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Institute of Arteriosclerosis Research and
* Institute of Clinical Chemistry and Laboratory Medicine, University of Muenster, Muenster, Germany; and
University of Applied Sciences, Muenster, Germany
1To whom correspondence should be addressed. E-mail: mkratz{at}u.washington.edu.
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • hypertriglyceridemia • lipoproteins • LDL • arteriosclerosis • diet
High serum triglyceride concentrations were recently recognized as an independent risk factor for cardiovascular disease (1), particularly when HDL-cholesterol concentrations are concomitantly low (2). Also, several studies show that pharmacological treatment of high serum triglyceride and low HDL-cholesterol concentrations lowers the risk of fatal and nonfatal cardiovascular events [reviewed in Sprecher et al. (2)].
Although a monogenic defect might be the cause of elevated triglyceride concentrations in some patients, most patients develop hypertriglyceridemia as a result of a genetic susceptibility combined with an unfavorable lifestyle. Particularly, diet has a huge impact on serum triglyceride levels, and dietary intervention is therefore the cornerstone of therapy in hypertriglyceridemia. Elevated serum triglyceride concentrations can be lowered effectively if the patient loses excess body weight, restricts the consumption of alcohol and simple carbohydrates, and increases the consumption of long-chain (n-3)-PUFAs, complex carbohydrates, and fiber. Because many patients also have increased concentrations of LDL-cholesterol, it is also appropriate to recommend a reduced intake of saturated and trans fatty acids.
It is less clear, however, whether the total fat content of such a diet should optimally be low or high. Various studies report higher triglyceride concentrations in normolipidemic (3–9) and hypertriglyceridemic (10–14) subjects consuming low-fat compared to higher-fat diets. Also, serum triglyceride levels are reported to be higher in populations that habitually consume low-fat diets (15,16). This is apparently due to the fact that low-fat diets usually contain higher amounts of carbohydrate. Carbohydrate-induced hypertriglyceridemia is a well known phenomenon, even in normolipidemic subjects [for a review see Hellerstein (17)]. However, the increase in serum triglyceride levels induced by consumption of a low-fat, high-carbohydrate diet is reported to be particularly distinct in hypertriglyceridemic subjects. Nevertheless, some experts and dietary guidelines still recommend low-fat diets for patients with hypertriglyceridemia (18,19). Others, apparently concerned about carbohydrate-induced hypertriglyceridemia, recommend higher-fat diets (20). Thus, it is still not entirely clear which diet is most suitable for the treatment of hypertriglyceridemia.
The present study compared the effects of a high-fat and a low-fat diet on the cardiovascular risk profiles of nonobese men with hypertriglyceridemia. Both diets were isocaloric; rich in monounsaturated fatty acids (MUFAs), long-chain (n-3)-PUFAs, fiber, and complex carbohydrates; and contained no alcohol. The absolute amounts of long-chain (n-3)-PUFAs and fiber were similar in both diets, and the fat and carbohydrate compositions were identical. The primary objective of this study was to compare the effects of these diets on serum triglyceride concentrations. Furthermore, serum concentrations of total, LDL-, and HDL-cholesterol were measured. Because both diets contained large amounts of unsaturated fatty acids, particularly highly unsaturated (n-3)-PUFAs, we were also interested in the effects of the diets on LDL susceptibility to oxidation and urinary isoprostanoid excretion as a measure of in vivo oxidative stress.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONLITERATURE CITED |
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30 kg/m2), did not present a history of symptoms or markers indicative of type III hyperlipidemia; apolipoprotein (apo) C-II deficiency; diabetes mellitus; liver, kidney, or thyroid dysfunction; pancreatitis; or coronary heart disease, and did not use tobacco products or regularly consume large amounts of alcohol. One participant withdrew during the study because of a conflict with employment demands, and 2 participants withdrew because they were unwilling or unable to comply with the dietary regimen. The anthropometric data and biochemical characteristics of the 14 men who finished the study are shown in Table 1. Six participants had been taking lipid-lowering drugs [atorvastatin (n = 3), simvastatin (n = 1), bezafibrate (n = 1), and fenofibrate and fluvastatin (n = 1)], and 2 were taking fish oil supplements on their initial visit; all were instructed to stop taking these drugs at least 4 wk before the beginning of the study. The participants were also asked to maintain their usual lifestyle and extent of physical activity throughout the study. The protocol and the objectives of the study were explained to the participants in detail. All gave written consent. The study protocol was approved by the Ethics Committee of the University of Muenster and was in accordance with the Helsinki Declaration of 1975, as revised in 1983 and 1989.
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The subjects and their wives received detailed dietary instructions from a trained nutritionist. They also received a study protocol booklet containing detailed information on the amounts and types of food items to be used in the preparation of meals or be chosen as snacks during the respective dietary periods. Alcoholic drinks, refined sugar, sweets, and soft drinks were not permitted for the entire duration of the study. To increase adherence to the dietary regimen, the subjects were permitted to consume 420 kJ (100 kcal) per day in the form of free-choice foodstuffs from an approved list.
To assess compliance, the participants completed a 3-d dietary protocol during the acclimation and washout-periods and two 3-d dietary protocols in both the high-fat and low-fat test diet periods. These records were coded and calculated on the basis of standard German food tables (Bundeslebensmittelschlüssel). A nutritionist was in regular contact with the subjects, both at their visits to the lipid clinic and by phone, to provide support and motivation. At each visit the subjects were weighed while wearing light clothes. During the entire length of the study, the subjects recorded their daily free-choice items and any deviations from the diets in the study protocol booklet.
Blood sampling. Blood samples were taken in the morning after an overnight fast of at least 10 h at the beginning of the acclimation period, before and after the high-fat diet period, and before and after the low-fat diet period. Additional fasting venous blood samples were taken on d 7 and 14 of the high-fat and low-fat diet periods to assess blood concentrations of triglycerides and pancreatic enzymes. After 30 to 60 min, serum and plasma containing EDTA were obtained by centrifugation at 2000 x g for 15 min at 10°C. Serum and EDTA plasma samples were immediately frozen at –80°C and stored until analysis.
Serum lipid variables. Serum concentrations of total cholesterol and triglycerides were measured using enzymatic assays (22,23). The HDL-cholesterol concentration was measured by a precipitation method (24), and the LDL-cholesterol concentration was measured after precipitation of LDL with dextran sulfate (25). Serum concentrations of apo A-I and apo B were measured using immunoturbidimetric assays (26). All these measurements were performed in series within 1 d, using a Hitachi 917 autoanalyzer (Roche Diagnostics). These methods were validated by regular analyses of reference serums supplied by the national German INSTAND proficiency testing program and the international quality assurance program of the U.S. Centers for Disease Control and Prevention. Because the serum triglyceride concentrations of 2 subjects were >11.25 mmol/L at baseline, HDL-cholesterol and apo B concentrations in serum could not be determined.
In addition to these in-series measurements at the end of the study, serum triglyceride and pancreatic enzyme concentrations were measured immediately after each clinic visit to detect critically high triglyceride levels.
LDL susceptibility to oxidation. LDL was separated from EDTA plasma by density gradient centrifugation in a single 2-h session, using a variation of the method described by Chung et al. (27). After centrifugation, the LDL was collected using a syringe and needle, then filtered through a sterile 0.22-µm filter (Renner) into sterile vacuum containers (Mallinckrodt Radio-Pharma). This preparation was stored in darkness at 4°C. Susceptibility to oxidation was measured on the following day.
Susceptibility to oxidation was measured from LDL by the method of Esterbauer et al. (28). Briefly, LDL was desalted by gel-filtration on an Econo-Pac 10DG column (Bio-Rad) and stored on ice for 60 min until oxidation was initiated. The concentration of the desalted LDL solution was assessed by measurement of the cholesterol content, using a commercially available assay (CHOD-PAP; Roche Diagnostics). The desalted LDL was diluted to 0.08 g cholesterol/L in PBS. Oxidation was initiated at 37°C by the addition of CuSO4 (final concentration 1.6 µmol/L) exactly 1 h after desalting. The formation of conjugated dienes was monitored by measurement of the change in absorbance over 3 h at 234 nm with a Uvikon 922 photometer (Kontron), resulting in a sigmoidal curve. A tangent to this curve was drawn at the point of inflection. The lag time was defined as the time from the addition of CuSO4 until the intersection of this tangent with the baseline. The rate of propagation was calculated from the slope of the tangent, and the maximum amount of conjugated diene formation was determined as the height of the maximum absorbance above baseline. All samples from each participant were measured in a single session, yielding intraassay CV values of 2.7, 3.8, and 4.5% for the measurements of lag time, rate of propagation, and maximum amount of conjugated diene formation, respectively.
Urinary isoprostanoid and creatinine concentrations.
Morning urine samples were collected at each visit, 0.002% butylated hydroxytoluene was added, and the samples were frozen at –80°C until analysis. Levels of 8-iso-prostaglandin F2
(8-iso-PGF2) were measured with a commercially available competitive enzyme immunoassay (Cayman Chemicals). The samples were first purified, using an affinity column specific for 8-iso-PGF2. Because some of the 8-iso-PGF2 content is lost during this procedure, recovery was assayed by adding [3H]-8-iso-PGF2 to the sample prior to purification and measuring scintillation in the sample with a LS 6500 scintillation counter (Beckman) before and after the purification step. All samples from each subject were measured on the same plate. The intraassay CV was 3.0%. Urinary creatinine was measured by an automated kinetic procedure according to the method of Jaffé, as described by Esterbauer et al. (28), using a Hitachi 747 autoanalyzer (Roche Diagnostics). This method was validated by regular analyses of reference samples supplied by the national German INSTAND proficiency testing program. All samples were measured within 1 d.
Statistical analysis. The appropriate number of study subjects was determined by a power analysis, using data from a previous study with a group of similar patients (10). This analysis showed that 24 subjects would be needed to detect a difference in serum triglyceride concentration of at least 0.56 mmol/L (50 mg/dL) between subjects consuming the 2 test diets with a power of 80%. However, after 14 subjects completed both dietary periods, a preliminary evaluation of the data showed that this comparison was not appropriate, because the effects of the diets on serum lipid concentrations differed distinctly between subjects. We therefore ended the study prematurely.
Statistical analyses were conducted using the Statistical Package for the Social Sciences (version 10; SPSS). The distribution of means was approximately normal for most variables, as shown by normal plots and histograms of the data and by Kolmogorov-Smirnov tests. In contrast, serum triglyceride concentrations did not appear to be normally distributed and so were logarithmically transformed. Mean differences and 95% CI values were calculated by two-tailed t tests of the logarithmically transformed triglyceride data and retransformation of the resulting means and 95% CI values. Triglyceride levels at the start of the high-fat and low-fat diet periods were compared by two-tailed paired t tests to assess the effect of diet order; levels did not differ between these 2 time points. Effects of the high-fat and low-fat diets and differences between them were assessed by two-tailed paired t tests. Results were considered significant at values of P < 0.05.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONLITERATURE CITED |
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Lipid peroxidation.
Urine concentrations of PGF2 did not differ among the acclimation, washout, and high-unsaturated-fat diet periods or between the high-fat and low-fat diets (Table 4). By contrast, consumption of the low-fat diet distinctly lowered the susceptibility of plasma LDL to oxidation in subjects compared to the high-fat diet, as indicated by a lower rate of propagation [mean difference = –2.07 nmol conjugated dienes/(min · mol LDL-cholesterol), 95% CI = –0.83 to –3.34 nmol conjugated dienes/(min · mol LDL-cholesterol)] and a lower maximal formation of conjugated dienes (mean difference = –106 nmol conjugated dienes/mol LDL-cholesterol, 95% CI = –21 to –191 nmol conjugated dienes/mol LDL-cholesterol). Also, the lag time until the start of oxidation tended to be longer (P = 0.06) after consumption of the low-fat diet (mean difference = +2.3 min, 95% CI = –0.11 to +4.69 min).
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONLITERATURE CITED |
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However, the most interesting finding of this study was that although mean triglyceride levels did not differ significantly between subjects that consumed the high- and low-fat diets, the individual serum triglyceride responses to these diets differed strongly. Whereas some subjects had distinctly lower serum triglyceride concentrations after consuming the high-fat diet, others had distinctly lower triglyceride concentrations after consuming the low-fat diet. These results suggest that many patients with hypertriglyceridemia are not treated optimally if general advice for either a low-fat diet or a high-fat diet is given. Instead, it appears to be more appropriate to fit any dietary recommendation to each patient individually.
At first glance, the present findings seem to be inconsistent with previously published data. Liu and colleagues (12,13) reported that slightly hypertriglyceridemic subjects (fasting serum triglyceride concentrations of 2.25 to 4.50 mmol/L) had distinctly lower serum triglyceride concentrations after consuming high-fat diets, compared with low-fat diets. Also, Hellerstein (17) recently concluded in a review of the effects of low-fat diets on serum triglyceride levels that individuals with higher baseline serum triglyceride levels are more likely to experience a further increase in plasma triglycerides when consuming a low-fat high-carbohydrate diet. The data summarized in this review and the data by Liu and colleagues are based on studies with either normolipidemic or slightly hypertriglyceridemic subjects. The present study supports the conclusion drawn by Hellerstein for slightly hypertriglyceridemic subjects, because in this study all individuals with baseline triglyceride concentrations below a threshold of 
4.5 mmol/L also had lower serum triglyceride concentrations after consuming the high-fat diet, compared with the low-fat diet. However, 5 of the 9 subjects with baseline levels above 4.5 mmol/L benefited more from the low-fat diet than from the high-fat diet.
We hypothesized that most patients with only slightly elevated serum triglyceride concentrations suffer from hypertriglyceridemia induced primarily by simple carbohydrates and/or alcohol. Advising these subjects to consume high-fat and therefore low-carbohydrate diets, to choose predominantly complex carbohydrates, and to refrain from drinking alcoholic beverages apparently eliminated the cause of the hypertriglyceridemia, inducing a fast and sustainable decrease in serum triglyceride concentrations. The cause for hypertriglyceridemia is apparently different at least in some of the subjects with more distinctly elevated triglyceride concentrations. The low-fat high-complex carbohydrate diet was much more effective in lowering serum triglyceride levels in some of these subjects. We therefore recommend a high-fat diet rich in unsaturated fatty acids [particularly long-chain (n-3)-PUFAs], fiber, and complex carbohydrates and low in SFAs, simple carbohydrates, and alcohol for patients with serum triglyceride concentrations < 4.5 mmol/L. However, a lower-fat diet should be considered for individuals with triglyceride concentrations above 4.5 mmol/L.
Nevertheless, the fat:carbohydrate ratio was second in importance to the carbohydrate and fat composition, which, together with alcohol restriction, likely accounted for most of the lowering of serum triglyceride levels. In particular, both the low-fat and high-fat diets contained similar high amounts of long-chain (n-3)-PUFAs. It is notable that the combination of the relatively low total fat content and the high content of (n-3)-PUFAs makes the low-fat diet much harder to implement than the high-fat diet, and might require more commitment on the part of the patient. Conversely, the high-fat diet provided an unusually high amount of fiber, which may have contributed to the good results seen in the subjects that consumed this diet. Clinicians might want to consider these points when implementing the diets.
Some years ago, Parks et al. (29) proposed the use of an algorithm to predict which patients would experience significant elevations in serum triglyceride concentration after consuming a low-fat diet. This algorithm was based on the baseline BMI and fasting triglyceride and insulin concentrations. In the present study, this algorithm did not help to predict the effects of the 2 diets on triglyceride levels in the subjects. For example, the algorithm indicated that only 1 of the study subjects would experience elevated triglyceride levels after consuming the low-fat diet. In fact, however, 7 participants had distinctly higher triglyceride concentrations after consuming the low-fat diet, compared to the high-fat diet. The inconsistency of the data with respect to the algorithm might be due to differences in study design. The low-fat diet used by Parks et al. (29) was extremely low in fat (10% of energy intake), and the subjects were normo- to only moderately hypertriglyceridemic, but the body weight range of the subjects was much wider than in the present study.
It might be argued that the low-fat diet would have lowered serum triglyceride concentrations even more if body weight loss had not been prevented (19). Although it is still unclear whether the fat content of the diet per se affects body weight (29,30), or whether the reduction in BMI frequently associated with low-fat diets is due to the generally higher fiber content of such diets, this possibility cannot be excluded. Thus, a study comparing the effects of free consumption of low-fat and high-fat diets in hypertriglyceridemic subjects would be interesting.
The susceptibility of LDL to oxidation was somewhat lower after subjects consumed the low-fat diet, compared to the high-fat diet. This was likely due to the lower absolute content of linoleic acid and -linolenic acid in the low-fat diet. We previously reported that linoleic acid particularly accumulates in LDL particles, rendering them more susceptible to oxidation (31). However, it remains unclear whether this difference affects risk for cardiovascular disease, especially in light of the fact that the test diets did not differ in their effect on urinary isoprostanoid excretion. It is interesting that the diets rich in highly unsaturated fatty acids did not increase either LDL susceptibility or urinary isoprostanoid excretion, 2 measures of in vivo oxidative stress.
In conclusion, the present study confirmed that a diet rich in unsaturated fatty acids [particularly long-chain (n-3)-PUFAs], fiber, and complex carbohydrates and low in saturated fatty acids, simple carbohydrates, and alcohol can be used effectively to treat hypertriglyceridemia. The study also confirmed previous findings that individuals with serum triglyceride concentrations < 4.5 mmol/L benefit more from such a diet if its fat content is relatively high. However, a considerable number of individuals with serum triglyceride concentrations > 4.5 mmol/L achieve lower serum triglyceride levels by consuming a low-fat diet. We therefore propose to fit the recommendation given to each patient individually, according to the patient’s baseline triglyceride concentration, dietary preferences, lifestyle, and overall cardiovascular risk profile.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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Manuscript received 8 September 2003. Initial review completed 8 October 2003. Revision accepted 3 March 2004.
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TOPABSTRACTMETHODSRESULTSDISCUSSIONLITERATURE CITED |
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high-fat diet