Untersuchungen zur Bedeutung der Kohlenhydrate in einer vollsynthetischen, fettfreien Diät

Förster, H.; Heller, G

doi:10.1055/s-0028-1106986

Cited by 33 publications

(3 citation statements)

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“…Fructose was administered in liquid, solid, or mixed formats at a mean dose of 94 g/d [25–213 g/d or 5–33% energy (E)] in the isocaloric trials and 215 g/d (213–219 g/d or +35% excess E) in the hypercaloric trials. Thirteen (72%) of the isocaloric trials and all 3 of the hypercaloric trials exceeded the dose threshold of 60 g/d proposed by the Canadian Diabetes Association (13, 15–17, 19, 20, 22, 23, 26). Nine (50%) isocaloric and all 3 hypercaloric trials used metabolically controlled designs.…”

Section: Resultsmentioning

confidence: 91%

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The Effects of Fructose Intake on Serum Uric Acid Vary among Controlled Dietary Trials

Wang

Sievenpiper

Souza

et al. 2012

The Journal of Nutrition

168

139

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Hyperuricemia is linked to gout and features of metabolic syndrome. There is concern that dietary fructose may increase uric acid concentrations. To assess the effects of fructose on serum uric acid concentrations in people with and without diabetes, we conducted a systematic review and meta-analysis of controlled feeding trials. We searched MEDLINE, EMBASE, and the Cochrane Library for relevant trials (through August 19, 2011). Analyses included all controlled feeding trials ≥7 d investigating the effect of fructose feeding on uric acid under isocaloric conditions, where fructose was isocalorically exchanged with other carbohydrate, or hypercaloric conditions, and where a control diet was supplemented with excess energy from fructose. Data were aggregated by the generic inverse variance method using random effects models and expressed as mean difference (MD) with 95% CI. Heterogeneity was assessed by the Q statistic and quantified by I2. A total of 21 trials in 425 participants met the eligibility criteria. Isocaloric exchange of fructose for other carbohydrate did not affect serum uric acid in diabetic and nondiabetic participants [MD = 0.56 μmol/L (95% CI: −6.62, 7.74)], with no evidence of inter-study heterogeneity. Hypercaloric supplementation of control diets with fructose (+35% excess energy) at extreme doses (213–219 g/d) significantly increased serum uric acid compared with the control diets alone in nondiabetic participants [MD = 31.0 mmol/L (95% CI: 15.4, 46.5)] with no evidence of heterogeneity. Confounding from excess energy cannot be ruled out in the hypercaloric trials. These analyses do not support a uric acid-increasing effect of isocaloric fructose intake in nondiabetic and diabetic participants. Hypercaloric fructose intake may, however, increase uric acid concentrations. The effect of the interaction of energy and fructose remains unclear. Larger, well-designed trials of fructose feeding at “real world” doses are needed.

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Section: Resultsmentioning

confidence: 91%

“…Although not tested formally in subgroup analyses, composition of the background diet in the trials also did not appear to have an effect. One of the included isocaloric trials, Forster et al (17), had a background diet devoid of fat. This study was included, because it met all eligibility criteria.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Fructose Intake on Serum Uric Acid Vary among Controlled Dietary Trials

Wang

Sievenpiper

Souza

et al. 2012

The Journal of Nutrition

168

139

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“…Indeed, as already noted, we have recently reported that consumption of beverages containing 17.5 or 25% Ereq as HFCS, the other commonly-consumed fructose-containing added sugar, increased both fasting and 24-h uric acids levels (58). In the other two studies it appears that both the fructose and control diets were energy-restricted (102, 103). Since uric acid production via the purine degradation pathway is increased by hepatic substrate overload leading to generation of excess AMP and a depletion of inorganic phosphate, energy-restricted diets are not likely to lead to increased uric acid levels.…”

Section: Introductionmentioning

confidence: 95%

Sugar consumption, metabolic disease and obesity: The state of the controversy

Stanhope

2015

Critical Reviews in Clinical Laboratory Sciences

566

390

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The impact of sugar consumption on health continues to be a controversial topic. The objective of this review is to discuss the evidence and lack of evidence that allows the controversy to continue, and why resolution of the controversy is important. There are plausible mechanisms and research evidence that support the suggestion that consumption of excess sugar promotes the development of cardiovascular disease (CVD) and type 2 diabetes (T2DM) both directly and indirectly. The direct pathway involves the unregulated hepatic uptake and metabolism of fructose, which leads to liver lipid accumulation, dyslipidemia, decreased insulin sensitivity and increased uric acid levels. The epidemiological data suggest that these direct effects of fructose are pertinent to the consumption of the fructose-containing sugars, sucrose and HFCS, which are the predominant added sugars. Consumption of added sugar is associated with development and/or prevalence of fatty liver, dyslipidemia, insulin resistance, hyperuricemia, cardiovascular disease and type 2 diabetes, and many of these associations are independent of body weight gain or total energy intake. There are diet intervention studies in which human subjects exhibited increased circulating lipids and decreased insulin sensitivity when consuming high sugar compared with control diets. Most recently, our group has reported that supplementing the ad libitum diets of young adults with beverages containing 0, 10, 17.5 or 25% of daily energy requirement (Ereq) as high fructose corn syrup (HFCS) increased lipid/lipoprotein risk factors for cardiovascular disease (CVD) and uric acid in a dose response manner. However, un-confounded studies conducted in healthy humans under a controlled, energy-balanced diet protocol that allow determination of the effects of sugar with diets that do not allow for body weight gain are lacking. Furthermore, there are recent reports that conclude that there are no adverse effects of consuming beverages containing up to 30% Ereq sucrose or HFCS, and the conclusions from several meta-analyses suggest that fructose has no specific adverse effects relative to any other carbohydrate. Consumption of excess sugar may also promote the development the development of CVD and T2DM indirectly by causing increased body weight and fat gain, but this is also a topic of controversy. Mechanistically, it is plausible that fructose consumption causes increased energy intake and reduced energy expenditure due to its failure to stimulate leptin production. Functional magnetic resonance imaging of the brain demonstrates that the brain responds differently to fructose or fructose-containing sugars compared with glucose or aspartame. There are epidemiological studies which show sugar consumption is associated with body weight gain, and there are intervention studies in which consumption of ad libitum high sugar diets promoted increased body weight gain compared with consumption of ad libitum low sugar diets. However, there are no studies in which energy intake and weight gai...

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References

Mäkinen

1978

Biochemical Principles of the Use of Xylitol in Medicine and Nutrition With Special Consideration of Dental Aspects

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Untersuchungen zur Bedeutung der Kohlenhydrate in einer vollsynthetischen, fettfreien Diät

Cited by 33 publications

References 0 publications

The Effects of Fructose Intake on Serum Uric Acid Vary among Controlled Dietary Trials

The Effects of Fructose Intake on Serum Uric Acid Vary among Controlled Dietary Trials

Sugar consumption, metabolic disease and obesity: The state of the controversy

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