Wikipedia

Oneirogen

Oneirogen
Drug class
Chemical structure of ibogaine, the main active constituent of Tabernanthe iboga and among the most well-known oneirogens.
Class identifiers
SynonymsOneirophrenic; Oneiric; Ibogaine-type hallucinogen; Harmaline-type hallucinogen
UseRecreational, spiritual, medical
Mechanism of actionUnknown
Biological targetUnknown
Chemical classAzepinoindoles (e.g., ibogaine), β-carbolines (e.g., harmaline)
Legal status
Legal status
In Wikidata

An oneirogen, from the Greek ὄνειρος óneiros meaning "dream" and gen "to create", is a drug that induces a dream-like state of consciousness, also known as oneirophrenia. The term oneirogen, oneirophrenic, or oneiric, was introduced to refer specifically to ibogaine- and harmaline-type hallucinogens by William Turner and Claudio Naranjo in the 1960s and 1970s.[1][2][3][4][5] Subsequently, the term has also sometimes been used to refer to non-hallucinogenic drugs that facilitate dreaming.[6][7]

Hallucinogenic oneirogens

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These compounds are notable in being structurally similar cyclized tryptamines and in being structurally related to psychedelic tryptamines.[8] For example, ibogaine is a cyclized derivative of 5-MeO-DMT, while harmaline is a cyclized derivative of 6-MeO-DMT.[8]

The hallucinogenic effects of these drugs are qualitatively unique and have been described as a "dream-like" altered state of consciousness.[9][2] Iboga alkaloids and β-carbolines or harmala alkaloids have similar qualitative effects, but show distinct subjective effects from those of serotonergic psychedelics.[10][11][9][2]

Ibogaine and noribogaine are so-called "dirty drugs" that are known to interact with numerous targets.[12][13][14][15][16][17] However, the precise mechanism of action of oneirogens like ibogaine, or whether their hallucinogenic effects are due to multiple concomitant activities, are unknown.[14][13] Unlike serotonergic psychedelics, while they can still bind to the serotonin 5-HT2A receptor, neither iboga alkaloids nor β-carbolines activate the receptor.[17][18][11][13][10][19] In addition, ibogaine does not produce the head-twitch response, a behavioral proxy of serotonergic psychedelic effects, in rodents.[18][11] Noribogaine, the major active metabolite and form of ibogaine, is known to be a potent atypical κ-opioid receptor agonist.[20] However, harmala alkaloids like harmaline do not interact with the κ-opioid receptor.[21] Similarly, the NMDA receptor and the sigma σ1 receptor do not appear to be involved in the subjective effects of ibogaine based on animal studies.[10][5]

Oral doses and durations of β-carbolines or harmala alkaloids
Compound Chemical name Dose (hallucinogen) Potency Dose (MAOI) Duration
Harman 1-Methyl-β-carboline >250 mg Unknown >250 mg Unknown
Harmine 7-Methoxyharman >300 mg ≤50% 140–250 mg 6–8 hours
Harmaline 7-Methoxy-3,4-dihydroharman 150–400 mg 100% 70–150 mg 5–8 hours
Tetrahydroharmine 7-Methoxy-1,2,3,4-tetrahydroharman ≥300 mg ~33% Unknown Unknown
6-Methoxyharmalan 6-Methoxy-3,4-dihydroharman ~100 mg ~150% Unknown Unknown
6-MeO-THH 6-Methoxy-1,2,3,4-tetrahydroharman ≥100 mg ~50% Unknown Unknown
P. harmala seeds – ≥5–28 ga – 3–5 ga Unknown
Footnotes: a = P. harmala seeds in ground form. They contain 2–7% harmala alkaloids, with 1 teaspoon ≈ 3 g ≈ 60–180 mg alkaloids; 1 tablespoon ≈ 9 g ≈ 200–600 mg alkaloids; and 1 large (OO) gelatin capsule ≈ 0.7 g ≈ 15–45 mg alkaloids. For comparison, B. caapi contains 0.05–1.95% (average 0.45%) harmala alkaloids. Note: Harmine and other β-carbolines have also been tested by non-oral routes such as sublingual, subcutaneous injection, intramuscular injection, and intravenous injection. Refs: See template page.

Dreaming-promoting oneirogens

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Claimed

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Possible

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Disputed

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  • Valerian (herb) – A study conducted in the UK in 2001 showed that valerian root significantly improved stress induced insomnia, but as a side effect greatly increased the vividness of dreams. This study concluded that valerian root affects REM due to natural chemicals and essential oils that stimulate serotonin and opioid receptors. Another study found no encephalographic changes in subjects under its influence.[30][31][32]

Non-pharmacological

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See also

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References

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  1. ^ Naranjo C (2020). My Psychedelic Explorations: The Healing Power and Transformational Potential of Psychoactive Substances. Inner Traditions/Bear. pp. 166–. ISBN 978-1-64411-059-1. Retrieved 26 December 2025. Fourthly, I dedicate some words to oneirophrenic substances—that is to say, beta-carbolines and ibogaine. [...] In The Healing Journey (1973) I proposed to call harmaline and ibogaine "fantasy-enhancers" to emphasize the property that led William Turner (1964) to coin the term oneirophrenic for yagé, after his pioneering self-experiment with a plant extract. This special term seemed justified in view of the fact that, while these substances may in a broad sense be called psychedelic, their effect is different enough from those of the LSD-like psychedelics and feeling-enhancers to distinguish them. Together with other harmala and iboga alkaloids, they constitute a group of "dream-inducing" drugs, as we might also call them if we were to adopt the language of South American Indians (who use the word dream in an extended sense, also applicable to dreams in the absence of sleep). [...] [Chapter] 4. Oneirophrenics. [...]
  2. ^ a b c Naranjo C (1969). "Psycotherapeutic Possibilities of New Fantasy-Enhancing Drugs". Clinical Toxicology. 2 (2): 209–224. doi:10.3109/15563656908990930. ISSN 0009-9309. [...] the subjective effect brought about by large doses [of ibogaine] has more resemblance to those of the hallucinogens than those of the hypnotics. Such a resemblance still is very fragmentary, for the effects of both harmaline and ibogaine is quite unique among the psychoactive drugs. No better term can be found to describe these effects than that proposed some years ago by Dr. William Turner, one of the pioneer investigators of the South American Banisteriopsis drink. That author [6] proposed to reintroducing the term oneirophrenia, first employed by Meduna, to designate drug-induced states that differ from the psychotomimetic by the absence of all symptoms of the psychotic range and yet share with the psychotic or psychotomimetic experience the prominence of primary process thinking. Harmaline [7] and ibogaine characteristically elicit such a state, for their psychological effect is one much like the bringing about of dream phenomena without loss of consciousness, changes in the perception of the environment, delusions, or formal alterations of thinking and depersonalization. In short, we may speak of an enhancement of fantasy which, remarkable as it may be, does not interfere with ego functions. Such an enhancement of fantasy, as we will see, is in the nature of both an increase in vividness of visual imagery (which takes on an eidetic quality) and an increased spontaneity of content, which resembles that of true dreams more than that of ordinary daydreams. [...] In fact, the effects of both types of drug seem to stand in polar opposition, those of the common hallucinogens [like mescaline and LSD] being a lofty and "angelic" domain of aesthetic feelings, empathy, and a sense of oneness with all things, whereas the domain of the oneirophrenics is that Freudian underworld of animal impulse and regression.
  3. ^ Naranjo, C. (1996). The Interpretation of Psychedelic Experience in Light of the Psychology of Meditation. Sacred Plants, Consciousness and Healing (pp. 75–90). https://www.claudionaranjo.net/pdf_files/psychedelics/psychedelics_and_meditation_english.pdf "Psychedelic substances differ in their psychological effects. I find it useful to classify them in three distinct groups: the LSD-like ones, which might also be called, in accordance with common usage “hallucinogens”; those like MDA (Methylene-dioxyamphetamine) and MMDA (Methoxy methylene-dioxy-amphetamine), which I proposed calling “feeling enhancers” (currently more referred to as entactogens); and the “fantasy enhancers” or oneirophrenics such as harmaline and ibogaine."
  4. ^ "Ibogaine: A Review of Contemporary Literature". Multidisciplinary Association for Psychedelic Studies – MAPS – Psychedelic Research for Psychological Healing. Retrieved 26 December 2025. In the 1960's, a Chilean psychiatrist named Claudio Naranjo began experiments to study the potential of ibogaine as a catalyst for the psychotherapeutic process. He found through case studies that, with a dosage range of between 3 and 5 mg/kg, ibogaine elicits an oneirogenic condition which facilitates long term memory retrieval and closure of unresolved emotional conflicts (Naranjo, 1974). The word "oneirogen" (from the Greek, meaning "dream") is used rather than "hallucinogen" in referring to ibogaine's psychological effects, because ibogaine is not truly psychomimetic; it does not produce loss of consciousness or any formal deterioration of thought (Goutarel, Gollnhofer, and Sillans, 1993). Naranjo noted, as did ethnographers who have studied the cultures of western Africa, that the imagery produced by ibogaine is largely Jungian in content. That is, it involves archetypes common to all humans, imagery that provides the basis for the human psyche. In a therapy session, this archetypal imagery is used as a medium for mitigating emotional insight in relation to memories most significant to the individual's condition (Naranjo, 1974).
  5. ^ a b Alper KR (2001). Alper KR, Glick SD (eds.). "Ibogaine: A Review" (PDF). The Alkaloids: Chemistry and Biology. 56. San Diego: Academic: 1–38. doi:10.1016/S0099-9598(01)56005-8. ISBN 978-0-12-469556-6. ISSN 1099-4831. OCLC 119074989. PMID 11705103. Archived from the original (PDF) on 27 September 2007. Ibogaine-related visual experiences are reported to be strongly associated with eye closure and suppressed by eye opening. The term "oneiric" (Greek, oneiros, dream) has been preferred to the term "hallucinogenic" in describing the subjective experience of the acute state. Not all subjects experience visual phenomena from ibogaine, which may be related to dose, bioavailability, and interindividual variation.
  6. ^ Naiman R (October 2017). "Dreamless: the silent epidemic of REM sleep loss". Ann N Y Acad Sci. 1406 (1): 77–85. Bibcode:2017NYASA1406...77N. doi:10.1111/nyas.13447. PMID 28810072. Using oneirogens For people who wish to boost their awareness and recall of REM/dreaming, there are many recipes available that use botanicals and nutraceuticals to promote dreaming.66 Melatonin supplementation is also a simple and generally safe way to optimize both sleep and dreams67 if used properly. Unfortunately, there is limited expert guidance available for melatonin use. Generally speaking, 0.3–1.0 mg of a time-released formulation is best. Nootropics that support healthy levels of acetylcholine can also function as oneirogens.
  7. ^ Mata R, Contreras-Rosales AJ, Gutiérrez-González JA, Villaseñor JL, Pérez-Vásquez A (2022). "Calea ternifolia Kunth, the Mexican "dream herb", a concise review". Botany. 100 (2): 261–274. doi:10.1139/cjb-2021-0063. ISSN 1916-2790. The more significant botanical and ethnomedical aspects were recorded including the discovery of the oneirogenic use (enhancer of dreams) of C. ternifolia by the Chontal Indigenous communities in Oaxaca, Mexico. The plant contains sesquiterpenes and flavonoids as the major constituents. Some properties associated with the plant's traditional uses have been demonstrated including spasmolytic, antidiabetic, antidepressant, anti-inflammatory, and antinociceptive effects. The plant's toxicity will be discussed in this paper. Solid pharmacological research provided evidence supporting the use of the dream herb for oneiromancy.
  8. ^ a b Shulgin A, Shulgin A (September 1997). TiHKAL: The Continuation. Berkeley, California: Transform Press. ISBN 0-9630096-9-9. OCLC 38503252.
  9. ^ a b Naranjo C (1973). "Ibogaine: Fantasy and Reality" (PDF). The Healing Journey: New Approaches to Consciousness. New York: Parthenon Books. pp. 174–228. ISBN 978-0-394-48826-4.
  10. ^ a b c Helsley S, Rabin RA, Winter J (2001). "Chapter 4 Drug discrimination studies with ibogaine". The Alkaloids: Chemistry and Biology (PDF). Vol. 56. Elsevier. pp. 63–77. doi:10.1016/s0099-9598(01)56008-3. ISBN 978-0-12-469556-6. PMID 11705117.
  11. ^ a b c González J, Prieto JP, Rodríguez P, Cavelli M, Benedetto L, Mondino A, Pazos M, Seoane G, Carrera I, Scorza C, Torterolo P (2018). "Ibogaine Acute Administration in Rats Promotes Wakefulness, Long-Lasting REM Sleep Suppression, and a Distinctive Motor Profile". Front Pharmacol. 9 374. doi:10.3389/fphar.2018.00374. PMC 5934978. PMID 29755349.
  12. ^ Sershen H, Hashim A, Lajtha A (2001). "Characterization of multiple sites of action of ibogaine". Alkaloids Chem Biol. 56: 115–133. doi:10.1016/s0099-9598(01)56010-1. PMID 11705104.
  13. ^ a b c Wasko MJ, Witt-Enderby PA, Surratt CK (October 2018). "DARK Classics in Chemical Neuroscience: Ibogaine". ACS Chem Neurosci. 9 (10): 2475–2483. doi:10.1021/acschemneuro.8b00294. PMID 30216039. Unlike LSD, mescaline, and psilocybin, the hallucinogenic properties of ibogaine cannot be ascribed to 5-HT2A receptor activation.
  14. ^ a b Iyer RN, Favela D, Zhang G, Olson DE (March 2021). "The iboga enigma: the chemistry and neuropharmacology of iboga alkaloids and related analogs". Natural Product Reports. 38 (2): 307–329. doi:10.1039/D0NP00033G. ISSN 0265-0568. OCLC 8646253022. PMC 7882011. PMID 32794540. Ibogaine—the prototypical iboga alkaloid with the most neurobiological data—still lacks a truly robust, scalable, enantioselective total synthesis. Moreover, its biological mechanism of action is completely opaque, pushing the limits of what traditional neuropharmacology is capable of explaining. [...] Ibogaine's mechanism of action is poorly defined, which has severely inhibited drug discovery efforts using it as a lead structure. Ibogaine and its active metabolite noribogaine bind to a number of targets with only modest affinities including serotonin, opioid, acetylcholine, sigma, and NMDA receptors as well as serotonin, dopamine, and norepinephrine transporters (Table S2).116 Without an obvious target-based assay to drive structure-activity relationship (SAR) studies, medicinal chemistry efforts have focused on producing antiaddictive ibogaine analogs (i.e., ibogalogs) lacking major side effects. [...] In standard assays, ibogaine appears to have weak affinity for a large number of neuroreceptors, which has hindered efforts to define its mechanism of action.165,166
  15. ^ Popik P, Layer RT, Skolnick P (June 1995). "100 years of ibogaine: neurochemical and pharmacological actions of a putative anti-addictive drug". Pharmacol Rev. 47 (2): 235–253. doi:10.1016/S0031-6997(25)06842-5. PMID 7568327.
  16. ^ Ray TS (February 2010). "Psychedelics and the human receptorome". PLOS ONE. 5 (2) e9019. Bibcode:2010PLoSO...5.9019R. doi:10.1371/journal.pone.0009019. PMC 2814854. PMID 20126400.
  17. ^ a b Cameron LP, Tombari RJ, Lu J, Pell AJ, Hurley ZQ, Ehinger Y, Vargas MV, McCarroll MN, Taylor JC, Myers-Turnbull D, Liu T, Yaghoobi B, Laskowski LJ, Anderson EI, Zhang G, Viswanathan J, Brown BM, Tjia M, Dunlap LE, Rabow ZT, Fiehn O, Wulff H, McCorvy JD, Lein PJ, Kokel D, Ron D, Peters J, Zuo Y, Olson DE (January 2021). "A non-hallucinogenic psychedelic analogue with therapeutic potential". Nature. 589 (7842): 474–479. Bibcode:2021Natur.589..474C. doi:10.1038/s41586-020-3008-z. PMC 7874389. PMID 33299186.
  18. ^ a b Ona G, Reverte I, Rossi GN, Dos Santos RG, Hallak JE, Colomina MT, Bouso JC (December 2023). "Main targets of ibogaine and noribogaine associated with its putative anti-addictive effects: A mechanistic overview". J Psychopharmacol. 37 (12): 1190–1200. doi:10.1177/02698811231200882. PMID 37937505.
  19. ^ Grella B, Teitler M, Smith C, Herrick-Davis K, Glennon RA (December 2003). "Binding of beta-carbolines at 5-HT(2) serotonin receptors". Bioorganic & Medicinal Chemistry Letters. 13 (24): 4421–4425. doi:10.1016/j.bmcl.2003.09.027. PMID 14643338. [...] several β-carbolines, including harmaline (1) and its positional isomer 6-methoxyharmalan (4) substituted for the hallucinogenic (5-HT2A agonist) phenylalkylamine [DOM] in a drug discrimination task with rats trained to discriminate DOM from saline vehicle.10 However, neither harmaline (1; Ki=7790 nM) nor 6-methoxyharmalan (4; Ki=5600 nM) binds with high affinity at 5-HT2A receptors, and both were found to lack action as 5-HT2A agonists in a phosphoinositol (PI) hydrolysis assay.5,9 [...] At this time, it is not known if the actions of 1 and 4 in the PI hydrolysis assay reflect their low affinity, low efficacy, or whether the actions of the β-carbolines (in drug discrimination and/or other assays) is attributable to, or compromised by, their actions at other populations of receptors—particularly 5-HT receptors—or by possible interactions with the serotonin transporter.
  20. ^ Maillet EL, Milon N, Heghinian MD, Fishback J, Schürer SC, Garamszegi N, Mash DC (Dec 2015). "Noribogaine is a G-protein biased κ-opioid receptor agonist". Neuropharmacology. 99: 675–688. doi:10.1016/j.neuropharm.2015.08.032. PMID 26302653.
  21. ^ Deecher DC, Teitler M, Soderlund DM, Bornmann WG, Kuehne ME, Glick SD (February 1992). "Mechanisms of action of ibogaine and harmaline congeners based on radioligand binding studies". Brain Res. 571 (2): 242–247. doi:10.1016/0006-8993(92)90661-r. PMID 1377086.
  22. ^ Mossoba ME, Flynn TJ, Vohra S, Wiesenfeld P, Sprando RL (2016). "Evaluation of "Dream Herb," Calea zacatechichi, for Nephrotoxicity Using Human Kidney Proximal Tubule Cells". J Toxicol. 2016 9794570. doi:10.1155/2016/9794570. PMC 5040790. PMID 27703475.
  23. ^ Sałaga M, Fichna J, Socała K, Nieoczym D, Pieróg M, Zielińska M, Kowalczuk A, Wlaź P (June 2016). "Neuropharmacological characterization of the oneirogenic Mexican plant Calea zacatechichi aqueous extract in mice". Metab Brain Dis. 31 (3): 631–41. doi:10.1007/s11011-016-9794-1. PMC 4863909. PMID 26821073.
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Further reading

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  • Media related to Oneirogens at Wikimedia Commons
  • Oneirogens: Substances That Make You Dream (Natural & Synthetic) - TripSitter