http://72.14.205.104/search?q=cache:1kN-7A5h7mAJ:teaboard.gov.in/pdf/stat/Consumption.pdf+tea+consumption+in+India+per+capita&hl=en&ct=clnk&cd=1&gl=us&client=firefox-a
http://en.wikipedia.org/wiki/List_of_countries_by_tea_consumption_per_capita
Carcinogenesis. 2007 Oct;28(10):2143-8. Epub 2007 Aug 27.
Green tea and black tea consumption in relation to colorectal cancer risk: the Singapore Chinese Health Study.
Sun CL, Yuan JM, Koh WP, Lee HP, Yu MC.
Division of Population Sciences, City of Hope National Medical Center and Beckman Research Institute, 1500 East Duarte Road, Duarte, CA 91010, USA.
The relationships between green tea and black tea consumption and colorectal cancer risk were examined within the Singapore Chinese Health Study, a prospective cohort study of diet and cancer involving >60,000 men and women. Intake of green tea and black tea was assessed through in-person interviews. Incident cancer cases and deaths among cohort members were identified through record linkage of the cohort database with respective databases from the nationwide Singapore Cancer Registry and the Singapore Registry of Births and Deaths. The proportional hazard regression method was used to examine the associations between intake of green and black tea separately and colorectal cancer risk with adjustment for potential confounders. After an average of 8.9 years of follow-up, 845 colorectal cancer cases were identified. Subjects who drank green tea exhibited a statistically non-significant increase in risk [relative risk (RR) = 1.12, 95% confidence interval (CI) = 0.97-1.29] relative to non-drinkers of green tea. This risk increase was mainly confined to men (RR = 1.31, 95% CI = 1.08-1.58); the comparable RR in women was 0.89 (95% CI = 0.71-1.12). In men, the green tea-colorectal cancer association was noted mainly in those with advanced disease (Duke C or D) (RR = 1.53, 95% CI = 1.19-1.97), and the association was dose dependent (P for trend = 0.0002). This latter association was especially strong within the colon subsite (RR = 1.75, 95% CI = 1.24-2.46; P for trend < 0.0001). Irrespective of gender, intake of black tea was not associated with risk of colorectal cancer (RR = 0.92, 95% CI = 0.79-1.07) in this Asian population.
Cancer Epidemiol Biomarkers Prev. 2007 Jun;16(6):1219-23.
Prospective cohort study of green tea consumption and colorectal cancer risk in women.
Yang G, Shu XO, Li H, Chow WH, Ji BT, Zhang X, Gao YT, Zheng W.
Department of Medicine, Vanderbilt Epidemiology Center and Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville TN 37232-2587, USA. Gong.Yang@vanderbilt.edu
Tea and its constituents have shown anticarcinogenic activities in in vitro and animal studies. Epidemiologic studies, however, have been inconsistent. We prospectively evaluated the association between green tea consumption and colorectal cancer (CRC) risk in a cohort of 69,710 Chinese women aged 40 to 70 years. Information on tea consumption was assessed through in-person interviews at baseline and reassessed 2 to 3 years later in a follow-up survey. During 6 years of follow-up, 256 incident cases of CRC were identified. The multivariate relative risk of CRC was 0.63 (95% confidence interval, 0.45-0.88) for women who reported drinking green tea regularly at baseline compared with nonregular tea drinkers. A significant dose-response relationship was found for both the amount of tea consumed (Ptrend = 0.01) and duration in years of lifetime tea consumption (Ptrend = 0.006). The reduction in risk was most evident among those who consistently reported to drink tea regularly at both the baseline and follow-up surveys (relative risk, 0.43; 95% confidence interval, 0.24-0.77). The inverse association with regular tea drinking was observed for both colon and rectal cancers. This study suggests that regular consumption of green tea may reduce CRC risk in women.
Biopharm Drug Dispos. 2008 Sep;29(6):335-48.
Influence of green and black tea on folic acid pharmacokinetics in healthy volunteers: potential risk of diminished folic acid bioavailability.
Alemdaroglu NC, Dietz U, Wolffram S, Spahn-Langguth H, Langguth P.
Institute of Pharmacy, Johannes Gutenberg-University, Mainz, Germany.
Previous in vitro studies using Caco-2 cell monolayers suggested a possible interaction between green and black tea and folic acid at the level of intestinal absorption. The main purpose of the present study was to investigate a possible pharmacokinetic interaction between tea and folic acid in healthy volunteers. In an open-labeled randomized cross-over study, the pharmacokinetic interaction between tea and folic acid (0.4 mg and 5 mg) was investigated in healthy volunteers. Water was used as the reference drink. Subjects ingested 0.4 mg folic acid tablets with water, green or black tea (0.3 g extract/250 ml) or 5 mg folic acid tablets with water or green tea (0.3 g extract/250 ml). Blood samples were collected over a period of 8 h. Serum folate analysis was carried out by a competitive immunoassay which uses direct chemiluminescent technology. At the 0.4 mg folic acid dose, green and black tea reduced the mean C(max) of serum folate by 39.2% and 38.6%, and the mean AUC(0 --> infinity) by 26.6% and 17.9%, respectively. At the 5 mg folic acid dose, the mean C(max) of serum folate was reduced by 27.4% and the mean AUC(0 --> infinity) was decreased significantly by 39.9% by the co-application of green tea. The present results suggest an in vivo interaction between tea and folic acid with even low concentrations of green and black tea extracts yielding decreased bioavailabilities of folic acid.
Int J Biochem Cell Biol. 2007;39(12):2215-25. Epub 2007 Jun 26.
Effects of folate cycle disruption by the green tea polyphenol epigallocatechin-3-gallate.
Navarro-Perán E, Cabezas-Herrera J, Campo LS, Rodríguez-López JN.
Departamento de Bioquímica y Biología Molecular A, Facultad de Biología, Universidad de Murcia, E-30100 Espinardo, Murcia, Spain.
We demonstrate that the tea polyphenol, epigallocatechin-3-gallate, is an efficient inhibitor of human dihydrofolate reductase. Like other antifolate compounds, epigallocatechin-3-gallate acts by disturbing folic acid metabolism in cells, causing the inhibition of DNA and RNA synthesis and altering DNA methylation. Epigallocatechin-3-gallate was seen to inhibit the growth of a human colon carcinoma cell line in a concentration and time dependent manner. Rescue experiments using leucovorin and hypoxanthine-thymine medium were the first indication that epigallocatechin-3-gallate could disturb the folate metabolism within cells. Epigallocatechin-3-gallate increased the uptake of [(3)H]-thymidine and showed synergy with 5-fluorouracil, while its inhibitory action was strengthened after treatment with hypoxanthine, which indicates that epigallocatechin-3-gallate decreases the cellular production of nucleotides, thus, disturbing DNA and RNA synthesis. In addition to its effects on nucleotide biosynthesis, antifolate treatment has been linked to a decrease in cellular methylation. Here, we observed that epigallocatechin-3-gallate altered the p16 methylation pattern from methylated to unmethylated as a result of folic acid deprivation. Finally, we demonstrate that epigallocatechin-3-gallate causes adenosine to be released from the cells because it disrupts the purine metabolism. By binding to its specific receptors, adenosine can modulate different signalling pathways. This proposed mechanism should help us to understand most of the molecular and cellular effects described for this tea polyphenol.
Ann Epidemiol. 2000 Oct 1;10(7):476-477.
Prenatal tea consumption and risks of anencephaly and spina bifida.
Correa A, Stolley A, Liu Y.
National Center for Environmental Health, Centers for Disease Control, Atlanta, GA, USA
PURPOSE: To evaluate the relationship between prenatal tea consumption and risk of anencephaly and spina bifida.METHODS: Data from the population-based Atlanta Birth Defects Case-Control Study were examined. Cases were infants with anencephaly (n = 122) or spina bifida (r = 154) and no other associated anomalies, and identified between 1968 and 1980. Controls were infants without birth defects (n = 3029) identified from birth certificates of the same birth cohort and frequency matched to cases by race, period of birth, and hospital of birth.RESULTS: Maternal tea consumption during the periconceptional period (3 months before through the first trimester of pregnancy) was reported at 82, 83.6, and 92.9% among controls, anencephaly, and spina bifida cases, respectively. With subjects whose mothers consumed no tea as a reference, odds ratios (OR) for tea consumption during the periconceptional period (adjusted for gender, race, period of birth, maternal age, education, alcohol consumption, smoking, and periconceptional multivitamins) were: anencephaly 0.9 (95% confidence limits (CI) 0.5-1.5); spina bifida 2.3 (CI 1.2-4.4). Odds ratios for spina bifida and number of cups of tea consumed/day were: 1-2 cups 2.1 (CI 1.1-4.0); 3+ cups 2.8 (CI 1.4-5.6). Consumption of other caffeinated beverages was not associated with risk for anencephaly or spina bifida.CONCLUSIONS: Further studies are warranted to corroborate and elucidate the observed association between tea consumption and spina bifida.
Environ Mol Mutagen. 2004;44(1):10-25.
Folate, colorectal carcinogenesis, and DNA methylation: Lessons from animal studies.
Kim YI.
Departments of Medicine and Nutritional Sciences, University of Toronto, Toronto, Ontario, Canada.
Folate, a water-soluble B vitamin and cofactor in one-carbon transfer, is an important nutritional factor that may modulate the development of colorectal cancer (CRC). Epidemiologic and clinical studies indicate that dietary folate intake and blood folate levels are inversely associated with CRC risk. Collectively, these studies suggest an approximately 40% reduction in the risk of CRC in individuals with the highest dietary folate intake compared with those with the lowest intake. Animal studies using chemical and genetically predisposed rodent models have provided considerable support for a causal relationship between folate depletion and colorectal carcinogenesis as well as a dose-dependent protective effect of folate supplementation. However, animal studies also have shown that the dose and timing of folate intervention are critical in providing safe and effective chemoprevention; exceptionally high supplemental folate levels and folate intervention after microscopic neoplastic foci are established in the colorectal mucosa promote, rather than suppress, colorectal carcinogenesis. These animal studies, in conjunction with clinical observations, suggest that folate possesses dual modulatory effects on carcinogenesis depending on the timing and dose of folate intervention. Folate deficiency has an inhibitory effect, whereas folate supplementation has a promoting effect on the progression of established neoplasms. In contrast, folate deficiency in normal epithelial tissues appears to predispose them to neoplastic transformation, and modest levels of folate supplementation suppress the development of tumors in normal tissues. Notwithstanding the limitations associated with animal models, these studies suggest that the optimal timing and dose of folate intervention must be established for safe and effective chemoprevention in humans. Folate is an important factor in DNA synthesis, stability, and integrity, the repair aberrations of which have been implicated in colorectal carcinogenesis. Folate may also modulate DNA methylation, which is an important epigenetic determinant in gene expression (an inverse relationship), in the maintenance of DNA integrity and stability, in chromosomal modifications, and in the development of mutations. A mechanistic understanding of how folate status modulates colorectal carcinogenesis further strengthens the case for a causal relationship and provides insight into a possible chemopreventive role of folate. Environ. Mol. Mutagen. 44:10-25, 2004. Copyright 2004 Wiley-Liss, Inc.
Cancer Epidemiol Biomarkers Prev. 2007 Jul;16(7):1325-9.
A temporal association between folic acid fortification and an increase in colorectal cancer rates may be illuminating important biological principles: a hypothesis.
Mason JB, Dickstein A, Jacques PF, Haggarty P, Selhub J, Dallal G, Rosenberg IH.
Jean Mayer U.S. Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA. joel.mason@tufts.edu
Nationwide fortification of enriched uncooked cereal grains with folic acid began in the United States and Canada in 1996 and 1997, respectively, and became mandatory in 1998. The rationale was to reduce the number of births complicated by neural tube defects. Concurrently, the United States and Canada experienced abrupt reversals of the downward trend in colorectal cancer (CRC) incidence that the two countries had enjoyed in the preceding decade: absolute rates of CRC began to increase in 1996 (United States) and 1998 (Canada), peaked in 1998 (United States) and 2000 (Canada), and have continued to exceed the pre-1996/1997 trends by 4 to 6 additional cases per 100,000 individuals. In each country, the increase in CRC incidence from the prefortification trend falls significantly outside of the downward linear fit based on nonparametric 95% confidence intervals. The statistically significant increase in rates is also evident when the data for each country are analyzed separately for men and women. Changes in the rate of colorectal endoscopic procedures do not seem to account for this increase in CRC incidence. These observations alone do not prove causality but are consistent with the known effects of folate on existing neoplasms, as shown in both preclinical and clinical studies. We therefore hypothesize that the institution of folic acid fortification may have been wholly or partly responsible for the observed increase in CRC rates in the mid-1990s. Further work is needed to definitively establish the nature of this relationship. In the meantime, deliberations about the institution or enhancement of fortification programs should be undertaken with these considerations in mind.
