In 2015 schreef Professor John Britton dit over het gateway argument
The gateway theory or hypothesis is commonly invoked in addiction discourse, broadly to suggest that the use of one drug (sometimes a legal one such as tobacco or alcohol) leads to the use of another drug (sometimes an illegal one) but its definition is contested. No clear provenance exists and its origin appears to derive from lay, academic and political models . It is apparent that discussions about the natural progression of drug use observed in longitudinal studies of young people appear to have morphed into implicit conclusions on causality without any evidential backing. Some have argued that the effect could be causal if the use of one drug, biochemically or pharmacologically, sensitises the brains of users to the rewarding effects of other drugs  making the dependent use of these other drugs more likely. However, there are many plausible competing hypotheses for such a progression  including i) shared networks and opportunities to purchase the drugs; and ii) individual characteristics such as genetic predispositions or shared problematic environment.
Academic experts have stated that the gateway concept “has been one of the most controversial hypotheses…in part because proponents and opponents of the hypothesis have not always been clear about what the hypothesis means and what policies it entails” . Indeed, a recent analysis of gateway concluded “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” .
Despite these serious and fatal flaws in the arguments, the use of the term ‘gateway’ is commonplace both in the academic literature and the lay press, particularly in relation to EC use and whether EC are a gateway to smoking. Some have suggested that if EC use increases at the same time as smoking increases then EC are acting as a gateway to smoking. Similarly, it’s been argued that if someone uses an EC first and then initiates smoking, EC are a gateway. These arguments are clearly erroneous. To give one example of the misuse of the gateway concept, a BMJ news item on the Moore et al., 2014  cross-sectional study discussed above commented that “[EC} could be a gateway into smoking” .
Kandel recently argued that evidence from mice offers a biological basis for the sequence of nicotine to cocaine use in people , but there is limited evidence for this. In reality, the gateway theory is extremely difficult to test in humans. For example, a clean test of the gateway hypothesis in relation to EC and smoking would require randomising people to an environment with EC and one without, and then following them up over a number of years to assess uptake of EC and smoking.
We strongly suggest that use of the gateway terminology be abandoned until it is clear how the theory can be tested in this field. Nevertheless, the use of EC and smoking requires careful surveillance in young people. The preferred option is that young people do not use EC but it would be preferable for a young person to use an EC instead of smoking, given the known relative risks of the EC and smoking cigarettes .