Draft:Hearing under the influence of a Psychedelic drug
The influence of Psychedelic drugs on hearing and langauge[edit]
The influence of Psychedelic drugs on hearing and language is a phenomenon that occurs when a human has an active Psychedelic drug in their body, such as Lysergic acid diethylamide, Psilocybin, or N,N-Dimethyltryptamine, and is described by measureable changes to the normal perception of sound, music, and language as well as language comprehension and production.
People have reported significant differences to their ability to perceive the internal and external environment with all senses when using psychedelics..[1] These include hearing sounds such as hissing, buzzing, whirring, singing, music, voices, and indistinct noises without apparent physical sources as well as hearing familiar sounds in a novel manner.[1] Language capabilities become enhanced under the influence of psychedelics; whole-brain dynamics change which allows for an expanded, more detailed vocabulary and emotional contribution to language production.[2][3][4][5]
Psychedelics and their effects on humans have been studied, but little work has been done to detail the alterations they cause to the neural pathways for hearing due to their classification as a restricted drug by many countries.[6] As these laws become less restrictive, more studies are being conducted which attempt to define the neural mechanisms by which psychedelics affect human hearing.[7]
Associated receptors[edit]
Psychedelic compounds are hallmarked by their actions on the Serotonin receptors in the nervous system, most notably the 5-HT2A receptor, which is a G-protein coupled receptor with extensive effects including CNS excitation, increases in hormone levels, and smooth muscle contraction 5-HT2A_receptor#Effects. The cognitive effects can be lessened or blocked with administration of the serotonergic antagonist Ketanserin, leading to the understanding that the serotonergic pathway plays a great role in the alterations these compounds cause.
Psychedelics also act upon the Dopamine#Reward system, contributing to the euphoric state most psychedelics induce but even fewer studies have been concerned with this cascade so the scientific knowledge of this system is tenuous.[8] Other factors such as the Alpha-1 adrenergic receptor and Sigma-1 receptor have been studied yet these are not understood to contribute to the cognitive changes psychedelics impress upon the senses.[9]
Natural stores of psychedelics can act on a separate system which administered compounds may not, specifically the Trace amine-associated receptors, further enhancing the range of symptoms an internal release can initiate.[10]
Biological activity[edit]
Humans naturally create N,N-Dimethyltryptamine from the essential amino acid precursor (Tryptophan)[11][8], it is synthesized and released in minute amounts during specific events such as REM sleep[12], near-death occasions[13], and spiritual experiences.[14]
While some associated machinery and mechanisms are defined, it is currently unknown what evolutionary purpose endogenous hallucinogens serve despite their occurrence among numerous lifeforms.[9] They act as perception modulators, with increasing concentrations leading to a dose-dependent dysfunction with reality-checking mechanisms in the human physiology and psyche [9] [11].
The changes in auditory and language capabilities due to psychedelics can either be from the natural release of stores in the body or from ingesting synthesized compounds [11]. It hasn't been demonstrated that any psychedelics act solely upon any single components of the neural pathways specific for hearing, but rather alter gross Monoamine neurotransmitter dynamics and neural communication patterns in the central nervous system [9].
Psychedelic drugs have been correlated with positive symptoms of Psychosis and Schizophrenia [15] as well as stress-induced heightened activity of endogenous N,N-Dimethyltryptamine in relation to psychosis-like symptoms.[16] This is related to altered dynamics between states of brain wave activity and the consequent perception of reality that can influence hearing and language abilities.[4]
In a study with Ayahuasca, brain wave states associated with top-down processing from conscious awareness were decreased, while bottom-up processes originating from the senses were strengthened (Top-down vs Bottom-up processing).[17]
Effects on hearing and language[edit]
The altered perceptual changes involves psychedelic compound activity in the body and fluctuations in a person's normal ability to perceive the environment, specifically with auditory stimuli. In 1996, a relationship between a hallucinogen, Psilocybin and enhanced Semantics activity was shown to broaden the consciously available spectrum of words a subject could produce in association with a given prime; the results found that response time under the influence increased but the number of errors across subjects did not.[2] This was one of the first experiments to demonstrate the ability of a hallucinogen to increase language-associative capabilities and the supplemented spread of cortical activity underlying enhanced lexical abilities.[2]
A PET scan imaging experiment was conducted in 2001, in which the authors concluded that consistent, increased activity was demonstrated in many cortical regions while under the influence of various hallucinogens.[18] Some indicated regions, such as the left dorsolateral prefrontal (Broca's area), left inferior temporal cortex, and bilateral temporo-parietal association cortex (Wernicke's area), are understood to be heavily involved with the comprehension and production of human language.[18]
In 2015, it was demonstrated that a significant statistical increase in the emotional response to music occurred with participants under the effect of administered LSD who were asked to rate the meaningfulness of different music clips, before and after administration.[19] The participants produced a measurably higher density of descriptive vocabulary when asked to freely self-report their experience while under the influence.[19] A similar conclusion was reached in a study which followed the same protocol while imaging the brain and saw changes in the functioning of the parahippocampal region, which is involved in Sentence processing and Language production.[20]
Another study conducted in 2016 was the first to demonstrate that administered LSD not only increased semantic activation similarly to Psilocybin, but increased errors among words considered to be in similar categories such as body parts and clothing as opposed to vehicles.[3] This demonstrates the decreased ability to sufficiently self-correct with respects to word matching, which is consistent with previous experiments suggesting that hallucinogens can impair attention capabilities.[2] However, the majority of experimental errors occurred when word associations were relatively close in meaning such as cat and dog compared to cat and car, participants under the effects of LSD did not present with any other statistical errors compared to controls.[3] This indicates that while it may be more difficult to focus attention while under the effects of a hallucinogen, errors involving hesitations and switched answered were no higher than control.[2][19][3]
Meta-Analyses and Prevailing Theories[edit]
Since the 1970's, studies have demonstrated that psychedelics induce an altered Default mode network based on primary process thinking which is a bottom-up, automatic mode of thinking.[21] The mechanisms underlying this change aren't fully understood but it likely involves a combination of reduced organizational function of metabolically-active regions and increased functioning of areas that are minimally active[22][4][21] as well as some contribution from activity of 5-HT2A receptors densely embedded within the neocortex.[5]
The default mode network states that there is a specific circuit within the nervous system that mediates the top-down, 'resting state' of the brain when not actively engaged in any physical actions; it underlies self-reflection, theory-of-mind, mental time-travel (memory recollection), day-dreaming, and is considered to be the neurological basis of the self.[21][22][4] Performing any physical actions or changing the mental state to being more in the present alters the activity of this network but only minimally; psychedelics can directly alter the functioning of the default mode network, leading to the changes in 'default state' experienced by someone under the influence of a psychedelic.[22] While many scientists agree that changes to the default mode network is involved in altered hearing and language capabilities, there have been several theories which hypothesize how this is mediated.
Entropic Brain Theory[edit]
Psychedelics alter the functioning of the default mode network such that increased Entropy, or chaos is imaged in subjects' brains under the influence as well as lasting changes to functional connectivity among subcortical regions.[22] This theory assumes that entropy is normally suppressed by both subconscious and conscious mechanisms which entrain thought processes to maintain a certain organization and form of neural communication. This ideology derives from Freud's line of thought in that secondary thinking, which is the default mode network, is the mediator of entropic suppression and the originator of the self-reflecting, evolved man yet it is the limiting factor in cognition as it 'filters' information received from the environment.[22]
This theory argues that psychedelics directly increase entropy in the nervous system by decoupling entrained activity or default mode network connectivity, especially in the medial temporal lobes, which are critical to hearing and language capabilities; this may explain the changes seen in hearing by subjects under the influence of psychedelics.[22] While EBT does well to explain the changes seen in hearing as a result of increased primary process thinking, it doesn't define the exact mechanisms by which psychedelics are specifically altering language functions other than stating that disorganizing effects of psychedelics changes the way the 'language centers' of our brain work.
Integrated Information Theory[edit]
IIT is a sub-shoot of EBT and takes into account that distinct brain states exist and are measurable by neuroimaging techniques such as EEGs, but extends the caveat that brain states are more likely to be hybrids and variations along a continuum as opposed to separate states.[4]. It is based on the presumption that the brain seeks to balance states to optimize the needs of the self based on past/present information and imagined future possibilities; as such, there must be a mediator between the primary and secondary thinking processes.
This theory states that there is a pas de trois between entropy, cognitive flexibility, and cause-effect information; psychedelics upset the delicate balance of this system to influence a person to become more mentally flexible and unconstrained yet less precise and controlled as organized structures become less organized and synergistic.[4] This theory also cannot explain the exact cause of neural entropy but it does validate previous findings seen with psychedelics and changes to language capabilities.[4]
Predictive Processing Theory[edit]
PP is an inter-disciplinary ideology which combines elements of Bayesian approaches to brain function, Predictive coding, and the Free energy principle [4]. The core tenet is that the human brain constantly makes predictions about future events and uses sensory feedback to self-correct or self-verify hypothesized information about the external environment and that the brain seeks to minimize prediction errors while optimizing prediction verifications, which is how the brain learns.[4] Higher-order neurons in the brain estimate possibilities while lower-order neurons receive them from the external world and communicate to the brain to 'constrain' the theorized possibilities to a single, actual event. Psychedelic drugs, through 5-HT2A receptor agonism, hyperexcite higher-order neurons so that range of imagined possibilities is enhanced, resulting in the hyper-vivid and/or otherworldly aspect usually accredited to serotonergic psychedelic drugs and may be the neural mechanism by which they can change the way humans hear, understand, and produce language.[4]
Future Studies[edit]
These studies and analyses offer insight into human psycholinguistics and even affords some support to language theories such as Distributional semantics yet there is still a deficit in the understanding of how language works at a precise level to fully explain how this system is affected by psychedelics.[2][19][3] For instance, the majority of statistical errors demonstrated by the subjects under the influence of hallucinogens were primarily exhibited when words or ideas were more similar, lending credence to the ideology that similar words are placed within phonological neighborhoods so that activation of a word may prime another closely positioned word.[3] Increasing numbers of controlled studies currently being conducted with psychedelics and brain imaging are being conducted to further define the mechanisms of how language works.[23]
Further Reading[edit]
- Psychedelic_microdosing
- Endogenous DMT and Inflammatory Response
- LSD and related compounds
- DMT: The Spirit Molecule
References[edit]
- ↑ 1.0 1.1 The American Heritage Dictionary of Medicine. Houghton Mifflin Publishing Company. Search this book on
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Spitzer, Manfred; Thimm, Markus; Hermle, Leo; Holzmann, Petra; Kovar, Karl-Artur; Heimann, Hans; Gouzoulis-Mayfrank, Euphrosyne; Kischka, Udo; Schneider, Frank (June 1996). "Increased activation of indirect semantic associations under psilocybin". Biological Psychiatry. 39 (12): 1055–1057. doi:10.1016/0006-3223(95)00418-1.
- ↑ 3.0 3.1 3.2 3.3 3.4 3.5 Family, Neiloufar; Vinson, David; Vigliocco, Gabriella; Kaelen, Mendel; Bolstridge, Mark; Nutt, David J.; Carhart-Harris, Robin L. (11 August 2016). "Semantic activation in LSD: evidence from picture naming". Language, Cognition and Neuroscience. 31 (10): 1320–1327. doi:10.1080/23273798.2016.1217030.
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 4.8 4.9 Swanson, LR (2018). "Unifying Theories of Psychedelic Drug Effects". Frontiers in pharmacology. 9: 172. doi:10.3389/fphar.2018.00172. PMID 29568270.
- ↑ 5.0 5.1 Kraehenmann, R; Pokorny, D; Aicher, H; Preller, KH; Pokorny, T; Bosch, OG; Seifritz, E; Vollenweider, FX (2017). "LSD Increases Primary Process Thinking via Serotonin 2A Receptor Activation". Frontiers in pharmacology. 8: 814. doi:10.3389/fphar.2017.00814. PMID 29167644.
- ↑ Bolstridge, M (March 2013). "The Psychedelic Renaissance: Reassessing the Role of Psychedelic Drugs in 21st Century Psychiatry and Society". British Journal of Psychiatry. 202 (3): 239. doi:10.1192/bjp.bp.112.122481.
- ↑ Johnson, MW; Richards, WA; Griffiths, RR (30 May 2008). "Human hallucinogen research: guidelines for safety". Journal of Psychopharmacology. 22 (6): 603–620. doi:10.1177/0269881108093587.
- ↑ 8.0 8.1 Barker, Steven A.; Borjigin, Jimo; Lomnicka, Izabela; Strassman, Rick (December 2013). "LC/MS/MS analysis of the endogenous dimethyltryptamine hallucinogens, their precursors, and major metabolites in rat pineal gland microdialysate". Biomedical Chromatography. 27 (12): 1690–1700. doi:10.1002/bmc.2981.
- ↑ 9.0 9.1 9.2 9.3 Nichols, David E (February 2004). "Hallucinogens". Pharmacology & Therapeutics. 101 (2): 131–181. doi:10.1016/j.pharmthera.2003.11.002.
- ↑ Wallach, J.V. (January 2009). "Endogenous hallucinogens as ligands of the trace amine receptors: A possible role in sensory perception". Medical Hypotheses. 72 (1): 91–94. doi:10.1016/j.mehy.2008.07.052.
- ↑ 11.0 11.1 11.2 Carbonaro, Theresa M.; Gatch, Michael B. (September 2016). "Neuropharmacology of N,N-dimethyltryptamine". Brain Research Bulletin. 126 (Pt 1): 74–88. doi:10.1016/j.brainresbull.2016.04.016. PMC 5048497. PMID 27126737.
- ↑ Callaway, J.C. (June 1988). "A proposed mechanism for the visions of dream sleep". Medical Hypotheses. 26 (2): 119–124. doi:10.1016/0306-9877(88)90064-3.
- ↑ Richard, Yensen, (1988). "Helping at the Edges of Life: Perspectives of a Psychedelic Therapist". Journal of Near-Death Studies. 6 (3). ISSN 0891-4494.
- ↑ Yaden, David B.; Le Nguyen, Khoa D.; Kern, Margaret L.; Belser, Alexander B.; Eichstaedt, Johannes C.; Iwry, Jonathan; Smith, Mary E.; Wintering, Nancy A.; Hood, Ralph W.; Newberg, Andrew B. (24 October 2016). "Of Roots and Fruits: A Comparison of Psychedelic and Nonpsychedelic Mystical Experiences". Journal of Humanistic Psychology. 57 (4): 338–353. doi:10.1177/0022167816674625.
- ↑ Murray, Robin M. (1 June 1979). "Increased Excretion of Dimethyltryptamine and Certain Features of Psychosis". Archives of General Psychiatry. 36 (6): 644–9. doi:10.1001/archpsyc.1979.01780060034003. PMID 286576.
- ↑ Grammenos, Dionysios; Barker, Steven A. (2 November 2014). "On the transmethylation hypothesis: stress, N,N-dimethyltryptamine, and positive symptoms. psychosis". Journal of Neural Transmission. 122 (6): 733–739. doi:10.1007/s00702-014-1329-5.
- ↑ Domínguez-Clavé, Elisabet; Soler, Joaquim; Elices, Matilde; Pascual, Juan C.; Álvarez, Enrique; de la Fuente Revenga, Mario; Friedlander, Pablo; Feilding, Amanda; Riba, Jordi (September 2016). "Ayahuasca: Pharmacology, neuroscience and therapeutic potential". Brain Research Bulletin. 126: 89–101. doi:10.1016/j.brainresbull.2016.03.002.
- ↑ 18.0 18.1 Vollenweider, FX (December 2001). "Brain mechanisms of hallucinogens and entactogens". Dialogues in clinical neuroscience. 3 (4): 265–79. PMC 3181663. PMID 22033605.
- ↑ 19.0 19.1 19.2 19.3 Kaelen, M.; Barrett, F.S.; Roseman, L.; Lorenz, R.; Family, N.; Bolstridge, M.; Curran, H. V.; Feilding, A.; Nutt, D. J.; Carhart-Harris, R. L. (11 August 2015). "LSD enhances the emotional response to music". Psychopharmacology. 232 (19): 3607–3614. doi:10.1007/s00213-015-4014-y.
- ↑ Kaelen, Mendel; Roseman, Leor; Kahan, Joshua; Santos-Ribeiro, Andre; Orban, Csaba; Lorenz, Romy; Barrett, Frederick S.; Bolstridge, Mark; Williams, Tim; Williams, Luke; Wall, Matthew B.; Feilding, Amanda; Muthukumaraswamy, Suresh; Nutt, David J.; Carhart-Harris, Robin (July 2016). "LSD modulates music-induced imagery via changes in parahippocampal connectivity". European Neuropsychopharmacology. 26 (7): 1099–1109. doi:10.1016/j.euroneuro.2016.03.018.
- ↑ 21.0 21.1 21.2 Preller, KH; Vollenweider, FX (2018). "Erratum to: Phenomenology, Structure, and Dynamic of Psychedelic States". Current topics in behavioral neurosciences. 36: 1. doi:10.1007/7854_2017_477. PMID 28710675.
- ↑ 22.0 22.1 22.2 22.3 22.4 22.5 Carhart-Harris, Robin L.; Leech, Robert; Hellyer, Peter J.; Shanahan, Murray; Feilding, Amanda; Tagliazucchi, Enzo; Chialvo, Dante R.; Nutt, David (2014). "The entropic brain: a theory of conscious states informed by neuroimaging research with psychedelic drugs". Frontiers in Human Neuroscience. 8. doi:10.3389/fnhum.2014.00020.
- ↑ Assi, Sulaf; Gulyamova, Nargilya; Ibrahim, Kinda; Kneller, Paul; Osselton, David (May 2017). "Profile, effects, and toxicity of novel psychoactive substances: A systematic review of quantitative studies". Human Psychopharmacology: Clinical and Experimental. 32 (3): e2607. doi:10.1002/hup.2607.
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