HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Abstract Full Text (PDF) Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ashton, E. L. Articles by Ball, M. J. Search for Related Content PubMed PubMed Citation Articles by Ashton, E. L. Articles by Ball, M. J.

Effects of Monounsaturated Enriched Sunflower Oil on CHD Risk Factors Including LDL Size and Copper-Induced LDL Oxidation

School of Biomedical Sciences, University of Tasmania, Tasmania (E.L.A., M.J.B.)
Department of Medicine, St. Vincent’s Hospital, Fitzroy, Victoria (J.D.B.), AUSTRALIA

Address reprint requests to: Madeleine J. Ball, M.D., School of Biomedical Sciences, University of Tasmania, PO Box 1214, Launceston, Tasmania 7250 AUSTRALIA. E-mail: Madeline.Ball{at}utas.edu.au

	ABSTRACT

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 
Objective: To compare the effects of a diet high in monounsaturated enriched sunflower oil and a low fat diet on CHD risk factors including in vitro Cu-induced LDL oxidation and LDL size, lipids, lipoproteins, glucose and insulin.

Design: A randomized crossover dietary intervention.

Setting: Free living individuals.

Subjects: Fourteen healthy males 35 to 55 years of age and 14 healthy postmenopausal women 50 to 60 years of age completed the dietary intervention. Two subjects did not complete the study, and their data were not included.

Interventions: A low fat, high carbohydrate diet (22% to 25% of energy from total fat, 7% to 8% of energy from monounsaturated fat and 55% to 60% of energy from carbohydrate) was compared to a monounsaturated enriched sunflower oil (MO) diet (40% to 42% of energy from fat, with 26% to 28% from monounsaturated fat and 40% to 45% of energy from carbohydrate) in an isocaloric substitution. Each dietary period was one month.

Results: Total cholesterol, LDL cholesterol, triglycerides and glucose were not significantly different between the two diets. HDL cholesterol, HDL₃ cholesterol and insulin were significantly higher on the MO diet, mean 7%, 7% and 17% higher respectively. Copper-induced LDL oxidation lag phase was significantly longer (mean 18%) after the MO diet compared to the low fat, high carbohydrate diet. LDL particle size was not significantly different.

Conclusions: The significant increase in LDL oxidation lag phase and the significantly higher HDL cholesterol on the MO diet would be expected to be associated with a decrease in CHD risk.

Key words: CHD, MUFA, LDL oxidation, LDL size

	INTRODUCTION

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 
Low fat, high carbohydrate diets are consumed by populations at low risk of coronary heart disease (CHD) and have been advised for those at high CHD risk, as they are associated with lower total cholesterol (TC) and low density lipoprotein (LDL) cholesterol concentrations. However the high carbohydrate diets can be associated with an increase in serum triglycerides (TG). A decrease in high density lipoprotein (HDL) cholesterol is also often seen when total fat is reduced and would be associated with an increased risk of CHD [1]. The optimum amount and type of fat intake that should be advised is controversial. Olive oil, which is 65% monounsaturated fatty acids (MUFA), has been studied as populations consuming this type of diet are generally at lower risk of developing CHD, despite consuming a diet high in total fat [2]. Some of the beneficial effects of olive oil may be due to the high oleic acid (C18:1) concentration. Sunola^TM oil is a MUFA enriched sunflower oil from specifically grown Australian sunflower plants and has a higher oleic acid concentration than olive oil. In addition, Sunola^TM oil has less saturated fat (SFA), which makes its use in line with dietary guidelines to reduce SFA intake [3], and less n-6 PUFA than olive oil, sunflower oil, canola oil and Trisun 80 (another oleic enriched sunflower oil), as shown in Table 1.

	METHODS

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 
Healthy, nonsmoking males 35 to 55 years of age and postmenopausal females 50 to 60 years of age, who were not taking hormone replacement therapy, were recruited by newspaper advertisement. Subjects were included if they were not taking medication or dietary supplements, had a body mass index between 20 and 35 kg/m², consistent physical activity, alcohol intake less than 12% of total energy and serum TC concentration less than 8 mmol/L, with serum TG concentration less than 4.5 mmol/L.

Deakin University Ethics Committee approved the study protocol, and each subject gave written, informed consent.

Study Design
The study was designed to compare the effects of two diets using a randomized crossover design. Prior to the commencement of the study, subjects were given detailed verbal and written instructions on completing a weighed food record, using accurate scales or household measures when weighing was not possible. Subjects then recorded their habitual diet for four days, including one weekend day, so their usual energy intake could be estimated [6].

Subjects were randomly assigned to either the low fat, high carbohydrate diet or the MO diet first. Each diet period was for one month with a two-week washout period between, during which subjects returned to their habitual diet. Both diets were designed to be nutritionally adequate and isocaloric with 15% to 18% of energy from protein, 7% to 8% of energy from PUFA and 7% to 8% of energy from SFA, with energy content appropriate to maintain subjects’ body weight throughout the study period. The MO diet was designed to have 40% to 42% of energy from fat, with 26% to 28% from MUFA, and 40% to 45% energy from carbohydrate. The added MUFA in the MO diet was largely Sunola^TM oil (Meadow Lea Foods Ltd, Mascot, Australia). The low fat, high carbohydrate diet was designed to have 22% to 25% of energy from total fat, with MUFA supplying only 7% to 8% of energy, and 55% to 60% of energy from carbohydrate, mainly from lemonade, yogurt and fruits. Meadowlea Sunflower oil was used in the low fat, high carbohydrate diet (composition given in Table 1). The two diets supplied different amounts of vitamin E, mainly due to the different amounts and types of oils. Vitamin E was not matched because foods that contain large amounts of vitamin E also contain fat and because supplemental vitamin E and food vitamin E do not necessarily exert the same effect on CHD risk [7]. Subjects weighed and recorded their dietary intake for seven days during the last week of each diet period, and the records were checked for completeness. These records were then analysed by Foodworks, (Version 1.05, 1997, Xyris Software, Queensland, Australia) using the NUTTAB 95 database. Vitamin E intake was calculated separately from the UK food composition tables [8].

Height and body weight were measured before starting the dietary intervention and weight was monitored, using electronic scales, at the end of each diet period. Venous blood was collected prior to commencing the study and at the end of each diet period, after an overnight fast and at approximately the same time. Serum and plasma aliquots were stored at -80°C for subsequent laboratory analysis.

Laboratory Analyses
Serum TC, TG, HDL cholesterol and plasma glucose were measured by enzymatic colorimetric tests using Boehringer Mannheim Gmbh calibrator, quality controls and reagents (Boehringer, Mannheim, Nunawading, Australia) on a Hitachi 704 autoanalyser (Hitachi, Tokyo Japan). LDL cholesterol was calculated using the Friedewald equation [9]. Using the calculated LDL, very low density lipoprotein (VLDL) cholesterol was calculated as TC- (LDL + HDL). HDL₂ and HDL₃, the major subfractions in the heterogenous HDL group of particles, were also measured using enzymatic methods and Boehringer kits. HDL₃ was directly measured then subtracted from the total HDL cholesterol values to determine HDL₂ concentration using a slight modification of the method of Widhalm and Pakosta [10].

Insulin was analysed by radioimmunoassay using the Linco Human Insulin Specific RIA Kit (Linco, Missouri, US), which included all standards, controls, human radioactive insulin (¹²⁵I) and reagents.

LDL was isolated by ultracentrifugation, and copper-induced oxidative modification was measured spectroscopically using a method previously described [11]. The maximum diene formation was calculated from the molar extinction coefficient for conjugated dienes (29,500 L·mol^-1·cm^-1) as described by Abbey et al. [12].

LDL particle diameter was determined by gel gradient electrophoresis using commercially available 3–13% non-denaturing native gels (Gradipore, Sydney, Australia) using a regression plot derived from standards of known diameter (28 nm latex beads (Duke Scientific, Palo Alto, CA), and high molecular weight standards of thyroglobulin 17 nm and ferritin 12.2 nm (Pharmacia, Piscataway, NJ) [13].

The two oils, Sunola^TM and Meadowlea Sunflower oil, used in the diets were analysed for their vitamin E content using the HPLC method described by Su et al. [14].

Statistical Analysis
Statistical analysis was performed using SPSS (Version 8.0.0, SPSS Inc., Chicago, IL). Paired t tests were used to investigate the differences between the two diets for normally distributed data (TC, LDL cholesterol and insulin), with log transformation for glucose values. Wilcoxon signed rank test was used to compare results at the end of the two diets for data that were not normally distributed (HDL cholesterol, HDL₂, TG, oxidation lag phase, maximum diene formation rate, oxidation rate and estimated VLDL). General linear model (GLM) was used to investigate the carry over and order effects by treating both time and diet as fixed factors and identification number as a random factor [15]. Pearson’s correlation was used to investigate the relationship between normally distributed data and Spearman’s correlation for non-normally distributed data.

	RESULTS

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 
Thirty subjects commenced the study and 28 subjects completed the two diet periods without significant problems; two subjects withdrew due to personal circumstances, and their data were excluded from the analysis. Subjects’ mean (SD) age was 48.3 (5.5) years and 54.8 (2.7) years for males and females, respectively. Mean ± SD (range) weights (kg) for males at the end of the low fat, high carbohydrate diet and MO diet were 85.1 ± 11.2 (61.4–99.9) and 85.1 ± 11.5 (61.0–103.0), respectively, and for females 70.2 ± 10.7 (54.3–92.1) and 70.6 ± 10.3 (54.6–92.1), respectively. Weight did not change significantly between diets in either group. There was no significant effect of order of diet on the variables measured.

The self-recorded dietary intakes for the 28 subjects are given in Table 2. The percentage of energy derived from protein was significantly lower on the MO diet, but the actual amount in grams was not significantly different. SFA was slightly higher on the MO diet in the total group; however, there was no significant difference in SFA or PUFA between the two diets in the males. In females, there were minor differences in PUFA and SFA, with the PUFA being 0.8% of energy lower on the MO diet and SFA 1% of energy higher on the MO diet [16].

The lipids and lipoproteins measured are given in Table 3, and results for LDL oxidation, glucose and insulin are given in Table 4. The mean LDL lag phase was 18.5% longer after the MO diet compared to the low fat diet, while maximum conjugated dienes concentration and oxidation rate were 10.3% and 12.4% lower after the MO diet. The mean insulin concentration increased significantly by 17% on the MO diet. Mean HDL cholesterol and HDL₃ were both 7% higher on the MO diet. There was no significant difference in TC, TG, LDL cholesterol, LDL size, glucose and glucose:insulin ratio between the two diets.

There was a significant correlation between the change in dietary MUFA and the change in TC (r = 0.76, p = 0.001), HDL cholesterol (r = 0.41, p = 0.032), HDL₂ (r = 0.46, p = 0.014) after the two diets, but not with LDL lag phase, oxidation rate or LDL size. There was no significant correlation between the change in LDL particle size between the two diets and change in TC, LDL, HDL or TG concentrations. However, LDL particle size was inversely correlated with TG concentration at baseline (r = -0.597, p = 0.040), on the low fat diet (r = -0.433, p = 0.027) and on the MO diet (r = -0.470, p = 0.018). LDL particle size was also significantly correlated with HDL cholesterol concentration at baseline (r = 0.527, p = 0.006), on the low fat diet (r = 0.637, p < 0.001) and on the MO diet (0.612, p < 0.001).

VLDL cholesterol estimates for baseline, low fat, high carbohydrate diet and MO diet were 0.63 ± 0.36, 0.67 ± 0.29 and 0.57 ± 0.30 mmol/L respectively. VLDL cholesterol was significantly different between the low fat and MO diet (p = 0.042). The male and female subjects studied did not respond differently to the two diets for any parameter.

	DISCUSSION

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 
The aim of the study was to compare the effects of a low fat, high carbohydrate diet with a MO diet on CHD risk factors in healthy subjects. Although the diets were designed to be isocaloric, the energy intake was significantly higher on the MO diet, largely due to three subjects with particularly high intakes on the MO diet. These individuals gained a little weight, but overall the reported energy difference was not reflected by a weight change, which is the best indicator of energy differences. The minor difference in PUFA and SFA in women compared to the large difference in MUFA (16% energy) is unlikely to greatly influence the results.

The significant difference in HDL cholesterol after the two diets may be due to an increase on the MO diet, a circumstance which is similar to that in several other studies that found a high MUFA diet increased HDL cholesterol compared to a low fat, high carbohydrate diet [17,18]. However, these findings have not been universal and other studies have found a high MUFA diet has no effect or negative effects on HDL cholesterol [19–22]. Alternatively, HDL cholesterol may have been reduced on the low fat, high carbohydrate diet due to the decrease in total fat [1] or possibly due to the high glycemic index carbohydrates used to replace the MUFA [23]. Few studies have measured the effects on HDL subfractions, although the HDL₂ subfraction is thought to have a stronger inverse relationship to CHD than HDL₃ [24]. Both subfractions increased on the MO diet, although only the HDL₃ subfraction significantly, so there is no evidence the results were due to a shift of cholesterol between subfractions.

In many studies a high carbohydrate diet induces hypertriglyceridemia; however, Parks and Hellerstein suggest in a recent review that there is no proof that hypertriglyceridemia induced by a low fat, high carbohydrate diet increases CHD risk [25]. Dietary factors that may influence TG and HDL levels on a low fat diet include the fiber, sucrose and starch content. In our study, the dietary fiber contents were similar, but both total sugars and starch were significantly higher on the low fat diet, and TG levels tended to be higher, although the difference was not statistically significant.

Many studies have compared the effects of high MUFA with low fat, high carbohydrate diets on TC and LDL [22,26–28]. However a meta-analysis by Clarke et al. [29] indicates that replacement of carbohydrates with MUFA produced no significant effect on TC or LDL cholesterol, as seen in this study. Compared with baseline values, both diets were effective in lowering LDL cholesterol, suggesting that either diet could be associated with a decreased risk compared to the baseline diet. The low fat diet resulted in higher estimated VLDL cholesterol compared to the MO diet, and it has been suggested that high carbohydrate diets lead to a decrease in clearance of VLDL, rather than an increase in VLDL production [30].

Of the two studies that have compared the effect of a high MUFA diet with a low fat, high carbohydrate diet on LDL oxidation [4,5], O’Byrne et al. showed that the lag time before the formation of conjugated dienes was significantly longer both in the six women consuming the low fat diet and the five women on a low fat MUFA enriched diet compared to baseline, which was a high SFA diet. Diets were not well controlled, as the "control" low fat group showed a significant decrease in PUFA from baseline to the end of the diet, as did the experimental group. There was also a significant decrease in total fat and SFA in the experimental group. Berry et al. found that LDL isolated after a high MUFA diet was less prone to peroxidation, as measured by thiobarbituric acid reactive substances [4]. In our study the lag phase for LDL isolated after the MO diet was on average 12 minutes longer than after the low fat, high carbohydrate diet, also suggesting that the LDL were less susceptible to oxidative modification. Maximum conjugated dienes formed were significantly lower on the MO diet than on the low fat, high carbohydrate diet, perhaps suggesting a lower PUFA concentration within the LDL particle, as PUFA is the primary substrate of oxidation.

The endogenous antioxidant concentrations of the LDL particle can influence the LDL oxidation [31,32]. In the present study the antioxidants in the background diet were similar, but the increase in LDL lag phase may be due to a number of components in the Sunola^TM, including the high MUFA content, the larger amounts of vitamin E supplied on the MO diet, their interactions or other unidentified components of the oil. Antioxidant and fatty acid analysis of the LDL particle would have provided insight into the changes in composition of the LDL, but would not have indicated the individual effects on LDL oxidation.

The subjects’ LDL particles in the present study were predominantly the larger, more buoyant subclass of LDL (diameter range 25.6–26.6 nm) [33]. Superko and Krauss [34] suggest that a threshold TG concentration exists (approximately 1.8064 mmol/L) where LDL particle size will change. However, only six subjects crossed this TG value, and these subjects were not statistically different from those that did not cross the threshold. There was an inverse relationship between the TG concentrations and LDL particle size, although there was no statistical difference in TG levels or LDL size between the two diets.

Insulin levels have been found to influence LDL oxidation [35,36]. Pelikanova et al. found that an induced state of hyperinsulinemia significantly decreased the lag time, suggesting enhanced LDL oxidizability, in healthy subjects [35]. Rifici et al. found that cell mediated oxidation of LDL was increased by incubation with supraphysiological insulin concentrations [36]. The mechanism or mechanisms of action of insulin on LDL oxidation are largely unknown; however, it is speculated to be through increased glucose utilisation by cells, resulting in increased O₂^- production which could initiate oxidation [37] or the conversion of cystine to thiols and the secondary generation of O₂^- by the reoxidation of thiols [38]. The slightly higher insulin levels on our MO diet were not associated with increased LDL oxidizability.

	CONCLUSION

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 
The LDL particles were less susceptible to oxidative modification on the MO diet, possibly due to a number of components of the oil. This finding, plus the higher HDL cholesterol, suggests that the MO diet could decrease CHD risk compared to the low fat, high carbohydrate diet. A MO diet may also be more palatable, a circumstance which may assist people in adhering to a healthy diet.

	ACKNOWLEDGMENTS

 
We thank Dr Dragicevic, St Vincent Hospital, for kindly performing the LDL sizing. We also thank Jane Foster for expert assistance with the dietary design and study management. We gratefully acknowledge the support of Meadow Lea Foods and of the Grains Research Development Corporation in providing the oils and funding towards this project.

	FOOTNOTES

 
Presented in part at the Twenty-third Annual Scientific meeting of the Nutrition Society, New Zealand, September 22, 1999.

Some financial assistance and foods were provided from Meadowlea Foods and the Grains Research Development Corporation.

Received April 6, 2000. Accepted March 27, 2001.

	REFERENCES

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 

1. Rubins HB, Robins SJ, Collins D, Fye CL, Anderson JW, Elam MB, Faas FH, Linares E, Schaefer EJ, Schectman G, Wilt TJ, Wittes J: Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial Study Group. N Engl J Med 341: 410–418, 1999.[Abstract/Free Full Text]
2. de Lorgeril M, Salen P, Martin JL, Mamelle N, Monjaud I, Touboul P, Delaye J: Effect of a Mediterranean type of diet on the rate of cardiovascular complications in patients with coronary artery disease. J Am Coll Cardiol 28: 1103–1108, 1996.[Abstract]
3. NHMRC: "Recommended Dietary Intakes for Use in Australia." Canberra: Australian Government Publishing Services, 1991.
4. Berry EM, Eisenberg S, Friedlander Y, Harats D, Kaufmann NA, Norman Y, Stein Y: Effects of diets rich in monounsaturated fatty acids on plasma lipoproteins—the Jerusalem Nutrition Study. Am J Clin Nutr 56: 394–403, 1992.[Abstract/Free Full Text]
5. O’Byrne DJ, O’Keefe SF, Shireman RB: Low-fat, monounsaturate-rich diets reduce susceptibility of low density lipoproteins to peroxidation ex vivo. Lipids 33: 149–157, 1998.[Medline]
6. Edington J, Thorogood M, Geekie M, Ball M, Mann J: Assessment of nutritional intake using dietary records with estimated weights. J Hum Nutr Diet 2: 407–414, 1989.
7. Kushi LH, Folsom AR, Prineas RJ, Mink PJ, Wu Y, Bostick RM: Dietary antioxidant vitamins and death from coronary heart disease in postmenopausal women. N Engl J Med 334: 1156–1162, 1996.[Abstract/Free Full Text]
8. McCance RA, Widdowson EM: "The Composition of Foods." B. Holland (ed.). Cambridge: Richard Clay Ltd, 1992.
9. Friedewald WT, Levy RI, Fredrickson DS: Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 18: 499–502, 1972.[Abstract]
10. Widhalm K, Pakosta R: Precipitation with polyethylene glycol and density-gradient ultracentrifugation compared for determining high-density lipoprotein subclasses HDL2 and HDL3. Clin Chem 37: 238–240, 1991.[Abstract/Free Full Text]
11. Ashton E, Dalais F, Ball M: Effect of meat replacement by tofu on CHD risk factors including copper induced LDL oxidation. J Am Coll Nutr 19: 761–767, 2000.[Abstract/Free Full Text]
12. Abbey M, Belling GB, Noakes M, Hirata F, Nestel PJ: Oxidation of low-density lipoproteins: intraindividual variability and the effect of dietary linoleate supplementation. Am J Clin Nutr 57: 391–398, 1993.[Abstract/Free Full Text]
13. O’Neal D, Lee P, Murphy B, Best J: Low-density lipoprotein particle size distribution in end-stage renal disease treated with hemodialysis or peritoneal dialysis. Am J Kidney Dis 27: 84–91, 1996.[Medline]
14. Su Q, Rowley KG, O’Dea K: Stability of individual carotenoids, retinol and tocopherols in human plasma during exposure to light and after extraction. J Chromatogr Biomed Sci Appl 729: 191–198, 1999.[Medline]
15. Fleiss JL: "The Design and Analysis of Clinical Experiments." New York: John Wiley and Sons Inc, 1986.
16. Ashton E, Pomeroy S, Foster J, Kaye R, Nestel P, Ball M: Diet high in monounsaturated fat does not have a different effect on arterial elasticity than a low fat, high-carbohydrate diet. J Am Diet Assoc 100: 537–542, 2000.[Medline]
17. Perez Jimenez F, Espino A, Lopez Segura F, Blanco J, Ruiz Gutierrez V, Prada JL, Lopez Miranda J, Jimenez Pereperez J, Ordovas JM: Lipoprotein concentrations in normolipidemic males consuming oleic acid-rich diets from two different sources: olive oil and oleic acid-rich sunflower oil. Am J Clin Nutr 62: 769–775, 1995.[Abstract/Free Full Text]
18. Garg A, Bonanome A, Grundy SM, Zhang ZJ, Unger RH: 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, 1988.[Abstract]
19. O’Byrne D, Knauft D, Shireman R: Low fat-monounsaturated rich diets containing high-oleic peanuts improved serum lipoprotein profiles. Lipids 32: 687–695, 1997.[Medline]
20. Morgan SA, O’Dea K, Sinclair AJ: A low-fat diet supplemented with monounsaturated fat results in less HDL-C lowering than a very-low-fat diet. J Am Diet Assoc 97: 151–156, 1997.[Medline]
21. Garg A, Grundy SM, Unger RH: Comparison of effects of high and low carbohydrate diets on plasma lipoproteins and insulin sensitivity in patients with mild NIDDM. Diabetes 41: 1278–1285, 1992.[Abstract]
22. Lehmann T, Golay A, James RW, Pometta D: Effects of two hypocaloric diets, fat restricted or rich in monounsaturated fat, on body weight loss and plasma lipoprotein distribution. Nutr Metab Cardiovasc Dis 5: 290–296, 1995.
23. Luscombe ND, Noakes M, Clifton PM: Diets high and low in glycemic index versus high monounsaturated fat diets: effects on glucose and lipid metabolism in NIDDM. Eur J Clin Nutr 53: 473–478, 1999.[Medline]
24. Hong ML, James RW, Grab B, Pometta D: High density lipoprotein (HDL) subfractions in cardiovascular patients with low levels of HDL-cholesterol. Influence of hypertriglyceridaemia on subfraction concentration and composition. Atherosclerosis 69: 241–248, 1988.[Medline]
25. Parks EJ, Hellerstein MK: Carbohydrate-induced hypertriacylglycerolemia: historical perspective and review of biological mechanisms. Am J Clin Nutr 71: 412–433, 2000.[Abstract/Free Full Text]
26. Grundy SM: Comparison of monounsaturated fatty acids and carbohydrates for lowering plasma cholesterol. N Engl J Med 314: 745–748, 1986.[Abstract]
27. Colquhoun DM, Moores D, Somerset SM, Humphries JA: Comparison of the effects on lipoproteins and apolipoproteins of a diet high in monounsaturated fatty acids, enriched with avocado, and a high-carbohydrate diet. Am J Clin Nutr 56: 671–677, 1992.[Abstract/Free Full Text]
28. Mensink RP, de Groot MJ, van den Broeke LT, Severijnen Nobels AP, Demacker PN, Katan MB: Effects of monounsaturated fatty acids v complex carbohydrates on serum lipoproteins and apoproteins in healthy men and women. Metabolism 38: 172–178, 1989.[Medline]
29. Clarke R, Frost C, Collins R, Appleby P, Peto R: Dietary lipids and blood cholesterol: quantitative meta-analysis of metabolic ward studies. BMJ 314: 112–117, 1997.[Abstract/Free Full Text]
30. Parks EJ, Krauss RM, Christiansen MP, Neese RA, Hellerstein MK: Effects of a low-fat, high-carbohydrate diet on VLDL-triglyceride assembly, production, and clearance. J Clin Invest 104: 1087–1096, 1999.[Medline]
31. Dieber Rotheneder M, Puhl H, Waeg G, Striegl G, Esterbauer H: Effect of oral supplementation with D-alpha-tocopherol on the vitamin E content of human low density lipoproteins and resistance to oxidation. J Lipid Res 32: 1325–1332, 1991.[Abstract]
32. Reaven P, Grasse B, Barnett J: Effect of antioxidants alone and in combination with monounsaturated fatty acid-enriched diets on lipoprotein oxidation. Arterioscler Thromb Vasc Biol 16: 1465–1472, 1996.[Abstract/Free Full Text]
33. Austin MA, King MC, Vranizan KM, Krauss RM: Atherogenic lipoprotein phenotype. A proposed genetic marker for coronary heart disease risk. Circulation 82: 495–506, 1990.[Abstract/Free Full Text]
34. Superko HR, Krauss RM: Differential effects of nicotinic acid in subjects with different LDL subclass patterns. Atherosclerosis 95: 69–76, 1992.[Medline]
35. Pelikanova T, Tvrzicka E, Kazdova L, Zak A: Relationships between fatty acid composition and insulin-induced oxidizability of low-density lipoproteins in healthy men. Ann N Y Acad Sci 827: 269–278, 1997.[Free Full Text]
36. Rifici VA, Schneider SH, Khachadurian AK: Stimulation of low-density lipoprotein oxidation by insulin and insulin like growth factor I. Atherosclerosis 107: 99–108, 1994.[Medline]
37. Heinecke JW, Rosen H, Suzuki LA, Chait A: The role of sulfur-containing amino acids in superoxide production and modification of low density lipoproteins by arterial smooth muscle cells. J Biol Chem 262: 10098–10103, 1987.[Abstract/Free Full Text]
38. Sparrow CP, Olszewski J: Cellular oxidation of low density lipoprotein is caused by thiol production in media containing transition metal ions. J Lipid Res 34: 1219–1228, 1993.[Abstract]

This article has been cited by other articles:

				W. R. Archer, B. Lamarche, A. C. St-Pierre, J.-F. Mauger, O. Deriaz, N. Landry, L. Corneau, J.-P. Despres, J. Bergeron, P. Couture, et al. High Carbohydrate and High Monounsaturated Fatty Acid Diets Similarly Affect LDL Electrophoretic Characteristics in Men Who Are Losing Weight J. Nutr., October 1, 2003; 133(10): 3124 - 3129. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ashton, E. L. Articles by Ball, M. J. Search for Related Content PubMed PubMed Citation Articles by Ashton, E. L. Articles by Ball, M. J.