The number of people with Alzheimer’s disease and other types of dementia is expected to triple by 2050. Researchers at the University of California, Davis, found that following a ketogenic (keto) diet may significantly decrease blood levels of tau protein in a rat model of Alzheimer’s disease. The keto diet also helped decrease blood lipid levels in the animal model. A new study in female rat models found that following the keto diet may significantly decrease blood levels of tau protein, which has been found to accumulate in the brains of people with Alzheimer’s disease. The study also found that animals in the Alzheimer’s disease model following the keto diet also experienced a decrease in their blood lipid levels.
Researchers are continuing to find new ways of preventing and treating Alzheimer’s disease. In this study, scientists focused on finding ways to improve cognitive behavior, motor function, and blood lipids, which can all play a role in Alzheimer’s disease development. Cognitive deficits are a hallmark of Alzheimer’s disease, and decreases in motor function occur as the disease progresses. Elevated levels of blood fatty acids and cholesterol are associated with the development of Alzheimer’s disease pathology. With the population of elderly people in the United States expanding, there is a need to identify viable strategies that can improve cognitive behavior, motor function, and blood lipids to increase the length of healthy life in humans.
Past studies have linked high levels of cholesterol to an increased risk of Alzheimer’s disease. The keto diet has been shown to potentially improve memory in mouse models of the disease. Researchers at the University of California, Davis, focused on examining which type of keto diet — continuous or intermittent — may have an impact. The TgF344-AD rat model of Alzheimer’s disease was used for this study. Rats on both types of keto diet did not show improved spatial learning memory or motor coordination compared to the control group. However, rats on the keto diet experienced decreased cholesterol levels and decreased blood levels of tau protein. Further research is needed to determine if the keto diet significantly alters markers of pathology and cellular processes that contribute to disease progression.
Monique Richard, a registered dietitian nutritionist, emphasized that while the keto diet can be effective for certain medical conditions when closely monitored, it is not suitable for everyone. For most individuals, the keto diet is difficult to follow, not sustainable long-term, and could have negative consequences. Individuals may experience negative effects on their lipid profiles, liver enzymes, digestive health, cognition, and satisfaction with eating after following the keto diet for an extended period of time. Proper nutrition and a standard lipid profile do not fully support brain health, and it would be important to consider the long-term effects of the keto diet on other aspects of health, like colon cancer or digestive impairment. Further research is needed to determine if the diet produces sufficient changes to warrant long-term diet studies in humans.
In conclusion, the keto diet showed promising results in reducing blood levels of tau protein and decreasing blood lipid levels in rat models of Alzheimer’s disease. While the diet may have potential benefits for slowing or mitigating some aspects of disease onset or progression, it is important to fully understand the implications of following a keto diet for an extended period of time. Proper monitoring and consideration of individual health needs are necessary when incorporating the keto diet into a lifestyle for potential Alzheimer’s disease prevention or treatment. Future studies may continue to explore the effects of the keto diet on cognitive behavior, motor function, and blood lipids in both animal models and human subjects.
