Myricetin (Hexahydroxy Flavonol · Antioxidant · Metabolic Support)
| CAS No. | 529-44-2 |
| Class | Polyphenol · Flavonol · Flavonoid |
| Source | Lycium barbarum (Goji berry); Myrica rubra (Bayberry); red wine grapes, cranberries, parsley, sage, oregano |
| Claim strength | Moderate |
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Name origin: Myricetin is named from Myrica rubra (bayberry), the plant from which it was historically isolated. Structural distinction: With six hydroxyl groups, it is the most hydroxylated of common dietary flavonols — one more than quercetin — giving it exceptional radical-scavenging capacity in ORAC and DPPH assays. Research interest areas: Glucose metabolism (inhibits intestinal SGLT1/GLUT2 and stimulates GLUT4 translocation in an insulin-mimetic manner), neuroprotection (inhibits amyloid-β and α-synuclein aggregation in Alzheimer's and Parkinson's models), and adipogenesis inhibition. Practical note: Its high degree of hydroxylation reduces aqueous solubility compared to quercetin, requiring formulation attention for adequate bioavailability.
Evidence for Antioxidant, Blood Glucose & Neuroprotective Activity
Antioxidant activity: Six hydroxyl groups produce exceptional radical-scavenging and metal-chelation capacity, along with Nrf2 upregulation in cell models. Claim strength: High (mechanistic); Moderate (clinical).
Blood glucose modulation: Inhibits SGLT1 and GLUT2 (slowing intestinal glucose absorption), stimulates GLUT4 translocation (insulin-mimetic effect), and inhibits aldose reductase (relevant to diabetic complications). Multiple rodent models show significant glucose reductions. Human data is limited. Claim strength: Moderate.
Neuroprotection: Inhibits aggregation of amyloid-β and α-synuclein — the proteins central to Alzheimer's and Parkinson's pathology. Crosses the blood-brain barrier and improves cognitive performance in animal neurodegeneration models. Claim strength: Emerging.
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Dosage & Formulator Notes
Dose range: No established human clinical dose. Preclinical studies use 50–200 mg/kg. Proposed supplement range: 100–500 mg/day. Dietary intake from flavonoid-rich diets is 0.5–3 mg/day — well below experimental doses.
Formulation: Low aqueous solubility requires lipid carrier, phytosome complex, or cyclodextrin inclusion for meaningful bioavailability. Minimise heat exposure during processing to reduce oxidative degradation.
Synergistic pairs: Quercetin (complementary flavonol antioxidant stack), berberine (AMPK + glucose metabolism), alpha-lipoic acid (antioxidant synergy), goji berry extract (natural food-matrix myricetin source with LBP polysaccharides).
Frequently Asked Questions — Myricetin
How does myricetin differ mechanistically from quercetin?
The additional 5′-hydroxyl group on myricetin's B-ring increases radical-scavenging capacity and metal chelation but reduces aqueous solubility. Myricetin has stronger documented effects on glucose transport proteins (SGLT1, GLUT2) and protein aggregation inhibition. Quercetin has stronger documented NF-κB inhibition and mast cell stabilisation, plus a broader overall evidence base.
Is myricetin relevant for diabetic health formulations?
Myricetin inhibits intestinal glucose absorption (SGLT1/GLUT2), stimulates GLUT4 translocation (insulin-mimetic), and inhibits aldose reductase — multiple complementary mechanisms relevant to blood glucose management. Preclinical evidence is compelling; isolated myricetin human trials are limited. Appropriate for comprehensive metabolic health formulations positioned as dietary supplement support.
Which food sources provide the most myricetin?
Bayberry bark and fruit are the richest botanical sources. Among commonly consumed foods: goji berries, cranberries, red wine grapes, walnuts. Culinary herbs including parsley, sage, oregano, and thyme contain notable concentrations. Most Western dietary intake is 0.5–3 mg/day from food.
Can myricetin be used in cognitive support formulations?
Myricetin crosses the blood-brain barrier and inhibits amyloid-β and α-synuclein aggregation — providing a mechanistic basis for neuroprotective positioning. Human cognitive evidence is early-stage. Best positioned as a complementary antioxidant and neuroprotective ingredient alongside compounds with stronger clinical evidence (Bacopa monnieri, ginkgo, phosphatidylserine).
Claim-strength scale – High = multiple human RCTs; Moderate = limited trials or strong preclinical convergence; Emerging = early-stage lab or animal data.
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