Study: Ancient Foraging Instinct Could Hold Alzheimer's Clues

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Key points:

  • An ancient response designed to ensure human ancestors did not starve may be fueling Alzheimer’s disease in today’s age of abundance.
  • Fructose in the brain helped ancestors focus solely on food gathering, but now may be leading to inflammation and Alzheimer’s disease.

An ancient human foraging instinct, fueled by fructose production in the brain, may hold clues to the development and possible treatment of Alzheimer’s disease, according to researchers at the University of Colorado Anschutz Medical Campus.

In the study published in The American Journal of Clinical Nutrition, the scientists suggest that Alzheimer’s disease is a harmful adaptation of an evolutionary survival pathway used in animals and distant human ancestors during times of scarcity.

When threatened with the possibility of starvation, early humans developed a survival response that sent them foraging for food. Yet, foraging is only effective if metabolism is inhibited in various parts of the brain. Foraging is enhanced by blocking whatever distractions get in the way, like recent memories and attention to time. Fructose, a kind of sugar, helps damp down these centers, allowing more focus on food gathering.

In fact, the researchers found 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 byproduct, intracellular uric acid, was critical to the survival of both humans and animals.

The researchers noted that fructose reduces blood flow to the brain’s cerebral cortex involved in self-control, as well as the hippocampus and thalamus. Meanwhile, blood flow increased around the visual cortex associated with food reward. All of this stimulated the foraging response.

“We believe that initially the fructose-dependent reduction in cerebral metabolism in these regions was reversible and meant to be beneficial,” said the study’s lead author Richard Johnson, MD, professor at the University of Colorado School of Medicine. “But chronic and persistent reduction in cerebral metabolism driven by recurrent fructose metabolism leads to progressive brain atrophy and neuron loss with all of the features of AD.”

Johnson suspects the survival response that helped ancient humans get through periods of scarcity is now stuck in the “on” position in a time of relative abundance. This leads to the overeating of high fat, sugary and salty food—prompting excess fructose production. Additionally, Johnson said the tendency of some AD patients to wander off might also be a vestige of the ancient foraging response.

The team says more research on the topic is needed.

“We suggest that both dietary and pharmacologic trials to reduce fructose exposure or block fructose metabolism should be performed to determine if there is potential benefit in the prevention, management or treatment of this disease,” Johnson said.

Information provided by University of Colorado Anschutz Medical Campus.

 

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