Quercetin

What quercetin is

Quercetin belongs to the flavonols, a subgroup of the polyphenols. In plants it is almost always bound to sugar — as a glucoside in onions, as a rutinoside in tea and buckwheat — and this binding determines how much reaches the body. Supplements, by contrast, mostly contain the pure aglycone, up to 1,000 milligrams a day — far above the intake from a normal diet.

How it is supposed to work

The common story is that of a powerful antioxidant. It only partly holds up to measurement in humans: in Edwards’ study, blood pressure in people with hypertension fell markedly, while the markers of oxidative stress in plasma and urine remained unchanged — the pressure fell, but not via the route usually held responsible for it.

On top of this comes a conversion problem: Olthof showed that quercetin-3-rutinoside is largely broken down by the gut flora into phenolic acids in humans, and that these breakdown products have weaker antioxidant activity than the parent substance. For the anti-allergic part, the target structure is the mast cell, whose histamine release quercetin inhibits in cell culture — supported in humans through symptom scores, not through the mechanism.

Blood pressure — the best-supported field

Three meta-analyses point in the same direction. Serban found a reduction of 3.04 mmHg systolic and 2.63 mmHg diastolic across 7 randomized studies with 587 patients, Huang 3.09 and 2.86 mmHg across 17 studies with 896 participants, Popiolek-Kalisz and Fornal 2.38 mmHg systolic across 10 studies with 841 participants.

Two patterns recur. First, the dose: in Serban’s analysis, the effect from 500 milligrams daily was 4.45 mmHg systolic, below that 1.59 mmHg and no longer significant — although the authors note that the direct comparison of the dose groups showed no difference. Second, the baseline value: Edwards treated 19 people with prehypertension and 22 with stage 1 hypertension. In stage 1, systolic pressure fell by 7 mmHg over 28 days; in those with prehypertension nothing changed.

Sport — measurable, but small

Two independent meta-analyses reach the same conclusion. Kressler included 11 studies with 254 subjects and found an effect size of 0.15, around 2 percent compared with placebo. Pelletier and colleagues analyzed 7 papers with 288 subjects: endurance performance plus 0.74 percent, VO2max plus 1.94 percent, both significant. But in untrained people 0.83 percent remained, in trained people 0.09 percent with a spread of 2.15 percent — in other words, nothing.

Recovery is more interesting. Rojano-Ortega and colleagues analyzed 13 randomized studies with 249 participants, almost all using 1,000 milligrams daily over seven days to 12 weeks. Muscle soreness in the first 24 hours after exertion was markedly lower, as was creatine kinase after 24 to 48 hours, and oxidative stress too — but there was no influence on interleukin-6.

The absorption problem

Hollman made the decisive measurement as early as 1995, in 9 people with an ileostomy — a setup in which it can be measured what leaves the small intestine unused. From onions, 52 percent was absorbed, from pure aglycone 24 percent, from rutinoside only 17 percent. The variation is not random; it follows the chemical form.

In 2025, Liu summarized across 31 human studies what improves absorption: oligoglucosides reach around 20 times that of the aglycone, a lecithin phytosome 20.1 times; dietary fat and fiber roughly double it. Bromelain and piperine, common absorption aids in guidebooks, do not appear in it, and no human study on them could be found. The advice to take quercetin with a fat-containing meal, on the other hand, is supported.

The senolytic story

Senescent cells no longer divide, but they do not die either, and they release pro-inflammatory substances. In 2015, Zhu described the first class of substances that removes them in a targeted way. Even then it was clear why two substances are needed: dasatinib hit senescent fat cell precursors, quercetin senescent endothelial cells. Neither reached all cell types on its own — and that is precisely why quercetin has never been tested on its own in humans.

In all five human studies — diabetic kidney disease, pulmonary fibrosis twice, bone metabolism and early Alzheimer’s disease — it was given alongside dasatinib. They provide proof that senescent cells can be removed in humans, but not the share that quercetin has in this. The only phase 2 trial so far also missed its endpoint.

What the studies show

Serban 2016 — blood pressure across 7 studies

Meta-analysis of placebo-controlled randomized studies, search up to January 2015, 7 studies with 9 treatment arms and 587 patients. The primary endpoint was the mean blood pressure difference versus placebo; it was met, at 3.04 mmHg systolic and 2.63 mmHg diastolic.

Farr 2024 — the only phase 2, endpoint missed

Randomized controlled trial in 60 postmenopausal women over 20 weeks, intermittent administration of dasatinib plus quercetin. The primary endpoint was the percentage change in the bone resorption marker CTx after 20 weeks: minus 4.1 percent on active treatment versus minus 7.7 percent in the control group, so no difference. The bone formation marker P1NP rose by 16 percent each after 2 and after 4 weeks, and stood at minus 9 percent after 20 weeks. No serious events occurred.

Hickson 2019 — the tissue evidence

Open-label phase 1 pilot study without a control group in 9 people with diabetic kidney disease. Over three days they received dasatinib and quercetin; tissue and blood were examined beforehand and 11 days after the end of treatment. In fat and skin tissue, cells with the aging markers p16 and p21 decreased, in the blood interleukin-1-alpha, interleukin-6 and two matrix metalloproteinases. The most convincing evidence that senescent cells can be removed in humans — without any statement about the share of quercetin.

Where the data stop

The senolytic effect of quercetin alone has not been tested in humans, and the one study with a predefined hard endpoint missed it. In Alzheimer’s patients, quercetin was not detectable at all in the cerebrospinal fluid, while dasatinib was — so even the basic evidence for an effect in the brain is missing. On inflammatory markers, two meta-analyses contradict each other: Mohammadi-Sartang and colleagues found CRP lowered by 0.33 milligrams per liter, Ou and colleagues found no relevant overall effects for CRP, interleukin-6 and TNF-alpha.

On the immune system, there is no meta-analysis of quercetin alone. Somerville and colleagues analyzed flavonoids as a whole substance group and found 33 percent fewer respiratory infections, with only trivial differences in immune markers. The most recent controlled test was negative: four weeks of quercetin glycoside before an mRNA booster vaccination changed neither the antibody nor the T-cell response in 50 participants. For allergies things look better, but there too polyphenols are analyzed together — Lai and colleagues rate confidence in their own results as low to very low.

Status, approval and legal

In Germany, quercetin may be marketed as an ingredient of food supplements and is not an approved medicine. It may not be advertised with a health claim: neither quercetin nor flavonol appears in the consolidated Union list of authorised claims, Regulation (EU) No 432/2012. In 2011, EFSA assessed four claims — oxidative damage to DNA, proteins and lipids, the cardiovascular system, mental state and performance, as well as liver and kidneys. None is on the positive list today. There is no official maximum level. Dasatinib, the partner in all senolytic human studies, by contrast is a prescription-only cancer drug approved in the EU since November 20, 2006.

Safety

The authoritative assessment of the isolated substance comes from the German Federal Institute for Risk Assessment (BfR). In the numerous human studies, adverse effects were rarely reported and were then mild. For use over more than 12 weeks at doses from 1,000 milligrams daily, however, sufficient data are not available. From animal studies, the BfR derives two critical points: quercetin could amplify kidney-damaging effects in a previously damaged kidney and promote tumor development in estrogen-dependent cancers. In addition, there are interactions with medicines whose bioavailability can change. For people with kidney disease, with a history of an estrogen-dependent tumor or on narrowly dosed long-term medication, this is not something for them. The International Society of Sports Nutrition also points out that antioxidants in very high doses can hinder training adaptations.

Sources

• Serban et al., J Am Heart Assoc 2016 (blood pressure meta-analysis)
• Huang et al., Nutrition Reviews 2020 (blood pressure, lipids, glucose)
• Popiolek-Kalisz & Fornal, Curr Probl Cardiol 2022 (blood pressure meta-analysis)
• Kressler et al., Med Sci Sports Exerc 2011 (endurance meta-analysis)
• Pelletier et al., Int J Sport Nutr Exerc Metab 2013 (performance and VO2max)
• Rojano-Ortega et al., Biology of Sport 2023 (recovery after exercise)
• Hollman et al., Am J Clin Nutr 1995 (absorption in humans)
• Liu et al., Food Chemistry 2025 (bioavailability, 31 human studies)
• Farr et al., Nature Medicine 2024 (phase 2 trial on bone metabolism)
• Andres et al., Mol Nutr Food Res 2018, German Federal Institute for Risk Assessment (safety)