Named Bioactive Compounds · Compound
Dihydromyricetin
Strong Evidenceflavonoid
Hermetica Superfood Encyclopedia
Dihydromyricetin is a flavonoid compound found in Hovenia dulcis that demonstrates hepatoprotective effects by modulating AMPK signaling pathways. Clinical research shows it reduces liver enzymes and improves insulin sensitivity in patients with metabolic disorders.
Dihydromyricetin (DHM) is a natural flavonoid primarily extracted from the leaves and stems of Ampelopsis grossedentata (Moyeam tea), a deciduous vine native to southern China. Commercial extraction typically uses ethanol or water-based solvents, followed by purification to produce a white to off-white powder standardized to ≥98% purity.
The primary human evidence comes from a double-blind RCT (PMID: 26032587) where 60 NAFLD patients received 300mg/day DHM or placebo for 3 months, showing significant improvements in liver enzymes and metabolic markers. Supporting preclinical research includes mouse NAFLD models demonstrating anti-inflammatory effects and gut microbiota modulation (PMC11729546).
Clinical studies used 300mg daily (150mg twice daily in capsules) for NAFLD management. Commercial supplements typically contain 100-300mg per capsule of purified DHM (≥98% purity). No other human dosing regimens have been clinically validated. Consult a healthcare provider before starting any new supplement.
Dihydromyricetin (DHM), also known as ampelopsin, is a flavanonol (dihydroflavonol) with the molecular formula C₁₅H₁₂O₈ and molecular weight 320.25 g/mol. It is not a food consumed for macronutrient content; rather, it is a bioactive polyphenolic compound typically consumed as a purified supplement or obtained from dietary sources. Key details: • Primary bioactive compound: Dihydromyricetin (ampelopsin) itself — a 3,5,7,3',4',5'-hexahydroxyflavanone. • Natural source concentration: Found abundantly in Ampelopsis grossedentata (vine tea/moyeam tea), where dried leaves contain approximately 20–40% DHM by weight, making it one of the richest natural sources of a single flavonoid. Also present in smaller quantities in Hovenia dulcis (Japanese raisin tree), Cedrus deodara, and certain Vitis species. • Supplement dosages typically range from 150–600 mg per dose, with clinical studies using 300–600 mg/day. • Macronutrients: Negligible — DHM is consumed in milligram quantities and contributes essentially zero calories, protein, fat, carbohydrate, or fiber. • Micronutrients (vitamins/minerals): None intrinsic to the purified compound. Vine tea extracts may contain trace minerals and other polyphenols (myricetin, gallic acid, quercetin derivatives) but these are incidental. • Key bioactive properties: DHM possesses six hydroxyl groups contributing to strong antioxidant capacity (ORAC and DPPH radical scavenging activity comparable to or exceeding that of many common flavonoids). It chelates metal ions (Fe²⁺, Cu²⁺) and modulates AMPK, SIRT1, Nrf2/ARE, and NF-κB signaling pathways. • Bioavailability notes: Oral bioavailability is relatively LOW, estimated at approximately 4–17% in animal models. DHM undergoes extensive first-pass metabolism including glucuronidation, sulfation, and methylation in the gut and liver. Absorption is primarily in the small intestine. Plasma half-life is short (~1.5–3 hours in animal studies). Bioavailability may be enhanced by co-administration with lipid-based carriers, phospholipid complexes (phytosomes), nanoformulations, or piperine. Gut microbiota metabolize unabsorbed DHM into smaller phenolic acids (e.g., phloroglucinol derivatives), which may contribute additional bioactivity. Peak plasma concentration (Tmax) occurs approximately 0.5–1.5 hours post-oral ingestion. Water solubility is limited (~20 mg/mL at room temperature), which partly explains the low bioavailability.
Dihydromyricetin activates AMP-activated protein kinase (AMPK) pathways, which regulate cellular energy metabolism and fatty acid oxidation. It inhibits hepatic lipogenesis by downregulating SREBP-1c and ACC enzymes while promoting fatty acid β-oxidation. The compound also enhances insulin signaling through PI3K/Akt pathway activation and reduces inflammatory cytokines like TNF-α and IL-6.
A randomized controlled trial with 60 NAFLD patients showed dihydromyricetin (300mg daily for 3 months) significantly reduced ALT, AST, and GGT liver enzymes compared to placebo. The same study demonstrated improved insulin sensitivity with HOMA-IR reductions of approximately 40%. Additional clinical research indicates benefits for glucose metabolism, though most studies involve small sample sizes of 50-80 participants. Evidence quality is moderate, with most trials lasting 8-12 weeks.
Dihydromyricetin appears generally well-tolerated with minimal reported side effects in clinical trials. Potential interactions may occur with diabetes medications due to glucose-lowering effects, requiring blood sugar monitoring. No specific drug interactions have been documented, but theoretical concerns exist with hepatically-metabolized medications. Safety during pregnancy and lactation has not been established, so use should be avoided in these populations.
