Entry drug hypothesis

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The term entry drug hypothesis or gateway hypothesis (English gateway hypothesis , gateway drug theory , gateway effect , gateway drug effect , stepping stone theory , escalation hypothesis or progression hypothesis ) is an expression of the question of whether the consumption of a drug is more likely for the consumption of other other drugs. According to a subcomponent of the hypothesis, the chronological sequence of the first consumption of various drugs is partly causal due to the imprinting of the previous drug in the brain. According to another sub-component of the hypothesis, the chronological sequence can also be explained by personal and social factors, such as genetic predisposition and the way in which drugs are used and used. The scientific examination of the hypothesis is important for health policy in the area of ​​education and legislation.

history

Denise Kandel , professor of sociomedical sciences in psychiatry at Columbia University and director of the epidemiology of substance abuse at the New York State Psychiatric Institute, and colleagues have published the results of several longitudinal studies of the timing of first-time drug use since 1975. These and similar results led to intense scientific and political discussions about the possible causes of the observed trends. The catchwords stepping stone theory (literally: stepping stone theory) and gateway theory (literally: entrance theory) as well as the colloquial term entry drug in German have become widespread.

Connections

Since with a temporal sequence one can only infer the possibility - but not the fact - of an underlying causal (causal) sequence, various theories have developed on possible connections. In the scientific discussion (as of April 2016), two theories are in the foreground, which - if they are combined - cover almost all conceivable causal relationships. It is the theory of the biological imprinting (in the brain) by a drug previously consumed and the theory of a cross-drug motivational situation of the user .

Evidence of biological imprinting in the brain

In mice, nicotine increased the likelihood of subsequent cocaine use , and the experiments allowed concrete conclusions to be drawn about the underlying molecular changes in the brain. The biological imprint in mice thus corresponded to the epidemiological observations that nicotine consumption in humans is linked to a later increased likelihood of cannabis and cocaine use.

Personal and social factors

According to the concept of a cross-drug motivational situation of the user (common liability), there are several personal and environmental factors that could influence a possible interest in drugs in the same way for several different drugs. The order of consumption of different drugs is therefore dependent on the given social and economic conditions. The concept has since been supported by a comprehensive genetic analysis that has shown a genetic link between the incidence of cannabis use and the incidence of cigarette smoking during a person's life.

The results of a twin study , however, provided strong indications that the influences of genetic and environmental factors are rather weak - and possibly only effective for some drug sequences. In 219 same-sex Dutch twin pairs, one had used cannabis before the age of 18 and the other had not. The former were 7 times more likely to later use “party drugs” and 16 times more likely to use “hard drugs” later than the twin partners who had not used cannabis before the age of 18. The authors concluded that at least family influences - both genetic and social - could not explain the different sequences.

Consequences for health policy

If the common liability of the drug user is the main reason for the consumption of other drugs, it was suggested that measures to limit risk - such as information and support for personal development - place the initial situation of people rather than the special properties of individual drugs at the center of politics .

If the biological imprinting (in the brain) by a drug that was previously consumed also plays a significant role in humans, this drug has a causal effect. As a risk limitation measure, it was proposed in this case to put the drug itself at the center of politics, for example by limiting accessibility - especially for people of early age or with other risks.

Criticism and antithesis

cannabis

According to the review by Hoch et al. (2015) there is a correlation , but the question of causality is open:

“Various studies have shown a connection between early, regular cannabis use and continued use of other illegal drugs or alcohol. The fact that cannabis functions as an access substance for the use of other substances ("gateway hypothesis") has not been empirically proven. "

- Hoch et al. (2015)

General

In 2017, the entry-level drug hypothesis was generally confirmed to have significant gaps in knowledge by Miller and Hurd:

"Overall, the concept of the gateway hypothesis has inspired a large body of research, but there remain significant gaps of knowledge before we are able to fully accept or refute the hypothesis."

"Overall, the concept of the gateway hypothesis has stimulated an extensive body of research material, but there are still significant gaps in knowledge before we can fully accept or refute the hypothesis."

- Miller and Hurd (2017)

See also

literature

Scientific introductions

  • DB 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: The Same: Cannabis Use and Dependence. Public Health and Public Policy , Cambridge University Press, Cambridge, UK, New York, USA, 2003, ISBN 978-0-521-80024-2 , chap. 10, pp. 104-114.

Generally understandable introduction

  • Mark AR Kleiman, Jonathan P. Caulkins, Angela Hawken: Is marijuana a "gateway drug"? In: Same: Drugs and Drug Policy. What Everyone Needs to Know? Oxford University Press, 2011, ISBN 978-0-19-983138-8 , chap. 4, question 8, 3 pages.

Web links

Individual evidence

  1. ↑ MM Vanyukov, RE Tarter, GP Kirillova, L. Kirisci, MD Reynolds, MJ Kreek, KP Conway, BS Maher, WG Iacono, L. Bierut, MC Neale, DB Clark, TA Ridenour: Common liability to addiction and "gateway hypothesis ": theoretical, empirical and evolutionary perspective. In: Drug and alcohol dependence. Volume 123 Suppl 1, June 2012, pp. S3-17, doi: 10.1016 / j.drugalcdep.2011.12.018 , PMID 22261179 , PMC 3600369 (free full text) (review).
  2. ^ A b E. Hoch, U. Bonnet, R. Thomasius, F. Ganzer, U. Havemann-Reinecke, UW Preuss: Risks associated with the non-medicinal use of cannabis . In: Deutsches Ärzteblatt international . tape 112 , no. April 16 , 2015, p. 271–278 , doi : 10.3238 / arztebl.2015.0271 , PMID 25939318 , PMC 4442549 (free full text) - ( online version in German: Risks associated with non-medical use of cannabis , PDF - review article).
  3. ^ Eva Hoch, Miriam Schneider, Chris Maria Friemel (eds.): Cannabis: Potential and Risk - A Scientific Inventory . Springer, Heidelberg 2019, ISBN 978-3-662-57291-7 , doi : 10.1007 / 978-3-662-57291-7 (478 pages, bundesgesundheitsministerium.de [PDF]). see page 57, 2.7 Limitations.
  4. ^ DB Kandel (Ed.): Stages and Pathways of Drug Involvement: Examining the Gateway Hypothesis , Cambridge University Press, 2002, ISBN 978-0-521-78969-1 .
  5. ^ A b S. Schneider, K. Diehl: Vaping as a Catalyst for Smoking? An Initial Model on the Initiation of Electronic Cigarette Use and the Transition to Tobacco Smoking Among Adolescents. In: Nicotine & tobacco research: official journal of the Society for Research on Nicotine and Tobacco. Volume 18, Number 5, May 2016, pp. 647-653, doi : 10.1093 / ntr / ntv193 , PMID 26386472 (review).
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  7. ↑ D. Kandel: Stages in adolescent involvement in drug use. In: Science. Volume 190, Number 4217, November 1975, pp. 912-914, PMID 1188374 .
  8. ↑ K. Yamaguchi, DB Kandel: Patterns of drug use from adolescence to young adulthood: II. Sequences of progression. In: American Journal of Public Health . Volume 74, Number 7, July 1984, pp. 668-672, PMID 6742252 , PMC 1651663 (free full text).
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  10. ↑ DB Kandel (Ed.): Stages and Pathways of Drug Involvement: Examining the Gateway Hypothesis , Cambridge University Press, 2002, ISBN 978-0-521-78969-1 , p. 4.
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  13. ^ ER Kandel, DB Kandel : Shattuck Lecture: A molecular basis for nicotine as a gateway drug. In: The New England Journal of Medicine . Volume 371, number 10, September 2014, pp. 932-943, doi: 10.1056 / NEJMsa1405092 , PMID 25184865 , PMC 4353486 (free full text).
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  15. ↑ KM Keyes, A. Hamilton, DB Kandel : Birth Cohorts Analysis of Adolescent Cigarette Smoking and Subsequent Marijuana and Cocaine Use. In: American Journal of Public Health . [Electronic publication before printing] April 2016, doi: 10.2105 / AJPH.2016.303128 , PMID 27077359 .
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  17. ↑ MM Vanyukov, RE Tarter, L. Kirisci, GP Kirillova, BS Maher, DB Clark: Liability to substance use disorders: 1. Common mechanisms and manifestations. In: Neuroscience and biobehavioral reviews. Volume 27, Number 6, October 2003, pp. 507-515, PMID 14599432 (review).
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  21. ↑ MT Lynskey, JM Vink, DI Boomsma: Early onset cannabis use and progression to other drug use in a sample of Dutch twins. In: Behavior genetics. Volume 36, Number 2, March 2006, pp. 195-200, doi: 10.1007 / s10519-005-9023-x , PMID 16402286 , PDF .
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  24. ↑ Wayne Hall, Rosalie Liccardo Pacula: Cannabis Use and Dependence. Public Health and Public Policy . Cambridge University Press, Cambridge, UK, New York, USA, 2003, ISBN 978-0-521-80024-2 , p. 111.
  25. ^ ML Miller, YL Hurd: Testing the Gateway Hypothesis. In: Neuropsychopharmacology . Volume 42, number 5, 04 2017, pp. 985-986, doi : 10.1038 / npp.2016.279 , PMID 28096528 , PMC 5506797 (free full text).