Objective To summarise evidence on the association between intake of dietary sugars and body weight in adults and children.Design Systematic review and meta-analysis of randomised controlled trials and prospective cohort studies.Data sources OVID Medline, Embase, PubMed, Cumulative Index to Nursing and Allied Health Literature, Scopus, and Web of Science (up to December 2011).Review methods Eligible studies reported the intake of total sugars, intake of a component of total sugars, or intake of sugar containing foods or beverages; and at least one measure of body fatness. Minimum duration was two weeks for trials and one year for cohort studies. Trials of weight loss or confounded by additional medical or lifestyle interventions were excluded. Study selection, assessment, validity, data extraction, and analysis were undertaken as specified by the Cochrane Collaboration and the GRADE working group. For trials, we pooled data for weight change using inverse variance models with random effects. We pooled cohort study data where possible to estimate effect sizes, expressed as odds ratios for risk of obesity or β coefficients for change in adiposity per unit of intake.Results 30 of 7895 trials and 38 of 9445 cohort studies were eligible. In trials of adults with ad libitum diets (that is, with no strict control of food intake), reduced intake of dietary sugars was associated with a decrease in body weight (0.80 kg, 95% confidence interval 0.39 to 1.21; P<0.001); increased sugars intake was associated with a comparable weight increase (0.75 kg, 0.30 to 1.19; P=0.001). Isoenergetic exchange of dietary sugars with other carbohydrates showed no change in body weight (0.04 kg, −0.04 to 0.13). Trials in children, which involved recommendations to reduce intake of sugar sweetened foods and beverages, had low participant compliance to dietary advice; these trials showed no overall change in body weight. However, in relation to intakes of sugar sweetened beverages after one year follow-up in prospective studies, the odds ratio for being overweight or obese increased was 1.55 (1.32 to 1.82) among groups with the highest intake compared with those with the lowest intake. Despite significant heterogeneity in one meta-analysis and potential bias in some trials, sensitivity analyses showed that the trends were consistent and associations remained after these studies were excluded.Conclusions Among free living people involving ad libitum diets, intake of free sugars or sugar sweetened beverages is a determinant of body weight. The change in body fatness that occurs with modifying intakes seems to be mediated via changes in energy intakes, since isoenergetic exchange of sugars with other carbohydrates was not associated with weight change.

Objective: To summarise evidence on the association between intake of dietary sugars and body weight in adults and children. Design: Systematic review and meta-analysis of randomised controlled trials and prospective cohort studies. Data sources: OVID Medline, Embase, PubMed, Cumulative Index to Nursing and Allied Health Literature, Scopus, and Web of Science (up to December 2011). Review methods: Eligible studies reported the intake of total sugars, intake of a component of total sugars, or intake of sugar containing foods or beverages; and at least one measure of body fatness. Minimum duration was two weeks for trials and one year for cohort studies. Trials of weight loss or confounded by additional medical or lifestyle interventions were excluded. Study selection, assessment, validity, data extraction, and analysis were undertaken as specified by the Cochrane Collaboration and the GRADE working group. For trials, we pooled data for weight change using inverse variance models with random effects. We pooled cohort study data where possible to estimate effect sizes, expressed as odds ratios for risk of obesity or β coefficients for change in adiposity per unit of intake. Results: 30 of 7895 trials and 38 of 9445 cohort studies were eligible. In trials of adults with ad libitum diets (that is, with no strict control of food intake), reduced intake of dietary sugars was associated with a decrease in body weight (0.80 kg, 95% confidence interval 0.39 to 1.21; P<0.001); increased sugars intake was associated with a comparable weight increase (0.75 kg, 0.30 to 1.19; P=0.001). Isoenergetic exchange of dietary sugars with other carbohydrates showed no change in body weight (0.04 kg, -0.04 to 0.13). Trials in children, which involved recommendations to reduce intake of sugar sweetened foods and beverages, had low participant compliance to dietary advice; these trials showed no overall change in body weight. However, in relation to intakes of sugar sweetened beverages after one year follow-up in prospective studies, the odds ratio for being overweight or obese increased was 1.55 (1.32 to 1.82) among groups with the highest intake compared with those with the lowest intake. Despite significant heterogeneity in one meta-analysis and potential bias in some trials, sensitivity analyses showed that the trends were consistent and associations remained after these studies were excluded. Conclusions: Among free living people involving ad libitum diets, intake of free sugars or sugar sweetened beverages is a determinant of body weight. The change in body fatness that occurs with modifying intakes seems to be mediated via changes in energy intakes, since isoenergetic exchange of sugars with other carbohydrates was not associated with weight change.

Stunting and underweight among under-five children in Indonesia are common, raising public health concerns. Whether inappropriate complementary feeding (CF) practices compromise optimal growth during late infancy in Indonesia is uncertain. Therefore we characterized and evaluated CF practices in Indonesian infants and investigated their relationship with subsequent growth. We enrolled breastfed infants at 6 months of age (n = 230); and followed them at 9 (n = 202) and 12 months of age (n = 190). We collected socio-demographic and anthropometric data and two-day in-home weighed food records. Relations between WHO CF indicators, sentinel foods, and energy and micronutrient intakes at 9 months and growth at 12 months were explored using multiple linear regression. Stunting and underweight increased from 15.8% and 4.4% at 6 months to 22.6% and 10.5% at 12 months, respectively. Median intakes of calcium, iron, zinc, and riboflavin were below WHO recommendations. Infants consuming fortified infant foods (FIFs) at 9 months had diets with a lower dietary diversity (DD) score (2.3 vs.3.0), energy density, median energy (250 vs. 310 kcal/d) and protein (6.5 vs. 9.1 g/d) intake than non-consumers (p<0.01), despite higher intakes of calcium, iron, and vitamins A and C (p<0.001). Positive relations existed for 9-month consumption of iron-rich/iron fortified infant foods with length-for-age Z-score (LAZ) at 12 months (β = 0.22; 95% CI: 0.01, 0.44; P = 0.04), and for fortified infant foods alone with both LAZ (β = 0.29; 95% CI: 0.09, 0.48; P = 0.04) and weight-for-age Z-score (β = 0.14; 95% CI: 0.02, 0.26; P = 0.02) at 12 months. The positive association of FIFs with subsequent growth may be attributed to their content of both powdered cow’s milk and multi-micronutrient fortificants. Nonetheless, mothers should not be encouraged to over-rely on FIFs as they reduce DD.

Our findings indicate that IYCF programs should be targeted toward the early period of complementary food introduction and that policies aimed at increasing formal maternal education may benefit child growth through improved feeding practices. This trial was registered at www.controlled-trials.com as ISRCTN37460449.

Our results indicate that vitamin D status may be marginally improved with weight loss in comparison with weight maintenance under similar conditions of supplemental vitamin D intake. Although additional studies in unsupplemented individuals are needed to confirm these findings, our results support the view that the association between obesity and lower serum 25-hydroxyvitamin D may be due to reversed causation with increased adiposity leading to suboptimal concentrations of circulating vitamin D. This trial was registered at www.crd.york.ac.uk/PROSPERO/ as CRD42015023836.