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Carbohydrates, glycemic index and diabetes mellitus

Glycemic index, glycemic load and their association with glycemic control among patients with type 2 diabetes

Abstract

Background/Objectives:

The aim was to investigate the associations of glycemic index (GI), glycemic load (GL), carbohydrate and fiber intakes with hyperglycemia in type 2 diabetic patients.

Subjects/Methods:

In a cross-sectional study of 640 type 2 diabetic patients aged 28–75 years, usual dietary intakes were assessed by validated food frequency questionnaire. We used published international and Iranian tables of GI based on the white bread. Multivariable logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CI).

Results:

High-GL diet was associated with higher risk of hyperglycemia in type 2 diabetic patients after controlling for potential confounders. In multivariable model, OR (95% CI) for the highest vs the lowest quartile of GL was 2.58 (1.08–6.15) for elevated fasting serum glucose (FSG) (>130 mg/dl) (Ptrend=0.02) and was 3.05 (1.33–7.03) for elevated HbA1c (>8.6%) (Ptrend=0.008). After additional adjusting for dietary fiber and protein intakes, the relation of GL with elevated FSG and HbA1c was stable. GI was not significantly associated with either elevated FSG or HbA1c. In multivariable model, OR (95% CI) for the highest vs lowest quartile of the substitution of dietary carbohydrate for fat intake was 2.32 (1.37–3.92) for elevated HbA1c (Ptrend=0.001). Higher intake of dietary fiber was associated with lower risk of elevated FSG (highest vs lowest quartile: OR, 0.53; 95% CI: 0.28–0.99; Ptrend=0.04), but not with lower risk of elevated HbA1c.

Conclusions:

GL and carbohydrate intake were positively associated with the risk of hyperglycemia in type 2 diabetic patients; but the benefit in pursuing a low-GI diet without considering carbohydrate and energy intakes in these patients should be further investigated.

Introduction

Diabetes is a chronic metabolic disease associated with long-term complications resulting from chronic hyperglycemia.1 Nutrition therapy is an integral part of diabetes care, and carbohydrate intake has the greatest impact on improving glycemic control.2 On the basis of American Diabetes Association’s (ADA) recommendations,3 there is no ideal percentage of energy from carbohydrate and other macronutrients for all diabetic patients. ADA proposes diabetic patients to monitor total carbohydrate intake via carbohydrate counting, exchanges or estimation.2 Foods containing equal amounts of carbohydrate induce a different effect on the postprandial blood glucose.4, 5 The glycemic index (GI), which quantifies the postprandial blood glucose and insulin responses to carbohydrate composition of diet,6 may have beneficial effects in addition to carbohydrate counting. On the other hand, the concept of glycemic load (GL), which represents both the quality and quantity of carbohydrate intake,7 has been developed to better represent overall glycemic effects of a particular food item.8 The effectiveness of low GI and GL diets in glycemic control has been examined in epidemiological, clinical trials and meta-analysis.9, 10, 11, 12, 13, 14 However, in some studies, diets with low GI or GL had no benefits in the management of diabetes.13, 14 On the basis of the current evidence, the ADA states that combined with carbohydrate counting, the use of GI and GL may provide a modest additional benefit in achieving blood glucose goals.3 On the other hand, the concept of the GI is considered as an important issue in the guidelines suggested by the European Association for the Study of Diabetes that recommends the substitution of low-GI foods with high-GI foods.15 Therefore, the aim of this study was to examine the potential association between dietary GI, GL, carbohydrate and fiber intakes, and the risk of hyperglycemia in men and women with type 2 diabetes.

Materials and methods

We conducted a cross-sectional study of 751 patients with type 2 diabetes who were randomly recruited via phone call from registered patients with diabetes at three major diabetes clinics located in Tehran: the Charity Foundation for Special Diseases, the Institute of Endocrinology and Metabolism, and the Iran Diabetes Association. Eligible participants were 25 years old and above with physician-diagnosed type 2 diabetes at least 1 year before data collection. We did not measure islet cell autoantibodies. Therefore, anyone with diabetes diagnosed before the age of 25 and taking only insulin therapy was considered to be having type 1 diabetes and was excluded from our sample.

Data on medical history, smoking addiction and medication were obtained from personal interview. We excluded those who did not meet the following criteria: taking insulin, altering medication regimen or dietary intake during 3 months before the study and having abnormal hepatic tests (n=30). We also excluded patients who did not live in Tehran (n=4), did not complete the food frequency questionnaire (FFQ) (n=48), those (n=11) who reported a total daily energy intake outside the range of 800–4200 kcal and those (n=18) who had missing data for confounding variables. After these exclusions, 640 type 2 diabetic patients aged 28–75 years remained.

Written informed consent was obtained from all participants. The research protocol was approved by the Ethics Committee of National Nutrition and Food Technology Research Institute.

We collected 20 ml blood samples from each participant between 0800 and 1000 hours, before taking any oral hypoglycemic agent(s) and after 12–14-h overnight fasting. Aliquots of serum and red pack cells were transferred to polystyrene tubes that were immediately stored at −70 °C until analysis. Fasting serum glucose (FSG) concentration was measured by the glucose oxidase method. HbA1c was measured by a chromatography method using the commercial kit (Globe Diagnostics, Rome, Italy).

The dietary intake of patients was assessed by interview using a 1-year validated 168-item semi-quantitative FFQ.16 It consisted of a list of foods with standard serving sizes according to Iranian meal patterns, and was designed to obtain information on usual food intake during the previous year. The reported frequency for each food item was then converted to a daily intake. Information on frequency of intake and portion size was converted to the number of grams of each food item consumed on average per day. To determine the total dietary carbohydrate, protein, fat, fiber and energy compositions of Iranian foods, we used the United States Department of Agriculture database17 and Iranian food composition tables. The validity and reproducibility of dietary GI and GL were similar to those of nutrients commonly studied in epidemiologic studies with the use of FFQs.18 Of the 168 food and beverage items included in the FFQ, 30 items (17.8%) contain no available carbohydrate. The calculation of dietary GL and GI was thus based on the remaining 138 items with GI values ranging from 10 to 123. We used published international5 and Iranian tables of GI.19 We calculated GL values by multiplying the available carbohydrate content of each food by its GI value and then multiplied the resultant value with the amount of consumption (divided by 100) and then summed the values from all food items.8 Each unit of dietary GL represents the equivalent of 1 g of carbohydrate from white bread. The overall GI for each participant was estimated by dividing the dietary GL by the total amount of carbohydrates consumed.8, 20 The calculated values of dietary GI, GL and total dietary carbohydrate, protein, fat and fiber were adjusted for total energy intake using the residual method.21

Height was measured to the nearest 0.1 cm and weight to the nearest 0.1 kg. Body mass index (BMI) was calculated as weight/height2 (kg/m2).

Data on physical activity were obtained using modified international physical activity questionnaire (publicly available at http://www.ipaq.ki.se/ipaq.htm) and expressed as metabolic equivalent h/day (MET-h/day).

Statistical analysis

The data were expressed as mean±s.d. or percentages. We divided GI and GL into quartiles and participants were categorized on the basis of GI and GL quartiles. Variables were compared across quartile categories of GI and GL by one-way analysis of variance with Tukey’s post hoc comparisons for quantitative variables and χ2-tests for qualitative variables. Logistic regression models were used to estimate odds ratio (OR) and 95% confidence intervals (CI) for each category using the lowest quartile of intake as the reference category, while controlling for potential confounding variables. FSG <130 mg/dl is recommended as a target of glycemic control by ADA2 and the expected HbA1c levels for normal glucose values are 6–8.6% by the commercial HbA1c kit.22 Therefore, we defined hyperglycemia with cutoff values of 130 mg/dl for FSG and 8.6% for HbA1c. All models were adjusted for age, sex and energy intake. Multivariable models included additional terms for duration of diabetes, smoking, physical activity, BMI, vitamin/mineral supplementation, total hypoglycemic medication, blood pressure-lowering drug and lipid-lowering drug. In additional analyses, we further adjusted for dietary protein and fiber intakes (multivariable model 2). Multivariable model 1 for total carbohydrate intake was fit without adjusting for protein and fat intake to simulate the substitution of carbohydrate for the average mixture of protein and fat in the study population and with the adjustment for protein (multivariable model 2) to simulate the substitution of carbohydrate with total fat intake.23 To examine whether the associations between GL and elevated FSG or HbA1c were modified by other measures of diabetes risk factors, a cross-product term for the level of each factor and intake of GL expressed as a continuous variable was included in the multivariable model. P-values for tests for interactions were obtained from a likelihood ratio test with 1 degree of freedom. IBM SPSS 21 was used for all analyses. All P-values were two-sided.

Results

The median index across quartile of GL ranged from 108.2 to 246.6 and across quartile of GI ranged from 50.6 to 66.7. The main contributors of GL were bread (31.3%), rice (23.4%), fruits (21.3%) and sweets (9.8%). Clinical characteristics and nutrient intakes data relating to the 640 type 2 diabetes patients studied based on GL and GI quartiles are shown in Table 1. The participants with a higher GL were more likely to be younger, to be male, to have higher intakes of energy, carbohydrate, fat, protein and fiber, and to be smokers than subjects with lower GL. The participants with higher GL also had lower duration of diabetes. In comparison with the subjects in the lowest quartile of the GI, those in the higher quartiles were more likely to be younger, to be male, to be smokers and to consume more energy, carbohydrate and fat (Table 1).

Table 1 Characteristics of type 2 diabetic patients according to quartile of glycemic load and glycemic index

From 640 type 2 diabetes patients, 440 of them had FSG >130 mg/dl and 378 of them had HbA1c >8.6%. The ORs of elevated FSG (>130 mg/dl) and HbA1c (>8.6%) according to quartile categories of GL, GI, total carbohydrate and fiber intakes are shown in Table 2. After making adjustment for demographic, anthropometric, medication and lifestyle factors, higher GL was associated with elevated FSG risk (the highest vs the lowest quartile: OR=2.58, 95% CI: 1.08, 6.15; Ptrend=0.02) and elevated HbA1c risk (the highest vs the lowest quartile: OR=3.05, 95% CI: 1.33, 7.03, Ptrend=0.008) (multivariable model 1, Table 2). To explore whether the association of hyperglycemia with the GL is independent of the dietary intakes of fiber and protein, we additionally adjusted for dietary fiber and protein intakes (multivariable model 2). The odds of having elevated FSG for the highest quartile vs the lowest quartile of GL were increased by 200% and OR (95% CI) for elevated HbA1c for the highest quartile vs the lowest quartile was 3.94 (1.66–9.31, Ptrend=0.002). The GI was not significantly related to either elevated FSG or elevated HbA1c. Substitution of carbohydrate for average intake of protein or fat (multivariable model 1) was not significantly associated with increased risk of elevated FSG, but increased the risk of elevated HbA1c by 127% in the highest vs the lowest quartile of carbohydrate intake. Because total energy intake, and percent of energy from carbohydrate and protein intakes were included simultaneously in the analysis, the OR for carbohydrate can be interpreted as the effect of substituting carbohydrate with an equivalent reduction in the percent of energy from total fat. Substitution of carbohydrate for fat intake was significantly associated with higher risk of hyperglycemia measured by HbA1c (multivariable model 2). Higher dietary fiber intake was related with lower risk of elevated FSG (highest vs lowest quartile: OR, 0.53; 95% CI: 0.28, 0.99; Ptrend=0.04). However, higher dietary fiber intake was not associated with lower risk of elevated HbA1c.

Table 2 Multivariate-adjusted ORs (95% CI) of elevated fasting serum glucose (>130 mg/dl) and HbA1c (>8.6%) according to quartile categories of glycemic load and glycemic index, carbohydrate and fiber intakes

We also examined whether the associations between GL and elevated FSG and HbA1c differed by levels of hyperglycemia risk factors including age, BMI, duration of diabetes and sex. We have not found any significant interaction.

Discussion

In this cross-sectional study, we examined the association of quality and quantity of dietary carbohydrate intake with risk of hyperglycemia in type 2 diabetic patients and found that dietary GL in people with type 2 diabetes was positively associated with risk of hyperglycemia after the adjustment for demographic, anthropometric, lifestyle, medication and dietary factors. These associations were independent of dietary fiber and protein intakes. However, no statistically significant association was observed for GI in relation to either FSG or HbA1c; either after adjustment for potential confounders or after further adjustment for dietary factors. In addition, we found that quantity of carbohydrate intake was positively associated with the risk of hyperglycemia measured by HbA1c. Higher intake of fiber was also associated with lower FSG, but not HbA1c.

The importance of low GL or GI diets in the management of diabetes is controversial.9, 10, 11, 12, 13, 14 A growing body of evidence supports a pivotal role for dietary GI and GL in the prevention of diabetes. In a recent meta-analysis of prospective cohort studies, high-GI and/or high-GL diets have been correlated with the risk of type 2 diabetes (GI: OR=1.16, 95% CI: 1.06–1.26; GL: OR=1.20, 95% CI: 1.11–1.30).10 In Greenland's Inuit population, after adjustment for age, sex, BMI, smoking status and energy intake, GI was positively associated with fasting plasma glucose and HbA1c, although this association was dependent on educational level and physical activity and after further adjustment, only the association with fasting plasma glucose remained statistically significant. The inverse associations of GL with fasting plasma glucose and HbA1c have been also attenuated after additional adjustment for BMI, education, smoking status, physical activity and energy intake.24 In contrast, in a Dutch population, neither GI nor GL was associated with fasting glucose and HbA1c after multivariable adjustment.25

Besides epidemiologic studies, an effect of low-GI diet was also demonstrated by clinical trials. Consumption of low-GI foods instead of traditional or high-GI foods has clinically useful benefits on glycemic control in diabetic patients.11 A recent meta-analysis of randomized controlled trials conducted in diabetes reported that consuming low-GI diets significantly decreased HbA1c levels by 0.4% compared with comparison diets.26 Jenkins et al.9 identified that 6-month treatment with a low-GI diet in type 2 diabetic patients reduced HbA1c levels compared with a high-cereal fiber diet even after controlling for dietary fiber or body weight. In contrast, Ma et al.13 compared the effects of a low-GI diet with the standard ADA guidelines on the HbA1c for patients with type 2 diabetes. They found that the effects of low-GI diet on HbA1c improvement was comparable with ADA diet. Mayer-Davis et al. evaluated GI and GL in relation to average fasting glucose, 2 h plasma glucose following 75-g glucose load and glycated hemoglobin in adult participants in the insulin resistance atherosclerosis study. The results did not support the correlation between dietary GI and any measure of glycemia.14 To compare the long-term effects of diets with different GI or carbohydrate amount on HbA1c and plasma glucose, type 2 diabetic patients received high-carbohydrate and high-GI, high-carbohydrate and low-GI, or low-carbohydrate and high-monounsaturated fat diets for 1 year. Although there has been higher intake of fiber and reduction in postprandial glucose by high-carbohydrate and low-GI diet, HbA1c was not improved by reductions in the GI or carbohydrate intakes.27

For GI, we found no association with glycemic control, as assessed by FSG and HbA1c. The present finding of null association is hardly due to the range of dietary GI. In our study, median index across quartile of GI ranged from 50.6 to 66.7 and these values did not differ much from the studies that have found a significant association between dietary GI and risk of diabetes.28, 29, 30, 31 Energy intake has a positive effect on glycemic control in diabetic patients32 and high intake of dietary fiber is associated with lower fasting blood glucose and HbA1c.33 However, after further adjustment for energy or dietary fiber intake, the results did not change. The association with GL but not GI suggests that the amounts of carbohydrate and GI of foods should be considered simultaneously, as represented by GL, in recommended diet to effectively manage glycemic control in diabetic patients.

This study had some limitations. We could not infer causality because of the observational nature of our study. We assessed diet using a validated FFQ. Measurement errors may be introduced by the under- or overreporting of the amounts of food groups usually eaten per day. GIs were estimated on the basis of the international and Iranian tables of GI. Thus, the effect of varying degree of ripeness, processing and chewing on food GIs is a concern.34 Another possible source of measurement error is that we focused only on dietary fiber consumption without regarding the amount of fiber supplements. However, we would expect these to bias results toward the null. In addition, one limitation of the study is the possibility of participant’s weight change before including in the study and our study only addresses the association controlling for weight at time of measuring dietary intake and glycemic control factors. However, we did not find any interaction between GL and BMI. This study had several strengths. We measured known potential confounders and were able to control for them in our analyses.

In conclusion, our findings suggest that GL which describes quality and quantity of carbohydrate consumption, and also the total carbohydrate intake significantly influence glycemic control in type 2 diabetic patients. But benefit in pursuing a low-GI diet without considering carbohydrate and energy intakes in patients with type 2 diabetes should be further investigated.

References

  1. 1

    Marcovecchio ML, Lucantoni M, Chiarelli F . Role of chronic and acute hyperglycemia in the development of diabetes complications. Diabetes Technol Ther 2011; 13: 389–394.

    CAS  Article  Google Scholar 

  2. 2

    American Diabetes Association. Standards of medical care in diabetes—2013. Diabetes Care 2013; 36: S11–S66.

    Article  Google Scholar 

  3. 3

    American Diabetes Association. Standards of medical care in diabetes—2014. Diabetes Care 2014; 37: S14–S80.

    Article  Google Scholar 

  4. 4

    O'Dea K, Nestel PJ, Antonoff L . Physical factors influencing postprandial glucose and insulin responses to starch. Am J Clin Nutr 1980; 33: 760–765.

    CAS  Article  Google Scholar 

  5. 5

    Foster-Powell K, Holt SH, Brand-Miller JC . International table of glycemic index and glycemic load values: 2002. Am J Clin Nutr 2002; 76: 5–56.

    CAS  Article  Google Scholar 

  6. 6

    Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H, Baldwin JM et al. Glycemic index of foods: a physiological basis for carbohydrate exchange. Am J Clin Nutr 1981; 34: 362–366.

    CAS  Article  Google Scholar 

  7. 7

    Liu S, Manson JE, Stampfer MJ, Holmes MD, Hu FB, Hankinson SE et al. Dietary glycemic load assessed by food-frequency questionnaire in relation to plasma high-density-lipoprotein cholesterol and fasting plasma triacylglycerols in postmenopausal women. Am J Clin Nutr 2001; 73: 560–566.

    CAS  Article  Google Scholar 

  8. 8

    Willett WC, Manson J, Liu S . Glycemic index, glycemic load, and risk of type 2 diabetes. Am J Clin Nutr 2002; 76: 274S–280S.

    CAS  Article  Google Scholar 

  9. 9

    Jenkins DJ, Kendall CW, McKeown-Eyssen G, Josse RG, Silverberg J, Booth GL et al. Effect of a low-glycemic index or a high-cereal fiber diet on type 2 diabetes: a randomized trial. JAMA 2008; 300: 2742–2753.

    CAS  Article  Google Scholar 

  10. 10

    Dong JY, Zhang L, Zhang YH, Qin LQ . Dietary glycaemic index and glycaemic load in relation to the risk of type 2 diabetes: a meta-analysis of prospective cohort studies. Br J Nutr 2011; 106: 1649–1654.

    CAS  Article  Google Scholar 

  11. 11

    Brand-Miller J, Hayne S, Petocz P, Colagiuri S . Low-glycemic index diets in the management of diabetes: a meta-analysis of randomized controlled trials. Diabetes Care 2003; 26: 2261–2267.

    Article  Google Scholar 

  12. 12

    Riccardi G, Rivellese AA, Giacco R . Role of glycemic index and glycemic load in the healthy state, in prediabetes, and in diabetes. Am J Clin Nutr 2008; 87: 269S–274S.

    CAS  Article  Google Scholar 

  13. 13

    Ma Y, Olendzki BC, Merriam PA, Chiriboga DE, Culver AL, Li W et al. A randomized clinical trial comparing low-glycemic index versus ADA dietary education among individuals with type 2 diabetes. Nutrition 2008; 24: 45–56.

    CAS  Article  Google Scholar 

  14. 14

    Mayer-Davis EJ, Dhawan A, Liese AD, Teff K, Schulz M . Towards understanding of glycaemic index and glycaemic load in habitual diet: associations with measures of glycaemia in the Insulin Resistance Atherosclerosis Study. Br J Nutr 2006; 95: 397–405.

    CAS  Article  Google Scholar 

  15. 15

    The Diabetes and Nutrition Study Group (DNSG) of the European Association for the Study of Diabetes. Recommendations for the nutritional management of patients with diabetes mellitus. Eur J Clin Nutr 2000; 54: 353–355.

    Article  Google Scholar 

  16. 16

    Mirmiran P, Esfahani FH, Mehrabi Y, Hedayati M, Azizi F . Reliability and relative validity of an FFQ for nutrients in the Tehran lipid and glucose study. Public Health Nutr 2010; 13: 654–662.

    Article  Google Scholar 

  17. 17

    USDA Nutrient Database for Standard Reference, Release 24: Department of Agriculture ARS 2011.

  18. 18

    Levitan EB, Westgren CW, Liu S, Wolk A . Reproducibility and validity of dietary glycemic index, dietary glycemic load, and total carbohydrate intake in 141 Swedish men. Am J Clin Nutr 2007; 85: 548–553.

    CAS  Article  Google Scholar 

  19. 19

    Taleban FA, Esmaeili M . Glycemic Index of Iranian Foods. National Nutrition and Food Technology Research Institute Press: Tehran, Iran, 1999.

    Google Scholar 

  20. 20

    Wolever TM, Nguyen PM, Chiasson JL, Hunt JA, Josse RG, Palmason C et al. Determinants of diet glycemic index calculated retrospectively from diet records of 342 individuals with non-insulin-dependent diabetes mellitus. Am J Clin Nutr 1994; 59: 1265–1269.

    CAS  Article  Google Scholar 

  21. 21

    Willett WC, Howe GR, Kushi LH . Adjustment for total energy intake in epidemiologic studies. Am J Clin Nutr 1997; 65: 1220S–1228S.

    CAS  Article  Google Scholar 

  22. 22

    Glycated HbA1c. Chromatographic determination in tube with preweighted resin of hemoglobin A1c in blood. REF GD541500, GD540500. http://www.gdsrl.com/upload/prodotti/gd5415_00_glycated_hba1c_0.pdf.

  23. 23

    Hu FB, Stampfer MJ, Manson JE, Rimm E, Colditz GA, Rosner BA et al. Dietary fat intake and the risk of coronary heart disease in women. N Engl J Med 1997; 337: 1491–1499.

    CAS  Article  Google Scholar 

  24. 24

    van Aerde MA, Witte DR, Jeppesen C, Soedamah-Muthu SS, Bjerregaard P, Jørgensen ME . Glycemic index and glycemic load in relation to glucose intolerance among Greenland's Inuit population. Diabetes Res Clin Pract 2012; 97: 298–305.

    CAS  Article  Google Scholar 

  25. 25

    Du H, van der A DL, van Bakel MM, van der Kallen CJ, Blaak EE, van Greevenbroek MM et al. Glycemic index and glycemic load in relation to food and nutrient intake and metabolic risk factors in a Dutch population. Am J Clin Nutr 2008; 87: 655–661.

    CAS  Article  Google Scholar 

  26. 26

    Thomas DE, Elliott EJ . The use of low-glycaemic index diets in diabetes control. Br J Nutr 2010; 104: 797–802.

    CAS  Article  Google Scholar 

  27. 27

    Wolever TM, Gibbs AL, Mehling C, Chiasson JL, Connelly PW, Josse RG et al. The Canadian Trial of Carbohydrates in Diabetes (CCD), a 1-y controlled trial of low-glycemic-index dietary carbohydrate in type 2 diabetes: no effect on glycated hemoglobin but reduction in C-reactive protein. Am J Clin Nutr 2008; 87: 114–125.

    CAS  Article  Google Scholar 

  28. 28

    Salmerón J, Ascherio A, Rimm EB, Colditz GA, Spiegelman D, Jenkins DJ et al. Dietary fiber, glycemic load, and risk of NIDDM in men. Diabetes Care 1997; 20: 545–550.

    Article  Google Scholar 

  29. 29

    Krishnan S, Rosenberg L, Singer M, Hu FB, Djoussé L, Cupples LA et al. Glycemic index, glycemic load, and cereal fiber intake and risk of type 2 diabetes in US black women. Arch Intern Med 2007; 167: 2304–2309.

    Article  Google Scholar 

  30. 30

    Salmerón J, Manson JE, Stampfer MJ, Colditz GA, Wing AL, Willett WC . Dietary fiber, glycemic load, and risk of non-insulin-dependent diabetes mellitus in women. JAMA 1997; 277: 472–477.

    Article  Google Scholar 

  31. 31

    Schulze MB, Liu S, Rimm EB, Manson JE, Willett WC, Hu FB . Glycemic index, glycemic load, and dietary fiber intake and incidence of type 2 diabetes in younger and middle-aged women. Am J Clin Nutr 2004; 80: 348–356.

    CAS  Article  Google Scholar 

  32. 32

    Heilbronn LK, Noakes M, Clifton PM . Effect of energy restriction, weight loss, and diet composition on plasma lipids and glucose in patients with type 2 diabetes. Diabetes Care 1999; 22: 889–895.

    CAS  Article  Google Scholar 

  33. 33

    Post RE, Mainous 3rd AG, King DE, Simpson KN . Dietary fiber for the treatment of type 2 diabetes mellitus: a meta-analysis. J Am Board Fam Med 2012; 25: 16–23.

    Article  Google Scholar 

  34. 34

    Ciok J, Dolna A . The role of glycemic index concept in carbohydrate metabolism. Przegl Lek 2006; 63: 287–291.

    PubMed  Google Scholar 

Download references

Acknowledgements

This work was supported by a grant from the National Nutrition and Food Technology Research Institute, Tehran, Iran.

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Correspondence to Maryam S Farvid.

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Farvid, M., Homayouni, F., Shokoohi, M. et al. Glycemic index, glycemic load and their association with glycemic control among patients with type 2 diabetes. Eur J Clin Nutr 68, 459–463 (2014). https://doi.org/10.1038/ejcn.2013.288

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Keywords

  • glycemic index
  • glycemic load
  • carbohydrate
  • fiber
  • hyperglycemia

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