A blinded randomised controlled trial of prescribed oral sip-feed supplements compared with routine hospital practice was undertaken in acute admissions to a geriatric medicine department. Patients were eligible for inclusion if they were admitted from home, were not obese (BMI>75th percentile), had no swallowing difficulties and were not deemed to be in the terminal stage of illness. On admission they were stratified by nutritional status (BMI<5th, >5th to <25th, >25th to <75th percentile) and randomised. The intervention group received 120 ml oral sip-feed supplement prescribed three times per d in the medicine prescription chart (22·5 g protein, 2260 kJ (540 kcal) energy/d) distributed at medication rounds for the duration of hospital stay. The control group received routine hospital care. Outcomes were patient compliance with supplement, total energy intake and nursing staff views of the method. Patients were randomised to receive supplements (n 186 of total n 381). Half had full compliance and three-quarters at least moderate compliance. Total energy intake was significantly increased, on average, in the intervention group (P=0·001). The proportion of patients meeting estimated minimum energy requirements was significantly increased (P=0·023), but was still <50 % for the sample of patients in the intervention group. The present study suggests this method is acceptable to patients and staff and improves total energy intake. However, the amount prescribed did not ensure minimum energy requirements were met in all cases.

The aim of the present study was to determine the relationship of BMI with other cardiovascular risk factors, leisure-time physical activity and diet. Participants were recruited in a cross-sectional population-based survey in a southern-Europe Mediterranean population (Spain); cardiovascular risk factors were measured, and leisure-time physical activity and diet intake were evaluated. Linear regression analysis adjusted for several confounders showed a significant, direct association of BMI and total cholesterol (P<0·005) and LDL-cholesterol (P<0·006), in men. HDL-cholesterol was inversely related to BMI in both sexes (P<0·0001). Higher BMI was more frequent in less-active men (P<0·04) but not in women. BMI increased significantly (P<0·0001) by 1·92 kg/m2 with each 4·18 MJ consumed in men but not in women. Dietary intakes of carbohydrate (P<0·03), total fat (P<0·03) and saturated fatty acids (P<0·02) were directly associated with BMI in men but not in women, in whom protein intake was correlated (P<0·001) with BMI. Linear regression models including dietary components explained up to 10·6 and 21·1 % of BMI variability in men and women, respectively. Sex differences in the association of BMI with total cholesterol, and LDL-cholesterol, may account for the lower risk for CHD in women compared with men of similar BMI reported in the literature for the southern-Europe Mediterranean region. An increases of BMI may be more deleterious in populations in which it is accompanied by other risk factors such as a higher intake of total fat and, particularly, of saturated fatty acids, or lower leisure-time physical activity.

The aim of the present analysis was to evaluate the effect of intake of added sugars on intakes of nutrients and food groups. We used a mixed linear model (PROC MIXED) to analyse data from the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) study (an ongoing longitudinal cohort study between infancy and adulthood). Between July 1985 and August 2001, 3 d weighed dietary records (n 4993) from 849 children and adolescents (416 male, 433 female) aged 2–18 years were collected and evaluated. Overall mean intake of added sugars was 12·4 (SD 5·3) (median 12·0) % energy. Fat intake (% energy) and intake of all analysed nutrients (as % reference values for nutrient intakes) fell across quintiles 1–5 of energy intake from added sugars (P<0·001). With the exception of ‘Sugary foods’ and ‘Beverages’ (significant increase, P<0·0001) and ‘Dairy’ (NS), intake of all other food groups decreased with increasing intake of added sugars (P<0·0001). In conclusion, we found a slight, but statistically significant, nutrient-dilution effect of added sugars and a significant reduction in intake of important nutrient-bearing food groups. However, the DONALD study gives no clear indicator on grounds of micronutrient dilution for a quantitative limit on intake of added sugars.

The increasing interest in a healthy diet is stimulating innovative development of novel scientific products in the food industry. The viable lactic acid bacteria in fermented milk products, such as yoghurt, have been associated with increased lactose tolerance, a well-balanced intestinal microflora, antimicrobial activity, stimulation of the immune system and antitumoural, anticholesterolaemic and antioxidative properties in human subjects. Recently, we have studied a human Lactobacillus spp. strain that possesses antioxidative activity. The aim of the present pilot study was to develop goats' milk fermented with the human antioxidative lactobacilli strain, Lactobacillus fermentum ME-3, and to test the effect of the fermented probiotic goats' milk on oxidative stress markers (including markers for atherosclerosis) in human blood and urine and on the gut microflora. Twenty-one healthy subjects were assigned to two treatment groups: goats' milk group and fermented goats' milk group (150 g/d) for a period of 21 d. Consumption of fermented goats' milk improved anti-atherogenicity in healthy subjects: it prolonged resistance of the lipoprotein fraction to oxidation, lowered levels of peroxidized lipoproteins, oxidized LDL, 8-isoprostanes and glutathione redox ratio, and enhanced total antioxidative activity. The consumption of fermented goats' milk also altered both the prevalence and proportion of lactic acid bacteria species in the gut microflora of the subjects. We conclude that the goats' milk fermented with our special antioxidative lactobacilli strain Lactobacillus fermentum ME-3 exhibits anti-atherogenic effects.

Epidemiological studies indicate that Asian women have a lower breast cancer incidence compared with their counterparts in the West, and the difference has been related to soya consumption. Animal studies have suggested that soya may prevent dimethylbenz[a]anthracene (DMBA)-induced carcinogenesis in the breast. In the present study a cell culture model was developed to address the effect of soya isoflavones on the DMBA-induced DNA damage. DMBA is metabolized into a DNA-attacking moiety by two phase I cytochrome P450 (CYP) enzymes CYP1A1 and CYP1B1. DNA mutation caused by this genotoxic agent is a crucial step in cancer initiation. Substances that interfere with the CYP1 enzyme activities can affect the initiation. In the present study, genistein was found to be an effective inhibitor of recombinant human CYP1A1 and CYP1B1 with Ki of 15·35 and 0·68 μmol/l. The other soya isoflavone daidzein, on the other hand, did not demonstrate any significant inhibition of the enzyme activities. At the transcriptional level, DMBA induced the CYP1 enzyme expressions by stimulating the xenobiotic response element (XRE)-dependent transactivation pathway. When genistein (25 μmol/l) was co-administered with DMBA, the XRE-Luc activity the CYP1 mRNA abundances were significantly suppressed. The present study illustrated that the soya isoflavone genistein, but not daidzein, protected against DMBA genotoxicity.

Epidemic spastic paraparesis (konzo) found in tropical and subtropical countries is known to be caused by long-term intake of cassava (Manihot esculenta Crantz), which contains a cyanoglucoside linamarin (α-hydroxyisobutyronitrile-β-D-glucopyranoside). It has been reported that linamarin is enzymatically converted to cyanide by bacteria in the intestine, and this is absorbed into the blood and then damages neural cells. However, unmetabolized linamarin was found in the urine after oral administration of cassava; thus, we hypothesized that konzo could be caused by direct toxicity of the unmetabolized linamarin that was transferred to the brain and could be transported into neural cells via a glucose transporter. In the present study it was confirmed that linamarin directly damaged neural culture pheochromocytoma cell (PC) 12 cells; 0·10 mM-linamarin caused cell death at 13·31 (SD 2·07) %, which was significantly different from that of control group (3·18 (SD 0·92) %, P=0·0004). Additional 10 μM-cytochalasin B, an inhibitor of a glucose transporter, prevented cell death: the percentage of dead cells significantly decreased to 6·06 (SD 1·98), P=0·0088). Furthermore, glucose also prevented cell death. These present results strongly suggest that linamarin competes with cytochalasin B and glucose for binding to a glucose transporter and enters into cells via glucose transporter.

The UK Food Standards Agency convened a group of expert scientists to review current research investigating folate bioavailability. The workshop aimed to overview current research and establish priorities for future research. Discrepancies were observed in the evidence base for folate bioavailability, especially with regard to the relative bioavailability of natural folates compared with folic acid. A substantial body of evidence shows folic acid to have superior bioavailability relative to food folates; however, the exact relative bioavailability still needs to be determined, and in particular with regard to mixed diets. The bioavailability of folate in a mixed diet is probably not a weighted average of that in the various foods consumed; thus the workshop considered that assessment of folate bioavailability of whole diets should be a high priority for future research.