Resveratrol
Also sold as: Trans-Resveratrol
Best-in-class: PolyResveratrol-SR
A sustained-release polyphenol (with added pterostilbene) studied as a sirtuin activator for cardiovascular and metabolic longevity.
Resveratrol quick facts
| Suggested dose | As directed (SR form for steadier exposure). |
| How often | Daily |
| Who it's for | Cardiovascular, metabolic and longevity experimenters. |
Honest summary: the story was better than the data. Human trials across metabolic and cardiovascular endpoints have been largely disappointing, and bioavailability is poor with rapid glucuronidation. It is a moderate CYP inhibitor and has antiplatelet activity. Kept because the mechanism debate is genuinely unresolved rather than settled against it, but expectations should be calibrated well below the marketing.
How Resveratrol actually works
Originally proposed as a direct SIRT1 activator, which is the entire basis of the red-wine longevity story. That specific finding was substantially challenged as an artifact of the fluorescent assay used, and current thinking favors indirect activation via AMPK and effects on phosphodiesterases. It has genuine antioxidant and anti-inflammatory activity independent of the sirtuin question.
Where to get Resveratrol
Buy PolyResveratrol-SR at Thorne →The evidence for Resveratrol
Graded by what exists behind each claim.
✅ Clinically validated
- RCTs show modest improvements in some metabolic and vascular markers (blood pressure, insulin sensitivity), with mixed results overall.
- Sustained-release aims to offset its very short half-life.
📊 Correlative data
- Polyphenol-rich diets are associated with cardiovascular and longevity benefits.
🧪 Theoretical / extrapolated benefits
- The 'sirtuin/longevity' promise from animal studies is much stronger than the human outcome data so far.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Resveratrol actually does
Two numbers decide whether anything else on this page matters, and both were measured in humans.
Number one. Ten healthy volunteers per dose level swallowed single doses of 0.5, 1, 2.5 or 5 grams of resveratrol. At the top dose — five grams, which is ten to fifty times what any capsule contains — peak plasma resveratrol was 539 ± 384 ng/mL, which the authors convert for you: 2.4 micromolar Boocock 2007.
Number two. Six volunteers took 25 mg. At least 70% of it was absorbed, and peak plasma resveratrol plus metabolites was 491 ± 90 ng/mL, with a plasma half-life of 9.2 ± 0.6 hours Walle 2004. Put the two side by side. A 200-fold larger dose produced roughly the same plasma number, because in the small-dose study almost all of what was circulating was sulfate and glucuronide rather than resveratrol itself. Absorption was never the problem. The problem is that the gut wall and the liver rewrite the molecule on the way through, and what arrives at the tissue is a conjugate with a sugar or a sulfate sitting on the hydroxyl that was doing the work.
Now the arithmetic for a real capsule. Thorne's PolyResveratrol-SR, which this site's card names, delivers 100 mg of trans-resveratrol per two-capsule serving Office of Dietary Supplements. That is one fiftieth of the five grams that reached 2.4 micromolar. Scale linearly and you land near 50 nanomolar — double digits, in the units of a hormone rather than of a nutrient. Treat that as an order of magnitude rather than a measurement, because the published dose–response is not perfectly proportional, but no reasonable correction moves it into micromolar. Cell work on sirtuins, AMPK and NF-kappaB in this literature runs at 10–100 micromolar. The gap between the dish and the capsule is two to three orders of magnitude.
And the mechanism the whole category is named after was an assay artifact. Resveratrol became famous as a SIRT1 activator, SIRT1 being the NAD+-dependent deacetylase that removes acetyl groups from PGC-1alpha, p53 and FOXO. Direct-activation testing against a panel including SRT1720, SRT2183 and SRT1460 concluded that none of them, resveratrol included, directly activates SIRT1 — the apparent activation depended on a fluorophore attached to the peptide substrate Pacholec 2010. Something is still happening in cells; the leading alternative is indirect, through phosphodiesterase inhibition raising cAMP and reaching AMPK by way of Epac1 and CaMKK-beta, with sirtuin signaling downstream rather than upstream. That is labeled extrapolation, and it has never been demonstrated in a human at any dose.
Cell, rodent, human — and where it stops
In cells. Hepatocytes, myotubes, endothelium and adipocytes, 10–100 micromolar unconjugated trans-resveratrol, 6–48 hours. Every headline mechanism in this literature was born in that window.
In rodents. Mice at 22–400 mg/kg/day in chow for weeks to months, which at the top end is a human-equivalent of roughly 32 mg/kg — about 2.2 grams a day for a 70 kg adult, taken every day for a year. Mice also conjugate resveratrol, but they were fed continuously rather than dosed once, which flattens the peak-and-trough problem a capsule creates.
In people, four trials that matter, and three of them are null or worse. Obese men, high-dose resveratrol, investigator-initiated, randomized and placebo-controlled: no improvement in insulin sensitivity, substrate metabolism or body composition Poulsen 2013. Nonobese women with normal glucose tolerance: no improvement in metabolic function Yoshino 2012. Aged men doing eight weeks of exercise training: the resveratrol group gained less than placebo on cardiovascular measures, which is the only trial in this cohort where a supplement made a training program work worse Gliemann 2013. And the epidemiology that was supposed to underwrite the whole red-wine story: urinary resveratrol metabolites in older community-dwelling adults were not associated with all-cause mortality, with inflammation, with cardiovascular disease or with cancer Semba 2014.
The specific obstacle, stated once and precisely. It is not that resveratrol is poorly absorbed — 70% of an oral dose gets in Walle 2004. It is that first-pass sulfation and glucuronidation convert almost all of it before it reaches the systemic circulation, so the parent compound peaks in the tens of nanomolar at a supplement dose while the biology was demonstrated in the tens of micromolar Boocock 2007. Every extrapolation from a dish to a bottle in this category has to cross that gap, and no published human study has shown it being crossed.
Resveratrol — which form, and does it matter
Trans, not cis, and the bottle should be opaque. Only trans-3,5,4'-trihydroxystilbene is the studied molecule. Ultraviolet light isomerizes trans to cis, and cis-resveratrol is not what any of the trials on this page administered. A clear jar in a lit shop window is a manufacturing defect wearing a merchandising costume; look for ‘trans-resveratrol’ stated explicitly and a purity figure, and note that the two on-market labels for the product this site names do say trans Office of Dietary Supplements.
The product this site links to is not a resveratrol supplement. It is a five-ingredient polyphenol blend. The filed Supplement Facts panel gives, per two-capsule serving: curcumin phytosome (Meriva) 100 mg, green tea phytosome (GreenSelect) 100 mg, quercetin phytosome 100 mg, trans-pterostilbene 100 mg and trans-resveratrol 100 mg Office of Dietary Supplements. The card on this site describes it as a sustained-release polyphenol with added pterostilbene, which accounts for two of the five actives and omits three. That matters in three directions at once: the pterostilbene carries its own measured LDL problem and has its own page here; the quercetin phytosome duplicates the ingredient on this site's quercetin page, so a reader following both takes it twice; and the green tea phytosome is a concentrated catechin extract, a class with its own liver-safety literature and its own page. Nobody buying ‘resveratrol’ expects four other polyphenols, and no trial has tested this combination against any endpoint.
Sustained release is a real idea aimed at a real number, and it is untested. The rationale is the 9.2-hour terminal half-life measured for resveratrol and its metabolites Walle 2004 sitting behind a very short-lived parent peak: spread the dose and you trade a high, brief parent concentration for a flatter, lower one. Whether that helps depends entirely on whether the active species is parent or conjugate, which nobody knows. No trial has compared a sustained-release resveratrol against an immediate-release one at matched daily milligrams for any endpoint.
Dose, plainly. The label's suggested use is two capsules once or twice daily Office of Dietary Supplements, which is 100–200 mg of trans-resveratrol a day. This site's card says only ‘as directed’. The human trials that found nothing were run at gram doses Poulsen 2013. A reader should know they are taking roughly a tenth of the dose that already failed.
What would have to be true, and how you would know it was not
1. Fasting insulin: no change at 12 weeks. This is the prediction that cuts against the product and it is the best-evidenced statement on the page. Two randomized trials at doses far above the label found no improvement in insulin sensitivity, in obese men and in normal-weight women Poulsen 2013Yoshino 2012. Draw fasting insulin and HbA1c before and at twelve weeks; predict both flat. If they move, look first at what else changed, because the trial evidence says this molecule did not do it.
2. If you are training, measure whether the training still works. Eight weeks of exercise in aged men produced smaller cardiovascular gains with resveratrol than with placebo Gliemann 2013. The read-out is the one you already have: a fixed workload, heart rate at that workload, and blood pressure, recorded weekly. If your usual training adaptation stalls in the first eight weeks on this compound, that is the published finding happening to you, not a coincidence.
3. ApoB and the full lipid panel, because of what is in the bottle rather than what is on the front of it. The blend contains 100 mg of trans-pterostilbene per serving Office of Dietary Supplements, and pterostilbene has its own measured LDL signal on its own page here. Lipid panel with ApoB before starting and at eight weeks; a rise of 15 mg/dL in LDL cholesterol is a reasonable pre-agreed line for stopping. Nobody taking a longevity blend should discover a lipid change by accident two years later.
4. Blood pressure down 2–4 mmHg systolic, at best, and attributable to the blend rather than to resveratrol. Home cuff, seven mornings averaged, before and at twelve weeks. State the confound out loud: four of the five actives in this product have vascular effects of their own, so a positive result identifies the capsule, not the molecule.
What will fool you: the story. Red wine, French paradox, sirtuins, yeast lifespan — it is the most attractive narrative in supplement science, and the urinary-metabolite cohort study that actually tested it in older adults found no association with mortality, cardiovascular disease, cancer or inflammation Semba 2014.
What nobody has tested yet
Nobody has done the experiment that would rescue this compound. Give a single oral dose, then measure free trans-resveratrol, resveratrol-3-O-sulfate and resveratrol-3-O-glucuronide separately in plasma and in a tissue biopsy — adipose is easy and skeletal muscle is standard in exercise physiology. If tissue sulfatase and beta-glucuronidase regenerate the parent locally, tissue concentrations could be far above plasma and the entire objection on this page collapses. If they do not, the objection is fatal. This costs one biopsy per subject and has never been published.
No human trial has ever measured a sirtuin substrate. Twenty years after the sirtuin claim was made and fifteen years after the direct-activation result went against it Pacholec 2010, no resveratrol trial has reported acetylated p53 or acetylated PGC-1alpha in peripheral blood mononuclear cells before and after dosing. That is one extra tube of blood and it is the direct read-out of the mechanism the whole product category is named after.
The exercise-blunting result has never been replicated or explained. One trial in aged men Gliemann 2013. The mechanistic hypothesis is that suppressing the transient oxidative signal produced by exercise removes the stimulus for adaptation, which would predict the effect is dose-dependent and timing-dependent — and therefore that taking it away from training might avoid it entirely. Nobody has tested a morning-dose versus evening-dose design against a training program, and that is a cheap, informative, and completely absent experiment.
And nobody has tested this blend as a blend. Five actives, one capsule, no trial Office of Dietary Supplements. The specific missing arm is the blend versus trans-resveratrol alone at matched resveratrol content, which would say whether the other four ingredients are doing the work, and whether the LDL and liver questions belong to them.
Resveratrol — its own safety story, not its category's
The antiplatelet effect is the one that actually reaches plasma. Stilbenes inhibit platelet aggregation, and unlike the sirtuin claim this one does not need micromolar tissue concentrations — platelets are in the compartment where the drug is. Additive with warfarin, apixaban, rivaroxaban, clopidogrel and aspirin at any dose. This is pharmacodynamic, not metabolic: it does not show up as a changed drug level, it shows up as bruising, nosebleeds or a raised INR. Stop at least two weeks before surgery or dental extraction and volunteer it, because the pre-operative form asks about prescriptions and not about polyphenols.
The CYP interaction is real and it is worst at the doses people use for longevity. Resveratrol inhibits CYP3A4 and CYP2C9 among others, so it raises exposure to the drugs those enzymes clear — and CYP2C9 is the enzyme that clears warfarin, which stacks a metabolic interaction on top of the pharmacodynamic one described above. Two mechanisms pointing the same way at the same drug is the definition of a combination worth avoiding without monitoring.
Weak estrogenicity, and the honest version of that sentence. Resveratrol is a stilbene, structurally related to diethylstilbestrol, and binds estrogen receptors weakly. In a hormone-sensitive cancer — breast, ovarian, uterine, prostate — that is an oncology conversation rather than a supplement decision. The awkward part is that the plasma-concentration argument running through this whole page cuts both ways: if the exposure is too low to activate a sirtuin, it is probably too low to matter at a receptor either. Both statements cannot be selectively true, and this page will not pretend otherwise.
The blend's risks are not resveratrol's risks. Four other actives ride in the same capsule Office of Dietary Supplements. The green tea phytosome puts a concentrated catechin extract into a daily longevity habit, a class this site covers separately and one whose liver-safety question is not resveratrol's to answer. The trans-pterostilbene carries a measured LDL effect discussed on its own page. And the quercetin phytosome brings quercetin's CYP3A4 and P-glycoprotein inhibition with it, so the drug-interaction section above understates this particular product. If you take a narrow-therapeutic-index drug, read the blend's whole panel, not the front of the bottle.
Gastrointestinal upset and diarrhea appear above about a gram a day, which is well above this label and well below the doses used in the trials that found nothing Poulsen 2013.
Sources read for this page
- Boocock DJ, et al. Phase I dose escalation pharmacokinetic study in healthy volunteers of resveratrol, a potential cancer chemopreventive agent.. Cancer Epidemiology, Biomarkers & Prevention 2007 · PMID 17548692
- Walle T, et al. High absorption but very low bioavailability of oral resveratrol in humans.. Drug Metabolism and Disposition 2004 · PMID 15333514
- Pacholec M, et al. SRT1720, SRT2183, SRT1460, and resveratrol are not direct activators of SIRT1.. Journal of Biological Chemistry 2010 · PMID 20061378
- Poulsen MM, et al. High-dose resveratrol supplementation in obese men: an investigator-initiated, randomized, placebo-controlled clinical trial of substrate metabolism, insulin sensitivity, and body composition.. Diabetes 2013 · PMID 23193181
- Yoshino J, et al. Resveratrol supplementation does not improve metabolic function in nonobese women with normal glucose tolerance. Cell Metabolism, 2012 · PMID 23102619
- Gliemann L, et al. Resveratrol blunts the positive effects of exercise training on cardiovascular health in aged men.. Journal of Physiology 2013 · PMID 23878368
- Semba RD, et al. Resveratrol levels and all-cause mortality in older community-dwelling adults.. JAMA Internal Medicine 2014 · PMID 24819981
- Office of Dietary Supplements, National Institutes of Health. PolyResveratrol-SR (Thorne) -- filed Supplement Facts panel: per 2-capsule serving, curcumin phytosome 100 mg, green tea phytosome 100 mg, quercetin phytosome 100 mg, trans-pterostilbene 100 mg, trans-resveratrol 100 mg. NIH Dietary Supplement Label Database, DSLD ID 336336
How you would know if it worked
The sirtuin story is why people buy this and it is not testable in a person. What the human trials measured is metabolic and vascular: modest changes in insulin sensitivity and blood pressure, mixed enough across trials that a null is an expected outcome rather than a disappointment. Fasting insulin is the sensitive end of that read and HbA1c is the confirmation, because insulin can wobble on one bad night of sleep and a three-month average cannot. Blood pressure is the other half and belongs to a cuff at home. If twelve weeks moves none of the three, you have the answer the animal data could not give you.
- Fasting Insulin Retest: Every 3–6 months, or 8–12 weeks after an intervention.
- HbA1c (Hemoglobin A1c) Retest: Every 3 months (matches red cell lifespan).
The cheapest panel carrying Fasting Insulin and at least one other of these is Am I Prediabetic?, at $19 — the panel is named for a different question, and the marker is the same marker. That is the whole cost of finding out.
Draw before you start, not after. A result with nothing to compare it to answers nothing.
Resveratrol — safety & side effects
- GI upset and diarrhea at high doses (above about 1 g).
- Antiplatelet activity and CYP inhibition — it raises levels of medications cleared by CYP3A4, CYP2C9 and others. Additive bleeding risk with anticoagulants and antiplatelets — warfarin, apixaban, rivaroxaban, clopidogrel, and aspirin at any dose. The interaction is pharmacodynamic rather than metabolic, so it does not show up as a changed drug level; it shows up as bruising, nosebleeds or a raised INR.
- Weakly estrogenic. Avoid if you have or have had a hormone-sensitive cancer (breast, ovarian, uterine, prostate) without oncology input. The mechanism that makes it useful is the mechanism that makes it a question in that setting.
- Poor oral bioavailability is the honest limit on the whole category — most of the impressive data comes from cells and animals at doses humans cannot reach.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this against it with a pharmacist or doctor — pharmacists are underused and free.
- When to take it, and what to take it with
- Which form actually absorbs
- Who it's worth it for
- Best-in-class brand pick
- Coach Cam's stacks and notes
- Fasted or with food, and when in the day
- Morning or night, and why that window
- Around training, or deliberately away from it
- What it must not share a window with
Everything above is free and stays free. Skool is where it becomes a plan — Resveratrol in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Resveratrol
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| Comprehensive Metabolic Panel (CMP) | Liver. Resveratrol inhibits CYP enzymes and interacts with a long drug list |
| hs-CRP (High-Sensitivity C-Reactive Protein) | The inflammation claim, measured |
| Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) | The cardiovascular claim, which trials treat far more cautiously |
The Longevity Baseline panel covers these in one order — 13 markers, $219.10 with the discount applied.
Check results you already have → · All 103 markers A–Z
Resveratrol — frequently asked questions
What is Resveratrol?
A sustained-release polyphenol (with added pterostilbene) studied as a sirtuin activator for cardiovascular and metabolic longevity.
What is the suggested dose of Resveratrol?
As directed (SR form for steadier exposure). This is a general reference for education only — statements have not been evaluated by the FDA and this is not medical advice.
Where can I find Resveratrol dosing and the full breakdown?
The suggested dose and the full evidence — clinical, correlative and theoretical — are on this page. What's inside Skool is when to take it, which form actually absorbs, the brand worth buying and Coach Cam's stacks.
Where can I buy Resveratrol?
Coach Cam sources Resveratrol from Thorne, with 10% off auto-applied at checkout — use the buy link on this page.
What Resveratrol is used for
Resveratrol appears under 2 goals in the goal router.
Related Longevity & Antioxidants supplements
Where this goes next
The pages here are the frameworks. The protocols — the dosing, the order to correct things in, the week-by-week schedule and what to retest — are inside Skool.