Fructose Consumption May Increase Risk of Alzheimer’s, Researchers Say

Researchers say an evolutionary foraging instinct that is dependent on the sugar fructose, may now be driving the formation of Alzheimer’s disease in the human body. Scientists at the University of Colorado Anschutz Medical Campus suggest that an ancient human foraging instinct, activated by the production of fructose in the brain, could hold clues to the development and treatment of Alzheimer’s disease.

The disease is characterized by an abnormal accumulation of proteins in the brain, leading to a slow erosion of memory and cognition. The study argues that Alzheimer’s disease is driven by diet, as it is an adaptation of an evolutionary survival pathway used by animals and our distant ancestors during times of scarcity. Early humans developed a survival response that sent them foraging for food when threatened with the possibility of starvation.

Foraging requires focus, impulsivity, exploratory behavior, and risk-taking, which is enhanced by blocking whatever gets in the way, like recent memories and attention to time. Fructose, a type of sugar, helps dampen these centers, allowing more focus on food gathering.

The researchers found that the entire foraging response was set in motion by the metabolism of fructose, whether it was eaten or produced in the body. Metabolizing fructose and its by-product, intracellular uric acid, was crucial to the survival of both humans and animals. Fructose produced in the brain can lead to swelling and thereby cause Alzheimer’s disease.

Fructose consumption can reduce blood flow to the brain’s cerebral cortex, hippocampus, and thalamus, while increasing blood flow around the visual cortex associated with food reward, thereby stimulating the foraging response.

The study argues that an ancient foraging instinct, activated by the production of fructose in the brain, is a harmful adaptation of an evolutionary survival pathway that is stuck in the “on” position in a time of relative abundance, leading to the overeating of high-fat, sugary and salty food, and prompting excess fructose production that can lead to inflammation and ultimately Alzheimer’s disease.

Animals who were given fructose show memory loss, a loss in the ability to navigate, and inflammation of the neurons. The study suggests that more research is needed on the role of fructose and uric acid metabolism in Alzheimer’s disease and that both dietary and pharmacologic trials to reduce fructose exposure or block fructose metabolism should be done to determine whether there is potential benefit in the prevention, management or treatment of this disease.