Scientific Name(s): 2-(3,4-Dihydroxyphenyl)-3,5,7-trihydroxy-4H-1-benzopyran-4-one, 3, 3′, 4′, 5, 7-pentahydroxy-2-phenylchromen-4-one, 3,3′,4′,5,7-pentahydroxyflavone
Common Name(s): Pentahydroxyflavone, Quercetin, Quercetine, Vitamin P
Medically reviewed by Drugs.com. Last updated on Jun 9, 2021.
Interest in quercetin as an antioxidant is ongoing. Chemoprotective and antihypertensive effects show promise, but clinical studies are limited. Preliminary data indicate potential benefit for improving adaptive and social functioning in children with autism.
Although specific evidence to support dosing recommendations is limited, most clinical studies use quercetin 500 to 1,000 mg per day in divided doses.
Contraindications have not been identified. Avoid coadministration with the cardiac glycoside digoxin.
Generally recognized as safe (GRAS) when consumed as food. Avoid dosages above those found in foods because information regarding safety and efficacy in pregnancy and lactation is lacking for such doses. Fetal growth retardation was observed in a study in rats exposed to quercetin by oral gavage.
A case report of a clinically relevant warfarin interaction resulting in supratherapeutic international normalized ratio (INR) values has been documented.
No clinically important adverse effects were reported in clinical studies.
Oral supplemental doses of up to 1,000 mg per day for as long as 12 weeks showed no evidence of toxicity. However, data on long-term safety at high doses are lacking, and concerns regarding carcinogenicity remain unresolved. Nephrotoxicity has been reported with high doses of intravenous (IV) quercetin.
The flavonol quercetin is found as glycosides in many vegetables and fruits, as well as in seeds, nuts, flowers, bark, and leaves. Rich sources of quercetin include apples, asparagus, berries, Brassica vegetables (eg, broccoli), capers, grapes, onions, shallots, tea, and tomatoes. Quercetin is also found in large amounts in ginkgo, St. John’s wort, and elder. The outermost layers of onions and dried, not fresh, shallots are rich in quercetin.1, 2, 3, 4, 5 See also Onion monograph.
Initially, quercetin was considered to be a vitamin and given the name "vitamin P." It was identified in the 1930s, but was slow to gain recognition because it did not seem to be an essential micronutrient. As epidemiological studies in the 1990s pointed to the benefits of flavonoids in cardiovascular health, more researchers started investigating quercetin in depth.6
Quercetin (3, 3′, 4′, 5, 7-pentahydroxy-2-phenylchromen-4-one) is a flavonol, sharing the common hydroxylated 3-ringed structure with attached hydroxyl groups of other flavonoids.2 Quercetin is bright yellow and soluble in alcohol and lipids, but poorly soluble in hot water and insoluble in water. The aglycone form is more lipophilic than quercetin glycosides such as rutinoside from tea, and is absorbed more readily than glycoside forms, which must be hydrolyzed to release quercetin. Analytical techniques for the identification of quercetin have been described.1, 5, 7, 8, 9
Uses and Pharmacology
Patients with sarcoidosis showed increased plasma antioxidant capacity and reduced markers of oxidative stress and inflammation with quercetin supplementation.7, 13 However, in a clinical study of quercetin's effect on hypertension, none was found on markers of oxidative stress,14 and no antioxidant effects were observed in healthy volunteers despite increased plasma quercetin levels.7
Data from a small, prospective, open-label trial (n = 40; 87.5% boys) in children with autism spectrum disorder showed significant improvement in adaptive functioning and overall behavior after 26-week administration of a supplement containing luteolin from chamomile (100 mg), quercetin (70 mg), and the quercetin glycoside rutin (30 mg); 1 capsule per 10 kg of weight was given daily with food. Changes in raw and age-equivalent scores were significant for all domains except communication raw scores and were greater than those expected by maturation per se. No major adverse effects were documented; however, 6 children from the original 50 enrolled withdrew due to increased irritability caused by the formulation.50
In vitro and animal studies have attempted to elucidate possible mechanisms of action for quercetin in cancer. Aside from its potent scavenging of reactive oxygen and nitrogen species and metal chelation, such mechanisms include antiproliferative, growth-suppressing, and antiangiogenesis activity; inhibition of telomerase and induction of senescence and cell death; and activation of immune and autophagic activity. Studies in rodents have included cancers of the colon, small intestine, tongue, skin, lung, and mammary gland. Other in vivo studies have used melanoma and prostate cancer cells. Quercetin also demonstrates estrogenic activity and may exert a direct effect on androgen receptors in prostate cancer cells.1, 8, 15, 16, 17, 18, 19, 20, 21
Clinical trials are lacking to support findings from epidemiological and animal studies. Phase 1 (safety) clinical studies have shown positive results; however, the number of participants was too small to draw conclusions. Other studies have used mixed preparations of quercetin with curcumin or are of limited robustness.1, 22
Animal models and studies using isolated cardiovascular tissues suggest a role for quercetin in cardiovascular disease.1, 15 However, not all effects observed in animal studies have translated to similar effects in humans.23, 24 Antioxidant effects, including reduced low-density lipoprotein oxidation, decreased experimental reperfusion injury, improved endothelial function, decreased inflammation, and anti-aggregating and antihypertensive effects of quercetin have been demonstrated mostly in rodents.1, 15, 24 Improved cholesterol profiles and decreased insulin resistance have also been demonstrated,6, 15 while a role for quercetin metabolites has also been suggested.25
Epidemiological studies on the role of flavonoids in decreasing risk factors of cardiovascular morbidity support a place for quercetin.1, 15 Studies in healthy volunteers and among patients with prehypertension (systolic blood pressure [BP] 120 to 139 mm Hg and diastolic BP 80 to 89 mm Hg) have found no effect of quercetin supplementation on blood pressure.14, 26 In 23 patients with stage 1 hypertension (systolic BP 140 to 159 mm Hg, diastolic BP 90 to 99 mm Hg), quercetin 730 mg per day over 28 days reduced systolic pressure by 7 mm Hg (±2) and diastolic pressure by 5 mm Hg (±2). Mean arterial pressure was also reduced. Measures of oxidative stress, however, were not affected.14 In a trial of overweight patients, systolic BP was reduced by 2.6 mm Hg (P < 0.01) in all participants and by 3.7 mm Hg (P < 0.01) in participants with hypertension who consumed quercetin 150 mg per day over 6 weeks.27 Another clinical trial suggested that the efficacy of quercetin is dependent on the apolipoprotein (Apo) genotype, with subjects presenting with subtype ApoE 3 demonstrating decreased systolic pressure, while those with subtype ApoE 4 did not.28 Inhibition of platelet aggregation and postulated reductions in the risk of thrombosis have been shown in healthy volunteers given quercetin alone and as onion soup.29, 30 Limited studies evaluating quercetin’s effect on lipids have produced equivocal results.28, 31
Endothelial dysfunction and inflammation biomarkers were evaluated after 35 prehypertensive adults ingested pure epicatechin 100 mg/day and quercetin-3-glucoside 160 mg/day for 4 weeks in a placebo-controlled, double-blind, crossover study. Of the 5 endothelial dysfunction biomarkers measured, soluble endothelial selectin was significantly reduced (P = 0.03) by epicatechin and quercetin supplementation. No other biomarkers were significantly affected by epicatechin; however, pure quercetin supplementation also reduced inflammatory markers (ie, interleukin [IL]-1-beta [P = 0.009], z score for inflammation [P = 0.02]). As a reference, it’s important to note that 4 cups of black tea contain about 19 mg of quercetin.53
The effects of quercetin supplementation on C-reactive protein (CRP) (a strong predictor of cardiovascular disease) were assessed in a systematic review and subsequent meta-analysis of 7 double-blind, randomized, placebo-controlled trials (N=549), including 4 crossovers. The studies had sample sizes of 40 to 93 adult participants (1 study enrolled only males, 2 studies enrolled only females) and administered quercetin at dosages of 150 to 500 mg/day for 6 to 10 weeks. Baseline CRP levels ranged from 1.28 to 5.7 mg/L (mean, 3.44 mg/L) in patients with body mass indices of 21.4 to 31.1 kg/m2 and who presented with a variety of conditions (eg, metabolic syndrome, pre-hypertension, mild hypertension, rheumatoid arthritis, type 2 diabetes, various apolipoprotein genotypes). Overall, data showed a statistically significant reduction in CRP (weight mean difference, −0.33 mg/L; P<0.001) in favor of quercetin. The effect size was robust; however, study heterogeneity was significant. Subgroup analysis revealed baseline CRP <3 mg/L, quercetin dose ≥500 mg, duration of treatment ≥8 weeks, mean age of participants ≤45 years, and a parallel study design to be variables that led to significant beneficial results of quercetin on CRP (P<0.001 to P=0.002).54
Studies in mice have shown efficacy of quercetin supplementation in enhancing physical activity; however, the relevance of data from animal studies is diminished by the availability of clinical trial data and a published meta-analysis.32, 33
A meta-analysis, which included 11 clinical trials conducted through July 2010, found that quercetin supplementation marginally improved physical endurance capacity by approximately 3%. Median treatment duration was 11 days, using a median dose of quercetin 1,000 mg per day.32 Improvement in endurance performance was additionally documented in a meta-analysis of 7 trials identified between 1966 and March, 2011. A significant improvement of 0.74% (P = 0.02) in endurance performance was noted; however, this result was influenced mostly by the positive effect attained in untrained subjects (0.83%) versus trained participants (0.09%). VO2max was also significantly increased (P = 0.02). No heterogeneity was noted among studies.51
Equivocal data have been published on the anti-inflammatory effects of quercetin13, 34, 35, 53 Reduced markers of inflammation with quercetin supplementation have been demonstrated in sarcoidosis patients and those with prehypertension.13, 53 However, no effect on immune measures or inflammation was found in healthy community-dwelling, adult women taking supplemental quercetin 1,000 mg per day over 12 weeks.34 In a similar study by the same researchers, no effect was found for all participants, although a reduction in sick days for respiratory illness was found in middle-aged and elderly subgroups.35 Antimicrobial effects against HIV and Helicobacter pylori have also been described.1
Studies suggestive of a neuroprotective role have been conducted in human and animal nervous system tissues and in vitro in animals.36 Clinical studies are lacking, except for a preliminary report on the role of quercetin in peripheral neuropathy due to diabetes, which found improvements in symptoms.37
Typical dietary quercetin intake based on fruit and vegetable consumption is estimated to be from 5 to 100 mg per day. Heavy consumption of foods rich in quercetin, such as apples or onions, could lead to daily intakes of up to 500 mg.1, 5, 7, 15 The effective dose is increased when eaten with a fatty meal or in the presence of apple pectin, oligosaccharides, and lecithin.3, 5
As a dietary supplement, 2 weeks of quercetin 50 mg achieved a 178% increase in serum levels, while quercetin 100 mg increased the levels by 359%, and quercetin 500 mg increased serum levels by 570%, although with wide individual variation.38 Based on animal studies, quercetin accumulates in the lungs, liver, kidneys, and small intestine, with lower levels seen in the brain, heart, and spleen. It is eliminated via the renal, fecal, and respiratory systems.7, 9, 15, 39
Pregnancy / Lactation
GRAS when consumed as food. Avoid dosages above those found in foods because information regarding safety and efficacy in pregnancy and lactation is lacking for such doses. Fetal growth retardation was observed in a study in rats exposed to quercetin by oral gavage. No signs of embryonic viability or morphology were apparent.40
Case reports are lacking.
Studies investigating the effects of quercetin on the cytochrome P450 (CYP-450) system have established that the potential for interactions exists; however, conflicting results between in vitro and in vivo studies have been found.41 Quercetin inhibits the P-glycoprotein transport system, as well as CYP3A4 and CYP1A2, while it enhances CYP2A6, N-acetyltransferase, and xanthine oxidase activity.41, 42
Studies in pigs have shown decreased bioavailability of cyclosporine and increased bioavailability of digoxin, doxorubicin, etoposide, fexofenadine, irinotecan, paclitaxel, pioglitazone, tamoxifen, and verapamil.41, 42, 43, 44 The interaction with digoxin in pigs was fatal.45
No effect on saquinavir, rosiglitazone, or resveratrol was found in studies in healthy volunteers.44, 46, 47 Rutin has been shown to decrease the anticoagulant effect of warfarin, and limited studies suggest quercetin similarly exhibits antiplatelet aggregation activity.1, 29, 30, 41 Synergism with moclobemide and levodopa/carbidopa has been postulated.48, 49
A supratherapeutic INR was reported in a case study of a 73-year-old female on warfarin who ate large quantities of scuppernongs, a quercetin-containing muscadine grape. She had a medical history of systolic and diastolic heart failure, pulmonary and cutaneous sarcoidosis, chronic low back pain and osteoarthritis. During the fruiting season, she consumed up to 75 scuppernongs a day with corresponding INRs as high as 8.2. Therapeutic INRs were achieved with concomitant reductions in both her warfarin dose and consumption of scuppernongs.52
At oral supplemental doses of up to 1,000 mg/day, taken for up to 12 weeks, no evidence of toxicity or clinically important adverse effects have been found; however, data on long-term safety at high doses are lacking.5, 7 Clinical studies report no clinically important adverse effects.14, 27
Quercetin shows in vitro mutagenicity in the Ames test, and reports of mutagenicity in the 1970s led to concerns about its safety.5, 7 Under certain circumstances, quercetin exhibits both radical scavenging and pro-oxidant activity.1, 5 In 1999, however, the International Agency for Research on Cancer classified quercetin as "not classifiable as to its carcinogenicity" to humans.5, 40 Most in vivo studies have shown that quercetin is not carcinogenic and may be protective against genotoxicants.1
Dietary quercetin undergoes first-pass metabolism in the gut and liver and is almost completely metabolized, reducing the potential for toxicity. At oral supplemental doses of up to 1,000 mg per day taken for up to 12 weeks, no evidence of toxicity has been found; however, data on long-term safety at high doses are lacking.5, 7 Nephrotoxicity was reported with the use of high-dose IV quercetin in a patient with compromised health.5, 15
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