Legality of Cannabis by U.S. Jurisdiction

Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
→‎Further reading: added "State of research before 1974"
New section "History"; deletion of text that is not specific to or unrelated to the subject of the article
Line 27: Line 27:
The results of a [[twin study]], however, presented strong indications that genetic and environmental factors may be rather weak, possibly only relevant for sequences of some drugs. In 219 same sex Dutch twin pairs one had used cannabis before the age of 18 whereas the other had not. In the cannabis group the rate of later use of party drugs was seven times higher and the rate of later use of hard drugs was 16 times higher than in the non-cannabis group. The authors concluded that at least family influences – both genetic and social ones – could not explain the differences.<ref name="PMID16402286">M. T. Lynskey, J. M. Vink, D. I. Boomsma: ''Early onset cannabis use and progression to other drug use in a sample of Dutch twins.'' In: ''Behavior genetics.'' Vol 36, nr 2, March 2006, pp.&nbsp;195–200, {{DOI|10.1007/s10519-005-9023-x}}, PMID 16402286.</ref>
The results of a [[twin study]], however, presented strong indications that genetic and environmental factors may be rather weak, possibly only relevant for sequences of some drugs. In 219 same sex Dutch twin pairs one had used cannabis before the age of 18 whereas the other had not. In the cannabis group the rate of later use of party drugs was seven times higher and the rate of later use of hard drugs was 16 times higher than in the non-cannabis group. The authors concluded that at least family influences – both genetic and social ones – could not explain the differences.<ref name="PMID16402286">M. T. Lynskey, J. M. Vink, D. I. Boomsma: ''Early onset cannabis use and progression to other drug use in a sample of Dutch twins.'' In: ''Behavior genetics.'' Vol 36, nr 2, March 2006, pp.&nbsp;195–200, {{DOI|10.1007/s10519-005-9023-x}}, PMID 16402286.</ref>


== History ==
== Electronic cigarettes as gateway to smoking ==
While the phrase ''gateway drug'' first appeared in the 1980s, the underlying ideas had already been discussed since the 1930s by using the phrases ''stepping-stone theory'', ''escalation hypothesis'', or ''progression hypothesis''.<ref>[[Denise Kandel|D. B. Kandel]] (Ed.): ''Stages and Pathways of Drug Involvement: Examining the Gateway Hypothesis'', Cambridge University Press, 2002, ISBN 978-0-521-78969-1, p. 4.</ref><ref>Erich Goode: ''Marijuana use and the progression to dangarous drugs'', in: {{cite book | last=Miller | first=Loren (Ed.) | title=Marijuana Effects on Human Behavior | publisher=Elsevier Science | location=Burlington | year=1974 | isbn=978-1-4832-5811-9 | page=303-338}}</ref>
Much of the literature on [[electronic cigarette]]s has expressed fears that they would, especially if marketed by [[big tobacco]], be a gateway to [[smoking]] tobacco for young people. In 2015 a report commissioned by [[Public Health England]], a government agency, examined the evidence for this, and concluded that "We strongly suggest that use of the gateway terminology be abandoned until it is clear how the theory can be tested in this field",<ref name=McNeill201576>{{cite web|last1=McNeill|first1=A, SC|title=E – cigarettes: an evidence update A report commissioned by Public Health England|url=https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/454516/Ecigarettes_an_evidence_update_A_report_commissioned_by_Public_Health_England.pdf|website=www.gov.uk|publisher=Public Health England|p=38|accessdate=24 August 2015|location=UK|date=2015}}</ref> They quoted a study which concluded that: "Although the concept of the gateway theory is often treated as a straightforward scientific theory, its emergence is rather more complicated. In effect, it is a hybrid of popular, academic and media accounts – a construct retroactively assembled rather than one initially articulated as a coherent theory”.<ref>Bell, K. and H. Keane, "All gates lead to smoking: The ‘gateway theory’, e-cigarettes and the remaking of nicotine"., ''Social Science & Medicine'', 2014. 119, quoted McNeill, pp. 37-38</ref>


The scientific and political discussion has intensified since 1975 after the publications of sereral longitudinal studies by [[Denise Kandel]] and others.<ref name="PMID1188374">D. Kandel: ''Stages in adolescent involvement in drug use.'' In: ''Science (New York, N.Y.).'' Vol 190, nr 4217, November 1975, pp.&nbsp;912–914, PMID 1188374.</ref><ref name="PMID6742252">K. Yamaguchi, D. B. Kandel: ''Patterns of drug use from adolescence to young adulthood: II. Sequences of progression.'' In: ''American journal of public health.'' Vol 74, nr 7, July 1984, pp.&nbsp;668–672, PMID 6742252, {{PMC|1651663}}.</ref><ref name="PMID8498623">D. Kandel, K. Yamaguchi: ''From beer to crack: developmental patterns of drug involvement.'' In: ''American journal of public health.'' Vol 83, nr 6, June 1993, pp.&nbsp;851–855, PMID 8498623, {{PMC|1694748}}.</ref> [[Denise Kandel]] is Professor of Sociomedical Sciences and Psychiatry at Columbia University and Head of the Department of Epidemiology of Substance Abuse at the [[New York State Psychiatric Institute]] (since 1956 married to [[Eric Kandel]], neurobiologist and recipient of the 2000 [[Nobel Prize in Physiology or Medicine]]).
== Prohibition ==
Another theory is that ''prohibition'' itself is a gateway to "hard" drug use. Many support this theory referencing the introduction to the black market. Once utilizing the black market, sellers have incentive to sell higher margin products, unrestricted by greater regulation on more harmful substances.<ref>{{cite web|title=Prohibition Is the Real "Gateway Drug"|url=http://www.huffingtonpost.com/inge-fryklund/prohibition-is-the-real-g_b_8210802.html|website=The Huffington Post|date=29 September 2015}}</ref> The research has found an increase of drug-related incidents in [[County (United States)|counties of the United States]] that ban alcohol as well.<ref>{{cite journal|url=http://ssrn.com/abstract=2650484|doi=10.2139/ssrn.2650484|title=Breaking Bad: Are Meth Labs Justified in Dry Counties?|journal=SSRN Electronic Journal|year=2015|last1=Fernandez|first1=Jose M.|last2=Gohmann|first2=Stephan|last3=Pinkston|first3=Joshua C.}}</ref><ref>Conlin, Michael; Dickert-Conlin, Stacy; Pepper, John. "Effect of Alcohol Prohibition on Illicit-Drug-Related Crimes, The." Journal of Law and Economics 48.1 (2005): 215-234.</ref>


== Criticisms ==
== Criticisms ==

Revision as of 11:46, 30 May 2016

The gateway drug theory (also called gateway theory, gateway hypothesis and gateway effect) states that use of less deleterious drugs precedes, and can lead to, future use of more dangerous hard drugs[1] or crime.[2] It is often attributed to the earlier use of one of several licit substances, including tobacco or alcohol, as well as cannabis.[1]

The reverse gateway theory posits that earlier regular cannabis use predicts later tobacco initiation and/or nicotine dependence in those who did not use tobacco before.[3]

Sequence of first-time use

General concept

The concept of gateway drug is based on observations that the sequence of first-time use of different drugs is not random but shows trends. On the basis of established techniques of longitudinal studies such trends can be described precisely in terms of statistical probability. As to the interpretation of the observed trends, it is important to note the difference between sequence and causation. Both may – but need not – be coupled, a question which is subject of further research, e.g., by physiological experiments.[4]

Examples of trends

From a sample of 6,624 persons who had not used other illegal drugs before their cannabis consumption the overall probability of later use of further illegal drugs was estimated to be 44.7%. Subgroup analyses showed that personal and social conditions, such as gender, age, Ethnicity, Urbanicity, and educational attainment influenced the height of probability.[5]

In a sample of 27,461 persons who showed no signs of alcohol use disorder (AUD) before their cannabis consumption a second examination three years later revealed a five times higher rate (500%) of AUD compared to a control group that had not consumed cannabis. In another sample of 2,121 persons who already had AUD at the first examination the rate of persistence of AUD three years later was 74% higher in the group of Cannabis consumers than in the group of non-consumers.[6]

A study of drug use of 14,577 US 12th graders showed that alcohol consumption was associated with an increased probability of later use of tobacco, cannabis, and other illegal drugs.[7]

Causes

Because a sequence of first-time use can only indicate the possibility – but not the fact – of an underlying causal relation, different theories concerning the observed trends were developed. The scientific discussion (state of 2016) is dominated by two concepts, which appear to cover almost all possible causal connections if appropriately combined. These are the theories of biological alterations in the brain due to an earlier drug use and the theory of similar attitudes across different drugs.[8][9]

Alterations in the brain

In animals it is relatively simple to determine if consumption of a certain drug increases the later attraction of another drug. For example, cannabis consumption – earlier in life – increased the self-administration of heroin,[10] morphine,[11] and also nicotine.[12] There were direct indications that the alteration consisted of lasting anatomical changes in the reward system of the brain.[10]

In mice nicotine increased the probability of later consumption of cocaine und the experiments permitted concrete conclusions on the underlying molecular biological alteration in the brain.[13] The biological changes in mice correspond to the epidemiological observations in humans that nicotine consumption is coupled to an increased probability of later use of cannabis and cocaine.[14]

Personal and social factors

According to the concept of similar attitudes across different drugs (common liability) several personal and environmental factors can lead to a generally increased interest in various drugs. The sequence of first-time use would then depend on the given social and economic conditions.[15][16] The concept received support from a large-scale genetic analysis that showed a genetic basis for the connection of the prevalence of cigarette smoking and cannabis use during the life of a person.[17]

The results of a twin study, however, presented strong indications that genetic and environmental factors may be rather weak, possibly only relevant for sequences of some drugs. In 219 same sex Dutch twin pairs one had used cannabis before the age of 18 whereas the other had not. In the cannabis group the rate of later use of party drugs was seven times higher and the rate of later use of hard drugs was 16 times higher than in the non-cannabis group. The authors concluded that at least family influences – both genetic and social ones – could not explain the differences.[18]

History

While the phrase gateway drug first appeared in the 1980s, the underlying ideas had already been discussed since the 1930s by using the phrases stepping-stone theory, escalation hypothesis, or progression hypothesis.[19][20]

The scientific and political discussion has intensified since 1975 after the publications of sereral longitudinal studies by Denise Kandel and others.[21][22][23] Denise Kandel is Professor of Sociomedical Sciences and Psychiatry at Columbia University and Head of the Department of Epidemiology of Substance Abuse at the New York State Psychiatric Institute (since 1956 married to Eric Kandel, neurobiologist and recipient of the 2000 Nobel Prize in Physiology or Medicine).

Criticisms

Alternative explanations for the correlation between the use of soft drugs (e.g., marijuana) and the use of hard drugs (e.g., cocaine, heroin) include, but are not limited to:

  • The Common Liability to Addiction theory (CLA) argues that a person's involvement with drugs and its various degrees, including potential development and severity of addiction, are based on biobehavioral mechanisms that are largely not drug-specific. Within the CLA framework, the sequence of drug use initiation – the essence of the "gateway theory" - is opportunistic and trivial: the "gateway" drugs, that is, the substances used first, are merely those that are (usually) available at an earlier age (thus usually licit) than those used later (usually, hard drugs). In an extensive review addressing the CLA and the "gateway" theory, it was pointed out[24] that the "gateway" sequence applies only to the initiation of use of different drugs rather than different levels or extent of drug involvement (from use to dependence), questioning its relevance to addiction as a medical problem. Despite that, the "gateway theory" has significantly and, arguably, adversely influenced policy formation, intervention, and research.[1]
  • Teenagers' trust of adults erodes when authority-figures exaggerate or make up the dangers of the "gateway" drugs, leading teenagers to regard all anti-drug messages as nonsense.[25]
  • The peer environments in which "gateway" drugs are used can sometimes overlap with the ones in which harder drugs are used, especially in societies that prohibit the substances or impose very high age-limits.[25]

See also

References

  1. ^ a b c Vanyukov MM, Tarter RE, Kirillova GP, et al. (June 2012). "Common liability to addiction and "gateway hypothesis": theoretical, empirical and evolutionary perspective". Drug Alcohol Depend (Review). 123 Suppl 1: S3–17. doi:10.1016/j.drugalcdep.2011.12.018. PMC 3600369. PMID 22261179.
  2. ^ Pudney, Stephen (December 2002). "The road to ruin? Sequences of initiation into drug use and offending by young people in Britain" (PDF). Home Office Research Study 253. London: Home Office Research, Development and Statistics Directorate. ISBN 1-84082-928-1. ISSN 0072-6435. Retrieved 2009-04-04.
  3. ^ Peters EN, Budney AJ, Carroll KM (August 2012). "Clinical correlates of co-occurring cannabis and tobacco use: a systematic review". Addiction (Review). 107 (8): 1404–17. doi:10.1111/j.1360-0443.2012.03843.x. PMC 3377777. PMID 22340422.
  4. ^ D. B. Kandel (Ed.): Stages and Pathways of Drug Involvement: Examining the Gateway Hypothesis, Cambridge University Press, 2002, ISBN 978-0-521-78969-1, pp. 3-10.
  5. ^ Secades-Villa, R; Garcia-Rodríguez, O; Jin, C. J.; Wang, S; Blanco, C (2015). "Probability and predictors of the cannabis gateway effect: A national study". International Journal of Drug Policy. 26 (2): 135–142. doi:10.1016/j.drugpo.2014.07.011. PMC 4291295. PMID 25168081.
  6. ^ Weinberger, A. H.; Platt, J; Goodwin, R. D. (2016). "Is cannabis use associated with an increased risk of onset and persistence of alcohol use disorders? A three-year prospective study among adults in the United States". Drug and Alcohol Dependence. 161: 363–7. doi:10.1016/j.drugalcdep.2016.01.014. PMID 26875671.
  7. ^ Kirby, T; Barry, A. E. (2012). "Alcohol as a gateway drug: A study of US 12th graders" (PDF). Journal of School Health. 82 (8): 371–9. doi:10.1111/j.1746-1561.2012.00712.x. PMID 22712674.
  8. ^ A. R. Morral, D. F. McCaffrey, S. M. Paddock: Reassessing the marijuana gateway effect. In: Addiction (Abingdon, England). Vol 97, nr 12, December 2002, pp. 1493–1504, PMID 12472629 (Review).
  9. ^ D. M. Fergusson, J. M. Boden, L. J. Horwood: Cannabis use and other illicit drug use: testing the cannabis gateway hypothesis. In: Addiction (Abingdon, England). Vol 101, nr 4, April 2006, pp. 556–569, doi:10.1111/j.1360-0443.2005.01322.x, PMID 16548935.
  10. ^ a b M. Ellgren, S. M. Spano, Y. L. Hurd: Adolescent cannabis exposure alters opiate intake and opioid limbic neuronal populations in adult rats. In: Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology. Vol 32, nr 3, March 2007, pp. 607–615, doi:10.1038/sj.npp.1301127, PMID 16823391.
  11. ^ C. Cadoni, A. Pisanu, M. Solinas, E. Acquas, G. Di Chiara: Behavioural sensitization after repeated exposure to Delta 9-tetrahydrocannabinol and cross-sensitization with morphine. In: Psychopharmacology. Vol 158, nr 3, November 2001, pp. 259–266, doi:10.1007/s002130100875, PMID 11713615.
  12. ^ Panlilio, L. V.; Zanettini, C; Barnes, C; Solinas, M; Goldberg, S. R. (2013). "Prior Exposure to THC Increases the Addictive Effects of Nicotine in Rats". Neuropsychopharmacology. 38 (7): 1198–1208. doi:10.1038/npp.2013.16. PMC 3656362. PMID 23314220.
  13. ^ E. R. Kandel; D. B. Kandel (2014). "A Molecular Basis for Nicotine as a Gateway Drug". New England Journal of Medicine. 371 (10): 932–943. doi:10.1056/NEJMsa1405092. PMC 4353486. PMID 25184865.
  14. ^ K. M. Keyes, A. Hamilton, D. B. Kandel: Birth Cohorts Analysis of Adolescent Cigarette Smoking and Subsequent Marijuana and Cocaine Use. In: American journal of public health. [electronic publication before print] April 2016, doi:10.2105/AJPH.2016.303128, PMID 27077359.
  15. ^ M. M. Vanyukov, R. E. Tarter, L. Kirisci, G. P. Kirillova, B. S. Maher, D. B. Clark: Liability to substance use disorders: 1. Common mechanisms and manifestations. In: Neuroscience and biobehavioral reviews. Vol 27, nr 6, October 2003, pp. 507–515, PMID 14599432 (Review).
  16. ^ Degenhardt, L; Dierker, L; Chiu, W. T.; Medina-Mora, M. E.; Neumark, Y; Sampson, N; Alonso, J; Angermeyer, M; Anthony, J. C.; Bruffaerts, R; De Girolamo, G; De Graaf, R; Gureje, O; Karam, A. N.; Kostyuchenko, S; Lee, S; Lépine, J. P.; Levinson, D; Nakamura, Y; Posada-Villa, J; Stein, D; Wells, J. E.; Kessler, R. C. (2010). "Evaluating the drug use "gateway" theory using cross-national data: Consistency and associations of the order of initiation of drug use among participants in the WHO World Mental Health Surveys". Drug and Alcohol Dependence. 108 (1–2): 84–97. doi:10.1016/j.drugalcdep.2009.12.001. PMC 2835832. PMID 20060657.
  17. ^ S. Stringer, C. C. Minică u. a.: Genome-wide association study of lifetime cannabis use based on a large meta-analytic sample of 32 330 subjects from the International Cannabis Consortium. In: Translational psychiatry. Vol 6, 2016, p. e769, doi:10.1038/tp.2016.36, PMID 27023175.
  18. ^ M. T. Lynskey, J. M. Vink, D. I. Boomsma: Early onset cannabis use and progression to other drug use in a sample of Dutch twins. In: Behavior genetics. Vol 36, nr 2, March 2006, pp. 195–200, doi:10.1007/s10519-005-9023-x, PMID 16402286.
  19. ^ D. B. Kandel (Ed.): Stages and Pathways of Drug Involvement: Examining the Gateway Hypothesis, Cambridge University Press, 2002, ISBN 978-0-521-78969-1, p. 4.
  20. ^ Erich Goode: Marijuana use and the progression to dangarous drugs, in: Miller, Loren (Ed.) (1974). Marijuana Effects on Human Behavior. Burlington: Elsevier Science. p. 303-338. ISBN 978-1-4832-5811-9.
  21. ^ D. Kandel: Stages in adolescent involvement in drug use. In: Science (New York, N.Y.). Vol 190, nr 4217, November 1975, pp. 912–914, PMID 1188374.
  22. ^ K. Yamaguchi, D. B. Kandel: Patterns of drug use from adolescence to young adulthood: II. Sequences of progression. In: American journal of public health. Vol 74, nr 7, July 1984, pp. 668–672, PMID 6742252, PMC 1651663.
  23. ^ D. Kandel, K. Yamaguchi: From beer to crack: developmental patterns of drug involvement. In: American journal of public health. Vol 83, nr 6, June 1993, pp. 851–855, PMID 8498623, PMC 1694748.
  24. ^ Vanyukov, M. M.; Tarter, R. E.; Kirillova, G. P.; Kirisci, L; Reynolds, M. D.; Kreek, M. J.; Conway, K. P.; Maher, B. S.; Iacono, W. G.; Bierut, L; Neale, M. C.; Clark, D. B.; Ridenour, T. A. (2012). "Common liability to addiction and "gateway hypothesis": Theoretical, empirical and evolutionary perspective". Drug and Alcohol Dependence. 123 (Suppl 1): S3–17. doi:10.1016/j.drugalcdep.2011.12.018. PMC 3600369. PMID 22261179.
  25. ^ a b Brecher, Edward M. (1972). "Heroin on the youth drug scene – and in Vietnam". Licit and illicit drugs; the Consumers Union report on narcotics, stimulants, depressants, inhalants, hallucinogens, and marijuana – including caffeine, nicotine, and alcohol. Boston: Little, Brown. ISBN 0-316-10717-4. {{cite book}}: External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)

Further reading

Scientific textbooks

  • D. B. Kandel (Ed.): Stages and Pathways of Drug Involvement: Examining the Gateway Hypothesis, Cambridge University Press, 2002, ISBN 978-0-521-78969-1.
  • Wayne Hall, Rosalie Liccardo Pacula: Is cannabis a gateway drug? In: Same authors: Cannabis Use and Dependence. Public Health and Public Policy, Cambridge University Press, Cambridge, UK, New York, USA, 2003, ISBN 978-0-521-80024-2, chapt. 10, pp. 104–114.

Lay scientific books

  • Mark A.R. Kleiman, Jonathan P. Caulkins, Angela Hawken: Is marijuana a "gateway drug"? In: Same authors: Drugs and Drug Policy. What Everyone Needs to Know, Oxford University Press, 2011, ISBN 978-0-19-983138-8, chapt. 4, question 8, pp. 81–83.

State of research before 1974

  • Erich Goode: Marijuana use and the progression to dangarous drugs, in: Miller, Loren (Ed.) (1974). Marijuana Effects on Human Behavior. Burlington: Elsevier Science. p. 303-338. ISBN 978-1-4832-5811-9.

External links

source: https://en.wikipedia.org/w/index.php?title=Gateway_drug_effect&diff=prev&oldid=722834844