Comparison of a Daily Steviol Glycoside Beverage compared with a Sucrose Beverage for Four Weeks on Gut Microbiome in Healthy Adults.

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.

Important food sources of fructose-containing sugars and adiposity: A systematic review and meta-analysis of controlled feeding trials.

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).

Different Food Sources of Fructose-Containing Sugars and Fasting Blood Uric Acid Levels: A Systematic Review and Meta-Analysis of Controlled Feeding Trials.

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.

Acute glycemic and insulin response of Fossence™ alone, or when substituted or added to a carbohydrate challenge: A three-phase, acute, randomized, cross-over, double blind clinical trial.

Short chain fructo-oligosaccharides (scFOS) are well-recognized prebiotic fibers. Fossence™ (FOSS) is a scFOS that has been produced from sucrose via a proprietary fermentation process and has not been tested for its digestibility or glucose/insulin response (GR and IR, respectively). The present randomized, controlled, cross-over study was conducted in 3 phases to explore GR and IR to ingestion of FOSS, when replaced by/added to available-carbohydrates (avCHO) among 25 healthy adults (40 ± 14years). In each phase GR and IR elicited by 3-4 test-meals were measured among the fasted recruited subjects. The interventional test meals were as follows: Phase-1, water alone or 10g FOSS or 10g Dextrose in 250ml water; Phase-2, 250ml water containing Dextrose:FOSS (g:g) in the content as 50:0 or 50:15 or 35:0 or 35:15; Phase-3 portions of white-bread (WB) containing avCHO:FOSS (g:g) in the content as 50:0 or 50:15 or 35:0 or 35:15. Blood samples (finger prick method) were collected at fasting and 15, 30, 45, 60, 90 and 120 min after start of test meal ingestion. Plasma glucose and serum insulin were analyzed utilizing standard methods. The primary endpoint was differences in glucose IAUC. All subjects provided their written consent to participate in the study (ClinicalTrials.gov: NCT03755232). The results demonstrated that FOSS, when consumed alone, showed no raise in glycaemia or insulinemia and was statistically equivalent to response of water alone. GR and IR elicited by dextrose:FOSS and WB:FOSS test-meals of Phase 2 and Phase 3, were statistically equivalent to the respective test-meals without FOSS. Result of the 3 phases support the hypothesis that FOSS is resistant to breakdown and is indigestible in the human small-intestine, and therefore can be classified as an unavailable carbohydrate that does not raise post prandial blood glucose or insulin. FOSS, being sweet to taste, may be an acceptable sugar replacer in beverages without compromising their taste and sensory qualities.

Effect of fructose and its epimers on postprandial carbohydrate metabolism: A systematic review and meta-analysis.

AIMS: To synthesize the evidence of the effect of small doses (≤30-g/meal) of fructose and its epimers (allulose, tagatose, and sorbose) on the postprandial glucose and insulin response to carbohydrate-containing meals. METHODS: MEDLINE, EMBASE, and the Cochrane Central Register of Controlled Trials were searched through to April 9, 2019. We included randomized (RCTs) and non-randomized acute, single-meal, controlled feeding trials that added ≤30-g of fructose or its epimers either prior to or with a carbohydrate-containing meal compared with the same meal alone. Outcomes included the incremental area under the curve (iAUC) for glucose and insulin, the Matsuda Insulin Sensitivity Index, and the Early Insulin Secretion Index. Data were expressed as ratio of means (RoM) with 95% CIs and pooled using the inverse variance method. The overall certainty of the evidence was evaluated using GRADE. RESULTS: Forty trial comparisons (n = 400) were included (none for sorbose). Allulose significantly reduced the postprandial iAUC glucose response by 10% (0.90 [0.84 to 0.96], P < 0.01). Tagatose significantly reduced the postprandial iAUC insulin response by 25% (0.75 [0.62 to 0.91], P < 0.01) and showed a non-significant 3% reduction in the postprandial iAUC glucose response (0.97 [0.94 to 1.00], P = 0.07). There was no effect of fructose on any outcome. The certainty of the evidence was graded as low to moderate for fructose, moderate for allulose, and low for tagatose. CONCLUSIONS: Small doses of allulose and tagatose, but not fructose, lead to modest improvements on postprandial glucose and insulin regulation. There is a need for long-term RCTs to confirm the sustainability of these improvements.

Important food sources of fructose-containing sugars and incident gout: a systematic review and meta-analysis of prospective cohort studies.

OBJECTIVE: Sugar-sweetened beverages (SSBs) are associated with hyperuricaemia and gout. Whether other important food sources of fructose-containing sugars share this association is unclear. DESIGN: To assess the relation of important food sources of fructose-containing sugars with incident gout and hyperuricaemia, we conducted a systematic review and meta-analysis of prospective cohort studies. METHODS: We searched MEDLINE, Embase and the Cochrane Library (through 13 September 2017). We included prospective cohort studies that investigated the relationship between food sources of sugar and incident gout or hyperuricaemia. Two independent reviewers extracted relevant data and assessed the risk of bias. We pooled natural-log transformed risk ratios (RRs) using the generic inverse variance method with random effects model and expressed as RR with 95% confidence intervals (CIs). The overall certainty of the evidence was assessed using the Grading of Recommendations Assessment, Development and Evaluation system. RESULTS: We identified three studies (1 54 289 participants, 1761 cases of gout), comparing the highest with the lowest level of exposure for SSBs, fruit juices and fruits. No reports were found reporting incident hyperuricaemia. Fruit juice and SSB intake showed an adverse association (fruit juice: RR=1.77, 95% CI 1.20 to 2.61; SSB: RR=2.08, 95% CI 1.40 to 3.08), when comparing the highest to lowest intake of the most adjusted models. There was no significant association between fruit intake and gout (RR 0.85, 95% CI 0.63 to 1.14). The strongest evidence was for the adverse association with SSB intake (moderate certainty), and the weakest evidence was for the adverse association with fruit juice intake (very low certainty) and lack of association with fruit intake (very low certainty). CONCLUSION: There is an adverse association of SSB and fruit juice intake with incident gout, which does not appear to extend to fruit intake. Further research is needed to improve our estimates. TRIAL REGISTRATION NUMBER: NCT02702375; Results.

Yogurt Is a Low-Glycemic Index Food.

High yogurt intake is associated with a reduced risk of type 2 diabetes (T2DM). Although several mechanisms could explain this association, this paper addresses the glycemic and insulinemic impact of yogurt. There is evidence that low-glycemic index (GI) and low-glycemic load (GL) diets are associated with a reduced risk of T2DM. The 93 GI values for yogurt in the University of Sydney's GI database have a mean ± SD of 34 ± 13, and 92% of the yogurts are low-GI (≤55). The 43 plain yogurts in the database have a lower GI than the 50 sweetened yogurts, 27 ± 11 compared with 41 ± 11 (P < 0.0001). This difference is not explained by sugar, per se, but rather by the higher protein-to-carbohydrate ratio in plain yogurt. Although yogurt has a low GI, its insulinemic index (II) is higher than its GI. High insulin responses may be deleterious because hyperinsulinemia is associated with an increased risk of T2DM. Nevertheless, this may not be a concern for yogurt because, although its II is higher than its GI, the II of yogurt is within the range of II values for nondairy low-GI foods. In addition, mixed meals containing dairy protein elicit insulin responses similar to those elicited by mixed meals of similar composition containing nondairy protein. Because the GI of yogurt is lower than that of most other carbohydrate foods, exchanging yogurt for other protein and carbohydrate sources can reduce the GI and GL of the diet, and is in line with recommended dietary patterns, which include whole grains, fruits, vegetables, nuts, legumes, fish, vegetable oils, and yogurt.

Reformulating cereal bars: high resistant starch reduces in vitro digestibility but not in vivo glucose or insulin response; whey protein reduces glucose but disproportionately increases insulin.

BACKGROUND: Resistant starch (RS) and whey protein are thought to be effective nutrients for reducing glycemic responses. OBJECTIVE: We aimed to determine the effect of varying the sucrose, RS, and whey protein content of cereal bars on glucose and insulin responses. DESIGN: Twelve healthy subjects [mean ± SD age: 36 ± 12 y; mean ± SD body mass index (in kg/m2): 24.9 ± 2.7] consumed 40 g available-carbohydrate (avCHO) portions of 5 whole-grain cereal bars that contained varying amounts of RS and whey protein concentrate [WPC; 70% protein; RS:WPC, %wt:wt: 15:0 (Bar15/0); 15:0, low in sucrose (Bar15/0LS); 15:5 (Bar15/5); 10:5 (Bar10/5); and 10:10 (Bar10/10)] and 2 portion sizes of a control bar low in whole grains, protein, and RS [control 1 contained 40 g avCHO (Control1); control 2 contained total carbohydrate equal to Bar15/0LS (Control2)] on separate days by using a randomized crossover design. Glucose and insulin responses in vivo and carbohydrate digestibility in vitro were measured over 3 h. RESULTS: Incremental area under the curve (iAUC) over 0-3 h for glucose (min × mmol/L) differed significantly between treatments (P < 0.001) [Bar15/0LS (mean ± SEM), 169 ± 14; Control2, 164 ± 20; Bar15/0, 144 ± 15; Control1, 140 ± 17; Bar10/5, 117 ± 12; Bar15/5, 116 ± 9; and Bar10/10, 100 ± 9; Tukey's least significant difference = 42, P < 0.05], but insulin iAUC did not differ significantly. Higher protein content was associated with a lower glucose iAUC (P = 0.028) and a higher insulin-to-glucose iAUC ratio (P = 0.002) All 5 RS-containing bars were digested in vitro ∼30% more slowly than the control bars (P < 0.05); however, in vivo responses were not related to digestibility in vitro. Glucose and insulin responses elicited by high-RS, whey protein-free bars were similar to those elicited from control bars. CONCLUSIONS: The inclusion of RS in cereal bar formulations did not reduce glycemic responses despite slower starch digestion in vitro. Thus, caution is required when extrapolating in vitro starch digestibility to in vivo glycemic response. The inclusion of whey protein in cereal bar formulations to reduce glycemic response requires caution because this may be associated with a disproportionate increase in insulin as judged by an increased insulin-to-glucose iAUC ratio. This trial was registered at clinicaltrials.gov as NCT02537587.

Whole Soy Flour Incorporated into a Muffin and Consumed at 2 Doses of Soy Protein Does Not Lower LDL Cholesterol in a Randomized, Double-Blind Controlled Trial of Hypercholesterolemic Adults.

BACKGROUND: Soy protein may reduce coronary heart disease (CHD) risk by lowering LDL cholesterol, but few studies have assessed whether whole soy flour displays a similar effect. OBJECTIVE: The aim of this study was to assess the dose effect of whole soy flour incorporated into muffins on plasma LDL cholesterol in hypercholesterolemic adults. METHODS: Adults aged 30-70 y (n = 243) with elevated LDL cholesterol (≥3.0 and ≤5.0 mmol/L) were stratified by LDL cholesterol and randomly assigned to consume 2 soy muffins containing 25 g soy protein [high-dose soy (HDS)], 1 soy and 1 wheat muffin containing 12.5 g soy protein and 12.5 g whey protein [low-dose soy (LDS)], or 2 wheat muffins containing 25 g whey protein (control) daily for 6 wk while consuming a self-selected diet. Fasting blood samples were collected at weeks 0, 3, and 6 for analysis of plasma lipids [total, LDL, and HDL cholesterol and triglycerides (TGs)], glucose, insulin, C-reactive protein (CRP), and isoflavones. Blood pressures also were measured. Dietary intake was assessed at weeks 0 and 4 with the use of 3 d food records. Treatment effects were assessed with the use of intention-to-treat analysis with multiple imputation and LDL cholesterol as the primary outcome. RESULTS: In total, 213 (87.6%) participants completed the trial. Participants were primarily Caucasian (83%) and mostly female (63%), with a mean ± SD body mass index (in kg/m2) of 28.0 ± 4.6 and systolic and diastolic blood pressures of 122 ± 16 and 77 ± 11 mm Hg, respectively. Despite a dose-dependent increase in plasma isoflavones (P < 0.001), neither HDS nor LDS had a significant effect on LDL cholesterol compared with control (mean ± SEM changes: control, -0.04 ± 0.05 mmol/L; HDS, 0.01 ± 0.05 mmol/L; and LDS, -0.04 ± 0.06 mmol/L). There were no significant treatment effects on total or HDL cholesterol, TGs, CRP, homeostatic model assessment of insulin resistance, blood pressure, or the Framingham 10-y CHD risk score. CONCLUSION: Consuming 12.5 or 25 g protein from defatted soy flour incorporated into muffins does not reduce LDL cholesterol or other CHD risk factors in hypercholesterolemic adults. This trial was registered at clinicaltrials.gov as NCT01547585.

Sugar-sweetened beverage consumption and incident hypertension: a systematic review and meta-analysis of prospective cohorts.

BACKGROUND: The role of sugar-sweetened beverages (SSBs) that contain free or bound fructose in the pathogenesis of hypertension remains unclear. OBJECTIVE: We conducted a systematic review and meta-analysis of prospective cohort studies to quantify the association between fructose-containing SSBs and risk of hypertension. DESIGN: MEDLINE, Embase, Cumulative Index to Nursing and Allied Health Literature, and the Cochrane registry were searched from conception through 11 November 2014. Two independent reviewers extracted data and assessed the quality of studies (with the use of the Newcastle-Ottawa Scale). Risk estimates of extreme quantiles of SSB intake (lowest compared with highest) for hypertension incidence were generated with the use of generic inverse-variance methods with random-effects models and expressed as risk ratios with 95% CIs. Heterogeneity was assessed with the Cochran Q statistic and quantified with the I(2) statistic. RESULTS: Six prospective cohort studies (n = 240,508) with 79,251 cases of hypertension observed over ≥3,197,528 person-years of follow-up were included. SSB consumption significantly increased the risk of developing hypertension by 12% (risk ratio: 1.12; 95% CI: 1.06, 1.17) with evidence of significant heterogeneity (I(2) = 62%, P = 0.02) when highest [≥1 serving (6.7, 8, or 12 oz)/d] and lowest (none) quantiles of intake were compared. With the use of a dose-response analysis, a significant 8.2% increase in risk of every additional SSB per day from none to ≥1 SSB/d (ß = 0.0027, P < 0.001) was identified. Limitations include unexplained heterogeneity and residual confounding. The results may also have been subject to collinearity effects from aspects of a Western dietary pattern. CONCLUSIONS: SSBs were associated with a modest risk of developing hypertension in 6 cohorts. There is a need for high-quality randomized trials to assess the role of SSBs in the development of hypertension and its complications. This study was registered at clinicaltrials.gov as NCT01608620.

Negative association of acetate with visceral adipose tissue and insulin levels.

BACKGROUND: The composition of gut flora has been proposed as a cause of obesity, a major risk factor for type 2 diabetes. The objective of this study was to assess whether serum short chain fatty acids, a major by-product of fermentation in gut flora, are associated with obesity and/or diabetes-related traits (insulin sensitivity and secretion). METHODS: The association of serum short chain fatty acids levels with measures of obesity was assessed using body mass index, computerized tomography scan, and dual photon X-ray absorptiometry scan. Insulin sensitivity and insulin secretion were both determined from an oral glucose tolerance test and insulin sensitivity was also determined from a hyperinsulinemic euglycemic clamp. RESULTS: In this population of young, obese women, acetate was negatively associated with visceral adipose tissue determined by computerized tomography scan and dual photon X-ray absorptiometry scan, but not body mass index. The level of the short chain fatty acids acetate, but not propionate or butyrate, was also negatively associated with fasting serum insulin and 2 hour insulin levels in the oral glucose tolerance test. CONCLUSIONS: In this population, serum acetate was negatively associated with visceral adipose tissue and insulin levels. Future studies need to verify these findings and expand on these observations in larger cohorts of subjects.

Plasma vitamin D levels and risk of metabolic syndrome in Canadians.

PURPOSE: Vitamin D deficiency has been implicated in susceptibility to the development of metabolic syndrome, obesity and type 2 diabetes mellitus. The present study aimed to quantify the association between vitamin D plasma level, the number of metabolic syndrome components and insulin resistance in Canadians. METHODS: Vitamin D plasma level and clinical data were determined from 1,818 subjects from the Canadian Health Measures Survey; a representative health survey of the general population of Canada conducted from 2007 to 2009. The definition of metabolic syndrome was based on the National Cholesterol Education Program, Adult Treatment Panel III criteria. Adjusted general linear models were used to estimate the association between vitamin D level and probability of having metabolic syndrome, as well as the association between plasma vitamin D and insulin resistance (homeostasis model assessment for insulin resistance, or HOMA-IR). RESULTS: The prevalence of metabolic syndrome in the study population was 8.9%. The number of metabolic syndrome components was inversely correlated with plasma vitamin D level (ρ= -0.1, p < 0.0001). Subjects in the highest vitamin D quartile had lower odds ratio of metabolic syndrome compared with their counterparts in the lowest vitamin D quartile (0.50, 95% CI= 0.24-1.06). Increasing plasma vitamin D level (by 10 nmol/L) was inversely associated with HOMA-IR score (ß= -0.08, p=0.006) in a model adjusted for physical activity, smoking status, month of interview, age, sex and ethnicity. CONCLUSION: Vitamin D plasma levels are associated with the occurrence of metabolic syndrome components and insulin resistance among Canadians and are linked to increased level of insulin resistance.

Informing food choices and health outcomes by use of the dietary glycemic index.

Considerable epidemiologic evidence links consuming lower glycemic index (GI) diets with good health, particularly upon aging. The GI is a kinetic parameter that reflects the ability of carbohydrate (CHO) contained in consumed foods to raise blood glucose in vivo. Newer nutritional, clinical, and experimental data link intake of lower dietary GI foods to favorable outcomes of chronic diseases, and compel further examination of the record. Based upon the new information there are two specific questions: 1) should the GI concept be promoted as a way to prolong health, and 2) should food labels contain GI information? Further, what are the remaining concerns about methodological issues and consistency of epidemiological data and clinical trials that need to be resolved in order to exploit the benefits of consuming lower GI diets? These issues are addressed in this review.

Effect of adding the novel fiber, PGX®, to commonly consumed foods on glycemic response, glycemic index and GRIP: a simple and effective strategy for reducing post prandial blood glucose levels--a randomized, controlled trial.

BACKGROUND: Reductions in postprandial glycemia have been demonstrated previously with the addition of the novel viscous polysaccharide (NVP), PolyGlycopleX® (PGX®), to an OGTT or white bread. This study explores whether these reductions are sustained when NVP is added to a range of commonly consumed foods or incorporated into a breakfast cereal. METHODS: Ten healthy subjects (4M, 6F; age 37.3 ± 3.6 y; BMI 23.8 ± 1.3 kg/m2), participated in an acute, randomized controlled trial. The glycemic response to cornflakes, rice, yogurt, and a frozen dinner with and without 5 g of NVP sprinkled onto the food was determined. In addition, 3 granolas with different levels of NVP and 3 control white breads and one white bread and milk were also consumed. All meals contained 50 g of available carbohydrate. Capillary blood samples were taken fasting and at 15, 30, 45, 60, 90 and 120 min after the start of the meal. The glycemic index (GI) and the glycemic reduction index potential (GRIP) were calculated. The blood glucose concentrations at each time and the iAUC values were subjected to repeated-measures analysis of variance (ANOVA) examining for the effect of test meal. After demonstration of significant heterogeneity, differences between individual means was assessed using GLM ANOVA with Tukey test to adjust for multiple comparisons. RESULTS: Addition of NVP reduced blood glucose response irrespective of food or dose (p < 0.01). The GI of cornflakes, cornflakes+NVP, rice, rice+NVP, yogurt, yogurt+NVP, turkey dinner, and turkey dinner+NVP were 83 ± 8, 58 ± 7, 82 ± 8, 45 ± 4, 44 ± 4, 38 ± 3, 55 ± 5 and 41 ± 4, respectively. The GI of the control granola, and granolas with 2.5 and 5 g of NVP were 64 ± 6, 33 ± 5, and 22 ± 3 respectively. GRIP was 6.8 ± 0.9 units per/g of NVP. CONCLUSION: Sprinkling or incorporation of NVP into a variety of different foods is highly effective in reducing postprandial glycemia and lowering the GI of a food. CLINICAL TRIAL REGISTRATION: NCT00935350.

Genetic variation in TAS1R2 (Ile191Val) is associated with consumption of sugars in overweight and obese individuals in 2 distinct populations.

BACKGROUND: Taste is an important determinant of food consumption, and genetic variations in the sweet taste receptor subunit TAS1R2 may contribute to interindividual variations in sugar consumption. OBJECTIVE: We determined whether Ser9Cys and Ile191Val variations in TAS1R2 were associated with differences in the consumption of sugars in 2 populations. DESIGN: Population 1 included 1037 diabetes-free young adults in whom we assessed dietary intake by using a 1-mo, 196-item food-frequency questionnaire. Population 2 consisted of 100 individuals with type 2 diabetes with dietary intakes assessed by using 2 sets of 3-d food records administered 2 wk apart. Dietary counseling was provided between food records 1 and 2. Dietary intakes between genotypes were compared by using analysis of covariance adjusted for potential confounders. RESULTS: In population 1, a significant Ile191Val × body mass index (BMI; in kg/m²) interaction was detected for the consumption of sugars, and the effect of genotype was significant only in individuals with a BMI ≥ 25 (n = 205). In comparison with individuals homozygous for the Ile allele, Val carriers consumed fewer sugars (122 ± 6 compared with 103 ± 6 g sugar/d, respectively; P = 0.01). Regression estimates that associated BMI with total sugar consumption by Ile/Ile and Val-carrier genotype intersected at a BMI of 23.5. In population 2, Val carriers also consumed less sugar than did individuals with the Ile/Ile genotype (99 ± 6 compared with 83 ± 6 g sugar/d, respectively; P = 0.04) on food record 2, and sugar was the only macronutrient that decreased significantly (-9 ± 4 g sugar/d, P = 0.02) in Val carriers who received dietary counseling. CONCLUSION: Our findings show that a genetic variation in TAS1R2 affects habitual consumption of sugars and may contribute to interindividual differences in changing behaviors in response to dietary counseling.

Reduction of postprandial glycemia by the novel viscous polysaccharide PGX, in a dose-dependent manner, independent of food form.

OBJECTIVE: Health benefits of viscous fiber intake are well established; nevertheless few effective and palatable preparations are available. The objective of the study therefore was to determine palatability and effectiveness of escalating doses of PGX, a novel viscous polysaccharide (NVP), in reducing postprandial glycemia when added to a liquid and a solid meal. DESIGN: Two open-label, randomized, controlled trials were undertaken. SETTING: Glycemic Index Laboratories, Inc, Toronto, Ontario, Canada. SUBJECTS: Two groups of 10 healthy subjects each (group 1: 5 M, 5 F; 35.6 +/- 13.2 y; 24.6 +/- 2.1 kg/m(2); and group 2: 3 M, 7 F; 33.5 +/- 11.1 y; 26.3 +/- 5.2 kg/m(2)) were studied. INTERVENTIONS: Zero, 2.5, 5, and 7.5 g of NVP were added to a glucose drink (group 1) or to white bread and margarine (WB + Marg) (group 2). Subjects repeated glucose control (group 1) or WB control (group 2) 3 times to allow calculation of the glycemic index (GI). Measures of Outcomes: Palatability of foods and capillary blood glucose concentrations were measured fasting and at 15, 30, 45, 60, 90, and 120 minutes after the start of the meal. RESULTS: Addition of NVP to the meal reduced blood glucose incremental areas under the curve irrespective of dose, reaching significance at the 7.5 g dose when added to glucose (p < 0.01), and at the 5 and 7.5 g doses when added to WB + Marg (p < 0.001). The GI values of glucose with 0, 2.5, 5, or 7.5 g of NVP were (mean +/- standard error of the mean [SEM]) 100.0 +/- 0.0, 83.7 +/- 9.0, 77.7 +/- 8.2, and 72.5 +/- 5.9, respectively; the GI of the WB alone, or of WB + Marg, with 0, 2.5, 5, or 7.5 g of NVP was 71.0 +/- 0.0, 66.8 +/- 3.0, 47.5 +/- 5.9, 37.3 +/- 5.9, and 33.9 +/- 3.6, respectively. CONCLUSION: Addition of NVP to different food matrices is highly effective in lowering the glycemic index of a food in a dose-responsive manner.