off. A friend, who is much smaller than I (5'11, 130lbs
perhaps) experienced similar intensity and effects, even though he had
taken the same dose as I did.
A slightly increased heart rate was also noted, as was a slight crawling
skin feeling, but these were probably because of the pseudoephedrine.
Near the end of the experience, I got a horrid bloated gassy stomach ache,
and spent the remainder of the 'trip' dealing with severe diarrhea. It
wasn't pleasant. The friend who also did it, didn't experience these
effects so it must have just been that my system can't handle the crap that
makes up cough syrup (flavors, sugars, perhaps the pseudoephedrine). Or
maybe I react badly to the DM itself. The entire experience lasted perhaps
6 hr.
Overall, somewhat pleasant and interesting, but nothing terribly
spectacular or insightful. Planned on taking a higher dose the next time,
to try for some actual hallucinogenic or psychedelic effects. It did almost
feel as if I was nearing a threshold of some sort, sort of similar to a
very low dose of LSD.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Sir Death (male), 240mg
Got ahold of 2 4-oz bottles of "Father John's Medicine"-10mg DXM per 5ml
"dose" = 236mg per bottle. It took me nearly 10 minutes to down the first
bottle-it was a thick black sludge that was supposed to be licorice but
smelled (&tasted) much like FlyNap (that stuff at school that we use to
temporarily knock out fruit-flies). Needless to say, I was already feeling
nauseous and decided against trying to consume the second bottle. By about
45 minutes after consuming the liquid, I began to notice some unusual
effects... the radio (I was listening to a talk show) began making weird
almost flange-like effects... I stuttered somewhat when I tried to speak (I
do not normally have this problem).
About an hour into this, I switched the radio over to an REM CD. The music
was more beautiful than I have ever heard it before-each note was intense
and vibrant. I stood up and discovered a floating, somewhat euphoric
feeling with a little cloudiness of thought. These effects seem to be
virtually identical to that of Vicodin (sp.?), a narcotic painkiller I had
had prescribed for me following outpatient ear surgery last spring.
The nausea became extremely intense over the next several minutes, and I
finally began vomiting violently into my trash can-however, almost
IMMEDIATELY afterwards, I felt much, much better. My head felt big and
swollen (not at all unpleasant, however) and the euphoria felt when walking
around was exponentially more intense. Coordination seemed to be
impaired-I tried playing "Tetris" on my computer only to find it impossible
to think and act properly. I definitely would not want to drive in this
condition.
After about four and a half hours, I began to come down gradually. No
"crash" at all-I didn't even fall asleep (as I do with almost every other
substance I've tried). By about six and a half hours, I was feeling no
effects whatsoever and was able to continue with the rest of my day.
In short, I would try DXM again (just not in that vile toxic waste form).
I'd recommend taking an meclizine antiemetic (e.g. Bonine or Dramamine
II)-NOT, however, a dimenhydrinate one (e.g. Dramamine) as this causes
drowsiness-to control the nausea.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
M. T. (male), 250mg
I felt confident and tried a low dose (250mg). I loved it! Everything I
read about it came true; music sounded "live", slight euphoria, etc. I did
250mg a few times before moving on to larger doses. Before long I had
turned a few friends on to DXM.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
B. D. (male) 250mg.
(I kept the original spelling and typing just to illustrate that DXM doesn't
always improve one's typing skills. :^) )
sorry abouyt not quoting, but i can't be bopthered. well, i'm currently on
the tail enbd of a 250 mg dose of dxm, and fuck i feel *GOOD*. i can't
imagine it being possible to have a bad trip on this shit.
oh, man, i feel so good.
well, if i can get this posted withougth screwing up roayally i will ta
leastr remewmber it when i read this, and probably regret it...it's neat...
ity's like being in a rpoom, with no lightsa except a whole bunch of tv's,
and each tv is a different sensory input, and i have a few outputs toom but
i can only play with ione atta time. so i cant think vetry well. oh,
plese flame me, i am too happy to care. having tried this, i would
definately reccomend it.
i walked through the woods for 2 hours with a freibnd who aslo tried dxm
for the first time... we had such fun, oh damn i can't see the keyboard
anymore am i typing still? oh, i can see the screen so i am. i am going
away. TRY DXM, IT'S FUN.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
J. W. (male), 300mg
Hello all. 2 hours and 8 minutes ago I ingested 300 mg of DXM, my first
trip on anything. I've never done acid or anything like that. This is the
most incredible thing I've ever experienced. Based on what I've read, I
think I must be peaking right now. This is simply incredible. I can't
even explain what's happening to me. I can't stay focused on anything, my
mind is racing, and I feel totally relaxed. I can feel my body swaying
back and forth to the music ( which DOES sound absolutely incredible on DXM
).
Okay now its 1:19 PM.... 3 hours and 25 minutes since I took 300mg of DXM.
I have felt a little sick occasionally, and have itched tremendously on
certain areas of my body for the past hour or so. There is a huge red rash
on my chest that itches incredibly, almost like a sunburn. I have no idea
what it is. I watched some television and that experience was very weird.
I didn't like it at all. The only thing on TV was "The Golden Girls" which
I find funny sober... It seemed very dumb and boring to me on this DXM.
Please realize that the DXM is still obviously going strong in my body and
my message may reflect it to some extent. However, since some people have
expressed interest in reading other people's experiences (and I love to
read other people's experiences myself ), I will now try to describe
exactly what is going on, so long as I can remain cognitive. Instead of
trying to remember what it was like and post it later, I will try to post
it as it happens. I'll devote the next 45 minutes to writing this
message...
Both of my eyes feel very puffy, like I get when I'm around cats. My head
spins occasionally, and the world around me seems to jitter every time I
move my head. While laying down on my bed listening to music, everything
was fine. In fact, I find that I am almost perfectly normal (feeling, not
thinking ) when I'm laying down. As soon as I get up and walk around,
things get crazy. The more I move my head or change my sense of balance,
the stranger things get. Neither of my eyes will focus on the same object.
I have lost almost all of my 3-dimensional perception. My right eye
stares straight ahead and so does my left. They no longer converge on an
object to present my brain with a 3d image. Everything is flat. This is
only when I let them go, however. I can control my vision. Perhaps with
greater dosages I will not have this luxury <G>
Keep in mind, please, that this is my first trip-at only 300mg. For $4.25
I got 300mg of pure DXM and I'd just like to tell you that it has been
nothing short of incredible. I read articles about people smoking pot
about 2 hours after taking DXM to get both drugs to peak at the same
time... I didn't mix anything with DXM (yet ).
Now its 1:24 PM and I have no idea how long this is gonna last. I think I
peaked about 2.5 hours into the experience, that would be maybe an hour and
a half ago. The peak was simply unexplainable. By far one of the most
incredible experiences of my life. There was, however, nothing 'profound'
about it. I didn't get any feelings of superiority or godlikeness, or
anything like that. Perhaps it was the low dosage. I'm going to go pick
up 750 mg's when I can finally drive <G> and take that sometime later this
week. Having never experimented with many drugs (I haven't done all that
many drugs like some of you veterans <G> ) I must say that DXM is probably
the strangest, most interesting thing I've done in my life. There's just
no easy way to explain it. On this low dosage, I didn't get any "pink
elephants." However, with my home stereo playing loudly, the bass shook my
head (which was laying on a pillow which would obviously absorb the bass)
and made the entire room shake. As I said, the bass could not have
physically made my head move as I was on a pillow. It was more likely an
affect of the drug/my eyes/the music. Music does certainly sound
incredible with DXM.
Its 1:37 now. I've been listening to the Natural Born Killers soundtrack,
Tori Amos' Under the Pink and Little Earthquakes, and "Chill Out," a
ambient 2-disc set. I have also listened to all of Yanni's CD's in the
past few hours. The music is simply incredible. I paged a friend of mine
and she called me back. I told her about what I had done (this was about
an hour ago when the peak was beginning to end) and we talked for a while.
Quite an interesting conversation. She and her friend are going to try DXM
with me next time I do it. I'm going to take probably 600 mg or so and
they will get 300mg each. We'll see how it all turns out. Well now its
1:43 and it seems like I've been sitting here for hours. Time looses its
meaning with DXM. Even in this low dosage, I guess. I could have been
sitting here for a day and would never have known it.
Anyway, my brother and his friends are over here. They don't know what
I've done. I find that when I smoke pot I tend to be more withdrawn and
afraid of people. They just walked into my room just now and I was not at
all alarmed. Personal interaction is very easy yet somehow complex. I
have not experienced the "dizzy" feelings everyone always talks about.
Perhaps, again, it is the low dosage.
I have heard that, after taking large dosages of DXM, people have
experienced gas for the next few days. My entire body feels very warm and
flush, but my pelvic area seems particularly warm. I have not "messed
myself" or anything of the like, but I can hear my stomach growling
constantly. My intestines must be doing something. Perhaps I should have
taken the DXM with orange juice or something similar to help with the pH
differences...
1:51 now. I'm wondering how long this stupid thing will end up being. My
apologies in advance if I begin to ramble on and on. A while ago I made
some cappuccino. I dipped my finger in the boiling water and felt NOTHING.
I only kept it in for a few seconds because I cognitively knew that, even
though I couldn't feel it, my skin was indeed burning. DXM certainly
alters your perception and consciousness. I've read articles about people
staring at trees, talking to dogs, thinking they were things other than
human, etc. on DXM. This whole time I have not forgotten than I am sitting
here in my room, listening to my CD player, etc. I never had any thoughts
of being something other than human or seen any wild hallucinations. The
dosage is again probably to blame.
1:55 now, I'll write until 2:00. To wrap up, I guess I'll talk about how I
felt when I first took it. I was not really nervous or concerned. I have
spent 3 months researching DXM. I always research something before I try
it. When I finally took all the pills, I grew impatient quickly. I had
eaten about 45 minutes before, so I think that had something to do with how
long it took to take affect. About 1 hour 20 minutes after I took the
pills I began to definitely feel something. If there is anyone out there
thinking of trying DXM, I suggest this: research it until _you_ feel you
know enough about it. Talk to people who have done it. Read the FAQs,
etc. If some guy came up to me on the street and said "There are 10 DXM
tabs here. Take them." I would have totally freaked out. I personally
need to know _everything_ about what I'm considering trying before I try
it. Better safe than sorry, I guess.
Well its 2:00 now and I apologize for the length of this thing. I hope you
all find at least something here useful or entertaining, as I don't want to
waste bandwidth.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
AN148627 (male, 73kg), 300mg (4.1mg/kg)
OK, I'll do that thing. Lately I've become a big fan of low-dosage (300 mg,
I weigh 160 lb., and have a very low threshold for every drug I've ever
tried) DXM trips. I guess "trip" isn't quite the right word...at that
dosage, it's more like a buzz, admittedly a buzz with interesting cognitive
effects.
Here is a log from a recent 300 mg experience:
3:30 - 4:00 PM - Took 10 Drixoral cough caps while reading alt.drugs. I
used the timer on my watch to give me a beep every 3 minutes. At each
beep, I took a cap, with water. This was about two hours after a light
lunch (a 6" veggie & cheese sub from Subway).
4:45 - Began to feel a bit dizzy. Noticed a tendency to smile at nothing.
5:15 - Definitely feeling a buzz. I played a computer game for 15 minutes.
When I stood up, I practically launched myself out of my chair! My
limbs felt very light. I felt like I could jump up and hit my head on
the ceiling (though I didn't...I was also feeling very relaxed.)
6:00 - Had dinner. Ate *very* slowly, and about half the usual amount.
Talked to my wife at great length about exponential growth (I think she
was laughing at me).
During this whole period (5:30 till I went to bed), I felt my thoughts
frequently "spinning off." Like I would be thinking about one thing, and it
would lead to a complicated spin-off, that in turn would lead to another
spin-off etc. I had a vision involving mathematical processes. Hmmm, how
to explain? Consider a convergent infinite sum (like 1/i^2, for I running
from 1 to infinity). The sum tells you to add a term, add another term, add
another and another and another, forever. But instead, you can just "do the
sum" and get the answer (2, in this case). By this act of abstraction, you
short circuit the process of infinitely adding terms. So I imagined doing
the same with the act of abstraction itself. This leads to an infinite
series of abstractions of abstractions. So do the same to that one! And so
forth... I guess you had to be there...
7:00 - 8:00 - While my wife put the kids to bed, I lay down on the floor
with the headphones, listening to Counting Crows, Dire Straits,
Koyaanisqatsi, and Brandenburg concertos. Really got into it. As has
frequently been noted on alt.drugs, music is greatly enhanced by DXM.
8:00 - 9:00 - Played a 2-player computer game with my wife (Oxyd). We had a
great time!
9:00 - Smoked a bowl. At first it seemed to cloud up my thoughts, but later
I felt even better than before. Watched some TV, but couldn't handle
the raw stupidity.
9:30 - Took a hot shower. Felt great. Afterwards, very relaxed. Talked with
my wife for about an hour, then just lay down on the couch with my eyes
closed.
12:00 - Went to bed, slept great.
That was it. Never felt any nausea. The next day I felt fine, the effects
were completely gone.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
J. R. (male, 60kg) + friend (male), 300mg each (J. R. 5mg/kg; friend
unknown)
10:03 Both: Took 300mg(10 capsules) each of Drixoral Cough Liquid Caps...
might have been a bit much for a first time try, but we were feeling
daring...(and we wanted it to be good) :)...
10:47 Both: Think we're starting to get a general 'nice' feeling
10:57 J.: Colors seem to be getting brighter. Listening to Nirvana's
Bleach album, music seems kind of 'thin' but it's pretty easy to get
into.
11:16 J.: Colors really brightening.
11:22 J.: Getting into it... K. doesn't seem to be having much fun yet..
11:53 Both: Went outside to have a smoke and walk around.
12:07 Both: came back in, J.: Things seemed to really be setting in. I
first noticed it when I walked back up the stairs to come back into
the house. I felt very bouncy, as if I were going to keep floating
up... I also felt it when I stood up from a chair. Around this time I
also started to notice things bouncing around a bit when I tried to
fix my eyes on them.
12:20 I'm definitely getting weird, K. still isn't getting anything...
12:26 Turned off the lights and the monitor, stopped writing this log as
things happened. Listened to music in the dark and had a pretty good
time singing along. Now I popped in Nirvana's Nevermind. It was more
melodic and cooler to listen to. I thought the more psychedelic parts
of the music would be more stimulating, but it was really basic song
structure and melody that got me going... Time started to get
distorted. Couldn't keep my eyes from wandering.
1:00(or so) J.: Time getting really distorted. Songs seem to last for
hours, still nothing really for K.. We just lied around and listened...
Things really hit around 1:30... All I can say is that I was FUCKED *UP*!!!
My memory from then on is really screwed up, but I remember realizing just
how fried I was when I found myself sitting up on the bed with my legs
shaking, and asking K. if they were shaking. He told me to stop shaking
them (By now he seemed pretty fried too) and when I stopped (it was fairly
hard, I couldn't quite remember 'how' to). It felt weird stopping, so I
just let them shake (They stopped when I laid back down). Standing up was
hard and so was talking (although that didn't stop me). Just laying down,
talking and listening was actually quite enjoyable.
Things I noticed: These things are DANGEROUS! I almost choked trying to
swallow one of the pills :) (Really though, Make sure you have something to
wash them down with). We were VERY heavily stoned. I remember K.
remarking 'This is what retarded people must feel like' :). I just couldn't
think straight at all...
I seemed to instantly verbalize most of my thoughts. According to K., I
talked almost the whole time about absolutely nothing... I wonder if I
would have talked so much if there weren't anyone there with me...I found
myself contradicting myself often. "I want to try and go outside. No I
don't." I also said completely senseless things. He would ask me a
question like "Do you want to try and stand up?" and I'd say something like
"No, because you'll try to kill me, and the windows can't handle that."
Weird...
Part of our talking was telling each other all of our deepest darkest
secrets. I can only remember a few of the milder ones, but I know I told
him things about myself I wouldn't tell ANYONE normally... Luckily our
memories of the experience are very bad, and many of the things we told
each other were absolute hogwash (I distinctly remember "Hey man, I gotta
tell you something. I have sex with furniture" "That's OK man, I have sex
with guitars..."). The next day however, we both felt like a tremendous
weight had been taken off of our chest, and I think we're much better
friends.
I didn't seem to hallucinate as I thought I would. In fact, I really
couldn't imagine anything visual at all. When I closed my eyes, I just saw
kind of a slightly more intense normal-closed-eye pattern, and I just felt
a general 'swirling' feeling in my mind. K., however, reported seeing Sonic
the Hedgehog come running at him a few times. :)
I noticed my body seemed generally numbed, and severely in my mouth and
face. The numbing of my mouth added to the difficulty of talking, and I
think I had cottonmouth, but it might have just been the numbness.
At one point, for some reason I told K. to make sure all of his fingers
were still on because DXM can me bad for them. He started nervously tugging
on them to see if they were loose. I really freaked him out :-).
Moving around and dancing was REALLY cool. I was very disoriented and had a
bit of a hard time standing up, but I didn't get motion sick or anything,
and moving felt great. Looking back, I'm glad nobody sober was watching me
dance, I pretty much made a fool of myself :)...
For part of the most intense part of the trip I seemed to be just 'Out of
my head', Like the rest of my mind just wandered off and left me to just
kinda lay there and stare at things. I also had a few 'waking up'
experiences. It's hard to explain, but it was if I were dreaming, and then
woke up to find things exactly as they were in the dream.
I only got nauseous twice for short periods, and it was very mild.
Sometime around 4:00, Both of us decided to go so sleep (I wasn't really
tired, it was a decision we just kinda made) No weird dreams or anything...
The next day, I didn't feel down after the trip, probably because I was
still feeling the effects quite a bit. My memory wasn't doing too good, I
felt mildly stoned, and I still got that funny feeling whenever I got up.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
AN165416 (male). 300mg + alcohol
Tonight I took 300mg of DXM after getting drunk and I really liked it. I
am sick and probably have the worst situation for having a "bad trip", if I
had dropped acid I definitely would have lost it and felt like shit all
night. But I got drunk and took 10 Drixoral cough caps and I really
enjoyed the whole thing, sickness and all. At first I was nauseous and
threw up a couple of times but it was very painless and left me with a
feeling of relief that was very pleasurable. Then I laid down and listened
to music for awhile as it kicked in and the only way to describe it was as
a religious experience. It was *awesome*. For the next few hours I was
restless and I walked around for awhile and just walking around was fun.
Feeling no pain, pretty much feeling *nothing* was just the effect I was
looking for. I had to take a shit a couple of times with the flu I have
but it was not really unpleasant even though I'm sick (get it?).
Now I'm starting to come down I guess, and I would have to say that DXM is
good for those who are looking for a kind of narcotic type high but with
some of the weird effects of the hallucinogenic type drugs. I think its
especially good for those who want to get more than pot has to offer but
for whom acid makes them anxious. At least for me DXM doesn't have that
"on edge" feeling that acid and shrooms have. Anyway, I'm hungry and I've
gotta get something in my stomach. Later.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Anonymous (male, age 16, 80kg). 350mg (4.4mg/kg) + cannabis
(Although generally positive, this user had an exceptionally long (3 day)
hangover which was definitely not an expected or pleasant experience.)
Recently I decided to experiment with DXM as a recreational drug. Although
the initial experience was not negative, I am now becoming a bit
frightened. You see, it has been more than 54 hours since I took the DXM,
and yet I am still feeling the effects. I'll get into the details of how I
feel right now at the end of this article, let me tell you that I am still
feeling slightly light-headed and numb.
Before I relate to you my story, however, let me tell you a bit about
myself. I am 16 years old, white, male, and I weigh about 80 kg (180 lb.).
I'm a good student, a junior in high school with a GPA of 3.8 and in many
honors/AP classes. I have experimented with marijuana and LSD in the past.
I'm not currently on any sort of medication.
And now my story: (all names are changed to protect the guilty.)
Wednesday, March 29th
3:00 PM: School gets out. After reading about dextromethorphan in the DXM
FAQ and some positive stories from someone I met up in the city, I decided
to go out to Long's drugs and buy some Drixoral gelcaps. I told my friend
(who will now be known as Andy) about DXM, and he was interested, too. I
drove Andy and myself over to Longs, where we split the cost of a 20 pack
of Drixoral Cough. We then drove back to Andy's house. Andy actually
lives with a foster family. Back at the house, Andy's foster brother Sam
was home with a female friend named Pam. We told Sam about the Drixoral,
but he scoffed at us for "stooping" to the level of cough syrup. This from
a guy who used to get high from Vick's inhalers.
4:30 PM: Since nothing important is happening at school the next day, we
decide to each take 5 caplets. That's 150 mg DXM, or 1.875 mg/kg. Andy
weighs less than I do. Regardless, we figured this to be a rather tame
dosage to take, so we swallowed the caplets with water and went outside
with Sam and Pam. We talked, listened to music, etc.
5:15 PM: We don't feel any affects. We get the idea that this isn't going
to work at all (we had a failed Morning Glory experience 5 days earlier) so
we each take 5 more gelcaps, finishing off the box. We have now taken a
total of 300 mg DXM, which for me is 3.75 mg/kg. Discouraged, we recall
that pot is supposed to help enhance the effects of DXM. We get out our
bong, and scrape out the resin so we can smoke it. Sam has some shake left
in the bottom of a suede leather bag, so we put it along with the scraped
off resin in cigarette paper and stick the whole wad in the bowl.
5:45 PM: All four of us smoke out, getting quite pleasantly stoned. Andy
and I have given up on the DXM, although we did notice that neither of us
coughed at all when we smoked, unlike Sam and Pam. It truly is a good
cough suppressant.
7:00 PM: We've been eating and watching TV for a bit, but nothing is on.
We get up. Andy and I look at each other. We don't feel stoned. We feel
something more. We go upstairs to Sam's room and listen to some music.
Andy and I feel good. Really good. Sam and Pam go out to have a walk. My
memory of the evening begins to get fuzzy
7:30 PM: I call my house and leave a message on the machine that I won't be
coming home at 8, but that I'll be home at 10.
8:00 PM: Music feels really good. I'm seeing hallucinations now. The neat
part about them is that I can control them, something I didn't experience
on LSD. I've also lost my appetite. I try to force down a cookie, but I
can't. I'm very thirsty, however. I drink some water.
8:30 PM: I'm completely delirious by now. I feel insanely good, and I'm
getting a definite visual flanging effect. We both feel feverish. I also
feel vasoconstricted in my lips and hands. Music is losing it's euphoric
quality, but movement is great. Andy and I go out for a walk in the hills.
Depth perception is gone, and I am getting double vision. Focusing on
things is difficult.
9:45 PM: We get back to the house, and I need to go home, as Sam's mother
has returned home. As usual, I am stuck driving in my VW Bug back home.
The drive in uneventful. I don't run any stop signs, I don't see any cops,
and I go the speed limit.
10:00 PM: I got home. I am able to talk with my father successfully. I am
still very thirsty, so I drink a couple more glasses of water. I brush my
teeth and at 10:30 I go to bed.
Thursday, March 30
6:30 AM: I haven't slept a wink. I am still tripping. Over the past 8
hours I have tossed and turned, feeling very good, although a bit anxious.
Getting up and walking around every so often has felt nice. I enjoy some
more hallucinations. Then I realize that I'm going to have to drive to
school still under the effects of DXM. I'm a bit worried now, but guess
I'm just experiencing the "hangover."
6:45 AM: I take a shower. Neat experience. Felt weird.
7:00 AM: I go to the kitchen to get breakfast. My parents are up. I
attempt to talk with them, but I have trouble forming sentences. I shut
up. I make myself half a quesadilla, and force down about half of it. I
have no appetite, but I don't want to come down not having eaten anything.
I drink some more water.
7:30 AM: I drive to school. Pretty easy, although I still have a hard time
focusing on things directly.
8:00 AM: School begins. I'm still light-headed and feeling "good." I want
it to stop. I take a math quiz on limits. I feel like I'm taking forever
to do it, but I finish in less than 10 minutes (about 10 minutes before
everyone else.) My perception of time is still a little strange.
10:00 AM: I confer with Andy. He is no longer feeling any effects. We
also come to believe that I felt it more strongly than he did the night
before. My eyes still move slightly independently.
3:00 PM: I return home from school. I'm still feeling strange.
3:30 PM: I finally take a nap, the first sleep I've gotten in 33 hours.
5:30 PM: I wake up. I feel much better. My vision is totally normal
again. I call Andy up, let him know I'm okay.
6:30 PM: Dinner. I interact with parents again and babble a bit.
9:00 PM: I make brownies. It's a lot of fun. I'm feeling the effects of
DXM a little stronger again. I'm getting a little frightened that my trip
has gone for over 24 hours, so I call Andy up. We talk. I continue to see
slight hallucinations in the dark (breathing walls, shifting shadows.)
10:45 PM: I've been watching TV with my Mom for a while, and now I'm
beginning to feel a little stranger. I'm twitching a bit. Having things
touch me feels very good.
11:15 PM: In bed. Fatigued, but not sleepy. I end up writing in bed for
about two hours. I'm in a state of what I would call ecstasy. The sheets
on my skin feel unbelievable good. Certain parts of me feel numb, however,
especially around my genitals. Hallucinations have stopped.
Friday, March 31
1:45 AM: This is the last time I remember looking at the clock for a while.
3:30 AM: I wake up for a bit. I've stopped writhing.
7:30 AM: My dad comes in, wakes me up. I'm late, having slept through my
alarm clock.
8:00 AM: I just make it to school on time. I'm very jittery. I blame all
my remaining symptoms on lack of sleep - I've gotten about 5 hours of sleep
in the past 48. I stutter a bit when I speak. My hands shake.
12:00 PM: I get progressively worse as the day goes on. I'm having
troubles coping with people. I go home.
2:00 PM: I nap until 5:00. I feel slightly better.
This all leads up to me now. I've been typing this up for about an hour.
I started at 11:15 PM. Here's my current situation. I am tired and woozy.
I feel numbish all over - not totally number, and I still feel pain
(pinching) just fine, but gently touching and squeezing of my body feels
strange. I am developing a headache, but I'm loathe to take any medication
right now. My hair is still sensitive to touch (scalp hair, arm hair,
etc.) but the actual skin underneath isn't. The effect is most pronounced
in my scalp skin, forehead, nose, face, arms and genitals. I still have
feeling in all these places, it is just a different type of "feel", but it
is different. I still feel pain normally, however.
Worst of all, I'm getting sort of used to feeling this way. I begin to
forget that I'm not quite all here. Then I'll realize that I don't feel
like I normally do.
I apologize if this gets harder to read as my article continues. I'm
finding it more and more difficult to type. Also I am having trouble
concentrating. I going to go to sleep.
I didn't get a chance to send this off last night. It is now 6:30 PM
Saturday, and I'm feeling better. I'm still lightheaded and slightly numb,
however.
Wow, a 72 hour "trip." I wasn't expecting this.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Raskolnikov (male). 350mg
(Note: this experience seems typical of day-time DXM trips. Most people's
DXM experiences have occurred at night.)
I've done 350mg during the day (before a lecture). What I noticed was that
everything was pretty bright, I felt a great buzz, and I was tremendously
relaxed. Since I could see everything, the feeling of disjointed limbs was
pretty intense, too. If you have roboed enough, I say go for it. I can
pass for sober at this level easily, too, so it's safe to do in public.
But YMMV.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
J. W. (male), 360mg
I tried my first robodose this Friday. I went up to Walmart's and bought
8oz of Vicks 44. I was planning on doing it with a friend, but right after
I had downed about 2oz(of the 4 that I did) a girl called and asked me on a
date.
Well, I asked my friend that I was dosing with if it would be all right if
I ditched him. He said it was fine(knowing that I don't get too many
dates, especially good looking ones). I finished off the other 2 oz, then
I met her at a smoking hall. We sat around and talked awhile, I told her
that I was drugged and that I may not be completely coherent throughout the
night ;)
We couldn't find a movie to watch, so we went back to my place(she was
driving, obviously) and talked a bit more. I was just beginning to feel
the effects when we were talking at my house. (The initial were having
trouble walking, and a slight distortion in background noise) During when
we talked, I had "Indiffence" by Pearl Jam on... the music felt great, it
just ran through my body. My whole body and mind felt as if they were new,
like I was five years old again. I actually managed to hold a decent
conversation.
I went to put in The Wall (movie) by Pink Floyd. We sat back on my bed and
watched it, this is when the visual distortions began to come on. At first
there were slight trails, then there were waves, like the fabric of the
universe was flowing. At about "Another Brick in the Wall part 3" I
couldn't get both my eyes in sync, one looked normal, the other was
rotated off at 45'. By the end of The Wall, the effects were lessening,
and I was still feeling good, no hard come down. She took me to get my
car(I felt as if I could drive now), and we went back to her place. We sat
down on her bed and talked for another 4 hours. A really good date, and a
very good trip. In the morning, I felt fresh, a little tired because of
only getting 3 hours of sleep, but no cotton mouth, no hang over.
Unfortunately, my friend, who I ditched :(, went to a party and started
puking. But he understood(although he says he'll never robodose again ;)
I would recommend robodosing to anyone who can hold down the syrup...I
think it was the best trip in my life.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Derf (male, age 21). 360mg + cannabis
I've posted a few DXM experiences a while back, and recently had another...
every time I think I have this drug figured out, something REALLY odd
happens! This time, it started at a friends house where we all smoked a
little pot. After that, I went home and ate 12 Drixorals. (good thing
that's all I had). I've experimented with a lot more than this, but I
didn't feel like going to get more caps! Anyway, after the caps started
working, my earlier high had settled into a really mellow feeling.
When the DXM peaked, the most I can remember is laying on my bed thinking
"wow, that's odd how I can still move my legs even though they aren't
attached to my body anymore!" This was WAY cool and didn't bother me in
the slightest bit at the time. I was totally convinced that my body had
separated into 2 parts, but I was amazed that I could still control them
both. I was laying there for a loooong time just wiggling my feet and
stuff just because it seemed so strange!!
Other than that and one other incident which I'll describe later, the trip
was just your standard flying around and stuff. The other weird thing that
happened to me was when I was just sitting and listening to some pink
floyd. All of a sudden, there was a lot of confusion in my mind of what I
was seeing, and what I was imagining. I've always been able to pretty much
distinguish the two before. this time, it felt a lot more like an acid trip
than usual. It felt like I discovered another set of "eyes" somewhere just
above my real eyes, and that these eyes were looking out at a different
reality. Once I straightened that out in my mind, I could switch back and
forth!
When I switched to the new reality, I remember at one point being confused
as to which was actually my original reality. I couldn't remember whether I
was sitting at home or standing in this long hallway. that's about all I
can remember tho. =(
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Derf (male, age 21). 420mg
I dunno if anyone has had similar experiences, but I started thinking ...
when I'm on a trip, I have a life in that reality. when the trip is over
and that reality disappears, that life must die, right? So... then I
started thinking about what if my life as I know it now is only a similar
sort of occurrence, then what will happen to me when this "trip" is over?
Hmm.... then I started thinking that it would be possible for me to be the
only person who is actually "real" in my reality, and that anyone and
everything else is just produced by my thoughts. This was a GREAT part of
the trip... I felt like I was a god. in fact... Later on I created a
reality for a small population of beings, then destroyed it... well, just
because I could. =)
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Derf (male, age 21). 420mg
Well, here goes my weekly DXM trip report! hehehehee... this one was
pretty boring.(420mg) it started getting good around 2:30am and I was
already REALLY tired, so I didn't get a lot of good visuals like I usually
do. Anyone else ever have this happen??? But the one cool thing that I
remember from last night was the conversation with my friends ducks. Yeah,
sounds odd... but these ducks convinced me that they were the keepers of
time or something to that effect, and that they could control time itself.
I remember chatting to these ducks at great length in my mind.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Derf (male, age 21). 420mg
Well, I had recently posted an article stating that my most recent DXM trip
was practically uneventful... I think I spoke too soon! Over the past few
days, I've slowly began to remember more and more of it! Now that I'm able
to recall a few strange new experiences, I'll try to describe them.
This is definitely a new feeling for me on a DXM trip... I remember at one
point I found myself living out one of my memories of when I was 5 years
old and staying at my grandparents house. I remember thinking I was
actually there again. I was outside on a bright, clear, summer day riding
my tricycle with a neighbor girl while my grandmother was watching me. This
was a really short memory, but it made me feel great being there again
since my grandmother died about 2 years after this. (I'm 21 now) for some
reason, I felt like the period of time while I was tripping was linked to
the time period of my memory... that's the only way I can describe what it
felt like immediately after living through the memory again.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
J. S. D. (male). 560mg
Hmmmm so far the max dosage I've taken has been 560mg (yesterday), and I
think I knew who I was . . but it got really strange. Having downed a
bottle of Formula 44, I put some Front 242 into my walkman (which I
listened to continually until dark when I switched to White Zombie) and
just took a long walk. As I walked down the trail near my house I began to
pace my walk to the beat of the song, snap my fingers, do little spins on
the road, none of which I normally don't do (no shit), but it just felt so
good to move. And when I think my trip was peaking I saw/felt something
invisible, yet incredibly large and fast, moving around me in the forest.
Very intense. So much more than an acid smurf, I felt as though it WAS the
forest, trying to contact me.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
D. M. (male). 600mg
I started my journey about 8pm. Finished the pills in a span of about 30
minutes. About 30-45 minutes later, I started feeling the familiar effects
of drowsiness. I decided that it would be best to get out and do something
before I fell asleep and wasted my time. It was about 9:00, so I went to
my favorite alternative club where there was an awesome "mind candy" band
called Mindseye playing. There weren't more than 20 people in the club
including the two bands that were playing. I just kicked back in a booth,
closed my eyes, and went on an internal trip that lasted at least 45
minutes, although it felt like hours.
I had a sensation of moving into a higher realm of thought. I was so
focused on the music that it became a part of my consciousness and my
being. Opening my eyes just became a letdown because it reminded me that I
was in reality. :) So I just closed them again and enjoyed the phosphenes
that were running rampant through my brain. The only part I didn't like
was the feeling of being in a Doom game without the monsters. I felt like
I was running through the corridors and riding the elevators. Oh, well.
Nobody promised that it would be COMPLETELY enjoyable.
Anyway, after the set, I went to the bar to order a Miller Lite. The
barkeep said that they didn't have Miller Lite. I asked for Coors Light.
He said he didn't have Coors Light. [blank stare with severely dilated
pupils] "What light beers do you have?" "Lite." "Lite?" "Lite." "Lemme
have that, then" "$1.50" ("Hey, great price", I thought) It was Miller
Lite. Oh, well. It felt like I was arguing for 30 minutes. Gawd, I hate
interacting with people in that condition.
I staggered back to my booth (at least it FELT like staggering ... it felt
REALLY weird to walk) and sipped my beer while watching the band take down
their equipment. They looked like a bunch of worker bees from my
perspective, and is was really interesting to watch. Drinking was an
unusual experience, too. It was like the first time I had ever drunk
anything. All my movements were very slow, methodical, and calculated.
After I finished my beer, I went down to a techno club I had been meaning
to visit. It was about midnight. I know that this is a big lapse in time.
I guess I wasted 2 1/2 hours in that bar listening to the jukebox and
watching the band. It was only 4 blocks, but the way my legs were moving,
it felt like I was walking stiff-legged the whole way. Fortunately, it was
a slow night on my city's version of Bourbon St., and I only passed about 5
people on the way.
The doorman was the next big hurdle. Actually, I managed to keep myself
fairly composed. He warned me that it was kinda slow, and I went into a
repeat of the beer discussion. "Slow?" "Slow." "Okay." (trying to avoid
giving myself away, even though my pupils filled my eyeballs) I handed him
the two bucks he asked for and walked in. I found an empty couch and
plopped down. It was heavily padded and had a low back. Perfect for
slouching. The DJ was playing a fantastic mix of techno and classic rock.
As the night wore on, she was playing almost constant techno. They have a
light show that is really something to be seen. The dance floor is
surrounded by mirrors that reflect the blue lights from the bar and make it
look like a cityscape from the year 2020. VERY impressive in my condition.
The only times I got up were to go to the john twice and to the bar once
for water. Walking got stranger and stranger. I think I was having
trouble keeping my balance, but I don't remember staggering. The worst
part was the feeling that I was choking on my uvula. My mouth felt dry,
and water wasn't helping. It must have been the anesthetic effects of DXM.
I stayed there for two hours in the same spot only moving the three times
I mentioned. I was still not bored, but I figured that since it was 2am,
it was about time to get home. This may have been a mistake. The
streetlights had started tracing, and the blinking lights were playing hell
on my perception.
In retrospect, I probably shouldn't have driven home, but I was broke, so a
cab was out of the question, and there was no way I could have sobered up.
I didn't feel drunk. It just felt like all my surroundings were foreign.
I paid extra-close attention to my driving, but still nearly jumped out of
my skin at the sight of police. I got home in one piece and fell asleep to
the mellow sounds of Pink Floyd's Ummagumma disc 2.
I woke up around 9:30am, fully alert. Checked my eyes. Fully dilated.
Made an excuse to get out of the house, wearing shades. Went to see a
movie with a friend, which was pretty fun. I was still feeling a bit
weird. The dark theater helped me relax. Got out of the movie and went
home. My eyes were normal by this time, although I still felt a little
strange. That feeling lasted until about 7pm. So the brunt of the trip
lasted about 12 hours and the after-effects lasted another 11. WOW!
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Anonymous (male). 600mg
I had just got home from work and decided to do DXM, so I took about 600mg
and went downstairs and turned on the radio to wait for it to begin. Well,
I guess what happened next is I fell asleep before I started tripping.
Boy, about 3-4 hours later I woke up from having the most incredible
dreams/hallucinations ever! The best part was that the dreams were under
my control {even the really funky ones}. While dreaming, I had started to
make my own, and have fun with the ~normal~ ones. They were very
imaginative, creative, and about the most visually clear dreams I have ever
had. And what is even better, the music on the radio, influenced my later
dreams so that the theme of the song was sometimes the visual side of the
dream I was having.
Well anyway, I later found out by experimenting, that if you choose songs
with good themes or stories in them you could almost live them while they
sang. I find that to be a very wonderful side of DXM, I can not wait until
next time.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
AN172244 (male, age 23, 82kg). 720mg (8.8mg/kg)
I felt heavily stoned. It was hard to track objects with my eyes, and I
often had double vision. Objects looked far away, but not out of
proportion (e.g. the small TV a few feet away looked like a HUGE TV many
feet away). Walking was difficult-I felt like a robot. I had preloaded my
5 disc changer (Pink Floyd Animals, Dark Side, Beethoven Sym #9,
Shostakovich #5, and Electric Ladyland). Laid on my couch w/ a good pair
of headphones, and only the light of the Xmas tree, and entered another
world. The music totally pulled me in, I could no longer feel my body or
the headphones, I felt like I was in some strange video game, flying over
computer generated terrain. I often felt like I was in a huge concert hall
listening to the music come from all around me. I was always in control,
though. If I opened my eyes I could return to 'reality'. Incredible!!
(side note: I _highly_ recommend the Shostakovich #5 for DXM trips. The
music has a real dramatic Russian flair, and is alternately dreamy and very
intense. Being a 'modern' classical piece, it is strange enough to sound
like it is from another world when on DXM. The Bernstein recording of it
should be less than 10 bucks.)
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
S. T. (male, age 28, 110kg). 960mg (8.7mg/kg) + cannabis
Starts real mellow. A body warming. Slightly drunk and dizzy. In a very
good way. A "boozy" drunken feeling it is not, maybe like Seconal. A
definite "in the body" thing. Started cutting corners close, bumping into
walls. Distortions in my spatial perception. Sight slightly blurry.
Impossible for me to read small print. Underlying calmness.
Music is much more enjoyable. A kind of craving for louder and harder
beats. Enjoying the textures of the tape hiss between tracks.
Strange disjointed thought process. Underlying calmness. Full warping of
subspace. Pin Head with expansive arms/legs. Incredible head size. Warping
and folding of body. Incredible spatial distortions.
Had to lie down on bed with no light. Wind was howling but I was calm.
Continued spatial and mental distortions, but with a calmness telling me
the trip was going to be okay. Never "totally" lost it like with LSD.
Underlying calmness throughout entire trip which is unlike LSD for me. LSD
tends to be a "speedy", tense kind of trip for me. Hard for me to ride an
LSD trip because of the tenseness.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
P. L. (male) Unspecified dosage of DXM
(I don't usually include unspecified dosage trip descriptions, but P. L.
writes exceptionally well, and I think this particular piece may capture
the essence of a high second plateau trip better than anything else I've
yet found. Though probably written after the trip itself, the form of his
writing is in many ways characteristic of the thought processes of a DXM
trip. Enjoy!)
Hello friends. Yesterday I was feeling a touch lethargic. I had woken up
only around 2pm and generally felt like a lazy bum. I messed around for a
while on the computer, reading email and news. Well not really a while
because I emerged from a semi-comatose state at around 6 PM. I decided
shutting the computer off would be the wise thing to do at that point so
that is what happened as it were.
Grabbing a bit or 10 from the cafeteria, I pondered the slogan of Jester
cafeteria: "What you Don't Know Can't Hurt You." I didn't know what I was
eating but so it didn't hurt me unless you count starch overload and
gaseous pain as bad, which I don't. Upon returning to my room I arrived.
The roommate of mine, Mr. James was entirely present at once giving
studying a go of it.
"James, I lamented," I said at the time, "Studying on a Saturday night?"
"Yeh," he said. Noting that he did not say "Yeah" but more of a "Yeh" with
a long uuuh sound. I seated myself on the seat infrontwise of the computer
and flicky the switch that turney it on. Reading news and mail for even
more longer periods of time I morosed at my situation again. Spotting the
presence of many drixoral cough caps in my desk drawer I suddenly developed
a rather severe cough requiring immedietly medical attendonitis.
Writing myself a perspiration is wont to help being the situation as it
pleased me so, I consumfed the pills regularly quick. Putting clothes on
(nekkid was I this whole time) rendered me fully clothed and I discovered
that my ears were detecting strains of bizarre religious Korean music
wafting from a box adorning Mr. James' desk. "Thinking this won't do," I
said quietly determined to find my own tunes. I put on the headphones and
started to play the Musak of all. Quickly finding the bright light
unappealing, and noticing I was on the higher floor of the dorm, I elected
to faraway to a more pastoral clime.
Gathering my belongs into a green bag that materialized in my paws, I
forgot to include a wonderfully handy Mini-Mag lite that would have solved
woeful problems I encountered later in the evening. Note the clever use of
foreshadowing in the previous passage. I included amongst these materials
a Walk-man and tapes of various important American rock-and-roll bands the
devil's music as it were. Also was cigarettes and the important useful
lighter, black in color. I considered flooding my guitar into my pocket
and percolating that too, but the accoustics were suffering as a result of
the stuffage so I left saying, "Good-bye, Mr. James! I will see you
later."
Shaky swagger down the hall stopping to release bladderfuls of concerns
into porcelain. My heart was heavy and my eyes were dim as I realized it
was almost 45 minutes since ingesting the ahem medicine and the
effectingness were starting to notice upon me. I stepped outside into the
lovely cool air noting the temperature was neither hot nor cold. It seemed
to me to be like one of the oft-remembered nights-on-the-town of Incline
yore.
I stooped beneath an old oak tree adorning the lawn at the corner of East
21st Street, Austin Texas 78705-9005 postal code and the nearby adjacent
San Jacinto street. I smoked a filthy cancer stick noting that the taste
was unusually pleasantly remindful of smoking past with the combination of
the evil grass leaf, cannabis sativa. You see, I usually smoked Camel
Special Lights (TM) (R) along with the bad mary jee-wana and the taste is
remindful as I was smoking the selfsame ciggies last night. The music was
continually playing note after note in my left and right ear, being the
Dead (who are ironically alive) playing a lovely China Cat Sunflower -> I
Know You Rider which is lovely. The notes started to close my eyes and I
rode along the golden crest of waves.
Simply sitting under the tree was the time first of all that I realized
that the miniature Mag-lite would have been useful to sort my assortment of
un-sorted musical tapes. As it was dark. I decided to move myself closer
to the light-source illuminating and perched high humpty-dumpty style on a
wall of sorts nearto and overlooking the street aforementioned. Many
people passed nearby (but never touching) as this was a busy sort of street
near many dorms including the one in which I lived. I looked at the popel
but touching was not done. Bored getting was I though I had only barely
begin to tripppp out.
In the U of T, A there is a feature architechtually or landscaping-known in
some circles considered to be a South Mall to which I decided to rest my
bones. In front of the largest Penis in the Sated of Texas is a large Lawn
named the South Mall. At the North End of the South Lawn is a statuesque
of Jefferson who is also holding a dildo in his left hand (this is true.)
Across the lawn is clearly visible the State Capitol of Texas forming a
large line across the city of Austin, Tekas. Walking wise the mile or less
to this site seemed to take a longishly short amount of time as my feet
moved very very fast it seemed. I knew at this point that the effects of
my uh cough medication were takingly effects. I found the South Mall where
I left it from Last Time which was friday. I walked across the ocean of
green (though sort of blue in the flourescent and moonlight) grass to the
exact center of the lawn. I was now part of the line betweenwixt the afro
mentioned objects. Laying on the underside of of my back I noticed the
milky way gladcy was lining up to me too.
My rain falls like crazy fingers. I straighting out my possesions
including the hat atop my head blocking my access to the ground. If not
for hair, we would all be bald so be thankful. Many times when you are
thinking about the Earthy you picture your place being that one of a flat
area plane. Rarely is it an enticing thought to actually see yourself in a
round sphere at the apex. Well my friends at this point in the Tale I will
draw a diagram:
/^\
ooooooo
(ooooooooo)
/ooooooooooo\
(ooooooooooooo)>-|o <- [Fig. 2: "Me"] *
\ooooooooooo/ |
(ooooooooo) [Fig. 3: "Nearest Star"]
ooooooo
\,/
[Fig. 1: "The Earth"]
In other words I was sitting at the very nearest point of the Eard to the
point in space I was looking straight up at. Believe me it took a long
time to draw that stupid Earth Fig 1. I don't even know what figs have to
do with it.
I thought of Sumner also at that instant, though , "This was all one song?! I thought it was, well," more
songs, I said. I lookie at all the peeplies walking aboust on a proustly
Saturday night. Many of them are perhaps wondering to themselves as, "Who
is this guy on the grass anywhays," or "Damn, my last joint," or perhaps
as, "I wonder if that guy on the grass has a really bad cough or
something?" But the answer was for none to see.
Rather surprising at once point was when a guy walking merrily about his
way down the bath suddenly stooped and did a cartwheel. As this person was
now spinning about a purple axis, I wondered, "Did my eyes just decieve me
or did that person suddenist spin around a pooply axis, bold as love?" Such
recriminations were nost in order though as I heard "Dancing in the
Streets" and "Morning Dew" in the next order. I had by now rolled around
considerably on the grass and perplexing the poor stuff. It felt rather
soft and nice to my trippy hands. Finally I took out my Dead 5/2/70h.
Wondering abits with nothing to do, I feeled the need to urinate again
(After all I had drank quite a bit of liquids in revealing the drixorals to
my stomach) so headed to the nearest Building. Which happened to be the
Undergrad Library, which happened to be closed. I proceeded to the NEXT
building, which was the infamous Student Union upon entering. Mostly it
was closed as well but some areas of the large structurly were open for
business of any ports. Finding it very berry difficult to walk at this
time, I turned off my headphones. It seems that the bassline of "All You
Need Is Love" was effecting the movements of my feet in such a way that
made walking impossible. The walls were beginning to melt and Greg Brady
was emerging from the woodwork in a way that I Wish he wouldn't. Feeling
OK Soda for the moment though, I thought about Where I found a Bathroom on
my Summer Vacation. Near the bowling alley.
Bowling Alley?! No bowling alley in a Student Union, were there? Sure
enough there was and it was quite packed with younders enjoying all sorts
of sports infolving throwing heavy balls at white pins. Luckily for me the
balls of all sorts were evading my head and extremities, but Not for Long!
I wondered how could that last after all I Was standing in the "alley" as
they termed it for throwing the balls at the pins. "Cries of," hey what's
that moron thinks he's doing, and Get out of the way, dummy! "Accompanied
my fusilade.he ralleying
cry.
Surely my eyes aren't decieving me, but I swore this girlie that I knew
from way back on the Island walks by and says, "Hallo" as she is want to
do. Me as I was fiddeling with stuff didn't realized it until after the
time, Butt I said "Hallo" anyway. Who knew? Maybe next year I will get a
right hook too. Walking down Guadalouppe (the Drag) why a drag it was,
too. I found myself in the West Mall this time, which is different from
the South Mall in that it plays to the West rather than Southerly, and
there is little to know grass here. Turn that damn guitar down! Well I
float in liquid gardens and Arizona's new red sands. I sat to recoup and
gain my senses and possibly replace the tape I am playtch to find out the answer to this
lovely question. It seems the watch face has melted onto my wrist. It is
therefore impossible to find out the time, but fortunately the U of T, A is
equipped with an extra-large Penis as noted before. This Penis chimes out
the hour every hour on the hour. I found it to be by now 12 midnightly by
my reckoning.
I found my way back to the South Mall and gave the damn grass a once-more
going over to find my lighter. No luck so I lay down on the grass. My
body quite literally melts into the earth, leaving the essence of my soul
clinging to the ground like a vapor. However, perhaps the source of this
disturbance can be found. You see I cannot verily go to French class on
Monday if my body has melted into the Earth, can I now? The musak goes out
of Space (for those of ye who don't know, a very bizarre sound-effects
weird thing done at Dead shows) and into a song, "The Other One." The
guitar notes emerging from Space into Other One is the life-force that
slowly ebbs back into my body. It rises from the ground, engulfs my body,
and I rise from the Dead so to speak.
I was very pleased that my soul found a home again, because I had a paper
due in English coming up and it's hard to type if your soul's body has
melted into the ground. I decide now would be a good time to return
sightly home again. I make my way back to the lovely Moore-Hill dorm (my
home). Smoking (en francais, fumar) is verboten dans el Universitudo, so
you have to smoke your dagga outside. I cleft a ciggie to my lips and
learn again that I have no light. Damn! However, there is a studnut run
radio station in the next building. some nasty hippie kids are standing by
the door smoking, so I figure how can I get a light from them? Being near
them would be a good start. I try to be near them but they have
disappered. They are gone. I go back to my corner of the universe, and
sure enough there they are again. I am a...............
Negative Experiences
Anonymous (male, 73kg). 135mg (1.85mg/kg)
(This experience is atypical for such a low dose, and I believe that this
unfortunate individual lacked the normal P450-2D6 enzyme. As a
consequence, the duration and strength of the trip were much greater than
usual, and very little of the DXM was converted into DXO. Thus, this may
be a good example of the effects of a sigma agonist with little or no NMDA
activity.)
It began OK about 40 minutes after taking the Robo, but without any
especially interesting effects. I began to feel very relaxed and warm,
almost feverish (although without a real fever). Talking tookI began to hallucinate in a completely boring way: I began
to see what seemed like many parallel streams of type, in a variety of
typefaces, sizes, and colors, emerging simultaneously from a multitude of
invisible sources. Most of the time they didn't seem to make any sense,
but sometimes I felt that there was a message in them that I should
understand. Later I could see, in brief flashes, brightly colored
cartoon-like moving faces and what seemed to be animated billboards or TV
commercials. Sometimes the streams of type would be replaced by streams of
musical notes on multiple musical staves, all in color (but without any
accompanying sound). The waves of nausea and fever also continued, though
more widely spaced and less severe.
All this I found very tiresome, though not frightening: I just wanted it
to go away so I could rest. I tried listening to the radio. Music was
impossible to take, but talk radio seemed to give me some distraction from
the hallucinations (even when I couldn't focus on the conversations).
Finally at about midnight it began to fade away. I dozed off several times
over the next 5 hours, once for as long as an hour; the first couple of
times, when I awoke, I had some trouble telling where I was.
All the next day I felt weak and nauseated, but my emotional disposition
was even better than usual (go figure!). I had to force myself to eat. By
9 PM that night (i.e., about 27 hours after the dose of DXM) I was feeling
about normal again, though nausea still came and went over the next 12
hours.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
A. L. (male, 68kg). 150mg (2.2mg/kg)
What I bought was a 10 pack of Contac CoughCaps, 30 mg per capsule. I read
the box over carefully and the instructions said that the product containeed off until five
minutes before the show. I swear we were standing in a hot, crowded, and
loud room for a day at least. (actual duration of the wait was about 45
minutes) This was when it really kicked in - not a good place to get very
high very quickly. I felt like I was PISSED OUT OF MY TREE. I started to
get really hot and I wanted to take off my jacket but I couldn't because I
was smuggling a couple bottles of pop in. I was getting dangerously close
to bugging out but managed to control it without too much difficulty. I
think I felt like bugging out because it was simply a new experience. I'd
never dosed on it before and the effects hit me far more quickly and
strongly than I had expected; based on the FAQ. I'm pretty experienced and
careful when it comes to drugs so that wasn't a factor in being unprepared.
Anyway, the staff moved the ropes and every stampeded to get into the
fucking theater. I felt like slammin' people. 8) Once we got a good seat
anoticed this when I got home. I never noticed any itching at all and had
only a mild cramp in one leg after the trip. I think another LactAid pill
would have been helpful. I felt great coming down; really smooth and
gradual compared to the initial shock. Had some great sex afterwards and
felt great in the morning.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
W. A. (male, age 19, 110kg). 150mg (1.4mg/kg)
An entire 100ml bottle of 15mg/10ml DM was ingested, in about the same
timeframe as the first experience. There was no pseudoephedrine (or any
other active ingredients) in the preparation - just DM, and I believe a bit
of alcohol, tho at the dose taken, I don't believe this altered the
experience any. The same friend who had tried it with me the first time,
also ingested it. (same amount as I used)
The effects came on in a similar fashion to the ones stated above, only the
drunkenness became much worse, as did the disassociated feeling (as if my
mind was separated from my body and the surrounding physical world).
Friend's condition appeared to be the same, perhaps a bit more intense.
The motion-perception became very very unusual, it really did feel as if I
were gliding smoothly along (like a slug), or hovering, when I walked.
For awhile this was interesting, we spent what felt like perhaps an hour in
subjective time (I'm not sure how much time actually passed) playing in a
park with all sorts of stone structures & fountains and waterfalls, and
twisting pathways, trees, and a big pond. (I love that place. Whoever
designed it had psychedelic users in mind ;) It was night-time.
Eventually the effects (especially the slowed down, drunken feeling)
started getting really intense, and we decided it would be best to return
to the apartment. Again, there were no significant visual or audio
hallucinations. There were some slight visual effects, similar to those
experienced on pot or hash. My thoughts still felt fairly clear and lucid,
although there was a very odd feeling, again it sorth times, so this may have delayed the start of
the effects. Perhaps there was a little bit left in my system from the day
before.
I was sitting down, doing some reading, and nothing happened for well over
an hour or maybe two hours. Then, all of the sudden, I got a severe heat
flash. It felt like a sick wave flowing over my entire body. I could even
feel a strong buzzing (almost like pain) in the roots of my teeth. Every
inch of skin on my body felt like it was next to a hot water bottle. I was
very light headed and thought I was going to die. I quickly scribbled
information on a piece of paper to tell anyone that found me what I had
taken. The heat flash went away after what seemed like 5 or 10 minutes.
Actually it was probably only a minute or two. I felt my forehead and it
was dripping with sweat.
I was OK for a while after that. I talked with a friend for about 10 or 15
minutes, but it seemed like hours. Again, I was very talkative. I felt
like I was making sense, and having an enjoyable time. I just felt spacy.
Tly frustrated because I knew I wanted to find a number to call to get
help, but all I could do was flip the pages. I couldn't figure out exactly
what to look up. Finally, I looked inside the front cover. 911 seemed a
little drastic. The only other number was poison control. After several
attempts, I finally dialed the number successfully. The problem was that I
couldn't remember which digit I had just dialed or which one to dial next.
I was quite incoherent on the phone, and had a lot of difficulty giving my
address, phone number, etc. The lady told me that I had taken quite a lot,
and that I should have someone take me to a hospital. I asked what might
happen to me if I didn't go, and she said that I possibly could go into a
coma and/or stop breathing. This scared me enough that I decided I needed
to go in.
I found a friend that was willing to take me in. Thank goodness for
friends. In the Emergency Room, I experienced several more heat flashes.
My heart rate was up to almost 120 beats per minute when I was at my
calmest point. They pumped my stomach and put activated charcoal down me
to absorb any remaining DM. That is an experience well worth avoiding! I
even preferred the blood and urine tests to the gastric lavage.
Masted for another day.
Three days later, I took half of an imipramine (a prescription
antidepressant left over from a legitimate prescription) because my head
felt a little foggy. A few hours later, I got a miniature heat flash, and
felt a little spacy. That never happened before when I was on these
antidepressants.
All in all, I think it was a VERY bad experience! Sure there were a few
weird effects, but the negatives far outweighed the positives. The dose I
took was significantly lower than what some people claim to have taken.
I'm just glad I didn't chug the whole bottle at once. Perhaps some
people's bodies can handle DM better than mine, but I have also noticed a
large increase in people telling about bad experiences with it.
I don't think it's a very good idea to take a chance with DM. But, if you
do, please start with lower doses, let a few days pass between doses, and
increase the doses gradually. Not like me where I took twice as much as
the time before. As for me, I don't thin days.
My friend did not like the experience and said that he would probably not
try DM again. Despite his stroke, my friend is a normal, intelligent guy
who does not seem prone to "bad" trips. He enjoys mushrooms and marijuana.
Neither of these drugs produce any activity in his blind spot, nor do they
have the de-personalizing effect of DM.
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
Anonymous 360mg
Let me provide my testimonial about roboing. Yesterday I picked up an 8
oz. bottle of generic brand extra-strength cough syrup, containing only
Dextro as its active ingredient. I immediately downed somewhere under 4
oz. of the stuff. Taste wasn't as bad as I expected. Chugged a good deal of
water to wash it down anyway, and nibbled on some bread. Nausea was not a
problem at all.
About an hour later it started to hit. Motor skills were definitely
impaired. Pupils were very large. I felt like I was on shrooms, but without
mood-alterations or significant visuals. Television images appeared to be
moving in slow motion like when on acid. Unlike what I've heard posted
here, music did not sound very interesting. This was a big disappointment
since claims to the contrary were what convinced me to give it .
0830: Took Drixoral (300 mg.)
0930: No effects, took Tussin (240 mg.)
1000: Difficulty walking without noticeable effects (but I think I was able
to.) Not unlike mild alcohol inebriation.
1030: Everything kicks in. (I think the caps took a while to dissolve).
Only severe motor control difficulties and a general loss of tactile
sensation. Lay down.
At this point I spent the next 3 hours lying in bed, not out of necessity,
I just didn't feel like moving. I alternated between eyes-open and
eyes-closed 'images'. Not acid-like hallucinations, more like visions.
Static, unchanging (as opposed to 'melting' or 'swirling') images. I
distinctly remember three: The bedspread looked like a far-off mountain
range; my leg looked like it was hundreds of feet long, and I remember the
peculiar feeling of rotating in a plane in both directions at once (like
alcohol 'spins') with no feeling of nausea. This was accompanied by the
inexplicable visual equivalent (of spinning both ways at once). There was
a period when I was beset by words rather than images. At some point I
crawled across the room and pet the cat. I boria. He started feeling his first
effects around 8:30, noting "definite rubber-body sensations." Half an hour
later, after a loud clap of (real) thunder "scared the living crap out of"
him, he noticed a surging, vibrating sensation in his muscles, and a
general body speediness. The effects were mostly physical at this point.
9:15: "Hey, what is this? I just coughed."
Perceptive effects started to become apparent. Music seemed to be less
ambient, more "attached" to the speakers; the room no longer contained
music as a whole but two units of music. He took a few more swigs from his
second bottle of cough syrup as he noticed his 3D perception deteriorating.
By 9:30 he was enjoying simply walking around. "I'm doing the grandfather
walk and waddling."
9:35: He finished the second bottle, for a total DXM dose of 700 mg.
Sometime around here his clothes felt uncomfortably warm, moist, and
sticky, and he changed into a T-shirt and shorts. Mental effects were
strong now; he began to write more, though writing itself was more
difficult since he was losing physical coordination.
"I feel really 'stoned' now, and it's always strange to see such facticity
as a toilet in this state."
The ambiance of music continued to diminish:
"Music really went away into its own sucking holes. It doesn't escape far
out into the room before it falls to the ground."
At 9:45 he went to the door to see if his cat wanted something I'd done today must have done
it. It was just toothpaste splatter. Flying toothpaste particles mixed with
water and being shot through the air by the toothbrush bristles."
In the next few minutes, the trip took on a different character. He became
physically inactive, lying down on the floor, and external events seemed to
matter less and less. Though music was still playing, he was barely
conscious of it. At around 10:20, he began to experience a fairly deep
dissociative effect, becoming a "free-floating 'I'," his body sinking back
into an indifferent realm of matter and flesh.
This free-floating "I" was unique in that, though it was definitely an "I",
it also lacked all subjectivity. He experienced this deeply, but feels it
isa day. Not
26 years. That is incomprehensible. Strange- work on the body for 26 years,
etc., - where is it? what is it?"
He then turned to other things. He developed a slight fear that a cop would
begin pounding on his door- he felt that his altered state was diffusing
through the walls of his apartment and into the outside world, where it
would surely attract attention.
By 11:15, he was noticing the physical again. His balance was severely
disrupted, and his visual field seemed to update with smearing
sluggishness. He sensed his mouth and teeth as a unit; he could no longer
discern anything but a unit when he moved his tongue around inside his
mouth. He felt a strange sensation he called "swimcap head."
The trip still seemed to be on the upswing. He wrote in short bursts-
"intense trip- extreme," "SEVERE loss of balance," "don't know if these
words are getting to paper," "just seems to keep increasing in intensity,
intensity."
He felt giddy and exuberant, but nonetheless wrote: "Anxiety: This is where
I live NOW! it's an apartment! People will see me living in it! Reminds me
of life, like a [illegible]." He can't remember what was going through his
head while he wrote this.
At 11:50 he noticed that his pupils were greatly dilated, and his eyes
seemed bugged out, making his appearance very strange and disturbing; later
he found that he would also unknowingly raise his eyebrows whenever he
looked in the miry night, the gelcaps, 600 mg. Took 'em at
8:30 with a friend, walked around till about 11:00, neither of us was
feeling anything and I was *most* disappointed. I caught a train back to my
house, and in the station waiting to change trains it started to hit