Excess dietary fructose does not alter gut microbiota or permeability in humans: A pilot randomized controlled study

Alemán, José O.; Henderson, Wendy A.; Walker, Joseph R.; Ronning, Andrea; Jones, Drew R.; Walter, Peter J.; Daniel, Scott G.; Bittinger, Kyle; Vaughan, Roger; MacArthur, Robert B.; Chen, Kun; Breslow, Jan L.; Holt, Peter R.

doi:10.1017/cts.2021.801

Cited by 15 publications

(11 citation statements)

References 52 publications

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“…These findings are in contrast to those recently published by others, reporting that in a double-blind, cross-over design study with 10 obese subjects, the isocaloric substitution of complex carbohydrates with 75 g of either fructose or glucose for 2 weeks had no effect on fecal microbiota composition, gut permeability, or indices of endotoxemia [156]. Differences between our study [7] and that of Alemán et al [156] might have resulted from the study design (standardized nutrition vs. exchange of parts of the complex carbohydrates), the dose of fructose (25E% vs. ~20E%) but also the parameters detected (bacterial endotoxin vs. CD14, intestinal fatty acid binding protein and LPS binding protein). However, the divagating results also underlie the need for further well-designed studies.…”

Section: How Could Dietary Fructose Add To the Development Of Nafld? ...contrasting

confidence: 99%

“…Results of studies of our own group suggest that in dietetically standardized young healthy adults, consumption of a fructose-rich diet (25% of total energy intake) for only 3 days results in significantly increased plasma endotoxin concentrations while similar effects were not found when the same subjects consumed isocaloric amounts of glucose [7]. These findings are in contrast to those recently published by others, reporting that in a double-blind, cross-over design study with 10 obese subjects, the isocaloric substitution of complex carbohydrates with 75 g of either fructose or glucose for 2 weeks had no effect on fecal microbiota composition, gut permeability, or indices of endotoxemia [156]. Differences between our study [7] and that of Alemán et al [156] might have resulted from the study design (standardized nutrition vs. exchange of parts of the complex carbohydrates), the dose of fructose (25E% vs. ~20E%) but also the parameters detected (bacterial endotoxin vs. CD14, intestinal fatty acid binding protein and LPS binding protein).…”

Section: How Could Dietary Fructose Add To the Development Of Nafld? ...contrasting

confidence: 70%

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Fructose, a trigger of metabolic diseases?—a narrative review

2022

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Worldwide the number of individuals being overweight or obese has dramatically increased during the last decades, which is also associated with a similar dramatic increase of individuals afflicted with metabolic disorders like dyslipidemia, hypertension, and non-alcoholic fatty liver disease (NAFLD). Genetic predisposition may account for some of the increases in body weight and the development of metabolic disorders; however, much is probably also related to the changes in physical activity and dietary pattern. Indeed, results of epidemiological studies suggest that a ‘western-type dietary pattern’ composed of highly processed foods, sweetened foods, and beverages, all adding to a low fiber but high sugar and saturated fat intake, may increase the odd of developing overweight and metabolic disorders. Consumption of sugar, and especially, fructose has repeatedly been discussed to be a key contributor to the development of health disturbances including hypertension, dyslipidemia, insulin resistance as well as NAFLD. However, despite intense research effort, the question if and how (high) dietary fructose intake interferes with human health has not yet been fully answered also as findings are sometimes contradictory. In the present narrative review, results of recent studies assessing the effect of fructose consumption on the development of metabolic disorders including hypertension, dyslipidemia, cardiovascular diseases (CVDs), hyperinsulinemia, and NAFLD as well as underlying molecular mechanisms are reviewed, thereby, aiming to further address the question if (high) fructose intake is a trigger of metabolic diseases.

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Section: How Could Dietary Fructose Add To the Development Of Nafld? ...contrasting

confidence: 99%

Section: How Could Dietary Fructose Add To the Development Of Nafld? ...contrasting

confidence: 70%

Fructose, a trigger of metabolic diseases?—a narrative review

2022

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“…We retrieved 4616 reports from databases and manual searches, 4433 of which were excluded based on the title or abstract. Of the 174 reports reviewed in full text, 51 reports of controlled feeding trials (75 trial comparisons, n = 2059) met the eligibility criteria [ 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 , 72 , 73 , 74 , 75 , 76 , 77 , 78 , 79 , 80 , 81 , 82 , 83 , 84 , 85 , 86 , 87 , 88 , 89 , 90 , 91 , 92 , 93 , 94 ]. These trials included ten different food sources of fructos...…”

Section: Resultsmentioning

confidence: 99%

Important Food Sources of Fructose-Containing Sugars and Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis of Controlled Trials

et al. 2022

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Background: Fructose providing excess calories in the form of sugar sweetened beverages (SSBs) increases markers of non-alcoholic fatty liver disease (NAFLD). Whether this effect holds for other important food sources of fructose-containing sugars is unclear. To investigate the role of food source and energy, we conducted a systematic review and meta-analysis of controlled trials of the effect of fructose-containing sugars by food source at different levels of energy control on non-alcoholic fatty liver disease (NAFLD) markers. Methods and Findings: MEDLINE, Embase, and the Cochrane Library were searched through 7 January 2022 for controlled trials ≥7-days. Four trial designs were prespecified: substitution (energy-matched substitution of sugars for other macronutrients); addition (excess energy from sugars added to diets); subtraction (excess energy from sugars subtracted from diets); and ad libitum (energy from sugars freely replaced by other macronutrients). The primary outcome was intrahepatocellular lipid (IHCL). Secondary outcomes were alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Independent reviewers extracted data and assessed risk of bias. The certainty of evidence was assessed using GRADE. We included 51 trials (75 trial comparisons, n = 2059) of 10 food sources (sugar-sweetened beverages (SSBs); sweetened dairy alternative; 100% fruit juice; fruit; dried fruit; mixed fruit sources; sweets and desserts; added nutritive sweetener; honey; and mixed sources (with SSBs)) in predominantly healthy mixed weight or overweight/obese younger adults. Total fructose-containing sugars increased IHCL (standardized mean difference = 1.72 [95% CI, 1.08 to 2.36], p < 0.001) in addition trials and decreased AST in subtraction trials with no effect on any outcome in substitution or ad libitum trials. There was evidence of influence by food source with SSBs increasing IHCL and ALT in addition trials and mixed sources (with SSBs) decreasing AST in subtraction trials. The certainty of evidence was high for the effect on IHCL and moderate for the effect on ALT for SSBs in addition trials, low for the effect on AST for the removal of energy from mixed sources (with SSBs) in subtraction trials, and generally low to moderate for all other comparisons. Conclusions: Energy control and food source appear to mediate the effect of fructose-containing sugars on NAFLD markers. The evidence provides a good indication that the addition of excess energy from SSBs leads to large increases in liver fat and small important increases in ALT while there is less of an indication that the removal of energy from mixed sources (with SSBs) leads to moderate reductions in AST. Varying uncertainty remains for the lack of effect of other important food sources of fructose-containing sugars at different levels of energy control.

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“…In view of this, a significant reduction in fructose, sucrose and HFCS in processed foods, beverages and a general ban on high-fructose corn syrup are advised [38,87,92,137,145,146,250]. The role of fructose in the intestinal microbiome and gut barrier function remains under debate [120,122].…”

Section: Discussionmentioning

confidence: 99%

“…reported that a high-fructose diet was associated with lower abundance of beneficial microbes (Eubacterium and Streptococcus), which are involved in carbohydrate metabolism, aiding dysbiosis [121]. A 2020 study by Aleman et al demonstrated that a daily dose of 75 g of fructose in obese patients did not cause increased gut permeability or endotoxemia [122]. This contradicts previous reports that stated that fructose causes bacterial overgrowth, an increase in intestinal permeability, precipitating endotoxemia and, hence, the initiation of an inflammatory cascade driving the progression of NAFLD [123,124].…”

Section: Fructose and Sucrose-fructose And Sucrose In The Epidemiolog...mentioning

confidence: 99%

The Role of Macronutrients in the Pathogenesis, Prevention and Treatment of Non-Alcoholic Fatty Liver Disease (NAFLD) in the Paediatric Population—A Review

Pixner

Stummer

Schneider

et al. 2022

Life

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Paediatric non-alcoholic fatty liver disease (NAFLD) has become the most common chronic liver disease in childhood. Obesity is the main risk factor. Nutrition and lifestyle are the key elements in preventing and treating NAFLD in the absence of approved drug therapy. Whilst recommendations and studies on macronutrients (carbohydrates, fat and protein) in adult NAFLD exist, the discussion of this topic in paediatric NAFLD remains contradictory. The purpose of this review is to provide state-of-the-art knowledge on the role of macronutrients in paediatric NAFLD regarding quality and quantity. PubMed was searched and original studies and review articles were included in this review. Fructose, sucrose, saturated fatty acids, trans-fatty acids and ω-6-fatty-acids are strongly associated with paediatric NAFLD. High consumption of fibre, diets with a low glycaemic index, mono-unsaturated-fatty-acids and ω-3-fatty-acids reduce the risk of childhood-onset NAFLD. Data regarding the role of dietary protein in NAFLD are contradictory. No single diet is superior in treating paediatric NAFLD, although the composition of macronutrients in the Mediterranean Diet appears beneficial. Moreover, the optimal proportions of total macronutrients in the diet of paediatric NAFLD patients are unknown. Maintaining a eucaloric diet and avoiding saturated fatty acids, simple sugars (mainly fructose) and a high-caloric Western Diet are supported by literature.

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Excess dietary fructose does not alter gut microbiota or permeability in humans: A pilot randomized controlled study

Abstract: This version may be subject to change during the production process.

Cited by 15 publications

References 52 publications

Fructose, a trigger of metabolic diseases?—a narrative review

Fructose, a trigger of metabolic diseases?—a narrative review

Important Food Sources of Fructose-Containing Sugars and Non-Alcoholic Fatty Liver Disease: A Systematic Review and Meta-Analysis of Controlled Trials

The Role of Macronutrients in the Pathogenesis, Prevention and Treatment of Non-Alcoholic Fatty Liver Disease (NAFLD) in the Paediatric Population—A Review

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