"[4] However, a 2018 literature review conducted by the National Institute of Justice, which analyzed 23 peer-reviewed research studies, concluded "that existing statistical research and analysis relevant to the "gateway" hypothesis has produced mixed results",[5] and that "no causal link between cannabis use and the use of other illicit drugs can be claimed at this time.
Alcohol and nicotine also prime the brain for a heightened response to other drugs and are, like marijuana, also typically used before a person progresses to other, more harmful substances.
Subgroup analyses showed that personal and social conditions, such as gender, age, marital status, mental disorders, family history of substance use, overlapping illegal drug distribution channels, alcohol use disorder, nicotine dependence, ethnicity, urbanicity, and educational attainment influenced the height of probability.
[15] Large-scale longitudinal studies in the U.K. and New Zealand from 2015 and 2017 showed an association between cannabis use and an increased probability of later disorders in the use of other drugs.
[16][17][18] Students who regularly consume caffeinated energy drinks have a greater risk of alcohol use disorder, cocaine use and misuse of prescription stimulants.
At the end of a three-year period, it found that those who had previously reported cannabis use were associated with a five times greater odds of being diagnosed with AUD than those who had not.
After adjustment for select confounders (age, race, marital status, income, and education), these odds were reduced to two times greater risk.
[23][24] 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.
[34][35][36][37] In mice, nicotine increased the probability of later consumption of cocaine, and the experiments permitted concrete conclusions on the underlying molecular biological alteration in the brain.
[38] 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,[39] as well as other drugs.
[40] In rats, alcohol increased the probability of later addiction to cocaine and again relevant alterations in the reward system were identified.
[45] These findings correspond to epidemiological data that people who consume energy drinks generally showed an increased tendency to take alcohol and other substances.