European Journal of Nutrition (Eur J Nutr)

Publisher: Springer Verlag

Journal description

The European Journal of Nutrition publishes original papers invited reviews and short communications in nutritional sciences. The major focus of manuscripts submitted to the Eur J Nutr should consequently be on: cellular and molecular aspects of nutrition mechanistic studies on interactions between nutrients and non-nutrient food components on cell organ and body functions epidemiology with emphasis on the use of biomarkers nutrient metabolism in humans studies on the relation between individual genetic susceptibility nutrition and disease regulation of gene expression through nutrients or non-nutrient food components Animal nutrition studies will only be considered for publication if a strong relation to actual problems in human nutrition is presented. Indexing and Abstract Services

Current impact factor: 3.47

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 3.467
2013 Impact Factor 3.84
2012 Impact Factor 3.127
2011 Impact Factor 2.75
2010 Impact Factor 3.343
2009 Impact Factor 2.866
2008 Impact Factor 1.899
2007 Impact Factor 2.098
2006 Impact Factor 2.356
2005 Impact Factor 2.257
2004 Impact Factor 2.098
2003 Impact Factor 1.684
2002 Impact Factor 1.644
2001 Impact Factor 2.13
2000 Impact Factor 2.059

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.26
Cited half-life 4.80
Immediacy index 0.93
Eigenfactor 0.01
Article influence 0.85
Website European Journal of Nutrition website
Other titles European journal of nutrition (Online)
ISSN 1436-6215
OCLC 42848305
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Springer Verlag

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Author's pre-print on pre-print servers such as arXiv.org
    • Author's post-print on author's personal website immediately
    • Author's post-print on any open access repository after 12 months after publication
    • Publisher's version/PDF cannot be used
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany link to published version (see policy)
    • Articles in some journals can be made Open Access on payment of additional charge
  • Classification
    green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Purpose: To estimate total sodium (Na) and potassium (K) intake using non-fasting morning urine specimens among Lebanese elementary (6-10 year old) schoolchildren. Method: A national cross-sectional study was conducted. A multistage cluster sampling procedure was used to select a representative sample of 1403 healthy children from the eight districts of Lebanon. Age, anthropometric measurements, and urine samples were collected and analyzed for Na, K, and creatinine (Cr). Results: The ratios of Na and K to Cr were 23.93 ± 15.54 mM/mM (4.86 ± 3.16 mg/mg) and 11.48 ± 5.82 mM/mM (3.97 ± 2.01 mg/mg), respectively, and showed differences (P value <0.001) between age groups. No differences were found between boys and girls in all the measured Na and K parameters. The estimated mean Na intake was 96.57 ± 61.67 mM/day (2.220 ± 1.418 g/day or 5.69 ± 3.64 g NaCl/day) and exceeded the upper limit of intake in half the children. Estimated K intake was 46.6 ± 23.02 mM/day (1.822 ± 0.900 g/day), and almost all children failed to meet the recommended daily K intake. The high Na/K ratio (2.361 ± 1.67 mM/mM or 1.39 ± 0.98 mg/mg) resulted from a combination of high Na and low K intake but was mostly affected by K intake. Conclusions: About 50 % of children exceeded the recommended daily upper intake for Na, while the majority was below K adequate intake. This unfavorable Na/K ratio is indicative of potentially negative health effects at later stages in life. Interventions aimed at reducing salt intake and increasing consumption of fruits and vegetables are warranted.
    No preview · Article · Feb 2016 · European Journal of Nutrition
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    ABSTRACT: Purpose: Telomere length is a biomarker for aging. It is known that oxidative stress can accelerate telomere shortening, whereas antioxidants can delay their shortening. Carotenoids as antioxidants are favorably associated with health- and aging-related diseases caused by oxidative stress, but their association with telomere length is less certain. We investigated the association between blood carotenoid levels and leukocyte telomere length in a representative sample of US adults. Methods: We analyzed 3660 participants aged 20 years and older in the 1999-2002 National Health and Nutrition Examination Survey. The levels of carotenoids-alpha-carotene, beta-carotene (trans + cis), beta-cryptoxanthin, combined lutein/zeaxanthin, and trans-lycopene-were measured using high-performance liquid chromatography. The leukocyte telomere length (T/S ratio) was assayed using the quantitative polymerase chain reaction method. Results: A doubling of blood alpha-carotene, beta-carotene (trans + cis), and beta-cryptoxanthin was associated with approximately 2 % longer telomeres. Compared with the lowest carotenoid quartile of alpha-carotene, beta-carotene (trans + cis), and beta-cryptoxanthin, telomere length for adults with the highest quartiles was significantly increased by 5-8 %. Conclusion: We found that increasing levels of blood carotenoid were significantly associated with longer leukocyte telomeres in US adults. High intake of carotenoid-rich food may play a role in protecting telomeres and regulating telomere length.
    No preview · Article · Jan 2016 · European Journal of Nutrition
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    ABSTRACT: Purpose: Studies suggest that long-chain ω-3 polyunsaturated fatty acid (LCω3PUFA) intake and its primary food source-fish-may have beneficial effects on the individual components of metabolic syndrome (MetS). We examined the longitudinal association between fish or LCω3PUFA intake and MetS incidence. Methods: We prospectively followed 4356 American young adults, free from MetS and diabetes at baseline, for incident MetS and its components in relation to fish and LCω3PUFA intake. MetS was defined by the National Cholesterol Education Program/Adult Treatment Panel III criteria. Cox proportional hazards model was used for analyses, controlling for socio-demographic, behavioral, and dietary factors. Results: During the 25-year follow-up, a total of 1069 incident cases of MetS were identified. LCω3PUFA intake was inversely associated with the incidence of MetS in a dose-response manner. The multivariable adjusted hazards ratio (HR) [95 % confidence interval (CI)] of incident MetS was 0.54 (95 % CI 0.44, 0.67; P for linear trend < 0.01) as compared the highest to the lowest quintile of LCω3PUFA intake. A threshold inverse association was found between non-fried fish consumption and the incidence of MetS. The multivariable adjusted HRs (95 % CIs) from the lowest to the highest quintile were 1.00, 0.70 (0.51, 0.95), 0.68 (0.52, 0.91), 0.67 (0.53, 0.86), and 0.71 (0.56, 0.89) (P for linear trend = 0.49). The observed inverse associations were independent of the status of baseline individual components of MetS. Conclusions: Our findings suggest that intakes of LCω3PUFAs and non-fried fish in young adulthood are inversely associated with the incidence of MetS later in life.
    No preview · Article · Jan 2016 · European Journal of Nutrition
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    ABSTRACT: Purpose: Evaluating early iron supplementation in non-anemic mothers with postpartum depression (PPD). Methods: This randomized, double-blind, placebo-controlled trial evaluated 70 mothers with PPD. One week after delivery, the mothers were randomly allocated in the iron-treated (50 mg elemental iron/daily) and placebo-treated groups. After 6 weeks, the improvement of PPD symptoms was compared between the groups. Results: Ferritin significantly increased in the iron-treated group (p < 0.001), but not in the placebo group (p = 0.09). After intervention, ferritin was higher in the iron-treated group (medians: 78.2 vs. 37 mg/dl, p = 0.01). The rate of iron deficiency significantly decreased in the iron-treated group (p = 0.009), but not in the placebo group (p = 0.4). After intervention, the rate of iron deficiency was higher in the placebo group (31.4 vs. 8.5 %, p = 0.01). The Edinburgh Postnatal Depression Scale (EPDS) score significantly decreased in the iron-treated group (p < 0.001), but not in the placebo group (p = 0.13). After intervention, the EPDS score was lower in the iron-treated group (medians 9 vs. 12, p = 0.01). The improvement rate for PPD was significantly higher in the iron-treated group (42.8 vs. 20 %, p = 0.03). After intervention, mothers with continued PPD had lower ferritin than the improved mothers (41.8 vs. 67 mg/dl, p = 0.03). Mothers with continued depression had higher rate of iron deficiency compared to the improved mothers (27.1 vs. 4.5 %, p = 0.02). Conclusions: Early iron supplementation in mothers with PPD significantly improves the iron stores and causes a significant improvement in PPD with a 42.8 % improvement rate during 6 weeks. Continued PPD might be related to the lower postpartum ferritin levels in untreated mothers.
    No preview · Article · Dec 2015 · European Journal of Nutrition
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    ABSTRACT: Purpose: A gluten-free diet (GFD) has been reported to negatively impact the quality of life (QoL) of coeliac disease (CD) patients. The gut-brain axis hormones ghrelin and leptin, with the brain-derived neurotrophic factor (BDNF), may affect QoL of CD patients undergoing GFD. Our aims were to evaluate whether: (a) the circulating concentrations of leptin, ghrelin and BDNF in CD patients were different from those in healthy subjects; (b) GFD might induce changes in their levels; (c) BDNF Val66Met polymorphism variability might affect BDNF levels; and (d) serum BDNF levels were related to dietary docosahexaenoic acid (DHA) as a neurotrophin modulator. Methods: Nineteen adult coeliac patients and 21 healthy controls were included. A QoL questionnaire was administered, and serum concentrations of ghrelin, leptin, BDNF and red blood cell membrane DHA levels were determined at the enrolment and after 1 year of GFD. BDNF Val66Met polymorphism was analysed. Results: Results from the questionnaire indicated a decline in QoL after GFD. Ghrelin and leptin levels were not significantly different between groups. BDNF levels were significantly (p = 0.0213) lower in patients after GFD (22.0 ± 2.4 ng/ml) compared to controls (31.2 ± 2.2 ng/ml) and patients at diagnosis (25.0 ± 2.5 ng/ml). BDNF levels correlated with DHA levels (p = 0.008, r = 0.341) and the questionnaire total score (p = 0.041, r = 0.334). Conclusions: Ghrelin and leptin seem to not be associated with changes in QoL of patients undergoing dietetic treatment. In contrast, a link between BDNF reduction and the vulnerability of CD patients to psychological distress could be proposed, with DHA representing a possible intermediate.
    No preview · Article · Dec 2015 · European Journal of Nutrition
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    ABSTRACT: Purpose: Epidemiological evidence on the association between fish consumption and risk of type 2 diabetes is heterogeneous across geographical regions. Differences related to fish consumption pattern could possibly help explain the discrepancy between the findings. We therefore aimed to investigate the association between fish consumption (total, fried, specific fish items) and type 2 diabetes incidence, taking exposure to contaminants present in fish (polychlorinated biphenyls and methyl mercury) into consideration. Methods: The population-based Cohort of Swedish Men, including 35,583 men aged 45-79 years, was followed from 1998 to 2012. We estimated hazard ratios (HRs) with 95 % confidence intervals (CIs) using Cox proportional hazards models. Results: During 15 years of follow-up, 3624 incident cases were identified. Total fish consumption (≥4 servings/week vs. <1 serving/week) was not associated with type 2 diabetes in multivariable-adjusted analysis (HR 1.00; 95 % CI 0.85-1.18); however, a statistically non-significant inverse association was observed after adjustment for dietary contaminant exposures (HR 0.79; 95 % CI 0.60-1.04). Fried fish (≥6 servings/month vs. ≤1 servings/month) and shellfish consumption (≥1 serving/week vs. never/seldom) were associated with HRs of 1.14 (95 % CI 1.03-1.31) and 1.21 (95 % CI 1.07-1.36), respectively. Conclusions: We observed no overall association between total fish consumption and type 2 diabetes. The results indicated that dietary contaminants in fish may influence the relationship. Fried fish and shellfish consumption were associated with higher type 2 diabetes incidence. These findings suggest that more specific advice on fish species sub-types (varying in contamination) and preparation methods may be warranted.
    No preview · Article · Dec 2015 · European Journal of Nutrition
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    ABSTRACT: Purpose: Selenium (Se) has a dual role in metabolic syndrome (MS) development as it has an antioxidant action against both "good" and "bad" reactive oxygen species. This study evaluates Se body profile in dams which present MS during gestation and lactation, in order to elucidate a normal dietary Se's implication in this pathology. Method: Rats were randomized into control (C) and fructose (F) groups. The rich fructose diet (65 %) during gestation and lactation periods induced MS in dams. Se body distribution was determined by atomic absorption spectrophotometry, and the hepatic activity of the four antioxidant enzymes and the bimolecular oxidation were determined by spectrophotometry. The cardiac activity was monitored using the indirect tail occlusion method. Lipid and glucidic profile was also analyzed. Results: Despite the fact that the diet supplied has 0.1 ppm of Se, the minimal dietary requirement for rats, F dams ate less amount of food, and therefore, they had lower Se retention. However, they had normal levels of Se in serum and milk. Dams with MS had Se depletion in heart and muscle joint to hypertension and a lower heart rate, and Se repletion in liver and kidney. Despite the increase in hepatic glutathione peroxidase (GPx) and catalase activity found, lipid oxidation occurred-probably because superoxide dismutase activity was diminished. In heart, the activity and expression of the selenoprotein GPx1 were decreased. Conclusion: With these results, it is not possible to elucidate whether a dietary Se supplementation or a Se-restricted diet are good for MS; because despite the fact that GPx activity is increased in liver, it is also found, for the first time, that heart Se deposits are significantly decreased during MS.
    No preview · Article · Dec 2015 · European Journal of Nutrition
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    ABSTRACT: Purpose: Nutrition is indispensable for cell survival and proliferation. Thus, loss of nutrition caused by serum starvation in cells could induce formation of reactive oxygen species (ROS), resulting in cell death. Liquiritigenin (LQ) is an active flavonoid in licorice and plays a role in the liver as a hepatic protectant. Methods: This study investigated the effect of LQ, metformin [an activator of activated AMP-activated protein kinase (AMPK)] and GW4064 [a ligand of farnesoid X receptor (FXR)] on mitochondrial dysfunction and oxidative stress induced by serum deprivation as well as its molecular mechanism, as assessed by immunoblot and flow cytometer assays. Results: Serum deprivation in HepG2, H4IIE and AML12 cells successfully induced oxidative stress and apoptosis, as indicated by depletion of glutathione, formation of ROS, and altered expression of apoptosis-related proteins such as procaspase-3, poly(ADP-ribose) polymerase, and Bcl-2. However, LQ pretreatment significantly blocked these pathological changes and mitochondrial dysfunction caused by serum deprivation. Moreover, LQ activated AMPK in HepG2 cells and mice liver, as shown by phosphorylation of AMPK and ACC, and this activation was mediated by its upstream kinase (i.e., LKB1). Experiments using a chemical inhibitor of AMPK with LKB1-deficient Hela cells revealed the role of the LKB1-AMPK pathway in cellular protection conferred by LQ. LQ also induced protein and mRNA expression of both FXR as well as small heterodimer partner, which is important since treatment with FXR ligand GW4064 protected hepatocytes against cell death and mitochondrial damage induced by serum deprivation. Conclusion: AMPK activators such as LQ can protect hepatocytes against oxidative hepatic injury and mitochondrial dysfunction induced by serum deprivation, and the beneficial effect might be mediated through the LKB1 pathway as well as FXR induction.
    No preview · Article · Dec 2015 · European Journal of Nutrition
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    ABSTRACT: Purpose: Growth hormone (GH) controls liver metabolism through the transcription factor signal transducer and activator of transcription 5 (STAT5). However, it remains to be fully understood to what extent other GH/STAT5 target tissues contribute to lipid and glucose metabolism. This question was now addressed in muscle-specific STAT5 knockout (STAT5 MKO) mice model. Methods: Changes in lipid and glucose metabolism were investigated at physiological and molecular levels in muscle and liver tissues of STAT5 MKO mice under normal diet or high-fat diet (HFD) conditions. Results: STAT5 MKO mice exhibited an increased intramyocellular lipid (IMCL) accumulation in the quadriceps in HFD group. Decreased lipolytic hormone-sensitive lipase transcript levels may contribute to the increased IMCL accumulation in STAT5 MKO mice. STAT5 MKO induced hepatic lipid accumulation without deregulated STAT5 signaling. The upregulation of lipoprotein lipase and Cd36 mRNA levels, an increased trend of very low-density lipoprotein receptor mRNA levels, and elevated circulating concentrations of free fatty acid, triglyceride, and total cholesterol support the increase in hepatic lipid accumulation. Conclusions: STAT5 MKO in conjunction with a HFD deregulated both lipid and glucose metabolism in skeletal muscle, and this deregulation induced hepatic fat accumulation via increased circulating glucose, FFA, and TG concentrations. Our study emphasizes that muscle-specific STAT5 signaling is important for balancing lipid and glucose metabolism in peripheral tissues, including muscle and liver and that the deregulation of local STAT5 signaling augments HFD-induced lipid accumulation in both muscle and liver.
    No preview · Article · Nov 2015 · European Journal of Nutrition
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    ABSTRACT: Purpose: The present placebo-controlled, double-blind, randomized trial aimed to investigate whether a natural mineral water rich in magnesium sulphate and sodium sulphate (Donat Mg) may help to improve bowel function. Methods: A total of 106 otherwise healthy subjects with functional constipation were randomly assigned to consume 300 or 500 mL of a natural mineral water as compared to placebo water, over a course of 6 weeks. The 300-mL arms were terminated due to the results of a planned interim analysis. Subjects documented the complete spontaneous bowel movements, spontaneous and overall bowel movements/week, stool consistency, gastrointestinal symptoms and general well-being in a diary. Change in the number of complete spontaneous bowel movements was defined as the primary outcome. Results: For the 75 subjects in the 500-mL arms, the change in the number of complete spontaneous bowel movements per week tended to be higher in the active group when compared to placebo after 6 weeks (T2 = 1.8; p value = 0.036; one-sided). The mean number of spontaneous bowel movements significantly increased over the course of the study, with significant differences between study arms considering the whole study time (F test = 4.743; p time × group = 0.010, 2-sided). Stool consistency of spontaneous bowel movements (p < 0.001) and the subjectively perceived symptoms concerning constipation (p = 0.005) improved significantly with the natural mineral water as compared to placebo. Conclusions: The daily consumption of a natural mineral water rich in magnesium sulphate and sodium sulphate improved bowel movement frequency and stool consistency in subjects with functional constipation. Moreover, the subjects' health-related quality of life improved. Clinical trial registration: EudraCT No 2012-005130-11.
    No preview · Article · Nov 2015 · European Journal of Nutrition
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    ABSTRACT: Purpose: Green tea may have a beneficial role of inhibiting leukemia. Glutathione S-transferases (GSTs) are known to detoxify certain carcinogens. We investigated the roles of green tea consumption and polymorphisms of GSTM1, GSTT1 and GSTP1 on the risk of adult leukemia, and to determine whether the associations varied within GSTs genotypes. Methods: A multicenter case-control study was conducted in China, 2008-2013. It comprised 442 incident, hematologically confirmed adult leukemia cases and 442 outpatient controls, individually matched to cases by gender, birth quinquennium and study site. Data were collected by face-to-face interview using a validated questionnaire. Genetic polymorphisms were assayed by PCR. Results: An inverse association between green tea consumption and adult leukemia risk was observed. Compared with non-tea drinkers, the adjusted odds ratios (95 % confidence intervals) were 0.50 (0.27-0.93), 0.31 (0.17-0.55) and 0.53 (0.29-0.99) for those who, respectively, consumed green tea >20 years, ≥2 cups daily and dried tea leaves >1000 g annually. In assessing the associations by GSTs genotypes, risk reduction associated with green tea consumption was stronger in individuals with the GSTT1-null genotype (OR 0.24; 95 % CI 0.11-0.53) than GSTT1-normal carriers (OR 0.67; 95 % CI 0.42-1.05; P interaction = 0.02). GSTM1 and GSTP1 did not significantly modify the inverse association of leukemia with green tea. Conclusions: The results suggest that regular daily green tea consumption may reduce leukemia risk in Chinese adults regardless of GSTM1 and GSTP1 polymorphic status. The association between green tea and adult leukemia risk varied with GSTT1 genotype and highlights further study.
    No preview · Article · Nov 2015 · European Journal of Nutrition