Originating from China Tea, a product made up from leaf and bud of the plant, Camellia sinensis, is the second most consumed beverage in the world, well ahead of coffee, beer, wine and carbonated soft drinks (1,2). Green tea is mainly produced from Camellia sinensis var. sinensis. The Assam type (Camellia sinensis var. assamica) has a too high content of polyphenols, which would make green tea taste excessively bitter (3). The production of green tea is characterized by an initial heating process, which kills the enzyme polyphenol oxidase, which is responsible for the conversion of the flavanols in the leaf into the dark polyphenolic compounds that colour black tea. The other important process is rolling, in which leaves are cut and twisted. The final form of green tea depends on the particular variant being produced. The rolling stage is very similar to the operation with the same name in black tea production. Green tea production is restricted mainly to China and Japan (3,4). Green tea has been considered a medicine and a healthful beverage since ancient times. The traditional Chinese medicine has recommended this plant for headaches, body aches and pains, digestion, depression, detoxification, as an energizer and, in general, to prolong life.
Green tea leaves contain three main components which act upon human health: xanthic bases (caffeine and theophylline), essential oils and especially, polyphenolic compounds. Caffeine acts mainly upon the central nervous system, stimulating wakefulness, facilitating ideas association and decreasing the sensation of fatigue (5). Some of the effects caused by caffeine are influenced by theophylline tea content. Theophylline induces psychoactive activity, it also has a slightly inotrope and vasodilator effect, and a much higher diuretic effect than caffeine. Green tea is the type of tea with the higher percentage of essential oils (5,6). However, green tea has received a great deal of attention especially due to its content of polyphenols (GTP) , which are strong antioxidants and present important biological properties. Among all GTP, catechins and gallic acid have been especially considered to be the main players in the beneficial effects on human health.
Green tea is considered a dietary source of antioxidant nutrients: green tea is rich in polyphenols, but it also contains carotenoids, tocopherols, ascorbic acid (vitamin C), minerals such as Cr, Mn, Se or Zn, and certain phytochemical com-pounds which enhance the GTP antioxidant potential.
A substantial number of human intervention studies with green tea demonstrate a significant increase in plasma antioxidant capacity in humans after consumption of moderate amounts (1–6 cups/day); there are also initial indications which show that the enhanced blood antioxidant potential leads to a reduced oxidative damage in macromolecules such as DNA and lipids (1, 7-10). McKay and Blumberg  reported that the repeated consumption of green tea and encapsulated green tea extracts for one to four weeks has been demonstrated to decrease biomarkers of oxidative status. Furthermore, Klaunig et al (11) observed in a study with 40 male smokers in China and 27 men and women (smokers and non- smokers) in the United States, that oxidative DNA damage, lipid peroxidation, and free radical generation were reduced after consuming 6 cups/day of green tea for seven days. Erba et al (12) suggest the ability of green tea, consumed within a balanced controlled diet, to improve overall the antioxidative status and to protect against oxidative damage in humans.
Negishi et al (13) observed that both black and green tea polyphenols attenuate blood pressure increases, through their antioxidant properties. Epidemiological studies indicate that green tea consumption slightly reduces blood pressure. Yang et al (14) concluded that habitual moderate strength green tea or oolong tea consumption for 1 year significantly reduces the risk of developing hypertension in the Chinese population. Hodgson et al (15) reported that long-term regular ingestion of green tea may have a favourable effect on blood pressure in older women. Singh et al (16), and Murakami and Ohsato (17) reported that dietary green tea intake preserves and improves arterial compliance and endothelial function. Data on green tea are reported by Sasazuki et al (18) who in a cross sectional study of 512 coronary patients established that green tea may be protective against coronary atherosclerosis in men, but not in women. Nakachi et al (19) in a prospective cohort study of 8522 men and women concluded that consuming 10 cups/day is linked with a 42% decreased relative risk of death from cardiovascular disease in men and 18% in women. Several studies have demonstrated that green tea may affect the cardiovascular function through mechanisms of action related to LDL-cholesterol oxidation (20). Trevisanato and Kim (21)] indicated that GTP may slow atherogenesis by reducing the oxidative modification of LDL-cholesterol and associated events such as foam cell formation, endothelial cytotoxicity and induction of pro-inflammatory cytokines. Thus, GTP may exert an anti-atherosclerotic action by virtue of its antioxidant properties and by increasing HDL-cholesterol levels. Consistent with these results are the data reported by Hertog et al (22) that demonstrated an inverse correlation between catechin intake and coronary heart disease mortality after a 25-year follow-up of 12763 men from seven different countries. Similarly, research showed that men and women from the Boston Area Health study who consumed one or more cups per day of green tea in the previous year had a 44% lower risk of myocardial infarction than those who drank no tea (23). Recently, Peters et al (24) have provided a meta- analysis that suggested a decrease in the rate of cardiovascular disease outcomes with increasing green tea consumption.
Body Weight Control
The effects of long-term feeding with tea catechins have been widely studied, and some investigators suggest a potential role of green tea in bodyweight control. In addition, caffeine and theanine have been found to strengthen polyphenol effects on body weight control and fat accumulation (25). In vitro studies with green tea extracts containing 25% of catechins have shown its capacity to significantly inhibit gastric lipase, and to a lower extent pancreatic lipase. Thus, the lipolysis of long-chain triglycerides is reduced by 37% (26). Dulloo et al (27) using a green tea extract rich in catechins and caffeine, concluded that green tea has thermogenic properties and promotes fat oxidation beyond those explained by its caffeine content per se; the green tea extract may play a role in the control of body composition via sympathetic activation of thermogenesis, fat oxidation, or both.
Glucose Tolerance and Insulin Sensitivity
Epidemiological observations and laboratory studies have shown that green tea has an effect on glucose tolerance and insulin sensitivity. Some investigations have also shown that EGCG does not only regulate the glucose level in blood, but also may rehabilitate damaged beta-cells, which are responsible for producing insulin (28).
The neuroprotective power of complex extracts rich in flavonoids like those of Ginkgo biloba, green tea or lyophilized red wine have been demonstrated in several studies (29,30). Recent studies suggest that GTP possibly protect against Parkinson’s and Alzheimer’s diseases and other neurodegenerative diseases (31). GTP have demonstrated neuroprotectant activity in cell cultures and animal models, such as the prevention of neurotoxin-induced cell injury; hence the biological effects of GTP may benefit patients with Parkinson’s disease (32). The neuroprotective effects of the theanine contained in green tea are also a focus of considerable attention (29). The European Medicines Agency has conferred traditional herbal medicinal product for status on Green Tea extract for relief of fatigue and sensation of weakness (33-35).
1. Costa LM, Gouveia ST, Nobrega JA:Ann Sci 18:313–318, 2002.
2. Rietveld A, Wiseman S: J Nutr 133:3275–3284, 2003.
3. Willson KC: “Coffee, Cocoa and Tea.” New York: CABI Publishing, 1999.
4. Zuo Y, Chen H, Deng Y: Talanta 57:307–316, 2002.
5. Varnam AH, Sutherland JP: “Beverages: Technology, Chemistry and Microbiology.” London: Chapman & Hall, 1994.
6. Bruneton J: “Pharmacognosie. Phytochimie. Plantes Me´dicinales.” Paris: Technique et Documentation-Lavoisier, 2001.
7. McKay DL, Blumberg JB: J Am Coll Nutr 21:1–13, 2002.
8. Henning SM, Fajardo-Lira C, Lee HW, Youssefian AA, Go VLW, Heber D: Nutr Cancer 45:226–235, 2003.
9. Higdon JV, Frei B: Crit Rev Food Sci Nutr 43:89–143, 2003.
10. Xu JZ, Yeung SY, Chang Q, Huang Y, Chen ZY: Br J Nutr 91:873–881, 2004.
11. Klaunig J, Xu Y, Han C, Kamendulis L, Chen J, Heiser C. Proc Soc Exp Biol Med 220:249–254, 1999.
12. Erba D, Riso P, Bordoni A, Foti P, Biagi PL, Testolin G: J Nutr Biochem 16: 144–149, 2005.
13. Negishi H, Xu JW, Ikeda K, Njelekela M, Nara Y, Yamory Y: J Nutr 134:38–42, 2004.
14. Yang YC, Lu FH, Wu JS, Wu CH, Chang CJ: Arch Intern Med 164:1534–1540, 2004.
15. Hodgson JM, Devine A, Puddey IB, Chan SY, Beilin LJ, Prince RL: J Nutr 133:2883–2886, 2003.
16. Singh AK, Seth P, Anthony P, Husain MM, Madhavan S,Mukhtar H, Maheshwari RK: Arch Biochem Biophys 401:29–37, 2002.
17. Murakami T, Oshato K: J Am Coll Cardiol 41:271–274, 2003.
18. Sasazuki S, Kodama H, Yoshimasu K, Liu Y, Washio M, Tanaka K, Ann Epidemiol 10:401–408, 2000.
19. Nakachi K, Matsuyama S, Miyake S, Suganuma M, Imai K: Biofactors 13:49–54, 2000.
20. Ishikawa T, Suzukawa M, Ito T, Yoshida H, Ayaori M, Nishiwaki. Am J Clin Nutr 66:261–266, 1997.
21. Trevisanato S, Kim Y: Tea and health. Nutr Rev 58:1–10, 2000.
22. Hertog M, Kromhout D, Aravanis C, Blackburn H, Buzina R, Arch Intern Med 155:381–386, 1995.
23. Sesso H, Gaziano J, Buring J, Hennekens C: Am J Epidemiol 149:162–169, 1999.
24. Peters U, Poole C, Arab L: Am J Epidemiol 154:495–503, 2001.
25. Zheng G, Sayama K, Okubo T, Junefa LR, Oguni I: In vivo 18:55–62, 2004.
26. Juhel C, Armand M, Pafumi Y, Rosier C, Vandermander J, J Nutr Biochem 11:45–51, 2000.
27. Dulloo AG, Duret C, Rohrer D, Girardier L, Mensi N, Fathi M, Am J Clin Nutr 70: 1040–1045, 1999.
28. Wu CH, Lu FH, Chang CS, Chang TC, Wang RH, Chang CJ: Obes Res 11:1088–1095, 2003a.
29. Kakuda T: Biol Pharm Bull 25:1513–1518, 2002.
30. Dajas F, Rivera F, Blasina F, Arredondo F, Echeverri C, Lafon L, Neurotox Res 5:425–432, 2003.
31. Weinreb O, Mandel S, Amit T, Youdim MB: J Nutr Biochem 15:506–516, 2004.
32. Pan TH, Jankovic J, Le WD: Drugs Aging 20: 711–721, 2003.