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Nutraceuticals and Functional Foods Institute, Laval University, Québec, Canada G1K 7P4;
* Lipid Research Center, CHUL Research Center, Québec, Canada G1V 4G2;
Québec Heart Institute, Laval Hospital Research Center, Québec, Canada G1V 4G5
6To whom correspondence should be addressed. E-mail: Nathalie.Bergeron{at}inaf.ulaval.ca.
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ABSTRACT |
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 TOP ABSTRACT SUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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KEY WORDS: • LDL peak particle diameter • low fat-high carbohydrate diet • high fat-high monounsaturated fatty acid diet • lipids
Whether reduced LDL particle size is an independent risk factor for future coronary artery disease (CAD)6 remains controversial. Several large cohort studies showed that a reduced LDL peak particle diameter (PPD), i.e., the diameter of the most abundant LDL subclass within an individual, was associated with an approximately threefold increase in the risk of developing CAD (1,2), although this is not a unanimous finding (3,4). These inconsistent observations led us to hypothesize that LDL-PPD per se may not represent the most adequate measure of the atherogenicity attributed to the small dense LDL phenotype. Further characterization of LDL particles on electrophoresis gels has allowed us to measure the cholesterol (C) concentration contained within small LDL [LDL-C (<25.5 nm)]. Although we showed recently that the more traditional LDL-PPD measure was only marginally associated with an increased risk of CAD in men of the Quebec Cardiovascular Study, an increased concentration of LDL-C (<25.5 nm) was associated with a fourfold increase in CAD risk, independent of other variables of the traditional lipid profile and of the LDL-PPD (5).
Dietary habits significantly affect coronary heart disease (CHD) risk (6,7). However, the determination of the macronutrient composition that will be most effective in reducing CHD risk remains the topic of intense debate. Although low fat, high complex carbohydrate (high CHO) diets have been extensively recommended, their overall benefit remains controversial because of their potentially deleterious triglyceride (TG)-raising effect (8–10) and their negative effect on LDL-PPD (11) and HDL-C levels (9,12,13). It is important to stress, however, that recognition of the potentially negative effect of low fat, high CHO diets on plasma lipids and LDL-PPD is based largely on studies conducted under isoenergetic conditions in which energy intake was artificially imposed to keep body weight constant (11,12,14). It has been argued that such experimental designs may not reflect "real life" ad libitum intake of food because low fat, high CHO diets promote body weight reduction by being associated with a spontaneous reduction of energy intake (9,15). To the best of our knowledge, studies have yet to investigate the effects of ad libitum consumption of low fat, high CHO diets on a large spectrum of LDL electrophoretic characteristics, including LDL-C (<25.5 nm).
In contrast to low fat, high CHO diets, high fat diets rich in monounsaturated fatty acids (high MUFA) have been reported to reduce total plasma and LDL-C levels without raising plasma TG or lowering HDL-C concentrations (8). Under isoenergetic conditions, the consumption of a MUFA-enriched sunflower oil diet had no effect on LDL-PPD compared with a low fat, high CHO diet (16). However, the effects of high fat, high MUFA diets consumed ad libitum on LDL-PPD and other electrophoretic characteristics of LDL particles remain to be documented.
The goal of this study was to compare the effect of ad libitum consumption of a low fat, high CHO diet with that of a high fat, high MUFA diet on specific electrophoretic characteristics of LDL particles including LDL-PPD and small LDL-C (<25.5 nm) levels in healthy men.
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SUBJECTS AND METHODS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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The study design was described in detail previously (17). Briefly, sedentary men [n = 65; age, 37.5 ± 11.2 (mean ± SD) y; Table 1] were recruited in the Québec metropolitan area. Exclusion criteria included endocrine, cardiovascular, hepatic and renal disorders, use of medication known to affect lipid metabolism, smoking and significant change in body weight within the year that preceded study onset. Individuals with excessive alcohol intake, unusual dietary habits and food aversions or allergies were also excluded. Each participant signed a consent form approved by the Clinical Research Ethical Committee of Laval University.
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As indicated in a previous report (17), subjects were randomly assigned to either a defined low fat, high carbohydrate diet or a defined high fat diet rich in MUFA, which they consumed for 6- 7 wk (Table 2). Subjects were instructed to maintain their usual level of physical activity except for the 3 d preceding the beginning and the end of the study, during which they were required to remain inactive. Participants and staff performing laboratory measures were unaware of dietary treatments. On weekdays, just before lunch, body weight was recorded while subjects stood backwards on the scale to avoid fixation on body weight fluctuations.
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The nutritional composition of the experimental diets was calculated with the Canadian Nutrient File database (Health Canada, Ottawa, 1997) and the Nutrition Data System for Research (NDS-R) software (Nutrition Coordinating Center, Minneapolis, Database version 4.03_30, 1999). The experimental diets consisted of usual solid foods that were prepared daily in our metabolic kitchen and weighed in individual portions. As much as possible, the experimental diets were formulated to have very similar food compositions, and differed mainly with respect to the proportion of the food items/ingredients and, thereby, macronutrients (Table 2). Both diets were composed of nonhydrogenated unsaturated fats, mostly olive oil, with whole grains and vegetables as the main forms of carbohydrates. Simple sugars were used only in the preparation of muffins and some desserts.
Dietary intervention.
On weekdays, subjects came to the metabolic unit daily to consume their noon meal under the supervision of at least one member of the staff, at which time they were also given their evening meals and the next day’s packaged breakfast to take home. On weekends, all meals were provided by the research unit but were packaged to take home. Each participant received food in quantities that met 150% of their habitual daily energy intake as assessed by the 3-d food records obtained before the study (2 weekdays and 1 weekend day). The breakfast meal represented 20% of the daily energy intake, whereas the lunch and dinner meals each provided 40% of daily energy intake. Subjects were instructed to consume their entire breakfast, but were asked to eat their lunches and dinners ad libitum, until they were satiated. To ensure that participants in a given diet group consumed adequate proportions of dietary fat, CHO and protein, foods in each meal were arranged on the participant’s plate so that it was easy for them to consume the same proportion of each component of the meal. For example, a participant who consumed 75% of the meal’s meat had to consume 75% of the pasta, 75% of the vegetable and 75% of the dessert, if any. Thus, all leftovers retained the preset macronutrient composition of the experimental diets. All leftovers were returned to the laboratory and weighed to calculate actual energy intakes. For participants used to eating between meals, 837-kJ snacks were provided on demand. These high CHO and high MUFA snacks were prepared in our kitchen and had the same macronutrient composition as the 2 experimental diets. Caffeine-containing beverages were restricted to 2 servings/d, but subjects had free access to water and diet, caffeine-free beverages. Dietary compliance was evaluated periodically by using riboflavin as previously described (17–19). All men included in the present analyses were judged to be compliant with the experimental diets.
Laboratory methods.
Blood samples were collected after a 12- h fast at the beginning and at the end of the study. Samples were then immediately centrifuged at 4°C for 10 min at 1500 x g, and stored at 4°C until processed. Plasma lipid and apolipoprotein levels were measured according to standardized procedures as described previously [Burstein (20) #162; Rush (21) #164; Landry et al. (17) #1310]. Distinct subpopulations of LDL particles were separated in whole plasma using nondenaturing 2–16% gradient gel electrophoresis as described previously (5). LDL-PPD was identified as the most important subclass of LDL in each individual and was calculated from calibration curves using plasma standards of known diameter. The CV of the calculated particle diameters was estimated to be 2%. The relative proportion of LDL particles with a diameter < 25.5 nm [LDL% (<25.5 nm)] was ascertained by computing the relative area of the densitometric scan < 25.5 nm as described previously (5). The absolute concentration of cholesterol among particles < 25.5 nm [LDL-C (<25.5 nm)] was calculated by multiplying the total plasma LDL cholesterol levels by the relative proportion of LDL with a diameter < 25.5 nm (5). A similar approach was used to assess the relative [LDL% (>26.0 nm)] and absolute concentrations of cholesterol in particles with a diameter > 26.0 nm [LDL-C (>26.0 nm)].
Statistical analyses.
Data were analyzed using both SAS (version 8.2, SAS Institute, Cary, NC) and JMP statistical software (version 4.0.5, SAS Institute). Plasma TG, VLDL-C and VLDL-TG data were log-transformed before statistical analyses. ANOVA for repeated-measures adjusted for baseline values were conducted to detect differences within and between dietary groups. Changes in lipid levels and in electrophoretic characteristics of LDL were further adjusted for the diet-induced changes in body weight. Spearman’s correlation coefficients were calculated to test for associations between diet-induced changes in lipids and in LDL electrophoretic characteristics. All results are reported as means ± SD. Differences were considered significant at P < 0.05.
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RESULTS |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Ad libitum consumption of the high fat, high MUFA diet was associated with reduced body weight (-2.1 kg ± 3.1 kg, P < 0.01) and waist circumference (-2.3 cm ± 3.2 cm, P < 0.01). The high MUFA diet also lowered plasma LDL-apoB (-14%), but this was not significant after adjustment for baseline levels and changes in body weight (P = 0.24). Plasma LDL-C levels were reduced (-16%, P = 0.03) in the high MUFA group, whereas none of the electrophoretic characteristics of LDL particles were affected. The high MUFA diet did not affect HDL-C levels (P = 0.88) but decreased plasma VLDL-TG concentrations (-18%, P = 0.02).
The effects of the two diets on the morphological characteristics of the participants were comparable (Table 1). Although the high fat, high MUFA diet had a more favorable effect on TG levels, the effects of both diets on LDL-C levels, LDL-PPD and on other LDL electrophoretic characteristics were not different (Table 3).
Diet-induced changes in plasma TG levels were correlated with variations in LDL-PPD (Fig. 1, upper panels) in the low fat, high CHO group (r = -0.65, P < 0.01) and in the high fat, high MUFA group (r = -0.36, P = 0.04). Diet-induced changes in LDL-apoB concentrations also correlated inversely with variations in LDL-PPD in the low fat, high CHO diet group (Fig. 1, lower panels; r = -0.40, P = 0.02) but not in the high fat, high MUFA diet group (r = +0.20, P = 0.28).
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To further our analysis in each dietary group, participants were categorized as having large or small LDL particles at baseline using the median LDL-PPD (50th percentile) within each dietary group. Ad libitum consumption of a low fat, high CHO diet was associated with a reduction in LDL-PPD (-0.25 ± 0.24 nm, P < 0.01) in men with large LDL-PPD at baseline, whereas no change in LDL-PPD (0.01 ± 0.45 nm, P = 0.94) occurred in men with small baseline LDL-PPD (Fig. 2, panel A, left side). On the other hand, the reduction in LDL-C (<25.5 nm) with the low fat, high CHO diet group was restricted to men with small LDL particles at baseline. In the high fat, high MUFA group, participants with small LDL particles at baseline tended to have a small elevation in LDL-PPD (P = 0.51). The diet-induced reduction in LDL-C (<25.5 nm) was apparent in both group of subjects with small and large LDL-PPD at baseline, but the change was significant in the former (-0.38 ± 0.17 nm, P < 0.01) but not the latter group (P = 0.06) (Fig. 2, panel B, right side).
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DISCUSSION |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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Numerous studies have investigated the effect of dietary fats and carbohydrates on LDL particle size phenotype (11,16,30–33). In general, diets rich in saturated fatty acids (SFA) are associated with an increase in LDL particle size, whereas low fat, high CHO diets have been shown to reduce LDL particle size and to increase its density. As indicated previously, the majority of the studies that have investigated the effect of dietary fat or CHO on LDL size phenotype have been conducted under isoenergetic conditions so that body weight was kept constant intentionally during the experiments. Such experimental conditions do not reflect "real life" situations in which individuals generally consume food ad libitum (14).
To the best of our knowledge, no study to date has documented the effects of ad libitum consumption of a low fat, high CHO diet composed of solid foods on a series of electrophoretic characteristics of LDL particles. This is an important issue because low fat, high CHO diets, particularly those rich in complex CHO and with a low glycemic index, generally promote body weight reduction. The present study therefore provides novel information on the effect of low fat, high CHO and high MUFA diets on LDL particle electrophoretic characteristics when consumed under ad libitum conditions. Indeed, consumption of a low fat, high CHO diet on an ad libitum basis, when associated with significant body weight loss, beneficially reduced LDL-C (<25.5 nm) levels and prevented the reduction in LDL-PPD that typically occurs when these diets are consumed under isoenergetic conditions (30,34).
Low fat, high CHO diets and LDL size.
In the study by Krauss and Dreon (30), 105 men were consecutively assigned to an isoenergetic high fat diet (46% fat, 38% CHO) followed by a low fat, high CHO diet (60% CHO, 24% fat) for 6 wk each. The low fat, high CHO diet significantly increased plasma TG levels and reduced LDL-PPD compared with the high fat diet. Interestingly, the baseline LDL phenotype modulated the diet-induced changes in LDL-PPD. Hence, although 36 of the 87 men who had large LDL after consuming the high fat diet had a reduction in LDL size when they consumed the high CHO diet, LDL size was not affected by low fat, high CHO consumption in men who initially had small LDL particles when they consumed the high fat diet, despite significant increases in plasma TG. These results (30) as well as those reported by Dreon et al. (11) suggest that isoenergetic consumption of a low fat diet may be associated with undesirable changes in LDL-PPD particularly in individuals with large LDL. Our results concurred with these previous observations. Indeed, the reduction in LDL-PPD in the high CHO group as a whole was largely attributable to the fact that men with larger LDL particles at baseline had a significant reduction in LDL-PPD, whereas men with smaller LDL at baseline did not (Fig. 2). However, it must be recognized that the LDL-PPD value during consumption of the diet in the entire high CHO group remained higher (25.73 nm) than the value that has been considered as an important threshold value (25.6 nm) below which the risk of CAD increases significantly (35). In addition, because the low fat, high CHO diet reduced plasma LDL-apoB levels and because the cholesterol level in small LDL particles was reduced [LDL-C (<25.5 nm)], we contend that the diet-induced decrease in LDL size in men with large LDL particles at baseline should not be interpreted as being clinically deleterious in terms of CAD risk. Finally, our results are consistent with data from previous isoenergetic studies on the association between LDL-PPD and low fat, high CHO diets (11). Indeed, men with no change in body weight after ad libitum consumption of the high CHO diet, thereby mimicking isoenergetic conditions, had a significant reduction in LDL-PPD, whereas those who lost weight did not (data not shown). The reduction vs. lack of change in body weight in response to the high CHO diet was also predictive of more favorable changes in the LDL-C (<25.5 nm) levels.
Beard et al. (32) investigated the effects of a very low fat, high CHO diet (<10% of energy from fat, >80% CHO) consumed ad libitum combined with an aerobic exercise training program on LDL-PPD. They reported that the 3-wk intervention protocol, which induced a 4% reduction in body weight, was associated with a significant increase in the LDL-PPD of 23 individuals with small dense LDL particles at baseline (32). They also reported that the percentage of LDL-C carried in the more dense subfractions fell significantly, whereas that carried by the less dense fractions increased (32). Although the study protocol did not allow the investigators to dissociate the specific effect of the diet from that of the exercise training protocol, these results are nevertheless consistent with our own findings that a low fat, high CHO diet, when consumed ad libitum and when associated with small but significant weight loss, leads to cardioprotective changes in LDL size characteristics.
High MUFA diets and LDL size.
To the best of our knowledge, the present study is the first to report the effect of a high MUFA diet consumed ad libitum on a series of LDL electrophoretic characteristics. Although the reduction in LDL-C (<25.5 nm) levels was not significant after adjustment for baseline levels and diet-induced changes in body weight, the high fat, high MUFA diet and the high CHO diet had a comparable effect on LDL-C and on electrophoretic characteristics of LDL particles. In contrast to the high CHO diet, variations in these variables were not modulated by concurrent changes in body weight. Many studies conducted under isoenergetic conditions have investigated the effects of high fat diets rich in MUFA on the plasma lipid profile (8,36–38). One recent study (16) compared the effects of an isoenergetic consumption of a MUFA-enriched sunflower oil diet (% of energy: CHO, 40–45; fat, 40–42; MUFA, 26–28) with a low fat, high CHO diet (% of energy: CHO, 55–60; fat, 22–25; MUFA, 7–8) on LDL size. Both diets significantly improved the lipid profile with no effect on plasma TG levels and LDL size. In addition, in both dietary groups, there was no correlation between variations in LDL size and changes in total cholesterol, LDL-C and TG levels. Earlier isoenergetic studies (33,39) evaluated the effect of a high fat diet rich in SFA on LDL-PPD in healthy men. Consistent with the inverse relationship between plasma TG concentrations and LDL-PPD, the latter study (39) reported that 6 wk of consumption of a high fat, high SFA diet (46% of energy from fat, 18% from SFA), was associated with increased LDL-PPD and decreased TG levels. On the other hand, 3 wk of isoenergetic consumption of a high fat (36% fat) high SFA (15%) diet did not affect LDL-PPD despite a reduction in plasma TG levels (33). Furthermore and consistent with our data, baseline LDL-PPD did not predict variations in LDL-PPD when men consumed the high fat diet (33). A more recent report indicated that isoenergetic consumption of a high MUFA diet compared with a high SFA diet had no effect on LDL-PPD (40). These observations along with our own data suggest that the cardioprotective properties of diets rich in MUFA are not mediated by beneficial changes in LDL-PPD.
In conclusion, results from the present study contrast with those generated in previous isoenergetic studies by showing that ad libitum consumption of a low fat, high CHO diet, which led to a moderate but significant weight loss, was associated with significant improvements in the LDL-C levels, with no deleterious change in either plasma TG levels or LDL electrophoretic characteristics. The fact that the effects of the high MUFA diet on body weight, plasma LDL-C levels, LDL particle number and other LDL electrophoretic characteristics were indistinguishable from those induced by the low fat, high CHO diet suggests that the two diets when consumed ad libitum and associated with weight loss are equally beneficial in the management of LDL-related atherogenic dyslipidemia. However, the high MUFA diet more favorably affected plasma TG concentrations than the low fat, high CHO diet, thus suggesting that from the viewpoint of cardiovascular risk, the high MUFA diet may be preferable.
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ACKNOWLEDGMENTS |
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FOOTNOTES |
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2 W.R.A. is the recipient of a research fellowship from the Réseau en Santé Cardiovasculaire du Québec of the Fonds de la Recherche en Santé du Québec (FRSQ) and Fonds québécois de la recherche sur la nature et les technologies.
3 B.L. is Chair Professor in Nutrition, Functional Food and Cardiovascular Health from the Canada Research Chair Program.
4 A.C.St-P. is the recipient of a training fellowship from la Fondation des Maladies du Coeur du Canada and Fonds pour la Formation de Chercheurs et l’Aide à la Recherche (FCAR).
5 J.B. and P.C. are Clinical Research Scholars from the FRSQ.
7 Abbreviations used: apoB, apolipoprotein B; C, cholesterol; CAD, coronary artery disease; CHD, coronary heart disease; CHO, carbohydrate; LDL-C (<25.5 nm), cholesterol in small LDL; LDL-C (25.5–26.0 nm), cholesterol in medium-sized LDL; LDL-C (>26.0 nm), cholesterol in large LDL; LDL-PPD, LDL peak particle diameter; MUFA, monounsaturated fatty acids; SFA, saturated fatty acids; TG, triglyceride.
Manuscript received 23 April 2003. Initial review completed 20 June 2003. Revision accepted 18 July 2003.
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LITERATURE CITED |
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TOPABSTRACTSUBJECTS AND METHODSRESULTSDISCUSSIONLITERATURE CITED |
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1. Austin, M. A., Breslow, J. L., Hennekens, C. H., Buring, J. E., Willett, W. C. & Krauss, R. M. (1988) Low-density lipoprotein subclass patterns and risk of myocardial infarction. J. Am. Med. Assoc. 260:1917-1921.
2. Lamarche, B., Tchernof, A., Moorjani, S., Cantin, B., Dagenais, G. R., Lupien, P. J. & Després, J. P. (1997) Small, dense low-density lipoprotein particles as a predictor of the risk of ischemic heart disease in men. Prospective results from the Québec Cardiovascular Study. Circulation 95:69-75.
3. Campos, H., Roederer, G. O., Lussier-Cacan, S., Davignon, J. & Krauss, R. M. (1995) Predominance of large LDL and reduced HDL2 cholesterol in normolipidemic men with coronary artery disease. Arterioscler. Thromb. Vasc. Biol. 15:1043-1048.
4. Sherrard, B., Simpson, H., Cameron, J., Wahi, S., Jennings, G. & Dart, A. (1996) LDL particle size in subjects with previously unsuspected coronary heart disease: relationship with other cardiovascular risk markers. Atherosclerosis 126:277-287.[Medline]
5. St-Pierre, A. C., Ruel, I. L., Cantin, B., Dagenais, G. R., Bernard, P.-M., Després, J.-P. & Lamarche, B. (2001) Comparison of various electrophoretic characteristics of LDL particles and their relationship to the risk of ischemic heart disease. Circulation 104:2295-2299.
6. Artaud-Wild, S., Connor, S. L., Sexton, G. & Connor, W. E. (1993) Differences in coronary mortality can be explained by differences in cholesterol and saturated fat intakes in 40 countries but not in France and Finland. A paradox. Circulation 88:2771-2779.
7. Krauss, R. M., Eckel, R. H., Howard, B., Appel, L. J., Daniels, S. R., Deckelbaum, R. J., Erdman, J. W., Kris-Etherton, P., Goldberg, I. J., Kotchen, T. A., Lichtenstein, A. H., Mitch, W. E., Mullis, R., Robinson, K., Wylie-Rosett, J., St. Jeor, S., Suttie, J., Tribble, D. L. & Bazzarre, T. L. (2000) AHA Dietary Guidelines. Revision 2000: a statement for healthcare professionals from the nutrition committee of the American Heart Association. Circulation 102:2284-2299.
8. Grundy, S. M. (1986) Comparison of monounsaturated fatty acids and carbohydrates for lowering plasma cholesterol. N. Engl. J. Med. 314:745-748.[Abstract]
9. Schaefer, E. J., Lichtenstein, A. H., Lamon-Fava, S., McNamara, J. R., Schaefer, M. M., Rasmussen, H. & Ordovas, J. M. (1995) Body weight and low-density lipoprotein cholesterol changes after consumption of a low-fat ad libitum diet. J. Am. Med. Assoc. 274:1450-1455.
10. Parks, E. J. & Hellerstein, M. K. (2000) Carbohydrate-induced hypertriacylglycerolemia: historical perspective and review of biological mechanisms. Am. J. Clin. Nutr. 71:412-433.
11. Dreon, D. M., Fernstrom, H. A., Williams, P. T. & Krauss, R. M. (1999) A very-low-fat diet is not associated with improved lipoproteins profiles in men with a predominance of large, low-density lipoproteins. Am. J. Clin. Nutr. 69:411-418.
12. Mensink, R. P. & Katan, M. B. (1992) Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials. Arterioscler. Thromb. Vasc. Biol. 12:911-919.
13. Williams, P. T., Dreon, D. M. & Krauss, R. M. (1995) Effects of dietary fat on high-density-lipoprotein subclasses are influenced by both apolipoprotein E isoforms and low-density-lipoprotein subclass patterns. Am. J. Clin. Nutr. 61:1234-1240.
14. Purnell, J. Q. & Brunzell, J. D. (1997) The central role of dietary fat, not carbohydrate, in the insulin resistance syndrome. Curr Opin Lipidol. 8:17-22.[Medline]
15. Lichtenstein, A. H., Ausman, L. M., Carrasco, W., Jenner, J. L., Ordovas, J. M. & Schaefer, E. J. (1994) Short-term consumption of a low-fat diet beneficially affects plasma lipid concentrations only when accompanied by weight loss. Arterioscler. Tromb. 14:1751-1760.
16. Ashton, E. L., Best, J. D. & Ball, M. J. (2001) Effects of monounsaturated enriched sunflower oil on CHD risk factors including LDL size and copper-induced LDL oxidation. J. Am. Coll. Nutr. 20:320-326.
17. Landry, N., Bergeron, N., Archer, R., Samson, P., Corneau, L., Bergeron, J. & Deriaz, O. (2003) Whole-body fat oxidation rate and plasma triacylglycerol concentrations in men consuming an ad libitum high-carbohydrate or low-carbohydrate diet. Am. J. Clin. Nutr. 77:580-586.
18. Dubbert, P. M., King, A., Rapp, S. R., Brief, D., Martin, J. E. & Lake, M. (1985) Riboflavin as a tracer of medication compliance. J. Behav. Med. 8:287-299.[Medline]
19. Babiker, I. E., Cooke, P. R. & Gillett, M. G. (1989) How useful is riboflavin as a tracer of medication compliance?. J. Behav. Med. 12:25-38.[Medline]
20. Burstein, M. & Samaille, J. (1960) Sur un dosage rapide du cholestérol lié aux a et aux b-lipoprotéines du sérum. Clin Chim Acta. 5:609.[Medline]
21. Rush, R. L., Leon, L. & Turrell, J. (1972) Automated simultaneous cholesterol and triglyceride determination on the AutoAnalyser II instrument. Barton, E. C. DuCros, M. J. Erdrich, M. M. Golin, J. E. eds. Advances in Automated Analysis 1972:503-507 Technicon International Congress 1970. Mount Kisco, New York: Futura Publishing Mount Kisco, NY. .
22. Austin, M. A. (2000) Triglyceride, small, dense low-density lipoprotein, and the atherogenic lipoprotein phenotype. Curr. Atheroscler. Rep. 2:200-207.[Medline]
23. La Belle, M. & Krauss, R. (1990) Differences in carbohydrate content of low density lipoproteins associated with low density lipoprotein subclass patterns. J. Lipid Res. 31:1577-1588.[Abstract]
24. Packard, C. J., Demant, T., Stewart, J. P., Bedford, D., Caslake, M. J., Schwertfeger, G., Bedynek, A., Shepherd, J. & Seidel, D. (2000) Apolipoprotein B metabolism and the distribution of VLDL and LDL subfractions. J. Lipid Res. 41:305-318.
25. Tribble, D. L., Rizzo, M., Chait, A., Lewis, D. M., Blanche, P. J. & Krauss, R. M. (2001) Enhanced oxidative susceptibility and reduced antioxidant content of metabolic precursors of small, dense low-density lipoproteins. Am. J. Med. 110:103-110.[Medline]
26. Berneis, K. K. & Krauss, R. M. (2002) Metabolic origins and clinical significance of LDL heterogeneity. J. Lipid Res. 43:1363-1379.
27. Stampfer, M. J., Krauss, R. M., Ma, J., Blanche, P. J., Holl, L. G., Sacks, F. M. & Hennekens, C. H. (1996) A prospective study of triglyceride level, low-density lipoprotein particle diameter, and risk of myocardial infarction. J. Am. Med. Assoc. 276:882-888.
28. Gardner, C. D., Fortmann, S. P. & Krauss, R. M. (1996) Association of small low-density lipoprotein particles with the incidence of coronary artery disease in men and women. J. Am. Med. Assoc. 276:875-881.
29. Lamarche, B., Lemieux, I. & Despres, J. P. (1999) The small, dense LDL phenotype and the risk of coronary heart disease: epidemiology, patho-physiology and therapeutic aspects. Diabetes Metab. 25:199-211.[Medline]
30. Krauss, R. M. & Dreon, D. M. (1995) Low-density-lipoprotein subclasses and response to a low-fat diet in healthy men. Am. J. Clin. Nutr. 62:478S-487S.
31. Campos, H., Dreon, D. M. & Krauss, R. M. (1995) Associations of hepatic and lipoprotein lipase activities with changes in dietary composition and low density lipoprotein subclasses. J. Lipid. Res. 36:462-472.[Abstract]
32. Beard, C. M., Barnard, R. J., Robbins, D. C., Ordovas, J. M. & Schaefer, E. J. (1996) Effects of diet and exercise on qualitative and quantitative measures of LDL and its susceptibility to oxidation. Arterioscler. Thromb. Vasc. Biol. 16:201-207.
33. Clifton, P. M., Noakes, M. & Nestel, P. J. (1998) LDL particle size and LDL and HDL cholesterol changes with dietary fat and cholesterol in healthy subjects. J. Lipid. Res. 39:1799-1804.
34. Dreon, D. M., Fernstrom, H. A., Miller, B. & Krauss, R. M. (1994) Low-density lipoprotein subclass patterns and lipoprotein response to a reduced-fat diet in men. FASEB J. 8:121-126.[Abstract]
35. Lamarche, B., St-Pierre, A. C., Ruel, I. L., Cantin, B., Dagenais, G. R. & Després, J.-P. (2001) A prospective, population-based study of low density lipoprotein particle size as a risk factor for ischemic heart disease in men. Can. J. Cardiol. 17:859-865.[Medline]
36. Garg, A., Bonanome, A., Grundy, S. M., Zhang, Z. J. & Unger, R. H. (1988) Comparison of a high-carbohydrate diet with a high-monounsaturated-fat diet in patients with non-insulin-dependent diabetes mellitus. N. Engl. J. Med. 319:829-834.[Abstract]
37. Kris-Etherton, P. M., Pearson, T. A., Wan, Y., Hargrove, R. L., Moriarty, K., Fishell, V. & Etherton, T. D. (1999) High-monounsaturated fatty acid diets lower both plasma cholesterol and triacylglycerol concentrations. Am. J. Clin. Nutr. 70:1009-1015.
38. Jansen, S., Lopez-Miranda, J., Castro, P., Lopez-Segura, F., Marin, C., Ordovas, J. M., Paz, E., Jiménez-Perepérez, J., Fuentes, F. & Perez-Jimenez, F. (2000) Low-fat and high-monounsaturated fatty acid diets decrease plasma cholesterol ester transfer protein concentrations in young, healthy, normolipemic men. Am. J. Clin. Nutr. 72:36-41.
39. Dreon, D. M., Fernstrom, H. A., Campos, H., Blanche, P., Williams, P. T. & Krauss, R. M. (1998) Change in dietary saturated fat intake is correlated with change in mass of large low-density-lipoprotein particles in men. Am. J. Clin. Nutr. 67:828-836.[Abstract]
40. Rivellese, A. A., Maffettone, A., Vessby, B., Uusitupa, M., Hermansen, K., Berglund, L., Louheranta, A., Meyer, B. J. & Riccardi, G. (2003) Effects of dietary saturated, monounsaturated and n-3 fatty acids on fasting lipoproteins, LDL size and post-prandial lipid metabolism in healthy subjects. Atherosclerosis 167:149-158.[Medline]
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