According to the researchers, excessive sugar consumption results in metabolic dysfunction that in turn increases one’s risk for developing serious cognitive conditions later in life. The data centers around a process called fructose metabolism, wherein the brain produces an abundance of simple carbohydrate.
When consumed in excess, (especially via processed sugars) fructose metabolism in the brain deprives the body of the cerebral energy it needs to perform other important neurological functions. Over time, this abnormality atrophies brain neurons.
“In essence, we propose that Alzheimer’s disease is a modern disease driven by changes in dietary lifestyle in which fructose can disrupt cerebral metabolism and neuronal function,” the authors write in the new report.
“The loss of cognitive function in Alzheimer’s disease is pathologically linked with neurofibrillary tangles, amyloid deposition, and loss of neuronal communication. Cerebral insulin resistance and mitochondrial dysfunction have emerged as important contributors to pathogenesis supporting our hypothesis that cerebral fructose metabolism is a key initiating pathway for Alzheimer’s disease.”
Fructose, a natural sugar, commonly found in fruit, processed foods, sodas, and corn syrup, is processed in the liver. Compared to glucose which is distributed throughout the body in the form of blood sugar, fructose doesn’t suppress one’s appetite. In fact, it has been reported to promote overeating, cause leptin resistance, hinder fat regulation, and increase one’s risk of developing obesity and type 2 diabetes.
“Fructose is unique among nutrients because it activates a survival pathway to protect animals from starvation by lowering energy in cells in association with adenosine monophosphate degradation to uric acid. The fall in energy from fructose metabolism stimulates foraging and food intake while reducing energy and oxygen needs by decreasing mitochondrial function, stimulating glycolysis, and inducing insulin resistance.”
With respect to dementia risk, high-fructose intake induces neural glycolysis, a process that denotes a provisional increase in brain excitation, that causes it to burn through fuel oxidation.
Medical experts recommend healthy adults derive the majority of their fructose intake from energy-dense fruits.
“Alzheimer’s disease may be driven by overactivation of cerebral fructose metabolism, in which the source of fructose is largely from endogenous production in the brain. Thus, the reduction in mitochondrial energy production is hampered by neuronal glycolysis that is inadequate, resulting in progressive loss of cerebral energy levels required for neurons to remain functional and viable,” the authors concluded.
“By outlining consistent evidence, we’re hoping to inspire researchers to continue exploring the relationship between fructose in the brain and Alzheimer’s disease,” Johnson says. “New treatments aimed at inhibiting intracerebral fructose metabolism could provide a novel way to prevent and treat this disease.”