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
Two independent
reviewers assessed the eligibility of studies to be included in the
paper. Data were extracted systematically by two independent reviewers
according to the patient characteristics, interventions, and results.
The methodological quality of all included studies was assessed by the
use of a quality assessment checklist adapted from the consolidated
standard of reporting trials (CONSORT) guidelines [12, 13]. Disagreements were resolved through discussion with the third author.
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.
A
forest plot (random-effect model) for the three trials is shown in
figure 2. The meta-analysis reveals a statistically significant
difference in body weight between GCE and placebo (MD: −2.47 kg; 95% CI:
−4.23, −0.72). The I
2 statistic of 97% suggests that there is considerable
heterogeneity amongst the studies. A further plot of two trials which
involved CGA-enriched GCE revealed a statistically nonsignificant
difference in body weight between GCE and placebo (MD: −1.92 kg; 95% CI:
−5.40, 1.56). Heterogeneity was also considerable in this analysis (I
2 statistic of 99%). One of the studies reported a
statistically significant decrease in the percentage of body fat in the
GCE group compared with baseline, but no significant difference in the
placebo group [5].
There was no mention of intergroup differences regarding the percentage
of body fat. None of the trials reported any adverse events associated
with the use of GCE.
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.
The
effective dosage of GCE for use as a weight loss supplement is also not
established. The dosages of GCE reported in most of the human trials
identified were estimated, as the GCE was a component of coffee. While 2
of the RCTs identified enriched their GCE with CGA [5, 17], the third trial did not report that the GCE used was fortified with CGA [18]. This warrants further investigation.
The
RCTs identified from our searches were not also clear on blinding
issues. None of the RCTs reported on how randomisation was carried out,
and none provided information regarding blinding of outcome assessors.
This casts doubt on the internal validity of these trials. Future trials
involving the use of GCE as a weight loss supplement should be
conducted in line with the CONSORT guidelines. This will ensure the
validity and applicability of study results. Two authors in one study
were affiliated to a company which markets Svetol [18] but did not specify whether or not they had any conflicts of interest.
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