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Could fructose contribute to development of Alzheimer?

Could fructose contribute to development of Alzheimer?

An increased risk of neurological disorders, such as Alzheimer’s disease, is connected with the shift in the global age demographic towards older ages. Dementia risk profiles may also be evolving. Over the past 50 years, the frequency of obesity and type 2 diabetes has increased, and these conditions have been linked to a higher risk of dementia.

Certain dietary modifications could potentially pose a direct danger. From an estimated 8.1 kg/person/year at the start of the XIX century to an estimated 65 kg/person/year today, there has been a diet change in the United States with regard to the consumption of refined sugar, notably high-fructose corn syrup (HFCS).

With an estimated 6 million people living with it, Alzheimer’s disease continues to be a serious health issue. The hypothesis that fructose, a prevalent sugar present in packaged foods and fruits worldwide, may contribute to the disease’s development has recently put forth in a narrative review.

Alzheimer’s disease is characterised by the production of aberrant beta-amyloid and tau protein clumps. Treatments aimed at these aberrant protein aggregates, however, have had mixed results.

Conversely, other scientists have suggested that changes in brain metabolism that take place before the formation of these protein aggregates may be to blame for the onset of Alzheimer’s.

According to studies, diets that cause the body to produce a lot of fructose or foods that contain a lot of fructose might cause metabolic problems like obesity, diabetes, and high blood pressure.

Fructose survival pathway

A glucose and a fructose molecule make up each mole of table sugar, also known as sucrose. Most cell types and tissues in the body use glucose as fuel.

Despite the fact that fructose can be used as energy, the body prefers to store it as fat or as the storage carbohydrate glycogen.

The authors’ theory states that an animal can survive for extended periods of time without food or water by activating a survival response when it consumes fructose in excess. During migration or hibernation, the animal may be able to survive thanks to this survival reaction.

Consuming fructose results in an increase in thirst and hunger instead of fullness, which is produced by consuming glucose. Animals’ urge to forage is thereby stimulated by fructose ingestion. The fructose survival pathway, in particular, entails saving energy for just required actions, such as foraging, and minimising energy expenditure for body processes at rest.

Reducing the sensitivity of tissues to insulin, such as muscles, leads to a decrease in glucose absorption and consumption, which lowers energy expenditure. Moreover, the liver stores extra energy in the form of fat and glycogen.

The main mediators of the survival response include fructose, uric acid, and vasopressin. When this fructose survival route is activated for an extended period of time, the metabolism is disrupted, mimicking a number of the symptoms of metabolic syndrome.

They include persistent low-level inflammation, insulin resistance, high blood pressure, and weight gain. The fructose survival pathway can potentially affect the metabolism of the brain.

Impact on the brain

While making up only 2% of the overall mass of the body, the human brain consumes almost 20% of the total energy used while at rest. Furthermore, glucose is the only fuel that can be used by neurons, which make up the majority of brain cells.

The fructose survival pathway alters the metabolism of the brain at the regional level while reducing energy expenditure to conserve glucose for the brain.

In particular, the scientists believe that activating the fructose survival pathway causes the brain’s food-seeking areas to become active. An increase in impulsive and exploratory actions that enable the animal to quickly investigate risky locations promotes this foraging response.

Meanwhile, the foraging response is linked to the inhibition of brain regions, such as those involved in logic, memory, and impulse control, that may decrease foraging activity.

In other words, the aforementioned brain areas involved in cognitive function experience a drop in energy metabolism when the foraging response is activated.

Evidence supporting the role of fructose

The rise in fructose levels in the brain, according to the researchers’ theory, may play a role in the onset of Alzheimer’s disease.

Nevertheless, given that individual fruits only contain a modest amount of fructose and that only 1% to 2% of ingested fructose reaches the brain, this rise is most certainly not attributable to fruit consumption as a whole.

However, it appears that ingestion of foods high in glucose, glycemic index, and salt may be more relevant in raising fructose levels in the brain.

The levels of fructose in the brain could therefore be increased by a diet heavy in salt and carbohydrates. Moreover, the uric acid that is created when fructose breaks down in the periphery can encourage the creation of fructose in the brain.

According to studies, consuming more high-fructose corn syrup or table sugar, foods with a high glycemic index, and salty foods is linked to a higher risk of Alzheimer’s disease.

In line with this, metabolic diseases linked to increased consumption of certain foods, such as obesity, insulin resistance, and diabetes, are also risk factors for Alzheimer’s disease.

The fructose metabolism

According to Dr. Johnson, treating fructose metabolism may be essential for the management or prevention of Alzheimer’s.

The majority of the evidence, he continued, “suggests three characteristic findings in early Alzheimer’s that seem to precede the end-stage presentation: these are the presence of insulin resistance associated with reduced glucose uptake in the brain, the fact that there is mitochondrial dysfunction in the brain, and that there is local inflammation, or “neuroinflammation,” in the brain.

Others are still attempting to cure this condition by administering intranasal insulin or by reducing inflammation. Yet once more, this only addresses the symptoms and not the root problem, according to Dr. Johnson.

Moreover, the metabolism of fructose raises the amounts of uric acid in the brain, which on its own can cause inflammation and memory problems. For instance, memory impairments and hippocampal inflammation are seen in hyperuricemic rats that produce too much uric acid.



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