A M Prentice

London School of Hygiene and Tropical Medicine, Londinium, England, United Kingdom

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Publications (481)3072.58 Total impact

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    ABSTRACT: This is the final published version. It first appeared at http://www.nature.com/ncomms/2015/150512/ncomms8000/full/ncomms8000.html.
    Nature Communications 05/2015; 6:7000. DOI:10.1038/ncomms8000 · 10.74 Impact Factor
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    Sarah Prentice · Momodou W Jallow · Andrew M Prentice
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    ABSTRACT: Bacillus Calmette-Guerin (BCG) vaccination has been reported to protect neonates from non-tuberculous pathogens, but no biological mechanism to explain such effects is known. We hypothesised that BCG produces broad-spectrum anti-microbial protection via a hepcidin-mediated hypoferraemia, limiting iron availability for pathogens. To test this we conducted a trial in 120 Gambian neonates comparing iron status in the first 5-days of life after allocation to: (1) All routine vaccinations at birth (BCG/Oral Polio Vaccine (OPV)/Hepatitis B Vaccine (HBV)); (2) BCG delayed until after the study period (at day 5); and (3) All routine vaccinations delayed until after the study period. Vaccine regime at birth did not significantly impact on any measured parameter of iron metabolism. However, the ability to detect an effect of BCG on iron metabolism may have been limited by short follow-up time and high activation of the inflammatory-iron axis in the study population. Copyright © 2015. Published by Elsevier Ltd.
    Vaccine 05/2015; 204(26). DOI:10.1016/j.vaccine.2015.04.087 · 3.49 Impact Factor
  • 05/2015; DOI:10.1530/endoabs.37.EP234
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    ABSTRACT: Choline is an essential nutrient, and the amount needed in the diet is modulated by several factors. Given geographical differences in dietary choline intake and disparate frequencies of single-nucleotide polymorphisms (SNPs) in choline metabolism genes between ethnic groups, we tested the hypothesis that 3 SNPs that increase dependence on dietary choline would be under negative selection pressure in settings where choline intake is low: choline dehydrogenase (CHDH) rs12676, methylenetetrahydrofolate reductase 1 (MTHFD1) rs2236225, and phosphatidylethanolamine-N-methyltransferase (PEMT) rs12325817. Evidence of negative selection was assessed in 2 populations: 1 in The Gambia, West Africa, where there is historic evidence of a choline-poor diet, and the other in the United States, with a comparatively choline-rich diet. We used 2 independent methods, and confirmation of our hypothesis was sought via a comparison with SNP data from the Maasai, an East African population with a genetic background similar to that of Gambians but with a traditional diet that is higher in choline. Our results show that frequencies of SNPs known to increase dependence on dietary choline are significantly reduced in the low-choline setting of The Gambia. Our findings suggest that adequate intake levels of choline may have to be reevaluated in different ethnic groups and highlight a possible approach for identifying novel functional SNPs under the influence of dietary selective pressure.-Silver, M. J., Corbin, K. D., Hellenthal, G., da Costa, K.-A., Dominguez-Salas, P., Moore, S. E., Owen, J., Prentice, A. M., Hennig, B. J., Zeisel, S. H. Evidence for negative selection of gene variants that increase dependence on dietary choline in a Gambian cohort. © FASEB.
    The FASEB Journal 04/2015; DOI:10.1096/fj.15-271056 · 5.48 Impact Factor
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    ABSTRACT: In populations of European ancestry, the genetic contribution to body mass index (BMI) increases with age during childhood but then declines during adulthood, possibly due to the cumulative effects of environmental factors. How the effects of genetic factors on BMI change with age in other populations is unknown. In a rural Gambian population (N=2535), we used a combined allele risk score, comprising genotypes at 28 'Caucasian adult BMI-associated' single nucleotide polymorphisms (SNPs), as a marker of the genetic influence on body composition, and related this to internally-standardised z-scores for birthweight (zBW), weight-for-height (zWT-HT), weight-for-age (zWT), height-for-age (zHT), and zBMI cross-sectionally and longitudinally. Cross-sectionally, the genetic score was positively associated with adult zWT (0.018±0.009 per allele, p=0.034, N=1426) and zWT-HT (0.025±0.009, p=0.006), but not with size at birth or childhood zWT-HT (0.008±0.005, p=0.11, N=2211). The effect of the genetic score on zWT-HT strengthened linearly with age from birth through to late adulthood (age interaction term: 0.0083 z-scores/allele/year; 95% CI 0.0048 to 0.0118, p=0.0000032). Genetic variants for obesity in populations of European ancestry have direct relevance to bodyweight in nutritionally deprived African settings. In such settings, genetic obesity susceptibility appears to regulate change in weight status throughout the life course, which provides insight into its potential physiological role. Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.
    Journal of Medical Genetics 04/2015; 52(6). DOI:10.1136/jmedgenet-2014-102784 · 5.64 Impact Factor
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    ABSTRACT: Early and chronic inflammation is a hallmark of HIV infection, and inflammation is known to increase hepcidin expression. Consequently, hepcidin may be a key determinant of the iron homeostasis and anemia associated with poorer HIV prognoses. The objective of this study was to understand how hepcidin is related to anemia, iron homeostasis, and inflammation at HIV diagnosis and to investigate associations between hepcidin and all-cause mortality in HIV infection. In a retrospective cohort, baseline plasma hepcidin was measured by competitive enzyme immunoassay within 3 mo of HIV diagnosis in 196 antiretroviral-naive Gambians. Iron homeostasis [hemoglobin, plasma transferrin, ferritin, iron, soluble transferrin receptor (sTfR)] and inflammation [α1-antichymotrypsin (ACT)] from the same plasma sample were available, as were absolute CD4 cell counts, age, gender, body mass index (BMI), and HIV type. Anemia was common across the spectrum of immunosuppression [CD4 cell counts (prevalence of anemia): >500 cells/μL (68%), 200-500 cells/μL (73%), and <200 cells/μL (89%); P = 0.032] and in men (81%) and women (76%). Increasing hepcidin was associated with iron homeostasis biomarkers (higher ferritin and lower transferrin, hemoglobin, and sTfR), inflammation (higher ACT), and key health indicators (lower CD4 or BMI, advancing age, and male gender; P < 0.001 except for hemoglobin, P = 0.021). Elevated hepcidin was associated with greater all-cause mortality in a dose-dependent manner [intermediate vs. lowest tertile: unadjusted HR (95% CI), 1.95 (1.22, 3.10); upper vs. lowest tertile: 3.02 (1.91, 4.78)]. Principal components analysis identified 2 patterns composed of hepcidin-ferritin-transferrin, with or without ACT, and iron-sTfR-hemoglobin that may distinguish inflammation and erythropoiesis iron functions. Elevated hepcidin is independently associated with greater mortality in men and women with HIV infection, and hepcidin is also part of a complex relation linking iron homeostasis, anemia, and HIV. Understanding the mechanisms and role of hepcidin modulation may further guide evidence-based interventions needed to counter detrimental iron homeostasis and anemia in HIV infection. © 2015 American Society for Nutrition.
    Journal of Nutrition 04/2015; 145(6). DOI:10.3945/jn.114.203158 · 4.23 Impact Factor
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    ABSTRACT: Exposure to environmental toxins during embryonic development may lead to epigenetic changes that influence disease risk in later life. Aflatoxin is a contaminant of staple foods in sub-Saharan Africa, is a known human liver carcinogen and has been associated with stunting in infants. We have measured aflatoxin exposure in 115 pregnant women in The Gambia and examined the DNA methylation status of white blood cells from their infants at 2-8 months old (mean 3.6 ± 0.9). Aflatoxin exposure in women was assessed using an ELISA method to measure aflatoxin albumin (AF-alb) adducts in plasma taken at 1-16 weeks of pregnancy. Genome-wide DNA methylation of infant white blood cells was measured using the Illumina Infinium HumanMethylation450beadchip. AF-alb levels ranged from 3.9 to 458.4 pg/mg albumin. We found that aflatoxin exposure in the mothers was associated to DNA methylation in their infants for 71 CpG sites (false discovery rate < 0.05), with an average effect size of 1.7% change in methylation. Aflatoxin-associated differential methylation was observed in growth factor genes such as FGF12 and IGF1, and immune-related genes such as CCL28, TLR2 and TGFBI. Moreover, one aflatoxin-associated methylation region (corresponding to the miR-4520b locus) was identified. This study shows that maternal exposure to aflatoxin during the early stages of pregnancy is associated with differential DNA methylation patterns of infants, including in genes related to growth and immune function. This reinforces the need for interventions to reduce aflatoxin exposure, especially during critical periods of fetal and infant development. © The Author 2015; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.
    International Journal of Epidemiology 04/2015; DOI:10.1093/ije/dyv027 · 9.20 Impact Factor
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    ABSTRACT: Vitamin D is well known for its role in promoting skeletal health. Vitamin D status is determined conventionally by circulating 25-dihydroxyvitamin D (25OHD) concentration. There is evidence indicating that circulating 25OHD concentration is affected by variation in Gc, the gene encoding the vitamin D binding protein (DBP). The composite genotype of two single nucleotide polymorphisms (rs7041 and rs4588) results in different DBP isotypes (Gc1f, Gc1s and Gc2). The protein configurational differences among DBP isotypes affect DBP substrate binding affinity. The aims of this study were to determine 1) Gc variant frequencies in a population from an isolated rural region of The Gambia, West Africa (n = 3129) with year-round opportunity for cutaneous vitamin D synthesis and 2) the effects of Gc variants on 25OHD concentration (n = 237) in a genetically representative sub-group of children (mean (SD) age: 11.9 (4.8) years). The distribution of Gc variants was Gc1f: 0.86, Gc1s: 0.11 and Gc2: 0.03. The mean (SD) concentration of 25OHD was 59.6 (12.9) nmol/L and was significantly higher in those homozygous for Gc1f compared to other Gc variants (60.7 (13.1) vs. 56.6 (12.1) nmol/L, P = 0.03). Plasma 25OHD and 1,25(OH)2D concentration was significantly associated with parathyroid hormone in Gc1f-1f but not in the other Gc variants combined. This study demonstrates that different Gc variants are associated with different 25OHD concentrations in a rural Gambian population. Gc1f-1f, thought to have the highest affinity for 25OHD, had the highest 25OHD concentration compared with lower affinity Gc variants. The considerable difference in Gc1f frequency observed in Gambians compared with other non-West African populations and associated differences in plasma 25OHD concentration, may have implications for the way in which vitamin D status should be interpreted across different ancestral groups.
    Bone 01/2015; 74. DOI:10.1016/j.bone.2014.12.068 · 4.46 Impact Factor
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  • Ka Ward · A Riddell · A Prentice
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    ABSTRACT: Ready-to-use supplementary food supplements improve endothelial function, hemoglobin and growth in Tanzanian children with sickle cell anaemia: The Vascular Function Intervention Study (V-FIT), a random order crossover trial
    American Society of Hematology; 12/2014
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    ABSTRACT: Hepcidin inhibits ferroportin-mediated iron efflux, leading to intracellular macrophage iron retention, possibly favoring Mycobacterium tuberculosis iron acquisition and tuberculosis (TB) pathogenesis. Plasma hepcidin was measured at human immunodeficiency virus (HIV) diagnosis in a retrospective HIV-prevalent, antiretroviral-naïve African cohort to investigate the association with incident pulmonary and/or extra-pulmonary TB. One hundred ninety-six participants were followed between 5 August 1992 and 1 June 2002, with 32 incident TB cases identified. Greater hepcidin was associated with significantly increased likelihood of TB after a median time to TB of 6 months. Elucidation of iron-related causal mechanisms and time-sensitive biomarkers that identify individual changes in TB risk are needed.
    The International Journal of Tuberculosis and Lung Disease 11/2014; 18(11). DOI:10.5588/ijtld.14.0143 · 2.76 Impact Factor
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    J Redmond · L Palla · L Yan · L M A Jarjou · A Prentice · I Schoenmakers
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    ABSTRACT: Ethnic differences in renal calcium and phosphate excretion exist, which may depend on differences in their dietary intakes and regulatory factors. We report highly significant differences in urinary calcium and phosphate excretion between white British and Gambian adults after statistical adjustment for mineral intakes, indicating an independent effect of ethnicity.
    Osteoporosis International 10/2014; 26(3). DOI:10.1007/s00198-014-2926-8 · 4.17 Impact Factor
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    ABSTRACT: Summary Predictors of 25(OH)D3 half-life were factors associated with vitamin D metabolism, but were different between people in The Gambia and the UK. Country was the strongest predictor of plasma 25(OH)D concentration, probably as a marker of UVB exposure. 25(OH)D3 half-life may be applied as a tool to investigate vitamin D expenditure. Introduction The aim of this study was to investigate predictors of 25(OH)D3 half-life and plasma 25(OH)D concentration. Methods Plasma half-life of an oral tracer dose of deuterated-25(OH)D3 was measured in healthy men aged 24–39 years, resident in The Gambia, West Africa (n = 18) and in the UK during the winter (n = 18), countries that differ in calcium intake and vitamin D status. Plasma and urinary markers of vitamin D, calcium, phosphate and bone metabolism, nutrient intakes and anthropometry were measured. Results Normally distributed data are presented as mean (SD) and non-normal data as geometric mean (95 % CI). Gambian compared to UK men had higher plasma concentrations of 25(OH)D (69 (13) vs. 29 (11) nmol/L; P 2D (181 (165, 197) vs. 120 (109, 132) pmol/L; P P 3 half-life (14.7 (3.5) days vs. 15.6 (2.5) days) between countries (P = 0.2). In multivariate analyses, 25(OH)D, 1,25(OH)2D, vitamin D binding protein and albumin-adjusted calcium (Caalb) explained 79 % of variance in 25(OH)D3 half-life in Gambians, but no significant predictors were found in UK participants. For the countries combined, Caalb, PTH and plasma phosphate explained 39 % of half-life variability. 1,25(OH)2D, weight, PTH and country explained 81 % of variability in 25(OH)D concentration; however, country alone explained 74 %. Conclusion Factors known to affect 25(OH)D metabolism predict 25(OH)D3 half-life, but these differed between countries. Country predicted 25(OH)D, probably as a proxy measure for UVB exposure and vitamin D supply. This study supports the use of 25(OH)D half-life to investigate vitamin D metabolism.
    Osteoporosis International 10/2014; 26(3). DOI:10.1007/s00198-014-2905-0 · 4.17 Impact Factor
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    ABSTRACT: During HIV type-1 (HIV-1), hepatitis C virus (HCV), and hepatitis B virus (HBV) infections, altered iron balance correlates with morbidity. The liver-produced hormone hepcidin dictates systemic iron homeostasis. We measured hepcidin, iron parameters, cytokines, and inflammatory markers in three cohorts: plasma donors who developed acute HIV-1, HBV, or HCV viremia during the course of donations; HIV-1-positive individuals progressing from early to chronic infection; and chronically HIV-1-infected individuals (receiving antiretroviral therapy or untreated). Hepcidin increased and plasma iron decreased during acute HIV-1 infection, as viremia was initially detected. In patients transitioning from early to chronic HIV-1 infection, hepcidin in the first 60 d of infection positively correlated with the later plasma viral load set-point. Hepcidin remained elevated in individuals with untreated chronic HIV-1 infection and in subjects on ART. In contrast to HIV-1, there was no evidence of hepcidin up-regulation or hypoferremia during the primary viremic phases of HCV or HBV infection; serum iron marginally increased during acute HBV infection. In conclusion, hepcidin induction is part of the pathogenically important systemic inflammatory cascade triggered during HIV-1 infection and may contribute to the establishment and maintenance of viral set-point, which is a strong predictor of progression to AIDS and death. However, distinct patterns of hepcidin and iron regulation occur during different viral infections that have particular tissue tropisms and elicit different systemic inflammatory responses. The hypoferremia of acute infection is therefore a pathogen-specific, not universal, phenomenon.
    Proceedings of the National Academy of Sciences 08/2014; 111(33). DOI:10.1073/pnas.1402351111 · 9.81 Impact Factor
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    ABSTRACT: Iron deficiency and malaria have similar global distributions, and frequently co-exist in pregnant women and young children. Where both conditions are prevalent, iron supplementation is complicated by observations that iron deficiency anaemia protects against falciparum malaria, and that iron supplements increase susceptibility to clinically significant malaria, but the mechanisms remain obscure. Here, using an in vitro parasite culture system with erythrocytes from iron-deficient and replete human donors, we demonstrate that Plasmodium falciparum infects iron-deficient erythrocytes less efficiently. In addition, owing to merozoite preference for young erythrocytes, iron supplementation of iron-deficient individuals reverses the protective effects of iron deficiency. Our results provide experimental validation of field observations reporting protective effects of iron deficiency and harmful effects of iron administration on human malaria susceptibility. Because recovery from anaemia requires transient reticulocytosis, our findings imply that in malarious regions iron supplementation should be accompanied by effective measures to prevent falciparum malaria.
    Nature Communications 07/2014; 5:4446. DOI:10.1038/ncomms5446 · 10.74 Impact Factor
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    ABSTRACT: Objectives: Whereas coverage of antenatal iron supplementation is low and benefits are uncertain, there are concerns that it can increase the burden of malaria, with potentially devastating effects on maternal and neonatal health outcomes. We aimed to measure the effect of iron supplementation during pregnancy on maternal Plasmodium infection assessed at delivery, birth weight, gestational age, fetal growth and maternal and infant iron status. Methods: Rural Kenyan women (n=470) with singleton pregnancies, gestational age 13─23 weeks and haemoglobin concentration ≥ 90 g/L were randomised to supervised daily supplementation with iron (60 mg as ferrous fumarate) or placebo until 1 month postpartum. To prevent severe anaemia, all women additionally received 5.7 mg iron/day through flour fortification. Intermittent preventive treatment against malaria was given as usual. Plasmodium infection was assessed at birth by dipstick tests, PCR and histological examination of placental biopsies. Results: There was no evident effect on Plasmodium infection (both intervention groups: 45%; difference, 95% CI: 0%, ─9% to 9%). Iron supplementation increased birth weight by 143g (95% CI: 58─228g) and reduced the prevalence of low birth weight (<2,500g) by 65% (95% CI: 13%─86%). The effect on birth weight was larger in women who were initially iron-deficient than in those who were iron-replete (250 g versus ─13 g; p-interaction=0.008), and the improved birth weight seemed achieved mostly through improved fetal growth. Iron supplementation resulted in improved maternal iron status at 1 month postpartum, and improved infant iron stores. Conclusion: Coverage of universal antenatal iron supplementation must be increased.
    Micronutrient Forum - 2014, Addis Ababa; 06/2014
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    ABSTRACT: Context: There is uncertainty over the equivalence of vitamins D2 and D3 to maintain plasma 25-hydroxyvitamin D (25(OH)D). Objective: To compare the plasma half-lives of 25(OH)D2 and 25(OH)D3 in two distinct populations with different dietary calcium intake and 25(OH)D status. Participants: Healthy men (aged 24 and 39 years), resident in The Gambia (n=18) or UK (n=18). Interventions: Oral tracer dose of deuterated-25(OH)D2 and deuterated-25(OH)D3 (both 40 nmol). Blood samples were collected over 33 days. Main outcome measures: 25(OH)D2 and 25(OH)D3 plasma half-lives, concentrations of 25(OH)D and DBP and DBP genotypes. Results: 25(OH)D2 half-life (mean (SD)) (13.9 (2.6) d) was shorter than 25(OH)D3 half-life (15.1 (3.1) d; P=0.001) for countries combined, and in Gambians (12.8 (2.3) d vs. 14.7 (3.5) d; P<0.001), but not in the UK (15.1 (2.4) d vs. 15.6 (2.5) d; P=0.3). 25(OH)D concentration was 69 (13) and 29 (11) nmol/L (P<0.0001) and DBP concentration was 259 (33) and 269 (23) mg/l (P=0.4) in The Gambia and UK, respectively. Half-lives were positively associated with plasma DBP concentration for countries combined: (25(OH)D2 half-life: regression coefficient (SE) 0.03 (0.01) d per 1 mg/l DBP; P=0.03; 25(OH)D3 half-life: 0.04 (0.02) d; P=0.02) and in Gambians (25(OH)D2 half-life: 0.04 (0.01) d; P=0.02; 25(OH)D3 half-life: 0.06 (0.02) d; P=0.01), but not in UK participants. DBP concentration*country interactions were not significant. DBP Gc1f/1f homozygotes had shorter 25(OH)D2 half-lives compared to other combined genotypes (P=0.007), after correction for country. Conclusions: 25(OH)D2 half-life was shorter than 25(OH)D3 half-life, and half-lives were affected by DBP concentration and genotype. Stable isotope 25(OH)D half-life measurements provide a novel tool to investigate vitamin D metabolism and vitamin D expenditure, and aid in the assessment of vitamin D requirements.
    Journal of Clinical Endocrinology &amp Metabolism 06/2014; 99(9):jc20141714. DOI:10.1210/jc.2014-1714 · 6.31 Impact Factor
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    Martha K Mwangome · Gregory Fegan · Andrew M Prentice · James A Berkley
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    ABSTRACT: Objective: To compare mothers' perceptions of their own infants' nutritional status with anthropometric indicators of undernutrition. Design: A qualitative study and cross-sectional quantitative survey. The qualitative study involved developing tools to assess mother's perception. Two methods of verbal description and a pictorial scale were developed. The quantitative survey involved measuring maternal perception and comparing it with the anthropometric measures of weight-for-age Z-score (WAZ) and mid-upper arm circumference-for-age Z-score (MUACZ). Setting: A rural community setting in Kenya. Subjects: Seventy-four infants aged between 4 and 6 months, and their mothers, living in rural Kenya were enrolled. Results: Using verbal description, the positive and negative likelihood ratios were 3.57 (95 % CI 1.44, 9.98) and 0.69 (95% CI 0.50, 0.96) respectively for MUACZ < -2; and 4.60 (95% CI 1.60, 13.3) and 0.67 (95% CI 0.49, 0.92) respectively for WAZ < -2. Using the pictorial scale, the positive and negative likelihood ratios were 8.30 (95% CI 1.91, 36.3) and 0.69 (95% CI 0.52, 0.93) respectively for MUACZ < -2; and 4.31 (95% CI 1.22, 15.0) and 0.78 (95% CI 0.61, 1.00) respectively for WAZ < -2. Conclusions: In a rural community, mothers better identify undernutrition in their infants using a pictorial scale than verbal description. However, neither can replace formal anthropometric assessment. Objective anthropometric tools should be validated for identification of severe acute malnutrition among infants aged less than 6 months.
    Public Health Nutrition 05/2014; 18(05):1-8. DOI:10.1017/S1368980014001074 · 2.48 Impact Factor
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    ABSTRACT: Childhood anemia is a major global health problem resulting from multiple causes. Iron supplementation addresses iron deficiency anemia but is undesirable for other types of anemia and may exacerbate infections. The peptide hormone hepcidin governs iron absorption; hepcidin transcription is mediated by iron, inflammation, and erythropoietic signals. However, the behavior of hepcidin in populations where anemia is prevalent is not well established. We show that hepcidin measurements in 1313 African children from The Gambia and Tanzania (samples taken in 2001 and 2008, respectively) could be used to identify iron deficiency anemia. A retrospective secondary analysis of published data from 25 Gambian children with either postmalarial or nonmalarial anemia demonstrated that hepcidin measurements identified individuals who incorporated >20% oral iron into their erythrocytes. Modeling showed that this sensitivity of hepcidin expression at the population level could potentially enable simple groupings of individuals with anemia into iron-responsive and non-iron-responsive subtypes and hence could guide iron supplementation for those who would most benefit.
    Science translational medicine 05/2014; 6(235):235re3. DOI:10.1126/scitranslmed.3008249 · 14.41 Impact Factor

Publication Stats

21k Citations
3,072.58 Total Impact Points


  • 1996–2015
    • London School of Hygiene and Tropical Medicine
      • • Department of Nutrition and Public Health Interventions Research
      • • Faculty of Epidemiology and Population Health
      Londinium, England, United Kingdom
    • University of the Witwatersrand
      • School of Physiology
      Johannesburg, Gauteng, South Africa
    • Sheba Medical Center
      Gan, Tel Aviv, Israel
  • 2012–2014
    • University of London
      Londinium, England, United Kingdom
  • 1980–2014
    • Medical Research Council Unit, The Gambia Unit
      Bakau, Banjul, Gambia
  • 2011
    • Muhimbili University of Health and Allied Sciences
      • Department of Haematology and Blood Transfusion
      Dar es Salaam, Dar es Salaam Region, Tanzania
    • Cranfield University
      Cranfield, England, United Kingdom
  • 2002–2011
    • Mrc Harwell
      Oxford, England, United Kingdom
    • University of Glasgow
      • Child Health Section
      Glasgow, SCT, United Kingdom
  • 2008
    • Oxford University Hospitals NHS Trust
      • Nuffield Department of Medicine
      Oxford, England, United Kingdom
  • 1995–2007
    • University of Cambridge
      Cambridge, England, United Kingdom
    • Papworth Hospital NHS Foundation Trust
      Papworth, England, United Kingdom
  • 2006
    • University of Gambia
      Bathurst, Banjul, Gambia
  • 2000–2005
    • MRC International Nutrition Group
      Londinium, England, United Kingdom
    • WWF United Kingdom
      Londinium, England, United Kingdom
  • 1990–2002
    • University of Ulster
      • Biomedical Sciences Research Institute
      Aontroim, Northern Ireland, United Kingdom
  • 1989–2000
    • Medical Research Council (UK)
      Londinium, England, United Kingdom
  • 1998
    • University of Auckland
      • Department of Medicine
      Окленд, Auckland, New Zealand
  • 1991–1996
    • MRC Clinical Sciences Centre
      London Borough of Harrow, England, United Kingdom
  • 1992
    • New York State
      New York, New York, United States
  • 1988
    • Spokane VA Medical Center
      Spokane, Washington, United States