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*
Institute of Arteriosclerosis Research at the University of Münster, Domagkstraße 3, 48149 Münster, Germany;
Institute of Clinical Chemistry and Laboratory Medicine, University of Münster, Albert-Schweitzer-Straße 33, 48129 Münster, Germany;
**
Institute of Pharmacological Sciences, University of Milan, Via Balzaretti, 9, 20133 Milan, Italy; and
University of Applied Sciences, Josefstraße 2, 48151 Münster, Germany
2To whom correspondence should be addressed. E-mail: mkratz{at}uni-muenster.de.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • monounsaturated fatty acids • polyunsaturated fatty acids • heterogeneity • lipoproteins • humans
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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) in cross-sectional (1
–6
) and case-control studies (7
–12
). Also, it was reported recently that hypercholesterolemic mice with predominantly small, dense LDL develop distinctly more atherosclerosis than mice with similar cholesterol levels but large, buoyant LDL particles (13
). Observations in patients with CHD, however, suggest that the association between small, dense LDL and cardiovascular diseases is due to confounding by other lipoprotein-related risk factors (14
,15
). In these patients, the authors even observed a positive association between large buoyant LDL and CHD. Thus, the relationship between the LDL subclass pattern and cardiovascular diseases is still not fully understood. Nevertheless, it is known from numerous studies that the small, dense LDL subspecies exhibit several properties that render them more atherogenic than large, buoyant LDL particles. Small, dense LDL have a reduced affinity for the LDL receptor (16
,17
), which results in a prolonged plasma half-life, and an increased affinity for receptor-independent cell-surface binding sites. This has been suggested to enhance the anchoring of LDL in the arterial wall (18
). Furthermore, small, dense LDL have been associated with impaired endothelial function in vivo (19
) and are more susceptible to oxidative modification (20
–23
). The latter effect might be due to a lower tocopherol content of small, dense LDL (24
) and/or to a larger amount of polyunsaturated fatty acids (PUFA) in the denser LDL subspecies (20
).
The latter point suggests that the LDL particle size and subclass pattern might be influenced by dietary fat. Until now, research on this topic has focused on the quantity rather than the quality of dietary fat. Several studies have consistently shown that low fat diets lead to a decrease in mean LDL size compared with high fat diets (25
–27
). Dreon and colleagues (28
) investigated the effect of nutrient intakes on LDL size and subclass pattern, and found a positive correlation between dietary saturated fatty acid (SFA) content and LDL peak particle diameter (i.e., the size of the major LDL fraction). Such an association was not apparent for monounsaturated fatty acids (MUFA) or PUFA. Up to now, however, the effect of dietary fat quality on LDL size has not been the scope of a controlled dietary study. We therefore investigated the effect of the dietary fatty acid composition on LDL peak particle diameter in healthy volunteers who participated in a strictly controlled dietary study. This study was designed initially to investigate the effect of refined olive oil (rich in MUFA), rapeseed oil [rich in MUFA and (n-3)-PUFA], and sunflower oil [rich in (n-6)-PUFA] on LDL susceptibility to oxidation (29
).
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Of 700 students living under boarding school–like conditions in a third-level technical college, 115 volunteers were screened for participation. Inclusion criteria were a body mass index < 27 kg/m2, serum cholesterol levels < 7.76 mmol/L and triglyceride levels < 3.39 mmol/L. Of the 115 volunteers, one was excluded because of diabetes mellitus, three because of hyperlipidemia, five because of thyroid disease, two because of intake of vitamin supplements, four because of hyperuricemia and 25 because of allergy, intolerance or aversion to foodstuffs contained in the study diets. Other exclusion criteria were smoking, drug or substance abuse, and malabsorption syndromes. Of the 75 students who qualified for participation in the study, 69 (35 men, 34 women), aged between 18 and 43 y were chosen for inclusion by drawing lots. Six subjects withdrew during the study because of illness and five withdrew because they were unwilling or unable to comply with the dietary regimen. In two participants, LDL concentrations were too low to allow determination of the peak particle diameter. The baseline characteristics of the 56 (30 men, 26 women) participants who finished the study are shown in Table 1
. Women who were taking oral contraceptives (n = 20) were instructed not to stop taking them and not to change to another pill. The participants were also asked not to change their regular lifestyles and their usual extent of physical activity throughout the study.
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Design and diets.
The study was conducted in a parallel design and consisted of two consecutive dietary periods for each subject. All participants consumed a baseline high fat diet rich in SFA for 2 wk and were then randomly divided into three groups. This was done using tables of random digits, separate for men and women, which were generated by a professional biostatistician. The study personnel and the participants were aware of group affiliations. Each group consumed a high fat diet containing refined olive oil (10 men, 8 women), sunflower oil (10 men, 10 women) or rapeseed oil (10 men, 8 women), respectively, as the principal source of fat for 4 wk. These diets were identical in every respect other than the fatty acid composition. Venous blood samples were obtained at the beginning of the study (visit 1), after the baseline period (visit 2), after 2 wk of consuming the study diets (visit 3) and at the end of the study (visit 4). All samples were drawn after an overnight fast of at least 12 h.
Before the study, the participants kept a careful 3-d dietary record. This was used to estimate each subject’s habitual energy and nutrient intake. The records were coded and calculated on the basis of German standard food tables. The study diets were calculated for 10 levels of energy intake ranging in steps of 0.84 MJ/d (200 kcal/d) from 7.52 to 15.05 MJ/d (1800–3600 kcal/d) by using a computer-based nutrient calculation program (EBIS, Nutrition Research Center, Esslingen, Germany). All participants were weighed twice per week while wearing light clothing, and energy intake was adjusted when necessary to maintain a stable body weight. During the study, the mean body weight decreased by 0.70 kg (SD 1.17 kg).
The composition of the participants’ habitual diet and the study diets is shown in Table 2
. The dietary treatments were described in more detail previously (29
).
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Measurement of LDL size.
The size of LDL was determined from plasma by the use of a commercially available polyacrylamide gradient gel electrophoresis kit in which lipoproteins are visualized by lipid staining (LFS Lipogel Assay Kit, LaboMed, Waldkirch, Germany). For calibration, every gel contained two standard plasma samples, one with large LDL (diameter 27.65 nm) and one with small LDL (diameter 24.46 nm). The size of these LDL was originally determined by electron microscopy of negatively stained LDL, which were isolated from the standard plasmas by sequential ultracentrifugation (30
). The size of the major LDL peak in samples was estimated by log-linear regression analysis of Rf values, which were calculated as the ratio of the electrophoretic migration distance of albumin (diameter 7.1 nm) to the electrophoretic migration distance of LDL. All four samples of each individual (visits 1–4) were analyzed within one gel.
Statistics.
All statistical calculations were performed using the Statistical Package for the Social Sciences (SPSS, version 10, Chicago, IL) computer program. Data were analyzed by repeated-measures ANOVA. Post-hoc comparisons of visits 2, 3 and 4 were done by paired t tests. These tests were two-tailed, and the multiple test situation was taken into account according to Bonferroni. The level of significance was P < 0.05.
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RESULTS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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LDL peak particle diameter was reduced significantly (-0.36 nm) during the oil diet phase [F(1,53) = 6.751, P = 0.012], with no significant difference among the three diet groups [F(2,53) = 0.976, P = 0.384] (Table 3)
. Comparison of the three time points (visits 2, 3 and 4) revealed that the reduction in LDL size was continuous throughout the 4 wk of the oil diet phase [-0.36 nm, T(55) = 2.626, P = 0.011, 95% confidence interval from -0.09 to -0.65 nm, visit 4 vs. visit 2], with no significant differences between visits 2 and 3 or visits 3 and 4. Furthermore, affiliation with one of the three diet groups did not contribute significantly to the observed variation in LDL size [F(2,53) = 0.374, P = 0.690].
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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It has been reported before that the concentration of PUFA in small, dense LDL is higher than in large, buoyant LDL (20
). Both the rapeseed oil and sunflower oil diets contained more PUFA than the baseline diet. We showed previously that the amount of PUFA in LDL increased due to both diets (29
). In particular, in subjects that consumed the rapeseed oil diet, the amount of linoleic acid in LDL remained constant, whereas the amount of 
-linolenic acid and eicosapentaenoic acid increased. In subjects that consumed the sunflower oil diet, the amount of linoleic acid increased further, despite an already high level (29
). Thus, the findings in these two groups are in agreement with the concept that dietary PUFA decrease LDL size by being incorporated into the particle. However, the olive oil diet, which contained less PUFA than the baseline diet, led to distinctly lower LDL-PUFA levels, whereas no significant increase in LDL size was observed in subjects that consumed this diet (29
). Thus, other mechanisms might contribute to the effect of dietary PUFA on LDL size. One such factor might be the effect of individual PUFA on the expression or activity of enzymes such as cholesterol ester transfer protein, lecithin cholesterol acyltransferase, lipoprotein lipase or hepatic lipase. In agreement with this concept, plasma activities of cholesterol ester transfer protein and lecithin cholesterol acyltransferase have been reported to be influenced by the content of MUFA and PUFA in the diet (31
–33
), and the activities of these enzymes have been associated with the LDL subclass pattern (34
–36
). However, because we have not measured enzyme activities, this hypothesis remains putative.
Changing the type of dietary fat had only a modest effect on LDL size. Would such a small difference have any clinical implications? Although the majority of the cross-sectional and prospective case-control studies conducted to date have shown a higher risk of CHD in patients with smaller and denser LDL, it is not known whether this association is independent of other factors such as serum triglyceride levels or serum HDL cholesterol concentrations. Because none of our participants fit into the classic small, dense LDL phenotype [i.e., LDL subclass phenotype B (peak particle diameter < 25.5 nm) combined with high serum triglyceride levels and low HDL cholesterol concentrations (37
)], it is hard to say on the basis of the available literature whether those of our subjects with smaller LDL indeed have a higher risk of CHD. In addition, it is not known whether a reduction in the peak particle diameter in response to diet increases the risk of CHD. There is, however, circumstantial evidence that this may be the case. Thus, it cannot be excluded that the small decrease in LDL peak particle diameter due to the diets rich in unsaturated fatty acids might by associated with an increase in atherosclerosis risk. On the other hand, research done by Rudel and colleagues (38
) in nonhuman primates offers a completely different perspective on our findings. These authors fed African green monkeys diets rich in SFA, MUFA or (n-6)-PUFA for 5 y, and investigated the effect of these dietary treatments on qualitative and quantitative aspects of lipoprotein metabolism as well as on coronary atherosclerosis directly. The monkeys fed the (n-6)-PUFA–rich diet developed less atherosclerosis than those fed the MUFA-rich diet despite a higher LDL cholesterol/HDL cholesterol ratio and smaller LDL size (38
). Although there might be metabolic differences between humans and the monkeys, these results show that extrapolating the effects of dietary fat on single risk factors to cardiovascular disease risk should be approached cautiously.
In conclusion, changing the quality of dietary fat from saturated to unsaturated fat slightly reduced the LDL peak particle diameter, with no significant difference between diets rich in MUFA, (n-6)-PUFA and (n-3)-PUFA. It is unclear, however, whether such a small decrease in LDL size has any effect on CHD risk. Furthermore, the small magnitude of this reduction suggests that the composition of dietary fat is not a major factor affecting LDL size.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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3 Abbreviations used: CHD: coronary heart disease, MUFA: monounsaturated fatty acids, PUFA: polyunsaturated fatty acids, SFA: saturated fatty acids.
Manuscript received 6 September 2001. Initial review completed 30 October 2001. Revision accepted 7 January 2002.
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LITERATURE CITED |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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