61 research outputs found

    Phytate degradation determines the effect of industrial processing and home cooking on iron absorption from cereal-based foods

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    The aim of the present study was to compare Fe absorption from industrially-manufactured and home-cooked cereal foods. Fe absorption was measured using the radiolabelled Fe extrinsic tag technique in thirty-nine adult human subjects from cereal porridges manufactured by extrusion cooking or roller-drying, and from the same cereal flours after home cooking to produce pancakes, chappattis or bread. One series of cereal porridges was amylase-treated in addition before roller-drying. Fe absorption was relatively low from all products, ranging from 1·8-5·5% for rice, 2·5-3·5% for maize, 4·9-13·6 % for low-extraction wheat, and <1% for high-extraction wheat foods. The phytic acid content remained high after drying of the cereal porridges being about 1·20, 1·70, 3·20, 3·30 mg/g in low-extraction wheat, rice, high-extraction wheat and maize products respectively, and could explain the low Fe absorption. There were little or no differences in Fe absorption between the extruded and roller-dried cereals, although amylase pre-treatment increased Fe absorption from the roller-dried rice cereal 3-fold. This was not due to phytate degradation but possibly because of the more liquid nature of the cereal meal as fed. There were similarly few or no differences in Fe absorption between the industrially-processed cereals and home-cooked cereals made into pancakes or chappattis. Bread-making, however, degraded phytic acid to zero in the low-extraction wheat flour and Fe absorption increased to 13·6%, the greatest from all cereal foods tested. It is concluded that Fe absorption from extruded, roller-dried or home-cooked cereal foods is similarly low and that only those cooking procedures such as bread-making, which extensively degrades phytic acid, or amylase pre-treatment, which substantially liquifies cereal porridges, improve Fe absorptio

    An evaluation of EDTA compounds for iron fortification of cereal-based foods

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    Fe absorption was measured in adult human subjects consuming different cereal foods fortified with radiolabelled FeSO4, ferrous fumarate or NaFeEDTA, or with radiolabelled FeSO4 or ferric pyrophosphate in combination with different concentrations of Na2EDTA. Mean Fe absorption from wheat, wheat-soyabean and quinoa (Chenopodium quinoa) infant cereals fortified with FeSO4 or ferrous fumarate ranged from 0·6 to 2·2 %. For each infant cereal, mean Fe absorption from ferrous fumarate was similar to that from FeSO4 (absorption ratio 0·91-1·28). Mean Fe absorption from FeSO4-fortified bread rolls was 1·0 % when made from high-extraction wheat flour and 5·7 % when made from low-extraction wheat flour. Fe absorption from infant cereals and bread rolls fortified with NaFeEDTA was 1·9-3·9 times greater than when the same product was fortified with FeSO4. Both high phytate content and consumption of tea decreased Fe absorption from the NaFeEDTA-fortified rolls. When Na2EDTA up to a 1:1 molar ratio (EDTA:Fe) was added to FeSO4-fortified wheat cereal and wheat-soyabean cereal mean Fe absorption from the wheat cereal increased from 1·0 % to a maximum of 5·7 % at a molar ratio of 0·67:1, and from the wheat-soyabean cereal from 0·7 % to a maximum of 2·9 % at a molar ratio of 1:1. Adding Na2EDTA to ferric pyrophosphate-fortified wheat cereal did not significantly increase absorption (P>0·05). We conclude that Fe absorption is higher from cereal foods fortified with NaFeEDTA than when fortified with FeSO4 or ferrous fumarate, and that Na2EDTA can be added to cereal foods to enhance absorption of soluble Fe-fortification compounds such as FeSO

    Ferrous fumarate fortification of a chocolate drink powder

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    An evaluation was made into the usefulness of ferrous fumarate as an iron fortificant for an experimental chocolate drink powder targetted to children and adolescents. Organoleptically ferrous fumarate was acceptable when the chocolate drink powder was reconstituted in milk or water that was heated to < 80°. Unacceptable colour changes occurred, however, when boiling milk or water were used. In human Fe absorption studies when the Fe compounds were added to the chocolate drink immediately before consumption, ferrous fumarate was 3.31 % absorbed compared with 2.82% for ferrous sulphate and 2.11 % for ferric pyrophosphate. When the Fe compounds were processed during the manufacture of the chocolate drink powder, the absorption of ferrous fumarate was 5.27 %, ferrous sulphate 2.62 % and ferric pyrophosphate 0.55 %. Ascorbic acid had little or no effect on the absorption of ferrous fumarate. It is concluded that food processing can influence the relative absorption of fortification Fe and that, if not reconstituted with boiling milk or water, ferrous fumarate could be a useful compound for the fortification of chocolate drink powder

    Oxalate and Phytate of Soy Foods

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    Neurodevelopmental disorders in children aged 2-9 years: Population-based burden estimates across five regions in India.

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    BACKGROUND: Neurodevelopmental disorders (NDDs) compromise the development and attainment of full social and economic potential at individual, family, community, and country levels. Paucity of data on NDDs slows down policy and programmatic action in most developing countries despite perceived high burden. METHODS AND FINDINGS: We assessed 3,964 children (with almost equal number of boys and girls distributed in 2-<6 and 6-9 year age categories) identified from five geographically diverse populations in India using cluster sampling technique (probability proportionate to population size). These were from the North-Central, i.e., Palwal (N = 998; all rural, 16.4% non-Hindu, 25.3% from scheduled caste/tribe [SC-ST] [these are considered underserved communities who are eligible for affirmative action]); North, i.e., Kangra (N = 997; 91.6% rural, 3.7% non-Hindu, 25.3% SC-ST); East, i.e., Dhenkanal (N = 981; 89.8% rural, 1.2% non-Hindu, 38.0% SC-ST); South, i.e., Hyderabad (N = 495; all urban, 25.7% non-Hindu, 27.3% SC-ST) and West, i.e., North Goa (N = 493; 68.0% rural, 11.4% non-Hindu, 18.5% SC-ST). All children were assessed for vision impairment (VI), epilepsy (Epi), neuromotor impairments including cerebral palsy (NMI-CP), hearing impairment (HI), speech and language disorders, autism spectrum disorders (ASDs), and intellectual disability (ID). Furthermore, 6-9-year-old children were also assessed for attention deficit hyperactivity disorder (ADHD) and learning disorders (LDs). We standardized sample characteristics as per Census of India 2011 to arrive at district level and all-sites-pooled estimates. Site-specific prevalence of any of seven NDDs in 2-<6 year olds ranged from 2.9% (95% CI 1.6-5.5) to 18.7% (95% CI 14.7-23.6), and for any of nine NDDs in the 6-9-year-old children, from 6.5% (95% CI 4.6-9.1) to 18.5% (95% CI 15.3-22.3). Two or more NDDs were present in 0.4% (95% CI 0.1-1.7) to 4.3% (95% CI 2.2-8.2) in the younger age category and 0.7% (95% CI 0.2-2.0) to 5.3% (95% CI 3.3-8.2) in the older age category. All-site-pooled estimates for NDDs were 9.2% (95% CI 7.5-11.2) and 13.6% (95% CI 11.3-16.2) in children of 2-<6 and 6-9 year age categories, respectively, without significant difference according to gender, rural/urban residence, or religion; almost one-fifth of these children had more than one NDD. The pooled estimates for prevalence increased by up to three percentage points when these were adjusted for national rates of stunting or low birth weight (LBW). HI, ID, speech and language disorders, Epi, and LDs were the common NDDs across sites. Upon risk modelling, noninstitutional delivery, history of perinatal asphyxia, neonatal illness, postnatal neurological/brain infections, stunting, LBW/prematurity, and older age category (6-9 year) were significantly associated with NDDs. The study sample was underrepresentative of stunting and LBW and had a 15.6% refusal. These factors could be contributing to underestimation of the true NDD burden in our population. CONCLUSIONS: The study identifies NDDs in children aged 2-9 years as a significant public health burden for India. HI was higher than and ASD prevalence comparable to the published global literature. Most risk factors of NDDs were modifiable and amenable to public health interventions

    Inflammatory Markers and Hepcidin are Elevated but Serum Iron is Lower in Obese Women of Reproductive Age

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    Limited evidence suggests that serum iron and hepcidin concentrations are dysregulated in obesity and inflammation. The objective of the present study was to compare C-reactive protein, interleukin-6, circulating levels of hepcidin, serum lipids, and iron status in obese vs. normal-weight women of childbearing age. Healthy women aged 18&ndash;30 years were recruited for the study (n = 47: 25 obese and 22 normal weight). Fasting blood samples were obtained to measure serum lipids (total cholesterol, HDL, LDL cholesterol, triglycerides, non-HDL cholesterol), complete blood count, serum iron, total iron-binding capacity, transferrin saturation, serum ferritin, hepcidin, C-reactive protein, and interleukin-6. Obese women had significantly higher mean serum C-reactive protein (p &lt; 0.001), interleukin-6 (p &lt; 0.001), hepcidin (p = 0.024), triglycerides (p &lt; 0.001) and total cholesterol/HDL ratio (p &lt; 0.001) but lower HDL (p = 0.001) and serum iron/hepcidin ratio (p = 0.011) compared with normal-weight women. BMI correlated positively with inflammatory markers, triglycerides, LDL and total cholesterol/HDL ratio, and negatively with HDL and serum iron/hepcidin ratio. Serum iron correlated negatively with ferritin in the obese group (p = 0.030) but positively in normal weight women (p = 0.002). BMI and ferritin were the only predictors of serum iron/hepcidin ratio accounting for 23% of the variation among subjects. Studies are needed to examine anti-inflammatory dietary approaches that can improve iron biomarkers in obese women

    Inflammatory Markers and Hepcidin are Elevated but Serum Iron is Lower in Obese Women of Reproductive Age

    No full text
    Limited evidence suggests that serum iron and hepcidin concentrations are dysregulated in obesity and inflammation. The objective of the present study was to compare C-reactive protein, interleukin-6, circulating levels of hepcidin, serum lipids, and iron status in obese vs. normal-weight women of childbearing age. Healthy women aged 18–30 years were recruited for the study (n = 47: 25 obese and 22 normal weight). Fasting blood samples were obtained to measure serum lipids (total cholesterol, HDL, LDL cholesterol, triglycerides, non-HDL cholesterol), complete blood count, serum iron, total iron-binding capacity, transferrin saturation, serum ferritin, hepcidin, C-reactive protein, and interleukin-6. Obese women had significantly higher mean serum C-reactive protein (p p p = 0.024), triglycerides (p p p = 0.001) and serum iron/hepcidin ratio (p = 0.011) compared with normal-weight women. BMI correlated positively with inflammatory markers, triglycerides, LDL and total cholesterol/HDL ratio, and negatively with HDL and serum iron/hepcidin ratio. Serum iron correlated negatively with ferritin in the obese group (p = 0.030) but positively in normal weight women (p = 0.002). BMI and ferritin were the only predictors of serum iron/hepcidin ratio accounting for 23% of the variation among subjects. Studies are needed to examine anti-inflammatory dietary approaches that can improve iron biomarkers in obese women

    The Protection of EGCG Against 6-OHDA-Induced Oxidative Damage by Regulating PPARγ and Nrf2/HO-1 Signaling

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    6-Hydroxydopamine (6-OHDA) is a classic neurotoxin that has been widely used in Parkinson’s disease research. 6-OHDA can increase intracellular reactive oxygen species (ROS) and can cause cell damage, which can be attenuated with (-)-Epigallocatechin-3-gallate (EGCG) treatment. However, the mechanism by which EGCG alters the 6-OHDA toxicity remains unclear; In this study, we found 6-OHDA (25 μM) alone increased intracellular ROS concentration in N27 cells, which was attenuated by pretreating with EGCG (100 μM). We evaluated the intracellular oxidative damage by determining the level of thiobarbituric acid reactive substances (TBARS) and protein carbonyl content. 6-OHDA significantly increased TBARS by 82.7% ( P  < .05) and protein carbonyl content by 47.8 ( P  < .05), compared to the control. Pretreatment of EGCG decreased TBARS and protein carbonyls by 36.4% ( P  < .001) and 27.7% ( P  < .05), respectively, compared to 6-OHDA alone treatment. Antioxidant effect was tested with E2-related factor 2 (Nrf2), heme oxygenase-1(HO-1) and peroxisome-proliferator activator receptor γ (PPARγ) expression. 6-OHDA increased Nrf2 expression by 69.6% ( P  < .001), HO-1 by 173.3% ( P  < .001), and PPARγ by 122.7% ( P  < .001), compared with untreatment. EGCG pretreatment stabilized these alterations induced by 6-OHDA. Our results suggested that the neurotoxicity of 6-OHDA in N27 cells was associated with ROS pathway, whereas pretreatment of EGCG suppressed the ROS generation and deactivated the Nrf2/HO-1 and PPARγ expression
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