In a recent study using a mouse model, researchers found that a ketogenic (keto) diet delayed the onset of Alzheimer’s disease (AD).
This delay in Alzheimer’s disease onset was attributed to a significant increase in the levels of the beta-hydroxybutyrate (BHB) molecule in the mice, which was observed to be sevenfold higher.
The BHB molecule has been linked to delaying the onset of mild cognitive dementia associated with the early stages of Alzheimer’s. This molecule is naturally present in humans and is produced when the body metabolizes fat for energy to fuel the mitochondria. It facilitates the transfer of energy from the liver to the rest of the body when glucose levels are insufficient.
Researchers from the University of California, Davis (UC Davis), who conducted the study, had previously published findings suggesting that BHB, depending on dosage, exhibits anti-inflammatory properties on brain cells inflamed by beta-amyloid plaques, which were once believed to be the primary cause of Alzheimer’s.
However, subsequent research discredited the notion that these plaques were the sole cause of Alzheimer’s, as some individuals with these plaques never develop the disease.
The study involved genetically modified APP/PS1 mice expressing both a mouse/human amyloid precursor protein and a mutant human presenilin 1 gene, targeting neurons in the central nervous system.
These mice, bred at UC Davis, were raised in a controlled environment with a standard mouse chow diet for six months before being assigned to weight-balanced groups and placed in individual enclosures to monitor food consumption.
The mice were then fed either a ketogenic diet or a carbohydrate-rich standard diet, with both diets providing the same number of calories. The researchers noted that female mice had higher levels of BHB in their bodies compared to males, along with increased brain enzymes associated with memory support.
Additionally, male mice switched to a ketogenic diet in late midlife showed improvements in spatial memory.
The Impact of Keto Diets on Neuroinflammation
A ketogenic diet, characterized by high fat and low carbohydrate intake, induces a metabolic state known as ketosis. In ketosis, the body primarily utilizes fat for energy production, resulting in the generation of ketone bodies as an alternative fuel source.
One concern associated with the increased consumption of fats in a ketogenic diet is the potential promotion of neuroinflammation, which can have detrimental effects on cognitive health. However, it’s worth noting that specific types of fats may actually help reduce neuroinflammation.
In the study, the lead author noted that when the same number of calories is provided by a ketogenic diet compared to a control diet, there is a significant reduction in systemic inflammatory cytokines.
Certain fats contain neuroprotective properties, such as omega-3 fatty acids, fat-soluble carotenoids, and vitamins, which can mitigate inflammation and oxidative stress in the brain.
However, it’s essential to strike a balance, as excessive consumption of saturated fats may potentially lead to elevated cholesterol levels and increase the risk of cardiovascular issues.
Therefore, while incorporating some fats into the diet can help alleviate inflammation and neuroinflammation, moderation and choosing the right types of fats are key to maintaining overall health.
Ways to Increase BHB Levels
After approximately 12 hours of fasting, human bodies experience a rise in beta-hydroxybutyrate (BHB) levels due to the depletion of carbohydrate stores. This phenomenon occurs because the body switches to utilizing fat stores for energy.
Individuals following a ketogenic (keto) diet typically exhibit significantly higher BHB levels compared to those on a standard carbohydrate-rich diet.
There are three primary methods to increase human BHB levels:
- Intermittent Fasting: Following a one-meal-a-day carbohydrate diet can also elevate BHB levels, albeit less effectively. However, BHB levels may rise slowly after the liver’s glycogen stores are depleted during fasting periods. It’s important to note that BHB levels may drop significantly when consuming a carbohydrate-rich meal after fasting.
- Keto Diet: Adopting a ketogenic diet, which involves consuming high levels of fats and minimal carbohydrates, leads to a notable increase in BHB levels.
- BHB Supplements: Another option is to take BHB supplements, which can directly elevate BHB levels in the bloodstream.
Before making any significant changes to your diet, it’s advisable to consult with a physician to ensure it aligns with your overall health and wellness goals.
Mice vs. Human Studies for Alzheimer’s Disease
It’s crucial to understand that the recent study discussed here was conducted using mice and cannot definitively prove the effects of a ketogenic diet on Alzheimer’s progression in humans.
This research was based on a mouse model of Alzheimer’s disease, which, while sharing some similarities with the human condition, does not perfectly replicate the disease as it occurs in humans.
Animal models are valuable tools for studying the basic biology of diseases, but findings from such studies must be further validated through human research involving representative populations.
While the findings of this study are intriguing, more extensive research is necessary to fully comprehend the potential impacts and outcomes of a ketogenic diet on individuals with Alzheimer’s disease or those at risk of developing it.
It’s important to emphasize that no one should adopt a ketogenic diet solely for the purpose of preventing or treating Alzheimer’s or other cognitive impairments without consulting with a healthcare professional first.
In 2025, the Alzheimer’s Association is expected to release the findings of the U.S. Study to Protect Brain Health Through Lifestyle Intervention to Reduce Risk (U.S. POINTER).
This two-year clinical trial involves a large, diverse group of Americans and aims to investigate whether lifestyle interventions targeting multiple risk factors, including diet, can safeguard cognitive function in older adults at heightened risk of cognitive decline.