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In 1999, a study by the Division of Neuroscience and Behavioral Health at the [[Institute of Medicine]] entitled "Marijuana and Medicine: Assessing the Science Base," found no evidence of a link between cannabis use and the subsequent abuse of other illicit drugs on the basis of its particular physiological effect.<ref name=IOM>{{cite web|url=http://books.nap.edu/readingroom/books/marimed/notice.html|title=Marijuana and Medicine: Assessing the Science Base|publisher=[[National Academies Press]]|year=1999|accessdate=2007-03-30}}</ref>
In 1999, a study by the Division of Neuroscience and Behavioral Health at the [[Institute of Medicine]] entitled "Marijuana and Medicine: Assessing the Science Base," found no evidence of a link between cannabis use and the subsequent abuse of other illicit drugs on the basis of its particular physiological effect.<ref name=IOM>{{cite web|url=http://books.nap.edu/readingroom/books/marimed/notice.html|title=Marijuana and Medicine: Assessing the Science Base|publisher=[[National Academies Press]]|year=1999|accessdate=2007-03-30}}</ref>


====United States Government Drug Scheduling Classification====
====United States Government Drug Scheduling Classification Studies====
In conflict with U.S. Governments own common propaganda, the United States Drug Enforcement Agency (DEA) has classified Cannabis / Marijuana as a Schedule 1 Drug <ref name="DEA Website">{{cite web|url=http://www.justice.gov/dea/pubs/scheduling.html|Publisher|United States Drug Enforcement Agency|accessdate=2011-05-08|title=DEA Website</ref>. This is the highest classification a drug can be scheduled as. Making the theory that Marijuana is a gateway drug to harder drugs simply false by DEA's statement of fact itself. If according to the DEA there is nothing harder than the classification schedule 1 drugs as of Marijuana, then it can't be a gateway drug to something more harmful. Instead it would have to be a gateway drug to something less harmful like; Opium, Peyote, Methamphetamine, etc. according the viewpoint of the highly educated and impartial minds of the DEA<ref name="DEA Website">{{cite web|url=http://www.justice.gov/dea/pubs/scheduling.html|Publisher|United States Drug Enforcement Agency|accessdate=2011-05-08|title=DEA Website</ref>.
In conflict with U.S. Governments own common propaganda, the United States Drug Enforcement Agency (DEA) studies have classified Cannabis / Marijuana as a Schedule 1 Drug <ref name="DEA Website">{{cite web|url=http://www.justice.gov/dea/pubs/scheduling.html|Publisher|United States Drug Enforcement Agency|accessdate=2011-05-08|title=DEA Website</ref>. This is the highest classification a drug can be scheduled as. Making the theory that Marijuana is a gateway drug to harder drugs simply false by DEA's statement of fact itself. If according to the DEA there is nothing harder than the classification schedule 1 drugs as of Marijuana, then it can't be a gateway drug to something more harmful. Instead it would have to be a gateway drug to something less harmful like; Opium, Peyote, Methamphetamine, etc. according the viewpoint of the highly educated and impartial minds of the DEA<ref name="DEA Website">{{cite web|url=http://www.justice.gov/dea/pubs/scheduling.html|Publisher|United States Drug Enforcement Agency|accessdate=2011-05-08|title=DEA Website</ref>.


====Mathematical Model====
====Mathematical Model====

Revision as of 08:08, 8 May 2011

The gateway drug theory (also called gateway theory, gateway hypothesis and gateway effect) is the hypothesis that the use of less deleterious drugs may lead to a future risk of using more dangerous hard drugs and/or crime.[1] It is often attributed to the use of several drugs, including tobacco,[2] alcohol,[3] black coffee and cannabis[citation needed].

While some research shows that many hard drug users used cannabis or alcohol before moving on to the harder substances, other research shows that some serious drug abusers have used other drugs before using cannabis or alcohol.[4] The former is particularly evident in individual drug-abuse histories which tend to show that "hard drug" users do progress from one drug to another.[5]

Variations of the theory

Several different hypotheses have been called "gateway" theories in popular discourse. These include (but are not limited to):

  • The gateway substance causes users to be at increased risk for abuse of other substances.[citation needed]
  • The gateway substance primes the brain for addiction to other substances (independent of becoming more likely to try other substances).[citation needed]
  • A rigid sequence of progression, starting with illicit drugs followed by (increasingly dangerous) illicit ones.[citation needed]
  • The gateway effect is pharmacological, rather than socially constructed.[citation needed]

Cannabis

Main article: Cannabis (drug)

Some scientific studies show that the consumption of cannabis can possibly predict a significant higher risk for the subsequent use of other "harder" illicit drugs, while other studies show that it cannot.[6][7] Two recent studies are from University of Pittsburgh's School of Pharmacy,[8] and from Dr. Michael Lynskey.[9][10]

Studies in favor of the gateway theory

Study of Australian Adolescents (10 years)

A stratified, random sample of 1,943 adolescents was recruited from secondary schools across Victoria, Australia at age 14–15 years. This cohort was interviewed on eight occasions until the age of 24–25 years. At age 24 years, 12% of the sample had used amphetamines in the past year, with 1%–2% using at least weekly. Young adult amphetamine use was predicted strongly by adolescent drug use and was associated robustly with other drug use and dependence in young adulthood. Associations were stronger for more frequent users. Among young adults who had not been using amphetamines at age 20 years, the strongest predictor of use at age 24 years was the use of other drugs, particularly cannabis, at 20 years.[11] Those who were smoking cannabis at the age of 15 were as much as 15 times more likely to be using amphetamines in their early 20s.[12]

Twin Study

A study by researchers at Virginia Commonwealth University attempted to dissect the contribution of genetic, shared environmental and unique environmental influences on the development of dependence on other drugs in those who had used cannabis.[13] The study found that while cannabis was strongly predictive of use of other drugs in the future, the main contributors to this effect were the shared environmental and genetic risk for all substances. However, there was "persisting evidence for some causal influences" of cannabis in the development of other drug dependencies, indicating that the gateway theory could be operative, although not the main cause of the association.

Study of rats

In 2006, the Karolinska Institute in Sweden used twelve rats to examine how adolescent use of cannabis affects subsequent abuse of other illicit drugs. The study gave six of the twelve "teenage" (28–49 days old, or 6.6–10.4 in human years) rats a small dose of THC, reportedly equivalent to one cannabis joint smoked by a human, every three days. The rats were allowed to self-administer heroin by pushing a lever and the study found the rats given THC took larger doses of heroin (but no such effect was found for amphetamines).

The current findings support the gateway hypothesis demonstrating that adolescence cannabis exposure has an enduring impact on hedonic processing resulting in enhanced opiate intake, possibly as a consequence of alterations in limbic opioid neuronal populations.[14]

The institute examined the brain cells in the rats and found THC alters the opioid system that is associated with positive emotions, which lessens the effects of opiates on rat's brain and thus causes them to use more heroin.[15] Paul Armentano, policy analyst for NORML, claimed because the rats were given THC at the young age of 28 days, is impossible to extrapolate the results of this study to humans. Also, the previously cannabis-exposed adult rats, despite being desensitized to heroin, were no more likely to get addicted (as measured by likelihood of self-administration) than the controls.[16] In addition, not all animal studies agree with the results found in this study (see below).

Studies not in favor of the gateway theory

In 1999, a study by the Division of Neuroscience and Behavioral Health at the Institute of Medicine entitled "Marijuana and Medicine: Assessing the Science Base," found no evidence of a link between cannabis use and the subsequent abuse of other illicit drugs on the basis of its particular physiological effect.[17]

United States Government Drug Scheduling Classification Studies

In conflict with U.S. Governments own common propaganda, the United States Drug Enforcement Agency (DEA) studies have classified Cannabis / Marijuana as a Schedule 1 Drug [18]. This is the highest classification a drug can be scheduled as. Making the theory that Marijuana is a gateway drug to harder drugs simply false by DEA's statement of fact itself. If according to the DEA there is nothing harder than the classification schedule 1 drugs as of Marijuana, then it can't be a gateway drug to something more harmful. Instead it would have to be a gateway drug to something less harmful like; Opium, Peyote, Methamphetamine, etc. according the viewpoint of the highly educated and impartial minds of the DEA[18].

Mathematical Model

In December 2002, a study by RAND regarding if cannabis use results in the subsequent use of cocaine and heroin was published in the British Journal of Addiction, a peer-reviewed scientific publication. The researchers created a mathematical model simulating adolescent drug use. National rates of cannabis and hard drug use in the model matched survey data collected from representative samples of youths from across the United States; the model produced patterns of drug use and abuse. Andrew Morral, associate director of RAND's Public Safety and Justice unit and lead author of the study stated:[19]

We've shown that the marijuana gateway effect is not the best explanation for the link between marijuana use and the use of harder drugs ... An alternative, simpler and more compelling explanation accounts for the pattern of drug use you see in this country, without resort to any gateway effects. While the gateway theory has enjoyed popular acceptance, scientists have always had their doubts. Our study shows that these doubts are justified.

One reason the risk factor for abusing drugs in cannabis users is higher is because few people try hard drugs prior to trying cannabis, not because cannabis users increasingly try hard drugs such as amphetamines. For example, cannabis is typically available at a significantly earlier age than other illicit drugs. Further research has shown that people with a disposition to resort to cannabis use are more likely to live longer and healthier lives than users of other "social drugs" such as alcohol.[20]

Study on American adolescents (12 years)

In December 2006, a 12 year gateway drug hypothesis study on 214 boys from ages 10–12 by the American Psychiatric Association was published in the American Journal of Psychiatry. The study concluded adolescents who used cannabis prior to using other drugs, including alcohol and tobacco, were no more likely to develop a substance abuse disorder than subjects in the study who did not use cannabis prior to using other drugs.[21] In other words, rearranging the order of the alleged "steppingstones" did not change the outcomes.

Study on San Francisco vs. Amsterdam

In 2004, a study comparing cannabis users in San Francisco to those in Amsterdam was done to test the effects of the differing drug policies in the two cities on drug use patterns. The Netherlands has a drug policy of decriminalization in which cannabis can be bought by adults over 18 in quasi-legal "coffee shops" and used publicly, while in the United States cannabis is criminalized and must be bought in the black market (often from the same dealers that sell hard drugs) and used "underground". The results found that, compared with their counterparts in Amsterdam the San Francisco cannabis users were significantly more likely to use cocaine, crack, amphetamines, ecstasy, and opiates despite similar cannabis use patterns and a more permissive drug policy in the Netherlands.[22] One plausible explanation is that the black market itself acts as a gateway to harder drugs, as opposed to the effects of cannabis per se.

Rat studies

A study in 3-4 month old rats actually found reduced reinforcing potential of cocaine in those rats pretreated with THC compared with those treated with vehicle only.[23] Another rat study (age unspecified) found that, while rats pretreated with THC consumed higher doses of heroin relative to controls, both groups took up self-administration of heroin at the same rate, and there was no significant difference between groups on the reinforcing effects of heroin.[24]

Alcohol

Both alcohol and tobacco tend to precede cannabis use, and it is rare for those who use hard drugs to not have used alcohol or tobacco first.[3] Data from the 2005 National Survey of Drug Use and Health (NSDUH) in the United States found that, compared with lifetime nondrinkers, adults who have consumed alcohol were statistically much more likely to currently use illicit drugs and/or abuse prescription drugs in the past year.[25] Effects were strongest for cocaine (26 times more likely), cannabis (14 times more likely), and psychedelics (13 times more likely). In addition, lifetime drinkers were also six times more likely to abuse or be dependent on illicit drugs than lifetime nondrinkers.[25]

As with cannabis, this correlation does not, however, necessarily mean that alcohol is a gateway drug (i.e. a causal relationship). In addition, whether one tries alcohol or cannabis first before the other does not accurately predict later substance use disorders.[21]

One study found that, in the United States, raising the drinking age to 21 in the 1980s was correlated with an increase in cannabis use among high school seniors, the opposite of what the gateway theory would predict. This suggests that the two substances are substitutes rather than complements. Interestingly, state decriminalization of cannabis did not predict an increase in cannabis use; rather, it predicted a mild decrease in both alcohol and cannabis use. Higher alcohol prices, however, appeared to reduce the use of both substances, suggesting at least partial complementarity (though not necessarily a gateway).[26]

Tobacco

According to the NIDA, "People who abuse drugs are also likely to be cigarette smokers. More than two-thirds of drug abusers are regular tobacco smokers, a rate more than triple that of the rest of the population."[27] One study found that cannabis use varies inversely with cigarette prices: the higher the cigarette price, the less cannabis use (though the association of cannabis use with later hard drug use was not robust).[28] Another study found that adolescents (especially the youngest ones) who smoke are 50% more likely to have drinking problems than those who do not.[29] Still another study finds that giving nicotine to early adolescent rats appears to increase the reinforcing (reward) effects of subsequent cocaine exposure, an effect that was not seen in adult rats.[30] However, as with the Karolinska study on cannabis given to adolescent rats, extrapolation to humans is difficult.

The price and tax of tobacco, particularly cigarettes, has been inversely associated with not just cigarette consumption but also that of alcohol[31][32] and cannabis.[32] This suggests complementarity between tobacco and alcohol and between tobacco and cannabis, but not necessarily a gateway effect.

Other drugs sometimes alleged to be gateway drugs

Due to the past decade's increase in prescription drug abuse, especially narcotic painkillers such as Vicodin and OxyContin, such substances have also been recently labeled as gateway drugs.[33] In the US, such substances appear to be more common than cannabis as the first "illicit" drug tried[citation needed], and are relatively easy to obtain by adolescents. Due to the similarity between narcotics, those who become addicted to prescription painkillers sometimes move on to heroin since the latter can actually be a cheaper habit to support.[34] In addition, a study on mice found that abusing oxycodone during adolescence may sensitize the brain's reward system, possibly predisposing to later addiction.[35]

Caffeine has also been alleged by some to be a gateway drug.[36][37][38] Being the most widely consumed psychoactive substance in the world, it is often the first one that people use, preceding even alcohol or tobacco if the latter two are used. However, the hypothesis of caffeine being a gateway drug has not been very well studied, and thus there is little to no evidence either way on this question.

Reverse gateway

In addition, there is a less-studied reverse gateway theory that earlier regular cannabis use predicts later tobacco initiation and/or nicotine dependence in those who did not use tobacco before. One Australian study[39] appears to have found such a correlation. However, they admittedly could not rule out the fact that cannabis is commonly (in many countries, including Australia and most of Europe) mixed with tobacco in joints to enhance burning and/or stretch supplies. Additionally, though not mentioned in the study, blunts (tobacco-leaf cigars filled with cannabis) are commonly used by some subcultures in the United States as well, despite tobacco-mixed joints being relatively uncommon there. Such "traditions," as opposed to cannabis per se, could plausibly act as a "Trojan horse" for developing a nicotine habit.[40]

Cannabis use only predicted later nicotine dependence in non-dependent tobacco smokers who also used cannabis daily, and even for them cannabis had no significant effect on the likelihood of quitting tobacco.[39]

An American study[41] also found a modest association between earlier cannabis use and later daily smoking (and nicotine dependence) as well, specifically among those who had smoked at least one tobacco cigarette. However, the results were not always statistically significant, and said nothing about the risk of initiating tobacco use. The smoking of blunts was also not addressed.

On the other hand, a more recent Australian twin study casts doubt on the hypothesis of a truly causal relationship between early (or any) cannabis use and later nicotine dependence. Rather, it was found to be largely due to common genetic factors, with no remaining evidence for a reverse gateway effect.[42]

Criticism

The gateway theory has been criticized,[19][22][43][44] mostly due to the existence of alternative explanations. These include (but are not limited to):

  • Some individuals are, for whatever reason, willing to try any substance, and the "gateway" drugs are merely the ones that are (usually) available at an earlier age than the harder drugs.[19]
  • Particularly for cannabis, which is illegal, exposure to the black market (where harder drugs are available) is suggested to be the real cause.[22][44]
  • For teenagers, credibility of adults is eroded when the dangers of the "gateway" drugs are exaggerated or made up, leading them to think all anti-drug messages are nonsense.[45]
  • 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.[45]

See also

References

  1. ^ Pudney, Stephen (2002). "The road to ruin? Sequences of initiation into drug use and offending by young people in Britain". Home Office.
  2. ^ The National Institute on Drug Abuse (NIDA), part of the NIH, a component of the U.S. Department of Health and Human Services.] – [http://web.archive.org/web/20051103184120/http://www.nida.nih.gov/nida_notes/NNVol15N5/Craving.html Nicotine Craving and Heavy Smoking May Contribute to Increased Use of Cocaine and Heroin
  3. ^ a b Golub, A.; Johnson, B. D. (2001). "Variation in youthful risks of progression from alcohol and tobacco to marijuana and to hard drugs across generations". American Journal of Public Health. 91 (2): 225–32. doi:10.2105/AJPH.91.2.225. PMC 1446541. PMID 11211630.
  4. ^ MacKesyamiti, M; Fendrich, M; Goldstein, PJ (1997). "Sequence of drug use among serious drug users: typical vs atypical progression". Drug and Alcohol Dependence. 45 (3): 185–96. doi:10.1016/S0376-8716(97)00032-X. PMID 9179520.
  5. ^ Contents | Marijuana and Medicine: Assessing the Science Base | Institute of Medicine
  6. ^ Mirken, Bruce (2006-12-19). "Why Smoking Marijuana Doesn't Make You a Junkie". AlterNet. Retrieved 2007-06-11.
  7. ^ Srikameswaran, Anita (2006-12-05). "Researchers say smoking pot not always path to hard drugs drug use". Pittsburgh Post-Gazette.
  8. ^ Tarter, R. E.; Vanyukov, M.; Kirisci, L.; Reynolds, M.; Clark, D. B. (2006). "Predictors of Marijuana Use in Adolescents Before and After Licit Drug Use: Examination of the Gateway Hypothesis". American Journal of Psychiatry. 163 (12): 2134–40. doi:10.1176/appi.ajp.163.12.2134. PMID 17151165.
  9. ^ Lynskey, M. T. (2003). "Escalation of Drug Use in Early-Onset Cannabis Users vs Co-twin Controls". JAMA: the Journal of the American Medical Association. 289: 427–33. doi:10.1001/jama.289.4.427. {{cite journal}}: Unknown parameter |laydate= ignored (help); Unknown parameter |laysource= ignored (help); Unknown parameter |laysummary= ignored (help)
  10. ^ Lynskey, Michael T.; Vink, Jacqueline M.; Boomsma, Dorret I. (2006). "Early Onset Cannabis Use and Progression to other Drug Use in a Sample of Dutch Twins". Behavior Genetics. 36 (2): 195–200. doi:10.1007/s10519-005-9023-x. PMID 16402286.
  11. ^ Degenhardt, Louisa; Coffey, Carolyn; Carlin, John B.; Moran, Paul; Patton, George C. (2007). "Who are the new amphetamine users? A 10-year prospective study of young Australians". Addiction. 102 (8): 1269–79. doi:10.1111/j.1360-0443.2007.01906.x. PMID 17624977.
  12. ^ ABC News Australia: Cannabis linked to use of amphetamines, 2007-07-18
  13. ^ Agrawal, Arpana; Neale, Michael C.; Prescott, Carol A.; Kendler, Kenneth S. (2004). "A twin study of early cannabis use and subsequent use and abuse/dependence of other illicit drugs". Psychological Medicine. 34 (7): 1227–37. doi:10.1017/S0033291704002545. PMID 15697049.
  14. ^ Ellgren, Maria: Neurobiological effects of early life cannabis exposure in relation to the gateway hypothesis
  15. ^ Ellgren, Maria; Spano, Sabrina M; Hurd, Yasmin L (2006). "Adolescent Cannabis Exposure Alters Opiate Intake and Opioid Limbic Neuronal Populations in Adult Rats". Neuropsychopharmacology. 32 (3): 607–15. doi:10.1038/sj.npp.1301127. PMID 16823391. {{cite journal}}: Unknown parameter |laydate= ignored (help); Unknown parameter |laysource= ignored (help); Unknown parameter |laysummary= ignored (help)
  16. ^ Smith, Jordan (2006-11-03). "Reefer Madness". The Austin Chronicle. Retrieved 2007-05-13. {{cite news}}: External link in |publisher= (help)
  17. ^ "Marijuana and Medicine: Assessing the Science Base". National Academies Press. 1999. Retrieved 2007-03-30.
  18. ^ a b {{cite web|url=http://www.justice.gov/dea/pubs/scheduling.html%7CPublisher%7CUnited States Drug Enforcement Agency|accessdate=2011-05-08|title=DEA Website
  19. ^ a b c "RAND Study Casts Doubt on Claims that Marijuana Acts as "Gateway" to the Use of Cocaine and Heroin". RAND. 2002-12-02. Retrieved 2007-07-11.
  20. ^ Morgan, John Jacob Brooke; Zimmer, Lynn Etta (1997). Marijuana myths, marijuana facts: a review of the scientific evidence. New York: Lindesmith Center. pp. 32–7. ISBN 978-0-9641568-4-5.{{cite book}}: CS1 maint: multiple names: authors list (link)
  21. ^ a b Tarter, R. E.; Vanyukov, M.; Kirisci, L.; Reynolds, M.; Clark, D. B. (2006). "Predictors of Marijuana Use in Adolescents Before and After Licit Drug Use: Examination of the Gateway Hypothesis". American Journal of Psychiatry. 163 (12): 2134–40. doi:10.1176/appi.ajp.163.12.2134. PMID 17151165. {{cite journal}}: Unknown parameter |laydate= ignored (help); Unknown parameter |laysource= ignored (help); Unknown parameter |laysummary= ignored (help)
  22. ^ a b c Reinarman, C.; Cohen, P. D. A.; Kaal, H. L. (2004). "The Limited Relevance of Drug Policy: Cannabis in Amsterdam and in San Francisco". American Journal of Public Health. 94 (5): 836–42. doi:10.2105/AJPH.94.5.836. PMC 1448346. PMID 15117709.
  23. ^ Panlilio, Leigh V; Solinas, Marcello; Matthews, Stephanie A; Goldberg, Steven R (2006). "Previous Exposure to THC Alters the Reinforcing Efficacy and Anxiety-Related Effects of Cocaine in Rats". Neuropsychopharmacology. 32 (3): 646–57. doi:10.1038/sj.npp.1301109. PMID 16738542.
  24. ^ Solinas, M; Panlilio, L V; Goldberg, S R (2004). "Exposure to Δ-9-Tetrahydrocannabinol (THC) Increases Subsequent Heroin Taking but not Heroin's Reinforcing Efficacy: A Self-Administration Study in Rats". Neuropsychopharmacology. 29 (7): 646–57. doi:10.1038/sj.npp.1300431.
  25. ^ a b Illicit Drug Use among Lifetime Nondrinkers and Lifetime Alcohol Users, NSDUH, 2005
  26. ^ Dinardo, J; Lemieux, T (2001). "Alcohol, marijuana, and American youth: the unintended consequences of government regulation" (PDF). Journal of Health Economics. 20 (6): 991–1010. doi:10.1016/S0167-6296(01)00102-3. PMID 11758056.
  27. ^ The National Institute on Drug Abuse (NIDA), part of the NIH, a component of the U.S. Department of Health and Human Services. – Nicotine Craving and Heavy Smoking May Contribute to Increased Use of Cocaine and Heroin [citation needed] – Patrick Zickler, NIDA NOTES Staff Writer. Retrieved October, 2006.
  28. ^ Beenstock, M; Rahav, G (2002). "Testing Gateway Theory: do cigarette prices affect illicit drug use?". Journal of Health Economics. 21 (4): 679–98. doi:10.1016/S0167-6296(02)00009-7. PMID 12146597.
  29. ^ Smoking May Boost Problem Drinking in Teens, HeathDay, 2006
  30. ^ McQuown, S; Belluzzi, J; Leslie, F (2007). "Low dose nicotine treatment during early adolescence increases subsequent cocaine reward". Neurotoxicology and Teratology. 29 (1): 66–73. doi:10.1016/j.ntt.2006.10.012. PMC 1847361. PMID 17174067.
  31. ^ Dee, T (1999). "The complementarity of teen smoking and drinking". Journal of Health Economics. 18 (6): 769–93. doi:10.1016/S0167-6296(99)00018-1. PMID 10847934.
  32. ^ a b Substitution of Marijuana For Alcohol: The Role of Perceived Access and Harm, Encyclopedia Britannica, Journal of Drug Education, 2006 by Robert Greene, David K. Lohrmann, Randi J. Alter
  33. ^ Prescription drugs a gateway for teen drug abuse, Cindy George, Houston Chronicle, September 2008
  34. ^ New drug rising: heroin by Scott Spjut, Toole Transcript Bulletin, Apr 01, 2010
  35. ^ Painkiller Abuse Can Predispose Adolescents to Lifelong Addiction Rockefeller University, 2008
  36. ^ Is Red Bull A Gateway Drug? Some John Hopkins Experts Say Caffeine Drinks Need Warning Labels, 2008
  37. ^ "ABC Discovers a New Gateway Drug for Kids: Caffeine". Businessandmedia.org. Retrieved 2010-07-29.
  38. ^ Reissig, C; Strain, E; Griffiths, R (2009). "Caffeinated energy drinks—A growing problem". Drug and Alcohol Dependence. 99 (1–3): 1–10. doi:10.1016/j.drugalcdep.2008.08.001. PMC 2735818. PMID 18809264.
  39. ^ a b Patton, George C.; Coffey, Carolyn; Carlin, John B.; Sawyer, Susan M.; Lynskey, Michael (2005). "Reverse gateways? Frequent cannabis use as a predictor of tobacco initiation and nicotine dependence". Addiction. 100 (10): 1518–25. doi:10.1111/j.1360-0443.2005.01220.x. PMID 16185213.
  40. ^ Australian Government Department of Health: National Cannabis Strategy Consultation Paper, page 4. "Cannabis has been described as a 'Trojan Horse' for nicotine addiction, given the usual method of mixing cannabis with tobacco when preparing marijuana for administration."
  41. ^ Timberlake, David S.; Haberstick, Brett C.; Hopfer, Christian J.; Bricker, Josh; Sakai, Joseph T.; Lessem, Jeffrey M.; Hewitt, John K. (2007). "Progression from marijuana use to daily smoking and nicotine dependence in a national sample of U.S. adolescents". Drug and Alcohol Dependence. 88 (2–3): 272–81. doi:10.1016/j.drugalcdep.2006.11.005. PMC 2596656. PMID 17174040.
  42. ^ Timberlake, David S.; Haberstick, Brett C.; Hopfer, Christian J.; Bricker, Josh; Sakai, Joseph T.; Lessem, Jeffrey M.; Hewitt, John K. (2007). "Progression from marijuana use to daily smoking and nicotine dependence in a national sample of U.S. adolescents". Drug and Alcohol Dependence. 88: 1896–1904. doi:10.1016/j.drugalcdep.2006.11.005. PMC 2596656. PMID 17174040.
  43. ^ Schaffer Library of Drug Policy
  44. ^ a b The "Gateway" theory: Does cannabis use lead to hard drugs? Drug use progression and the gateway effect
  45. ^ 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)
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