
Scientists have discovered a surprising connection between alcohol use and the way the body handles sugar—one that could reshape how we treat addiction and liver disease. A new study from the University of Colorado Anschutz Medical Campus reveals that alcohol doesn’t just harm the liver directly; it triggers the body to make a form of sugar that reinforces the urge to drink.
Researchers found that alcohol activates a metabolic pathway that leads to the internal production of fructose, the same sugar found in many sweetened foods. This process depends on an enzyme called ketohexokinase (KHK). Once produced, the fructose seems to intensify alcohol cravings and worsen liver stress, creating a cycle where drinking promotes even more drinking—and more damage.
To test the enzyme’s impact, scientists studied mice with KHK genetically removed or medically blocked. The results were dramatic. These mice showed:
Essentially, removing KHK broke the biological loop connecting sugar metabolism and alcohol dependence.
The findings highlight a shared metabolic pathway behind alcohol-associated liver disease (ALD) and metabolic dysfunction-associated steatotic liver disease (MASLD). Both conditions rely heavily on fructose-driven processes, suggesting that targeting KHK could help patients regardless of whether their liver damage is caused by alcohol, diet, or both.
This metabolic insight opens a promising new door: instead of treating the consequences of alcohol, scientists may be able to stop the cycle at its source.