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It has been postulated that fructose-induced triglyceride synthesis is augmented when accompanied by glucose. Chronic elevations could lead to excess fat accumulation in the liver and ectopic fat deposition in muscles, which in turn could contribute to the induction of abnormalities in glucose homeostasis, insulin resistance, and the subsequent development of type 2 diabetes. Our objective was to evaluate the effect of the addition of commonly consumed fructose- and (or) glucose-containing sugars in the usual diet on liver fat content and intramuscular adipose tissue. For 10 weeks, 64 individuals (mean age, 42.16 ± 11.66 years) consumed low-fat milk sweetened with either high-fructose corn syrup (HFCS) or sucrose; the added sugar matched consumption levels of fructose in the 25th, 50th, and 90th percentiles of the population. The fat content of the liver was measured with unenhanced computed tomography imaging, and the fat content of muscle was assessed with magnetic resonance imaging. When the 6 HFCS and sucrose groups were averaged, there was no change over the course of 10 weeks in the fat content of the liver (13.32% ± 10.49% vs. 13.21% ± 10.75%; p > 0.05), vastus lateralis muscle (3.07 ± 0.74 g per 100 mL vs. 3.15 ± 0.84 g per 100 mL; p > 0.05), or gluteus maximus muscle (4.08 ± 1.50 g per 100 mL vs. 4.24 ± 1.42 g per 100 mL; p > 0.05). Group assignment did not affect the result (interaction > 0.05). These data suggest that when fructose is consumed as part of a typical diet in normally consumed sweeteners, such as sucrose or HFCS, ectopic fat storage in the liver or muscles is not promoted.

The American Heart Association (AHA) and World Health Organization (WHO) have recommended restricting calories from added sugars at lower levels than the Institute of Medicine (IOM) recommendations, which are incorporated in the Dietary Guidelines for Americans 2010 (DGAs 2010). Sucrose (SUC) and high fructose corn syrup (HFCS) have been singled out for particular concern, because of their fructose content, which has been specifically implicated for its atherogenic potential and possible role in elevating blood pressure through uric acid-mediated endothelial dysfunction. This study explored the effects when these sugars are consumed at typical population levels up to the 90th percentile population consumption level for fructose. Three hundred fifty five overweight or obese individuals aged 20–60 years old were placed on a eucaloric diet for 10 weeks, which incorporated SUC- or HFCS-sweetened, low-fat milk at 8%, 18% or 30% of calories. There was a slight change in body weight in the entire cohort (169.1 ± 30.6 vs. 171.6 ± 31.8 lbs, p < 0.01), a decrease in HDL (52.9 ± 12.2 vs. 52.0 ± 13.9 mg/dL, p < 0.05) and an increase in triglycerides (104.1 ± 51.8 vs. 114.1 ± 64.7 mg/dL, p < 0.001). However, total cholesterol (183.5 ± 42.8 vs. 184.4 mg/dL, p > 0.05), LDL (110.3 ± 32.0 vs. 110.5 ± 38.9 mg/dL, p > 0.05), SBP (109.4 ± 10.9 vs. 108.3 ± 10.9 mmHg, p > 0.05) and DBP (72.1 ± 8.0 vs. 71.3 ± 8.0 mmHg, p > 0.05) were all unchanged. In no instance did the amount or type of sugar consumed affect the response to the intervention (interaction p > 0.05). These data suggest that: (1) when consumed as part of a normal diet, common fructose-containing sugars do not raise blood pressure, even when consumed at the 90th percentile population consumption level for fructose (five times the upper level recommended by the AHA and three times the upper level recommended by WHO); (2) changes in the lipid profile are mixed, but modest.

SUMMARY Twenty eight patients with classical irritable bowel syndrome completed a double blind placebo controlled crossover trial in which they added to their normal diet a daily supplement of either 12 bran biscuits (1 = 1. 3 g fibre) or 12 placebo biscuits (1 =0 23 g fibre). Each biscuit was given for three months in random order with crossover to the alternative biscuit at three months. After the initial three months therapy, there was a significant symptomatic improvement compared with pretreatment in both the bran treated (p<001) and placebo treated groups (p<001), but there was no significant difference in symptom scores between these two groups. There was no further improvement in either group after the second three months treatment with the alternative therapy. When crossover data for all 28 subjects were combined, symptoms scores after three months bran therapy and after three months placebo therapy did not differ significantly. Twenty four patients completed three day stool collections in both treatment periods. When the symptomatic response to bran among 15 subjects in whom stool weights rose on bran was compared with that among nine subjects whose stool weights were static or fell on the bran, it was shown that symptomatic improvement was independent of an increase in stool weight. These data suggest that in irritable bowel syndrome, especially that associated with abdominal pain, the beneficial effects of bran are due to a placebo response which is independent of an increase in stool weight.Standard treatment of irritable bowel syndrome (IBS) includes increasing the oral intake of fibre.' In 1977, Manning et al reported that the addition of 7 g fibre in the form of wheat bran for six weeks to the diet of patients with IBS resulted in a significant improvement in symptoms.2 Subsequent studies in IBS, however, have either failed to show a therapeutic benefit of bran compared with placebo34 or have suggested that bran is of only limited value.5Interpretation of these clinical trials of dietary fibre is confounded by short duration of study which, as Ritchie and Truelove have shown, can significantly influence the apparent symptomatic response to treatment in IBS.6 We, therefore, conducted a double blind placebo controlled crossover study of the efficacy of a three month course of bran supplements in patients with classical IBS.7