A study from the University of Colorado has found a fascinating link between the evolutionary survival response of early humans to forage for food and the development of Alzheimer’s disease.
Researchers have suggested that Alzheimer’s is a harmful adaptation of an evolutionary survival pathway used by animals and humans during times of scarcity.
Foraging is a survival response that sends humans looking for food, but it requires focus, rapid assessment, impulsivity, exploratory behavior, and risk-taking.
Researchers have found that fructose, a kind of sugar, helps to dampen down these centers in the brain, allowing more focus on food gathering.
The study has discovered that the entire foraging response was set in motion by the metabolism of fructose, whether it was eaten or produced in the body.
The metabolism of fructose and its byproduct, intracellular uric acid, was critical to the survival of both humans and animals.
However, the 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 Alzheimer’s disease.
The researchers believe that the survival response, known as the “survival switch,” 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 foods, prompting excess fructose production, which can lead to inflammation and ultimately Alzheimer’s disease.
The study has also shown that animals that were given fructose showed memory lapses, a loss in the ability to navigate a maze, and inflammation of the neurons.
These findings suggest that there is a link between our ancient foraging instincts and the development of Alzheimer’s disease, which could pave the way for new treatments for the disease.
While more research is needed to confirm these findings, this study offers a new way of looking at Alzheimer’s disease, which is characterized by abnormal accumulations of proteins in the brain that slowly erodes memory and cognition.
By understanding the evolutionary basis for the development of the disease, researchers may be able to find new treatments to slow or prevent its progression.
How to prevent Alzheimer’s disease
While there is no known cure for Alzheimer’s disease, there are steps individuals can take to reduce their risk of developing the disease or to slow its progression:
Stay physically active: Regular exercise, especially aerobic exercise, can help improve brain function and reduce the risk of Alzheimer’s.
Eat a healthy diet: A healthy diet, such as the Mediterranean diet, which is rich in fruits, vegetables, whole grains, fish, and healthy fats, has been linked to a reduced risk of Alzheimer’s.
Stay mentally active: Engage in mentally stimulating activities, such as reading, doing crossword puzzles, or learning a new skill, to keep your brain active and healthy.
Socialize: Staying socially active can also help keep your brain healthy, as social interactions help keep the mind active and engaged.
Get enough sleep: Sleep is essential for good brain function and can help reduce the risk of Alzheimer’s. Aim for 7-8 hours of sleep each night.
Manage chronic conditions: Certain chronic conditions, such as diabetes, high blood pressure, and obesity, have been linked to an increased risk of Alzheimer’s. Managing these conditions can help reduce the risk.
Reduce stress: Chronic stress can have a negative impact on brain function and has been linked to an increased risk of Alzheimer’s. Find ways to manage stress, such as meditation, exercise, or therapy.
If you care about brain health, please read studies about vitamin D deficiency linked to Alzheimer’s and vascular dementia, and blood pressure problem at night may increase Alzheimer’s risk.
For more information about brain health, please see recent studies about antioxidants that could help reduce dementia risk, and epilepsy drug may help treat Alzheimer’s disease.
The study was conducted by Richard Johnson et al and published in The American Journal of Clinical Nutrition.
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