For years now, scientific research has found evidence that moderate drinking has heart-health benefits—now researchers are focusing on why those benefits exist. A recent study conducted at Brazil’s University of São Paulo Biomedical Science Institute has found one possible way alcohol can boost cardiovascular health. Ironically, it appears that the stress of metabolizing alcohol may prepare your heart to fight off bigger health threats.
The study, published in the June 2018 issue of the European Society of Cardiology's journal Cardiovascular Research, suggests that alcohol’s cardioprotective effects are associated with aldehyde dehydrogenase-2 (ALDH2), an enzyme that helps process harmful chemicals brought on by various forms of cardiovascular stress, and acetaldehyde, a toxic byproduct of metabolizing alcohol that ALDH2 helps process.
Past research has shown that when the heart endures certain types of injury, ALDH2 activity is significantly decreased, leading to a higher chance of cell damage and cell death. But the new study found that previous exposure to acetaldehyde from drinking alcohol could actually prepare the body to produce more ALDH2 when it faces other types of damage later on down the road.
"Our data suggest moderate exposure to ethanol causes minor stress in heart cells, but not enough to kill them,” Julio Cesar Batista Ferreira, principal investigator for the research project, said in press release. “Intracellular signaling is reorganized as a result, and heart cells eventually create a biochemical memory to protect against stress, also known as preconditioning.”
To test this "memory," the researchers studied mouse hearts in an ex-vivo, or out of the body, model. One group of hearts was exposed to ethanol for 10 minutes, at a dose equivalent to two glasses of wine for an average-size man, according to each animal’s mass.
Next, the researchers simulated cardiovascular stress in the hearts of the treated group, plus a group that had not previously been exposed to ethanol. In the group that had the ethanol exposure, after an hour, an average of 30 percent of the cells in their hearts had died. By comparison, the group that did not receive ethanol treatment prior to the heart-damage simulation lost approximately 50 percent of their cells. An analysis also revealed that ALDH2 activity was twice as high in the ethanol-treated group as in the untreated group, and the treated group’s ALDH2 activity was equivalent to the level measured in a control group, which was not exposed to alcohol nor injury.
To examine the phenomenon further, another group of mouse hearts was treated with both ethanol and a drug that inhibits ALDH2 activity. In this group, cell death rose to 80 percent after the simulated heart damage, which reinforces the idea that alcohol’s cardioprotective effects do indeed depend on ALDH2.
While these results do indicate a heart-helping potential of alcohol—and more important, ALDH2 and previous exposure to acetaldehyde—this protective "memory" effect won’t occur in every case.
“It all depends on people's DNA," Ferreira said. "The acetaldehyde that results from digesting ethanol may protect most people if a small amount is produced, but it can also maximize the damage done by a heart attack in an individual with the ALDH2 gene mutation.” This mutation, especially common in those of East Asian descent, inhibits the body from properly processing acetaldehyde after drinking and can lead to higher rates of cell death. Ferreira also warns about overconsumption of alcohol, which can have a negative cardiovascular impact even in those without the ALDH2 deficiency.
The final group of hearts tested in the study came from mice that were genetically modified to have a mutation that reduced ALDH2 activity by roughly 80 percent. "In this group, when we exposed the hearts to ethanol, the [simulated heart] damage … was greater. The rate of cell death rose from 50 percent to 70 percent," Ferreira said. However, when the researchers treated this group's hearts with an experimental drug that activates ALDH2, cell death fell to 35 percent.
The researchers are now working to determine how the presence of acetaldehyde creates this “memory” that keeps ALDH2 more active during times of future stress, with the goal of developing a drug that mimics the mechanism, so that this cardioprotective effect of alcohol can be enjoyed by all.
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