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The Impact of Dietary Glycemic Index and Glycemic Load on Postprandial Lipid Kinetics, Dyslipidemia and Cardiovascular Risk.
Lambadiari, V, Korakas, E, Tsimihodimos, V
Nutrients. 2020;(8)
Abstract
Many recent studies have acknowledged postprandial hypetriglyceridemia as a distinct risk factor for cardiovascular disease. This dysmetabolic state is the result of the hepatic overproduction of very low-density lipoproteins (VLDLs) and intestinal secretion of chylomicrons (CMs), which leads to highly atherogenic particles and endothelial inflammation. Postprandial lipid metabolism does not only depend on consumed fat but also on the other classes of nutrients that a meal contains. Various mechanisms through which carbohydrates exacerbate lipidemia have been identified, especially for fructose, which stimulates de novo lipogenesis. Glycemic index and glycemic load, despite their intrinsic limitations, have been used as markers of the postprandial glucose and insulin response, and their association with metabolic health and cardiovascular events has been extensively studied with contradictory results. This review aims to discuss the importance and pathogenesis of postprandial hypertriglyceridemia and its association with cardiovascular disease. Then, we describe the mechanisms through which carbohydrates influence lipidemia and, through a brief presentation of the available clinical studies on glycemic index/glycemic load, we discuss the association of these indices with atherogenic dyslipidemia and address possible concerns and implications for everyday practice.
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The Role of Health Literacy in Diabetes Knowledge, Self-Care, and Glycemic Control: a Meta-analysis.
Marciano, L, Camerini, AL, Schulz, PJ
Journal of general internal medicine. 2019;(6):1007-1017
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Abstract
BACKGROUND Empirical evidence on how health literacy affects diabetes outcomes is inconsistent. The purpose of this meta-analysis was to quantitatively summarize the findings on the associations between health literacy and diabetes knowledge, self-care activities, and glycemic control as disease-related outcomes, with specific focus on the type of health literacy assessment. DATA SOURCES Nine databases (MEDLINE, CINAHL, Communication and Mass Media Complete, PsychInfo, PsychArticles, Psychology and Behavioral Sciences Collection, ERIC, Sociology, Embase) were searched for peer-reviewed original research articles published until 31 March 2018. METHODS Studies with type 1 and/or type 2 diabetes patients aged 18 or older, providing a calculable baseline effect size for functional health literacy and diabetes knowledge, self-care activities, or HbA1C were included. RESULTS The meta-analysis includes 61 studies with a total of 18,905 patients. The majority were conducted in the USA, on type 2 diabetes patients, and used the S-TOFHLA as a performance-based or the BHLS as a perception-based measure of functional health literacy. Meta-analytic results show that all three outcomes are related to health literacy. Diabetes knowledge was best predicted by performance-based health literacy measures, self-care by self-report measures, and glycemic control equally by both types of health literacy assessment. DISCUSSION Health literacy plays a substantial role in diabetes knowledge. Findings for the role of health literacy in self-care and glycemic control remain heterogeneous, partly due to the type of health literacy assessment (performance- vs. perception-based). This has implications for the use of health literacy measures in clinical settings and original research. This meta-analysis was limited to functional health literacy and, due to the paucity of studies, did not investigate the role of other dimensions including communicative and critical health literacy.
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Dietary support in insulin resistance: An overview of current scientific reports.
Gołąbek, KD, Regulska-Ilow, B
Advances in clinical and experimental medicine : official organ Wroclaw Medical University. 2019;(11):1577-1585
Abstract
Over the past 30 years, a significant increase in the prevalence of insulin resistance (IR) has been observed. It is associated with more frequent occurrence of impaired glucose tolerance, diabetes, excessive weight, cardiovascular diseases, and endocrine disorders. The results of current studies do not indicate a necessity to exclude dairy products from the diet of insulin-resistant individuals. In addition, it has been found that moderate amounts of alcohol as part of a balanced, low-energy diet do not have a negative effect on insulin sensitivity. The authors of recent studies emphasize the importance of reducing the intake of simple sugars, especially from sweet drinks, sweets and excessive fruit juice consuption. Many studies have demonstrated the beneficial effects of consuming complex, low-glycemic-index carbohydrates that are rich in dietary fiber. An insulin-resistant patient's diet should be rich in whole grains and high amounts of non-starchy vegetables and raw fruit. The beneficial effect of the Dietary Approaches to Stop Hypertension (DASH diet) and the Mediterranean diet has been confirmed. The positive correlation between low-carbohydrate and very-low-carbohydrate diets requires confirmation in long-term studies with the participation of insulin-resistant patients. Research shows the benefits of increased calorific intake during the first half of the day, especially from a high-energy and low-glycemic-index breakfast. Furthermore, many researchers indicate that slow and mindful eating is a significant component of an appropriate diet for insulin-resistant individuals.
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Effect of pasta in the context of low-glycaemic index dietary patterns on body weight and markers of adiposity: a systematic review and meta-analysis of randomised controlled trials in adults.
Chiavaroli, L, Kendall, CWC, Braunstein, CR, Blanco Mejia, S, Leiter, LA, Jenkins, DJA, Sievenpiper, JL
BMJ open. 2018;(3):e019438
Abstract
OBJECTIVE Carbohydrate staples such as pasta have been implicated in the obesity epidemic. It is unclear whether pasta contributes to weight gain or like other low-glycaemic index (GI) foods contributes to weight loss. We synthesised the evidence of the effect of pasta on measures of adiposity. DESIGN Systematic review and meta-analysis using the Grading of Recommendations Assessment, Development, and Evaluation (GRADE) approach. DATA SOURCES MEDLINE, Embase, CINAHL and the Cochrane Library were searched through 7 February 2017. ELIGIBILITY CRITERIA FOR SELECTING STUDIES We included randomised controlled trials ≥3 weeks assessing the effect of pasta alone or in the context of low-GI dietary patterns on measures of global (body weight, body mass index (BMI), body fat) and regional (waist circumference (WC), waist-to-hip ratio (WHR), sagittal abdominal diameter (SAD)) adiposity in adults. DATA EXTRACTION AND SYNTHESIS Two independent reviewers extracted data and assessed risk of bias. Data were pooled using the generic inverse-variance method and expressed as mean differences (MDs) with 95% CIs. Heterogeneity was assessed (Cochran Q statistic) and quantified (I2 statistic). GRADE assessed the certainty of the evidence. RESULTS We identified no trial comparisons of the effect of pasta alone and 32 trial comparisons (n=2448 participants) of the effect of pasta in the context of low-GI dietary patterns. Pasta in the context of low-GI dietary patterns significantly reduced body weight (MD=-0.63 kg; 95% CI -0.84 to -0.42 kg) and BMI (MD=-0.26 kg/m2; 95% CI -0.36 to -0.16 kg/m2) compared with higher-GI dietary patterns. There was no effect on other measures of adiposity. The certainty of the evidence was graded as moderate for body weight, BMI, WHR and SAD and low for WC and body fat. CONCLUSIONS Pasta in the context of low-GI dietary patterns does not adversely affect adiposity and even reduces body weight and BMI compared with higher-GI dietary patterns. Future trials should assess the effect of pasta in the context of other 'healthy' dietary patterns. TRIAL REGISTRATION NUMBER NCT02961088; Results.
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The influence of glycemic index on cognitive functioning: a systematic review of the evidence.
Philippou, E, Constantinou, M
Advances in nutrition (Bethesda, Md.). 2014;(2):119-30
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The impact of the rate of carbohydrate absorption, as measured by the carbohydrate's glycemic index (GI) on cognitive performance, is not clear. The aim of this review was to systematically assess the relevant research studies. A systematic review of English-language articles using Medline, Cochrane Central Register of Controlled Trials, EMBASE, PsycINFO, and PsycARTICLES (up to July 2012) using the search terms "glyc(a)emic index" or "glycaemic load" combined with "cognitive function" or "cognition" or "memory" was carried out. Inclusion and exclusion criteria were prespecified. Eligibility of the identified studies was assessed independently by the 2 reviewers. Independent extraction of data was carried out by the 2 authors using predefined data fields. The primary outcome measure was the effect on cognitive function (CF) after the consumption of meals varying in GI. Eleven eligible studies were identified. The age range of the participants varied from 6 to 82 y old. Overall, the findings were inconsistent, with some studies showing benefits toward either the high-GI or the low-GI meal, others not finding any differences between the 2 meals, and other studies showing a positive or negative effect on performance on only some cognitive domain or domains after consumption of 1 of the 2 meals. A number of methodologic and confounding factors were identified that could explain these inconsistencies. These include the study design, the selected sample (size, age, blood glucose regulation), the timing of testing, the cognitive domain being examined, the number and type of cognitive tests used, the meals provided (composition, size), the timing of blood samples collected, as well as the possibility of bias because participants and investigators were not blinded to randomization. A low-GI meal may favor CF in adults, but the findings at present are inconclusive. On the basis of this review, it is suggested that future studies address the identified methodologic issues and some recommendations are proposed to this effect.
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Clinical review: Consensus recommendations on measurement of blood glucose and reporting glycemic control in critically ill adults.
Finfer, S, Wernerman, J, Preiser, JC, Cass, T, Desaive, T, Hovorka, R, Joseph, JI, Kosiborod, M, Krinsley, J, Mackenzie, I, et al
Critical care (London, England). 2013;(3):229
Abstract
The management reporting and assessment of glycemic control lacks standardization. The use of different methods to measure the blood glucose concentration and to report the performance of insulin treatment yields major disparities and complicates the interpretation and comparison of clinical trials. We convened a meeting of 16 experts plus invited observers from industry to discuss and where possible reach consensus on the most appropriate methods to measure and monitor blood glucose in critically ill patients and on how glycemic control should be assessed and reported. Where consensus could not be reached, recommendations on further research and data needed to reach consensus in the future were suggested. Recognizing their clear conflict of interest, industry observers played no role in developing the consensus or recommendations from the meeting. Consensus recommendations were agreed for the measurement and reporting of glycemic control in clinical trials and for the measurement of blood glucose in clinical practice. Recommendations covered the following areas: How should we measure and report glucose control when intermittent blood glucose measurements are used? What are the appropriate performance standards for intermittent blood glucose monitors in the ICU? Continuous or automated intermittent glucose monitoring - methods and technology: can we use the same measures for assessment of glucose control with continuous and intermittent monitoring? What is acceptable performance for continuous glucose monitoring systems? If implemented, these recommendations have the potential to minimize the discrepancies in the conduct and reporting of clinical trials and to improve glucose control in clinical practice. Furthermore, to be fit for use, glucose meters and continuous monitoring systems must match their performance to fit the needs of patients and clinicians in the intensive care setting.
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Dietary glycemic index, glycemic load, and risk of coronary heart disease, stroke, and stroke mortality: a systematic review with meta-analysis.
Fan, J, Song, Y, Wang, Y, Hui, R, Zhang, W
PloS one. 2012;(12):e52182
Abstract
BACKGROUND The relationship between dietary glycemic index, glycemic load and risk of coronary heart disease (CHD), stroke, and stroke-related mortality is inconsistent. METHODS We systematically searched the MEDLINE, EMBASE, and Science Citation Index Expanded databases using glycemic index, glycemic load, and cardiovascular disease and reference lists of retrieved articles up to April 30, 2012. We included prospective studies with glycemic index and glycemic load as the exposure and incidence of fatal and nonfatal CHD, stroke, and stroke-related mortality as the outcome variable. Pooled relative risks (RR) and 95% confidence intervals (CI) were calculated using random-effects models. RESULTS Fifteen prospective studies with a total of 438,073 participants and 9,424 CHD cases, 2,123 stroke cases, and 342 deaths from stroke were included in the meta-analysis. Gender significantly modified the effects of glycemic index and glycemic load on CHD risk, and high glycemic load level was associated with higher risk of CHD in women (RR=1.49, 95%CI 1.27-1.73), but not in men (RR=1.08, 95%CI 0.91-1.27). Stratified meta-analysis by body mass index indicated that among overweight and obese subjects, dietary glycemic load level were associated with increased risk of CHD (RR=1.49, 95%CI 1.27-1.76; P for interaction=0.003). Higher dietary glycemic load, but not glycemic index, was positively associated with stroke (RR=1.19, 95% CI 1.00-1.43). There is a linear dose-response relationship between dietary glycemic load and increased risk of CHD, with pooled RR of 1.05 (95%CI 1.02-1.08) per 50-unit increment in glycemic load level. CONCLUSION High dietary glycemic load is associated with a higher risk of CHD and stroke, and there is a linear dose-response relationship between glycemic load and CHD risk. Dietary glycemic index is slightly associated with risk of CHD, but not with stroke and stroke-related death. Further studies are needed to verify the effects of gender and body weight on cardiovascular diseases.
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Associations of glycemic index and load with coronary heart disease events: a systematic review and meta-analysis of prospective cohorts.
Mirrahimi, A, de Souza, RJ, Chiavaroli, L, Sievenpiper, JL, Beyene, J, Hanley, AJ, Augustin, LS, Kendall, CW, Jenkins, DJ
Journal of the American Heart Association. 2012;(5):e000752
Abstract
BACKGROUND Glycemic index (GI) and glycemic load (GL) have been associated with coronary heart disease (CHD) risk in some but not all cohort studies. We therefore assessed the association of GI and GL with CHD risk in prospective cohorts. METHODS AND RESULTS We searched MEDLINE, EMBASE, and CINAHL (through April 5, 2012) and identified all prospective cohorts assessing associations of GI and GL with incidence of CHD. Meta-analysis of observational studies in epidemiology (MOOSE) methodologies were used. Relative measures of risk, comparing the group with the highest exposure (mean GI of cohorts=84.4 GI units, range 79.9 to 91; mean GL of cohorts=224.8, range 166 to 270) to the reference group (mean GI=72.3 GI units, range 68.1 to 77; mean GL=135.4, range 83 to 176), were pooled using random-effects models, expressed as relative risk (RR) with heterogeneity assessed by χ(2) and quantified by I(2). Subgroups included sex and duration of follow-up. Ten studies (n=240 936) were eligible. Pooled analyses showed an increase in CHD risk for the highest GI quantile compared with the lowest, with RR=1.11 (95% confidence interval [CI] 0.99 to 1.24) and for GL, RR=1.27 (95% CI 1.09 to 1.49), both with evidence of heterogeneity (I(2)>42%, P<0.07). Subgroup analyses revealed only a significant modification by sex, with the female cohorts showing significance for GI RR=1.26 (95% CI 1.12 to 1.41) and for GL RR=1.55 (95% CI 1.18 to 2.03). CONCLUSIONS High GI and GL diets were significantly associated with CHD events in women but not in men. Further studies are required to determine the relationship between GI and GL with CHD in men.
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Dietary hyperglycemia, glycemic index and metabolic retinal diseases.
Chiu, CJ, Taylor, A
Progress in retinal and eye research. 2011;(1):18-53
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Abstract
The glycemic index (GI) indicates how fast blood glucose is raised after consuming a carbohydrate-containing food. Human metabolic studies indicate that GI is related to patho-physiological responses after meals. Compared with a low-GI meal, a high-GI meal is characterized with hyperglycemia during the early postprandial stage (0-2h) and a compensatory hyperlipidemia associated with counter-regulatory hormone responses during late postprandial stage (4-6h). Over the past three decades, several human health disorders have been related to GI. The strongest relationship suggests that consuming low-GI foods prevents diabetic complications. Diabetic retinopathy (DR) is a complication of diabetes. In this aspect, GI appears to be useful as a practical guideline to help diabetic people choose foods. Abundant epidemiological evidence also indicates positive associations between GI and risk for type 2 diabetes, cardiovascular disease, and more recently, age-related macular degeneration (AMD) in people without diabetes. Although data from randomized controlled intervention trials are scanty, these observations are strongly supported by evolving molecular mechanisms which explain the pathogenesis of hyperglycemia. This wide range of evidence implies that dietary hyperglycemia is etiologically related to human aging and diseases, including DR and AMD. In this context, these diseases can be considered as metabolic retinal diseases. Molecular theories that explain hyperglycemic pathogenesis involve a mitochondria-associated pathway and four glycolysis-associated pathways, including advanced glycation end products formation, protein kinase C activation, polyol pathway, and hexosamine pathway. While the four glycolysis-associated pathways appear to be universal for both normoxic and hypoxic conditions, the mitochondria-associated mechanism appears to be most relevant to the hyperglycemic, normoxic pathogenesis. For diseases that affect tissues with highly active metabolism and that frequently face challenge from low oxygen tension, such as retina in which metabolism is determined by both glucose and oxygen homeostases, these theories appear to be insufficient. Several lines of evidence indicate that the retina is particularly vulnerable when hypoxia coincides with hyperglycemia. We propose a novel hyperglycemic, hypoxia-inducible factor (HIF) pathway, to complement the current theories regarding hyperglycemic pathogenesis. HIF is a transcription complex that responds to decrease oxygen in the cellular environment. In addition to playing a significant role in the regulation of glucose metabolism, under hyperglycemia HIF has been shown to increase the expression of HIF-inducible genes, such as vascular endothelial growth factor (VEGF) leading to angiogenesis. To this extent, we suggest that HIF can also be described as a hyperglycemia-inducible factor. In summary, while management of dietary GI appears to be an effective intervention for the prevention of metabolic diseases, specifically AMD and DR, more interventional data is needed to evaluate the efficacy of GI management. There is an urgent need to develop reliable biomarkers of exposure, surrogate endpoints, as well as susceptibility for GI. These insights would also be helpful in deciphering the detailed hyperglycemia-related biochemical mechanisms for the development of new therapeutic agents.
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Is glycemic index of food a feasible predictor of appetite, hunger, and satiety?
Niwano, Y, Adachi, T, Kashimura, J, Sakata, T, Sasaki, H, Sekine, K, Yamamoto, S, Yonekubo, A, Kimura, S
Journal of nutritional science and vitaminology. 2009;(3):201-7
Abstract
This review assesses the feasibility of using glycemic index (GI) as a predictor of appetite, hunger and satiety by surveying published human intervention studies. We also discuss the relationship between GI and two appetite/satiety control hormones, leptin and ghrelin. Ingestion of high-GI food increased hunger and lowered satiety in short-term human intervention studies. This effect may be attributed to the rapid decline in blood glucose level following a hyperinsulinemic response caused by a sharp and transient increase in blood glucose level that occurs after the ingestion of high-GI food, which is defined as the glucostatic theory. However, appetite, hunger and satiety after the ingestion of foods with varying GI were inconsistent among long-term human intervention studies. From the few relevant long-term studies available, we selected two recent well-designed examples for analysis, but they failed to elicit clear differences in glycemic and insulinemic responses between high- and low-GI meals (consisting of a combination of different foods or key carbohydrate-rich foods incorporated into habitual diets). One of the reasons that these studies could not predict glycemic response to mixed meals is presumably that the GI of each particular food was not reflected in that of the mixed meals as a whole. Thus, it is difficult to conclude that the GI values of foods or mixed meals are a valid long-term predictor for appetite, hunger and satiety. Both insulin and insulin-mediated glucose uptake and metabolism in adipose tissue affect blood leptin concentration and its diurnal pattern. Circulating ghrelin level is suppressed by carbohydrate-rich meals, presumably via glycemia and insulinemia. Accordingly, low-GI foods may not necessarily increase satiety or suppress appetite and/or hunger because of the lack of insulin-mediated leptin stimulation and ghrelin suppression. However, insulin-mediated leptin stimulation and ghrelin suppression per se is not consistent among studies; thus we were not able to identify a clear relationship among GI, satietogenic leptin, and appetitic ghrelin.