ABSTRACT
BACKGROUND: Protein influences acute postprandial glucose and insulin responses, but the effects of dose, protein type, and health status are unknown. OBJECTIVES: We aimed to determine the acute effect of adding protein to carbohydrate on postprandial responses and identify effect modifiers. METHODS: We searched MEDLINE, EMBASE, and Cochrane databases through 30 July, 2023 for acute, crossover trials comparing acute postprandial responses elicited by carbohydrate-containing test meals with and without added protein in adults without diabetes or with type 2 (T2DM) or type 1 (T1DM) diabetes mellitus. Group data were pooled separately using generic inverse variance with random-effects models and expressed as the ratio of means with 95% confidence interval. Risk of bias and certainty of evidence (Grading of Recommendations Assessment, Development, and Evaluation) were assessed. RESULTS: In 154 trial comparisons of animal, dairy, and plant proteins (without diabetes, n = 22, 67, 32, respectively; T2DM, n = 14, 16, 3, respectively), each gram protein per gram available carbohydrate (g/g) reduced the glucose area under the curve (AUC) less in adults with T2DM than in those without diabetes (-10% compared with -50%, P < 0.05) but increased the insulin AUC similarly (+76% compared with +56%). In subjects without diabetes, each g/g of dairy and plant protein reduced glucose AUC by 52% and 55%, respectively, and increased the insulin AUC by 64% and 45%, respectively (all P < 0.05). Animal proteins significantly reduced the glucose AUC by 31% and increased the insulin AUC by 37% (pooled effects) but without a significant dose-response. In adults with T2DM, animal protein reduced the glucose AUC by 13% and increased the insulin AUC by 105%, with no significant dose-response. Dairy protein reduced the glucose AUC by 18% (no dose-response), but each g/g increased the insulin AUC by 34% (P < 0.05). In adults with T1DM, protein increased the glucose AUC by 40% (P < 0.05, n = 5). Data source (reported AUC compared with calculated AUC) and study methodology quality significantly modified some outcomes and contributed to high between-study heterogeneity. CONCLUSIONS: In people without diabetes, adding dairy or plant protein to a carbohydrate-containing meal elicits physiologically significant reductions in glucose AUC and increases insulin AUC. Animal protein may slightly reduce the glucose AUC and may increase the insulin AUC. In people with T2DM, protein may not have such large and consistent effects. Further research is needed to determine if the effects of protein differ by health status and protein source. This study was registered at PROSPERO as CRD42022322090.
ABSTRACT
BACKGROUND: Recent studies suggest that some nonnutritive sweeteners (NNS) have deleterious effects on the human gut microbiome (HGM). The effect of steviol glycosides on the HGM has not been well studied. OBJECTIVE: We aimed to evaluate the effects of stevia- compared with sucrose-sweetened beverages on the HGM and fecal short-chain fatty acid (SCFA) profiles. METHODS: Using a randomized, double-blinded, parallel-design study, n = 59 healthy adults [female/male, n = 36/23, aged 31±9 y, body mass index (BMI): 22.6±1.7 kg/m2] consumed 16 oz of a beverage containing either 25% of the acceptable daily intake (ADI) of stevia or 30 g of sucrose daily for 4 weeks followed by a 4-week washout. At weeks 0 (baseline), 4, and 8, the HGM was characterized via shotgun sequencing, fecal SCFA concentrations were measured using ultra-high performance liquid chromatography-tandem mass spectrometry and anthropometric measurements, fasting serum glucose, insulin and lipids, blood pressure, pulse, and 3-d diet records were obtained. RESULTS: There were no significant differences in the HGM or fecal SCFA between the stevia and sucrose groups at baseline (P > 0.05). At week 4 (after intervention), there were no significant differences in the HGM at the phylum, family, genus, or species level between the stevia and sucrose groups and no significant differences in fecal SCFA. At week 4, BMI had increased by 0.3 kg/m2 (P = 0.013) in sucrose compared with stevia, but all other anthropometric and cardiometabolic measures and food intake did not differ significantly (P > 0.05). At week 8 (after washout), there were no significant differences in the HGM, fecal SFCA, or any anthropometric or cardiometabolic measure between the stevia and sucrose groups (P > 0.05). CONCLUSIONS: Daily consumption of a beverage sweetened with 25% of the ADI of stevia for 4 weeks had no significant effects on the HGM, fecal SCFA, or fasting cardiometabolic measures, compared with daily consumption of a beverage sweetened with 30 g of sucrose. TRIAL REGISTRATION: clinicaltrials.gov as NCT05264636.
Subject(s)
Cardiovascular Diseases , Diterpenes, Kaurane , Gastrointestinal Microbiome , Glucosides , Non-Nutritive Sweeteners , Stevia , Adult , Humans , Male , Female , Sucrose , Beverages/analysis , Stevia/chemistryABSTRACT
AIMS: We aimed to determine if ketone production and excretion are increased even at mild fasting hyperglycemia in type 1 diabetes (T1D) and if these are modified by ketoacidosis risk factors, including sodium-glucose co-transporter inhibition (SGLTi) and female sex. METHODS: In secondary analysis of an 8-week single-arm open-label trial of empagliflozin (NCT01392560) we evaluated ketone concentrations during extended fasting and clamped euglycemia (4-6 mmol/L) and mild hyperglycemia (9-11 mmol/L) prior to and after treatment. Plasma and urine beta-hydroxybutyrate (BHB) concentrations and fractional excretion were analyzed by metabolomic analysis. RESULTS: Forty participants (50 % female), aged 24 ± 5 years, HbA1c 8.0 ± 0.9 % (64 ± 0.08 mmol/mol) with T1D duration of 17.5 ± 7 years, were studied. Increased BHB production even during mild hyperglycemia (median urine 6.3[3.5-13.6] vs. 3.5[2.2-7.0] µmol/mmol creatinine during euglycemia, p < 0.001) was compensated by increased fractional excretion (0.9 % [0.3-1.6] vs. 0.4 % [0.2-0.9], p < 0.001). SGLTi increased production and attenuated the increased BHB fractional excretion (decreased to 0.3 % during mild hyperglycemia, p < 0.001), resulting in higher plasma concentrations (increased to 0.21 [0.05-0.40] mmol/L, p < 0.001), particularly in females (interaction p < 0.001). CONCLUSIONS: Even mild hyperglycemia is associated with greater ketone production, compensated by urinary excretion, in T1D. However, SGLTi exaggerates production and partially reduces compensatory excretion, particularly in women.
Subject(s)
Diabetes Mellitus, Type 1 , Hyperglycemia , Symporters , Humans , Female , Male , Diabetes Mellitus, Type 1/drug therapy , Ketones/therapeutic use , Hyperglycemia/drug therapy , 3-Hydroxybutyric Acid , Glucose , Sodium , Blood Glucose/analysisABSTRACT
Beans elicit lower glycemic responses (GRs) than other starchy foods, but the minimum effective dose (MED) to reduce GR is unknown. We sought to determine the MED of beans compared to common starchy foods. Overnight-fasted healthy volunteers consumed »c (phase 1, n = 24) or ½c (phase 2, n = 18) of black, cranberry, great northern, kidney, navy and pinto beans and corn, rice, pasta and potato (controls), with blood glucose measured before and for 2 h after eating. GRs (incremental areas under the curves, iAUCs) after beans were consumed were compared to those of controls by ANOVA followed by Dunnett's test. To qualify for MED, beans had to elicit an effective reduction in GR, defined as a statistically significant reduction in iAUC of ≥20% (i.e., a relative glycemic response, RGR, ≤80). Outcomes from in vitro digestion were compared with in vivo RGR. Both doses of all six beans effectively reduced GR versus all four starchy controls, except for »c and ½c cranberry and pinto vs. corn, »c great northern and navy vs. corn and »c navy and pinto vs. potato. MED criteria were met for 18 comparisons of the »c servings, with four of the remaining six met by the ½c servings. The overall mean ± SEM RGR vs. controls was similar for the »c and ½c servings: 53 ± 4% and 56 ± 3%, respectively. By multiple regression analysis, RGR = 23.3 × RDS + 8.3 × SDS - 20.1 × RS + 39.5 × AS - 108.2 (rapidly digested starch, p < 0.001; slowly digested starch, p = 0.054; resistant starch, p = 0.18; available sugars, p = 0.005; model r = 0.98, p = 0.001). RGR correlated with in vitro glucose release (r = 0.92, p < 0.001). The MED of beans is » cup. For n = 30 comparisons (n = 24 beans vs. controls, n = 6 controls vs. each other), an effective reduction in GR was predicted from in vitro carbohydrate analysis with 86% sensitivity and 100% specificity.
Subject(s)
Fabaceae , Glycemic Index , Humans , Blood Glucose , Starch , Fruit , Digestion , Dietary CarbohydratesABSTRACT
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.
Subject(s)
Fructose , Hypertension , Adult , Humans , Blood Pressure , Fruit , SugarsABSTRACT
When this project was designed, there was no evidence that adding resistant starch to available carbohydrate (avCHO) reduced glycaemic and insulinaemic responses (GIR). We compared GIR elicited by a cookie containing cross-linked phosphorylated RS4 wheat starch (Fibersym®) (RS4XL) versus an avCHO-matched control-cookie (CC) after n = 15 adults had consumed RS4XL or CC daily for 3-days using a double-blind, randomised, cross-over design. The difference in glucose iAUC over 0-2 h (primary endpoint) (mmol × min/L) after RS4XL, (mean ± SEM) 106 ± 16, versus CC, 124 ± 16, was not significant (p = 0.087). However, RS4XL reduced 0-90 min glucose iAUC (72 ± 9 vs 87 ± 9, p = 0.022), peak glucose concentration (6.05 ± 0.36 vs 6.57 ± 0.31 mmol/L, p = 0.017) and 0-2 h insulin iAUC (189 ± 21 vs 246 ± 24 nmol × h/L, p = 0.020). These results show that RS4XL reduced postprandial glycaemic and insulinaemic responses when added to avCHO, but do not prove that the products of its colonic fermentation are required for this effect.
Subject(s)
Insulin , Starch , Humans , Adult , Glucose , Triticum , Blood Glucose , Glycemic Index , Dietary Carbohydrates , Postprandial Period , Cross-Over StudiesABSTRACT
Women with gestational diabetes (GD) have reduced antioxidant capacity; however, the relationship between maternal diet, maternal biochemical capacity, breast milk concentration, and infant intake has not been adequately explored in the literature. An exploration of underlying mechanism(s) is warranted, particularly for nutrient antioxidants impacted by maternal intake. These nutrients may provide a means for modifying maternal and infant antioxidant capacity. Oxygen radical absorbance capacity (ORAC), alpha-tocopherol, ascorbic acid, and beta-carotene concentrations were measured in breast milk of women with and without GD. Plasma, three-day diet records, and breast milk were collected at 6 to 8 weeks postpartum. Student's t-test was used to compare breast milk ORAC, nutrient antioxidant concentration and plasma ORAC between women with and without GD. Pearson correlations were used to determine associations among antioxidant concentrations in breast milk and dietary antioxidant intake. Breast milk antioxidant concentrations were associated with maternal intake of beta-carotene (r = 0.629, p = 0.005). Breast milk and plasma ORAC and antioxidant vitamin concentrations were not significantly different between GD and NG women. Breast milk ORAC associated with breast milk alpha-tocopherol for NG (r = 0.763, p = 0.010), but not GD women (r = 0.385, p = 0.35), and with breast milk ascorbic acid for GD (r = 0.722, p = 0.043) but not NG women (r = 0.141, p = 0.70; interaction p = 0.041). In GD participants, breast milk ORAC was significantly associated with plasma ORAC (r = 0.780, p = 0.039). ORAC and antioxidant vitamin concentrations in breast milk in women with GD were comparable to women with NG; however, the relationships between breast milk ORAC and vitamin concentrations differed in GD versus NG women for alpha-tocopherol and ascorbic acid.
ABSTRACT
BACKGROUND: Sugar-sweetened beverages (SSBs) providing excess energy increase adiposity. The effect of other food sources of sugars at different energy control levels is unclear. OBJECTIVES: To determine the effect of food sources of fructose-containing sugars by energy control on adiposity. METHODS: In this systematic review and meta-analysis, MEDLINE, Embase, and Cochrane Library were searched through April 2022 for controlled trials ≥2 wk. We prespecified 4 trial designs by energy control: substitution (energy-matched replacement of sugars), addition (energy from sugars added), subtraction (energy from sugars subtracted), and ad libitum (energy from sugars freely replaced). Independent authors extracted data. The primary outcome was body weight. Secondary outcomes included other adiposity measures. Grading of Recommendations Assessment, Development, and Evaluation (GRADE) was used to assess the certainty of evidence. RESULTS: We included 169 trials (255 trial comparisons, n = 10,357) assessing 14 food sources at 4 energy control levels over a median 12 wk. Total fructose-containing sugars increased body weight (MD: 0.28 kg; 95% CI: 0.06, 0.50 kg; PMD = 0.011) in addition trials and decreased body weight (MD: -0.96 kg; 95% CI: -1.78, -0.14 kg; PMD = 0.022) in subtraction trials with no effect in substitution or ad libitum trials. There was interaction/influence by food sources on body weight: substitution trials [fruits decreased; added nutritive sweeteners and mixed sources (with SSBs) increased]; addition trials [dried fruits, honey, fruits (≤10%E), and 100% fruit juice (≤10%E) decreased; SSBs, fruit drink, and mixed sources (with SSBs) increased]; subtraction trials [removal of mixed sources (with SSBs) decreased]; and ad libitum trials [mixed sources (with/without SSBs) increased]. GRADE scores were generally moderate. Results were similar across secondary outcomes. CONCLUSIONS: Energy control and food sources mediate the effect of fructose-containing sugars on adiposity. The evidence provides a good indication that excess energy from sugars (particularly SSBs at high doses ≥20%E or 100 g/d) increase adiposity, whereas their removal decrease adiposity. Most other food sources had no effect, with some showing decreases (particularly fruits at lower doses ≤10%E or 50 g/d). This trial was registered at clinicaltrials.gov as NCT02558920 (https://clinicaltrials.gov/ct2/show/NCT02558920).
Subject(s)
Adiposity , Fructose , Humans , Obesity , Body Weight , Fruit , BeveragesABSTRACT
To determine the minimum amount of oat ß-glucan (OBG) required to reduce glycaemic responses (MinDose), we conducted a systematic review and meta-regression analysis of acute, crossover, single-meal feeding trials that examined the effects of adding OBG or oat bran to a carbohydrate-containing test-meal versus a control test-meal containing an equivalent amount of available-carbohydrate (avCHO) from the same or similar source. Medline, Embase, and Cochrane Library were searched up to 18 August 2021. The primary outcome was glucose incremental-area-under-the-curve (iAUC). Secondary outcomes included insulin iAUC, and glucose and insulin incremental peak-rise (iPeak). Two independent reviewers extracted data. Results were expressed as ratio-of-means (RoM) with 95% confidence intervals (CIs). Linear associations were assessed by random effects meta-regression. MinDose was defined as the dose at which the upper 95% CI of the regression line cut the line of no effect (i.e., RoM = 1). Fifty-nine comparisons (n = 340) were included; 57 in healthy subjects without diabetes and two in subjects with diabetes; 24 high-MW (>1000 kg/mol), 22 medium-MW (300-1,000 kg/mol), and 13 low-MW (<300 kg/mol). In healthy subjects without diabetes the associations between OBG dose and glucose iAUC and iPeak were linear (non-linear p value >0.05). MinDoses for glucose iAUC for high-MW, medium-MW and low-MW OBG, respectively, were estimated to be 0.2 g, 2.2 g and 3.2 g per 30 g avCHO; MinDoses for glucose iPeak were less than those for iAUC. Insufficient data were available to assess MinDose for insulin, however, there was no evidence of a disproportionate increase in insulin. More high-quality trials are needed to establish MinDose in individuals with diabetes.
Subject(s)
Blood Glucose , Diabetes Mellitus , Humans , Blood Glucose/analysis , Molecular Weight , Healthy Volunteers , Avena , Insulin , Regression Analysis , GlucoseABSTRACT
BACKGROUND: Fructose-containing sugars as sugar-sweetened beverages (SSBs) may increase inflammatory biomarkers. Whether this effect is mediated by the food matrix at different levels of energy is unknown. To investigate the role of food source and energy, we conducted a systematic review and meta-analysis of controlled trials on the effect of different food sources of fructose-containing sugars on inflammatory markers at different levels of energy control. METHODS: MEDLINE, Embase, and the Cochrane Library were searched through March 2022 for controlled feeding trials ≥ 7 days. Four trial designs were prespecified by energy control: substitution (energy matched replacement of sugars); addition (excess energy from sugars added to diets); subtraction (energy from sugars subtracted from diets); and ad libitum (energy from sugars freely replaced). The primary outcome was C-reactive protein (CRP). Secondary outcomes were tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6). Independent reviewers extracted data and assessed risk of bias. GRADE assessed certainty of evidence. RESULTS: We identified 64 controlled trials (91 trial comparisons, n = 4094) assessing 12 food sources (SSB; sweetened dairy; sweetened dairy alternative [soy]; 100% fruit juice; fruit; dried fruit; mixed fruit forms; sweetened cereal grains and bars; sweets and desserts; added nutritive [caloric] sweetener; mixed sources [with SSBs]; and mixed sources [without SSBs]) at 4 levels of energy control over a median 6-weeks in predominantly healthy mixed weight or overweight/obese adults. Total fructose-containing sugars decreased CRP in addition trials and had no effect in substitution, subtraction or ad libitum trials. No effect was observed on other outcomes at any level of energy control. There was evidence of interaction/influence by food source: substitution trials (sweetened dairy alternative (soy) and 100% fruit juice decreased, and mixed sources (with SSBs) increased CRP); and addition trials (fruit decreased CRP and TNF-α; sweets and desserts (dark chocolate) decreased IL-6). The certainty of evidence was moderate-to-low for the majority of analyses. CONCLUSIONS: Food source appears to mediate the effect of fructose-containing sugars on inflammatory markers over the short-to-medium term. The evidence provides good indication that mixed sources that contain SSBs increase CRP, while most other food sources have no effect with some sources (fruit, 100% fruit juice, sweetened soy beverage or dark chocolate) showing decreases, which may be dependent on energy control. CLINICALTRIALS: gov: (NCT02716870).
Subject(s)
Fructose , Interleukin-6 , Beverages , Biomarkers , C-Reactive Protein/metabolism , Sweetening Agents , Tumor Necrosis Factor-alphaABSTRACT
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.
Subject(s)
Non-alcoholic Fatty Liver Disease , Sugar-Sweetened Beverages , Adult , Beverages/analysis , Fructose/adverse effects , Fruit , Fruit and Vegetable Juices/analysis , Humans , Non-alcoholic Fatty Liver Disease/etiology , Randomized Controlled Trials as TopicABSTRACT
Dietary starch contains rapidly (RAG) and slowly available glucose (SAG). To establish the relationships between the RAG:SAG ratio and postprandial glucose, insulin and hunger, we measured postprandial responses elicited by test meals varying in the RAG:SAG ratio in n 160 healthy adults, each of whom participated in one of four randomised cross-over studies (n 40 each): a pilot trial comparing six chews (RAG:SAG ratio 2·4-42·7) and three studies comparing a test granola (TG1-3, RAG:SAG ratio 4·5-5·2) with a control granola (CG1-3, RAG:SAG ratio 54·8-69·3). Within studies, test meals were matched for fat, protein and available carbohydrate. Blood glucose, serum insulin and subjective hunger were measured for 3 h. Data were subjected to repeated-measures analysis of variance (ANOVA). The relationships between the RAG:SAG ratio and postprandial end points were determined by regression analysis. In the pilot trial, 0-2 h glucose incremental areas under the curve (iAUC0-2; primary end point) varied across the six chews (P = 0·014) with each 50 % reduction in the RAG:SAG ratio reducing relative glucose response by 4·0 %. TGs1-3 elicited significantly lower glucose iAUC0-2 than CGs1-3 by 17, 18 and 17 %, respectively (similar to the 15 % reduction predicted by the pilot trial). The combined means ± sem (n 120) for TC and CG were glucose iAUC0-2, 98 ± 4 v. 118 ± 4 mmol × min/l (P < 0·001), and insulin iAUC0-2, 153 ± 9 v. 184 ± 11 nmol × h/l (P < 0·001), respectively. Neither postprandial hunger nor glucose or hunger increments 2 h after eating differed significantly between TG and CG. We concluded that TGs with RAG:SAG ratios <5·5 predictably reduced glycaemic and insulinaemic responses compared with CGs with RAG:SAG ratios >54. However, compared with CG, TG did not reduce postprandial hunger or delay the return of glucose or hunger to baseline.
Subject(s)
Edible Grain , Insulin , Adult , Blood Glucose/metabolism , Edible Grain/chemistry , Edible Grain/metabolism , Glucose , Glycemic Index , Humans , Postprandial PeriodABSTRACT
BACKGROUND: Practical risk reduction strategies are needed to address cardiovascular disease. Beans can decrease LDL cholesterol; however, research into different daily amounts and varieties is warranted. OBJECTIVES: To examine the effects of canned beans (daily rotation of black, navy, pinto, dark red kidney, white kidney) in 1-cup (1CB, 180 g) and ½-cup (½CB, 90 g) daily amounts compared with a 1-cup white rice (WR) control on serum lipid and glycemic biomarkers in adults with elevated LDL cholesterol. METHODS: Adults [n = 73, mean ± SD age: 48.1 ± 14.2 y; BMI (in kg/m2): 25.9 ± 4.22; fasting serum LDL cholesterol: 3.0-5.0 mmol/L] consumed 1CB, ½CB, and WR for 4-wk treatment periods separated by ≥4-wk washouts in a multicenter, randomized, crossover study. Fasting serum LDL cholesterol (primary outcome) and other lipids and glycemic biomarkers (secondary outcomes) were measured on study days 1 and 29 of each treatment period with study day 29 values compared using repeated-measures ANCOVA, including study day 1 values as covariates. RESULTS: Treatment completion was n = 66 for 1CB, n = 68 for ½CB, and n = 64 for WR. Total cholesterol on study day 29 was lower for 1CB (P = 0.04) but not ½CB (P = 0.77) compared with WR (-5.46%, -2.74%, -0.65% changes from study day 1, respectively) and did not differ between 1CB and ½CB (P = 0.17). LDL cholesterol on study day 29 was also lower for 1CB (P = 0.002) but not ½CB (P = 0.30) compared with WR (-8.08%, -3.84%, +0.49% changes from study day 1, respectively) and did not differ between 1CB and ½CB (P = 0.11). Other lipids and glycemic biomarkers did not differ among treatments. CONCLUSIONS: Consumption of 1 cup (180 g) of canned beans of multiple varieties decreased total and LDL cholesterol in adults with elevated LDL cholesterol, supporting a practical strategy for cardiovascular disease risk reduction. This trial was registered at clinicaltrials.gov as NCT03830970.
Subject(s)
Cardiovascular Diseases , Vegetables , Adult , Biomarkers , Cardiovascular Diseases/prevention & control , Cholesterol, LDL , Cross-Over Studies , Humans , Middle AgedABSTRACT
The glycaemic index (GI) is a food metric that ranks the acute impact of available (digestible) carbohydrates on blood glucose. At present, few countries regulate the inclusion of GI on food labels even though the information may assist consumers to manage blood glucose levels. Australia and New Zealand regulate GI claims as nutrition content claims and also recognize the GI Foundation's certified Low GI trademark as an endorsement. The GI Foundation of South Africa endorses foods with low, medium and high GI symbols. In Asia, Singapore's Healthier Choice Symbol has specific provisions for low GI claims. Low GI claims are also permitted on food labels in India. In China, there are no national regulations specific to GI; however, voluntary claims are permitted. In the USA, GI claims are not specifically regulated but are permitted, as they are deemed to fall under general food-labelling provisions. In Canada and the European Union, GI claims are not legal under current food law. Inconsistences in food regulation around the world undermine consumer and health professional confidence and call for harmonization. Global provisions for GI claims/endorsements in food standard codes would be in the best interests of people with diabetes and those at risk.
Subject(s)
Diet , Food Analysis , Global Health , Glycemic Index , Food Labeling , HumansABSTRACT
OBJECTIVE: To inform the update of the European Association for the Study of Diabetes clinical practice guidelines for nutrition therapy. DESIGN: Systematic review and meta-analysis of randomised controlled trials. DATA SOURCES: Medline, Embase, and the Cochrane Library searched up to 13 May 2021. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Randomised controlled trials of three or more weeks investigating the effect of diets with low glycaemic index (GI)/glycaemic load (GL) in diabetes. OUTCOME AND MEASURES: The primary outcome was glycated haemoglobin (HbA1c). Secondary outcomes included other markers of glycaemic control (fasting glucose, fasting insulin); blood lipids (low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), non-HDL-C, apo B, triglycerides); adiposity (body weight, BMI (body mass index), waist circumference), blood pressure (systolic blood pressure (SBP) and diastolic blood pressure (DBP)), and inflammation (C reactive protein (CRP)). DATA EXTRACTION AND SYNTHESIS: Two independent reviewers extracted data and assessed risk of bias. Data were pooled by random effects models. GRADE (grading of recommendations assessment, development, and evaluation) was used to assess the certainty of evidence. RESULTS: 29 trial comparisons were identified in 1617 participants with type 1 and 2 diabetes who were predominantly middle aged, overweight, or obese with moderately controlled type 2 diabetes treated by hyperglycaemia drugs or insulin. Low GI/GL dietary patterns reduced HbA1c in comparison with higher GI/GL control diets (mean difference −0.31% (95% confidence interval −0.42 to −0.19%), P<0.001; substantial heterogeneity, I2=75%, P<0.001). Reductions occurred also in fasting glucose, LDL-C, non-HDL-C, apo B, triglycerides, body weight, BMI, systolic blood pressure (dose-response), and CRP (P<0.05), but not blood insulin, HDL-C, waist circumference, or diastolic blood pressure. A positive dose-response gradient was seen for the difference in GL and HbA1c and for absolute dietary GI and SBP (P<0.05). The certainty of evidence was high for the reduction in HbA1c and moderate for most secondary outcomes, with downgrades due mainly to imprecision. CONCLUSIONS: This synthesis suggests that low GI/GL dietary patterns result in small important improvements in established targets of glycaemic control, blood lipids, adiposity, blood pressure, and inflammation beyond concurrent treatment with hyperglycaemia drugs or insulin, predominantly in adults with moderately controlled type 1 and type 2 diabetes. The available evidence provides a good indication of the likely benefit in this population. STUDY REGISTRATION: ClinicalTrials.gov NCT04045938.
Subject(s)
Diabetes Mellitus, Type 1/prevention & control , Diabetes Mellitus, Type 2/prevention & control , Glycemic Index , Glycemic Load , Cardiometabolic Risk Factors , Diet, Diabetic , Glycemic Control , HumansABSTRACT
BACKGROUND: It was suggested that low salivary-amylase activity (SAA) and cooling or stir-frying cooked starch decreases its digestibility and glycemic index. OBJECTIVE: We determined the effects of SAA, cooling, and single-nucleotide polymorphisms (SNPs) in the salivary amylase (AMY1), pancreatic amylase (AMY2A, AMY2B), maltase-glucoamylase (MGAM), and sucrase-isomaltase (SI) genes on starch digestibility and glycemic index of cooked polished rice. METHODS: Healthy subjects [pilot, n = 12; main, n = 20 with low-SAA (<50 U/mL), and n = 20 with high-SAA (>105 U/mL)] consumed test meals containing 25 g (pilot) or 50 g (main) available carbohydrate at a contract research organization using open-label (pilot) or assessor-blinded (main), randomized, crossover, Latin-square designs (trial registration: NCT03667963). Pilot-trial test meals were dextrose, freshly cooked polished rice, cooked rice cooled overnight, stir-fried hot rice, or stir-fried cold rice. Main-trial test meals were dextrose, dextrose plus 10 g lactulose, plain hot rice, or plain cold rice. In both trials, blood glucose was measured fasting and at intervals over 2 h. In the main trial, breath hydrogen was measured fasting and hourly for 6 h to estimate in vivo starch digestibility. Data were analyzed by repeated-measures ANOVA for the main effects of temperature and stir-frying (pilot trial) or the main effects of SAA and temperature (main trial) and their interactions. Effects of 24 single nucleotide polymorphisms (SNPs) were assessed separately. Means were considered to be equivalent if the 95% CI of the differences were within ±20% of the comparator mean for glucose response/glycemic index or ±7% for digestibility. RESULTS: Pilot: neither temperature nor stir-frying significantly affected glucose incremental AUC (primary endpoint, n = 12). Main: mean ± SEM glycemic index (primary endpoint, n = 40) was equivalent for low-SAA compared with high-SAA (73 ± 3 vs. 75 ± 4) and cold rice compared with hot rice (75 ± 3 vs. 70 ± 3). Estimated starch digestibility (n = 39) was equivalent for low-SAA compared with high-SAA (95% ± 1% vs. 92% ± 1%) and hot rice compared with cold rice (94% ± 1% vs. 93% ± 1%). No meaningful associations were observed between genotypes and starch digestibility or glycemic index for any of the SNPs. CONCLUSIONS: The results do not support the hypotheses that low-SAA, cooling, and common genetic variations in starch-digesting enzymes affect the glycemic index or in vivo carbohydrate digestibility of cooked polished rice. This trial was registered at clinicaltrials.gov as NCT03667963.
Subject(s)
Amylases/metabolism , Glycemic Index , Oryza , Polymorphism, Single Nucleotide , Saliva/enzymology , Starch/metabolism , Adult , Aged , Amylases/genetics , Blood Glucose/analysis , Cross-Over Studies , Digestion , Female , Humans , Male , Middle Aged , Sucrase-Isomaltase Complex/genetics , alpha-Glucosidases/geneticsABSTRACT
BACKGROUND: High-molecular-weight (MW) oat ß-glucan (OBG), consumed at 3-4 g/d, in solid foods reduces LDL cholesterol by a median of â¼6.5%. OBJECTIVES: We evaluated the effect of a beverage providing 3 g/d high-MW OBG on reduction of LDL cholesterol (primary endpoint) when compared with placebo. METHODS: We performed a parallel-design, randomized clinical trial at a contract research organization; participants, caregivers, and outcome assessors were blinded to treatment allocation. Participants with LDL cholesterol between 3.0 and 5.0 mmol/L, inclusive [n = 538 screened, n = 260 ineligible, n = 23 lost, n = 48 withdrawn (product safety); n = 207 randomly assigned, n = 7 dropped out, n = 9 withdrawn (protocol violation); n = 191 analyzed; n = 72 (37.7%) male, mean ± SD age: 43.3 ± 14.3 y, BMI: 29.7 ± 5.2 kg/m2], were randomly assigned to consume, 3 times daily for 4 wk, 1 g OBG (n = 104, n = 96 analyzed) or rice powder (Control, n = 103, n = 95 analyzed) mixed into 250 mL water. Treatment effects were assessed as change from baseline and differences analyzed using a 2-sided t test via ANOVA with baseline characteristics as covariates. RESULTS: After 4 wk, change from baseline least-squares-mean LDL cholesterol on OBG (-0.195 mmol/L) was less than on Control (0.012 mmol/L) by mean: 0.207 mmol/L (95% CI: 0.318, 0.096 mmol/L; P = 0.0003); the following secondary endpoints were also reduced as follows: total cholesterol (TC) (0.226 mmol/L; 95% CI: 0.361, 0.091 mmol/L; P = 0.001), TC:HDL cholesterol ratio (0.147; 95% CI: 0.284, 0.010; P = 0.036), non-HDL cholesterol (0.194 mmol/L; 95% CI: 0.314, 0.073 mmol/L; P = 0.002), and Framingham cardiovascular disease (CVD) risk (0.474; 95% CI: 0.900, 0.049, P = 0.029). Changes in HDL cholesterol, triglycerides, glucose, and insulin did not differ between treatment groups (P > 0.05). Lipid treatment effects were not significantly modified by age, sex, BMI, or hypertension treatment. There were no major adverse events, but both treatments transiently increased gastrointestinal symptoms. CONCLUSIONS: Consuming a beverage containing 1 g high-MW OBG 3 times daily for 4 wk significantly reduced LDL cholesterol by â¼6% and CVD risk by â¼8% in healthy adults with LDL cholesterol between 3 and 5 mmol/L.This trial was registered at clinicaltrials.gov as NCT03911427.
Subject(s)
Cardiovascular Diseases , Adult , Beverages , Cardiovascular Diseases/prevention & control , Cholesterol , Cholesterol, HDL , Cholesterol, LDL , Double-Blind Method , Female , Humans , Male , Middle Aged , Triglycerides , beta-GlucansABSTRACT
The gastrointestinal (GI) side-effects of dietary fibers are recognized, but less is known about their effects on non-GI symptoms. We assessed non-GI symptoms in a trial of the LDL-cholesterol lowering effect of oat ß-glucan (OBG). Participants (n = 207) with borderline high LDL-cholesterol were randomized to an OBG (1 g OBG, n = 104, n = 96 analyzed) or Control (n = 103, n = 95 analyzed) beverage 3-times daily for 4 weeks. At screening, baseline, 2 weeks and 4 weeks participants rated the severity of 16 non-GI symptoms as none, mild, moderate or severe. The occurrence and severity (more or less severe than pre-treatment) were compared using chi-squared and Fisher's exact test, respectively. During OBG treatment, the occurrence of exhaustion and fatigue decreased versus baseline (p < 0.05). The severity of headache (2 weeks, p = 0.032), anxiety (2 weeks p = 0.059) and feeling cold (4 weeks, p = 0.040) were less on OBG than Control. The severity of fatigue and hot flashes at 4 weeks, limb/joint pain at 2 weeks and difficulty concentrating at both times decreased on OBG versus baseline. High serum c-reactive-protein and changes in c-reactive-protein, oxidized-LDL, and GI-symptom severity were associated with the occurrence and severity of several non-GI symptoms. These data provide preliminary, hypothesis-generating evidence that OBG may reduce several non-GI symptoms in healthy adults.
Subject(s)
Affect/drug effects , Dietary Fiber/pharmacology , Eating/psychology , beta-Glucans/pharmacology , Adolescent , Adult , Aged , Anxiety/therapy , C-Reactive Protein/analysis , Chi-Square Distribution , Cholesterol, LDL/blood , Double-Blind Method , Fasting/blood , Fatigue/therapy , Female , Gastrointestinal Tract/drug effects , Headache/therapy , Healthy Volunteers , Humans , Male , Middle Aged , Musculoskeletal Pain/therapy , Nutritional Physiological Phenomena , Severity of Illness Index , Young AdultABSTRACT
BACKGROUND: Although fructose as a source of excess calories increases uric acid, the effect of the food matrix is unclear. OBJECTIVES: To 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. METHODS: MEDLINE, 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. RESULTS: We 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. CONCLUSIONS: Food 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.