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Dietary intake/status of the trace mineral Se may affect the risk of developing hypertensive conditions of pregnancy, i.e. pre-eclampsia and pregnancy-induced hypertension (PE/PIH). In the present study, we evaluated Se status in UK pregnant women to establish whether pre-pregnant Se status or Se supplementation affected the risk of developing PE/PIH. The samples originated from the SPRINT (Selenium in PRegnancy INTervention) study that randomised 230 UK primiparous women to treatment with Se (60 μg/d) or placebo from 12 weeks of gestation. Whole-blood Se concentration was measured at 12 and 35 weeks, toenail Se concentration at 16 weeks, plasma selenoprotein P (SEPP1) concentration at 35 weeks and plasma glutathione peroxidase (GPx3) activity at 12, 20 and 35 weeks. Demographic data were collected at baseline. Participants completed a FFQ. UK pregnant women had whole-blood Se concentration lower than the mid-range of other populations, toenail Se concentration considerably lower than US women, GPx3 activity considerably lower than US and Australian pregnant women, and low baseline SEPP1 concentration (median 3·00, range 0·90–5·80 mg/l). Maternal age, education and social class were positively associated with Se status. After adjustment, whole-blood Se concentration was higher in women consuming Brazil nuts (P= 0·040) and in those consuming more than two seafood portions per week (P= 0·054). A stepwise logistic regression model revealed that among the Se-related risk factors, only toenail Se (OR 0·38, 95 % CI 0·17, 0·87, P= 0·021) significantly affected the OR for PE/PIH. On excluding non-compliers with Se treatment, Se supplementation also significantly reduced the OR for PE/PIH (OR 0·30, 95 % CI 0·09, 1·00, P= 0·049). In conclusion, UK women have low Se status that increases their risk of developing PE/PIH. Therefore, UK women of childbearing age need to improve their Se status.

Purpose A vegan diet is associated with health benefits but may also lead to inadequate intake of essential nutrients. Due to the lower selenium content in plant-based compared to animal-based foods, many vegans do not reach the recommended selenium intake in Europe. The only plant-based food with high selenium content is the Brazil nut, even though there is also a high variability. Therefore, we investigated the effectiveness of Brazil nut butter compared to a dietary supplement as selenium source to improve the selenium status of vegans and omnivores. Methods 44 vegans and 42 omnivores were randomly assigned to one of three intervention groups, either receiving placebo or consuming additional 55 µg of selenium daily as Brazil nut butter or supplement for two weeks. Serum selenium concentrations, glutathione peroxidase 3 (GPX3), and selenoprotein P (SELENOP) were measured at baseline and after intervention. Additionally, dietary selenium intake was estimated using a five-day dietary protocol. Results The estimated selenium intake was significantly lower in vegans compared to omnivores and correlated with all three selenium biomarkers. Independent of the dietary pattern (vegan or omnivore), Brazil nut butter as well as supplement significantly increased serum selenium and SELENOP concentrations, while there were no changes in the placebo groups. Both interventions were equally effective in increasing selenium levels, but the upregulation of SELENOP was more pronounced in vegans than in omnivores. Conclusion Brazil nuts are a plant-based source of selenium suitable for vegans and omnivores to improve their selenium status when consumed once in a while. Trial registration number and date of registration Clinical trials registration number: NCT05814874, April 18 2023.

PURPOSE: Oxidative stress is closely related to cognitive impairment, and the antioxidant system may be a potential therapeutic target to preserve cognitive function in older adults. Selenium plays an important antioxidant role through selenoproteins. This controlled trial aimed to investigate the antioxidant and cognitive effects of the consumption of Brazil nuts, the best selenium food source. METHODS: We enrolled 31 older adults with mild cognitive impairment (MCI) who were randomly assigned to ingestion of Brazil nuts or to the control group. Participants of the treatment group consumed one Brazil nut daily (estimated 288.75 µg/day) for 6 months. Blood selenium concentrations, erythrocyte glutathione peroxidase (GPx) activity, oxygen radical absorbance capacity, and malondialdehyde were evaluated. Cognitive functions were assessed with the CERAD neuropsychological battery. RESULTS: Eleven participants of the treated group and nine of the control group completed the trial. The mean age of the participants was 77.7 (±5.3) years, 70 % of whom were female. We observed increased selenium levels after the intervention, whereas the control group presented no change. Among the parameters related to the antioxidant system, only erythrocyte GPx activity change was significantly different between the groups (p = 0.006). After 6 months, improvements in verbal fluency (p = 0.007) and constructional praxis (p = 0.031) were significantly greater on the supplemented group when compared with the control group. CONCLUSION: Our results suggest that the intake of Brazil nut restores selenium deficiency and provides preliminary evidence that Brazil nut consumption can have positive effects on some cognitive functions of older adults with MCI.

Although cross-sectional studies have shown a positive association between Se and cholesterol concentrations, a recent randomised controlled trial in 501 elderly UK individuals of relatively low-Se status found that Se supplementation for 6 months lowered total plasma cholesterol. The Danish PRECISE (PREvention of Cancer by Intervention with Selenium) pilot study (ClinicalTrials.gov ID: NCT01819649) was a 5-year randomised, double-blinded, placebo-controlled trial with four groups (allocation ratio 1:1:1:1). Men and women aged 60–74 years (n 491) were randomised to 100 (n 124), 200 (n 122) or 300 (n 119) μg Se-enriched yeast or matching placebo-yeast tablets (n 126) daily for 5 years. A total of 468 participants continued the study for 6 months and 361 participants, equally distributed across treatment groups, continued for 5 years. Plasma samples were analysed for total and HDL-cholesterol and for total Se concentrations at baseline, 6 months and 5 years. The effect of different doses of Se supplementation on plasma lipid and Se concentrations was estimated by using linear mixed models. Plasma Se concentration increased significantly and dose-dependently in the intervention groups after 6 months and 5 years. Total cholesterol decreased significantly both in the intervention groups and in the placebo group after 6 months and 5 years, with small and nonsignificant differences in changes in plasma concentration of total cholesterol, HDL-cholesterol, non-HDL-cholesterol and total:HDL-cholesterol ratio between intervention and placebo groups. The effect of long-term supplementation with Se on plasma cholesterol concentrations or its sub-fractions did not differ significantly from placebo in this elderly population.

Pre-eclampsia is a serious hypertensive condition of pregnancy associated with high maternal and fetal morbidity and mortality. Se intake or status has been linked to the occurrence of pre-eclampsia by our own work and that of others. We hypothesised that a small increase in the Se intake of UK pregnant women of inadequate Se status would protect against the risk of pre-eclampsia, as assessed by biomarkers of pre-eclampsia. In a double-blind, placebo-controlled, pilot trial, we randomised 230 primiparous pregnant women to Se (60 μg/d, as Se-enriched yeast) or placebo treatment from 12 to 14 weeks of gestation until delivery. Whole-blood Se concentration was measured at baseline and 35 weeks, and plasma selenoprotein P (SEPP1) concentration at 35 weeks. The primary outcome measure of the present study was serum soluble vascular endothelial growth factor receptor-1 (sFlt-1), an anti-angiogenic factor linked with the risk of pre-eclampsia. Other serum/plasma components related to the risk of pre-eclampsia were also measured. Between 12 and 35 weeks, whole-blood Se concentration increased significantly in the Se-treated group but decreased significantly in the placebo group. At 35 weeks, significantly higher concentrations of whole-blood Se and plasma SEPP1 were observed in the Se-treated group than in the placebo group. In line with our hypothesis, the concentration of sFlt-1 was significantly lower at 35 weeks in the Se-treated group than in the placebo group in participants in the lowest quartile of Se status at baseline ( P = 0·039). None of the secondary outcome measures was significantly affected by treatment. The present finding that Se supplementation has the potential to reduce the risk of pre-eclampsia in pregnant women of low Se status needs to be validated in an adequately powered trial.

Blood selenium (Se) concentrations differ substantially by population and could be influenced by genetic variants, increasing Se deficiency-related diseases. We conducted a genome-wide association study (GWAS) to identify single nucleotide polymorphisms (SNPs) associated with serum Se deficiency in 382 adults with admixed ancestry. Genotyping arrays were combined to yield 90,937 SNPs. R packages were applied to quality control and imputation. We also performed the ancestral proportion analysis. The Search Tool for the Retrieval of Interacting Genes was used to interrogate known protein–protein interaction networks (PPIs). Our ancestral proportion analysis estimated 71% of the genome was from Caucasians, 22% was from Africans, and 8% was from East Asians. We identified the SNP rs1561573 in the TraB domain containing 2B (TRABD2B), rs425664 in MAF bZIP transcription factor (MAF), rs10444656 in spermatogenesis-associated 13 (SPATA13), and rs6592284 in heat shock protein nuclear import factor (HIKESHI) genes. The PPI analysis showed functional associations of Se deficiency, thyroid hormone metabolism, NRF2-ARE and the Wnt pathway, and heat stress. Our findings show evidence of a genetic association between Se deficiency and metabolic pathways indirectly linked to Se regulation, reinforcing the complex relationship between Se intake and the endogenous factors affecting the Se requirements for optimal health.

Background We studied the efficacy and safety of selenium supplementation in patients who had peripartum cardiomyopathy (PPCM) and selenium deficiency. Methods We randomly assigned 100 PPCM patients with left ventricular ejection fraction (LVEF) < 45% and selenium deficiency (< 70 μg/L) to receive either oral Selenium (L-selenomethionine) 200 μg/day for 3 months or nothing, in addition to recommended therapy, in an open-label randomised trial. The primary outcome was a composite of persistence of heart failure (HF) symptoms, unrecovered LV systolic function (LVEF < 55%) or death from any cause. Results Over a median of 19 months, the primary outcome occurred in 36 of 46 patients (78.3%) in the selenium group and in 43 of 54 patients (79.6%) in the control group (hazard ratio [HR] 0.69; 95% confidence interval [CI] 0.43–1.09; p  = 0.113). Persistence of HF symptoms occurred in 18 patients (39.1%) in the selenium group and in 37 patients (68.5%) in the control group (HR 0.53; 95% CI 0.30–0.93; p  = 0.006). LVEF < 55% occurred in 33 patients (71.7%) in the selenium group and in 38 patients (70.4%) in the control group (HR 0.91; 95% CI 0.57–1.45; p  = 0.944). Death from any cause occurred in 3 patients (6.5%) in the selenium group and in 9 patients (16.7%) in the control group (HR 0.37; 95% CI 0.10–1.37; p  = 0.137). Conclusions In this study, selenium supplementation did not reduce the risk of the primary outcome, but it significantly reduced HF symptoms, and there was a trend towards a reduction of all-cause mortality. Clinical trial registration ClinicalTrials.gov Identifier: NCT03081949.

Purpose This study aims to explore the interaction of Selenium (Se) deficiency and HT-2 toxin on cartilage homeostasis and the effect of Notch signaling pathway in this process. Methods Male C57BL/6 mice were randomly assigned to different dietary groups and subjected to either a Se-deficiency diet or a control diet for 4 weeks, followed by exposure to varying doses of HT-2 toxin for 4 weeks. Primary mouse chondrocytes were extracted and treated with DAPT (N-[N-(3,5-Difluorophenacetyl)-L-alanyl]-S-phenylglycine t-butyl ester), a γ-secretase inhibitor for the Notch signaling pathway, before combined intervention. Histological evaluation and transmission electron microscopy (TEM) were applied to assess cartilage damage, while immunohistochemical (IHC) analysis and Quantitative real-time polymerase chain reaction (qRT-PCR) were performed to detect extracellular matrix (ECM) metabolism and Notch signaling. Results HT-2 toxin, alone or in combination with Se deficiency, led to significant cartilage injury characterized by chondrocyte necrosis and ultrastructural abnormalities. IHC revealed increased expression of Adamts5 and decreased expression of Col2a1 and Acan in cartilage following exposure to HT-2 toxin, indicative of ECM degradation, which could be aggravated under Se deficiency. Additionally, activation of the Notch signaling pathway was observed in response to HT-2 toxin and Se deficiency, with upregulation of Notch pathway-related components. In vitro experiments further confirmed the role of the Notch pathway in ECM metabolism regulation, with partial protection against ECM depletion caused by HT-2 toxin and Se deficiency observed upon inhibition of the Notch pathway using DAPT. Conclusion This study demonstrate that Se deficiency exacerbates HT-2 toxin-induced cartilage degradation via Notch signaling activation, highlighting the interplay of environmental mycotoxins and nutritional deficits in KBD etiology and identify Notch signaling as a therapeutic target to mitigate disease progression.

Hydrogen sulfide (H2S), an endogenous gasotransmitter, plays an important role in apoptosis. Exudative diathesis (ED) disease is associated with dietary selenium (Se) deficiency in broilers. The liver is one of the target organs of Se deficiency; however, little is known about the effect of H2S on apoptosis via mitochondrial pathways in the livers of broilers with ED disease. In the present study, we aimed to investigate the correlation between endogenous H2S and mitochondrial-mediated apoptosis in the livers of broilers with ED disease, as induced by Se deficiency. One hundred twenty healthy, 1-day-old broilers were randomly assigned to one of two groups (60 each) based on diet: Basal diet (control group, 0.2 mg/kg Se) or a low-Se diet (−Se group, 0.033 mg/kg Se). At day 20, 15 broilers of a similar weight were sacrificed from the control group, while the same number of broilers were euthanatized from the −Se group when displaying typical symptoms of ED between days 18 and 25. The livers were collected, and apoptosis was measured using a TUNEL assay. Additionally, H2S concentration, the expression of H2S synthases of cystathionine γ-lyase (CSE), cystathionine β-synthase (CBS), and 3-mercaptopyruvate sulfurtransferase (3-MST), as well as mitochondrial apoptosis-related genes of Bcl-2, Bax, Bak, Cyt-C, Caspase-9, Caspase-3, and p53, were examined in livers. The results indicated that Se deficiency could induce apoptosis in the livers of broilers. Swelling, fractures, and vacuolization were visible in the mitochondrial cristae in the livers of the −Se group. The expression of H2S synthase-related genes and H2S concentration was significantly enhanced (P < 0.05) in the livers of the −Se group compared to controls. Moreover, a low-Se diet downregulated (P < 0.05) the level of Bcl-2 and upregulated (P < 0.05) the levels of Bax, Bak, Cyt-C, Caspase-9, Caspase-3, and p53. These results suggest that an H2S increase in the livers of ED broilers, which was induced by Se deficiency, is related to apoptosis mediated by mitochondrial pathways.

The study aimed to determine if selenium deficiency, serum ceruloplasmin and traditional birth practices are risk factors for peripartum cardiomyopathy (PPCM), in Kano, Nigeria. This is a case-control study carried out in three hospitals, and PPCM patients were followed up for six months. Critically low serum selenium concentration was defined as <70 µg/L. A total of 39 PPCM patients and 50 controls were consecutively recruited after satisfying the inclusion criteria. Mean serum selenium in patients (61.7 ± 14.9 µg/L) was significantly lower than in controls (118.4 ± 45.6 µg/L) (p < 0.001). The prevalence of serum selenium <70 µg/L was significantly higher among patients (76.9%) than controls (22.0%) (p < 0.001). The mean ceruloplasmin and prevalence of socio-economic indices, multiparity, pregnancy-induced hypertension, obesity and twin pregnancy were not different between the groups (p > 0.05). Logistic regression showed that rural residency significantly increased the odds for serum selenium <70 µg/L by 2.773-fold (p = 0.037). Baseline serum levels of selenium and ceruloplasmin were not associated with six-month mortality. This study has shown that selenium deficiency is a risk factor for PPCM in Kano, Nigeria, and is related to rural residency. However, serum ceruloplasmin, customary birth practices and some other characteristics were not associated with PPCM in the study area.