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Acute glycemic and insulinemic effects of low-energy sweeteners: a systematic review and meta-analysis of randomized controlled trials.
Greyling, A, Appleton, KM, Raben, A, Mela, DJ
The American journal of clinical nutrition. 2020;(4):1002-1014
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Abstract
BACKGROUND It has been suggested that low-energy sweeteners (LES) may be associated with an increased risk of metabolic diseases, possibly due to stimulation of glucose-responsive mechanisms. OBJECTIVE We conducted a systematic review and meta-analysis of human intervention studies examining the acute effect of LES intake on postprandial glucose (PPG) and postprandial insulin (PPI) responses, in order to comprehensively and objectively quantify these relations. METHODS We systematically searched the Medline, OVID FSTA, and SCOPUS databases until January 2020. Randomized controlled trials comparing acute postprandial effects on PPG and/or PPI after exposure to LES, either alone, with a meal, or with other nutrient-containing preloads to the same intervention without LES were eligible for inclusion. PPG and PPI responses were calculated as mean incremental area under the curve divided by time. Meta-analyses were performed using random effects models with inverse variance weighing. RESULTS Twenty-six papers (34 PPG trials and 29 PPI trials) were included. There were no reports of statistically significant differences in the effects of LES on PPG and PPI responses compared with control interventions. Pooled effects of LES intake on the mean change difference in PPG and PPI were -0.02 mmol/L (95% CI: -0.09, 0.05) and -2.39 pmol/L (95% CI: -11.83, 7.05), respectively. The results did not appreciably differ by the type or dose of LES consumed, cointervention type, or fasting glucose and insulin levels. Among patients with type 2 diabetes, the mean change difference indicated a smaller PPG response after exposure to LES compared with the control (-0.3 mmol/L; 95% CI: -0.53, -0.07). CONCLUSIONS Ingestion of LES, administered alone or in combination with a nutrient-containing preload, has no acute effects on the mean change in postprandial glycemic or insulinemic responses compared with a control intervention. Apart from a small beneficial effect on PPG (-0.3 mmol/L) in studies enrolling patients with type 2 diabetes, the effects did not differ by type or dose of LES, or fasting glucose or insulin levels. This review and meta-analysis was registered at PROSPERO as CRD42018099608.
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New insight into human sweet taste: a genome-wide association study of the perception and intake of sweet substances.
Hwang, LD, Lin, C, Gharahkhani, P, Cuellar-Partida, G, Ong, JS, An, J, Gordon, SD, Zhu, G, MacGregor, S, Lawlor, DA, et al
The American journal of clinical nutrition. 2019;(6):1724-1737
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Abstract
BACKGROUND Individual differences in human perception of sweetness are partly due to genetics; however, which genes are associated with the perception and the consumption of sweet substances remains unclear. OBJECTIVE The aim of this study was to verify previous reported associations within genes involved in the peripheral receptor systems (i.e., TAS1R2, TAS1R3, and GNAT3) and reveal novel loci. METHODS We performed genome-wide association scans (GWASs) of the perceived intensity of 2 sugars (glucose and fructose) and 2 high-potency sweeteners (neohesperidin dihydrochalcone and aspartame) in an Australian adolescent twin sample (n = 1757), and the perceived intensity and sweetness and the liking of sucrose in a US adult twin sample (n = 686). We further performed GWASs of the intake of total sugars (i.e., total grams of all dietary mono- and disaccharides per day) and sweets (i.e., handfuls of candies per day) in the UK Biobank sample (n = ≤174,424 white-British individuals). All participants from the 3 independent samples were of European ancestry. RESULTS We found a strong association between the intake of total sugars and the single nucleotide polymorphism rs11642841 within the FTO gene on chromosome 16 (P = 3.8 × 10-8) and many suggestive associations (P < 1.0 × 10-5) for each of the sweet perception and intake phenotypes. We showed genetic evidence for the involvement of the brain in both sweet taste perception and sugar intake. There was limited support for the associations with TAS1R2, TAS1R3, and GNAT3 in all 3 European samples. CONCLUSIONS Our findings indicate that genes additional to those involved in the peripheral receptor system are also associated with the sweet taste perception and intake of sweet-tasting foods. The functional potency of the genetic variants within TAS1R2, TAS1R3, and GNAT3 may be different between ethnic groups and this warrants further investigations.
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Association between soft drinks consumption and asthma: a systematic review and meta-analysis.
Al-Zalabani, AH, Noor Elahi, I, Katib, A, Alamri, AG, Halawani, A, Alsindi, NM, Almatrafi, M, Wesselius, A, Stewart, KFJ
BMJ open. 2019;(10):e029046
Abstract
OBJECTIVES To carry out meta-analysis and systematic review on the association between soft drinks consumption and asthma prevalence among adults and children. DESIGN Systematic review and meta-analysis of observational research. DATA SOURCES Medline, Scopus, ISI Web of Science and the Cochrane Library were searched up to December 2018. ELIGIBILITY CRITERIA We included observational studies investigating the association between soft drinks consumption (including maternal consumption during pregnancy) and asthma or wheeze. DATA EXTRACTION AND SYNTHESIS Data were extracted by one author and reviewed independently by two other authors. The most adjusted estimate from each original study was used in the meta-analysis. Meta-analysis was conducted using random-effects model. The quality of studies was assessed using the Newcastle-Ottawa scale and heterogeneity was evaluated using I2 statistic. RESULTS Of 725 publications originally identified, 19 were included in this systematic review, including 3 cohort studies and 16 cross-sectional studies. Ten articles reported on children up to 18 years, 5 articles on adults (>18 years) and 2 articles on prenatal exposure. In total, 468 836 participants were included, with more than 50 000 asthma cases. Soft drinks consumption was associated with significantly increased odds of asthma in both adults (OR=1.37; 95% CI, 1.23 to 1.52) and children (OR=1.14; 95% CI, 1.06 to 1.21). Prenatal exposure had marginally statistically significant association (OR=1.11; 95% CI, 1.00 to 1.23) with asthma in children. In subgroup analysis for childhood exposure, the association persists for sugar-sweetened soft drinks but not for carbonated drinks. CONCLUSION Our findings show a positive association between soft drinks consumption and asthma prevalence, mostly from cross-sectional studies. Therefore, more longitudinal research is required to establish causality.