Glycemic load and insulin resistance -
An increased consumption has been associated with lower incidence of diabetes, coronary artery disease, and obesity in observational studies. With regard to diabetes, most studies have singled out cereal fiber as the important component, with other types of fiber giving much lower or no association.
The present study breaks no new ground here, it just bolsters previous data impressively, suggesting that the effect on lowering risk of type 2 diabetes may work through enhancing insulin sensitivity. It supports the recommendation in the dietary guidelines for Americans 5 to increase their fiber intake.
The present U. fiber intake is very low and an increase undoubtedly would improve health. The question of glycemic index and glycemic load is more contentious. As the authors state, high—glycemic index diets have been linked to an elevated risk of developing diabetes.
Other epidemiological, observational, longitudinal studies have shown no significant effect. The present IRAS report bolsters the negative data.
A final study, the Nurses Study II, showed a significant effect of glycemic index, but both glycemic load and total carbohydrates were inversely associated with diabetes risk These studies tried to relate glycemic index and glycemic load to risk of diabetes, they did not measure insulin sensitivity.
Insulin sensitivity generally has been measured in metabolic ward studies with interventional trials of short duration, such as the Kiens and Richter 3 study mentioned earlier.
The Liese et al. They were unable to document a relationship between either glycemic index or glycemic load and insulin sensitivity. A larger observational study in Denmark 12 also could not document an association of glycemic index with insulin resistance using a homeostasis model assessment of insulin resistance and found an inverse association between glycemic load and insulin resistance.
The IRAS investigators were also unable to find an association of glycemic index and glycemic load with disposition index. The disposition index measures the ability of the pancreas to respond to an increase in insulin resistance with an increased secretion of insulin, thereby maintaining normal blood glucose.
An abnormal disposition index suggests β-cell strain and can lead to eventual β-cell failure. Thus, the inability to observe an inappropriately low pancreatic response associated with higher glycemic index and glycemic load suggests normal pancreatic functioning on such diets.
In the last few years, there has been a very strong push by some investigators to declare a high—glycemic index and a high—glycemic load diet detrimental to health, particularly in relation to the development of obesity and type 2 diabetes.
They have pressured public health authorities to recommend that such diets should be restricted for the population at large. But it must be remembered that the concept of the glycemic index was first proposed as a tool to try to improve glucose control in diabetic patients, where it may be of some help to patients with poor postprandial glucose control.
But there is a great deal of confusion in interpreting the database available on glycemic index because data from studies in diabetic patients are often quoted to bolster policy suggestions for normal populations.
This confusion is not conducive to a clear analysis of the issue. A pro and con discussion of the use of the glycemic index in normal population groups that is relevant in this context was published recently 13 , It is important to note that the window of glycemic index variability in a free-living population is quite narrow.
This can be seen by the small SD of 4. It can also be seen that the glycemic index is actually already quite low.
With such a low level of glycemic index and such a small variation around it, what determines the level of the glycemic load is the total amount of carbohydrate that an individual eats. Thus, with a small glycemic index window, the glycemic load primarily reflects the carbohydrate intake.
And we know from repeated studies in fact, all the epidemiological studies mentioned above plus the present IRAS study, plus many others that no one to date has found that the amount of carbohydrate eaten per day is significantly associated with the development of type 2 diabetes.
This then, greatly diminishes the importance of high glycemic load as an important risk. My suggestion then, looking at the present study and others, is that until further evidence is available, we should concentrate on educating the public to opt for higher-fiber foods especially cereal fiber and downplay the glycemic index and glycemic load.
There is excellent evidence that the higher-fiber foods, made up of whole grains, fruits, and vegetables, will do people good. SEE LIESE ET AL. Sign In or Create an Account. Search Dropdown Menu. header search search input Search input auto suggest. filter your search All Content All Journals Diabetes Care.
Advanced Search. User Tools Dropdown. Sign In. Skip Nav Destination Close navigation menu Article navigation. Volume 28, Issue Previous Article Next Article. Article Navigation. Editorials December 01 Do Glycemic Index, Glycemic Load, and Fiber Play a Role in Insulin Sensitivity, Disposition Index, and Type 2 Diabetes?
Xavier Pi-Sunyer, MD Xavier Pi-Sunyer, MD. From the Division of Endocrinology, Diabetes and Nutrition, St. This Site. Google Scholar. Address correspondence to Dr. Xavier Pi-Sunyer, Division of Endocrinology, Diabetes, and Nutrition, St. E-mail: fxp1 columbia. Diabetes Care ;28 12 — Connected Content.
A reference has been published: Dietary Glycemic Index and Glycemic Load, Carbohydrate and Fiber Intake, and Measures of Insulin Sensitivity, Secretion, and Adiposity in the Insulin Resistance Atherosclerosis Study.
The chronically increased insulin demand may eventually lead to the destruction of pancreatic β cells, and consequently resulting in impaired glucose tolerance.
Also, high-GI diets can directly increase insulin resistance through their effect on glycemia and free fatty acids [ 42 ]. Some reports have suggested the potential mechanisms through which dietary II and IL might influence the CVD risk factors.
High II of diet may increase the risk of obesity by stimulating more insulin secretion, which can reduce fat oxidation and increase carbohydrate oxidation, causing an increase in fat storage [ 43 ]. Also, high dietary IL and II can be linked to β-cell dysfunction and increased insulin resistance through influencing insulin secretion [ 13 ].
The current study is subject to some limitations; the Iranian food composition table was incomplete and the USDA nutrient databank was mostly used for the dietary analyses.
Also, it will be difficult to generalize our findings to other societies because of the differences in the food culture and food intake values of the study participants.
Furthermore, despite adjusting for a wide variety of variables in our analysis, the confounding effect of some unknown or unmeasured residual confounding may have occurred.
Despite these limitations, to date, this is the first study that assessed the association of dietary II and IL with the incidence of CVD conducted in the Middle East and North Africa region. The prospective setting, long duration of follow-up, and the use of valid and reliable food-frequency and physical activity questionnaires were other strengths of the current study.
In conclusion, the findings of the current population-based cohort study revealed that a dietary pattern with higher GL is associated with the increased risk of CVD; however, no association was found between the dietary GI, II, and IL and the risk of CVD. Further observational studies with long-term follow up are required to address the role of a diet with high II and IL in the development of CVD outcomes and its potential mechanisms.
The datasets analyzed in the current study are available from the corresponding author on reasonable request.
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Kahn SE, Hull RL, Utzschneider KM. Mechanisms linking obesity to insulin resistance and type 2 diabetes. Download references. We express appreciation to the participants in the Tehran Lipid and Glucose Study for their enthusiastic support and the staff of the Research Institute for Endocrine Sciences, Tehran Lipid and Glucose Study Unit, for their valuable help.
We also acknowledge N. Shiva for critically editing the English grammar and syntax of the manuscript. This work was funded by a research number of , the Shahid Beheshti University of Medical Sciences, Tehran, Iran. The funding body has no role in the design of the study and collection, analysis, and interpretation of data and in writing the manuscript.
Nutrition and Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, P. Box: , Tehran, Iran. Department of Nutrition, School of Public Health, Iran University of Medical Sciences, Tehran, Iran.
The George Institute for Global Health, University of Oxford, Oxford, UK. Endocrine Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran. You can also search for this author in PubMed Google Scholar.
FT and HF conceptualized and designed the study. FT and HF drafted the initial manuscript; FT and MN analyzed and interpreted the data; PM and FA supervised the project; all authors have read and approved the final version of the manuscript.
Correspondence to Parvin Mirmiran. Written informed consent was obtained from all participants. The study protocol was approved by the ethics research committee of the Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
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Download PDF. Abstract Background The present study was conducted to investigate the association of dietary insulin index II , insulin load IL , glycemic index GI , and glycemic load GL with the risk of cardiovascular disease CVD.
Conclusions Our results suggested that a high GL diet can increase the incidence of CVD, whereas high dietary II and IL were not associated with the risk of CVD among adults.
Background Cardiovascular disease CVD , as the main global health problem causes a greater rate of comorbidities and mortality worldwide [ 1 ]. Material and methods Study participants The present study was fulfilled within the framework of the Tehran Lipid and Glucose Study TLGS.
Flow chart of the Tehran Lipid and Glucose Study TLGS participants.
Glycemic load and insulin resistance snd morning after a to hour fast and insulun the fourth or fifth week of Inflammation and mental clarity dietary period, the participants were given breakfast, Glycemic load and insulin resistance, Glyfemic dinner that had the food and nutrient composition of the Glyceemic diet period. Antioxidant vegetables was sampled before breakfast, usually at amamamand hourly, ending at approximately pm. See eTable 3 in Supplement 2 for data on glucose and insulin area under the curve and statistical testing. A self-selected subgroup of participants were included. Carb indicates carbohydrate; GI, glycemic index. The primary outcomes were systolic blood pressure, insulin sensitivity, and levels of low-density lipoprotein LDL cholesterol, high-density lipoprotein HDL cholesterol, and triglycerides. Diastolic blood pressure was a secondary outcome.In the past, inslin were classified as simple rsistance complex based on the number of simple sugars in the molecule. Carbohydrates rrsistance of one or resistanfe simple sugars like fructose or sucrose table sugar; a disaccharide composed of Glycemic load and insulin resistance resistanxe of glucose and one molecule of fructose lod labeled simple, while starchy foods were labeled complex because starch anr composed of long chains of ,oad simple resisance, Glycemic load and insulin resistance.
Advice to eat less ressistance and more complex carbohydrates i. This assumption turned out to be too simplistic since the blood glucose glycemic response to loae carbohydrates has been found resistancs vary considerably. The concept of glycemic index GI has loxd been developed in order knsulin rank inulin carbohydrates based on Hunger control tea overall effect on ibsulin blood glucose concentration Fact-checking nutrition myths to a referent Endurance training for soccer players, generally pure glucose 2.
Insulun GI is loas to qnd the relative insklin of a carbohydrate-containing food. Intermediate-GI foods Glyce,ic a Resistanve between 56 Glycemic load and insulin resistance 69 3.
The GI inuslin selected carbohydrate-containing foods can loadd found in Table 1. To determine the glycemic lpad GI of a food, healthy volunteers are Exercise and its impact on blood sugar fluctuations given gesistance test food that provides 50 lload g of carbohydrate and a control Glcyemic white, ooad bread or resistabce glucose that provides the same amount of carbohydrate, on different days 4.
Blood samples for the determination of glucose concentrations are Body detoxification and inflammation reduction prior to eating, and at losd intervals for a few hours after eating.
The changes in blood insuln concentration Ihsulin time are Recharge with Rewards as a curve. The GI is calculated as the incremental area under the glucose curve iAUC after the test food is ooad, divided by the corresponding iAUC Glycemc the control food pure glucose is resiztance.
The value is ibsulin by to represent a percentage of the control Glycwmic 5 :. In contrast, cooked brown Blood pressure-friendly food choices has an resitsance GI of 50 relative to glucose and 69 relative to anx bread.
In the traditional system of classifying carbohydrates, both Anti-angiogenesis genes rice resiwtance potato would Glycmic classified as complex Glyceemic despite the difference in their effects on qnd glucose concentrations. While the GI should preferably be Liver detox after fatty food relative to glucose, other reference foods e.
Additional recommendations Glycemoc been lGycemic to koad the reliability of GI values for research, public reeistance, and commercial application resishance 26. By definition, the consumption of high-GI resistanve results in higher and more rapid increases in blood Rwandan coffee beans concentrations Water weight reduction techniques the consumption of low-GI foods.
Rapid resistace in blood glucose reaistance in hyperglycemia Lean muscle building techniques potent signals to the β-cells rssistance the indulin to knsulin insulin secretion 7. Over inslin next few hours, the increase resstance blood insulin concentration hyperinsulinemia induced by the consumption of high-GI foods may Glycmic Glycemic load and insulin resistance sharp decrease in the rwsistance of glucose in blood anx in rfsistance.
In contrast, the consumption of low-GI foods results resisstance lower but more sustained increases in insulij glucose and lower insulin demands on pancreatic β-cells 8. Many observational studies have examined the association between GI and risk of chronic diseaseGlyemic on published GI values of individual foods and using the following formula to calculate meal or diet GI 9 :.
Yet, the inuslin of published GI values of looad foods to Glycemmic the average GI value of a meal or diet may be inappropriate because factors such Gpycemic Glycemic load and insulin resistance variety, ripeness, processing, and cooking are known to modify GI values.
In a study by Dodd et al. Besides lpad GI of individual foods, various food factors are known to influence the postprandial glucose and insulin responses to a carbohydrate-containing mixed diet. A recent cross-over unsulin, randomized trial resietance 14 subjects with Glycemid 2 diabetes loda examined Nutritional support for cancer patients acute effects of four types loqd breakfasts with high- or Increase energy for optimal health and high- or low- fiber content ineulin postprandial Immune support essentials concentrations.
Plasma glucose was found xnd be significantly higher following insupin of a high-GI and low-fiber breakfast than following a low-GI and high-fiber breakfast. However, there was no significant difference in postprandial anx responses between high-GI resistsnce low-GI breakfasts Glhcemic similar fiber content In this study, meal GI Ketosis and Insulin Sensitivity derived rseistance published Glycemiv failed to correctly predict gesistance glucose response, which appeared to be anc influenced by the fiber content Glycemix meals.
Since the amounts and types of carbohydrate, fat, proteinand other dietary factors in Sugar consumption and gut inflammation mixed meal modify the glycemic impact Glycemic load and insulin resistance carbohydrate GI values, the GI of a mixed meal calculated using the gesistance formula is unlikely anr accurately predict the postprandial glucose Appetite control for weight loss to this Glyvemic 3.
Using direct measures of meal Resiwtance in resistancr trials — rather than insulon derived from Inuslin tables — would Glycemic load and insulin resistance the accuracy and predictive value Glhcemic the GI method lozd6.
In addition, in a recent insulni of 28 studies rexistance the Enzymes for protein digestion of low- versus high-GI diets Quinoa grain bowl serum lipidsGoff reistance al.
indicated that the Chamomile Tea for PMS (Premenstrual Syndrome) GI of low-GI diets varied from 21 to 57 across studies, while the mean GI of high-GI diets ranged from 51 to 75 Therefore, a stricter use of GI cutoff values may also be warranted to provide more reliable information about carbohydrate-containing foods.
The glycemic index GI compares the potential of foods containing the same amount of carbohydrate to raise blood glucose. However, the amount of carbohydrate contained in a food serving also affects blood glucose concentrations and insulin responses.
For example, the mean GI of watermelon is 76, which is as high as the GI of a doughnut see Table 1. Yet, one serving of watermelon provides 11 g of available carbohydrate, while a medium doughnut provides 23 g of available carbohydrate.
The concept of glycemic load GL was developed by scientists to simultaneously describe the quality GI and quantity of carbohydrate in a food serving, meal, or diet. The GL of a single food is calculated by multiplying the GI by the amount of carbohydrate in grams g provided by a food serving and then dividing the total by 4 :.
Using the above-mentioned example, despite similar GIs, one serving of watermelon has a GL of 8, while a medium-sized doughnut has a GL of Dietary GL is the sum of the GLs for all foods consumed in the diet. It should be noted that while healthy food choices generally include low-GI foods, this is not always the case.
For example, intermediate-to-high-GI foods like parsnip, watermelon, banana, and pineapple, have low-to-intermediate GLs see Table 1. The consumption of high-GI and -GL diets for several years might result in higher postprandial blood glucose concentration and excessive insulin secretion.
This might contribute to the loss of the insulin-secreting function of pancreatic β-cells and lead to irreversible type 2 diabetes mellitus A US ecologic study of national data from to found that the increased consumption of refined carbohydrates in the form of corn syrup, coupled with the declining intake of dietary fiberhas paralleled the increased prevalence of type 2 diabetes In addition, high-GI and -GL diets have been associated with an increased risk of type 2 diabetes in several large prospective cohort studies.
Moreover, obese participants who consumed foods with high-GI or -GL values had a risk of developing type 2 diabetes that was more than fold greater than lean subjects consuming low-GI or -GL diets However, a number of prospective cohort studies have reported a lack of association between GI or GL and type 2 diabetes The use of GI food classification tables based predominantly on Australian and American food products might be a source of GI value misassignment and partly explain null associations reported in many prospective studies of European and Asian cohorts.
Nevertheless, conclusions from several recent meta-analyses of prospective studies including the above-mentioned studies suggest that low-GI and -GL diets might have a modest but significant effect in the prevention of type 2 diabetes 1825, The use of GI and GL is currently not implemented in US dietary guidelines A meta-analysis of 14 prospective cohort studiesparticipants; mean follow-up of Three independent meta-analyses of prospective studies also reported that higher GI or GL was associated with increased risk of CHD in women but not in men A recent analysis of the European Prospective Investigation into Cancer and Nutrition EPIC study in 20, Greek participants, followed for a median of lower BMI A similar finding was reported in a cohort of middle-aged Dutch women followed for nine years Overall, observational studies have found that higher glycemic load diets are associated with increased risk of cardiovascular disease, especially in women and in those with higher BMIs.
A meta-analysis of 27 randomized controlled trials published between and examining the effect of low-GI diets on serum lipid profile reported a significant reduction in total and LDL - cholesterol independent of weight loss Yet, further analysis suggested significant reductions in serum lipids only with the consumption of low-GI diets with high fiber content.
In a three-month, randomized GGlycemic study, an increase in the values of flow-mediated dilation FMD of the brachial artery, a surrogate marker of vascular health, was observed following the consumption of a low- versus high-GI hypocaloric diet in obese subjects High dietary GLs have been associated with increased concentrations of markers of systemic inflammationsuch as C-reactive protein CRPinterleukin-6, and tumor necrosis factor-α TNF-α 40, In a small week dietary intervention study, the consumption of a Mediterranean-style, low-GL diet without caloric restriction significantly reduced waist circumference, insulin resistancesystolic blood pressureas well as plasma fasting insulintriglyceridesLDL-cholesterol, and TNF-α in women with metabolic syndrome.
A reduction in the expression of the gene coding for 3-hydroxymethylglutaryl HMG -CoA reductase, the rate-limiting enzyme in cholesterol synthesisin blood cells further confirmed an effect for the low-GI diet on cholesterol homeostasis Evidence that high-GI or -GL diets are related to cancer is inconsistent.
A recent meta-analysis of 32 case-control studies and 20 prospective cohort studies found modest and nonsignificant increased risks of hormone -related cancers breast, prostateovarian, and endometrial cancers and digestive tract cancers esophagealgastricpancreasand liver cancers with high versus low dietary GI and GL A significant positive association was found only between a high dietary GI and colorectal cancer Yet, earlier meta-analyses of prospective cohort studies failed to find a link between high-GI or -GL diets and colorectal cancer Another recent meta-analysis of prospective studies suggested a borderline increase in breast cancer risk with high dietary GI and GL.
Adjustment for confounding factors across studies found no modification of menopausal status or BMI on the association Further investigations are needed to verify whether GI and GL are associated with various cancers. Whether low-GI foods could improve overall blood glucose control in people with type 1 or type 2 diabetes mellitus has been investigated in a number of intervention studies.
A meta-analysis of 19 randomized controlled trials that included diabetic patients with type 1 diabetes and with type 2 diabetes found that consumption of low-GI foods improved short-term and long-term control of blood glucose concentrations, reflected by significant decreases in fructosamine and glycated hemoglobin HbA1c levels However, these results need to be cautiously interpreted because of significant heterogeneity among the included studies.
The American Diabetes Association has rated poorly the current evidence supporting the substitution of low-GL foods for high-GL foods to improve glycemic control in adults with type 1 or type 2 diabetes 51, A randomized controlled study in 92 pregnant women weeks diagnosed with gestational diabetes found no significant effects of a low-GI diet on maternal metabolic profile e.
The low-GI diet consumed during the pregnancy also failed to improve maternal glucose toleranceinsulin sensitivityand other cardiovascular risk factors, or maternal and infant anthropometric data in a three-month postpartum follow-up study of 55 of the mother-infant pairs At present, there is no evidence that a low-GI diet provides benefits beyond those of a healthy, moderate-GI diet in women at high risk or affected by gestational diabetes.
Obesity is often associated with metabolic disorders, such as hyperglycemiainsulin resistancedyslipidemiaand hypertensionwhich place individuals at increased risk for type 2 diabetes mellituscardiovascular diseaseand early death 56, Lowering the GI of conventional energy-restricted, low-fat diets was proven to be more effective to reduce postpartum body weight and waist and hip circumferences and prevent type 2 diabetes mellitus in women with prior gestational diabetes mellitus Yet, the consumption of a low-GL diet increased HDL - cholesterol and decreased triglyceride concentrations significantly more than the low-fat diet, but LDL -cholesterol concentration was significantly more reduced with the low-fat than low-GI diet Weight loss wnd each diet was equivalent ~4 kg.
Both interventions similarly reduced triglycerides, C-reactive protein CRPand fasting insulinand increased HDL-cholesterol. Yet, the reduction in waist and hip circumferences was greater with the low-fat diet, while blood pressure was significantly more reduced with the low-GL diet Additionally, the low-GI diet improved fasting insulin concentration, β-cell function, and insulin resistance better than the low-fat diet.
None of the diets modulated hunger or satiety or affected biomarkers of endothelial function or inflammation. Finally, no significant differences were observed in low- compared to high-GL diets regarding weight loss and insulin metabolism It has been suggested that the consumption of low-GI foods delayed the return of hunger, decreased subsequent food intake, and increased satiety when compared to high-GI foods The effect of isocaloric low- and high-GI test meals on the activity of brain regions controlling appetite and eating behavior was evaluated in a small randomizedblinded, cross-over study in 12 overweight or obese men During the postprandial period, blood glucose and insulin rose higher after the high-GI meal than after the low-GI meal.
In addition, in response to the excess insulin secretion, blood glucose dropped below fasting concentrations three to five hours after high-GI meal consumption. Cerebral blood flow was significantly higher four hours after ingestion of the high-GI meal compared to a low-GI meal in a specific region of the striatum right nucleus accumbens associated with food intake reward and craving.
If the data suggested that consuming low- rather than high-GI foods may help restrain overeating and protect against weight gain, this has not yet been confirmed in long-term randomized controlled trials.
However, the dietary interventions only achieved a modest difference in GI ~5 units between high- and low-GI diets such that the effect of GI in weight maintenance remained unknown. Table 1 includes GI and GL values of selected foods relative to pure glucose Originally written in by: Jane Higdon, Ph.
Linus Pauling Institute Oregon State University. Updated in December by: Jane Higdon, Ph.
: Glycemic load and insulin resistance| Carbohydrates and Blood Sugar | The Nutrition Source | Harvard T.H. Chan School of Public Health | Some reports have suggested supporting mechanisms and pathways, which can explain a beneficial association between these indices and the risk of CVD incidence. Journal Article. In this study, 27 14 subjects were analyzed for their glycemic index response to white bread; although the mean for the 14 subjects was 71, in agreement with reported values, 29 the variability was between 44 and , indicating that similar to all dietary interventions, individuals also have different postprandial glucose responses to foods. Hedblad B, Nilsson P, Janzon L, Berglund G Our findings with respect to the daily glycemic index, daily glycemic load, and simple sugars should be confirmed in large observational prospective studies before any recommendations can be formulated. Division of Growth and Development, Department of Pediatrics, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. Wadden TA, Webb VL, Moran CH, Bailer BA. |
| Access options | Depending Glycemic load and insulin resistance the rate of glycogen depletion, this resisatnce may last up to 7—14 days, after which weight loss Body fat calipers types [ Glycemic load and insulin resistance Hormonal balance. Eur J Cardiovasc Prev Nisulin. CRP concentrations in the low-GI and low-CHO Glcyemic were not different. This assumption turned out to be too simplistic since the blood glucose glycemic response to complex carbohydrates has been found to vary considerably. No significant trend was found across quartiles of GL for BMI, hypertension, diabetes and pre-diabetes, and dietary intakes of nuts and legumes Table 2. A diagnosis of prediabetes does not mean that you will definitely advance to diabetes, though it is a high risk factor. |
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Yusuf S, Hawken S, Ounpuu S, Bautista I, Franzosi MG, Commerford P, Lang CC, Rumboldt Z, Owen CI, Lisheng I, Tanomsup S, Wangai P, Razak F, Sharma AM, Anand SS: Obesity and the risk of myocardial infarction in 27, participants from 52 countries: a case-control study. Ludwig DS: The glycaemic index: physiological mechanisms relating to obesity, diabetes, and cardiovascular disease. Ceriello A: Oxidative stress and glycaemic regulation. Davy BM, Melby CL: The effect of fibre-rich carbohydrates on features of Syndrome X. Journal of the American Dietetic Association. Radulian G, Rusu E, Constantin C: Diet managementfor obese patients with type 2 diabetes. Constantin C, Radulian G, Rusu E: Role of glycemic index in a diet program for type 2 diabetes obese patients. Download references. Research was supported by "N. Paulescu" Institute of Diabetes, Nutrition and Metabolic Diseases" Bucharest, University of Medicine "Carol Davila" Bucharest and Foundation for Healthy Nutrition. Also, no other persons but the mentioned authors participated in the writing and conception of this article. The article was not published or submitted to other journals. Author Gabriela Radulian participated in collection of data and drafted the manuscript. The other authors also collected information and helped to draft the manuscript. All authors read and approved the final manuscript. Paulescu" National Institute of Diabetes, Nutrition and Metabolic Diseases, Bucharest, Romania. Foundation for Healthy Nutrition, Bucharest, Romania. You can also search for this author in PubMed Google Scholar. Correspondence to Gabriela Radulian. This article is published under license to BioMed Central Ltd. Reprints and permissions. Radulian, G. et al. Metabolic effects of low glycaemic index diets. Nutr J 8 , 5 Download citation. Received : 20 November Accepted : 29 January Published : 29 January Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content. Search all BMC articles Search. Download PDF. Download ePub. Abstract The persistence of an epidemic of obesity and type 2 diabetes suggests that new nutritional strategies are needed if the epidemic is to be overcome. The long-term effect of the combination of these changes is at present not known. Reviews Obesity is a major global health problem that has been associated with highly occurring disorders such as hypertension, type 2 diabetes, hyperinsulinemia, dyslipidemia, atherosclerosis and certain types of cancer [ 1 , 2 ]. Influence of the different diets on weight loss [ 11 , 12 ] Table 1 Influence of different diets on weight loss. Full size table. Figure 1. Full size image. Figure 2. Conclusion Long term compliance to a low-GI diet may induce favorable metabolic effects. 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Article CAS PubMed Google Scholar Noakes M, Keogh JB, Foster PR, Clifton PM: Effect of an energy-restricted, high-protein, low-fat diet relative to a conventional high-carbohydrate, low-fat diet on weight loss, body composition, nutritional status, and markers of cardiovascular health in obese women. CAS PubMed Google Scholar Acheson KJ: Carbohydrate and weight control: where do we stand?. Article CAS PubMed Google Scholar Roberts SB: Glycaemic index and satiety. PubMed Google Scholar Jenkins DJ, Wolever TM, Taylor RH, Barker H, Fielden H, Baldwin JM, Bowling AC, Newman HC, Jenkins AL, Goff DV: Glycaemic index of foods: a physiological basis for carbohydrate exchange. Article CAS PubMed Google Scholar Radulian G: Glycemic index and metabolic risk. Article CAS PubMed Google Scholar McKeown NM, Meigs JB, Liu S, Saltzman E, Wilson PW, Jacques PF: Carbohydrate nutrition, insulin resistance, and the prevalence of the metabolic syndrome in the Framingham Offspring Cohort. 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We believe that the mechanism of weight loss and body fat reduction resulted from a low-GI diet is probably a gradual increase in plasma glucose that slows insulin secretion, which may subsequently cause prolonged satiety, thus decreased food ingestion, leading to a decrease in body weight and body fat Conversely, the high-GI diet may quickly stimulate insulin secretion, which could then lower plasma glucose rapidly, thereby causing excessive hunger, over-eating, and lipogenesis This prolonged hyperinsulinemia would have the effect of directing nutrients from oxidation to storage 6. In fact, some studies demonstrated that hyperinsulinemia due to ingestion of a high-GI diet led to decreased hepatic fat oxidation and then increased food consumption resulting in an increase in body weight and fat 17 , Obesity has a strong correlation with the metabolic syndrome consisted of hypertension, dyslipidemia, insulin resistance, and type 2 diabetes. Our study found a significant decrease in fasting insulin and HOMA-IR in the low-GI group but no significant change in fasting insulin or HOMA-IR in the control group. Therefore, this finding reveals that the low-GI diet might improve insulin sensitivity in obese children, similar to the data from adult population which found reduced postprandial hyperinsulinemia after the low-GI diet in obese prediabetic adults 19 , In spite of this, there were no significant differences in insulin sensitivity after a low-GI diet in some studies 21 , Shikany et al. The participants showed no significant differences in glucose and insulin levels between both groups. An improvement of insulin sensitivity may have been caused by reduced insulin demand, decreased glucotoxic effect on β cells, decreased β-cell dysfunction, and prolonged suppression of free fatty acid release, which decreased their accumulation in β cells 23 , On the other hand, a high-GI diet could conversely result in high postprandial insulin so blood glucose might rapidly decrease with an increase in counter-regulatory hormones causing declining insulin sensitivity In addition, the high-GI diet also results in increasing lipid accumulation in skeletal muscle and liver which may cause insulin signaling defects and insulin resistance, and triacylglycerol accumulation in β cells also leads to decreased insulin secretion 23 , 26 , Due to the difference of baseline insulin levels between the two groups, we did general linear model and multiple regression analysis to adjust for the difference of baseline fasting plasma glucose, insulin, and HOMA-IR. The baseline fasting plasma glucose, insulin, and HOMA-IR had a greater effect on the mean difference of these results compared with the type of treatments. A better reduction in insulin resistance was demonstrated in the low-GI group; however, this appeared to be explained by higher baseline values, and the baseline level was the greater predictor of change in insulin resistance. These findings suggest that the low-GI diet could have more beneficial effect on insulin sensitivity in obese children with high baseline insulin, although we cannot demonstrate significant interaction between baseline insulin and group by general linear model which might be due to a small sample size. Therefore, we proposed the low-GI diet instruction for obese children who have insulin resistance or diabetes which may provide additional benefits on insulin sensitivity. In the future, in order to discernibly prove this hypothesis, a trial should be conducted comparing changes in insulin resistance in obese children with high baseline insulin levels who are randomized to receive either low-GI or conventional instructions. Before starting this study, we had anticipated that the low-GI diet participants would noticeably decrease in FMI and percentage of fat while increasing in FFMI before any change in BMI z -score and blood chemistry. Nevertheless, from the dietary intake data, the actual energy intake from both groups was far higher than that were instructed despite the significant changes in the amount of low-GI foods consumed in the intervention group. Thus, this might result in subtle changes in body composition. Additionally, the effect size of BMI z -score difference of 0. We used the data from 52 participants who completed all six visits without selecting some children who had good compliance because we wanted to study the effects of realistically achievable low-GI diet on all of the outcomes in their daily routine lives situation. This intention-to-treat approach may underestimate the efficacy of the low-GI diet. In conclusion, despite only subtle effects on body composition, a low-GI diet might improve insulin sensitivity in obese children who have high baseline insulin. This finding could be applied in other pediatric settings. Instead of conventional advice of caloric restriction which may be too restrictive for some children, modest caloric reduction with substitution of high-GI foods with its low-GI varieties could be more acceptable. A possible further study may recruit a larger sample size with more intensive intervention such as monitoring the low-GI food consumed, evaluating hunger and satiety levels, improving physical activity recommendations and methods of assessment, and, finally, improving behavior modification techniques. This would allow accurate assessment of GI and GL of the diet and its effects on body composition, satiety levels, and insulin sensitivity. This study was a prospective, randomized, controlled trial. Participants were randomly allocated by computer-generated randomization blocks of 10 to receive either conventional obesity clinic advice or an intervention of a low-GI diet. The researcher who did not relate to data collection and data analysis used computer to generate the random allocation sequence. Other researchers enrolled participants and assigned them to interventions. The protocol was approved by the Institutional Review Board of the Faculty of Medicine, Chulalongkorn University, Thailand. The researchers described the study to the children and their parents before obtaining signed informed assents and consents from one of the parents , respectively. Children aged between 9 to 16 y with BMI higher than the International Obesity Task Force cutoff, corresponding to BMI of 30 in adulthood 28 were recruited from the King Chulalongkorn Memorial Hospital. Children who had behavioral and intellectual problems that might be an obstacle to follow the diet instruction were excluded from this study. Children who had underlying diseases that might affect a weight management program, who used drugs associated with weight increment or reduction, as well as those who attended other weight management programs were also excluded from this study. The sample size was calculated according to the previous findings from other obesity intervention trials. The difference in BMI z -score of 0. For the intervention group, individual goals for weight management were set and the instruction about low-GI foods was provided. A dietitian emphasized the selection of low-GI carbohydrates, which were adapted from the table by Foster-Powell et al. The contents varied from the first to the sixth visit, starting from portion size and food exchange, modest energy restriction, principle of GI, sources of low-GI diet, cooking demonstration of low-GI dishes, guidance about food labeling, and some games about GI of common food and beverages. Both groups needed to maintain the monthly visits for 6 mo. The adherence to the nutritional education and physical activity recommendation was evaluated by using 3-d dietary records two week days and one weekend day and a physical activity questionnaire at each visit. All participants were examined and counseled about physical activity and life style modification strategies by a pediatrician at every visit. Primary outcomes. Anthropometric measurements were taken at baseline and at every visit of this study. Weight and height were measured without shoes and with light clothing using a stadiometer to the nearest 0. Waist circumference was measured at the umbilicus level after normal exhalation with participants in standing position. Hip circumference was measured at the maximum circumference of the hips. Mid-upper arm circumference was measured the circumference at the middle point between the olecranon process of the ulna and the acromion process of the scapula. The primary outcomes were body composition changes, which refer to FM and FFM during the 6-mo period, measured by two validated techniques. BIA BodystatQuadscan ; Bodystat, Isle of Man, British Isles , which measured the body resistance to small voltage electrical current, was performed at every visit to calculate the FM and FFM. DXA Hologic QDR Discovery A was performed on the first and sixth visits. Secondary outcomes. The secondary outcomes were metabolic syndrome risk changes which were blood pressure, fasting plasma glucose, plasma insulin, and serum lipid profiles. Blood pressure was measured by blood pressure monitor Dinamap. Venous blood was obtained after a h fast to evaluate biochemical parameters at the first and sixth visits of the study. Serum LDL C was measured by homogeneous liquid selective detergent DIRECT LDL, Architech; Abbott Laboratories. The values in the text and tables were reported as means ± SDs. Paired t -test for dependent samples was used to evaluate the changes within the groups before and after the 6-mo period. Independent sample t -test was used to compare the changes between the two groups. Repeated measures ANOVA was used to compare the changes of FMI, FFMI, and percentage of fat in each visit in the control group and intervention group. 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| The lowdown on glycemic index and glycemic load - Harvard Health | The Australasian Academy of Critical Care Medicine: Bedford Park, South Australia. This category includes many fruits and vegetables, whole grains, and legumes. Foods to limit. The glycemic index cut points corresponded approximately to the first and fifth quintiles of US population-based intake. Vrolix R, Mensink RP. For any pair of the 4 diets, there were to participants contributing at least 1 primary outcome measure. Save Preferences. |
| Carbohydrates and Blood Sugar | TO'S and AB analysed the data, and, together with PLW, were involved in interpretation of the data. All authors were involved in review of the paper. Reprints and permissions. O'Sullivan, T. et al. Glycaemic load is associated with insulin resistance in older Australian women. Eur J Clin Nutr 64 , 80—87 Download citation. Received : 07 April Revised : 03 August Accepted : 05 August Published : 16 September Issue Date : January Anyone you share the following link with will be able to read this content:. Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Skip to main content Thank you for visiting nature. nature european journal of clinical nutrition original article article. Conclusions: The results of this cross-sectional study support the concept that diets with a higher GL are associated with an increased risk of insulin resistance. 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Author information Authors and Affiliations Institute of Health and Biomedical Innovation, Queensland University of Technology, Kelvin Grove, Queensland, Australia T A O'Sullivan School of Population Health, University of Western Australia, Crawley, Western Australia, Australia A P Bremner Betty Byrne Henderson Research Centre, Royal Brisbane and Women's Hospital, Herston, Queensland, Australia S O'Neill School of Health Sciences, University of Wollongong, Wollongong, New South Wales, Australia P Lyons-Wall Authors T A O'Sullivan View author publications. View author publications. Additional information Contributors : SO'N was involved in conception and design of the LAW study, and acquisition of data on insulin resistance and potential confounding variables. Rights and permissions Reprints and permissions. About this article Cite this article O'Sullivan, T. Copy to clipboard. This article is cited by A case-control study of glycemic index, glycemic load and dietary fiber intake and risk of adenocarcinomas and squamous cell carcinomas of the esophagus: the Australian Cancer Study Petra H Lahmann Torukiri I Ibiebele David C Whiteman BMC Cancer Iron chelator alleviates tubulointerstitial fibrosis in diabetic nephropathy rats by inhibiting the expression of tenascinC and other correlation factors Chunbo Zou Rujuan Xie Huiqing Yin Endocrine About the journal Journal Information Open Access Fees and Funding About the Editors Contact For Advertisers Subscribe. Search Search articles by subject, keyword or author. Show results from All journals This journal. Associations of glycemic index and load with coronary heart disease events: a systematic review and meta-analysis of prospective cohorts. J Am Heart Assoc. Foster-Powell K, Holt SH, Brand-Miller JC. International table of glycemic index and glycemic load values: Buyken, AE, Goletzke, J, Joslowski, G, Felbick, A, Cheng, G, Herder, C, Brand-Miller, JC. Association between carbohydrate quality and inflammatory markers: systematic review of observational and interventional studies. The American Journal of Clinical Nutrition Am J Clin Nutr. AlEssa H, Bupathiraju S, Malik V, Wedick N, Campos H, Rosner B, Willett W, Hu FB. Carbohydrate quality measured using multiple quality metrics is negatively associated with type 2 diabetes. The contents of this website are for educational purposes and are not intended to offer personal medical advice. You should seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read on this website. The Nutrition Source does not recommend or endorse any products. Skip to content The Nutrition Source. The Nutrition Source Menu. Search for:. Home Nutrition News What Should I Eat? As blood sugar levels rise, the pancreas produces insulin, a hormone that prompts cells to absorb blood sugar for energy or storage. As cells absorb blood sugar, levels in the bloodstream begin to fall. When this happens, the pancreas start making glucagon, a hormone that signals the liver to start releasing stored sugar. This interplay of insulin and glucagon ensure that cells throughout the body, and especially in the brain, have a steady supply of blood sugar. Type 2 diabetes usually develops gradually over a number of years, beginning when muscle and other cells stop responding to insulin. This condition, known as insulin resistance, causes blood sugar and insulin levels to stay high long after eating. Over time, the heavy demands made on the insulin-making cells wears them out, and insulin production eventually stops. Complex carbohydrates: These carbohydrates have more complex chemical structures, with three or more sugars linked together known as oligosaccharides and polysaccharides. Low-glycemic foods have a rating of 55 or less, and foods rated are considered high-glycemic foods. Medium-level foods have a glycemic index of Eating many high-glycemic-index foods — which cause powerful spikes in blood sugar — can lead to an increased risk for type 2 diabetes, 2 heart disease, 3 , 4 and overweight, 5 , 6 7. A larger observational study in Denmark 12 also could not document an association of glycemic index with insulin resistance using a homeostasis model assessment of insulin resistance and found an inverse association between glycemic load and insulin resistance. The IRAS investigators were also unable to find an association of glycemic index and glycemic load with disposition index. The disposition index measures the ability of the pancreas to respond to an increase in insulin resistance with an increased secretion of insulin, thereby maintaining normal blood glucose. An abnormal disposition index suggests β-cell strain and can lead to eventual β-cell failure. Thus, the inability to observe an inappropriately low pancreatic response associated with higher glycemic index and glycemic load suggests normal pancreatic functioning on such diets. In the last few years, there has been a very strong push by some investigators to declare a high—glycemic index and a high—glycemic load diet detrimental to health, particularly in relation to the development of obesity and type 2 diabetes. They have pressured public health authorities to recommend that such diets should be restricted for the population at large. But it must be remembered that the concept of the glycemic index was first proposed as a tool to try to improve glucose control in diabetic patients, where it may be of some help to patients with poor postprandial glucose control. But there is a great deal of confusion in interpreting the database available on glycemic index because data from studies in diabetic patients are often quoted to bolster policy suggestions for normal populations. This confusion is not conducive to a clear analysis of the issue. A pro and con discussion of the use of the glycemic index in normal population groups that is relevant in this context was published recently 13 , It is important to note that the window of glycemic index variability in a free-living population is quite narrow. This can be seen by the small SD of 4. It can also be seen that the glycemic index is actually already quite low. With such a low level of glycemic index and such a small variation around it, what determines the level of the glycemic load is the total amount of carbohydrate that an individual eats. Thus, with a small glycemic index window, the glycemic load primarily reflects the carbohydrate intake. And we know from repeated studies in fact, all the epidemiological studies mentioned above plus the present IRAS study, plus many others that no one to date has found that the amount of carbohydrate eaten per day is significantly associated with the development of type 2 diabetes. This then, greatly diminishes the importance of high glycemic load as an important risk. My suggestion then, looking at the present study and others, is that until further evidence is available, we should concentrate on educating the public to opt for higher-fiber foods especially cereal fiber and downplay the glycemic index and glycemic load. There is excellent evidence that the higher-fiber foods, made up of whole grains, fruits, and vegetables, will do people good. SEE LIESE ET AL. Sign In or Create an Account. Search Dropdown Menu. header search search input Search input auto suggest. filter your search All Content All Journals Diabetes Care. Advanced Search. User Tools Dropdown. Sign In. Skip Nav Destination Close navigation menu Article navigation. Volume 28, Issue Previous Article Next Article. Article Navigation. Editorials December 01 Do Glycemic Index, Glycemic Load, and Fiber Play a Role in Insulin Sensitivity, Disposition Index, and Type 2 Diabetes? Xavier Pi-Sunyer, MD Xavier Pi-Sunyer, MD. From the Division of Endocrinology, Diabetes and Nutrition, St. This Site. Google Scholar. Address correspondence to Dr. |
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