Understanding Alcohol as a Gateway Drug and Why Early Treatment is Essential

Gateway drug theory maintains that use of particular psychoactive substances will eventually escalate to use of more addictive and damaging drugs. While the ideas underlying this theory have been in circulation for nearly a century under names like the stepping-stone theory and the escalation hypothesis, the phrase gateway drug only entered the mainstream lexicon in the 1980s. It quickly became a central feature in anti-drug campaigns such as Drug Abuse Resistance Education (D.A.R.E.) and a driving force in national drug policy.

For years, the gateway drug theory proponents held marijuana as its central focus. And at first glance, it appeared to make sense: people who use marijuana are more likely to use other illicit drugs than people who don’t use marijuana. However, as German Lopez notes in an article for Vox, “There doesn’t have to be a causal link between marijuana and harder drugs to explain this; it could just be that the things that drive someone to marijuana—boredom, depression, social circles—can just as easily drive them to other drugs.” Indeed, as early as 1999, the Institute of Medicine of the National Academy of Sciences noted, “There is no conclusive evidence that the drug effects of marijuana are causally linked to the subsequent use of other drugs.” Today, the scientific community largely rejects the idea of marijuana as a gateway drug, at least in the simplistic form in which it was initially popularized.

One of the reasons marijuana has, to a large extent, been discarded as the star of gateway drug theory is that research on progression of drug use shows that while, yes, people who use marijuana are more likely to use other drugs, marijuana use was overwhelmingly preceded by the use of alcohol, a perfectly legal substance consumed by a large majority of people. If we are going to claim that marijuana use opened up the path to cocaine and heroin addiction, we also have to say the same of alcohol, and that would be absurd, right?

Maybe not.

In recent years, alcohol has increasingly become a site of inquiry in gateway drug theory. On the surface, it may appear that theory of alcohol as a gateway drug suffers from the same lack of causal evidence as marijuana does. After all, the vast majority of people drink, but most of those people will not go on to try hard drugs, and even fewer go on to become addicted to the hard drugs they do try. Of those who do graduate to hard drug use and develop addiction, there are myriad biological and environmental factors that may influence this progression, including association with people who use hard drugs, mental illness, and genetic propensity for substance abuse. Now, however, a new study suggests that there may indeed be a causal relationship between drinking and addiction to hard drugs.

Earlier this month, a study by researchers at Columbia University was published in Science Advances. The study sought to understand how alcohol may function to set cocaine addicts apart from casual cocaine users, using rats as their test subjects. When rats were given cocaine without trying alcohol, they continued to seek out more cocaine by “pressing a lever to administer doses to themselves.” In other words, drug-seeking behavior was observed, sometimes to a high degree. However, their efforts were dwarfed by those observed in rats who engaged in heavy drinking prior to cocaine use:

When rats were allowed to drink alcohol every day for nearly two weeks—a considerable length of time in the lifespan of a rat—then given access to a dose of cocaine, they engaged in drug-seeking behavior with such determination that they were barely deterred by painful electric shocks. As researchers required more work for the cocaine, the alcohol-treated rats pressed a lever an average of 563 times—much more than the average 310 lever presses mustered by […] rats with no alcohol history. Days after cocaine administration had ceased, the rats exposed to alcohol pressed the lever 58 times, on average—far more than the 18 lever presses averaged by rats that were not primed with alcohol.

Only 14% of rats who had not been exposed to alcohol continued their drug seeking when electric shocks were administered. In contrast, most alcohol-primed rats “were willing to endure several sets of shocks before giving up” and 29% continued even when shocked at the highest level possible.

In addition to behavioral differences, researchers also observed significant chemical differences the brains of alcohol-treated vs untreated rats. These changes were particularly striking in the brain’s reward center as well as the epigenome, which is responsible for activating and deactivating gene expression. The findings make a strong case for the idea that alcohol—specifically alcohol in high amounts and for sustained periods—primes the brain for an addictive response to cocaine by creating meaningful neurological changes. “A rat is not necessarily a good model for the behavior of a human, but their neurons do things very similar to our neurons,” says John Dani, a neuroscientist specializing in addiction research at the University of Pennsylvania. Although Dani was not involved in the study, he believes the results are revealing. “We have those same enzymes and the same epigenetic processes in our neurons, and that’s where this has real value. At this molecular level, they’re very similar to us.”