Eliseo Guallar
Eliseo Guallar
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Chair and Professor of the Department of Epidemiology
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Professional overview
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Dr. Guallar is an epidemiologist whose research is focused on the study of cardiovascular disease epidemiology and prevention, with an emphasis on evaluating the role of environmental and nutritional exposures in the development of cardiovascular disease. This research has made critically important and novel contributions to our understanding of risk factors for chronic disease both in the US and globally. He has published seminal articles and is a leading figure in an emerging field highlighting the risks of exposure to levels of metals previously considered safe for cardiovascular health. In addition to his work in toxic metals, Dr. Guallar has made important contributions to understanding the effects of certain micronutrients and vitamin supplements on cardiovascular disease risk and outcomes. Publications in this area were influential in changing consumer habits and attitudes towards these products. Much of this research has been funded by the National Institutes of Health, the Agency for Healthcare Research and Quality, the American Heart Association, the CDC, and other funders.
Dr. Guallar was the founding director of the Center for Clinical Epidemiology at the Samsung Medical Center and a lead investigator of the Kangbuk Samsung Cohort Study at the Kangbuk Samsung Hospital since its inception in 2010. Dr. Guallar has published over 500 research papers in peer-reviewed journals. He is also a Deputy Editor for Methods at the Annals of Internal Medicine and a past member and Chair of the Cancer, Heart, and Sleep Study Section at the National Institutes of Health.
Prior to teaching at NYU, Dr. Guallar was a Professor of Epidemiology and Medicine at the Johns Hopkins University Bloomberg School of Public Health and a core faculty member of the Welch Center for Prevention, Epidemiology, and Clinical Research at Johns Hopkins. In the Department of Epidemiology, Dr. Guallar was the Director of the Environmental and Occupational Area of Concentration and the Co-Director of the PhD Program. Dr. Guallar was also an adjunct Professor at the Department of Clinical Research Design and Evaluation of the Samsung Advanced Institute for Health Science and Technology, Sungkyunkwan University, in Seoul, Korea.
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Education
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Diploma of English, Spanish Official School of Languages at Zaragoza (Escuela Oficial de Idiomas de Zaragoza), Zaragoza, SpainMD, University of Zaragoza, Zaragoza, SpainMPH, University of Minnesota, Minneapolis, MNDrPH, Harvard University, Boston, MA
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Honors and awards
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Six Honor Calls in the MD Program, University of Zaragoza School of Medicine (1981)Fellow of Spain’s Program of Training of Graduate Research of the Ministry of Education and Science, University of Zaragoza (1988)Fulbright Scholar, sponsored by Spain’s Ministry of Health and Consumer Affairs (1989)Faculty Innovation Award, Johns Hopkins University Bloomberg School of Public Health (2001)Scientist Development Award, American Heart Association (2002)Fellow of the American Heart Association, Council on Epidemiology and Prevention (2013)Advising, Mentoring, and Teaching Recognition Award 2014 – 2015, Johns Hopkins University Bloomberg School of Public Health (2015)High Impact Research Icon, University of Malaya (2015)
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Publications
Publications
Serum selenium concentrations and diabetes in U.S. adults : National health and nutrition examination survey (NHANES) 2003-2004
AbstractLaclaustra, M., Navas-Acien, A., Stranges, S., Ordovas, J. M., & Guallar, E. (n.d.).Publication year
2009Journal title
Environmental health perspectivesVolume
117Issue
9Page(s)
1409-1413AbstractBackground: Increasing evidence suggests that high selenium levels are associated with diabetes and other cardiometabolic risk factors. Objectives: We evaluated the association of serum selenium concentrations with fasting plasma glucose, glycosylated hemoglobin levels, and diabetes in the most recently available representative sample of the U.S. population. Methods: We used a cross-sectional analysis of 917 adults ≥ 40 years of age who had a fasting morning blood sample in the National Health and Nutrition Examination Survey 2003-2004. We evaluated the association of serum selenium, measured by inductively coupled plasma-dynamic reaction cell-mass spectrometry, and diabetes, defined as a self-report of current use of hypoglycemic agents or insulin or as fasting plasma glucose ≥ 126 mg/dL. Results: Mean serum selenium was 137.1 μg/L. The multivariable adjusted odds ratio [95% confidence interval (CI)] for diabetes comparing the highest quartile of serum selenium (≥ 147 μg/L) with the lowest (< 124 μg/L) was 7.64 (3.34-17.46). The corresponding average differences (95% CI) in fasting plasma glucose and glycosylated hemoglobin were 9.5 mg/dL (3.4-15.6 mg/dL) and 0.30% (0.14-0.46%), respectively. In spline regression models, the prevalence of diabetes as well as glucose and glycosylated hemoglobin levels increased with increasing selenium concentrations up to 160 μg/L. Conclusions: In U.S. adults, high serum selenium concentrations were associated with higher prevalence of diabetes and higher fasting plasma glucose and glycosylated hemoglobin levels. Given high selenium intake in the U.S. population, further research is needed to determine the role of excess selenium levels in the development or the progression of diabetes.Serum selenium concentrations and hypertension in the US population
AbstractLaclaustra, M., Navas-Acien, A., Stranges, S., Ordovas, J. M., & Guallar, E. (n.d.).Publication year
2009Journal title
Circulation: Cardiovascular Quality and OutcomesVolume
2Issue
4Page(s)
369-376AbstractBackground-Selenium is an antioxidant micronutrient with potential interest for cardiovascular disease prevention. Few studies have evaluated the association between selenium and hypertension, with inconsistent findings. We explored the relationship of serum selenium concentrations with blood pressure and hypertension in a representative sample of the US population. Methods and Results-We undertook a cross-sectional analysis of 2638 adults ≥40 years old who participated in the 2003 to 2004 National Health and Nutrition Examination Survey. Serum selenium was measured by inductively coupled plasma-dynamic reaction cell-mass spectrometry. Hypertension was defined as blood pressure ≥140/90 mm Hg or current use of antihypertensive medication. Mean serum selenium was 137.1 μg/L. The multivariable adjusted differences (95% CIs) in blood pressure levels comparing the highest (≥150 μg/L) to the lowest (The association of biomarkers of iron status with peripheral arterial disease in US adults
AbstractMenke, A., Fernández-Real, J. M., Muntner, P., & Guallar, E. (n.d.).Publication year
2009Journal title
BMC Cardiovascular DisordersVolume
9AbstractBackground: Several studies have examined the association of biomarkers of iron metabolism with measures of carotid artery atherosclerosis, with inconsistent results. Few studies, however, have evaluated the association between biomarkers of iron metabolism and peripheral arterial disease (PAD). The purpose of this study is to examine the association of ferritin and transferrin saturation with PAD. Methods: Serum ferritin, transferrin saturation, and PAD, defined as having an ankle-brachial blood pressure indexThe effect of n-3 long-chain polyunsaturated fatty acid supplementation on urine protein excretion and kidney function : Meta-analysis of clinical trials
AbstractMiller, E. R., Juraschek, S. P., Appel, L. J., Madala, M., Anderson, C. A., Bleys, J., & Guallar, E. (n.d.).Publication year
2009Journal title
American Journal of Clinical NutritionVolume
89Issue
6Page(s)
1937-1945AbstractBackground: Chronic kidney disease is a major worldwide problem. Although epidemiologic and experimental studies suggest that n-3 long-chain polyunsaturated fatty acid (n-3 LCPUFA) supplementation may prevent or slow the progression of kidney disease, evidence from clinical trials is inconsistent. Objective: The objective was to combine evidence from controlled clinical trials to assess the effect of n-3 LCPUFA supplementation on the change in urine protein excretion (UPE) and on glomerular filtration rate (GFR). Design: We performed a meta-analysis of clinical trials that tested the effect of n-3 LCPUFA supplementation on UPE, a marker of kidney damage, and on GFR, a marker of kidney function. A random-effects model was used to pool SD effect size (Cohen's d) across studies. Results: Seventeen trials with 626 participants were included in the meta-analysis. Most trials focused on patients with a single underlying diagnosis: IgA nephropathy (n = 5), diabetes (n = 7), or lupus nephritis (n = 1). The dose of n-3 LCPUFAs ranged from 0.7 to 5.1 g/d, and the median follow-up was 9 mo. In the pooled analysis, there was a greater reduction in UPE in the n-3 LCPUFA group than in the control group: Cohen's d for all trials was 20.19 (95% CI: -0.34, -0.04; P = 0.01). In a patient with 1 g UPE/d , this corresponds to a reduction of 190 mg/d. Effects on GFR were reported in 12 trials. The decline in GFR was slower in the n-3 LCPUFA group than in the control group, but this effect was not significant (0.11; 95% CI: -0.07, 0.29; P = 0.24). Conclusions: In our meta-analysis, use of n-3 LCPUFA supplements reduced UPE but not the decline in GFR. However, small numbers of participants in trials, different methods of assessing proteinuria and GFR, and inconsistent data reporting limit the strength of these conclusions. Large, high-quality trials with clinical outcomes are warranted.Urine arsenic concentrations and species excretion patterns in American Indian communities over a 10-year period : The strong heart study
AbstractNavas-Acien, A., Umans, J. G., Howard, B. V., Goessler, W., Francesconi, K. A., Crainiceanu, C. M., Silbergeld, E. K., & Guallar, E. (n.d.).Publication year
2009Journal title
Environmental health perspectivesVolume
117Issue
9Page(s)
1428-1433AbstractBackground: Arsenic exposure in drinking water disproportionately affects small communities in some U.S. regions, including American Indian communities. In U.S. adults with no seafood intake, median total urine arsenic is 3.4 μg/L. Objective: We evaluated arsenic exposure and excretion patterns using urine samples collected over 10 years in a random sample of American Indians from Arizona, Oklahoma, and North and South Dakota who participated in a cohort study from 1989 to 1999. Methods: We measured total urine arsenic and arsenic species [inorganic arsenic (arsenite and arsenate), methylarsonate (MA), dimethylarsinate (DMA), and arsenobetaine] concentrations in 60 participants (three urine samples each, for a total of 180 urine samples) using inductively coupled plasma/mass spectrometry (ICPMS) and high-performance liquid chromatography/ICPMS, respectively. Results: Median (10th, 90th percentiles) urine concentration for the sum of inorganic arsenic, MA, and DMA at baseline was 7.2 (3.1, 16.9) μg/g creatinine; the median was higher in Arizona (12.5 μg/g), intermediate in the Dakotas (9.1 μg/g), and lower in Oklahoma (4.4 μg/g). The mean percentage distribution of arsenic species over the sum of inorganic and methylated species was 10.6% for inorganic arsenic, 18.4% for MA, and 70.9% for DMA. The intraclass correlation coefficient for three repeated arsenic measurements over a 10-year period was 0.80 for the sum of inorganic and methylated species and 0.64, 0.80, and 0.77 for percent inorganic arsenic, percent MA, and percent DMA, respectively. Conclusions: This study found low to moderate inorganic arsenic exposure and confirmed long-term constancy in arsenic exposure and urine excretion patterns in American Indians from three U.S. regions over a 10-year period. Our findings support the feasibility of analyzing arsenic species in large population-based studies with stored urine samples.Vitamin E supplementation : What's the harm in that?
AbstractMiller, E. R., & Guallar, E. (n.d.).Publication year
2009Journal title
Clinical TrialsVolume
6Issue
1Page(s)
47-49Abstract~Arsenic exposure and diabetes mellitus in the United States - Reply
AbstractNavas-Acien, A., & Guallar, E. (n.d.).Publication year
2008Journal title
JAMAVolume
300Issue
23Page(s)
2728-2729Abstract~Arsenic exposure and prevalence of type 2 diabetes in US adults
AbstractNavas-Acien, A., Silbergeld, E. K., Pastor-Barriuso, R., & Guallar, E. (n.d.).Publication year
2008Journal title
JAMAVolume
300Issue
7Page(s)
814-822AbstractContext: High chronic exposure to inorganic arsenic in drinking water has been related to diabetes development, but the effect of exposure to low to moderate levels of inorganic arsenic on diabetes risk is unknown. In contrast, arsenobetaine, an organic arsenic compound derived from seafood intake, is considered nontoxic. Objective: To investigate the association of arsenic exposure, as measured in urine, with the prevalence of type 2 diabetes in a representative sample of US adults. Design, Setting, and Participants: Cross-sectional study in 788 adults aged 20 years or older who participated in the 2003-2004 National Health and Nutrition Examination Survey (NHANES) and had urine arsenic determinations. Main Outcome Measure: Prevalence of type 2 diabetes across intake of arsenic. Results: The median urine levels of total arsenic, dimethylarsinate, and arsenobetaine were 7.1, 3.0, and 0.9 μg/L, respectively. The prevalence of type 2 diabetes was 7.7%. After adjustment for diabetes risk factors and markers of seafood intake, participants with type 2 diabetes had a 26% higher level of total arsenic (95% confidence interval [CI], 2.0%-56.0%) and a nonsignificant 10% higher level of dimethylarsinate (95% CI, -8.0% to 33.0%) than participants without type 2 diabetes, and levels of arsenobetaine were similar to those of participants without type 2 diabetes. After similar adjustment, the odds ratios for type 2 diabetes comparing participants at the 80th vs the 20th percentiles were 3.58 for the level of total arsenic (95% CI, 1.18-10.83), 1.57 for dimethylarsinate (95% CI, 0.89-2.76), and 0.69 for arsenobetaine (95% CI, 0.33-1.48). Conclusions: After adjustment for biomarkers of seafood intake, total urine arsenic was associated with increased prevalence of type 2 diabetes. This finding supports the hypothesis that low levels of exposure to inorganic arsenic in drinking water, a widespread exposure worldwide, may play a role in diabetes prevalence. Prospective studies in populations exposed to a range of inorganic arsenic levels are needed to establish whether this association is causal.Arsenic in drinking water and lung cancer : A systematic review
AbstractCelik, I., Gallicchio, L., Boyd, K., Lam, T. K., Matanoski, G., Tao, X., Shiels, M., Hammond, E., Chen, L., Robinson, K. A., Caulfield, L. E., Herman, J. G., Guallar, E., & Alberg, A. J. (n.d.).Publication year
2008Journal title
Environmental ResearchVolume
108Issue
1Page(s)
48-55AbstractExposure to inorganic arsenic via drinking water is a growing public health concern. We conducted a systematic review of the literature examining the association between arsenic in drinking water and the risk of lung cancer in humans. Towards this aim, we searched electronic databases for articles published through April 2006. Nine ecological studies, two case-control studies, and six cohort studies were identified. The majority of the studies were conducted in areas of high arsenic exposure (100 μg/L) such as southwestern Taiwan, the Niigata Prefecture, Japan, and Northern Chile. Most of the studies reported markedly higher risks of lung cancer mortality or incidence in high arsenic areas compared to the general population or a low arsenic exposed reference group. The quality assessment showed that, among the studies identified, only four assessed arsenic exposure at the individual level. Further, only one of the ecological studies presented results adjusted for potential confounders other than age; of the cohort and case-control studies, only one-half adjusted for cigarette smoking status in the analysis. Despite these methodologic limitations, the consistent observation of strong, statistically significant associations from different study designs carried out in different regions provide support for a causal association between ingesting drinking water with high concentrations of arsenic and lung cancer. The lung cancer risk at lower exposure concentrations remains uncertain.Bone lead levels and blood pressure endpoints : A meta-analysis
AbstractNavas-Acien, A., Schwartz, B. S., Rothenberg, S. J., Hu, H., Silbergeld, E. K., & Guallar, E. (n.d.).Publication year
2008Journal title
EpidemiologyVolume
19Issue
3Page(s)
496-504AbstractBACKGROUND: Previous reviews have shown increases in blood pressure and hypertension associated with increases in lead levels in blood. We performed a meta-analysis of the association of bone lead levels with systolic blood pressure, diastolic blood pressure, and hypertension using published data. METHODS: We searched Medline, Embase, and Toxline for epidemiologic studies on bone lead levels and blood pressure endpoints. We used inverse-variance weighted random-effects models to summarize the association of tibia or patella lead levels with blood pressure endpoints. RESULTS: We summarized data from 3 prospective studies and 5 cross-sectional studies. All studies measured lead levels in tibia bone and 3 studies measured lead levels in patella. For a 10 μg/g increase in tibia lead, the cross-sectional summary increases in blood pressure were 0.26 mm Hg for systolic (95% confidence interval = 0.02 to 0.50) and 0.02 mm Hg for diastolic (-0.15 to 0.19). The summary odds ratio for hypertension was 1.04 (1.01 to 1.07). For a 10 μg/g increase in patella lead, the summary odds ratio for hypertension was 1.04 (0.96 to 1.12). CONCLUSION: Systolic blood pressure and hypertension risk were associated with lead levels in tibia bone, but the magnitude of the summary estimates was small. These summary estimates, however, were based on published data and we could not evaluate nonlinear dose-response relationships, the relative contribution of bone and blood lead levels, or the influence of differences in study populations. A more detailed characterization of the association of bone lead levels and blood pressure endpoints would require a pooled analysis of individual participant data from existing studies.C-reactive protein and colorectal cancer risk : A systematic review of prospective studies
AbstractTsilidis, K. K., Branchini, C., Guallar, E., Helzlsouer, K. J., Erlinger, T. P., & Platz, E. A. (n.d.).Publication year
2008Journal title
International Journal of CancerVolume
123Issue
5Page(s)
1133-1140AbstractC-reactive protein is a sensitive but nonspecific systemic marker of inflammation. Several prospective studies have investigated the association of prediagnostic circulating C-reactive protein concentrations with the development of colorectal cancer, but the results have been inconsistent. We performed a systematic review of prospective studies of the association between prediagnostic measurements of circulating high-sensitivity C-reactive protein and development of invasive colorectal cancer. Authors of original studies were contacted to acquire uniform data. We combined relative risks (RR) for colorectal cancer associated with a one unit change in natural logarithm-transformed high-sensitivity C-reactive protein using inverse variance weighted random effects models. We identified eight eligible studies, which included 1,159 colorectal cancer cases and 37,986 controls. The summary RR per one unit change in natural log-transformed high-sensitivity C-reactive protein was 1.12 (95% confidence intervals [CI], 1.01-1.25) for colorectal cancer, 1.13 (95% CI, 1.00-1.27) for colon cancer, and 1.06 (95 % CI, 0.86-1.30) for rectal cancer. The association was stronger in men (RR, 1.18; 95% CI, 1.04-1.34) compared to women (RR, 1.09; 95% CI, 0.93-1.27) but this difference was sensitive to the findings from a single study. Prediagnostic high-sensitivity C-reactive protein concentrations were weakly associated with an increased risk for colorectal cancer. More work is needed to understand the extent to which circulating high-sensitivity C-reactive protein or other blood inflammatory markers are related to colonic inflammation.Cadmium exposure and hypertension in the 1999-2004 National Health and Nutrition Examination Survey (NHANES).
AbstractTellez-Plaza, M., Navas-Acien, A., Crainiceanu, C. M., & Guallar, E. (n.d.).Publication year
2008Journal title
Environmental health perspectivesVolume
116Issue
1Page(s)
51-56AbstractINTRODUCTION: Cadmium induces hypertension in animal models. Epidemiologic studies of cadmium exposure and hypertension, however, have been inconsistent. OBJECTIVE: We aimed to investigate the association of blood and urine cadmium with blood pressure levels and with the prevalence of hypertension in U.S. adults who participated in the 1999-2004 National Health and Nutrition Examination Survey (NHANES). METHODS: We studied participants > or = 20 years of age with determinations of cadmium in blood (n = 10,991) and urine (n = 3,496). Blood and urine cadmium were measured by atomic absorption spectrometry and inductively coupled plasma-mass spectrometry, respectively. Systolic and diastolic blood pressure levels were measured using a standardized protocol. RESULTS: The geometric means of blood and urine cadmium were 3.77 nmol/L and 2.46 nmol/L, respectively. After multivariable adjustment, the average differences in systolic and diastolic blood pressure comparing participants in the 90th vs. 10th percentile of the blood cadmium distribution were 1.36 mmHg [95% confidence interval (CI), -0.28 to 3.00] and 1.68 mmHg (95% CI, 0.57-2.78), respectively. The corresponding differences were 2.35 mmHg and 3.27 mmHg among never smokers, 1.69 mmHg and 1.55 mmHg among former smokers, and 0.02 mmHg and 0.69 mmHg among current smokers. No association was observed for urine cadmium with blood pressure levels, or for blood and urine cadmium with the prevalence of hypertension. CONCLUSIONS: Cadmium levels in blood, but not in urine, were associated with a modest elevation in blood pressure levels. The association was stronger among never smokers, intermediate among former smokers, and small or null among current smokers. Our findings add to the concern of renal and cardiovascular cadmium toxicity at chronic low levels of exposure in the general population.Carotenoids and the risk of developing lung cancer : A systematic review
AbstractGallicchio, L., Boyd, K., Matanoski, G., Tao, X., Chen, L., Lam, T. K., Shiels, M., Hammond, E., Robinson, K. A., Caulfield, L. E., Herman, J. G., Guallar, E., & Alberg, A. J. (n.d.).Publication year
2008Journal title
American Journal of Clinical NutritionVolume
88Issue
2Page(s)
372-383AbstractBackground: Carotenoids are thought to have anti-cancer properties, but findings from population-based research have been inconsistent. Objective: We aimed to conduct a systematic review of the associations between carotenoids and lung cancer. Design: We searched electronic databases for articles published through September 2007. Six randomized clinical trials examining the efficacy of β-carotene supplements and 25 prospective observational studies assessing the associations between carotenoids and lung cancer were analyzed by using random-effects meta-analysis. Results: The pooled relative risk (RR) for the studies comparing β-carotene supplements with placebo was 1.10 (95% confidence limits: 0.89, 1.36; P = 0.39). Among the observational studies that adjusted for smoking, the pooled RRs comparing highest and lowest categories of total carotenoid intake and of total carotenoid serum concentrations were 0.79 (0.71, 0.87; P < 0.001) and 0.70 (0.44, 1.11; P = 0.14), respectively. For β-carotene, highest compared with lowest pooled RRs were 0.92 (0.83, 1.01; P = 0.09) for dietary intake and 0.84 (0.66, 1.07; P = 0.15) for serum concentrations. For other carotenoids, the RRs comparing highest and lowest categories of intake ranged from 0.80 for β-cryptoxanthin to 0.89 for α-carotene and lutein-zeaxanthin; for serum concentrations, the RRs ranged from 0.71 for lycopene to 0.95 for lutein-zeaxanthin. Conclusions: β-Carotene supplementation is not associated with a decrease in the risk of developing lung cancer. Findings from prospective cohort studies suggest inverse associations between carotenoids and lung cancer; however, the decreases in risk are generally small and not statistically significant. These inverse associations may be the result of carotenoid measurements' function as a marker of a healthier lifestyle (higher fruit and vegetable consumption) or of residual confounding by smoking.Dietary iron and blood pressure
AbstractStranges, S., & Guallar, E. (n.d.).Publication year
2008Journal title
BMJVolume
337Issue
7663Page(s)
183-184Abstract~HFE C282Y homozygotes have reduced low-density lipoprotein cholesterol : the Atherosclerosis Risk in Communities (ARIC) Study
AbstractPankow, J. S., Boerwinkle, E., Adams, P. C., Guallar, E., Leiendecker-Foster, C., Rogowski, J., & Eckfeldt, J. H. (n.d.).Publication year
2008Journal title
Translational ResearchVolume
152Issue
1Page(s)
3-10AbstractRecent studies have raised questions about the long-term health risks for individuals with mutations in the HFE gene, although previous studies may have been plagued by selection bias or lack of population-based comparison groups. We examined cardiovascular disease risk factors and iron and liver biomarkers, as well as morbidity and mortality associated with the C282Y and H63D variants of HFE in the Atherosclerosis Risk in Communities (ARIC) study, which is a population-based cohort of nearly 16,000 U.S. white and black men and women who were 45-64 years old at baseline. Subjects were followed for an average of 15 years for death, incident coronary heart disease, stroke, and heart failure, and an average of 8 years for incident diabetes. The prevalence of C282Y homozygosity was 0.42% (45/10,800) in whites, which is similar to other North American population-based studies. C282Y homozygotes had significantly lower mean low-density lipoprotein (LDL) cholesterol and fibrinogen as well as higher mean levels of iron (ferritin, transferrin saturation) and liver biomarkers (alanine aminotransferase, Hepascore) compared with HFE wild-type subjects. Rates of all-cause mortality, cardiovascular disease, and diabetes were similar across HFE genotypes. These prospective, population-based data indicate higher serum iron indices and possible mild liver dysfunction or disease in some C282Y homozygotes, but they provide little evidence that HFE C282Y or H63D mutations are related to all-cause mortality, cardiovascular disease, or diabetes. Reduced LDL in C282Y homozygotes may be because of effects of excess iron on cholesterol metabolism and lipoprotein formation in the liver.Measuring arsenic exposure, metabolism, and biological effects : The role of urine proteomics
AbstractNavas-Acien, A., & Guallar, E. (n.d.).Publication year
2008Journal title
Toxicological SciencesVolume
106Issue
1Page(s)
1-4Abstract~Selenium intake and cardiovascular risk : What is new?
AbstractNavas-Acien, A., Bleys, J., & Guallar, E. (n.d.).Publication year
2008Journal title
Current Opinion in LipidologyVolume
19Issue
1Page(s)
43-49AbstractPURPOSE OF REVIEW: Selenium is an essential element with a narrow safety margin. Adequate selenium intake is needed to maximize the activity of glutathione peroxidases and other selenoproteins. This review discusses recent experimental and epidemiologic contributions on the role of selenium for the prevention of atherosclerotic cardiovascular disease. RECENT FINDINGS: Few randomized trials have evaluated the efficacy of selenium supplementation on cardiovascular endpoints. Most trials, conducted in selenium-replete populations, found no evidence of cardiovascular protection. A meta-analysis of 13 prospective cohort studies found a moderate inverse relationship between plasma/serum selenium and coronary heart disease. The interpretation of these data is complicated, however, by potential residual confounding and publication bias. In contrast, recent data from trials of selenium-containing supplements and from epidemiologic studies suggest that chronically increased selenium intake in selenium-replete populations can induce diabetes and maybe also hypercholesterolemia. SUMMARY: Current evidence is insufficient to support a protective role for selenium in cardiovascular prevention. Large high-quality randomized controlled trials and observational studies are needed across populations with different levels of selenium intake. Furthermore, subjects living in regions with high selenium intake should be aware that selenium supplements may increase their risk of diabetes and hypercholesterolemia.Serum selenium and serum lipids in US adults
AbstractBleys, J., Navas-Acien, A., Stranges, S., Menke, A., Miller, E. R., & Guallar, E. (n.d.).Publication year
2008Journal title
American Journal of Clinical NutritionVolume
88Issue
2Page(s)
416-423AbstractBackground: Selenium, an essential micronutrient, has received considerable attention for its antioxidant properties. In addition, selenium may affect several cardiometabolic risk factors, such as glucose homeostasis and lipid concentrations. However, the effects of selenium intake on the lipid profile in selenium-replete populations, such as the United States, are largely unknown. Objective: We examined the relation of serum selenium concentrations with serum lipids in a representative sample of US adults. Design: This was a cross-sectional analysis of 5452 men and women aged ≥ 20 y participating in the third National Health and Nutrition Examination survey. Serum selenium was measured by atomic absorption spectrometry. Results: The multivariable adjusted differences in total cholesterol, LDL cholesterol, HDL cholesterol, apolipoprotein B (apo B), and apolipoprotein A-I (apo A-I) comparing the highest with the lowest quartile of serum selenium were 16.6 mg/dL (95% CI: 11.6, 21.4 mg/dL), 10.9 mg/dL (95% CI: 6.4, 15.4 mg/dL), 3.2 mg/dL (95% CI: 1.6, 5.0 mg/dL), 8.9 mg/dL (95% CI: 5.6, 12.2 mg/dL), and 6.9 mg/dL (95% CI: 1.7, 12.1 mg/dL), respectively. Participants in the highest quartile of serum selenium had 10% higher concentrations of triacylglycerols than did participants in the lowest quartile (ratio of triacylglycerol concentrations: 1.10; 95% CI: 1.05, 1.17). The difference in the ratios of LDL cholesterol to HDL cholesterol and apo B to apo A-I that compared the highest with the lowest selenium quartiles were 0.11 (95% CI: -0.02, 0.25) and 0.03 (95% CI: 0.00, 0.06), respectively. Conclusion: Elevated serum selenium was associated with elevated serum concentrations of total cholesterol, LDL cholesterol, HDL cholesterol, triacylglycerols, apo B, and apo A-I among US adults, a selenium-replete population. Experimental studies are needed to determine cause and effect relations and the potential mechanisms underlying these associations.Serum selenium levels and all-cause, cancer, and cardiovascular mortality among US adults
AbstractBleys, J., Navas-Acien, A., & Guallar, E. (n.d.).Publication year
2008Journal title
Archives of Internal MedicineVolume
168Issue
4Page(s)
404-410AbstractBackground: Selenium, an essential trace element involved in defense against oxidative stress, may prevent cancer and cardiovascular disease. We evaluated the association between selenium levels and all-cause and cause-specific mortality in a representative sample of US adults. Methods: Serum selenium levels were measured in 13 887 adult participants in the Third National Health and Nutrition Examination Survey. Study participants were recruited from 1988 to 1994 and followed up for mortality for up to 12 years. Results: The mean serum selenium level was 125.6 ng/mL. The multivariate adjusted hazard ratios comparing the highest (≥130.39 ng/mL) with the lowest (The association of urinary cadmium with sex steroid hormone concentrations in a general population sample of US adult men
AbstractMenke, A., Guallar, E., Shiels, M. S., Rohrmann, S., Basaria, S., Rifai, N., Nelson, W. G., & Platz, E. A. (n.d.).Publication year
2008Journal title
BMC public healthVolume
8AbstractBackground. Studies investigating the association of cadmium and sex steroid hormones in men have been inconsistent, but previous studies were relatively small. Methods. In a nationally representative sample of 1,262 men participating in the morning examination session of phase I (1998-1991) of the third National Health and Nutrition Examination Survey, creatinine corrected urinary cadmium and serum concentrations of sex steroid hormones were measured following a standardized protocol. Results. After adjustment for age and race-ethnicity, higher cadmium levels were associated with higher levels of total testosterone, total estradiol, sex hormone-binding globulin, estimated free testosterone, and estimated free estradiol (each p-trend < 0.05). After additionally adjusting for smoking status and serum cotinine, none of the hormones maintained an association with urinary cadmium (each p-trend > 0.05). Conclusion. Urinary cadmium levels were not associated with sex steroid hormone concentrations in a large nationally representative sample of US men.A prospective study of plasma ferritin level and incident diabetes : The Atherosclerosis Risk in Communities (ARIC) Study
AbstractJehn, M. L., Guallar, E., Clark, J. M., Couper, D., Duncan, B. B., Ballantyne, C. M., Hoogeveen, R. C., Harris, Z. L., & Pankow, J. S. (n.d.).Publication year
2007Journal title
American Journal of EpidemiologyVolume
165Issue
9Page(s)
1047-1054AbstractThe authors performed a case-cohort study nested within the Atherosclerosis Risk in Communities (ARIC) Study to determine the association between plasma ferritin level and risk of type 2 diabetes mellitus. Persons with incident cases of type 2 diabetes diagnosed over an average follow-up period of 7.9 years (n = 599) were compared with a random sample of the cohort (n = 690). After adjustment for age, gender, menopausal status, ethnicity, center, smoking, and alcohol intake, the hazard ratio for diabetes, comparing the fifth quintile of ferritin with the first quintile, was 1.74 (95% confidence interval: 1.14, 2.65; p-trend < 0.001). After further adjustment for body mass index and components of the metabolic syndrome, the hazard ratio was 0.81 (95% confidence interval: 0.49, 1.34; p-trend = 0.87). From a causal perspective, there are two alternative interpretations of these findings. Elevated iron stores, reflected in elevated plasma ferritin levels, may induce baseline metabolic abnormalities that ultimately result in diabetes. Alternatively, elevated ferritin may be just one of several metabolic abnormalities related to the underlying process that ultimately results in diabetes, rather than a causal factor for diabetes. Longitudinal studies with repeated measurements of glucose and iron metabolism parameters are needed to establish the role of iron stores and plasma ferritin in diabetes development.Efficacy and safety of statin monotherapy in older adults : A meta-analysis
AbstractRoberts, C. G., Guallar, E., & Rodriguez, A. (n.d.).Publication year
2007Journal title
Journals of Gerontology - Series A Biological Sciences and Medical SciencesVolume
62Issue
8Page(s)
879-887AbstractBackground. Statin therapy significantly reduces cardiovascular events. Older patients, however, are less likely to be prescribed statins than younger patients due to concern over lack of indication, lower predictive value of cholesterol levels, and increased risk of adverse events. To determine the effect of statins on all-cause mortality and on major cardiovascular events, including stroke, we performed a meta-analysis of statin trials that included older adult participants. Methods. Mortality, cardiovascular events, and adverse event outcomes were extracted from published randomized, placebo-controlled clinical trials of persons aged 60 years and older. Results. Data on 51,351 patients were evaluated. Statins reduced all-cause mortality by 15% (95% confidence interval, 7%-22%), coronary heart disease (CHD) death by 23% (15%-29%), fatal or nonfatal myocardial infarction (MI) by 26% (22%-30%), and fatal or nonfatal stroke by 24% (10%-35%). The relative risk of cancer comparing statins to placebo was 1.06 (0.95-1.18). Adverse event data were not consistently reported. Conclusions. Statin therapy significantly reduced all-cause and CHD mortality, as well as risk of stroke and MI. Statin therapy should be offered to older patients at high risk of atherosclerotic disease events.Impact of energy intake, physical activity, and population-wide weight loss on cardiovascular disease and diabetes mortality in Cuba, 1980-2005
AbstractFranco, M., Orduñez, P., Caballero, B., Tapia Granados, J. A., Lazo, M., Bernal, J. L., Guallar, E., & Cooper, R. S. (n.d.).Publication year
2007Journal title
American Journal of EpidemiologyVolume
166Issue
12Page(s)
1374-1380AbstractCuba's economic crisis of 1989-2000 resulted in reduced energy intake, increased physical activity, and sustained population-wide weight loss. The authors evaluated the possible association of these factors with mortality trends. Data on per capita daily energy intake, physical activity, weight loss, and smoking were systematically retrieved from national and local surveys. National vital statistics from 1980-2005 were used to assess trends in mortality from diabetes, coronary heart disease, stroke, cancer, and all causes. The crisis reduced per capita daily energy intake from 2,899 calories to 1,863 calories. During the crisis period, the proportion of physically active adults increased from 30% to 67%, and a 1.5-unit shift in the body mass index distribution was observed, along with a change in the distribution of body mass index categories. The prevalence of obesity declined from 14% to 7%, the prevalence of overweight increased 1%, and the prevalence of normal weight increased 4%. During 1997-2002, there were declines in deaths attributed to diabetes (51%), coronary heart disease (35%), stroke (20%), and all causes (18%). An outbreak of neuropathy and a modest increase in the all-cause death rate among the elderly were also observed. These results suggest that population-wide measures designed to reduce energy stores, without affecting nutritional sufficiency, may lead to declines in diabetes and cardiovascular disease prevalence and mortality.Physical activity and white matter lesion progression : Assessment using MRI
AbstractPodewils, L. J., Guallar, E., Beauchamp, N., Lyketsos, C. G., Kuller, L. H., Scheltens, P., & Guallar, E. (n.d.).Publication year
2007Journal title
NeurologyVolume
68Issue
15Page(s)
1223-1226AbstractWe evaluated the association between physical activity and changes in white matter lesions (WMLs) on MRI in a sample of 179 older adults comprising 59 incident cases of Alzheimer disease, 60 persons with mild cognitive impairment, and 60 persons who remained cognitively stable over a median 5-year follow-up. Physical activity was not significantly associated with a decreased rate of periventricular or deep WML progression.Rapid response systems : A systematic review
AbstractWinters, B. D., Pham, J. C., Hunt, E. A., Guallar, E., Berenholtz, S., & Pronovost, P. J. (n.d.).Publication year
2007Journal title
Critical care medicineVolume
35Issue
5Page(s)
1238-1243AbstractCONTEXT: Rapid response systems have been advocated as a potential model to identify and intervene in patients who are experiencing deterioration on general hospital wards. OBJECTIVE: To conduct a meta-analysis to evaluate the impact of rapid response systems on hospital mortality and cardiac arrest rates. DATA SOURCE: We searched MEDLINE, EMBASE, and the Cochrane Library from January 1, 1990, to June 30, 2005, for all studies relevant to rapid response systems. We restricted the search to the English language and by age category (all adults: ≥19 years). STUDY SELECTION: We selected observational and randomized trials of rapid response systems that provided empirical data on hospital mortality and cardiac arrest in control and intervention groups. We reviewed 10,228 abstracts and identified eight relevant studies meeting these criteria. DATA SYNTHESIS: Of the included studies, five used historical controls, one used concurrent controls, and two used a cluster-randomized design. The pooled relative risk for hospital mortality comparing rapid response teams to control was 0.76 (95% confidence interval, 0.39-1.48) between the two randomized studies and 0.87 (95% confidence interval, 0.73-1.04) among the five observational studies. The pooled relative risk for cardiac arrest comparing rapid response systems to control was 0.94 (95% confidence interval, 0.79-1.13) in the single randomized study and 0.70 (95% confidence interval, 0.56-0.92) in four observational studies. CONCLUSIONS: We found weak evidence that rapid response systems are associated with a reduction in hospital mortality and cardiac arrest rates, but limitations in the quality of the original studies, the wide confidence intervals, and the presence of heterogeneity limited our ability to conclude that rapid response systems are effective interventions. Large randomized controlled trials are needed to clarify the efficacy of rapid response systems before they should become standard of care.