Talk:Ketamine

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Potential references

Medical applications

  • Wilkinson, S. T., Ballard, E. D., Bloch, M. H., Mathew, S. J., Murrough, J. W., Feder, A., … Sanacora, G. (2017). The Effect of a Single Dose of Intravenous Ketamine on Suicidal Ideation: A Systematic Review and Individual Participant Data Meta-Analysis. American Journal of Psychiatry. https://doi.org/10.1176/appi.ajp.2017.17040472

Research

Intravenous administration

In medical settings, ketamine is usually injected intravenously or intramuscularly.[1] However, intravenous self-injection of ketamine is very dangerous. Karl Jansen warns: "If ketamine is taken by a rapid .i.v injection, it can sometimes cause the person to stop breathing for a short time (up to a minute). 2 mg/kg given i.v. as a fast injection produced a significant fall in blood oxygen lasting about 10 minutes. When given slowly (over 1.5 minutes), breathing is well maintained and may even increase slightly. However, the self-injector may then pass out before the injection is complete. Any desire to experiment with i.v. use should be resisted for as long as possible. As noted above, ketamine does not usually suppress breathing, but exceptions occur after rapid i.v. injection. This is safer when the psrson is lying down, or at least not sitting on an edge. Bathrooms are dangerous because the surface are hard and angular, there is a risk of drowing, and bleeding is more likely in warm water."[2]

Intravenous infusion in research labs has produced a very high correlation between blood levels and psychedelic effects.[3] The intravenous administration of 50 - 100 mg of ketamine can reproduce all of the features which have commonly been associated with NDE's. Intramuscular administration also results in NDE's, but events evolve at a slower pace and are longer lasting (Domino et al., 1965; Rumpf ,1969; Collier, 1972; Siegel,1978, 1980,1981; Stafford, 1977; Lilly, 1978; Grinspoon and Bakalar, 1981; White, 1982; Ghoniem et al., 1985; Sputz, 1989; Jansen, 1989a,b, 1990b, 1993, 1995, 1996).[4]

The typical intravenous antidepressant dosage of ketamine used to treat depression is low and results in maximal plasma concentrations of 70 to 200 ng/mL (294–841 nM).[5]

Ketamine can reproduce every feature of the near death experience

p. 26 “It [Ketamine] can reproduce every feature of the NDE, from rapid trips through dark tunnels into light and the conviction that one is dead, to ‘seeing spirits’, ‘telepathic communion with God’, out-of-body experiences, mystical states, peace and tranquillity (5, 7, 32-34, 44).“[6]

“The K-hole experience appears to vary with the individual, but can sometimes reproduce the features of a ‘near-death experience’ (NDE), including buzzing/ringing/whistling sounds at the beginning, travel through a dark tunnel into light at a high speed, the conviction that one is dead, apparent telepathic communion with God, intense visions and out-of-body experiences (Jansen, 2000).”[7]

Ketamine is a primary predictor of out-of-body experiences

“Self-report data (N = 192) from an online survey indicate that both lifetime frequency of ketamine use and OBEs during ketamine intoxication were more strongly related to the frequency of OBEs and related phenomena than other drugs.“[8]

References

  1. ↑ Lankenau, SE; Sanders, B; Bloom, JJ; Hathazi, D; et al. (March 2007). "First injection of ketamine among young injection drug users (IDUs) in three U.S. cities". Drug and Alcohol Dependence. 87 (2–3): 183–93. doi:10.1016/j.drugalcdep.2006.08.015. PMC 1852477 Freely accessible. PMID 16979848. 
  2. ↑ Ketamine: Dreams and Realities, p276-277
  3. ↑ [Ketamine: Dreams and Realities, p73]
  4. ↑ http://www.near-death.com/experiences/lsd03.html
  5. ↑ Sanacora G, Frye MA, McDonald W, Mathew SJ, Turner MS, Schatzberg AF, Summergrad P, Nemeroff CB (2017). "A Consensus Statement on the Use of Ketamine in the Treatment of Mood Disorders". JAMA Psychiatry. 74 (4): 399–405. doi:10.1001/jamapsychiatry.2017.0080. PMID 28249076. 
  6. ↑ Jansen, K. L. R. (1990). Neuroscience and the near-death experience: roles for the NMSA-PCP receptor, the sigma receptor and the endopsychosins. Medical Hypotheses, 31(1), 25-29. https://doi.org/10.1016/0306-9877(90)90048-J
  7. ↑ Dillon, P., Copeland, J., & Jansen, K. (2003). Patterns of use and harms associated with non-medical ketamine use. Drug & Alcohol Dependence, 69(1), 23-28. https://doi.org/10.1016/S0376-8716(02)00243-0
  8. ↑ Wilkins, L. K., Girard, T. A., & Cheyne, J. A. (2011). Ketamine as a primary predictor of out-of-body experiences associated with multiple substance use. Consciousness and cognition, 20(3), 943-950. https://doi.org/10.1016/j.concog.2011.01.005
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