Longitudinal Associations of Dietary Sugars and Glycaemic Index with Indices of Glucose Metabolism and Body Fatness during 3-Year Weight Loss Maintenance: A PREVIEW Sub-Study.

BACKGROUND: Dietary sugars are often linked to the development of overweight and type 2 diabetes (T2D) but inconsistencies remain. OBJECTIVE: We investigated associations of added, free, and total sugars, and glycaemic index (GI) with indices of glucose metabolism (IGM) and indices of body fatness (IBF) during a 3-year weight loss maintenance intervention. DESIGN: The PREVIEW (PREVention of diabetes through lifestyle Intervention and population studies in Europe and around the World) study was a randomised controlled trial designed to test the effects of four diet and physical activity interventions, after an 8-week weight-loss period, on the incidence of T2D. This secondary observational analysis included pooled data assessed at baseline (8), 26, 52, 104 and 156 weeks from 514 participants with overweight/obesity (age 25-70 year; BMI ≥ 25 kg⋅m-2) and with/without prediabetes in centres that provided data on added sugars (Sydney and Helsinki) or free sugars (Nottingham). Linear mixed models with repeated measures were applied for IBF (total body fat, BMI, waist circumference) and for IGM (fasting insulin, HbA1c, fasting glucose, C-peptide). Model A was adjusted for age and intervention centre and Model B additionally adjusted for energy, protein, fibre, and saturated fat. RESULTS: Total sugars were inversely associated with fasting insulin and C-peptide in all centres, and free sugars were inversely associated with fasting glucose and HbA1c (Model B: all p < 0.05). Positive associations were observed between GI and IGM (Model B: fasting insulin, HbA1c, and C-peptide: (all p < 0.01), but not for added sugars. Added sugar was positively associated with body fat percentage and BMI, and GI was associated with waist circumference (Model B: all p < 0.01), while free sugars showed no associations (Model B: p > 0.05). CONCLUSIONS: Our findings suggest that added sugars and GI were independently associated with 3-y weight regain, but only GI was associated with 3-y changes in glucose metabolism in individuals at high risk of T2D.

Relevance of dietary glycemic index, glycemic load and fiber intake before and during pregnancy for the risk of gestational diabetes mellitus and maternal glucose homeostasis.

BACKGROUND & AIMS: To date, the prevalence of Gestational diabetes mellitus (GDM) in China was 17.5%. Given the substantial relevance of GDM for medium- and long-term health of both mother and offspring and the paucity of existing data on the link between maternal diet and glucose homeostasis during pregnancy in Asian population, additional studies are needed. To examine the relevance of dietary glycemic index (GI), glycemic load (GL) and fiber intake before and during pregnancy for the development of GDM and glucose homeostasis over the course of pregnancy. METHODS: Cox proportional hazards analysis and linear mixed effects regressions were performed on data from 9317 women for whom three food frequency questionnaires (pre-pregnancy, 1st and 2nd trimesters) and biochemical measures during pregnancy were available. Investigated outcome variables included GDM risk, fasting plasma glucose (FPG), glycated hemoglobin (HbA1C), and homeostasis model assessment insulin resistance (HOMA-IR) in the 1st, 2nd and 3rd trimesters. RESULTS: Women in the highest tertile of dietary GI (or GL) before pregnancy, in the 1st, or the 2nd trimester respectively had a 12% (15%), 25% (23%) or 29% (25%) higher risk of developing GDM than those in the lowest tertile (all p for trend ≤ 0.02). Women with the highest dietary fiber intake before pregnancy, in the 1st or 2nd trimester had a 11%, 17% or 18% lower GDM risk (all p for trend ≤ 0.03). Moreover, increases in GI or GL and decreases in fiber intake over the course of pregnancy (1st to 3rd trimesters) were independently associated with adverse concurrent developments in FPG, HbA1C and HOMA-IR (p ≤ 0.03). CONCLUSIONS: Our study indicates that dietary GI, GL and fiber intake before and during pregnancy affects glucose homeostasis of pregnant Chinese women.

Relevance of fructose intake in adolescence for fatty liver indices in young adulthood.

PURPOSE: To examine the association between fructose intake in adolescence and fatty liver indices (hepatic steatosis index (HSI), fatty liver index (FLI)) in young adulthood. METHODS: Overall, 246 participants of the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) study who had a fasting blood sample in adulthood (18-36 years), at least two 3-day weighed dietary records for calculating fructose intakes and other fructose-containing sugars (total (TS), free (FS), added sugar (AS)) as well as two complete 24-h urine samples for calculating sugar excretion (fructose excretion (FE), fructose + sucrose excretion (FE + SE)) in adolescence (males: 9.5-16.5 years; females: 8.5-15.5 years) were analysed using multivariable linear regression analyses. RESULTS: On the level of dietary intake, no prospective associations were observed between adolescent fructose intake and both adult fatty liver indices, whereas higher FS intakes were associated with lower levels of HSI (Ptrend = 0.02) and FLI (Ptrend = 0.03). On the urinary excretion level, however, a higher FE (Ptrend = 0.03) and FE + SE (Ptrend = 0.01) in adolescence were prospectively related to higher adult FLI values. No associations were observed between adolescent sugar excretion and adult HSI. CONCLUSION: The present study does not provide unambiguous support for a detrimental impact of adolescent fructose intake on adult liver health. Nonetheless, further examinations estimating exposure by means of urinary excretion as well as dietary intake levels appear warranted.

World trends in sugar-sweetened beverage and dietary sugar intakes in children and adolescents: a systematic review.

OBJECTIVE: To provide a systematic overview of world dietary sugar and sugar-sweetened beverage (SSB) intake trends in children and adolescents. DATA SOURCES: Medline, Embase, and the Cochrane Central Register of Controlled Trials in the Cochrane Library were searched through January 2019 to identify longitudinal follow-up studies with time-trend data and repeated cross-sectional studies. DATA EXTRACTION: Data from studies reporting ≥ 2 measurements (sugars, SSB, or sweets/candy) over ≥ 2 years and included ≥ 20 healthy, normal- or overweight children or adolescents aged 1-19 years. DATA ANALYSIS: Data from 43 articles (n = 4 prospective cohort studies; n = 39 repeated cross-sectional studies) from 15 countries (n = 8 European countries plus Australia, Canada, China, South Korea, Mexico, Russia, and the United States) are presented narratively. According to the risk of bias in nonrandomized studies of interventions tool, 34 studies were judged to have a moderate risk of bias, and 5 to have a serious risk of bias. CONCLUSIONS: Consumption among US children and adolescents increased substantially in the decades preceding 2000, followed by a faster and continued decline. As a whole, other international intake trends did not reveal drastic increases and decreases in SSB and dietary sugars; they tended to change only slightly across 3 decades.

The Prospective Association of Dietary Sugar Intake in Adolescence With Risk Markers of Type 2 Diabetes in Young Adulthood.

Purpose: To examine the prospective relevance of dietary sugar intake (based on dietary data as well as urinary excretion data) in adolescent years for insulin sensitivity and biomarkers of inflammation in young adulthood. Methods: Overall 254 participants of the DONALD study who had at least two 3-day weighed dietary records for calculating intakes of fructose, glucose, sucrose, total, free, added sugars, total sugars from sugar-sweetened beverages (SSB), juice, and sweets/sugar or at least two complete 24 h urine samples (n = 221) for calculating sugar excretion (urinary fructose and urinary fructose + sucrose) in adolescence (females: 9-15 years, males: 10-16 years) and a fasting blood sample in adulthood (18-36 years), were included in multivariable linear regression analyses assessing their prospective associations with adult homeostasis model assessment insulin sensitivity (HOMA2-%S) and a pro-inflammatory score (based on CRP, IL-6, IL-18, leptin, chemerin, adiponectin). Results: On the dietary intake level, no prospective associations were observed between adolescent fructose, sucrose, glucose, added, free, total sugar, or total sugar from SSB, juice or sweets/sugar intake and adult HOMA2-%S (p > 0.01). On the urinary level, however, higher excreted fructose levels were associated with improved adult HOMA2-%S (p = 0.008) among females only. No associations were observed between dietary or urinary sugars and the adult pro-inflammatory score (p > 0.01). Conclusion: The present study did not provide support that dietary sugar consumed in adolescence is associated with adult insulin sensitivity. The one potential exception was the moderate dietary consumption of fructose, which showed a beneficial association with adult fasting insulin and insulin sensitivity.

Age and time trends in sugar intake among children and adolescents: results from the DONALD study.

PURPOSE: To describe age and time trends in added sugar, free sugar and total sugar intake among German 3-18-year-olds. METHODS: Overall, 10,761 3-day dietary records kept between 1985 and 2016 by 1312 DONALD participants (660 boys, 652 girls) were analysed (%E) using polynomial mixed-effects regression models. RESULTS: TS intake decreased with age (♂: linear, quadratic and cubic trend all p < 0.0098; ♀: linear trend p < 0.0001). While the oldest children had the lowest FS intake (linear, quadratic trend: p < 0.0001), the youngest children had the lowest AS intake (linear, quadratic trend p < 0.0001, cubic trend p = 0.0004). In terms of time trends, TS (♂: cubic trend p = 0.0052; ♀: quadratic trend p = 0.0608, cubic trend p = 0.0014) and FS (quadratic trend p = 0.0163, cubic trend p < 0.0001) intake increased between 1985 and 2005 and decreased thereafter, most notably since 2010. AS intake decreased between 1985 and 1995, increased slightly until 2005 and decreased thereafter, most notably since 2010 (linear, quadratic, cubic trend p < 0.0001). FS intake exceeded 10%E/day throughout the 30-year study period. CONCLUSION: Our results do not support the common assumptions that sugar intake is on the rise and generally higher among adolescents than among younger children. Of note, TS, AS and FS intakes have decreased in the last decade among all age groups. Nevertheless, FS intake still exceeds the intake level recommended by the WHO.

Effect of Dietary Sugar Intake on Biomarkers of Subclinical Inflammation: A Systematic Review and Meta-Analysis of Intervention Studies.

It has been postulated that dietary sugar consumption contributes to increased inflammatory processes in humans, and that this may be specific to fructose (alone, in sucrose or in high-fructose corn syrup (HFCS)). Therefore, we conducted a meta-analysis and systematic literature review to evaluate the relevance of fructose, sucrose, HFCS, and glucose consumption for systemic levels of biomarkers of subclinical inflammation. MEDLINE, EMBASE, and Cochrane libraries were searched for controlled intervention studies that report the effects of dietary sugar intake on (hs)CRP, IL-6, IL-18, IL-1RA, TNF-α, MCP-1, sICAM-1, sE-selectin, or adiponectin. Included studies were conducted on adults or adolescents with ≥20 participants and ≥2 weeks duration. Thirteen studies investigating 1141 participants were included in the meta-analysis. Sufficient studies (≥3) to pool were only available for (hs)CRP. Using a random effects model, pooled effects of the interventions (investigated as mean difference (MD)) revealed no differences in (hs)CRP between fructose intervention and glucose control groups (MD: −0.03 mg/L (95% CI: −0.52, 0.46), I² = 44%). Similarly, no differences were observed between HFCS and sucrose interventions (MD: 0.21 mg/L (−0.11, 0.53), I² = 0%). The quality of evidence was evaluated using Nutrigrade, and was rated low for these two comparisons. The limited evidence available to date does not support the hypothesis that dietary fructose, as found alone or in HFCS, contributes more to subclinical inflammation than other dietary sugars.