Polyphenol-Rich Foods and Nrf2 Activation

For a generation, mainstream nutrition advice has been to "eat the rainbow" and consume a wide variety of brightly colored fruits and vegetables. That folk wisdom turns out to be precisely correct biochemistry — the pigment compounds responsible for the colors (anthocyanins in berries, carotenoids in orange and red plants, chlorophyll and sulforaphane in greens, curcuminoids in turmeric) are polyphenols and isothiocyanates that activate the body's master antioxidant transcription factor, Nrf2. Activated Nrf2 enters the cell nucleus and transcribes more than 200 cytoprotective genes including glutathione synthesis enzymes, Phase II detoxification enzymes, and NADPH-generating enzymes. Polyphenol-rich foods therefore do not just provide direct antioxidant chemistry — they upregulate the body's endogenous antioxidant capacity. This is why diet-based interventions consistently outperform isolated antioxidant supplements in cardiovascular and neurodegenerative outcomes. This deep-dive walks through the Nrf2 mechanism, the most potent polyphenol activators, the bioavailability problem, and the practical food sources.

Table of Contents

1. The Nrf2/Keap1 Pathway — How Foods Talk to Cellular Antioxidant Genes
2. Sulforaphane (Cruciferous Vegetables) — The Most Potent Nrf2 Activator
3. Curcumin (Turmeric) — The Anti-Inflammatory Polyphenol
4. EGCG (Green Tea) and Catechins
5. Resveratrol and Stilbenes
6. Anthocyanins (Berries, Pomegranate, Dark Grapes)
7. Quercetin, Hesperidin, and Other Flavonoids
8. The Bioavailability Problem and Gut Microbiota
9. Why Whole Foods Outperform Isolated Antioxidant Supplements
10. Practical Daily Targets and Food Sources
11. Key Research Papers
12. Connections

The Nrf2/Keap1 Pathway — How Foods Talk to Cellular Antioxidant Genes

Nuclear factor erythroid 2-related factor 2 (Nrf2) is the master transcriptional regulator of the cellular antioxidant response. Under normal resting conditions, Nrf2 is held in the cytoplasm by its partner protein Keap1 (Kelch-like ECH-associated protein 1). The Keap1-Nrf2 complex is constantly tagged with ubiquitin and degraded by the proteasome, keeping baseline cytoplasmic Nrf2 low.

The trick is that Keap1 has approximately 25 cysteine residues that act as molecular sensors. When an oxidant or electrophilic molecule reaches the cytoplasm, it modifies one or more of these reactive Keap1 cysteines (the most sensitive are Cys-151, Cys-273, Cys-288), changing Keap1's conformation. The modified Keap1 releases Nrf2, which translocates to the nucleus, dimerizes with small Maf proteins, and binds antioxidant response elements (AREs) in the promoter regions of more than 200 cytoprotective genes.

The genes turned on by Nrf2 include:

• Glutathione synthesis — GCLC, GCLM (the rate-limiting gamma-glutamyl cysteine ligase subunits), GSS (glutathione synthetase)
• Antioxidant enzymes — glutathione peroxidases, peroxiredoxins, thioredoxin, thioredoxin reductase
• NADPH-generating enzymes — G6PD (glucose-6-phosphate dehydrogenase, the pentose phosphate pathway), 6PGD, ME1 (malic enzyme), IDH1 (isocitrate dehydrogenase)
• Phase II detoxification enzymes — NQO1 (NAD(P)H quinone dehydrogenase 1), GSTs (glutathione-S-transferases), UGTs (UDP-glucuronosyltransferases), SULTs (sulfotransferases)
• Heme and iron metabolism — HO-1 (heme oxygenase-1, the textbook Nrf2 target), ferritin (sequesters free iron that catalyzes Fenton chemistry)
• Metal-binding proteins — metallothionein

The net effect of Nrf2 activation is therefore not just "more antioxidant" — it is a coordinated cellular shift toward enhanced detoxification, ROS neutralization, glutathione synthesis, and iron sequestration. This is qualitatively different from giving a megadose of one antioxidant. The food compounds that activate Nrf2 are not themselves the active antioxidants; they are signaling molecules that tell the cell to upregulate its own antioxidant defenses.

An important nuance: Nrf2 activation should be intermittent and pulse-like rather than continuous. Sustained Nrf2 activation has been associated in some cancers with chemotherapy resistance (the tumor uses Nrf2 to detoxify chemotherapeutic agents) and accelerated tumor growth in established cancers. The food-derived activation is naturally pulse-like — you eat broccoli, sulforaphane spikes, Nrf2 activates for hours, then returns to baseline. This is how you want the system to work.

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Sulforaphane (Cruciferous Vegetables) — The Most Potent Nrf2 Activator

Sulforaphane is an isothiocyanate (R-N=C=S) released from cruciferous vegetables (broccoli, broccoli sprouts, brussels sprouts, cabbage, cauliflower, kale, bok choy, watercress, arugula) when the precursor glucoraphanin is hydrolyzed by the myrosinase enzyme. The hydrolysis happens when the vegetable is chopped, chewed, or crushed — myrosinase is sequestered in different cells from glucoraphanin until tissue damage brings them together.

Sulforaphane is the most potent natural Nrf2 activator known — effective at low micromolar concentrations. The mechanism is direct covalent modification of Keap1 Cys-151 by the reactive isothiocyanate carbon. The Talalay laboratory at Johns Hopkins (Paul Talalay, who died in 2019) was the foundational research group, demonstrating sulforaphane's chemoprotective effects in animal cancer models in the 1990s and going on to develop standardized broccoli sprout extract preparations.

Practical sulforaphane sources, ranked by content:

• Broccoli sprouts (3-day-old) — the densest source by 20-100x. Approximately 1 g of fresh sprouts equals the sulforaphane content of 50 g of mature broccoli. Easy home-growth: soak broccoli seeds 8 hours, drain twice daily in a sprouting jar, ready in 3-4 days. 30 g of sprouts (about 1/4 cup) delivers a substantial Nrf2-activating dose.
• Standardized broccoli sprout extract supplements — sold by Thorne (Crucera-SGS), Pure Encapsulations, Jarrow, others. Look for products that contain both glucoraphanin and active myrosinase, or are standardized to deliver sulforaphane equivalents. 10-30 mg sulforaphane per dose is typical for clinical-trial-equivalent dosing.
• Mature broccoli, steamed lightly — light steaming preserves myrosinase activity (boiling destroys it). 1-2 cups daily provides meaningful but lower-dose sulforaphane.
• Other cruciferous vegetables — kale, cabbage, cauliflower, brussels sprouts — contain related isothiocyanates (with similar Nrf2 activation but different potency). The well-studied compound from watercress is gluconasturtiin; from horseradish, sinigrin.

The clinical evidence for sulforaphane is among the most positive of any nutraceutical. Studies have shown effects on Helicobacter pylori clearance (Yanaka 2009), modulation of autism behavior (Singh 2014 PNAS), reduced systemic inflammation markers, improved insulin sensitivity, hepatic detoxification capacity, and ongoing chemopreventive trials in bladder cancer, prostate cancer, and Barrett's esophagus.

A practical preparation tip: if you boil broccoli (destroying myrosinase), sprinkling raw mustard powder (which contains active myrosinase) over the cooked broccoli before eating restores sulforaphane generation in the digestive tract.

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Curcumin (Turmeric) — The Anti-Inflammatory Polyphenol

Curcumin is the yellow polyphenol pigment of turmeric (Curcuma longa), the principal spice in curry. It is one of the most studied phytochemicals in the world — PubMed lists more than 25,000 publications on curcumin.

Curcumin's effects are pleiotropic, but the dominant mechanisms relevant to oxidative stress are:

1. Nrf2 activation — curcumin's alpha-beta unsaturated carbonyl system modifies Keap1 cysteine residues, releasing Nrf2 to activate the antioxidant response.
2. NF-kappaB inhibition — curcumin inhibits the inflammatory transcription factor NF-kappaB, reducing TNF-alpha, IL-6, IL-1beta, and other inflammatory cytokines.
3. Direct ROS scavenging — curcumin's phenolic hydroxyl groups directly quench reactive oxygen species, though this is a minor effect compared to Nrf2-mediated upregulation of endogenous defenses.
4. 5-LOX and COX-2 inhibition — reducing prostaglandin and leukotriene production for an anti-inflammatory effect similar to (but milder than) NSAIDs.

The clinical applications with the strongest evidence:

• Osteoarthritis — multiple meta-analyses (Daily 2016 J Med Food, Liu 2018) of curcumin extracts at 1,000-1,500 mg/day show pain reduction comparable to ibuprofen with better GI tolerance.
• Rheumatoid arthritis — smaller trials show benefit as adjunct to standard DMARDs.
• Inflammatory bowel disease — some evidence for benefit in mild-to-moderate ulcerative colitis as adjunct to mesalamine.
• Major depression — meta-analyses show modest antidepressant effect; benefits the "treatment-resistant" phenotype with elevated inflammatory markers more than melancholic depression.
• Hyperlipidemia — modest reductions in LDL and triglycerides; less impressive than statins.

Bioavailability is curcumin's biggest practical problem. Plain curcumin has <1% oral bioavailability due to poor solubility, rapid hepatic glucuronidation, and biliary excretion. Several formulation strategies dramatically improve bioavailability:

• Piperine combination (BCM-95, Bioperine) — black pepper extract inhibits glucuronidation. 2,000% bioavailability increase.
• Phospholipid complex (Meriva) — ~30x bioavailability increase.
• Nanoparticle formulations (TheraCurmin) — ~27x bioavailability increase.
• Liposomal curcumin — ~20x increase.

The clinical-trial-equivalent dose for plain curcumin is approximately 1,000-1,500 mg/day; for bioavailability-enhanced formulations, 200-500 mg/day is roughly equivalent. See our detailed Turmeric page for the full clinical profile.

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EGCG (Green Tea) and Catechins

Green tea (Camellia sinensis processed without fermentation) is the dominant dietary source of catechins, particularly epigallocatechin-3-gallate (EGCG), epicatechin (EC), epigallocatechin (EGC), and epicatechin-3-gallate (ECG). EGCG is the most abundant and most studied.

EGCG activates Nrf2 through Keap1 modification and additionally activates AMPK, inhibits the mTOR pathway (mimicking caloric restriction), and modulates the gut microbiome to favor beneficial taxa. The pleiotropic effects translate to evidence for:

• Cardiovascular benefit — large prospective cohorts (Japanese Ohsaki Study, others) show inverse association between green tea consumption and CVD mortality. Mechanisms include improved endothelial function, modest LDL reduction, blood pressure reduction, and platelet inhibition.
• Metabolic benefit — modest reductions in body weight and improved insulin sensitivity, especially with the combination of EGCG and caffeine in green tea.
• Cancer chemoprevention — large observational evidence; intervention trials less consistent.
• Cognitive function — modest evidence for cognitive benefit in older adults, with L-theanine (also abundant in green tea) contributing.

Dose-response: 3-5 cups of brewed green tea per day (providing 200-400 mg EGCG) is the typical effective dose in epidemiological studies. Concentrated EGCG supplements (300-500 mg/day) approximate this exposure but carry a rare hepatotoxicity risk (idiosyncratic, dose-related, usually reversible) that is not seen with brewed tea.

For more on green tea, see our Green Tea page.

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Resveratrol and Stilbenes

Resveratrol is a stilbene phytoalexin produced by grapevines, peanuts, knotweed, and a handful of other plants in response to pathogen stress. It was popularized by red wine research in the early 2000s as a potential explanation for the "French paradox" (low CVD mortality despite high saturated fat intake) and subsequently by David Sinclair's work suggesting resveratrol mimics caloric restriction through SIRT1 activation.

Mechanistically, resveratrol activates Nrf2, activates SIRT1 (a NAD+-dependent histone deacetylase involved in longevity pathways), activates AMPK (the cellular energy sensor), and has direct antioxidant effects. The cross-talk between Nrf2 and SIRT1 has been a fruitful area of recent research.

The clinical translation has been less dramatic than the early enthusiasm. Trials of high-dose resveratrol have shown modest improvements in insulin sensitivity and lipid profiles in metabolic syndrome, modest cognitive benefits in some studies, and no dramatic longevity effect in humans (the mouse longevity data on high-fat diets did not translate to chow-fed mice or to humans).

Bioavailability is poor (1-2%) due to rapid Phase II glucuronidation. Trans-resveratrol (the bioactive isomer) is the form to look for in supplements. Typical dose: 150-500 mg/day. The Sinclair-popular "1 g per day" doses produce more bioavailability problems and have shown adverse effects on insulin sensitivity in some studies. Dietary sources include red wine (1-3 mg per glass — not enough for the supplement-trial effects but contributing to the cardiovascular benefit of moderate red wine consumption), red grapes, blueberries, peanuts, and Japanese knotweed extract.

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Anthocyanins (Berries, Pomegranate, Dark Grapes)

Anthocyanins are the polyphenol pigments responsible for the red, blue, and purple color of berries (blueberries, blackberries, raspberries, strawberries, cranberries, elderberries), pomegranate, dark grapes, purple cabbage, eggplant skin, purple sweet potato, black rice, and red wine. They activate Nrf2 and have well-documented vascular benefits.

The strongest clinical evidence is for cardiovascular outcomes. The Nurses' Health Study and Health Professionals Follow-up Study both found inverse associations between anthocyanin intake and CVD events. Intervention trials of anthocyanin-rich extracts (Cassidy 2013, Cassidy 2014 American Journal of Clinical Nutrition) showed improved endothelial function, reduced blood pressure, and reduced arterial stiffness within weeks of starting daily berry consumption.

Mechanisms include direct Nrf2 activation, enhanced endothelial nitric oxide bioavailability (reducing vascular oxidative stress), reduced platelet aggregation, modest LDL reduction, and gut microbiota modulation. The gut microbiota plays a major role — anthocyanins are themselves poorly absorbed but are metabolized by gut bacteria into smaller phenolic acids (protocatechuic acid, ferulic acid, vanillic acid) that are well-absorbed and themselves bioactive.

Practical sources, ranked by anthocyanin density:

• Aronia berries (chokeberries) — the highest anthocyanin density of any common food (~1,500 mg per 100 g). Tart enough that they are usually consumed as concentrate or in juice blends.
• Elderberries — 700-1,000 mg per 100 g, plus immune-supportive sambucus compounds.
• Black raspberries — ~600 mg per 100 g.
• Blackberries, blueberries (wild > cultivated) — 300-500 mg per 100 g.
• Black currants — 300-500 mg per 100 g.
• Pomegranate — rich in punicalagins (related compounds) and ellagic acid plus anthocyanins.
• Red wine — 20-35 mg per 6 oz glass.

The typical effective dose in studies is approximately 200-500 mg of anthocyanins per day — achievable with 1 cup of berries daily, or 1-2 tablespoons of aronia concentrate. For more on berries, see our Berries page.

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Quercetin, Hesperidin, and Other Flavonoids

Beyond the headline polyphenols above, several other flavonoids contribute meaningfully to the dietary antioxidant effect:

• Quercetin — abundant in onions, apples, capers, dill, kale, red wine, green tea. Anti-inflammatory and antihistamine effects in addition to Nrf2 activation. 500-1,000 mg/day supplemental doses have been studied for exercise recovery, allergic rhinitis, and cardiovascular health. Combines well with bromelain (improves absorption) and Vitamin C.
• Hesperidin and naringin — citrus flavonoids. Improve endothelial function and capillary fragility. Found in the white pith of citrus fruits.
• Apigenin — chamomile, parsley, celery. Anti-inflammatory and modest sedative effects.
• Luteolin — celery, parsley, broccoli, peppers, thyme. Strong Nrf2 activator and anti-inflammatory.
• Kaempferol — kale, broccoli, dill, chives, beans, leeks, tea.
• Catechins beyond EGCG — in cocoa (epicatechin contributes to dark chocolate's vascular benefit) and apples.
• Proanthocyanidins (condensed tannins) — in grape seeds, pine bark (Pycnogenol), cocoa, cinnamon. Strong antioxidant capacity and vascular benefits.

The take-home is that polyphenol benefit comes from variety. No single flavonoid is uniquely necessary; multiple polyphenols delivered together (as in whole-food consumption) activate Nrf2 more reliably and at lower individual doses than any single compound.

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The Bioavailability Problem and Gut Microbiota

One of the great puzzles of polyphenol research has been the disconnect between in-vitro potency and in-vivo bioavailability. Many polyphenols have less than 5% bioavailability for the parent compound, are rapidly conjugated by Phase II enzymes (glucuronidated and sulfated within minutes), and yet produce measurable clinical effects in human trials. The resolution to this paradox is the gut microbiota.

Most polyphenols are not absorbed intact — they reach the colon, where gut bacteria deglycosylate them, cleave their ring structures, and produce smaller phenolic acid metabolites that are well-absorbed and bioactive. For example:

• Anthocyanins are metabolized to protocatechuic acid, vanillic acid, gallic acid, syringic acid.
• Ellagitannins (from pomegranate, walnuts, raspberries) are metabolized to urolithin A and urolithin B — the latter compounds being responsible for much of the systemic anti-inflammatory and mitophagy effect attributed to the parent ellagitannins. Urolithin A is now sold as a stand-alone supplement (Mitopure).
• Isoflavones (soy) are metabolized to equol by approximately 30% of Western adults (the "equol producers") who get more benefit from soy than non-producers.
• Catechins are metabolized to phenyl-valerolactones with their own activity.

This means that:

1. The relevant exposures in human polyphenol studies are not just the parent compounds but the microbiota-derived metabolites.
2. Individual variability in gut microbiota produces variable response to polyphenol foods. A person with a urolithin-producing microbiota gets more out of walnuts and pomegranate than a non-producer.
3. Antibiotic exposure or severe gut dysbiosis temporarily reduces polyphenol efficacy until the relevant bacteria recolonize.
4. Direct supplementation with the post-microbial metabolite (e.g., urolithin A) bypasses the variability.

The practical implication is that polyphenol-rich diet works synergistically with gut microbiome health — fermented foods, fiber, prebiotic-rich vegetables, and avoiding unnecessary antibiotics all amplify the antioxidant benefit of polyphenols.

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Why Whole Foods Outperform Isolated Antioxidant Supplements

One of the most important and humbling stories in clinical nutrition is the consistent failure of isolated antioxidant supplements in large RCTs:

• ATBC trial (1994) — alpha-tocopherol and beta-carotene supplementation in 29,000 Finnish smokers. Beta-carotene increased lung cancer incidence by 18% and overall mortality by 8%.
• CARET trial (1996) — beta-carotene + Vitamin A in 18,000 smokers and asbestos workers. Trial stopped early due to 28% increase in lung cancer.
• HOPE trial (2000) — high-dose Vitamin E in 9,500 CVD patients. No reduction in cardiovascular events; trend toward increased heart failure.
• SELECT trial (2008) — selenium and Vitamin E for prostate cancer prevention in 35,000 men. Vitamin E increased prostate cancer risk by 17% over 7 years.
• Bjelakovic meta-analysis JAMA 2007 — pooled 47 RCTs of 232,000 participants. Antioxidant supplementation (beta-carotene, Vitamin A, Vitamin E) was associated with increased mortality. Vitamin C and selenium were neutral.

In contrast, intake of antioxidant-rich whole foods (Mediterranean diet pattern, high fruit and vegetable consumption, regular berry consumption) consistently associates with reduced CVD events, reduced cancer incidence, reduced cognitive decline, and reduced all-cause mortality in both observational studies and intervention trials (PREDIMED).

Why the discrepancy? Several reasons:

1. Hormesis — ROS at low concentrations are essential signaling molecules. Megadose antioxidants disrupt this signaling. Foods deliver polyphenols in pulse-like patterns that activate Nrf2 transiently without sustained suppression of normal redox signaling.
2. Nrf2 activation versus direct scavenging — food polyphenols upregulate the endogenous antioxidant system rather than substituting for it. The result is durable cellular antioxidant capacity rather than transient direct ROS absorption.
3. Antioxidant network synergy — foods deliver dozens of polyphenols that interact synergistically; isolated single compounds at megadose can become pro-oxidant under specific conditions (the beta-carotene problem in smokers).
4. Cofactors and matrix — whole foods deliver minerals, B-vitamins, fiber, and other compounds that support the antioxidant system. Isolated supplements lack this context.
5. Gut microbiota processing — food polyphenols are processed by gut bacteria into bioactive metabolites. Isolated chemical supplements bypass this important biological filtering.

This does not mean every supplement is bad — NAC, glutathione precursors, CoQ10, Vitamin D in deficient populations, and curcumin all have positive supplement evidence. But the broad lesson is that the default position for oxidative stress management is dietary, with isolated supplements reserved for specific clinical indications rather than as a substitute for diet.

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Practical Daily Targets and Food Sources

A practical polyphenol-rich diet aiming at maximum Nrf2 activation looks like:

• Cruciferous vegetables daily — 1 cup of broccoli, kale, brussels sprouts, cabbage, cauliflower, or bok choy. Lightly steam or eat raw to preserve myrosinase. Add 1-2 tablespoons of broccoli sprouts (homegrown) for highest sulforaphane density. See our Broccoli page and Kale page.
• Berries daily — 1 cup of mixed berries (frozen are fine and often more anthocyanin-dense than out-of-season fresh). Blueberries, blackberries, raspberries, strawberries, pomegranate seeds. Berries deep-dive.
• Turmeric in cooking — 1/2 to 1 teaspoon turmeric (curcumin source) per day with black pepper for absorption. Turmeric page.
• Green tea — 3-5 cups daily; matcha (powdered whole leaf) for highest EGCG density. Green Tea page.
• Allium vegetables — onions, garlic, leeks, scallions, shallots daily for quercetin and organosulfur compounds.
• Dark leafy greens — spinach, chard, beet greens, mustard greens.
• Olive oil — extra virgin (not refined) for oleocanthal and oleuropein polyphenols. 2-4 tablespoons daily.
• Dark chocolate — 70%+ cacao, 20-30 g daily for epicatechin and proanthocyanidins.
• Coffee — 2-4 cups daily delivers chlorogenic acid and cafestol with documented cardiovascular and metabolic benefits in habitual consumers.
• Spices broadly — cinnamon, ginger, rosemary, thyme, oregano, sage, clove, allspice all are concentrated polyphenol sources.
• Walnuts and pecans — 1 ounce daily for ellagitannins (precursor to urolithin A).
• Red wine (optional, moderate) — 1 glass with dinner; benefit fades above moderate intake and is absent in non-drinkers who should not start.

This pattern overlaps almost exactly with the Mediterranean diet (PREDIMED), the Okinawan diet (longevity cohort), and the MIND diet (cognitive decline prevention). The single most important shift for someone starting from a typical Western diet is to add 2-3 servings daily of brightly colored fruits and vegetables, not as a side dish but as a substantial portion of caloric intake.

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Key Research Papers

1. Itoh K et al. (1997). An Nrf2/small Maf heterodimer mediates the induction of phase II detoxifying enzyme genes through antioxidant response elements. Biochem Biophys Res Commun. — PubMed
2. Hayes JD, Dinkova-Kostova AT (2014). The Nrf2 regulatory network provides an interface between redox and intermediary metabolism. Trends in Biochemical Sciences. — PubMed
3. Fahey JW, Talalay P (1999). Antioxidant functions of sulforaphane: a potent inducer of Phase II detoxication enzymes. Food and Chemical Toxicology. — PubMed
4. Yanaka A et al. (2009). Dietary sulforaphane-rich broccoli sprouts reduce colonization and attenuate gastritis in Helicobacter pylori-infected mice and humans. Cancer Prevention Research. — PubMed
5. Singh K et al. (2014). Sulforaphane treatment of autism spectrum disorder (ASD). PNAS. — PubMed
6. Daily JW et al. (2016). Efficacy of turmeric extracts and curcumin for alleviating the symptoms of joint arthritis: A systematic review and meta-analysis of randomized clinical trials. J Med Food. — PubMed
7. Estruch R et al. (2018). Primary prevention of cardiovascular disease with a Mediterranean diet supplemented with extra-virgin olive oil or nuts (PREDIMED). NEJM. — PubMed
8. Cassidy A et al. (2013). High anthocyanin intake is associated with a reduced risk of myocardial infarction in young and middle-aged women. Circulation. — PubMed
9. Bjelakovic G et al. (2007). Mortality in randomized trials of antioxidant supplements for primary and secondary prevention: systematic review and meta-analysis. JAMA. — PubMed
10. Omenn GS et al. (1996). Effects of a combination of beta carotene and vitamin A on lung cancer and cardiovascular disease (CARET). NEJM. — PubMed
11. Lippman SM et al. (2009). Effect of selenium and vitamin E on risk of prostate cancer and other cancers (SELECT). JAMA. — PubMed
12. Ristow M et al. (2009). Antioxidants prevent health-promoting effects of physical exercise in humans. PNAS. — PubMed

PubMed Topic Searches

• PubMed: Nrf2/Keap1 polyphenol activation
• PubMed: Sulforaphane clinical trials
• PubMed: Curcumin clinical inflammation
• PubMed: Anthocyanins cardiovascular
• PubMed: Polyphenols and gut microbiota

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Connections

• Oxidative Stress Hub
• Oxidative Stress Benefits Hub
• Glutathione Master Antioxidant
• NAC and Precursors
• Mitochondrial Health
• Turmeric (Curcumin)
• Green Tea (EGCG)
• Berries (Anthocyanins)
• Broccoli (Sulforaphane)
• Kale
• Onions (Quercetin)
• Vitamin C
• Vitamin E
• Mediterranean Diet
• Cardiovascular Disease

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