scholarly journals Important Food Sources of Sugars and Body Weight: A Systematic Review and Meta-Analysis of Controlled Feeding Trials

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 1620-1620
Author(s):  
Annette Cheung ◽  
Danielle Lee ◽  
Nema McGlynn ◽  
Sabrina Ayoub-Charette ◽  
Fei Au-Yeung ◽  
...  

Abstract Objectives Sugar-sweetened beverages (SSBs) have been linked to weight gain, and it is unclear if other food sources of fructose-containing sugars behave similarily. We conducted a systematic review and meta-analysis of controlled feeding trials to assess the effect of different food sources of fructose-containing sugars on body weight. Methods MEDLINE, EMBASE, and The Cochrane library were searched through January 2019. We included controlled feeding trials of ≥2 weeks investigating the effect of different food sources of sugars. Four levels of energy control were prespecified: substitution (energy-matched comparisons); addition (energy from sugars added to diet); subtraction (energy from sugars subtracted from diet); or ad libitum (energy from sugars freely replaced). The primary outcome was body weight. Two independent reviewers extracted data and assessed risk of bias. Data were pooled using random effects models and expressed as mean differences (MDs) with 95% confidence intervals (CIs). GRADE assessed the certainty of evidence. Results We identified 110 controlled trials (N = 5133) assessing the effect of 7 different food sources of fructose-containing sugars (SSBs, fruit, fruit juice, dried fruit; baked goods, sweets, & desserts; mixed sources; added caloric sweeteners). No effect on body weight was observed in substitution trials, whereas there was an increasing effect in addition trials (MD, 0.23 kg [95% CI, 0.06 to 0.40]) and ad libitum trials (1.43 kg [0.78 to 2.16]), and a decreasing effect in subtraction trials (–0.52 kg [–1.02 to −0.02]). There was evidence of interaction by food source with fruit showing weight loss in substitution trials and SSBs showing weight gain in addition trials. The certainty of evidence was moderate for the effects in the addition and subtraction trials and high for the effects in the substitution and ad libitum trials. Conclusions Energy control and food source appear to mediate the effect of fructose-containing sugars on body weight. Food sources of fructose-containing sugars adding excess energy to diets (especially sugars-sweetened beverages) appear to lead to weight gain. There is low to moderate likelihood that more research will substantially alter our estimates (ClinicalTrials.gov Identifier, NCT02558920) Funding Sources American Society for Nutrition Foundation (commissioned and funded), Diabetes Canada.

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1017-1017
Author(s):  
Laura Chiavaroli ◽  
Annette Cheung ◽  
Sabrina Ayoub-Charette ◽  
Amna Ahmed ◽  
Danielle Lee ◽  
...  

Abstract Objectives Sugar-sweetened beverages (SSBs) have been linked to weight gain. It is unclear if other food sources of fructose-containing sugars behave similarly. We conducted a systematic review and meta-analysis of controlled feeding trials to assess the effect of different food sources of fructose-containing sugars on body weight and markers of adiposity. Methods MEDLINE, Embase, and the Cochrane Library were searched through January 2020 for controlled feeding trials ≥2 weeks on the effect of fructose-containing sugars. Trial designs were prespecified by energy control: substitution (energy matched replacement of sugars in diets); addition (excess energy from sugars added to diets); subtraction (energy from sugars subtracted from diets); and ad libitum (energy from sugars freely replaced in diets). The primary outcome was body weight. Secondary outcomes were body mass index, body fat and waist circumference. Independent reviewers extracted data and assessed risk of bias. Certainty of evidence was assessed using GRADE. (NCT02558920) Results We identified 119 controlled trials (368 trial comparisons, N = 5263) assessing the effect of 10 food sources (SSBs, sweetened dairy alternative (soy), fruit juice, fruit drink, fruit, dried fruit, sweetened cereal grains/bars, sweets, added sweeteners and mixed sources). Total fructose-containing sugars increased body weight (mean difference, 0.29 kg [95% confidence interval, 0.05 to 0.53 kg], P = 0.017) and body fat in addition trials with no effect in other analyses or outcomes. There was evidence of interaction by food source in substitution trials with fruit reducing and mixed sources increasing some outcomes and in addition trials with 100% fruit juice reducing and SSBs and mixed sources increasing some outcomes. The overall certainty of evidence was moderate for the decreasing effect of fruit and fruit juice and the increasing effect of SSBs and mixed sources and high-to-very low for other comparisons. Conclusions Energy control and food source may mediate the effect of fructose-containing sugars on adiposity. The evidence provides good indication that fruit and 100% fruit juice decrease and SSBs and mixed sources increase markers of adiposity. More high-quality randomized trials of different foods are needed to improve our estimates. Funding Sources American Society for Nutrition, Diabetes Canada, CIHR, Mitacs.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1010-1010
Author(s):  
Fei Au-Yeung ◽  
Laura Chiavaroli ◽  
Tauseef Khan ◽  
Andreea Zurbau ◽  
Sabrina Ayoub-Charette ◽  
...  

Abstract Objectives Fructose providing excess calories has been shown to increase postprandial triglycerides (TAG). Whether this effect holds for different food sources of fructose-containing sugars is unclear. We conducted a systematic review and meta-analysis of controlled feeding trials on the effect of different food sources of fructose-containing sugars at different levels of energy control on postprandial blood lipids (NCT02716870). Methods MEDLINE, EMBASE, and Cochrane Library were searched through June 1st, 2020 for controlled feeding trials ≥7-days assessing the effect of food sources of fructose-containing sugars on postprandial lipids. Trial designs were prespecified based on energy control: substitution (energy matched replacement of sugars by other macronutrients); addition (excess energy from sugars added to diets); subtraction (energy from sugars subtracted from diets); and ad libitum (energy from sugars freely replaced by other macronutrients) trials. Independent reviewers extracted data and assessed risk of bias. Outcomes were postprandial TAG and apoB48. Certainty of evidence was assessed using GRADE. Results We included 29 trials (60 trial comparisons, N = 943) assessing 5 food sources (SSBs, fruit, sweets and desserts, added caloric sweetener and mixed sources) across 4 levels of energy control. Total fructose-containing sugars increased postprandial TAG in substitution (MD: 0.17 mmol/L [95% CI: 0.05, 0.30], P = 0.007), addition (0.38 mmol/L [0.13, 0.62], P = 0.003), and ad libitum (0.17 mmol/L [0.02, 0.31], P = 0.024) trials and increased apoB48 in addition trials (0.12 g/L [0.07, 0.18], P < 0.001).There was evidence of interaction by food source with SSBs increasing postprandial TAG and apoB48 in addition trials and mixed sources increasing postprandial TAG in ad libitum trials. The certainty of the evidence was “moderate” for SSBs increasing TAG in addition trials and mixed sources increasing TAG in ad libitum trials and “low” for all other comparisons. Conclusions Food source more than energy control appears to mediate fructose-containing sugars on postprandial lipids. Good evidence suggests that SSBs and mixed sources increase postprandial lipids while evidence is less certain for the lack of effect of other food sources. More high-quality trials of different food sources are needed. Funding Sources Primary: Diabetes Canada.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1052-1052
Author(s):  
Danielle Lee ◽  
Laura Chiavaroli ◽  
Sabrina Ayoub-Charette ◽  
Tauseef Khan ◽  
Andreea Zurbau ◽  
...  

Abstract Objectives Fructose as a source of excess calories increases non-alcoholic fatty liver disease (NAFLD) markers. Whether this effect is mediated by the food matrix is unknown. We thus conducted a systematic review and meta-analysis of controlled feeding trials assessing the effect of important food sources of fructose-containing sugars at different energy control levels on NAFLD markers. Methods MEDLINE, Embase, and Cochrane Library were searched through January 18, 2021 for controlled trials ≥7-days. Four trial designs were prespecified based on energy control: substitution (energy-matched replacement of sugars by other macronutrients); addition (excess energy from sugars added to diets); subtraction (energy from sugars subtracted from diets); and ad libitum (energy from sugars freely replaced by other macronutrients). The primary outcome was intrahepatocellular lipid (IHCL). Secondary outcomes were alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Independent reviewers extracted data and assessed risk of bias. Certainty of evidence was assessed by GRADE. Results We included 44 trials (65 trial comparisons, n = 1941) assessing the effect of 8 food sources (sugar-sweetened beverages [SSBs]; sweetened dairy alternative [soy]; fruit juice; fruit; dried fruit; baked goods, desserts and sweets; added nutritive sweetener; and mixed sources) across 4 energy levels. Total fructose-containing sugars increased IHCL in addition trials (standardized mean difference = 1.69 [95% CI, 1.00–2.37], P < 0.001), but no effect in substitution, subtraction and ad libitum trials. There was evidence of interaction by food source in addition trials with SSBs increasing IHCL and ALT, and mixed sources increasing AST. The overall certainty of evidence was high for SSBs on IHCL and ALT in addition trials and high to very low for all other comparisons. Conclusions Energy control and food source appear to mediate the effect of fructose-containing sugars on NAFLD markers. High certainty evidence suggests that SSBs providing excess energy increase NAFLD markers, while the evidence is less certain that mixed sources share the same effect and other food sources do not. More high-quality randomized trials of different food sources are needed to improve our estimates (ClinicalTrials.gov identifier, NCT02716870). Funding Sources Primary funding: Diabetes Canada.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1011-1011
Author(s):  
Sabrina Ayoub-Charette ◽  
Laura Chiavaroli ◽  
Qi Liu ◽  
Tauseef Khan ◽  
Andreea Zurbau ◽  
...  

Abstract Objectives Fructose as a source of excess calories increases uric acid. Whether this effect is mediated by the food matrix at different levels of energy is unknown. We aim to conduct a systematic review and meta-analysis of controlled feeding trials on the effect of food sources of fructose-containing sugars at different energy levels on uric acid (NCT02716870). Methods MEDLINE, Embase and the Cochrane Library were searched through January 27, 2020 for controlled trials ≥7-days assessing the effect of food sources of fructose-containing sugars on uric acid. Trial designs were prespecified based on energy control: substitution (energy matched replacement of sugars by other macronutrients); addition (excess energy from sugars added to diets); subtraction (energy from sugars subtracted from diets); and ad libitum (energy from sugars freely replaced by other macronutrients) trials. Independent reviewers extracted data and assessed risk of bias. Certainty of evidence was assessed using the GRADE approach. Results Eligibility was met by 41 trials (72 trial comparisons, N = 2109) assessing the effect of 9 food sources (sugar-sweetened beverages [SSBs], sweetened dairy, fruit drink [lemonade], 100% fruit juice, fruit, dried fruit [raisins], baked goods desserts and sweets, added nutritive [caloric] sweetener and mixed sources) across the 4 energy levels. Total fructose-containing sugars increased uric acid in substitution trials (mean difference, 0.15 mg/dL [95% confidence interval, 0.03 to 0.27 mg/dL], P = 0.012) with no effect in addition, subtraction or ad libitum trials. There was evidence of interaction by food source with SSBs and baked goods, desserts and sweets increasing uric acid in substitution and SSBs increasing and 100% fruit juice decreasing uric acid in addition trials. The overall certainty of evidence was moderate for the increasing effect of SSBs in substitution and addition trials and low to very low for all other comparisons. Conclusions Food source more than energy control mediate the effect of fructose-containing sugars on uric acid. SSBs and baked goods, desserts and sweets appear to increase, and 100% fruit juice appear to decrease uric acid. More high-quality trials of different food sources of fructose-containing sugars are needed to improve our estimates. Funding Sources Diabetes Canada.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1083-1083
Author(s):  
XinYe Qi ◽  
Laura Chiavaroli ◽  
Danielle Lee ◽  
Sabrina Ayoub-Charette ◽  
Tauseef Khan ◽  
...  

Abstract Objectives Excess calories as fructose may initiate pathways increasing biomarkers of inflammation. Whether this effect is mediated by the food matrix at different energy levels is unknown. We conducted a systematic review and meta-analysis of controlled feeding trials of the effect of food sources of fructose-containing sugars at different energy control levels on biomarkers of inflammation (NCT02716870). Methods We searched MEDLINE, Embase, and the Cochrane Library through January 15 2020 for controlled trials ≥7d. Trial designs were prespecified based on energy control: substitution (energy-matched replacement of sugar in the diet); addition (excess energy from sugar added to diets); subtraction (energy from sugar subtracted from diets); ad libitum (energy from sugar freely replaced in the diet). The primary outcome was C-reactive protein (CRP). Secondary outcomes were tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6). Independent reviewers extracted data and assessed the risk of bias. Certainty of evidence was assessed by GRADE. Results We included 48 trials (109 trial comparisons, n = 2108) assessing the effect of 10 food sources (SSBs, sweetened dairy, sweetened dairy alternatives (soy), fruit, 100% fruit juice, dried fruit, sweetened cereal grains/bars, sweets, added nutritive sweetener, and mixed sources) across the 4 levels of energy control. Total fructose-containing sugars had no effect on any outcome in any level of energy control. There was evidence of interaction by food source; in substitution trials, sweetened dairy alternative (soy) decreased CRP. In addition trials, fruit decreased while added nutritive sweetener increased TNF-α. The certainty of evidence was low for the effect of sweetened dairy alternative (soy) on CRP in substitution trials, and generally moderate for all other comparisons. Conclusions Food source more than energy control appears to mediate the effect of fructose-containing sugars on inflammation. The evidence provides some indication that sweetened dairy alternatives (soy) and fruit decrease and added nutritive sweeteners increase biomarkers of inflammation. More high-quality randomized trials of different fructose containing food sources are needed to improve our estimates. Funding Sources Diabetes Canada.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1056-1056
Author(s):  
Qi Liu ◽  
Laura Chiavaroli ◽  
Sabrina Ayoub-Charette ◽  
Tauseef Khan ◽  
Fei Au-Yeung ◽  
...  

Abstract Objectives Overconsumption of fructose-containing sugars may increase blood pressure. Whether this effect is mediated by the food matrix is unclear. We conducted a systematic review and meta-analysis of controlled feeding trials of the effect of food sources of fructose-containing sugars at different levels of energy control on blood pressure (NCT02716870). Methods We searched MEDLINE, Embase and the Cochrane Library through January, 2020 for controlled trials ≥7d. Trial designs were prespecified based on energy control: substitution (energy matched replacement of sugars in the diet); addition (excess energy from sugars added to diets); subtraction (energy from sugars subtracted from diets); and ad libitum (energy from sugars freely replaced in the diet) trials. Outcomes were systolic blood pressure (SBP) and diastolic blood pressure (DBP). Independent reviewers extracted data and assessed risk of bias. Certainty of evidence was assessed by GRADE. Results We included 76 trials (121 trial comparisons, N = 4 302) assessing 9 food sources (sugar-sweetened beverages [SSBs], sweetened dairy alternatives, 100% fruit juice, fruit, dried fruit, sweets, added nutritive sweetener, sweetened cereal grains/bars, and mixed sources) across the 4 levels of energy control. Total fructose-containing sugars decreased SBP (mean difference, −2.76 mmHg [95% CI, −4.36, −1.16], P = 0.001) and DBP (−1.26 mmHg [−2.29, −0.23], P = 0.016) in addition trials and the removal of these sugars decreased SBP (−1.79 mmHg [−3.36, −0.21], P = 0.026) in subtraction trials. There was evidence of interaction by food source with fruit decreasing and sweets and mixed sources increasing SBP and DBP in addition trials and the removal of SSBs decreased SBP in subtraction trials. The certainty of evidence was generally moderate to low for all food source-outcome relationships, except for the decreasing-effect of fruit on DBP in addition trials (high). Conclusions Food source and energy control appear to mediate the effect of fructose-containing sugars on blood pressure. The evidence provides a good indication that fruit decreases while excess calories from SSBs, sweets and mixed sources increase blood pressure. More high-quality trials of different food sources are needed to improve our estimates. Funding Sources Diabetes Canada.


2015 ◽  
Vol 39 ◽  
pp. S57
Author(s):  
Vivian L. Choo ◽  
Russell J. de Souza ◽  
Shana J. Kim ◽  
Adrian I. Cozma ◽  
Arash Mirrahimi ◽  
...  

2021 ◽  
Author(s):  
Nithya Neelakantan ◽  
Su Hyun Park ◽  
Guo-Chong Chen ◽  
Rob M van Dam

Abstract Context The prevalence of type 2 diabetes mellitus (T2DM) and cardiovascular diseases (CVDs) is increasing in Asia and several countries are adopting preventive policies to reduce consumption of sugar-sweetened beverages (SSBs). However, evidence on the relation between SSB consumption and cardiometabolic health in Asian populations has not been summarized. Objective In this systematic review, the associations between consumption of SSBs and cardiometabolic outcomes, including obesity, T2DM, and CVD, are examined in Asian populations. Data sources The PubMed, Scopus, and Web of Science databases, and gray literature were searched up to October, 2020 to identify relevant articles. Data extraction Two investigators independently extracted data from included studies. Data analysis When sufficient studies were available, a random-effects meta-analysis was used to calculate the pooled estimates (expressed as risk ratio [RR] and 95% confidence interval [CI]). Heterogeneity was tested and quantified using the Cochrane Q test and I2 statistic, respectively. Results Of the 17 studies included, 8 provided results about measures of adiposity (3 on weight change, 4 on body mass index (BMI), 2 on percent body fat, and 1 on abdominal obesity), 6 reported results about T2DM, and 3 reported on different CVD outcomes. High SSB consumption was significantly associated with greater weight gain and with a higher risk of selected CVD outcomes as compared with low consumption. In the meta-analysis, high SSB consumption was associated with greater T2DM risk before (RR, 1.51; 95%CI, 1.15–1.98 for highest vs lowest category; I2 = 76%) and after (RR, 1.38; 95%CI, 1.09–1.73; I2 = 56%) adjustment for BMI. Conclusions These findings suggest that high SSB consumption is directly associated with weight gain, risk of T2DM, and, possibly, selected CVD outcomes in Asian populations. Public health strategies to reduce SSB consumption in Asian countries are warranted. Systematic Review Registration PROSPERO registration no. CRD42019129456.Keywords: adiposity. cardiovascular disease, Asia, sugar-sweetened beverages, type 2 diabetes.


2015 ◽  
Vol 16 (7) ◽  
pp. 607-619 ◽  
Author(s):  
S. Schlesinger ◽  
W. Lieb ◽  
M. Koch ◽  
V. Fedirko ◽  
C. C. Dahm ◽  
...  

2020 ◽  
Author(s):  
LT Morenga ◽  
S Mallard ◽  
J Mann

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.


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