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Prospective study of dietary energy density and weight gain in women^1,2,3,4

¹ From the Department of Nutrition, Harvard School of Public Health, Boston, MA (MB-R, RMvD, TYL, LLS, and FBH); the Department of Preventive Medicine and Public Health, University of Navarra, Navarra, Spain (MAM-G and MB-R); and the Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, MA (RMvD and FBH)

² The funding organizations had no role in the design and conduct of the study; in the collection, analysis, and interpretation of the data; and in the preparation, review, or approval of the manuscript.

³ Supported by NIH grants CA50385, HL60712, and P30 DK46200. MB-R was supported by a grant from the Spanish Ministry of Education, Fundacion Caja Madrid, and Amigos de la Universidad de Navarra. FBH was the recipient of an American Heart Association–established Investigator Award.

⁴ Reprints not available. Address correspondence to FB Hu, Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA. E-mail: frank.hu{at}channing.harvard.edu.

	ABSTRACT

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

 
Background: Little is known about the long-term effects of dietary energy density (ED) on weight gain.

Objective: The objective was to assess the long-term relation between changes in dietary ED and age-related weight gain.

Design: We conducted a prospective study of 50 026 women ( ± SD age: 36.5 ± 4.6 y) in the Nurses’ Health Study II followed from 1991 to 1999. Dietary ED and body weight were ascertained in 1991, 1995, and 1999. Total dietary ED was calculated by dividing each subject's daily energy intake (kcal) by the reported weight (g) of all foods consumed.

Results: Dietary ED was positively correlated with saturated fat (r = 0.16), trans fat (r = 0.15), and the glycemic index (r = 0.16), but was inversely correlated with vegetable protein (r = –0.30), vegetables (r = –0.27), and fruit (r = –0.17). ED was not significantly correlated with total fat intake as a percentage of energy (r = 0.08). Women who increased their dietary ED during follow-up the most (5th quintile) had a significantly greater multivariate-adjusted weight gain than did those who decreased their dietary ED (1st quintile) (8-y time period: 6.42 kg compared with 4.57 kg; P for trend < 0.001). However, the amount of weight change over time varied considerably according to the ED values of individual foods and beverages.

Conclusion: A high dietary ED reflects a dietary pattern higher in saturated and trans fats and refined carbohydrates. Increases in dietary ED were associated with greater weight gain among middle-aged women during 8 y of follow-up. However, public health recommendations cannot be made simply on the basis of ED values of individual foods and beverages.

	INTRODUCTION

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Currently, obesity is one of the most important public health problems worldwide (1, 2). According to the latest estimates from the World Health Organization (WHO), 1.6 billion adults were overweight and 400 million were obese in 2005 (3). Because of the magnitude of the problem, it is important to develop effective practical strategies to prevent age-related weight gain (4). Obesity is the result of a long-term and sustained energy imbalance. Therefore, there has been an increasing interest in understanding factors that contribute to positive energy balance. One factor has been the energy density (ED) of the diet, which is defined as the amount of energy in a given weight of food (5). Diets with a low ED provide less energy per gram than do diets with a high ED (5). In short-term laboratory studies, subjects tended to consume a similar weight of food rather than a constant amount of energy (6). Consequently, high-ED diets may lead to "passive over-consumption" and increases in body weight. The WHO suggests that increased consumption of energy-dense diets contributes to the obesity epidemic (7). Likewise, the 2005 US Department of Agriculture Dietary Guidelines for Americans and the Centers for Disease Control and Prevention recommend consuming low-ED diets as an important part of a weight-management strategy (8, 9).

Despite these recommendations, surprisingly little is known about the long-term relation between dietary ED and subsequent weight gain in free-living populations (10). Whereas some cross-sectional studies have found a positive association between ED and body mass index (BMI) or body weight (11-16), others have not (17-19). In addition, despite a positive short-term relation between ED and energy intake, it is unclear whether compensation (ie, reduction in subsequent energy intake) occurs over the long term. So far, only 2 prospective studies have examined the relation between ED and weight change, and the results are inconsistent (20, 21). Therefore, the objective of this study was to assess the long-term relation between changes in dietary ED and age-related weight gain in a large prospective cohort of young and middle-aged women.

	SUBJECTS AND METHODS

TOP ABSTRACT INTRODUCTION SUBJECTS AND METHODS RESULTS DISCUSSION REFERENCES

 
Study population
The Nurses’ Health Study II is a prospective cohort study of 116 671 female US nurses aged 24–44 y at study initiation in 1989. This cohort was followed via the use of biennially mailed questionnaires with a follow-up rate exceeding 90% for every 2-y period. Participants completed self-administered food-frequency questionnaires (FFQs) in 1991, 1995, and 1999. For the present analysis, women were excluded from the baseline population if they did not complete dietary questionnaires in 1991, if >9 food items were left blank (participants with 1–9 missing items were retained in the analytic sample and were treated as non-consumers for the missing items); if they reported unreasonable energy intakes (<500 or >3500 kcal/d); if they had a history of diabetes or cardiovascular disease or reported a diagnosis of cancer (except nonmelanoma skin cancer) before 1999; if they had no data on physical activity assessed in 1991 or 1997; if they were pregnant at the time of the 1991, 1995, or 1999 questionnaire administration; or if they provided only 1991 baseline data. Those who did not provide information on weight at any time period were also excluded. These exclusions left a total of 50 026 women for the analyses. The Human Subjects Committees of the Harvard School of Public Health and Brigham and Women's Hospital approved the study protocol.

Dietary assessment
In 1991, the mailed questionnaire included a 133-item semiquantitative FFQ to obtain dietary information. Women were asked how often they had consumed a commonly used unit or portion size of each food on average over the previous year. The participants chose from 9 possible responses ranging from never to 6 times/d. Similar FFQs (more detailed items on low-fat foods were included in later FFQs) were used to collect dietary information in 1995 and 1999. Dietary ED was calculated by dividing each subject's daily intake (kcal) by the reported weight (g) of all foods consumed based on the serving size and daily frequency of consumption. Caloric and noncaloric beverages were excluded from the calculation (22) because energy intake from beverages is regulated differently from energy intake from foods (23). In addition, this method of calculating dietary ED has been demonstrated to provide the best correlations to measures of obesity in previous cross-sectional studies (12, 22). However, in a secondary analysis, we included caloric beverages in the calculation of dietary ED. We calculated the energy intake by multiplying the frequency of consumption by the calorie content of each food item and then adding the contribution from all food items. To assess the weight of all food consumed, we multiplied the frequency of consumption by the specified portion size of each food item (in g) and then summed all values. The food-composition database used to calculate the caloric values was based primarily on US Department of Agriculture data (24) and was supplemented with the manufacturers’ data. The validity and reliability of FFQs similar to those used in the Nurses’ Health Study II were described elsewhere (25).

Assessment of nondietary exposures
Through biennial questionnaires, we collected information on age, weight, smoking status, oral contraceptive use, hormone replacement therapy, and pregnancies. The validity of self-reported weight was evaluated previously in the original Nurses’ Health Study (26). The correlation coefficient between self-reported weight measurements and the average of 2 technician measurements was 0.97.

Physical activity was assessed with the 1991 and 1997 questionnaires and was computed as a metabolic equivalent (MET) index per week by multiplying the time spent engaging in various forms of exercise by the MET score specific for each activity. MET-hours for all activities were combined to obtain a value of total weekly MET-hours, which adequately correlated with energy expenditure measured in diaries or by recalls (0.62 and 0.79, respectively) (27).

Statistical analysis
We calculated Pearson correlation coefficients between dietary ED and consumption of each food item. We presented the top 15 positive and negative correlations. We used multiple approaches to assess the relation between dietary ED and body weight or BMI. In all analyses, we modeled the main exposure variable in quintiles (by including 4 dichotomous indicator variables in the model) to avoid a linearity assumption and to reduce the effect of outliers. First, we calculated the least-squares means for changes in body weight from 1991 to 1995, 1995 to 1999, and 1991 to 1999 across quintiles of changes in dietary ED for each period. We adjusted for age, alcohol intake, physical activity, smoking, and other lifestyle and dietary confounders at baseline for each time period. We also adjusted for changes in these covariates and changes in soft drink consumption, which were associated with weight gain in this cohort (28) and other cohorts (29). Tests of linear trend across quintiles of dietary ED were performed by assigning the median values for each quintile and treating them as continuous variables.

We also classified participants according to categories of changes in ED across 3 time periods (1991–1995, 1995–1999, and 1991–1999): consistent in the lowest quintile, consistent in the highest quintile, moving from the lowest to the highest quintiles (Q4 or Q5), and moving from the highest to the lowest quintiles (Q1 or Q2) and others. We estimated the mean weight change for each of these groups and conducted a stratified analysis by baseline BMI.

To take into account the effects of overall dietary patterns, we conducted additional analyses to adjust for changes in prudent and Western dietary patterns based on the results from principal component analysis of the 39 predefined food groups using the PROC FACTOR procedure in SAS (version 9; SAS Institute, Cary, NC) (30, 31).

To differentiate the effects of overall dietary ED and specific ED values of individual food items, we ranked the foods from the lowest to the highest ED values. For each food item, we fitted a linear regression model with weight change as the outcome and tertiles of change in the consumption of each food as the exposure, adjusting for relevant confounders. We represented graphically in the y axis the regression coefficients (β) and their 95% CIs of the weight gain for the highest tertile of change in each food item consumption during follow-up (1991–1999) relative to the first tertile of change. The purpose of this analysis was to assess whether there was any clear pattern between ED values of individual foods and beverages and the magnitude of weight change. All P values presented are 2-sided, and P values < 0.05 were considered statistically significant.

	RESULTS

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The mean (± SD) 8-y (1991–1999) weight gain was 5.44 ± 7.37 kg among 50 026 women ( ± SD age: 36.5 ± 4.6 y). The mean (± SD) baseline ED was 1.15 ± 0.39 kcal/g. During 8 y of follow-up, the average change in dietary ED was 0.47 ± 0.44 kcal/g. Participants with a higher dietary ED consumed more calories and a lower total weight of food than participants with a lower ED (Table 1). Saturated fat, trans fat, and the glycemic index were positively correlated with dietary ED (r = 0.16, 0.15, and 0.16, respectively), whereas vegetable protein intake, vegetables, and fruit consumption were inversely associated with ED (r = –0.30, –0.27, and –0.17, respectively). Total fat (as a percentage of energy) was minimally correlated with dietary ED (r = 0.08). A higher dietary ED was associated with a higher consumption of soda and red meat and lower consumption of fruit, vegetables, legumes, whole grains, and white meat (poultry) (Table 1). The types of food most inversely related to dietary ED were fruit and vegetables. By contrast, sweets and processed meat were most positively associated with dietary ED (Table 2).

Table 3

Table 4

Table 5

In addition, we conducted a secondary analysis by including caloric beverages in the definition of ED and found somewhat weaker associations. During the 8-y period, the mean adjusted weight changes were 5.23, 5.19, 5.38, 5.46, and 5.93 kg, respectively, across the quintiles of change in dietary ED (P for trend < 0.001). When we included in the definition of ED all beverages, similar results were obtained: for the 8-y period, the mean adjusted weight changes were 4.71, 5.08, 5.40, 5.70, and 6.30 kg (P for trend < 0.001), respectively, across the quintiles of change in dietary ED.

The amount of weight change over time varied considerably according to the ED of individual foods and beverages (Figure 1). The top food and beverage items that were associated with the greatest weight gain included regular soda, white bread, caffeine-free soda, French fried potatoes, fruit punches, chowder, crackers, candy bars, doughnuts, and bacon. Some foods with relatively high ED values, such as oil and vinegar salad dressing, olive oil salad dressing, and nuts, were not associated with greater weight gain or were associated with slightly reduced weight.

View larger version (13K): [in this window] [in a new window]   FIGURE 1.. Adjusted estimates [regression coefficients (β) and 95% CIs] of 8-y weight change (kg) for the highest tertile of change in consumption of each food item compared with the lowest tertile. Food items were ranked from the lowest (left) to the highest (right) energy density values. Estimates were adjusted for age, physical activity, smoking, postmenopausal hormone use, oral contraceptive use, baseline BMI, and changes in confounders between time periods (except BMI).

	DISCUSSION

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Several cross-sectional studies have evaluated the association between dietary ED and body weight. In the Multiethnic Cohort, Howarth et al (11) calculated ED from responses to an FFQ in 191 023 participants. After potential confounders were adjusted for, a higher ED was associated with a higher current BMI in each ethnic-sex group. In an analysis of US adults older than 20 y from the 1999–2002 National Health and Nutrition Examination Survey (n = 9688), dietary ED was independently associated with a higher BMI (12). Ledikwe et al (13) conducted a cross-sectional survey of adults (n = 7356) from the 1994–1996 Continuing Survey of Food Intakes by Individuals and found that the ED for obese subjects tended to be slightly higher than that for normal-weight people. A similar association was found among participants from the NHANES III (14), in a free-living sample of Chinese adults (15), and in 1136 female Japanese dietetic students (16). However, 3 cross-sectional studies reported no appreciable association between dietary ED and weight, percentage body fat, or BMI (17-19). Cross-sectional studies may have been affected by reverse causation bias: individuals who increased their weight may have reduced their dietary ED in the belief that it will help them to reduce energy intake and lose more weight.

Limited prospective data are available on the relation between dietary ED and subsequent weight gain. Iqbal et al (20) examined this association among Danish participants of the MONICA study (n = 862 men and 900 women). In the overall cohort, ED at baseline was not substantially associated with 5-y weight gain. In women, ED was positively associated with 5-y weight gain among the obese and was inversely associated with weight gain in normal-weight women, whereas no significant interaction with baseline weight was observed among men. However, this study measured dietary intake at baseline only. Our results showed that women who increased their dietary ED had a greater weight gain than did those who decreased their ED. Interestingly, women who maintained a high ED experienced a lower weight gain than did women who maintained a low ED. It is possible that participants with a constantly high dietary ED might compensate better for the energy intake from a high-ED diet. Another possibility is that the trajectory of weight gain for those participants has already reached a steady state after long-term consumption of a high-ED diet.

In the post hoc analyses of the PREMIER trial, Ledikwe et al (21) found that reductions in dietary ED were associated with greater weight loss in overweight and obese participants with prehypertension or hypertension (n = 658) during 6 mo of follow-up. The reductions in ED were primarily achieved by the implementation of the Dietary Approaches to Stop Hypertension Trial (DASH) diet, which promotes a higher intake of fruit and vegetables. In a 1-y randomized trial, Ello-Martin et al (33) found that reductions in dietary ED via reductions in fat intake and increases in intakes of water-rich foods, particularly fruit and vegetables, led to a greater weight reduction in obese women. However, interpretation of this study was complicated by the lack of a control group with high ED and a substantial increase in physical activity levels in both intervention groups. In a recent randomized clinical trial of breast cancer survivors, reducing dietary ED had no appreciable effects on body weight (34).

The cross-sectional analysis of baseline characteristics showed an inverse association between weight or BMI and dietary ED (Table 1). This cross-sectional correlation should be interpreted cautiously because it might be a result of reverse causation: subjects who are overweight or obese tend to reduce their ED. Therefore, it is important to assess changes in ED as the relevant exposure in relation to weight change over time using prospective data.

Some degree of measurement error in the assessment of dietary ED by a semiquantitative FFQ is inevitable. This is expected in nutritional assessments in free-living populations, no matter what types of instrument are used. However, the FFQ remains the best available method for assessing long-term diet in large epidemiologic studies such as ours (35). It should be noted that several previous studies have also used FFQs to assess ED (11, 16).

A major consideration in evaluating ED and obesity in epidemiologic studies is whether or not to include beverages in the calculation of dietary ED. We conducted secondary analyses by including caloric beverages in the definition of ED and found somewhat weaker associations. Because of the large amount of water in beverages, they typically have a very low ED, even though their sugar and calorie content is high (eg, sugar-sweetened beverages).

Translating the results of short-term studies on the relation between ED and body weight into dietary practice is challenging because of the large variability of ED values of individual foods and beverages that may comprise a high- or a low-ED diet. Freely selected high-ED diets may differ considerably in foods and nutrient composition between populations. Energy-dense diets are often high in refined grains, added sugars, and added fats (12). In fact, foods with the highest positive correlations with dietary ED were generally highly processed products low in fiber and rich in saturated and trans fats (eg, cookies, crackers, pancakes, waffles, and processed meats). Therefore, they have been associated with increased energy intake and poor diet quality (36, 37). From this perspective, a high-ED diet may represent poor diet quality. However, diets with a moderately high-fat content are not necessarily energy-dense. For example, the traditional Mediterranean diet is largely based on energy-diluted foods such as vegetables, fruit, and legumes. Indeed, the consumption of olive oil–based salad dressings in our cohort was negatively associated with dietary ED (r = –0.10). These results suggest that the effects of ED for individual foods depend on the context of their use. An increase in the consumption of nuts, which are energy-dense, was also not associated with greater weight gain. These findings are consistent with results from a Mediterranean cohort in which higher consumption of olive oil was not associated with weight gain (38), whereas a higher consumption of nuts was actually associated with less weight gain in the same cohort (39). Moreover, many processed foods high in fat and sugar are energy-dense, but at the same time are palatable, convenient, and inexpensive. Thus, ecological analyses have suggested a close relation between high-ED diets and low-energy cost (dollars per megajoule), which may contribute to higher obesity rates among socioeconomically disadvantaged populations (40).

The results of this study suggest that dietary ED reflects a poor diet quality characterized by higher intakes of saturated and trans fats and a higher glycemic load. The positive association between changes in dietary ED and weight gain observed in this study is thus likely to represent the effects of an overall dietary pattern rather than physiologic effects of ED per se. When each food and beverage was evaluated individually, the amount of weight changes over time varied considerably according to the ED value of individual foods and beverages. Changes in the consumption of some foods and beverages with low ED values, such as soda, fruit punches, and potatoes, were associated with greater weight gain, whereas changes in consumption of some foods with relatively higher ED values, such as olive oil and nuts, were not associated with weight gain. Therefore, it would be misleading to recommend foods solely based on ED values of individual foods and beverages. On the basis of our data, the best way to reduce total dietary ED is to reduce consumption of foods with a high amount of saturated fats and refined carbohydrates and to increase the consumption of fruit and vegetables. However, a reduction in the total amount of fat is unlikely to alter the overall dietary ED value. Furthermore, reducing the consumption of soft drinks, which have a low ED, is associated with lower weight gain in both children and adults (41).

In conclusion, an increase in dietary ED over 8 y was independently associated with a significantly higher weight gain in healthy middle-aged women. These results suggest that a reduction in the overall dietary ED, through a decreased consumption of foods with a high amount of saturated fats and refined carbohydrates and an increased consumption of fruit and vegetables, may be beneficial for weight control, especially for overweight and obese individuals.

	ACKNOWLEDGMENTS

 
The authors’ responsibilities were as follows—MB-R: participated in the conception and design, statistical analysis, data interpretation, manuscript writing, and critical revision of the manuscript for important intellectual content; RMvD and MAM-G: participated in the conception and design, data interpretation, and critical revision of the manuscript for important intellectual content; TYL: participated in the statistical analyses; LLS: participated in the data collection and interpretation; and FBH: obtained funding and participated in the concept and design, data interpretation, and critical revision of the manuscript for important intellectual content. All authors approved the final version of the manuscript.

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