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*
Division of Human Nutrition and Epidemiology, Wageningen University, Wageningen, the Netherlands and
The Wageningen Center for Food Sciences, Wageningen, the Netherlands
2To whom correspondence should be addressed at Division of Human Nutrition and Epidemiology, Wageningen University, Bomenweg 2, 6703 HD Wageningen, or P.O. Box 8129, 6700 EV Wageningen, the Netherlands. E-mail: nicole.deroos{at}staff.nutepi.wau.nl
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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KEY WORDS: • lipoproteins • HDL • trans-fatty acids • saturated fatty acids • humans
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). The intake of vegetable
shortenings exceeds that of margarines and is likely to increase even
further because of their use in ready-to-eat foods (Katan 2000
) and for deep-fat frying. This is an undesirable
development, because the intake of trans-fatty acids is
related to an increased risk of cardiovascular disease (Hu et al. 1997
, Kromhout et al. 1995
, Willett et al. 1993
). Experimental studies support this relation: many
metabolic studies showed that trans-fatty acids have an
unfavorable effect on blood lipids because, like saturated fatty acids,
they increase serum low density lipoprotein (LDL) cholesterol
(Judd et al. 1994
, Mensink and Katan 1990
, Nestel et al. 1992
, Zock and Katan 1992
). Moreover, the replacement of saturated by
trans-fatty acids was shown to decrease serum high density
lipoprotein
(HDL)3
cholesterol in many studies (Almendingen et al. 1995
,
Kris-Etherton and Yu 1997
, Müller et al. 1998
, Sundram et al. 1997
), which suggests an
additional increase in the risk of cardiovascular disease (Aro et al. 1997
, Ballantyne et al. 1999
,
Castelli et al. 1992
, de Backer et al. 1998
, Gordon et al. 1989
, Kitamura et al. 1994
, Pearson et al. 1979
, Sharrett et al. 1999
, Sorlie et al. 1999
). In response to
the negative health effects of trans-fatty acids, many
European manufacturers have decreased the trans-fatty acid
content of most stick margarines to <2% of energy (Katan 1995
, Michels and Sacks 1995
). The
trans-fatty acid content can be decreased by reducing the
degree of hydrogenation, which results in softer margarines.
Alternatively, solid margarines can be produced from tropical fats
instead of from partially hydrogenated vegetable oils: the amount of
saturated fatty acids will then be higher but the amount of
trans-fatty acids will be negligible (Michels and Sacks 1995
). Studies suggest that the replacement of 10% of
energy from trans-fat by saturated fat will increase serum
HDL cholesterol by 0.15 mmol/L (Zock et al. 1995
,
Zock and Katan 1992
). However, this prediction is based
on studies in which palmitic acid is the major saturated fatty acid,
and some, although not all (Kris-Etherton and Yu 1997
),
studies suggest that lauric acid might increase serum HDL cholesterol
more than palmitic acid (Temme et al. 1996
, Zock and Katan 1992
). Palm kernel fat and coconut fat are rich
sources of lauric acid (U.S. Department of Agriculture
).
We investigated whether replacement of a margarine rich in
trans-fatty acids by a margarine rich in lauric acid would
produce a stronger increase in serum HDL cholesterol than the 0.15
mmol/L per 10% of energy that was estimated previously. |
MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Subjects.
We enrolled 11 men and 21 women with a mean age of 30 y (range, 18–69 y) in the study. All of the volunteers were nonsmokers, and all were healthy as assessed by means of a medical questionnaire. The initial serum cholesterol concentration was 5.0 mmol/L (range, 3.0 to 7.1 mmol/L), and the body mass index 22.8 ± 2.5 kg/m2. The volunteers had no history of any chronic illness and were not taking any medication known to affect blood lipid metabolism. They all completed the study.
Study design.
We provided two controlled diets for 4 wk each in a randomized crossover design. One diet was rich in trans-fatty acids (trans-diet), and one was diet rich in saturated fatty acids (Sat-diet). There was no washout period between the two diets. The two diets were equal except for supplemental margarines, which were given in a 28-d menu cycle. The background diet consisted of conventional food items.
The margarine that was used in the diet rich in
trans-fatty acids was a blend of 70 parts of partially
hydrogenated soybean oil, containing 44% trans-C18:1
(Gouda’s Glorie; Van Dijk Foods, Lopik, the Netherlands); 14 parts of
a vegetable oil containing 63% linoleic acid and 23% oleic acid
(Becel; Unilever, Vlaardingen, the Netherlands) and 16 parts of water
(Table 1
). The margarine that was used in the diet rich in saturated fat was a
blend of 60 parts of palm kernel fat (Loders Croklaan, Wormerveer, the
Netherlands) and 40 parts of commercially available margarine made from
a blend of unhydrogenated rapeseed oil, soybean oil, sunflower oil,
palm kernel fat, coconut oil and palm oil (Blue Band; Van den Bergh BV,
Rotterdam, the Netherlands) (Table 1)
. Both supplemental margarines
were produced at NIZO Food Research (Ede, the Netherlands). The
margarines were used as a spread, as shortening in bread and cookies
and as fat in sauce and gravy. They supplied 77% of total fat in the
trans-diet and 68% of total fat in the Sat-diet. The
composition of the experimental diets was calculated using food
composition tables (Anonymous 1996
; Hulshof et al. 1999
, van Poppel et al. 1998
). To check the
composition of the diets, we collected duplicates of all meals
(Table 2
). The analyzed values were similar to the calculated composition.
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We weighed the subjects twice a week and increased or decreased their energy intakes as needed to maintain stable body weights.
Biochemical analysis.
We took blood samples on two separate days after d 19 of each diet. All four blood samples of each subject were analyzed in duplicate within one assay. Serum total cholesterol and triglycerides (Cholesterol Flex and Triglycerides Flex reagent cartridge; Dade Behring, Newark, NJ) and HDL cholesterol (liquid N-geneous HDL-C assay; Instruchemie BV, Hilversum, the Netherlands) were measured, and LDL cholesterol was calculated with the Friedewald formula. The coefficient of variation of 64 duplicate measurements was 0.4% for total cholesterol, 1.5% for triglycerides and 1.1% for HDL cholesterol.
The fatty acid composition of the margarines and the experimental diets
was analyzed by gas-liquid chromatography of the fatty acid methyl
esters (Metcalfe 1966) and, for 18 carbon
trans-fatty acids, by gas-liquid chromatography of
fatty acid 4,4-dimethyloxazoline derivatives (Fay and Richli 1991
).
Statistics.
We averaged the duplicate measurements in each dietary period and then calculated for each subject the difference between diets. We tested whether these differences were significantly different from zero by the Student’s t test for paired samples. We give two-sided 95% confidence intervals (CI) for the differences.
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Changes in body weight during the study were small and nonsignificant: -0.4 ± 0.9 kg during the trans-diet and -0.6 ± 0.9 kg during the Sat-diet (P > 0.5). We checked the diaries for deviations from the study protocol, but only minor deviations, which were unlikely to interfere with the results of the study, had been reported.
Serum lipids.
Serum total cholesterol was 0.31 mmol/L (95% CI, 0.14–0.48 mmol/L,
P = 0.0007) or 12.0 mg/dL lower at the end of the
trans-diet period than at the end of the Sat-diet period
(Fig. 1
). This difference was mainly due to a difference in HDL cholesterol,
which was 1.89 ± 0.46 mmol/L (73.1 ± 17.8 mg/dL) at the end
of the Sat-diet and 1.46 ± 0.33 mmol/L (56.5 ± 12.8
mg/dL) at the end of the trans-diet, for a difference of
0.36 mmol/L (95% CI, 0.26–0.46, P < 0.0001) (Fig. 1)
. Serum LDL cholesterol did not differ between the diet periods and
was 3.05 ± 0.81 mmol/L at the end of the Sat-diet and 3.04
± 0.80 mmol/L at the end of the trans-diet
(P = 0.64). Serum triglycerides were slightly lower at
the end of the Sat-diet, with a concentration of 0.90 ± 0.36
mmol/L, than at the end of the trans-diet, when the
concentration was 0.98 ± 0.41 mmol/L (P = 0.66)
(Fig. 1)
. The order of consumption of the two diets did not affect the
change in HDL cholesterol: the mean change was 0.33 ± 0.26 mmol/L
in subjects who switched from the trans-diet to the
Sat-diet and 0.39 ± 0.31 mmol/L in the subjects who received
the diets in the reverse order (P = 0.5).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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). Indeed, serum HDL cholesterol was 0.36 mmol/L
higher at the end of a 4-wk period in which 9.2% of energy was
provided by trans-fatty acids and 12.9% was provided by
saturated fatty acids than after a 4-wk period in which energy intake
from trans-fatty acids was 0% and that from saturated fatty
acids was 22.9%. Although the diets did not provide equal amounts of
polyunsaturated fatty acids (a difference of 2.2% energy), this
difference could only account for 
0.015 mmol/L in HDL cholesterol
according to the Mensink and Katan (1992
) equation.
Thus, lauric acid (or C12:0) appears to increase serum HDL cholesterol
more than does myristic (or C16:0) and palmitic acid (or C14:0)
(Sundram et al. 1997
, Temme et al. 1996
,
Zock and Katan 1992
). The major trans-fatty
acids in our study were the (n-10), (n-9) and (n-11) isomers of C18:1,
as is usual in partially hydrogenated soybean oil. These
trans-fatty acids were also the major trans-fatty
acids that were used in many other studies (Almendingen et al. 1995
, Judd et al. 1994
, Lichtenstein et al. 1993
, Mensink and Katan 1990
).
The difference in serum HDL cholesterol at the end of the two diets is
in line with results of epidemiological studies that suggest that the
risk of cardiovascular disease is increased more by the consumption of
trans-fatty acids than by the consumption of saturated fatty
acids (Ascherio et al. 1999
). For example, in the Health
Professionals follow-up study, the multivariate relative risk for
myocardial infarction was 1.12 (95% CI, 0.97–1.28) for each 5%
increase in intake of saturated fatty acids and 1.36 (95% CI,
1.03–1.81) for each 2% increase in intake of trans-fatty
acids (Ascherio et al. 1996
). In the Nurses’ Health
Study, the intake of foods rich in trans-fatty acids, such
as margarines, was also significantly associated with a higher risk of
coronary heart disease (Willett et al. 1993
). In the
same study, each increase of 5% in energy intake from saturated fat
was associated with a multivariate relative risk of coronary heart
disease of 1.17 (95% CI, 0.97–1.41). This was less than the relative
risk associated with a 2% increase in energy intake from
trans-fatty acids, which was 1.93 (95% CI, 1.43–2.61)
(Hu et al. 1997
). These studies show that the intake of
saturated and especially trans-unsaturated fatty acids
should be reduced to reduce the risk of coronary heart disease.
Moreover, we found that the LDL/HDL ratio was significantly higher
after the diet rich in trans-fatty acids than after the diet
rich in saturated fatty acids, indicating a higher risk of coronary
heart disease.
The consumption of saturated fatty acids and trans-fatty acids should not be encouraged. However, in products that require solid fats for their texture or firmness, the replacement of trans-fat with solid, tropical fats rich in lauric acids appears to be prudent.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: CI, confidence interval; HDL, high density lipoprotein; LDL, low density lipoprotein.
Manuscript received July 24, 2000. Initial review completed September 7, 2000. Revision accepted November 17, 2000.
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