Scientists have for years known that drinking moderately protects the heart, and they are now a step closer to understanding why.
Researchers behind a study in mice believe consuming small amounts of alcohol could protect the heart because it activates an enzyme which puts the organ under a healthy level of stress and makes it stronger.
According to the team at the Biomedical Science Institute of the University of Sao Paulo, Brazil, and Stanford University in the U.S., an enzyme called aldehyde dehydrogenase-2 (ALDH2) appears to both help process the toxic byproducts of alcohol digestion, and get rid of a molecule our heart cells create when they undergo major damage such as a heart attack.
When heart cells face stress, they create a large amount of a type of compound called an aldehyde which is toxic in excess and can torpedo the structure of cells. ALDH2 clears the aldehydes from the heart, including the form of the compound created by the liver after we drink.
“Intracellular signaling is reorganized as a result, and heart cells eventually create a biochemical memory to protect against stress, also known as preconditioning. When the cells are submitted to a higher level of stress, they know how to deal with it.”
The study suggests drinking moderately could protect the heart, but "it all depends on people's DNA."
"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," he said. "It's easy to identify these people. After one glass of beer, they get flushed and complain of a headache. Their resistance to alcohol doesn't improve over time."
In order to investigate why alcohol seems to be “cardioprotective,” the team triggered heart attacks in ex vivo mouse hearts. One group of hearts was untreated as a control. Another four groups were dosed with an amount of ethanol equivalent to two cans of beer or two glasses of wine; the recommended maximum alcohol allowance for the average man set by the World Health Organization.
They then recreated an ischemia-reperfusion injury, the type of damage caused when blood flows back into tissue after it is starved of oxygen for a period of time, by blocking oxygen and nutrients to the organ for 30 minutes before reintroducing the flow. The team noted that around half of cardiac cells died unless they intervened.
The researchers found that hearts whose ALDH2 was blocked or inhibited experienced greater cell death. But when they were treated with an experimental drug that activates ALDH2, cell death dropped to 35 percent.
Scientists used to believe a lack of oxygen damaged the heart during events such as heart attacks. But new evidence suggests damage is caused by the metabolism of heart cells collapsing as nutrients and oxygen re-enter the tissue, Ferreira said.
"In our new study, we observed that ALDH2 activity in the heart exposed to ethanol before ischemia-reperfusion injury remained equal to that seen in a healthy heart. We believe the stress caused by a moderate dose of ethanol leaves a memory and that the cell learns to keep ALDH2 more active,” Ferreira said.
The drug which activates ALDH2 has passed phase one clinical trials in the U.S., and will next be tested in patients with heart disease in the hope it will become a widely used treatment.
The findings were published in the journal Cardiovascular Research.