Fructose containing sugars do not raise blood pressure or uric acid at normal levels of human consumption.
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ABSTRACT:
SUBMITTER: Angelopoulos TJ
PROVIDER: S-EPMC8032165 | biostudies-literature | 2015 Feb
REPOSITORIES: biostudies-literature
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Fructose containing sugars do not raise blood pressure or uric acid at normal levels of human consumption.
Angelopoulos Theodore J TJ Lowndes Joshua J Sinnett Stephanie S Rippe James M JM
Journal of clinical hypertension (Greenwich, Conn.) 20141215 2
The impact of fructose, commonly consumed with sugars by humans, on blood pressure and uric acid has yet to be defined. A total of 267 weight-stable participants drank sugar-sweetened milk every day for 10 weeks as part of their usual, mixed-nutrient diet. Groups 1 and 2 had 9% estimated caloric intake from fructose or glucose, respectively, added to milk. Groups 3 and 4 had 18% of estimated caloric intake from high fructose corn syrup or sucrose, respectively, added to the milk. Blood pressure ...[more]
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Project description:BackgroundAlthough fructose as a source of excess calories increases uric acid, the effect of the food matrix is unclear.ObjectivesTo assess the effects of fructose-containing sugars by food source at different levels of energy control on uric acid, we conducted a systematic review and meta-analysis of controlled trials.MethodsMEDLINE, Embase, and the Cochrane Library were searched (through 11 January 2021) for trials ≥ 7 days. We prespecified 4 trial designs 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) designs. Independent reviewers (≥2) extracted data and assessed the risk of bias. Grading of Recommendations, Assessment, Development, and Evaluation was used to assess the certainty of evidence.ResultsWe included 47 trials (85 comparisons; N = 2763) assessing 9 food sources [sugar-sweetened beverages (SSBs), sweetened dairy, fruit drinks, 100% fruit juice, fruit, dried fruit, sweets and desserts, added nutritive sweetener, and mixed sources] across 4 energy control levels in predominantly healthy, mixed-weight adults. Total fructose-containing sugars increased uric acid levels in substitution trials (mean difference, 0.16 mg/dL; 95% CI: 0.06-0.27 mg/dL; P = 0.003), with no effect across the other energy control levels. There was evidence of an interaction by food source: SSBs and sweets and desserts increased uric acid levels in the substitution design, while SSBs increased and 100% fruit juice decreased uric acid levels in addition trials. The certainty of evidence was high for the increasing effect of SSBs in substitution and addition trials and the decreasing effect of 100% fruit juice in addition trials and was moderate to very low for all other comparisons.ConclusionsFood source more than energy control appears to mediate the effects of fructose-containing sugars on uric acid. The available evidence provides reliable indications that SSBs increase and 100% fruit juice decreases uric acid levels. More high-quality trials of different food sources are needed. This trial was registered at clinicaltrials.gov as NCT02716870.
| S-EPMC8349131 | biostudies-literature
Project description:The objective of the current study was to explore our hypothesis that average consumption of fructose and fructose containing sugars would not increase risk factors for cardiovascular disease (CVD) and the metabolic syndrome (MetS). A randomized, double blind, parallel group study was conducted where 267 individuals with BMI between 23 and 35 kg/m² consumed low fat sugar sweetened milk, daily for ten weeks as part of usual weight-maintenance diet. One group consumed 18% of calories from high fructose corn syrup (HFCS), another group consumed 18% of calories from sucrose, a third group consumed 9% of calories from fructose, and the fourth group consumed 9% of calories from glucose. There was a small change in waist circumference (80.9 ± 9.5 vs. 81.5 ± 9.5 cm) in the entire cohort, as well as in total cholesterol (4.6 ± 1.0 vs. 4.7 ± 1.0 mmol/L, p < 0.01), triglycerides (TGs) (11.5 ± 6.4 vs. 12.6 ± 8.9 mmol/L, p < 0.01), and systolic (109.2 ± 10.2 vs. 106.1 ± 10.4 mmHg, p < 0.01) and diastolic blood pressure (69.8 ± 8.7 vs. 68.1 ± 9.7 mmHg, p < 0.01). The effects of commonly consumed sugars on components of the MetS and CVD risk factors are minimal, mixed and not clinically significant.
| S-EPMC4848648 | biostudies-literature
Project description: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.
| S-EPMC8181250 | biostudies-literature
Project description: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.
| S-EPMC8181005 | biostudies-literature
Project description:Whether food source or energy mediates the effect of fructose-containing sugars on blood pressure (BP) is unclear. We conducted a systematic review and meta-analysis of the effect of different food sources of fructose-containing sugars at different levels of energy control on BP. We searched MEDLINE, Embase and the Cochrane Library through June 2021 for controlled trials ≥7-days. We prespecified 4 trial designs: substitution (energy matched substitution of sugars); addition (excess energy from sugars added); subtraction (excess energy from sugars subtracted); and ad libitum (energy from sugars freely replaced). Outcomes were systolic and diastolic BP. Independent reviewers extracted data. GRADE assessed the certainty of evidence. We included 93 reports (147 trial comparisons, N = 5,213) assessing 12 different food sources across 4 energy control levels in adults with and without hypertension or at risk for hypertension. Total fructose-containing sugars had no effect in substitution, subtraction, or ad libitum trials but decreased systolic and diastolic BP in addition trials (P<0.05). There was evidence of interaction/influence by food source: fruit and 100% fruit juice decreased and mixed sources (with sugar-sweetened beverages [SSBs]) increased BP in addition trials and the removal of SSBs (linear dose response gradient) and mixed sources (with SSBs) decreased BP in subtraction trials. The certainty of evidence was generally moderate. Food source and energy control appear to mediate the effect of fructose-containing sugars on BP. The evidence provides a good indication that fruit and 100% fruit juice at low doses (up to or less than the public health threshold of ~10% E) lead to small, but important reductions in BP, while the addition of excess energy of mixed sources (with SSBs) at high doses (up to 23%) leads to moderate increases and their removal or the removal of SSBs alone (up to ~20% E) leads to small, but important decreases in BP in adults with and without hypertension or at risk for hypertension. Trial registration: Clinicaltrials.gov: NCT02716870.
| S-EPMC10427023 | biostudies-literature
Project description:Sugars have replaced fat as the dominant public health nutrition concern. A fructose-centric view of cardiometabolic disease has emerged whereby fructose-containing sugars are thought to have deleterious effects on body weight, fasting and postprandial blood lipids, glycemia, blood pressure, uric acid, and markers of nonalcoholic fatty liver disease. Long-term prospective cohort studies have not supported these associations when assessing the relation between total fructose-containing sugars at any amount of intake and incident cardiometabolic disease. Conversely, a consistent signal for harm has been reported for sugary beverages when comparing the highest with the lowest intakes. These associations, however, do not hold at moderate intakes, which are more reflective of real-world intakes, are subject to important collinearity effects, and have small risk estimates with modest population-attributable risk fractions. Higher-level evidence from controlled feeding trials shows that fructose-containing sugars in either liquid or solid form have adverse cardiometabolic effects only when they supplement diets with excess calories compared with the same diets without the excess calories. In the absence of harm when fructose-containing sugars are exchanged for other sources of carbohydrate under energy-matched conditions, excess calories appear to be the dominant consideration. Like with the earlier fat story, it is difficult to separate the contribution of fructose-containing sugars from that of other sources of excess calories in the epidemic of obesity and cardiometabolic disease. Attention needs to remain focused on reducing the overconsumption of all caloric foods associated with obesity and cardiometabolic disease, including sugary beverages and foods, and promoting greater physical activity.
| S-EPMC4496733 | biostudies-literature
Project description:SubjectThis study aimed to establish a normal range for ankle systolic blood pressure (SBP).MethodsA total of 948 subjects who had normal brachial SBP (90-139 mmHg) at investigation were enrolled. Supine BP of four limbs was simultaneously measured using four automatic BP measurement devices. The ankle-arm difference (An-a) on SBP of both sides was calculated. Two methods were used for establishing normal range of ankle SBP: the 99% method was decided on the 99% reference range of actual ankle BP, and the An-a method was the sum of An-a and the low or up limits of normal arm SBP (90-139 mmHg).ResultsWhether in the right or left side, the ankle SBP was significantly higher than the arm SBP (right: 137.1 ± 16.9 vs 119.7 ± 11.4 mmHg, P<0.05). Based on the 99% method, the normal range of ankle SBP was 94~181 mmHg for the total population, 84~166 mmHg for the young (18-44 y), 107~176 mmHg for the middle-aged(45-59 y) and 113~179 mmHg for the elderly (≥ 60 y) group. As the An-a on SBP was 13 mmHg in the young group and 20 mmHg in both middle-aged and elderly groups, the normal range of ankle SBP on the An-a method was 103-153 mmHg for young and 110-160 mmHg for middle-elderly subjects.ConclusionA primary reference for normal ankle SBP was suggested as 100-165 mmHg in the young and 110-170 mmHg in the middle-elderly subjects.
| S-EPMC4459970 | biostudies-literature
Project description:Elevated serum levels of uric acid consistently correlate with hypertension, but the directionality of the association remains debated. To help define this relationship, we used a controlled setting within a homogeneous Amish community and the Mendelian randomization of a nonsynonymous coding single-nucleotide polymorphism, rs16890979 (Val253Ile), in the SLC2A9 gene. This gene expresses the GLUT9 transporter that also transports uric acid and is associated with lower serum uric acid levels. We studied the unconfounded association between genotype and blood pressure in 516 Amish adults, each placed for 6 days on standardized diets, first with high sodium, followed by low sodium, with an intervening washout period. Blood pressure, measured using 24-h ambulatory monitoring, during both diet periods was used as the primary outcome. All participants were free of diuretic or other antihypertensive medications and the relationships between GLUT9 genotype and both serum uric acid and blood pressure were assessed. Each copy of the GLUT9 minor Ile allele was found to confer a significant 0.44 mg/dl reduction in serum uric acid and was associated with a significant mean decrease in the systolic blood pressure of 2.2 and 1.5 mm Hg on the high- and low-sodium diet, respectively. Thus, a Mendelian randomization analysis using variants in the GLUT9 gene indicates that a decrease in serum uric acid has a causal effect of lowering blood pressure.
| S-EPMC3640827 | biostudies-literature
Project description:ObjectiveTo assess the effect of different food sources of fructose-containing sugars on glycaemic control at different levels of energy control.DesignSystematic review and meta-analysis of controlled intervention studies.Data sourcesMedine, Embase, and the Cochrane Library up to 25 April 2018.Eligibility criteria for selecting studiesControlled intervention studies of at least seven days' duration and assessing the effect of different food sources of fructose-containing sugars on glycaemic control in people with and without diabetes were included. Four study designs were prespecified on the basis of energy control: substitution studies (sugars in energy matched comparisons with other macronutrients), addition studies (excess energy from sugars added to diets), subtraction studies (energy from sugars subtracted from diets), and ad libitum studies (sugars freely replaced by other macronutrients without control for energy). Outcomes were glycated haemoglobin (HbA1c), fasting blood glucose, and fasting blood glucose insulin.Data extraction and synthesisFour independent reviewers extracted relevant data and assessed risk of bias. Data were pooled by random effects models and overall certainty of the evidence assessed by the GRADE approach (grading of recommendations assessment, development, and evaluation).Results155 study comparisons (n=5086) were included. Total fructose-containing sugars had no harmful effect on any outcome in substitution or subtraction studies, with a decrease seen in HbA1c in substitution studies (mean difference -0.22% (95% confidence interval to -0.35% to -0.08%), -25.9 mmol/mol (-27.3 to -24.4)), but a harmful effect was seen on fasting insulin in addition studies (4.68 pmol/L (1.40 to 7.96)) and ad libitum studies (7.24 pmol/L (0.47 to 14.00)). There was interaction by food source, with specific food sources showing beneficial effects (fruit and fruit juice) or harmful effects (sweetened milk and mixed sources) in substitution studies and harmful effects (sugars-sweetened beverages and fruit juice) in addition studies on at least one outcome. Most of the evidence was low quality.ConclusionsEnergy control and food source appear to mediate the effect of fructose-containing sugars on glycaemic control. Although most food sources of these sugars (especially fruit) do not have a harmful effect in energy matched substitutions with other macronutrients, several food sources of fructose-containing sugars (especially sugars-sweetened beverages) adding excess energy to diets have harmful effects. However, certainty in these estimates is low, and more high quality randomised controlled trials are needed.Study registrationClinicaltrials.gov (NCT02716870).
| S-EPMC6247175 | biostudies-literature
Project description:Obesity and sleeping blood pressure (BP) abnormalities are well recognized as some of the main risk factors for hypertension and cardiovascular diseases (CVDs). The primary objective of this study was to evaluate the prevalence of hypertension and non-dipping profile in overweight/obese subjects. A sample of 100 consecutive healthy overweight/obese subjects, aged 20-69 years and never treated with antihypertensive drugs was examined. Ambulatory 24 h BP monitoring was performed to diagnose hypertension and a non-dipping profile. Anthropometric, metabolic and routine hematochemical parameters were assessed. All subjects underwent ultrasound measurement of common carotid intima-media thickness. Hypertension was demonstrated in 69% (n = 69) and 27% of the sample (n = 27) had a non-dipping profile. Among the hematochemical variables, estimated glomerular filtration rate (eGFR) (p = 0.02) and FT4 (p = 0.01) serum levels were higher in the hypertensive group than in the normotensive group. Lower potassium and uric acid serum levels (p = 0.05) were independent predictive factors of a non-dipping BP profile. This study shows, for the first time, that 1) an unexpectedly high percentage (69%) of overweight/obese subjects is affected by hypertension; 2) early hypertensive subjects have an increased eGFR and higher FT4 serum levels; 3) lower potassium and uric acid levels are independent predictors of pathological nocturnal non-dipping.
| S-EPMC6950029 | biostudies-literature