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3 Institute of Human Nutrition and Food Science, Christian-Albrechts-University, 24118 Kiel, Germany; 4 Hugh Sinclair Human Nutrition Group, School of Chemistry, Food Biosciences and Pharmacy, University of Reading, Reading RG6 6AP, United Kingdom; and 5 Division of Nutritional Sciences, Faculty of Health and Medical Sciences, University of Surrey, Guildford GU2 7HX, United Kingdom
* To whom correspondence should be addressed. E-mail: frank{at}foodsci.uni-kiel.de.
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ABSTRACT |
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 TOP ABSTRACT IntroductionMethodsResultsDiscussionLITERATURE CITED |
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Introduction |
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150 mg/kg were lethal (3). The limited data on hepatotoxicity induced by dietary GTP in humans are based on case reports of abnormally high concentrations of liver injury markers. In these patients, cessation of green tea consumption normalized liver function and resumption of green tea drinking again elevated these biomarkers (4,5). Impaired liver function was observed in participants regularly consuming as little as 6 cups (
900-1200 mL) per day of green tea or 720 mg/d GTE (2). On the other hand, GTP were also suggested to protect from hepatic injury. For example, ingestion of 1 or 2% GTE in the diet for 6 wk reduced ALT and aspartate transaminase (AST) serum activities in obese but not in lean mice compared with control animals (6). Many of the human intervention studies reporting biological effects of green tea or GTP supplements have been performed in at-risk populations such as obese and/or hypercholesterolemic participants or smokers (7,8). Hence, little is known regarding the potential biological effects of dietary GTP on biomarkers of liver function and cardiovascular disease (CVD) risk in healthy individuals. Our aim was to test whether the daily consumption of a dose of GTP that was high yet achievable by dietary intake over a period of 3 wk would affect liver and kidney function and/or improve biomarkers of CVD risk in healthy men.
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Methods |
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Capsules. An aqueous GTE prepared from the leaves of Camellia sinensis L. (a gift of Cognis Deutschland) was used to make the GTE capsules. The GTE consisted of 88% native dry extract and 12% maltodextrin. GTE capsules were filled with 384 mg GTE containing 119 mg polyphenols (in mg: epigallocatechin, 47; epigallocatechingallate, 25; epicatechingallate, 14; gallocatechin, 9; gallocatechingallate, 8; epicatechin, 5; catechingallate, 3; catechin, 1; and ellagic acid, 7) and 19 mg caffeine. Placebo capsules were filled with 369 mg maltodextrin (a kind gift of Cognis) and 19 mg caffeine (Synopharm) each. Both the GTE and placebo powders were mixed with the flow regulating excipient silicium dioxide (0.1% by weight) to improve flow properties prior to filling the gelatin capsules. Capsules were sealed in 6 capsule blister packs (kindly provided by Alcan Packaging Singen GmbH).
Study protocol.
The trial was designed as a double-blind, placebo-controlled parallel study. The 35 eligible volunteers were randomized (stratified for age and BMI) into 1 of 2 treatment groups [GTP (n = 18) or placebo (n = 17)] with similar BMI (GTP, 26.0 ± 3.0 kg/m2; placebo, 25.1 ± 3.0 kg/m2; mean ± SD) and age (GTP, 41.0 ± 9.5 y; placebo, 40.8 ± 9.5 y). Participants took a total of 6 capsules per day, 2 capsules, together with a glass of water, before each principal meal, for 3 wk and were instructed to limit their daily tea and coffee consumption to 
3 cups (200 mL each) but to otherwise maintain their normal diet and exercise patterns. The 6 GTP capsules per day provided 714 mg GTP, of which 670 mg were flavanols. Compliance was determined by counting the returned capsules at the end of the trial and was high (GTP, >99.4%; placebo, >99.2%). Participants collected 24-h urine samples (50 mg sodium azide was added as a preservative to the urine containers) starting with the first urination of the day prior to commencement of supplementation and of the last day of the intervention period. Aliquots of the urine samples were stored at –20°C until analysis. Participants were instructed to refrain from strenuous physical activity and alcohol consumption on the day prior to blood sampling. Blood samples were drawn into tubes containing 0.05 mL 15% K3 EDTA (Vacutainer; Becton Dickinson UK) after an overnight fast on the first and last days of the 3-wk intervention period. Plasma was obtained by centrifugation at 1000 x g for 10 min and aliquots were stored at –80°C until analysis. Two participants dropped out because of insomnia due to caffeine sensitivity and their data were excluded from all analyses and are not presented herein.
Urinary flavanols and metabolites. Urine samples were enzyme treated with β-glucuronidase as described elsewhere (9). Samples were analyzed using an Agilent 1100 liquid chromatography system with a Nova-Pak C18 column (particle size, 4 µm; length x i.d., 250 x 4.6 mm) and guard column (4 µm, 15 x 4.6 mm). Mobile phase A consisted of methanol:water:5 mol/L HCl (5:94.9:0.1, v:v:v) and mobile phase B of acetonitrile:water:5 mol/L HCl (50:49.9:0.1, v:v:v). The following gradient system was used (min/% mobile phase B): 0/0, 5/0, 40/50, 60/100, 65/100, and 65.1/0 with a flow rate of 0.7 mL/min. The eluent was monitored by photodiode array detection at 280 nm with spectra of products obtained over the 220- to 600-nm range and by fluorescent detection (excitation wavelength, 276 nm; emission wavelength, 316 nm). Calibration curves were obtained using authentic standards and were linear over the entire range with CV > 0.995. O-methylated flavanols were generated as described previously (10).
Laser Doppler imaging with iontophoresis. We took laser Doppler imaging measurements with each participant in a supine position after 30 min of acclimatization in a quiet room with an ambient temperature of 22 ± 1°C prior to blood sampling. Two ION6 perspex chambers (Moor Instruments) with an internal platinum wire electrode were placed on the volar aspect of the forearm and attached to the skin using double-sided adhesive discs (MIC-1AD; Moor Instruments). Care was taken to avoid hair, broken skin, and superficial veins. The arm was supported on an armrest and a Velcro band was fastened around the wrist to prevent movement of the arm out of the scan area. The chambers were connected to a MIC2 iontophoresis controller (Moor Instruments). Then 2.5 mL of 1% acetylcholine chloride (Sigma-Aldrich) in 0.5% NaCl solution was placed in the anodal chamber and 2.5 mL of 1% sodium nitroprusside (Sigma-Aldrich) in 0.5% NaCl solution was placed in the cathodal chamber. Circular glass coverslips were placed over each chamber to prevent loss of solutions. Current delivery was controlled by laser Doppler imager software 3.08ib (Moor Instruments). We measured skin perfusion using a moorLDI2-VR laser Doppler imager (Moor Instruments) equipped with a red laser (wavelength 690 nm; maximum accessible power of 2.5 mW). The scanner head was positioned 30 cm above the chambers. The laser light was directed by a moving mirror in a raster fashion over both chambers. The backscattered light was then directed by the moving mirror onto the detectors and converted into a signal proportional to tissue blood flow (flux) and the concentration of moving blood cells. Twenty repeat scans were taken, the first with no current to act as a control, then 4 scans at 5 µA, 4 at 10 µA, 4 at 15 µA, and 2 at 20 µA to give a total charge of 8 mC; the final 5 scans were measured without any current. The area under the flux vs. time curve over the 20 scans was deemed to indicate the microvascular response.
Anthropometric measurements. Body weight, body height, and blood pressure were determined by a trained technician after the laser Doppler imaging measurements and blood draws were completed.
Liver and kidney function.
Plasma concentrations of total bilirubin, albumin, uric acid, and urea as well as enzyme activities of 
-glutamyl-transpeptidase (GGT), ALT, and AST were determined with enzymatic photometric kits on a Hitachi Modular P autoanalyzer (Roche Diagnostics) at the central laboratory of the university hospital in Kiel.
Plasma asymmetric dimethylarginine. Plasma concentrations of asymmetric dimethylarginine (ADMA) were measured with a commercial kit (catalog no. EA201/96; DLD Diagnostika) according to the manufacturer's protocol.
Plasma, lipids, glucose, and tocopherols. Total cholesterol, HDL cholesterol, nonesterified fatty acids (NEFA), triacylglycerols (TAG), and glucose concentrations in the plasma samples were determined using an ILab 600 biochemical analyzer and enzymatic colorimetric kits (Instrumentation Laboratories). Tocopherols were analyzed using HPLC with fluorescence detection and were quantified against tocopherol standards (catalog no. 613424; Merck) as described elsewhere (11).
Urinary creatinine and carboxyethyl hydroxychromanols.
Concentrations of creatinine in the 24-h urine samples were measured on a SPACE automatic biochemical analyzer (Alfa-Wasserman) using a colorimetric kit (Randox). Urinary carboxyethyl hydroxychromanols (CEHC) were quantified by HPLC with amperometric electrochemical detection using 
-CEHC (BASF AG) and -CEHC (Cayman Chemical) as external standards following the method of Lodge et al. (12).
Statistical analyses. Data passing a Kolmogorov-Smirnov test for Gaussian distribution were analyzed with GraphPad Prism software (version 4.0; GraphPad Software) by means of 2-way repeated-measures ANOVA, with Bonferroni post hoc correction for significant interactions using treatment and time as main factors. Statistical comparisons of skewed data were made using the statistical software Instat 3 for Macintosh (version 3.0b; GraphPad Software) by way of a Mann-Whitney U test for differences between the experimental groups (GTP vs. placebo) and a Wilcoxon's matched-pairs Signed Rank test for comparison of data obtained at baseline and after intervention (within experimental groups). Differences were considered significant at P < 0.05 and reported values represent means ± SD unless otherwise noted.
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Results |
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- and -tocopherol metabolites -CEHC and -CEHC, respectively, and the kidney function biomarker creatinine were not affected by dietary intervention (Table 1).
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Concentrations of total cholesterol, HDL cholesterol, NEFA, TAG, - and -tocopherol, and glucose in plasma obtained from fasting participants were not affected by the treatments. Time (P < 0.04) and the time x treatment interaction (P < 0.03) affected the ratio of total:HDL cholesterol (Table 1).
Systolic and diastolic blood pressure, plasma ADMA concentrations (Table 1), and endothelium-dependent and -independent vascular relaxation did not differ between treatments at baseline and postintervention (data not shown).
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Discussion |
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TOPABSTRACTIntroductionMethodsResultsDiscussionLITERATURE CITED |
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Because the uptake of GTP into the organism is a prerequisite for any potential biological function, we determined the urinary excretion of epicatechin and its 3'-O- and 4'-O-methylated metabolites as a bioavailability indicator. The significant increases in urinary excretion of epicatechin and its metabolites in participants ingesting GTP [consistent with ranges reported in the literature (20,21)] but not in those taking placebo supplements were indicative of the absorption and subsequent excretion of catechins in the GTP group (Fig. 1).
The applied dose is comparable to approximately twice the estimated mean daily intake of catechins in the UK (22) and 16–17 times that in a Dutch cohort (23). Daily consumption of this high dose of GTP, equivalent to 6–8 cups of green tea (24), for 3 wk did not affect markers of liver (AST, ALT, GGT, and bilirubin) and kidney function (urea, uric acid, albumin, and urinary creatinine) in our healthy men (Table 1), consistent with a comparable trial in healthy Japanese men who consumed 690 mg/d (treatment) or 22 mg/d catechins (control) for 12 wk (25). Our findings are further supported by trials in which obese participants ingested green tea beverages or supplements (daily catechin intake: treatment, 491–583 mg; control, 75–96 mg; duration: 12 or 24 wk) (7,26,27) and smokers ingested 8 g/d powdered green tea for 2 wk (28). Our placebo capsules were free of GTP but contained similar amounts of caffeine to our GTP capsules; the daily caffeine dose was comparable to 1 cup (200 mL) of coffee (29). The above studies, on the contrary, either used relatively high concentrations of GTP (22–96 mg/d) in their control treatments (7,25,27), did not use caffeine in their placebos (26), or were uncontrolled (28). Overall, the above findings from human trials are in agreement with epidemiological studies reporting no significant correlation of green tea consumption with serum activities of GGT, AST, and ALT (30,31).
The isolated cases of acute liver failure due to GTP consumption (4,5,32,33), when weighed against the number of participants involved in controlled human intervention trials (7,25–27) and epidemiological studies (30,31), suggest that other unknown factors may have contributed to hepatotoxicity. In this context, the individual genetic makeup might be of particular importance (4). Genetic variations (single nucleotide polymorphisms) in metabolic (phase I and II) enzymes, for example, may be responsible for the generation and/or reduced clearance of toxic intermediates in some individuals, whereas others are unaffected (34).
In our healthy participants, daily consumption of GTP reduced the ratio of total cholesterol:HDL cholesterol but did not affect fasting concentrations of blood lipids (total cholesterol, HDL cholesterol, TAG, NEFA) or glucose (Table 1) in agreement with other human intervention studies of healthy participants, smokers, and type 2 diabetics (25,28,35–40). A change by 1 unit in the ratio of total:HDL cholesterol was previously associated with a 53% change in risk of myocardial infarction (41). Hence, the decrease of the total:HDL cholesterol ratio (by 0.3 units) in our participants might represent a significant risk reduction.
GTP did not alter plasma tocopherol or urinary CEHC concentrations in men (Table 1) despite our previous findings of increased -tocopherol concentrations in epicatechin- and catechin-fed rats (42) and the reported reduction of the lymphatic absorption of -tocopherol in GTE-fed rats (43).
We did not observe a chronic effect of GTP intake on endothelium-dependent or -independent vascular function (data not shown). In healthy smokers, on the other hand, intake of 8 g/d powdered green tea (740 mg GTP/d) improved endothelial function (28). Increased vascular relaxation was also reported for women ingesting GTE for 5 wk (44). The observed discrepancies may be due to the different study cohorts (men vs. women and smokers, respectively). Consistent with the lack of effect on vascular function, blood pressure and ADMA plasma concentrations were unaffected by GTP treatment in our healthy participants (Table 1). In support of our findings, supplementation of obese women with caffeine-containing GTE capsules 3 times/d for 12 wk, despite the absence of caffeine in the placebo capsules, did not affect blood pressure (26). In obese participants ingesting 583 mg/d catechins for 12 wk, systolic blood pressure decreased in only those participants whose initial blood pressure at baseline was 130 mm Hg (7).
In conclusion, supplementation of healthy men for 3 wk with a high daily dose of 714 mg GTP did not cause adverse effects or impair liver and kidney function and did not improve CVD risk biomarkers other than the ratio of total:HDL cholesterol. Therefore, despite isolated reports of acute liver failure, a high intake of green tea for 3 wk appears to be safe for healthy men.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 Author disclosures: J. Frank, T. W. George, J. K. Lodge, A. Rodriguez-Mateos, J. P. E. Spencer, A. M. Minihane, and G. Rimbach, no conflicts of interest.
6 Abbreviations used: ADMA, asymmetric dimethylarginine; ALT, alanine transaminase; AST, aspartate transaminase; CEHC, carboxyethyl hydroxychromanol; CVD, cardiovascular disease; GGT, -glutamyl-transpeptidase; GTE, green tea extract; GTP, green tea polyphenol; NEFA, nonesterified fatty acid; TAG, triacylglycerol.
Manuscript received 15 July 2008. Initial review completed 27 August 2008. Revision accepted 3 November 2008.
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1. Higdon JV, Frei B. Tea catechins and polyphenols: health effects, metabolism, and antioxidant functions. Crit Rev Food Sci Nutr. 2003;43:89–143.[CrossRef][Medline]
2. Sarma DN, Barrett ML, Chavez ML, Gardiner P, Ko R, Mahady GB, Marles RJ, Pellicore LS, Giancaspro GI, et al. Safety of green tea extracts: a systematic review by the us pharmacopeia. Drug Saf. 2008;31:469–84.[Medline]
3. Galati G, Lin A, Sultan AM, O'Brien PJ. Cellular and in vivo hepatotoxicity caused by green tea phenolic acids and catechins. Free Radic Biol Med. 2006;40:570–80.[CrossRef][Medline]
4. Federico A, Tiso A, Loguercio C. A case of hepatotoxicity caused by green tea. Free Radic Biol Med. 2007;43:474.[Medline]
5. Jimenez-Saenz M, Martinez-Sanchez Mdel C. Acute hepatitis associated with the use of green tea infusions. J Hepatol. 2006;44:616–7.[Medline]
6. Bruno RS, Dugan CE, Smyth JA, DiNatale DA, Koo SI. Green tea extract protects leptin-deficient, spontaneously obese mice from hepatic steatosis and injury. J Nutr. 2008;138:323–31.
7. Nagao T, Hase T, Tokimitsu I. A green tea extract high in catechins reduces body fat and cardiovascular risks in humans. Obesity (Silver Spring). 2007;15:1473–83.[Medline]
8. Nagaya N, Yamamoto H, Uematsu M, Itoh T, Nakagawa K, Miyazawa T, Kangawa K, Miyatake K. Green tea reverses endothelial dysfunction in healthy smokers. Heart. 2004;90:1485–6.
9. Rechner AR, Kuhnle G, Bremner P, Hubbard GP, Moore KP, Rice-Evans CA. The metabolic fate of dietary polyphenols in humans. Free Radic Biol Med. 2002;33:220–35.[CrossRef][Medline]
10. Spencer JP, Schroeter H, Kuhnle G, Srai SK, Tyrrell RM, Hahn U, Rice-Evans C. Epicatechin and its in vivo metabolite, 3'-o-methyl epicatechin, protect human fibroblasts from oxidative-stress-induced cell death involving caspase-3 activation. Biochem J. 2001;354:493–500.[Medline]
11. Augustin K, Blank R, Boesch-Saadatmandi C, Frank J, Wolffram S, Rimbach G. Dietary green tea polyphenols do not affect vitamin e status, antioxidant capacity and meat quality of growing pigs. J Anim Physiol Anim Nutr (Berl). 2008;92:705–11.[Medline]
12. Lodge JK, Traber MG, Elsner A, Brigelius-Flohe R. A rapid method for the extraction and determination of vitamin e metabolites in human urine. J Lipid Res. 2000;41:148–54.
13. Manolio TA, Burke GL, Savage PJ, Jacobs DR Jr, Sidney S, Wagenknecht LE, Allman RM, Tracy RP. Sex- and race-related differences in liver-associated serum chemistry tests in young adults in the cardia study. Clin Chem. 1992;38:1853–9.
14. Heinig M, Johnson RJ. Role of uric acid in hypertension, renal disease, and metabolic syndrome. Cleve Clin J Med. 2006;73:1059–64.
15. Kutzing MK, Firestein BL. Altered uric acid levels and disease states. J Pharmacol Exp Ther. 2008;324:1–7.
16. Siest G, Schiele F, Galteau MM, Panek E, Steinmetz J, Fagnani F, Gueguen R. Aspartate aminotransferase and alanine aminotransferase activities in plasma: Statistical distributions, individual variations, and reference values. Clin Chem. 1975;21:1077–87.[Abstract]
17. Morgan DB, Carver ME, Payne RB. Plasma creatinine and urea: creatinine ratio in patients with raised plasma urea. BMJ. 1977;2:929–32.
18. Orrell JM, Neithercut WD, Henderson J, Spooner RJ, McGuire G, Frier BM. Raised liver associated enzyme activity and post-prandial bile acid concentrations in sera from treated diabetic outpatients. Diabetes Res Clin Pract. 1990;10:51–7.[Medline]
19. McPherson K, Healy MJ, Flynn FV, Piper KA, Garcia-Webb P. The effect of age, sex and other factors on blood chemistry in health. Clin Chim Acta. 1978;84:373–97.[CrossRef][Medline]
20. Baba S, Osakabe N, Yasuda A, Natsume M, Takizawa T, Nakamura T, Terao J. Bioavailability of (-)-epicatechin upon intake of chocolate and cocoa in human volunteers. Free Radic Res. 2000;33:635–41.[CrossRef][Medline]
21. Chow HH, Hakim IA, Vining DR, Crowell JA, Ranger-Moore J, Chew WM, Celaya CA, Rodney SR, Hara Y, et al. Effects of dosing condition on the oral bioavailability of green tea catechins after single-dose administration of polyphenon e in healthy individuals. Clin Cancer Res. 2005;11:4627–33.
22. Khokhar S, Magnusdottir SG. Total phenol, catechin, and caffeine contents of teas commonly consumed in the united kingdom. J Agric Food Chem. 2002;50:565–70.[Medline]
23. Arts IC, Hollman PC, Feskens EJ, Bueno de Mesquita HB, Kromhout D. Catechin intake and associated dietary and lifestyle factors in a representative sample of Dutch men and women. Eur J Clin Nutr. 2001;55:76–81.[CrossRef][Medline]
24. Henning SM, Fajardo-Lira C, Lee HW, Youssefian AA, Go VL, Heber D. Catechin content of 18 teas and a green tea extract supplement correlates with the antioxidant capacity. Nutr Cancer. 2003;45:226–35.[CrossRef][Medline]
25. Nagao T, Komine Y, Soga S, Meguro S, Hase T, Tanaka Y, Tokimitsu I. Ingestion of a tea rich in catechins leads to a reduction in body fat and malondialdehyde-modified ldl in men. Am J Clin Nutr. 2005;81:122–9.
26. Hsu CH, Tsai TH, Kao YH, Hwang KC, Tseng TY, Chou P. Effect of green tea extract on obese women: a randomized, double-blind, placebo-controlled clinical trial. Clin Nutr. 2008;27:363–70.[Medline]
27. Matsuyama T, Tanaka Y, Kamimaki I, Nagao T, Tokimitsu I. Catechin safely improved higher levels of fatness, blood pressure, and cholesterol in children. Obesity (Silver Spring). 2008;16:1338–48.[Medline]
28. Kim W, Jeong MH, Cho SH, Yun JH, Chae HJ, Ahn YK, Lee MC, Cheng X, Kondo T, et al. Effect of green tea consumption on endothelial function and circulating endothelial progenitor cells in chronic smokers. Circ J. 2006;70:1052–7.[CrossRef][Medline]
29. Nawrot P, Jordan S, Eastwood J, Rotstein J, Hugenholtz A, Feeley M. Effects of caffeine on human health. Food Addit Contam. 2003;20:1–30.[Medline]
30. Tanaka K, Tokunaga S, Kono S, Tokudome S, Akamatsu T, Moriyama T, Zakouji H. Coffee consumption and decreased serum gamma-glutamyltransferase and aminotransferase activities among male alcohol drinkers. Int J Epidemiol. 1998;27:438–43.
31. Imai K, Nakachi K. Cross sectional study of effects of drinking green tea on cardiovascular and liver diseases. BMJ. 1995;310:693–6.
32. Gloro R, Hourmand-Ollivier I, Mosquet B, Mosquet L, Rousselot P, Salame E, Piquet MA, Dao T. Fulminant hepatitis during self-medication with hydroalcoholic extract of green tea. Eur J Gastroenterol Hepatol. 2005;17:1135–7.[CrossRef][Medline]
33. Molinari M, Watt KD, Kruszyna T, Nelson R, Walsh M, Huang WY, Nashan B, Peltekian K. Acute liver failure induced by green tea extracts: case report and review of the literature. Liver Transpl. 2006;12:1892–5.[CrossRef][Medline]
34. Ingelman-Sundberg M, Oscarson M, McLellan RA. Polymorphic human cytochrome p450 enzymes: an opportunity for individualized drug treatment. Trends Pharmacol Sci. 1999;20:342–9.[CrossRef][Medline]
35. Princen HM, van Duyvenvoorde W, Buytenhek R, Blonk C, Tijburg LB, Langius JA, Meinders AE, Pijl H. No effect of consumption of green and black tea on plasma lipid and antioxidant levels and on ldl oxidation in smokers. Arterioscler Thromb Vasc Biol. 1998;18:833–41.
36. Ryu OH, Lee J, Lee KW, Kim HY, Seo JA, Kim SG, Kim NH, Baik SH, Choi DS, et al. Effects of green tea consumption on inflammation, insulin resistance and pulse wave velocity in type 2 diabetes patients. Diabetes Res Clin Pract. 2006;71:356–8.[Medline]
37. Young JF, Dragstedt LO, Haraldsdottir J, Daneshvar B, Kal MA, Loft S, Nilsson L, Nielsen SE, Mayer B, et al. Green tea extract only affects markers of oxidative status postprandially: lasting antioxidant effect of flavonoid-free diet. Br J Nutr. 2002;87:343–55.[CrossRef][Medline]
38. de Maat MP, Pijl H, Kluft C, Princen HM. Consumption of black and green tea had no effect on inflammation, haemostasis and endothelial markers in smoking healthy individuals. Eur J Clin Nutr. 2000;54:757–63.[CrossRef][Medline]
39. Inami S, Takano M, Yamamoto M, Murakami D, Tajika K, Yodogawa K, Yokoyama S, Ohno N, Ohba T, et al. Tea catechin consumption reduces circulating oxidized low-density lipoprotein. Int Heart J. 2007;48:725–32.[Medline]
40. van het Hof KH, de Boer HS, Wiseman SA, Lien N, Westrate JA, Tijburg LB. Consumption of green or black tea does not increase resistance of low-density lipoprotein to oxidation in humans. Am J Clin Nutr. 1997;66:1125–32.
41. Stampfer MJ, Sacks FM, Salvini S, Willett WC, Hennekens CH. A prospective study of cholesterol, apolipoproteins, and the risk of myocardial infarction. N Engl J Med. 1991;325:373–81.[Abstract]
42. Frank J, Budek A, Lundh T, Parker RS, Swanson JE, Lourenco CF, Gago B, Laranjinha J, Vessby B, et al. Dietary flavonoids with a catechol structure increase -tocopherol in rats and protect the vitamin from oxidation in vitro. J Lipid Res. 2006;47:2718–25.
43. Ikeda I, Imasato Y, Sasaki E, Nakayama M, Nagao H, Takeo T, Yayabe F, Sugano M. Tea catechins decrease micellar solubility and intestinal absorption of cholesterol in rats. Biochim Biophys Acta. 1992;1127:141–6.[Medline]
44. Tinahones FJ, Rubio MA, Garrido-Sanchez L, Ruiz C, Gordillo E, Cabrerizo L, Cardona F. Green tea reduces ldl oxidability and improves vascular function. J Am Coll Nutr. 2008;27:209–13.
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Different from GTP at that time, P < 0.0001; #P < 0.0003.