Recreational use of dextromethorphan


Recreational use of dextromethorphan
Dextromethorphan in gel cap form.
For general information on this drug, including medical usage, see dextromethorphan.

Dextromethorphan (DXM), an active ingredient found in many cough suppressant cold medicines, is commonly[citation needed] used as a recreational drug.[1] It has almost no psychoactive effects at medically-recommended doses. Dextromethorphan has euphoric, psychedelic, and dissociative properties when administered in doses well above those which are considered therapeutic medically for cough suppression.[1] Recreational use of DXM is sometimes referred to in slang form as "robo-tripping", whose prefix is derived from the Robitussin brand name of cough medicine, or "Triple Cs" which is derived from the Coricidin brand name of cough & cold medicine (since the pills were printed with CCC on them).

An online essay first published in 1995 entitled "The DXM FAQ" described dextromethorphan’s potential for recreational use, and classified its effects into plateaus.[citation needed]

Owing to its recreational use and theft concerns,[citation needed] many retailers in the US have moved dextromethorphan-containing products behind the counter so that one must ask a pharmacist to receive them or be 18 years (19 in New Jersey and Alabama, 21 in Mississippi) or older to purchase them. Some retailers also give out printed recommendations about the potential for abuse with the purchase of products containing dextromethorphan.

Contents

Classification

At high doses, dextromethorphan is classified as a dissociative general anesthetic and hallucinogen, similar to the controlled substances ketamine and phencyclidine (PCP).[2] Also like those drugs, dextromethorphan is an NMDA receptor antagonist.[3][4] Dextromethorphan generally does not produce withdrawal symptoms characteristic of physically addictive substances, but there have been cases of psychological addiction.[5][6]

Effects

Dextromethorphan, when consumed in low "recreational doses" (between 100 & 200 mg), is described as having a euphoric effect. With middle doses (about 400 mg, or 2.5 to 7.5 mg/kg), intense euphoria, vivid imagination, and closed-eye hallucinations may occur. With high doses (600 mg, or 7.5 mg/kg and over), profound alterations in consciousness have been noted, and users often report out-of-body experiences or temporary psychosis.[7][8] Most users find such high doses to be extremely uncomfortable and are unwilling to repeat them.[citation needed] Flanging (speeding up or slowing down) of sensory input is also a characteristic effect of recreational use.

There is also a marked difference between dextromethorphan hydrobromide, contained in most cough suppressant preparations, and dextromethorphan polistirex, contained in the brand name preparation Delsym. Polistirex is polymer that is bonded to the dextromethorphan that requires more time for the stomach to digest it as it requires that an ion exchange reaction take place prior to its dissolution into the blood. Because of this, dextromethorphan polistirex takes considerably longer to absorb, resulting in more gradual and longer lasting effects reminiscent of time release pills. As a cough suppressant, the polistirex version lasts up to 12 hours. This duration also holds true when used recreationally.

In 1981, a paper by Gosselin estimated the lethal dose to be between 50 and 500 mg/kg. Doses as high as 15–20 mg/kg are taken by some recreational users. It is suggested by a single case study that the antidote to dextromethorphan overdose is naloxone, administered intravenously.[9]

In addition to producing PCP-like mental effects, high doses may cause a false-positive result for PCP and opiates in some drug tests.[2][10]

The "DXM FAQ"

A document entitled "The DXM FAQ," by William E. White, classified dextromethorphan's high-dose effects into four or five plateaus, each defined by a dosing range. The dosages are specified in ratios of milligrams (of the drug) per kilogram (of one's body mass). Doses are experientially, not scientifically derived. According to the FAQ, the plateaus occur as follows:[11]

  • First plateau: At a dosage of 1.5 to 2.5 mg/kg, effects include alertness, restlessness, increased heartbeat, increased body temperature, intensification of emotions, euphoria, loss of balance, and slight intoxication.
  • Second plateau: At 2.5 to 7.5 mg/kg, effects are similar to the first plateau, but with heavier intoxication, choppy sensory input, a dreamlike state of consciousness, some detachment from outside world, and closed-eye hallucinations.
  • Third plateau: At 7.5 to 15.0 mg/kg, effects include flanging of visual effects, difficulty recognizing people or objects, chaotic blindness, dreamlike vision, inability to comprehend language, abstract hallucinations, delayed reaction time, decision making impairment, feelings of peace and quiet, near complete loss of motor coordination, short-term memory impairment, and/or feelings of rebirth.
  • Fourth plateau: At 15.0 mg/kg or more, an individual may experience a perceived loss of contact and control with their own body, changes in visual perception, out-of-body experiences, perceptions of contact with "superior" beings, other miscellaneous delusions, lack of movement or desire to move, rapid heart rate, complete blindness, increased hearing, and intensification of third plateau effects.
  • Plateau Sigma: 2.5-7.5 mg/kg every three hours for 9–12 hours; occurs by prolonging dosage. Plateau sigma is marked by the presence of psychosis with visual and auditory hallucinations. Users have reported that inclinations manifest as auditory hallucinations; rather than simply feeling tired and sitting down, a user might hear a voice saying, "sit down now, you're tired," and feel inclined to obey. White says that of all the reports of Plateau Sigma experiences he received, over half were described as unpleasant.

Risks associated with use

Dextromethorphan has been shown to cause vacuolization, also known as Olney's lesions, in rats,[12] however oral administration of dextromethorphan did not cause vacuolization in laboratory tests.[13] Oral administration of dextromethorphan repeatedly during adolescence, however, has been shown to impair learning in those rats during adulthood.[14] The occurrence of Olney's lesions in humans, however, has not been proven or disproven. William E. White, author of the DXM FAQ, has compiled informal research from correspondence with dextromethorphan users suggesting that heavy abuse may result in various deficits corresponding to the brain areas affected by Olney's lesions; these include loss of episodic memory, decline in ability to learn, abnormalities in some aspects of visual processing, and deficits of abstract language comprehension.[15]

A formal survey of dextromethorphan users[16] showed that more than half of users reported experience of the following symptoms individually for the first week after dextromethorphan use: fatigue, apathy, flashbacks, and constipation. Over a quarter reported insomnia, nightmares, anhedonia, impaired memory, attention deficit and decreased libido. Rarer side effects included panic attacks, impaired learning, tremor, jaundice, urticaria (hives) and myalgia. Frequent and long-term usage at very high doses could possibly lead to toxic psychosis and other permanent psychological problems.[1]

Erectile dysfunction and diminished libido can be a longer-term effect (years to decades) of many narcotic analgesics due to development of central hypogonadism; this appears to be especially common in individuals with significant melanin deficiencies, as the hormones tied to melanin production affect the absorption and conversion of these analgesics into progesterone.[17] Additionally, the haplotypes of about 48% of the indigenous population of Great Britain aggravate the condition, as the E647 sequence underwent epigenetic degradation and became a pseudogene. The chance of vulnerability is doubled for males, as the critical sequence is located on the X chromosome.[18]

Misuse of multi-symptom cold medications, rather than using a cough suppressant whose sole active ingredient is dextromethorphan, carries significant risk of fatality or serious illness. Multi-symptom cold medicines contain other active ingredients, such as acetaminophen (paracetamol), chlorpheniramine, and phenylephrine, any of which can cause permanent bodily damage such as kidney failure, or even death, if taken on the generally-accepted recreational dosing scale of dextromethorphan. Sorbitol, an artificial sweetener found in many cough syrups containing dextromethorphan, can also have negative side effects including diarrhea and nausea when taken at recreational dosages of dextromethorphan.[19][20][21] Guaifenesin, an expectorant commonly accompanying dextromethorphan in cough preparations, can cause unpleasant symptoms including vomiting, nausea, and headache.

Combining dextromethorphan with other substances can compound risks. CNS stimulants such as amphetamine and/or cocaine can cause a dangerous rise in blood pressure and heart rate. CNS depressants such as ethanol (drinking alcohol) will have a combined depressant effect, which can cause a decreased respiratory rate. Combining dextromethorphan with other CYP2D6 substrates can cause both drugs to build to dangerous levels in the bloodstream.[22][23]

Combining dextromethorphan with other serotonergic drugs could possibly cause serotonin toxicity, an excess of serotonergic activity in the central nervous system (CNS) and peripheral nervous system (PNS).

Pharmacology

Dextromethorphan's hallucinogenic and dissociative effects can be attributed largely to dextrorphan (DXO), a metabolite produced when dextromethorphan metabolizes within the body. Both dextrorphan and dextromethorphan are NMDA receptor antagonists,[24] just like the dissociative hallucinogenic drugs ketamine and phencyclidine (PCP); however for that purpose, dextrorphan is more potent than dextromethorphan.[25]

Just like all NMDA receptor antagonists, dextrorphan and dextromethorpan inhibit a neurotransmitter called glutamate from activating receptors in the brain. This can effectively slow or even shut down certain neural pathways, preventing areas of the brain from communicating with each other. This leaves the user feeling dissociated (disconnected) or potentially "out-of-body."[26][27]

Dextromethorphan's euphoric effects have sometimes been attributed to the triggering of an increase in dopamine levels, since such an increase generally correlates to a pleasurable response to a drug, as is observed with some antidepressants and recreational drugs. However the effect of dextrorphan and dextromethorphan on dopamine levels is a disputed subject. Studies show that some NMDA receptor antagonists, like ketamine and PCP, do raise dopamine levels.[28][29] Other studies show that dizocilpine, another NMDA receptor antagonist, has no effect on dopamine levels. Some findings even suggest that dextromethorphan actually counters the dopamine increase caused by morphine.[30][31][32][33] Due to these conflicting results, the actual effect of dextromethorphan on dopamine levels is yet to be determined.

Legality

Antitussive preparations containing dextromethorphan are legal to purchase from pharmacies in most countries, with some exceptions being Sweden,[34] Estonia and Latvia.[citation needed]

United States

No legal distinction currently exists in the United States between medical and recreational use, sale, or purchase. Some states and/or store chains have implemented restrictions, such as requiring signatures for DXM sale, limiting quantities allowable for purchase, and requiring purchasers to be over the age of majority in their state.

The sale of dextromethorphan in its pure powder form may incur penalties, although no explicit law exists prohibiting its sale. There have been cases of individuals being sentenced to time in prison and other penalties for selling pure dextromethorphan in this form, because of the incidental violation of more general laws for the sale of legitimate drugs — such as resale of a medication without proper warning labels.[3]

Dextromethorphan was excluded from the Controlled Substances Act (CSA) of 1970 and was specifically excluded from the Single Convention on Narcotic Drugs. Dextromethorphan is still excluded from the CSA (as of 2010); however, officials have warned that it could still be added if increased abuse warrants its scheduling.[2] The motivation behind its exclusion from the CSA was that, under the CSA, all optical isomers of listed Schedule II opiates are automatically Schedule II substances. Since dextromethorphan is an optical isomer of the Schedule II opiate levomethorphan (but does not act like an opiate), an exemption was necessary to keep it a non-controlled substance. Because of its chemical similarity to levomethorphan, DXM could also be treated as a Schedule II drug under the Federal Analog Act.

See also

References

  1. ^ a b c Dextromethorphan (DXM) | CESAR
  2. ^ a b c DEXTROMETHORPHAN (Street Names: DXM, CCC, Triple C, Skittles, Robo, Poor Man’s PCP)
  3. ^ a b http://www.erowid.org/psychoactives/research_chems/research_chems_law3.pdf
  4. ^ Erowid DXM Vault : Effects
  5. ^ Drug Abuse Help: DXM Information
  6. ^ :: Cough Syrup and Dextromethorphan (DXM) Addiction and Abuse - Drug Rehab Information ::
  7. ^ Bornstein, S; Czermak, M; Postel, J., (1968). "Apropos of a case of voluntary medicinal intoxication with dextromethorphan hydrobromide". Annales Medico-Psychologiques 1 (3): 447–451. PMID 5670018. 
  8. ^ Dodds A, Revai E (1967). "Toxic psychosis due to dextromethorphan". Med J Aust 2: 231. 
  9. ^ Schneider SM, Michelson EA, et al. (1991). "Dextromethorphan poisoning reversed by naloxone". Am. J. Emerg. Med. 9 (3): 237–238. doi:10.1016/0735-6757(91)90085-X. PMID 2018593. 
  10. ^ Erowid DXM Vault : Drug Tests
  11. ^ Erowid DXM Vault : DXM FAQ - The Experience
  12. ^ Hashimoto, K; Tomitaka, S; Narita, N; Minabe, Y; Iyo, M; Fukui, S (1996). "Induction of heat shock protein Hsp70 in rat retrosplenial cortex following administration of dextromethorphan". Environmental Toxicology and Pharmacology 1 (4): 235–239. doi:10.1016/1382-6689(96)00016-6. 
  13. ^ Carliss RD, Radovsky A, Chengelis CP, O'neill TP, Shuey DL (2007). "Oral administration of dextromethorphan does not produce neuronal vacuolation in the rat brain". NeuroToxicology 28 (4): 813. doi:10.1016/j.neuro.2007.03.009. PMID 17573115. 
  14. ^ Zhang TY, Cho HJ, Lee S, Lee JH, Choi SH, Ryu V, Yoo SB, Lee JY, Kim DG, Jahng JW (2006). "Impairments in water maze learning of aged rats that received dextromethorphan repeatedly during adolescent period.". Psychopharmacology 191 (1): 171–9. doi:10.1007/s00213-006-0548-3. PMID 17021924. 
  15. ^ Erowid DXM Vault : This is your brain on dissociatives, the bad news is finally in, by William E. White
  16. ^ [Ziaee V, Akbari Hamed E, Hoshmand A, Amini H, Kebriaeizadeh A, Saman K. Side effects of dextromethorphan abuse, a case series. Addictive Behavior 2005 Sep;30(8):1607-13.]
  17. ^ Advanced Hormone Physiology
  18. ^ Busch and Grenfield, et al.
  19. ^ Kirages T, Sulé H, Mycyk M (2003). "Severe manifestations of coricidin intoxication". Am J Emerg Med 21 (6): 473–5. doi:10.1016/S0735-6757(03)00168-2. PMID 14574654. 
  20. ^ Kintz, P. and Mangin, P. (December 1992). "Toxicological findings in a death involving dextromethorphan and terfenadine". Am J Forensic Med Pathol. 13 (4): 351–352. doi:10.1097/00000433-199212000-00018. PMID 1288270. 
  21. ^ Erowid DXM Vault : Guide to DXM in Non-Prescription Drugs
  22. ^ Drugs and Human Performance FACT SHEETS - Dextromethorphan
  23. ^ Erowid DXM Vault : DXM FAQ - Side Effects
  24. ^ Cat.Inist
  25. ^ Comparison of the Effects of Dextromethorphan, Dextrorphan, and Levorphanol on the Hypothalamo-Pituitary-Adrenal Axis - Pechnick and Poland 309 (2): 515 - Journal of Pharmacology And Experimental Therapeutics
  26. ^ Muir, KW; Lees KR (1995). "Clinical experience with excitatory amino acid antagonist drugs". Stroke 26 (3): 503–513. doi:10.1161/01.STR.26.3.503. PMID 7886734. http://stroke.ahajournals.org/cgi/content/full/26/3/503. Retrieved 2007-01-17. 
  27. ^ Kristensen, JD; Svensson B, and Gordh T Jr (1992). "The NMDA-receptor antagonist CPP abolishes neurogenic 'wind-up pain' after intrathecal administration in humans". Pain 51 (2): 249–253. doi:10.1016/0304-3959(92)90266-E. PMID 1484720. 
  28. ^ NMDA receptor antagonists ketamine and PCP have direct effects on the dopamine D2 and serotonin 5-HT2receptorsimplications for models of schizophrenia
  29. ^ Verma A, Moghaddam B (16 January 1996). "NMDA receptor antagonists impair prefrontal cortex function as assessed via spatial delayed alternation performance in rats: modulation by dopamine". Journal of Neuroscience 1: 373–9. PMID 8613804. 
  30. ^ "Dextromethorphan". NHTSA. http://www.nhtsa.dot.gov/PEOPLE/injury/research/job185drugs/dextromethorphan.htm. 
  31. ^ Steinmiller, CL; Maisonneuve IM, Glick SD. (2003). "Effects of dextromethorphan on dopamine release in the nucleus accumbens: Interactions with morphine". Pharmacol Biochem Behav. (Center for Neuropharmacology and Neuroscience (MC-136)) 74 (4): 803–10. doi:10.1016/S0091-3057(02)01080-8. PMID 12667894. 
  32. ^ Carrozza, DP; Ferraro TN, Golden GT, Reyes PF, Hare TA. (1992). "In vivo modulation of excitatory amino acid receptors: microdialysis studies on N-methyl-D-aspartate-evoked striatal dopamine release and effects of antagonists". Brain Res. 74 (4): 803–10. doi:10.1016/0006-8993(92)90797-D. PMID 1353403. 
  33. ^ Huang, EY; Liu TC, Tao PL. (2003). "Co-administration of dextromethorphan with morphine attenuates morphine rewarding effect and related dopamine releases at the nucleus accumbens". Brain Res. 368 (5): 386–92. doi:10.1007/s00210-003-0803-7. PMID 14564449. 
  34. ^ Erowid DXM Vault : Legal Status

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