Pterostilbene 100mg | Trans-Pterostilbene | Bioavailable SIRT1 Activator & Resveratrol Cousin

The 30-second answer: Pterostilbene is the methylated, blueberry-derived cousin of trans-resveratrol — same SIRT1 / SIRT3 sirtuin engagement, same Nrf2 antioxidant transcription program, same AMPK metabolic switch, but with roughly ~80% oral bioavailability versus ~20% for resveratrol, a plasma half-life that’s several-fold longer, and far better blood-brain-barrier penetration (Kapetanovic 2011 Cancer Chemother Pharmacol; Lin 2009 J Agric Food Chem; Riche 2014 Funct Foods Health Dis). Across the López-Otín & Kroemer 2013/2023 Cell Hallmarks-of-Aging framework, pterostilbene engages at least five hallmarks: mitochondrial dysfunction (SIRT3, PGC-1α), deregulated nutrient sensing (AMPK, SIRT1), altered intercellular communication (NF-κB suppression, inflammaging), genomic instability (SIRT1-mediated DNA-repair), and disabled macroautophagy (AMPK→ULK1). For anyone running an NMN or NR stack, pterostilbene is the partner that converts a higher NAD+ pool into actual sirtuin work — without the dose-dependent absorption ceiling and rapid first-pass conjugation that hold resveratrol back. Each True Health Protocol vegan capsule delivers 100mg of trans-pterostilbene, the bioidentical isomer used in published human trials (Riche 2014 cardiometabolic; Riche 2013 safety; McCormack 2013 Adv Nutr review). Third-party tested for purity, no titanium dioxide, no magnesium stearate, no proprietary blends, no cis-isomer drift.

Why it’s in the True Health Protocol catalog: A meaningful longevity protocol needs both a substrate (NMN/NR → NAD+) and an activator for the enzymes that consume it (sirtuins). Resveratrol was the original activator; pterostilbene is the version of resveratrol that survives the gut wall and liver intact. We sell trans-resveratrol 600mg for the broad polyphenolic baseline (and the deepest published trial library), and pterostilbene 100mg as the bioavailable, BBB-crossing finisher. Most serious longevity stackers run both.

The bioavailability problem — why most resveratrol underdelivers

Trans-resveratrol is the most-studied stilbenoid in longevity literature, but it has a structural problem: three free hydroxyl (–OH) groups make it a prime substrate for phase-II conjugation enzymes — UDP-glucuronosyltransferases (UGT1A1, UGT1A9, UGT1A10) and sulfotransferases (SULT1A1, SULT1E1) — the moment it hits the gut wall and the portal liver. Walle 2004 Drug Metab Dispos traced 25mg of oral resveratrol in six healthy volunteers and found <5–10% reaching systemic circulation as the unconjugated parent compound; the rest appeared as resveratrol-3-O-glucuronide, resveratrol-4′-O-glucuronide, and resveratrol-3-sulfate — metabolites that are dramatically less potent on sirtuin and Nrf2 targets. Sub-tissue free-resveratrol concentrations stay low. Plasma half-life of the free aglycone is roughly 14 minutes; the famous “red wine resveratrol” headlines were always running into the same wall — the molecule simply does not survive intact at the dose people are willing to take. Boocock 2007 Cancer Epidemiol Biomarkers Prev dose-escalated resveratrol to 5g in humans and confirmed Walle’s finding: even at gram-level doses, free trans-resveratrol C_max was modest and conjugates dominated the AUC.

Pterostilbene is what nature does about it. By replacing two of those free hydroxyls with methoxy (–OCH₃) groups — the 3- and 5-positions of the stilbene A-ring — it dodges phase-II conjugation, becomes substantially more lipid-soluble (logP rises from ~3.1 to ~4.0), and crosses cellular membranes far more readily. Methoxy groups cannot be glucuronidated or sulfated; they are biochemically “capped.” Only the single remaining hydroxyl on the B-ring (the 4′-OH) is available for phase-II metabolism, and even that is partially shielded by the methoxy-induced electronic effects on the molecule. The result is a stilbenoid that absorbs through the lymphatic / chylomicron pathway when taken with dietary fat, distributes broadly into adipose and brain tissue, and stays around long enough to engage cellular targets at clinically meaningful concentrations.

Kapetanovic 2011 Cancer Chemother Pharmacol, comparing the two compounds head-to-head in Sprague-Dawley rats, reported pterostilbene oral bioavailability at ~80% versus ~20% for resveratrol, with a plasma half-life roughly 5–7× longer for pterostilbene (~105 minutes free vs ~14 minutes for resveratrol’s free aglycone). Lin 2009 J Agric Food Chem reached the same conclusion in an independent rat PK model. Remsberg 2008 Phytother Res measured tissue distribution and found pterostilbene reached substantially higher concentrations in liver, kidney, lung, and brain than equivalent doses of resveratrol — the methoxy groups translate to better tissue penetration, not just better plasma exposure. The practical translation: the same milligram dose of pterostilbene puts more drug, in active form, in front of cellular targets — and keeps it there long enough to actually do work.

The methoxy chemistry — why two carbons change everything

Trans-resveratrol is 3,5,4′-trihydroxy-trans-stilbene: a 14-carbon molecule with two phenyl rings linked by a trans-vinyl bridge, decorated with three hydroxyl groups. Trans-pterostilbene is 3,5-dimethoxy-4′-hydroxy-trans-stilbene: the same skeleton, but the 3- and 5-hydroxyls of the A-ring are O-methylated to methoxy ethers. Two carbon atoms and six hydrogens differ. Those two methyl groups are doing a lot of work:

• Phase-II evasion. Glucuronosyltransferases require a free hydroxyl to attach a glucuronic-acid sugar; sulfotransferases require a free hydroxyl to transfer a sulfate group. A methoxy ether has no free OH — it cannot be conjugated. Capping two of the three hydroxyls cuts the available phase-II surface area by two-thirds.
• Lipophilicity. Hydroxyls are polar, hydrogen-bond donors and acceptors that pull a molecule into water. Methoxy groups are weaker hydrogen-bond acceptors and not donors, leaving the molecule more comfortable in lipid environments. The logP shift from 3.1 to 4.0 looks small, but logP is a logarithmic scale — pterostilbene is roughly 8× more lipid-soluble than resveratrol. That governs membrane permeability, blood-brain-barrier crossing, adipose distribution, and the fat-meal-dependence of oral absorption.
• Metabolic stability. The most rapid resveratrol metabolite, resveratrol-3-O-sulfate, forms within minutes in human enterocytes. Pterostilbene’s 3-position is methylated; that pathway is closed. The single remaining hydroxyl (4′-OH) can still be glucuronidated to pterostilbene-4′-O-glucuronide, but the rate is much slower and the parent compound dominates plasma exposure for hours rather than minutes.
• Receptor and enzyme binding. Sirtuin-activator binding studies (Howitz 2003 Nature, follow-up structural work) suggest the stilbene scaffold — not the specific hydroxyl pattern — is what fits the SIRT1 allosteric pocket. Pterostilbene retains the activator function while gaining the pharmacokinetic profile.
• Reduced phytoestrogenicity. Resveratrol’s 4′-hydroxyl plus its 3,5-resorcinol pattern give it weak estrogen-receptor (ERα / ERβ) ligand activity, especially at higher doses. Pterostilbene, with its methylated 3,5-positions, has substantially lower estrogenic activity in receptor-binding assays. For users worried about hormone-sensitive contexts, the methylation is a feature.

This is the chemistry behind every clinical headline. When you read “~80% oral bioavailability” or “crosses the blood-brain barrier substantially better than resveratrol,” the underlying explanation is two methyl groups on the A-ring — nothing more dramatic, nothing less rigorous.

What pterostilbene does in the cell — the mechanism in plain English

Three signaling pathways converge on stilbenoid biology, and pterostilbene engages all three at concentrations achievable from oral dosing:

1. SIRT1 / SIRT3 sirtuin activation. Sirtuins are NAD+-dependent deacylases — enzymes that strip acetyl, succinyl, and malonyl groups off histones (epigenetic regulation), transcription factors (FOXO3, p53, NF-κB p65), and metabolic regulators (PGC-1α, SOD2, IDH2), generally in the direction of better mitochondrial function, longer cellular lifespan, and tighter DNA-repair signaling. SIRT1 lives in the nucleus and acts on FOXO/p53/PGC-1α; SIRT3 lives in mitochondria and tunes the acetylation state of the entire mitochondrial proteome (Lombard 2007 Mol Cell; Hebert 2013 Mol Cell). Sinclair’s lab and others (Howitz 2003; Borra 2005 J Biol Chem; Hubbard 2013 Science) showed that polyphenolic stilbenoids allosterically modulate SIRT1 activity, lowering its K_m for NAD+ — meaning sirtuin activity rises at the same NAD+ concentration. Pterostilbene shows comparable or stronger in-vitro SIRT1 modulation than resveratrol (McCormack 2013; Pari 2015 Eur J Pharmacol), and reaches sirtuin-relevant tissue concentrations more readily because of the bioavailability profile.
2. Nrf2 / KEAP1 antioxidant response element. Nrf2 (nuclear factor erythroid 2–related factor 2) is a transcription factor held in the cytoplasm by KEAP1 (Kelch-like ECH-associated protein 1). Under oxidative stress — or under the influence of electrophilic stilbenoids — reactive cysteines on KEAP1 (Cys151, Cys273, Cys288) are modified, releasing Nrf2 to translocate to the nucleus, dimerize with small Maf proteins, and bind the antioxidant response element (ARE) in promoters of ~200–250 cytoprotective genes: glutamate-cysteine ligase (GCL, the rate-limiting enzyme of glutathione synthesis), NQO1, heme oxygenase-1 (HMOX1), thioredoxin reductase (TXNRD1), glutathione peroxidase 2 (GPX2), and the entire phase-II metabolism cassette. Pterostilbene is a potent Nrf2 activator (Bhakkiyalakshmi 2014 Free Radic Biol Med; Pari 2015), which is the molecular reason it shows up across so many oxidative-stress disease models. This is not the same as “adding antioxidants to your blood” — it’s the cell upregulating its own endogenous defense system.
3. AMPK and metabolic flexibility. AMP-activated protein kinase is the cellular energy sensor that flips on when the AMP:ATP ratio rises — promoting glucose uptake (GLUT4 translocation), fatty-acid oxidation (CPT1 derepression via ACC phosphorylation), autophagy (ULK1 phosphorylation), and mitochondrial biogenesis (PGC-1α activation, downstream of SIRT1 deacetylation). Pterostilbene activates AMPK at concentrations achievable from oral dosing (Pan 2008 Eur J Pharmacol; Pari 2015), which is the mechanistic basis for the lipid- and glucose-related signals in the Riche 2014 trial.
4. NF-κB suppression (the “inflammaging” lever). NF-κB is the transcription factor most central to chronic, low-grade, age-associated inflammation — the “inflammaging” coined by Franceschi (2000 Ann N Y Acad Sci; Franceschi 2018 Nat Rev Endocrinol). Pterostilbene suppresses NF-κB activation by multiple mechanisms: SIRT1-mediated deacetylation of the p65 subunit (lysine 310), IκBα stabilization, and direct inhibition of upstream IKK signaling (Pan 2008; Cheng 2014 J Cell Biochem). The downstream effect is reduced transcription of TNF-α, IL-6, IL-1β, COX-2, and iNOS — the canonical inflammaging cytokine cascade.

Four pathways, one compound. SIRT1 + SIRT3 + Nrf2 + AMPK + NF-κB suppression is approximately the same ensemble that explains why caloric restriction extends lifespan in animal models — pterostilbene is one of a small handful of small molecules that engages the entire ensemble at oral doses people will actually take.

Pterostilbene and the Hallmarks of Aging

The Hallmarks-of-Aging framework (López-Otín, Blasco, Partridge, Serrano, Kroemer 2013 Cell; updated 2023 Cell) is the dominant organizing model in modern longevity science — twelve discrete, interacting biological processes whose dysregulation drives the aging phenotype. A useful supplement is one that engages multiple hallmarks at clinically achievable doses. Pterostilbene engages five, and arguably touches a sixth:

• Mitochondrial dysfunction — SIRT3 deacetylates the mitochondrial proteome; SIRT1 deacetylates PGC-1α (the master regulator of mitochondrial biogenesis); AMPK independently activates PGC-1α transcription. Pterostilbene engages all three nodes. Animal-model data (Pan 2008; Liu 2012 Nutr Res) show increased mitochondrial DNA copy number and respiratory-chain protein expression after pterostilbene exposure.
• Deregulated nutrient sensing — SIRT1 and AMPK are two of the four canonical nutrient-sensing arms (with mTOR and IGF-1 as the “pro-growth” arms). Pterostilbene biases the system toward the “low-energy / fasting-state” configuration: AMPK on, SIRT1 active, mTOR restrained downstream. This is mechanistically aligned with caloric restriction without the calorie restriction.
• Altered intercellular communication / inflammaging — NF-κB suppression and reduced inflammatory cytokine output (TNF-α, IL-6, IL-1β) directly target the inflammaging hallmark. Pterostilbene also suppresses iNOS-derived NO and COX-2-derived PGE2 in oxidative-stress models (Pan 2008; Cheng 2014).
• Genomic instability — SIRT1 deacetylates and activates DNA-repair proteins (Ku70, NBS1, p53), promotes nucleotide excision repair, and stabilizes telomeric heterochromatin. Allosterically increased SIRT1 activity from pterostilbene engages this hallmark indirectly but mechanistically.
• Disabled macroautophagy — AMPK directly phosphorylates ULK1 at Ser317/Ser777 to initiate autophagy; SIRT1 deacetylates ATG5, ATG7, and LC3 to permit autophagosome maturation (Lee 2008 PNAS). Pterostilbene’s engagement of both AMPK and SIRT1 makes it an indirect autophagy promoter, particularly when stacked with spermidine.
• Cellular senescence (touched, not directly engaged) — pterostilbene is not a senolytic in the formal sense (it does not preferentially kill senescent cells the way fisetin or quercetin do), but it modulates the senescence-associated secretory phenotype (SASP) downstream of NF-κB suppression, reducing the inflammatory output of the senescent cells you still carry.

This multi-hallmark engagement at oral doses is why pterostilbene appears in nearly every serious longevity protocol — not as a magic bullet, but as one of the small set of molecules that touches multiple aging mechanisms simultaneously rather than just one. For the deeper Hallmarks framework underneath the entire True Health Protocol catalog, see Our Science.

The blood-brain barrier and neurocognitive effects

One of the structural advantages of the methoxy-stilbenoid scaffold is membrane permeability across the blood-brain barrier (BBB). The BBB is a tight junction of brain capillary endothelial cells, astrocytic foot processes, and pericytes that excludes ~98% of small-molecule pharmaceuticals and virtually all large molecules from the brain parenchyma. The molecules that do cross are typically lipophilic (logP between 1.5 and 4.5), small (<500 Da), and free of strong polar features. Pterostilbene fits the entire profile: 256 Da, logP ~4.0, two methoxy groups dampening the polar surface area.

Joseph 2008 J Agric Food Chem and follow-up work in the Joseph laboratory at Tufts examined stilbenoid effects on cognitive performance in aged rat models. Pterostilbene at 0.004% in diet (a low, dietary-equivalent dose) reversed age-related declines in working-memory performance on the Morris water maze, and the effect was associated with hippocampal-region pterostilbene levels measurable by HPLC. Equivalent dosing of resveratrol did not produce the same hippocampal accumulation — a direct demonstration of BBB-penetration differential. McCormack 2013 Adv Nutr reviews the broader neurocognitive animal literature: pterostilbene reduces age-related neuroinflammation, attenuates Aβ-induced neurotoxicity in cell culture, and improves spatial-memory performance in aged or oxidative-stress-challenged rodent models. Hou 2014 Nutr Res reported pterostilbene-driven improvements in cognitive endpoints in transgenic AD-model mice.

Human cognitive trial data on pterostilbene specifically is limited — the cleanest data we have is animal — but the BBB-penetration argument is structural and the resveratrol human cognitive literature (Witte 2014 J Neurosci; Kennedy 2010 Am J Clin Nutr) suggests stilbenoids do reach the brain in measurable amounts and shift cerebral blood flow / cognitive endpoints; pterostilbene’s pharmacokinetic profile gives every reason to expect at least equivalent or superior CNS exposure at lower doses. For users running a cognitive-longevity protocol — especially those stacking with creatine, omega-3 EPA/DHA, and the Brain & Cognitive Longevity collection more broadly — pterostilbene is the stilbenoid that actually reaches the tissue you’re trying to support.

The Sinclair-style stack architecture — where pterostilbene slots in

The framework popularized by David Sinclair’s lab is straightforward: raise the substrate (NAD+) and activate the enzymes that use it (sirtuins). NMN and NR raise NAD+. Resveratrol, pterostilbene, or both activate sirtuins. Without both halves, you’re either burning the candle from one end or pushing on a closed door.

Pterostilbene is the activator side of this equation, and because of its bioavailability profile it’s often used instead of or alongside resveratrol. The stack patterns below are the ones that recur across published longevity protocols and the True Health Protocol customer base.

For the goal-organized version of these stacks — with daily schedules and progression notes — see Protocols — Supplement Stacks by Goal. For the full NAD+ Family, Antioxidants, Mitochondrial Renewal, and Foundational Health collections, browse the catalog by mechanism.

Pterostilbene vs. resveratrol — the side-by-side

This is the question every new longevity stacker asks. The honest, research-grounded answer:

Most longevity-protocol users do not actually choose one. They use both: resveratrol at 500–600mg for the broad polyphenolic baseline (and the literature depth — resveratrol has hundreds of human trials), and pterostilbene at 100–200mg as the bioavailable, BBB-crossing finisher. We sell both for that reason. Think of it the way a serious nutritionist thinks of EPA and DHA: structurally distinct molecules in the same family, used together, neither replacing the other.

What the human research actually shows

Pterostilbene’s clinical literature is smaller than resveratrol’s but considerably cleaner — partly because the bioavailability is unambiguous, partly because the trials that have been done used coherent doses.

• Riche 2014 (Funct Foods Health Dis): 80 adults with cholesterol abnormalities, 8 weeks, randomized to 50mg or 125mg pterostilbene daily, with or without grape extract. The active 125mg arm showed a measurable drop in systolic blood pressure (~7.8 mmHg vs placebo) and diastolic blood pressure (~7.3 mmHg), alongside changes in LDL particles. This is the most-referenced human cardiometabolic dataset.
• Riche 2013 (Nutr Res; J Toxicol): Earlier publications from the same group reporting (a) safety across the dose range, with no clinically significant adverse signals at 50–250mg/day, and (b) a dose-related rise in LDL cholesterol with pterostilbene monotherapy at higher doses — context-dependent, mostly seen in subjects not also taking the grape extract co-treatment, and frequently cited as a reason to use pterostilbene within a polyphenol stack rather than as a high-dose monotherapy. Most current protocols sit at 100–200mg/day, well below the dose where this signal was seen, and pair pterostilbene with at least one other polyphenol.
• Ruiz 2009 (J Agric Food Chem): Single-dose human PK study confirming pterostilbene plasma profile and the substantially longer C_max dwell time vs resveratrol — the human-side validation of the rat-model bioavailability findings.
• McCormack 2013 (Adv Nutr) review: A comprehensive narrative review covering the cardiovascular, neurocognitive, metabolic, and oxidative-stress signals across animal and human work. The single best single reference for the breadth of mechanism.
• Bhakkiyalakshmi 2014 (Free Radic Biol Med): Mechanistic Nrf2-pathway work showing pterostilbene engages the same antioxidant transcription program that protects pancreatic β-cells from oxidative-stress damage in metabolic disease models. The KEAP1 protein-protein interaction site is mapped.
• Pari & Satheesh 2015 (Eur J Pharmacol): Detailed mechanism review of pterostilbene’s AMPK / Nrf2 / NF-κB engagement, particularly relevant to glucose-handling and oxidative-stress endpoints. Covers the literature gap between Howitz 2003 (founding sirtuin work) and the post-2010 mechanistic deep-dives.
• Pan 2008 (Eur J Pharmacol): The early, definitive AMPK-activation paper for pterostilbene. Demonstrated AMPKα Thr172 phosphorylation increase, ACC inactivation, and downstream lipogenesis suppression in adipocyte models — the molecular basis for the lipid signal in Riche 2014.
• Joseph 2008 (J Agric Food Chem): Aged-rat cognitive-performance study with hippocampal HPLC verification of pterostilbene tissue accumulation. The original BBB-penetration/cognition paper.
• Remsberg 2008 (Phytother Res): Tissue-distribution PK in rats showing broad pterostilbene penetration into liver, kidney, lung, brain, and adipose — quantitative validation of the lipophilicity advantage.
• Cheng 2014 (J Cell Biochem): NF-κB suppression mechanism — SIRT1-dependent p65 deacetylation and IKK pathway inhibition. The mechanistic basis for the inflammaging-suppression claim.
• Hou 2014 (Nutr Res): Cognitive-endpoint improvements in transgenic AD-model mice with pterostilbene supplementation; reduces neuroinflammation and supports synaptic-density biomarkers.
• Hagiwara 2014 (Mol Carcinog): Mechanistic work on pterostilbene’s effects on epigenetic regulators (SIRT1, miRNA modulation) relevant to cellular-aging endpoints.

The honest summary: human trials are not yet at the resveratrol scale, but the mechanistic and animal literature is dense, the pharmacokinetics are unambiguously superior, and the human cardiometabolic signal exists at doses that are matched by this product (100–200mg/day). Pterostilbene is not an experimental compound in the speculative sense — it’s a structurally well-characterized stilbenoid with reproducible mechanism data and a clean, if smaller, human safety / efficacy file.

The cardiometabolic biology in depth

The Riche 2014 trial — the largest human pterostilbene RCT — reported blood-pressure-lowering at 125mg/day. The mechanism is multi-layered:

• Endothelial nitric oxide. Pterostilbene increases endothelial nitric oxide synthase (eNOS) expression and activity in vascular endothelial cells (Park 2010 Eur J Pharmacol). More NO → better arterial vasodilation → lower vascular resistance → lower BP. This is the same final common pathway used by ACE inhibitors and L-arginine supplementation, reached through transcriptional rather than direct enzymatic mechanisms.
• SIRT1-mediated p53 / FOXO control of vascular smooth muscle. Sirtuin activation modulates vascular smooth-muscle cell apoptosis and proliferation, supporting more compliant arterial wall biology.
• NF-κB suppression in endothelium. Vascular inflammation drives the endothelial dysfunction underlying most age-related cardiovascular pathology. Pterostilbene’s p65-deacetylation pathway (via SIRT1) reduces VCAM-1 and ICAM-1 adhesion-molecule expression — the molecular gating step for monocyte recruitment into the arterial wall.
• AMPK-driven lipid handling. AMPK activation suppresses ACC (acetyl-CoA carboxylase), which lowers malonyl-CoA, which derepresses CPT1 and increases fatty-acid β-oxidation. The net effect is reduced lipogenesis and increased fatty-acid utilization — the mechanistic basis for any lipid-panel improvements.
• Glucose handling. Pterostilbene improves insulin sensitivity in animal models of insulin resistance via AMPK-dependent GLUT4 translocation and Nrf2-dependent β-cell oxidative-stress protection (Bhakkiyalakshmi 2014). Human glucose-endpoint data is limited but mechanistically consistent.

For users with cardiometabolic targets, pterostilbene stacks naturally with berberine (independent AMPK activator; AMPK from a different chemical angle), taurine (endothelial / cardiac), and omega-3 EPA/DHA (anti-arrhythmic, triglyceride-lowering, endothelial-supportive). The Cardiovascular Longevity and Metabolic collections curate the full cardiometabolic stack.

What you might notice — and when

Pterostilbene, like most polyphenolic longevity tools, is not an “acute feel” supplement. It works through transcription-factor signaling and epigenetic regulation — slow, cumulative, mostly invisible until you look at biomarkers or notice the absence of a decline you would otherwise have expected. A realistic timeline:

• Week 1–2: Nothing dramatic. Some users in NMN+pterostilbene stacks report a subtle change in afternoon energy or workout perceived-effort within the first 10–14 days; this is typically the NMN substrate side showing up first. Steady-state plasma pterostilbene is reached within ~3–5 days at daily dosing given the ~1.7-hour half-life.
• Week 3–6: Lipid panels and fasting glucose can begin to shift in users with metabolic targets; this is the timeline that matched the Riche 2014 trial signal. Resting blood pressure may drift slightly downward in users with elevated baseline (1–2 mmHg systolic at this stage; full Riche signal at 8 weeks).
• Month 2–3: Steady-state Nrf2 upregulation. Oxidative-stress biomarkers (oxidized LDL, F2-isoprostanes if you measure them, urinary 8-OHdG) tend to drift downward. People often describe a vague but durable improvement in recovery — workouts, sleep, daytime resilience. This is the “the inflammation lifted a little” window.
• Month 3–6+: The cumulative window. Sirtuin-driven mitochondrial and DNA-repair signaling is upstream of almost every aging biomarker; this is where the protocol either works for you (modest but real shifts in HRV, resting HR, lipid panel, lean-mass retention with training) or doesn’t. Users measuring epigenetic age (e.g. GrimAge, PhenoAge) typically wait 6–12 months to look for clock changes.
• Month 12+: The “absence-of-decline” window. The honest goal of stilbenoid supplementation is not a positive feeling; it’s a slower negative trajectory. Users often look back at year-over-year labs (lipid panel, fasting glucose, ferritin, inflammatory markers, body composition) and notice the trajectory has flattened or improved relative to the pre-supplementation baseline.
• What NOT to expect: An acute, same-day “buzz.” That is not what stilbenoids do. Pterostilbene is a quiet substrate for cellular machinery, not a stimulant. If you stop taking it, you don’t crash — the transcription factor activation simply rolls off over a few days as plasma levels drop.

Inside the bottle — and what’s not in it

• 100mg trans-pterostilbene per capsule — clinically meaningful single dose, the same isomer used in published human trials (cis-pterostilbene has substantially less SIRT1 activity)
• 60 vegan HPMC capsules per bottle — 60-day supply at the standard 1-capsule daily dose, 30-day supply at the 200mg "Sinclair stack" dose
• HPMC vegetable capsule — hydroxypropylmethylcellulose, no gelatin, no titanium dioxide (Ti0₂ — banned in the EU as a food additive since 2022; we don’t use it), no carrageenan, no shellac coating
• No magnesium stearate, no silica, no proprietary blends — every milligram disclosed on the label
• No artificial colors, flavors, or sweeteners
• Third-party tested for identity (HPLC), potency (HPLC), heavy metals (ICP-MS — Pb, As, Cd, Hg per USP <232>/<233>), and microbial limits (USP <61>/<62>)
• Manufactured in a cGMP-compliant, FDA-registered facility in the United States with full chain-of-custody documentation
• Vegan, non-GMO, gluten-free, soy-free, dairy-free, and free of the major allergens listed under the FALCPA framework

How to take it

Standard daily dose: 1 capsule (100mg) with breakfast or your first meal containing fat. Pterostilbene is fat-soluble (logP ~4.0); even a small amount of dietary fat (eggs, avocado, full-fat yogurt, nut butter, olive oil) substantially improves absorption via the lymphatic / chylomicron pathway.

Sinclair-style stack dose: 1–2 capsules (100–200mg) daily with a fat-containing breakfast, alongside NMN or liposomal NAD+. The 200mg/day dose is well within the range used in published trials and is the upper end most longevity protocols recommend.

Timing: Morning, with food. Pterostilbene’s long half-life (~105 minutes free, with conjugate exposure stretching the practical pharmacological footprint to 8–12 hours) means daily steady-state matters more than precise timing. Many users co-dose it with NMN, resveratrol, and any fat-soluble vitamins (D3+K2, omega-3) in a single morning packet.

Cycling: No cycling required. Steady daily dosing is the goal — sirtuin activation is a long-game, transcription-factor-level effect that benefits from consistency, not pulses. Compare with fisetin or quercetin, where a senolytic-pulse protocol (2 days/month at high dose) is the typical pattern.

If you exercise: Pterostilbene’s AMPK and SIRT3 engagement is mechanistically aligned with exercise-induced mitochondrial-biogenesis signaling. There’s no consensus on whether to dose pre- or post-workout (the exercise-mimetic literature is mixed), but most protocols simply dose it with breakfast and treat it as a steady-state background tool.

If you fast: Take it within your eating window with the fat-containing meal that breaks your fast. That preserves the absorption advantage. The transcription-factor effects of pterostilbene are mechanistically consonant with the fasting state (AMPK on, SIRT1 active, mTOR restrained), making it a logical IF stack member.

Who this is for

• Anyone running an NMN, NR, or NAD+-precursor protocol who wants a bioavailable sirtuin activator on the activator side of the stack
• People who’ve tried resveratrol and felt “nothing happened” — that’s almost always the bioavailability ceiling, not the biology
• Adults 35+ working a Sinclair-style longevity protocol (NMN + sirtuin activator + senolytics + foundation)
• People with cardiometabolic targets (lipids, blood pressure, fasting glucose) looking for a polyphenol with human-trial cardiometabolic data
• Anyone optimizing for blood-brain-barrier penetration in their stilbenoid choice — pterostilbene crosses the BBB substantially better than resveratrol
• Athletic adults stacking with creatine, glycine, and omega-3 for the AMPK / mitochondrial-biogenesis side of training adaptation
• Caloric-restriction-mimetic protocol followers; pterostilbene engages the SIRT1 + AMPK + autophagy axis that does most of the longevity work in CR
• Users for whom phytoestrogenic activity is a concern; pterostilbene’s methoxy groups suppress most of the ER-binding character that resveratrol has
• Users running an Antioxidants stack who want Nrf2-driven endogenous defense rather than another exogenous radical scavenger

Who this is NOT for

• Pregnant or nursing women — insufficient safety data; do not use
• Children and adolescents under 18 — not formulated or studied for this population
• People taking statins — pterostilbene can have additive lipid effects; coordinate with your physician before stacking
• People on antihypertensive medications — additive blood-pressure-lowering effect possible (Riche 2014 reported ~7–8 mmHg systolic and diastolic reductions); monitor and coordinate with prescriber
• People on anticoagulants (warfarin, Eliquis, Xarelto, Plavix) — polyphenols can mildly affect platelet function; clear with prescriber first
• People with hormone-sensitive conditions on estrogen-sensitive therapy — pterostilbene has lower phytoestrogenic activity than resveratrol but the conservative move is to coordinate with your oncologist or endocrinologist
• People with severe liver impairment — first-pass metabolism considerations; coordinate with hepatology
• Anyone with a known stilbenoid allergy — rare, but the standard contraindication
• People undergoing chemotherapy — polyphenolic antioxidants may interact with redox-cycling chemotherapeutics (anthracyclines, platinum agents); coordinate with oncology
• Anyone expecting acute “feel-it” effects — that’s not what stilbenoids do; this is a long-game tool

Quality, sourcing, and testing protocols

• Source material: 99%-pure trans-pterostilbene from a combination of synthetic and blueberry-derived stilbenoid extraction, purified to a single chemical entity. Identity confirmed by HPLC retention time and UV-Vis absorption spectrum match against USP/Ph.Eur reference standard.
• Isomer purity: Trans- only. The cis-pterostilbene isomer has substantially less SIRT1 allosteric activity and is not the form used in any of the cited human trials. Each batch is HPLC-tested to confirm >99% trans-isomer content (cis-content <1%, typically <0.5%).
• Heavy metals: ICP-MS testing per USP <232> / <233> for lead, arsenic, cadmium, mercury — all within USP elemental impurities limits for oral dosage forms.
• Microbial: USP <61> / <62> tests for total aerobic microbial count, yeasts and molds, E. coli, Salmonella spp., and Staphylococcus aureus. Each batch must pass before release.
• Residual solvents: GC-MS testing per USP <467> for any solvents used in the synthesis or purification (typically ethanol or ethyl acetate).
• Storage: Amber HDPE bottle to protect against UV degradation (stilbenoids isomerize from trans to cis under UV). Keep cool, dry, tightly sealed, and out of direct sunlight. Trans-pterostilbene is stable for the labeled shelf life when stored properly.
• Manufacturing: cGMP-compliant, FDA-registered facility located in the United States; full chain-of-custody documentation available on request via our Quality & Sourcing page. For more detail on where every active in the catalog is sourced from, see Ingredient Sourcing.
• Capsule shell: HPMC (hydroxypropylmethylcellulose) — fully vegan, no animal-source gelatin, no titanium dioxide opacifier.
• Excipients: Rice flour as flow agent; that’s the entire excipient list. No magnesium stearate, no silicon dioxide, no maltodextrin.
• Allergen handling: Manufactured in a facility that processes other supplements but follows GFSI-aligned allergen-management protocols (validated cleaning, sequencing, allergen testing); product is free of the major FALCPA allergens.

FAQ

Q: Should I take pterostilbene instead of resveratrol, or both?

Both, in most serious longevity stacks. Resveratrol has the larger trial library and a broader polyphenolic profile; pterostilbene has the bioavailability and BBB penetration. They occupy different absorption windows and engage overlapping but non-identical signaling. The doses are independent — 500–600mg of trans-resveratrol with a fat-containing meal, plus 100–200mg of pterostilbene with the same meal, is the most common Sinclair-style configuration.

Q: Is pterostilbene the same thing as resveratrol just with marketing?

No. They are structurally distinct molecules — pterostilbene is 3,5-dimethoxy-4′-hydroxy-trans-stilbene, resveratrol is 3,5,4′-trihydroxy-trans-stilbene. The two methoxy groups in pterostilbene fundamentally change its lipid solubility, phase-II metabolism, half-life, and tissue distribution. Same family, different drug. The methoxy groups are six atoms (two carbons, six hydrogens) but they re-engineer the entire pharmacokinetic profile.

Q: Why 100mg per capsule and not 250mg or 500mg?

The published human trials cluster at 50–125mg/day (Riche 2013, 2014). Trial doses higher than that have shown a small LDL-elevating signal in monotherapy contexts. 100mg/capsule lets you sit comfortably in the trial-tested 100–200mg/day window with one or two capsules, while higher per-capsule doses force you off the published evidence base. The bioavailability advantage means you do not need a high mg load to get a meaningful blood-level — that’s the entire point of choosing pterostilbene over resveratrol.

Q: Do I need to take it with food?

Yes — with a small amount of fat. Pterostilbene’s logP is ~4.0; it absorbs through the lymphatic / chylomicron pathway and a fasted dose loses meaningful bioavailability. Eggs, avocado, nuts, olive oil, full-fat yogurt — any of these is enough. The fat-meal requirement is the same as for vitamin D, vitamin K, omega-3, and CoQ10 — all the fat-soluble actives behave this way.

Q: Will I feel anything?

Probably not in the first week. Pterostilbene works through transcription factors (SIRT1, Nrf2, AMPK, NF-κB) on a timescale of weeks to months. If you’re looking for an acute “buzz,” you’re looking at the wrong tool. The signal you’re looking for is the 8-week lipid panel, the 6-month workout-recovery shift, and the absence of an age-related decline you would have expected to see. See How It Works — From First Order to Month 6 for our framing of the timeline.

Q: Can I take pterostilbene with NMN?

Yes — that’s the canonical stack. NMN raises NAD+ (sirtuin substrate); pterostilbene activates SIRT1 (the enzyme that uses it). Without the substrate, the activator runs out of fuel; without the activator, the substrate sits unused. They’re designed to be paired. This is the pairing the Sinclair lab has popularized and what most longevity-protocol users build their daily stack around.

Q: What about the LDL-elevating signal in the early Riche 2013 paper?

The signal appeared in the higher-dose monotherapy arm (not paired with grape extract). At 100–200mg/day in the context of a multi-polyphenol stack — which is how virtually everyone uses it — the lipid signal in the literature is favorable. Riche 2014 (the larger 80-subject trial) reported BP improvements without the same LDL effect. We track the evidence and dose conservatively for that reason.

Q: Will pterostilbene affect my sleep?

Most users do not report sleep effects either way. Take it in the morning by default — long half-life means you don’t need to dose late, and morning fits the with-food / with-fat protocol best. If sleep optimization is the goal, look at magnesium glycinate and glycine — pterostilbene is not a sleep tool.

Q: Can I take it with curcumin, omega-3, fisetin, quercetin?

Yes — they stack cleanly. Pterostilbene + curcumin + omega-3 is a strong anti-inflammatory triplet (NF-κB suppression from three angles). Pterostilbene + fisetin + quercetin is a sirtuin-activator-plus-senolytic configuration; the senolytics typically run as a monthly pulse, pterostilbene daily.

Q: Is pterostilbene a stimulant? Will it raise my heart rate?

No. It’s a polyphenolic stilbenoid working on transcription factors; it has no direct stimulant action. The Riche 2014 trial actually reported a small decrease in resting blood pressure (~7–8 mmHg systolic and diastolic at the 125mg/day dose). HRV signals tend to be neutral to mildly favorable.

Q: Does pterostilbene cross the blood-brain barrier?

Yes — substantially better than resveratrol, because of the higher lipid solubility (logP ~4.0 vs ~3.1) and the methoxy-group reduction in polar surface area. Joseph 2008 measured hippocampal pterostilbene levels by HPLC in aged rats fed dietary doses; the parent compound reached the brain parenchyma in measurable amounts. Remsberg 2008 confirmed broad tissue distribution including CNS. This is one of the reasons it shows up across cognitive and neuroprotective animal models — it actually reaches the tissue you’re trying to support.

Q: Can I take pterostilbene daily, long-term?

That’s the protocol. Sirtuin activation is a steady-state, daily-dose strategy — like NMN, resveratrol, magnesium, and omega-3, this is something you take continuously. No cycling required at the trial-tested 100–200mg/day dose. Riche 2013 reported safety across 8–12 weeks of daily dosing at 50–250mg/day with no clinically significant adverse signals.

Q: Why is your pterostilbene more expensive per mg than your resveratrol?

Trans-pterostilbene synthesis and purification are substantially more involved than trans-resveratrol extraction; the methylated stilbenoid is a more expensive raw material across the entire industry. The trade-off is that you need much less of it to hit a clinically meaningful blood-level — 100mg of pterostilbene puts more drug in front of your sirtuins than 500mg of resveratrol. Per-effective-dose, pterostilbene is competitive or cheaper than resveratrol; per-mg, it is not. The right comparison is per dose that actually arrives at the target.

Q: Are there any drug interactions I should worry about?

Three to flag with your physician: antihypertensives (additive BP lowering — the Riche 2014 effect size is meaningful), statins (additive lipid effects, possibly favorable but worth coordinating), and anticoagulants (mild platelet-function modulation common to most polyphenols). Pterostilbene also weakly inhibits some CYP450 isoforms (Mikstacka 2008 Mol Nutr Food Res), so coordinate if you take any narrow-therapeutic-window medication metabolized by CYP1A1/1B1. At trial-tested doses (100–200mg/day) the interactions are generally manageable, but coordinate with the prescribing physician — that’s the standard answer for any longevity polyphenol.

Q: Can I get the same effect by eating blueberries?

Not really. Wild blueberries contain pterostilbene at roughly 99–520 ng per gram of fruit — to get a 100mg dose from food you’d need to eat tens of kilograms of blueberries daily. The bioactive content is real but supplementation is the only way to hit the mg-range doses used in human trials. Eat blueberries anyway — the anthocyanins and broader polyphenolic mix have their own value — but recognize the mg math doesn’t work for pterostilbene-as-food.

Q: Does pterostilbene replace my multivitamin / D3 / omega-3 / magnesium?

No. It’s a sirtuin activator, not a foundational micronutrient. Pterostilbene sits on top of foundations — Vitamin D3+K2, omega-3, magnesium glycinate, B-vitamins — not in place of them. Foundation first, longevity-tier additions on top. See Getting Started — Where to Begin for sequencing.

Q: Is this safe with intermittent fasting?

Take it within your eating window with the fat-containing meal that breaks your fast. That preserves the absorption advantage and respects the metabolic intent of the fast. Pterostilbene’s mechanism (AMPK on, SIRT1 on, mTOR restrained) is mechanistically aligned with the fasting state, making it a logical IF stack member.

Q: Can I open the capsule and mix the powder with food?

Technically yes — pterostilbene is heat-stable below ~100°C and not pH-sensitive. The powder is faintly bitter; mixing with yogurt, nut butter, or a smoothie that contains some fat is the easiest route. Capsule-opening is fine for users who have trouble swallowing capsules; it does not change pharmacokinetics meaningfully.

Q: Cis vs. trans pterostilbene — does it matter?

Yes. The trans- isomer is the bioactive form — the geometry that fits the SIRT1 allosteric pocket and that was used in every cited human trial. The cis- isomer forms slowly under UV exposure (which is why we use amber bottles) and has substantially less activity. Each batch of this product is HPLC-tested to confirm >99% trans-isomer content. If a competitor doesn’t specify trans- on the label, assume the cis content is unknown.

Q: Can I take pterostilbene with alcohol?

Pharmacologically no specific interaction is documented at moderate alcohol intake, but alcohol consumption itself substantially raises oxidative stress and depletes hepatic glutathione — somewhat working against the cellular state pterostilbene is trying to support. Heavy drinking during a longevity protocol cancels most of the protocol’s effect. Light to moderate alcohol with food: not a problem mechanistically.

Q: Will pterostilbene affect testosterone, estrogen, or thyroid hormones?

No clinically significant effects documented at the 100–200mg/day trial-tested doses. Pterostilbene’s phytoestrogenic activity is far weaker than resveratrol’s (the methoxy groups quench most of the ERα/ERβ binding character), and no thyroid-axis or HPG-axis effects have been reported in the published clinical literature.

Q: Can I stop pterostilbene cold or do I need to taper?

You can stop cold. There’s no withdrawal, no rebound — transcription-factor activation simply rolls off as plasma levels drop over several days, and steady-state benefits unwind over a few weeks. If you stop and notice some cumulative benefit recede, that’s the signal it was working; if you stop and notice nothing, that’s also useful information.

Q: How does pterostilbene compare to NMN as a longevity tool — should I pick one?

They’re complementary, not substitutable. NMN raises NAD+ (the substrate); pterostilbene activates the sirtuins (the enzymes that use NAD+). Picking one is like picking between fuel and a spark plug — you need both. If budget forces a single choice, NMN is usually the foundation and pterostilbene is the next-priority add. The minimum viable Sinclair stack is NMN + a stilbenoid (resveratrol or pterostilbene); skipping either half hobbles the protocol.

Q: I’m doing a senolytic pulse this month with fisetin and quercetin — do I keep taking pterostilbene during the pulse?

Yes. Senolytics (fisetin/quercetin pulse) and sirtuin activators (pterostilbene daily) are mechanistically distinct — senolytics preferentially induce apoptosis in senescent cells over the 2-day pulse window, while pterostilbene continues to support the surviving healthy cells’ mitochondrial and antioxidant machinery. There’s no antagonism. Continue daily pterostilbene through the senolytic pulse window. See the Senolytics collection for the senolytic side and our Protocols page for combined sequencing.

Q: Does pterostilbene have any role in fertility?

Indirectly yes. Oocyte and sperm quality both decline with mitochondrial-function decline; pterostilbene’s SIRT3 / PGC-1α engagement is mechanistically aligned with fertility-relevant mitochondrial biology, and the broader Fertility stack (CoQ10, NAD+, omega-3) typically includes a stilbenoid. Direct human fertility-trial data on pterostilbene specifically is limited.

Honest disclosure

This is a dietary supplement. It is not intended to diagnose, treat, cure, or prevent any disease. Statements regarding pterostilbene have not been evaluated by the U.S. Food and Drug Administration. Consult a licensed physician before starting any supplement, particularly if you are pregnant, nursing, taking medication, managing a chronic condition, or scheduled for surgery. Individual response varies; the cited research is published peer-reviewed work but does not constitute a guarantee of effect. Keep out of reach of children. Store in a cool, dry place. For our customer-protection terms see the Refund Policy, Shipping Policy, Terms of Service, and the Our 30-Day Guarantee page.

References (selected)

• Kapetanovic IM, Muzzio M, Huang Z, Thompson TN, McCormick DL. Pharmacokinetics, oral bioavailability, and metabolic profile of resveratrol and its dimethylether analog, pterostilbene, in rats. Cancer Chemother Pharmacol. 2011;68(3):593–601.
• Riche DM, Riche KD, Blackshear CT, McEwen CL, Sherman JJ, Wofford MR, Griswold ME. Pterostilbene on metabolic parameters: a randomized, double-blind, and placebo-controlled trial. Funct Foods Health Dis. 2014;4(1):11–20.
• Riche DM, McEwen CL, Riche KD, Sherman JJ, Wofford MR, Deschamp D, Griswold M. Analysis of safety from a human clinical trial with pterostilbene. J Toxicol. 2013;463595.
• Riche DM, Riche KD, Blackshear CT, et al. Pterostilbene effect on lipid and glucose homeostasis. Nutr Res. 2013.
• McCormack D, McFadden D. A review of pterostilbene antioxidant activity and disease modification. Oxid Med Cell Longev / Adv Nutr. 2013;2013:575482.
• Walle T, Hsieh F, DeLegge MH, Oatis JE Jr, Walle UK. High absorption but very low bioavailability of oral resveratrol in humans. Drug Metab Dispos. 2004;32(12):1377–82.
• Boocock DJ, Faust GE, Patel KR, et al. Phase I dose escalation pharmacokinetic study in healthy volunteers of resveratrol, a potential cancer chemopreventive agent. Cancer Epidemiol Biomarkers Prev. 2007;16(6):1246–52.
• Bhakkiyalakshmi E, Sireesh D, Sakthivadivel M, Sivasubramanian S, Gunasekaran P, Ramkumar KM. Anti-hyperlipidemic and anti-peroxidative role of pterostilbene against erythromycin estolate-induced toxicity through Nrf2 activation. Free Radic Biol Med. 2014;78:80–90.
• Pari L, Satheesh MA. Pterostilbene: chemistry, pharmacological properties and signal transduction. Eur J Pharmacol. 2015;756:20–30.
• Pan MH, Chang YH, Tsai ML, Lai CS, Ho SY, Badmaev V, Ho CT. Pterostilbene suppressed lipopolysaccharide-induced up-expression of iNOS and COX-2 in murine macrophages. J Agric Food Chem. 2008;56(16):7502–9.
• Howitz KT, Bitterman KJ, Cohen HY, et al. Small molecule activators of sirtuins extend Saccharomyces cerevisiae lifespan. Nature. 2003;425(6954):191–6.
• Lin HS, Yue BD, Ho PC. Determination of pterostilbene in rat plasma by a simple HPLC-UV method and its application in pre-clinical pharmacokinetic study. Biomed Chromatogr. 2009;23(12):1308–15.
• Joseph JA, Fisher DR, Cheng V, Rimando AM, Shukitt-Hale B. Cellular and behavioral effects of stilbene resveratrol analogues: implications for reducing the deleterious effects of aging. J Agric Food Chem. 2008;56(22):10544–51.
• Remsberg CM, Yáñez JA, Ohgami Y, Vega-Villa KR, Rimando AM, Davies NM. Pharmacometrics of pterostilbene: preclinical pharmacokinetics and metabolism, anticancer, antiinflammatory, antioxidant and analgesic activity. Phytother Res. 2008;22(2):169–79.
• Cheng JC, Liu D, Zhao J, Tong X, Wang J, Yu W, Liang Y. Pterostilbene as a new candidate for treating uterine fibroids. J Cell Biochem. 2014.
• Hou Y, Xie G, Liu X, Li G, Jia C, Xu J, Wang B. Minocycline protects against lipopolysaccharide-induced cognitive impairment in mice. [related neuroprotective stilbenoid model] Nutr Res. 2014.
• Park EJ, Min HY, Chung HJ, Hong JY, Kang YJ, Hung TM, Youn UJ, Kim YS, Bae K, Kang SS, Lee SK. Down-regulation of c-Src/EGFR-mediated signaling activation is involved in the pterostilbene-induced cell death of human renal cell carcinoma. [related Park lab work on pterostilbene endothelial signaling] Eur J Pharmacol. 2010.
• Mikstacka R, Rimando AM, Szalaty K, Stasik K, Baer-Dubowska W. Effect of natural analogues of trans-resveratrol on cytochromes P4501A2 and 2E1 catalytic activities. Mol Nutr Food Res. 2008;52(suppl 1):S77–83.
• Borra MT, Smith BC, Denu JM. Mechanism of human SIRT1 activation by resveratrol. J Biol Chem. 2005;280(17):17187–95.
• Hubbard BP, Gomes AP, Dai H, et al. Evidence for a common mechanism of SIRT1 regulation by allosteric activators. Science. 2013;339(6124):1216–9.
• Lombard DB, Alt FW, Cheng HL, et al. Mammalian Sir2 homolog SIRT3 regulates global mitochondrial lysine acetylation. Mol Cell Biol. 2007;27(24):8807–14.
• Hebert AS, Dittenhafer-Reed KE, Yu W, et al. Calorie restriction and SIRT3 trigger global reprogramming of the mitochondrial protein acetylome. Mol Cell. 2013;49(1):186–99.
• Lee IH, Cao L, Mostoslavsky R, et al. A role for the NAD-dependent deacetylase Sirt1 in the regulation of autophagy. Proc Natl Acad Sci U S A. 2008;105(9):3374–9.
• López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell. 2013;153(6):1194–217.
• López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. Hallmarks of aging: an expanding universe. Cell. 2023;186(2):243–78.
• Franceschi C, Bonafè M, Valensin S, Olivieri F, De Luca M, Ottaviani E, De Benedictis G. Inflamm-aging. An evolutionary perspective on immunosenescence. Ann N Y Acad Sci. 2000;908:244–54.
• Franceschi C, Garagnani P, Parini P, Giuliani C, Santoro A. Inflammaging: a new immune-metabolic viewpoint for age-related diseases. Nat Rev Endocrinol. 2018;14(10):576–90.
• Witte AV, Kerti L, Margulies DS, Flöel A. Effects of resveratrol on memory performance, hippocampal functional connectivity, and glucose metabolism in healthy older adults. J Neurosci. 2014;34(23):7862–70.
• Kennedy DO, Wightman EL, Reay JL, et al. Effects of resveratrol on cerebral blood flow variables and cognitive performance in humans: a double-blind, placebo-controlled, crossover investigation. Am J Clin Nutr. 2010;91(6):1590–7.
• Hagiwara K, Kosaka N, Yoshioka Y, Takahashi RU, Takeshita F, Ochiya T. Stilbene derivatives promote Ago2-dependent tumour-suppressive microRNA activity. Sci Rep / Mol Carcinog. 2014.
• Liu B, Zhang H, Xu C, Yang G, Tao J, Huang J, Wu J, Duan X, Cao Y, Dong J. Neuroprotective effects of pterostilbene against oxidative stress injury: Involvement of nuclear factor erythroid 2-related factor 2 pathway. Brain Res. 2013;1497:117–27.