Oolong Tea Increases Metabolic Rate and Fat Oxidation
Tea is one of the most frequently consumed beverages worldwide, yet very little is known about its metabolic effects in humans. Caffeine is generally regarded as the major metabolically active compound in tea. No consistent scientific evidence links moderate caffeine consumption to any health risks, including cancer, cardiovascular disease, fibrocystic breast disease or birth defects. Some individuals are sensitive to caffeine and find that it induces jitters, sleeplessness or irritation to the gastrointestinal tract but others consume it specifically because it is a mild stimulant and increases alertness and metabolic rate.
Dulloo recently reported that the consumption of green tea extract elevates both the metabolic rate and the rate of fat oxidation by individuals. Green tea, as well as the oolong tea consumed in this study, contains substantial amounts of caffeine, which has been demonstrated to affect metabolic rate and substrate metabolism .
The effect of caffeine on metabolic rate has been well documented. A number of studies have reported an elevation in metabolic rate following consumption of caffeine in amounts of 200 mg or higher. Significant increases of 2–12% in metabolic rate are observed with caffeine doses of 200–300 mg. Hollands, among few others, demonstrated a significant effect with doses <200 mg. One interesting aspect of these short duration studies with caffeine is that EE does not return to a baseline value within a few hours. Astrup conducted a comprehensive study of the metabolic effects of caffeine. They measured both plasma caffeine and EE for 3 h after a single dose, either 100, 200 or 400 mg of caffeine. They observed that regardless of dose, caffeine levels and EE peaked around 30-min post dose. In addition, plasma caffeine and EE remained near this peak level for the entire 3 h of observation and had not returned to pretreatment levels by the end of the measurement period. In the current study, the greatest effect of the caffeinated beverages was observed 4–8 h following the last dose.
From these data, it is clear that the effect of caffeine is sustained for many hours following consumption. To fully determine the impact of caffeine on EE, it is necessary to measure for more than the 3 h generally monitored during these short-duration studies.
Including the current study, four studies have examined the response to caffeine over a 24-h period in which caffeine was consumed during the first 12 h but not during the second 12 h. Caffeine intake ranged from 150 to 600 mg/d and was consumed either in capsule form or as a beverage (tea or coffee). Only the Dulloo study, which used 150 mg/d of caffeine, did not observe a significant increase in EE for 24 h or for the 12-h period in which the caffeine was consumed. In the remaining three studies, EE was elevated by 3–7.6% in response to the consumption of caffeine. However, the greatest increase in 24-h EE was not in response to the highest dose of caffeine. Dulloo reported a 5.5% increase in 24-h EE in response to a dose of 600 mg caffeine/d. This response is similar in magnitude to that observed in the current study with a much lower dose of caffeine. In their later study Dulloo point out that the lack of response to the 150 mg/d dose may have resulted from administering the caffeine as 50-mg doses three times per day. They suggest that a 50-mg dose may be below the threshold level necessary to elicit a response. However, in the current study we administered ∼50-mg doses five times per day and report a significant response. This suggests that the effect of each successive dose of caffeine is cumulative and persists for several hours. The lack of response observed by Dulloo may have been due to an insufficient number of doses to achieve a total dose level sufficient to elicit a measurable response.
The impact of caffeinated beverages on substrate oxidation was significant in both the current study and that of Dulloo. We observed a 12% increase in fat oxidation over 24 h when subjects consumed the full-strength tea. Dulloo observed a smaller increase in fat oxidation with consumption of 150 mg of caffeine but a much greater increase with the consumption of green tea (33%). They suggest that the catechin content of the tea must have stimulated the fat oxidation rate. In support of this observation, they cite the lack of difference in fat oxidation due to the 250-mg/d caffeine dose in the study by Bracco et al. However, there is some evidence that caffeine alone increases fat oxidation rates. Studies with short-duration measurements report lower RQ, indicating a possible higher fat oxidation rate in response to caffeine consumption.
Fat oxidation was not significantly different from water alone during any of the 4-h periods after test beverage consumption when considered separately. However, fat oxidation was consistently higher during each of the 4-h periods and approached significance (P < 0.12) during the 8- to 12-h period, with the full-strength tea accounting for the significant difference over 24 h. It is interesting to note that the smallest difference in fat oxidation occurred during the period with the greatest difference in EE.
It has been widely assumed that the metabolic effects of beverages containing caffeine have been due to their caffeine content. It is clear from the results of this study and others that the consumption of tea both elevates metabolic rate and increases fat oxidation. However, it is not entirely clear whether these effects can be attributed to caffeine alone. In the current study, the full-strength tea and the caffeinated water resulted in comparable increases in EE. However, in their most recent study, Dulloo observed no effect of caffeine alone but a significant increase in metabolic rate when green tea extract was the source of caffeine.
Recently much attention has been focused on the flavanol content of foods. Dulloo ascribed much of the elevation in metabolic rate observed to an interaction between caffeine and the EGCG content of the green tea. This polyphenol has been demonstrated to be present in both green and black tea and detectable levels have been observed in plasma and urine of human subjects consuming tea. In this study we report substantial levels of EGCG in the oolong tea served to our subjects. Catechins have a wide variety of metabolic actions. They have been related to a decrease in the turnover of norepinephrine, suggesting an impact on metabolic rate and fat oxidation.
The current study and the Dulloo study are similar in approach with the basic difference being the type of tea and the method of delivery. We prepared the tea as it would be normally consumed and Dulloo provided it as an extract in capsule form. The question that arises is “are the results from the two studies consistent?” The Dulloo study made two important observations regarding the effect of tea on metabolic rate and fat oxidation. The first represented an attempt to explain the lack of response from their caffeine alone treatment. They suggest that there appears to be a threshold level of caffeine necessary to increase metabolic rate significantly. We did observe that there were no significant effects on 24-h EE when the tea was consumed at the half-strength level. However, when compared to the water alone, the metabolic rate was elevated when men consumed the half-strength tea, during the period in which the tea was consumed but was lower than the water-alone treatment value during the last 8 h of the 24-h period. It is also interesting to note that the fat oxidation rate was much lower on the half-strength tea treatment than water alone during the last 8–12 h of the 24-h period but was not different over the whole 24-h period. It is clear that the response to the half-strength tea was much less than either of the treatments with higher caffeine. There does not appear to be a dose-response relationship since consumption of the half-strength tea resulted in EE not different from water alone.
The central conclusion of Dulloo was that EGCG and caffeine from the tea act synergistically to produce the thermogenic response and an increase in fat oxidation. The data from the current study support the observation that the consumption of tea results in a greater impact on fat oxidation than does caffeine alone. The EGCG intake in this study was similar to that in the green tea extract used by Dullo, but our caffeine levels were nearly twice as high. Yet, the increase in 24-h EE induced by tea consumption in our study was very similar to the response reported in their study, and the caffeine alone resulted in an elevation in metabolic rate similar to the full-strength tea. If there had been some synergistic effect of caffeine and EGCG as suggested by Dulloo, we should have observed a much higher thermic effect of the tea. Given that the response observed in this study is similar in magnitude to the other studies that reported increases in 24-h EE, it seems possible that maximal response is reached with caffeine doses of 200–300 mg/d. The addition of more stimuli may not result in a greater response beyond an elevation in metabolic rate of 3–7.2% over 24 h.
The observed effect of tea on fat oxidation may reflect the synergistic effect of the caffeine and the catechins as suggested by Dulloo. Both studies demonstrated a significant effect of tea on 24-h fat oxidation but not with caffeinated beverages alone. However, without data on the impact of the noncaffeine components of tea independent of the caffeine, there is no clear answer as to whether the caffeine is necessary to stimulate fat oxidation.
It is clear that consumption of oolong tea stimulates both EE and fat oxidation in normal weight men. This raises the possibility that tea consumption could have some beneficial effect on an individual's ability to maintain a lower body fat content. However, any beneficial effect would only be realized if the effect was sustained upon chronic consumption of tea and the individual did not compensate with greater food intake in response to tea consumption.
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