среда, 26 июля 2017 г.

The Use of Green Coffee Extract as a Weight Loss Supplement: A Systematic Review and Meta-Analysis of Randomised Clinical Trials



1. Introduction

Overweight and obesity have become a serious health concern [1]. Different weight management strategies are presently utilised, and a variety of weight loss supplements sold as “slimming aids” are readily available. However, the efficacy of some of these food supplements remains uncertain. One such supplement is the green coffee extract (GCE).
GCE is present in green or raw coffee [2]. It is also present in roasted coffee, but much of the GCE is destroyed during the roasting process. Some GCE constituents, such as chlorogenic acid (CGA) can also be found in a variety of fruits and vegetables [3]. The daily intake of CGA in persons drinking coffee varies from 0.5 to 1 g [4]. The traditional method of extraction of GCE from green coffee bean, Coffea canephora robusta, involves the use of alcohol as a solvent [5]. Extracted GCE is marketed as a weight loss supplement under a variety of brand names as a weight loss supplement such as “Coffee Slender”, and “Svetol”.
Evidence is accumulating from animal studies regarding the use of GCE as a weight loss supplement [6, 7]. In human subjects, coffee intake has been reported to be inversely associated with weight gain [8]. Consumption of coffee has also been shown to produce changes in several glycaemic markers in older adults [9]. Similarly, other research has indicated that the consumption of caffeinated coffee can lead to some reductions in long-term weight gain, an effect which is likely to be due to the known thermogenic effects of caffeine intake as well as effects of GCE and other pharmacologically active substances present in coffee [10]. GCE has also been postulated to modify hormone secretion and glucose tolerance in humans [11]. This effect is accomplished by facilitating the absorption of glucose from the distal, rather than the proximal part of the gastrointestinal tract.

2. Methods

Data are presented as means with standard deviations. Mean changes in body weight were used as common endpoints to assess the differences between GCE and placebo groups. Using the standard meta-analysis software [14], we calculated mean differences (MD) and 95% confidence intervals (CI). The I 2 statistic was used to assess for statistical heterogeneity amongst studies.

3. Results

Our searches produced 2160 “hits”. 328 articles were excluded because they were duplicate citations, while 767 articles were excluded because of wrong titles and abstracts. Another 598 articles were excluded because they did not investigate a food supplements, and 454 articles excluded due to no report on clinical outcome. A further 13 articles were excluded due to unsuitable study design. Thus, 5 potentially relevant articles were identified (Figure 1). One trial was excluded because it involved only normal weight individuals, and did not measure weight as an outcome [15]. Another trial was excluded because it was not randomised [16]. In effect, 3 randomised clinical trials (RCTs) including a total of 142 participants met our inclusion criteria, and were included in this systematic paper [5, 17, 18]. Their key details are summarized in Tables Tables1 and1 and and22.

4. Discussion

In animals, GCE has been reported to influence postprandrial glucose concentration and blood lipid concentration [5]. This is thought to be via reduction in the absorption of glucose in the intestine; a mechanism achieved by promoting dispersal of the Na+ electrochemical gradient. This dispersal leads to an influx of glucose into the enterocytes [19]. GCE is also thought to inhibit the enzymatic activity of hepatic glucose-6-phosphatase, which is involved in the homeostasis of glucose [20]. Reports from animal studies have suggested that GCE mediates its antiobesity effect possibly by suppressing the accumulation of hepatic triglycerides [6]. Some authors have also posited that the antiobesity effect of GCE may be mediated via alteration of plasma adipokine level and body fat distribution and downregulating fatty acid and cholesterol biosynthesis, whereas upregulating fatty acid oxidation and peroxisome proliferator-activated receptor alpha (PPARα) expression in the liver [7].
Diets rich in polyphenols may help to prevent various kinds of diseases associated with oxidative stress, including coronary heart disease and some forms of cancer [21, 22]. GCE has been reported to have antioxidant activity, demonstrated by its ability to scavenge free radicals in vitro, and to increase the antioxidant capacity of plasma in vivo [16, 23]. There is also evidence that certain dietary phenols, including GCE, may modify intestinal glucose uptake in a number of ways [8, 24]. This activity might provide a basis for explaining its effects on body weight. The purported slimming effect of GCE would have a protective effect against diabetes mellitus, via changes in gastrointestinal hormone secretion [10]. A few questions, however, arise from the RCTs which involve the use of GCE as a weight loss aid.
All the RCTs involving the use of GCE which have been conducted so far have very small sample sizes, with the largest number of participants being 62 in one trial [17]. These small sample sizes increase the possibility of spurious or false positive results. Two of the RCTs were unclear about drop-outs of participants from the trial; neither did they report on intention-to-treat analysis [17, 18]. All of the trials so far identified have been of very short duration. This makes it difficult to assess the efficacy and safety of GCE as a weight reduction agent on the medium to long-term. Although none of the RCTs identified reported any adverse events, this does not indicate that GCE intake is “risk-free”. Two participants in a study report dropped out due to adverse events associated with the intake of GCE [16]. These included headache and urinary tract infection. Thus, the safety of this weight loss aid is not established.

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