Can flavonols prevent Alzheimer’s disease?

Flavonols are a class of flavonoids^?, which are compounds found naturally in many fruits, vegetables, tea, and wine, and have antioxidant^? and anti-inflammatory properties. A recent observational study reported that people with high intakes of flavonols had a significantly lower rate of developing Alzheimer’s disease compared to people with low intakes [1].

Findings come from a study of 921 elderly participants (average age of 81.2 years old) who were free of dementia at the time of enrollment. Every year, participants received clinical neurologic examinations while also being interviewed on the frequency and amounts of different food items and beverages they consumed. Participants were followed for up to 12 years (average of 6.1 years), during which 220 participants developed Alzheimer’s disease.

Researchers found that participants who were in the top 20% in total flavonol intake had a 48% lower rate of developing Alzheimer’s disease compared to those in the bottom 20%, after controlling for major lifestyle and other factors associated with dementia, such as age, education, genetic risk factor (ApoE), cognitive activity (e.g., reading, playing games, and writing letters), and physical activity (e.g., walking, biking, yard work). Interestingly, the association between higher flavonol intake and reduced Alzheimer’s risk was stronger in men compared to women, such that men who were in the top 20% in total flavonol intake had a 76% lower rate of developing Alzheimer’s compared to men in the bottom 20%. The reasons for this sex difference are unknown.

Researchers further evaluated the different subclasses of flavonols, called kaempferol, myricetin, isorhamnetin, and quercetin.

• Kaempferol is abundant in kale, beans, tea, spinach, broccoli, capers, ginger, and dried goji berries [2]. Participants who were in the top 20% in kaempferol intake had a 50% lower rate of developing Alzheimer’s disease compared to those in the bottom 20%.
• Myricetin is rich in tea, wine, kale, oranges, nuts, berries, and tomatoes [2]. Participants who were in the top 20% in myricetin intake had a 38% lower rate of developing Alzheimer’s disease compared to those in the bottom 20%.
• Isorhamnetin is abundant in pears, olive oil, wine, and tomato sauce. Participants who were in the top 20% in isorhamnetin intake had a 38% lower rate of developing Alzheimer’s disease compared to those in the bottom 20%.
• Quercetin is rich in tomatoes, capers, red onions, kale, berries, apples, and tea [2]. Dietary intake of quercetin was not associated with a lower rate of developing Alzheimer’s disease.

Because this study was an observational study and not a randomized clinical trial, it was not designed to prove that flavonols, or specific subclasses of flavonols like kaempferol, prevent Alzheimer’s disease. People who eat a diet rich in flavonols may be more likely to practice other healthy habits that are good for the brain. However, it is worth emphasizing that the associations between high flavonol intake and reduced Alzheimer’s disease risk remained significant even after controlling for some of these brain-healthy habits, such as cognitive and physical exercise.

Findings from this current study is consistent with previous ones reporting that greater flavonoid intake is associated with higher cognitive scores and slower cognitive decline [3; 4]. Thus, a diet rich in fruits, dark-colored vegetables, and legumes appears to be beneficial for brain health and dementia prevention.

1. Holland TM, Agarwal P, Wang Y et al. (2020) Dietary flavonols and risk of Alzheimer dementia. Neurology.
2. Bhagwat S, Haytowitz DB, Holden JM (2011) USDA Database for the Flavonoid Content of Selected Foods Release 3 US Department of Agriculture.
3. Devore EE, Kang JH, Breteler MM et al. (2012) Dietary intakes of berries and flavonoids in relation to cognitive decline. Annals of neurology  72, 135-143.
4. Letenneur L, Proust-Lima C, Le Gouge A et al. (2007) Flavonoid intake and cognitive decline over a 10-year period. American journal of epidemiology  165, 1364-1371.

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