Mathews Journal of Forensic Research

2692-8442

Previous Issues Volume 1, Issue 1 - 2018

Review Article Abstract PDF  

Overdose Toxic Effect of Hallucinogenic Drug: Lysergic Acid Diethylamide

Rohit Kumar Verma1 , Mahipal Singh Sankhla2 , Rajeev Kumar3

1Student of B.Sc. (Hons.) Forensic Science,

2Research Scholar, Division of Forensic science, Galgotias University, Greater Noida.

3Associate Professor, Division of Forensic science, Galgotias University, Greater Noida.

Corresponding Author: Mahipal Singh Sankhla, Research Scholar, Division of Forensic science, Galgotias University, Greater Noida, Tel: +91-9818019674; E-Mail: [email protected]

Received Date:  22 Sep 2018   Accepted Date:  02 Oct 2018   Published Date: 05 Oct 2018

Copyright © 2018 Sankhla MS

Citation: Verma RK, Sankhla MS, and Kumar R. (2018). Overdose Toxic Effect of Hallucinogenic Drug: Lysergic Acid Diethylamide. Mathews J Foren. 1(1): 004.

ABSTRACT

In today's world major problem youth intake of drugs are increasing day by day. Lysergic acid Diethylamide (LSD) is a synthetic hallucinogenic drug.LSD is derived from lysergic acid compound found in Ergot, a fungus that develops on moldy rye plant and different grains. It can be taken in the form of stamps (microdots), tablets, capsules, windowpanes (gelatin squares) etc. It increases blood pressure, heart rate and body temperature, loss of appetite, dry mouth, and sweating etc.LSD causes stimulating impacts by disturbing the interaction of the neurotransmitter serotonin and nerve cells which effects the brain. LSD is promptly consumed by the gastrointestinal tract with ingestion being the most widely route of exposure.LSD also uses in major date rape drug in sexual assault cases. It also effect the various parts of the body physically as well as mentally. It plays a major role in physiological effect and psychological effect. The overdose of toxic effect of LSD a person was in coma and sometimes death may occur.

KEYWORDS

LSD; Hallucinogenic; Toxic; Effect; Drugs; etc.

INTRODUCTION

Lysergic acid diethylamide (LSD) is a synthetic hallucinogenic drug. LSD is derived from the from lysergic acid, which is found in Ergot a fungus that develop on moldy rye and different grains. There was a Swiss scientist Albert Hofmann first orchestrated LSD in 1938 as a worker of the Sandoz Laboratories. Hofmann was leading exploration on the helpful estimation of the lysergic acid mixes as a circulatory and respiratory stimulant, however no extraordinary impacts were found and his research was discontinued. Hofmann found the hallucinogenic effect of LSD in 1943 when he coincidentally ingested a portion of the drug. This discovery reestablished interest for the drug as a conceivable treatment for schizophrenia and as an examination instrument in concentrate mental illness [1]. During the 1950s LSD (Delysid c Sandoz) was acquainted to the therapeutic community as an experimental tool to induce temporary psychotic-like states in normals ("model psychosis") and later to enhance psychotherapeutic treatments ("psycholytic" or "psychedelic" therapy)[2]. During the end of the 1960s, people begin using LSD for recreational and religious purposes, [3] prompting the arrangement of a "psychedelic movement" during the international student's complaints of that time [4,5]. In spite of the fact that the complaints progress declined, the utilization of LSD sustained. It is still a most important hallucinogen, illicitly utilized around the world. The National Survey on Drug Use and Health [6] has, for instance, announced LSD as a major drug of abuse in every yearly survey since the 1970s. In the 1990, LSD was amongst the position of "club drugs" that, along with MDMA and ketamine, were establish at dance clubs and large secretive parties recognized as raves [7]. A current national study suggest LSD utilize amongst high school students is declining, and may be at its lowest point in several years [8].

LSD's Use of Sexual Assault as a Date Rape Drug Date Rape Drugs are very normal and on the increase in developed as well as developing countries. Under the influence of LSD, the capacity to make reasonable judgment and see common date rape drug which can be lethal in quantity was taken in the drink and other forms. After an LSD trip, the abuser may suffer acute unconsciousness, anxiety, and depression may also use in the sexual assaults flashbacks, which are recurrences of the effects of LSD days or still months after captivating the last dosage. A flashback occurs abruptly, often without caution, usually in people who use hallucinogens constantly or have a sexual assault individuality problem. Bad trips and flashbacks are single part of the risk of LSD utilize. LSD users may also manifest relatively long-lasting psychoses, such as schizophrenia or brutal despair.LSD produce patience, so some users who take the drug repeatedly must take increasingly higher doses to attain the condition of intoxication that they had formerly achieved. [9].

Toxic Effect of Lysergic Acid Diethylamide on Human Health LSD's Effects on the Brain user experience the effects of LSD within 30 to 90 minutes after intake, and these effects may last as long as 12 hours. LSD causes hallucinogenic effects by disturbing the contact of the neurotransmitter serotonin and nerve cells. Serotonin is concerned in the control of behavioral, perceptual, and regulatory system, for example mood, hunger, body temperature, sexual behavior, and muscle control.[1] LSD's impact on serotonin also affect an region of the brain that detect exterior stimuli from all above the body, make it more approachable to effort from the surroundings. [10] LSD's effects on brain functioning are multifaceted and not fully understand. LSD influence various neurotransmitter systems [11,12].

Psychological Effect of LSD A modest dosage ((75–150 μg p.o.) of LSD will considerably change condition of consciousness. This modification is characterize by a stimulation of affect (mostly experience as euphoria), improved ability for introspection, and changed psychological functioning in the course of Freudian major processes, known or else as hypnagogic understanding and thoughts [13]. Particularly notable are perceptual change such as illusion, pseudo-hallucinations, synesthesias, and alteration of thinking and instance understanding. Changes of body-image and ego function also frequently take place [14,15].The acute psychological effects of LSD last between 6and 10 h, depending on the dose apply. The negligible identifiable dose of LSD in humans is about 25 μg p.o. [16,17]. The "optimal" dose for a characteristic completely outspread LSD reaction is predictable to be in the range of 100–200 μg [18,16,19].shocking experience (called "bad trips") can have long-lasting effects on LSD users, include mood swing and rarely flashback phenomenon [20]. It must be noted, however, that these usually take place in unrestrained circumstances. On the other hand, it has been exposed that under controlled and helpful conditions, the LSD experience may have permanent positive effects on attitude and personality [21].The psychologic effects of LSD are dosage related and effect change in stimulation, emotion, perception, thought processes, and self-image. The reply to the drug is connected to the person's state of mind, emotion, or expectations at the time and can be changed by the collection or location [22].Psychological effects were alike to those of lysergic acid diethylamide (LSD), with psilocybin careful to be more powerfully illustration, fewer sensitively strong, more euphoric, and with fewer panic reaction and less possibility of paranoia than LSD [23,24]. LSD has been describe as a "non-specific amplifier of the unconscious" since it promote the dormant psychodynamics of the patients and enable right of entry to thoughts, relations, feelings and inner processes, which are more often than not barred from consciousness. [25,26]. current scientific examination of psilocybin have indicate that it is not dangerous to bodily physical condition [27].

Neurobiological Effects of Lysergic Acid Diethylamide  The huge development that has been complete in our sympathetic of the mechanism of action of psychedelics[11,28-31]. The neurobiology of emotional disorders has enable us to assume new hypothesis concerning the therapeutic mechanism of psychedelics and their scientific application. At this point we focus on the glutamatergic and serotonergic mechanism of action of psychedelics with look upon to their most promising indication n — that is, their utilize in the action of depression and anxiety [32-34]. LSD given to normal's (0.5 to 1 μg/ kg p.o.) abridged the excretion of inorganic phosphate (as establish also with these other hallucinogens mescaline and psilocybin), suggestive of that LSD might take action on enzymatic systems to make easy the binding of phosphate [35]. Though this reduce is constantly observed, its consequence in regard to the action of LSD is indistinct, and it might just be a simple nonspecific manifestation of psychological pressure [36].These change were connected with events of psychological condition and constant with potential neurobiological substrates of main mental illness [37].

Somatic Effects of Lysergic acid diethylamide Cerletti report an LD-50 for mice with intravenous function of 280mg/kg which might involve an LD-50 of several grams of psilocybin in human [38]. The threshold dosage for considerable sympathomimetic effects in humans is 0.5–1.0 μg/kg LSD p.o. [39].These change can be the consequence of an excitatory syndrome cause by innermost stimulation of the sympathetic system. lower of blood pressure and Brady Cardiac was establish in the affected animals, and it was finished that the sympathomimetic effects of LSD require the commencement of higher cortical centers [40]. The somatic effects in humans were investigate first by Quetin in a non-blind study in healthy volunteers (n = 29, 8–12mg p.o., i.m.) [41]. mainly somatic effects credited to LSD, and report mostly in fewer methodologically complicated studies, may be secondary effects cause by the psychological response to the drug (i.e., the physiological and CNS response to the psychological experience) [42].

Pharmacological Effects of Lysergic Acid Diethylamide The pharmacology of LSD is difficult but the mechanism of action is still not understandable [43]. After make use of of LSD psychological and sympathomimetic effects continue for 30– 45min, reaching their peak after 1.5–2.5 h[44,45].A important pharmacological difference between LSD and other type of hallucinogens is the straight dopaminergic effect of LSD, which is not a component of the pharmacology of phenethylamineand tryptamine-type hallucinogens. Dopaminergic effects of LSD have been documented for many years [46].

DISCUSSION

In this review study Lysergic acid diethylamide is most common drug was taken by youth. It is a hallucinogenic and psychotropic drug. In overdose toxic effect, the person may go to coma and sometime death may occur. Human health is directly affected by Neurological dysfunction and hallucinogen. Earlier study have shown, exceed LSD mixes with drink uses as a sexual assault cases. The disease is basically related to chronic toxicity of LSD gastrointestinal effect, tremors, high blood pressure, bad trip, etc. This was a major essential growing problem that provides us to keep the use of LSD in differential for any patient who present with symptoms described about. The lack of scientific research in human awareness about the risk of LSD and youth will continuously use and particularly by those who have already experienced the effect of LSD.

CONCLUSION

The toxicologists have detected the chronic and acute toxic effect of LSD in various parts of human body. Analytical instrument are use for detection of concentration in blood, saliva, urine, sweat of LSD by using GC-MS, HPLC, LC-MS. In nowadays youth are rapidly increasing use of LSD drug in developing countries. Benzodiazepines (diazepam) is the treatment alternative for sedation of LSD drug. The LSD is illicit drug in India and most of the countries the world. Some of the countries use these drugs as medicinal purposes. Further related study agreed out in the future with sample detained in different states, will allow a quantitative report of the drug in these samples to be defined at the national level.

REFERENCES

  1. National Institute on Drug Abuse. (2001). Research Report Series: Hallucinogens and Dissociative Drugs (NIH Publication number 01-4209). Washington, DC: US.
  2. Passie T. (1997). Psycholytic and psychedelic therapy research: A complete international bibliography 1931 1995. Hannover: Laurentius Publishers.
  3. Lee MA and Shlain B. Acid dreams, the CIA, LSD, and the sixties rebellion. New York: Grove Press, 1985.
  4. Boskin J and Rosenstone RA. (1969). Protest in the sixties. Ann Am Acad Pol SocSci. 382:1-219.
  5. Hunter R. The storming of the mind. Toronto, Montreal:Doubleday, SAMHSA. Available at: http://www. oas.samhsa.gov/ ecstasy.htm, 2006. Accessed 13 July 2008.
  6. National Drug Intelligence Center. (April 2001). Information Bulletin: Raves (Product no. 2001-L0424-004). Washington, DC:US
  7. National Institute on Drug Abuse. (12/16/02). 2002 Monitoring the Future Survey: Decreasing in Use of Marijuana, Club Drugs, and Tobacco. Retrieved February 11, 2003.
  8. Sankhla MS, Kumari M, Nandan M and Kumar R. (2017). Forensic Identification of Sexual Assault by use of Date Rape Drugs. Journal of Recent Research and Applied Studies. 4, 7(9): 42-46.
  9. Carson-Dewitt R. (2001). Encyclopedia of Drugs, Alcohol, & Addictive Behavior, 2nd edition (vol. 2). Macmillan Reference USA. New York, NY: US
  10. Nichols DE Pharmacol Ther. 2004. The pharmacology of lysergic acid diethylamide: a review. 101(2):131-81.
  11. Passie T, Halpern JH, Stichtenoth DO, Emrich HM, Hintzen A CNS NeurosciTher. (2008)Winter; 14(4):295-314.
  12. Farthing GW. (1992).The Psychology of Consciousness. EnglewoodCliffs: Prentice Hall. (26).
  13. Katz MM, Waskow IE and Olsson J. (1968).Characterizing the psychological state produced by LSD. J AbnormPsychol. 73(1):1-14.
  14. Savage C. (1955).Variations in ego feeling induced by D-lysergic acid diethylamide (LSD-25). Psychoanal Rev. 42(1):1-16.
  15. Hoffer A. (1965). LSD: A review of its present status. ClinPharmacolTher. 6:183-255.
  16. Stoll WA. (1947). Lysergs"auredi"athylamid, einPhantastikumaus der Mutterkorngruppe. Schweiz Arch NeurolPsychiatr. 60: 279-323
  17. Leuner H. (1962). Die experimentellePsychose. Berlin, G" ottingen, Heidelberg: Springer,
  18. Grof S. (1980). The effects of LSD on chromosomes, genetic mutation, fetal development and malignancy. In: Grof S. LSD psychotherapy. Pomoma, CA: Hunter House. 320-347.
  19. Strassman RJ. (1984). Adverse reactions to psychedelic drugs: A review of the literature. J Nerv Ment Dis. 172(10): 577-595.
  20. McGlothlin WH, Cohen S and McGlothlin MS. (1967). Long lasting effects of LSD on normals. Arch Gen Psychiatry. 17:521-532.
  21. Bowers MB and Freedman DX. (1966). Psychedelic experiences in acute psychoses. Arch Gen Psychiatry. 15(3): 240-248.
  22. Passie T, Seifert J, Schneider U and Emrich HM. (2002). The pharmacology of psilocybin. Addict Biol. 7(4):357- 364.
  23. Passie T. (2004). A history of the use of psilocybin in psychotherapy. In: Metzner R, ed. Teonanacatl: Sacred Mushroom of Vision. El Verano, CA: Four Trees. 109-134.
  24. Grof S. (1975). Realms of the Human Unconscious. New York, NY: Viking.
  25. Leuner H. (1981). Halluzinogene. Bern: Huber.
  26. Hasler F, Grimberg U, Benz MA, Huber T, et al. (2004). Acute psychological and physiological effects of psilocybin in healthy humans: a double-blind, placebo controlled dose-effect study. Psychopharmacology (Berl). 172(2):145-156.
  27. Gonzalez-Maeso J and Sealfon SC. (2009). Agonist-trafficking and hallucinogens. Curr. Med. Chem. 16(8): 1017- 1027.
  28. Winter JC. (2009). Hallucinogens as discriminative stimuli in animals: LSD, phenethylamines, and tryptamines. Psychopharmacology (Berlin). 203(2): 251-263.
  29. Large CH. (2007). Do NMDA receptor antagonist models of schizophrenia predict the clinical efficacy of antipsychotic drugs? J. Psychopharmacol. 21(3): 283-301.
  30. Quirk MC, Sosulski DL, Feierstein CE, Uchida N. et al. (2009). A defined network of fastspiking interneurons in orbitofrontal cortex: responses to behavioral contingencies and ketamine. 3(3).
  31. Sanacora G, Zarate CA, Krystal JH. (2008). Targeting the glutamatergic system to develop novel, improved therapeutics for mood disorders. NatureRev. Drug Discov. 7(5): 426-437.
  32. DeRubeis RJ, Siegle GJ and Hollon SD. (2008). Cognitive therapy versus medication for depression: treatment outcomes and neural mechanisms. Nature Rev.Neurosci. 9(10): 788-796.
  33. Clark L, Chamberlain SR and Sahakian BJ. (2009). Neurocognitive mechanisms in depression: implications for treatment. Annu. Rev. Neurosci. 32: 57-74
  34. Pincus G and Hoagland H. (1950). Adrenal cortical responses to stress in normal and psychotic subjects. Am J Psychiatry. 106(9): 651-659.
  35. Hollister Le and Moore FF. (1965). Increased plasma free fatty acids following psychotomimetic drugs. J Psychiat Res. 3:199-203.
  36. Vollenweider FX, Leenders KL, Scharfetter C, Maguire P, et al. (1997). Positron emission tomography and fluorodeoxyglucose studies of metabolic hyperfrontality and psychopathology in the psilocybin model of psychosis. Neuropsychopharmacology.16(5):357-372
  37. Cerletti A. (1958). Etude pharmacologique de la psilocybine. In: Heim R, Wasson RG, editors. Les champignons hallucinogenes du mexique. Paris: Museum de historienaturelle. 268-271.
  38. Greiner TH, Burch NR and Edelberg R. (1958). Psychopathologyand psychophysiology of minimal LSD-25 dosage. AMAArch Neurol Psychiatry. 79(2): 208-210.
  39. Tauberger G and Klimmer OR. (1968). Effects of high doses of d-lysergic acid diethylamide on the respiration, blood circulation and central sympathicus tone of cats. Arzneimittelforschung. 18(12):1489-1491.
  40. Quetin AM. (1960). La Psilocybineenpsychiatrie Clinique etexperimentale. Paris: Medical Dissertation University of Paris.
  41. Kornetsky C. (1957). Relation of physiological and psychological effects of lysergic acid diethylamide. AMA Arch NeurolPsychiat. 77(6):657-658.
  42. Passie T, Halpern JH, Stichtenoth DO, Emrich HM, et al. (2008). The pharmacology of lysergic acid diethylamide: a review. CNS Neuroscience & Therapeutics. 14(4): 295- 314.
  43. Leuner H. (1962). Die experimentellePsychose. Berlin, Gottingen, " Heidelberg: Springer.
  44. Rinkel M, Hyde RW, Solomon HC and Hoagland H. (1955). Experimental psychiatry. II. Clinical and physio-chemical observations in experimental psychosis. Am J Psychiatry 111(12): 881- 895.
  45. Watts VJ, Lawler CP, Fox DR, Neve KA, et al. (1995). LSD and structural analogs: pharmacological evaluation at D1 dopamine receptors. Psychopharmacology 118(4): 401- 409.

Creative Commons License

© 2015 Mathews Open Access Journals. All Rights Reserved.

Open Access by Mathews Open Access Journals is licensed under a
Creative Commons Attribution 4.0 International License.
Based On a Work at Mathewsopenaccess.com