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* Beltsville Human Nutrition Research Center, ARS-U.S. Department of Agriculture, Beltsville, MD;
Unilever Research Laboratory, Vlaardingen, The Netherlands;
** The George Washington University Lipid Research Clinic, Washington, DC;
Unilever Bestfoods NA, Englewood Cliffs, NJ
2To whom correspondence should be addressed. E-mail: judd{at}bhnrc.arsusda.gov.
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • black tea • cholesterol • lipoproteins • antioxidant status • caffeine
Flavonoids, polyphenolic compounds found naturally in various plant materials, possess antioxidant properties in vitro and ex vivo and cholesterol-lowering effects in humans and animals (1–4). Black tea is a major source of flavonoids in Western diets (3). Several recent epidemiological studies have examined the relationship between black tea or flavonoid consumption and the risk of cardiovascular disease (CVD)2 (1) including coronary heart disease (CHD) or ischemic stroke (5), but the results from these studies are not consistent. Most studies report an apparent protective effect for CHD or stroke with high intakes of black tea or flavonoids (6–10). Conversely, no protective effects from tea intake were noted in a large cohort study (11), and in another study an increased risk of death from CHD was found with increased tea consumption (12).
Most free-living studies have observed that ingestion of black tea did not improve plasma or lipoprotein antioxidant status (13–17). However, some researchers have found that acute consumption of black tea increases antioxidant activity (18–20). Moreover, chronic consumption of tea reduced the susceptibility of LDL to oxidation ex vivo in a cross-sectional study (21). Two randomized trials did not detect an effect of tea drinking on total LDL or HDL cholesterol (15,22). These studies did not control for diet and thus may not have been able to detect small alterations in antioxidant status and blood lipids. Therefore, the purpose of the present study was to examine the effects of black tea ingestion on blood lipid profiles and markers of oxidative stress and antioxidant status in a controlled dietary setting with mildly hypercholesterolemic volunteers.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONLITERATURE CITED |
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Men and women were selected based on the following criteria: mildly elevated total cholesterol, 35 y-of-age or older, 90–140% of ideal body weight, no major health problems such as diabetes, heart disease, stroke, or cancer and not taking prescription medications that could interfere with lipid metabolism. Women had to be postmenopausal (last menses at least 1 y earlier) and not undergoing hormone replacement therapy. Volunteers had to be willing to consume all foods and beverages supplied by the study. The Committee on Human Research, Johns Hopkins University School of Hygiene and Public Health approved the study. All volunteers provided written consent for participation in the study. They also received monetary compensation commensurate with the effort required of them by the study.
Study design.
Volunteers were recruited to participate in a randomized double-blind crossover study of black tea (T) compared with a placebo having no added caffeine (P). To assess caffeine effects, a third period was added post hoc in which all subjects received the placebo with caffeine added (PC) at a concentration equivalent to that in T. Volunteers for the third study period were recruited from participants who completed periods 1 and 2 of the study. Beverages for T, P and PC treatments were prepared from dry powders similar to instant tea.
Prior to the first treatment period volunteers were placed in a 2-wk run-in period. Additionally, treatments were separated by a 4-wk washout period. During these times, alcohol and tea consumption were not allowed. During all phases of the study (run-in, wash-out and treatment periods) volunteers ingested either one cup of caffeinated coffee or two caffeinated diet sodas daily thus establishing a consistent baseline level of caffeine intake and preventing possible caffeine withdrawal symptoms. Subjects eliminated other caffeine-containing foods and medications throughout the study. As an indicator of compliance, intake of caffeine-containing beverages and medications was assessed from daily forms completed by the volunteers. Urinary caffeine excretion was determined as an indirect marker of intake.
Controlled diet.
During the three treatment periods, volunteers consumed the same background-controlled diet. All foods and beverages were prepared and supplied by the Human Studies Facility at the Beltsville Human Nutrition Research Center (Beltsville, MD). Food items were weighed, served in proportion to caloric requirements and color-coded according to the treatment beverage. Dietitians monitored food and treatment beverage selections at each meal. Composites of foods in the 7-d menu cycle were prepared and analyzed for macronutrients and fatty acids (Covance Laboratories, Madison, WI). Seven-day menus were prepared in 200-kcal increments and designed to follow a National Cholesterol Education Program (NCEP) Step I-type diet (23). The diets provided 58% of calories from carbohydrates, 26% from fat and 16% from protein. The fat had a ratio of polyunsaturated to monounsaturated to saturated fatty acids of 1:1:0.8. The diet provided 71 mg of cholesterol, 13.6 g of dietary fiber and 8.5 mg of iron per 1000 kcal. At the average energy intake for the study of 2760 kcal, this translates to a daily intake of 196 mg of cholesterol, 33.6 g of dietary fiber and 23.5 g of iron. The amount of dietary caffeine in the background diet, i.e., not associated with the treatment beverages, coffee or sodas, was 26.3 mg/1000 kcal (72.6 mg/d). During P, caffeine excretion was approximately equal in the prestudy baseline level. During T and PC, caffeine excretion increased by 2.6 and 3.0 times the level of excretion during P. Except for calcium and iron when prescribed by the volunteer’s personal physician, vitamin and mineral supplementation was not permitted.
Each weekday, volunteers were weighed and energy intake was adjusted as needed to keep body weight constant. Dinner and breakfast were consumed at the Center during the week; carryout lunches and snacks were provided. Weekend foods and treatment beverages were packaged with instructions for home consumption. Blood pressure was monitored weekly to assess the effects of T, P and PC.
Blinding.
During the first two periods of the study, investigators, volunteers and kitchen staff were blinded to the T or P treatments. Because of the post hoc addition of a third treatment period, only the kitchen staff and volunteers were blinded to the PC treatment in the third study period. Treatments were blinded to investigators and kitchen staff by placing powdered drink mixtures in numbered and color-coded packets and to volunteers by color coding and the addition of artificial fruit flavors (apple or lemon), artificial sweetener and coloring to mask the appearance and distinctive taste of black tea. Treatment packets were coded, analyzed and supplied by Unilever Bestfoods NA [Englewood Cliffs, NJ (Table 1)]. Black tea was provided as lyophilized tea solids in packets that contained the amount of tea solids that approximated that which would come from one regular tea bag, i.e., one serving of tea. Black tea and P were prepared daily by the kitchen staff and served with breakfast and dinner. Volunteers consumed two servings of T or P (apple-flavored) with breakfast and the equivalent of three servings of T or P (lemon-flavored) with dinner for a total of five servings per day. All beverages were prepared with 180 mL of room temperature spring water per serving. Volunteers were allowed to chill, heat or add additional artificial sweetener to their treatment beverage as desired. Volunteers consumed 71% of the treatment beverages (25 out of 35 drinks per week) under supervision of a dietitian in the Beltsville human study facility during breakfast and dinner on weekdays. The remaining 10 drinks per week were consumed at home during the weekends.
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Procedures for blood sampling and processing were those described in the protocol for the Lipid Research Clinics Program (24). Blood samples were drawn during the last week of the study on two different days and after an overnight fast (minimum 12 h). Plasma (from EDTA tubes) or serum was harvested from whole blood collected by venipuncture and divided into cryogenic vials for storage at -80°C. LDL, for use in oxidation assays, was isolated from 4 mL of fresh plasma. Briefly, the triglyceride-rich (d < 1.0063 g/mL) and LDL (d < 1.065 g/mL) fractions of plasma were isolated and removed sequentially by standard ultracentrifugation techniques (25). Both centrifugation runs were performed at 10°C and 187,000 x g for 14 h using a 50.4 Ti rotor (Beckman Instruments, Palo Alto, CA). Once isolated, LDL was brought to 4 mL, portioned as one mL aliquots, purged with nitrogen and stored at -80°C. For the TBARS assay, glutathione was added to the LDL fraction to minimize oxidation and stored at -80°C under nitrogen. After the final blood collection, plasma, serum or LDL samples were analyzed with all samples for a subject included in the same analytical run. Complete urine collections were obtained on three consecutive days at the end of each treatment period. An aliquot of urine was frozen each day. Subsequently, samples were thawed on ice and an amount of urine from each day’s collection proportional to that day’s total volume was pooled for analysis.
Lipid and apolipoprotein profiles.
Prior to freezing, plasma aliquot was precipitated for HDL determination using the sequential precipitation procedure of Gidez et al. (26). Lipid analyses were performed at the Lipid Research Clinic Laboratory, The George Washington University Medical Center, which maintains standardization with the Centers for Disease Control and Prevention, U.S. Department of Health and Human Services, for the analysis of total cholesterol, triglycerides and HDL cholesterol. Plasma total cholesterol, HDL cholesterol and triglycerides were determined enzymatically using commercial kits (Sigma Chemical Company, St. Louis, MO) on an Abbott VP analyzer (Abbott Laboratories, Chicago, IL). LDL cholesterol was calculated by the Friedewald procedure (27). Plasma apolipoprotein A-I and B concentrations were determined by rate nephelometry (Beckman ICS Immunochemical Analyzer; Beckman Instruments, Fullerton, CA).
Lp(a) was analyzed as described previously (28,29) by using a commercially available enzyme-linked immunosorbent assay (Strategic Diagnostics, Newark, DE).
Oxidative stress.
Oxidized LDL concentration was measured in plasma with a commercial ELISA (Mercodia AB, Uppsala, Sweden). Total F2-isoprostanes were measured in plasma with a commercial ELISA (Cayman Chemical Co., Ann Arbor, MI). Urinary 8-hydroxy-2'-deoxyguanosine (8OhdG) was determined using a commercially available competitive ELISA assay (OxisResearch, Portland, OR).
Antioxidant status.
Plasma antioxidant capacity was measured using the ferric-reducing ability of plasma (FRAP) assay as described by Benzie and Strain (30). Lipid peroxidation in the LDL fraction was determined spectrophometrically by measuring the amount of malondialdehyde (MDA) equivalents using thiobarbituric acid and expressed as TBARS according to the method of Fogelman et al. (31). LDL protein content was determined by the Lowry method (32) and used to normalize MDA equivalents for comparisons.
Statistics.
Statistical analyses were performed using SAS-PC version 8.2 (SAS Institute, Cary, NC). All variables from the start (baseline) and end of each treatment period were compared with a mixed model ANOVA that included fixed terms for treatment (i.e., T, P or PC) and period with a repeated term for volunteer. BMI and baseline value of the variable were included in the model as covariates to adjust for differences among the subjects for these parameters. Data are presented as least-square means ± SEE unless otherwise stated in the text. Values were considered statistical significant at P 
0.05.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONLITERATURE CITED |
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Sixteen volunteers (8 men and 8 women) completed the first two randomized dietary periods and 13 out of 16 elected to participate in the third treatment period. After lipid analyses, one male volunteer was found to have had a hypertriglyceridemic response to the reduced fat controlled diet and his data were excluded from further analyses. Baseline physical characteristics for the 15 volunteers included in the final data are shown in Table 2. Body weight was determined each weekday morning, and once the energy level needed to maintain weight was established, stability of body weight without further caloric change was considered to be an indicator of compliance. Compliance was also assessed through a daily questionnaire that included questions on general health and on consumption of foods or drinks not provided by the study. Body weights did not change significantly from the prestudy level throughout the study (data not shown). Weekly blood pressure measurements were not different among treatments (data not shown).
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Total and LDL cholesterol concentrations were reduced by 3.8% (P = 0.0589, trend) and 7.5% (P = 0.0140), respectively, after consumption of 5 servings/d of T compared with P (Table 3). Compared with PC, consumption of T reduced total and LDL cholesterol by 6.5% (P = 0.0007) and 11.1% (P = 0.0002), respectively. Although the total and LDL cholesterol concentrations were numerically higher after PC than P, the differences were not significant at the 0.05 probability level. Apolipoprotein B was not significantly different between T and P. However, compared with PC, T lowered apo B by 5.0% (P = 0.0322) and P by 4.7% (P = 0.0371). There was no difference in Lp(a) concentration between T and P. However, Lp(a) was significantly lower after T (16.4%, P = 0.0085) and P (13.0%, P = 0.0321) than after PC. There were no effects of T, P or PC consumption on HDL cholesterol, apolipoprotein A-I or triglyceride concentrations.
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No treatment effects were found for plasma concentration of oxidized LDL, plasma F2-isoprostane concentration or urinary excretion of 8OhdG (Table 4). Antioxidant status or capacity indicated by FRAP or TBARS in LDL were not different following consumption of T, P or PC.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONLITERATURE CITED |
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A possible mechanism for the cholesterol-lowering effect of tea may be that tea limits cholesterol absorption in the intestine. Tea catechins, specifically gallate esters, were shown to be hypocholesterolemic in rats by reducing cholesterol absorption in vivo and by precipitating cholesterol from micelles in vitro (34). The hypolipidemic effect of green tea extracts was not associated with reduced cholesterol or fatty acid synthesis in hamsters, thus leading the authors to suggest that the effect of green tea extract on cholesterol reduction was on absorption (35). It has not been determined if a similar mechanism occurs in humans.
Oxidative modification of LDL is thought to play an important role in the development of atherosclerosis (36). We measured markers of antioxidant status and oxidative stress by various methods: FRAP, LDL TBARS, oxidized LDL and F2-isoprostanes and 8OhdG. Our findings are not in agreement with the findings of those that have demonstrated that acute and chronic consumption of tea improved antioxidant status (18–21). However, only one study included a caffeine control group (19), and the other studies utilized water as the control treatment (18,20,21). Furthermore, Hodgson et al. (19) reported that lipid oxidation was similar between black tea and caffeine treatments.
We conclude that the addition of five servings of black tea per day to an NCEP Step I-type diet appreciably reduces total and LDL cholesterol in mildly hypercholesterolemic volunteers. According to the new NCEP Adult Treatment Panel III classification, consumption of black tea results in improving LDL cholesterol classification from borderline high to near optimal/above optimal (37). While questions remain regarding some of the beneficial effects tea may have as part of a prudent diet, based on our study, the inclusion of tea in the diet has the potential to significantly reduce blood cholesterol and thereby reduce the risk of CVD and should be encouraged.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: 8OhdG, 8-hydroxy-2'-deoxyguanosine; CHD, coronary heart disease; CVD, cardiovascular disease; FRAP, ferric reducing ability of plasma; MDA, malondialdehyde; NCEP, National Cholesterol Education Program; P, placebo having no added caffeine; PC, placebo with caffeine added; T, black tea.
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LITERATURE CITED |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONLITERATURE CITED |
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