Intermittent Fasting

Intermittent Fasting and Alzheimer's

Intermittent fasting has been recommended by Dr. Bredesen and others as a way to combat Alzheimer’s disease. In his book The End of Alzheimer’s, Dale Bredesen recommends a 12/3 ketoflex diet and the 12/3 refers to twelve hours of fasting between dinner and breakfast and three hours minimum between the end of dinner and bedtime. For Apoe4 carriers, Bredesen recommends 14 to 16 hours of fasting. Animal studies have shown that intermittent fasting reduces oxidative stress, promotes autophagy, reduces insulin resistance, increases the health of the gut microbiome, increases ketone bodies, reduces inflammation, improves cognition, and delays aging. But, let’s take a look at the human data to see if randomized clinical trials can back up the animal data on intermittent fasting.1,2,3

Intermittent Fasting and Alzheimer Studies

Intermittent fasting does a couple important things to help prevent Alzheimer’s. One way that intermittent fasting helps is by decreasing insulin resistance. A systematic review and meta-analysis conducted in 2019 using twelve different randomized trials showed that BMI decrease, fasting glucose levels decrease, insulin resistance decreased, and fat mass decreased. All of that add up to improved glycemic control and reduced insulin resistance.4

One small study of human subjects (asthma patients) showed a decrease in oxidative stress and inflammation after intermittent fasting. Another very small study of 11 human subjects found that the SIRT genes (responsible for longevity) were activated during intermittent fasting. SIRT activation promotes autophagy. We discussed SIRT genes and autophagy in the calorie restriction section, but to remind you autophagy is the term used to describe the degradation and recycling of cellular components within cells as well as removing protein aggregates like amyloid plaques. There is evidence suggesting that promoting autophagy could help prevent Alzheimer’s disease in the early stages of the disease, but may also expedite neuronal degeneration at later stages of the disease.3,5,6,7