Trip killer

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A trip killer, or hallucinogen antidote, is a drug that aborts or reduces the effects of a hallucinogenic drug experience (or 'trip'). [1] [2] [3] [4] [5] As there are different types of hallucinogens that work in different ways, there are different types of trip killers. [6] [7] [8] They can completely block or reduce the effects of hallucinogens [6] or they can simply provide anxiety relief and sedation. [3] Examples of trip killers, in the case of serotonergic psychedelics, include serotonin receptor antagonists, like antipsychotics and certain antidepressants, and benzodiazepines. [4] [6] Trip killers are sometimes used by recreational psychedelic users as a form of harm reduction to manage so-called bad trips, for instance difficult experiences with prominent anxiety. [2] [4] They can also be used clinically to manage effects of hallucinogens, like anxiety and psychomotor agitation, for instance in the emergency department. [3] [9]

Contents

Serotonergic psychedelic antidotes

Serotonergic psychedelics, such as psilocybin (found in psilocybin mushrooms), lysergic acid diethylamide (LSD), mescaline (found in peyote cactii), and dimethyltryptamine (DMT) (found in ayahausca), are thought to produce their hallucinogenic effects via activation of the serotonin 5-HT2A receptor. [10] [11] [6] As a result, serotonin 5-HT2A receptor antagonists would theoretically be expected to block the hallucinogenic effects of serotonergic psychedelics. [6] Accordingly, the serotonin 5-HT2A receptor antagonists ketanserin, an antihypertensive agent, and risperidone, an antipsychotic, have been shown to block the effects of serotonergic psychedelics in clinical studies. [6] [12] [13] [14] This includes the effects of psilocybin, [15] [16] [17] LSD, [18] [19] mescaline, [20] and ayahausca. [21] Conversely, the antipsychotic chlorpromazine has shown inconsistent effects in reversing psychedelic effects, [6] while the antipsychotic haloperidol, which is a dopamine D2 receptor antagonist but not a serotonin 5-HT2A receptor antagonist, is ineffective. [6] [22] [15]

Cyproheptadine, a non-selective serotonin receptor antagonist (including of the serotonin 5-HT2A receptor), is used as an antidote in the treatment of serotonin syndrome (or serotonin toxicity) caused by serotonergic drugs, including the toxicity of serotonergic psychedelics like the NBOMe drugs. [23] [24] [25] Certain other serotonin receptor antagonists, like chlorpromazine, have also been used for such purposes. [25] [26]

Recreational psychedelic users sometimes employ trip killers to abort psychedelic trips. [2] [4] [5] The most commonly encountered putative trip killers in a 2024 online study of Reddit social media postings were the benzodiazepines alprazolam and diazepam, the antipsychotic quetiapine, the antidepressant trazodone, and alcohol. [4] [5] [27] Others used less frequently included the benzodiazepines lorazepam, clonazepam, and etizolam, the antipsychotic olanzapine, and the antidepressant mirtazapine, among others. [4] [5] Antipsychotics like quetiapine and olanzapine and antidepressants like trazodone and mirtazapine are all potent serotonin 5-HT2A receptor antagonists. [6] [28] [29] Conversely, benzodiazepines and alcohol act as positive allosteric modulators of the GABAA receptor and have anxiolytic and sedative effects. [30] Such effects can be useful in managing the effects of serotonergic psychedelics, including clinically in the case of benzodiazepines. [3] [31] While employed by recreational users for harm-reduction purposes, the use of trip killers to abort the effects of psychedelics and other hallucinogens is not fully characterized and could pose medical risks. [1] [4] [5] [27]

Other serotonin 5-HT2A receptor antagonists that may block or reduce the effects of serotonergic psychedelics include other antipsychotics, like pipamperone, other antidepressants, like mianserin, nefazodone, and etoperidone, and the antimigraine agent pizotifen, among others. [6] The selective serotonin 5-HT2A receptor antagonist pimavanserin is also been studied as a blocker of the effects of psychedelics. [32] Conversely, in spite of variably acting as serotonin 5-HT2A receptor antagonists, tricyclic antidepressants (TCAs), including desipramine, imipramine, and clomipramine, have paradoxically been reported to potentiate the effects of serotonergic psychedelics rather than diminish them. [6] Other drugs that have been reported to potentiate rather than inhibit the effects of serotonergic psychedelics include lithium, reserpine, pindolol, and methysergide. [6] Pindolol, a beta blocker and serotonin 5-HT1A receptor antagonist, has been reported to potentiate the hallucinogenic effects of DMT by 2- to 3-fold in humans. [33] [34]

High-dose niacin (vitamin B3) was reported to reduce and block the effects of LSD in one early clinical study. [6] [35] [36] However, a subsequent clinical study attempting to replicate the findings found that it was not effective for this purpose. [35] Azacyclonol, a claimed ataractive (i.e., non-antipsychotic hallucination-suppressing medication) that is no longer marketed, likewise seems to be ineffective. [6]

Besides serotonin 5-HT2A receptor antagonists, other serotonergic drugs may also diminish the effects of serotonergic psychedelics. [6] Examples include serotonin 5-HT1A receptor agonists like buspirone, serotonin reuptake inhibitors like the selective serotonin reuptake inhibitors (SSRIs) (e.g., fluoxetine, paroxetine, sertraline) and serotonin–norepinephrine reuptake inhibitors (SNRIs), and monoamine oxidase inhibitors (MAOIs) (e.g., phenelzine, nialamide, isocarboxazid). [6] Buspirone, a partial agonist of the serotonin 5-HT1A receptor, has specifically been found to markedly attenuate the visual and certain other effects of psilocybin, although it did not completely block the hallucinogenic effects of psilocybin. [6] [37] [33] The reduced effects of psychedelics in the case of concomitant drugs that elevate serotonin levels may be due to desensitization of serotonin 5-HT2A receptors. [6] Although MAOIs can diminish the effects of serotonergic psychedelics, it must be noted that some serotonergic psychedelics, such as DMT, are highly susceptible substrates for monoamine oxidase (MAO), and hence can simultaneously be greatly potentiated by MAOIs (as in ayahausca). [6] [38]

Antidotes of other hallucinogens

Cannabinoid CB1 receptor antagonists like rimonabant, drinabant, and surinabant have been found to block or reduce the psychoactive effects of cannabinoids in clinical studies and could be useful as antidotes against cannabinoid toxicity. [7] [39] Likewise, the hallucinogenic and other effects of κ-opioid receptor agonists like salvinorin A (found in Salvia divinorum ), butorphanol, and pentazocine have been shown to be blocked by the non-selective opioid receptor antagonist naltrexone in clinical studies. [8] [40] [41] [42] Although clinical management of antimuscarinic deliriant intoxication and poisoning, for instance due to scopolamine, is usually supportive, acetylcholinesterase inhibitors, such as physostigmine, have sometimes been used in this context as well. [43] [44] Benzodiazepines and antipsychotics have also been used in such situations. [43] [44]

Although trip killers exist for certain types of hallucinogens, antidotes do not exist for all types of hallucinogens, for instance NMDA receptor antagonist dissociatives like ketamine and phencyclidine (PCP). [45] [3] [46] NMDA receptor agonists, which theoretically could reverse the effects of NMDA receptor antagonists, can produce excitotoxic neurotoxicity and convulsions, which limits their potential medical use. [47] [48] [49] In any case, benzodiazepines can be useful in managing dissociative intoxication. [9] [45] As with NMDA receptor antagonists, there is no antidote for Amanita muscaria intoxication. [50] [51]

Related Research Articles

<span class="mw-page-title-main">Psychedelic drug</span> Hallucinogenic class of psychoactive drug

Psychedelics are a subclass of hallucinogenic drugs whose primary effect is to trigger non-ordinary mental states and a perceived "expansion of consciousness". Also referred to as classic hallucinogens or serotonergic hallucinogens, the term psychedelic is sometimes used more broadly to include various types of hallucinogens, such as those which are atypical or adjacent to psychedelia like salvia and MDMA, respectively.

<span class="mw-page-title-main">Empathogen</span> Class of psychoactive drugs that produce empathic experiences

Empathogens or entactogens are a class of psychoactive drugs that induce the production of experiences of emotional communion, oneness, relatedness, emotional openness—that is, empathy or sympathy—as particularly observed and reported for experiences with 3,4-methylenedioxymethamphetamine (MDMA). This class of drug is distinguished from the classes of hallucinogen or psychedelic, and amphetamine or stimulants. Major members of this class include MDMA, MDA, MDEA, MDOH, MBDB, 5-APB, 5-MAPB, 6-APB, 6-MAPB, methylone, mephedrone, GHB, αMT, and αET, MDAI among others. Most entactogens are phenethylamines and amphetamines, although several, such as αMT and αET, are tryptamines. When referring to MDMA and its counterparts, the term MDxx is often used. Entactogens are sometimes incorrectly referred to as hallucinogens or stimulants, although many entactogens such as ecstasy exhibit psychedelic or stimulant properties as well.

<span class="mw-page-title-main">Azapirone</span> Drug class of psycotropic drugs

Azapirones are a class of drugs used as anxiolytics, antidepressants, and antipsychotics. They are commonly used as add-ons to other antidepressants, such as selective serotonin reuptake inhibitors (SSRIs).

<span class="mw-page-title-main">5-Hydroxytryptophan</span> Chemical compound

5-Hydroxytryptophan (5-HTP), used medically as oxitriptan, is a naturally occurring amino acid and chemical precursor as well as a metabolic intermediate in the biosynthesis of the neurotransmitter serotonin.

<span class="mw-page-title-main">Psilocin</span> Chemical compound

Psilocin, also known as 4-hydroxy-N,N-dimethyltryptamine (4-OH-DMT), is a substituted tryptamine alkaloid and a serotonergic psychedelic. It is present in most psychedelic mushrooms together with its phosphorylated counterpart psilocybin. Psilocin is a Schedule I drug under the Convention on Psychotropic Substances. Acting on the serotonin 5-HT2A receptors, psilocin's psychedelic effects are directly correlated with the drug's occupancy at these receptor sites. The subjective mind-altering effects of psilocin are highly variable and are said to resemble those of lysergic acid diethylamide (LSD) and N,N-dimethyltryptamine (DMT).

<span class="mw-page-title-main">Ketanserin</span> Antihypertensive agent

Ketanserin, sold under the brand name Sufrexal, is an antihypertensive agent which is used to treat arterial hypertension and vasospastic disorders. It is also used in scientific research as an antiserotonergic agent in the study of the serotonin system; specifically, the 5-HT2 receptor family. The drug is taken by mouth.

<span class="mw-page-title-main">5-MeO-MiPT</span> Chemical compound

5-MeO-MiPT is a psychedelic and hallucinogen of the tryptamine family. It used by some as an entheogen. It has structural and pharmacodynamic properties similar to the drugs 5-MeO-DiPT, DiPT, and MiPT. It is commonly used as a "substitute" for 5-MeO-DiPT because of the very similar structure and effects.

<span class="mw-page-title-main">Trazodone</span> Antidepressant medication

Trazodone, sold under many brand names, is an antidepressant medication, used to treat major depressive disorder, anxiety disorders, and insomnia. It is a phenylpiperazine compound of the serotonin antagonist and reuptake inhibitor (SARI) class. The medication is taken orally.

<span class="mw-page-title-main">Lisuride</span> Chemical compound

Lisuride, sold under the brand name Dopergin among others, is a monoaminergic medication of the ergoline class which is used in the treatment of Parkinson's disease, migraine, and high prolactin levels. It is taken by mouth.

5-HT<sub>2A</sub> receptor Subtype of serotonin receptor

The 5-HT2A receptor is a subtype of the 5-HT2 receptor that belongs to the serotonin receptor family and is a G protein-coupled receptor (GPCR). The 5-HT2A receptor is a cell surface receptor, but has several intracellular locations.

<span class="mw-page-title-main">Etoperidone</span> Chemical compound

Etoperidone, associated with several brand names, is an atypical antidepressant which was developed in the 1970s and either is no longer marketed or was never marketed. It is a phenylpiperazine related to trazodone and nefazodone in chemical structure and is a serotonin antagonist and reuptake inhibitor (SARI) similarly to them.

<span class="mw-page-title-main">Serotonin receptor agonist</span> Neurotransmission-modulating substance

A serotonin receptor agonist is an agonist of one or more serotonin receptors. They activate serotonin receptors in a manner similar to that of serotonin, a neurotransmitter and hormone and the endogenous ligand of the serotonin receptors.

<span class="mw-page-title-main">Pipamperone</span> Antipsychotic drug

Pipamperone, sold under the brand name Dipiperon, is a typical antipsychotic of the butyrophenone family used in the treatment of schizophrenia and as a sleep aid for depression. It is or has been marketed under brand names including Dipiperon, Dipiperal, Piperonil, Piperonyl, and Propitan. Pipamperone was discovered at Janssen Pharmaceutica in 1961, and entered clinical trials in the United States in 1963.

<span class="mw-page-title-main">Aeruginascin</span> Chemical compound

Aeruginascin, also known as 4-phosphoryloxy-N,N,N-trimethyltryptamine (4-PO-TMT), is an indoleamine derivative which occurs naturally within the mushrooms Inocybe aeruginascens, Pholiotina cyanopus, and Psilocybe cubensis.

<span class="mw-page-title-main">1-Methylpsilocin</span> Chemical compound

1-Methylpsilocin (developmental code names CMY, CMY-16) is a tryptamine derivative developed by Sandoz which acts as a selective agonist of the serotonin 5-HT2C receptor (IC50Tooltip half-maximal inhibitory concentration of 12 nM, vs. 633 nM at 5-HT2A), and an inverse agonist at 5-HT2B (Ki of 38 nM). While 1-methylpsilocin does have higher affinity for 5-HT2C than 5-HT2A, it does produce a head-twitch response in mice that is dependent on 5-HT2A, so it is not entirely free of effects on 5-HT2Ain vivo. In contrast to psilocin, 1-methylpsilocin did not activate 5-HT1A receptors in mice.

ITI-1549 is a putatively non-hallucinogenic serotonin 5-HT2A receptor agonist which is under development for the treatment of mood disorders and other psychiatric disorders. In addition to acting at the serotonin 5-HT2A receptor, it is also an antagonist of the serotonin 5-HT2B receptor and an agonist of the serotonin 5-HT2C receptor. The drug's route of administration has not been specified.

References

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  2. 1 2 3 Bellanavidanalage Gothami Ayanthie Vis Jayasinha (8 February 2024). Towards Safer Trips: Exploring Harm Reduction Strategies for Recreational Psychedelic Use in Aotearoa New Zealand (Thesis). University of Otago. Retrieved 3 October 2024. Another form of mixing substances involves the use of trip killers; a pharmacological coping strategy aimed to reduce the negative effects of a psychedelic experience by consuming a different substance (Suran, 2024). While this is a new concept and an under researched area, there are reports of trip killers being effective in reducing the negative effects of a psychedelic experience (Suran, 2024). One study gathered research from reddit, an online social media platform, investigating the usage of trip killers during challenging psychedelic experiences (Suran, 2024). The most popular and effective trip killers used were prescription medication, with 47% reporting the use of benzodiazepines as they reduce anxiety, followed by the use of antipsychotic and antidepressant medication (Suran, 2024). However, there are risks in mixing substances with psychedelic drugs, and subjectivity in the effectiveness. As some individuals may experience positive effects, while for others it may lead to negative effects (Suran, 2024). Therefore, it is recommended that before using trip killers, individuals should try other non- pharmacological coping strategies to reduce the negative effects of the psychedelic drug (Gable, 2004; Van Amsterdam et al., 2011). These factors discussed above, demonstrate the effectiveness of protective behaviours and harm reduction practices, in promoting safe psychedelic use and reducing harm.
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  36. ↑ Agnew N, Hoffer A (January 1955). "Nicotinic acid modified lysergic acid diethylamide psychosis". J Ment Sci. 101 (422): 12–27. doi:10.1192/bjp.101.422.12. PMID   14368207.
  37. ↑ Brandt SD, Kavanagh PV, Twamley B, Westphal F, Elliott SP, Wallach J, Stratford A, Klein LM, McCorvy JD, Nichols DE, Halberstadt AL (February 2018). "Return of the lysergamides. Part IV: Analytical and pharmacological characterization of lysergic acid morpholide (LSM-775)". Drug Test Anal. 10 (2): 310–322. doi:10.1002/dta.2222. PMC   6230476 . PMID   28585392. Additionally, pretreatment with the 5‐HT1A agonist buspirone (20 mg p.o.) markedly attenuates the visual effects of psilocybin in human volunteers.59 Although buspirone failed to completely block the hallucinogenic effects of psilocybin, the limited inhibition is not necessarily surprising because buspirone is a low efficacy 5‐HT1A partial agonist.60 The level of 5‐HT1A activation produced by buspirone may not be sufficient to completely counteract the stimulation of 5‐HT2A receptors by psilocin (the active metabolite of psilocybin). Another consideration is that psilocin acts as a 5‐HT1A agonist.30 If 5‐HT1A activation by psilocin buffers its hallucinogenic effects similar to DMT58 then competition between psilocin and a weaker partial agonist such as buspirone would limit attenuation of the hallucinogenic response.
  38. ↑ Egger, Klemens; Aicher, Helena D.; Cumming, Paul; Scheidegger, Milan (10 September 2024). "Neurobiological research on N,N-dimethyltryptamine (DMT) and its potentiation by monoamine oxidase (MAO) inhibition: from ayahuasca to synthetic combinations of DMT and MAO inhibitors". Cellular and Molecular Life Sciences. 81 (1). Springer Science and Business Media LLC. doi: 10.1007/s00018-024-05353-6 . ISSN   1420-682X. PMC   11387584 .
  39. ↑ Bosquez-Berger, Taryn; Szanda, Gergő; Straiker, Alex (30 August 2023). "Requiem for Rimonabant: Therapeutic Potential for Cannabinoid CB1 Receptor Antagonists after the Fall". Drugs and Drug Candidates. 2 (3): 689–707. doi: 10.3390/ddc2030035 . ISSN   2813-2998.
  40. ↑ Maqueda AE, Valle M, Addy PH, Antonijoan RM, Puntes M, Coimbra J, Ballester MR, Garrido M, González M, Claramunt J, Barker S, Lomnicka I, Waguespack M, Johnson MW, Griffiths RR, Riba J (July 2016). "Naltrexone but Not Ketanserin Antagonizes the Subjective, Cardiovascular, and Neuroendocrine Effects of Salvinorin-A in Humans". Int J Neuropsychopharmacol. 19 (7): pyw016. doi:10.1093/ijnp/pyw016. PMC   4966277 . PMID   26874330.
  41. ↑ Walsh SL, Chausmer AE, Strain EC, Bigelow GE (January 2008). "Evaluation of the mu and kappa opioid actions of butorphanol in humans through differential naltrexone blockade". Psychopharmacology (Berl). 196 (1): 143–155. doi:10.1007/s00213-007-0948-z. PMC   2766188 . PMID   17909753.
  42. ↑ Preston KL, Bigelow GE (February 1993). "Differential naltrexone antagonism of hydromorphone and pentazocine effects in human volunteers". J Pharmacol Exp Ther. 264 (2): 813–823. PMID   7679737.
  43. 1 2 Shim KH, Kang MJ, Sharma N, An SS (September 2022). "Beauty of the beast: anticholinergic tropane alkaloids in therapeutics". Nat Prod Bioprospect. 12 (1): 33. doi:10.1007/s13659-022-00357-w. PMC   9478010 . PMID   36109439. The treatment of TA poisoning including gastric emptying, use of activated charcoal (0.5 to 1 g/kg in children or 25 to 100 g in adults) to absorb the drug and benzodiazepines for managing agitation [157, 158]. Physostigmine (an AChE inhibitor) is recommended in the case when both PNS and CNS are afected by anticholinergic poisoning [159, 160]. In such cases, intravenous dose of physostigmine (0.02 mg/kg for children and 0.5 to 2 mg/ kg for adults) is recommended [159]. Physostigmine is helpful in restoring the level of consciousness to its baseline [157] which is diferent from sedative action of benzodiazepines.
  44. 1 2 Bulut NS, Arpacıoğlu ZB (September 2022). "Acute onset psychosis with complex neurobehavioural symptomatology following the intramuscular injection of hyoscine butylbromide: a case report with an overview of the literature". Eur J Hosp Pharm. 29 (5): 294–297. doi:10.1136/ejhpharm-2020-002583. PMC   9660700 . PMID   33376193. The most crucial intervention in the treatment of anticholinergic intoxication is without doubt the discontinuation of the suspected agent. Hospitalisation may be necessary for the close monitoring of severe cases. While physostigmine is commonly used as a specific antidote for anticholinergic toxicity, benzodiazepines and antipsychotics can prove to be useful in managing agitation, hallucinations, and agressive and self-mutilative behaviours as in our case.2
  45. 1 2 Schep LJ, Slaughter RJ, Watts M, Mackenzie E, Gee P (June 2023). "The clinical toxicology of ketamine". Clin Toxicol (Phila). 61 (6): 415–428. doi:10.1080/15563650.2023.2212125. PMID   37267048.
  46. ↑ Jenkins, Amanda J.; Gates, Madeleine J. (2020). "Hallucinogens and Psychedelics". Principles of Forensic Toxicology. Cham: Springer International Publishing. pp. 467–489. doi:10.1007/978-3-030-42917-1_26. ISBN   978-3-030-42916-4.
  47. ↑ Gonda X (2012). "Basic pharmacology of NMDA receptors". Curr Pharm Des. 18 (12): 1558–1567. doi:10.2174/138161212799958521. PMID   22280436.
  48. ↑ Rana V, Ghosh S, Bhatt A, Bisht D, Joshi G, Purohit P (2024). "N-Methyl-D-Aspartate (NMDA) Receptor Antagonists and their Pharmacological Implication: A Medicinal Chemistry-oriented Perspective Outline". Curr Med Chem. 31 (29): 4725–4744. doi:10.2174/0109298673288031240405061759. PMID   38638036.
  49. ↑ Rothman, Steven M.; Olney, John W. (1987). "Excitotoxity and the NMDA receptor". Trends in Neurosciences. 10 (7). Elsevier BV: 299–302. doi:10.1016/0166-2236(87)90177-9. ISSN   0166-2236.
  50. ↑ Mitchel DH (1980). "Amanita mushroom poisoning". Annu Rev Med. 31: 51–57. doi:10.1146/annurev.me.31.020180.000411. PMID   6772091.
  51. ↑ Rampolli FI, Kamler P, Carnevale Carlino C, Bedussi F (2021). "The Deceptive Mushroom: Accidental Amanita muscaria Poisoning". Eur J Case Rep Intern Med. 8 (3): 002212. doi:10.12890/2021_002212. PMC   7977045 . PMID   33768066.
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