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Quercetin and Hypertension by Dr Neil McKinney, ND (non-practicing)

Quercetin is the most abundant flavonol in the human diet and is also medically active in several diseases.  It is clinically valuable as an anti-histamine, notably in allergic rhinitis. Quercetin significantly impacts cancer stem cells and metabolism. It is known to modulate cardiovascular inflammation.

This systematic review and meta‐analysis of randomized controlled trials assessed the impact of quercetin on hypertension. A substantial reduction in both systolic and diastolic blood pressure was noted at doses of 500 mg or higher. Minor side effects such as headache, nausea, and tingling of the extremities were observed in long‐term quercetin supplementation at 1000 mg/day. In fact, it is commonly used now at 1,000 mg 3 times daily in acute allergy, with only the rarest of adverse effects.

Bioavailability of oral doses is severely limited by rapid glucuronidation, sulfation and methylation in the gut. Very little unconjugated quercetin reaches the plasma. Quercetin is particularly active in patients with apo E3 phenotype, who have altered β-glucoronidases. While reducing gut glucuronidation would enhance absorption, our experience with such agents, e.g. piperine from black pepper, is that they increase absorption of biotoxins from the gut that normally would be detoxified in the gut and liver by glucuronidation. The most useful tactic to safely improve quercetin bioavailability appears to be liposomal delivery. It is possible that liposomal doses of 50 – 70 mg twice daily may be clinically efficacious. 

Multiple mechanisms of action for its antihypertensive effect are described. Quercetin may be of particular benefit in diabetic hypertension. Quercetin has hypoglycemic and insulin‐sensitizing activities in diabetes, which can attenuate diabetes‐induced vasoconstriction. Inflammation increases β-glucuronidase activity, and inflammation is a comorbidity in diabetic cardiovascular disease. Quercetin blocks tumor necrosis factor‐α (TNFα)‐mediated inflammatory cascades. Quercetin prevents TNF‐α from directly activating nuclear factor‐κB (NF‐κB), a potent inducer of inflammatory gene expression and protein secretion. In addition, quercetin may indirectly prevent inflammation by increasing peroxisome proliferator‐activated receptor c (PPARγ) activity, thereby antagonizing NF‐κB or activator protein‐1(AP‐1) transcriptional activation of inflammatory genes.

This common nutrient, generally regarded as safe, may be a useful add-on to hypertensive protocols, particularly in those with inflammatory co-morbidities such as diabetes, obesity or rheumatoid disorders.


Serban, MC., et al., Effects of Quercetin on Blood Pressure: A Systematic Review and Meta‐Analysis of Randomized Controlled Trials, J. Amer. Heart Assoc. 2016; 5 (7): e002713.

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