Benefits
Free radical scavenging in laboratory studies
In test-tube work dihydroquercetin donates hydrogen atoms to free radicals and binds iron, which is the basis of its antioxidant reputation. In one electron-spin-resonance ranking of 15 flavonoids it was a weaker radical quencher than quercetin, rutin and vitamin E. These are chemistry assays, not effects measured in people taking it.
Lipid peroxidation readings in a human study
A 21-person non-randomized study of a dihydroquercetin plus vitamin C combination, in people with age-related vascular changes, reported lower lipid-peroxidation readings in red-cell membranes and blood plasma over three weeks than in an untreated comparison group. It tested a combination product rather than the isolated compound, and was not placebo-controlled.
Antioxidant activity in animal tissue
In animal studies taxifolin lowered reactive oxygen and nitrogen species in the wall of the aorta and helped restore antioxidant activity in organs placed under stress. These are findings in rodents given the compound by injection or diet, and have not been confirmed as antioxidant effects in people who swallow it.
Blood flow and circulation support
In the same small combination study, whole-blood viscosity fell and red blood cells became less clumped and more flexible over three weeks. Laboratory blood samples and animal models of sluggish circulation point the same way. The research used dihydroquercetin together with vitamin C, so the effect of the compound on its own is unclear.
Fat-packaging enzymes in liver cell studies
In cultured human liver cells taxifolin lowered the activity of two enzymes, DGAT and MTP, that help assemble and export fats, which reduced the output of apolipoprotein B, the protein that carries LDL cholesterol. This is a cell-culture finding about how fats are handled, and it has not been shown to change blood cholesterol in people.
Mechanism of action
Donates hydrogen to free radicals and binds metals
Like other flavonoids, dihydroquercetin can hand a hydrogen atom to an unstable free radical and can bind transition metals such as iron that would otherwise speed up oxidation. In cell and chemistry studies this lowers markers of oxidative damage, though it is a comparatively modest radical quencher next to quercetin.
Lowers reactive oxygen species in blood vessels (animal studies)
In the aorta of aging rats and of rats given a nitric oxide blocker, taxifolin lowered reactive oxygen and nitrogen species and brought angiotensin-converting enzyme activity back toward that of young animals. This is a proposed vascular mechanism from animal work, not something measured in people.
Poorly absorbed from the gut
Dihydroquercetin dissolves poorly in water and is pushed back out of intestinal cells by a transporter called P-glycoprotein, so only a small fraction is absorbed. This is why makers package it in microcapsules, liposomes and other delivery forms, and it is one reason human effects are hard to pin down.
Clinical trials
Randomized, double-blind, placebo-controlled crossover study of a single intake of taxifolin-containing food versus placebo, with cognitive tests and whole-blood gene expression. (Shinozaki et al. 2023, Food Funct)
Healthy young adults, each receiving placebo and the taxifolin-rich food on separate occasions.
After the taxifolin food, calculation scores improved and rated mental fatigue fell, and whole-blood gene expression showed more activity in genes tied to clearing foreign substances. This was a single serving of a food rather than a measured dose of the isolated compound, and antioxidant blood markers were not the endpoint.
Non-randomized clinical study of ascovertin, a combination of dihydroquercetin and ascorbic acid, for 21 days versus an untreated comparison group. (Plotnikov et al. 2004, Zh Nevrol Psikhiatr Im S S Korsakova)
21 patients aged 45 to 65 with early vascular changes on a background of atherosclerosis, plus 10 untreated age-matched comparison patients.
The combination group had lower whole-blood viscosity, less red-cell clumping and more flexible red cells, and lower lipid-peroxidation readings in red-cell membranes and plasma; the comparison group did not. It tested a dihydroquercetin plus vitamin C combination, was small and not placebo-controlled, and was reported in Russian.
Laboratory study of dihydroquercetin added to neutrophils isolated from the blood of patients with type 2 diabetes. (Fedosova et al. 2004, Bull Exp Biol Med)
White blood cells (neutrophils) taken from patients with non-insulin-dependent diabetes, tested in the test tube.
Added to the cells in the test tube, dihydroquercetin lowered production of anion radicals, hypochlorous acid and malondialdehyde and reduced protein kinase C and myeloperoxidase activity, and it bound iron. This is a test-tube effect on cells taken from people, not the result of anyone swallowing the compound.
Animal study of taxifolin at 30 to 100 micrograms per kilogram per day on aortic angiotensin-converting enzyme and reactive oxygen and nitrogen species. (Arutyunyan et al. 2013, Age (Dordr))
Aging rats and rats given a nitric oxide synthase blocker or dexamethasone.
Taxifolin lowered angiotensin-converting enzyme activity in the aorta toward the level of young animals and reduced reactive oxygen and nitrogen species raised by the nitric oxide blocker. These are animal results describing a possible vascular mechanism, not an outcome measured in people.
Cell-culture study of taxifolin on diacylglycerol acyltransferase and microsomal triglyceride transfer protein in HepG2 liver cells. (Casaschi et al. 2004, Atherosclerosis)
Cultured human HepG2 liver cells.
Taxifolin lowered the activity of DGAT and MTP, two enzymes that assemble and export fats, and reduced secretion of apolipoprotein B, the carrier protein of LDL cholesterol. This is a cell-culture finding about fat handling and does not show a change in blood cholesterol in people.