Dietary Fibre Consensus from the International Carbohydrate Quality Consortium (ICQC).

Dietary fibre is a generic term describing non-absorbed plant carbohydrates and small amounts of associated non-carbohydrate components. The main contributors of fibre to the diet are the cell walls of plant tissues, which are supramolecular polymer networks containing variable proportions of cellulose, hemicelluloses, pectic substances, and non-carbohydrate components, such as lignin. Other contributors of fibre are the intracellular storage oligosaccharides, such as fructans. A distinction needs to be made between intrinsic sources of dietary fibre and purified forms of fibre, given that the three-dimensional matrix of the plant cell wall confers benefits beyond fibre isolates. Movement through the digestive tract modifies the cell wall structure and may affect the interactions with the colonic microbes (e.g., small intestinally non-absorbed carbohydrates are broken down by bacteria to short-chain fatty acids, absorbed by colonocytes). These aspects, combined with the fibre associated components (e.g., micronutrients, polyphenols, phytosterols, and phytoestrogens), may contribute to the health outcomes seen with the consumption of dietary fibre. Therefore, where possible, processing should minimise the degradation of the plant cell wall structures to preserve some of its benefits. Food labelling should include dietary fibre values and distinguish between intrinsic and added fibre. Labelling may also help achieve the recommended intake of 14 g/1000 kcal/day.

Commercial complementary food consumption is prospectively associated with added sugar intake in childhood.

Given that commercial complementary food (CF) can contain high levels of added sugar, a high consumption may predispose to a preference for sweet taste later in life. This study examined cross-sectional associations between commercial CF consumption and added sugar intake in infancy as well as its prospective relation to added sugar intake in pre-school and primary-school age children. In all, 288 children of the Dortmund Nutritional and Anthropometric Longitudinally Designed Study with 3-d weighed dietary records at 0·5 and 0·75 (infancy), 3 and 4 (pre-school age) and 6 and 7 years of age (primary-school age) were included in this analysis. Individual commercial CF consumption as percentage of total commercial CF (%cCF) was averaged at 0·5 and 0·75 years. Individual total added sugar intake (g/d, energy percentage/d) was averaged for all three age groups. Multivariable logistic and linear regression models were used to analyse associations between %cCF and added sugar intake. In infancy, a higher %cCF was associated with odds for high added sugar intake from CF and for high total added sugar intake (>75th percentile, P<0·033). Prospectively, a higher %cCF was related to higher added sugar intake in both pre-school (P<0·041) and primary-school age children (P<0·039), although these associations were attenuated in models adjusting for added sugar intake in infancy. A higher %cCF in infancy may predispose to higher added sugar intake in later childhood by virtue of its added sugar content. Therefore, offering home-made CF or carefully chosen commercial CF without added sugar might be one strategy to reduce sugar intake in infancy and later on.

Direction of associations between added sugar intake in early childhood and body mass index at age 7 years may depend on intake levels.

Dietary factors, especially during early childhood, have been discussed as potentially critical for the development of childhood overweight. This study evaluated associations between added sugar intake during early childhood and BMI and body fat at age 7 y. Analysis was based on data from 216 participants of the Dortmund Nutritional and Anthropometric Longitudinally Designed (DONALD) Study. Life-course plots were constructed to evaluate the association between added sugar intake at different ages (0.5, 1, 1.5, and 2 y) and BMI SD score (BMI-SDS) and % body fat (%BF) at age 7 y. Multivariable analyses were performed for the periods identified as critical for later BMI and body fat. Added sugar intake at age 1 y and the change in intake levels during the second year of life emerged as potentially critical. At age 1 y, a higher total added sugar intake was related to a lower BMI-SDS at age 7 y [adjusted ß ± SE: -0.116 ± 0.057 BMI-SDS/percent energy (%En) added sugar; P = 0.04]. Conversely, an increase in total added sugar in the second year of life (Δ%En between age 1 and 2 y) tended to be associated with a higher BMI-SDS (adjusted ß ± SE: 0.074 ± 0.043 BMI-SDS/Δ%En added sugar; P = 0.09). No associations were observed with %BF. In conclusion, added sugar intake at low intake levels during early childhood does not appear to be critical for BMI and body fat at age 7 y. However, detrimental effects on BMI development may emerge when added sugar intakes are increased to higher levels.

Consumption of polyunsaturated fatty acids, fish, and nuts and risk of inflammatory disease mortality.

BACKGROUND: n-3 (omega-3) Polyunsaturated fatty acids (PUFAs), fish, and nuts can regulate inflammatory processes and responses. OBJECTIVE: We investigated whether dietary intakes of PUFAs [n-3, n-6 (omega-6), and α-linolenic acid], fish, and nuts were associated with 15-y mortality attributed to noncardiovascular, noncancer inflammatory diseases. DESIGN: The analyses involved 2514 participants aged ≥49 y at baseline. Dietary data were collected by using a semiquantitative food-frequency questionnaire, and PUFA, fish, and nut intakes were calculated. Inflammatory disease mortality was confirmed from the Australian National Death Index. RESULTS: Over 15 y, 214 subjects died of inflammatory diseases. Women in the highest tertiles of total n-3 PUFA intake, compared with those in the lowest tertile of intake at baseline, had a 44% reduced risk of inflammatory disease mortality (P for trend = 0.03). This association was not observed in men. In both men and women, each 1-SD increase in energy-adjusted intake of α-linolenic acid was inversely associated with inflammatory mortality (hazard ratio: 0.83; 95% CI: 0.71, 0.98). Subjects in the second and third tertiles of nut consumption had a 51% and 32% reduced risk of inflammatory disease mortality, respectively, compared with those in the first tertile (reference). Dietary intakes of long-chain n-3 and n-6 PUFAs and fish were not associated with inflammatory disease mortality. CONCLUSIONS: We report on a novel link between dietary intake of total n-3 PUFA and risk of inflammatory disease mortality in older women. Furthermore, our data indicate a protective role of nuts, but not fish, against inflammatory disease mortality.

Urinary isoflavone phytoestrogens in German children and adolescents--a longitudinal examination in the DONALD cohort.

SCOPE: In light of concerns about hormonally active agents, it is important to assess human exposure to such compounds, especially in children as a susceptible subgroup. Estrogenic plant constituents are present in the human diet in varying levels, in particular the isoflavones daidzein (DAI) and genistein (GEN). We aimed to examine age-dependent and secular trends in phytoestrogen exposures and to investigate equol (EQ) excretion of German children using biomarker analysis in 24-h urine samples from a longitudinally designed study. METHODS AND RESULTS: The concentrations of DAI, its metabolite EQ and GEN were determined by GC-MS analysis in 24-h urines (510 samples) collected between 1985 and 2000 in 90 (47 boys) German children (6-18 years old), who are participants in the Dortmund Nutritional and Anthropometric Longitudinally Designed study. The results from the urinary biomarker analysis indicate isoflavone exposures at quite variable levels in German children: Analyte concentrations in over 500 urine samples cover the range reported previously in adults on typical German diet and with soy intake. EQ, the DAI metabolite produced by the gastrointestinal microflora, was detected in a high fraction of all samples, with 28/90 children (31%) excreting EQ in all their urines, and 62/90 children (68%) in at least one sample. Interestingly, when multiple urines obtained from individuals at different ages (6-18 years) were analyzed, EQ formation did not appear to be a constant trait over time. When stratified by sex, DAI, EQ and GEN concentrations (ng/mL) in urines and excretion rates (µg/day) were similar in boys and girls. Total isoflavone excretion rates (µg/day) increased during childhood (6-12 years) (p=0.02) and were constant during adolescence (13-18 years) (p=0.6). No clear trend for changes in dietary isoflavone exposure over the total study period was seen (p=0.7). CONCLUSIONS: In conclusion, biomarkers in urine of German children and adolescents indicate a frequent, but widely variable dietary isoflavone intake and suggest no secular increase (1985-2000) in the exposure to isoflavone phytoestrogens among German children and adolescents.

Relation of isoflavones and fiber intake in childhood to the timing of puberty.

BACKGROUND: It has been suggested that phytoestrogens and dietary fiber can affect puberty timing. OBJECTIVE: We examined whether intake of isoflavone and fiber in healthy white children before their pubertal growth spurt [age at take-off (ATO)] was associated with puberty timing. DESIGN: Multivariate regression analyses were performed in 227 DONALD (DOrtmund Nutritional and Anthropometric Longitudinally Designed) Study participants with 3-d weighed dietary records and information on potential confounders at baseline (1 and 2 y before ATO). In a subsample (n = 111), urinary isoflavones were determined in 24-h urine samples by gas chromatography-mass spectrometry analysis. Puberty timing was examined by using ATO and chronologic ages at pubertal stage 2 for breast development (B2) or gonadal development, peak height velocity (PHV), and menarche or voice break. RESULTS: Girls whose diet was in the highest dietary isoflavone tertile experienced Tanner stage 2 for breast development ap 0.7 y later and reached PHV ap 0.6 y later than did girls whose diet was in the lowest isoflavone tertile [age (95% CI) at B2: 10.7 y (10.4, 10.9 y) compared with 10.0 y ( 9.7, 10.3 y), respectively; P for trend = 0.04; age at PHV: 11.9 y (11.6, 12.2 y) compared with 11.3 y (11.0, 11.6 y), respectively; P for trend = 0.04; adjusted for body mass index z score and fiber intake]. In boys, dietary isoflavones were not associated with pubertal markers. Urinary isoflavone and dietary fiber intakes were not associated with pubertal markers. CONCLUSIONS: Girls, but not boys, with higher prepubertal isoflavone intakes appear to enter puberty at a later age. Fiber intake in this sample of healthy white girls and boys was not relevant for puberty timing.

A new FFQ designed to measure the intake of fatty acids and antioxidants in children.

OBJECTIVE: The present paper describes the systematic development of an FFQ to assess the intake of fatty acids and antioxidants in school-aged children. In addition, a validation study applying 24 h dietary recalls was performed. DESIGN: Using the variance-based Max_r method, a list of eighty-two foods was compiled from data obtained by 3 d weighed dietary records. The foods were used to design an FFQ, the comprehensibility of which was evaluated in a feasibility study. In addition, the FFQ was validated in a subset of 101 children from the German Infant Nutritional Intervention Study (GINI PLUS) against one 24 h dietary recall. RESULTS: The feasibility study attested a good acceptance of the FFQ. Mean intake of foods compared well between the FFQ and the 24 h dietary recall, although intake data generated from the FFQ tended to be higher. This difference became less apparent at the nutrient level, although the estimated average consumption of arachidonic acid and EPA using the FFQ still exceeded values recorded with the 24 h recall method by 45 % and 29 %, respectively. CONCLUSIONS: On the basis of the systematic selection process of the food list, the established practicability of the FFQ and the overall plausibility of the results, the use of this FFQ is justified in future epidemiological studies.

Modifications in dietary fat quality are associated with changes in serum lipids of older adults independently of lipid medication.

Prospective evidence on the extent to which serum lipid concentrations in older persons respond to dietary modification is scarce. It is not clear whether such behavioral changes are relevant in the context of more commonly initiated treatments with lipid-lowering drugs. We therefore examined whether individual changes in the consumption of dietary fatty acids or main food sources were associated with changes in the serum lipid profile of older Australians. A total of 903 participants (> or =49 y) in the Blue Mountains Eye Study had complete data on fasting lipids and dietary intake from a validated FFQ at baseline (1992-1994) and 5- and 10-y follow-up examinations. Decreasing consumption of SFA and butter during the 10-y period were associated with moderate decreases in serum total cholesterol independently of initiation of lipid-lowering drug treatment [adjusted estimates were 0.018 +/- 0.007 mmol/(L x % energy (%en) from SFA (P = 0.01) and 0.055 +/- 0.015 mmol/(L x 5 g butter) (P = 0.0003), respectively]. Increased consumption of (n-3) fatty acids and fish was independently related to modest increases in serum HDL-cholesterol [0.067 +/- 0.026 mmol/(L x %en from (n-3) fatty acids) (P = 0.01) and 0.010 +/- 0.004 mmol/(L x 20 g fish) (P = 0.02)] and decreases in log-transformed serum triglyceride concentrations [P = 0.02 for (n-3) fatty acids and P = 0.02 for fish intake]. Hence, 10-y changes in the intake of dietary fatty acids and their food sources appear to have contributed to concurrent improvements in the serum lipid profile of older Australians, independent of concomitantly initiated lipid-lowering drug treatment.