Effects of processing methods on amaranth starch digestibility and predicted glycemic index

Amaranth has attracted a great deal of interest in recent decades due to its valuable nutritional, functional, and agricultural characteristics. Amaranth seeds can be cooked, popped, roasted, flaked, or extruded for consumption. This study compared the in vitro starch digestibility of processed amaranth seeds to that of white bread. Raw seeds yielded rapidly digestible starch content (RDS) of 30.7% db and predicted glycemic index (pGI) of 87.2, the lowest among the studied products. Cooked, extruded, and popped amaranth seeds had starch digestibility similar to that of white bread (92.4, 91.2, and 101.3, respectively), while flaked and roasted seeds generated a slightly increased glycemic response (106.0 and 105.8, respectively). Cooking and extrusion did not alter the RDS contents of the seeds. No significant differences were observed among popped, flaked, and roasted RDS contents (38.0%,46.3%, and 42.9%, respectively), which were all lower than RDS content of bread (51.1%). Amaranth seed is a high glycemic food most likely because of its small starch granule size, low resistant starch content (< 1%), and tendency to completely lose its crystalline and granular starch structure during those heat treatments.

Glycemic index, glycemic load, and risk of digestive tract neoplasms: a systematic review and meta-analysis

Background: Habitual consumption of diets with a high glycemic index (GI) and a high glycemic load (GL) may influence cancer risk via hyperinsulinemia and the insulin-like growth factor axis.
Objective: The objective was to conduct a systematic review to assess the association between GI, GL, and risk of digestive tract cancers.
Design: Medline and Embase were searched for relevant publications from inception to July 2008. When possible, adjusted results from a comparison of cancer risk of the highest compared with the lowest category of GI and GL intake were combined by using random-effects meta-analyses.
Results: Cohort and case-control studies that examined the risk between GI or GL intake and colorectal cancer (n = 12) and adenomas (n = 2), pancreatic cancer (n = 6), gastric cancer (n = 2), and squamous-cell esophageal carcinoma (n = 1) were retrieved. Most case-control studies observed positive associations between GI and GL intake and these cancers. However, pooled cohort study results showed no associations between colorectal cancer risk and GI intake [relative risk (RR): 1.04; 95% CI: 0.92, 1.12; n = 7 studies] or GL intake (RR: 1.06; 95% CI: 0.95, 1.17; n = 8 studies). Furthermore, no significant associations were observed in meta-analyses of cohort study results of colorectal cancer subsites and GI and GL intake. Similarly, no significant associations emerged between pancreatic cancer risk and GI intake (RR: 0.99; 95% CI: 0.83, 1.19; n = 5 studies) or GL intake (RR: 1.01; 95% CI: 0.86, 1.19; n = 6 studies) in combined cohort studies.
Conclusions: The findings from our meta-analyses indicate that GI and GL intakes are not associated with risk of colorectal or pancreatic cancers. There were insufficient data available regarding other digestive tract cancers to make any conclusions about GI or GL intake and risk.

Glycemic index, carbohydrate and fiber intakes and risk of reflux esophagitis, Barrett’s esophagus, and esophageal adenocarcinoma

Objective: To examine the association between dietary glycemic index (GI), glycemic load (GL), total carbohydrate, sugars, starch, and fiber intakes and the risk of reflux esophagitis, Barrett’s esophagus, and esophageal adenocarcinoma.

Methods: In an all-Ireland study, dietary information was collected from patients with esophageal adenocarcinoma (n = 224), long-segment Barrett’s esophagus (n = 220), reflux esophagitis (n = 219), and population-based controls (n = 256). Multiple logistic regression analysis examined the association between dietary variables and disease risk by tertiles of intake and as continuous variables, while adjusting for potential confounders.

Results: Reflux esophagitis risk was positively associated with starch intake and negatively associated with sugar intake. Barrett’s esophagus risk was significantly reduced in people in the highest versus the lowest tertile of fiber intake (OR 0.44 95%CI 0.25–0.80). Fiber intake was also associated with a reduced risk of esophageal adenocarcinoma, as was total carbohydrate intake (OR 0.45 95%CI 0.33–0.61 per 50 g/d increase). However, an increased esophageal adenocarcinoma risk was detected per 10 unit increase in GI intake (OR 1.42 95%CI 1.07–1.89).

Conclusions: Our findings suggest that fiber intake is inversely associated with Barrett’s esophagus and esophageal adenocarcinoma risk. Esophageal adenocarcinoma risk is inversely associated with total carbohydrate consumption but positively associated with high GI intakes.

Dietary Carbohydrate Intake, Glycemic Index, and Glycemic Load and Endometrial Cancer Risk: A Prospective Cohort Study

Endometrial cancer risk has been directly associated with glycemic load. However, few studies have investigated this link, and the etiological role of specific dietary carbohydrate components remains unclear. Our aim was to investigate associations of carbohydrate intake, glycemic index, and glycemic load with endometrial cancer risk in the US Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial. Recruitment took place in 1993-2001. Over a median of 9.0 years of follow-up through 2009, 386 women developed endometrial cancer among 36,115 considered in the analysis. Dietary intakes were assessed using a 124-item diet history questionnaire. Cox proportional hazards models were applied to calculate hazard ratios and 95% confidence intervals. Significant inverse associations were detected between endometrial cancer risk and total available carbohydrate intake (hazard ratio (HR) = 0.66, 95% confidence interval (CI): 0.49, 0.90), total sugars intake (HR = 0.71, 95% CI: 0.52, 0.96), and glycemic load (HR = 0.63, 95% CI: 0.46, 0.84) when women in the highest quartile of intake were compared with those in the lowest. These inverse associations were strongest among overweight and obese women. No associations with endometrial cancer risk were observed for glycemic index or dietary fiber. Our findings contrast with previous evidence and suggest that high carbohydrate intakes and glycemic loads are protective against endometrial cancer development. Further clarification of these associations is warranted.

Dietary glycemic index and glycemic load in relation to changes in body composition measures during adolescence:Northern Ireland Young Hearts Study

Background: Epidemiologic evidence on the influence of dietary glycemic index (GI) and glycemic load (GL) on the development of obesity is limited.

Objective: This prospective study examined the associations between dietary GI and GL and changes in body composition measures during adolescence.

Design: In a representative sample of Northern Irish adolescents aged 12 years at baseline and 15 years at follow-up (n=426), dietary intake was assessed by a diet history interview. Body composition measures included body mass index (BMI; kg m(-2)), BMI z-score, sum of four skinfold thicknesses, percentage body fat, fat mass index (FMI; kg m(-2)) and fat-free mass index (kg m(-2)).

Results: After adjustment for potential confounding factors, baseline GI was associated with increased change in FMI. Mean (95% confidence interval) values of changes in FMI according to tertiles of baseline GI were 0.41 (0.25, 0.57), 0.42 (0.26, 0.58) and 0.67 (0.51, 0.83) kg m(-2), respectively (P for trend=0.03). There was no significant association of baseline GI with changes in other body composition measures (P for trend0.054). Conversely, baseline GL showed no association with changes in any of the measures (P for trend0.41). Furthermore, changes in GI or GL were not associated with changes in any of the measures (P for trend0.16).

Conclusion: Dietary GI at age 12 years was independently associated with increased change in FMI between ages 12 and 15 years in a representative sample from Northern Ireland, whereas dietary GL showed no association with changes in any of the body composition measures examined.

Influence of dietary protein intake and glycemic index on the association between TCF7L2 HapA and weight gain

BACKGROUND: Genetic polymorphisms of transcription factor 7-like 2 (TCF7L2) have been associated with type 2 diabetes and BMI. OBJECTIVE: The objective was to investigate whether TCF7L2 HapA is associated with weight development and whether such an association is modulated by protein intake or by the glycemic index (GI). DESIGN: The investigation was based on prospective data from 5 cohort studies nested within the European Prospective Investigation into Cancer and Nutrition. Weight change was followed up for a mean (±SD) of 6.8 ± 2.5 y. TCF7L2 rs7903146 and rs10885406 were successfully genotyped in 11,069 individuals and used to derive HapA. Multiple logistic and linear regression analysis was applied to test for the main effect of HapA and its interaction with dietary protein or GI. Analyses from the cohorts were combined by random-effects meta-analysis. RESULTS: HapA was associated neither with baseline BMI (0.03 ± 0.07 BMI units per allele; P = 0.6) nor with annual weight change (8.8 ± 11.7 g/y per allele; P = 0.5). However, a previously shown positive association between intake of protein, particularly of animal origin, and subsequent weight change in this population proved to be attenuated by TCF7L2 HapA (P-interaction = 0.01). We showed that weight gain becomes independent of protein intake with an increasing number of HapA alleles. Substitution of protein with either fat or carbohydrates showed the same effects. No interaction with GI was observed. CONCLUSION: TCF7L2 HapA attenuates the positive association between animal protein intake and long-term body weight change in middle-aged Europeans but does not interact with the GI of the diet.

Glycemic Index, glycemic control and beyond

It is currently estimated that over 370 million individuals have diabetes, making diabetes a major public health issue contributing significantly to global morbidity and mortality. The steep rise in diabetes prevalence over the past decades is attributable, in a large part, to lifestyle changes, with dietary habits and behaviour significant contributors. Despite the relatively wide availability of anti-diabetic medicine, it is lifestyle approaches that still remain the cornerstone of diabetes prevention and treatment. Glycemic index (GI) is a nutritional tool, which represents the glycemic response to carbohydrate ingestion. In light of the major impact of nutrition on diabetes pathophysiology, with the rising need to combat the escalating diabetes epidemic, this review will focus on the role of GI in glycemic control, the primary target of diabetic treatment and beyond. The review will present the evidence relating GI and diabetes treatment and prevention, as well as weight loss, weight maintenance and CVD risk factors.

Diet compounds, glycemic index and obesity-related cardiac effects

Background: Diet compounds may influence obesity-related cardiac oxidative stress and metabolic sifting. Carbohydrate-rich diet may be disadvantageous from fat-rich diet to cardiac tissue and glycemic index rather than lipid profile may predict the obesity-related cardiac effects.Materials and methods: Male Wistar rats were divided into three groups (n=8/group): (C) receiving standard chow (3.0 kcal/g); (CRD) receiving carbohydrate-rich diet (4.0 kcal/g), and (FRD) receiving fat-rich diet (4.0 kcal/g). Rats were sacrificed after the oral glucose tolerance test (OGTT) at 60 days of dietary treatments. Lipid profile and oxidative stress parameters were determined in serum. Myocardial samples were used to determine oxidative stress, metabolic enzymes, glycogen and triacylglycerol.Results: FRD rats showed higher final body weight and body mass index than CRD and C. Serum cholesterol and low-density lipoprotein were higher in FRD than in CRD, while triacylglycerol and oxidized low-density lipoprotein cholesterol were higher in CRD than in FRD. CRD rats had the highest myocardial lipid hydroperoxide and diminished superoxide dismutase and catalase activities. Myocardial glycogen was lower and triacylglycerol was higher in CRD than in C and FRD rats. Although FRD rats had depressed myocardial-reducing power, no significant changes were observed in myocardial energy metabolism. Myocardial beta-hydroxyacyl coenzyme-A dehydrogenase and citrate synthase, as well as the enhanced lactate debydrogenase/citrate synthase ratio indicated that fatty acid degradation was decreased in CRD rats. Glycemic index was positively correlated with obesity-related cardiac effects.Conclusions: Isoenergetic carbohydrate-rich and fat-rich diets induced different degree of obesity and differently affected lipid profile. Carbohydrate-rich diet was deleterious relative to fat-rich diet in the heart enhancing lipoperoxidation and shifting the metabolic pathway for energy production. Glycemic index rather than dyslipidemic profile may predict the obesity effects on cardiac tissue. (C) 2007 Elsevier B.V. All rights reserved.

Rutin ameliorates glycemic index, lipid profile and enzymatic activities in serum, heart and liver tissues of rats fed with a combination of hypercaloric diet and chronic ethanol consumption

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Association between glycemic index and glycemic load and the risk of incident coronary heart disease among whites and African Americans with and without type 2 diabetes: The Atherosclerosis Risk in Communities study

Several studies have examined the association between high glycemic index (GI) and glycemic load (GL) diets and the risk for coronary heart disease (CHD). However, most of these studies were conducted primarily on white populations. The primary aim of this study was to examine whether high GI and GL diets are associated with increased risk for developing CHD in whites and African Americans, non-diabetics and diabetics, and within stratifications of body mass index (BMI) and hypertension (HTN). Baseline and 17-year follow-up data from ARIC (Atherosclerosis Risk in Communities) study was used. The study population (13,051) consisted of 74% whites, 26% African Americans, 89% non-diabetics, 11% diabetics, 43% male, 57% female aged 44 to 66 years at baseline. Data from the ARIC food frequency questionnaire at baseline were analyzed to provide GI and GL indices for each subject. Increases of 25 and 30 units for GI and GL respectively were used to describe relationships on incident CHD risk. Adjusted hazard ratios for propensity score with 95% confidence intervals (CI) were used to assess associations. During 17 years of follow-up (1987 to 2004), 1,683 cases of CHD was recorded. Glycemic index was associated with 2.12 fold (95% CI: 1.05, 4.30) increased incident CHD risk for all African Americans and GL was associated with 1.14 fold (95% CI: 1.04, 1.25) increased CHD risk for all whites. In addition, GL was also an important CHD risk factor for white non-diabetics (HR=1.59; 95% CI: 1.33, 1.90). Furthermore, within stratum of BMI 23.0 to 29.9 in non-diabetics, GI was associated with an increased hazard ratio of 11.99 (95% CI: 2.31, 62.18) for CHD in African Americans, and GL was associated with 1.23 fold (1.08, 1.39) increased CHD risk in whites. Body mass index modified the effect of GI and GL on CHD risk in all whites and white non-diabetics. For HTN, both systolic blood pressure and diastolic blood pressure modified the effect on GI and GL on CHD risk in all whites and African Americans, white and African American non-diabetics, and white diabetics. Further studies should examine other factors that could influence the effects of GI and GL on CHD risk, including dietary factors, physical activity, and diet-gene interactions. ^

Effect of a Mediterranean Diet Intervention on Dietary Glycemic Load and Dietary Glycemic Index: The PREDIMED Study

[EN]To compare the one year effect of two dietary interventions with MeDiet on GL and GI in the PREDIMED trial. Methods. Participants were older subjects at high risk for cardiovascular disease. This analysis included 2866 nondiabetic subjects. Diet was assessed with a validated 137-item food frequency questionnaire (FFQ). The GI of each FFQ item was assigned by a 5-step methodology using the International Tables of GI and GL Values. Generalized linear models were fitted to assess the relationship between the intervention group and dietary GL and GI at one year of follow-up, using control group as reference.