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White rice, brown rice and the risk of type 2 diabetes: a systematic review and meta-analysis.
Yu, J, Balaji, B, Tinajero, M, Jarvis, S, Khan, T, Vasudevan, S, Ranawana, V, Poobalan, A, Bhupathiraju, S, Sun, Q, et al
BMJ open. 2022;12(9):e065426
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The prevalence of type 2 diabetes (T2D) has continued to increase worldwide, especially in low-income and middle-income countries. Since rice is a staple food in many cultures and is predominant in most Asian diets, it is hypothesised that improving diet quality by replacing white rice with brown rice could play an important role in the prevention of T2D. The aim of this study was to assess the relationship between rice intake and the risk of T2D. This study is a systematic review and meta-analysis of nineteen studies – 8 cohort studies and 11 randomised controlled trials. Results from the meta-analyses of the cohort studies show a positive association between intake of white rice and risk of T2D. The associations were stronger in women compared with men. Additionally, brown rice was inversely associated with risk of T2D however, the results are based on limited data. Furthermore, the randomised controlled trials showed that the between-group difference in high-density lipoprotein cholesterol was statistically significant in favour of the brown rice group. Authors conclude that replacing white rice with brown rice or other whole grains has the potential to be a low-cost and feasible lifestyle strategy to improve diet quality and help reduce T2D risk.
Abstract
OBJECTIVE Intake of white rice has been associated with elevated risk for type 2 diabetes (T2D), while studies on brown rice are conflicting. To inform dietary guidance, we synthesised the evidence on white rice and brown rice with T2D risk. DESIGN Systematic review and meta-analysis. DATA SOURCES PubMed, EMBASE and Cochrane databases were searched through November 2021. ELIGIBILITY CRITERIA Prospective cohort studies of white and brown rice intake on T2D risk (≥1 year), and randomised controlled trials (RCTs) comparing brown rice with white rice on cardiometabolic risk factors (≥2 weeks). DATA EXTRACTION AND SYNTHESIS Data were extracted by the primary reviewer and two additional reviewers. Meta-analyses were conducted using random-effects models and reporting followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Risk of bias was assessed using the Newcastle Ottawa Scale for prospective cohort studies and the Cochrane Risk of Bias Tool for RCTs. Strength of the meta-evidence was assessed using NutriGrade. RESULTS Nineteen articles were included: 8 cohort studies providing 18 estimates (white rice: 15 estimates, 25 956 cases, n=5 77 426; brown rice: 3 estimates, 10 507 cases, n=1 97 228) and 11 RCTs (n=1034). In cohort studies, white rice was associated with higher risk of T2D (pooled RR, 1.16; 95% CI: 1.02 to 1.32) comparing extreme categories. At intakes above ~300 g/day, a dose-response was observed (each 158 g/day serving was associated with 13% (11%-15%) higher risk of T2D). Intake of brown rice was associated with lower risk of T2D (pooled RR, 0.89; 95% CI: 0.81 to 0.97) comparing extreme categories. Each 50 g/day serving of brown rice was associated with 13% (6%-20%) lower risk of T2D. Cohort studies were considered to be of good or fair quality. RCTs showed an increase in high-density lipoprotein-cholesterol (0.06 mmol/L; 0.00 to 0.11 mmol/L) in the brown compared with white rice group. No other significant differences in risk factors were observed. The majority of RCTs were found to have some concern for risk of bias. Overall strength of the meta-evidence was moderate for cohort studies and moderate and low for RCTs. CONCLUSION Intake of white rice was associated with higher risk of T2D, while intake of brown rice was associated with lower risk. Findings from substitution trials on cardiometabolic risk factors were inconsistent. PROSPERO REGISTRATION NUMBER CRD42020158466.
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Food sources of fructose-containing sugars and glycaemic control: systematic review and meta-analysis of controlled intervention studies.
Choo, VL, Viguiliouk, E, Blanco Mejia, S, Cozma, AI, Khan, TA, Ha, V, Wolever, TMS, Leiter, LA, Vuksan, V, Kendall, CWC, et al
BMJ (Clinical research ed.). 2018;363:k4644
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With increasing evidence linking fructose to metabolic disease, current dietary guidelines recommend a reduction of added free sugars, especially fructose-containing sugars from sugars-sweetened beverages (SSBs). However, it is currently unclear whether the negative impact of fructose on metabolic health is as implicative in the context of an overall dietary consumption pattern. The aim of this study was to assess the effect of different sources of fructose-containing sugars on glycaemic control in people with and without diabetes. This review analysed 155 controlled intervention studies and found that fructose-containing sugars in the form of fruit do not have a harmful effect on glycaemic control when compared to energy-matched macronutrient substitutions. Further, harmful effects on glycaemic control were found when excess energy in the form of fructose-containing sugars from SSBs were added to the diet. The authors conclude the food source of fructose-containing sugars on glycemic control is important in the conversation of metabolic health and glycaemic control. While further research is needed to assess a wider variety of food sources, public health professionals should consider the influence of food sources when developing dietary recommendations for the prevention and management of diabetes and other metabolic conditions.
Abstract
OBJECTIVE To assess the effect of different food sources of fructose-containing sugars on glycaemic control at different levels of energy control. DESIGN Systematic review and meta-analysis of controlled intervention studies. DATA SOURCES Medine, Embase, and the Cochrane Library up to 25 April 2018. ELIGIBILITY CRITERIA FOR SELECTING STUDIES Controlled intervention studies of at least seven days' duration and assessing the effect of different food sources of fructose-containing sugars on glycaemic control in people with and without diabetes were included. Four study designs were prespecified on the basis of energy control: substitution studies (sugars in energy matched comparisons with other macronutrients), addition studies (excess energy from sugars added to diets), subtraction studies (energy from sugars subtracted from diets), and ad libitum studies (sugars freely replaced by other macronutrients without control for energy). Outcomes were glycated haemoglobin (HbA1c), fasting blood glucose, and fasting blood glucose insulin. DATA EXTRACTION AND SYNTHESIS Four independent reviewers extracted relevant data and assessed risk of bias. Data were pooled by random effects models and overall certainty of the evidence assessed by the GRADE approach (grading of recommendations assessment, development, and evaluation). RESULTS 155 study comparisons (n=5086) were included. Total fructose-containing sugars had no harmful effect on any outcome in substitution or subtraction studies, with a decrease seen in HbA1c in substitution studies (mean difference -0.22% (95% confidence interval to -0.35% to -0.08%), -25.9 mmol/mol (-27.3 to -24.4)), but a harmful effect was seen on fasting insulin in addition studies (4.68 pmol/L (1.40 to 7.96)) and ad libitum studies (7.24 pmol/L (0.47 to 14.00)). There was interaction by food source, with specific food sources showing beneficial effects (fruit and fruit juice) or harmful effects (sweetened milk and mixed sources) in substitution studies and harmful effects (sugars-sweetened beverages and fruit juice) in addition studies on at least one outcome. Most of the evidence was low quality. CONCLUSIONS Energy control and food source appear to mediate the effect of fructose-containing sugars on glycaemic control. Although most food sources of these sugars (especially fruit) do not have a harmful effect in energy matched substitutions with other macronutrients, several food sources of fructose-containing sugars (especially sugars-sweetened beverages) adding excess energy to diets have harmful effects. However, certainty in these estimates is low, and more high quality randomised controlled trials are needed. STUDY REGISTRATION Clinicaltrials.gov (NCT02716870).