Why do some people develop alcohol use disorder (AUD)? And why do other stay sober – even when they come from the same environment?
Questions like these drove the research behind a sweeping new study appearing in JAMA Psychiatry. In it, the authors suggest that (at least part of) the answer stems from the drinker’s intelligence – in more ways than one.
Drawing on data culled from more than half a million Swedish men and several international genetic datasets, researchers found that lower IQ at age 18 predicted a dramatically higher lifetime risk of alcohol use disorder. Those in the lowest IQ bracket faced a 43% higher adjusted risk than their average peers, even after accounting for socioeconomic background, family history, and coexisting psychiatric conditions.
But it wasn’t just behavioral – or even psychological – for that matter. It stretched well into biology. Subsequent analyses revealed that lower genetic liability for cognitive performance directly boosted the risk of alcohol use disorder. And the researchers confirmed this pattern across several large genome-wide association studies (GWAS).
60 Years of Follow-Up
Researchers based the primary analysis on a uniquely comprehensive source: Sweden’s Military Conscription Register. Between 1950 and 1962, nearly 650,000 men underwent standardized IQ testing around age 18. Researchers then tied those records back to national medical and mortality registers, following each participant for an average of 60 years.
The results stunned the team.
As IQ scores climbed, lifetime incidence of AUD fell in a near-linear pattern. Men with low IQ scores endured nearly two-thirds higher crude lifetime risk than average. Those with high IQ, on the other hand, boasted a 40% lower risk.
Even among siblings, where genes and home environments overlapped, those with lower IQ appeared to be much more likely to develop an alcohol problem later on in life.
Education accounted for only about 14% of that effect, suggesting that intelligence shapes alcohol-related vulnerability through multiple pathways – cognitive, behavioral, and social.
Parsing Causality
To figure out whether cognitive ability drives lower AUD risk – or just coexists with it – the team ran a series of Mendelian randomization (MR) analyses using data from over a million participants across Europe, the U.S., and Australia.
These analyses supported a causal direction. Genes tied to better cognitive performance also seemed to extend protection against alcohol use disorder. Even so, results varied based on the national context.
In the U.S.- and U.K.-based datasets, education appeared to mediate much of this effect, implying that higher intelligence reduces AUD risk largely by enabling better educational and occupational outcomes.
Standing in stark contrast, the Finnish data told a different story. Once the researchers accounted for education, the genetic link between cognitive performance and AUD grew stronger, suggesting education might buffer genetic risk rather than simply explain it.
The Role of Polygenic Scores
In a separate U.S. cohort (the Yale-Penn study) participants’ polygenic scores for cognitive performance also forecast their likelihood of AUD. Those in the highest decile of genetic cognitive ability had 35% lower odds of developing AUD than those in the lowest decile.
And yet, despite the Swedish data, the U.S. pattern was asymmetrical. Higher scores conferred protection, but lower scores didn’t necessarily amplify risk.
This nuance, the authors argue, underscores how “genetic liability interacts with social structure.” In short, what protects one population might not apply to another.
Social Context, Policy Implications
The findings land squarely in a broader debate about nature, nurture, and inequality. AUD has a heritability of roughly 50%, but environmental forces – from education and employment to access to healthcare – shape how that genetic risk unfolds.
In Sweden, where educational and health disparities remain relatively narrow, lower IQ still predicted higher risk, but the gap was smaller. In more stratified systems like the United States, the same genetic and cognitive factors might magnify risk through wildly unequal opportunities and stress exposure.
“Cognitive performance may confer resilience through enhanced problem-solving and adaptive coping,” the authors wrote, “but educational attainment reflects a broader constellation of traits – including self-regulation and access to supportive environments – that determine whether that resilience translates into healthier outcomes.”
If intelligence and education help defend against alcohol addiction, then it isn’t about innate ability. It’s all about opportunity. Societies that foster cognitive development and educational equity might (indirectly) help curb a population’s addiction risk.
Brains and environments don’t just interact. They negotiate. And when it comes to addiction, smarter policy might be as important as smarter minds.
Further Reading
Even Moderate Alcohol Consumption Drives Up Dementia Risk
