Scientists have long known that many bone fractures are alcohol-related, whether the break results from minor accidents like trips and falls, or major ones that involve heavy machinery. What remained unclear was the underlying mechanism. Scientists have now discovered through tests on ordinary lab mice what it is about binge drinking that causes slow bone healing.

The answer, the team found, lies at the cellular and molecular levels. Broken bones heal themselves with reactive tissue formation and then reparative callus formation. In the group of mice given large quantities of alcohol, this callus formation was less mineralized — meaning it wasn’t forming properly. Even after the bone refashioned its original contours, the newly formed bone wasn’t as strong as the bone of sober mice, prompting researchers to further advise people against alcohol abuse.

"Many bone fractures are alcohol-related, due to car accidents, falls, shootings, etc.," Dr. Roman Natoli, of Loyola University’s Stritch School of Medicine, said in a statement. "In addition to contributing to bone fractures, alcohol also impairs the healing process. So add this to the list of reasons why you should not abuse alcohol."

The researchers behind the study, working out of Loyola University Medical Center, emphasized curbing abuse in adolescents especially, as growing bones are already more susceptible to fracture, so any depletion of long-term calcium stores would negatively impact the bone’s ability to self-repair.

Natoli and his colleagues also found the effect to be dose-dependent, so the more alcohol that the mice consumed, the more difficult it was for their bones to repair themselves.

The mice in the team’s study were split into two groups: one received no alcohol, while the other had their blood alcohol levels raised to human equivalents of .20, or 2.5 times the legal limit. Researchers induced tibia fractures in both groups to observe the way each group’s bones healed. In addition to softer, weaker callus formation in “binge-drinking” mice, the team saw less production of a protein called osteopontin, which the body rushes to a fracture site with the help of immature stem cells.

Worse, the bone cells in mice that were exposed to alcohol showed greater concentrations of oxidative stress, a process of degrading cell components from an overabundance of free radicals and peroxides that fight against antioxidants. Due to its ability to break down proteins and DNA, oxidative stress has been implicated in cancer, Alzheimer’s disease, and heart failure.

Binge drinking has health risks that extend far beyond slow bone healing, of course. Alcohol abuse can lead to cirrhosis of the liver, liver failure, depression and anxiety, sleep disorders, and increased risk of type 2 diabetes, among other diseases.

Luckily, as binge drinking pertains to slow bone healing, the dose-dependent risks also work in the opposite direction. Once a person stops drinking in excess, his or her bones can gradually restore themselves back to normal health.

“The basic goal,” Natoli said, “is to get these fractures to heal normally.”