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Original Investigation |

The National Cholesterol Education Program Diet vs a Diet Lower in Carbohydrates and Higher in Protein and Monounsaturated Fat:  A Randomized Trial FREE

Y. Wady Aude, MD; Arthur S. Agatston, MD; Francisco Lopez-Jimenez, MD, MSc; Eric H. Lieberman, MD; Marie Almon, MS, RD; Melinda Hansen, ARNP; Gerardo Rojas, MD; Gervasio A. Lamas, MD; Charles H. Hennekens, MD, DrPH
[+] Author Affiliations

Author Affiliations: Agatston Research Institute (Drs Aude, Agatston, and Hennekens and Ms Almon); the Division of Cardiovascular Research, Mount Sinai Medical Center–Miami Heart Institute (Drs Aude, Lopez-Jimenez, Lieberman, Rojas, and Lamas, and Ms Hansen); and the Departments of Medicine (Drs Agatston, Lamas, and Hennekens) and Epidemiology and Public Health (Dr Hennekens), University of Miami School of Medicine, Miami Beach, Fla.


Arch Intern Med. 2004;164(19):2141-2146. doi:10.1001/archinte.164.19.2141.
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Background  In the United States, obesity is a major clinical and public health problem causing diabetes, dyslipidemia, and hypertension, as well as increasing cardiovascular and total mortality. Dietary restrictions of calories and saturated fat are beneficial. However, it remains unclear whether replacement of saturated fat with carbohydrates (as in the US National Cholesterol Education Program [NCEP] diet) or protein and monounsaturated fat (as in our isocaloric modified low-carbohydrate [MLC] diet, which is lower in total carbohydrates but higher in protein, monounsaturated fat, and complex carbohydrates) is optimal.

Methods  We randomized 60 participants (29 women and 31 men) to the NCEP or the MLC diet and evaluated them every 2 weeks for 12 weeks. They were aged 28 to 71 years (mean age, 44 years in the NCEP and 46 years in the MLC group). A total of 36% of participants from the NCEP group and 35% from the MLC group had a body mass index (calculated as weight in kilograms divided by the square of height in meters) greater than 27. The primary end point was weight loss, and secondary end points were blood lipid levels and waist-to-hip ratio.

Results  Weight loss was significantly greater in the MLC (13.6 lb) than in the NCEP group (7.5 lb), a difference of 6.1 lb (P = .02). There were no significant differences between the groups for total, low density, and high-density lipoprotein cholesterol, triglycerides, or the proportion of small, dense low-density lipoprotein particles. There were significantly favorable changes in all lipid levels within the MLC but not within the NCEP group. Waist-to-hip ratio was not significantly reduced between the groups (P = .27), but it significantly decreased within the MLC group (P = .009).

Conclusions  Compared with the NCEP diet, the MLC diet, which is lower in total carbohydrates but higher in complex carbohydrates, protein, and monounsaturated fat, caused significantly greater weight loss over 12 weeks. There were no significant differences between the groups in blood lipid levels, but favorable changes were observed within the MLC diet group.

In the United States, obesity is a major clinical and public health problem causing diabetes, hypertension, and abnormalities in lipid metabolism1,2 as well as higher cardiovascular36 and total mortality.47 Nearly 55% of the US population has a body mass index (BMI, calculated as weight in kilograms divided by the square of height in meters) of 25 to 30 (overweight) or greater than 30 (obese).8,9 Despite many available diet programs, the prevalence of obesity continues to rise. While reduction of calories and saturated fat are generally accepted as beneficial, it is unclear whether replacement of saturated fat with either carbohydrates or protein and monounsaturated fat is optimal. The American Heart Association (AHA) has classified obesity as a major modifiable risk factor for coronary heart disease.10 Furthermore, even modest weight loss (5%-10% of body weight) has beneficial effects on blood pressure as well as lipid1113 and glucose levels.12

For many years the US National Cholesterol Education Program (NCEP) and the AHA have advocated low-calorie and low-fat diets that are high in carbohydrates.14,15 Adherence to such diets up to 1 year reduces high-density lipoprotein (HDL) cholesterol1620 and increases triglyceride levels.20 Because elevated HDL and triglyceride levels appear to be independent risk factors for cardiovascular disease, a controversy has arisen about whether to replace saturated fat with carbohydrates.21 In its recent revision, the AHA continues to recommend a lower intake of calories and saturated fat but encourages the substitution of carbohydrates for unsaturated fat.22 It remains unclear, however, whether an isocaloric diet lower in carbohydrates and higher in protein and monounsaturated fat would have a more favorable effect on weight loss than the NCEP Step II diet. To test this hypothesis, we randomized patients to the NCEP diet or an isocaloric modified low-carbohydrate (MLC) diet lower in total carbohydrates but higher in protein, monounsaturated fat, and complex carbohydrates.

PARTICIPANTS

The institutional review board of Mount Sinai Medical Center–Miami Heart Institute reviewed and approved the trial. Subjects were recruited by media announcements. The inclusion criteria were age older than 18 years, a BMI of 27 or greater, and the willingness and stated ability to adhere to a prescribed diet for 3 months at home without alteration in levels of physical activity. The exclusion criteria were a history of thyroid disease or insulin-dependent diabetes mellitus, pregnancy, unstable medical conditions, and current use of oral or parenteral corticosteroids, testosterone, appetite suppressants, or other medications known to affect weight or appetite. The use of lipid-lowering agents was permitted if it had not been changed during the 3 months prior to participation. The 2 participants meeting this criterion agreed not to change their medication or dosage during the 12 weeks of the trial. Each eligible participant gave written informed consent.

TRIAL DESIGN

Randomization was done using a block design by sex to achieve an equal sex distribution. The 60 participants (29 women and 31 men) enrolled to the NCEP or the MLC diet were between 27 and 71 years old (mean age, 44 years in the NCEP and 46 years in the MLC group), with a BMI greater than 27 (35.5 in the NCEP and 34.9 in the MLC group). For issues of feasibility and compliance, 2 couples sharing a household were randomized to the NCEP diet and 2 to the MLC diet.

Follow-up visits for diet counseling and anthropometric measurements occurred every 2 weeks.

CLINICAL PROCEDURES

The baseline evaluation, randomization, and first session of dietary counseling were completed on the first day. Weight was measured with indoor clothing and without shoes on a single scale. Height was measured with all subjects standing erect without shoes, using the same vertical rod. Hip girth was measured at the largest horizontal circumference around the buttocks and waist girth at the narrowest circumference viewed from the front. Both were taken with a nonelastic tape measure with the subjects standing. All anthropometric measurements were obtained by an observer blinded to the treatment assignment. At 12 weeks, participants also completed validated questionnaires to evaluate their level of satisfaction with diet and counseling.23,24

DIETARY INTERVENTION

A single specially trained dietitian and nurse practitioner instructed participants about their assigned diet and provided them with written guidelines. All participants, regardless of their assignment, met with the dietitian or the nurse practitioner for 1 hour at the first visit and 30 minutes at subsequent visits. To assess the appropriateness of the foods consumed, 24-hour food recalls were obtained. Because the goal of the 24-hour food recalls was to provide feedback to the participants, the information was insufficient to perform any quantitative analysis.

In the NCEP diet the percentages of calories from fat (30%), carbohydrate (55%), and protein (15%) were unchanged throughout the trial. Saturated fat comprised less than 7% of the total fat intake, and monounsaturated fat between 10% and 15%. The diet was tailored to provide approximately 1300 calories for women and 1600 calories for men.

The MLC diet consisted of 2 phases of 2 weeks’ duration and of a third or maintenance phase of 8 weeks. The first phase was characterized by higher intake of fat (62%), very low intake of carbohydrates (10%), and an intake of protein of 28%. In the second phase fat intake was decreased to 43% whereas carbohydrate intake was increased to 27% and protein intake to 30%. In the third phase, the percentages of calories were 39% from fat, 28% from carbohydrates, and 33% from protein. The percentages of calories from monounsaturated fats were 13% in phase 1 and 8% in phases 2 and 3. In the maintenance phase the approximate numbers of calories consumed based on the recommended guidelines were also about 1300 for women and 1600 for men (Table 1).

Table Graphic Jump LocationTable 1. Composition of the Study Diet*

Foods recommended in the MLC diet included those high in protein (ie, lean meats), monounsaturated fats (ie, olive, canola, and sunflower oils as well as peanuts, almonds, pecans, and avocado), and fibers but with a low glycemic index. The glycemic index is a measure of the level to which a food raises blood glucose and elicits an insulin response compared with pure glucose (100%). Therefore, foods with a low glycemic index are those that produce a slow and more sustained rise in blood glucose, and thus potentially provide a greater sensation of satiety (eg, soy beans and peanuts have a glycemic index between 10% and 19%).25 Participants assigned to the MLC diet were advised to avoid simple sugars, which have a high glycemic index, as well as refined or highly processed foods. All MLC participants were also encouraged to eat vegetables in unlimited quantities and snack on foods containing protein (eg, yogurt) and/or with a low glycemic index (eg, peanuts). Additional fiber in the form of psyllium (1 teaspoon in a half glass of water before lunch and dinner) was also recommended.

The goal of the 3 phases in the MLC diet was to gradually introduce carbohydrates into the diet, beginning with more complex carbohydrates (with a lower glycemic index) and following with foods containing less complex carbohydrates (with a higher glycemic index). Because foods with a higher glycemic index may be associated with a feeling of early hunger or “craving,” it was expected that this type food would give a feedback signal that would help the participants in their future selection of food. This approach was effective in one of our earlier trials.26

LABORATORY PROCEDURES

At the beginning and end of the trial, blood was collected from the antecubital vein after a 12- to 14-hour fast. Plasma was separated within 2 hours and kept at 4°C until it was processed. Total cholesterol and triglyceride concentrations were measured by enzymatic procedures27 and HDL cholesterol by dextran–sulfate-magnesium precipitation28; LDL cholesterol was calculated as total cholesterol minus the sum of HDL cholesterol and very-low-density lipoprotein (VLDL) cholesterol29 and VLDL as the triglyceride concentration divided by 5. Serum was also obtained and samples stored at −70° to analyze LDL subclasses by gradient gel electrophoresis (performed by Berkeley HeartLab, Berkeley, Calif), with particular focus on particle diameter of major LDL peak and the proportion of small, dense LDL subclasses (sum of peaks IIIA, IIIB, IVA, IVB). Based on the availability of remaining stored serum, gradient gel electrophoresis could be performed for 45 randomized participants (23 in the NCEP and 22 in the MLC group).

END POINTS

The primary end point was weight loss and secondary end points were various lipid parameters as well as waist-to-hip ratio.

STATISTICAL ANALYSIS

The size of the sample was chosen to provide more than 90% power to detect a difference of 10 lb in weight loss between the NCEP and MLC groups at a 2-sided α level of significance of 5%. For the significance of differences between the groups, t tests for continuous variables and χ2 tests for discrete variables were used. For triglycerides, a continuous variable not normally distributed and skewed toward higher values, logarithmic transformations were performed. For discrete variables in which the sample size was 5 or less, the Fisher exact test was used. All P values were 2-sided.

From January 1998 to January 1999, 60 subjects, 29 men and 31 women, were randomized for the trial. Their mean age was 45 years and mean BMI was 35. At the end of the trial, complete data obtained for 54 participants (25 in the NCEP and 29 in the MLC group) formed the basis for these analyses. Of the 6 participants who did not complete the study, 5 were in the NCEP and 1 in the MLC group. The mean follow-up duration for the NCEP and the MLC groups were 90 and 92 days, respectively (P was not significant), and the mean numbers of visits were 5.5 and 6.1 (P was not significant).

At baseline, there were no significant differences in age, weight, BMI, waist-to-hip ratio, and any of the lipid variables between the NCEP and MLC groups (Table 2). The frequencies of myocardial infarction, stroke, congestive heart failure, hypertension, and non–insulin-dependent diabetes mellitus, and use of lipid-lowering agents were low, and not significantly different between the groups.

Table Graphic Jump LocationTable 2. Baseline Characteristics of Study Subjects*

Weight loss was significantly greater in the MLC (13.6 lb) than in the NCEP group (7.5 lb, a difference of 6.1 lb (P = .02) (Table 3). Although the waist-to-hip ratio was not significantly different between the groups, it was significantly reduced within the MLC but not in the NCEP group. Total cholesterol levels were similarly reduced by both diets, and LDL cholesterol levels were not significantly different between the 2 groups. However, LDL cholesterol levels were significantly reduced within the NCEP group (−6.4 mg/dL [−0.17 mmol/L]; P = .05) but not the MLC group (−3.9 mg/dL [−0.10 mmol/L]; P = .48). There were no significant differences between groups regarding HDL values. The NCEP group experienced a significant reduction in HDL levels (−3.8 mg/dL [−0.10 mmol/L]; P = .006) but the MLC group did not (−1.3 mg/dL [0.03 mmol/L]; P = .46). Triglyceride levels were not significantly different between the groups. They were significantly lowered within the MLC group (−42.0 mg/dL [−10.88 mmol/L]; P = .003) but not the NCEP group (−15.2 mg/dL [3.89 mmol/L]; P = .20). The ratio of total cholesterol concentration to HDL cholesterol concentration was not significantly changed by either diet.

Table Graphic Jump LocationTable 3. Randomized Comparisons Between the MLC and NCEP Step 2 Diets Within and Between Groups*

Regarding the LDL subclasses, there were no significant differences between the MLC and NCEP groups. At baseline, particle size of the major LDL peak correlated with triglyceride (R = −0.65; P<.001) and HDL (R = 0.51; P<.001) concentrations but not with total or LDL cholesterol. At 3 months, the increase in LDL particle size correlated with magnitude of triglyceride reduction (R = −0.47; P<.001). The particle size of the major LDL peak in patients adhering to the NCEP diet did not change significantly (from 262.2 to 263.4 nm; P = .20). In contrast, the particle size of the major LDL peak increased significantly in the MLC group (from 259.4 to 264.2 nm; P = .001) (Table 3). In addition, the proportion of small, dense LDL subclasses (sum of IIIA, IIIB, IVA, and IVB) decreased significantly in the MLC (by 6.1%; P = .02) but not in the NCEP group (by 1.4%; P = .29).

Plasma ketone body concentrations were measured at the end of the trial and all participants were found without ketosis. In addition, there were no significant differences in glucose, insulin, and C-reactive protein levels between the NCEP and MLC groups. Satisfaction with the diet and counseling were similar in both groups (Table 4).

Table Graphic Jump LocationTable 4. Participant Satisfaction Scores Regarding Diet and Diet Counseling*

In this randomized trial the MLC diet low in carbohydrates and relatively high in predominantly monounsaturated fat and protein caused more weight loss than the NCEP diet, had no adverse effects, and improved lipid variables after 12 weeks.

The MLC diet was designed based on observations that rapid and significant weight loss occurred in patients adhering to popular high-fat, low-carbohydrate diets. However, the most popular of these diets emphasizes the consumption of saturated fats. Although fat content in the MLC diet was relatively high, the fats consumed were mostly monounsaturated. Diets rich in monounsaturated fatty acids lower total and LDL cholesterol while preserving HDL cholesterol levels.3033 The beneficial effect of diets rich in unsaturated fats on lipoprotein levels may extend to benefits on cardiovascular disease.21 The MLC diet recommended lower total carbohydrate intake but a higher consumption of complex carbohydrates, those with a low glycemic index, given the known detrimental effect of foods with a high glycemic index on HDL34 and triglyceride levels.35,36

There were no significant differences between the MLC and NCEP groups regarding waist-to-hip ratio. Within the MLC group, however, there was a significant decrease. It should be noted that this trial was designed with sufficient statistical power to assess between-group differences in weight but not in other anthropometric measures or lipid variables. Nonetheless, it is interesting to note that the preferential deposition of abdominal fat (the central or android pattern) is an independent cardiovascular risk factor.3739 Central obesity is often associated with hyperinsulinemia, glucose intolerance, high triglyceride and low HDL cholesterol levels, and hypertension,4042 which contributes to the metabolic syndrome. The metabolic syndrome is a major clinical and public health problem. It is a clinical problem because, for those who have it, the overall risk of coronary heart disease is far greater than the simple arithmetic sum of the individual risks4345; it is a public health problem because, in the United States, 40% of adults older than 40 years are affected.46

Hypertriglyceridemia is an independent risk factor for coronary heart disease.4750 Overweight individuals, especially those with central obesity, often have hypertriglyceridemia, a component of the metabolic syndrome. Although there were no significant differences between the groups, the MLC diet markedly and significantly reduced triglycerides. This finding in the MLC diet group may be a consequence of the patients’ greater weight loss and their consumption of foods with a low glycemic index.

There were no significant differences between the 2 groups for any lipid variables. Nonetheless, the NCEP, but not the MLC diet, significantly reduced HDL as well as LDL cholesterol levels. Diets low in saturated fats but high in carbohydrates may result in a reduction in HDL cholesterol levels. The clinical relevance of reducing HDL cholesterol levels by dieting is not clear. For example, in a small randomized trial,51 patients who followed a low-fat diet for 5 years experienced regression of coronary atherosclerosis. These patients had a significant, long-term reduction in HDL cholesterol level without any apparent adverse consequences. However, in that trial, other intense lifestyle changes, including smoking cessation and increased levels of exercise, may have confounded the lipid results. Although the NCEP diet significantly reduced LDL cholesterol, the effect size was small, and neither diet significantly changed the total cholesterol-to-HDL ratio.

There were additional significant changes in lipid variables within the MLC but not within the NCEP diet group. Specifically, the MLC diet was associated with increased particle size of the major LDL peak and a reduction in the proportion of small, high-density LDL particles. The clinical implications of a change in LDL particle size and density without a change in overall concentration of LDL cholesterol is not clear. However, a preponderance of small, dense LDL particles is commonly associated with hypertriglyceridemia.52 Indeed, the marked reduction in triglyceride levels in the MLC diet group was associated with an increase in the particle size of the major LDL peak. This finding was not present in the NCEP diet group, possibly because of the more modest reduction in triglyceride levels.

The rationale for the stepped approach of the MLC diet included motivation and education. In the first stage, patients promptly lose weight because of the significant reduction in calories. This motivates them to proceed to the later stages of the diet. The educational aspects of the stepped approach to diet are also important. Patients learn the effects of different foods on their weight and how to identify foods higher in monounsaturated fat and with a lower glycemic index to reduce postprandial craving.

Overall, despite the added complexity of the MLC diet, with its stepped approach, both groups of patients were similarly satisfied with their assigned diets and the dietary counseling. Of interest, 5 of the 6 participants who did not complete the trial were assigned to the NCEP diet. This may reflect a lack of early weight loss or dissatisfaction with the diet. The latter possibility is supported by long-term data from a randomized trial, which demonstrated significantly less weight loss as well as lower compliance with a low-protein, high-carbohydrate diet.53

In recently revised dietary guidelines the AHA recommended a diet low in saturated but high in monounsaturated fat as an option for individuals with low HDL-cholesterol, elevated triglyceride, and elevated small, dense LDL-cholesterol levels. The AHA recognized that LDL cholesterol levels might be reduced by substituting either carbohydrates or monounsaturated fat for saturated fat, and that this approach lacks the potentially detrimental effect of high-carbohydrate, lower-fat diets on HDL and triglyceride levels.22 The data from the present trial are compatible with this recent AHA revision.

Popular low-carbohydrate, high-fat diets have been criticized for promoting ketosis, a sign of metabolic derangements. We were unable to detect ketone bodies in any of the study participants. However, the tests for ketosis were performed at the end of the trial, during the maintenance phase of the MLC diet, when calories from carbohydrates were much less restricted. Thus, we cannot exclude the possiblilty of ketosis during the early phase of the MLC diet.

The trial was intended to be isocaloric in both randomized groups. Because of limitations inherent in food diaries and calorie counts, we cannot exclude small differences in overall caloric intake between groups.

The trial duration of 12 weeks was relatively short but sufficient to observe a greater decrease in body weight in the MLC than in the NCEP diet group. It remains unclear whether this beneficial effect would be maintained over a prolonged period of years. It is also unclear whether the observed apparently beneficial but nonsignificant changes in blood lipid concentration and waist-to-hip ratio would increase, decrease, or remain the same.

Overweight and obesity have reached epidemic proportions in the United States. Approximately $68 billion per year are spent on health problems directly associated with excessive body weight. Weight reduction programs and special food regimens represent an incremental additional societal cost of $30 billion per year.54 Traditionally, low-fat diets with a high carbohydrate content have been recommended as healthier diets to promote weight loss,55,56 but their effect on weight is modest, and they may increase triglyceride and lower HDL cholesterol levels.

While any expected incremental benefits of different diets are small to moderate, the clinical and public health implications are very large for a condition as common and serious as obesity. Thus, randomized trials of large sample size and long duration of dietary interventions represent the most reliable design strategy to provide data on obesity and weight loss likely to have an impact on the health and health care expenditures of the US population. Further randomized trials of sufficient size and duration are necessary to confirm or refute the current findings.

Correspondence: Charles H. Hennekens, MD, DrPH, 2800 S Ocean Blvd, PH-A, Boca Raton, FL 33432 (profchhmd@prodigy.net).

Accepted for Publication: November 25, 2003.

Acknowledgment: We thank Danielle Hollar, PhD, for her advice and help.

Financial Interest: Dr Hennekens is funded by the Agatston Research Institute, a nonprofit foundation, as Director of Research.

Ashley  FW  JrKannel  WB Relation of weight change to changes in atherogenic traits: the Framingham Study. J Chronic Dis 1974;27103- 114
PubMed
Kannel  WBD’Agostino  RBCobb  JL Effect of weight on cardiovascular disease. Am J Clin Nutr 1996;63 ((3 suppl)) 419S- 422S
PubMed
Willett  WCManson  JEStampfer  MJ  et al.  Weight, weight change, and coronary heart disease in women: risk within the “normal” weight range. JAMA 1995;273461- 465
PubMed
Calle  EEThun  MJPetrelli  JMRodriguez  CHeath  CW Body-mass index and mortality in a prospective cohort of US adults. N Engl J Med 1999;3411097- 1105
PubMed
Stevens  JCai  JPamuk  ERWilliamson  DFThun  MJWood  JL The effect of age on the association between body-mass index and mortality. N Engl J Med 1998;3381- 7
PubMed
Manson  JEWillett  WCStampfer  MJ  et al.  Body weight and mortality among women. N Engl J Med 1995;333677- 685
PubMed
Lee  IMManson  JEHennekens  CHPaffenbarger  RS  Jr Body weight and mortality: a 27-year follow-up of middle-aged men. JAMA 1993;2702823- 2828
PubMed
Kuczmarski  RJCarroll  MDFlegal  KMTroiano  RP Varying body mass index cutoff points to describe overweight prevalence among US adults: NHANES III (1988 to 1994). Obes Res 1997;5542- 548
PubMed
National Institutes of Health, National Heart, Lung, and Blood Institute, Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report.  Bethesda, Md National Institutes of Health1998;
Eckel  RHKrauss  RMAHA Nutrition Committee, American Heart Association Call to Action: obesity as a major risk factor for coronary artery disease. Circulation 1998;972099- 2100
PubMed
Wood  PDStefanick  MLDreon  DM  et al.  Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise. N Engl J Med 1988;3191173- 1179
PubMed
Van Gaal  LFWauters  MADe Leeuw  IH The beneficial effects of modest weight loss on cardiovascular risk factors. Int J Obes Relat Metab Disord 1997;21 ((suppl)) S5- S9
PubMed
Goldstein  DJ Beneficial health effects of modest weight loss. Int J Obes Relat Metab Disord 1992;16397- 415
PubMed
 Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults: the Expert Panel. Arch Intern Med 1988;14836- 69
PubMed
Grundy  SMBilheimer  DBlackburn  H  et al.  Rationale of the diet-heart statement of the American Heart Association: report of nutrition committee. Circulation 1982;65 ((suppl)) 839A- 854A
PubMed
Wood  PDStefanick  MLWilliams  PTHaskell  WL The effects on plasma lipoproteins of a prudent weight-reducing diet, with or without exercise, in overweight men and women. N Engl J Med 1991;325461- 466
PubMed
Hunninghake  DBStein  EADujovne  CA  et al.  The efficacy of intensive dietary therapy alone or combined with lovastatin in outpatients with hypercholesterolemia. N Engl J Med 1993;3281213- 1219
PubMed
Schaefer  EJLichtenstein  AHLamon-Fava  S  et al.  Efficacy of a National Cholesterol Education Program NCEP diet in normolipidemic and hypercholesterolemic middle-aged and elderly men and women. Arterioscler Thromb Vasc Biol 1995;151079- 1085
PubMed
Mensink  RPKatan  MB Effect of dietary fatty acids on serum lipids and lipoproteins: a meta-analysis of 27 trials. Arterioscler Thromb 1992;12911- 919
PubMed
Mensink  RPKatan  MB Effect of monounsaturated fatty acids versus complex carbohydrates on high-density lipoproteins in healthy men and women. Lancet 1987;1122- 125
PubMed
Katan  MBGrundy  SMWillet  WC Beyond low-fat diets. N Engl J Med 1997;337563- 566
PubMed
Krauss  RMEckel  RHHoward  B  et al.  AHA Dietary Guidelines: Revision 2000: a statement for healthcare professionals from the nutrition committee of the American Heart Association. Circulation 2000;1022284- 2299
PubMed
Trudeau  EDube  L Moderators and determinants of satisfaction with diet counseling for patients consuming a therapeutic diet. J Am Diet Assoc 1995;9534- 39
PubMed
The Cleveland Clinic Foundation, Modification of Diet in Renal Disease (MDRD) Study: Dietary Satisfaction Questionnaire.  Cleveland, Ohio The Cleveland Clinic Foundation1989;
Williams  SR Inequality of Carbohydrates: The Glycemic Index: Nutrition and Diet Therapy.  Boston, Mass Times Mirror/Mosby College Publishing1989;60- 61
Lopez-Jimenez  FHeilbron  RAlmon  MKorn  HLamas  GAAgatston  AS The beneficial effect of a high-fat, high-protein, low-carbohydrate diet on body weight and HDL cholesterol. J Am Coll Cardiol 1998;31 ((suppl)) 343A
Warnick  GR Enzymatic methods for quantification of lipoproteins lipids: methods. Methods Enzymol 1986;129101- 123
PubMed
Warnick  GRBenderson  JAlbers  JJ Dextran sulfate-Mg2+ precipitation procedure or quantification of high-density-lipoprotein cholesterol. Clin Chem 1982;281379- 1388
PubMed
Friedewald  WTLevy  RIFredrickson  DS Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972;18499- 502
PubMed
Mattson  FHGrundy  SM Comparison of effects of dietary saturated, mono-unsaturated, and polyunsaturated fatty acids on plasma lipids and lipoproteins in man. J Lipid Res 1985;26194- 202
PubMed
Grundy  SM Comparison of monounsaturated fatty acids and carbohydrates for lowering plasma cholesterol. N Engl J Med 1986;314745- 748
PubMed
Spiller  GAJenkins  DABosello  OGates  JECragen  LNBruce  B Nuts and plasma lipids: an almond-based diet lowers LDL-C while preserving HDL-C. J Am Coll Nutr 1998;17285- 290
PubMed
Spiller  GAJenkins  DACragen  LN  et al.  Effect of a diet high in mono-unsaturated fat from almonds on plasma cholesterol and lipoproteins. J Am Coll Nutr 1992;11126- 130
PubMed
Frost  GLeeds  AADore  CJMadeiros  SBrading  SDornhorst  A Glycemic index as a determinant of serum HDL-cholesterol concentration. Lancet 1999;3531045- 1048
PubMed
Frost  GWilding  JBeecham  J Dietary advice based on the glycemic index improves dietary profile and metabolic control in type 2 diabetic patients. Diabet Med 1994;11397- 401
PubMed
Jenkins  DJWolever  TMKalmusky  J  et al.  Low-glycemic index diet in hyperlipidemia: use of traditional starchy foods. Am J Clin Nutr 1987;4666- 71
PubMed
Rexrode  KMCarey  VJHennekens  CH  et al.  Abdominal adiposity and coronary heart disease in women. JAMA 1998;2801843- 1848
PubMed
Daniels  SRMorrison  JASprecher  DLKhoury  PKimball  TR Association of body fat distribution and cardiovascular risk factors in children and adolescents. Circulation 1999;99541- 545
PubMed
Casassus  PFontbonne  AThibult  N  et al.  Upper-body fat distribution: a hyperinsulinemia-independent predictor of coronary heart disease mortality: the Paris prospective study. Arterioscler Thromb 1992;121387- 1392
PubMed
Despres  JP Obesity and lipid metabolism: relevance of body fat distribution. Curr Opin Lipidol 1991;25- 15
Despres  JPMoorjani  SLupien  PJTremblay  ANadeau  ABouchard  C Regional distribution of body fat, plasma lipoproteins, and cardiovascular disease. Arteriosclerosis 1990;10497- 511
PubMed
Grundy  SM Small LDL, atherogenic dyslipidemia, and metabolic syndrome. Circulation 1997;951- 4
PubMed
Lempiäinen  PMykkänen  LPyörälä  KLakkso  MKuusisto  J Insulin resistance syndrome predicts coronary heart disease events in elderly nondiabetic men. Circulation 1999;100123- 128
PubMed
Gaudet  DVohl  MCPerron  P  et al.  Relationships of abdominal obesity and hyperinsulinemia to angiographically assessed coronary artery disease in men with known mutations in the LDL receptor gene. Circulation 1998;97871- 877
PubMed
Haffner  SM Impaired glucose tolerance, insulin resistance and cardiovascular disease. Diabet Med 1997;14 ((suppl)) S12- S18
PubMed
Eidelman  RLamas  GAHennekens  CH The new National Cholesterol Education Program guidelines: clinical challenges for more widespread therapy of lipids to treat and prevent coronary heart disease. Arch Intern Med 2002;1622033- 2036
PubMed
Jeppesen  JHein  HOSuadicani  PGyntelberg  F Triglyceride concentration and ischemic heart disease: an eight-year follow-up in the Copenhagen male study. Circulation 1998;971029- 1036
PubMed
Hokanson  JEAustin  MA Plasma triglyceride level as a risk factor for cardiovascular disease independent of high-density lipoprotein level: a meta-analysis of population-based prospective studies. J Cardiovasc Risk 1996;3213- 219
PubMed
Austin  MA Plasma triglyceride and coronary artery disease. Arterioscler Thromb 1991;112- 14
PubMed
Miller  MSeidler  AMoalemi  APearson  TA Normal triglyceride levels and coronary artery disease events: the Baltimore Coronary Observational Long-term Study. J Am Coll Cardiol 1998;311252- 1257
PubMed
Ornish  DScherwitz  LWBillings  JH  et al.  Intensive lifestyles changes for reversal of coronary heart disease. JAMA 1998;2802001- 2007
PubMed
Superko  RH Lipoprotein subclasses and atherosclerosis. Front Biosci 2001;6D355- D365
PubMed
McManus  KAntinoro  LSacks  F A randomized controlled trial of a moderate-fat, low-energy diet compared with a low-fat, low-energy diet for weight loss in overweight adults. Int J Obes Relat Metab Disord 2001;251503- 1511
PubMed
National Task Force on the Prevention and Treatment of Obesity, Long-term pharmacotherapy in the management of obesity JAMA 1996;2761907- 1915
PubMed
Kennedy  EMeyers  LLayden  W The 1995 dietary guidelines for Americans: an overview. J Am Diet Assoc 1996;96234- 237
PubMed
Krauss  RMDeckelbaum  RJErnst  N  et al.  Dietary guidelines for healthy American adults: a statement for health professionals from the nutrition committee, American Heart Association. Circulation 1996;941795- 1800
PubMed

Figures

Tables

Table Graphic Jump LocationTable 1. Composition of the Study Diet*
Table Graphic Jump LocationTable 2. Baseline Characteristics of Study Subjects*
Table Graphic Jump LocationTable 3. Randomized Comparisons Between the MLC and NCEP Step 2 Diets Within and Between Groups*
Table Graphic Jump LocationTable 4. Participant Satisfaction Scores Regarding Diet and Diet Counseling*

References

Ashley  FW  JrKannel  WB Relation of weight change to changes in atherogenic traits: the Framingham Study. J Chronic Dis 1974;27103- 114
PubMed
Kannel  WBD’Agostino  RBCobb  JL Effect of weight on cardiovascular disease. Am J Clin Nutr 1996;63 ((3 suppl)) 419S- 422S
PubMed
Willett  WCManson  JEStampfer  MJ  et al.  Weight, weight change, and coronary heart disease in women: risk within the “normal” weight range. JAMA 1995;273461- 465
PubMed
Calle  EEThun  MJPetrelli  JMRodriguez  CHeath  CW Body-mass index and mortality in a prospective cohort of US adults. N Engl J Med 1999;3411097- 1105
PubMed
Stevens  JCai  JPamuk  ERWilliamson  DFThun  MJWood  JL The effect of age on the association between body-mass index and mortality. N Engl J Med 1998;3381- 7
PubMed
Manson  JEWillett  WCStampfer  MJ  et al.  Body weight and mortality among women. N Engl J Med 1995;333677- 685
PubMed
Lee  IMManson  JEHennekens  CHPaffenbarger  RS  Jr Body weight and mortality: a 27-year follow-up of middle-aged men. JAMA 1993;2702823- 2828
PubMed
Kuczmarski  RJCarroll  MDFlegal  KMTroiano  RP Varying body mass index cutoff points to describe overweight prevalence among US adults: NHANES III (1988 to 1994). Obes Res 1997;5542- 548
PubMed
National Institutes of Health, National Heart, Lung, and Blood Institute, Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults: The Evidence Report.  Bethesda, Md National Institutes of Health1998;
Eckel  RHKrauss  RMAHA Nutrition Committee, American Heart Association Call to Action: obesity as a major risk factor for coronary artery disease. Circulation 1998;972099- 2100
PubMed
Wood  PDStefanick  MLDreon  DM  et al.  Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise. N Engl J Med 1988;3191173- 1179
PubMed
Van Gaal  LFWauters  MADe Leeuw  IH The beneficial effects of modest weight loss on cardiovascular risk factors. Int J Obes Relat Metab Disord 1997;21 ((suppl)) S5- S9
PubMed
Goldstein  DJ Beneficial health effects of modest weight loss. Int J Obes Relat Metab Disord 1992;16397- 415
PubMed
 Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults: the Expert Panel. Arch Intern Med 1988;14836- 69
PubMed
Grundy  SMBilheimer  DBlackburn  H  et al.  Rationale of the diet-heart statement of the American Heart Association: report of nutrition committee. Circulation 1982;65 ((suppl)) 839A- 854A
PubMed
Wood  PDStefanick  MLWilliams  PTHaskell  WL The effects on plasma lipoproteins of a prudent weight-reducing diet, with or without exercise, in overweight men and women. N Engl J Med 1991;325461- 466
PubMed
Hunninghake  DBStein  EADujovne  CA  et al.  The efficacy of intensive dietary therapy alone or combined with lovastatin in outpatients with hypercholesterolemia. N Engl J Med 1993;3281213- 1219
PubMed
Schaefer  EJLichtenstein  AHLamon-Fava  S  et al.  Efficacy of a National Cholesterol Education Program NCEP diet in normolipidemic and hypercholesterolemic middle-aged and elderly men and women. Arterioscler Thromb Vasc Biol 1995;151079- 1085
PubMed
Mensink  RPKatan  MB Effect of dietary fatty acids on serum lipids and lipoproteins: a meta-analysis of 27 trials. Arterioscler Thromb 1992;12911- 919
PubMed
Mensink  RPKatan  MB Effect of monounsaturated fatty acids versus complex carbohydrates on high-density lipoproteins in healthy men and women. Lancet 1987;1122- 125
PubMed
Katan  MBGrundy  SMWillet  WC Beyond low-fat diets. N Engl J Med 1997;337563- 566
PubMed
Krauss  RMEckel  RHHoward  B  et al.  AHA Dietary Guidelines: Revision 2000: a statement for healthcare professionals from the nutrition committee of the American Heart Association. Circulation 2000;1022284- 2299
PubMed
Trudeau  EDube  L Moderators and determinants of satisfaction with diet counseling for patients consuming a therapeutic diet. J Am Diet Assoc 1995;9534- 39
PubMed
The Cleveland Clinic Foundation, Modification of Diet in Renal Disease (MDRD) Study: Dietary Satisfaction Questionnaire.  Cleveland, Ohio The Cleveland Clinic Foundation1989;
Williams  SR Inequality of Carbohydrates: The Glycemic Index: Nutrition and Diet Therapy.  Boston, Mass Times Mirror/Mosby College Publishing1989;60- 61
Lopez-Jimenez  FHeilbron  RAlmon  MKorn  HLamas  GAAgatston  AS The beneficial effect of a high-fat, high-protein, low-carbohydrate diet on body weight and HDL cholesterol. J Am Coll Cardiol 1998;31 ((suppl)) 343A
Warnick  GR Enzymatic methods for quantification of lipoproteins lipids: methods. Methods Enzymol 1986;129101- 123
PubMed
Warnick  GRBenderson  JAlbers  JJ Dextran sulfate-Mg2+ precipitation procedure or quantification of high-density-lipoprotein cholesterol. Clin Chem 1982;281379- 1388
PubMed
Friedewald  WTLevy  RIFredrickson  DS Estimation of the concentration of low-density lipoprotein cholesterol in plasma, without use of the preparative ultracentrifuge. Clin Chem 1972;18499- 502
PubMed
Mattson  FHGrundy  SM Comparison of effects of dietary saturated, mono-unsaturated, and polyunsaturated fatty acids on plasma lipids and lipoproteins in man. J Lipid Res 1985;26194- 202
PubMed
Grundy  SM Comparison of monounsaturated fatty acids and carbohydrates for lowering plasma cholesterol. N Engl J Med 1986;314745- 748
PubMed
Spiller  GAJenkins  DABosello  OGates  JECragen  LNBruce  B Nuts and plasma lipids: an almond-based diet lowers LDL-C while preserving HDL-C. J Am Coll Nutr 1998;17285- 290
PubMed
Spiller  GAJenkins  DACragen  LN  et al.  Effect of a diet high in mono-unsaturated fat from almonds on plasma cholesterol and lipoproteins. J Am Coll Nutr 1992;11126- 130
PubMed
Frost  GLeeds  AADore  CJMadeiros  SBrading  SDornhorst  A Glycemic index as a determinant of serum HDL-cholesterol concentration. Lancet 1999;3531045- 1048
PubMed
Frost  GWilding  JBeecham  J Dietary advice based on the glycemic index improves dietary profile and metabolic control in type 2 diabetic patients. Diabet Med 1994;11397- 401
PubMed
Jenkins  DJWolever  TMKalmusky  J  et al.  Low-glycemic index diet in hyperlipidemia: use of traditional starchy foods. Am J Clin Nutr 1987;4666- 71
PubMed
Rexrode  KMCarey  VJHennekens  CH  et al.  Abdominal adiposity and coronary heart disease in women. JAMA 1998;2801843- 1848
PubMed
Daniels  SRMorrison  JASprecher  DLKhoury  PKimball  TR Association of body fat distribution and cardiovascular risk factors in children and adolescents. Circulation 1999;99541- 545
PubMed
Casassus  PFontbonne  AThibult  N  et al.  Upper-body fat distribution: a hyperinsulinemia-independent predictor of coronary heart disease mortality: the Paris prospective study. Arterioscler Thromb 1992;121387- 1392
PubMed
Despres  JP Obesity and lipid metabolism: relevance of body fat distribution. Curr Opin Lipidol 1991;25- 15
Despres  JPMoorjani  SLupien  PJTremblay  ANadeau  ABouchard  C Regional distribution of body fat, plasma lipoproteins, and cardiovascular disease. Arteriosclerosis 1990;10497- 511
PubMed
Grundy  SM Small LDL, atherogenic dyslipidemia, and metabolic syndrome. Circulation 1997;951- 4
PubMed
Lempiäinen  PMykkänen  LPyörälä  KLakkso  MKuusisto  J Insulin resistance syndrome predicts coronary heart disease events in elderly nondiabetic men. Circulation 1999;100123- 128
PubMed
Gaudet  DVohl  MCPerron  P  et al.  Relationships of abdominal obesity and hyperinsulinemia to angiographically assessed coronary artery disease in men with known mutations in the LDL receptor gene. Circulation 1998;97871- 877
PubMed
Haffner  SM Impaired glucose tolerance, insulin resistance and cardiovascular disease. Diabet Med 1997;14 ((suppl)) S12- S18
PubMed
Eidelman  RLamas  GAHennekens  CH The new National Cholesterol Education Program guidelines: clinical challenges for more widespread therapy of lipids to treat and prevent coronary heart disease. Arch Intern Med 2002;1622033- 2036
PubMed
Jeppesen  JHein  HOSuadicani  PGyntelberg  F Triglyceride concentration and ischemic heart disease: an eight-year follow-up in the Copenhagen male study. Circulation 1998;971029- 1036
PubMed
Hokanson  JEAustin  MA Plasma triglyceride level as a risk factor for cardiovascular disease independent of high-density lipoprotein level: a meta-analysis of population-based prospective studies. J Cardiovasc Risk 1996;3213- 219
PubMed
Austin  MA Plasma triglyceride and coronary artery disease. Arterioscler Thromb 1991;112- 14
PubMed
Miller  MSeidler  AMoalemi  APearson  TA Normal triglyceride levels and coronary artery disease events: the Baltimore Coronary Observational Long-term Study. J Am Coll Cardiol 1998;311252- 1257
PubMed
Ornish  DScherwitz  LWBillings  JH  et al.  Intensive lifestyles changes for reversal of coronary heart disease. JAMA 1998;2802001- 2007
PubMed
Superko  RH Lipoprotein subclasses and atherosclerosis. Front Biosci 2001;6D355- D365
PubMed
McManus  KAntinoro  LSacks  F A randomized controlled trial of a moderate-fat, low-energy diet compared with a low-fat, low-energy diet for weight loss in overweight adults. Int J Obes Relat Metab Disord 2001;251503- 1511
PubMed
National Task Force on the Prevention and Treatment of Obesity, Long-term pharmacotherapy in the management of obesity JAMA 1996;2761907- 1915
PubMed
Kennedy  EMeyers  LLayden  W The 1995 dietary guidelines for Americans: an overview. J Am Diet Assoc 1996;96234- 237
PubMed
Krauss  RMDeckelbaum  RJErnst  N  et al.  Dietary guidelines for healthy American adults: a statement for health professionals from the nutrition committee, American Heart Association. Circulation 1996;941795- 1800
PubMed

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