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Dietary Fructose and the Metabolic Syndrome.
Taskinen, MR, Packard, CJ, Borén, J
Nutrients. 2019;11(9)
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Fructose is a naturally occurring sugar in carbohydrate foods and is often used as an ingredient in foods and sugar sweetened beverages (SSB) such as sport and energy drinks. The consumption of these drinks accounts for up to 15-17% of calorie intake in the modern western diet. Excessive sugar consumption is becoming a major public health issue with high sugar intake linked to Metabolic Syndrome (MetS), cardiovascular disease, type II diabetes and non-alcoholic fatty liver disease. Fructose is largely absorbed in the small intestines however the liver is considered the major organ for fructose metabolism. Too much fructose in the diet appears to stimulate the liver to produce more sugars and triglyceride fats which can raise cholesterol levels and promote insulin resistance. This partially explains the role of fructose in promoting a build-up of fat around the liver leading to non-alcoholic fatty liver disease and central obesity. Too much fructose is also linked to unfavourable changes in gut bacteria which may contribute to obesity and MetS. Overall the study concludes that too much fructose contributes to an unhealthy lifestyle and is a risk factor for metabolic disturbances.
Abstract
Abstract: 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.
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Relation of total sugars, fructose and sucrose with incident type 2 diabetes: a systematic review and meta-analysis of prospective cohort studies.
Tsilas, CS, de Souza, RJ, Mejia, SB, Mirrahimi, A, Cozma, AI, Jayalath, VH, Ha, V, Tawfik, R, Di Buono, M, Jenkins, AL, et al
CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne. 2017;189(20):E711-E720
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Sugars, particularly fructose-containing sugars, have been implicated as an important driver in the rise in incidence of type 2 diabetes. The aim of this study was to determine the role of fructose-containing sugars independent of food form in the development of type 2 diabetes. This study is a systemic review and meta-analysis of prospective cohort studies. The study included 15 cohorts from 9 studies. Results indicate that intakes of total sugars and fructose were not associated with type 2 diabetes, whereas intake of sucrose was associated with an 11% decrease in type 2 diabetes. Authors conclude that in the absence of a clear signal for harm, sugars alone do not appear to explain the relation between sugar-sweetened beverages and type 2 diabetes.
Abstract
BACKGROUND Sugar-sweetened beverages are associated with type 2 diabetes. To assess whether this association holds for the fructose-containing sugars they contain, we conducted a systematic review and meta-analysis of prospective cohort studies. METHODS We searched MEDLINE, Embase, CINAHL and the Cochrane Library (through June 2016). We included prospective cohort studies that assessed the relation of fructose-containing sugars with incident type 2 diabetes. Two independent reviewers extracted relevant data and assessed risk of bias. We pooled risk ratios (RRs) using random effects meta-analyses. The overall quality of the evidence was assessed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system. RESULTS Fiffeen prospective cohort studies (251 261 unique participants, 16 416 cases) met the eligibility criteria, comparing the highest intake (median 137, 35.2 and 78 g/d) with the lowest intake (median 65, 9.7 and 25.8 g/d) of total sugars, fructose and sucrose, respectively. Although there was no association of total sugars (RR 0.91, 95% confidence interval [CI] 0.76-1.09) or fructose (RR 1.04, 95% CI 0.84-1.29) with type 2 diabetes, sucrose was associated with a decreased risk of type 2 diabetes (RR 0.89, 95% CI 0.80-0.98). Our confidence in the estimates was limited by evidence of serious inconsistency between studies for total sugars and fructose, and serious imprecision in the pooled estimates for all 3 sugar categories. INTERPRETATION Current evidence does not allow us to conclude that fructose-containing sugars independent of food form are associated with increased risk of type 2 diabetes. Further research is likely to affect our estimates. TRIAL REGISTRATION ClinicalTrials.gov, no. NCT01608620.