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Garlic Powder Has no Anti-Inflammatory, Hypolipidemic, or Blood Pressure Lowering
Effects in Subjects with Risk Factors for Atherosclerosis
Sonia M.S. Espirito Santo*, MSc.; Martijn B.A. van Doorn*, MD; Piet Meijer, PhD; Ingrid Kamerling,
PhD; Rik C. Schoemaker, PhD; Verena Dirsch, PhD; Angelika Vollmar, PhD; Thomas Haffner,
PhD; Rolf Gebhardt, PhD; Adam F. Cohen, MD, PhD; Hans M.G. Princen, PhD; Jacobus Burggraaf,
MD, PhD.
*Both authors contributed equally
TNO Prevention and Health, Gaubius Laboratory, Leiden, The Netherlands (S.M.S.E.S., H.M.G.P.);
Department of General Internal Medicine, Leiden University Medical Center, Leiden, The Netherlands
(S.M.S.E.S.); Centre for Human Drug Research, Leiden, The Netherlands (M.B.A.D., I.K., R.S., A.C.,
J.B.); Department of Pharmacy, University of Munich, Munich, Germany (V.D., A.V.); Lichtwer AG,
Berlin, Germany (T.H.); Institute of Leipzig, University of Leipzig, Leipzig, Germany (R.G.).
All correspondence addressed to:
M.B.A. van Doorn, M.D.
Centre for Human Drug Research,
Zerrnikedreef 10
2333 CL Leiden, The Netherlands
Tel: + 31 71 5246419
mdoorn@chdr.nl
Text word count: 4352
Abstract word count: 244
ABSTRACT
Context Epidemiological studies suggest that garlic may have beneficial effects on risk factors
associated with cardiovascular disease (CVD). However, these findings are not unambiguously
supported by randomized placebo controlled clinical trials.
Objective To investigate the effects of a well-characterized enteric coated garlic preparation on
relevant biomarkers in subjects with risk factors for CVD. Efficacy parameters included: markers of
inflammation, endothelial function, lipid metabolism, and haemodynamic parameters.
Design, Setting, Participants, and Interventions Double-blind, randomized placebo-controlled
trial in 90 obese (BMI >24.5 kg.m-2) subjects aged 40-75 years, who smoked >10 cigarettes.day-1.
Subjects were randomly assigned to 3 parallel treatment groups: the garlic powder Printanor (2.1
g.day-1), atorvastatin (40 mg.day-1) or placebo. Measurements were performed at baseline, after 1
month and 3 months of treatment. Treatments were compared with ANOVA and differences
between treatments were reported as mean percentage difference and corresponding 95%
confidence interval (95% CI).
Results None of the efficacy parameters showed significant changes between the garlic treated
group versus placebo. In contrast, significant decreases were observed in the atorvastatin treated
group in plasma concentrations of CRP (20%; 95%CI: 4-34%), total cholesterol (37%; 95%CI: 34-
41%), LDL-cholesterol (52%; 95% CI: 49-57%), triglycerides (32%; 95%CI: 22-40%) and TNF
(42%; 95%CI: 22-56%). In addition, atorvastatin increased the ratio of ex vivo whole blood LPS-
stimulated over non-stimulated TNF concentrations by 110% (95%CI: 46-202%).
Conclusion A well-characterized enteric coated garlic preparation has no significant effect on a
comprehensive array of relevant biomarkers in subjects with risk factors for cardiovascular
disease.
KEYWORDS: Garlic, C-reactive protein (CRP), lipids, blood pressure, and humans.
2
INTRODUCTION
Beneficial effects of garlic on human health have been claimed for decades. However, none
of these claims are unambiguously supported by results from placebo controlled clinical trials. One
of these health claims entails the beneficial effects of garlic on risk factors associated with
atherosclerosis and consequently the occurrence of cardiovascular events. In support of this
notion, a number of studies reported a lowering of plasma lipids, systolic blood pressure, and
enhanced fibrinolytic activity associated with garlic use.1-7 Through these actions, garlic is believed
to protect the vessel wall from progressive atherosclerotic changes and consequently reduce the
incidence of cardiovascular events.1-3 However, a number of other studies do not support these
observations and showed no significant effects on these parameters.1-3,8-16 These conflicting
findings may be ascribed to the use of different study designs (e.g. lack of placebo group), different
patient inclusion criteria, as well as to the use of different garlic derived-material, such as raw
garlic, garlic powders, and garlic oil, all of which carry variation in production conditions and
chemical composition.1-3 Hence, from these reports it remains difficult to conclude whether garlic
can truly exert beneficial effects on clinical risk factors associated with atherosclerosis.
In order to adequately investigate the effects of garlic on various human health parameters,
a major collaborative EU program entitled “Garlic and Health” was started. This program aimed to
identify garlic species containing the highest content of the compounds believed to be responsible
for the claimed health effects. Subsequently, this garlic preparation was used to perform pre-
clinical experiments in order to better define the role of garlic on presumed pharmacological
targets. Moreover, the program aimed to investigate the effects of the garlic preparation on a
comprehensive array of cardiovascular biomarkers in a well-powered clinical trial (‘Human
Intervention Study’) of which the results are described in the current article.
A growing body of evidence suggests that inflammation may play an important role in the
pathophysiology of atherosclerosis. This is illustrated by the results from a number of recent
studies, which have shown C-reactive protein (CRP) te be one of the strongest predictors for the
risk of atherosclerosis and cardiovascular events in subjects with and without cardiovascular
disease.17-18 Remarkably, there are no studies reporting on CRP or other markers of inflammation
3
in subjects treated with garlic. Only in vitro studies have shown that high concentrations of garlic
can decrease cytokine production in endothelial cells suggesting anti-inflammatory properties.19-21
Hence, the importance of investigating the effects of garlic on markers of inflammation in addition
to traditional markers (plasma lipids and blood pressure) is evident.
We investigated the effects of a chemically well-characterized and production-controlled
garlic powder (Printanor) on plasma CRP concentrations (primary endpoint) in subjects with known
risk factors for CVD, during 12 weeks of treatment. In addition, we determined the effects of
Printanor on plasma markers of endothelial function (von Willebrand factor (vWF), soluble vascular
cell adhesion molecule (s-VCAM), soluble intercellular adhesion molecule (s-ICAM), and s-
selectine) and general inflammation (fibrinogen), sensitivity of leukocytes to an inflammatory
stimulus, plasma lipid levels and blood pressure.
4
METHODS
Subjects
The European Union Garlic Intervention Study (EUGIS) was a double-blind, randomized placebo-
controlled trial in which atorvastatin was used as positive control. The study protocol was approved
by the Committee on Medical Ethics of Leiden University Medical Center (LUMC) and conducted in
the Netherlands. Subjects were recruited by advertisements in local newspapers. The participants
were of either gender in general good health with known risk factors for atherosclerosis, i.e. aged
40-75 years, smoking >10 cigarettes.day-1, and a body mass index of >24.5 kg.m-2. Subjects were
excluded if they used chronic (i.e. hormone replacement therapy) or any other medication (i.e.
aspirin or NSAIDs) interfering with the measures of the study. Eligibility was assessed using a
general health questionnaire, by measurement of body weight, height, and routine laboratory
parameters including a urine pregnancy test for female subjects. A total of 150 subjects were
informed about the study of which 142 signed the informed consent. Ninety subjects were eligible
and entered the study.
Study design
Eligible subjects started with a 2-week placebo run-in period after which blood samples for
determination of liver enzymes, creatine phosphokinase (CPK), hemoglobin, viral serology
(Hepatitis B/C, HIV), and a urine sample for pregnancy testing (for females) were collected. If all
parameters were still within the inclusion range, subjects were randomized to one of the three
treatment groups in this parallel design study. Characteristics of the study population are listed in
Table 1. The treatments were given in a double-dummy design. Thus, the subjects received either
the garlic preparation (daily dose of 2.1 g; three 300 mg garlic tablets in the morning and four 300
mg garlic tablets in the evening plus one Atorvastatin-matching placebo tablet), or atorvastatin
(daily dose of 40 mg; 3 garlic-matching placebo tablets in the morning and 4 garlic-matching
placebo tablets in the evening plus a 40 mg atorvastatin tablet), or placebo (3 garlic-matching
placebo tablets in the morning and 4 garlic-matching placebo tablets in the evening plus one
5
atorvastatin-matching placebo tablet in the evening). The total treatment period was 12 weeks with
follow-up visits scheduled after 4, 5, 11, and 12 weeks. On these visits, fasting blood samples for
safety measurements and plasma biomarkers were collected, adverse events were recorded, and
study medication was counted. In addition, on each visit blood pressure, and heart rate were
measured.
Treatments
The garlic powder (Printanor) was produced under high sulfur-fertilization levels during the
cultivation procedures as a part of European Union research program entitled “Garlic and Health”
carried out by a consortium of 15 independent research groups from six countries. This garlic
powder was produced and supplied by one of the participants (INRA, Dijon, France) and analyzed
by standard high performance liquid chromatography (HPLC) procedure for the content of garlic
sulfur-containing compounds, i.e. alliin content and allicin liberation capacity.22 The garlic powder
contained 313.413.6 nmol of alliin per mg of garlic powder with the capacity to liberate 4.5 µg of
allicin per mg of garlic powder. This means that in this study the subjects had a daily intake of
107.3 mg of alliin in the form of garlic powder. Subsequently, 300 mg tablets of this garlic powder
and matching placebo tablets were produced under good manufacturing practice (GMP) standards
by Lichtwer Pharma AG, Berlin, Germany. These tablets were coated such that the tablets were
(gastric) acid resistant for at least 2 hours.
Atorvastatin (Lipitor®40 mg) tablets were purchased by the LUMC pharmacy and the matching
placebo tablets were produced and supplied by Katwijk Pharma, The Netherlands.
All study medication was packed, labeled, and dispensed by the LUMC pharmacy.
Measurements
Tolerability assessment consisted of adverse event assessment, measurements of vital signs, 12-
lead ECG recordings (Cardiofax V equipped with ECAPS12 analysis program, Nihon Kohden,
Tokyo, Japan) and routine laboratory safety measurements (aspartate aminotransferase (ASAT),
alanine aminotransferase (ALAT), alkaline phosphatase (ALKPHOS), -glutamyl transpeptidase
6
(GT), lactate dehydrogenase (LDH), CPK, total bilirubin and conjugated bilirubin) on all visits. At
these time points automated measurements of blood pressure and heart rate were made.
Blood sampling and sample handling
All blood samples collected at screening, randomization, after 4 and 5 weeks, and after 11 and 12
weeks of treatment, were taken after an overnight fast and at least 10 minutes of supine rest.
Blood samples for haemoglobin concentration (at screening) were collected in tubes containing
EDTA and analysed by the Central Clinical Haematology Laboratory (CKHL) of LUMC using a
standard automated assay. Blood samples for ASAT, ALAT, ALKPHOS, GT, LDH, CPK, bilirubin,
cholesterol, HDL-cholesterol, LDL-cholesterol and triglycerides (at screening and during study)
were collected in plain serum tubes and analysed by the Central Clinical Chemistry Laboratory
(CCCL) of LUMC using a standard automated assay.5 Blood samples for C-reactive protein23, von
Willebrand factor24, and fibrinogen (STA fibrinogen methods, Roche Diagnostics, Mannheim,
Germany) were collected on ice in tubes containing 0.105 M citrate and processed within 60
minutes. Blood samples for tumor necrosis factor-α (TNFα) were collected in EDTA-tubes, stored
at 37ºC and processed within 30 minutes. TNFα was measured using the Quantikine TNFα elisa
(R&D systems, Abington, United Kingdom) in EDTA plasma of a whole blood lipopolysaccharide
(LPS)-stimulation test using 0 and 10 ng/mL LPS (final concentration) and overnight incubation at
37°C in a 5% CO2 incubator.25 Blood samples for markers of vessel wall activation (soluble
vascular cell adhesion molecule, soluble intercellular adhesion molecule, and s-selectine) were
collected on ice in Li-Heparin tubes, processed within 60 minutes, and analysed by the department
of Pharmacy at the University of Munich as previously described.26
Statistics
The a priori power of the study was calculated using data from an earlier experiment investigating
the effects of atorvastatin on plasma CRP concentrations.23 Based upon these data this study had
a power of 0.72/0.80 to detect a 25/30% decrease in CRP (at a 2-sided alpha level of 0.05) in each
treatment group of 30 subjects.
7
The endpoints were analysed separately by mixed model analyses of variance (using SAS PROC
MIXED with an unstructured covariance matrix) with subject as random effect and treatment, time
and treatment by time as fixed effects, with baseline as covariate. Additionally, for graphical
purposes, an analysis was performed with change from baseline values using baseline as
covariate. This leads to statistically identical results compared with the alternate analysis, but
allows graphs of change from baseline to be generated. Data were analyzed log-transformed and
the analysis results were back-transformed and presented as geometric mean and percentage
difference and the corresponding 95% confidence interval (95% CI) for the treatment contrasts.
Calculation of time and treatment by time effects was performed for graphical presentation
purposes only. All calculations were performed using SAS for Windows V8.2 (SAS Institute, Inc.,
Cary, NC).
8
RESULTS
Adverse events and safety parameters
Ten subjects (3 subjects in statin group, 5 subjects in garlic group and 2 subjects in placebo group)
did not complete the study because of personal reasons (n=3) or adverse events (n=7). Two of
these adverse events were possibly related to the study medication (abdominal discomfort (garlic
group) and severe garlic odor (garlic group)), while the remaining five events were considered
unrelated. Four subjects were replaced (2 subjects in statin arm and 2 subjects in garlic arm) with
newly recruited volunteers. Therefore, the final study population consisted of 84 subjects; 29
subjects in the statin group, 27 subjects in the garlic group and 28 subjects in the placebo group.
All other adverse events reported in the course of this study were mild or moderate and considered
unrelated to study drug administration. In addition, vital signs, electrocardiogram (ECG), and
routine laboratory parameters were virtually unchanged apart from a mild rise in liver enzyme
levels noted in the atorvastatin treated group. This rise in liver enzyme levels is commonly seen in
patients treated with statins and was considered not clinically significant.
Compliance
The compliance data showed only minor differences between subjects in tablet counts of returned
study medication on each visit. The average daily intake of garlic was 7.1 ± 0.1 tablets (range 6.9-
7.2) and the average daily intake of atorvastatin was 1.0 ± 0.1 tablets (range: 0.9-1.2).
Inflammation markers
After 12 weeks of garlic treatment, the mean plasma C-reactive protein (CRP) concentration
increased by approximately 18% (95% CI: -2, -42%) compared with placebo. Atorvastatin
treatment resulted in a 20% decrease (95% CI: 4, 34%) in mean CRP concentrations compared
with placebo. Results are summarized in Table 2 and Figure 1.
After garlic treatment, plasma (non-stimulated) tumor necrosis factor- (TNF) concentrations and
the ratio between lipopolysaccharide (LPS)-stimulated over non-stimulated TNF concentrations
9
remained virtually unchanged. In contrast, atorvastatin treatment significantly decreased the mean
plasma (non-stimulated) TNF concentration and increased the ratio of the LPS-stimulated over
non-stimulated mean TNF concentration (Figure 2). The plasma fibrinogen concentrations were
unaffected in both garlic and atorvastatin treatment groups.
Endothelial function markers
Both garlic and atorvastatin treatments did not affect the mean plasma concentrations of von
Willebrand factor (vWF), soluble vascular cell adhesion molecule (s-VCAM), soluble intercellular
adhesion molecule (s-ICAM), and soluble selectin (s-selectin). However, in the atorvastatin treated
group the mean s-selectin concentration decreased by 9.8% (95% CI: -0.1, 18.7%) nearly reaching
statistical significance (p=0.051). Results are summarized in Table 2.
Lipids and Lipoproteins
Garlic treatment did not influence the mean plasma cholesterol, high-density lipoprotein (HDL)-
cholesterol, low-density lipoprotein (LDL)-cholesterol and triglyceride concentrations when
compared with placebo treatment. In contrast, atorvastatin treatment resulted in a decrease of total
cholesterol (37%; 95%CI: 34, 41%), LDL-cholesterol (52%; 95% CI: 49, 57%) and triglycerides
(32%; 95%CI: 22, 40%) when compared with placebo, while HDL-cholesterol concentrations
remained unaffected (p=0.32). Results are summarized in Table 2 and Figure 3.
Blood pressure and heart rate
Neither treatment affected blood pressure or heart rate at one and three months.
10
DISCUSSION
This clinical study investigated the effects of a chemically well-characterized and
production-controlled garlic powder (2.1 g.day-1) and atorvastatin as positive control on a wide and
comprehensive array of relevant biomarkers in subjects with known risk factors for CVD. Taken
together, our data show that the garlic powder has no beneficial effects on a wide variety of
important biomarkers for atherosclerosis in man. This makes it unlikely that garlic exerts a
beneficial effect on CVD unless some other hitherto unknown biological effect is the basis of its
purported epidemiological effects. However some other associated lifestyle effect is more likely to
be the cause than a biological effect of garlic.
The garlic dose administered in this study was chosen using information from the pertaining
literature. Previous studies that focused on the effects of garlic on lipid metabolism, blood
pressure, and heart rate in humans used garlic powder doses that varied from 0.3 g.day -1 to 1
g.day-1 (approximately equivalent to 5.1 mg alliin.day-1 to 17 mg alliin.day-1). None of these studies
reported beneficial effects of garlic on any of these parameters.8-10,12-15 However, one study
investigated the effects of a considerably higher dose of a garlic-derived material (7.2 g.day-1 of
aged garlic extract which is mainly composed of S-allylcysteine and S-allylmercaptocysteine) and
showed a significant decrease in plasma lipids, LDL-cholesterol, and blood pressure in
hypercholesterolemic subjects.5 Therefore, in the present study, we choose a relatively high dose
of the garlic powder (2.1 g.day -1; approximately equivalent to 107 mg alliin.day-1 or 5.2 g.day-1 of
fresh garlic) to be able to detect potentially beneficial effects of garlic powder on inflammation
and/or atherosclerosis related markers. Furthermore, a pharmaceutical formulation was used that
complies with all requirements for optimal release and bioavailability of the supposedly active
compounds of garlic.28
The compliance data suggest that the adherence to the dosing regimens was good.
Obviously, measurement of garlic components and atorvastatin plasma concentrations could have
corroborated this observation, but unfortunately these data are not available. The effects of
atorvastation were as expected supporting the notion that compliance was good at least in the
positive control group.
11
Previously, in vitro studies showed that high concentrations of garlic decreased cytokine
production in endothelial cells suggesting anti-inflammatory properties of garlic.19-21 In addition, a
growing body of evidence suggests that inflammatory processes play an important role in the
pathophysiology of atherosclerosis. Therefore, several markers of inflammation have been
evaluated in the past years as risks markers, including C-reactive protein. Since CRP is one of the
strongest predictors for the risk of atherosclerosis and cardiovascular events in subjects with and
without cardiovascular disease17,18 this marker was chosen as primary endpoint. It is important to
note that our study had an a priori power to detect a 25-30% decrease in CRP in a study
population with known risk factors for CVD. This percentage decrease was considered relevant
since other studies have shown similar effects of atorvastatin on CRP.23 Since this population had
a relatively high plasma concentration of CRP (>2 mg/l) when compared with health volunteers (<2
mg/l), this allowed us to detect possible effects of garlic and atorvastatin treatment on the
inflammatory status of these subjects. Furthermore, we measured other markers of inflammation
(fibrinogen and leukocyte TNF production in response to LPS) and markers of endothelial
function. Our data showed that the garlic powder Printanor had no significant effects on any of
these markers (Table 2). This suggests that garlic has no significant effect on the inflammatory
processes associated with atherosclerosis.
Alternatively, the potentially lipid and lipoprotein lowering properties of garlic have been
raised as a mechanism by which garlic could exert a beneficial effect on atherogenesis.4-6
However, recent placebo-controlled studies failed to show significant effects of garlic on these
parameters.8-15 In fact, our data appear to be in keeping with these findings since we did not
observe any effect of garlic on plasma lipids and lipoproteins (Table 2, Figure 3). In contrast,
atorvastatin treatment significantly decreased mean plasma CRP, total cholesterol, LDL-
cholesterol, triglycerides, and increased the sensitivity of leukocytes to LPS.
In summary, our data show that 12 weeks of treatment with a high dose chemically well-
characterized and production-controlled garlic powder has no anti-inflammatory, lipid lowering, or
blood pressure lowering effect in a population with known risk factors for CVD. As such we
conclude that there is no evidence that the garlic powder Printanor, and possibly garlic in general,
12
has beneficial effects on atherogenesis and consequently cardiovascular events in a relevant
population through anti-inflammatory processes, lipid lowering effects or blood pressure reduction.
In the future, it may be of interest to further advance our understanding on the effects of
garlic in atherosclerosis and consequently CVD in humans, by focusing on other potentially
beneficial effects of garlic on other risk factors for atherosclerosis. This may for instance be the
antantioxidant or anti-proliferative effects of garlic on vascular smooth muscle cells for which some
recent in vitro evidence exists.
13
ACKNOWLEDGEMENTS
This work was partly supported by the European Union research project QLK1-CT-1999-498. We
thank all the people involved in the EU project “Garlic and Health” for their collaboration and
Lilianna Schyschka from the University of Munich for technical assistance.
ABBREVIATIONS
Cardiovascular disease, CVD; C-reactive protein, CRP: tumor necrosis factor-, TNF;
lipopolysaccharide, LPS; soluble vascular cell adhesion molecule, s-VCAM; soluble intercellular
adhesion molecule, s-ICAM; low-density lipoprotein, LDL; high-density lipoprotein, HDL.
14
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17
Table 1. Characteristics of the study population
Gender Female Male
Age range (years) 40-67 40-63
Body Mass Index (kg/m2) 29.6 4.1 29.3 3.2
Systolic Blood Pressure (mm Hg) 124 18 130 11
Diastolic Blood pressure (mm Hg) 76 12 82 :10
Data are n or means SD.
19
Table 2. Average treatment effects of placebo, garlic and atorvastatin treatments on inflammation markers, markers of endothelial function and
vessel wall activation, lipids and lipoproteins; LS means are geometric means (data were analysed after log-transformation)
Parameter Comparison Garlic LS mean Statin LS mean Placebo LS mean % Change 95% CI Pr > |t|C-Reactive protein (mg/L)
Garlic vs Placebo 2.522 2.141 17.8% ( -2.3%, 42.0%) 0.0859
C-Reactive protein (mg/L)
Statin vs Placebo 1.709 2.141 -20.2% ( -33.5%, -4.3%) 0.0158
TNF alpha (pg/mL) Garlic vs Placebo 44.6 57.8 -22.9% ( -42.8%, 4.1%) 0.0883
TNF alpha (pg/mL) Statin vs Placebo 33.6 57.8 -41.9% ( -56.4%, -22.4%) 0.0004
TNF alpha after LPS (pg/mL)
Garlic vs Placebo 220 221 -0.5% ( -19.6%, 23.2%) 0.9644
TNF alpha after LPS (pg/mL)
Statin vs Placebo 270 221 22.1% ( -0.4%, 49.6%) 0.0547
TNF alpha LPS ratio Garlic vs Placebo 4.87 3.85 26.6% ( -13.2%, 84.5%) 0.2172
TNF alpha LPS ratio Statin vs Placebo 8.07 3.85 109.7% ( 45.6%, 202.1%) 0.0001
von Willebrand factor (%) Garlic vs Placebo 132.8 127.0 4.6% ( -6.2%, 16.8%) 0.4150
von Willebrand factor (%) Statin vs Placebo 123.6 127.0 -2.6% ( -12.7%, 8.5%) 0.6246
Fibrinogen (g/L) Garlic vs Placebo 3.839 3.769 1.9% ( -2.3%, 6.3%) 0.3860
Fibrinogen (g/L) Statin vs Placebo 3.899 3.769 3.4% ( -0.8%, 7.8%) 0.1080
s-ICAM (ng/mL) Garlic vs Placebo 215.5 215.9 -0.2% ( -8.6%, 8.9%) 0.9651
s-ICAM (ng/mL) Statin vs Placebo 204.4 215.9 -5.3% ( -13.3%, 3.3%) 0.2156
s-Selectine (ng/mL) Garlic vs Placebo 29.05 30.41 -4.5% ( -13.8%, 5.8%) 0.3739
s-Selectine (ng/mL) Statin vs Placebo 27.42 30.41 -9.8% ( -18.7%, 0.1%) 0.0513
s-VCAM (ng/mL) Garlic vs Placebo 575.2 557.0 3.3% ( -6.6%, 14.2%) 0.5252
s-VCAM (ng/mL) Statin vs Placebo 558.1 557.0 0.2% ( -9.4%, 10.8%) 0.9666
20
Table 3. Average treatment effects after 3 months treatment with placebo, garlic or atorvastatin on lipids and lipoproteins; the data are
presented as geometric means and the comparisons are shown as the percentage change from baseline of the percentage difference between
treatments.
Placebo Garlic StatinGarlic vs Placebo
%Change; (95%CI); p-valueStatin vs Placebo
%Change; (95%CI); p-valueCholesterol (mmol/L)
5.53 5.59 3.47 0.9%; (-4.7%, 6.9%); p= 0.7516 -37.2%; (-40.6%, -33.7%); p<0.0001
HDL (mmol/L)
1.20 1.19 1.23 -1.1% (-6.3%, 4.2%); p= 0.6680 2.5%; (-2.6%, 7.9%); p=0.3427
LDL (mmol/L)
3.33 3.37 1.57 1.3% (-7.1%, 10.6%); p= 0.7638 -52.7% (-56.5%, -48.6%); p<0.0001
Triglycerides (mmol/L)
1.69 1.64 1.15 -2.8% (-15.4%, 11.6%); p= 0.6795
-31.9% (-40.4%, -22.3%); p<0.0001)
LS means are geometric means (data were analysed after log-transformation)
21
FIGURE LEGENDS
Figure 1. Plasma CRP concentrations during 12 weeks of treatment. The figure represents the
time course of the mean % change from baseline of the parameter (with 95% CI error bars). The
occasions indicated at the horizontal axis correspond with the subjects visits by which visit 1 is the
mean value of the two pre-treatment values, visit 2 is the value of week 4, visit 3 is the value of
week 5, visit 4 is the value of week 11, and visit 5 is the value of week 12. Significant differences
as compared with placebo are indicated *P0.05.
Figure 2. TNF- concentrations after 12 weeks of treatment. The figure shows the mean %
change from baseline of the mean (non-stimulated) TNF- concentrations (left panel) and mean %
change from baseline in ratio of LPS stimulated (10 ng/ml) over non-stimulated (0 ng/ml) TNF-
(right panel) for the different treatments.
Figure 3. Plasma cholesterol and triglyceride concentrations during 12 weeks of treatment.
The figure represents the time course of the mean absolute change from baseline of the parameter
(with 95% CI error bars). The occasions indicated at the horizontal axis correspond with the visits
by which visit 1 is the mean value of the two pre-treatment values, visit 2 is the value of week 4,
visit 3 is the value of week 5, visit 4 is the value of week 11, and visit 5 is the value of week 12.
Significant differences as compared with placebo are indicated *P0.05.
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