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Effects of fructose restriction on liver steatosis (FRUITLESS); a double-blind randomized controlled trial.
Simons, N, Veeraiah, P, Simons, PIHG, Schaper, NC, Kooi, ME, Schrauwen-Hinderling, VB, Feskens, EJM, van der Ploeg, EMCL, Van den Eynde, MDG, Schalkwijk, CG, et al
The American journal of clinical nutrition. 2021;113(2):391-400
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The use of fructose in the food industry may have contributed to the increase in non-alcoholic fatty liver disease (NAFLD) in the general population. Consequently, obesity and associated comorbidities like type 2 diabetes, dyslipidaemia, NAFLD, and cardiovascular disease have increased. Although glucose and fructose are both sugars, they are metabolised differently by the body. The overfeeding of fructose may contribute to steatosis or accumulation of fat in the liver than glucose. The aim of this randomised, double-blind trial was to measure intrahepatic lipid content in 44 overweight subjects with high fatty liver index following fructose restriction for six weeks. In this study, fructose restriction resulted in a small but significant reduction in intrahepatic lipid content with a small effect size of 0.7% point. Fructose restriction did not seem to affect glucose tolerance, serum lipid concentration or HOMA-IR, variables related to intrahepatic lipid content. As a supplement, fructose may have a different metabolic profile than when taken as a food component. The study found no effect on glucose tolerance or serum lipid levels. The results of this study may help healthcare professionals to comprehend the role of fructose in steatosis and NAFLD.
Abstract
BACKGROUND There is an ongoing debate on whether fructose plays a role in the development of nonalcoholic fatty liver disease. OBJECTIVES The aim of this study was to investigate the effects of fructose restriction on intrahepatic lipid (IHL) content in a double-blind randomized controlled trial using an isocaloric comparator. METHODS Between March 2017 and October 2019, 44 adult overweight individuals with a fatty liver index ≥ 60 consumed a 6-wk fructose-restricted diet (<7.5 g/meal and <10 g/d) and were randomly assigned to supplementation with sachets of glucose (= intervention group) or fructose (= control group) 3 times daily. Participants and assessors were blinded to the allocation. IHL content, assessed by proton magnetic resonance spectroscopy, was the primary outcome and glucose tolerance and serum lipids were the secondary outcomes. All measurements were conducted in Maastricht University Medical Center. RESULTS Thirty-seven participants completed the study protocol. After 6 wk of fructose restriction, dietary fructose intake and urinary fructose excretion were significantly lower in the intervention group (difference: -57.0 g/d; 95% CI: -77.9, -39.5 g/d; and -38.8 μmol/d; 95% CI: -91.2, -10.7 μmol/d, respectively). Although IHL content decreased in both the intervention and control groups (P < 0.001 and P = 0.003, respectively), the change in IHL content was more pronounced in the intervention group (difference: -0.7% point, 95% CI: -2.0, -0.03% point). The changes in glucose tolerance and serum lipids were not significantly different between groups. CONCLUSIONS Six weeks of fructose restriction per se led to a small, but statistically significant, decrease in IHL content in comparison with an isocaloric control group.This trial was registered at clinicaltrials.gov as NCT03067428.
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Acute responses of hepatic fat content to consuming fat, glucose and fructose alone and in combination in non-obese non-diabetic individuals with non-alcoholic fatty liver disease.
Kovar, J, Dusilova, T, Sedivy, P, Bruha, R, Gottfriedova, H, Pavlikova, P, Pitha, J, Smid, V, Drobny, M, Dezortova, M, et al
Journal of physiology and pharmacology : an official journal of the Polish Physiological Society. 2021;72(1)
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Non-alcoholic fatty liver disease (NAFLD) is often associated with obesity or conditions related to obesity, such as type 2 diabetes. Steatosis is one of the four stages of NAFLD, where there is a small layer of fat build-up on the liver. Currently, one in three people in the UK has simple fatty liver or steatosis. A fascinating aspect of this study is exploring the long-term cumulative effects of daily fat intake when consumed with glucose or fructose and in the pathogenesis of steatosis. In this randomised controlled study, the researchers examined the immediate impact of high-fat loads on hepatic fat content (HFC) when administered with glucose or fructose in eight healthy overweight males with NFALD. The experiments lasted only eight hours. HFC was only transiently elevated by co-administration of glucose and high-fat loading. However, fructose co-administration with multiple high-fat loads promoted HFC. Small sample size and short duration are the limitations of this study. Long-term robust studies are needed to confirm the findings. Yet, healthcare professionals can use this study to distinguish between the immediate effects of fructose or glucose when combined with multiple doses of high fat on HFC in healthy and NAFLD subjects.
Abstract
We have recently demonstrated that a high-fat load can induce immediate increase in hepatic fat content (HFC) and that such an effect can be modified differently by co-administration of fructose or glucose in healthy subjects. Therefore, we addressed the question how consumption of these nutrients affects changes in HFC in subjects with non-alcoholic fatty liver disease (NAFLD). Eight male non-obese non-diabetic patients with NAFLD underwent 6 experiments each lasting 8 hours: 1. fasting, 2. high-fat load (150 g of fat (dairy cream) at time 0), 3. glucose (three doses of 50 g at 0, 2, and 4 hours), 4. high-fat load with three doses of 50 g of glucose, 5. fructose (three doses of 50 g at 0, 2, and 4 hours), 6. high-fat load with three doses of 50 g of fructose. HFC was measured using magnetic resonance spectroscopy prior to meal administration and 3 and 6 hours later. Plasma triglycerides, non-esterified fatty acids, glucose and insulin were monitored throughout each experiment. HFC increased by 10.4 ± 6.9% six hours after a high-fat load and by 15.2 ± 12.5% after high-fat load with fructose. When co-administering glucose with fat, HFC rose only transiently to return to baseline at 6 hours. Importantly, NAFLD subjects accumulated almost five times more fat in their livers than healthy subjects with normal HFC. Consumption of a high-fat load results in fat accumulation in the liver of NAFLD patients. Fat accumulation after a fat load is diminished by glucose but not fructose co-administration.
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Decreased Consumption of Added Fructose Reduces Waist Circumference and Blood Glucose Concentration in Patients with Overweight and Obesity. The DISFRUTE Study: A Randomised Trial in Primary Care.
Domínguez-Coello, S, Carrillo-Fernández, L, Gobierno-Hernández, J, Méndez-Abad, M, Borges-Álamo, C, García-Dopico, JA, Aguirre-Jaime, A, León, AC
Nutrients. 2020;12(4)
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Cardiovascular disease, diabetes and obesity have increased in recent decades and some studies have established a direct link between insulin resistance (IR) and these conditions. Currently, the relationship between sugar intake and the risk of obesity and diabetes remains controversial. However, some studies involving overweight or obese participants without diabetes concluded that increasing fructose intake under certain conditions lead to the development of hepatic IR in adults. The primary objective of this randomised controlled study was to determine whether decreasing the consumption of foods with high amounts of fructose, independent of a reduction in calorie intake, led to a decrease in IR after 24 weeks. 438 adults who were obese or overweight but not diabetic, took part in the 24-week study, one group ate a low fructose diet and the other a standard diet. The low fructose diet did not reduce IR but it reduced waist circumference and fasting blood glucose. The authors conclude that in overweight and obese non-diabetic primary care patients, a small decrease in the consumption of added fructose in a sustained manner may be enough to achieve metabolic benefits. New studies with larger number of patients are needed.
Abstract
The relationship between fructose intake and insulin resistance remains controversial. Our purpose was to determine whether a reduction in dietary fructose is effective in decreasing insulin resistance (HOMA2-IR). This field trial was conducted on 438 adults with overweight and obese status, without diabetes. A total of 121 patients in a low fructose diet (LFD) group and 118 in a standard diet (SD) group completed the 24-week study. Both diets were prescribed with 30-40% of energy intake restriction. There were no between-group differences in HOMA2-IR. However, larger decreases were seen in the LFD group in waist circumference (-7.0 vs. -4.8 = -2.2 cms, 95% CI: -3.7, -0.7) and fasting blood glucose -0.25 vs. -0.11 = -0.14 mmol/L, 95% CI: -0.028, -0.02). The percentage of reduction in calorie intake was similar. Only were differences observed in the % energy intake for some nutrients: total fructose (-2 vs. -0.6 = -1.4, 95% CI: -2.6, -0.3), MUFA (-1.7 vs. -0.4 = -1.3, 95% CI: -2.4, -0.2), protein (5.1 vs. 3.6 = 1.4, 95% CI: 0.1, 2.7). The decrease in fructose consumption originated mainly from the reduction in added fructose (-2.8 vs. -1.9 = -0.9, 95% CI: -1.6, -0.03). These results were corroborated after multivariate adjustments. The low fructose diet did not reduce insulin resistance. However, it reduced waist circumference and fasting blood glucose concentration, which suggests a decrease in hepatic insulin resistance.
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Effects of Periodic Fasting on Fatty Liver Index-A Prospective Observational Study.
Drinda, S, Grundler, F, Neumann, T, Lehmann, T, Steckhan, N, Michalsen, A, Wilhelmi de Toledo, F
Nutrients. 2019;11(11)
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Non-alcoholic fatty liver disease (NAFLD) comprises a number of liver disorders and is thought to have a prevalence of 20% in industrialised countries. NAFLD has been associated with dietary excess of saturated fatty acids, refined carbohydrates, and fructose. This prospective observational study evaluated the effects of periodic fasting on the fatty liver index (FLI), a combination of waist circumference, body mass index (BMI) and biochemical characteristics, which has been shown to closely correlate to magnetic resonance imaging (MRI) results, the gold standard for NAFLD diagnosis. 697 subjects fasted for 6-38 days (mean 8.5 days) in a clinical setting, whilst also engaging in an exercise programme, mindfulness and relaxation. Study subjects included both non-diabetics and type 2 diabetics. There were significant decreases in FLI, weight, BMI and waist circumference, as well as improvements in a number of metabolic blood parameters, in both diabetics and non-diabetics. There were no serious side effects and the intervention was well tolerated. The authors conclude that periodic fasting is an easily realisable, well-tolerated, non-pharmaceutical intervention, which effectively reduces the FLI.
Abstract
This prospective observational trial investigated effects and safety of periodic fasting in subjects with and without type 2 diabetes mellitus (T2DM). The primary end point was set as the change of fatty liver index (FLI) as a surrogate parameter of non-alcoholic fatty liver disease (NAFLD). Six-hundred and ninety-seven subjects (38 with T2DM) were enrolled. A baseline FLI ≥ 60 (the threshold for fatty liver) was found in 264 subjects (37.9%). The mean duration of fasting was 8.5 ± 4.0 days (range 6-38). FLI decreased significantly (-14.02 ± 11.67; p < 0.0001), with a larger effect in individuals with T2DM (-19.15 ± 11.0; p < 0.0001; p = 0.002 compared to non-diabetic subjects). Body mass index (BMI) decreased by -1.51 ± 0.82 kg/m2, and 49.9% of the subjects lost ≥5% body weight. After fasting, nearly half of the 264 subjects with FLI ≥ 60 (highest risk category) shifted to a lower category. The improvement of FLI correlated with the number of fasting days (r = -0.20, p < 0.0001) and with the magnitude of BMI reduction (r = 0.14, p = 0.0001). Periodic fasting with concomitant weight reduction leads to significant rapid improvement of FLI in subjects with and without T2DM.
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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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Effects of Dietary Protein and Fat Content on Intrahepatocellular and Intramyocellular Lipids during a 6-Day Hypercaloric, High Sucrose Diet: A Randomized Controlled Trial in Normal Weight Healthy Subjects.
Surowska, A, Jegatheesan, P, Campos, V, Marques, AS, Egli, L, Cros, J, Rosset, R, Lecoultre, V, Kreis, R, Boesch, C, et al
Nutrients. 2019;11(1)
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High sugar diets can lead to increased fat accumulation in the liver and skeletal muscles, as intrahepatocellular lipid (IHCL) and intramyocellular lipid (IMCL) respectively. Elevation in these lipid concentrations is associated with an increased risk of various chronic diseases. The aim of this randomised crossover trial was to assess whether the consequences of a high sugar diet differed according to the protein and fat composition in 12 healthy adults. At the beginning of each trial period, participants consumed a 3-day weight maintenance diet followed by a 6-day high calorie, high sugar diet consisting of either low protein-high fat or high protein-low fat with a 4-8 week washout period. IHCL and IMCL concentrations, energy expenditure and blood metabolites were monitored after each weight maintenance diet and after each 6-day intervention diet period. This study found that both diets led to increased lipid concentrations, most notably the in liver cells. Lipid increases induced by the high protein-low fat diet were significantly lower than those induced by the low protein-high fat diet. Based on these results, the authors conclude that when overfed on a high sugar diet, high protein-low fat markedly reduces the amount of fat accumulation in liver and muscle cells and suggest that either dietary protein may have a protective effect of sugar and fat may have an additive adverse effect.
Abstract
Sucrose overfeeding increases intrahepatocellular (IHCL) and intramyocellular (IMCL) lipid concentrations in healthy subjects. We hypothesized that these effects would be modulated by diet protein/fat content. Twelve healthy men and women were studied on two occasions in a randomized, cross-over trial. On each occasion, they received a 3-day 12% protein weight maintenance diet (WM) followed by a 6-day hypercaloric high sucrose diet (150% energy requirements). On one occasion the hypercaloric diet contained 5% protein and 25% fat (low protein-high fat, LP-HF), on the other occasion it contained 20% protein and 10% fat (high protein-low fat, HP-LF). IHCL and IMCL concentrations (magnetic resonance spectroscopy) and energy expenditure (indirect calorimetry) were measured after WM, and again after HP-LF/LP-HF. IHCL increased from 25.0 ± 3.6 after WM to 147.1 ± 26.9 mmol/kg wet weight (ww) after LP-HF and from 30.3 ± 7.7 to 57.8 ± 14.8 after HP-LF (two-way ANOVA with interaction: p < 0.001 overfeeding x protein/fat content). IMCL increased from 7.1 ± 0.6 to 8.8 ± 0.7 mmol/kg ww after LP-HF and from 6.2 ± 0.6 to 6.9 ± 0.6 after HP-LF, (p < 0.002). These results indicate that liver and muscle fat deposition is enhanced when sucrose overfeeding is associated with a low protein, high fat diet compared to a high protein, low fat diet.
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Sugar-Sweetened Beverage Consumption in Relation to Obesity and Metabolic Syndrome among Korean Adults: A Cross-Sectional Study from the 2012⁻2016 Korean National Health and Nutrition Examination Survey (KNHANES).
Shin, S, Kim, SA, Ha, J, Lim, K
Nutrients. 2018;10(10)
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Obesity and Metabolic Syndrome (MetS) in Korea has increased significantly in the last decade and dietary factors, including the consumption of sugar sweetened drinks, is considered one of the key drivers. Soft drinks, soda coffee, fruit juices, sports drinks and sweetened rice drinks are popular beverages in Asia. Consumption of these is a major source of sugar intake for the Korean population. This study analysed data from over 12,112 participants of the Korean National Health and Nutrition Examination Survey (KNHANES) to see if the consumption of sugar sweetened beverages was causally linked to obesity and MetS. Food questionnaires were used in the original study to assess which foods and drinks the participants consumed during a 1-year period. Within the study group the number of participants with obesity was 34.9% and MetS was 26.7% respectively. They found that the participants who regularly consumed >4 sugar sweetened beverages per week consumed more calories on average than those who did not drink these beverages. In men, it was linked to higher blood pressure and blood glucose levels whilst in women it linked to a higher body mass index (BMI), increased waist circumference, and elevated cholesterol. Overall drinking 1 sugar sweetened beverage per day increased the risks of obesity in women by 59% and MetS by 61% whilst in men it increased the prevalence of obesity by 41% and MetS by 7%. Therefore drinking sugar sweetened beverages increases the risk of both obesity and MetS.
Abstract
It is well known that the consumption of sugar-sweetened beverages (SSBs) increases the risk of developing obesity and metabolic syndrome (MetS). However, there are not many studies investigating the link between SSBs and increased incidences of diseases in the Asian population, and in particular, in Korea. We explored the association of SSB consumption with the risk of developing obesity and MetS among Korean adults (12,112 participants from the 2012⁻2016 Korean National Health and Nutrition Examination Survey). We calculated the total SSB consumption frequency by counting each beverage item, including soda beverages, fruit juices, and sweetened rice drinks. Obesity was defined as a body mass index ≥25 kg/m², and MetS was defined using the National Cholesterol Education Program, Adult Treatment Panel III. A survey logistic regression analyses was conducted to examine the association of SSB consumption with obesity and MetS, adjusting for related confounders such as age, energy intake, household income, education, alcohol drinking, smoking status, and physical activity. The SSB consumption was positively associated with an increased risk of the prevalence for obesity (Odd ratio (OR): 1.60; 95% confidence interval (CI): 1.23⁻2.09; p for trend = 0.0009) and MetS (OR: 1.61; 95% CI: 1.20⁻2.16; p for trend = 0.0003) among women. In men, SSB consumption only contributed to a higher prevalence of obesity (OR: 1.38; 95% CI: 1.11⁻1.72; p for trend = 0.0041). In conclusion, increased consumption of SSBs was closely linked with a higher prevalence of obesity and MetS in the Korean population.
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Fructose metabolism and metabolic disease.
Hannou, SA, Haslam, DE, McKeown, NM, Herman, MA
The Journal of clinical investigation. 2018;128(2):545-555
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Sugar consumption is thought to be a contributing factor in the increase in diabetes and obesity and the associated risk of cardiovascular disease worldwide. Sucrose (table sugar) and high fructose corn syrup contain almost equal amounts of fructose and glucose and are commonly added to processed foods. Whilst long-term studies are lacking, some short-term intervention studies show that fructose can impair lipid metabolism and insulin sensitivity in humans. This article reviews the biochemistry and molecular genetics of fructose metabolism as well as potential mechanisms by which excessive fructose consumption contributes to cardiometabolic disease. Fructose absorption in the human intestine is saturable, and there is a large range in capacity to absorb fructose between individuals, and unabsorbed fructose may contribute to gastrointestinal symptoms including pain and bloating. Fructose concentrations in the blood can increase 10-fold after consumption, but are rapidly cleared, mostly by the liver, where it provides substrate for metabolic processes, but may also be involved in signalling functions. Fructose may enhance glucose uptake by the liver and storage as glycogen and lipids. It may also increase production of uric acid which is implicated with gout. Excessive fructose consumption affects lipid metabolism and may contribute to fat accumulation in the liver and increase circulating triglycerides, a risk factor for heart disease. In animal models it also induces increased insulin levels. Fructose is one of the sweetest sugars which may affect appetite and overeating. It may also induce addiction-like behaviours such as binging and dependence in part by stimulating dopaminergic pathways. It also appears to induce leptin resistance which further increases food intake and obesity.
Abstract
Increased sugar consumption is increasingly considered to be a contributor to the worldwide epidemics of obesity and diabetes and their associated cardiometabolic risks. As a result of its unique metabolic properties, the fructose component of sugar may be particularly harmful. Diets high in fructose can rapidly produce all of the key features of the metabolic syndrome. Here we review the biology of fructose metabolism as well as potential mechanisms by which excessive fructose consumption may contribute to cardiometabolic disease.
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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).
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Self-reported dietary fructose intolerance in irritable bowel syndrome: Proposed diagnostic criteria.
Berg, LK, Fagerli, E, Myhre, AO, Florholmen, J, Goll, R
World journal of gastroenterology. 2015;21(18):5677-84
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The mechanisms for fructose malabsorption (FM) are not clearly understood and the diagnostic techniques are suboptimal. There is increasing interest to use self-reported responses to a fructose-reduced diet (FRD) as a diagnostic tool, however there is no standardised procedure for performing FRD tests. The aim of this study was to define the criteria for self-reported dietary fructose intolerance and to evaluate subjective global assessment as an outcome measure in 182 IBS patients. Participants were randomised to either consume a fructose-reduced diet or maintain a normal IBS diet, and record their symptoms and stool movements daily. After 12 weeks, a fructose-rich provocation test was performed. This study found that a fructose-reduced diet improves symptoms in a subgroup of IBS patients, and proposes a new diagnostic standard for self-reported fructose intolerance.
Abstract
AIM: To study the criteria for self-reported dietary fructose intolerance (DFI) and to evaluate subjective global assessment (SGA) as outcome measure. METHODS Irritable bowel syndrome (IBS) patients were randomized in an open study design with a 2 wk run-in on a habitual IBS diet, followed by 12 wk with/without additional fructose-reduced diet (FRD). Daily registrations of stool frequency and consistency, and symptoms on a visual analog scale (VAS) were performed during the first 4 wk. SGA was used for weekly registrations during the whole study period. Provocation with high-fructose diet was done at the end of the registration period. Fructose breath tests (FBTs) were performed. A total of 182 subjects performed the study according to the protocol (88 FRD, 94 controls). RESULTS We propose a new clinically feasible diagnostic standard for self-reported fructose intolerance. The instrument is based on VAS registrations of symptom relief on FRD combined with symptom aggravation upon provocation with fructose-rich diet. Using these criteria 43 of 77 patients (56%) in the present cohort of IBS patients had self-reported DFI. To improve the concept for clinical evaluation, we translated the SGA scale instrument to Norwegian and validated it in the context of the IBS diet regimen. The validation procedures showed a sensitivity, specificity and κ value for SGA detecting the self-reported DFI group by FRD response within the IBS patients of 0.79, 0.75 and 0.53, respectively. Addition of the provocation test yielded values of 0.84, 0.76 and 0.61, respectively. The corresponding validation results for FBT were 0.57, 0.34 and -0.13, respectively. CONCLUSION FRD improves symptoms in a subgroup of IBS patients. A diet trial followed by a provocation test evaluated by SGA can identify most responders to FRD.