Etiology of Anemia in Older Mexican Adults: The Role of Hepcidin, Vitamin A and Vitamin D.
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SUBMITTER: De la Cruz-Gongora V
PROVIDER: S-EPMC8622982 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Few studies assess the malnutrition risk of older Mexican adults because most studies do not assess nutritional status. This study proposes a modified version of the Mini Nutritional Assessment (MNA) to assess the risk of malnutrition among older Mexicans adults in the Mexican Health and Aging Study (MHAS). Data comes from the 2012, 2015, and 2018 waves of the MHAS, a nationally representative study of Mexicans aged 50 and older. The sample included 13,338 participants and a subsample of 1911 with biomarker values. ROC analysis was used to calculate the cut point for malnutrition risk. This cut point was compared to the definition of malnutrition from the ESPEN criteria, BMI, low hemoglobin, or low cholesterol. Logistic regression was used to assess predictors of malnutrition risk. A score of 10 was the optimal cut point for malnutrition risk in the modified MNA. This cut point had high concordance to identify malnutrition risk compared to the ESPEN criteria (97.7%) and had moderate concordance compared to BMI only (78.6%), and the biomarkers of low hemoglobin (56.1%) and low cholesterol (54.1%). Women, those older than 70, those with Seguro Popular health insurance, and those with fair/poor health were more likely to be malnourished. The modified MNA is an important tool to assess malnutrition risk in future studies using MHAS data.
| S-EPMC8151238 | biostudies-literature
Project description:Hepcidin, the master regulator of systemic iron homeostasis, tightly influences erythrocyte production. High hepcidin levels block intestinal iron absorption and macrophage iron recycling, causing iron restricted erythropoiesis and anemia. Low hepcidin levels favor bone marrow iron supply for hemoglobin synthesis and red blood cells production. Expanded erythropoiesis, as after hemorrhage or erythropoietin treatment, blocks hepcidin through an acute reduction of transferrin saturation and the release of the erythroblast hormone and hepcidin inhibitor erythroferrone. Quantitatively reduced erythropoiesis, limiting iron consumption, increases transferrin saturation and stimulates hepcidin transcription. Deregulation of hepcidin synthesis is associated with anemia in three conditions: iron refractory iron deficiency anemia (IRIDA), the common anemia of acute and chronic inflammatory disorders, and the extremely rare hepcidin-producing adenomas that may develop in the liver of children with an inborn error of glucose metabolism. Inappropriately high levels of hepcidin cause iron-restricted or even iron-deficient erythropoiesis in all these conditions. Patients with IRIDA or anemia of inflammation do not respond to oral iron supplementation and show a delayed or partial response to intravenous iron. In hepcidin-producing adenomas, anemia is reverted by surgery. Other hepcidin-related anemias are the "iron loading anemias" characterized by ineffective erythropoiesis and hepcidin suppression. This group of anemias includes thalassemia syndromes, congenital dyserythropoietic anemias, congenital sideroblastic anemias, and some forms of hemolytic anemias as pyruvate kinase deficiency. The paradigm is non-transfusion-dependent thalassemia where the release of erythroferrone from the expanded pool of immature erythroid cells results in hepcidin suppression and secondary iron overload that in turn worsens ineffective erythropoiesis and anemia. In thalassemia murine models, approaches that induce iron restriction ameliorate both anemia and the iron phenotype. Manipulations of hepcidin might benefit all the above-described anemias. Compounds that antagonize hepcidin or its effect may be useful in inflammation and IRIDA, while hepcidin agonists may improve ineffective erythropoiesis. Correcting ineffective erythropoiesis in animal models ameliorates not only anemia but also iron homeostasis by reducing hepcidin inhibition. Some targeted approaches are now in clinical trials: hopefully they will result in novel treatments for a variety of anemias.
| S-EPMC6794341 | biostudies-literature
Project description:Anemia is prevalent in patients with infections and other inflammatory conditions. Induction of the iron regulatory hormone hepcidin has been implicated in the pathogenesis of anemia of inflammation. This review outlines recent discoveries in understanding how hepcidin and its receptor ferroportin are regulated, how they contribute to anemia of inflammation, and how this knowledge may help guide new diagnostic and therapeutic strategies for this disease.IL-6 is a primary driver for hepcidin induction in many models of anemia of inflammation, but the SMAD1/5/8 pathway also contributes, likely via Activin B and SMAD-STAT3 interactions at the hepcidin promoter. Hepcidin has an important functional role in many, but not all forms of anemia of inflammation, although hepcidin-independent mechanisms also contribute. In certain populations, hepcidin assays may help target therapy with iron or erythropoiesis-stimulating agents to patients who may benefit most. New therapies targeting the hepcidin-ferroportin axis have shown efficacy in preclinical and early clinical studies.Recent studies confirm an important role for the hepcidin-ferroportin axis in the development of anemia of inflammation, but also highlight the diverse and complex pathogenesis of this disorder depending on the underlying disease. Hepcidin-based diagnostic and therapeutic strategies offer promise to improve anemia treatment, but more work is needed in this area.
| S-EPMC4993159 | biostudies-literature
Project description:ObjectivesTo create a risk index (Mexican American Dementia Nomogram (MADeN)) that predicts dementia over a 10-year period for Mexican Americans aged 65 and older.DesignRetrospective cohort study with longitudinal analysis.SettingTexas, New Mexico, Colorado, Arizona, and California.ParticipantsHispanic Established Populations for the Epidemiologic Study of the Elderly (H-EPESE) participants (n = 1,739).MeasurementsDementia was defined as a decline of three or more points per year on the Mini-Mental State Examination and inability to perform one or more daily activities. Candidate risk factors included demographic characteristics, measures of social engagement, self-reported health conditions, ability to perform daily activities, and physical activity.ResultsThe MADeN comprised the following risk factors: age, sex, education, not having friends to count on, not attending community events, diabetes mellitus, feeling the blues, pain, impairment in instrumental activities of daily living, and unable to walk a half-mile. The area under the receiver operating characteristic curve was 0.74 (95% confidence interval (CI) = 0.70-0.78) and a score of 16 points or higher had a sensitivity of 0.65 (95% CI = 0.59-0.72) and specificity of 0.70 (95% CI = 0.67-0.73) in predicting dementia.ConclusionThe MADeN was able to predict dementia in a population of older Mexican-American adults with moderate accuracy. It has the potential to identify older Mexican-American adults who may benefit from interventions to reduce dementia risk and to educate this population about risk factors for dementia.
| S-EPMC5180363 | biostudies-literature
Project description:ObjectiveThe aim of this study was to determine the risk factors associated with severe influenza-like illness (ILI) in Mexican adults that could be useful to clinicians when assessing patients with ILI.MethodsData from adult patients enrolled from 2010 through 2014 in ILI002 - a prospective hospital-based observational cohort study - were analyzed. Etiology and clinical characteristics were compared between cases of severe ILI (defined as hospitalization and/or death) and cases of non-severe ILI.ResultsOverall, 1428 (39.0%) out of a total 3664 cases of ILI were classified as severe. Adjusted analyses showed a higher risk of severe ILI associated with signs and symptoms related to lower tract infection, i.e. cough with sputum (odds ratio (OR) 2.037, 95% confidence interval (CI) 1.206-3.477; P = 0.008), dyspnea (OR 5.044, 95% CI 2.99-8.631; and shortness of breath (OR 5.24, 95% CI 3.0839.124; P < 0.001), and with increases in lactate dehydrogenase (OR 4.426, 95% CI 2.321-8.881; P < 0.001) and C-reactive protein (OR 3.618, 95% CI 2.5955.196; P < 0.001). Further, there was an increased risk of severe ILI with a longer time between symptom onset and inclusion (OR 1.108, 95% CI 1.049-1.172; P < 0.001) and with chronic steroid use (OR 14.324, 95% CI 8.059-26.216; P < 0.001).ConclusionsRespiratory viruses can cause severe ILI. The results of this study highlight the importance of evaluating data compatible with lower tract involvement and previous use of immunosuppressants at baseline, because patients meeting these conditions may develop severe illness.
| S-EPMC9972394 | biostudies-literature
Project description:Vitamin D deficiency is common among older adults and has been linked to muscle weakness. Vitamin D supplementation has been proposed as a strategy to improve muscle function in older adults. The aim of this study was to investigate the effect of calcifediol (25-hydroxycholecalciferol) on whole genome gene expression in skeletal muscle of vitamin D deficient frail older adults. A double-blind placebo controlled trial was conducted in vitamin D deficient frail older adults (aged above 65), characterized by blood 25-hydroxycholecalciferol concentrations between 20 and 50 nmol/L. Subjects were randomized across the placebo group (n=12) and the calcifediol group (n=10, 10 µg per day). Muscle biopsies were obtained before and after six months of calcifediol or placebo supplementation and subjected to whole genome gene expression profiling using Affymetrix HuGene 2.1ST arrays. Expression of the vitamin D receptor gene was virtually undetectable in human skeletal muscle biopsies. Calcifediol supplementation led to a significant increase in blood 25-hydroxycholecalciferol levels compared to the placebo group. No difference between treatment groups was observed on strength outcomes. The whole transcriptome effects of calcifediol and placebo were very weak. Correcting for multiple testing using false discovery rate did not yield any differentially expressed genes using any sensible cut-offs. P-values were uniformly distributed across all genes, suggesting that low p-values are likely to be false positives. Partial least squares-discriminant analysis and principle component analysis was unable to separate treatment groups. Calcifediol supplementation did not affect the skeletal muscle transcriptome in frail older adults. Our findings indicate that vitamin D supplementation has no effects on skeletal muscle gene expression, suggesting that skeletal muscle may not be a direct target of vitamin D in older adults.
2019-06-10 | GSE123993 | GEO
Project description:BackgroundA growing body of research suggests exposure to high levels of outdoor air pollution may negatively affect cognitive functioning in older adults, but less is known about the link between indoor sources of air pollution and cognitive functioning. We examine the association between exposure to indoor air pollution and cognitive function among older adults in Mexico, a developing country where combustion of biomass for domestic energy remains common.MethodData come from the 2012 Wave of the Mexican Health and Aging Study. The analytic sample consists of 13 023 Mexican adults over age 50. Indoor air pollution is assessed by the reported use of wood or coal as the household's primary cooking fuel. Cognitive function is measured with assessments of verbal learning, verbal recall, attention, orientation and verbal fluency. Ordinary least squares regression is used to examine cross-sectional differences in cognitive function according to indoor air pollution exposure while accounting for demographic, household, health and economic characteristics.ResultsApproximately 16% of the sample reported using wood or coal as their primary cooking fuel, but this was far more common among those residing in the most rural areas (53%). Exposure to indoor air pollution was associated with poorer cognitive performance across all assessments, with the exception of verbal recall, even in fully adjusted models.ConclusionsIndoor air pollution may be an important factor for the cognitive health of older Mexican adults. Public health efforts should continue to develop interventions to reduce exposure to indoor air pollution in rural Mexico.
| S-EPMC5796803 | biostudies-literature
Project description:ObjectiveTo explore the association between US migration, chronic conditions (diabetes, stroke, heart attack, cancer, and hypertension), and mental health (depressive symptoms, and depression).Materials and methodsWe assessed average changes in depressive symptom scores as well as depression over time and their link with migration experience controlling for health and sociodemographic factors among older Mexican adults (50+) using 2012, 2015, and 2018 waves of the Mexican Health and Aging Study (MHAS).ResultsNon-migrants had higher average depressive symptom scores and prevalence of depression (5+ score) in 2012 and 2015, but there was no significant difference in either measure in 2018 or on changes over time.ConclusionAlthough there were no significant differences in average depressive symptoms and depression over time by migration history, this study highlights some differences in 2012 and 2015. Comparing groups across migration histories allowed the researchers to examine how life course differences impact mental health outcomes.
| S-EPMC10751990 | biostudies-literature
Project description:BackgroundIron is crucial for survival and growth of microbes. Consequently, limiting iron availability is a human antimicrobial defense mechanism. We explored iron and iron-related proteins as potential biomarkers in community-acquired pneumonia and hypothesized that infection-induced changes in these potential biomarkers differ between groups of pathogens and could predict microbial etiology.MethodsBlood samples from a prospective cohort of 267 patients with community-acquired pneumonia were analyzed for hepcidin, ferritin, iron, transferrin, and soluble transferrin receptor at admission, clinical stabilization, and a 6-week follow-up. A total of 111 patients with an established microbiological diagnosis confined to 1 microbial group (atypical bacterial, typical bacterial, or viral) were included in predictive analyses.ResultsHigh admission levels of ferritin predicted atypical bacterial versus typical bacterial etiology (odds ratio [OR], 2.26; 95% confidence interval [CI], 1.18-4.32; P = .014). Furthermore, hepcidin and ferritin predicted atypical bacterial versus viral etiology (hepcidin: OR = 3.12, 95% CI = 1.34-7.28, P = .008; ferritin: OR = 2.38, 95% CI = 1.28-4.45, P = .006). The findings were independent of C-reactive protein and procalcitonin.ConclusionsHepcidin and ferritin are potential biomarkers of microbial etiology in community-acquired pneumonia.
| S-EPMC8043258 | biostudies-literature
Project description:Chronic kidney disease affects 40% of adults aged 65 and older. Anemia of CKD is present in 30% of patients with CKD and is associated with increased cardiovascular risk, decreased quality of life, and increased mortality. Hepcidin-25 (hepcidin), the key iron regulating hormone, prevents iron egress from macrophages and thus prevents normal recycling of the iron needed to support erythropoiesis. Hepcidin levels are increased in adults and children with CKD. Vitamin D insufficiency is highly prevalent in CKD and is associated with erythropoietin hyporesponsiveness. Recently, hepcidin levels were found to be inversely correlated with vitamin D status in CKD. The aim of this study was to investigate the role of vitamin D in the regulation of hepcidin expression in vitro and in vivo. This study reports that 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), the hormonally active form of vitamin D, is associated with decreased hepcidin and increased ferroportin expression in lipopolysaccharide (LPS) stimulated THP-1 cells. 1,25(OH)2D3 also resulted in a dose-dependent decrease in pro-hepcidin cytokines, IL-6 and IL-1β, release in vitro. Further, we show that high-dose vitamin D therapy impacts systemic hepcidin levels in subjects with early stage CKD. These data suggest that improvement in vitamin D status is associated with lower systemic concentrations of hepcidin in subjects with CKD. In conclusion, vitamin D regulates the hepcidin-ferroportin axis in macrophages which may facilitate iron egress. Improvement in vitamin D status in patients with CKD may reduce systemic hepcidin levels and may ameliorate anemia of CKD.
| S-EPMC4119757 | biostudies-literature