This Hidden Sugar in Your Body May Trigger Alcoholism

Alcoholism is not just a matter of will or social context. Its anchoring in the body goes further than we imagined. Once absorbed, ethanol triggers an unsuspected metabolic mechanism capable of transforming the body into an independent sugar producer. This internal manufacturing would not be without consequences, as it could fuel both the desire to drink and the silent progression of alcohol-related liver disease.

When alcohol transforms the body into a sugar factory

Alcohol doesn't just damage the liver. According to a team from the University of Colorado Anschutz, it also changes the way the body handles sugar. When circulating in the blood, ethanol activates a metabolic pathway known as the “polyol pathway.” This mechanism pushes the body to make its own fructose from glucose, a process normally reserved for certain situations of stress or energy imbalance.

This endogenous fructose is then metabolized by an enzyme called ketohexokinase (KHK). However, this enzyme seems to play a dual role. It stimulates the brain's reward system and accelerates liver inflammation. In other words, the body transforms into an internal sugar factory, the production of which feeds both the desire to consume and the deterioration of tissues.

The researchers, relayed by SciTechDaily, observed in mice that the absence of KHK prevented this cycle from starting. Animals deprived of this enzyme spontaneously drank less alcohol and showed reduced brain activity in regions associated with addiction. These findings suggest that alcohol works by hijacking a biological mechanism designed to manage energy, turning it into an addictive drive.

The little-known link between addiction and alcohol-related liver disease

This same mechanism could also explain why liver damage is so common in dependent people. In their experiments, the researchers showed that blocking KHK (either through genetic modification or drug treatment) almost completely prevented the occurrence of liver damage. Protected mice had fewer fatty deposits, reduced inflammation and no fibrosis.

This discovery links two pathologies previously thought to be distinct: alcohol-related liver disease (ALD) and sugar-induced metabolic disorders, such as metabolic fatty liver disease. In both cases, fructose appears to be a central player in the inflammatory process. The metabolism of sugar and that of alcohol therefore share a biological point of convergence, which could explain the frequency of liver diseases in heavy drinkers.

Professor Richard Johnson, co-author of the study, points out that this intersection between alcohol and fructose opens up an entirely new perspective. That of simultaneously treating the effects of alcohol and sugar by targeting a single metabolic pathway. These observations, reported by News Medical, mark a major advance in understanding the link between addiction and liver degeneration.

Towards a new therapeutic lever to break the vicious circle

By acting on the production and metabolism of fructose, it would therefore be possible to interrupt the biological loop which links pleasure, addiction and cellular destruction. In rodents, blocking KHK not only reduced alcohol consumption, but also protected the liver from chronic damage. Scientists believe that inhibitors of this enzyme could constitute a new generation of treatments, capable of acting on both behavior and internal lesions.

The idea may seem daring, yet it traces a new path. By limiting sugar at the source, we act at the root. The body regains balance, and the addictive impulse loses its strength. Ultimately, this approach could lighten the load on the liver, while calming the mind. A double promise which, if confirmed, would change the situation.