Gateway drug theory

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The gateway drug theory (also called gateway theory, gateway hypothesis and gateway effect) is the theory 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] and cannabis.

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]

Contents

Variations of the theory

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

Cannabis

Some scientific studies show that the consumption of cannabis can possibly predict a significant higher risk for the subsequent use of "harder" illicit drugs, while other studies show that it cannot.[7][8] Two recent studies are from University of Pittsburgh's School of Pharmacy,[9] and from Dr. Michael Lynskey.[10][11]

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.[12] 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.[13]

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.[14] 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.[15]

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.[16] 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.[17] 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.[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 using 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]

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 (28–49 days old, or 6.6–10.4 in human years) 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 use 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.

A more recent US-Finnish twin study found that those who started smoking tobacco by the age of 12 were 26 times more likely to start using cannabis or other illcit drugs by age 17, compared to those who never smoked. In fact, early tobacco smoking was one of the most powerful predictors of later use of illicit drugs.[33]

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.[34] 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.[35] In addition, a study on mice found that using oxycodone during adolescence may sensitize the brain's reward system, possibly predisposing to later addiction.[36]

Caffeine has also been alleged by some to be a gateway drug.[37][38][39] 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[40] 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 smokers 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.[41]

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.[40]

An American study[42] 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.[43]

Criticisms

The gateway theory has been the subject of much criticism. Perhaps most common is the claim that gateway theory proponents commit either the post hoc ergo propter hoc or the cum hoc ergo propter hoc logical fallacies. In the latter case, it is argued, proponents of the gateway theory invalidly infer a causal relationship between two variables (in this case, the relationship between the use of less harmful soft drugs and the use of more dangerous hard drugs) from a relationship between the two variables that is strictly correlational.[19][22][44][45]

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:

See also

References

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