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In general, green tea intake significantly lowered the total cholesterol (TC); WMD: − 4.66 mg/dL; 95% CI: − 6.36, − 2.96 mg/dL; P < 0.0001) and low-density lipoprotein (LDL) cholesterol (WMD:− 4.55 mg/dL; 95% CI: − 6.31, − 2.80 mg/dL; P < 0.0001) levels compared with those in the control.
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Read More »The present meta-analysis evaluated the association between green tea consumption and reduction in serum lipid concentrations based on published results from 31 studies comprising 3216 subjects. The results suggest that green tea supplementation significantly lowered both serum TC and LDL cholesterol concentrations. In addition, we demonstrated a trend toward decrease in triglyceride concentrations, although it did not attain significance, presumably because of the limited participants or duration for which the triglyceride concentrations were reported; however, green tea did not significantly affect the levels of HDL cholesterol. These findings are generally in accordance with the results from previous meta-analyses, which also identified a significant correlation between green tea supplementation and improvements in TC and LDL cholesterol concentration [13]. Recent mechanistic studies have examined the effects of green tea intake on lipid control and provide further evidence for the biological plausibility of these findings. In accordance with our results, several animal studies have reported that green tea supplementation significantly improved hyperlipidemia status in high-fat diet induced rats, including lowering TC, LDL cholesterol, and triglycerides [54]. Moreover, recent animal studies have indicated that green tea catechins could significantly inhibit atherosclerotic plaque formation, lower liver fat accumulation, and increase HDL cholesterol in hyperlipidemic rats induced by high-fat andhigh-cholesterol diet [55]. The mechanism underlying the beneficial effect of green tea on lipid control may be attributed to the high concentration of green tea catechins, which involve the following aspects: (1) EGCG could attenuate the endothelial dysfunction induced by oxidized-LDL via the Jagged-1/Notch signaling pathway in human umbilical vein endothelial cells, which provides a beneficial effect by inhibiting the atherosclerotic plaque formation [56]. (2) Tea catechins are powerful antioxidants that prevent LDL oxidation by incorporating themselves into LDL particles in nonconjugated forms in vitro [57]. (3) These are responsible for LDL receptor binding activity upregulation in HepG2 cells in a dose-dependent manner by regulating the SREBP-1 (sterol regulatory binding protein-1) pathway [58]. (4) Green tea might also inhibit intestinal lipid absorption by interfering with micelle formation [59]. Observational studies have also indicated that green tea intake is inversely related to a risk of CVD. A large, 11-year population-based study involving > 40,000 middle-aged individuals from Japan revealed that, compared with non-tea drinkers, those with habitual green tea intake (over two cups daily, approximately 7 oz/day for 10 years) reduced their risk of death from CVD by 22–33% [7]. Randomized controlled trials have been performed to determine the effect of green tea on cholesterol concentration; however, the results are conflicting. Some studies have revealed that green tea intake significantly reduced the TC and LDL cholesterol [24, 53]. In contrast, several other studies reported no positive correlations between green tea intake and reduction in TC and LDL cholesterol [23, 52]. In addition, most studies suggested that no effect was seen for HDL cholesterol or triglycerides [35, 39], whereas only a few studies suggested a beneficial effect on HDL cholesterol or triglycerides levels [24]. The weighted mean reductions in TC and LDL cholesterol appearing due to green tea supplementation as observed in the present study (TC: 4.66 mg/dL; LDL cholesterol: 4.55 mg/dL), corresponding to reductions of 2–5%, might be important for primary prevention of cardiovascular health. Studies have reported that a 1% reduction in TC or LDL cholesterol was clinically associated with a 2–3% or 1% decreased risk of CVD, respectively [60]. Importantly, green tea intake did not negatively affect the serum HDL cholesterol levels. Thus, green tea supplementation mainly reduces the serum TC and LDL cholesterol concentrations but has limited effect on HDL cholesterol.
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Read More »In this meta-analysis, subgroup analyses suggest that the beneficial effect of green tea was consistent in all the subgroup analyses except for the crossover design subgroups; however, only three trials were included in the crossover design, which were insufficient to make a significant conclusion. In addition, the beneficial effect of green tea intake on LDL cholesterol was also consistently observed in most subgroup analyses except for the caffeine subgroup. A significant reduction in LDL cholesterol was observed in the decaffeination subgroup instead of the caffeine subgroup. As caffeine is naturally present in green tea, whether caffeine intake affects lipid reduction is another potential issue, which continues to have conflicting opinions among previous studies [61, 62]. The meta-analysis indicated that green tea has no beneficial effect on serum HDL cholesterol, a finding that was consistent in all subgroup analyses. Green tea consumption has a beneficial effect on triglyceride levels in subjects with a longer duration of consumption (≥12 weeks); however, the benefit was not significant in other subgroup analyses. Because the number of trials available for subgrouping was limited, such analyses should be interpreted with caution. In addition, meta-regression found no significant relations between net change in serum lipid and intervention dose, treatment duration, caffeine content, different ethnicity, intervention type and study design. Larger and longer duration trials with optimally designed treatments and controls are required in the future research. Our study has certain strengths. First, we only selected RCTs in this meta-analysis, which ensured relatively high-quality data and provided reliable inference about causality. Second, the relatively large number of pooled participants provided us higher statistical power to detect a small treatment effect. Third, results were unlikely to be influenced by publication bias. The results of Egger’s regression tests suggested no significant asymmetry of the funnel plot for the overall effect estimation of mean differences in TC, LDL cholesterol, HDL cholesterol, and triglyceride levels. Our analyses did have a few limitations. First, the studies had relatively short duration of follow-up, ranging from 3 weeks to 12 months, with a median of 11 weeks, so presumed health benefits cannot be extrapolated beyond the duration of these studies; however, long-term effects are clinically important for lipid profiles and other CVD risk factors. Second, although considerable lowering of TC and LDL cholesterol by green tea intake was observed in our study, we could not determine the optimal dosage of green tea supplementation that would have the greatest impact on improving lipid metabolism, as the catechin dosage varied from 80 to 2488.7 mg/day (median: 630.9 mg/day). Third, our meta-analysis did not recognize a safety margin in this study, however, in some studies; concern has been raised as to the safety of high-dose green tea catechin supplementation. Mild side effects were reported in some clinical studies, including gastric upset, mild skin rashes, and abdominal bloating [26, 33]. In addition, green tea was known to be the major dietary source of oxalate in some patients with kidney oxalate stones [63]. Fourth, we identified large variations in study designs, catechin dosage, ethnic groups, green tea type, baseline health status, and trial quality. Although we did not identify these variations as statistically significant sources of heterogeneity, such heterogeneity may limit the validity of the overall pooled results. In addition, the articles included were all published in English; limited resources prevented us from including articles published in other languages.
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