-_-Moltres-_- Posted April 8, 2021 Posted April 8, 2021 A recent study out of BYU has linked lifestyle choice to Alzheimer’s disease, at least to some degree, through findings that show a possible energy gap between the amount of glucose and ketones being used to power the brain. BYU professor Ben Bikman, who studies diabetes and insulin resistance, thought of a fundamental question surrounding Alzheimer’s disease and insulin resistance in the brain. Bikman said there has been growing evidence that the brains in humans with Alzheimer’s disease are deficient in the use of glucose. “The brain has a certain energy demand, let’s say that is 100%,” Bikman said. “In most instances, glucose is providing virtually all of that energy, nearly 100% all of the time. There is a secondary fuel known as ketones, so the average brain is consuming almost all of its energy from glucose with a little bit of energy coming from ketones at any moment. In some individuals, the brain starts to become deficient in its ability to use glucose. So now glucose can only provide about 60% of that energy, and then ketones would be expected to fill up the rest of that energy. The tragedy is that the average individual has almost undetectable levels of ketones and that’s entirely a matter of lifestyle.” This lack of ketones as well as the brain’s resistance to insulin is linked to lifestyle. Insulin is expected to stimulate tissues or cells to take in the glucose and use it for energy. As the brain becomes more insulin resistant, it can’t take in glucose anymore and this is something Bikman said has been shown in other research. The BYU research expanded on some of those findings. “We found that indeed the expression of genes involved in glucose metabolism was significantly down, very broad across every cell type we looked at in the brain,” Bikman said. “All of the cell types we looked at had significant reductions in glucose-related genes, but the ketone-related genes were almost totally normal.” This is key because it shows that if the brain can receive more ketones, there is a possibility that one could overcome that energy gap. While it may not be able to be filled in with glucose, it can be with ketones but ketones need to be produced by one’s body. With many people having diets that are high in refined sugars and starches, insulin is elevated all of the time, and ketones are only produced when insulin levels are low. These conditions include fasting or low-carb diets, also known as keto diets. Ph.D. student Erin Saito is another one of the lead authors of the study and is doing this project as her dissertation. Another collaborator included Washington University of Saint Louis, which gave the BYU research team access to various brain banks. “BYU is a wonderfully collaborative environment, not only encouraging collaborations within the university but also outside of the university,” Bikman said. “Thus communicating with our internal and external collaborators was very easy and very natural. There was very much a common interest to work on this project together, a common enthusiasm for answering a question that had not been asked yet. It would not have been possible without that mutual collaboration and enthusiasm.” He added that managing the project with enthusiastic students was a delight, making it easy because of the enthusiasm surrounding the project. Bikman said it is gratifying for him to be able to contribute to what little is known about Alzheimer’s disease, because traditional strategies and approaches have continued to fail. “Looking at Alzheimer’s disease as a metabolic problem, I would say, is the greatest breakthrough in our understanding of the disease in decades,” Bikman said. Looking at it through the metabolic side of things allows people to possibly detect the problem years in advance, looking at changes in brain glucose metabolism long before Alzheimer’s sets in. Bikman believes that someday the metabolic approach to Alzheimer’s will be the standard of care. Moving forward, Bikman said he hopes that people feel empowered when it comes to Alzheimer’s disease. He wants people to not look at it as a passive process where they are the victim, but rather acknowledging that their lifestyle choices can either act as the culprit or the cure. “For too long we have viewed Alzheimer’s disease as a disease that is no respecter of person, no respecter of choices and that is simply not true,” Bikman said. “We have long known that people with metabolic disorders, like type 2 diabetes and insulin resistance, are at significantly greater risk of developing Alzheimer’s disease and we have more evidence suggesting that dietary choices and changes do make significant improvements in someone’s cognition.” Even someone in the midst of Alzheimer’s disease can see improvements in memory and learning with a lifestyle change, according to Bikman, and he added that he hopes this evidence will help to strengthen that view and empower individuals to take matters into their own hands.
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