Glycemic index, glycemic load and glycemic response: An International Scientific Consensus Summit from the International Carbohydrate Quality Consortium (ICQC).

BACKGROUND AND AIMS: The positive and negative health effects of dietary carbohydrates are of interest to both researchers and consumers. METHODS: International experts on carbohydrate research held a scientific summit in Stresa, Italy, in June 2013 to discuss controversies surrounding the utility of the glycemic index (GI), glycemic load (GL) and glycemic response (GR). RESULTS: The outcome was a scientific consensus statement which recognized the importance of postprandial glycemia in overall health, and the GI as a valid and reproducible method of classifying carbohydrate foods for this purpose. There was consensus that diets low in GI and GL were relevant to the prevention and management of diabetes and coronary heart disease, and probably obesity. Moderate to weak associations were observed for selected cancers. The group affirmed that diets low in GI and GL should always be considered in the context of diets otherwise understood as healthy, complementing additional ways of characterizing carbohydrate foods, such as fiber and whole grain content. Diets of low GI and GL were considered particularly important in individuals with insulin resistance. CONCLUSIONS: Given the high prevalence of diabetes and pre-diabetes worldwide and the consistency of the scientific evidence reviewed, the expert panel confirmed an urgent need to communicate information on GI and GL to the general public and health professionals, through channels such as national dietary guidelines, food composition tables and food labels.

Evidence for greater production of colonic short-chain fatty acids in overweight than lean humans.

BACKGROUND: Short-chain fatty acids (SCFA) are produced by colonic microbiota from dietary carbohydrates and proteins that reach the colon. It has been suggested that SCFA may promote obesity via increased colonic energy availability. Recent studies suggest obese humans have higher faecal SCFA than lean, but it is unclear whether this difference is due to increased SCFA production or reduced absorption. OBJECTIVES: To compare rectal SCFA absorption, dietary intake and faecal microbial profile in lean (LN) versus overweight and obese (OWO) individuals. DESIGN: Eleven LN and eleven OWO individuals completed a 3-day diet record, provided a fresh faecal sample and had SCFA absorption measured using the rectal dialysis bag method. The procedures were repeated after 2 weeks. RESULTS: Age-adjusted faecal SCFA concentration was significantly higher in OWO than LN individuals (81.3±7.4 vs 64.1±10.4 mmol kg(-1), P=0.023). SCFA absorption (24.4±0.8% vs 24.7±1.2%, respectively, P=0.787) and dietary intakes were similar between the groups, except for a higher fat intake in OWO individuals. However, fat intake did not correlate with SCFAs or bacterial abundance. OWO individuals had higher relative Firmicutes abundance (83.1±4.1 vs 69.5±5.8%, respectively, P=0.008) and a higher Firmicutes:Bacteriodetes ratio (P=0.023) than LN individuals. There was a positive correlation between Firmicutes and faecal SCFA within the whole group (r=0.507, P=0.044), with a stronger correlation after adjusting for available carbohydrate (r=0.615, P=0.005). CONCLUSIONS: The higher faecal SCFA in OWO individuals is not because of differences in SCFA absorption or diet. Our results are consistent with the hypothesis that OWO individuals produce more colonic SCFA than LN individuals because of differences in colonic microbiota. However, further studies are needed to prove this.

Altering source or amount of dietary carbohydrate has acute and chronic effects on postprandial glucose and triglycerides in type 2 diabetes: Canadian trial of Carbohydrates in Diabetes (CCD).

BACKGROUND AND AIMS: Nutrition recommendations for type 2 diabetes (T2DM) are partly guided by the postprandial responses elicited by diets varying in carbohydrate (CHO). We aimed to explore whether long-term changes in postprandial responses on low-glycemic-index (GI) or low-CHO diets were due to acute or chronic effects in T2DM. METHODS AND RESULTS: Subjects with diet-alone-treated T2DM were randomly assigned to high-CHO/high-GI (H), high-CHO/low-GI (L), or low-CHO/high-monounsaturated-fat (M) diets for 12-months. At week-0 (Baseline) postprandial responses after H-meals (55% CHO, GI = 61) were measured from 0800 h to 1600 h. After 12 mo subjects were randomly assigned to H-meals or study diet meals (L, 57% CHO, GI = 50; M, 44% CHO, GI = 61). This yielded 5 groups: H diet with H-meals (HH, n = 34); L diet with H- (LH, n = 17) or L-meals (LL, n = 16); and M diet with H- (MH, n = 18) or M meals (MM, n = 19). Postprandial glucose fluctuations were lower in LL than all other groups (p < 0.001). Changes in postprandial-triglycerides differed among groups (p < 0.001). After 12 mo in HH and MM both fasting- and postprandial-triglycerides were similar to Baseline while in MH postprandial-triglycerides were significantly higher than at Baseline (p = 0.028). In LH, triglycerides were consistently (0.18-0.34 mmol/L) higher than Baseline throughout the day, while in LL the difference from Baseline varied across the day from 0.04 to 0.36 mmol/L (p < 0.001). CONCLUSION: Low-GI and low-CHO diets have both acute and chronic effects on postprandial glucose and triglycerides in T2DM subjects. Thus, the composition of the acute test-meal and the habitual diet should be considered when interpreting the nutritional implications of different postprandial responses.

Sugars and fat have different effects on postprandial glucose responses in normal and type 1 diabetic subjects.

BACKGROUND AND AIMS: We aimed to determine the effects on glycemic responses and potential risk of hypoglycaemia in type 1 diabetic subjects of replacing half the starch in a meal with sugars, and of adding fat to the low-sugar and high-sugar meals. METHODS AND RESULTS: We studied overnight fasted subjects with type 1 diabetes (n = 11) and age-, BMI- and ethnicity-matched controls (n = 11) using a 2 × 2 factorial design. The low-sugar/low-fat meal was 110 g white-bread. In the high-sugar/low-fat meal half the white-bread starch replaced by sugars (jam and orange juice). The high-fat meals consisted of the low-fat meals plus 20 g fat (margarine). The significance of the main effects of sugars and fat and the sugar × fat, group × sugar and group × fat interactions were determined by ANOVA. In control and diabetic subjects, respectively, high-sugar significantly reduced time to peak rise by 13% (P = 0.004) and 32% (P = 0.004; group × sugar: P = 0.01) and increased peak rise by 14% and 10% (ns). Adding fat increased time to peak rise by 17-19% in both groups (P = 0.003), reduced peak rise by 31% in normal (P < 0.001) but increased peak rise in diabetic subjects by 3% (ns) (group × fat: P = 0.022). Blood glucose nadir and occurrence of hypoglycaemia were similar among the 4 meals. CONCLUSIONS: In type 1 diabetes, insulin adjustment to avoid hypoglycemia may be useful for meals in which the proportion of carbohydrate absorbed as glucose is <0.75, however the precise level which increases hypoglycaemic risk requires further research. The results suggest that people with type 1 diabetes should not be advised to add fat to meals to reduce glycemic responses.

Effects of sucromalt on postprandial responses in human subjects.

BACKGROUND/OBJECTIVE: To compare postprandial responses elicited by sucromalt, a nutritive sweetener produced by treating a blend of sucrose and corn syrup with an enzyme from Leuconostoc mesenteroides, with those after 42% of high-fructose corn syrup (HFCS), and to see if the reduced responses after sucromalt could be accounted for by carbohydrate malabsorption. SUBJECT AND METHODS: Three experiments were performed in separate groups of normal subjects studied after overnight fasts using double-blind, randomized, cross-over designs. HFCS was used as the control because it contained a similar amount of fructose as sucromalt. Experiment 1 (n = 10): plasma glucose and insulin were measured after 50 g sucromalt and 50 g HFCS. Experiment 2 (n = 10): metabolic profiles were measured after 80 g HFCS, 80 g sucromalt or 56 g fructose/glucose blend plus 24 g inulin. Experiment 3 (n = 20): the glycaemic indices of sucromalt and HFCS were determined. RESULTS: Mean glucose and insulin responses after sucromalt were 66 and 62%, respectively, of those after HFCS (P < 0.05). The inulin treatment, used to mimic the effects of carbohydrate malabsorption, elicited higher breath hydrogen (H2), lower glucose and insulin responses, and a significantly earlier rise in serum free fatty acids (FFA) than those of HFCS (all P < 0.05). Sucromalt elicited no rise in breath H2, and delayed falls in glucose and insulin, and a delayed rebound of FFA compared to HFCS (all P < 0.05). CONCLUSIONS: The reduced glucose and insulin responses elicited by sucromalt are not explained by malabsorption and are more likely related to differences in either rate of digestion and absorption or postabsorptive handling by body.

Acute increases in serum colonic short-chain fatty acids elicited by inulin do not increase GLP-1 or PYY responses but may reduce ghrelin in lean and overweight humans.

BACKGROUND: Colonic fermentation of dietary fibre to short-chain fatty acids (SCFA) influences appetite hormone secretion in animals, but SCFA production is excessive in obese animals. This suggests there may be resistance to the effect of SCFA on appetite hormones in obesity. OBJECTIVES: To determine the effects of inulin (IN) and resistant starch (RS) on postprandial SCFA, and gut hormone (glucagon-like peptide (GLP-1), peptide-tyrosine-tyrosine (PYY) and ghrelin) responses in healthy overweight/obese (OWO) vs lean (LN) humans. SUBJECTS/METHODS: Overnight-fasted participants (13 OWO and 12 LN) consumed 300 ml water containing 75 g glucose (GLU) as control or 75 g GLU plus 24 g IN, or 28.2 g RS using a randomised, single-blind, cross-over design. Blood for appetite hormones and SCFA was collected at intervals over 6 h. A standard lunch was served 4 h after the test drink. RESULTS: Relative to GLU, IN, but not RS, significantly increased SCFA areas under the curve (AUC) from 4-6 h (AUC4-6). Neither IN nor RS affected GLP-1 or PYY-AUC4-6. Although neither IN nor RS reduced ghrelin-AUC4-6 compared with GLU, ghrelin at 6 h after IN was significantly lower than that after GLU (P<0.05). After IN, relative to GLU, the changes in SCFA-AUC4-6 were negatively related to the changes in ghrelin-AUC4-6 (P=0.017). SCFA and hormone responses did not differ significantly between LN and OWO. CONCLUSIONS: Acute increases in colonic SCFA do not affect GLP-1 or PYY responses in LN or OWO subjects, but may reduce ghrelin. The results do not support the hypothesis that SCFA acutely stimulate PYY and GLP-1 secretion; however, a longer adaptation to increased colonic fermentation or a larger sample size may yield different results.

The acute effects of inulin and resistant starch on postprandial serum short-chain fatty acids and second-meal glycemic response in lean and overweight humans.

BACKGROUND/OBJECTIVES: Colonic fermentation of dietary fiber to short-chain fatty acids (SCFA) may protect against obesity and diabetes, but excess production of colonic SCFA has been implicated in the promotion of obesity. We aimed to compare the effects of two fermentable fibers on postprandial SCFA and second-meal glycemic response in healthy overweight or obese (OWO) vs lean (LN) participants. SUBJECTS/METHODS: Using a randomized crossover design, 13 OWO and 12 LN overnight fasted participants were studied for 6 h on three separate days after consuming 300 ml water containing 75 g glucose (GLU) as control or with 24 g inulin (IN) or 28 g resistant starch (RS). A standard lunch was served 4 h after the test drink. RESULTS: Within the entire group, compared with control, IN significantly increased serum SCFA (P<0.001) but had no effect on free-fatty acids (FFA) or second-meal glucose and insulin responses. In contrast, RS had no significant effect on SCFA but reduced FFA rebound (P<0.001) and second-meal glucose (P=0.002) and insulin responses (P=0.024). OWO had similar postprandial serum SCFA and glucose concentrations but significantly greater insulin and FFA than LN. However, the effects of IN and RS on SCFA, glucose, insulin and FFA responses were similar in LN and OWO. CONCLUSIONS: RS has favorable second-meal effects, likely related to changes in FFA rather than SCFA concentrations. However, a longer study may be needed to demonstrate an effect of RS on SCFA. We found no evidence that acute increases in SCFA after IN reduce glycemic responses in humans, and we were unable to detect a significant difference in SCFA responses between OWO vs LN subjects.

Glycaemic index methodology.

The glycaemic index (GI) concept was originally introduced to classify different sources of carbohydrate (CHO)-rich foods, usually having an energy content of >80 % from CHO, to their effect on post-meal glycaemia. It was assumed to apply to foods that primarily deliver available CHO, causing hyperglycaemia. Low-GI foods were classified as being digested and absorbed slowly and high-GI foods as being rapidly digested and absorbed, resulting in different glycaemic responses. Low-GI foods were found to induce benefits on certain risk factors for CVD and diabetes. Accordingly it has been proposed that GI classification of foods and drinks could be useful to help consumers make 'healthy food choices' within specific food groups. Classification of foods according to their impact on blood glucose responses requires a standardised way of measuring such responses. The present review discusses the most relevant methodological considerations and highlights specific recommendations regarding number of subjects, sex, subject status, inclusion and exclusion criteria, pre-test conditions, CHO test dose, blood sampling procedures, sampling times, test randomisation and calculation of glycaemic response area under the curve. All together, these technical recommendations will help to implement or reinforce measurement of GI in laboratories and help to ensure quality of results. Since there is current international interest in alternative ways of expressing glycaemic responses to foods, some of these methods are discussed.

Effect of ethnicity on glycaemic index: a systematic review and meta-analysis.

OBJECTIVES: Low glycaemic index (GI) foods are recommended to improve glycaemic control in diabetes; however, Health Canada considers that GI food labeling would be misleading and unhelpful, in part, because selected studies suggest that GI values are inaccurate due to an effect of ethnicity. Therefore, we conducted a systematic review and meta-analysis to compare the GI of foods when measured in Caucasians versus non-Caucasians. METHODS: We searched MEDLINE, EMBASE and Cochrane databases for relevant articles. GI differences were aggregated using the generic inverse variance method (random effects model) and expressed as mean difference (MD) with 95% confidence intervals (95% CI). Study quality was assessed based on how well studies complied with official international GI methodology. RESULTS: Review of 1288 trials revealed eight eligible studies, including 28 comparisons of GI among 585 non-Caucasians and 971 Caucasians. Overall, there was borderline significant evidence of higher GI in non-Caucasians than Caucasians (MD, 3.3 (95% CI, -0.1, 6.8); P=0.06) with significant heterogeneity (I(2), 46%; P=0.005). The GI of eight types of rice was higher in non-Caucasians than Caucasians (MD, 9.5 (95% CI, 3.7, 23.1); P=0.001), but there was no significant difference for the other 20 foods (MD, 1.0 (95% CI, -2.5, 4.6); P=0.57). MD was significantly greater in the four low-quality studies (nine comparisons) than the four high-quality studies (19 comparisons; 7.8 vs 0.7, P=0.047). CONCLUSIONS: With the possible exception of rice, existing evidence suggests that GI values do not differ when measured in Caucasians versus non-Caucasians. To confirm these findings high-quality studies using a wide range of foods are required.

Acarbose in the treatment of elderly patients with type 2 diabetes.

AIMS: To study the effect of acarbose, an alpha-glucosidase inhibitor, on glycemic control in elderly patients with type 2 diabetes. METHODS: Elderly patients with type 2 diabetes treated with diet alone were randomly treated in a double-blind fashion with placebo (n=99) or acarbose (n=93) for 12 months. RESULTS: After 12 months of therapy, there was a statistically significant difference in the change in glycated haemoglobin (HbA(1c)) (-0.6%) in the acarbose group versus placebo, as well as in the incremental post-prandial glucose values (-2.1 mmol h/l) and mean fasting plasma glucose (-0.7 mmol/l). Although there was no effect of acarbose on insulin release, there was a clear effect of acarbose to decrease relative insulin resistance (-0.8) (HOMA method). In addition, acarbose was generally well tolerated and safe in the elderly; most discontinuations were due to gastrointestinal side effects such as flatulence and diarrhea. There were no cases of hypoglycemia reported, and no clinically relevant changes in laboratory abnormalities or vital signs during the study. CONCLUSIONS: Acarbose improves the glycemic profile and insulin sensitivity in elderly patients with type 2 diabetes who are inadequately controlled on diet alone.

Determination of the glycaemic index of foods: interlaboratory study.

OBJECTIVE: Practical use of the glycaemic index (GI), as recommended by the FAO/WHO, requires an evaluation of the recommended method. Our purpose was to determine the magnitude and sources of variation of the GI values obtained by experienced investigators in different international centres. DESIGN: GI values of four centrally provided foods (instant potato, rice, spaghetti and barley) and locally obtained white bread were determined in 8-12 subjects in each of seven centres using the method recommended by FAO/WHO. Data analysis was performed centrally. SETTING: University departments of nutrition. SUBJECTS: Healthy subjects (28 male, 40 female) were studied. RESULTS: The GI values of the five foods did not vary significantly in different centres nor was there a significant centrexfood interaction. Within-subject variation from two centres using venous blood was twice that from five centres using capillary blood. The s.d. of centre mean GI values was reduced from 10.6 (range 6.8-12.8) to 9.0 (range 4.8-12.6) by excluding venous blood data. GI values were not significantly related to differences in method of glucose measurement or subject characteristics (age, sex, BMI, ethnicity or absolute glycaemic response). GI values for locally obtained bread were no more variable than those for centrally provided foods. CONCLUSIONS: The GI values of foods are more precisely determined using capillary than venous blood sampling, with mean between-laboratory s.d. of approximately 9.0. Finding ways to reduce within-subject variation of glycaemic responses may be the most effective strategy to improve the precision of measurement of GI values.

Effects of a beverage containing an enzymatically induced-viscosity dietary fiber, with or without fructose, on the postprandial glycemic response to a high glycemic index food in humans.

OBJECTIVE: Dietary supplementation with guar gum or fructose has been reported to reduce the postprandial glycemic response to an oral glucose challenge. As a result of the poor palatability of most foods containing guar gum, a novel low-viscosity beverage with guar gum was developed that becomes viscous in vivo through an enzymatic induction. The primary study objective was to determine the effect of an amylase-induced viscosity (I-V) product, with or without supplemental fructose, on the postprandial glycemic response to a high glycemic index test meal in healthy nondiabetic subjects. DESIGN: The study was a four-treatment, placebo-controlled, double-blind, randomized block protocol. SETTING: The study was performed at Glycaemic Index Testing, Inc., Toronto, Ontario, Canada. SUBJECTS: A total of 30 healthy nondiabetic volunteers (13 male, 17 female, mean+/-s.e.m. age of 51+/-3 y and body mass index of 24.2+/-0.4 kg/m(2)) participated in the study. INTERVENTION: In the morning after an overnight fast, subjects participated in four 3-h meal glucose tolerance tests on separate occasions. The test meals contained 50 g of available carbohydrate from maltodextrin and white bread (control) or the same meal with either 5 g of guar gum (3.6 g galactomannan), 5 g of fructose, or 5 g of guar gum +5 g of fructose. RESULTS: Treatments containing guar gum had a reduced (P<0.01) baseline-adjusted peak glucose response and incremental area under the glucose curve. In contrast to previous studies, fructose increased (P<0.05) the baseline-adjusted peak glucose concentration. CONCLUSIONS: Guar gum incorporated into an amylase I-V product provided a means to stabilize blood glucose levels by reducing the early phase excursion and then by appropriately maintaining the later phase excursion in healthy nondiabetic humans.

Kinetic model of acetate metabolism in healthy and hyperinsulinaemic humans.

BACKGROUND/OBJECTIVES: The short chain fatty acid acetate (AC), may have a role in increasing insulin sensitivity, thus lowering risk for obesity and type 2 diabetes mellitus. It is unclear if AC kinetics is similar in normal (NI) and hyperinsulinaemic (HI) participants. Therefore, we studied AC absorption from the distal colon in participants with normal (<40 pmol/l) and high (≥40 pmol/l) plasma insulin. This work was a part of a series of studies conceived to compute a kinetic model for AC. Kinetic parameters such as estimates of rate of entry into peripheral blood, hepatic uptake and endogenous/exogenous production were compared in the groups. SUBJECTS/METHODS: Overnight fasted NI (n=9) and HI (n=8) participants were given rectal infusions containing sodium AC (90 mmol/l). The solutions were retained for 40 min, then voided for AC measurement. Total amount of AC infused was 27 mmols. RESULTS: AC absorption from the distal colon (279±103 vs 322±91 µmol/min, P=0.76) and hepatic uptake of AC (155±101 vs 146±85 µmol/min, P=0.94) were similar in the groups. Endogenous and exogenous AC production was significantly higher in NI than HI participants. Plasma AC was inversely proportional to plasma insulin concentrations in the entire cohort (y=k/x, where k=1813). CONCLUSIONS: There was low power to detect differences in AC absorption rate and hepatic AC uptake in NI vs HI. The rate of entry of AC into peripheral blood was similar in NI and HI participants. However, hyperinsulinaemia may alter endogenous and exogenous AC metabolism.

Adiposity, gut microbiota and faecal short chain fatty acids are linked in adult humans.

BACKGROUND/OBJECTIVES: High dietary fibre intakes may protect against obesity by influencing colonic fermentation and the colonic microbiota. Though, recent studies suggest that increased colonic fermentation contributes to adiposity. Diet influences the composition of the gut microbiota. Previous research has not evaluated dietary intakes, body mass index (BMI), faecal microbiota and short chain fatty acid (SCFA) in the same cohort. Our objectives were to compare dietary intakes, faecal SCFA concentrations and gut microbial profiles in healthy lean (LN, BMI⩽25) and overweight or obese (OWOB, BMI>25) participants. DESIGN: We collected demographic information, 3-day diet records, physical activity questionnaires and breath and faecal samples from 94 participants of whom 52 were LN and 42 OWOB. RESULTS: Dietary intakes and physical activity levels did not differ significantly between groups. OWOB participants had higher faecal acetate (P=0.05), propionate (P=0.03), butyrate (P=0.05), valerate (P=0.03) and total short chain fatty acid (SCFA; P=0.02) concentrations than LN. No significant differences in Firmicutes to Bacteroides/Prevotella (F:B) ratio was observed between groups. However, in the entire cohort, Bacteroides/Prevotella counts were negatively correlated with faecal total SCFA (r=-0.32, P=0.002) and F:B ratio was positively correlated with faecal total SCFA (r=0.42, P<0.0001). Principal component analysis identified distinct gut microbiota and SCFA-F:B ratio components, which together accounted for 59% of the variation. F:B ratio loaded with the SCFA and not with the microbiota suggesting that SCFA and F:B ratio vary together and may be interrelated. CONCLUSIONS: The results support the hypothesis that colonic fermentation patterns may be altered, leading to different faecal SCFA concentrations in OWOB compared with LN humans. More in-depth studies looking at the metabolic fate of SCFA produced in LN and OWOB participants are needed in order to determine the role of SCFA in obesity.

Effect of fructose on markers of non-alcoholic fatty liver disease (NAFLD): a systematic review and meta-analysis of controlled feeding trials.

BACKGROUND/OBJECTIVES: In the absence of consistent clinical evidence, there are concerns that fructose contributes to non-alcoholic fatty liver disease (NAFLD). To determine the effect of fructose on markers of NAFLD, we conducted a systematic review and meta-analysis of controlled feeding trials. SUBJECTS/METHODS: We searched MEDLINE, EMBASE, CINAHL and the Cochrane Library (through 3 September 2013). We included relevant trials that involved a follow-up of ≥ 7 days. Two reviewers independently extracted relevant data. Data were pooled by the generic inverse variance method using random effects models and expressed as standardized mean difference (SMD) for intrahepatocellular lipids (IHCL) and mean difference (MD) for alanine aminotransferase (ALT). Inter-study heterogeneity was assessed (Cochran Q statistic) and quantified (I(2) statistic). RESULTS: Eligibility criteria were met by eight reports containing 13 trials in 260 healthy participants: seven isocaloric trials, in which fructose was exchanged isocalorically for other carbohydrates, and six hypercaloric trials, in which the diet was supplemented with excess energy (+21-35% energy) from high-dose fructose (+104-220 g/day). Although there was no effect of fructose in isocaloric trials, fructose in hypercaloric trials increased both IHCL (SMD=0.45 (95% confidence interval (CI): 0.18, 0.72)) and ALT (MD=4.94 U/l (95% CI: 0.03, 9.85)). LIMITATIONS: Few trials were available for inclusion, most of which were small, short (≤ 4 weeks), and of poor quality. CONCLUSIONS: Isocaloric exchange of fructose for other carbohydrates does not induce NAFLD changes in healthy participants. Fructose providing excess energy at extreme doses, however, does raise IHCL and ALT, an effect that may be more attributable to excess energy than fructose. Larger, longer and higher-quality trials of the effect of fructose on histopathological NAFLD changes are required.

Glycemic index claims on food labels: review of Health Canada's evaluation.

Recently Health Canada (HC) published its opinion that including glycemic index (GI) values on food labels would be misleading and not add value to nutrition labeling and dietary guidelines to help consumers make healthier food choices. Important areas of concern were identified by HC, but the discussion of them is scientifically invalid. HC concluded that GI has poor precision for labeling purposes based on incorrect application of the standard deviation. In fact, GI methodology is precise enough to distinguish, with high probability, low-GI (GI ≤ 55) from high-GI (GI ≥ 70) foods and to pass the Canadian Food Inspection Agency Nutrition Compliance Test procedure. HC rightly concluded that GI does not respond to portion size, whereas glycemic response does, but no valid evidence was provided to support the assertion that a lower-GI food could have a higher glycemic response. HC's focus on glycemic response could promote a low-carbohydrate diet inconsistent with nutrition recommendations. HC correctly concluded that GI is unresponsive to the replacement of available- with unavailable-carbohydrate but this is irrelevant to GI labeling. HC is rightly concerned about promoting unhealthy low-GI foods; however, this could be avoided by prohibiting GI labeling on such foods. Therefore, HC has provided neither a helpful nor scientifically valid evaluation of GI for labeling purposes but has contributed to the wealth of misinformation about GI in the literature. Currently, Canadian consumers only have access to unregulated and misleading information about GI; well-crafted guidelines for GI labeling would provide consumers accurate information about GI and help them make healthier food choices.

Is glycaemic index (GI) a valid measure of carbohydrate quality?

Recent criticisms of the glycaemic index (GI) focus on its validity with assertions that GI methodology is not valid, GI values are inaccurate and imprecise, GI does not predict what foods are healthy and that whole grain and fibre are better markers of carbohydrate quality than GI. None of the critics provide sound reasons for rejecting GI because some of their arguments are based on flagrant errors in understanding and interpretation while others are not supported by current data or are inconsistent with other nutritional recommendations. This paper addresses current criticisms of GI and outlines reasons why GI is valid: (1) GI methodology is accurate and precise enough for practical use; (2) GI is a property of foods; and (3) GI is biologically meaningful and relevant to virtually everyone. Current dietary guidelines recommend increased consumption of whole grains and dietary fibre but do not mention GI. However, this is illogical because the evidence that GI affects health outcomes is at least as good or better than that for whole grains and fibre. GI is a novel concept from a regulatory point of view and a number of problems need to be addressed to successfully translate GI knowledge into practice. The problems are not insurmountable but no progress can be made until bias and misunderstanding about GI can be overcome and there is better agreement about what is the actual state of knowledge on GI so that the real issues can be identified and addressed.

Intravenous acetate elicits a greater free fatty acid rebound in normal than hyperinsulinaemic humans.

BACKGROUND/OBJECTIVES: Colonic fermentation of dietary fiber may improve insulin sensitivity by the metabolic effects of short chain fatty acids (SCFA) in reducing free fatty acids (FFA). The main objectives of this study were to compare peripheral uptake of acetate (AC) in participants with normal (<40 pmol/l, NI) and high (≥ 40 pmol/l, HI) plasma insulin, and the ability of AC to reduce FFA in both the groups. SUBJECTS/METHODS: Overnight fasted NI (n=9) and HI (n=9) participants were given an intravenous (IV) infusion of 140 mmol/l sodium acetate at three different rates over 90 min. The total amount of AC infused was 51.85 mmols. RESULTS: AC clearance in NI participants was not significantly different than that in HI participants (2.11 ± 0.23 vs 2.09 ± 0.24 ml/min). FFA fell in both the groups, but rebounded to a greater extent in NI than HI participants (time × group interaction, P=0.001). Significant correlations between insulin resistance (IR) indices (homeostasis model assessment of insulin resistance (HOMA-IR), Matsuda and insulinogenic index) vs FFA rebound during IV AC infusion were also observed. CONCLUSIONS: These findings suggest that AC uptake is similar in both the groups. Participants with lower plasma insulin and lower IR indices had a greater FFA rebound. These results support the hypothesis that increasing AC concentrations in the systemic circulation may reduce lipolysis and plasma FFA concentrations and thus improve insulin sensitivity. More in-depth studies are needed to look at the effects of SCFA on FFA metabolism in insulin-resistant participants.