Light-to-moderate drinking has long been linked to better heart health, but scientists have never been sure why. More clear are the health risks of alcohol, including an increased chance of cancer, neurological aging, and more—so why would alcohol’s effect on the heart be different?
Now, in a new study published in the Journal of the American College of Cardiology, researchers at Massachusetts General Hospital explained one reason why alcohol might be linked to better heart health: it reduces stress signals in the brain in a sustained way, leading to less of a burden on the heart.
First, the scientists looked at data from more than 50,000 people in the Mass General Brigham Biobank, a large research database created by the hospital, and confirmed that light-to-moderate drinking was indeed associated with marked reductions in people’s risk of cardiovascular disease. The large size of the study let them determine that this effect was not caused by people’s socioeconomic statuses, activity levels, or even genetics—factors that are difficult to control for in smaller studies. Something else appeared to be at work, which they discovered by looking at people’s brain scans. These suggested that drinking alcohol eases the brain’s stress levels in a lasting way, which lightens the stress load placed on the heart even days after someone’s last drink.
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The brain’s stress network operates like a game of tug-of-war. On one side is the amygdala, which controls emotions, and on the other is the prefrontal cortex, which controls executive functioning. During times of stress, the amygdala sends out panic signals, and the prefrontal cortex can help block that alarm bell from ringing throughout the whole body—including in the heart. Drinking alcohol is known to ease the amygdala’s alarm effect, says Dr. Ahmed Tawakol, a study author and co-director of the Cardiovascular Imaging Research Center at Massachusetts General Hospital. “But we asked a different question: Does it have long-lasting effects on those systems?”
Looking at brain scans from more than 1,000 study participants, the team discovered that light-to-moderate drinkers experienced an ongoing dampening of activity in the amygdala, while the activity of the prefrontal cortex was normal when alcohol was not in their systems. Though the data didn’t let the researchers see whether or not this effect on the amygdala faded eventually if people stopped drinking entirely, this dampening of the amygdala’s activity was associated with a 22% reduction in cardiovascular disease.
When the researchers looked specifically at light-to-moderate drinkers with a history of anxiety—a condition characterized by an overactive stress network—the effect doubled. Rather than the 22% reduction, “people with prior anxiety had a 40% reduction in heart disease,” says Tawakol. “That gave us support for what we found on imaging.”
“I know that a lot of people will hear that and say, ‘Well, I’m anxious. That’s why I drink—I guess there’s a benefit,’” he adds. “But there is no safe quantity of alcohol.”
There are better ways than alcohol to take advantage of this stress-reducing pathway. One is exercise, which Tawakol is studying now and says increases prefrontal cortex activity rather than decreasing amygdala activity, to the same effect. “A substantial portion of the benefits of exercise can be explained by the brain,” he says. Getting enough sleep works in a similar way, he says.
Still, Tawakol’s ultimate goal is to find a pharmacological way to safely reduce activity in the amygdala. “It’s not enough for us to simply say sleep better and exercise more, because we’ve been saying that, and there’s a limited utility,” Tawakol says. “Now that we’ve highlighted a pathway that, when interrupted, doubles the risk reduction of cardiovascular disease, we need to go and find interventions that actually work.”
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