Resveratrol

Pharmacology & Research

Resveratrol is the famous stilbene of red wine — and the cleanest example in this whole database of the gap between reputation and evidence. The story begins with the “French paradox” (low heart-disease mortality despite a high-fat diet, attributed in 1992 to wine) ^{1Reference 1Renaud S · 1992Wine, alcohol, platelets, and the French paradox for coronary heart diseaseView study →} and accelerated when a 2003 paper proposed resveratrol as a SIRT1-activating calorie-restriction mimic and possible longevity molecule ^{3Reference 3Howitz KT et al. · 2003Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespanView study →}. Almost everything since has complicated that picture. Oral bioavailability is near zero — resveratrol is well absorbed but so rapidly conjugated that free resveratrol is barely detectable in blood ^{2Reference 2Walle T et al. · 2004High absorption but very low bioavailability of oral resveratrol in humansView study →}; the direct SIRT1-activation claim turned out to be largely an assay artifact ^{4Reference 4Pacholec M et al. · 2010SRT1720, SRT2183, SRT1460, and resveratrol are not direct activators of SIRT1View study →}; the human trials are small, dose- and subgroup-dependent, and frequently null in healthy people; and the field carries two serious credibility scars — a failed drug-development program and a major research-fraud scandal (both below). The form that is studied is trans-resveratrol, and the supplements are extracted from Japanese knotweed, not grapes.

1. Metabolic — glucose, insulin & lipids

This is resveratrol’s most-studied domain, and the honest summary is “small, and only where there’s already dysfunction.” A meta-analysis of 11 RCTs found significant improvements in fasting glucose, insulin, HbA1c and HOMA-IR — but only in participants with diabetes, with no significant effect in non-diabetics ^{5Reference 5Liu K et al. · 2014Meta-analysisEffect of resveratrol on glucose control and insulin sensitivity: a meta-analysis of 11 randomized controlled trialsView study →}. The famous 30-day pilot in obese men (calorie-restriction-like metabolic changes, less liver fat) is real but tiny (n≈11) and mechanistic ^{6Reference 6Timmers S et al. · 2011Calorie restriction-like effects of 30 days of resveratrol supplementation on energy metabolism and metabolic profile in obese humansView study →}, and it is directly contradicted by a better-powered high-dose RCT that found no improvement in insulin sensitivity or body composition in obese men ^{7Reference 7Poulsen MM et al. · 2013RCTHigh-dose resveratrol supplementation in obese men — an investigator-initiated, randomized, placebo-controlled clinical trial of substrate metabolism, insulin sensitivity, and body compositionView study →}, and by a clean RCT showing no metabolic benefit in metabolically healthy women ^{8Reference 8Yoshino J et al. · 2012Resveratrol supplementation does not improve metabolic function in nonobese women with normal glucose toleranceView study →}. Blood lipids are unaffected in meta-analysis ^{9Reference 9Sahebkar A · 2013Meta-analysisEffects of resveratrol supplementation on plasma lipids: a systematic review and meta-analysis of randomized controlled trialsView study →}.

Gap: the benefit is confined to diabetic/dysregulated subgroups and is modest; the strongest “wow” pilots are small and don’t replicate at higher power; the red-wine lipid story is not supported ^{5,7,9Reference 5Liu K et al. · 2014Meta-analysisEffect of resveratrol on glucose control and insulin sensitivity: a meta-analysis of 11 randomized controlled trialsView study →Reference 7Poulsen MM et al. · 2013RCTHigh-dose resveratrol supplementation in obese men — an investigator-initiated, randomized, placebo-controlled clinical trial of substrate metabolism, insulin sensitivity, and body compositionView study →Reference 9Sahebkar A · 2013Meta-analysisEffects of resveratrol supplementation on plasma lipids: a systematic review and meta-analysis of randomized controlled trialsView study →}.

2. Cognitive & cerebrovascular

Resveratrol’s most consistent positive human signal is here — but narrowly. A single group’s program in postmenopausal women found improved cerebrovascular responsiveness, cognition and mood over 14 weeks ^{15Reference 15Evans HM et al. · 2017RCTEffects of resveratrol on cognitive performance, mood and cerebrovascular function in post-menopausal women — a 14-week randomised placebo-controlled intervention trialView study →} and sustained benefit over 24 months (the RESHAW trial) ^{16Reference 16Thaung Zaw JJ et al. · 2021RCTLong-term effects of resveratrol on cognition, cerebrovascular function and cardio-metabolic markers in postmenopausal women — a 24-month randomised, double-blind, placebo-controlled, crossover studyView study →}. Acutely, a single dose raises cerebral blood flow but does not improve cognitive performance — blood flow is not the same as thinking better ^{14Reference 14Kennedy DO et al. · 2010RCTEffects of resveratrol on cerebral blood flow variables and cognitive performance in humans — a double-blind, placebo-controlled, crossover investigationView study →}.

Gap: the positive cerebrovascular body of work is largely one research team (Wong/Howe/Thaung Zaw) and needs independent replication; and in Alzheimer’s disease the definitive RCT was essentially negative for clinical/cognitive benefit despite moving a CSF amyloid marker (with slightly greater brain-volume loss) ^{13Reference 13Turner RS et al. · 2015RCTA randomized, double-blind, placebo-controlled trial of resveratrol for Alzheimer diseaseView study →}. So: a promising postmenopausal-vascular niche, not a proven cognitive enhancer ^{13,15,16Reference 13Turner RS et al. · 2015RCTA randomized, double-blind, placebo-controlled trial of resveratrol for Alzheimer diseaseView study →Reference 15Evans HM et al. · 2017RCTEffects of resveratrol on cognitive performance, mood and cerebrovascular function in post-menopausal women — a 14-week randomised placebo-controlled intervention trialView study →Reference 16Thaung Zaw JJ et al. · 2021RCTLong-term effects of resveratrol on cognition, cerebrovascular function and cardio-metabolic markers in postmenopausal women — a 24-month randomised, double-blind, placebo-controlled, crossover studyView study →}.

3. Cardiovascular & endothelial

Genuinely mixed. A blood-pressure meta-analysis found that only high doses (≥150 mg/day) significantly reduced systolic BP, with no effect on diastolic and none at lower doses ^{10Reference 10Liu Y et al. · 2015Meta-analysisEffect of resveratrol on blood pressure: a meta-analysis of randomized controlled trialsView study →}. Endothelial function (flow-mediated dilation) improved in obese adults in one RCT ^{11Reference 11Wong RH et al. · 2013Chronic resveratrol consumption improves brachial flow-mediated dilatation in healthy obese adultsView study →} — but another RCT in postmenopausal women found resveratrol did not improve (and appeared to blunt) post-exercise endothelial function relative to estradiol ^{12Reference 12Ozemek C et al. · 2020Effects of resveratrol or estradiol on postexercise endothelial function in estrogen-deficient postmenopausal womenView study →}.

Gap: dose-gated and cohort-dependent; the vascular benefits are modest where present and absent or possibly counter-productive elsewhere. No consistent outcome-level cardiovascular benefit is established ^{10,11,12Reference 10Liu Y et al. · 2015Meta-analysisEffect of resveratrol on blood pressure: a meta-analysis of randomized controlled trialsView study →Reference 11Wong RH et al. · 2013Chronic resveratrol consumption improves brachial flow-mediated dilatation in healthy obese adultsView study →Reference 12Ozemek C et al. · 2020Effects of resveratrol or estradiol on postexercise endothelial function in estrogen-deficient postmenopausal womenView study →}.

4. Anti-inflammatory & other

A scatter of meta-analyses and small RCTs. Resveratrol reduces some inflammatory markers (TNF-α, CRP) but heterogeneously ^{17Reference 17Koushki M et al. · 2018Meta-analysisEffect of resveratrol supplementation on inflammatory markers — a systematic review and meta-analysis of randomized controlled trialsView study →}; in NAFLD the evidence is inconsistent with no robust conclusion ^{18Reference 18Elgebaly A et al. · 2017Meta-analysisResveratrol supplementation in patients with non-alcoholic fatty liver disease — systematic review and meta-analysisView study →}; in PCOS a meta-analysis found preliminary metabolic/androgen signals from small trials ^{19Reference 19Larik MO et al. · 2024Meta-analysisEffects of resveratrol on polycystic ovarian syndrome — a systematic review and meta-analysis of randomized controlled trialsView study →}. A bone-turnover RCT is often cited, but it tested equol + resveratrol together, so the effect can’t be assigned to resveratrol ^{20Reference 20Corbi G et al. · 2023Clinical trialEquol and resveratrol improve bone turnover biomarkers in postmenopausal women — a clinical trialView study →}.

Gap: heterogeneous, condition-restricted, small trials; at least one headline result is a combination product. Preliminary, not established ^{17,18,19,20Reference 17Koushki M et al. · 2018Meta-analysisEffect of resveratrol supplementation on inflammatory markers — a systematic review and meta-analysis of randomized controlled trialsView study →Reference 18Elgebaly A et al. · 2017Meta-analysisResveratrol supplementation in patients with non-alcoholic fatty liver disease — systematic review and meta-analysisView study →Reference 19Larik MO et al. · 2024Meta-analysisEffects of resveratrol on polycystic ovarian syndrome — a systematic review and meta-analysis of randomized controlled trialsView study →Reference 20Corbi G et al. · 2023Clinical trialEquol and resveratrol improve bone turnover biomarkers in postmenopausal women — a clinical trialView study →}.

Mechanisms

Target / pathway	Effect	Relevant to	Evidence
SIRT1 (proposed activation)	CR-mimetic / metabolic	metabolic, ageing	contested — not a direct activator in clean assays 3,4Reference 3Howitz KT et al. · 2003Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespanView study →Reference 4Pacholec M et al. · 2010SRT1720, SRT2183, SRT1460, and resveratrol are not direct activators of SIRT1View study →
AMPK activation; ↑ mitochondrial biogenesis (PGC-1α)	improved energy metabolism	metabolic	animal + small human 6Reference 6Timmers S et al. · 2011Calorie restriction-like effects of 30 days of resveratrol supplementation on energy metabolism and metabolic profile in obese humansView study →
eNOS / nitric-oxide↑	vasodilation, endothelial function	cardiovascular	human (mixed) 11,12Reference 11Wong RH et al. · 2013Chronic resveratrol consumption improves brachial flow-mediated dilatation in healthy obese adultsView study →Reference 12Ozemek C et al. · 2020Effects of resveratrol or estradiol on postexercise endothelial function in estrogen-deficient postmenopausal womenView study →
Estrogen-receptor agonism (phytoestrogen)	mixed agonist/antagonist	safety, postmenopausal	in vitro 25Reference 25Gehm BD et al. · 1997Resveratrol, a polyphenolic compound found in grapes and wine, is an agonist for the estrogen receptorView study →
NF-κB inhibition (↓ TNF-α, CRP)	anti-inflammatory	inflammation	human (heterogeneous) 17Reference 17Koushki M et al. · 2018Meta-analysisEffect of resveratrol supplementation on inflammatory markers — a systematic review and meta-analysis of randomized controlled trialsView study →
Platelet aggregation / eicosanoid inhibition	antiplatelet	safety	in vitro 27Reference 27Pace-Asciak CR et al. · 1995The red wine phenolics trans-resveratrol and quercetin block human platelet aggregation and eicosanoid synthesis — implications for protection against coronary heart diseaseView study →

Pharmacokinetics

Resveratrol’s pharmacokinetics are the reason its dramatic laboratory activity has never cleanly translated. The molecule is well absorbed — about 70% of an oral dose crosses the gut — yet its oral bioavailability is essentially zero, because it is conjugated so extensively and rapidly (sulfation and glucuronidation, beginning in the enterocyte itself) that peak free trans-resveratrol in plasma is only a few nanograms per millilitre ^{2Reference 2Walle T et al. · 2004High absorption but very low bioavailability of oral resveratrol in humansView study →}. The landmark human study’s title says it outright: “high absorption but very low bioavailability” ^{2Reference 2Walle T et al. · 2004High absorption but very low bioavailability of oral resveratrol in humansView study →}. Even single doses up to 5 grams leave parent-drug levels low and highly variable, with conjugates dominating ^{21Reference 21Boocock DJ et al. · 2007ObservationalPhase I dose escalation pharmacokinetic study in healthy volunteers of resveratrol, a potential cancer chemopreventive agentView study →}. What the tissues mostly see, therefore, is resveratrol glucuronides and sulfates, plus microbial metabolites — gut bacteria convert a portion to dihydroresveratrol, with large person-to-person variation ^{22Reference 22Bode LM et al. · 2013In vitroIn vivo and in vitro metabolism of trans-resveratrol by human gut microbiotaView study →}. Formulation attempts to fix this — notably the micronised SRT501 — raised parent levels somewhat but did not overcome the conjugation bottleneck ^{23Reference 23Howells LM et al. · 2011RCTPhase I randomized, double-blind pilot study of micronized resveratrol (SRT501) in patients with hepatic metastases — safety, pharmacokinetics, and pharmacodynamicsView study →}.

Two further chemistry facts matter. Resveratrol exists as trans and cis isomers; the trans form is the one in supplements and trials, and it isomerises to cis on exposure to UV light ^{28Reference 28Nour V et al. · 2012Ultraviolet irradiation of trans-resveratrol and HPLC determination of trans- and cis-resveratrol in Romanian red winesView study →}, which is why material and formulations are light-protected. The net PK picture: the concentrations that drive resveratrol’s in-vitro SIRT1, anti-inflammatory and anticancer effects are far above what an oral dose — let alone a glass of wine — delivers to human tissue ^{2,21Reference 2Walle T et al. · 2004High absorption but very low bioavailability of oral resveratrol in humansView study →Reference 21Boocock DJ et al. · 2007ObservationalPhase I dose escalation pharmacokinetic study in healthy volunteers of resveratrol, a potential cancer chemopreventive agentView study →}.

Clinical trials

Resveratrol has a large but inconsistent human literature. Meta-analyses converge on “small, dose- and subgroup-dependent, often null”:

Positive (narrow)	Null / negative	Mixed
Glucose in diabetics 5Reference 5Liu K et al. · 2014Meta-analysisEffect of resveratrol on glucose control and insulin sensitivity: a meta-analysis of 11 randomized controlled trialsView study →; postmenopausal cerebrovascular 15,16Reference 15Evans HM et al. · 2017RCTEffects of resveratrol on cognitive performance, mood and cerebrovascular function in post-menopausal women — a 14-week randomised placebo-controlled intervention trialView study →Reference 16Thaung Zaw JJ et al. · 2021RCTLong-term effects of resveratrol on cognition, cerebrovascular function and cardio-metabolic markers in postmenopausal women — a 24-month randomised, double-blind, placebo-controlled, crossover studyView study →; systolic BP at high dose 10Reference 10Liu Y et al. · 2015Meta-analysisEffect of resveratrol on blood pressure: a meta-analysis of randomized controlled trialsView study →	Healthy-population metabolism 7,8Reference 7Poulsen MM et al. · 2013RCTHigh-dose resveratrol supplementation in obese men — an investigator-initiated, randomized, placebo-controlled clinical trial of substrate metabolism, insulin sensitivity, and body compositionView study →Reference 8Yoshino J et al. · 2012Resveratrol supplementation does not improve metabolic function in nonobese women with normal glucose toleranceView study →; lipids 9Reference 9Sahebkar A · 2013Meta-analysisEffects of resveratrol supplementation on plasma lipids: a systematic review and meta-analysis of randomized controlled trialsView study →; Alzheimer’s cognition 13Reference 13Turner RS et al. · 2015RCTA randomized, double-blind, placebo-controlled trial of resveratrol for Alzheimer diseaseView study →	Endothelial function 11,12Reference 11Wong RH et al. · 2013Chronic resveratrol consumption improves brachial flow-mediated dilatation in healthy obese adultsView study →Reference 12Ozemek C et al. · 2020Effects of resveratrol or estradiol on postexercise endothelial function in estrogen-deficient postmenopausal womenView study →; inflammation 17Reference 17Koushki M et al. · 2018Meta-analysisEffect of resveratrol supplementation on inflammatory markers — a systematic review and meta-analysis of randomized controlled trialsView study →; NAFLD 18Reference 18Elgebaly A et al. · 2017Meta-analysisResveratrol supplementation in patients with non-alcoholic fatty liver disease — systematic review and meta-analysisView study →

Last checked: July 2026.

Isolate vs. Plant Studies

Resveratrol is mis-sold in three ways worth stating plainly. “Red wine’s healthy molecule” oversells the dose: a 150 mL glass delivers only ~0.3 mg resveratrol (even a high Pinot Noir ~2 mg), while trials use hundreds of milligrams to grams — you would need hundreds to thousands of glasses to reach a studied dose, so the wine framing is biologically hollow ^{2Reference 2Walle T et al. · 2004High absorption but very low bioavailability of oral resveratrol in humansView study →}. The supplement isn’t from grapes: commercial resveratrol is extracted from Japanese knotweed (Polygonum cuspidatum) root, the one source concentrated enough to be economic — grapes and food are trace-level by comparison. And the mechanism story is contested: the direct SIRT1-activation that launched the longevity narrative was shown to depend on a fluorophore artifact in the original assay ^{3,4Reference 3Howitz KT et al. · 2003Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespanView study →Reference 4Pacholec M et al. · 2010SRT1720, SRT2183, SRT1460, and resveratrol are not direct activators of SIRT1View study →}, so “resveratrol activates the longevity enzyme” should be read as an unresolved hypothesis, not a fact. Within this database resveratrol appears as a genuine constituent of sarsaparilla (with oxyresveratrol; Smilax stilbenes shown in vitro to modulate nicotine-related CYP2A6 and oxidative stress ^{35Reference 35Kim JY et al. · 2014In vitroEffects of Smilax china L. stilbenes on nicotine-induced oxidative stress and CYP2A6 in vitro. (stilbene / oxyresveratrol study). https://pubmed.ncbi.nlm.nih.gov/25220663/View study →}) and is the signature compound of the Polygonaceae; those are legitimate occurrence-level entries, not evidence for the supplement claims.

Prevalence in Nature

Resveratrol is a phytoalexin — a stress-and-defence compound plants synthesise in response to fungal attack, UV and injury — which is why its levels are so variable and why it concentrates in skins and roots rather than flesh. In the food supply it is genuinely trace. Grape skin (not the flesh, which has almost none) carries ~50–100 µg/g, and red wine — because fermentation extracts the skins — is the best-known dietary source at roughly 0.1–14 mg/L (typically ~1–3 mg/L; Pinot Noir highest, white wine near-zero because the skins are removed early) ^{29Reference 29Pezzuto JM · 2019Resveratrol — twenty years of growth, development and controversyView study →}. Peanuts contribute a little (raw ~0.02–1.9 µg/g; boiled peanuts higher), and berries (blueberry, bilberry, cranberry) and dark chocolate carry only fractions of a µg/g ^{31,32,33Reference 31Burns J et al. · 2002Plant foods and herbal sources of resveratrolView study →Reference 32Lyons MM et al. · 2003Resveratrol in raw and baked blueberries and bilberriesView study →Reference 33Hurst WJ et al. · 2008Survey of the trans-resveratrol and trans-piceid content of cocoa-containing and chocolate productsView study →}. A minor botanical footnote for this database: resveratrol was reported for the first time in camu-camu seed coat in 2018 ^{34Reference 34Fidelis M et al. · 2018Camu-camu seed (Myrciaria dubia) — from side stream to an antioxidant, antihyperglycemic, antiproliferative, antimicrobial, antihemolytic, anti-inflammatory, and antihypertensive ingredientView study →}.

The number that matters, though, is the one off the top of this chart: Japanese knotweed (Polygonum cuspidatum) root contains on the order of 500–3,000 µg/g of free resveratrol (plus more as the glucoside polydatin/piceid) — roughly 1,000 times or more the concentration in any food tissue ^{29Reference 29Pezzuto JM · 2019Resveratrol — twenty years of growth, development and controversyView study →}. That single fact explains the entire supplement industry: essentially all commercial resveratrol is extracted from knotweed root, standardised to 50–98%, because you physically cannot concentrate a meaningful dose from grapes or wine. (The chart above deliberately shows only foods, on a µg/g scale; knotweed would flatten every other bar to invisibility.) There are no non-plant sources.

Discovery & Synthesis

Resveratrol is reported to have been first isolated in 1939 by Michio Takaoka from the roots of white hellebore (Veratrum grandiflorum) — the name being built from Veratrum + resorcinol (its resorcinol-type A-ring) + the “-ol” of a phenol. That origin is documented only in a pre-MEDLINE Japanese journal, so it is best treated as reported rather than primary-sourced ^{29Reference 29Pezzuto JM · 2019Resveratrol — twenty years of growth, development and controversyView study →}. It was later found in the roots of Polygonum cuspidatum (Japanese knotweed, “Ko-jo-kon” in traditional East-Asian medicine) — now the commercial source — and, famously, in grape skin and red wine, the finding that connected it to the 1992 “French paradox” ^{1Reference 1Renaud S · 1992Wine, alcohol, platelets, and the French paradox for coronary heart diseaseView study →}. Structurally resveratrol is 3,4′,5-trihydroxystilbene, a stilbenoid built from two phenolic rings joined by an ethylene bridge, and in plants it is the branch-point of a small family: the glucoside polydatin (piceid), the dimethyl ether pterostilbene, and oxyresveratrol are all close relatives (each with its own entry).

Its modern fame is a cautionary tale, and the page states it plainly. In 2003 a Sinclair-lab paper reported resveratrol as a small-molecule SIRT1 activator that extended yeast lifespan, seeding a decade of “longevity molecule” interest ^{3Reference 3Howitz KT et al. · 2003Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespanView study →}; in 2010 a careful study showed the apparent activation was an artifact of the fluorescent assay substrate, and that resveratrol is not a direct SIRT1 activator ^{4Reference 4Pacholec M et al. · 2010SRT1720, SRT2183, SRT1460, and resveratrol are not direct activators of SIRT1View study →} — a debate the field still hasn’t fully closed. The field also carries an outright fraud scar: a prolonged University of Connecticut investigation concluded in 2012 that a prominent resveratrol/red-wine cardiovascular researcher had fabricated and falsified data across some 145 counts, triggering a wave of retractions ^{30Reference 30Roehr B · 2012Cardiovascular researcher fabricated data in studies of red wineView study →}. None of that erases the legitimate resveratrol literature, but it is part of why claims about this molecule deserve unusually careful reading. Commercial resveratrol is made almost entirely by extraction from knotweed root (acid or enzymatic work-up); chemical syntheses and yeast-fermentation routes exist but are minor. Isolated trans-resveratrol is a pale solid that must be protected from light to prevent trans→cis isomerisation ^{28Reference 28Nour V et al. · 2012Ultraviolet irradiation of trans-resveratrol and HPLC determination of trans- and cis-resveratrol in Romanian red winesView study →}.

Patents: not yet researched (future patent-loop pass).

Toxicity & Safety

At the doses in food and typical supplements, resveratrol is well tolerated and low in toxicity. The caveats attach to high-dose supplemental and pharmaceutical use, and to a few specific interactions.

Gastrointestinal upset is the common dose-limiter — nausea, diarrhoea and abdominal discomfort appear at gram-scale doses ^{21Reference 21Boocock DJ et al. · 2007ObservationalPhase I dose escalation pharmacokinetic study in healthy volunteers of resveratrol, a potential cancer chemopreventive agentView study →}. More seriously, the pharmaceutical micronised form SRT501 was trialled at 5 g/day in multiple myeloma and the study was halted for lack of efficacy and unacceptable toxicity — including a renal safety signal (cast nephropathy / renal failure events) ^{24Reference 24Popat R et al. · 2013A phase 2 study of SRT501 (resveratrol) with bortezomib for patients with relapsed and/or refractory multiple myelomaView study →}; this is a caution against very-high-dose use, particularly in people with renal risk or paraproteins. Resveratrol is also a phytoestrogen — an estrogen-receptor agonist (with mixed, context-dependent agonist/antagonist behaviour) in vitro — which is a reason for caution with concentrated supplements in hormone-sensitive conditions ^{25Reference 25Gehm BD et al. · 1997Resveratrol, a polyphenolic compound found in grapes and wine, is an agonist for the estrogen receptorView study →}. It modulates drug-metabolising enzymes (CYP1A2, CYP2D6, CYP3A4 and phase-II enzymes) in a human volunteer study, so interactions with CYP-metabolised medications are plausible ^{26Reference 26Chow HH et al. · 2010Resveratrol modulates drug- and carcinogen-metabolizing enzymes in a healthy volunteer studyView study →}, and it inhibits platelet aggregation in vitro, giving a theoretical additive bleeding risk with antiplatelet/anticoagulant drugs ^{27Reference 27Pace-Asciak CR et al. · 1995The red wine phenolics trans-resveratrol and quercetin block human platelet aggregation and eicosanoid synthesis — implications for protection against coronary heart diseaseView study →}.

Dosage

There is no established dose of resveratrol. Human trials have used roughly 150 mg to 1 g per day (with single tolerability doses up to 5 g), and consumer supplements are typically 250–500 mg/day ^{10,21Reference 10Liu Y et al. · 2015Meta-analysisEffect of resveratrol on blood pressure: a meta-analysis of randomized controlled trialsView study →Reference 21Boocock DJ et al. · 2007ObservationalPhase I dose escalation pharmacokinetic study in healthy volunteers of resveratrol, a potential cancer chemopreventive agentView study →}. The key context is that all of these are far above dietary intake — a glass of red wine provides only about 0.3 mg — so any “resveratrol from your diet” framing is meaningless at the doses that have any measured effect ^{2Reference 2Walle T et al. · 2004High absorption but very low bioavailability of oral resveratrol in humansView study →}.

These are research figures, not a recommendation — the honest position is that resveratrol’s clinical effects are small, inconsistent, and mostly confined to specific subgroups.

References