Role of Dietary Factors and Food Habits in the Development… : Journal of Pediatric Gastroenterology and Nutrition


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    Obesity is the most prevalent nutritional disorder among children and adolescents throughout the world (1,2). Notwithstanding recent reports suggesting a levelling off of the prevalence of obesity in some countries (3–5), the burden of paediatric obesity for society is still high (6–8). In addition to short-term complications such as psychosocial disturbances or orthopaedic problems, the origins of potential long-term metabolic consequences are also identifiable in many obese children (9). It is well established that obesity is a multifactorial disease in which genetic as well as psychological and environmental causative factors are implicated, with diet and physical inactivity looming large.

    The focus of this comment is to assess the role of dietary factors and food habits in the prevention of obesity in childhood. For the roles of physical activity and sedentary behaviour, we refer readers to available reviews and position papers (10–13). The treatment of obesity is also beyond the scope of this Comment. For the role of dietary interventions in the treatment of obese children, we refer readers to a recent Cochrane review (14). Finally, the role of early nutrition in obesity development is not covered because nutrition during the first year of life has been extensively discussed in 2 recent comments published by the European Society for Paediatric Gastroenterology, Hepatology, and Nutrition Committee on Nutrition (15,16). In summary, it was stated that the potential for breast-feeding to contribute to reduction of later obesity should be explored in more detail, and that the available evidence on how complementary feeding influences later obesity risk is not conclusive.

    This Comment aims to provide a state-of-the-art summary on the role of nutrition-related factors that may contribute to the development of obesity in children ages 2 to 18 years. This Comment also provides recommendations on healthy nutrition patterns with the potential to decrease obesity risk to be promoted by paediatricians and other health care professionals.


    Although the gap between energy input and energy expenditure plays a major role in the development of obesity (17), energy balance is far more complex than this model suggests (18). There are paradoxical reports of reduced energy intakes in children who were already obese and/or overweight, pointing to the importance of energy expenditure (19) and the possibility of reverse causation. Reports on preventive interventions have also emphasized the role of a regular decreased daily energy intake (ranging from 100 to 150 kcal/day) to counterbalance the energy gap and its possible role in obesity (20,21). Lack of consistency between observations has raised methodological questions with regard to the adequacy of dietary surveys, given the trend to underreport dietary intakes in obese subjects, and the possible role of nutrient imbalances (eg, the quality of fats vs their quantity) (22,23). Because fats are the major source of energy, inaccurate recording of intake could lead to as much as a 2-fold error when determining their contribution to overall energy intake. Nevertheless, examining the differences in energy intakes and/or energy balance should be given priority in studies on the dietary determinants of overweight and obesity.

    Recommendation Considering the multiple factors involved in energy balance, energy intake should be individually determined, taking into account energy expenditure and growth.


    The role of particular macronutrients (as total or relative percentage of energy intake) in the aetiology of obesity is poorly understood. This is due in part to the complex interrelation between dietary carbohydrate (CHO), protein, and fat, given that when the intake of 1 macronutrient changes, the intake of the other 2 also changes as a consequence.

    Carbohydrates and Fibre

    The intake of simple CHO has been proposed to be associated with adiposity development, whereas slowly absorbed CHO (low glycaemic index) could be protective (24). In adults, observational studies suggest a possible relation between consumption of sugar-sweetened beverages and body weight, but there is insufficient supporting evidence from randomised controlled trials of adequate size and duration (25).

    Rapidly digested carbohydrates produced lower satiety in normal-weight and obese children (26), whereas low-glycaemic-index foods eaten at breakfast had a significant impact on food intake at lunch, when intake was reduced after low- compared with after high-glycaemic-index breakfasts (27). Accordingly, the independent roles of breakfast and CHO-based foods within breakfast in satiety need to be defined to develop obesity prevention strategies (28).

    Buyken et al (29) prospectively examined whether dietary glycaemic index, glycaemic load, added sugar intake, or fibre intake between ages 2 and 7 years is associated with the development of a particular body composition, and if so, to ascertain whether these associations are modified by meal frequency. They observed that neither dietary glycaemic index nor glycaemic load or added sugar intake appeared to significantly influence changes in body composition. It is possible that potential benefits associated with increasing fibre intake throughout childhood could be limited to toddlers with a lower meal frequency (29).

    Recommendation The ingestion of slowly absorbed CHO should be promoted, while limiting the supply of rapidly absorbed CHO and simple sugars.


    Fats are the main energy contributors to the diet on a volume intake basis: They are twice as energy dense as carbohydrates or proteins, and the energy cost of storage of the energy contained in fats is about one-tenth that for carbohydrates or proteins (30).

    Enhanced percentage fat intake was significantly related to increased relative body weight (31), body fat mass (32), and body fat content (33) in large groups of children. However, equivocal results were found when groups of children were subdivided according to sex: significant positive correlations were found between dietary fat intakes and body fat mass in boys, but not in girls (3,34,35). It is important to note that other observational studies failed to find a relation between fat intake and the development of obesity (36,37).

    The only available intervention study suggests that modification of fat intake may decrease the risk of obesity. When infants were randomly assigned at the age of 7 months to dietary counselling with the aim of reducing total fat and substituting unsaturated products instead of saturated fats, the proportion of overweight girls was significantly lower in the intervention group than in the control group when followed up at the age of 10 years (38).

    Experimental evidence suggests that polyunsaturated fatty acids of the omega-6 series may promote both adipogenesis in vitro and adipose tissue development in vivo in rodents during the gestation/lactation period (39). Small observational studies found significant differences in plasma linoleic acid, arachidonic acid, and the sum of omega-3 polyunsaturated fatty acids between obese and nonobese children (40,41), but these data do not allow inferences on causality considering also the potential role of the subinflammatory status associated with obesity (42).

    A review concluded that the role of dietary fat types as early determinants of childhood obesity is poorly understood (43). The potential for medium-chain triglycerides, conjugated linoleic acid (CLA), and omega-3 long-chain polyunsaturated fatty acids to modulate food intake has been explored (44), and supplementation of CLA was recently reported to significantly attenuate body fat deposition in overweight or obese prepubertal children (45). However, safety and efficacy of such interventions require careful scrutiny in the paediatric age group (46,47).

    Further paediatric data are needed on the effects of total fat consumption and the potential role of dietary fat quality and composition on the development of childhood obesity.

    Recommendation It is likely that total fat intake and specific dietary lipids play a role in the development of obesity. However, the paucity of available data does not support recommendations on fat quantity and quality in relation to obesity prevention.


    Dietary proteins and specific amino acids (particularly arginine, alone or in combination with lysine) have been shown to stimulate the somatotropic axis and may thereby influence body composition (48,49). Growth hormone (GH) plays an important role in reducing fat mass, with studies showing increased lipolysis and decreased fat mass after GH administration (50).

    Agostoni et al (51) suggested that a positive correlation between high protein intake and later obesity occurs mainly in populations with protein intake higher than 15% to 16% of total energy intake. When compared with a low-protein, high-fat intake diet, a high-protein, low-fat diet was associated with an earlier adiposity rebound (defined as the rise in body mass index [BMI] curve normally occurring at 5–7 years of age), which has been shown to be associated with the development of obesity (52). The analysis of data from the German DONALD study suggests that animal but not vegetable protein intakes in early childhood may play a role in later overweight and adiposity (53).

    In contrast, in a cohort of healthy Danish girls, a high protein intake was associated with a decrease in body fat and an increase in fat-free mass, depending on the available amounts and combinations of arginine and lysine (49). In another Danish cohort study (54), linear growth in prepubertal girls was influenced by habitual arginine intake, whereas body fat gain was inhibited by the intake of arginine and lysine. Further research should explore the role of specific amino acids on weight gain and body composition.

    Recommendation The evidence associating protein intake and obesity in children older than 2 years of age is inconsistent and does not allow firm conclusions and recommendations.



    Dietary calcium intake has been suggested to be negatively associated with the development of obesity. One possible mechanism is reduced intestinal fat absorption. Several studies in both animals and humans have shown that calcium increases the excretion of fat, presumably by formation of insoluble calcium fatty acid soaps or binding of bile acids that impair the formation of micelles (55–57). Another mechanism could be the regulatory influence of intracellular calcium on fat metabolism by modifying lipolysis, fat oxidation, and lipogenesis (55–58).

    Despite the above, findings in children and adolescents are inconsistent. Epidemiological data both support (59–63) and refute (64–66) an association between calcium or dairy product intake and the development of obesity. In a cross-sectional study in healthy premenarcheal girls (67), an inverse association between calcium intake and body fat content appeared to result from avoidance of foods high in calcium by girls who were concerned about their body weight or shape. In the longitudinal part of this study, calcium intake was not associated with changes in body fat content over time (67).

    Randomised trials conducted to examine the effects of calcium or dairy product supplementation on bone mineral accretion have not detected differences in weight gain between supplemented and control children (68,69). Studies that supplemented the diet of children with dairy products instead of elemental calcium are difficult to interpret, because energy and protein intakes may have also increased in the supplemented groups, thus obscuring any differential effects on changes in weight or body fat.

    Recommendation Available evidence does not allow recommendations on the role of calcium or dairy products in the development of obesity.

    Dietary Modulators of Gut Microbiota

    Recent evidence, primarily from investigations in animal models, suggests that the gut microbiota affects nutrient acquisition and energy regulation (70). In both animals and humans its composition has been shown to differ in the lean and obese (71,72). Interestingly, the gut bacterial flora of obese mice and humans include fewer Bacteroidetes and correspondingly more Firmicutes than that of their lean counterparts, suggesting that caloric extraction of ingested food may indeed be influenced by the composition of the gut microbiota (73). There are no data on the effect of any dietary factor, including prebiotics and probiotics, on the prevention of obesity by modulating gut microbiota.

    Recommendation No dietary modulators of gut microbiota can be recommended for obesity prevention.

    Plant Foods: Vegetarian Diets

    Plant-based diets are low in energy density and high in complex carbohydrates, fibre, and water, which may increase satiety and resting energy expenditure. Two recent reviews deal with the relation between plant food and childhood obesity (74,75). Newby concluded there was no relation between childhood obesity and fruit and vegetables; insufficient evidence regarding beans, legumes, and soy; and slight protection with grains and breakfast cereals, fibre, and plant-based dietary patterns (74). Most of the studies reviewed were cross-sectional, failed to adequately adjust for potential confounders, and did not consider the influence of reporting errors.

    Sabaté and Wien (75) explored the concept of plant-based diets because several studies showed that vegetarians were leaner than their nonvegetarian peers (76,77). In their review, they concluded that animal foods (meats and dairy products/eggs) were associated with an increased risk of overweight, whereas plant foods were either protective (cereals, legumes, and nuts) or showed no association (fruit/vegetables and vegetable protein products).

    Inadequate intake of energies, protein, calcium, zinc, iron, vitamin B12, and vitamin D related to plant-based diets may occur on a vegetarian diet because of a poor choice of foods and because of high nutritional requirements related to growth and development. Thus, when implementing such diets, appropriate planning (taking into account recommended macro- and micronutrient intakes) and monitoring (growth, zinc, iron, vitamin B12, and vitamin D) should be undertaken by a health care professional.

    Recommendation Plant foods can be used as the main food contributors to a well-balanced diet. When a vegetarian diet is practiced, appropriate planning (taking into account recommended macro- and micronutrient intakes) and monitoring (growth, zinc, iron, vitamin B12, and vitamin D) should be undertaken by a health care professional.


    The majority of studies classify the following as sugar-added beverages: any sugar-sweetened or artificially sweetened fruit-flavoured drinks, sports (natural or artificial) drinks, and drinks that contain 100% fruit juice; carbonated sodas that include sugar or artificial sweetener, caffeinated or decaffeinated; and sugar-sweetened or artificially sweetened, caffeinated or decaffeinated tea or coffee (78).

    Two reviews (79,80) systematically addressed the relation between sugar-added beverages and obesity. The first (79) included cross-sectional, longitudinal, and intervention studies, both in children and in adults, and the second (80) included only longitudinal and randomised controlled trials in children and adolescents. Malik et al (79) concluded that sufficient evidence exists for public health strategies to discourage consumption of sugary drinks. Forshee et al (80) concluded that both quantitative meta-analysis and qualitative review found practically no association between sweetened beverage consumption and BMI. The different conclusions can be explained by different study populations, different methodology, and confounding variables. For example, the randomised controlled trial of James et al (81) showed that the percentage of overweight and obese children increased in the control group by 7.5%, and decreased in the intervention group (reduced sweetened beverage consumption) by 0.2%; however, those differences could not simply be attributed to a decline in the consumption of high-calorie sodas. Moreover, Ebbeling et al (82) observed that although energy intakes from high-calorie beverages dropped by 82% in the intervention group, the difference in BMI gain was not significant.

    Since these 2 reviews have been made available, other longitudinal and intervention studies on this topic have been published. Some support the association between sugar-sweetened beverages consumption and BMI (78,83,84), whereas other studies found no association (85,86). Recently, Muckelbauer et al (87) performed a combined environmental and educational intervention promoting water consumption among children in elementary school in a population from socially deprived areas. The intervention was successful in increasing water consumption and preventing overweight without an effect on juice and soft drink consumption.

    Overall, results are not conclusive. It is uncertain whether the critical factor is the sugar, energies, or behaviours related to beverage consumption. In addition, some foods frequently accompany certain sugar-sweetened beverages (88), and drinking these beverages may also lead to higher subsequent energy intakes due to producing lower satiety than energy consumed in solid form (89,90). Sugar-added beverages may also encourage additional energy intake because of their high glycaemic index (91). In addition, the high fructose content of many sweetened beverages has been linked to the obesity epidemic (92,93), although it is uncertain whether fructose itself is the culprit (93,94).

    Fruit juice also contains sugar and a similar energy density as many sugar-added beverages, but there is uncertainty on their effects. Although it is difficult to separate juices with or without added sugar using the conventional dietary assessment methods, fruit juice intake was not associated with obesity development in several longitudinal studies (78,85,95–100).

    Recommendation A relation between sugar-sweetened beverage consumption and development of obesity in children and adolescents has been reported in some studies, although conclusive evidence is not available. Sugar-sweetened beverages are a significant contributor to energy intake. The Committee therefore considers that plain water should be promoted as the main source of fluids for children.


    Eating Frequency

    Observations both in adult and child populations associate a lower number of daily meals with a higher risk of obesity (101,102). Several cross-sectional (103–107) and longitudinal studies (108,109) have addressed this issue in children. Cross-sectional studies showed inconsistent results. In the longitudinal studies, Thompson et al (108) observed that eating occasions between 4.0 and 5.9 times per day were negatively associated with changes in BMI z score, after controlling for baseline BMI z score. In both black and white girls ages 9 to 10 years, followed up for 10 years, Franko et al (109) found that participants who frequently ate more than 3 meals per day had lower BMI-for-age z scores than those eating fewer meals. Black, but not white girls, who frequently ate more than 3 meals per day, were less likely to meet criteria for overweight.

    Adolescents or adults who eat more frequently also exercise more and make healthier food choices (110), a possible source of confounding. Increased thermogenesis from consuming more meals could be a potential explanation, linking fat mass and meal frequency. However, there is ongoing controversy regarding this mechanism because studies on thermic effects of food do not point to different degrees of thermogenesis when comparing “nibbling” (consuming frequent small meals) and “gorging” (consuming infrequent large meals) (111).

    Recommendation Given the apparent inverse association between number of daily meals and obesity development, it is appropriate that children older than 2 years of age eat at least 4 meals per day. Whether eating 5 or more meals per day provides an additional contribution to the prevention of overweight/obesity remains to be elucidated.

    Skipping Breakfast

    Breakfast is usually defined as the meal eaten in the morning and the first meal of the day. Skipping breakfast has been suggested to be a risk factor for obesity (112). One systematic review (113) found that although breakfast eaters consumed more daily calories, they were less likely to be overweight. In a recent systematic review of studies performed in Europe, observational studies have consistently shown that children and adolescents who eat breakfast have a reduced risk of being overweight or obese and have a lower BMI compared with those who skip breakfast (114). Three of 4 longitudinal studies performed in the United States (115–118) also showed a relation between skipping breakfast and BMI gain (115–117).

    Children who skip breakfast regularly were found to consume a greater percentage of energy from fat (119) and snacks that are higher in fat (120). Skipping breakfast may be followed by increased appetite later in the day, producing overeating, or may promote choice of foods with higher energy density, leading to greater overall intake (121). Alternatively, because a person consumed a nutrient-dense diet, eating breakfast may boost the person’s ability to engage in regular physical activity (121).

    Recommendation Children should be encouraged to eat breakfast every day.

    Family Dinner

    Eating family dinner has been linked to healthy dietary intake patterns (122). Two longitudinal studies assessed the relation between family dinner and obesity development. One observed a positive relation, but only in whites, and the other only in the cross-sectional analysis and not in the longitudinal one.

    In adolescents between 12 and 15 years of age from the 1997 survey of the National Longitudinal Survey of Youth, Sen (123) observed that, for whites, higher frequency of eating dinner as a family was associated with reduced odds of being overweight, reduced odds of becoming overweight, and increased odds of ceasing to be overweight by 2000. No such associations were found for blacks and Hispanics. Taveras et al (124) found that young respondents who reported eating dinner with families all or most of the time were less likely to be overweight than counterparts who did so only some or none of the time at the baseline, but there was no statistical relation between family dinners and becoming overweight within 1 year. Conversely, in a 5-year longitudinal study of adolescents, Fulkerson et al (125) did not find any significant association between family dinner and obesity development.

    Family meals may therefore have relevance for the prevention and correction of childhood overweight. Regular family meals give parents the scope to provide their children with nutritious and healthy fare, to monitor and limit children’s intake of calorically dense and “junk” food, and to serve as role models for healthy eating behaviour (126).

    Recommendation Regular family meals should be encouraged.

    Consumption of Food From Fast-food Restaurants

    Characteristic qualities of fast foods include large portion size, high energy density, high content of saturated and trans fats, high glycaemic load, low content of fibre, and palatability (appealing to primordial taste preferences for fats, sugar, and salt), which may cause excessive weight gain (88). Few studies have examined the effects of fast-food consumption on any nutrition or health-related outcome. Three studies on the relation between fast food and obesity in children have been identified.

    Taveras et al (127) investigated a large cohort of children ages 9 to 14 years at baseline; BMI was obtained from self-reported height and weight. During a period of 1 year, high consumption of fried food away from home was associated with rising BMI compared with those with low consumption at baseline and 1 year later. In a prospective study of adolescents participating in surveys II and III of the National Longitudinal Study of Adolescent Health (116), more numerous days of fast-food consumption at survey II predicted increased BMI z score at survey III. Among healthy girls between the ages of 8 and 12 years at baseline and 11 and 19 years at follow-up, those who ate fast food twice per week or more at baseline had the greatest mean increase in BMI z score compared to those who ate fast food once per week or not at all (128). From the reviewed studies it can be concluded that increasing consumption of food from fast-food outlets is associated with excess weight gain.

    Recommendation Regular consumption of fast food with large portion sizes and high energy density should be avoided.



    Snacks can be defined as eating episodes, generally smaller and less structured than meals (129). Snack foods can be energy dense and of little nutritional value. They are readily available and consumed by children and adolescents in a variety of settings. Data from 3 cross-sectional studies showed that more frequent snacking intake was associated with a smaller risk of overweight or obesity in children (107,130,131). However, another cross-sectional study in schoolchildren from Colombia showed that the prevalence of overweight was positively associated with snack food intake. In that case, snack food consisted of high-energy sweets and beverages (132).

    Three longitudinal studies analysing the effect of snacking on obesity development suggest that low-nutritional-value snack foods were not an independent determinant of weight gain among children and adolescents (133–135). Overall, the available evidence is too limited to establish a relation between snack foods and obesity in children.

    Recommendation Healthy food options should be promoted for snacking.

    Food Portion Size

    The extent to which excessive food portions contribute to children’s energy intake and body weight has not been studied extensively. Some studies showed that portion size influence energy intake in children (136,137). In an experimental school lunch situation, the effect of portion size on food intake was influenced by age (138). In a similar study model, doubling an age-appropriate portion of an entrée increased entrée and total energy intakes at lunch by 25% and 15%, respectively; changes were attributable to increases in the average size of the children’s bites of the entrée without compensatory decreases in the intake of other foods served at the meal (139). In addition, 1 study showed that meal portion sizes were associated with BMI percentile in boys 6 to 11 years old and in children 12 to 19 years old (140) and another study showed that portion size and energy intake were positively associated with body weight (141).

    Recommendation Food portion sizes should be appropriate for age and body size.


    1. The origin of obesity is multifactorial. Dietary interventions should be incorporated into a multidisciplinary strategy for obesity prevention.
    2. No single nutrient has been unequivocally associated with the development of overweight and obesity.
    3. Methodological limitations in study design and the complex nature of obesity must be taken into account when interpreting the association with some of the reported dietary factors.
    4. Energy intake should be individually determined, taking into account energy expenditure and growth.
    5. Preferential intake of slowly absorbed carbohydrates, along with limiting the supply of rapidly absorbed carbohydrates and simple sugars, should be promoted.
    6. With respect to obesity prevention, no recommendations on fat quantity and quality, protein or amino acid intake, or calcium and dairy product intake can be made.
    7. No dietary modulators of gut microbiota can be recommended for obesity prevention.
    8. Plant foods can be used as the main food contributors to a well-balanced diet. When a vegetarian diet is practiced, appropriate planning (taking into account recommended macro- and micronutrient intakes) and monitoring (growth and potentially zinc, iron, vitamin B12, and vitamin D status) should be executed by a health care professional.
    9. Sugar-sweetened beverages are a significant contributor to energy intake. Plain water should be promoted as the main source of fluids for children.
    10. Children should eat at least 4 meals, including breakfast, every day. Regular family meals should be encouraged.
    11. Fast food with large portion sizes and high energy density should be avoided.
    12. Healthy food options should be promoted for snacking.
    13. Food portion sizes should be appropriate for age and body size.
    14. Nutrition and lifestyle education aimed at the prevention of obesity should be included in the routine care of children by general paediatricians and other health professionals.


    1. Wang Y, Lobstein T. Worldwide trends in childhood overweight and obesity. Int J Pediatr Obes 2006; 1:11–25. 2. Moreno LA, Pigeot I, Ahrens W. Epidemiology of Obesity in Children and Adolescents: Prevalence and Etiology. New York: Springer; 2011. 3. Ogden CL, Carroll MD, Flegal KM. High body mass index for age among US children and adolescents, 2003-2006. JAMA 2008; 299:2401–2405. 4. Sundblom E, Petzold M, Rasmussen F, et al. Childhood overweight and obesity prevalences levelling off in Stockholm but socioeconomic differences persist. Int J Obes (Lond) 2008; 32:1525–1530. 5. Péneau S, Salanave B, Maillard-Teyssier L, et al. Prevalence of overweight in 6- to 15-year-old children in central/western France from 1996 to 2006: trends toward stabilization. Int J Obes (Lond) 2009; 33:401–407. 6. Lobstein T, Baur L, Uauy R. Obesity in children and young people: a crisis in public health. Obes Rev 2004; 5(suppl 1):4–104. 7. Koletzko B, Girardet JP, Klish W, et al. Obesity in children and adolescents worldwide: current views and future directions—Working Group Report of the First World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition. J Pediatr Gastroenterol Nutr 2002; 35(suppl 2):S205–S212. 8. Fisberg M, Baur L, Chen W, et al. Obesity in children and adolescents: Working Group report of the second World Congress of Pediatric Gastroenterology, Hepatology, and Nutrition. J Pediatr Gastroenterol Nutr 2004; 39:S678–S687. 9. Ebbeling CB, Pawlak DB, Ludwig DS. Childhood obesity: public-health crisis, common sense cure. Lancet 2002; 360:473–482. 10. Reichert FF, Baptista Menezes AM, Wells JC, et al. Physical activity as a predictor of adolescent body fatness: a systematic review. Sports Med 2009; 39:279–294. 11. Strong WB, Malina RM, Blimkie CJ, et al. Evidence based physical activity for school-age youth. J Pediatr 2005; 146:732–737. 12. Rey-López JP, Vicente-Rodríguez G, Biosca M, et al. Sedentary behaviour and obesity development in children and adolescents. Nutr Metab Cardiovasc Dis 2008; 18:242–251. 13. Marshall SJ, Biddle SJ, Gorely T, et al. Relationships between media use, body fatness and physical activity in children and youth: a meta-analysis. Int J Obes Relat Metab Disord 2004; 28:1238–1246. 14. Oude Luttikhuis H, Baur L, Jansen H, et al. Interventions for treating obesity in children. Cochrane Database Syst Rev 2009;(1):CD001872. 15. Agostoni C, Decsi T, Fewtrell M, et al. Complementary feeding: a commentary by the ESPGHAN Committee on Nutrition. J Pediatr Gastroenterol Nutr 2008; 46:99–110. 16. Agostoni C, Braegger C, Decsi T, et al. Breast-feeding: a commentary by the ESPGHAN Committee on Nutrition. J Pediatr Gastroenterol Nutr 2009;49:112–25. 17. Wang YC, Gortmaker SL, Sobol AM, et al. Estimating the energy gap among US children: a counterfactual approach. Pediatrics 2006; 118:e1721–e1733. 18. Reilly JJ, Ness AR, Sherriff A. Epidemiological and physiological approaches to understanding the etiology of pediatric obesity: finding the needle in the haystack. Pediatr Res 2007; 61:646–652. 19. Troiano RP, Briefel RR, Carroll MD, et al. Energy and fat intakes of children and adolescents in the United States: data from the National Health and Nutrition Examination Surveys. Am J Clin Nutr 2000; 72(5 suppl):S1343–S1353. 20. Hill JO, Wyatt HR, Reed GW, et al. Obesity and the environment: where do we go from here? Science 2003; 299:853–855. 21. Plachta-Danielzik S, Landsberg B, Bosy-Westphal A, et al. Energy gain and energy gap in normal-weight children: longitudinal data of the KOPS. Obesity (Silver Spring) 2008; 16:777–783. 22. Voss S, Kroke A, Klipstein-Grobusch K, et al. Is macronutrient composition of dietary intake data affected by underreporting? Results from the EPIC-Potsdam Study. European Prospective Investigation into Cancer and Nutrition. Eur J Clin Nutr 1998; 52:119–126. 23. Goris AH, Westerterp-Plantenga MS, Westerterp KR. Undereating and underrecording of habitual food intake in obese men: selective underreporting of fat intake. Am J Clin Nutr 2000; 71:130–134. 24. Gibson LJ, Peto J, Warren JM, et al. Lack of evidence on diets for obesity for children: a systematic review. Int J Epidemiol 2006; 35:1544–1552. 25. Van Baak MA, Astrup A. Consumption of sugars and body weight. Obes Rev 2009; 10(suppl 1):9–23. 26. Alvina M, Araya H. Rapid carbohydrate digestion rate produced lesser short-term satiety in obese preschool children. Eur J Clin Nutr 2004; 58:637–642. 27. Warren JM, Henry CJ, Simonite V. Low glycemic index breakfasts and reduced food intake in preadolescent children. Pediatrics 2003; 112:e414. 28. Timlin MT, Pereira MA. Breakfast frequency and quality in the etiology of adult obesity and chronic diseases. Nutr Rev 2007; 65:268–281. 29. Buyken AE, Cheng G, Günther ALB, et al. Relation of dietary glycemic index, glycemic load, added sugar intake, or fiber intake to the development of body composition between ages 2 and 7 y. Am J Clin Nutr 2008; 88:755–762. 30. Pi-Sunyer FX. Metabolic efficiency of macronutrient utilization in humans. Crit Rev Food Sci Nutr 1993; 33:359–361. 31. Wardle J, Guthrie C, Sanderson S, et al. Food and activity preferences in children of lean and obese parents. Int J Obes Relat Metab Disord 2001; 25:971–977. 32. Johnson L, Mander AP, Jones LR, et al. Energy-dense, low-fiber, high-fat dietary pattern is associated with increased fatness in childhood. Am J Clin Nutr 2008; 87:846–854. 33. McGloin AF, Livingstone MB, Greene LC, et al. Energy and fat intake in obese and lean children at varying risk of obesity. Int J Obes Relat Metab Disord 2002; 26:200–207. 34. Nguyen VT, Larson DE, Johnson RK, et al. Fat intake and adiposity in children of lean and obese parents. Am J Clin Nutr 1996; 63:507–513. 35. Maffeis C, Provera S, Filippi L, et al. Distribution of food intake as a risk factor for childhood obesity. Int J Obes Relat Metab Disord 2000; 24:75–80. 36. Brixval CS, Andersen LB, Heitmann BL. Fat intake and weight development from 9 to 16 years of age: the European youth heart study—a longitudinal study. Obes Facts 2009; 2:166–170. 37. Alexy U, Sichert-Hellert W, Kersting M, et al. Pattern of long-term fat intake and BMI during childhood and adolescence—results of the DONALD Study. Int J Obes Relat Metab Disord 2004; 28:1203–1209. 38. Hakanen M, Lagström H, Kaitosaari T, et al. Development of overweight in an atherosclerosis prevention trial starting in early childhood. The STRIP study. Int J Obes (Lond) 2006; 30:618–626. 39. Ailhaud G, Guesnet P. Fatty acid composition of fats is an early determinant of childhood obesity: a short review and an opinion. Obes Rev 2004; 5:21–26. 40. Decsi T, Molnár D, Koletzko B. Long-chain polyunsaturated fatty acids in plasma lipids of obese children. Lipids 1996; 31:305–311. 41. Decsi T, Csábi G, Török K, et al. Polyunsaturated fatty acids in plasma lipids of obese children with and without metabolic cardiovascular syndrome. Lipids 2000; 35:1179–1184. 42. Klein-Platat C, Drai J, Oujaa M, et al. Plasma fatty acid composition is associated with the metabolic syndrome and low-grade inflammation in overweight adolescents. Am J Clin Nutr 2005; 82:1178–1184. 43. Macé K, Shahkhalili Y, Aprikian O, et al. Dietary fat and fat types as early determinants of childhood obesity: a reappraisal. Int J Obes (Lond) 2006; 30(suppl 4):S50–S57. 44. Li JJ, Huang CJ, Xie D. Anti-obesity effects of conjugated linoleic acid, docosahexaenoic acid, and eicosapentaenoic acid. Mol Nutr Food Res 2008; 52:631–645. 45. Racine NM, Watras AC, Carrel AL, et al. Effect of conjugated linoleic acid on body fat accretion in overweight or obese children. Am J Clin Nutr 2010; 91:1157–1164. 46. Wang YW, Jones PJ. Conjugated linoleic acid and obesity control: efficacy and mechanisms. Int J Obes Relat Metab Disord 2004; 28:941–955. 47. Toomey S, McMonagle J, Roche HM. Conjugated linoleic acid: a functional nutrient in the different pathophysiological components of the metabolic syndrome? Curr Opin Clin Nutr Metab Care 2006; 9:740–747. 48. van Vught AJ, Nieuwenhuizen AG, Brummer RJ, et al. Effects of oral ingestion of amino acids and proteins on the somatotropic axis. J Clin Endocrinol Metab 2008; 93:584–590. 49. van Vught AJ, Heitmann BL, Nieuwenhuizen AG, et al. Association between dietary protein and change in body composition among children (EYHS). Clin Nutr 2009; 28:684–688. 50. Buijs MM, Burggraaf J, Langendonk JG, et al. Hyposomatotropism blunts lipolysis in abdominally obese women. J Clin Endocrinol Metab 2002; 87:3851–3858. 51. Agostoni C, Scaglioni S, Ghisleni D, et al. How much protein is safe? Int J Obes (Lond) 2005; 29(suppl 2):S8–S13. 52. Rolland-Cachera MF, Deheeger M, Maillot M, et al. Early adiposity rebound: causes and consequences for obesity in children and adults. Int J Obes (Lond) 2006; 30(suppl 4):S11–S17. 53. Gunther AL, Buyken AE, Kroke A. Protein intake during the period of complementary feeding and early childhood and the association with body mass index and percentage body fat at 7 y of age. Am J Clin Nutr 2007; 85:1626–1633. 54. van Vught AJ, Heitmann BL, Nieuwenhuizen AG, et al. Association between intake of dietary protein and 3-year-change in body growth among normal and overweight 6-year-old boys and girls (CoSCIS). Public Health Nutr 2010; 13:647–653. 55. Zemel MB, Shi H, Greer B, et al. Regulation of adiposity by dietary calcium. FASEB J 2000; 14:1132–1138. 56. Jacobsen R, Lorenzen JK, Toubro S, et al. Effect of short-term high dietary calcium intake on 24-h energy expenditure, fat oxidation, and fecal fat excretion. Int J Obes (Lond) 2005; 29:292–301. 57. Welberg JW, Monkelbaan JF, de Vries EG, et al. Effects of supplemental dietary calcium on quantitative and qualitative fecal fat excretion in man. Ann Nutr Metab 1994; 38:185–191. 58. Zemel MB. Role of dietary calcium and dairy products in modulating adiposity. Lipids 2003; 38:139–146. 59. Carruth BR, Skinner JD. The role of dietary calcium and other nutrients in moderating body fat in preschool children. Int J Obes Relat Metab Disord 2001; 25:559–566. 60. Skinner JD, Bounds W, Carruth BR, et al. Longitudinal calcium intake is negatively related to children’s body fat indexes. J Am Diet Assoc 2003; 103:1626–1631. 61. Barba G, Troiano E, Russo P, et al. Inverse association between body mass and frequency of milk consumption in children. Br J Nutr 2005; 93:15–19. 62. Novotny R, Daida YG, Acharya S, et al. Dairy intake is associated with lower body fat and soda intake with greater weight in adolescent girls. J Nutr 2004; 134:1905–1909. 63. Moore LL, Bradlee ML, Gao D, et al. Low dairy intake in early childhood predicts excess body fat gain. Obesity (Silver Spring) 2006; 14:1010–1018. 64. Phillips SM, Bandini LG, Cyr H, et al. Dairy food consumption and body weight and fatness studied longitudinally over the adolescent period. Int J Obes Relat Metab Disord 2003; 27:1106–1113. 65. Newby PK, Peterson KE, Berkey CS, et al. Beverage consumption is not associated with changes in weight and body mass index among low income preschool children in North Dakota. J Am Diet Assoc 2004; 104:1086–1094. 66. Berkey CS, Rockett HR, Willett WC, et al. Milk, dairy fat, dietary calcium, and weight gain: a longitudinal study of adolescents. Arch Pediatr Adolesc Med 2005; 159:543–550. 67. Barr SI. Calcium and body fat in peripubertal girls: cross-sectional and longitudinal observations. Obesity (Silver Spring) 2007; 15:1302–1310. 68. Chan GM, Hoffman K, McMurry M. Effects of dairy products on bone and body composition in pubertal girls. J Pediatr 1995; 126:551–556. 69. Lorenzen JK, Mølgaard C, Michaelsen KF, et al. Calcium supplementation for 1 y does not reduce body weight or fat mass in young girls. Am J Clin Nutr 2006; 83:18–23. 70. Reinhardt C, Reigstad CS, Bäckhed F. Intestinal microbiota during infancy and its implications for obesity. J Pediatr Gastroenterol Nutr 2009; 48:249–256. 71. Turnbaugh PJ, Ley RE, Mahowald MA, et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature 2006; 444:1027–1031. 72. DiBaise JK, Zhang H, Crowell MD, et al. Gut microbiota and its possible relationship with obesity. Mayo Clin Proc 2008; 83:460–469. 73. Ley RE, Turnbaugh PJ, Klein S, et al. Microbial ecology: human gut microbes associated with obesity. Nature 2006; 444:1022–1023. 74. Newby PK. Plant foods and plant-based diets: protective against childhood obesity? Am J Clin Nutr 2009; 89:S1572–S2187. 75. Sabaté J, Wien M. Vegetarian diets and childhood obesity prevention. Am J Clin Nutr 2010; 91(suppl):S1525–S1529. 76. Sabaté J, Lindsted KD, Harris RD, et al. Anthropometric parameters of schoolchildren with different life-styles. Am J Dis Child 1990; 144:1159–1163. 77. Grant R, Bilgin A, Zeuschner C, et al. The relative impact of a vegetable-rich diet on key markers of health in a cohort of Australian adolescents. Asia Pac J Clin Nutr 2008; 17:107–115. 78. Fiorito LM, Marini M, Francis LA, et al. Beverage intake of girls at age 5 y predicts adiposity and weight status in childhood and adolescence. Am J Clin Nutr 2009; 90:935–942. 79. Malik VS, Schulze MB, Hu FB. Intake of sugar-sweetened beverages and weight gain: a systematic review. Am J Clin Nutr 2006; 84:274–288. 80. Forshee RA, Anderson PA, Storey ML. Sugar-sweetened beverages and body mass index in children and adolescents: a meta-analysis. Am J Clin Nutr 2008; 87:1662–1671. 81. James J, Thomas P, Cavan D, et al. Preventing childhood obesity by reducing consumption of carbonated drinks: cluster randomised controlled trial. BMJ 2004; 328:1237. 82. Ebbeling CB, Feldman HA, Osganian SK, et al. Effects of decreasing sugar-sweetened beverage consumption on body weight in adolescents: a randomized, controlled pilot study. Pediatrics 2006; 117:673–680. 83. Libuda L, Alexy U, Sichert-Hellert W, et al. Pattern of beverage consumption and long-term association with body-weight status in German adolescents—results from the DONALD study. Br J Nutr 2008; 99:1370–1379. 84. Nissinen K, Mikkilä V, Männistö S, et al. Sweets and sugar-sweetened soft drink intake in childhood in relation to adult BMI and overweight. The Cardiovascular Risk in Young Finns Study. Public Health Nutr 2009; 12:2018–2026. 85. Johnson L, Mander AP, Jones LR, et al. Is sugar-sweetened beverage consumption associated with increased fatness in children? Nutrition 2007; 23:557–563. 86. Vanselow MS, Pereira MA, Neumark-Sztainer D, et al. Adolescent beverage habits and changes in weight over time: findings from Project EAT. Am J Clin Nutr 2009; 90:1489–1495. 87. Muckelbauer R, Libuda L, Clausen K, et al. Promotion and provision of drinking water in schools for overweight prevention: randomized, controlled cluster trial. Pediatrics 2009; 123:e661–e667. 88. French SA, Story M, Neumark-Sztainer D, et al. Fast food restaurant use among adolescents: associations with nutrient intake, food choice and behavioral and psychosocial variables. Int J Obes Relat Metab Disord 2001; 25:1823–1833. 89. Bellisle F, Rolland-Cachera MF. How sugar-containing drinks might increase adiposity in children. Lancet 2001; 357:490–492. 90. Mattes RD. Dietary compensation by humans for supplemental energy provided as ethanol or carbohydrate in fluids. Physiol Behav 1996; 59:179–187. 91. Ludwig DS. The glycemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. JAMA 2002; 287:2414–2423. 92. Bray GA, Nielsen SJ, Popkin B. Consumption of high-fructose corn syrup in beverages may play a role in the epidemic of obesity. Am J Clin Nutr 2004; 79:537–543. 93. Morabia A, Constanza MC. Sodas, high fructose corn syrup, and obesity: let’s focus on the right target. Prev Med 2010; 51:1–2. 94. Libuda L, Kersting M. Soft drinks and body weight development in childhood: is there a relationship? Curr Opin Clin Nutr Metab Care 2009; 12:596–600. 95. Skinner JD, Carruth BR. A longitudinal study of children’s juice intake and growth: the juice controversy revisited. J Am Diet Assoc 2001; 101:432–437. 96. Berkey CS, Rockett HR, Field AE, et al. Sugar-added beverages and adolescent weight change. Obes Res 2004; 12:778–788. 97. Tam CS, Garnett SP, Cowell CT, et al. Soft drink consumption and excess weight gain in Australian school students: results from the Nepean study. Int J Obes (Lond) 2006; 30:1091–1093. 98. Blum JW, Jacobsen DJ, Donnelly JE. Beverage consumption patterns in elementary school aged children across a two-year period. J Am Coll Nutr 2005; 24:93–98. 99. Field AE, Gillman MW, Rosner B, et al. Association between fruit and vegetable intake and change in body mass index among a large sample of children and adolescents in the United States. Int J Obes Relat Metab Disord 2003; 27:821–826. 100. Striegel-Moore RH, Thompson D, Affenito SG, et al. Correlates of beverage intake in adolescent girls: the National Heart, Lung, and Blood Institute Growth and Health Study. J Pediatr 2006; 148:183–187. 101. Fabry P, Hejl Z, Fodor J, et al. The frequency of meals. Its relation to overweight, hypercholesterolaemia, and decreased glucose-tolerance. Lancet 1964; 2:614–615. 102. Koletzko B, Toschke AM. Meal patterns and frequencies: do they affect body weight in children and adolescents? Crit Rev Food Sci Nutr 2010; 50:100–105. 103. Toschke AM, Küchenhoff H, Koletzko B, et al. Meal frequency and childhood obesity. Obes Res 2005; 13:1932–1938. 104. Barba G, Troiano E, Russo P, et al. Total fat, fat distribution and blood pressure according to eating frequency in children living in southern Italy: the ARCA Project. Int J Obes (Lond) 2006; 30:1166–1169. 105. Nicklas TA, Yang SJ, Baranowski T, et al. Eating patterns and obesity in children. The Bogalusa Heart Study. Am J Prev Med 2003; 25:9–16. 106. Nicklas TA, Morales M, Linares A, et al. Children’s meal patterns have changed over a 21-year period: the Bogalusa Heart Study. J Am Diet Assoc 2004; 104:753–761. 107. Lioret S, Touvier M, Lafay L, et al. Are eating occasions and their energy content related to child overweight and socioeconomic status? Obesity (Silver Spring) 2008; 16:2518–2523. 108. Thompson OM, Ballew C, Resnicow K, et al. Dietary pattern as a predictor of change in BMI z-score among girls. Int J Obes (Lond) 2006; 30:176–182. 109. Franko DL, Striegel-Moore RH, Thompson D, et al. The relationship between meal frequency and body mass index in black and white adolescent girls: more is less. Int J Obes (London) 2008; 32:23–29. 110. Croll JK, Neumark-Sztainer D, Story M, et al. Adolescents involved in weight-related and power team sports have better eating patterns and nutrient intakes than non-sport-involved adolescents. J Am Diet Assoc 2006; 106:709–717. 111. Bellisle F, McDevitt R, Prentice AM. Meal frequency and energy balance. Br J Nutr 1997; 77(suppl 1):S57–S70. 112. Moreno LA, Rodriguez G, Fleta J, et al. Trends of dietary habits in adolescents. Crit Rev Food Sci Nutr 2010; 50:106–112. 113. Rampersaud GC, Pereira MA, Girard BL, et al. Breakfast habits, nutritional status, body weight, and academic performance in children and adolescents. J Am Diet Assoc 2005; 105:743–760. 114. Szajewska H, Ruszczynski M. Systematic review demonstrating that breakfast consumption influences body weight outcomes in children and adolescents in Europe. Crit Rev Food Sci Nutr 2010; 50:113–119. 115. Berkey CS, Rockett HR, Gillman MW, et al. Longitudinal study of skipping breakfast and weight change in adolescents. Int J Obes Relat Metab Disord 2003; 27:1258–1266. 116. Niemeier HM, Raynor HA, Lloyd-Richardson EE, et al. Fast food consumption and breakfast skipping: predictors of weight gain from adolescence to adulthood in a nationally representative sample. J Adolesc Health 2006; 39:842–849. 117. Timlin MT, Pereira M, Story M, et al. Breakfast eating and weight change in a 5-year prospective analysis of adolescents: Project EAT (Eating Among Teens). Pediatrics 2008; 121:e638–e645. 118. Affenito SG, Thompson DR, Barton BA, et al. Breakfast consumption by African-American and white adolescent girls correlates positively with calcium and fiber intake and negatively with body mass index. J Am Diet Assoc 2005; 105:938–945. 119. Nicklas TA, Reger C, Myers L, et al. Breakfast consumption with and without vitamin-mineral supplement use favorably impacts daily nutrient intake of ninth-grade students. J Adolesc Health 2000; 27:314–321. 120. Resnicow K. The relationship between breakfast habits and plasma cholesterol levels in schoolchildren. J Sch Health 1991; 61:81–85. 121. Wyatt HR, Grunwald GK, Mosca CL, et al. Long-term weight loss and breakfast in subjects in the National Weight Control Registry. Obes Res 2002; 10:78–82. 122. Gillman MW, Rifas-Shiman SL, Frazier AL, et al. Family dinner and diet quality among older children and adolescents. Arch Fam Med 2000; 9:235–240. 123. Sen B. Frequency of family dinner and adolescent body weight status: evidence from the national longitudinal survey of youth, 1997. Obesity (Silver Spring) 2006; 14:2266–2276. 124. Taveras EM, Rifas-Shiman SL, Berkey CS, et al. Family dinner and adolescent overweight. Obes Res 2005; 13:900–906. 125. Fulkerson JA, Neumark-Sztainer D, Hannan PJ, et al. Family meal frequency and weight status among adolescents: cross-sectional and 5-year longitudinal associations. Obesity (Silver Spring) 2008; 16:2529–2534. 126. Pearson N, Biddle SJ, Gorely T. Family correlates of breakfast consumption among children and adolescents. A systematic review. Appetite 2009; 52:1–7. 127. Taveras EM, Berkey CS, Rifas-Shiman SL, et al. Association of consumption of fried food away from home with body mass index and diet quality in older children and adolescents. Pediatrics 2005; 116:e518–e524. 128. Thompson OM, Ballew C, Resnicow K. et al Food purchased away from home as a predictor of change in BMI z-score among girls. Int J Obes Relat Metab Disord 2004; 28:282–289. 129. Gatenby SJ. Eating frequency: methodological and dietary aspects. Br J Nutr 1997; 77(suppl 1):S7–S20. 130. Aounallah-Skhiri H, Romdhane HB, Traissac P, et al. Nutritional status of Tunisian adolescents: associated gender, environmental and socio-economic factors. Publ Health Nutr 2008; 11:1306–1317. 131. Keast DR, Nicklas TA, O’Neil CE. Snacking is associated with reduced risk of overweight and reduced abdominal obesity in adolescents: National Health and Nutrition Examination Survey (NHANES) 1999-2004. Am J Clin Nutr 2010; 92:428–435. 132. McDonald CM, Baylin A, Arsenault JE, et al. Overweight is more prevalent than stunting and is associated with socioeconomic status, maternal obesity, and a snacking dietary pattern in school children from Bogota, Colombia. J Nutr 2009; 139:370–376. 133. Phillips SM, Bandini LG, Naumova EN, et al. Energy-dense snack food intake in adolescence: longitudinal relationship to weight and fatness. Obes Res 2004; 12:461–472. 134. Field AE, Austin SB, Gillman MW, et al. Snack food intake does not predict weight change among children and adolescents. Int J Obes Relat Metab Disord 2004; 28:1210–1216. 135. Francis LA, Lee Y, Birch LL. Parental weight status and girls’ television viewing, snacking, and body mass indexes. Obes Res 2003; 11:143–151. 136. McConahy KL, Smicklas-Wright H, Mitchell DC, et al. Portion size of common foods predicts energy intake among preschool-aged children. J Am Diet Assoc 2004; 104:975–979. 137. Fisher JO, Liu Y, Birch LL, et al. Effects of portion size and energy density on young children’s intake at a meal. Am J Clin Nutr 2007; 86:174–179. 138. Rolls BJ, Engell D, Birch LL. Serving portion size influences 5-year-old but not 3-year old children’s food intakes. J Am Diet Assoc 2000; 100:232–234. 139. Orlet Fisher JO, Rolls BJ, Birch LL. Children’s bite size and intake of an entrée are greater with large portions than with age-appropriate or self-selected portions. Am J Clin Nutr 2003; 77:1164–1170. 140. Huang TT, Howarth NC, Lin BH, et al. Energy intake and meal portions: associations with BMI percentile in U.S. children. Obes Res 2004; 12:1875–1885. 141. McConahy KL, Smiciklas-Wright H, Birch LL, et al. Food portions are positively related to energy intake and body weight in early childhood. J Pediatr 2002; 140:340–347.



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