Search

Background: Sorghum is the fifth most consumed cereal grain but limiting in the indispensable amino acid lysine. Complementing sorghum with lentils can improve the quality of sorghum-based diets. However, knowledge of lysine bioavailability in sorghum is lacking.Objectives: The study objectives were to determine the bioavailability of lysine in sorghum and to assess the effect of complementation of sorghum and lentils in a mixed-meal format.Methods: We studied 5 healthy young men (≤30 years; BMI <25 kg/m2) in a repeated-measure design using the indicator amino acid oxidation (IAAO) method, with L-[1-13C] phenylalanine as the indicator. Each subject participated in 8 determinations in random order. On the reference diet, subjects received 4 amounts of L-lysine (5, 8, 12, and 15 mg. kg-1 . d-1) from a crystalline amino acid mixture patterned after egg protein. On the test diet, they received 3 levels of lysine (8.2, 12.5, and 15.7 mg. kg-1 . d-1) from sorghum, and on the complementation diet they received 1 level of lysine from a mixed meal of sorghum and lentils. The bioavailability of lysine in sorghum was estimated by comparing the IAAO response to the test diet with the IAAO response to the reference diet using the slope-ratio method. Effectiveness of complementation was assessed by comparing the IAAO response to the mixed meal to the IAAO response to the test protein.Results: The bioavailability of lysine from sorghum was 94%. Upon complementation with lentils, there was a decline in the oxidation of L-[1-13C] phenylalanine by 19% (P < 0.0495), reflecting an improvement in available lysine in the mixed meal due to increased lysine intake.Conclusions: Although the bioavailability of lysine in sorghum is high, its lysine content is limiting. Complementation with lentils in a 1:1 ratio is recommended to achieve the lysine requirement for adult men consuming a sorghum-based diet. This trial was registered at clinicaltrials.gov as NCT03411005. [ABSTRACT FROM AUTHOR]

Background: Accurate measurement of dietary intake is vital for providing nutrition interventions and understanding the complex role of diet in health. Traditional dietary assessment methods are very resource intensive and burdensome to participants. Technology may help mitigate these limitations and improve dietary data capture.Objective: Our objective was to evaluate the accuracy of a novel mobile application (PIQNIQ) in capturing dietary intake by self-report. Our secondary objective was to assess whether food capture using PIQNIQ was comparable with an interviewer-assisted 24-h recall (24HR).Methods: This study was a single-center randomized clinical trial enrolling 132 adults aged 18 to 65 y from the general population. Under a provided-food protocol with 3 menus designed to include a variety of foods, participants were randomly assigned to 1 of 3 food capture methods: simultaneous entry using PIQNIQ, photo-assisted recall using PIQNIQ, and 24HR. Primary outcomes were energy and nutrient content (calories, total fat, carbohydrates, protein, added sugars, calcium, dietary fiber, folate, iron, magnesium, potassium, saturated fat, sodium, and vitamins A, C, D, and E) captured by the 3 methods.Results: The majority of nutrients reported were within 30% of consumed intake in all 3 food capture methods (n = 129 completers). Reported intake was highly (>30%) overestimated for added sugars in both PIQNIQ groups and underestimated for calcium in the photo-assisted recall group only (P < 0.001 for all). However, in general, both PIQNIQ methods had similar levels of accuracy and were comparable to the 24HR except in their overestimation (>30%) of added sugars and total fat (P < 0.001 for both).Conclusions: Our results suggest that intuitive, technology-based methods of dietary data capture are well suited to modern users and, with proper execution, can provide data that are comparable to data obtained with traditional methods. This trial was registered at clinicaltrials.gov as NCT03578458. [ABSTRACT FROM AUTHOR]

Background: Inflammation, both acute and chronic, is associated with reductions in the synthesis of retinol-binding protein (RBP) and the concentration of retinol in plasma. Consequently, it is currently recommended that the retinol isotope dilution (RID) method not be used to estimate vitamin A total body stores (TBS) in subjects with inflammation.Objectives: To apply compartmental analysis to study the effects of inflammation on hepatic apo-RBP input, plasma retinol pool size, and RID-predicted TBS in theoretical subjects with known steady state values for these parameters.Methods: We selected 6 previously generated hypothetical subjects who ingested a dose of stable isotope-labeled vitamin A (day 0). Starting with each subject's published steady state model for retinol tracer kinetics, we developed a parallel model for unlabeled retinol and RBP that incorporated links between these entities and tied liver retinol secretion to RBP availability. Then we perturbed the steady state model by initiating chronic or acute inflammation on day 0 or acute inflammation on day 3 or 9 and simulating results for RBP, plasma retinol, and TBS.Results: Chronic inflammation led to substantial reductions in RID-predicted TBS for at least 2 weeks after tracer administration. In contrast, acute inflammation induced on day 0 or 3 resulted in less dramatic impacts on TBS (37% or 20% reduction, respectively, from steady state levels, with levels rebounding by 14 days). When inflammation was induced 9 days after administration of the tracer, the effects on predicted TBS were minimal. Overall, for acute inflammation initiated at 0, 3, or 9 days, accurate predictions of TBS were obtained by 2 weeks.Conclusions: Compartmental analysis can be applied in the novel way described here to study the influence of perturbations such as inflammation on predictions of vitamin A status using RID. Such an approach has potential value for studying other perturbations and different nutrients. [ABSTRACT FROM AUTHOR]

Background: Descriptive and quantitative information on β-carotene whole-body kinetics in humans is limited.Objectives: Our objective was to advance the development of a physiologically based, working hypothesis compartmental model describing the metabolism of β-carotene and β-carotene-derived retinol.Methods: We used model-based compartmental analysis (Simulation, Analysis and Modeling software) to analyze previously published data on plasma kinetics of [2H8]β-carotene, [2H4]β-carotene-derived retinol, and [2H8]retinyl acetate-derived retinol in healthy, older US adults (3 female, 2 male; 50-68 y); subjects were studied for 56 d after consuming doses of 11 μmol [2H8]β-carotene and, 3 d later, 9 μmol [2H8]retinyl acetate in oil.Results: We developed a complex model for labeled β-carotene and β-carotene-derived retinol, as well as preformed vitamin A, using simulations to augment observed data during model calibration. The model predicts that mean (range) β-carotene absorption (bioavailability) was 9.5% (5.2-14%) and bioefficacy was 7.3% (3.6-14%). Of the absorbed β-carotene, 41% (25-58%) was packaged intact in chylomicrons and the balance was converted to retinol, with 58% (42-75%) transported as retinyl esters in chylomicrons and 0-2% by retinol-binding protein. Most (95%) chylomicron β-carotene was cleared by the liver. Later data revealed differences in the metabolism of retinyl acetate- versus β-carotene-derived retinol; data required that both β-carotene and derived retinol be recycled from extrahepatic tissues (e.g. adipose) in HDL. Of total bioconversion [73% (47-99%)], 82% occurred in the intestine, 17% in the liver, and 0.83% in other tissues.Conclusions: Our model advances knowledge about whole-body β-carotene metabolism in healthy adults, including the kinetics of transport in all lipoprotein species, and suggests hypotheses to be tested in future studies, such as the possibility that retinol derived from hepatic conversion over a long period of time might contribute to plasma retinol homeostasis and total body vitamin A stores. [ABSTRACT FROM AUTHOR]

Background: Pearl millet is the chief source of energy in the diet in some developing regions, but has a limited amount of indispensable amino acid lysine. Complementation with pulses like lentils can improve the protein quality of millet diets, but the knowledge of lysine bioavailability (BA) in millet and lentils is lacking.Objectives: The study objectives were to determine the BA of lysine in millet and lentils separately and to assess the effect of complementation of millet and lentils in a mixed meal format.Methods: We studied 9 healthy young men (≤30 y; BMI <25) in a repeated-measure design using the indicator amino acid oxidation (IAAO) method, with L-[1-13C] phenylalanine as the indicator. Each subject completed 7 or 8 experiments in random order. On the reference diet, subjects received 4 graded levels of L-lysine (5, 8, 12, and 15 mg·kg-1.d-1) from a crystalline amino acid mixture patterned after egg protein; on the test diets, they received 3 levels of lysine (10, 12, and 15 mg·kg-1.d-1) from either steamed millet or stewed lentils; and on the complementation diet, they received 1 level of lysine from a mixed meal of steamed millet and stewed lentils. The BA of lysine and the effect of complementation were assessed by comparing the IAAO responses to the test diets and the complementation diet with the IAAO response to L-lysine intakes in the reference protein, using the slope ratio method.Results: The BA of lysine was 97% from millet and 80% from lentils. Complementation of steamed millet with stewed lentils decreased the oxidation of L-[1-13C] phenylalanine by 27% (P < 0.05), signifying improved quality of the combined millet and lentil protein.Conclusions: Lysine has high BA but is still limiting in steamed pearl millet. Complementation with lentils in a 2:1 ratio is recommended to meet the lysine and protein requirements for adult men consuming a millet-based diet. This trial was registered at clinicaltrials.gov as NCT03674736 and NCT03339167. [ABSTRACT FROM AUTHOR]

Background: Better methods are needed for determining vitamin A absorption efficiency in humans to support development of dietary recommendations and to improve the accuracy of predictions of vitamin A status.Objectives: We developed and evaluated a method for estimating vitamin A absorption efficiency based on compartmental modeling of theoretical data on postprandial plasma retinyl ester (RE) kinetics.Methods: We generated data on plasma RE and retinol kinetics (30 min to 8 h or 56 d, respectively) after oral administration of labeled vitamin A for 12 theoretical adults with a range of values assigned for vitamin A absorption (55-90%); we modeled all data to obtain best-fit values for absorption and other parameters using Simulation, Analysis, and Modeling software. We then modeled RE data only (16 or 10 samples), with or without added random error, and compared assigned to predicted absorption values. We also compared assigned values to areas under RE response curves (RE AUCs).Results: We confirmed that a unique value for vitamin A absorption cannot be identified by modeling plasma retinol tracer kinetics. However, when RE data were modeled, predicted vitamin A absorptions were within 1% of assigned values using data without error and within 12% when 5% error was included. When the sample number was reduced, predictions were still within 13% for 10 of the 12 subjects and within 23% overall. Assigned values for absorption were not correlated with RE AUC (P = 0.21).Conclusions: We describe a feasible and accurate method for determining vitamin A absorption efficiency that is based on compartmental modeling of plasma RE kinetic data collected for 8 h after a test meal. This approach can be used in a clinical setting after fasting subjects consume a fat-containing breakfast meal with a known amount of vitamin A or a stable isotope label. [ABSTRACT FROM AUTHOR]

Background: Chronically higher inflammation, which may partly result from diet and lifestyle, is implicated in risk for multiple chronic diseases. The dietary inflammatory index (DII) and empirical dietary inflammatory pattern (EDIP), developed to characterize dietary contributions to systemic inflammation, have several limitations. There are no scores to characterize contributions of lifestyle to inflammation.Objectives: To reflect dietary/lifestyle contributions to inflammation, we developed novel, inflammation biomarker panel-weighted, dietary (DIS) and lifestyle (LIS) inflammation scores in a subset (n = 639) of the Reasons for Geographic and Racial Differences in Stroke Study (REGARDS) cohort.Methods: We selected a priori 19 food groups and 4 lifestyle characteristics to comprise the DIS and LIS, respectively. We calculated the components' weights based on their strengths of association with an inflammation biomarker score [comprising high-sensitivity C-reactive protein (hsCRP), IL-6, IL-8, and IL-10] using multivariable linear regression. The sums of the weighted components constitute the scores, such that higher scores reflect, on balance, more proinflammatory exposures. We calculated the DIS, LIS, DII, and EDIP with cross-sectional data from the remaining REGARDS cohort (  n = 14,210 with hsCRP measurements) and 2 other study populations with hsCRP and/or an 8-component inflammation biomarker panel, and investigated their associations with circulating inflammation biomarker concentrations using multivariable logistic regression.Results: In REGARDS, those in the highest relative to the lowest DIS, LIS, DII, and EDIP quintiles had statistically significant 1.66-, 4.29-, 1.56-, and 1.32-fold higher odds of a high hsCRP concentration (>3 mg/dL), respectively (all P-trend < 0.001). Those in the highest relative to the lowest joint DIS/LIS quintile had a statistically significant 7.26-fold higher odds of a high hsCRP concentration. Similar findings were noted in the other 2 validation populations.Conclusion: Our results support that dietary and lifestyle exposures collectively contribute substantially to systemic inflammation, and support the use of our novel DIS and LIS. [ABSTRACT FROM AUTHOR]

Background: Sampling times and study duration impact estimates of kinetic parameters and variables including total body stores (TBS) and disposal rate (DR) when compartmental analysis is used to analyze vitamin A kinetic data.Objective: We hypothesized that inclusion of dietary intake (DI) of vitamin A as an additional input would improve confidence in predictions of TBS and DR when modeling results appear to indicate that studies are not long enough to accurately define the terminal slope of the plasma retinol isotope response curve.Methods: We reanalyzed previously published data on vitamin A kinetics monitored over 52 d in 7 US and 6 Chinese adults (means: 56 y, BMI 26.6 kg/m2, 38% males), adding an estimate for vitamin A intake [2.8 µmol/d (mean RDA)] as an input during application of the Simulation, Analysis and Modeling software.Results: Use of a model with 1 extravascular compartment (1 EV), as in the original analysis, resulted in predictions of vitamin A intake that were higher than physiologically reasonable; inclusion of intake data in a model with 2 extravascular compartments (2 EV DI) resulted in more realistic estimates of intake and DR. Specifically, predictions of DR by the 2 EV DI (versus 1 EV) model were 2.10 compared with 12.2 µmol/d (US) and 2.21 compared with 5.13 µmol/d (Chinese). Predictions of both TBS [2056 compared with 783 µmol (US) and 594 compared with 219 µmol (Chinese)] and days of vitamin A stores [981 compared with 64 d (US) and 269 compared with 43 d (Chinese)] were higher using the new approach.Conclusions: Inclusion of vitamin A intake as additional data input when modeling vitamin A kinetics can compensate for less-than-optimal study duration, providing more realistic predictions of vitamin A TBS and DR. This approach advances the application of compartmental analysis to the study of vitamin A and, potentially, other nutrients. [ABSTRACT FROM AUTHOR]

Background: Height is an indicator of nutritional status; linear growth faltering has recognized consequences for cognitive, emotional, and chronic disease risk. Although height is routinely studied in developing countries, less attention is given to height in the United States.Objective: The objective of this study was to identify longitudinal associations between childhood and adolescent beverage intakes, nutrient adequacy, or energy intake and height in a birth cohort.Methods: Data for participants through ages 2-17 y (n = 717; 353 males, 364 females) recruited at birth for the longitudinal Iowa Fluoride Study (IFS) were used in the current cohort analyses. Beverage intakes (n = 708) were collected by beverage-frequency questionnaires at 3- to 6-mo intervals, whereas nutrient data (n = 652) were obtained from 3-d food diaries completed at 3- to 6-mo intervals through age 8.5 y and from Block Kids' food-frequency questionnaires at 2-y intervals after age 8.5 y. Nutrient adequacy ratios were calculated with the use of age- and sex-specific Estimated Average Requirements. Height was measured at clinic visits when the participants were approximately ages 5, 9, 11, 13, 15, and 17 y. Linear mixed models were used to identify longitudinal associations between dietary variables and height. A baseline model that adjusted for changing growth patterns during adolescence was established. Dietary and potential confounding variables were added to this baseline model.Results: Milk intake adjusted for mean adequacy ratio, energy intake, and baseline socioeconomic status was associated with height; for each additional 8 ounces (236 mL) of milk consumed per day throughout childhood and adolescence, height increased, on average, by 0.39 cm (95% CI: 0.18, 0.60 cm; P < 0.001).Conclusions: IFS participants' height increased by 0.39 cm for each additional 8 ounces (236 mL) of milk consumed throughout childhood and adolescence. The clinical implications of the mild linear growth faltering observed in healthy youth are unknown. This trial was registered at www.clinicaltrials.gov as 199112665. [ABSTRACT FROM AUTHOR]

Background: A meal rich in saturated fatty acids induces a postprandial metabolic challenge. The type of dietary protein may modulate postprandial metabolism.Objective: We studied the effect of dietary protein type on postprandial changes in the metabolome after a high-fat meal.Methods: In a 3-period, crossover, postprandial study, 10 healthy overweight men with an elevated waist circumference (>94 cm) ingested high-fat meals made up of cream fat (70% of energy), sucrose (15% energy), and protein (15% energy) from either casein (CAS), whey protein (WHE), or α-lactalbumin-enriched whey protein (LAC). Urine collected immediately before and 2, 4, and 6 h after the meal was analyzed for metabolomics, a secondary outcome of the clinical study. We used mixed-effect models, partial least-square regression, and pathway enrichment analysis.Results: At 4 and 6 h after the meal, the postprandial metabolome was found to be fully discriminated according to protein type. We identified 17 metabolites that significantly explained the effect of protein type on postprandial metabolomic changes (protein-time interaction). Among this signature, acylcarnitines and other acylated metabolites related to fatty acid or amino acid oxidation were the main discriminant features. The difference in metabolic profiles was mainly explained by urinary acylcarnitines and some other acylated products (protein type, Ps < 0.0001), with a dramatically greater increase (100- to 1000-fold) after WHE, and to a lesser extent after LAC, as compared with CAS. Pathway enrichment analysis confirmed that the type of protein had modified fatty acid oxidation (P < 0.05).Conclusion: Taken together, our results indicate that, in healthy overweight men, the type of protein in a high-fat meal interplays with fatty acid oxidation with a differential accumulation of incomplete oxidation products. A high-fat meal containing WHE, but not CAS, resulted in this outpacing of the tricarboxylic acid cycle. This study was registered at clinicaltrials.gov as NCT00931151. [ABSTRACT FROM AUTHOR]

Background: Provitamin A carotenoids are an important source of dietary vitamin A for many populations. Thus, accurate and simple methods for estimating carotenoid bioefficacy are needed to evaluate the vitamin A value of test solutions and plant sources. β-Carotene bioefficacy is often estimated from the ratio of the areas under plasma isotope response curves after subjects ingest labeled β-carotene and a labeled retinyl acetate reference dose [isotope reference method (IRM)], but to our knowledge, the method has not yet been evaluated for accuracy.Objectives: Our objectives were to develop and test a physiologically based compartmental model that includes both absorptive and postabsorptive β-carotene bioconversion and to use the model to evaluate the accuracy of the IRM and a simple plasma retinol isotope ratio [(RIR), labeled β-carotene-derived retinol/labeled reference-dose-derived retinol in one plasma sample] for estimating relative bioefficacy.Methods: We used model-based compartmental analysis (Simulation, Analysis and Modeling software) to develop and apply a model that provided known values for β-carotene bioefficacy. Theoretical data for 10 subjects were generated by the model and used to determine bioefficacy by RIR and IRM; predictions were compared with known values. We also applied RIR and IRM to previously published data.Results: Plasma RIR accurately predicted β-carotene relative bioefficacy at 14 d or later. IRM also accurately predicted bioefficacy by 14 d, except that, when there was substantial postabsorptive bioconversion, IRM underestimated bioefficacy. Based on our model, 1-d predictions of relative bioefficacy include absorptive plus a portion of early postabsorptive conversion.Conclusion: The plasma RIR is a simple tracer method that accurately predicts β-carotene relative bioefficacy based on analysis of one blood sample obtained at ≥14 d after co-ingestion of labeled β-carotene and retinyl acetate. The method also provides information about the contributions of absorptive and postabsorptive conversion to total bioefficacy if an additional sample is taken at 1 d. [ABSTRACT FROM AUTHOR]

We discuss whether dietary vitamin A intake should be restricted or maintained at balance when retinol isotope dilution equations are applied to estimate an individual's vitamin A total body stores (TBS) after oral administration of a labeled dose of vitamin A. Although, at first glance, restriction makes sense as a way to prevent dilution of tracer in plasma, further investigation of the assumptions underlying the widely used isotope dilution equation presented by Olson's laboratory in 1989, as well as the compartmental modeling results presented in this article, indicate that, in fact, restriction leads to an incorrect prediction of TBS if steady state retinol isotope dilution equations are applied at the traditional time (21 d). Our results show that newly ingested vitamin A is a minor contributor to total plasma retinol turnover and that restriction of vitamin A intake leads to a higher plasma retinol specific activity than the value obtained when vitamin A input equals output (balance). When that higher specific activity is used in the traditional retinol isotope dilution equation, it results in a small but notable underestimation of vitamin A TBS. We conclude that, especially if blood is sampled at the traditional time, the most accurate results will be obtained when vitamin A balance is maintained. If sampling is done soon after dosing (e.g., 4 d), dietary intake has less effect on plasma retinol specific activity and thus on predictions of vitamin A status. Vitamin A status can also be estimated if intake is completely restricted and a different (non-steady state) equation is applied at an appropriate time after isotopic equilibrium has been reached. [ABSTRACT FROM AUTHOR]

Background: Zinc and copper have many physiologic functions and little or no functional storage capability, so persistent losses of either element present health concerns, especially during extended-duration space missions.Objectives: We evaluated the effects of short-term bed rest (BR), a spaceflight analog, on copper and zinc metabolism to better understand the role of these nutrients in human adaptation to (simulated) spaceflight. We also investigated the effect of artificial gravity on copper and zinc homeostasis.Methods: Zinc and copper balances were studied in 15 men [mean ± SD age: 29 ± 3 y; body mass index (in kg/m2): 26.4 ± 2.2] before, during, and after 21 d of head-down tilt BR, during which 8 of the participants were subjected to artificial gravity (AG) by centrifugation for 1 h/d. Control subjects were transferred onto the centrifuge but were not exposed to centrifugation. The study was conducted in a metabolic ward; all urine and feces were collected. Data were analyzed by 2-factor repeated-measures ANOVA.Results: Urinary zinc excretion values for control and AG groups were 33% and 14%, respectively, higher during BR than before BR, and fecal zinc excretion values for control and AG groups were 36% and 19%, respectively, higher during BR, resulting in 67% and 82% lower net zinc balances for controls and AG, respectively (both P < 0.01), despite lower nutrient intake during BR. Fecal copper values for control and AG groups were 40% and 33%, respectively, higher during BR than before BR (P < 0.01 for both). Urinary copper did not change during BR, but a 19% increase was observed after BR compared with before BR in the AG group (P < 0.05).Conclusions: The increased fecal excretion of copper and zinc by men during BR suggests that their absorption of these minerals from the diet was reduced, secondary to the release of minerals from bone and muscle. These findings highlight the importance of determining dietary requirements for astronauts on space missions and ensuring provision and intake of all nutrients. [ABSTRACT FROM AUTHOR]

Over the past 50 y, tryptophan has been ingested in amounts well in excess of its dietary requirement. This use is based on extensive findings that ingesting tryptophan increases brain tryptophan concentrations, which stimulates the synthesis and release of the neurotransmitter serotonin, from which it is derived. Such increases in serotonin function may improve mood and sleep. However, tryptophan ingestion has other effects, such as increasing serotonin production in the gut, increasing serotonin concentrations in blood, stimulating the production of the hormone melatonin (a tryptophan metabolite), stimulating tryptophan metabolism via the kynurenine pathway, and possibly stimulating the production of tryptophan metabolites in the gut microbiome. Several of the kynurenine metabolites have actions on excitatory glutamate receptors in the gut and brain and on cells of the immune system. In addition, metabolites of tryptophan produced by colonic bacteria are reported to cause adverse effects in some species. This review examines each of these tryptophan pathways to determine if any of the metabolites increase after tryptophan ingestion, and if so, whether effects are seen on target body functions. In this regard, recent research suggests that it may be useful to examine kynurenine pathway metabolites and some microbial tryptophan metabolites to determine whether supplemental tryptophan consumption increases their concentrations in the body and amplifies their actions. [ABSTRACT FROM AUTHOR]

Background: Retinol isotope dilution (RID) equations are used to determine vitamin A status and the efficacy of vitamin A intervention programs. Recent work related to RID methods has focused on modifying the "Olson equation" to improve the accuracy of predictions of vitamin A total body stores (TBS) in individual subjects.Objective: We investigated the hypothesis that short-term restriction of vitamin A intake would result in accurate RID prediction of vitamin A TBS in individuals.Methods: We applied model-based compartmental analysis to a 6-component model derived from published retinol kinetic studies on 12 individuals with a wide range of vitamin A stores and determined vitamin A TBS in the steady state. Then we simulated the impact of eliminating or strictly limiting vitamin A intake at the time of isotope administration, while maintaining plasma retinol homeostasis, on retinol specific activity in plasma (SAp; fraction of dose/μmol retinol) and stores, and we calculated TBS using the simplified RID equation TBS = 0.75 × 1/SAp, where the fractional absorption of tracer was set at 0.75 and SAp was simulated 5 d after dosing.Results: When vitamin A intake was zero or strictly limited (0.25 μmol/d), mean TBS predicted by the equation at 5 d after dose administration divided by TBS determined by using the model was 1.00 (range: 0.959-1.04) or 1.02 (range: 0.983 - 1.06), respectively.Conclusions: By eliminating or strictly limiting vitamin A input, isotopic equilibrium was reached by 5 d. At isotopic equilibrium, SAp is the same as that in the body's exchangeable vitamin A pools; under these conditions, SAp may be measured at any time from 5 d on and used to calculate TBS. [ABSTRACT FROM AUTHOR]

Background: Model-based compartmental analysis of data on plasma retinol kinetics after administration of labeled retinol provides unique information about whole-body vitamin A metabolism. If labeled β-carotene is coadministered, its bioefficacy relative to the retinol reference dose can also be estimated.Objectives: The objectives were to model plasma retinol kinetics after administration of labeled preformed vitamin A and provitamin A β-carotene and to determine relative β-carotene bioefficacy.Methods: We used the Simulation, Analysis and Modeling software (WinSAAM version 3.0.8; http://www.WinSAAM.org) to analyze previously collected data on plasma [13C10]- and [13C5]retinol kinetics for 14 d after oral administration of 1 mg [13C10]retinyl acetate and 2 mg [13C10]β-carotene in oil to 30 healthy young adults of European ancestry [13 men, 17 women; mean ± SD age: 24.5 ± 4.2 y; mean ± SD body weight: 65.2 ± 10 kg; mean ± SD body mass index (in kg/m2): 22.5 ± 1.9] with moderate vitamin A intakes.Results: A 6-component model provided the best fit to the data, including compartments for initial metabolism of vitamin A, plasma retinol, and extravascular vitamin A storage. The disposal rate was 6.7 ± 3.1 μmol/d, fractional catabolic rate was 6.0% ± 2.3%/d, and vitamin A stores were 123 ± 71 μmol. Relative β-carotene bioefficacy, based on the ratio of the areas under the fraction of dose curves calculated by WinSAAM, averaged 13.5% ± 6.02% (retinol activity equivalents = 7.7:1.0 μg). Interindividual variation in relative β-carotene bioefficacy was high (CV: 44%).Conclusions: Vitamin A kinetics in these young adults were best described by essentially the same model that had been previously developed by using data for older adults with higher vitamin A stores; differences in parameter values reflected differences in vitamin A status. Estimated β-carotene bioefficacy was relatively low but similar to previously reported estimates obtained by graphical methods. This trial was registered at the UK Clinical Research Network as UKCRN 7413. [ABSTRACT FROM AUTHOR]

Background: Retinol isotope dilution (RID) is used to determine vitamin A total body stores (TBS) after an oral dose of a vitamin A stable isotope. The generally accepted prediction equation proposed by Olson's group in 1989 (Furr et al. Am J Clin Nutr 1989;49:713-6) includes factors related to dose absorption and retention, isotope equilibration in plasma compared with stores, catabolism during the mixing period, and the optimal time for measuring plasma isotope enrichment.Objectives: The objectives were 1) to develop a modified RID equation and identify an earlier sampling time for predicting TBS and 2) to improve prediction in individuals as well as groups.Methods: To develop a modified RID equation, we used results of model-based compartmental analysis [the Simulation, Analysis and Modeling software (WinSAAM version 3.0.8; http://www.WinSAAM.org)] of plasma [13C10]retinol kinetic data from 32 previously studied, healthy young adults of European ancestry who had moderate vitamin A intakes and who ingested 2.95 μmol [13C10]retinyl acetate.Results: We examined the time dependence of factors in the prediction equation related to absorption/retention (Fa) and isotope equilibration (S) and determined that 4 or 5 d postdosing was the optimal sampling time. TBS calculated by the equation TBS = Fa x S x (1/SAp), where SAp is plasma retinol specific activity (fraction of dose/μmol), were highly correlated with model-predicted TBS (r = 0.95 and 0.96 for 4 and 5 d, respectively; P < 0.001); predictions for individuals were also highly correlated (Rs = 0.94 and 0.94; P < 0.001).Conclusion: The equation TBS ≈ 0.5 × (1/SAp) accurately predicted vitamin A TBS in this group of 32 healthy young adults and its individual members with the use of data from 1 blood sample taken 4 d after isotope administration. [ABSTRACT FROM AUTHOR]

Background: Postprandial lipemia is a risk factor for cardiovascular disease. The potential impacts of the type/nature of dietary protein on postprandial lipemia and associated dysregulations have been insufficiently investigated.Objective: We investigated the postprandial effect of including in a high-fat meal some milk protein fractions that markedly differ in their physicochemical properties and composition [either casein (CAS), whey protein (WHE), or α-lactalbumin-enriched whey protein (LAC)].Methods: The protein fractions were incorporated as 15% energy in a high-fat meal in a 3-period, crossover postprandial study of 10 healthy overweight men with an elevated waist circumference (>94 cm). We measured postprandial changes in plasma lipids, amino acids, glucose, and oxidative stress markers, vascular function (using pulse contour analysis), and low-grade inflammation (using plasma markers). We also characterized in vitro the meal structures, including the size of the fat globule, and possible changes during digestion.Results: The type of protein did not affect postprandial plasma glucose, amino acids, insulin, or nonesterified fatty acids, but, compared with WHE and LAC, which did not differ, CAS markedly reduced postprandial triglycerides (TGs), achieving a 22 ± 10% reduction in the 6-h area under the curve (P < 0.05). Similar trends were shown for plasma chylomicrons [apolipoprotein (apo)B-48; P < 0.05]. However, there were no significant differences between the meals regarding postprandial oxidative stress (plasma hydroperoxides and malondialdehyde), endothelial dysfunction (salbutamol-induced changes in pulse contour analysis), or low-grade inflammation. In vitro studies showed that when the pH of the meal decreased to stomach pH values, the reduction in the solubility of casein resulted in a phase separation between fat and protein, whereas the proteins in the other meals remained suspended with fat globules.Conclusion: In healthy overweight men, casein has specific physical interactions with fat that affect postprandial TGs, leading to the formation of fewer chylomicrons or an increase in chylomicron clearance. This trial was registered at clinicaltrials.gov as NCT00931151. [ABSTRACT FROM AUTHOR]

Background: Postprandial lipemia represents a risk factor for chronic diseases, including type 2 diabetes. Little is known about the effect of dietary fat on the plasma lipidome in the postprandial period. Objective: The objective of this study was to assess the effect of dairy fat and soy oil on circulating postprandial lipids in men. Methods: Men (40-60 y old, nonsmokers; n = 16) were randomly assigned in a crossover design to consume 2 breakfast meals of dairy-based or soy oil-based foods. The changes in the plasma lipidome during the 4-h postprandial period were analyzed with electrospray ionization tandem mass spectrometry and included 316 lipid species in 23 classes and subclasses, representing sphingolipids, phospholipids, glycerolipids, and sterols. Results: Nonparametric Friedman tests showed significant changes in multiple plasma lipid classes, subclasses, and species in the postprandial period after both dairy and soy meals. No difference was found in triglyceridemia after each meal. However, 6 endogenous lipid classes increased after dairy but decreased after soy (P < 0.05), including ether linked phospholipids and plasmalogens and sphingomyelin (not present in soy), dihexosylceramide, and GM3 ganglioside. Phosphatidylcholine and phosphatidylinositol were not affected by the soy meal but were significantly elevated after the dairy meal (8.3% and 16%, respectively; P < 0.05). Conclusions: The changes in postprandial plasma phospholipids in men relate to the diet composition and the relative size of the endogenous phospholipid pools. Despite similar lipemic responses as measured by changes in triglyceride concentrations, the differential responses to dairy and soy meals derived through lipidomic analysis of phospholipids suggest differences in the metabolism of soybean oil and dairy fat. The increased concentrations of plasmalogens, with potential antioxidant capacity, in the postprandial period after dairy but not soy meals may represent a further important difference in the response to these sources of fat. The trial was registered at www.anzctr.org.au as ACTRN12610000562077. [ABSTRACT FROM AUTHOR]

Background: Disrupting the physical structure of pulses by blending them or by using a digestive supplement (α-galactosidase) to reduce intestinal discomfort could potentially negate the previously observed bene?cial effects of whole pulses of lowering appetitive and glycemic responses because of more rapid digestion. Objective: We hypothesized that blended lentils, a-galactosidase, or both increase postprandial appetite and blood glucose responses vs. whole lentils. Methods:Me na n dw o m e n[n = 12; means ± SDs body mass index (kg/m²): 23.3 ± 3.1; aged 28 ± 10 y] consumed breakfast meals containing whole (W), blended (B), or no lentils [control (C)], each with 3 α-galactosidase or placebo capsules in a randomized, crossover, double-blind placebo-controlled trial. Between each test day there was a 3- to 5-d washout period. Results: Mixed-model ANOVA showed effects of meal on postprandial appetite and glucose (P = 0.0001-0.031). The B meal resulted in higher postprandial appetite ratings than did theWmeal but not the C meal for hunger, desire to eat, and prospective consumption (Δ = 0.4-0.5 points; P = 0.002-0.044). Postprandial glucose concentrationwas 4.5mg/dL lower for the Bmeal than for the C meal (P < 0.0001) but did not differ from the W meal. There were no main effects of a-galactosidase, but there were meal 3 α-galactosidase interaction effects, with a greater postprandial desire to eat and lower postprandial fullness with the B meal than with the 2 other meals in the placebo condition but not in the α-galactosidase condition. Conclusions: Blending lentils increased appetite (;6%), but not glycemic response, compared with whole lentils, whereas α-galactosidase did not. Both B andWmealsmay be consumed (with or without an α-galactosidase supplement) with little impact on appetite, without increasing glycemic response. This trial was registered at clinicaltrials.gov as NCT02110511. [ABSTRACT FROM AUTHOR]

The Hordaland Homocysteine Study (HHS) is a population-based study of more than 18,000 men and women in the county of Hordaland in Western Norway. The first investigation (HHS-I) took place in 1992-93, when the subjects were aged 40-67 y. In 1997-99, a follow-up study (HHS-II) of 7,053 subjects was carried out. In this large population, plasma levels of total homocysteine (tHcy) are associated with several physiologic and lifestyle factors and common diseases. Increasing age, male sex, smoking, coffee consumption, high blood pressure, unfavorable lipid profile, high creatinine, and the MTHFR 677C > T polymorphism are among the factors associated with increased tHcy levels; physical activity, moderate alcohol consumption, and a good folate or vitamin B-12 status are associated with lower tHcy levels. Subjects with raised tHcy levels have increased risk of cardiovascular morbidity, cardiovascular and noncardiovascular mortality, and are more likely to suffer from depression and from cognitive deficit (elderly). Among women, raised tHcy levels are associated with decreased bone mineral density and increased risk of osteoporosis. Women with raised tHcy levels also have an increased risk of having suffered from pregnancy complications and an adverse pregnancy outcome. Significant associations between tHcy and clinical outcomes are usually observed for tHcy levels > 15 micromol/L, but for most conditions, there is a continuous concentration-response relation with no apparent threshold concentration. Overall, the findings from HHS indicate that a raised tHcy level is associated with multiple clinical conditions, whereas a low tHcy level is associated with better physical and mental health. [ABSTRACT FROM AUTHOR]

A lignan complex rich in the plant lignan secoisolariciresinol diglucoside (SDG) was isolated from flaxseed. SDG is metabolized by the colonic microflora to the mammalian lignans enterodiol (END) and enterolactone (ENL), and was hypothesized to reduce plasma lipid concentrations and improve antioxidant capacity. The aim of this study was to investigate the effects of a lignan complex, providing 500 mg/d of SDG, on serum concentration and urinary excretion of ENL, plasma lipids, serum lipoprotein oxidation resistance, and markers of antioxidant capacity. Healthy postmenopausal women (n = 22) completed a randomized, double-blind, placebo-controlled, crossover study. Women consumed daily a low-fat muffin, with or without a lignan complex, for 6 wk, separated by a 6-wk washout period. Serum ENL concentration, urinary ENL excretion, plasma concentrations of total cholesterol (TC), LDL cholesterol (LDL-C), HDL cholesterol (HDL-C), triacylglycerol (TAG), serum lipoprotein oxidation lag time, plasma Trolox-equivalent antioxidant capacity (TEAC), and ferric reducing ability of plasma (FRAP) were measured at the beginning and end of each intervention period. ENL concentrations in serum (P < 0.001) and ENL urinary excretion (P < 0.001) were significantly higher after the lignan complex intervention period compared with placebo. Plasma concentrations of TC, LDL-C, HDL-C, TAG, lipoprotein oxidation lag time, TEAC and FRAP were not affected. Daily consumption for 6 wk of a low-fat muffin enriched with a lignan complex significantly increased serum ENL concentrations and urinary ENL excretion in healthy postmenopausal women, but had no effect on plasma lipid concentrations, serum lipoprotein oxidation resistance, or plasma antioxidant capacity. [ABSTRACT FROM AUTHOR]

In contrast to most expectations, we showed previously that dietary fructooligosaccharides (FOS) stimulate intestinal colonization and translocation of invasive Salmonella enteritidis in rats. Even before infection, FOS increased the cytotoxicity of fecal water, mucin excretion, and intestinal permeability. In the present study, we tested whether FOS has these effects in humans. A double-blind, placebo-controlled, crossover study of 2 × 2 wk, with a washout period of 2 wk, was performed with 34 healthy men. Each day, subjects consumed lemonade containing either 20 g FOS or placebo and the intestinal permeability marker chromium EDTA (CrEDTA). On the last 2 d of each supplement period, subjects scored their gastrointestinal complaints on a visual analog scale and collected feces and urine for 24 h. Fecal lactic acid was measured using a colorimetric enzymatic kit. The cytotoxicity of fecal water was determined with an in vitro bioassay, fecal mucins were quantified fluorimetrically, and intestinal permeability was determined by measuring urinary CrEDTA excretion. In agreement with our animal studies, FOS fermentation increased fecal wet weight, bifidobacteria, lactobacilli, and lactic acid. Consumption of FOS increased flatulence and intestinal bloating. In addition, FOS consumption doubled fecal mucin excretion, indicating mucosal irritation. However, FOS did not affect the cytotoxicity of fecal water and intestinal permeability. The FOS-induced increase in mucin excretion in our human study suggests mucosal irritation in humans, but the overall effects are more moderate than those in rats. [ABSTRACT FROM AUTHOR]

The precise role that isoflavones play in the health-related effects of soy foods, and their potential for adverse effects are controversial. This may be due in part to a lack of basic knowledge regarding their bioavailability and metabolism, particularly as it relates to the soy source. To date, there is little information concerning possible differences in the bioavailability of isoflavones derived from natural soy foods consumed at physiologically relevant intakes and whether age- or gender-related differences influence that bioavailability. In the current study of healthy adults [premenopausal (n = 21) and postmenopausal (n = 17) women and a group of men (n = 21)], we examined the effect of age, gender, and the food matrix on the bioavailability of isoflavones for both the aglycon and glucoside forms that are naturally present in 3 different soy foods, soy milk, textured vegetable protein, and tempeh. The study was designed as a random crossover trial so that all individuals received each of the 3 foods. The dose of isoflavones administered to each individual as a single bolus dose was 0.44 mg/kg body weight. Pharmacokinetic parameters were normalized to mg of each isoflavone ingested per kilogram body weight to account for differences in daidzein and genistein content between the diets. Serum isoflavone concentrations in all individuals and groups increased rapidly after the ingestion of each soy food; as expected, genistein concentrations exceeded daidzein concentrations in serum. In this small study, gender differences in peak concentrations of daidzein were observed, with higher levels attained in women. Consumption of tempeh (mainly isoflavone aglycon) resulted in higher serum peak levels of both daidzein (P < 0.001) and genistein (P < 0.01) and the associated area under the curve (P < 0.001 and P < 0.03, respectively) compared with textured vegetable protein (predominantly isoflavone glucosides). However, soy milk was absorbed faster and peak levels of isoflavones were attained earlier than with the other soy foods. Only 30% of the subjects were equol producers and no differences in equol production with age or gender were observed. [ABSTRACT FROM AUTHOR]

The health consequences of mild copper excess in humans are unknown. In a previous study, 2 mg of supplementation with up to 6 mg Cu/L in drinking water did not induce detectable changes. Here we assessed a copper supplement at the upper level of dietary recommendations for "healthy" adults. The study was a prospective controlled trial; participants (women and men, 18-50 y old), represented the upper and lower 5% of the ceruloplasmin distribution curve obtained from a community-based sample of 800 healthy adults (n = 41/ group, each ∼50% men). Individuals received a single daily dose of 10 mg Cu for 60 d. Before and after supplementation, blood [copper, ceru loplasmin protein, homocysteine, liver aminot ranferases, Cu-Zn -superoxide dismutase activity in erythrocytes (eSOD), and glutathione in peripheral mononuclear cells] and urine [copper excretion after a 5-h administration of a chelator 2,3-dimercapto-1 -propano-sodium sulfonate (DMPS)] analyses were performed. After 2 mo, liver enzyme activities remained below the clinical cutoff value used to diagnose liver dysfunction, but had increased significantly in both groups and genders. These increases were no longer present 12 mo after the copper loading period was completed. Glutathione in mononuclear cells (mmol/g of protein) also increased after the 2-mo copper loading in both groups and in both genders (P = 0.01). eSOD activity, serum homocysteine concentration, and urinary copper excretion 5 h after DMPS administration were not affected. We conclude that copper administered as described induced a transient, mild, but significant elevation of aminotrans-ferases. [ABSTRACT FROM AUTHOR]

D-Lactate is normally present in the blood of mammals at nanomolar concentrations due to methyl-glyoxal metabolism; millimolar D-lactate concentrations can arise due to excess gastrointestinal microbial production. Grain overload in ruminants, short-bowel syndrome in humans, and diarrhea in calves can all result in profound D-lactic acidemia, with remarkably similar neurological manifestations. In the past, D-lactate was thought to be excreted mainly in the urine, and metabolized slowly by the enzyme D-α-hydroxy acid dehydrogenase. More recent studies reported that mammals have a relatively high capacity for D-lactate metabolism and identified a putative mammalian u-lactate dehydrogenase. A growing body of literature is also emerging describing subclinical elevation of D-lactate as an indicator of sepsis and trauma. This article describes advances in the understanding of D-lactate metabolism, D-lactic acidosis in ruminants and humans, and subclinical elevation of D-lactate. [ABSTRACT FROM AUTHOR]

Choline is an essential nutrient for humans that is used to synthesize membrane phospholipids and the neurotransmitter acetylcholine. Betaine. a metabolite of choline, functions as a methyl-group donor in the conversion of homocysteine to methionine, and is important for renal function. Accurate analysis of choline intake was previously not possible because the choline content of most foods was not known. Using new and recently published data on the concentrations of choline in common foods, we measured the choline content of diets consumed ad libitum by healthy adult volunteers housed in a clinical research center and compared these with estimates of choline intake derived from 3-d food records kept by subjects immediately before study enrollment. Mean choline intake in this subject population met or slightly exceeded the current Adequate Intake (AI) of 7 mg/(kg · d) set by the Institute of Medicine. Men and women consumed similar amounts of choline per day (8.4 and. 6.7 mg/kg, respectively; P = 0.11). Choline intakes estimated from the 3-d food records were significantly lower than this (when expressed as mg/kg, or as total rag, but not when normalized to energy intake), suggesting underreporting of food intake. Intake of betaine, which may spare choline utilization as a methyl-group donor, was 5.3 mg/(kg · d) in men and 4.7 mg/(kg · d) in women. Intake of folate, vilamin B-12, and methionine + cysteine, were similar and sufficient in all subjects. The current recommended AI for choline seems to be a good approximation of the actual intake of this nutrient. [ABSTRACT FROM AUTHOR]

Defining optimal nutrient requirements is critical for ensuring crew health during long-duration space exploration missions. Data pertaining to such nutrient requirements are extremely limited. The primary goal of this study was to better understand nutritional changes that occur during long-duration space flight. We examined body composition, bone metabolism, hematology, general blood chemistry, and blood levels of selected vitamins and minerals in 11 astronauts before and after long-duration (128-195 d) space flight aboard the International Space Station. Dietary intake and limited biochemical measures were assessed during flight. Crew members consumed a mean of 80% of their recommended energy intake, and on landing day their body weight was less (P = 0.051) than before flight. Hematocrit, serum iron, ferritin saturation, and transferrin were decreased and serum ferritin was increased after flight (P < 0.05). The finding that other acute-phase proteins were unchanged after flight suggests that the changes in iron metabolism are not likely to be solely a result of an inflammatory response. Urinary 8-hydroxy-2'-deoxyguanosine concentration was greater and RBC superoxide dismutase was less after flight (P < 0.05), indicating increased oxidative damage. Despite vitamin D supplement use during flight, serum 25-hydroxycholecalciferol was decreased after flight (P < 0.01). Bone resorption was increased after flight, as indicated by several markers. Bone formation, assessed by several markers, did not consistently rise 1 d after landing. These data provide evidence that bone loss, compromised vitamin D status, and oxidative damage are among critical nutritional concerns for long-duration space travelers. [ABSTRACT FROM AUTHOR]

Dietary lipids are hypothesized to be an important factor for carotenoid bioavailability. However, most carotenoid-rich fruits and vegetables are low in lipids. The objective of this study was to assess whether the addition of avocado fruit as a lipid source enhances carotenoid absorption in humans. Healthy subjects (n = 11/study) were recruited for 2 crossover, postprandial studies. The effect of avocado addition (150 g) to salsa on lycopene and beta-carotene absorption was examined in Study 1, and the absorption of lutein, alpha-carotene, and beta-carotene from salad in Study 2. Furthermore, the effects of avocado dose (75 vs. 150 g containing 12 vs. 24 g lipid, respectively) and of lipid source (avocado fruit vs. avocado oil) on carotenoid absorption were examined in Study 2. Intact carotenoids were quantified in the plasma triacylglycerol-rich lipoprotein (TRL) fraction during the 9.5 h after consumption of the test meal and expressed as baseline-corrected area under the concentration-vs.-time curve (AUC). The addition of avocado to salsa enhanced lycopene and beta-carotene absorption (P < 0.003), resulting in 4.4 and 2.6 times the mean AUC after intake of avocado-free salsa, respectively. In Study 2, supplementing 150 g avocado or 24 g avocado oil to salad similarly enhanced alpha-carotene, beta-carotene, and lutein absorption (P < 0.01), resulting in 7.2, 15.3, and 5.1 times the mean AUC after intake of avocado-free salad, respectively (150 g avocado). Neither the avocado dose nor the lipid source affected carotenoid absorption. In conclusion, adding avocado fruit can significantly enhance carotenoid absorption from salad and salsa, which is attributed primarily to the lipids present in avocado. [ABSTRACT FROM AUTHOR]

In evaluating potential indicators of biotin status, we quantitated the expression of biotin-related genes in leukocytes from human blood of normal subjects before and after inducing marginal biotin deficiency. Biotin deficiency was induced experimentally by feeding an egg-white diet for 28 d. Gene expression was quantitated for the following biotin-related proteins: methylcrotonyl-CoA carboxylase chains A (MCCA) and B (MCCB); propionyl-CoA carboxylase chains A (PCCA) and B (PCCB); pyruvate carboxylase (PC); acetyl-CoA carboxylase isoforms A (ACCA) and B (ACCB); holocarboxylase synthetase (HCS); biotinidase; and 2 potential biotin transporters: sodium-dependent multivitamin transporter (SMVT) and solute carrier family 19 member 3 (SLC19A3). For 7 subjects who successfully completed the study, the abundance of the specific mRNAs was determined by quantitative real-time RT-PCR at d 0 and 28. At d 28, SLC19A3 expression had decreased to 33% of d 0 (P < 0.02 by two-tailed, paired t test). Expression of MCCA, PCCA, PC, ACCA, ACCB, HCS, biotinidase, and SMVT decreased to approximately 80% of d 0 (P < 0.05). Expression of the MCCB and PCCB chains that do not carry the biotin-binding motif did not change significantly; we speculate that expression of the biotin-binding chains of biotin-dependent carboxylases is more responsive to biotin status changes. These data provide evidence that expression of SLC19A3 is a relatively sensitive indicator of marginal biotin deficiency. [ABSTRACT FROM AUTHOR]

Young and Nestle suggested that the increase in the portion size of food products evident in the United States during the past 20 years may be responsible for the epidemic of overweight and obesity. They based their conclusion on statistical correlations. The purpose of the present study was to provide experimental evidence to support their proposal. Cornell undergraduate students were given access to a buffet lunch on Monday, Wednesday, and Friday and were told this was a test of flavor enhancers. They were instructed to eat as much or as little as they wanted. On the same days of the following week, the subjects were divided into 3 groups. Each group was served either 100%, 125%, or 150% of the amount of food they had consumed the previous week. When larger amounts were served, significantly greater amounts of food were consumed. Each of the 4 foods that comprised the meal (soup, pasta, breadsticks, ice cream) increased significantly in proportion to the portion size. The data clearly support the hypothesis proposed by Young and Nestle and support the powerful role that environment plays in determining energy intake and potential increases in body weight. [ABSTRACT FROM AUTHOR]

Previous studies indicated that physical characteristics of food influence satiety, but the relative importance of the oral, gastric, and intestinal behaviors of the food is unclear. The aim of this study was to investigate the satiating effects of 2 types of alginates, which gel weakly or strongly on exposure to acid, compared with guar gum whose viscosity is unaffected by acid. Subjects (n = 12; 3 men, 9 women) ingested a 325-mL sweetened, milk-based meal replacer beverage on 4 separate occasions, either alone as a control or including 1% by weight alginate or guar gum. Intragastric gelling, gastric emptying, and meal dilution were assessed by serial MRI while satiety was recorded for 4 h. MR images showed that all of the meals became heterogeneous in the stomach except for guar, which remained homogeneous. The alginate meals formed lumps in the stomach, with the strong-gelling alginate producing the largest volume. Although gastric emptying was similar for all 4 meals, the sense of fullness at the same gastric volume was significantly greater for all 3 viscous meals than for the control. Compared with the control meal, the strong-gelling alginate (P = 0.031) and guar (P = 0.041) meals increased fullness at 115 min, and the strong-gelling alginate decreased hunger by the 115-min (P = 0.041) and 240-min (P = 0.041) time points. Agents that gel on contact with acid may be useful additions to weight-reducing diets. We hypothesize that this effect is due to distension in the gastric antrum and/or altered transport of nutrients to the small intestine in the lumps. [ABSTRACT FROM AUTHOR]

Population-based studies report differences in folate status indicators among Mexican American (MA), African American (AA) and Caucasian (CA) women. It is unclear, however, whether these differences are due to variations in dietary folate intake. The present study was designed to investigate the influence of ethnicity/race on folate status parameters in MA, AA, and CA women (18-45 y; n = 14 in each group) under conditions of strictly controlled folate intake. In addition, the adequacy of the 1998 folate U.S. recommended dietary allowance (RDA), 400 micro g/d as dietary folate equivalents (DFE), for non-Caucasian women was assessed. Subjects (n = 42) with the methylenetetrahydrofolate reductase 677 CC genotype consumed a low-folate diet (135 micro g DFE/d) for 7 wk followed by repletion with 400 (7 MA, 7 AA, 7 CA) or 800 micro g DFE/d (7 MA, 7 AA, 7 CA) for 7 wk. AA women had lower (P

A bioassay for zinc status in humans has been sought due to the importance of zinc, an essential trace metal, for many divergent functions in the human body; however, a sensitive bioassay for zinc status in humans is lacking. To address this issue, we established gene expression profiles of human lymphoblastoid cells treated with 0 or 30 micro mol/L ZnSO(4) using microarray technology. A limited number of genes were responsive to 30 micro mol/L zinc based on the analysis of Affymetrix human genome U133A GeneChips. We also examined the gene expression patterns of zinc transporters in human lymphoblastoid cells using quantitative RT-PCR analysis. ZNT1 was upregulated in lymphoblastoid cells, whereas ZIP1 was downregulated in response to the increased zinc concentrations in the culture media. To evaluate the potential applications of using both zinc transporter genes as biomarkers of zinc status, we measured the expression levels of ZIP1 and ZNT1 in the peripheral leukocytes collected from 2 different age groups of Korean women. After administration of a zinc supplement (22 mg zinc gluconate/d for 27 d), ZIP1 expression decreased by 17% (P < 0.01) and 21% (P < 0.05) in the peripheral leukocytes collected from 15 young (20-25 y) and 10 elderly (64-75 y) subjects, respectively. ZNT1 expression was not affected by taking the zinc supplement. These data suggest a potential application of ZIP1 as a biomarker of zinc status in humans. [ABSTRACT FROM AUTHOR]

ABSTRACT When free phytosterols are adequately heated and then cooled in fat, they recrystallize and are rendered bioavailable for blocking cholesterol absorption. To extend the application of phytosterols to fried foods, the activity of these modified crystals was assessed in 2 experiments with 26 male gerbils fed purified diets containing 0.15 g/100 g cholesterol with or without 0.75 g/100 g free phytosterols. The heat-modified soybean sterols were added directly to the diet (Expt. 1) or as phytosterol-enriched potato chips (Expt. 2). In the gerbil experiments, only the diet containing phytosterols significantly reduced plasma cholesterol (35-48%) and the total cholesterol/HDL cholesterol (HDL-C) ratio (40%), as well as hepatic cholesterol esters (80%). In a subsequent human study, subjects (n = 7) consumed two 28-g servings of tortilla chips fried in oil with or without phytosterols that provided 0 or 1.5 g/d for 4-wk periods in a crossover design (Expt. 3). During consumption of the phytosterolenriched chips, significant reductions in plasma cholesterol (10%) and LDL cholesterol (15%) were achieved without affecting HDL-C. This novel means of delivering free phytosterols proved to be both functionally efficient and effective. [ABSTRACT FROM AUTHOR]

ABSTRACT Soy proteins have been shown to result in lower postprandial nitrogen retention than milk proteins, Milk protein Soy protein Milk group Soy group Milk group Soy group Milk group Soy group Milk group Soy group N]-labeled milk protein nitrogen is influenced by diet compo-. [Extracted from the article]

Of the dried culinary herbs tested, oregano, sage, peppermint, garden thyme, lemon balm, clove, Herbs are most often defined as any part of a plant that is Tansy is a wild herb that grows in Norway. Herb varieties collected in the fall contained higher values Herbs may therefore make a relevant contribution (1 mmol). [Extracted from the article]

In addition to pelargonidin-3-glucoside, five anthocyanin metabolites were identified in urine: three Tion of strawberry anthocyanin metabolites corresponded to 1.80 0.29% (mean SEM, n 6) of pelargonidin- Glucuro- and sulfo-conjugated in humans and that the main metabolite of strawberry anthocyanins in human urine Urinary excretion of anthocyanin metabolites in humans after consumption of 200 g strawberries. [Extracted from the article]

In mammals, biotin serves as a coenzyme for carboxylases such as propionyl-CoA carboxylase. The expression of genes encoding interleukin-2 (IL-2) and IL-2 receptor (IL-2R)gamma also depends on biotin. Biotin metabolites are structurally similar to biotin, and their concentrations in tissues are quantitatively important. Here, the hypothesis was tested that biotin metabolites can mimic the effects of biotin on gene expression and thus have biotin-like activities. A human T-cell line (Jurkat cells) was used to model effects of biotin and synthetic metabolites (diaminobiotin and desthiobiotin) on the expression of genes encoding IL-2 and IL-2Rgamma. Cells were cultured in biotin-deficient medium (0.025 nmol/L biotin) for 35 d; controls were cultured in medium containing 10 nmol/L biotin. The biotin-deficient medium was supplemented with 10 nmol/L of diaminobiotin, desthiobiotin, biotin or no biotin 24 h before gene expression analyses. Transcriptional activities of genes encoding IL-2 and IL-2Rgamma were increased up to 43% in cells supplemented with diaminobiotin, desthiobiotin or biotin compared with biotin-deficient cells, as judged by luciferase activities after transfection with reporter-gene constructs. These findings are consistent with the hypothesis that diaminobiotin and desthiobiotin mimic the effects of biotin on gene expression and thus have biotin-like activities. Supplementation of cells with diaminobiotin and desthiobiotin did not affect abundances of holocarboxylases and activities of propionyl-CoA carboxylase, suggesting that effects of synthetic biotin metabolites on gene expression are not mediated by carboxylase-dependent pathways. It is not known whether naturally occurring biotin metabolites also have biotin-like activities. [ABSTRACT FROM AUTHOR]

The purpose of this study was to determine a cut-off value of the molar ratio of retinol-binding protein to transthyretin (RBP:TTR) to indicate marginal vitamin A (VA) deficiency. Plasma RBP and TTR were measured by radial immunodiffusion in two groups of patients, i.e., surgical patients with known hepatic VA stores, and a cohort of children residing in a malaria-endemic area of Papua New Guinea who had received placebo or 210 micro mol of VA every 3 mo for 9 mo. A RBP:TTR ratio < or =0.36 selectively detected five of seven patients (71% sensitivity) with hepatic VA stores < or =69.9 nmol/g of tissue (i.e., < or =20 micro g/g), indicative of marginal VA deficiency. Using this cut-off value, 28% (n = 245) of children from Papua New Guinea had marginal VA deficiency before supplementation. After 7 mo, a low ratio persisted in 29% (n = 92) of placebo-treated children but in only 11% (n = 83) of those receiving VA supplements (chi(2), P < 0.01). At the end of the study, 13 mo after initiation or 4 mo after the last dose of VA, the percentage of children with a low ratio was still lower (chi(2), P < 0.02) in the VA group, 42.5% (n = 113) than in the placebo group, 58.6% (n = 118). These results demonstrate that a cut-off value < or =0.36 is indicative of marginal VA deficiency and can be used as an indirect method of VA assessment. [ABSTRACT FROM AUTHOR]

Age-related macular degeneration (ARMD) is inversely associated with the accumulation of lutein + zeaxanthin in the macula, but higher lutein intakes are inconsistently related to reduced risk of ARMD in epidemiologic studies. Resolution of efficacy awaits clinical trials designed with knowledge of lutein supplement pharmacokinetics. Lutein bioavailability was determined for lutein diester and unesterified lutein formulations as they might be incorporated into dietary supplements. Healthy subjects (n = 18) consumed a single dose of each formulation (either 0.5 or 0.67 micro mol lutein/kg body, 10 and 8 subjects, respectively) in random order, and the appearance of free lutein + zeaxanthin was measured in serum from 0 to 408 h. Areas under the serum concentration x time curves (AUC), as a measure of bioavailability, were independent of gender, body mass index and lutein dose. The lutein diester formulation was 61.6% more bioavailable than the unesterified lutein formulation with higher mean AUC, maximum serum concentration and ascending slope (P < 0.05). The AUC was greater in 14 of 18 subjects when they consumed the lutein diester formulation. Comparison with data from previous studies suggested that dissolution was a greater limitation to bioavailability than lutein ester hydrolysis because an oil-solubilized unesterified lutein preparation, given at 0.5 micro mol/kg body, resulted in greater mean peak concentrations and AUC compared with either the unesterified or lutein diester formulations used in our study. In conclusion, the lutein diester formulation poses no impediment to lutein bioavailability at the doses tested, but formulation dissolution is an important factor in lutein bioavailability and should be evaluated before a supplement and dose are selected for use in clinical trials. [ABSTRACT FROM AUTHOR]

Flavonoids and related polyphenolics with antioxidant and anti-inflammatory activities may play a role in the prevention of cardiovascular disease by decreasing oxidative stress and inflammation. We wished to determine the effects of cocoa extract supplementation on markers of oxidative stress and inflammation. Healthy subjects (n = 25) were studied at baseline, after cocoa supplementation (36.9 g of dark chocolate bar and 30.95 g of cocoa powder drink) for 6 wk and after a 6-wk washout period. Fasting blood and early morning urine were collected at the three time points. Two indices of flavonoid intake, total phenols and oxygen radical absorbance capacity of plasma, were measured after an overnight fast. Neither was affected by supplementation. Measures of oxidative stress included copper-catalyzed LDL oxidation kinetics and urinary F(2) isoprostanes. LDL oxidizability was lower after chocolate supplementation as evidenced by a longer lag time (P < 0.05) of conjugated diene formation (101.0 +/- 20.7 min) compared with baseline (91.3 +/- 18.0 min) and washout (96.4 +/- 7.5 min) phases. There was no effect of chocolate on urinary F(2) isoprostane levels or on markers of inflammation including the whole-blood cytokines, interleukin-1 beta, interleukin-6 and tumor necrosis factor-alpha, high sensitivity C-reactive protein and P-selectin. In conclusion, cocoa products supplementation in humans affects LDL oxidizability, but not urinary F(2) isoprostanes or markers of inflammation. [ABSTRACT FROM AUTHOR]

Oral exposure to dietary fat (through modified sham feeding, which entails mastication and expectoration of foods) augments the postprandial triacylglycerol (TAG) concentration, in part, though augmented lipid absorption. This study was designed to characterize early events in this process. At 2200 h, 25 healthy adults (13 men, 12 women) consumed 80 g of almonds (high oleic acid content) and fasted until approximately 0700 h. After placement of a catheter in a hand vein and 4 blood draws at 10-min intervals, 50 1-g safflower oil (high linoleic acid content) capsules were consumed. After another blood draw, modified sham feeding was initiated with a cracker only or cracker with cream cheese in random order with 1 wk between trials. Oral exposures occurred at 5-min intervals for 60 min then at 15-min intervals from min 60 to 120. Additional blood draws occurred at 2, 4, 6, 8, 10, 12, 14, 30, 60, 120, 240, 360 and 480 min. Oral stimulation, especially by fat, prompted the rapid (mean approximately 23 min) release of lipid stored from the previous meal (almonds) in all participants. This resulted in multimodal postprandial triacylglycerol (TAG) peaks generally occurring at 0-30 min, 60-120 min and 240-480 min after loading and initiation of oral stimulation. TAG magnitudes during these times were correlated (r = 0.40-0.89, P < 0.001-P = 0.053). It is proposed that the sensory-enhanced release of lipid from the residual pool initiates an early TAG rise, which augments the peak attributable to absorption of meal lipid; this in turn supplements a later peak associated with release of endogenously synthesized TAG because lipid from all three sources competed for a common clearance mechanism. If substantiated, additional understanding of the behavioral factors (e.g., eating patterns) that initiate this cascade will be warranted. [ABSTRACT FROM AUTHOR]

The goal of this study was to investigate the effect of the dietary fat composition on LDL peak particle diameter. Therefore, we measured LDL size by gradient gel electrophoresis in 56 (30 men, 26 women) healthy participants in a controlled dietary study. First, all participants received a baseline diet rich in saturated fat for 2 wk; they were then randomly assigned to one of three dietary treatments, which contained refined olive oil [rich in monounsaturated fatty acids (MUFA), n = 18], rapeseed oil [rich in MUFA and (n-3)-polyunsaturated fatty acids (PUFA), n = 18], or sunflower oil [rich in (n-6)-PUFA, n = 20] as the principal source of fat for 4 wk. Repeated-measures ANOVA revealed a small, but significant reduction in LDL size during the oil diet phase (-0.36 nm, P = 0.012), which did not differ significantly among the three groups (P = 0.384). Furthermore, affiliation with one of the three diet groups did not contribute significantly to the observed variation in LDL size (P = 0.690). In conclusion, our data indicate that dietary unsaturated fat similarly reduces LDL size relative to saturated fat. However, the small magnitude of this reduction also suggests that the composition of dietary fat is not a major factor affecting LDL size. [ABSTRACT FROM AUTHOR]

Soy contains the isoflavone phytoestrogens, genistein and daidzein. These isoflavones are partial estrogen agonists in cell and animal models, but effects from dietary soy in humans are unclear. Experiments were conducted in pre- and postmenopausal women to examine whether dietary isoflavones from soy behave as estrogen agonists, antagonists or have no effect on the estrogen-sensitive pituitary. Pituitary sensitivity to gonadotropin-releasing hormone (GnRH), an estrogen-sensitive endpoint, was measured during GnRH challenge tests administered before, during and after dietary soy consumption. The response to an isoflavone-rich soy food diet was examined in five premenopausal and seven postmenopausal women using transdermal estrogen replacement therapy. Estrogen agonists suppress gonadotropin concentrations and enhance GnRH priming (enhanced gonadotropin secretion in response to repeated doses of GnRH), whereas antagonists elevate gonadotropin concentrations and have no effect on GnRH priming. Each subject consumed 50 g textured soy protein containing 60 mg total isoflavones daily for 10-14 d. Baseline estradiol concentrations were consistent among study periods. In both pre- and postmenopausal women, soy consumption did not affect mean baseline or peak luteinizing hormone (LH) concentrations, indicating a lack of estrogen-like effect at the level of the pituitary. However, in postmenopausal subjects, mean LH secretion decreased after discontinuing soy, suggesting a residual estrogenic effect. In one premenopausal woman, enhanced LH secretion was observed after soy treatment, suggesting there may be subpopulations of women who are highly sensitive to isoflavones. [ABSTRACT FROM AUTHOR]

Epidemiologic and clinical studies have shown that nut consumption is associated with favorable plasma lipid profiles and reduced cardiovascular risk. These effects may result from their high monounsaturated fat (MUFA) content but nuts contain constituents other than fatty acids that might be cardioprotective. We conducted a study to compare the effects of whole-almond vs. almond oil consumption on plasma lipids and LDL oxidation in healthy men and women. Using a randomized crossover trial design, 22 normolipemic men and women replaced half of their habitual fat (approximately 14% of approximately 29% energy) with either whole almonds (WA) or almond oil (AO) for 6-wk periods. Compliance was ascertained by monitoring dietary intake via biweekly 5-d food records, return of empty almond product packages and weekly meetings with a registered dietitian. Fat replacement with either WA and AO resulted in a 54% increase in percentage of energy as MUFA with declines in both saturated fat and cholesterol intake and no significant changes in total energy, total or polyunsaturated fat intake. The effects of WA and AO on plasma lipids did not differ compared with baseline; plasma triglyceride, total and LDL cholesterol significantly decreased, 14, 4 and 6% respectively, whereas HDL cholesterol increased 6%. Neither treatment affected in vitro LDL oxidizability. We conclude that WA and AO do not differ in their beneficial effects on the plasma lipid variables measured and that this suggests that the favorable effect of almonds is mediated by components in the oil fraction of these nuts. [ABSTRACT FROM AUTHOR]

The effects of long-term supplementation with pharmacologic doses of zinc oxide on serum levels of zinc, lipids and hematocrit have not been studied systematically to date. Eleven Clinical Centers enrolled 4757 participants from 1992 to 1998 as part of the Age-Related Eye Disease Study (AREDS). Of these, 3640 participants, aged 55-80 y, who had early-to-late age-related macular degeneration (AMD) were randomly assigned to daily supplementation with or without 80 mg of zinc as zinc oxide plus 2 mg of copper as cupric oxide to study the effects of zinc supplementation on the progression to late AMD. This paper reports on the effect of a 5-y supplementation with zinc oxide and cupric oxide on serum zinc, copper, lipids, and hematocrit for 717 participants from three clinical centers. At the 5-y exam, the median increase in serum zinc levels for participants assigned to zinc formulations was 17% compared with a 2% increase for participants not assigned to zinc (P < 0.001). The differential effect on serum zinc was observed at 1 y and remained fairly constant over the 5-y period. After 5 y, no significant differences in changes in serum hematocrit, copper or lipids were found between participants assigned to formulations containing zinc and copper, and those assigned to formulations without zinc and copper. Estimates from a modified Block Food-Frequency Questionnaire suggest the AREDS population at baseline had a zinc intake from diet similar to that of the general population. [ABSTRACT FROM AUTHOR]

The U.S. Department of Agriculture 1994-1996 Continuing Survey of Food Intakes by Individuals was used to estimate the intake of naturally occurring inulin and oligofructose by the U.S. population. Two nonconsecutive 24-h dietary recalls from >15,000 Americans of all ages were conducted, and a special database of inulin and oligofructose was developed specifically for the analyses. American diets provided on average 2.6 g of inulin and 2.5 g of oligofructose. Intakes varied by gender and age, ranging from 1.3 g for young children to 3.5 g for teenage boys and adult males. When standardized for amount of food consumed, the intakes showed little difference across gender and age. Significant differences in intake of these components were seen between categories within region of the country, season, income, and race and origin; however, the actual differences were relatively small. Major food sources of naturally occurring inulin and oligofructose in American diets were wheat, which provided about 70% of these components, and onions, which provided about 25% of these components. The estimation of the presence of inulin and oligofructose in the diets of Americans has not been published to date. [ABSTRACT FROM AUTHOR]

The most recent survey effort to determine the extent of food insecurity and hunger in the United States, the Food Security Supplement, included a series of questions to assess this complex phenomenon. The primary measure developed from this Food Security Supplement was based on measurement concepts, methods and items from two previously developed measures. This paper presents the evidence available that questionnaire-based measures, in particular the national food security measure, provide valid measurement of food insecurity and hunger for population and individual uses. The paper discusses basic ideas about measurement and criteria for establishing validity of measures and then uses these criteria to structure an examination of the research results available to establish the validity of food security measures. The results show that the construction of the national food security measure is well grounded in our understanding of food insecurity and hunger, its performance is consistent with that understanding, it is precise within usual performance standards, dependable, accurate at both group and individual levels within reasonable performance standards, and its accuracy is attributable to the well-grounded understanding. These results provide strong evidence that the Food Security Supplement provides valid measurement of food insecurity and hunger for population and individual uses. Further validation research is required for subgroups of the population, not yet studied for validation purposes, to establish validity for monitoring population changes in prevalence and to develop and validate robust and contextually sensitive measures in a variety of countries that reflect how people experience and think about food insecurity and hunger. [ABSTRACT FROM AUTHOR]

In previous studies, the bioavailability of biotin in humans was estimated from the recovery of biotin in urine; urinary biotin was measured by microbial growth assays or assays of avidin-binding activity. These assays underestimate concentrations of biotin metabolites, which originate from beta-oxidation, sulfur oxidation or a combination. We have developed an HPLC/avidin-binding assay that is specific for biotin and its metabolites. With the use of the HPLC/avidin-binding assay, TLC and derivatization with p-dimethylaminocinnamaldehyde, we have identified and quantitated biotin and metabolites in urine from six healthy adults. Of that total, biotin accounted for 32+/-12%, bisnorbiotin for 52+/-15%, bisnorbiotin methyl ketone for 7.9+/-5.8%, biotin-d,l-sulfoxide for 4.0+/-3.2% and biotin sulfone for 3.6+/-1.9%. After intravenous administration of 18.4 micromol of biotin, the urinary excretion of biotin metabolites increased 21-130 times above baseline values. Because the biliary excretion of biotin is quantitatively minor (1.9+/-0.2% of an intravenous [14C]biotin dose in rats), intravenously administered biotin is not exposed to intestinal microorganisms. Thus we conclude that biotin metabolites in human urine originate from biotin catabolism in human tissues rather than biotin catabolism by intestinal microorganisms. With the use of the HPLC/avidin-binding assay, we estimated the bioavailability of biotin in adults from the urinary excretion of biotin and metabolites after ingestion of 2.1, 8.2 and 81.9 micromol of biotin. These data provide evidence that biotin is nearly completely absorbed. [ABSTRACT FROM AUTHOR]