Does Drug Use Lead to Addiction, or Are Some Brains More Prone To Use Drugs?

Does using alcohol, nicotine, or cannabis engender addiction by changing the structure of brains, or does the structure of brains incline some people toward using those substances? In standard brain disease models of addiction, the neurotoxic effects of abused psychoactive substances are thought to cause brain changes that spur compulsive cravings for drink, smokes, or dope.

A recent study in JAMA Network Open, an open-access, peer-reviewed, international medical journal published by the American Medical Association, challenges that model and suggests that brain differences associated with addiction precede rather than result from substance abuse. A team of neuroscientists examined associations between brain structure and substance use initiation in nearly 10,000 children enrolled in the ongoing Adolescent Brain Cognitive Development (ABCD) Study.

Children aged 9 to 11 years were enrolled in the study. MRIs of each child’s brain were taken at that time. None of the kids in the initial cohort reported using alcohol, nicotine, cannabis, or other psychoactive substances. During the next three years, the researchers periodically asked the kids, all still below age 15, if they had used any of those substances. Roughly a third of the kids (3,460), with some overlap, owned up to using either alcohol (3,123), nicotine products (431), cannabis (212), and other substances (213), such as inhalants, prescription sedatives, and hallucinogens.

The researchers then compared the brain MRIs of the kids who consumed psychoactive substances with those who did not. Remember, these MRIs were taken before any of the now adolescents had used any psychoactive substances. The researchers identified eight “neuroanatomical features associated with substance use initiation that were present before substance exposure.”

Prior studies of adult addicts have found that they generally have lower overall brain  volumes than nonabusers do. In their study of the ABCD cohort, the researchers were surprised to find the contrary to be the case. Bigger adolescent brains with more gray matter were significantly associated with early substance-use initiation. Interestingly, neurological research suggests that bigger brains somewhat correlate with higher intelligence.

Another difference in brain structures coincident with early substance use is a thinner prefrontal cortex, which is associated with impaired emotional regulation and working memory. Early users also have larger globus pallidus volumes, which lessens impulse control. The researchers
suggest their study may be capturing brain variability related to exploration and risk-taking that motivates precocious psychoactive substance use.

An earlier study using data from the ABCD cohort asked if cannabis use contributes to psychosis in adolescents or if adolescents use cannabis to self-medicate their emerging psychotic symptoms. The researchers did not find evidence that early cannabis use contributed to the risk of experiencing psychotic symptoms.

Instead, they suggest there may be a shared vulnerability in which genetic, gestational, or environmental factors may confer vulnerability for both cannabis use and psychosis. They further found, consistent with the self-medication hypothesis, that worsening symptoms motivated the initiation of cannabis use and that the users experienced reduced symptom distress.

In their commentary on the adolescent substance use initiation study, two University of Minnesota cognitive neuroscientists observed that the brain differences found in the new study “reflect predispositional risk for substance use initiation—and that we may need to reevaluate the causal assumptions that underlie brain disease models of addiction.”

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