Evolutionary Foraging Instinct Fueled by Fructose Production Linked to Alzheimer’s Disease Formation, Researchers Say
According to a recent study conducted by scientists at the University of Colorado Anschutz Medical Campus, the formation of Alzheimer’s disease (AD) may be fueled by an ancient human foraging instinct that relied on fructose production in the brain. It is believed that this instinct, which was used during times of scarcity by animals and our distant ancestors, could offer new insights into the development and treatment of AD.
The case that diet drives Alzheimer’s disease is made by the study’s lead author, Richard Johnson, MD, who is a professor at the University of Colorado School of Medicine specializing in renal disease and hypertension, along with co-author Maria Nagel, MD, a research professor of neurology at the CU School of Medicine. AD is characterized by the abnormal accumulation of proteins in the brain, which slowly erode memory and cognition.
It is suggested by Johnson and his team that AD is a harmful adaptation of an evolutionary survival pathway.
Fructose’s Role in Early Human Survival Response and Foraging Behavior Explored by Researchers
According to a recent study, one of the basic tenets of life is to ensure enough food, water, and oxygen for survival. The study notes that nature has developed a clever way to protect animals before they face starvation or hypoxia. The study also reveals that early humans developed a survival response when threatened with the possibility of starvation, which sent them foraging for food. Foraging is only effective if metabolism is inhibited in different parts of the brain.
The entire foraging response, the researchers found, was set in motion by the metabolism of fructose, whether it was consumed or produced in the body. Fructose and its byproduct, intracellular uric acid, were critical to the survival of both humans and animals.
The researchers also observed that fructose reduces blood flow to the brain’s cerebral cortex involved in self-control, as well as the hippocampus and thalamus, while blood flow increases around the visual cortex associated with food reward. All of this stimulated the foraging response. Fructose helps to dampen these centers, enabling greater concentration on food gathering.
It is worth noting that foraging requires a great deal of focus, rapid assessment, impulsivity, exploratory behavior, and risk-taking. To enhance foraging, whatever hinders it, such as recent memories and attention to time, needs to be blocked.
Fructose Metabolism and Alzheimer’s Disease: The Survival Switch Hypothesis
According to lead author Richard Johnson and his team, the fructose-dependent reduction in cerebral metabolism in certain regions was initially beneficial and reversible. However, persistent reduction in cerebral metabolism caused by recurrent fructose metabolism can result in progressive brain atrophy, neuron loss, and all the characteristics of Alzheimer’s disease (AD).
The survival switch, which aided early humans during times of scarcity, is now stuck in the on position, leading to overeating of high-fat, sugary, and salty foods that promote excess fructose production. Fructose produced in the brain can cause inflammation and ultimately lead to Alzheimer’s disease. Memory lapses, an inability to navigate a maze, and neuron inflammation have been observed in animals given fructose.
According to Johnson, high levels of fructose can also be found in the brains of Alzheimer’s patients, and the wandering tendencies of some patients may be a remnant of the ancient foraging response. The study recommends further research into the role of fructose and uric acid metabolism in AD.
To establish the potential for prevention, management, or treatment of the disease, both dietary and pharmacologic trials to reduce fructose exposure or block fructose metabolism should be conducted, according to Johnson.
Reference: “Could Alzheimer’s disease be a maladaptation of an evolutionary survival pathway mediated by intracerebral fructose and uric acid metabolism?” by Richard J. Johnson, Dean R. Tolan, Dale Bredesen, Maria Nagel, Laura G. Sánchez-Lozada, Mehdi Fini, Scott Burtis, Miguel A. Lanaspa and David Perlmutter, 11 January 2023, American Journal of Clinical Nutrition.
DOI: 10.1016/j.ajcnut.2023.01.002
