Siv K.
Bøhn‡
*a,
Kevin D.
Croft
b,
Sally
Burrows
b,
Ian B.
Puddey
b,
Theo P. J.
Mulder
c,
Dagmar
Fuchs
c,
Richard J.
Woodman
d and
Jonathan M.
Hodgson
b
aDepartment of Nutrition, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Norway. E-mail: s.k.bohn@medisin.uio.no; Tel: +47 22851516
bSchool of Medicine and Pharmacology, University of Western Australia, WAIMR Centre for Food and Genomic Medicine, Perth, Western Australia, Australia
cUnilever Research and Development, Vlaardingen, The Netherlands
dDiscipline of General Practice, Flinders University, Adelaide, South Australia, Australia
First published on 12th May 2014
There is increasing evidence that tea and its non-caffeine components (primarily flavonoids) contribute to cardiovascular health. Randomized controlled trials have shown that tea can improve cardiovascular disease risk factors. We have previously reported a non-caffeine associated beneficial effect of regular black tea consumption on blood pressure and its variation. Objective: To explore the non-caffeine associated effects of black tea on body weight and body fat distribution, and cardiovascular disease related metabolic outcomes. Design: regular tea-drinking men and women (n = 111; BMI 20–35 kg m−2) were recruited to a randomized controlled double-blind 6 month parallel-designed trial. Participants consumed 3 cups per day of either powdered black tea solids (tea) or a flavonoid-free flavour- and caffeine-matched placebo (control). Body weight, waist- and hip-circumference, endothelial function and plasma biomarkers were assessed at baseline, 3 months and 6 months. Results: Compared to control, regular ingestion of black tea over 3 months inhibited weight gain (−0.64 kg, p = 0.047) and reduced waist circumference (−1.88 cm, P = 0.035) and waist-to-hip ratio (−0.03, P = 0.005). These effects were no longer significant at 6 months. There were no significant effects observed on fasting glucose, insulin, plasma lipids or endothelial function. Conclusion: Our study suggests that short-term regular ingestion of black tea over 3 months can improve body weight and body fat distribution, compared to a caffeine-matched control beverage. However, there was no evidence that these effects were sustained beyond 3 months.
Epidemiological data suggest that black and green tea may reduce the risk of both coronary heart disease and stroke by between 10 and 20%.2 Experimental and clinical trial data generally indicate either neutral or beneficial effects on risk factors and pathways linked to the development of CVD.2 While there is growing evidence that regular ingestion of green tea catechins with caffeine can reduce body weight and visceral fatness3–9 there is only one study linking black tea with body weight and body fat distribution.10
In this trial we have previously demonstrated that regular ingestion of black tea can result in lower blood pressure11 and lower blood pressure variation.12 The objective of the current analysis was to assess the effects of longer-term regular consumption of black tea, over 6 months, on body weight and body fat distribution. We also assessed effects of tea on several other cardiovascular disease-related metabolic outcomes.
Participants were enrolled in the study by a clinical trials coordinator. Prior to the 4 week run-in period volunteers were randomized (1:1) using computer generated random numbers. Randomization codes were generated by a statistician working with Unilever Research and Development, Vlaardingen independent of study investigators. Randomization codes consisted of a four-digit number linked to the study products: either control or active tea. Study products were sachets labeled with 10 different randomly generated numbers of four digits: five linked to control and five linked to active tea. This prevented volunteers from finding out what product they were consuming by talking to each other. This also maintained blinding of researchers performing measurements during the study. A total of 120 envelopes, numbered 1 to 120, each containing one of those 4 digit numbers, 60 linked to control and 60 linked to active tea, were produced independent of study researchers. These envelopes were then provided to the lead investigator (JMH) who was not involved directly in performing any outcome measurements. Envelopes were opened in consecutive order by the lead investigator as each participant entered into the study.
Of the 111 recruited participants 56 were randomly chosen to consume 3 cups per day of black tea. The tea was prepared from a single batch of powdered black tea provided to participants as single serve sachets. Each sachet contained black tea solids containing 429 mg of polyphenols assessed as gallic acid equivalents measured using the folin–ciocalteu reagent with gallic acid as a standard13 and 96 mg of caffeine (measured by HPLC).14 The contents of each sachet were dissolved in hot water prior to ingestion. 55 participants were randomly chosen to consume the placebo beverage, which was matched in flavour and caffeine content, containing no tea solids (Table 1).
Ingredient (mg) | Control | Tea |
---|---|---|
Polyphenols | 0 | 143 |
Total caffeine | 33 | 32 |
Tea solids | — | 498 |
Caffeine added | 37 | — |
Caramel colour | 90 | — |
Tea flavour | 10 | — |
Sugar [sucrose] | 1363 | 1403 |
Total weight of sachet | 1500 | 1900 |
Following randomization, participants followed a low-flavonoid diet during a 4 week run-in period and throughout the 6 month intervention. During run-in, the participants consumed 3 cups per day of regular leaf tea.
A total of 77 participants completed the trial (Fig. 1). The reasons for withdrawal in the control group were medical issues unrelated to the trial (n = 5), moving interstate (n = 1), unable to drink the beverage (n = 2) and personal issues (n = 8). The reasons for withdrawal in the tea group were incomplete baseline data (n = 1), medical issues unrelated to the trial (n = 6), moving interstate (n = 1), unable to drink the beverage (n = 2) and personal issues (n = 8).
All procedures followed were in accordance with the ethical standards of the University of Western Australia Ethics Committee and the trial was registered at the Australian New Zealand Clinical trials Registry ACTRN12607000543482.
Endothelial function measurement and analysis was performed by a trained technician, who was blinded to the treatment allocation according to a previously published method.18,19 Endothelium-dependent flow-mediated dilatation of the brachial artery (FMD) was measured following an ischemic stimulus. Analysis was carried out using a semi-automated edge detection software system. Measurements of endothelium-dependent flow-mediated dilatation of the brachial artery were performed at 30 second intervals for 4 minutes. Peak response was also assessed and was used for analysis of differences.
The effect of black tea on BMI, waist to hip circumference ratio, waist circumference, hip circumference, glucose, insulin, HOMA, triglycerides, cholesterol, HDL and LDL were analysed using mixed model analysis for longitudinal data sets i.e. each subject was measured repeatedly on the same outcome (at baseline, 3 and 6 months). The “mixed” command for linear mixed models in STATA 12 (StataCorp) with a random intercept was used treating time as a categorical parameter, with the following parameterization: β0month+ β1treatment+ β2(month*treatment). Where the month*treatment was significant the difference between the treatment groups with regards to changes in the fitted mean over time are given in the text. The difference between each group at each time point was tested using model-based contrasts. All models were applied on per protocol samples. Fitted means and SE for each time and group generated by the mixed model analysis are reported. Significance was determined by P < 0.05.
Control (n=39) | Tea (n = 38) | |||
---|---|---|---|---|
Mean | SD | Mean | SD | |
a 4OMGA; urinary 4-O-methylgallic acid, HDL; high density lipoprotein, LDL; high density lipoprotein; FMD; flow-mediated dilatation. p < 0.005. | ||||
Age | 55.4 | 9.8 | 55.9 | 10.9 |
Gender | ||||
Males (n) | 14 | 13 | ||
Females (n) | 25 | 25 | ||
Tea biomarker | ||||
4OMGA (μg mmol−1 creatinine) | 43 | 25 | 51 | 33 |
Body weight and anthropometry | ||||
Waist-to-hip ratio | 0.8 | 0.1 | 0.8 | 0.1 |
Waist-circumference (cm) | 80.9 | 10.2 | 81.5 | 10.6 |
Hip-circumference (cm) | 100.4 | 5.9 | 98.4 | 7.9 |
BMI (kg m−2) | 25.0 | 3.1 | 24.8 | 3.5 |
Weight (kg) | 72.4 | 11.0 | 71.2 | 11.6 |
Glucose metabolism | ||||
Glucose (mmol L−1) | 5.1 | 0.5 | 5.3 | 0.9 |
Insulin (mU L−1) | 6.5 | 3.6 | 8.1 | 9.2 |
HOMA | 1.5 | 1.0 | 2.2 | 3.4 |
Blood lipids/lipoproteins | ||||
Triglycerids (mmol L−1) | 1.1 | 0.6 | 1.2 | 0.5 |
Cholesterol (mmol L−1) | 5.2 | 0.8 | 5.1 | 0.8 |
HDL (mmol L−1) | 1.4 | 0.1 | 1.4 | 0.1 |
LDL (mmol L−1) | 3.3 | 0.1 | 3.1 | 0.1 |
Endothelial function | ||||
Peak FMD (%) | 7.8 | 2.9 | 8.2 | 3.8 |
Max FMD diameter (mm) | 3.6 | 0.5 | 3.5 | 0.5 |
t | Control | Tea | Mixed model | ||||||
---|---|---|---|---|---|---|---|---|---|
n | Fitted mean | SE | n | Fitted mean | SE | Time*group | p | ||
a Fitted means from the mixed models with SE. The p values are obtained from the month*treatment interaction for 3 and 6 months respectively. Time*group corresponds to the difference in slopes (effects of time) between tea and controls. t = Time (months). *p-value < 0.05. | |||||||||
Tea biomarker | |||||||||
4OMGA μg mmol−1 creatinine | 0 | 39 | 43 | 4 | 38 | 51 | 4 | ||
3 | 39 | 7 | 4 | 36 | 61 | 4 | 45 | <0.001* | |
6 | 39 | 7 | 4 | 37 | 70 | 4 | 55 | <0.001* | |
Anthropometry | |||||||||
Waist-to-hip ratio | 0 | 39 | 0.81 | 0.02 | 38 | 0.83 | 0.02 | ||
3 | 38 | 0.82 | 0.02 | 38 | 0.82 | 0.02 | −0.03 | 0.005* | |
6 | 39 | 0.80 | 0.02 | 36 | 0.81 | 0.02 | −0.02 | 0.129 | |
Waist (cm) | 0 | 39 | 80.91 | 1.69 | 38 | 81.50 | 1.71 | ||
3 | 38 | 81.72 | 1.69 | 38 | 80.43 | 1.71 | −1.88 | 0.035* | |
6 | 39 | 79.78 | 1.69 | 36 | 80.30 | 1.71 | −0.07 | 0.937 | |
Hip (cm) | 0 | 39 | 100.41 | 1.08 | 38 | 98.38 | 1.10 | ||
3 | 38 | 99.46 | 1.09 | 38 | 98.45 | 1.10 | 1.01 | 0.272 | |
6 | 39 | 99.12 | 1.08 | 36 | 98.89 | 1.10 | 1.80 | 0.051 | |
BMI (kg m−2) | 0 | 39 | 24.97 | 0.52 | 38 | 24.76 | 0.53 | ||
3 | 39 | 25.19 | 0.52 | 38 | 24.76 | 0.53 | −0.22 | 0.042* | |
6 | 39 | 25.02 | 0.52 | 37 | 24.94 | 0.53 | 0.13 | 0.225 | |
Weight (kg) | 0 | 39 | 72.44 | 1.80 | 38 | 71.17 | 1.83 | ||
3 | 39 | 73.08 | 1.80 | 38 | 71.17 | 1.83 | −0.64 | 0.047* | |
6 | 39 | 72.56 | 1.80 | 37 | 71.70 | 1.83 | 0.41 | 0.207 |
There was no significant difference between groups in the change between baseline and 6 months (Table 3). ESI Table 1† shows the total output from the mixed model analysis. There were no significant differences between groups with regard to changes in energy intakes throughout the study (P = 0.42 at 3 months, P = 0.40 at 6 months, data not shown). In addition macro-nutrient intakes were not significantly altered during the intervention.
t | Control | n | Tea | SE | Mixed model | ||||
---|---|---|---|---|---|---|---|---|---|
n | Fitted mean | SE | Fitted mean | Time* group | p | ||||
a Fitted means from the mixed models with SE. The p values are obtained from the month*treatment interaction for 3 and 6 months respectively. Time*group shows the difference in effects of time between tea and controls. Tests for absolute difference between treatment groups at 3 and 6 months. Trig = triglycerides; Chol = cholesterol. | |||||||||
Glucose metabolism | |||||||||
Glucose (mmol L−1) | 0 | 39 | 5.09 | 0.09 | 38 | 5.31 | 0.09 | ||
3 | 39 | 5.10 | 0.09 | 38 | 5.12 | 0.09 | −0.20 | 0.089 | |
6 | 39 | 5.09 | 0.09 | 37 | 5.24 | 0.09 | −0.07 | 0.572 | |
Insulin (mU L−1) | 0 | 39 | 6.53 | 0.82 | 38 | 8.11 | 0.83 | ||
3 | 39 | 6.53 | 0.82 | 38 | 6.89 | 0.83 | −1.22 | 0.238 | |
6 | 39 | 6.15 | 0.82 | 37 | 6.80 | 0.83 | −0.94 | 0.367 | |
HOMA | 0 | 39 | 1.52 | 0.26 | 38 | 2.16 | 0.27 | ||
3 | 39 | 1.52 | 0.26 | 38 | 1.60 | 0.27 | −0.55 | 0.177 | |
6 | 39 | 1.42 | 0.26 | 37 | 1.62 | 0.27 | −0.43 | 0.294 | |
Blood lipids/lipoproteins | |||||||||
Trig (mmol L−1) | 0 | 39 | 1.12 | 0.09 | 38 | 1.15 | 0.09 | ||
3 | 39 | 1.03 | 0.09 | 38 | 1.08 | 0.09 | 0.02 | 0.819 | |
6 | 39 | 1.12 | 0.09 | 37 | 1.11 | 0.09 | −0.05 | 0.566 | |
Total Chol (mmol L−1) | 0 | 39 | 5.24 | 0.13 | 38 | 5.08 | 0.13 | ||
3 | 39 | 5.30 | 0.13 | 38 | 5.27 | 0.13 | 0.13 | 0.263 | |
6 | 39 | 5.28 | 0.13 | 37 | 5.15 | 0.13 | 0.03 | 0.764 | |
HDL-Chol (mmol L−1) | 0 | 39 | 1.42 | 0.05 | 38 | 1.40 | 0.05 | ||
3 | 39 | 1.49 | 0.05 | 38 | 1.48 | 0.05 | 0.01 | 0.760 | |
6 | 39 | 1.47 | 0.05 | 37 | 1.46 | 0.05 | 0.01 | 0.850 | |
LDL-Chol (mmol L−1) | 0 | 39 | 3.30 | 0.12 | 38 | 3.14 | 0.12 | ||
3 | 39 | 3.34 | 0.12 | 38 | 3.29 | 0.12 | 0.11 | 0.246 | |
6 | 39 | 3.29 | 0.12 | 37 | 3.18 | 0.12 | 0.05 | 0.609 |
t | Control | n | Tea | SE | Mixed model | ||||
---|---|---|---|---|---|---|---|---|---|
n | Fitted mean | SE | Fitted mean | Time* group | p | ||||
a Fitted means from the mixed models with SE. The p values are obtained from the month*treatment interaction for 3 and 6 months respectively. Time*group corresponds to the difference in slopes (effects of time) between tea and controls. | |||||||||
Endothelial function | |||||||||
Peak FMD (%) | 0 | 39 | 3.57 | 0.08 | 38 | 3.50 | 0.08 | ||
3 | 39 | 3.58 | 0.08 | 38 | 3.53 | 0.08 | 0.02 | 0.244 | |
6 | 39 | 3.62 | 0.08 | 37 | 3.53 | 0.08 | −0.02 | 0.294 | |
Max FMD diam. (mm) | 0 | 39 | 7.82 | 0.53 | 38 | 8.21 | 0.54 | ||
3 | 39 | 8.14 | 0.53 | 38 | 7.94 | 0.54 | −0.6 | 0.710 | |
6 | 39 | 8.23 | 0.53 | 37 | 8.08 | 0.54 | −0.5 | 0.573 |
Adverse CVD risk is associated with obesity and particularly with abdominal obesity.21 In addition, waist circumference and waist to hip circumference ratio have been suggested to reflect the amount of visceral fatness.22 Compared to the control group the tea group had a small reduction in body weight, waist circumference and waist-to-hip ratio over time, up to 3 months, suggesting that tea intake may potentially benefit visceral fat deposits. There are several reports on the effects of green tea intake on body weight and body composition.3–9,23,24 Several of these studies were up to 12 weeks in duration. However, the only controlled clinical study on black tea and effects on anthropometry published so far is a 12 week double blind randomized controlled trial of 36 pre-obese Japanese adults intervened with black tea extract (BTE).10 In line with our findings, they found a significant decrease in visceral fatness as measured by computed tomography scanning. In addition they found that BMI decreased significantly in the BTE group compared to controls.10 Our results were not able to provide evidence that these potential benefits were maintained beyond 3 months, out to 6 months. The reason for this is not clear.
There are limited studies on the effect of tea on blood glucose. Intake of black tea has been reported to lower blood glucose in healthy subjects and improve scores of insulin sensitivity.25 A short-term clinical trial of healthy volunteers showed that intake of instant black tea decreased fasting blood glucose and increased fasting insulin in response to an oral glucose load.25 A clinical intervention study with oolong tea demonstrated a lowering of blood glucose in type 2 diabetic subjects.26In vitro studies suggest a mechanism for how tea catechins can promote blood glucose regulation through induction of glucose transporter (GLUT)4 translocation in skeletal muscle.27 Our results provide only weak evidence for a benefit of black tea on glucose concentrations. We did not find any differential effects on serum cholesterol levels between the tea group and the caffeine controlled placebo. Most human intervention studies with black tea or tea extracts have found little or no change in total serum cholesterol levels. Out of the seven randomised controlled trials on black tea only one showed cholesterol lowering effects.28
Interestingly, in the present study, the control group and the tea group had a similar pattern of increased HDL level over time. Conflicting results have been reported on the effect of black tea on HDL. Some studies find no effect of black tea intake on HDL29,30 while others have reported moderate increase in HDL when comparing a group consuming black tea to controls consuming hot water (without caffeine)31.
FMD is used to directly assess the function of the arterial wall. In the present study we did not find any effects on FMD. In the tea group, compared to control, neither Max FMD diameter nor Peak FMD was altered. This finding contradicts most other studies on black tea and FMD.32 A meta-analysis from 2011 of 9 human intervention studies where the effect of green and black tea on endothelial function had been measured by FMD concluded that moderate consumption of tea substantially and significantly enhances FMD.33 The reason for the lack of benefit in the current study may relate to the level of FMD at baseline, which was close to 8%. In our hands, a healthy normolipidaemic, normotensive population has an FMD of approximately 8% (unpublished data). Thus, the FMD in the current population was essentially normal. There is evidence that it is difficult to chronically improve already normal endothelial function.34 In addition, the majority of studies reported in the literature measured the acute effect of tea on FMD, which has not been determined in the current study. Therefore, an acute-on-chronic effect of tea on FMD in the current study cannot be excluded. An improved FMD after chronic tea consumption (i.e. 4 weeks) has been demonstrated in subjects with impaired endothelial function (baseline FMD ∼6.0%).35,36
Due to the long period of the intervention regular tea drinkers were recruited for this study. However, the amount of tea consumed daily varied between the volunteers. This made it necessary to standardise the tea intake to 3 cups of regular tea daily during the 4 week run-in period. Subsequently, subjects were randomised to the placebo or tea group. As a consequence the current study design combines the overall effect of standardised ingestion of tea in the tea group and tea withdrawal in the placebo group. It is not clear whether similar effects might be seen in a non-tea-drinking group.
Footnotes |
† Electronic supplementary information (ESI) available: Supplemental files: ESI Table 1, Total output from the mixed model analysis. See DOI: 10.1039/c4fo00209a |
‡ Present address: Department of Nutrition, Institute of Basic Medical Sciences, Faculty of Medicine, University of Oslo, Norway. |
This journal is © The Royal Society of Chemistry 2014 |