A Randomized Study of the Effect of Replacing Sugar-Sweetened Soda by Reduced Fat Milk on Cardiometabolic Health in Male Adolescent Soda Drinkers

Chiu, Sally; Siri-Tarino, Patty W.; Bergeron, Nathalie; Suh, Jung Hee; Krauss, Ronald M.

doi:10.3390/nu12020405

Cited by 17 publications

(10 citation statements)

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“…We retrieved 4616 reports from databases and manual searches, 4433 of which were excluded based on the title or abstract. Of the 174 reports reviewed in full text, 51 reports of controlled feeding trials (75 trial comparisons, n = 2059) met the eligibility criteria [ 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 ]. These trials included ten different food sources of fructos...…”

Section: Resultsmentioning

confidence: 99%

Important Food Sources of Fructose-Containing Sugars and Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis of Controlled Trials

et al. 2022

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Background: Fructose providing excess calories in the form of sugar sweetened beverages (SSBs) increases markers of non-alcoholic fatty liver disease (NAFLD). Whether this effect holds for other important food sources of fructose-containing sugars is unclear. To investigate the role of food source and energy, we conducted a systematic review and meta-analysis of controlled trials of the effect of fructose-containing sugars by food source at different levels of energy control on non-alcoholic fatty liver disease (NAFLD) markers. Methods and Findings: MEDLINE, Embase, and the Cochrane Library were searched through 7 January 2022 for controlled trials ≥7-days. Four trial designs were prespecified: substitution (energy-matched substitution of sugars for other macronutrients); addition (excess energy from sugars added to diets); subtraction (excess 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. The certainty of evidence was assessed using GRADE. We included 51 trials (75 trial comparisons, n = 2059) of 10 food sources (sugar-sweetened beverages (SSBs); sweetened dairy alternative; 100% fruit juice; fruit; dried fruit; mixed fruit sources; sweets and desserts; added nutritive sweetener; honey; and mixed sources (with SSBs)) in predominantly healthy mixed weight or overweight/obese younger adults. Total fructose-containing sugars increased IHCL (standardized mean difference = 1.72 [95% CI, 1.08 to 2.36], p < 0.001) in addition trials and decreased AST in subtraction trials with no effect on any outcome in substitution or ad libitum trials. There was evidence of influence by food source with SSBs increasing IHCL and ALT in addition trials and mixed sources (with SSBs) decreasing AST in subtraction trials. The certainty of evidence was high for the effect on IHCL and moderate for the effect on ALT for SSBs in addition trials, low for the effect on AST for the removal of energy from mixed sources (with SSBs) in subtraction trials, and generally low to moderate for all other comparisons. Conclusions: Energy control and food source appear to mediate the effect of fructose-containing sugars on NAFLD markers. The evidence provides a good indication that the addition of excess energy from SSBs leads to large increases in liver fat and small important increases in ALT while there is less of an indication that the removal of energy from mixed sources (with SSBs) leads to moderate reductions in AST. Varying uncertainty remains for the lack of effect of other important food sources of fructose-containing sugars at different levels of energy control.

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Section: Resultsmentioning

confidence: 99%

Important Food Sources of Fructose-Containing Sugars and Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis of Controlled Trials

et al. 2022

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“…In our work, high SSB intake was associated with increased systolic blood pressure and odds of hypertension; numerous trials also evaluated the effects of reduced SSB intake on blood pressure; in the study by Chen L et al reduction in SSB intake of 1 serving/day over 18 months was associated with a 1.8 and 1.1 mmHg reduction in SBP and DBP, respectively [43]. Chiu S et al also reported reduced systolic blood pressure after replacing sugar sweetened sodas with milk in young male adolescents [44]. Accumulating evidence has linked SSB consumption during childhood to unhealthy weight gain which itself associated with risk of health outcomes such as type 2 diabetes, metabolic syndrome, cardiovascular diseases and other obesity-related disorders in later life [45].…”

Section: Discussionmentioning

confidence: 99%

Sugar-sweetened beverages increases the risk of hypertension among children and adolescence: a systematic review and dose–response meta-analysis

2020

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Background: In the current systematic review and meta-analysis, we summarized the studies that evaluated the effects of sugar-sweetened beverages (SSBs) intake on blood pressure among children and adolescents. Methods: In a systematic search from PubMed, Scopus, Embase and Cochrane electronic databases up to 20 April 2020, the observational studies that evaluated the association between sugar-sweetened beverages intake and hypertension, systolic or diastolic blood pressure (SBP, DBP) were retrieved. Results: A total of 14 studies with 93873 participants were included in the current meta-analysis. High SSB consumption was associated with 1.67 mmHg increase in SBP in children and adolescents (WMD: 1.67; CI 1.021-2.321; P < 0.001). The difference in DBP was not significant (WMD: 0.313; CI −0.131-0.757; P = 0.108). High SSB consumers were 1.36 times more likely to develop hypertension compared with low SSB consumers (OR: 1.365; CI 1.145-1.626; P = 0.001). In dose-response meta-analysis, no departure from linearity was observed between SSB intake and change in SBP (P-nonlinearity = 0.707) or DBP (P-nonlinearity = 0.180). Conclusions: According to our finding, high SSB consumption increases SBP and hypertension in children and adolescents.

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“…On the other hand, in young adults an increase in triglycerides and VLDL is associated with both acute and chronic fructose consumption ( 28 , 116 , 117 ), even at relatively low doses ( 118 ). Regarding the hypothesis of an association between consumption of SSBs and triglycerides in pediatric age, data are conflicting: some studies show an increase in triglyceridemia in children and adolescents with higher consumption of SSBs ( 113 , 115 , 118 ), whereas others studies do not show any significant differences ( 119 , 120 ).…”

Section: Fructose and Cardiometabolic Risk Factors In Pediatric Age: ...mentioning

confidence: 98%

“…The study included a cross-over phase between the two groups after a washout period. The SBP z-score and uricemia were significantly lower when milk was taken instead of SSBs ( 120 ). Only one study evaluated the consumption of sugars taken via solid foods (sugary snacks) and confirmed that the subjects with the highest level of consumption had an increased risk of being hypertensive.…”

Section: Fructose and Cardiometabolic Risk Factors In Pediatric Age: ...mentioning

confidence: 99%

Fructose Intake, Hypertension and Cardiometabolic Risk Factors in Children and Adolescents: From Pathophysiology to Clinical Aspects. A Narrative Review

et al. 2022

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Arterial hypertension, dyslipidemia, alterations in glucose metabolism and fatty liver, either alone or in association, are frequently observed in obese children and may seriously jeopardize their health. For obesity to develop, an excessive intake of energy-bearing macronutrients is required; however, ample evidence suggests that fructose may promote the development of obesity and/or metabolic alterations, independently of its energy intake. Fructose consumption is particularly high among children, because they do not have the perception, and more importantly, neither do their parents, that high fructose intake is potentially dangerous. In fact, while this sugar is erroneously viewed favorably as a natural nutrient, its excessive intake can actually cause adverse cardio-metabolic alterations. Fructose induces the release of pro-inflammatory cytokines, and reduces the production of anti-atherosclerotic cytokines, such as adiponectin. Furthermore, by interacting with hunger and satiety control systems, particularly by inducing leptin resistance, it leads to increased caloric intake. Fructose, directly or through its metabolites, promotes the development of obesity, arterial hypertension, dyslipidemia, glucose intolerance and fatty liver. This review aims to highlight the mechanisms by which the early and excessive consumption of fructose may contribute to the development of a variety of cardiometabolic risk factors in children, thus representing a potential danger to their health. It will also describe the main clinical trials performed in children and adolescents that have evaluated the clinical effects of excessive intake of fructose-containing drinks and food, with particular attention to the effects on blood pressure. Finally, we will discuss the effectiveness of measures that can be taken to reduce the intake of this sugar.

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A Randomized Study of the Effect of Replacing Sugar-Sweetened Soda by Reduced Fat Milk on Cardiometabolic Health in Male Adolescent Soda Drinkers

Cited by 17 publications

References 58 publications

Important Food Sources of Fructose-Containing Sugars and Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis of Controlled Trials

Important Food Sources of Fructose-Containing Sugars and Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis of Controlled Trials

Sugar-sweetened beverages increases the risk of hypertension among children and adolescence: a systematic review and dose–response meta-analysis

Fructose Intake, Hypertension and Cardiometabolic Risk Factors in Children and Adolescents: From Pathophysiology to Clinical Aspects. A Narrative Review

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