Condiciones de salud que galato de epigalocatequina (EGCG) puede ayudar a apoyar.
EGCG, the primary bioactive polyphenol in green tea, has been directly studied for acne, showing antimicrobial, anti-inflammatory, and sebum-suppressing effects. Clinical and in vitro evidence demonstrates it reduces C. acnes biofilm, suppresses sebocyte lipogenesis, and inhibits inflammatory cytokines. A 2019 mini-review confirmed clinical evidence for EGCG in inflammatory acne.
EGCG (epigallocatechin gallate), the major catechin of green tea, stabilizes mast cells, attenuates FcεRI signaling, and reduces airway inflammation and IgE levels in preclinical allergic asthma models. A 2025 comprehensive systematic review (MDPI Nutrients) summarized EGCG's mechanistic anti-allergic activity, noting preclinical models show decreased specific IgE and increased IL-10 in bronchoalveolar lavage. Clinical data for EGCG alone in respiratory allergy remain scarce.
EGCG, the principal catechin in green tea, is identified in multiple peer-reviewed reviews as a phytochemical with ALS activity. It reduces oxidative stress and protects motor neurons in organotypic spinal cord cultures relevant to ALS. EGCG modulates iron homeostasis, inhibits protein aggregation, and activates Nrf2 antioxidant pathways. Evidence is primarily preclinical.
EGCG (Epigallocatechin Gallate) is the predominant catechin in green tea and is extensively studied for its antioxidant properties. It directly scavenges reactive oxygen species (ROS) and activates the Nrf2/ARE signaling pathway to upregulate endogenous antioxidant enzymes. Multiple human and clinical studies confirm measurable reductions in oxidative stress biomarkers following EGCG supplementation, supporting its role in antioxidant defense. Evidence is primarily mechanistic and biomarker-based, with some clinical trials in populations with metabolic disease.
Multiple preclinical studies show EGCG reduces anxiety-like behavior via anti-inflammatory and neuroprotective mechanisms in hippocampal tissue. A small 8-week randomized, double-blind, placebo-controlled human trial in schizophrenia/bipolar disorder patients measured anxiety symptoms using the Hamilton Rating Scale-Anxiety. Both EGCG and placebo groups showed reductions, but EGCG's specific anxiolytic signal was not statistically differentiated from placebo.
EGCG, the primary catechin in green tea, delays gastric emptying in a double-blind RCT in healthy women, prolonging satiety. It also inhibits COMT, potentiating norepinephrine-mediated thermogenesis and appetite suppression. Effects on appetite are enhanced in combination with caffeine.
EGCG is the principal catechin in green tea responsible for its arterial benefits, including eNOS upregulation, NO production, inhibition of endothelial adhesion molecules, and reduction of LDL oxidation. Clinical studies confirm improvements in endothelial function (FMD) and blood pressure reduction. The 2024 PMC vascular nutraceutical review included green tea polyphenols (primarily EGCG) among arterial health nutraceuticals.
EGCG markedly reduces arthritic symptoms in the pristane-induced arthritis rat model, with effects comparable to methotrexate when administered early and continuously. It suppresses synovial inflammation, joint destruction, and cartilage damage via anti-inflammatory and anti-oxidative mechanisms relevant to both rheumatoid and osteoarthritis.
EGCG, the primary catechin in green tea, stabilizes mast cells, attenuates FcεRI (IgE receptor) signaling, and reduces airway inflammation in preclinical asthma models. A 2025 systematic review confirmed EGCG stabilizes mast cells and reduces airway inflammation in preclinical models, though clinical data in asthma remain limited.
EGCG, the principal catechin in green tea, has been studied in autoimmune conditions including rheumatoid arthritis, multiple sclerosis, inflammatory bowel disease, and lupus. It inhibits NF-κB, reduces pro-inflammatory cytokines, and suppresses Th17 differentiation. Animal studies show significant disease attenuation in EAE (MS model) and collagen-induced arthritis.
EGCG, the principal catechin of green tea, directly neutralizes methyl mercaptan by chemical reaction and suppresses the mgl gene in Porphyromonas gingivalis that encodes the enzyme responsible for methyl mercaptan production. In vitro studies confirm EGCG inhibits growth and VSC production by multiple halitogenic bacteria including Solobacterium moorei and P. gingivalis. Research published in Journal of Dental Research (2010) confirmed bactericidal and mgl-suppressing effects at clinically relevant concentrations.
EGCG is the most abundant and potent catechin in green tea with documented antiplatelet activity. It inhibits platelet aggregation by suppressing TXA2 synthesis, modulating calcium signaling, and reducing collagen-receptor platelet activation. A 2022 systematic review included green tea/EGCG among herbs with RCT-demonstrated platelet aggregation inhibition.
EGCG is the primary active catechin in green tea, responsible for much of its antihypertensive effect. Clinical studies show it reduces both SBP and DBP through ACE inhibition, NO upregulation, and vascular oxidative stress reduction. Evidence derives from both isolated EGCG trials and green tea extract RCTs.
EGCG is the predominant catechin in green tea and has been studied for its effects on insulin sensitivity and blood glucose. Meta-analyses of clinical trials show green tea/EGCG supplementation significantly reduces fasting blood glucose. It enhances insulin signaling, inhibits alpha-glucosidase, and reduces hepatic glucose output.
Epidemiological studies show habitual tea drinkers have higher bone mineral density and lower hip fracture risk. EGCG promotes osteoblast differentiation and mineralization while suppressing osteoclastogenesis via the RANKL/OPG pathway in multiple cell and animal studies. Human population data are supportive but isolated EGCG RCT data for bone density specifically remain limited.
EGCG has demonstrated improvements in cognitive performance and cerebral blood flow parameters in human double-blind crossover studies. It inhibits amyloid-beta aggregation, reduces tau phosphorylation, and activates BDNF pathways relevant to cognitive clarity. Clinical evidence from Down syndrome trials also shows improved adaptive cognitive function.
EGCG activates AMPK, the master cellular energy sensor, promoting mitochondrial biogenesis and glucose uptake. It modulates mitochondrial function, and at low therapeutic doses enhances antioxidant protection of mitochondria, though at high doses can uncouple oxidative phosphorylation.
EGCG, the principal catechin of green tea, is cited in MDPI Cosmetics (2026) as widely researched for antifibrotic, antioxidant, and lipolytic action in cellulite treatment. It inhibits COMT to amplify lipolytic norepinephrine signaling, activates AMPK, and reduces adipogenesis.
EGCG, the principal polyphenol in green tea, has been tested in clinical trials for HPV-related cervical lesions. A pilot study of 51 women found a 69–74% response rate with topical polyphenon E (EGCG-rich) ointment versus 10% in untreated controls. A phase II RCT (n=98) showed oral EGCG was safe but did not significantly outperform placebo for CIN1 with HR-HPV.
EGCG, the most bioactive green tea catechin, inhibits micellar cholesterol absorption and HMG-CoA reductase, and upregulates hepatic LDL receptors. A meta-analysis of 14 RCTs confirmed significant TC and LDL-C reductions. Studied doses: 224–674 mg/day.
EGCG (Epigallocatechin Gallate), the predominant polyphenol in green tea, has documented anti-inflammatory activity supported by both mechanistic research and human clinical data. Its primary molecular targets include NF-κB suppression, inhibition of pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), and NLRP3 inflammasome attenuation. A clinical study in 50 diabetic patients showed that 300 mg/day of EGCG for eight weeks significantly reduced high-sensitivity C-reactive protein (hs-CRP). However, human trial results are inconsistent, with at least one large RCT finding no significant effect on CRP, IL-6, or TNF-α at higher doses over 12 months.
EGCG is under investigation as an anti-nociceptive agent, addressing nociceptive, neuropathic, and nociplastic pain through anti-inflammatory, antioxidant, and neuroprotective mechanisms. A 2025 systematic review identified it as a promising adjunct to conventional pain management, though clinical bioavailability limitations constrain translation.
EGCG, the primary polyphenol in green tea, has demonstrated neuroprotective mechanisms in preclinical models including antioxidant activity, inhibition of amyloid-beta aggregation, and tau phosphorylation reduction. Human clinical trials exist but are limited in number and scope: the most positive results come from Down syndrome populations, while trials in healthy adults and other neurological conditions show minimal or no benefit. No long-term RCT has yet confirmed that EGCG alone protects against cognitive decline or dementia in the general aging population.
EGCG is the principal bioactive catechin of green tea with well-documented anti-influenza and antiviral activity. It inhibits influenza hemagglutinin and neuraminidase, blocking viral entry and release. Clinical RCTs of green tea catechin preparations (predominantly EGCG) reduced influenza incidence by ~90% in healthcare workers in one RCT. It also modulates innate immune responses relevant to cold/flu defense.
EGCG, the principal bioactive catechin in green tea, inhibits tyrosinase, suppresses melanogenesis, and exerts antioxidant and anti-inflammatory effects relevant to periorbital hyperpigmentation. It is listed among natural ingredients studied for hyperpigmentation management in a PMC systematic review. Its anti-melanogenic mechanism is well-characterized in vitro and supported by clinical evidence for hyperpigmentation.
Multiple preclinical studies in rodent CUMS (chronic unpredictable mild stress) models demonstrate EGCG alleviates depression-like behaviors through inhibition of NLRP3 inflammasome activation, NF-κB/caspase-1 pyroptosis, and mTOR autophagy dysregulation. Epidemiological data link regular tea consumption to reduced depression risk. One small human RCT reported reductions in Hamilton Depression Scale scores in psychiatric patients, though not statistically differentiated from placebo.
EGCG, the principal catechin of green tea, has clinical evidence for radiation-induced dermatitis from multiple trials, including a 2:1 randomized controlled study in 165 breast cancer patients where topical EGCG spray delayed onset of radiodermatitis by 2–3 weeks and significantly reduced severity. It is also studied for atopic and seborrheic dermatitis.
EGCG, the principal active catechin in green tea, is the key constituent in MighTeaFlow, a clinically validated xerostomia formula. Research at the Dental College of Georgia found EGCG may partially restore salivary gland function and delay progression of salivary gland dysfunction through molecular and cellular mechanisms in gland acinar cells.
EGCG, the primary catechin in green tea, exerts potent anti-angiogenic effects by inhibiting VEGF expression and signaling in endometriotic lesions, demonstrated in multiple in vitro and animal studies. It also decreased endometriotic lesion size in animal models. No published RCTs in humans exist yet; one large registered RCT (185 women) completed enrollment but has not published results as of 2025.
EGCG is the predominant catechin in green tea and contributes to its thermogenic and energy expenditure-enhancing effects. In combination with caffeine, EGCG has been shown in RCTs and meta-analyses to significantly increase resting energy expenditure and fat oxidation during exercise, making it a well-studied ingredient for energy metabolism support.
EGCG protects sperm from oxidative DNA damage, reduces sperm deformity, inhibits spermatogenic cell apoptosis, and at low concentrations improves sperm motility and capacitation. Addition of EGCG to thawed sperm for IVF after chemotherapy significantly increased penetration and fertilization rates in human studies.
EGCG has been shown to improve oocyte maturation quality and developmental capacity in vitro, support ovarian function, and reduce oxidative stress in female reproductive tissues. Preclinical evidence also suggests benefits for pregnancy complications such as preeclampsia via the eNOS/Nrf2/HO-1 pathway.
EGCG is the primary bioactive catechin in green tea with documented effects on brain alpha-wave activity, working memory circuitry, and neuroprotection. A placebo-controlled crossover RCT found EGCG (135 mg) significantly increased occipital and posterior alpha activity associated with attentional engagement. It also modulates acetylcholinesterase, BDNF, and oxidative stress relevant to sustained focus.
EGCG, the main bioactive catechin in green tea, stabilizes mast cells and attenuates FcεRI signaling, reducing IgE-mediated allergic responses. It inhibits antigen-stimulated mast cell degranulation through 67LR-mediated signaling. A 2025 comprehensive allergy review confirmed EGCG's preclinical anti-allergic evidence including reduction of airway inflammation, though human clinical trial data remain limited.
EGCG, the principal catechin of green tea, has demonstrated gallstone-preventing effects in a mouse model of gallstone disease, possibly through anti-inflammatory activity. Life Extension's PubMed-supported gallstones protocol includes EGCG among natural interventions that may reduce gallstone formation risk. Population-based studies suggest green tea consumption (source of EGCG) is associated with reduced gallstone risk.
EGCG is the major catechin in green tea and has demonstrated in vitro anti-H. pylori activity including inhibition of urease and reduction of bacterial adherence to gastric mucosa. It also reduces pro-inflammatory cytokine expression in gastric epithelial cells relevant to gastritis pathogenesis.
EGCG protects retinal pigment epithelial cells from oxidative stress-induced death, slows photoreceptor degeneration in animal models of retinitis pigmentosa, and has demonstrated beneficial effects across multiple ocular pathologies including glaucoma, diabetic retinopathy, dry eye, and cataracts in preclinical studies. Human clinical evidence remains limited but mechanistic and animal data are substantial.
EGCG, the major catechin in green tea, has shown IOP-lowering effects in human volunteers and neuroprotection in glaucoma animal models. A randomized placebo-controlled trial found EGCG supplementation (200 mg/day for 3 months) improved pattern electroretinogram amplitudes in early-to-moderate POAG patients. A 2022 clinical study confirmed EGCG 400 mg reduced IOP significantly in healthy volunteers.
EGCG, the primary catechin in green tea, has been shown to stimulate GLP-1 secretion in intestinal enteroendocrine cells (NCI-H716) in vitro. It is used as a positive control in GLP-1 secretion assays and has supporting evidence from in vitro and animal models for GLP-1-mediated satiety.
EGCG, the major catechin of green tea, specifically inhibits IL-1β expression, blocks ROS production, and limits leukocyte infiltration in MSU crystal-induced peritonitis models directly replicating acute gout inflammation. EGCG also suppresses NLRP3 inflammasome and NF-κB, key molecular drivers of gouty arthritis. Tea leaf extracts consistently show high XO inhibitory activity in comparative plant extract studies.
EGCG is the predominant and most bioactive catechin in green tea, directly responsible for much of its periodontal benefit. It inhibits P. gingivalis at 250–500 μg/ml, suppresses NF-κB, COX-2, and MMP-1 expression, and inhibits osteoclast-mediated alveolar bone resorption. Clinical investigations confirm its efficacy as an adjuvant therapy for periodontal disease.
EGCG, the major polyphenol in green tea, modulates gut microbiota by inhibiting potentially harmful Bacteroidetes and Firmicutes while preserving Lactobacillus, and by being extensively biotransformed by gut bacteria into bioactive metabolites. Multiple studies document its bidirectional gut microbiome interactions.
EGCG promotes hair follicle growth by stimulating proliferation of dermal papilla cells and outer root sheath cells via Sonic Hedgehog (Shh) and AKT signaling pathways. It also inhibits 5α-reductase, the enzyme that converts testosterone to DHT, a key driver of androgenic alopecia.
EGCG, the major polyphenol of green tea, promotes hair growth by stimulating proliferation and inhibiting apoptosis of dermal papilla cells, and selectively inhibiting 5-alpha reductase. In vitro and in vivo studies confirm these mechanisms. A systematic review of 16 RCTs identified green tea among the natural products with meaningful evidence for hair loss.
EGCG is the principal catechin of green tea and one of the most studied plant bioactives for healthy aging. It activates AMPK and autophagy, inhibits mTOR and NF-κB, and peer-reviewed studies confirm cardiovascular benefits, metabolic support, and longevity pathway activation. ConsumerLab and multiple systematic reviews confirm its safety and activity.
EGCG is the principal bioactive catechin in green tea responsible for thermogenic and fat-oxidizing effects via COMT inhibition and TRPV1/AMPK pathway activation. Clinical studies at doses of 270–600 mg/day demonstrate modest reductions in body weight, body fat, and waist circumference compared to placebo.
EGCG (epigallocatechin gallate), the principal catechin in green tea, has clinical and meta-analytic evidence supporting cardiovascular benefits including LDL cholesterol reduction, blood pressure lowering, and improved endothelial function. A systematic review of 17 RCTs found that 107–856 mg/day for 4–14 weeks reduced LDL-C by approximately 9.3 mg/dL. A separate crossover trial in coronary artery disease patients showed acute endothelial function improvement following a single 300 mg dose. Evidence is promising but not yet conclusive across all populations.
EGCG, the primary bioactive catechin in green tea, has been shown in a randomized controlled pilot trial to reduce uterine fibroid volume and associated heavy menstrual bleeding. Women with symptomatic fibroids receiving 800 mg/day green tea extract (45% EGCG) for 4 months experienced a 32.6% reduction in fibroid volume and 32.4% reduction in symptom severity including blood loss, compared to placebo. Fibroids are a leading structural cause of heavy periods.
EGCG, the major catechin in green tea, reduces HSV-1 titers by 3,000-fold and HSV-2 by 10,000-fold in vitro by binding viral glycoproteins B and D to block cell entry. EGCG-stearate topical preparation reduced inflammation in two recurrent HSV-1 patients. It is active at vaginal pH, suggesting potential as a topical microbicide against HSV-2.
EGCG is the predominant catechin in green tea with documented anti-estrogenic effects including inhibition of estrogen-induced receptor signaling and suppression of estrogen-dependent cell proliferation. It inhibits nicotine- and estrogen-induced receptor upregulation in breast cancer cells and is included in evidence-based estrogen-control supplement protocols.
EGCG, the principal catechin in green tea, inhibits tyrosinase and melanin synthesis, and has been identified in systematic reviews as a natural depigmenting agent. It reduces UV-induced pigmentation through antioxidant and anti-inflammatory mechanisms.
EGCG, the predominant catechin in green tea, improves insulin sensitivity through multiple mechanisms including GLUT4 translocation promotion, PTP1B inhibition, and anti-inflammatory actions in skeletal muscle, liver, and adipose tissue. In vitro studies confirm suppression of insulin resistance and glucose uptake enhancement; human evidence from green tea studies shows reductions in fasting glucose in some populations.
EGCG is the major catechin of green tea and is identified in a PMC systematic review as one of the phytochemicals effective for prevention of urolithiasis. It inhibits calcium oxalate crystal formation and reduces oxidative stress in renal cells, protecting against crystal-induced cell injury and adhesion. Multiple preclinical studies in hyperoxaluric animal models support its antiurolithic action.
Epigallocatechin gallate (EGCG), the major catechin in green tea, has documented effects on intestinal barrier function. A 2023 review in MDPI Molecules specifically listed EGCG among polyphenols studied for leaky gut-related diseases. EGCG reduces intestinal inflammation, modulates tight junction protein expression, and supports beneficial gut microbiota composition in multiple in vitro and animal studies.
EGCG is the most abundant and bioactive catechin in green tea, with neuroprotective, anti-neuroinflammatory, and pro-neurogenic properties. It inhibits acetylcholinesterase, prevents amyloid-beta aggregation, and upregulates BDNF. Clinical studies with green tea extracts containing EGCG show improvements in memory and cognitive function.
A randomized, double-blind trial (NCT02147041, n=102 women with central obesity, 856.8 mg EGCG/day for 12 weeks) found significantly lower ghrelin levels and higher adiponectin in the EGCG group versus placebo, along with significant weight loss and reduced BMI and waist circumference. EGCG is the primary bioactive catechin in green tea proposed to mediate these appetite-hormone effects.
EGCG is the principal hepatoprotective polyphenol in green tea, demonstrating antioxidant, anti-inflammatory, antiviral, and anti-fibrotic activity in the liver. Research confirms EGCG inhibits hepatitis B and C viral replication, reduces hepatic lipid accumulation, and activates Nrf2-mediated phase II detoxification pathways. Clinical trial reviews confirm it reduces liver enzymes in liver disease.
EGCG is the primary bioactive catechin of green tea with strong preclinical evidence for lung anti-inflammatory and antifibrotic effects. It inhibits NF-κB, reduces MMP-9-mediated tissue destruction in COPD emphysema models, and shows antiviral activity against respiratory pathogens. Epidemiological data supports association with lower lung cancer risk.
EGCG protects retinal pigment epithelial (RPE) cells from oxidative damage central to AMD pathogenesis, downregulates VEGFA to suppress neovascularization in wet AMD, and protects against UV-induced retinal cell damage. Preclinical evidence is substantial; controlled clinical trials are still needed.
EGCG, the major catechin of green tea, selectively inhibits 5α-reductase and stimulates dermal papilla cell proliferation and survival. PMC reviews (PMC11549889, PMC9963650) and a 2025 Frontiers in Nutrition systematic review confirm EGCG among phytochemicals with documented beneficial effects in AGA. In vitro and preclinical studies consistently support its DHT-reducing and follicle-promoting mechanisms.
EGCG, the major catechin in green tea, inhibits mast cell histamine release by blocking tyrosine phosphorylation of focal adhesion kinase pp125(FAK) and suppressing intracellular Ca2+ influx, as documented in PubMed (PMID 10924324). Both in vitro (RBL-2H3, rat peritoneal mast cells) and in vivo animal studies confirm dose-dependent suppression of degranulation and histamine. EGCG also inhibits histidine decarboxylase, reducing histamine biosynthesis.
EGCG is the predominant polyphenol catechin in green tea with documented neuroprotective and pro-cognitive effects. It reduces amyloid-β aggregation, inhibits acetylcholinesterase mildly, and supports hippocampal neurogenesis. Epidemiological studies link regular green tea consumption to reduced cognitive decline. Human trial evidence for EGCG specifically on memory is emerging but limited compared to the broader green tea literature.
EGCG, the principal catechin in green tea, has neuroprotective and cognitive-enhancing properties. It modulates BDNF signaling, reduces neuroinflammation, and studies show it supports attention and cognitive processing. Often studied alongside caffeine and L-theanine as part of the green tea complex.
EGCG (Epigallocatechin Gallate), the primary bioactive polyphenol in green tea, has been investigated in multiple human randomized controlled trials (RCTs) and systematic reviews for its effects on metabolic syndrome components, including dyslipidemia, insulin resistance, hypertension, and visceral adiposity. Clinical evidence shows modest but meaningful improvements in triglycerides, LDL cholesterol, blood pressure, and inflammatory markers, particularly with doses of 150–800 mg/day over 8–16 weeks. Results are mixed across trials, with some parameters (e.g., HbA1c, fasting insulin) showing only modest or non-significant effects. Overall, the evidence base is scientific but not yet conclusive enough to support EGCG as a standalone intervention for metabolic syndrome.
EGCG, the predominant catechin in green tea, has human clinical evidence supporting its role in modulating metabolism, primarily through effects on energy expenditure, lipid metabolism, and fat oxidation. Multiple randomized controlled trials and systematic reviews confirm modest but measurable metabolic effects. Mechanistically, EGCG activates AMP-activated protein kinase (AMPK) and inhibits catechol-O-methyltransferase (COMT), both of which shift substrate utilization toward fat oxidation and reduce lipogenesis. Evidence is strongest for improvements in lipid profiles and body composition, though effect sizes are generally modest.
EGCG, the major catechin of green tea, competitively inhibits DNMT1 and DNMT3 (DNA methyltransferases), reactivating epigenetically silenced genes. A 2025 PMC systematic review (PMC12554032) of 76 studies identifies EGCG as the most frequently studied food-derived DNMT modulator. Evidence is primarily from in vitro and animal studies.
EGCG, the principal catechin in green tea, enhances mitochondrial electron transport and oxidative phosphorylation efficiency, promotes mitochondrial biogenesis via AMPK activation, and induces mitophagy. Studies show it increases PGC-1α, NRF-1, and mtDNA replication, making it one of the better-characterized natural mitochondrial modulators.
EGCG is one of the most studied natural neuroprotective compounds, inhibiting amyloid-beta and alpha-synuclein aggregation, reducing neuroinflammation, promoting mitochondrial health, and activating neuronal survival pathways. Clinical studies demonstrate reductions in neurodegenerative biomarkers and improvements in cognitive and motor function.
EGCG, the primary catechin of green tea, modulates GABAergic and dopaminergic neurotransmission, upregulates BDNF, and exerts antioxidant neuroprotection supporting synaptic plasticity. The 2017 Neural Plasticity review (Sangiovanni et al.) identified EGCG as a BDNF modulator from Camellia sinensis. Multiple preclinical studies confirm hippocampal neurogenesis promotion.
EGCG, the primary catechin in green tea, increases eNOS phosphorylation, vascular cGMP, and BH4 levels while reducing oxidative stress in animal hypertension models. It is recognized among natural polyphenols that positively modulate eNOS activity and endothelial NO production in peer-reviewed literature.
EGCG, the primary catechin in green tea, has demonstrated broad-spectrum antimicrobial activity against oral disease-associated microbes including S. mutans, P. gingivalis, A. actinomycetemcomitans, and Solobacterium moorei (halitosis). Multiple in vitro studies confirm inhibition of biofilm formation and virulence factors. Human studies of green tea consumption show measurable shifts in oral microbiota taxa.
EGCG inhibits osteoclast formation via the RANKL/OPG axis, promotes osteoblast proliferation and bone mineralization, and protects against glucocorticoid-induced bone loss. Population data show habitual tea drinkers have measurably higher BMD and lower fracture rates, and animal studies confirm direct EGCG-mediated protection.
EGCG, the major polyphenol in green tea, has demonstrated neuroprotective effects in multiple experimental PD models through inhibition of α-synuclein aggregation, MAO-B inhibition, antioxidant activity, and iron chelation. Epidemiological studies link regular green tea consumption to reduced PD risk. Robust clinical trials specific to EGCG in PD are limited.
EGCG, the major bioactive catechin from green tea, has insulin-sensitizing, anti-inflammatory, and anti-androgenic properties relevant to PCOS. It activates AMPK, reduces oxidative stress, and has shown improvements in fasting insulin, BMI, and androgen levels in PCOS-related studies.
EGCG is the primary bioactive catechin in green tea that activates AMPK, promotes mitochondrial biogenesis, and enhances fat oxidation during exercise—effects that spare glycogen and improve endurance capacity. Multiple human studies show EGCG supplementation improves aerobic performance, reduces exercise-induced oxidative stress, and supports endurance adaptations when combined with training.
EGCG, the principal catechin from green tea, has demonstrated direct antimicrobial activity against Streptococcus pneumoniae and antiviral activity against influenza and SARS-CoV-2. It inhibits pneumococcal adhesion to host cells and modulates pneumonia-associated inflammatory cascades through NF-κB and NLRP3 inhibition. It is a documented antiviral component in propolis-related COVID-19 pneumonia research.
A Korean randomized clinical trial found green tea extract (containing EGCG) reduced recurrent colorectal adenoma incidence from 31% to 15% at 1 year post-polypectomy. The MIRACLE trial (n=1,001, 41 German centres) examined 300 mg EGCG daily for 3 years after polypectomy. The J-FAPP Study I (2026, n=160 FAP patients) formally evaluated green tea extract (1.5 g/day, 2 years) for suppressing colorectal polyp development in FAP.
EGCG, the principal catechin of green tea, has antiviral activity against SARS-CoV-2 (inhibiting spike protein-ACE2 binding) and potent anti-inflammatory and antioxidant effects relevant to post-viral recovery. It is included in a post-COVID recovery formulation (MitoCore, Holistic Primary Care 2023 protocol) recommended for 90 days.
EGCG, the principal catechin in green tea, is identified by the NCI's PDQ as one of the most potent modulators of molecular pathways relevant to prostate carcinogenesis. It inhibits androgen receptor signaling, suppresses PSA production, induces apoptosis, and reduces prostate tumor size in preclinical models. Early-phase clinical trials confirm accumulation in prostate tissue.
EGCG, the major catechin in green tea, has been studied in preclinical psoriasis models. Mouse studies show it attenuates skin inflammation, reduces T-cell infiltration, and suppresses IL-17, IL-22, and IL-23. A nanoparticle EGCG formulation produced a 20-fold stronger therapeutic effect in a murine psoriasis model compared to free EGCG. No human clinical RCTs are available.
EGCG is the principal bioactive catechin in green tea with potent anti-inflammatory effects in RA, including inhibition of NF-κB, COX-2, TNF-α, IL-6, and matrix metalloproteinases. Multiple preclinical studies in collagen-induced arthritis models and cell culture work with RA synoviocytes demonstrate significant anti-arthritic activity.
EGCG, the primary bioactive catechin of green tea, has been shown to reduce papulopustular rosacea lesion count. Topical green tea polyphenols (predominately EGCG) produced ~25% reduction in rosacea symptoms (PMID 23346663). Reviewed as an evidence-based complementary rosacea therapy in J Drugs Dermatol 2018.
EGCG, the primary catechin of green tea, has demonstrated anti-scarring effects by inhibiting the Akt/PI3K pathway, suppressing fibroblast proliferation, reducing TGF-β1 expression, and decreasing collagen synthesis in hypertrophic scar and keloid models. One RCT rated 1b supports its clinical use for scar management.
EGCG is the primary catechin in green tea (~59% of catechin content) and the most studied individual tea polyphenol for skin anti-aging. A controlled human clinical trial using topical green tea extract showed 36–63% wrinkle improvement. EGCG inhibits MMP-1, -2, and -9 via MAPK/MEK-ERK and NF-κB pathways, protecting dermal collagen from UV-induced degradation.
EGCG is the primary bioactive catechin of green tea with clinical evidence for protecting dermal collagen and elastin from UV-induced degradation. An RCT of 50 adults found oral green tea extract with vitamin C mitigated UV-induced degradation of skin elastin fibers and preserved elasticity. EGCG inhibits MMP activity, stimulates elastin and fibronectin production, and has emerging clinical use in aesthetic medicine for loss of elasticity.
EGCG mitigates physiological and behavioral consequences of chronic stress in multiple rodent CUMS models, including reversing hypothalamic-pituitary-adrenal axis dysregulation markers, neuroinflammation, and depressive behavior. The stress-reducing effect is tied to its modulation of the NF-κB/caspase-1 pathway and NLRP3 inflammasome.
EGCG, the major catechin in green tea, has extensive evidence for skin photoprotection in preclinical and some human studies. It inhibits UV-induced leukocyte infiltration, antigen-presenting cell depletion, and oxidative stress in skin. Human studies combining green tea polyphenols showed reduced UV-induced erythema and decreased pro-inflammatory 12-LOX metabolites.
EGCG is the major bioactive catechin in green tea and is the primary thermogenic compound in green tea extract. It increases 24-hour energy expenditure and fat oxidation, partly by inhibiting catechol-O-methyltransferase (COMT) to prolong norepinephrine signaling. Human RCTs confirm effects on energy expenditure, especially when combined with caffeine.
EGCG, the major active catechin in green tea, supports tooth remineralization through MMP inhibition (protecting dentinal collagen), S. mutans biofilm suppression, dentinal tubule occlusion, and optimization of the mineralization microenvironment. Multiple in vitro and in situ studies document its protective effects on dental hard tissues.
Two clinical trials found EGCG significantly reduced fasting plasma triglyceride levels in obese subjects after 8 weeks of supplementation. A meta-analysis confirmed that green tea extract supplementation for more than 8 weeks at doses exceeding 800 mg/day significantly reduced serum triglyceride concentrations in type 2 diabetes patients.
EGCG is the primary catechin in green tea responsible for antiviral activity against influenza, RSV, and other respiratory viruses. Green tea EGCG supplementation significantly reduced laboratory-confirmed influenza infections in a double-blind RCT of healthcare workers (n=197, OR 0.27). It inhibits viral neuraminidase, hemagglutinin, and RNA polymerase.
EGCG from green tea has demonstrated anti-uterine fibroid activity in both preclinical models and a human pilot RCT. A randomized controlled trial found that 800 mg/day EGCG over 4 months significantly reduced uterine fibroid volume and improved anemia and quality of life in premenopausal women compared to placebo.
EGCG is the most abundant and bioactive catechin in green tea, with well-documented broad-spectrum antiviral activity including against influenza A, HSV, HIV, HCV, and SARS-CoV-2. It inhibits viral attachment to heparan sulfate and sialic acid on host cells and suppresses viral 3CL-protease activity. Both in vitro and preliminary human-level evidence support antiviral immune benefits.
EGCG, the primary bioactive catechin in green tea, demonstrates antioxidant and cytoprotective effects on melanocytes in vitro, protecting against H2O2-induced cell death. Combined with quercetin and folic acid it shows synergistic melanocyte protection in cell culture. A 2023 Mendelian randomization study found standard tea consumption may causally reduce vitiligo risk.
EGCG is the primary catechin (>55%) in FDA-approved sinecatechins ointment (Veregen®) for external genital and perianal warts. Phase 3 RCTs in 1,000+ patients achieved 54–57% complete clearance vs ~34% with placebo. EGCG inhibits HPV-activated cell proliferation and induces apoptosis in HPV-positive cell lines; HeLa cells showed 75% growth inhibition at 313 µM.
Volver