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. -----BEGIN PGP PUBLIC KEY BLOCK----- Version: 2.6.2 mQCNAi1lhpkAAAEEALzR0vS+W7qdMjQJz0Lc+TQm86HMpHu1ZEGDtGHcZShBy/tB xoDueEe7vy0nPJpvrfoEUjp8KhR55/Eb1i27CCTP47+5IvJNlV+1D0xrnaX6gSWr OVPjz/rLOvi8BHQxu7XNQ1BfUaaV0CPs8McPSUyeEqzNNadKouCp8NBoN4HlAAUR tC5XaWxsaWFtIEUuIFdoaXRlIDxid2hpdGVAb3Vjc2FjZS5jcy5vaGlvdS5lZHU+ =qyt4 -----END PGP PUBLIC KEY BLOCK----- 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 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 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 ) 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 *hard*. I was hanging out alone in the station, hacky-sacking, and the walls started to bend to greet me. By the time I got to my local station, things were getting pretty intense. I *floated* home, as far as I could tell at the time. Two hours later I was hanging out with a bunch of friends, one of whom was also on. I was warm, I was fuzzy, I loved everyone, and I was directly aware of being a higher being making its temporary abode in this body and this mind. Oh; and I *itched* like nobody's business. Anyone else had this? I forgot a lot of things on my way down, but based on what I did bring back I think that the forgetting was because the normal ego-bound me couldn't have understood too much of what was happening. I realize I'm waiting to digest it well before I start. Topical antihistamine spray sits nearby in case of itching. [Note: I never used it.] Setting: Apartment is lit subtly by overhead lights on dimmer switch. Music is playing - radio now. Selected tapes + CDs are laid out for later on. [Note: I never got to them.] I have chosen strongly thematic themes as suggested, while avoiding anything that might be a 'downer'. There is also some lighter, mood-lifting stuff like pop + techno. I cleaned the apartment today to make things seem more cheerful. [Note: I don't think it made a difference. A book of ancient Chinese philosophical verse...] sits before me to read while waiting for the onset - only because I find it comforting and familiar. Set: I began 'psyching' myself up yesterday. I feel confident and fairly at ease. Also curious. Curiosity, I think, is my main reason for doing this. Perhaps I'll even learn something about myself? I don't know. [Note: I still don't.] The journal goes on to note the circumstances of the ingestion of the caps. I note that I found it both physically and psychologically easier to down them than I expected, though there was a transient problem with gas (which I eventually dealt with by taking the caps with milk). To keep my mood up I sang with the radio and read. It took from 5:55 to 6:46 to down them all (with a few long pauses to burp up gas and let md against the night sky. Yet they seem somehow absurd in proportion, like children's toys blown up to gratuitous scale. Stars were clear and bright. Reaching the pond, I gazed out across the water at the surrounding city scape. I noticed the first 'tracing' effects. As I swept my gaze from left to right or vice versa, the lights would pan not continuously, but in blocks - about four blocks per 120 degree sweep. A mildly unpleasant phenomenon, and one which was to last the length of the trip. It was as if my brain were no longer able to keep up with the sudden changes in scene causes by rapidly moving my eyes or head. I stayed at the pond only minutes. On the way back, I was feeling fairly good. I was substantially stoned. I wasn't really euphoric, just upbeat and at peace. Everything seemed exceptionally clear and still, as though viewed through a layer of deep, limpid water. Contrasts seemed much starker. I briefly lost track of where I was a time or two but quickly reoriented myself and proceeded home. Arriving at my apartment, I made the following journal entry in rather scrawling letters: I have returned. I visited the pond several blocks away. Dark, with city lights shining about. [No duh. No-one ever accused DXM of improving mental acuity.] Noticed tracing effects. Immediately following two or three thoughts were started and aborted in succession: Profoundly everything seemed dar [This line is crossed out.] Jy - spectacular, bioluminescent, massy things that churned like thick, boiling, liquid. They came in various colors - white, black, dark blue, and purple, mainly. Some were like churning walls of gel. Some were like complex blobs, jellyfish, or worms with thousands of pseudopodia. All were constantly writhing and huge. I could sense they were intelligent. I seemed to be an interesting specimen to them. They approached freely. Some of them picked me up and passed me around. But I never felt as if I were in danger. These things seemed not only friendly, but affectionate. I felt affectionate toward them as well. Their appearances were not monstrous so much as stunningly beautiful. I was in awe, really. "Glorious" was the word that came to mind at the time. One by one, an 'entity' would come over and 'play' with me, like a child with a new toy. They would touch me, sensing my thoughts. There were immensely powerful yet gentle. It was somehow very pleasurable. Each entity had it'my double vision, I could see how incredibly screwed up all proportions were. I felt like a big insect. My body seemed proportioned vaguely like some kind of praying mantis in human skin. And yet it was all so consistent. Proportions were screwed up in a very stable manner. I could look at something, look back, and it would look the same. Distances seemed exaggerated and contrasts were abnormally sharp. Outlines, while similarly sharpened, were made up of more than just one line (probably due to my double vision). This gave the illusion that I could see a little more of the sides of an object than would be normally visible. It was a little like looking through everything through the wrong end of a misaligned pair of binoculars. I thought of it as "insect vision". My steps were short and slow. I shuffled to the bathroom automaton-like and took a wizz. Then I emerged to make my journal entry, in childish, blocky letters. The M's in "mother", "human", and "almost" have 3 humps instead of two. I could really barely see what I was writing, and couldn't be sure it would be readable the next day. 10:51. I LOVE THE GREAT QUEEN MOTHER. ACCCPT [= "accept"] THE LOVE I OFFER. I OFFER ALL MY HUMAN LOVE. [Such was my song.] THIS IS MOST INTERESTING. [Referring to my 'insect vision'.] ALMOST CUBIST! Things were getting more 'rigid' somehow. My thinking and movement were both very stiltn, then went back to bed to catch some sleep, praying that my vision and movement would be back to normal when I awoke. As I waited for sleep, I watched some entertaining hallucinations. One was like sliding down a tunnel of molten bronze. Another was like gliding over a weird, undersea city. Occasionally something playing on the radio seemed particularly stirring, especially if it had heavy electric guitar riffs, but that's as close as I ever came to DXM music euphoria. Then I slept. My next journal entry says, in almost normal looking cursive: 2:33. Wake up. Dread to open eyes proves unfounded when I look at clock and see double vision is gone. I had actually been awake for 15 minutes or more, but had dreaded to open my eyes and see two of that damn LED clock. My heart had been beating rapidly as if in anxiety. Getting up to make that entry, proportions seemed normal again and I felt much more human (though not entirely back to normal). It was quite a relief. I relaxed and realized I'd be O.K.. I took another wizz, went back to bed, and said my good-byes to the Queen Mother and her brood (yes, really). They were forming into a sort of fleet and preparing to fly away. It was rather touching in it's way, though of course utterly insane. The Q.M. understood that I had to return to the human world, and bid me farewell. I promised to remember her. My next (and last) entry: 2:55. The Queen Mother has departed. I have pn and her brood. What did they represent? Fragments of my own psyche? The fevered attempts of a stoned brain to codify sensory data and enhanced emotional states it no longer comprehended? I don't know (though offhand I would consider the latter explanation more likely). My sober thoughts about this experience are on the whole positive. There were only a few slightly scary or disconcerting moments. I'm not sorry I did it, but I have no real desire to do it again anytime soon, nor would I urge others to try it. Curiosity was my main motivation, and my curiosity has been satisfied. Moreover, the experience was overpowering in a way - too much so to be repeated lightly. I can see how had it turned out badly, it could t nothing. I then moved myself closer to the stereo. There I fell backward (not far since I had crawled) and became, sorry for the blasphemy, Jesus himself. I was on the cross and floating up toward heaven. I passed through clouds as the music lifted me up. I believe Pink Floyd's COMFORTABLY NUMB had just begun... Anyway, I saw god and many people behind him (prophets I assume). I really did not know where I was or how fast time was moving. Again I stress that closed eyes make the trip MUCH more visual. Not once did I feel like I was overdosing, it was beautiful... Then I became, brace yourself, 3 different people. I truly believed that I was 3 separate entities and each one was communicating with the others. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . J. W. (male). 900mg Well, I dosed 900mg this morning at 8:00 am and was done by 1:00pm. Anyhow, the stuff hit me REALLY hard ( I did it on an empty stomach :) ) and I ralfed three times. Oh well. I wrapped myself in a blanket for like 2 hours because I was FREEZING. I felt like I was naked at the north pole, man. You know how the outdoors look when the sun goes under a cloud ( the light level increases and decreases, etc. )? Well I've experienced that every time I dose DXM. Way phat. Anyhow, I also made a trippy phone call to my friend, told him some dude was experimenting on my brother (who was 70 . . . . . . . . . . . . . . . . . . . . . . . . . D. P. (male). 900mg I went down to the lake one Saturday morning and took a few boxes of Drixoral cough liqui-caps. Invited some friends along, but nobody could come with me, so I took ALL the little motherfuckers. I walked along the side of the lake for a few miles, not feeling any major effects yet. Then, suddenly, it hit. I felt very dizzy, and very out of place. I couldn't walk so I sat down on a park bench. It was foreign... here I was on a park bench in some strange place, with everything spinning around me. Cars hissed by on lake shore drive, seem like some kind of deadly monster, or dangerous presence. I was very confused & decided to walk back. It was hard to walk when everything was twisting in strange directions, but I made it all the way down to where there was a tree in the sand. (I'm not sure if there really WAS a tree there, but at the time there seemed to be). Walked down to the tree and collapsed beneath it. Looking at the sky thru its bnormal. later that night there were some kind of weak residual visuals (fireworks)... who knows? Maybe I still AM on that rock... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . P. L. (male). 900mg; friend (male), 600mg Around 9 PM I took 30 drixorals, around 900 mg. My friend, T, took 20, which is 600 mg. I was experienced, he was not. 9:30: The power goes off! It's a really intense thunderstorm, even for Texas. The lights (and my computer, which was playing Acid Warp) shut down. My sister calls T and I into her room to watch the thunderstorm. I start to realize I am a bit fucked up (like stoned on pot.) 10:00 T and I retire to my room again. Am I tripping now. I leave the window open so I can watch the beautiful lightning... let me tell you that is a trip on any drug! I have a perfect little tripping environment set up. My friend T is visiting me from out of town, and he is sleeping in my bed. I am laying on a few blankets on the floor. I have a CD player, a stack of Hendrix, Beatles, and THE GRATEFUL DEAD (emphasis to show that this is the all-time great tripping band) and a really good set of headphones. Also I have a journal and a few pens. I decide to start writing down random thoughts. After checking to see if T is tripping or not (he isn't) I turn out the light and put in Jimi Hendrix's Electric Ladyland. Oh my god. If any of you aren't experienced with this album, GET IT. It's availible on a CD reissue with good liner notes. By the time the actual song "Electric Ladyland" came on, I was on the upswing of my trip. Since I was on a rather large amount of DXM, let me tell you I was flying. Literally. I closed my eyes and entered a new universe of Jimi. I started on a tall cliff overlooking a craggy valley. The sky was a deep purple. I took a single step off the cliff and dropped many hundreds of feet. Eventually my fall turned into a gentle swn entirely new, and pleasant, thing for him. He was listening to a "trip mix" that I had crafted for him of a lot of Grateful Dead and Beatles. I opened my journal and scrawled (it's hard to write on DXM) something to the effect of describing what had just happened. Then I went back into the dream. I finished exploring 1983 (the ocean) and listening to the rest of Electric Ladyland. Of course a lot of stuff "happened" in between that but I won't cover it here. I put in the White Album by the Beatles and affirmed the reasons why I have listened to them for so many years. The White Album is another must-have, BTW. It seems to fit roboing so well, because it is at times harsh and at others gentle. The imagery of the lyrics and music are conducive to tripping. I guess this is why it's considered Psychedelic... Dear Prudence is a fantastic song. Later I listened to Europe '72 by the Dead. Like the images of the Beatles from A Hard Day's Night, the Dead have a very carefree fun image in my mind. In other words they are a bunch of guys (and gals if you include Donna) that you would just want to hang around with. Well, that's what I did. :) DuThen I buggged out. 8) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anonymous 1100mg We had just gotten back from a football game, and we decided to stop at the drug store on the way home for some tussin. I was with 3 friends, Joe, Eli, and Matt. We got back to my house, and me and Joe started drinking. Eli just wanted to smoke, so I hooked him up on my vaporizer. Matt is a straight edge, so he just sat watching us. I finished off 12 oz, and Joe had about 6. He's much less tolerant than me, so that put as at the same level. I noticed the effects in 30 min. I have discovered, that unlike most other drugs, DXM comes on quicker if my stomach is full. NO idea why this happens. I started to feel very drunk. Joe has described the initial effects of DXM "I feel like I'm so drunk, that if I had drunken alcohol, I'd be dead". I was quite dizzy, and the room was spinning slightly. Getting up and moving around was initially an effort, but it also felt GREAT. I had a great urge to dance to techno music. We decided to go take a walk around and have a cigarette. We got up, and walked out, with incidentally, my parents and younger sister all home and awake at the time. We got back and I felt that I was starting to peak. It felt A LOT like acid in may respects. I had just received a package from my girlfriend in Cal, and when I opened it up, she spilled all over the floor. What I actually think this was, was me recalling a whole lot of memories about her at once. So many, and so intense, that I forgot they werenly for a second. I had this problem, that if I tried to fall asleep, I would suddenly hear jazz music playing loudly. VERY loudly. It was more real than normally hearing music in my head, and it sounded just like it was coming out of my stereo. After I have no idea how long, I eventually drifted off. The next morning I felt just fine. Lots of fun. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . T. M. (male). 1560mg + cannabis (Another long description, characteristic of the fourth plateau.) It was an interesting experience to say the least. I had been going through some of my old Amiga disks and came across the game 'Lemmings' and popped it in the drive. I started from the very beginning (since I no longer have any idea where the sheet of paper is that I wrote the level codes down on when I first played it a few years ago) and alternated swallowing Drixorals and smoking bowls in between levels. (I never realized that that game would be so much fun when stoned!). Later, I n my memory and what I do remember I just remember as events without any kind of time stamp on them) I was lying down listening to music and I had another full blown vision like the pink space one... oh boy, this is gonna be hard to describe.. hummm I was no longer in my body - I was just a consciousness floating in space - and I was looking at a spiral. It was like a spring but instead of each loop being circular, they were perfect squares. This square spring extend out to infinity in both directions. Each square loop was flat on the top and bottom and thick.. as if someone had cut a square spiral out of paper and pulled it out. The loops were divided into sections and each section was a window into another reality. I was looking at a portion of the spiral that had the window to this world. Each window opened onto a different part of my existence: moving down the coil, the window adjacent to the one I was looking at opened onto the world of my life before this one and the next window after that revealed my life before that and so on. Likewise, moving up the coil, the window adjacent to the one I was looking at revealed the my next life after this one and the next window after that revealed one more life and so on. So, up were my future lives and down were my past lives.. The next thing that happened to me I'd like to mention because it was rather scary. Normally, I use the music coming through my headphones as that one last thread of this reality. I know that no matter what happens, if I can still hear music then (a) my body is still alive and functioning properly no matter what I may think and (b) I will always be able to find my way back; there's no possibility of getting lost. It's like a security blanket. I had been looking at a large blue shape that was a sphere with a concave trench dug out around than I had come. I found myself floating above my body and looking down at it. It was then that I realized that I wasn't hearing any music.. In fact, when I thought about it, I couldn't remember hearing any music during that entire trip.. my security blanket was gone and I freaked out. In a frenzy I forced myself back into my body and with some difficulty managed to open my eyes. I could hear the music once again but this was little consolation since my body was cold.. felt like I had been lying outside with my clothes off. And I couldn't feel any part of it.. not even the familiar beating of my heart (yes, I know this is normal for robo but I was in a big paranoia fit at the time and the MJ wasn't helping). I tried to reach over and feel my heart, but I only got my arm a few inches off the bed before it feel limply at my side. That did it.. I was really scared now and I was sure that my heart had stopped and if it hadn't yet it was real close to it and I only had seconds left on this earth. I decided my only chance at survival was to try and get my body moving to keep my heart stimulated. I gathered up all my willpower and with one big effort managed to sit up. I pulled the headphones off, got out of bed and started jumping up and down.. Then I did some push ups.. I did those push ups like a wild m 5 days since then, and my body still feels different. My overactive senses have managed to return to normal, but I still feel like I'm sloshing around in my body.. even now while I'm sitting down. And I still have that helium feeling only it's no longer all over my whole body at once.. it's localized to various areas and those areas are constantly moving around. I played some vball and it doesn't seem to affect my coordination.. in fact I feel that I can use my body better now than I could before (a good thing too 'cause I've gotta play away games in Reno and Chico this weekend.. I'd hate to have to explain to the team that I can no longer play ball because I roboed to hard and fucked my body up!) I wasn't expecting this to turn out to be so long.. but I just had to share this experience.. I couldn't keep it to myself any longer. I hope I didn't bore y'all too much! 8) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Repo Man (male). 1050mg When I was stationed in Korea, we could buy these little yellow pills over the counter that we only knew as Romilars. We had no idea what they were and because the people selling them to us wanted to keep the mystery up (I guess so we didn't just go to another store and order whole caseload of them) they just gave them to us in little paper bags. anted to talk to them but was afraid to and so quickly walked away to the drug store which was a mile or two away in my bedroom slippers to buy more DXM (at this point I was not yet completely gone). I was very dizzy and the sea legs had just hit me. (Before my walk, I sat in the sun and enjoyed the light-headedness. My body felt very light.) By the time I made it to the shopping center, it was just like being a ghost. On the way, I knew I was dying but it was very pleasant. My soul gradually dissociated from my body and the world seemed so strange, uncertain and mysterious. I remember seeing a leaf blowing in the wind and I knew that it and I (along with everything else) were really the same thing. Near the end, however, my hands and arms started to tingle a lot (the same feeling that you get if you wake up after having slept on one of your limbs), my face and neck were getting paralyzed, my heart was beating very fast, and I was having severe robo movements. Added to all this, it was getting harder to move but I was at McDonald's by myself and had to get home. I kept thinking, "I have to call my friend, I have to call my friend" (who I had told about my plans). My life started to flash in front of me and for a second I saw myself from the outside (although I think id three times in front of all these cars and rushed into the motel's men's room. I threw up some more. I was in a cold sweat and felt very sick. the room was dizzy and if I hadn't been already familiar with the place I wouldn't have recognized it. I sat for about 5 or 10 minutes and then robotically walked back home, where I called my friend, who was an absolute blessing. I told him everything and soon started to come back, although I could only lie down and was breathing very heavy with a fast heartbeat. My experience was horrible (except for the brief insights) and I'm truly convinced that the DXM high is identical to dying. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Anonymous (male, age 19, 55kg). 600mg (10.9mg/kg) A few weekends ago, none of my friends were available to do anything, so I decided to try some DXM. I had eaten about 4 hours before, and had a Super Big Gulp, but I was bored and had time to waste. I bought a package of generic DXM liquicapsI could think of who I was, and say who I was, but I didn't feel like that person. I lost track of time. I lost track of what was happening to me. I wanted to know what happened to me. It was like I somehow got into a different dimension, with strange things going on in my head, and I didn't know what. "WHAT IS HAPPENING?" I soon figured out that I had taken something called DXM, and that was the cause of my confusion. But it was bizarre. I went to my bed to lay down to sleep. I fell asleep. Then, I was flying in the air - actually, I was being suspended by my shoulders. I was being lifted up in the air by my shoulders, and it was dark out. I was lifted over buildings. The buildings were really simple (skyscrapers). I opened my eyes, and I wasn't flying. I closed my eyes, and I was being suspended in the air again. Then, I was going down a slide. But it wasn't like an ordinary slide at a park, it was like a slide in a totally abstract world. Everything around me was black and grey and maybe there were a few white lines around. But I was in this strange world, and I couldn't stop myself from falling down this slide. I was on my stomach, and I kept falling down, and down. It was really disturbing. I woke up after feeling this. I had to think who I was again. I had to think what was happening. I was out of control, and I didn't like all the intense hallucinations, since they were more than visual, as I _was_ being lifted in the air, or going down the slide. I didn't like any of this at the time. I got to sleep again. I felt something warm, then hot in my chest. I grabbed the garbage can sitting next to the bed (how convenient) and pukede usually prefaced with a good deal of anxiety. 3:00pm: Shortly before arriving home at 3pm, I started noticing a tingling sensation in my head - a "pins and needles" effect. Started keeping a diary of what takes place. 3:10pm: Taking a shower. Physical sensations are were intensified on my head: washing my hair, rinsing, and shaving my face seemed unusual. I heard myself say "wow" a couple times. 3:15pm: A heightened awareness of the opinions of my body. I was choosing clothes based on how they would sense during the day. 3:20pm: I began to notice motor control problems, similar to having a beer or two. I knew something was not quite right with my coordination but was not sure exactly what it was. 3:35pm: Detail work with my hands was becoming difficult. I had bought a thermometer with the Drixoral to make sure I could have some objective measure of my temperature during the day, and found it quite difficult to open the case. 3:40ad were reporting "pins & needles" (hereafter referred to as "P&N"). Total effect reminds me of having a bad hangover. Had the thought, "do I really want to do this?" Noticed imagination of being found dead, choked on my own vomit. 4:05pm: Water difficult to drink, because it was reminding me of the nasty taste in my mouth. Ate four crackers, and was amazed at how incredibly dry my mouth became, literally needing water to swallow. Starting to feel better after getting sick. The crackers seemed to "ground" me and help me feel a little more normal. My eyeglasses seemed oppressive, and I turned off the TV. 4:10pm: Realized that my penis and balls had become incredibly small. There is usually "shrinkage" (in the Seinfeld sense of the word) after riding my bike, but this was spooky. Felt the urge to have fresh air, so I went out onto my apartment's balcony (third floor). My vision was definitely affected, and I had difficulty focusing m, but I now knew for sure that DXM was in the alcohol-class of drugs that just brings your awareness to a lower level. (For me.)) 4:38pm: P&N throughout my body. Came inside the apartment again. Ate four more crackers. 4:41pm: Starting to miss normal functional vision. Wrote "wish my eyes worked again!" 4:45pm: Temperature: 97.8 Pulse: about 132/minute (33 in 15 seconds) Tried playing guitar. Unlike herb, I felt somewhat indifferent to it, and music was not feeding me emotionally. Realized for the first time that I tend to avoid certain guitar chords because they are connected to certain sad memories in my past when I was learning them. 4:47pm: "There is a deadness to this drug." I was feeling broken, in the sense that my body and mind were operating wrongly. (Contrast to feeling of intensified sensitivity with other drugs.) Felt that I knew what deranged street people must be experiencing, with both their minds and bodies irreparably damaged. (This is not a fun thought.) 4:55pm: Staring at my face in the mirror. Realized that inside the abstract thing I call "my head" is actually a lot of bone. Fascinated briefly by my jawbone. Felt strange to "be me", as though I usually interpret my Wrote, "Jim, if you read this later, do not do this drug, it sucks!" 5:45pm: Again, felt that this was the experience of being insane. Realized simultaneously how long life is, and how short it is. The day seemed to be passing super-slowly. Brushing my teeth after vomiting was another "grounding" event, making me feel better. Had to stop listening to music, it was too intense and was becoming oppressive. 5:50pm: Turning on the computer, hoping it will "ground" me more. Still feeling crazy in an unhealthy way. 5:55pm: Since puking, my breathing has been quite deep and has attracted my attention. Noticed a certain amount of background fear that thinks I will always be this messed up. Hard to focus on the screen. 6:06pm: Felt sad for humanity without knowing why. Felt "bad" for being human, the same feeling of "badness" as when your father yells at you. Felt that we ought not to be human. Felt guilty, ashamed of myself for trying DXM, felt ashamed to "something higher" or god. (I hardly ever have feelings of being in the presence of a higher intelligence, so this was odd for me.) 6:10pm: Wondered who looks out for the people on the Earth. 6:20pm: Wondered if this is how it feels to die. Time seeming to go on and on... Last ten minutes since my last entry seems like an hour. Ate eight more crackers. 6:25pm: Starting to feel as though I am heading back towards mental health. Felt strong urge to read messages on a Usenet group relating to a particular system of ceither a good or a bad one depending on your point of view, but I put it here to illustrate Torch's friend's negative experience as a "mescalibur worm". Note that I'm fairly certain Torch miscalculated the dosage; 1/3 of 16oz of DXM-only cough syrup should be 480mg each, not 157mg each, bringing the dosages to 570mg for Torch and 675 for each of his friends, which is consistent with a third plateau trip level.) I had a verweird shit - "I'm gonna ram your boat! Watch out!" We'd say back to him, "Ram it! Ram it!" Then he started babbling about how he was a mescalibur worm. We didn't know what the hell he was talking about but I was extremely tired so I told my other friend to tell him a story that ended in him sleeping. At this point my tripping friend was flying through space as this worm, so my other friend told him a story about going into a space station and seeing NASA beds. He laid down in the NASA beds, they were very comfortable, and he fell soundly asleep. He was quiet for a little while and we thought it worked, but then he started screaming "Oh, shit! Oh, shit!" We were worried about him so we tapped him trying to wake him up but he wouldn't stop and he kept talking about how he was a mescalibur worm and his job was to go through the green tunnels very fast. We stood him up and he still thought he was that worm, so we started to freak out recalling stories about people who have tripped on acid and thought they were a dog or an orange for the rest of their life. We held him and started saying "Your name is X, and you're not a worm, your a human being. You're a HUMAN BEING. Now what are you?" And he would reply "A human being." We said "Not a mescalibur worm.." and he would gasp and look really scared... It took us about 30 minutes to convince him that he was a human and not a worm. We turned on the TV and had him watch it, explaining that the animals he saw on it were humans, just like he was. Then we started playing Piggy by NIN and let him sing along to it so he could participate in something familiar to him (we got kind of worried when the lyrics were 'nothing can stop me now, 'cause I don't care,ffects from his experience, but he is reluctant to try DXM again. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . S. C. 700mg The dosage was about 700 mg - the most FOAF had ever choked down. After experiencing the normal start-up body stone and perceptual distortions, he fell asleep. Now picture yourself waking up in the Abyss. You are an amnesiac. You can remember only the following facts: 1) You are something called a "human being" (although you're not quite sure what that is). 2) Your name, and how to spell it. 3) The name of your employer. 4) The fact that it is something called "Saturday night" - or is it "Sunday night"? This is important because you must be back to something called "work" on Monday! Except for this disconcerting notion, the concept of time is irrelevant to you. 5) Vague awareness of the fact that the reason you are here (in this Abyss) is because you took some sort of drug. 6) Vague awareness that there is another reality somewhere, reality by which you could compare them). Flowing columns of streaky, stainy gunk are common, dismal sights. Yuck. This is experience FOAF is not eager to repeat. The amnesia was definitely something he'd not experienced (at least, not to the point of crises) in previous trips. FOAF intends to lay off the "dark hallucinogen" for a while. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . AN17016. 720mg. It hit pretty fast (within a half an hour) with light headedness and slight disorientation. After an hour there was SEVERE disorientation and depersonalization. He felt almost as if he were outside himself looking in. There weren't especially harsh visual effects as in real hallucinations. Things were very grainy and somewhat distorted. Unable to keep focus on much of anything. He got severe itching fits several times (the only way around it was to ignore the itching, stop and wait til you forget about it). Breathing often felt slightly constricted as if you were wearing a tight shirt collar. There were severe heat flashes so that we had to turn a fan on high in an air conditioned house. Walking was very difficult. Hard to keep a balance. Time was VERY distorted. The whole trip lasted about an 1.5-2 hr. for the strong effects but it seemed like FOREVER. He was also very dehydrated and found it hard to get the damn cherry taste out of his mouth. Also, this person has taken many trips on acid and several shroom trips and has never had any + 1 joint cannabis Needless to say, many of my would-be companions to the outer planes of consciousness faltered somewhere along this path-not many could keep up past step 2. In fact, once we were watching the "Grateful Dead Movie" and, at the first there's this little animation sequence that's kinda neat but not too heavy, and, just as the robo was beginning to take effect, one unfortunate traveler arose suddenly, and proclaimed that he "could not take it anymore", then fled from the room at approximately 4 am, alone. To this day, neither I nor my other companions of that fateful night have seen him since. Wherever he is, may his road be clear and burdens be light. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Roto (98kg male). 800mg (8.2mg/kg), "some" cannabis Friday evening I took about 800mg of DXM HBr. About one hour later I smoked some marihuana (I could feel the effects of DXM coming) and some minute later my heart rate jumped to almost 200 and stood there for about one hour. I was really scared and had some moments of true panic. Afterward my pulse stabilized at about 130. Now... Since Saturday morning I feel a pain in my chest and in the back, between the shoulders. I saw three (3) doctors, had an EKG and everything seems to be OK. Anyway, I have an appointment for tomorrow with a fourth doctor and I wanna ask for a EKG under load. Today my situation seems improved a bit. By the way, I weigh about 98 Kg, am pretty fit and absolutely healthy (until Saturday, at least). During this experience I've never lost consciousness, I never felt any acute pain (at least not acute enough to be felt in the conditions I was), I didn't bleed from the nose neither I had blood in the urine/feces or broken blood vessels in my eyes. (Note: it's my general conclusion that Roto suffered from a panic attack, and that the chest and back pains were a combination of muscle soreness and possibly indigestion. The physicians basically came to the same conclusion, and eventually told him that he had probably not been in any serious danger. One physician pointed out that stomach pain can appear to come from the chest area.) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . le, but then I would fall back into endless loops of thinking. During the whole trip, I was in complete darkness. On other DXM voyages, I have always had nice visual impressions, fractals floating by, or when I was listening to music, it converted itself to beautiful images in my field of vision. But not this time. No lights, no sights at all. This wasn't really helping to improve my mood, too. Several times, I felt the presence of "beings". Some of them seemed to watch me; well, not really watch, because it was all dark, but I could feel their stare, or rather their interest in me. They knew what I was experiencing. Others didn't seem to bother at all. Those were just there. When I finally got back to this world, I immediately took some notes. It was 1:10am. I was still tripping hard, but I suddenly remembered that I had puked at some point, and I had spilt the rest of the drink which I had used to wash the pills down. I sat up on my bed in order to see whether there was a mess... Somehow, I had managed to reach the dustbin before shouting buick. For the rest of the night, the flight went on; I was having a rather good time again. I listened to some music for a while, and finally fell asleep. The next morning, I was perfectly myself again. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . AN17016. Unspecified amount of DXM, probably 3rd plateau Last night, while I was tripping, 2 of my 3 companions for the evening decided they'd get in on the excitement a bit with some handy Robitussin. The third was a) not interested, and b) the requisite babysitter/driver. Anyway, At some time in the chronological blur of last night, the Tussin user at whose we were decided that he wanted to try to astrally project. After this, he started acting strangely, and in a verlso, I was amazed that he wasn't tired. DM _should_, in my understanding, produce a sedating effect. He couldn't fall asleep, though, and didn't know whether or not he wanted to. He eventually did, with the help of the Valerian root that is kept around to cushion the "ride back down". The only problem is that he awoke in seemingly the same state. Through the entire drive to get me home, he seemed very disturbed, crossing his eyebrows and looking around a lot, sitting in a contorted position. The other person in the car, [Driver's name here], asked if I was used to it lasting this long. I wasn't, and I reminded them that even if I was, I wasn't used to any of the other properties of his experience. The only thing any of us could think of was getting me home without causing alarm, and probing for information, specifically on the 'net. ------------------------------------------------------------------------------ [10.3] Long-term Use Experiences I'd like to point out once again that long-term use of DXM may cause tolerance and lead to very unpf times, large doses, and it had _no_ effect whatsoever, save heavy perspiration and giddiness. Was my town unique, or was "robing" something most kids in the 80's did? .............................................................................. Positive Experiences P. M. (male). 1200mg per day I'm up to 40 gels (30mg or 1200 per trip) per day (or every other day). I've since passed the hallucination stage, and it's pretty much white light proper, and no more of that endless infinity stuff. I certainly don't tell people (other than a few on the net) about this stuff, and I don't recommend it in the kind of doses I do. I've had maybe 5 out of 300 trips go slightly bad. Usually these happened when I was in need of sleep. Essentially I lost my core identity and was basically fair game for whatever entity wanted to possess my being. This also bought grand delusions of making me think a lot of stuff was happening that really wasn't (even though I was sitting in a chair the whole time). I used to meditate a lot, and I'm sure that is why I've had such great success with this stuff - it is really a drug that forces one to stay in the moment if it is to be enjoyed properly. Oh, and I used to take acid a lot, so that also did a good job DXM experience. It was neither as euphorically pleasing nor did it (and I say this with a bit of skepticism, now) seem to offer the insight into the inner workings of the universe that DXM seemed to afford at times. However, I found that the experiences that I sought from DXM became fewer and farther between as I grew older. Eventually I stopped using it altogether because my trips no longer had the shamanic quality that I sought, but rather became dull, shallow highs that had little if any psychedelic character at all- in fact, the effect was almost like codeine, and not as intensively euphoric. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . C. D. (male): The second point that I would like to bring up is a hacking dry cough as a result to chronic usage. I've had this happen to me from using the drug twice a week for two to three months. I also know personally several other people who experienced this exact same reaction to repeated close range usage of the drug, one of whom who actually had to visit a doctor about it. Unfortunately I don't know any details about this doctors visit, I just used it to illustrate DXM's cough inducing affect. ------------------------------------------------------------------------------ [10.4] Multiple Drug Experiences (This section covers some of the more interesting multiple drug combinations; generally I placed DXM + cannabis and DXM + alcohol in the above sections. Note that I do not advise any of these combinations, and some - such as combining DXM with an opiate or any kind of depressant - may be a very bad idea.) moked that bowl, and then finished off another, this time mostly just bud. I also finished off another beer. At this point it had been about 1 hour since I took the DXM, and I still wasn't feeling much other than being stoned. I took four gelcaps, for a total of 120mg. We started watching Beavis and Butthead, and spent the next 30 minutes laughing like idiots at Cornholio needing cappuccino for his bung-hole. And then the DXM kicked in, and it felt like I'd been jerked up into the air and was soaring. The ordinary "buzz" feeling of being stoned was suddenly enhanced and deepened, and everything around me looked like it was under a strobe light. Evidently I acted kinda weird for awhile, staring off into space with an ecstatic look on my face. We smoked another bowl, smaller, this time about half hash and half bud. I drank the other bottle, bringing my total up to 840mg of DXM. I could barely manage to work the pipe; by the end, I collapsed on the couch and was only semi-conscious. It was weird - the strobe action effect seemed to slow down more and more, and ever so often it would seem like the strobing would merge together into a moment of lucidity. I was reminded of a spinning fan under a strobe or a fluorescent light At one point the strobing slowed down and stopped, and everything went grey and then white. I don't know how long I was in that state, nor do I remember much about what happened there. I do recall a feeling that I was navigating a realm of probabilities, connections, and synchronicity. And then, suddenly, consciousness came back to me, and I was awake. At that point the more interesting aspects of the trip ended, and yet my senses were still weird. Sight worked, and yet it seemed like a dream sight, where everything was fuzzy. It felt more than anything like I was really just dreaming with my eyes closed, and yet I knew that they were open. I finally went to sleep, and awoke the next day. It was another day and a half before vision and my other senses returned to normal; in the mean time I felt like I was stuck at the bottom of a very deep well, or perhaps manipulating my body via remote control. All in all the trip was pleasant, or at least interesting, but I wouldn't advise combining this many intoxicants. .............................................................................. DXM + Cyclizine Anonymous (male, 84kg). 600mg (7.1mg/kg) + 150mg cyclizine I'd been playing with the combination of DXM and Cyclizine. I took 600mg of DXM (I weigh 84kg) over a period of about 2 hours. I was going slow because I wasn't sure in formed around the road and I took off along it zooming up and down over hills and hitting turns at immense speeds (I was surpassed that I didn't go flying from the bed at each turn). Then a brick wall appeared across the road on the horizon and I was approaching it quickly. I tried to will myself to stop but couldn't. There was nothing I could do. I thought "Oh shit I'm gonna hit the wall and get plastered all over it!" I gritted my teeth, grabbed the blankets, and watched as I zoomed toward certain death. At the last second, the bed started braking. I slowed down and came to a halt with my nose kissing the wall. It was such a thrill.. better than any amusement park! I looked over the wall and tried to will myself over il of clothes and my sister was no where in sight. 8) A friend of my had brought some beer and a bong over a few days before. We had left several empty beer cans scattered about and I had been too lazy to deal with them. While I was tripping, he came back. He walked into my room (right through the closed door), gathered up all the beer cans and left. The next morning, I got up to find all the cans still in the same places they've always been in... it came as quite a shock. I was sure he had taken them. As I was coming down I went out for a smoke. I was sitting on the steps watching some formless jelly shit moving about in the bushes when a cat came out of the bushes to my left (I think it was a real cat... I'll never know for sure tho). It stared at the jelly stuff I was looking at and crouched down and tensed up in the standard kitty ready-to-pounce position. I found this to be rather curious.. After all, I'm the only one who should be seeing my hallucinations right? As I puzzled about this, the cat darted headlown and do the 2 whippets one after the other. 7. Make sure you pay attention because you only get about 10 seconds. ============================================================================== [A] APPENDICES [A.1] Appendix 1: P450 Inhibiting Drugs This is a partial list of recreational and medical drugs which inhibit the P450 enzymes. Not all of them will inhibit all of the P450 enzymes, but it's safe to say that a substantial number of these will interact with DXM. [This section to be inserted when paper is received] ------------------------------------------------------------------------------ [A.2] Appendix 2: Receptor Binding of Recreational Drugs alcohol Targets and blocks GABA and NMDA channels, as well as probably having an effect on other ion channels (voltage-dependent and receptors). Actually, alcohol is not well understood in comparison to other drugs. amphetamine Causes a non-vesicular release of dopamine and noradrenaline by neurons which normally secrete them. May have some direct effect on dopamine and noradrenaline receptors, but this is insignificant compared to its neurotransmitter releasing effect. barbiturates Targets and binds to a specific site on GABA receptors, which activates them. This site is called the barbiturate binding site (appropriately enough). This is a different site from alcohol and benzodiazepines, so that if you combine any of these three, they will not compete for the same binding sites. Consequently, there is a synergistic effect, which can be quite dangerous. benzodiazepines Similar to barbiturates, except for two factors. First, the binding site is the ber (or family of receptors) designated anandamide. It is not yet known whether cannabis (actually, THC) is an agonist or antagonist at this receptor. codeine See morphine. coffee See caffeine. cocaine A dopamine reuptake inhibitor; cocaine blocks the transporter which takes used dopamine out of the way. Thus, dopamine secreted by a neuron keeps activating receptors over and over. Cocaine is also a sigma1 agonist, and has blocking abilities on certain ion channels (by which it exerts its local anesthetic effects). Demerol See morphine. glue See solvents. heroin See morphine. LSD Targets 5HT2A and 5HT2C, where it acts either as an antagonist or a partial agonist. Also has some dopaminergic activity; however, the majority of its effects are mediated through the 5HT receptors. marijuana See cannabis. MDA See MDMA. Release binding spectrum is probably different, and MDA may have additional effects on receptors. MDMA Similar to amphetamine, except that MDMA causes a nonvesicular release of dopamine and serotonin (5HT). Probably has other effects as well, some of which may be significant. methamphetamine Similar to amphetamine, possibly with more dopamine release. morphine Targets opio================ [R] REFERENCES Note: due to a hard drive crash, some of the information for this section was lost; in particular, I am missing the authors for about 20 or so papers. Hopefully this information will be corrected in the next release. 1 Fleeger CA (ed.). USAN and the USP Dictionary of Drug Names. USP Convention Inc. 1993 (Rockville). 2 McEnvoy GK (ed.). AHFS Drug Information. ASHP Inc. 1993 (Bethesda). 3 Bem JL, Peck R. Dextromethorphan. An overview of safety issues. Drug Saf. 1992;7:190-199. 4 Murray S, Brewerton T. Abuse of over-the-counter dextromethorphan by teenagers. South. Med. J. 1993;86:1151-1153. 5 Schadel M, Romach MK, Sellers EM. Mania and cough syrup [letter]. J. Clin. Psychiatry 1993;54:200. 6 Craig DF. Psychosis with Vicks Formula 44-D abuse. Can. Med. Assoc. J. 1992;146:1199-1200. 7 Jacobs MR, Fehr KO. Drugs and Drug Abuse. 1987 (Toronto). 8 Dukes, MNG (ed.). Meyler's Side Effects of Drugs. E to the administration of encainide in humans. J. Pharmacol. & Exp. Therapeutics 1992;263:780-786. 16 Mura C, Panserat S, et al. DNA haplotype dependency of debrisoquine 4-hydroxylase (CYP2D6) expression among extensive metabolisers. Human Gen. 1993;92:367-372. 17 Jacqz-Aigrain E, Funck-Brentano C, Cresteil T. CYP2D6- and CYP3A- dependent metabolism of dextromethorphan in humans. Pharmacogenetics 1993;3:197-204. 18 Evans WE, Relling MV. Concordance of P450 2D6 (debrisoquine hydrox- ylase) phenotype and genotype: inability of dextromethorphan metabolic ratio to discriminate r. Brain Res. 1992;594:323-326. 26 Lancaster FE. Alcohol, nitric oxide, and neurotoxicity: is there a connection? - a review. Alcohol Clin. Exp. Res. 1992;16:539-541. 27 Morgan PF. Is quinolinic acid an endogenous excitotoxin in alcohol withdrawal? Med. Hypotheses 1991;36:118-121. 28 Danysz W, Dyr W, et al. The involvement of NMDA receptors in acute and chronic effects of ethanol. Alcohol Clin. Exp. Res. 1992;16: 499-504. 29 Morgan PF, Nadi NS, et al. Mapping rat brain structures activated during ethanol withdrawal: role of glutamate and NMDA receptors. Eur. J. Pharmacol. 1992;225:217-223. 30 Heyes MP, Saito K, Markey SP. Human macrophages convert L-tryptophan into the neurotoxin quinolinic acid. Biochem. J. 1992;283(pt 3): 633-635. 31 Heyes MP, Satio K, et al. Poliovirus induces indolamine-2,3-dioxygenase and t from those in rat brain are expressed on human lung cancer cells. Mol. Biol. Cell. 1992;3:613-619. 39 Otton SV, Wu D, et al. Inhibition by fluoxetine of cytochrome P450 2D6 activity. Clin. Pharmacol. & Therapeutics 1993;53:401- 409. 40 Achamallah NS. Visual hallucinations after combining fluoxetine and dextromethorphan [letter]. Am. J. Psychiatry 1992;149:1406. 41 Kintz P, Mangin P. Toxicological findings in a death involving dextro- methorphan and terfenadine. Am. J. Forensic Med. Pathol. 1992;13: 351-352. 42 Kamei J, Iwamoto Y, Misawa M, Kasuya Y. Effects of rimcazole, a specific antagonist of sigma sites, on the antitussive effects of non- n 1993;18:157-172. 50 Micheletti G, Lannes B, et al. Chronic administration of NMDA antag- onists induces D2 receptor synthesis in rat striatum. Brain. Res. Mol. Brain Res. 1992;14:362-368. 51 Wolfe SA Jr, De Souza EB. Sigma and phencyclidine receptors in the brain-endocrine-immune axis. [Review]. NIDA Res. Monograph Ser. 1993; 133:95-123. 52 Huang X, Nichols DE. 5-HT2 receptor-mediated potentiation of dopamine synthesis and central serotonergic deficits. Eur. J. Pharmacol. 1993; 238:291-296. 53 Khanna JM, Shah G, Weiner J, et al. Effect of NMDA receptor antagonists on rapid tolerance to ethanol. Eur. J. Pharmacol. 1993;230:23-31. 54 Schneider SM, Michelson EA, et al. Dextromethorphan poisoning reversed by naloxone. [Review]. Am. J. Emerg. Med. 1991;9:237- 238. 55 Kamei J, Iwamoto Y, et al. Involvement of haloperidol-sensitive sigma- sites in antitussive effects. Eur. J. Pharmacol. 1992;224:39-43. 56 Kamei J, Mori T, et al. Serotonin release in nucleus of the solitary tract and its modulation by antitussive drugs. Res. Commun. Chem. Pathol. Pharmacol. 1992;76:371-374. 57 Kamei J, Mori T, et al. Effects of 8-hydroxy-2-(dDA receptor antagonists in rats. Eur. J. Pharmacol. 1992;229:75-82. 64 Oye I, Paulsen O, et al. Effects of ketamine on sensory perception: evidence for a role of N-methyl-D-aspartate receptors. Pharmacol. Exp. Ther. 1992;260:1209-1213. 65 Miller CL, Bickford PC, et al. Phencyclidine and auditory sensory gating in the hippocampus of the rat. Neuropharmacology 1992;31: 1041-1048. 66 Mayer ML, Benveniste M, et al. Pharmacologic properties of NMDA receptors. Ann. N.Y. Acad. Sci. 1992;648:194-204. 67 Gasic GP, Heinemann S. Receptors coupled to ionic channels: the glutamate receptor family. Curr. Opin. Neurobiol. 1991;1:20-26. 68 Bortolotto ZA, Collingridge GL. Activation of glutamate metabotropic receptors induces long-term potentiation. Eur. J. Pharmacol. 1992; 214:297-298. 69 Walker JM, Bowen WD, et al. A comparison of (-)-deoxybenzomorphans devoid of opiate activity with their dextrorotary phenolic counterparts suggests role of sigma-2 receptors in motor function. Eur. J. Pharmacol. 1993;231:61-68. 70 Akunne HC, Johannessen JN, et al. MPTP lesions of the nigrostriatal dopaminergic projection decrease [3H]1-[1-(2- thienyl)cyclohexyl) piperidine binding to PCP site 2: further evidence that PCP site 2 is associated with the biogenic amine reuptake complex. Neurochem. Res. 1992;17:261-264. 71 Rogers C, Lemaire S. Characterization of [3H]desmethylimipramine binding in bovine adrenal medulla: interactions with sigma- and (or) phencyclidine-receptor ligands. Can. J. Physiol. Pharmacol. 1992;70: 1508-1514. 72 Izenwasser S, Newman AH, Katz JL. Cocaine and several sigma receptor ligands inhibit nsitive sigma 2 receptor in rat brain. Mol. Pharmacol. 1992;42:471-479. 79 Jeanjean AP, Mestre M, Maloteaux JM, et al. Is the sigma-2 receptor in rat brain related to the K+ channel of class III antiarrhythmic drugs? Eur J. Pharmacol. 1993;241:111-116. 80 Itzhak Y. Repeated methamphetamine-treatment alters brain sigma receptors. Eur. J. Pharmacol. 1993;230:243-244. 81 Mash DC, Zabetian CF. Sigma receptors are associated with cortical limbic areas in the primate brain. Synapse 1992;12:195-205. 82 Roman FJ, Martin B, Junien JL. In vivo interaction of neuropeptide Y and peptide YY with sigma receptor sites in the mouse brain. Eur. J. Pharmacol. 1993;242:305-307. 83 Karbon EW, Enna SJ. Pharmacological characterization of sigma binding sites in guinea pig brain membranes. Adv. Exp. Med. Biol. 1991;287: 51-59. 84 Klein M, Canoll PD, Musacchio JM. SKF 525-A and cytochrome P-450 ligands inhibit with high affinity the binding of [3H]dextrometh- orphan and sigma ligands to guinea pig brain. Life Sci. 1991;48: 543-550. 85 Larson AA, Sun X. Regulation of sigma activity by amine-terminus of substance P in the mouse spinal cord: involvement of phencyclidine (PCP) sites not linked to N-methyl-D-aspartate (NMDA) activity. Neuropharmacology 1993;32:909-917. 86 Su TP. Deliniating biochemical and functional properties of sigma receptors: emerging concepts. [Review]. Crit801, a non-competative antagonist of NMDA receptor, prevents methamphetamine-induced decrease of striatal dopamine uptake sites in the rat striatum. Neurosci. Lett. 1992;136: 39-42. 94 Koyuncuoglu H, Aricioglu F. Previous chronic blockade of NMDA receptors intensifies morphine dependence in rats. 95 Simpson MD, Slater P, et al. Regionally selective deficits in uptake sites for glutamate and gamma-aminobutyric acid in the basal ganglia in schizophrenia. Psychiatry Res. 1992;42:273-282. 96 Shinn AF (ed.). Evaluations of Drug Interactions. Macmillan, 1988 (NY). 97 Newman AH, Bevan K, et al. Synthesis and Evaluation of 3-Substituted 17-Methylmorphinan Analogs as Potential Anticonvulsant Agents. J. Med. Chem. 1992;35:4135-4142. 98 Su, Tsung-Ping. Pharmacologic Characterizations of Sigma Receptors. Sigma, PCP, and NMDA Receptors. NIDA Research Monograph 133 (1993). 99 Quirion R, DiMaggio DA, et al. Evidence for an endogenous peptide ligand for the phencyclidine receptor. Peptides 1984;5:967-973. 100 DiMaggio DA, Contreras PC, et al. Biological and chemical characterization of the endopsychosins: Distinct ligands for PCP and sigma sites. Sigma and Phencyclidine-Like Compounds as Molecular Probes in Biology. NPP Books 1988 (Ann Arbor). 101 Rothman SM, Olney JW. Excitotoxicity and the NMDA Receptor - still lethal after eight years. Trends in Neurosci. 1995;18:57-58. 102 Vilner et al. Sigma receptor mediated morphologic and cytotoxic effects. J. Neurosci. 1995;15(1):118-134. 103 Yamada M, Nishigami T, et al. Relationship between sigma-like site and progesterone-binding site of adult male rat liver microsomes. Hepatology 1994;Nov:1271-1280. 104 Cocaine-sensitive sigma receptor and its interaction with steroid hormones in the human placental syncytiotrophoblast and in chorio- carcinoma cells. Endocrinology 1995;136(3):924-923. 105 A role of sigma receptors on hypoxia/hypoglycemia-induced decrease in CA1 presynaptic fiber spikes in rat hippocampal slices. Brain Res. 1995;67 molecular field analysis of ligands for the neuromodulatory sigma 3 receptor. J. Medicinal Chem. 1994;37(24):4109-4117. 116 Discriminative stimulus effects of dextromethorphan in rats. Psycho- pharmacol. 1994;116(3):249-254. 117 Behavioral evidence for a modulating role of sigma ligands in memory process. I. Attenuation of dizocilpine (MK-801)-induced amnesia. Brain Res. 1994;647(1):44-56. 118 Behavioral evidence for a modulating role of sigma ligands in memory process. II. Reversion of carbon monoxide-induced amnesia. Brain Res 1994;647(1):57-64. 119 Chein CC, Pasternak GW. Functional antagonism of morphine analgesia by (+)-pentazocine: evidence for an anti-opioid sigma 1 system. Eur. J. Pharmacol 1993;250(1):R7-R8. 120 Jansen KL, Faull RL, et al. Loss of sigma binding sites in the CA1 area of the anterior hippocampus in Alzheimer's disease correlates with CA1 pyramidal cell loss. Brain Res. 1993;632(2):299-302. 121 Pharmacological characteristics of hyperambulation induced by the sigma ligand (+)-3-PPP in rats. Japanese J. Pharmacol. 1994;65(1): 1-7. 122 4-Methoxyphenyl 4-(3,4,5-trimethoxybenzyl)-1-piperazineacetate monofumarate monohydrate (KB-5492), a new anti-ulcer agent with a selective affinity for the sigma receptor, prevents cysteamine- induced duodenal ulcers in rats by a mechanism different from that of cimetidine. Japanese J. Pharmacol 1994;64(3):22189. 131 Ameliorating effects of sigma receptor ligands on the impairment of passive avoidance tasks in mice: involvement in the central acetyl- cholinergic system. Eur J Pharmacol 1994;261(1-2):43-51. 132 Low dose of 1,3-di(2-tolyl)guanidine (DTG) attenuates MK-801 induced spatial working memory impairment in mice. Psychopharmacol 1994; 114(3):520-522. 133 Massive dextromethorphan ingestion and abuse. Am J. Emerg. Med 1995;13(2):174-176. 134 The combination of tizanidine markedly improves the treatment with dextromethorphan of heroin addicted outpatients. Int. J Clin Pharmacol & Therapeutics 1995;33(1):13-19. 135 Neuroprotection by N-methyl-D-aspartate antagonists in focal cerebral ischemia is dependent on continued maintenance dosing. Neuroscience 1995;64(1):99-107. 136 N„kki R, Koistinaho J, et al. Cerebellar toxicity of phencyclidine. J. Neurosci. 1995;15(3):2097-2108 137 Hinsberger A, Sharma V, Mazimian D. Cognitive deterioration from long-term abuse of dextromethorphan: a case report. J. Psychiatry & Neurosci. 1994;19(5):375-377. 138 [This reference unintentionally left blank] 139 Hofstadter DR. G”del, Escher, Bach: an eternal golden braid. Basic Books; 1979 (New York) 140 [This reference unintentionally left blank] 141 Itzhak Y (editor). Sigma receptors. Academic Press; 1994 (Sof an agonist. A competitive antagonist works by competing with an agonist for the same location on the receptor; it is like a key which fits into a lock but cannot open it. A noncompetitive antagonist binds somewhere else on the receptor, temporarily changing the receptor so that the agonist won't work. An irreversible antagonist destroys the receptor. cannabis Marijuana, ganja, hemp, dope, grass, weed, doobage, etc. Everyone's favorite anandamide agonist. cytochrome A specific type of enzyme containing iron ions, generally found in the mitochondria of cells, but occasionally found elsewhere. delta An opiate neuroreceptor. dextromethorphan A cough suppressant drug commonly used in over-the- counter medications, which has dissociative effects at recreational doses. The subject of this text. dissociation A feeling of being disconnected from one's body and/or from reality, both in a physical and a psychological sense. dissociative A drug producing dissociation; this term is usually reserved for the dissociative anesthetics, even though most recreational drugs are to some degree dissociative. As an adjective, see dissociation. dissociative anesthetic An anesthetic which works by dissociating the patient from the body. Most anesthetics work by lowering brain function overall, bringing the patient to a near-comatose level; dissociative anesthetics selectively shrs with alien or spiritual beings, and that sort of thing. Nobody really knows why this occurs, nor does anyone know if this phenomenon occurs during the anesthesia, or when coming out of it. The emergence phenomenon is often very intense, and like near-death experiences, can occasionally have lasting effects on personality. enzyme A biological catalyst molecule which speeds up (usually significantly) the transformation of one chemical into another. endogenous Produced by the body. For example, endorphins are endogenous substances that fits into the opioid receptors. -ergic Activating or pertaining to the system of (whatever neurotransmitter). For example, a dopaminergic is a substance which activates the dopamine system (possibly by triggering dopamine secretion, possibly by activating dopamine receptors. Note that a substance which activates the serotonin (5HT) system is occasionally called a serotonergic (instead of serotoninergic). GABA Gamma-aminobutyric acid, a neurotransmitter derived from the amino acid glutamine. The GABA-ergic system is generally responsible for lowering the activity of neurons, and provide the negative inputs to most of the neural nets in the brain. Alcohol, benzodiazepines, and barbiturates all activate GABA receptors (thus being "downers") through different locations, which is why combining these drugs is exceedingly dangerous and stupid. GABA receptors are very plastic, and will downregulate as a result of too much activity, and cutting off a GABA-ergic "cold turkey" can cause a rebound effect where neurons burn themselves out as a result of too much activity, leading tohetic. Very frequently used in veterinary medicine, infrequently used (as an anesthetic) in humans. Recreationally used, it goes by street names such as "Vitamin K" and "Special K", and usually appears as a liquid solution or a white powder. It is typically injected intramuscularly (IM), but can also be smoked or snorted. Although generally regarded as safer than PCP, ketamine can be dangerous, both physically and psychologically. mu An opiate neuroreceptor. The primary site where endorphins act. Also one of the targets of morphine and its derivatives. neuron A nerve cell. neuroreceptor A structure, generally on the surface of a neuron, which can be activated by a neurotransmitter to produce any number of effects (such as stimulating or inhibiting the neuron). A neuroreceptor can be compared to a lock, with the neuro- transmitter being the key. In order to be an actual neuro- receptor, several conditions must be met, and the term is occasionally used somewhat loosely, both in this text and in common use. For example, the sigma receptor may not actually be a neuroreceptor. neurotransmitter A chemical which activates a neuroreceptor. Generally, neurotransmitters are specific for a family of neuroreceptors -- for example, the neurotransmitter dopamine acwithdrawal symptoms from alcohol (see GABA). It is probable that chronic use of dextromethorphan, ketamine, or PCP may lead to tolerance and withdrawal symptoms. PCP A dissociative anesthetic, sometimes called phencyclidine (which is short for 1-(1-phenylcyclohexyl)piperidine, the chemical name). Unlike ketamine, PCP is not used medically in humans, although it occasionally sees veterinary use. As a street drug, PCP goes by such names as "angel dust", "green", and numerous others. PCP is usually considered a hard drug with a bad reputation (partly deserved) for inducing violent psychotic reactions. In reality, most PCP users don't tend to move around a lot, and the average alcohol-intoxicated user is probably more likely to be violent. Many people find PCP to be distinctly unpleasant, and it probably has more bad trip potential than any other street drug. In addition to occasionally inducing delusions of the "I can fly off this building" sort, PCP can also block pain, leading to people doing all sorts of stupid things. Definitely not for beginners. PCP is usually smoked, often with marijuana. It can also be snorted, injected, or taken orally. plateau As used in this text, a tier or level at which the effects of a drug increase or decrease, but do not significantly change. Between plateaus, however, the effects can change significantly. Dextromethorphan exhibits up to four plateaus. quinolinic acid An extremely potent neurotoxin produced from trypto- phan. This conversion is greatly enhanced by the action of immune cells, and in the body, quinolinic acid is probably used to attack diseased cells and/or invading bacteria. In the brain or spinal column, however, quinolinic acid can have devastating effects on neurons (which is one of the reasons why immune cells aren't supposed to be there). Quinolinic acid is entirely responsible for the crippling damage of polio; it is the body's response to the virus that causes all the trouble. Dextromethorphan may be able to block quinolinic acid's toxic effects on nerve tissue. receptor Generally, but not always, used in this text to mean a neuro- receptor; however, some receptors are not neuroreceptors. For example, steroid receptors, thyroid hormone receptors, and various intracellular messenger receptors exist. The sigma receptor may not be a true neuroreceptor. sigma A family of neuroreceptors, originally classified with the opiate receptors (mu, kappa, and delta), but which has since been given its own category. There are at least two different sigma receptors (numbered 1 and 2, strangely enough), possibly a third. Currently, nobody's sure what the endogenous ligands for the sigma receptors are; in fact, it's not even certain that the sigma receptors are really n the Internet). Press RETURN to finish