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Scandinavian Clinical Research AS, N-2027 Kjeller, Norway;
**
Parexel Medstat AS, Lillestrøm, Norway;
Scandinavian Statistical Services AS, N-2027 Kjeller, Norway;
*
Cecor AS, Haugesund, Norway; and
Natural AS, Oslo, Norway
2To whom correspondence should be addressed. E-mail: ola{at}scr.no
 |
ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • conjugated linoleic acid • body composition • body fat mass • lean body mass • humans
|
INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). CLA (mainly
cis-9, trans-11 but also trans-10,
cis-12 and other isomers) is readily formed in the first
biohydrogenation step of linoleic acid by the action of linoleic acid
isomerase of the bacterium Butyrivibrio fibrisolvens
(Kepler et al. 1970
and 1971
).
Consistent and convincing effects of CLA on body composition have been
documented in several animal models, i.e., CLA has been shown to reduce
body fat and to increase lean body mass (LBM) in pigs (Dugan et al. 1997
), mice (Pariza et al. 1996
, Park et al. 1997
), rats and chicks (Pariza et al. 1996
). The CLA-induced changes have been linked to
increased lipolysis in adipocytes and enhanced fatty acid oxidation in
both adipocytes and skeletal muscle cells (Pariza et al. 1997
, Park et al. 1999b
). Park et al. (1999a)
showed that in mice, dietary CLA significantly
increased total carnitine palmitoyltransferase activity in both fat pad
and skeletal muscle, but not in the liver. In addition, hormone
sensitive lipase activity was increased in adipocytes from CLA-fed
mice (Pariza et al. 1997
). In 3T3-L1 adipocytes, CLA
reduced heparin-releasable lipoprotein lipase activity and
intracellular concentration of triacylglycerol and glycerol
(Park et al. 1997
).
The consistent and well-documented data from both animal and in vitro studies have led to an increased interest in whether CLA exhibits the same fat-to-lean body mass repartitioning property in humans. The scope of this study was to investigate the putative beneficial effects of CLA on overweight or obese humans in relation to body fat mass (BFM), LBM, weight reductions and blood lipids.
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Subjects participating in the study were healthy men and women recruited after an announcement in the local newspaper at the study site. The subjects were referred to the research center (CECOR AS, Haugesund, Norway).
Inclusion criteria.
All subjects were >18 y old and had a body mass index (BMI) > 25
kg/m2 and < 35 kg/m2. The range for BMI
was chosen in accordance with the World Health Organization definition
for grading overweight and obesity (WHO 1997
).
Exclusion criteria.
Subjects who had used drug therapy for weight loss the previous week, subjects using adrenergic stimulating medication or undergoing insulin treatment, or subjects with any unstable medical or psychiatric illness or with any clinical condition that rendered the subject unfit to participate were excluded from the study. In addition, pregnant lactating women were excluded.
Ethics.
Approval from the Regional Ethics Committee was given before the onset of the study. Written informed consent was obtained from all participating volunteers. The study was conducted in agreement with the current version of the declaration of Helsinki.
Study design.
The trial was performed as a single-center, randomized, double-blind, placebo-controlled study with five parallel groups. Precise sample size estimation was problematic due to the limited data available. Sixty subjects were allocated to two strata, men or women in the ratios of 1/3 (n = 20) and 2/3 (n = 40), respectively, and within strata randomized to placebo (9 g olive oil) or 1.7, 3.4, 5.1 or 6.8 g CLA/d. The daily dosage was divided into three doses taken at breakfast, lunch and dinner. The treatment lasted for 12 wk. To ensure the double-blinding, a double-dummy technique was used. Each subject received four boxes (marked A, B, C and D) containing either placebo or CLA capsules. The subjects took one capsule from each of the four boxes at each intake. Thus, in the highest dosage group, all boxes contained CLA capsules and in the placebo group, all boxes contained placebo capsules. The total intake was 12 capsules per day for each subject. The active capsules contained 750 mg oil of which 75% was CLA (Tonalin, Natural Lipids, Norway). The CLA preparation consisted of equal parts of the cis-9, trans-11 isomer and the trans-10, cis-12 isomer. As placebo, olive oil capsules were chosen because this oil is regarded as relatively inactive in this context. All capsules were opaque soft gel capsules of identical appearance. Both active capsules and placebo capsules were supplied by Natural Lipids, Hovdebygda, Norway.
Clinical assessment.
The study required three visits to the clinic. Measurements of BFM, LBM
(total mass minus both fat mass and bone mineral content), weight,
blood pressure, heart rate and recording of possible confounding
factors such as physical exercise were made at each visit. Blood
samples for safety assessment and physical examinations were scheduled
for the first and third visit. In addition, baseline characteristics
and demographic data such as gender, height, smoking and alcohol
consumption were recorded on the first visit. Adverse events were
monitored throughout the study. For every adverse event, a rating of
severity, frequency, drug relation, action taken and subject outcome
was recorded. Compliance during the trial was expressed as the
discrepancy between the expected number of capsules taken and the
actual number of capsules used, divided by the expected number of
capsules taken. Blood samples were analyzed by validated methods at a
commercial clinical laboratory accredited for all tests performed
(Fürst Medical Laboratory, Oslo, Norway). The following blood
variables were analyzed: hemoglobin, erythrocytes, white blood cells,
platelets, serum creatinine, calcium, sodium, chloride, potassium,
serum creatine phosphokinase, lactate dehydrogenase, alanine
transaminase, aspartate transaminase, serum ferritine, 
-glutamyl
transferase, bilirubin, glucosylated hemoglobin A1c, serum
lipase (activity), triglycerides, total cholesterol, LDL cholesterol,
HDL cholesterol and lipoprotein (a).
Measurement of body composition.
Dual-energy X-ray absorptiometry (DXA) was used to measure body composition. The DXA measurement was performed with a Hologic QDR-2000, (Hologic, Waltham, MA).
Self-evaluation of quality of life.
Possible treatment effects on working capacity, general vitality and some other aspects of quality of life were assessed by a quality of life questionnaire using visual analog scales (VAS) of 100 mm. The VAS registration was comprised of seven questions related to sleep, gain from training, appetite, mood, stress, working capacity and leisure activity during the last 14 d. The subjects assessed these questions twice during the study (at baseline and at 12 wk).The subjects were asked to score the different categories by putting a mark between the end points [not at all satisfied (0 mm) or completely satisfied (100 mm)]. Scores at baseline were then compared with scores after 12 wk by taking the difference between the wk 0 (baseline) and the wk 12 values for each category. This difference was used for the statistical analysis.
Physical training.
The subjects received an offer by a local training center in Haugesund to follow a standard training program. The training was registered as light (without sweat) or intensive (with sweat).
Statistical analysis.
Means were used for estimation of the expected value for continuously
distributed variables, and are given with SD and number of
subjects. Most variables, including main variables, were considered
normally distributed; thus parametric methods were used for estimation
and statistical significance testing. Frequency rates were used for
estimation of categorical variables. Changes from wk 0 to 6 and from wk
0 to 12 within treatment groups were tested with a paired
t test; however, in some cases in which a large
proportion of subjects showed no change, the Sign test or Wilcoxon
Rank-Sum test was used. Differences among the five treatment groups
were analyzed with ANOVA test (demographic and clinical variables at
inclusion), repeated-measures ANOVA (clinical variable differences
between wk 0 and 6 or 12) and analysis of covariance (laboratory
variables measured at wk 0 and 6 with wk 0 value as cofactor). The null
hypothesis stated equal changes between treatment groups vs. at least
one of the active groups different from placebo. Dunnett’s
test was used for testing each of the four active groups pair wise
against placebo, controlling for type-I error. Categorical
variables were analyzed using Fisher’s exact test. A
P-value 
0.05 was regarded as significant, and
all tests were performed two-sided. The statistical analyses were
performed using the Statistical Analysis Systems version 6.12 (SAS
Institute, Cary, NC).
Subjects with two visits or more (at least wk 0 and 6) were included in the main analysis, whereas subjects with only the wk 0 visit were not included. A few subjects missed some of the wk 6 values. For these subjects, values were interpolated by taking the mean of the wk 0 and 12 values. Last-value-carried-forward was not applied here because the number of subject visits was limited.
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RESULTS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The number of subjects included in the study was 60 (5 x 12
subjects). The data analyzed in the main analysis were from 52 subjects
because 8 subjects withdrew during the first 6 wk of the study. There
were no differences in baseline registrations of height, weight and BMI
or in demographic variables such as gender, age, smoking and alcohol
habits when subjects included in the main analyses were examined
(Table 1
). Moreover, demographic data and baseline characteristics of the eight
subjects that withdrew were not different from the data obtained from
the main analyses. Five subjects withdrew from the study between wk 6
and 12; these subjects were not included in the analyses performed for
the final visit. Thus, 47 of 60 subjects completed the study. The
reasons for subject withdrawals from the study were adverse events for
eight subjects and five subjects did not return even after reminders
(Fig. 1
). The rates of adverse events did not differ significantly among
treatment groups.
|
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Effects of CLA on weight and body composition.
None of the groups had a significant reduction in weight or BMI after
12 wk of treatment (Table 2
). No differences were observed among the different treatment groups for
these variables. However, when BFM over the course of the study was
analyzed (Table 3
), differences among treatment groups were found. When active groups
were tested pairwise against placebo, significant differences in favor
of the 1.7, 3.4 and 6.8 g CLA groups were found. Within the
different groups, a significant reduction in BFM was found in the 3.4
and 6.8 g CLA groups (Table 3)
after 12 wk of treatment.
|
|
. However, only the 6.8 g CLA group
showed a significant increase in LBM from wk 0 (baseline) to wk 12
(Table 3)
(Fig. 2
).
|
). No significant differences were found among the groups regarding
either intensive or light training.
|
Blood samples were analyzed to monitor safety and effects of the CLA
treatment. Some changes were observed within each group. In the placebo
group, a significant increase in glucose after 12 wk was found
(P = 0.02). In all CLA-treated groups, significant
reductions in blood lipids (total cholesterol, HDL cholesterol or LDL
cholesterol) were found (Table 5
). Additionally, a significant increase in potassium (P
= 0.02), and a decrease in serum creatinine (P = 0.004) and platelets (P = 0.02) were found in the
3.4 g CLA group. In the 5.1 g CLA group, significant
reductions in serum creatinine (P = 0.05) and bilirubin
(P = 0.05) were found. A significant reduction in
creatine-phosphokinase (P = 0.03) was found in the
6.8 g CLA group. None of these changes, however, were considered
clinically important.
|
Adverse events.
The frequency of adverse events in the original 60 subjects was 60% (36/60), and no significant differences among the different treatment groups were observed. In eight subjects, adverse events resulted in subject withdrawals, but the treatment groups did not differ significantly regarding rate of withdrawal related to adverse event. One of these adverse events was serious because the subject was hospitalized due to a relapse of asthma, but this adverse event was not judged to be drug related (the subject was in the 3.4 g CLA group). Of all adverse events reported, one was considered to be severe (fatigue); the remainder were of a mild-to-moderate character. The most frequent adverse events were gastrointestinal symptoms. These events could be drug related. The numbers of possibly drug related adverse events were 3, 5, 9, 8 and 11 in the placebo, 1.7, 3.4, 5.1 and 6.8 g CLA groups, respectively. Of these 36 adverse events, 20 were gastrointestinal symptoms. Altogether, 55% of the adverse events were considered to have a possible connection to the study treatment. No difference was found among the groups regarding the frequency of possible drug-related events.
As pointed out above, adverse events resulted in eight subject withdrawals; seven of these were in active treatment groups and one in the placebo treatment group. The other subjects had transient adverse events that disappeared during continuous treatment without any dose adjustments.
Quality of life.
The VAS assessed possible treatment effects on some aspects of the
quality of life. Positive changes i.e., a subjective experience of
improvement of the conditions monitored by the VAS were observed only
in the CLA-treated groups (Table 6
).
|
|
DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONREFERENCES |
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, who did not find any differences between the CLA group
(2.7 g CLA) and the placebo group in a 6-mo placebo-controlled,
randomized, double-blind study in obese volunteers. However, some
studies have been performed in subjects of normal weight that
demonstrate an effect of CLA on body composition. In a
placebo-controlled, double-blind trial by Vessby and Smedman (1999),
the reduction of body fat after 12 wk of treatment with
4.2 g CLA/d was 1.2% (P < 0.0001). On the other
hand, Kreider [reviewed in Doyle (1998)
] did not find
that CLA affected body fat in weight lifters with an initially low body
fat percentage (14%). However, CLA had a positive effect on muscle
strength and the ability to handle training and immune stress. This is
interesting because the only group in this study that had a significant
increase in LBM was the group that had intensified their training.
Whether the increased LBM is an effect of the increased training
activities or an effect of CLA intake is difficult to decide. However,
a small, albeit not significant increase was seen in all
CLA-treated groups.
The CLA preparation used in this study contained equal amounts of the
cis-9, trans-11 isomer and the
trans-10, cis-12 isomer. The effects of CLA
presented in this study could therefore result from either or both of
these isomers. The cis-9, trans-11 isomer has
been regarded as the biologically most active isomer because of its
abundance relative to the other isomers in biological membranes of mice
and rats (Ha et al. 1990
, Ip et al. 1991
). However, the trans-10, cis-12
isomer has been associated with reduced BFM and enhanced body protein
in mice, whereas no such changes in body composition have been found
due to the cis-9, trans-11 isomer (Park et al. 1999b
). Furthermore, the trans-10,
cis-12 isomer, but not the cis-9,
trans-11 isomer has been found to reduce lipoprotein lipase
activity, intracellular triacylglycerol and glycerol, and to enhance
glycerol release into the medium in cultured 3T3-L1 adipocytes
(Park et al. 1999b
). Interestingly, the ratio of
cis-9, trans-12 and trans-10,
cis-12 varies dependent on the tissue (Park et al. 1995
). This means that individual CLA isomers may trigger
different responses in different tissues. Thus, the effect of CLA on
LBM may be uncoupled from the effect of CLA on BFM.
In this study, blood CLA levels were not measured. This may be of importance because the subjects may vary with respect to the quantity of CLA-rich food they ingest per day.
An effect of CLA on early arteriosclerosis, concomitant with a
reduction in plasma total and LDL cholesterol levels, was reported in
rabbits (Lee et al. 1994
) and hamsters (Nicolosi et al. 1993
). Clinically important reductions in total or LDL
cholesterol were not seen in this study. It may be that the treatment
period was too short for such reductions to appear, but divergent
responses in different species and the initial level of cholesterol may
also play a role.
A reduction in the HDL level was found in all the CLA-treated groups after 12 wk of treatment. This reduction might be of importance and should be investigated in future studies. In addition, the reduced LDL cholesterol level found in the 1.7 and 3.4 g CLA-treated groups after 12 wk might be of some importance.
Both withdrawal rates and the occurrence of adverse events were quite
high in the study. This may be caused by the number of capsules that
were to be taken each day (12 capsules). As reported by Vessby and Smedman (1999)
, the dominant nuisances reported were of
gastrointestinal origin. These events could have been caused by the
capsules or the oil per se rather than the high content of CLA.
In general, the subjects in the present trial participated with the goal of improving some aspect of their quality of life. These results may be of importance, and future CLA studies should include validated measurements to investigate further the effects of CLA on general well-being.
In conclusion, we want to emphasize that the beneficial effects of CLA with regard to BFM and LBM are promising. The number of subjects in this study was relatively small and may thus be a limiting factor in reaching general conclusions. However, at present, a dose of 3.4 g CLA/d for 12 wk seems to be sufficient to reduce BFM significantly in overweight and obese humans. A conclusion regarding the optimal dose of CLA and duration of treatment cannot be made on the basis of these limited data, but the current data provide a solid platform for future studies.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: BFM, body fat mass; BMI,
body mass index; CLA, conjugated linoleic acid; DXA, dual-energy
X-ray absorptiometry; LBM, lean body mass; VAS, visual analog scale.
Manuscript received March 13, 2000. Initial review completed June 14, 2000. Revision accepted September 4, 2000.
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17. Vessby B., Smedman A. Conjugated linoleic acid (CLA) reduces the body fat content in humans.. Chem. Phys. Lipids 1999;101:AT2./01abs.
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S. Tricon, G. C Burdge, S. Kew, T. Banerjee, J. J Russell, E. L Jones, R. F Grimble, C. M Williams, P. Yaqoob, and P. C Calder Opposing effects of cis-9,trans-11 and trans-10,cis-12 conjugated linoleic acid on blood lipids in healthy humans Am. J. Clinical Nutrition, September 1, 2004; 80(3): 614 - 620. [Abstract] [Full Text] [PDF]
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U. Riserus, B. Vessby, J. Arnlov, and S. Basu Effects of cis-9,trans-11 conjugated linoleic acid supplementation on insulin sensitivity, lipid peroxidation, and proinflammatory markers in obese men Am. J. Clinical Nutrition, August 1, 2004; 80(2): 279 - 283. [Abstract] [Full Text] [PDF]
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J.-M. Gaullier, J. Halse, K. Hoye, K. Kristiansen, H. Fagertun, H. Vik, and O. Gudmundsen Conjugated linoleic acid supplementation for 1 y reduces body fat mass in healthy overweight humans Am. J. Clinical Nutrition, June 1, 2004; 79(6): 1118 - 1125. [Abstract] [Full Text] [PDF]
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U. Riserus, A. Smedman, S. Basu, and B. Vessby Metabolic effects of conjugated linoleic acid in humans: the Swedish experience Am. J. Clinical Nutrition, June 1, 2004; 79(6): 1146S - 1148S. [Abstract] [Full Text] [PDF]
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Y. Wang and P. J. Jones Dietary conjugated linoleic acid and body composition Am. J. Clinical Nutrition, June 1, 2004; 79(6): 1153S - 1158S. [Abstract] [Full Text] [PDF]
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R. S McLeod, A. M LeBlanc, M. A Langille, P. L Mitchell, and D. L Currie Conjugated linoleic acids, atherosclerosis, and hepatic very-low-density lipoprotein metabolism Am. J. Clinical Nutrition, June 1, 2004; 79(6): 1169S - 1174S. [Abstract] [Full Text] [PDF]
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G. C. Burdge, B. Lupoli, J. J. Russell, S. Tricon, S. Kew, T. Banerjee, K. J. Shingfield, D. E. Beever, R. F. Grimble, C. M. Williams, et al. Incorporation of cis-9,trans-11 or trans-10,cis-12 conjugated linoleic acid into plasma and cellular lipids in healthy men J. Lipid Res., April 1, 2004; 45(4): 736 - 741. [Abstract] [Full Text] [PDF]
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A. H. Terpstra Effect of conjugated linoleic acid on body composition and plasma lipids in humans: an overview of the literature Am. J. Clinical Nutrition, March 1, 2004; 79(3): 352 - 361. [Abstract] [Full Text] [PDF]
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T. M. Larsen, S. Toubro, and A. Astrup Efficacy and safety of dietary supplements containing CLA for the treatment of obesity: evidence from animal and human studies J. Lipid Res., December 1, 2003; 44(12): 2234 - 2241. [Abstract] [Full Text] [PDF]
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J. M. Brown and M. K. McIntosh Conjugated Linoleic Acid in Humans: Regulation of Adiposity and Insulin Sensitivity J. Nutr., October 1, 2003; 133(10): 3041 - 3046. [Abstract] [Full Text] [PDF]
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A. H. M. Terpstra, M. Javadi, A. C. Beynen, S. Kocsis, A. E. Lankhorst, A. G. Lemmens, and I. C. M. Mohede Dietary Conjugated Linoleic Acids as Free Fatty Acids and Triacylglycerols Similarly Affect Body Composition and Energy Balance in Mice J. Nutr., October 1, 2003; 133(10): 3181 - 3186. [Abstract] [Full Text] [PDF]
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