Pterostilbene
Pterostilbene, the dimethyl ether analogue of resveratrol
Written by Aaron CuhaReviewed Sep 2026
Also known as: trans-pterostilbene, 3,5-dimethoxy-4'-hydroxystilbene, Pteropure
One randomised human trial, 80 adults with raised cholesterol. At 250 mg a day it lowered systolic blood pressure by 7.8 mmHg and raised LDL cholesterol by 17.1 mg/dL in the same people. No human trial has measured an ageing endpoint of any kind.
Overview
Pterostilbene is sold as the better resveratrol, and on one narrow measure that claim is defensible. In rats given equimolar oral doses, resveratrol was about 20 percent bioavailable and pterostilbene about 80 percent, because replacing two hydroxyl groups with methoxy groups slows the glucuronidation that destroys resveratrol on its first pass through the liver.
That is a pharmacokinetic fact in rats, and it is where the case rests. The human evidence is a single randomised, double blind, placebo-controlled trial of 80 adults with total cholesterol at or above 200 mg/dL or LDL at or above 100 mg/dL, run in four arms for six to eight weeks. It measured lipids, blood pressure and weight.
It found two things. Systolic blood pressure fell 7.8 mmHg and diastolic 7.3 mmHg on the high dose, which is a real effect in the size range of a low dose antihypertensive. And LDL cholesterol rose by 17.1 mg/dL on pterostilbene alone (p = 0.001), an effect not seen when pterostilbene was combined with grape extract and attenuated in people already on a cholesterol medication. The authors' own one-sentence conclusion is that pterostilbene increases LDL and reduces blood pressure in adults.
A separate safety analysis of the same trial found no signal on liver, kidney or glucose markers at up to 250 mg a day, and concluded the compound is generally safe for use in humans at that dose. Safe and beneficial are different findings, and only one of them was demonstrated.
Mechanism of action
Structurally, resveratrol with two of its three hydroxyl groups replaced by methoxy groups. That change makes the molecule more lipophilic and a much poorer substrate for the phase 2 conjugation enzymes that clear resveratrol, which is the entire pharmacokinetic argument for it. The downstream biology attributed to it is the same list attributed to resveratrol: SIRT1 activation, AMPK signalling, NRF2 induction and antioxidant activity, most of it established in cell culture at concentrations well above what oral dosing produces in human plasma. Why it raises LDL cholesterol in people is not established. The trial that found the effect was not designed to explain it, and the observation that combining it with grape extract abolished the rise, and that background statin therapy attenuated it, has not been followed up.
Human evidence
One randomised controlled trial of 80 adults, reported across two papers, one for efficacy and one for safety. It ran six to eight weeks and measured lipids, blood pressure and weight. That is the entire human record.
- LDL cholesterol rose 17.1 mg/dL on pterostilbene monotherapy (p = 0.001), and lower doses also raised LDL without reaching significance.
- The LDL rise was not seen when pterostilbene was combined with grape extract, and was attenuated in participants already taking a cholesterol medication.
- Systolic blood pressure fell 7.8 mmHg and diastolic 7.3 mmHg on 125 mg twice daily.
- Participants not on a cholesterol medication showed a small reduction in body mass index of 0.62 kg per square metre (p = 0.012).
- No adverse drug reactions on hepatic, renal or glucose markers at up to 250 mg a day.
- No human trial has measured cognition, lifespan, healthspan, cardiovascular events or any ageing endpoint.
What this does not tell you: Eighty people split across four arms means roughly twenty per arm, six to eight weeks of exposure, and no follow-up. Both the benefit and the harm signal come from the same small trial and neither has been replicated. Blood pressure and LDL are both surrogates, and this is an unusual case where the compound moved one in the direction you want and the other in the direction you do not, in the same people, over the same weeks. Nobody has run the trial that would tell you which one matters more.
Reading the research record
A surrogate endpoint is a measurement that stands in for the thing you care about, on the assumption that moving it moves the outcome. That assumption has failed often enough to be treated as a claim rather than a given. Homocysteine is the canonical case: it predicts cardiovascular disease strongly in observational data, it can be lowered reliably by several cheap interventions, and when trials lowered it and then counted heart attacks, the events did not fall. The lesson is not that markers are worthless. It is that a trial reporting a marker has answered a smaller question than the one the buyer is asking, and the page should say which question was answered.
Pterostilbene is the clearest illustration in this batch of selective reporting by omission. The trial has two findings of similar statistical strength. One of them, the blood pressure reduction, is quoted constantly in product copy. The other, a 17.1 mg/dL rise in LDL cholesterol, is quoted almost nowhere, despite appearing first in the results section, first in the abstract conclusion, and in the paper's own title-level summary sentence.
There is no lifespan data for this compound in any species that this entry could locate. Its parent molecule, resveratrol, was tested by the Interventions Testing Program and did not extend lifespan in mice. Pterostilbene is better absorbed than a compound that failed, which is an argument about delivery and not about effect.
This archive's stated position on supplements is that you take something because a number on your bloodwork is out of range, and that you retest and stop if the number does not move. Applying that rule to this group is uncomfortable, because for most of them there is no deficiency state to correct and therefore no marker that tells you whether the bottle is doing anything. Where a compound here does move a readable number, the number is a surrogate rather than a deficiency, so moving it is not the same as fixing something that was broken.
The evidence, charted
Fig. 1 · evidence composition
2of 4 citations (50%) are in people
Counted from the citation list on this page. The Human count is the same number shown in the badge at the top. Both understate any literature larger than the sources we cite.
Fig. 2 · evidence over time
Evidence spans 4 distinct years, 2008 to 2014, counted from the citation list on this page. The newest citation on file is from 2014, more than five years ago; the published record may have gone quiet.
Fig. 3 · legal status at a glance
US
Not approved
UK
Not approved
AU
Not approved
CA
Not approved
Not approved in any of the four jurisdictions shown. A jurisdiction's classification is a regulatory fact, not a verdict on the science; see Legal status below for the full text and any notes.
Key studies & citations
- Human2014
Pterostilbene on metabolic parameters: a randomized, double-blind, and placebo-controlled trial.
80 adults with total cholesterol at or above 200 mg/dL and/or LDL at or above 100 mg/dL, in four arms for 6 to 8 weeks: pterostilbene 125 mg twice daily, 50 mg twice daily, 50 mg plus grape extract 100 mg twice daily, or placebo. LDL rose 17.1 mg/dL on pterostilbene monotherapy (p = 0.001), an effect not seen with the grape extract combination (p = 0.47) and attenuated by background cholesterol medication. Systolic blood pressure fell 7.8 mmHg (p < 0.01) and diastolic 7.3 mmHg (p < 0.001) on the high dose. Registered as NCT01267227.
Evidence-Based Complementary and Alternative Medicine - Human2013
Analysis of safety from a human clinical trial with pterostilbene.
The safety report from the same 80-patient trial, 91.3 percent completion, average age 54, 71 percent female. No adverse drug reactions on hepatic, renal or glucose markers and no statistically significant self-reported or major adverse reactions. The stated conclusion is that pterostilbene is generally safe for use in humans up to 250 mg a day. It reports safety only and makes no efficacy claim.
Journal of Toxicology - Animal2011
Pharmacokinetics, oral bioavailability, and metabolic profile of resveratrol and its dimethylether analog, pterostilbene, in rats.
Rats dosed orally for 14 consecutive days at equimolar levels. Resveratrol was approximately 20 percent bioavailable and pterostilbene approximately 80 percent, with markedly higher plasma levels of parent compound and sulfate metabolite for pterostilbene. This is the source of the better-absorbed-than-resveratrol claim, and it is a rat study. NIH funded.
Cancer Chemotherapy and Pharmacology - Animal2008
Cellular and behavioral effects of stilbene resveratrol analogues: implications for reducing the deleterious effects of aging.
19 month old Fischer 344 rats fed diets containing 0.004 or 0.016 percent pterostilbene, selected as the most effective of seven stilbenes in a cell screen. Pterostilbene reversed cognitive behavioural deficits and dopamine release deficits, and working memory correlated with pterostilbene levels in the hippocampus. Aged rats, not people, and a cognition endpoint rather than a lifespan one.
Journal of Agricultural and Food Chemistry
Frequently asked questions
Is pterostilbene better than resveratrol?
Better absorbed, in rats: about 80 percent oral bioavailability against about 20 percent for resveratrol at equimolar doses. Whether that translates into a better outcome in a person is untested. Resveratrol itself did not extend lifespan in multi-site mouse testing, so being a better-absorbed version of it is not in itself a reason to expect more.
Does pterostilbene raise cholesterol?
In the one human trial, yes. LDL cholesterol rose 17.1 mg/dL on pterostilbene alone at 250 mg a day, p = 0.001, and lower doses raised it too without reaching significance. The rise did not occur when it was combined with grape extract, and was smaller in people already on a cholesterol medication. This is a single trial of 80 people and has not been replicated in either direction.
Does it lower blood pressure?
In the same trial, systolic fell 7.8 mmHg and diastolic 7.3 mmHg at 125 mg twice daily. That is a meaningful size. It is also a six to eight week result in about twenty people on that dose, measuring a surrogate, with no cardiovascular event data of any kind.
Is there any anti-ageing evidence?
Not in humans, and not in the form of a lifespan result in any species that this entry could verify. The closest is a 2008 study in 19 month old rats where the compound reversed cognitive and dopamine release deficits, with working memory correlating with hippocampal levels. That is a cognition finding in aged rats.
How much has been tested in people?
Up to 250 mg a day for six to eight weeks, in 80 adults, in one trial. The safety analysis of that trial found no liver, kidney or glucose signal at that dose. Nothing is known about longer exposures or higher doses in humans.