United Kingdom Prospective Diabetes Study(UKPDS)からのメッセージとその解釈

Consumption of fructose, the sweetest of all naturally occurring carbohydrates, has increased dramatically in the last 40 years and is today commonly used commercially in soft drinks, juice, and baked goods. These products comprise a large proportion of the modern diet, in particular in children, adolescents, and young adults. A large body of evidence associate consumption of fructose and other sugar-sweetened beverages with insulin resistance, intrahepatic lipid accumulation, and hypertriglyceridemia. In the long term, these risk factors may contribute to the development of type 2 diabetes and cardiovascular diseases. Fructose is absorbed in the small intestine and metabolized in the liver where it stimulates fructolysis, glycolysis, lipogenesis, and glucose production. This may result in hypertriglyceridemia and fatty liver. Therefore, understanding the mechanisms underlying intestinal and hepatic fructose metabolism is important. Here we review recent evidence linking excessive fructose consumption to health risk markers and development of components of the Metabolic Syndrome.

https://www.mdpi.com/2072-6643/11/9/1987/pdf

Dietary Fructose and the Metabolic Syndrome

Background Fructose consumption increases risk factors for cardiometabolic disease. It is assumed that the effects of free sugars on risk factors are less potent because they contain less fructose. We compared the effects of consuming fructose, glucose or their combination, high fructose corn syrup (HFCS), on cardiometabolic risk factors. Methods Adults (18–40 years; BMI 18–35 kg/m2) participated in a parallel, double-blinded dietary intervention during which beverages sweetened with aspartame, glucose (25% of energy requirements (ereq)), fructose or HFCS (25% and 17.5% ereq) were consumed for two weeks. Groups were matched for sex, baseline BMI and plasma lipid/lipoprotein concentrations. 24-h serial blood samples were collected at baseline and at the end of intervention. Primary outcomes were 24-h triglyceride AUC, LDL-cholesterol (C), and apolipoprotein (apo)B. Interactions between fructose and glucose were assessed post hoc. Findings 145 subjects (26.0 ± 5.8 years; body mass index 25.0 ± 3.7 kg/m2) completed the study. As expected, the increase of 24-h triglycerides compared with aspartame was highest during fructose consumption (25%: 6.66 mmol/Lx24h 95% CI [1.90 to 11.63], P = 0.0013 versus aspartame), intermediate during HFCS consumption (25%: 4.68 mmol/Lx24h 95% CI [−0.18 to 9.55], P = 0.066 versus aspartame) and lowest during glucose consumption. In contrast, the increase of LDL-C was highest during HFCS consumption (25%: 0.46 mmol/L 95% CI [0.16 to 0.77], P = 0.0002 versus aspartame) and intermediate during fructose consumption (25%: 0.33 mmol/L 95% CI [0.03 to 0.63], P = 0.023 versus aspartame), as was the increase of apoB (HFCS-25%: 0.108 g/L 95%CI [0.032 to 0.184], P = 0.001; fructose 25%: 0.072 g/L 95%CI [−0.004 to 0.148], P = 0.074 versus aspartame). The post hoc analyses showed significant interactive effects of fructose*glucose on LDL-C and apoB (both P  Conclusion A significant interaction between fructose and glucose contributed to increases of lipoprotein risk factors when the two monosaccharides were co-ingested as HFCS. Thus, the effects of HFCS on lipoprotein risks factors are not solely mediated by the fructose content and it cannot be assumed that glucose is a benign component of HFCS. Our findings suggest that HFCS may be as harmful as isocaloric amounts of pure fructose and provide further support for the urgency to implement strategies to limit free sugar consumption.

Synergistic effects of fructose and glucose on lipoprotein risk factors for cardiovascular disease in young adults.

Metabolism of sugars: A window to the regulation of glucose and lipid homeostasis by splanchnic organs.

Currently, there is considerable emphasis on the relationship between dietary sugar consumption and various health outcomes, with some countries and regions implementing national sugar reduction campaigns. This has resulted in significant efforts to quantify dietary sugar intakes, to agree on terms to describe dietary sugars and to establish associated recommendations. However, this information is infrequently collated on a global basis and in a regularised manner. The present review provides context regarding sugar definitions and recommendations. It provides a global review of the available data regarding dietary sugar intake, considering forms such as total, free and added sugars. A comprehensive breakdown of intakes is provided by age group, country and sugar form. This analysis shows that free sugar intakes as a percentage of total energy (%E) are the highest for children and adolescents (12-14%E) and the lowest for older adults (8%E). This trend across lifecycle stages has also been observed for added sugars. The available data also suggest that, while some reductions in sugar intake are observed in a few individual studies, overall intakes of free/added sugars remain above recommendations. However, any wider conclusions are hampered by a lack of detailed high-quality data on sugar intake, especially in developing countries. Furthermore, there is a need for harmonisation of terms describing sugars (ideally driven by public health objectives) and for collaborative efforts to ensure that the most up-to-date food composition data are used to underpin recommendations and any estimates of intake or modelling scenarios.

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Current perspectives on global sugar consumption: definitions, recommendations, population intakes, challenges and future direction.

This article presents a systematic review of the scientific evidence linking sugar consumption and health in the adult population performed by a group of experts, mandated by the French Agence nationale de securite sanitaire de l'alimentation, de l'environnement, et du travail (ANSES). A literature search was performed by crossing search terms for overweight/obesity, diabetes/insulin resistance, dyslipidemia/cardiovascular diseases, non-alcoholic fatty liver diseases (NAFLD), and uric acid concentrations on one hand and for intake of sugars on the other. Controlled mechanistic studies, prospective cohort studies, and randomized clinical trials were extracted and assessed. A literature analysis supported links between sugar intake and both total energy intake and body weight gain, and between sugar intake and blood triglycerides independently of total energy intake. The effects of sugar on blood triglycerides were shown to be mediated by the fructose component of sucrose and were observed with an intake of fructose >50 g/day. In addition, prospective cohort studies showed associations between sugar intake and the risk of diabetes/insulin resistance, cardiovascular diseases, NAFLD, and hyperuricemia. Based on these observations, ANSES proposed to set a maximum limit to the intake of total sugars containing fructose (sucrose, glucose⁻fructose syrups, honey or other syrups, and natural concentrates, etc.) of 100 g/day.

https://www.mdpi.com/2072-6643/10/8/989/pdf

Gérard Slama

Papers

French Recommendations for Sugar Intake in Adults: A Novel Approach Chosen by ANSES