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] 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. [32] [33]

High-dose niacin (vitamin B3) was reported to reduce and block the effects of LSD in one early clinical study. [6] [34] [35] However, a subsequent clinical study attempting to replicate the findings found that it was not effective for this purpose. [34] 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] [32] The reduced effects in the case of 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] [36]

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] [37] 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] [38] [39] [40] 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. [41] [42] Benzodiazepines and antipsychotics have also been used in such situations. [41] [42]

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). [43] [3] [44] 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. [45] [46] [47] In any case, benzodiazepines can be useful in managing dissociative intoxication. [9] [43] As with NMDA receptor antagonists, there is no antidote for Amanita muscaria intoxication. [48] [49]

Related Research Articles

<span class="mw-page-title-main">Psilocybin</span> Chemical compound found in some species of mushrooms

Psilocybin, also known as 4-phosphoryloxy-N,N-dimethyltryptamine (4-PO-DMT), and formerly sold under the brand name Indocybin, is a naturally occurring psychedelic prodrug compound produced by more than 200 species of fungi. Psilocybin is itself biologically inactive but is quickly converted by the body to psilocin, which has mind-altering effects similar, in some aspects, to those of other classical psychedelics. In general, the effects include euphoria, visual and mental hallucinations, changes in perception, a distorted sense of time, and perceived spiritual experiences. It can also cause adverse reactions such as nausea and panic attacks.

<span class="mw-page-title-main">Psychopharmacology</span> Study of the effects of psychoactive drugs

Psychopharmacology is the scientific study of the effects drugs have on mood, sensation, thinking, behavior, judgment and evaluation, and memory. It is distinguished from neuropsychopharmacology, which emphasizes the correlation between drug-induced changes in the functioning of cells in the nervous system and changes in consciousness and behavior.

<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">Mirtazapine</span> Antidepressant medication

Mirtazapine, sold under the brand name Remeron among others, is an atypical tetracyclic antidepressant, and as such is used primarily to treat depression. Its effects may take up to four weeks but can also manifest as early as one to two weeks. It is often used in cases of depression complicated by anxiety or insomnia. The effectiveness of mirtazapine is comparable to other commonly prescribed antidepressants. It is taken by mouth.

<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.

α-Ethyltryptamine Chemical compound

α-Ethyltryptamine, also known as etryptamine, is an entactogen and stimulant drug of the tryptamine family. It was originally developed and marketed as an antidepressant under the brand name Monase by Upjohn in the 1960s before being withdrawn due to toxicity.

<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.

Cross-tolerance is a phenomenon that occurs when tolerance to the effects of a certain drug produces tolerance to another drug. It often happens between two drugs with similar functions or effects—for example, acting on the same cell receptor or affecting the transmission of certain neurotransmitters. Cross-tolerance has been observed with pharmaceutical drugs such as anti-anxiety agents and illicit substances, and sometimes the two of them together. Often, a person who uses one drug can be tolerant to a drug that has a completely different function. This phenomenon allows one to become tolerant to a drug that they have never used before.

<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.

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">Pizotifen</span> Drug used to reduce frequency of headaches

Pizotifen (INN) or pizotyline (USAN), trade name Sandomigran, is a benzocycloheptene-based drug used as a medicine, primarily as a preventive to reduce the frequency of recurrent migraine headaches.

<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">Quipazine</span> Chemical compound

Quipazine is a serotonergic drug of the piperazine group which is used in scientific research. It was originally intended as an antidepressant but never developed for medical use.

Hallucinogens are a large and diverse class of psychoactive drugs that can produce altered states of consciousness characterized by major alterations in thought, mood, and perception as well as other changes. Most hallucinogens can be categorized as either being psychedelics, dissociatives, or deliriants.

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

Pirenperone (INNTooltip International Nonproprietary Name, USANTooltip United States Adopted Name, BANTooltip British Approved Name; developmental code names R-47456, R-50656) is a serotonin receptor antagonist described as an antipsychotic and tranquilizer which was never marketed. It is a relatively selective antagonist of the serotonin 5-HT2 receptors and has been used in scientific research to study the serotonin system. In the 1980s, the drug was found to block the effects of the lysergic acid diethylamide (LSD) in animals, and along with ketanserin, led to the elucidation of the 5-HT2A receptor as the biological mediator of the effects of serotonergic psychedelics.

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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  41. 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. 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.
  42. 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. 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
  43. 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.
  44. ↑ 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.
  45. ↑ Gonda X (2012). "Basic pharmacology of NMDA receptors". Curr Pharm Des. 18 (12): 1558–1567. doi:10.2174/138161212799958521. PMID   22280436.
  46. ↑ 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.
  47. ↑ 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.
  48. ↑ Mitchel DH (1980). "Amanita mushroom poisoning". Annu Rev Med. 31: 51–57. doi:10.1146/annurev.me.31.020180.000411. PMID   6772091.
  49. ↑ 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. PMID   33768066.
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