Myricetin: Food Sources, Flavonols & What Research Shows

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What Is Myricetin?

Myricetin is a naturally occurring flavonol flavonoid.

Its chemical name is 3,3′,4′,5,5′,7-hexahydroxyflavone.

It shares the basic flavonol structure found in compounds such as:

• quercetin;
• kaempferol;
• isorhamnetin; and
• other related dietary flavonols.

Myricetin contains three hydroxyl groups on its B-ring, whereas quercetin contains two and kaempferol contains one.

These structural differences influence chemical reactivity and help explain why the compounds can behave differently in laboratory antioxidant and enzyme experiments.

However, structural activity in a chemical system does not establish that the same response occurs after a person consumes myricetin as part of food.

Is Myricetin a Flavonoid or a Flavonol?

Both terms are correct at different levels of classification.

Flavonoids are the larger family of plant compounds.

Flavonols are one subclass within the flavonoid family.

Myricetin is therefore a flavonol flavonoid.

Other flavonoid subclasses include anthocyanins, flavan-3-ols, flavanones, flavones, and isoflavones.

Learn more in our Flavonols and Flavonoids guides.

What Are Myricetin Glycosides?

Myricetin does not always occur in plants as the free aglycone.

Plants commonly attach sugars to the myricetin structure, forming myricetin glycosides.

Reported forms include myricetin attached to sugars such as:

• glucose;
• galactose;
• rhamnose;
• arabinose;
• xylose; and
• other sugar or substituted groups.

Examples include:

• myricetin-3-O-glucoside;
• myricetin-3-O-galactoside;
• myricetin-3-O-rhamnoside; and
• additional myricetin glycosides identified in specific berries and plant species.

The attached sugar can affect solubility, stability, digestion, absorption, and metabolism.

That means a measurement of total myricetin after chemical hydrolysis is not necessarily the same thing as measuring the individual myricetin glycosides naturally present in a food.

Myricetin vs. Myricitrin: What Is the Difference?

Myricitrin is not another name for free myricetin.

Myricitrin is a myricetin glycoside commonly identified as myricetin-3-O-rhamnoside.

In other words:

• Myricetin — the flavonol aglycone.
• Myricitrin — myricetin attached to the sugar rhamnose.

This is similar to the distinction between quercetin and rutin, where the underlying flavonol structure is chemically modified by an attached sugar group.

Because glycosylation can affect absorption and metabolism, research involving myricitrin should not automatically be described as research involving free myricetin.

Myricetin vs. Quercetin: What Is the Difference?

Myricetin and quercetin are closely related flavonols, but they are different molecules.

Both share the same general flavonol backbone.

The principal structural difference is that myricetin contains an additional hydroxyl group on the B-ring.

That difference can influence:

• redox behavior;
• chemical stability;
• binding to proteins and enzymes;
• solubility;
• metabolism; and
• activity observed in laboratory assays.

Quercetin has a substantially larger controlled human supplementation literature than myricetin.

Research findings from quercetin therefore should not be transferred to myricetin simply because both are flavonols.

See our Quercetin guide for the human evidence on that compound.

Myricetin vs. Dihydromyricetin: Are They the Same?

No. Myricetin and dihydromyricetin are different compounds.

Dihydromyricetin is also known as ampelopsin and is particularly associated with vine tea and certain other plants.

The compounds have closely related names and chemical structures, but dihydromyricetin has a saturated bond within its central ring that changes its classification and chemical properties.

Myricetin is classified as a flavonol.

Dihydromyricetin is classified as a dihydroflavonol or flavanonol.

This distinction matters because a supplement or research paper involving dihydromyricetin should not automatically be cited as evidence for myricetin.

The confusion is especially common online because both compounds are discussed in supplement and laboratory research.

What Foods Contain Myricetin?

Myricetin and its glycosides occur in a variety of plant foods.

Reported dietary sources include:

• Cranberries
• Black currants
• Blueberries
• Bilberries
• Aronia berries or chokeberries
• Crowberries
• Some grapes and grape-derived foods
• Tea
• Wine
• Leafy vegetables and herbs
• Certain nuts and other plant foods

The amount of myricetin in a food can differ substantially according to species, cultivar, maturity, growing environment, plant tissue, storage, processing, and analytical method.

Which Foods Are Highest in Myricetin?

There is no single universal ranking of foods by myricetin concentration.

A comparative study of 25 edible berries reported myricetin concentrations ranging from approximately 14 to 142 mg/kg fresh weight in berries including cranberry, black currant, crowberry, bog whortleberry, blueberry, and bilberry.

A later study examining 28 wild and cultivated berry species found that myricetin glycosides occurred in a more restricted group of berries than quercetin glycosides.

Myricetin glycosides were identified in species including:

• chokeberry or aronia;
• cranberry and other Vaccinium species;
• black currant and related currants and gooseberries;
• elderberry and related species; and
• several other berries included in the analysis.

These studies also demonstrate why one number from one cultivar should not be treated as the universal myricetin content of an entire fruit category.

Myricetin in FruitFast-Relevant Fruits

Myricetin is particularly relevant to FruitFast through several berries and dark-colored fruits used in our product portfolio.

The relevant scientific connection is the chemistry of the fruit itself. It does not establish a particular amount in a finished FruitFast juice concentrate.

Cranberries

Cranberries contain myricetin glycosides alongside substantial quercetin-derived flavonols.

Berry-composition studies have repeatedly identified cranberry as a source of myricetin or myricetin-related compounds.

Cranberries also contain:

• anthocyanins;
• proanthocyanidins;
• quercetin glycosides;
• phenolic acids;
• naturally occurring benzoic acid; and
• other plant constituents.

A cranberry study therefore should not automatically be described as a myricetin study.

Black Currants

Black currants contain myricetin glycosides as part of a broader flavonol profile.

Earlier analytical research isolated compounds including myricetin-3-glucoside from black currant fruit.

Modern analyses also show that black currants contain quercetin-related flavonols and substantial anthocyanins.

The chemistry of whole black currant is therefore considerably broader than myricetin alone.

Wild Blueberries

Blueberries can contain myricetin and myricetin glycosides.

Their flavonol profile can also include quercetin, isorhamnetin, syringetin, laricitrin, and other related compounds depending on species and cultivar.

Blueberries are especially rich in chemical diversity because their anthocyanin profile can include compounds derived from several different anthocyanidins.

Whole-blueberry research therefore should not automatically be attributed to myricetin.

Aronia Berries

Aronia berries, or chokeberries, contain myricetin glycosides in addition to quercetin derivatives.

Aronia is also notable for its anthocyanins and high-molecular-weight proanthocyanidins.

These compound families differ structurally and metabolically, so an outcome observed with whole aronia cannot be assigned to myricetin unless the study specifically isolates that relationship.

Explore our Aronia educational guide →
That guide covers aronia as a fruit and juice ingredient; it should not be read as evidence that myricetin alone explains whole-aronia research.

Grapes

Myricetin and myricetin-derived flavonols have been identified in grapes and grape products, particularly in pigmented grape tissues.

Grapes can also contain quercetin, kaempferol, anthocyanins, flavan-3-ols, proanthocyanidins, phenolic acids, and stilbenes such as resveratrol.

A result from grape seed extract, red wine, whole grapes, Concord grape juice, or isolated myricetin therefore represents very different scientific evidence.

Is Myricetin an Antioxidant?

Myricetin demonstrates strong antioxidant and redox activity in laboratory chemical systems.

Its multiple hydroxyl groups allow it to participate in reactions involving reactive chemical species and metal ions.

Researchers often find strong activity when purified myricetin is tested using laboratory antioxidant assays.

But this does not establish that consuming a myricetin-containing food produces the same reaction throughout the human body.

The distinction matters because:

• food myricetin frequently occurs as glycosides rather than free myricetin;
• digestion can change those chemical forms;
• absorption of intact myricetin appears limited;
• phase-II metabolism can produce sulfate and glucuronide conjugates;
• gut microorganisms can transform flavonoids into smaller metabolites; and
• circulating metabolites may behave differently from purified myricetin in a test tube.

Learn more about this distinction in our Antioxidants, Free Radicals & Oxidative Stress guide.

How Is Myricetin Absorbed and Metabolized?

Myricetin's bioavailability is one of the major limitations discussed in the scientific literature.

The free compound has relatively poor water solubility, and reviews describe limited oral bioavailability and substantial metabolism after ingestion.

Potential metabolic transformations include:

• glucuronidation;
• sulfation;
• methylation;
• degradation into smaller phenolic compounds; and
• transformations involving intestinal microorganisms.

Much of the detailed pharmacokinetic information still comes from laboratory and animal studies rather than large human pharmacokinetic trials.

What Has Human Cranberry Research Shown About Myricetin Absorption?

A human study examined the absorption and excretion of phenolic compounds after healthy volunteers consumed cranberry juice, cranberry sauce, and cranberry fruit.

The cranberry foods contained numerous phenolic compounds, including flavonols.

Researchers detected significant increases in multiple smaller phenolic compounds and conjugated metabolites in plasma and urine after consumption.

However, the researchers did not detect intact quercetin or myricetin in plasma or urine using the analytical methods employed in that study, despite those flavonols being present in the cranberry foods.

This does not prove that myricetin from cranberry has zero absorption or biological relevance.

Analytical sensitivity, chemical transformation, glycoside identity, conjugation, microbial metabolism, and the compounds selected for measurement all affect what a pharmacokinetic study can detect.

It does demonstrate why the amount of intact myricetin present in a food should not be assumed to equal the amount of free myricetin circulating in human blood.

What Role Might the Gut Microbiome Play?

Like other flavonoids, myricetin glycosides and breakdown products can interact with intestinal microorganisms.

The microbiome can contribute to:

• removal of sugar groups;
• ring-cleavage reactions;
• formation of smaller phenolic metabolites; and
• differences in metabolite exposure among individuals.

Research into myricetin–microbiome interactions is still developing.

It is therefore premature to describe myricetin as having an established “gut health” effect simply because microbial metabolism occurs.

Myricetin Research: What Has Actually Been Studied?

The phrase “myricetin benefits” can give the impression that the compound has a large established clinical evidence base.

It does not.

Myricetin has been studied extensively in:

• chemical assays;
• cultured cells;
• isolated tissues;
• animal models; and
• mechanistic experiments.

Direct controlled human clinical research on isolated myricetin is much more limited.

A 2020 review specifically noted that few clinical trials had been performed using myricetin as a nutraceutical.

A newer 2026 review reaches a similar practical conclusion: extensive pharmacological research exists, but limited bioavailability and a shortage of strong clinical evidence remain important barriers to translating preclinical findings into established human applications.

Inflammatory & Oxidative-Stress Research

Laboratory and animal studies have investigated myricetin in numerous pathways related to oxidative and inflammatory processes.

Research includes effects on:

• reactive chemical species;
• antioxidant enzymes;
• cell-signaling pathways;
• cytokines;
• transcription factors; and
• other mechanistic endpoints.

These experiments can help identify possible mechanisms.

They do not establish that dietary myricetin treats inflammation, inflammatory diseases, pain, or oxidative-stress-related conditions in humans.

Neurological & Neuroprotection Research (Mostly Preclinical)

Myricetin has received substantial attention in experimental neurological research.

Cell and animal studies have investigated mechanisms involving:

• neuronal oxidative stress;
• protein aggregation;
• neuroinflammatory signaling;
• mitochondrial function;
• cell survival; and
• experimental models of neurological disease.

This research explains why reviews frequently use terms such as “neuroprotective” when describing experimental myricetin.

However, preclinical neuroprotection is not evidence that myricetin-containing foods preserve cognition, prevent dementia, or treat neurological disease in people.

Direct human evidence is far too limited for those conclusions.

Cardiovascular Research

Experimental studies have also examined myricetin in pathways involving:

• endothelial signaling;
• platelet function;
• lipid oxidation;
• blood-vessel responses; and
• cardiac injury models.

Again, most of this evidence is mechanistic or preclinical.

It does not establish that consuming myricetin lowers blood pressure, prevents cardiovascular disease, or improves circulation in humans.

Glucose & Lipid Metabolism Research

Myricetin has been widely studied in experimental models of glucose and lipid metabolism.

A 2024 systematic review and meta-analysis reported favorable differences in glucose, insulin, triglycerides, total cholesterol, and LDL cholesterol.

But there is a crucial detail:

All 21 studies in that meta-analysis were mouse studies.

The review included 514 mice with experimental metabolic-disease models—not human participants.

The authors themselves concluded that further research is needed to confirm the findings in humans.

This is an important example of why the existence of a meta-analysis does not automatically mean there is strong clinical evidence.

Cancer-Related Preclinical Research

Myricetin has also been investigated extensively in cancer-cell and animal models.

Researchers have studied cell proliferation, apoptosis, cell-cycle signaling, enzyme activity, oxidative processes, and numerous molecular pathways.

These experiments are relevant to drug-discovery and mechanistic research.

They do not establish that dietary myricetin, berries containing myricetin, or FruitFast products prevent or treat cancer.

What Human Clinical Research Exists?

The direct clinical literature is small compared with the large laboratory and animal literature.

Some human studies have used preparations containing myricetin along with other active compounds.

Those trials are particularly difficult to interpret as “myricetin studies” because an observed outcome cannot be assigned to myricetin when chlorogenic acid, plant extracts, vitamins, or other ingredients are administered at the same time.

For this reason, evidence reviews repeatedly distinguish the large preclinical literature from the much smaller clinical evidence base.

At present, there is not a robust body of replicated randomized human trials demonstrating that isolated dietary myricetin produces the broad cardiovascular, cognitive, immune, inflammatory, or metabolic benefits commonly listed on supplement and wellness websites.

Myricetin Research vs. Whole-Berry Research

This distinction is especially important for FruitFast.

A cranberry, wild blueberry, black currant, aronia berry, or grape contains far more than myricetin.

Depending on the fruit, it may also contain:

• anthocyanins;
• proanthocyanidins;
• quercetin and other flavonols;
• phenolic acids;
• flavan-3-ols;
• organic acids;
• vitamins and minerals;
• sugars;
• fiber when whole fruit is consumed; and
• numerous other plant compounds.

If a human study reports an effect from blueberries, cranberry juice, aronia, black currant, or grapes, that result belongs to the specific fruit preparation tested.

It does not automatically establish that myricetin caused the outcome.

Likewise, a cell or animal experiment using purified myricetin should not automatically be used to claim that a fruit juice or concentrate produces the same biological effect.

How Processing & Storage Affect Myricetin

The amount and form of myricetin measured in foods can change during processing and storage.

Relevant factors include:

• fruit tissue — skin, flesh, seeds, and other tissues can have different flavonol profiles;
• pressing and extraction;
• clarification and filtration;
• heat exposure;
• pH;
• oxygen exposure;
• enzymatic reactions;
• fermentation;
• storage time and temperature; and
• analytical method.

Myricetin itself has limited water solubility and can be chemically sensitive to environmental conditions.

Processing can therefore change both total flavonol measurements and the distribution of individual glycosides.

Does Fruit Juice Concentrate Contain Myricetin?

A juice concentrate made from fruit containing myricetin compounds can contain myricetin-derived flavonols from the starting fruit.

However, the amount and glycoside profile in the finished concentrate depend on factors such as:

• fruit species and cultivar;
• starting-fruit composition;
• fruit tissue entering the juice;
• pressing and extraction;
• clarification and filtration;
• processing conditions;
• degree of concentration;
• storage;
• age of the finished product; and
• analytical method.

How Is Myricetin Measured?

Food researchers commonly use chromatographic techniques to identify and quantify myricetin and its glycosides.

Methods can include:

• high-performance liquid chromatography, or HPLC;
• ultra-performance liquid chromatography, or UPLC;
• diode-array detection;
• liquid chromatography coupled with mass spectrometry; and
• tandem mass-spectrometry methods.

Some methods directly measure individual myricetin glycosides.

Other methods hydrolyze glycosides and report a total value expressed as myricetin aglycone.

These approaches do not necessarily produce directly comparable numbers.

That is another reason to review analytical methods before comparing claims about which food contains “more myricetin.”

Is Myricetin Safe?

Myricetin compounds occur naturally in commonly consumed fruits, vegetables, tea, and other plant foods.

Ordinary dietary exposure should be distinguished from concentrated isolated-myricetin supplements.

Human safety data for high-dose, long-term isolated myricetin supplementation remain limited.

Much of the toxicology and pharmacology literature is based on cell and animal experiments rather than long-duration human supplementation trials.

Therefore, research doses used experimentally should not automatically be interpreted as safe or appropriate daily intake recommendations.

People considering concentrated myricetin supplements—particularly those who are pregnant, breastfeeding, managing a medical condition, or taking medications—should discuss individual questions with an appropriate healthcare professional.

Frequently Asked Questions About Myricetin

How to Evaluate Myricetin Research

When reading a study about myricetin, first determine exactly what was tested.

A study may involve:

• free myricetin aglycone;
• a myricetin glycoside;
• myricitrin;
• dihydromyricetin;
• a berry extract;
• whole fruit;
• fruit juice or concentrate;
• a multi-ingredient supplement;
• a cell-culture experiment; or
• an animal model.

These materials and study designs are not interchangeable.

It is also useful to consider:

• Compound identity — Was the research actually about myricetin?
• Glycoside form — Was a sugar attached to the compound?
• Study type — Chemical assay, cell experiment, animal model, observational study, or randomized human trial?
• Dose — Was the amount comparable with food exposure or a concentrated experimental dose?
• Population — Healthy people, a clinical population, laboratory animals, or isolated cells?
• Bioavailability — Was intact myricetin actually detected in circulation?
• Other compounds — Did the intervention also contain anthocyanins, quercetin, chlorogenic acid, other flavonoids, or additional supplement ingredients?
• Outcome — Chemical antioxidant activity, cell signaling, a biomarker, symptoms, or a demonstrated clinical outcome?

A strong antioxidant result in a test tube, improved glucose measurements in mice, a molecular effect in cultured neurons, and a clinical benefit in humans represent very different levels of evidence.

For myricetin in particular, maintaining that distinction is essential because the preclinical literature is much larger than the direct human evidence base.