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American Journal of Clinical Nutrition, Vol. 88, No. 5, 1232-1241, November 2008
© 2008 American Society for Nutrition

ORIGINAL RESEARCH COMMUNICATION

Comparison of 3 ad libitum diets for weight-loss maintenance, risk of cardiovascular disease, and diabetes: a 6-mo randomized, controlled trial1,2,3,4

Anette Due, Thomas M Larsen, Huiling Mu, Kjeld Hermansen, Steen Stender and Arne Astrup

1 From the Department of Human Nutrition, Centre for Advanced Food Studies, Faculty of Life Sciences, University of Copenhagen, Frederiksberg C, Denmark (AD, TML, and AA); Biocentrum DTU, Technical University of Denmark, Lyngby, Denmark (HM); the Department of Endocrinology and Metabolism, Århus University Hospital, Århus, Denmark (KH); and the Department of Clinical Chemistry, Copenhagen University Hospital, Gentofte, Denmark (SS)

See corresponding editorial on page 1185.

2 AD and TML contributed equally to the manuscript.

3 Supported by the HA Foundation, The Danish Heart Association, The Danish Diabetes Association, Centre for Advanced Food Research, The state Research Councils, and The Danish Pork Council foundations, associations, and research councils: www.mufobes.dk/?show=sponsorer. Foods in the supermarket and low-calorie diets were sponsored by Nutrillett, the HA Foundation, KGT/DEG, The Danish Pork Council, Danisco FDB, Arla Foods, The Danish Heart Association, and LMC Rådighedsfond. Food sponsors: 3-Stjernet, Aarhus United, Allara, Ardo/Frigodan, Beauvais, Bæchs Conditori, Bähncke, Cadiso, Cerealia, Daloon, Danisco, FDB, Flensted, Frisko, G-kartofler, Gamba Food, Jan Import, Kelloggs, Kims, Kraft Foods, Kryta, Københavns Engros Grønttorv, Kødbranchens Fællesråd, LCH catering, Lykkeberg, Malaco Leaf, Nutana, Nutrillett, Odense Marcipan, Polar Is, Puratos, Rose Poultry, Rynkeby, Saeby, Santa Maria, Schulstad, Svansø, Sønderjysk Kål, Tholstrup Cheese, Toms, Tulip, Unilever, Urtekram, and Wasa: www.mufobes.dk/?show=kostsponsorer.

4 Address reprint requests and correspondence to A Astrup, Department of Human Nutrition, Centre for Advanced Food Studies, Faculty of Life Sciences, University of Copenhagen, Rolighedsvej 30, DK-1958 Frederiksberg C, Denmark. E-mail: ast{at}life.ku.dk.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Background: The optimal dietary content and type of fat and carbohydrate for weight management has been debated for decades.

Objective: The objective was to compare the effects of 3 ad libitum diets on the maintenance of an initial weight loss of ≥8% and risk factors for CVD and diabetes during a 6-mo controlled dietary intervention.

Design: Nondiabetic overweight or obese [mean ± SD body mass index (in kg/m2): 31.5 ± 2.6] men (n = 55) and women (n = 76) aged 28.2 ± 4.8 y were randomly assigned to a diet providing a moderate amount of fat (35–45% of energy) and >20% of fat as monounsaturated fatty acids (MUFA diet; n = 54), to a low-fat (20–30% of energy) diet (LF diet; n = 51), or to a control diet (35% of energy as fat; n = 26). Protein constituted 10–20% of energy in all 3 diets. All foods were provided free of charge from a purpose-built supermarket.

Results: More subjects dropped out of the MUFA (28%) group than out of the LF group (16%) and control group (8%) (MUFA compared with control: P < 0.05). All groups regained weight (MUFA: 2.5 ± 0.7 kg; LF: 2.2 ± 0.7 kg; and control: 3.8 ± 0.8 kg; NS). Body fat regain was lower in the LF (0.6 ± 0.6%) and MUFA (1.6 ± 0.6%) groups than in the control group (2.6 ± 0.5%) (P < 0.05). In the MUFA group, fasting insulin decreased by 2.6 ± 3.5 pmol/L, the homeostasis model assessment of insulin resistance by 0.17 ± 0.13, and the ratio of LDL to HDL by 0.33 ± 0.13; in the LF group, these variables increased by 4.3 ± 3.0 pmol/L (P < 0.08) and 0.17 ± 0.10 (P < 0.05) and decreased by 0.02 ± 0.09 (P = 0.005), respectively; and in the control group, increased by 14.0 ± 4.3 pmol/L (P < 0.001), 0.57 ± 0.17 (P < 0.001), and 0.05 ± 0.14 (P = 0.036), respectively. Dietary adherence was high on the basis of fatty acid changes in adipose tissue.

Conclusions: Diet composition had no major effect on preventing weight regain. However, both the LF and MUFA diets produced less body fat regain than did the control diet, and the dropout rate was lowest in the LF diet group, whereas fasting insulin decreased and the homeostasis model assessment of insulin resistance and ratio of LDL to HDL improved with the MUFA diet. This trial was registered at clinicaltrials.gov as NCT00274729.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The prevalence of obesity has increased worldwide during the past decades. Although the cause of obesity is complex, much attention has been paid to dietary composition. The Nordic (1) and US Department of Agriculture (USDA) 2004 (2) (ie, those available until January 2005) official dietary recommendations aim to decrease total fat in the diet to <30% of energy, increase carbohydrates to 55–60% of energy, increase protein from lean meat and dairy products to 10–20% of energy, and limit the intake of sugar-sweetened soft drinks. Meta-analyses of intervention studies show that a low-fat diet can induce weight loss (3) and decrease cardiovascular disease risk (3, 4). However, a recent meta-analysis found little evidence to support the consumption of a low-fat diet for weight reduction (5). Inspired by the apparent lack of effect of the USDA dietary recommendations on health, Willett and coworkers have developed new guidelines: the new Healthy Eating Pyramid (6). These guidelines recommend a diet that is high in vegetable oil, whole grains, nuts, legumes, fruit, and vegetables; is low in carbohydrates with a high glycemic index (GI); and is low in meat and dairy products (even low-fat versions). However, opponents have expressed concern that the increased intake in total fat will increase energy density and lead to weight gain. The intake of dietary fat, irrespective of its composition, has been associated with weight gain (7), although some studies indicate that the intake of unsaturated fat may not lead to the same weight gain as does an isocaloric diet high in saturated fatty acid (SFA) (8-10).

The challenge is not really to lose weight but to prevent weight gain and weight regain after weight loss. There is much contradictory data in this area and a lack of data from well-controlled trials about the most effective dietary approaches to maintaining a weight loss in overweight individuals.

The purpose of the present study was to compare the effect on weight-loss maintenance and change in cardiovascular disease and diabetic risk factors of 3 different ad libitum diets in a 6-mo controlled dietary maintenance intervention in healthy subjects. The diets compared are Willett's new Healthy Eating Pyramid [high in monounsaturated fat (MUFA) and a low GI], the Official Nordic Dietary Guidelines (similar to the USDA 2004 Food Pyramid—low in fat and a medium GI), and the average Danish diet (similar to the Western diet—high in SFA and a high GI).


   SUBJECTS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Subjects and experimental design
A total of 169 subjects aged 18–35 y with a body mass index (BMI; in kg/m2) of 28–36 were recruited from the Copenhagen area. Recruitment and additional inclusion criteria were previously described (11). A total of 154 participants fulfilled the inclusion criteria and were put on an 8-wk low-calorie diet (LCD; 800–1000 kcal/d) consisting primarily of shakes and bars with a composition of {approx}40%, 40%, and 20% of energy from protein, carbohydrate, and fat, respectively (Figure 1Go). Only subjects who lost ≥8% of their initial body weight were subsequently allocated to 1 of the 3 intervention diets using a simple block randomization procedure in which sex and an initial BMI < 32 were used as stratification criteria (Table 1Go). The procedure was carried out independently by 2 of the study personnel. All the participants were counseled by dietitians and instructed to follow an energy-restricted control diet (described below) for a 3-wk standardization and weight stabilization period before the examinations at baseline. The study was a parallel, randomized, 6-mo dietary intervention trial, and the allocation ratio was 2:2:1 for the MUFA:LF:control groups.


Figure 1
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  		FIGURE 1.. Organization chart of participant flow throughout the study. MUFA, diet with a moderate amount of fat (35–45% of energy) and >20% of fat as monounsaturated fatty acids (the new Healthy Eating Pyramid); LF, diet low in fat (USDA Food Pyramid); CTR, control diet; LCD, low-calorie diet.

 

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  		TABLE 1. Characteristics of the study participants by diet group at screening1

 
Experimental diets, supermarket model, and dietary compliance
The 3 prescribed ad libitum diets were as follows: 1) The new Healthy Eating Pyramid—moderate amount of fat (35–45% of energy) and high amount (>20% of energy) of MUFAs (MUFA diet), 2) The USDA Food Pyramid—low amount (20–30% of energy) of fat (LF diet), or 3) a control diet (35% of energy as fat) with >15% of energy as SFA. Protein was 10–20% of energy in all diets (Table 2Go). The MUFA diet also included more whole-grain foods, nuts, and legumes and had a lower GI, whereas the control diet included more sugar-containing foods than the other diets. Alcohol consumption was allowed in accordance with the current Danish guidelines, ie, <14 units/wk for women and <21 units/wk for men (1 unit = 12 g alcohol). Subjects were encouraged to eat until they were comfortably satiated, and they were instructed to maintain their habitual physical activity level to achieve energy balance and weight maintenance and/or further weight loss.


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  		TABLE 2. Prescribed and actual dietary intakes during the 6-mo controlled dietary intervention for the MUFA, LF, and control groups1

 
To control dietary composition and to monitor energy intake, the supermarket model was used (12). A 70-m2 shop was established at the Department. The study participants collected all foods (ie, 100% of their energy needs) free of charge from the supermarket during the 3-wk standardization period and the 6-mo dietary intervention. The supermarket product database included {approx}800 food items. A separate list of {approx}380 food items was also incorporated in the computer program to allow registration of foods reported being eaten from outside the supermarket (nonsupermarket foods). The supermarket facilities and computer program were described previously (11).

At each shopping session, educated project personnel scanned the barcodes of all the chosen food items and assisted the subjects in altering the selection made to meet the prescribed macronutrient composition (Appendix AGo). Subjects were not allowed to leave the supermarket until the food selection met the prescribed macronutrient composition. The subjects were carefully instructed to eat the foods themselves. Foods that they had not eaten themselves, waste and leftovers from the previous shopping session, and intake of nonsupermarket foods were registered at the start of each shopping session. Food intake was permitted ad libitum, and the energy content was not shown to the subjects. During the shopping period, all subjects were allowed a 21-d break (eg, for holidays and illness) during which no shopping or registration of dietary intake was required, although they were still instructed to follow the diet. All subjects received dietary counseling during the shopping period and had a minimum of 2 private counseling sessions with a dietitian during the 6 mo. The dietitian also arranged lectures and cooking classes relevant to each diet group, and they uploaded recipes on the website. Books with recipes of the respective diets were available in the supermarket for inspiration. Dietary compliance was assessed by fatty acid analyses from subcutaneous adipose tissue biopsy samples (<1 g) taken from the buttock at screening and at 6 mo.


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  		APPENDIX A. Foods recommended for the groups consuming the monounsaturated fatty acid (MUFA), low-fat (LF), and control diets (tool for dietary counseling during dietary intervention)

 
Study protocol
The primary outcome measure was change in body weight from 0 to 6 mo after the LCD weight-loss intervention. Secondary weight-related outcomes included changes in body composition (measured by dual-energy X-ray absorptiometry; DXA) and maintenance of >10% weight loss achieved during the 8-wk LCD. Body weight was measured with DXA (Lunar Radiation Co, GE, Madison, WI) at months 0 and 6. For repeated-measurement analyses, monthly weights were obtained with a single calibrated scale (Lindell Tronic 8000; Samhall Lavi, Christianstad, Sweden). Body composition (body fat and fat-free mass) measured with DXA and waist and hip circumferences measured with a tape measure on subjects in standing posture wearing only underwear was measured before weight loss and before and after the 6-mo intervention. Secondary endpoints were changes in diabetes and cardiovascular disease risk factors measured in fasting blood samples taken before and after the 6-mo intervention. Subjects had to consume their evening meal before 2000 and subsequently fast for 12 h before blood sampling. Venous blood samples from the antecubital vein and a fat biopsy sample from the buttock were obtained after the subject remained in a supine position for ≥10 min.

Laboratory analyses
Blood samples were kept on ice and centrifuged at 2800 x g for 10 min at 4 °C. All blood samples were kept at –20 °C, except for insulin (–80 °C), until analyzed. Serum glucose concentration was analyzed by standard end-point methods with a Vitros 950 (Johnson & Johnson, Ortho-Clinical Diagnostics, Birkerød, Denmark) with an intraassay CV of 1.1%. Serum insulin concentrations were measured by enzyme-linked immunosorbent assay (13) and then batched and analyzed at the same time. An insulin resistance score—the homeostasis model assessment of insulin resistance (HOMA-IR)—was computed by using the following formula: fasting glucose (mmol/L) x fasting insulin (mU/L)/22.5 (14). Plasma cholesterol, HDL cholesterol, and triglycerides were measured enzymatically with a COBAS INTEGRA 400 (Roche Diagnostic Systems, Basel, Switzerland), and the LDL concentration was calculated as follows: LDL = total cholesterol – HDL – (triglycerides/2.2). C-reactive protein concentrations were measured using the CRP (Latex) ultrasensitive assay. The fatty acid composition of fat biopsy samples was analyzed by gas chromatograph (Hewlett-Packard, Waldbronn, Germany). The fatty acid methyl esters were identified by comparing their retention times with those of authentic standards (Sigma Chemical Co, St Louis, MO).

Statistical analysis
The primary statistical analyses were done on completers only, and no differences were seen in age, sex, or BMI at baseline between completers and those who dropped out. An expected number of completers of 25 participants in each group gave the study enough power (80%) to detect a significant mean (± SD) difference (P < 0.05) in change in body weight of 2.0 ± 2.5 kg. To account for an expected drop-out during the LCD ({approx}15%) and during the dietary maintenance intervention ({approx}20%), the sample size estimation was increased to 50 in the MUFA and LF groups; 25 subjects were allocated to the control group.

Differences between groups before the dietary intervention were tested by one-factor analysis of variance. Differences between groups in changes from month 0 to 6 for all variables were tested by analysis of covariance with baseline values as covariates. Repeated measurements analyses were done for body weight over time and diet x month with baseline as covariate for both completers only and for the whole population in an intention-to-treat (ITT) analysis. For the ITT analysis, multiple imputation (MI) via Markov chain Monte Carlo was conducted assuming that the missing values are missing at random. The means were adjusted by the covariate. The ITT analysis was conducted with SAS 9.1 (SAS Institute Inc, Cary, NC). Differences in sex, the proportion of drop-outs, and the number of participants maintaining a weight loss >10% or achieving further weight loss were tested with chi-square tests. Correlations analyses were done with Pearson's correlation coefficient. Stepwise multiple regression analysis was performed to examine independent predictors of the changes in different outcome variables. The independent variables used in all models were the dietary components energy density, total fat, SFA, MUFA, polyunsaturated fatty acid (PUFA), total carbohydrates, fiber, sugar, protein, and alcohol (in % of energy). Fiber was assumed to provide 10 kJ/g. All results are presented as mean values with 95% CIs or means ± SEMs. The statistical analyses were conducted by using SPSS 13 (SPSS Inc, Chicago, IL).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Dietary intake and compliance
Dietary intake during the 3-wk supermarket standardization period was considered the control diet, and no differences between groups were seen (data not shown). The total dietary intake (foods from the supermarket and not from the supermarket) during the dietary intervention period is shown in Table 2Go. Dietary composition corresponded to the prescribed diets for all 3 groups. Highly significant differences in the amount and type of fat intake between all 3 groups (P < 0.001) and in intake of carbohydrate (P < 0.001) were obtained. Pairwise analyses showed that protein intake was slightly lower in the MUFA group than in the LF and control groups (P < 0.05), energy density was lower in the LF group than in the MUFA (P < 0.001) and control (P < 0.05) groups, and fiber intake was lower in the control group than in the MUFA and LF groups (P < 0.001). No differences in energy intake or alcohol consumption were seen between the groups. GI was prescribed to be low in the MUFA diet, moderate in the LF diet, and high in the control diet.

Dietary compliance, assessed by fat biopsy, showed that the MUFA group had a higher concentration of oleic acid (18:1) and linoleic acid and a lower concentration of myristic acid than did the LF and control groups after 6 mo (Table 3Go). Furthermore, the control group had a lower concentration of total PUFAs than did the MUFA and LF groups. A positive correlation between the dietary intake of oleic acid and oleic acid from the fat biopsy sample (r = 0.228, P < 0.04) was found after the 6-mo intervention.


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  		TABLE 3. Dietary compliance assessed from fat biopsy samples before a low-calorie diet (LCD) and after 6 mo of the dietary intervention1

 
Body weight and body composition
Body weight and body composition before and after the 6-mo dietary intervention are shown in Table 4Go. During the LCD, a mean (± SEM) weight loss of 12.1 ± 0.5 kg in the MUFA group, 13.1 ± 0.6 kg in the LF group, and 13.2 ± 1.0 kg in the control group was achieved, and no differences between groups were observed (P = 0.43). An average weight regain of 1.0 ± 0.01 kg was observed during the 3-wk standardization period, and no difference between groups was seen before the onset of testing the 3 diets at month 0. After 6 mo, weight regains of 2.5 ± 0.7 kg in the MUFA group, 2.2 ± 0.7 kg in the LF group, and 3.8 ± 0.8 kg in the control group were found (P = 0.31). A completer analysis showed no differences between groups in changes in weight regain during the 6-mo intervention as tested by repeated measurements (diet x month: P = 0.63; Figure 2Go). Similarly, the ITT analysis including all 125 subjects showed no significant differences in weight regain between groups (data not shown). After 6 mo, 73%, 56%, and 43% among groups maintained 5%, 8%, and 10% of the achieved weight loss during the LCD, respectively, with no difference between groups. The number of subjects losing additional body weight during the 6-mo intervention tended to be greater in the LF group (33%) than in the control group (13%) (P = 0.06), and no differences were found compared with the MUFA group (29%).


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  		TABLE 4. Body composition and diabetic and cardiovascular disease risk factors at baseline (month 0) and after 6 mo of the dietary intervention1

 

Figure 2
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  		FIGURE 2.. Change in body weight (A) and in body fat (B) from screening to after 6 mo of the MUFA, LF, and control (CTR) diets. MUFA, diet with a moderate amount of fat (35-45% of energy) and >20% of fat as monounsaturated fatty acids (the new Healthy Eating Pyramid); LF, diet low in fat (USDA Food Pyramid). No diet x month interaction was observed for changes in body weight by repeated measurement (P = 0.63; ANOVA). LCD: 8-wk low-calorie diet period. Stand., 3-wk standardization period. Different lowercase letters indicate significant differences between groups (P < 0.05).

 
The body fat regains of 1.3 ± 0.6 kg in the LF group and of 2.2 ± 0.7 kg in the MUFA group were significantly lower than the 3.5 ± 0.8 kg regain in the control group (P < 0.01 and P < 0.05, respectively; Figure 2Go). The estimated between-diet differences in changes in body fat were as follows: 1.9 (95% CI: 0.1, 3.7) for the control compared with the MUFA group, 2.5 (95% CI: 0.7, 4.4) for the control group compared with the LF group, and 0.7 (95% CI: –0.9, 2.2) for the MUFA group compared with the LF group. The increase in total lean mass in the LF group (0.9 ± 0.3 kg) was also higher than that in the control group (0.2 ± 0.3 kg) with post hoc pairwise analyses (P = 0.02). The estimated between-diet differences in changes in lean body mass were as follows: 0.5 (95% CI: –3.5, 1.3) for the MUFA group compared with the control group, 1.0 (95% CI: 0.1, 1.8) for the LF group compared with the control group, and 0.5 (95% CI: –0.2, 1.2) for the LF group compared with the MUFA group.

Multiple regression analyses including all groups showed that an increase in fiber intake of 1% of energy could predict a 1.4-kg lower increase in body weight. For the control group, an increase of 1 kJ/g in energy density could predict a 4-kg increase in body fat, whereas an increase in PUFA intake of 1% of energy could predict a lower regain in body weight and body fat of 2.6 and 2.7 kg, respectively, for the MUFA group.

Cardiovascular disease and diabetes risk factors
A reduction in fasting insulin of 2.6 ± 3.5 pmol/L was induced by the MUFA diet, whereas increases of 4.3 ± 3.0 by the LF diet and 14.0 ± 4.3 by the control diet were found, leading to a significant difference between all groups after the 6-mo intervention (P < 0.001; Table 4Go). Pairwise analyses showed differences in changes in fasting insulin between the control and MUFA groups of 17.8 (95% CI: 8.3, 27.3; P < 0.001), between the control and LF groups of 10.7 (95% CI: 1.4, 19.9; P < 0.01), and a tendency between the LF and MUFA groups of 7.1 (95% CI: –0.9, 15.1; P < 0.08). Correspondingly, HOMA-IR improved more in the MUFA group than in the control group (0.7; 95% CI: 0.3, 1.0; P < 0.001), more in the LF group than in the control group (0.4; 95% CI: 0.1, 0.7; P < 0.01), and more in the MUFA group than in the LF group (0.3; 95% CI: 0.01, 0.6; P < 0.06).

After adjustment for changes in body fat, the overall difference in change in fasting insulin was still significant (P = 0.019), and the pairwise analysis showed a 15.7 (95% CI: 4.7, 26.7; P = 0.006) difference between the control and MUFA groups, whereas the difference of 8.9 (95% CI: –2.2, 20.1; P = 0.115) between the control and LF groups seemed less convincing. Similarly, the overall difference in HOMA-IR was significant (P = 0.010), and the pairwise analysis showed a 3.9 (95% CI: 1.3, 6.4; P = 0.004) difference between the control and MUFA groups and no significant difference (1.8; 95% CI: –0.8, 4.4; P = 0.164) between the control and LF groups, whereas a difference of 2.0 (95% CI: –0.1, 4.1; P = 0.057) between the LF and MUFA groups was nearly significant. After adjustment for changes in body weight during the 6-mo intervention, the overall differences in change in fasting insulin (P = 0.040) and HOMA-IR (P = 0.031) were significant. Pairwise analyses showed significant differences only for the comparison between the MUFA and control groups for changes in fasting insulin of 15.0 (95% CI: 3.4, 26.7; P = 0.012) and for HOMA-IR of 3.6 (95% CI: 0.9, 6.3, P = 0.010). No significant difference in the change in fasting glucose was found between groups after adjustment for changes in body weight or body fat.

No significant differences in blood lipids or in high-sensitivity CRP were seen after the 6-mo dietary intervention. However, a reduction in the ratio of LDL to HDL of –0.33 ± 0.13 was induced by the MUFA diet, whereas almost no changes were seen in the LF (–0.02 ± 0.09) and control (0.05 ± 0.14) groups, which led to a significant difference between all groups after 6 mo (P = 0.011; Table 4Go). Pairwise analyses showed differences in changes in the ratio of LDL to HDL between the MUFA and control groups of 0.41 (95% CI: 0.03, 0.79; P = 0.036) and between the MUFA and LF groups of 0.44 (95% CI: 0.14, 0.75; P = 0.005). Multiple regression analyses showed that an increase in PUFA intake of 1% of energy could predict a lower increase of {approx}0.5 mmol/L glucose, of 4 pmol/L insulin, and of 1 score in HOMA-IR when all groups were analyzed together.

Withdrawal and dropout
One-hundred thirty-one participants were randomly assigned to the dietary intervention, and 25 of 131 participants (19%) did not complete the 6-mo intervention: 15 of 54 (28%) in the MUFA group, 8 of 51 (16%) in the LF group, and 2 of 26 (8%) in the control group. The number of dropouts in the MUFA group was significantly greater than that in the control group (P = 0.03). Personal reasons (divorce) and disease (eg, depression and illness) were the primary reasons for dropout, but the demanding nature of the project was also a reason (Figure 1Go).


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The present study showed that diet composition had no major effect on maintenance of weight loss during the 6-mo controlled dietary intervention. However, both the officially recommended low-fat diet and the new Healthy Eating Pyramid diet, which is high in MUFA, caused a lower regain in body fat than did a typical Western diet. Moreover, the novel Healthy Eating Pyramid diet seems to have a more favorable effect on diabetes risk factors.

In the present trial, >50% of the 106 completers maintained a weight loss of >8%, but the finding that none of the tested diets were significantly superior in preventing weight regain suggests that the type of diet followed may not be particularly important for weight-loss maintenance. This finding agrees with the findings of some (15-19) but not all (7, 20, 21) trials that compared the effects of low-fat and moderate-fat diets on body weight. The study most comparable with the present study was that by McManus et al (17), who also found equal weight loss (5%) with a moderate-fat diet (35% of total energy) and a lower-fat control diet (20% of total energy) after the first 6 mo of intervention. However, after 18 mo, a greater reduction in percentage body fat and waist circumference was observed in the moderate-fat group. This difference may be due in part to the fact that the diets were energy restricted (women were instructed to consume 1200 kcal/d and men 1500 kcal/d) and therefore not ad libitum and comparable with the free-living conditions of the present trial and to an unintentional higher fiber intake in the moderate-fat group.

Several short-term studies have shown that dietary fat is proportional with energy intake (22, 23). However, energy density rather than fat content has been suggested to determine energy intake (24). Even though energy density was higher in the MUFA diet, it was only in the control group that a 1-kJ/g increment in energy density was associated with a 4-kg regain of body fat. On the other hand, an increase in PUFA intake of 1% of energy predicted a lower regain of 2.7 kg body fat in only the MUFA group, which suggested that the type of fat could have an effect on body fat. In animal studies, less accumulation of body fat has been found in rats fed a PUFA-rich diet compared with an SFA rich diet (25, 26). Furthermore, MUFA intake has been found to induce a lower satiety level and a larger subsequent energy intake than do PUFA and SFA intakes (27) and to increase body weight more than PUFA intake (25). Other studies have found a more favorable effect of unsaturated fat than of SFA on body fat (8-10). However, the evidence linking particular fatty acids to body fatness is still weak and, thus far, no ad libitum dietary intervention study has proven that a diet high in unsaturated fatty acid is equivalent or superior to a low-fat diet in the prevention of weight gain.

In the present trial, the MUFA diet caused a greater reduction in fasting insulin and an improvement in HOMA-IR. This favorable effect may have been caused by the higher intake of PUFA, because it was shown that an increase in PUFA intake of 1% of energy predicted an improvement of {approx}0.5 mmol/L glucose, of 4 pmol/L insulin, and of 1 score in HOMA-IR. This is in line with other findings showing that a diet higher in unsaturated fat may improve insulin resistance (28, 29) compared with a diet high in carbohydrate, even though the total fat content increased. Other trials have failed to find an effect of macronutrient composition on glucose metabolism (20, 30). Moreover, the MUFA diet may have exerted favorable effects on cardiovascular disease risk because the ratio of LDL to HDL improved significantly more with the MUFA diet than with either the LF diet or the control diet. Although no difference in energy intake was found between groups in the present study, long-term studies are needed to see whether a greater intake of MUFAs and PUFAs results in a higher energy intake and thus may counteract the potential favorable effects on risk of diabetes and cardiovascular disease.

The fatty acid composition in buttock fat was used as a dietary compliance marker, although this method has not yet been validated. The analyses showed a good correlation between the dietary fat and the fatty acid composition of the buttock, and we believe that this method is representative of the recent intake of fat. The fatty acid composition in fat biopsy samples is believed to reflect the intake of dietary fat over a long period, especially with regard to PUFAs (31-35). SFAs and MUFAs are not generally considered to be good biomarkers of intake, because they are also endogenously synthesized. However, changes can be reflected if the diets are controlled for all macronutrients and if the fatty acids of interest differ considerably between the diets (36). In the present trial, the dietary fat intake monitored in the supermarket during the first 6 mo of the intervention generally correlated well with changes in the fatty acid composition of body tissue. The fatty acid composition of the tissue was also expected to reflect the dietary fat intake because (on average) a net regain in body fat occurred in all groups during the dietary intervention after the initial {approx}30% loss of body fat mass. Compliance was also aided by the fact that all of the diets were ad libitum, all of the foods were free of charge, and the use of the supermarket model made it possible to create an environment similar to free-living conditions for prolonged study periods (12). Additional strengths of this study include its study design, the number of diets compared simultaneously, and the relatively high overall retention rate after 6 mo (81%).

The larger drop-out rate in the MUFA group than in the control group was presumably due to a lower acceptance of a less common diet that was high in vegetable fat by our northern European population. In contrast, a 19% lower completion rate was seen in the low-fat group than in the moderate-fat group in a similar trial by McManus et al (17). These observations support the premise that one diet does not fit all and that it is important to consider cultural habits and food preferences to maximize long-term adherence (37).

In conclusion, none of the tested diets were superior to one another in maintaining weight loss. The favorable effects of a low-fat diet (ie, lower body fat regain) and of the new Healthy Eating Pyramid diet (on diabetes and cardiovascular disease risk factors) may not turn out to be very important if the weight is eventually regained. The real challenge is to maintain body weight loss and to prevent subsequent relapse. We need to look further than diet composition and other factors such as physical activity, and eating behavior needs to be taken into consideration for the prevention of obesity.


   ACKNOWLEDGMENTS
 
We thank the project staff of the Department of Human Nutrition. Special thanks go to Walter Willett (Department of Epidemiology and Nutrition, Harvard School of Public Health, Boston, MA) and David Ludwig (Department of Medicine, Children's Hospital, Boston, MA) for participating in the design of the project and David Allison and Miguel Padilla (Department of Biostatistics, University of Alabama at Birmingham) for the ITT analysis.

The authors' responsibilities were as follows—AD and TML: had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis; AA, TML, and AD: study concept and design; AD and TML: data acquisition; AD, TML, HM, KH, SS, and AA: analysis and interpretation of data; AD, TML, and AA: drafting of the manuscript; AD, TML, HM, KH, SS, and AA: critical revision of the manuscript for important intellectual content; AD: statistical analysis; AA, TML and AD: obtained funding; AD, TML, HM, KH, SS, and AA: administrative, technical, or material support; and AA: study supervision. No sponsor participated in the analysis or interpretation of the data, manuscript preparation, review, or approval, or the decision to publish. None of the authors reported any conflicts of interest.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
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Received for publication November 29, 2007. Accepted for publication June 16, 2008.


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