Alzheimer’s disease is a progressive and deadly neurodegenerative disorder characterized by the accumulation of misfolded proteins in the brain, leading to the loss of cognitive function and memory. Despite decades of research, the exact causes of Alzheimer’s disease remain elusive. However, a team of researchers at the University of Colorado Anschutz Medical Campus has recently found evidence that the disease may be driven by a survival strategy inherited from early humans.
According to the study, which was led by Dr. Richard Johnson and published in The American Journal of Clinical Nutrition, Alzheimer’s disease may be a negative consequence of an evolutionary survival strategy utilized by animals and our distant ancestors to preserve their bodies and brains during times of shortage. The prospect of famine, the researchers argue, necessitated a foraging response, which was activated by fructose metabolism. Fructose is a simple sugar found in many fruits, vegetables, and processed foods.
The researchers found that fructose metabolism triggers the foraging response, which involves shutting off distractions like recent memories and concentrating on the present moment to improve the ability to forage. The calming effects of fructose on certain areas of the brain facilitate a heightened capacity for foraging. This foraging response was shown to be triggered by fructose metabolism, whether ingested or generated endogenously.
The study also found that blood flow decreases in regions of the brain related to self-control, such as the cerebral cortex, hippocampus, and thalamus, and rises around the visual cortex, which is linked to food reward. All of these factors prompt foraging behavior.
At first, the fructose-dependent decrease in metabolism in certain parts of the brain was thought to be advantageous and reversible. However, the study suggests that the hallmarks of Alzheimer’s disease, such as progressive brain shrinkage and cell loss, are the result of a chronic and persistent decline in cerebral metabolism caused by recurrent fructose metabolism.
The researchers argue that overeating high-fat, sugary, and salty food, which in turn prompts excess fructose production, is a result of the survival reaction, which Johnson refers to as the “survival switch.” This switch helped ancient humans get through moments of shortage by promoting foraging behavior and conserving energy. However, in modern times, where food is abundant, this survival switch may contribute to the development of Alzheimer’s disease and other chronic diseases associated with high fructose consumption.
The study also suggests that inflammation caused by the brain’s own production of fructose is a key factor in the development of Alzheimer’s disease. Animals that have been fed fructose exhibit memory impairment, a decline in maze-navigating ability, and neuronal inflammation. In animal studies, prolonged exposure to fructose results in the development of tau and amyloid beta proteins in the brain, which are also characteristic of Alzheimer’s disease in humans. Alzheimer’s patients also tend to have high quantities of fructose in their brains.
Some Alzheimer’s patients’ propensity to wander out may be a holdover from the primitive foraging reaction, says Johnson. The fructose and uric acid metabolic pathways in Alzheimer’s disease need more investigation. The authors recommend more investigation into the potential benefits of pharmacologic and nutritional interventions to minimize fructose consumption or inhibit fructose metabolism for the prevention, management, and treatment of this condition.
The study sheds new light on the possible causes and progression of Alzheimer’s disease, a condition that affects millions of people worldwide. The findings may lead to novel treatments and interventions that target the underlying mechanisms of the disease. However, the study also highlights the need for a more comprehensive understanding of the complex interplay between genetics, environment, and lifestyle factors in the development of chronic diseases.
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