Pamela L. Lutsey
University of Minnesota
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Featured researches published by Pamela L. Lutsey.
Circulation | 2008
Pamela L. Lutsey; Lyn M. Steffen; June Stevens
Background— The role of diet in the origin of metabolic syndrome (MetSyn) is not well understood; thus, we sought to evaluate the relationship between incident MetSyn and dietary intake using prospective data from 9514 participants (age, 45 to 64 years) enrolled in the Atherosclerosis Risk in Communities (ARIC) study. Methods and Results— Dietary intake was assessed at baseline via a 66-item food frequency questionnaire. We used principal-components analysis to derive “Western” and “prudent” dietary patterns from 32 food groups and evaluated 10 food groups used in previous studies of the ARIC cohort. MetSyn was defined by American Heart Association guidelines. Proportional-hazards regression was used. Over 9 years of follow-up, 3782 incident cases of MetSyn were identified. After adjustment for demographic factors, smoking, physical activity, and energy intake, consumption of a Western dietary pattern (Ptrend=0.03) was adversely associated with incident MetSyn. After further adjustment for intake of meat, dairy, fruits and vegetables, refined grains, and whole grains, analysis of individual food groups revealed that meat (Ptrend<0.001), fried foods (Ptrend=0.02), and diet soda (Ptrend=< 0.001) also were adversely associated with incident MetSyn, whereas dairy consumption (Ptrend=0.006) was beneficial. No associations were observed between incident MetSyn and a prudent dietary pattern or intakes of whole grains, refined grains, fruits and vegetables, nuts, coffee, or sweetened beverages. Conclusions— These prospective findings suggest that consumption of a Western dietary pattern, meat, and fried foods promotes the incidence of MetSyn, whereas dairy consumption provides some protection. The diet soda association was not hypothesized and deserves further study.
Diabetes Care | 2009
Jennifer A. Nettleton; Pamela L. Lutsey; Youfa Wang; Joao A.C. Lima; Erin D. Michos; David R. Jacobs
OBJECTIVE We determined associations between diet soda consumption and risk of incident metabolic syndrome, its components, and type 2 diabetes in the Multi-Ethnic Study of Atherosclerosis. RESEARCH DESIGN AND METHODS Diet soda consumption was assessed by food frequency questionnaire at baseline (2000–2002). Incident type 2 diabetes was identified at three follow-up examinations (2002–2003, 2004–2005, and 2005–2007) as fasting glucose >126 mg/dl, self-reported type 2 diabetes, or use of diabetes medication. Metabolic syndrome (and components) was defined by National Cholesterol Education Program Adult Treatment Panel III criteria. Hazard ratios (HRs) with 95% CI for type 2 diabetes, metabolic syndrome, and metabolic syndrome components were estimated, adjusting for demographic, lifestyle, and dietary confounders. RESULTS At least daily consumption of diet soda was associated with a 36% greater relative risk of incident metabolic syndrome and a 67% greater relative risk of incident type 2 diabetes compared with nonconsumption (HR 1.36 [95% CI 1.11–1.66] for metabolic syndrome and 1.67 [1.27–2.20] for type 2 diabetes). Of metabolic syndrome components, only high waist circumference (men ≥102 cm and women ≥88 cm) and high fasting glucose (≥100 mg/dl) were prospectively associated with diet soda consumption. Associations between diet soda consumption and type 2 diabetes were independent of baseline measures of adiposity or changes in these measures, whereas associations between diet soda and metabolic syndrome were not independent of these factors. CONCLUSIONS Although these observational data cannot establish causality, consumption of diet soda at least daily was associated with significantly greater risks of select incident metabolic syndrome components and type 2 diabetes.
Circulation | 2018
Emelia J. Benjamin; Salim S. Virani; Clifton W. Callaway; Alanna M. Chamberlain; Alex R. Chang; Susan Cheng; Stephanie E. Chiuve; Mary Cushman; Francesca N. Delling; Rajat Deo; Sarah D. de Ferranti; Jane F. Ferguson; Myriam Fornage; Cathleen Gillespie; Carmen R. Isasi; Monik Jimenez; Lori C. Jordan; Suzanne E. Judd; Daniel T. Lackland; Judith H. Lichtman; Lynda D. Lisabeth; Simin Liu; Chris T. Longenecker; Pamela L. Lutsey; Jason S. Mackey; David B. Matchar; Kunihiro Matsushita; Michael E. Mussolino; Khurram Nasir; Martin O’Flaherty
Each chapter listed in the Table of Contents (see next page) is a hyperlink to that chapter. The reader clicks the chapter name to access that chapter. Each chapter listed here is a hyperlink. Click on the chapter name to be taken to that chapter. Each year, the American Heart Association (AHA), in conjunction with the Centers for Disease Control and Prevention, the National Institutes of Health, and other government agencies, brings together in a single document the most up-to-date statistics related to heart disease, stroke, and the cardiovascular risk factors listed in the AHA’s My Life Check - Life’s Simple 7 (Figure1), which include core health behaviors (smoking, physical activity, diet, and weight) and health factors (cholesterol, blood pressure [BP], and glucose control) that contribute to cardiovascular health. The Statistical Update represents …
British Journal of Nutrition | 2007
Pamela L. Lutsey; David R. Jacobs; Sujata Kori; Elizabeth J. Mayer-Davis; Steven Shea; Lyn M. Steffen; Moyses Szklo; Russell P. Tracy
We examined the relationship between whole grain intake and obesity, insulin resistance, inflammation, diabetes and subclinical CVD using baseline data from the Multi-Ethnic Study of Atherosclerosis. Whole grain intake was measured by a 127-item FFQ in 5496 men and women free of CHD and previously known diabetes. Mean whole grain intake was 0.5 (sd 0.5) servings per d; biochemical measures reflect fasting levels. After adjustment for demographic and health behaviour variables, mean differences for the highest quintile of whole grain intake minus the lowest quintile of intake were 0.6 kg/m2 for BMI, 0.36 mg/l for C-reactive protein, 0.82 micromol/l for homocysteine, 0.15 mU/l*mmol/l for homeostasis model assessment (HOMA), 0.48 mU/l for serum insulin, 2.0 mg/dl for glucose and 5.7 % for prevalence of newly diagnosed impaired fasting glucose (glucose >or= 100 mg/dl or diabetes medication). These differences represent 11-13 % of a standard deviation of BMI, HOMA, glucose and impaired fasting glucose, but 23 %, 52 % and 80 % of a standard deviation of homocysteine, C-reactive protein and insulin, respectively. An inverse association between whole grains and urine albumin excretion was suggested but retained statistical significance after adjustment only in Chinese and Hispanic participants. No associations were observed between whole grain intake and two subclinical disease measures: carotid intima-media thickness and coronary artery calcification. Concordant with previous research, whole grain intake was inversely associated with obesity, insulin resistance, inflammation and elevated fasting glucose or newly diagnosed diabetes. Counter to hypothesis, however, whole grain intake was unrelated to subclinical CVD.
Journal of Thrombosis and Haemostasis | 2006
Pamela L. Lutsey; Mary Cushman; Lyn M. Steffen; David Green; R. G. Barr; David M. Herrington; Pamela Ouyang; Aaron R. Folsom
Summary. Background: Hemostatic factors and endothelial markers may play some role in racial/ethnic differences in cardiovascular disease (CVD) rates. However, little information exists on hemostatic factors and endothelial markers across racial/ethnic groups. Objectives: To describe, in four American racial/ethnic groups (Caucasian, Black, Hispanic, and Chinese), mean levels of selected hemostatic factors and endothelial markers. Patients and methods: Multi‐ethnic Study of Atherosclerosis baseline data were used (participant age: 45–84 years). Sex‐specific analysis of covariance models, and t‐tests for pairwise comparisons, were used to compare means of factors and markers. Adjustments were made for demographics and traditional CVD risk factors. Differences were significant at P < 0.05. Results: Blacks had the highest levels of factor VIII, D‐Dimer, plasmin–antiplasmin (PAP), and von Willebrand factor, among the highest levels of fibrinogen and E‐selectin (women only), but among the lowest levels of intercellular adhesion molecule 1 (ICAM‐1), and, in men, the lowest levels of plasminogen activator inhibitor‐1 (PAI‐1). Whites and Hispanics tended to have intermediate levels of factors and markers, although they had the highest levels of ICAM‐1, and Hispanics had the highest mean levels of fibrinogen and E‐selectin (women only). Chinese participants had among the highest levels of PAI‐1, but the lowest, or among the lowest, of all other factors and markers. No soluble thrombomodulin differences were observed. Conclusions: In this large cohort, hemostatic factor and endothelial marker mean levels varied by race/ethnicity, even after adjustment for traditional CVD risk factors.
Sleep | 2015
Xiaoli Chen; Rui Wang; Phyllis C. Zee; Pamela L. Lutsey; Sogol Javaheri; Carmela Alcántara; Chandra L. Jackson; Michelle A. Williams; Susan Redline
OBJECTIVES There is limited research on racial/ethnic variation in sleep disturbances. This study aimed to quantify the distributions of objectively measured sleep disordered breathing (SDB), short sleep duration, poor sleep quality, and self-reported sleep disturbances (e.g., insomnia) across racial/ethnic groups. DESIGN Cross-sectional study. SETTING Six US communities. PARTICIPANTS Racially/ethnically diverse men and women aged 54-93 y in the Multi-Ethnic Study of Atherosclerosis Sleep Cohort (n = 2,230). INTERVENTIONS N/A. MEASUREMENTS AND RESULTS Information from polysomnography-measured SDB, actigraphy-measured sleep duration and quality, and self-reported daytime sleepiness were obtained between 2010 and 2013. Overall, 15.0% of individuals had severe SDB (apnea-hypopnea index [AHI] ≥ 30); 30.9% short sleep duration (< 6 h); 6.5% poor sleep quality (sleep efficiency < 85%); and 13.9% had daytime sleepiness. Compared with Whites, Blacks had higher odds of sleep apnea syndrome (AHI ≥ 5 plus sleepiness) (sex-, age-, and study site-adjusted odds ratio [OR] = 1.78, 95% confidence interval [CI]: 1.20, 2.63), short sleep (OR = 4.95, 95% CI: 3.56, 6.90), poor sleep quality (OR = 1.57, 95% CI: 1.00, 2.48), and daytime sleepiness (OR = 1.89, 95% CI: 1.38, 2.60). Hispanics and Chinese had higher odds of SDB and short sleep than Whites. Among non-obese individuals, Chinese had the highest odds of SDB compared to Whites. Only 7.4% to 16.2% of individuals with an AHI ≥ 15 reported a prior diagnosis of sleep apnea. CONCLUSIONS Sleep disturbances are prevalent among middle-aged and older adults, and vary by race/ethnicity, sex, and obesity status. The high prevalence of sleep disturbances and undiagnosed sleep apnea among racial/ethnic minorities may contribute to health disparities.
Thrombosis and Haemostasis | 2009
Aaron R. Folsom; Pamela L. Lutsey; Brad C. Astor; Mary Cushman
The role of inflammation in the causation of venous thromboembolism (VTE) is uncertain. In 10,505 participants of the Atherosclerosis Risk in Communities (ARIC) Study, we assessed the association of the systemic inflammation marker, elevated C-reactive protein (CRP), with incidence of VTE (n=221) over a median of 8.3 years of follow-up. Adjusted for age, race, and sex, the hazard ratios of VTE across quintiles of CRP were 1.0, 1.61, 1.16, 1.56, and 2.31 (p for trend p<0.0007). For CRP above the upper 10 percentile (> or = 8.55 mg/L), compared with the lowest 90% of CRP values, the hazard ratio of VTE was 2.07 (95% CI 1.47, 2.94). Further adjustment for baseline hormone replacement therapy, diabetes, and body mass index attenuated the hazard ratios only slightly. For example, the adjusted hazard ratio of VTE was 1.76 (95% CI 1.23, 2.52) for CRP above versus below the 90(th) percentile. In conclusion, this prospective, population-based study suggests elevated CRP is independently associated with increased risk of VTE.
Neurobiology of Aging | 2011
Stefan Walter; Gil Atzmon; Ellen W. Demerath; Melissa Garcia; Robert C. Kaplan; Meena Kumari; Kathryn L. Lunetta; Yuri Milaneschi; Toshiko Tanaka; Gregory J. Tranah; Uwe Völker; Lei Yu; Alice M. Arnold; Emelia J. Benjamin; Reiner Biffar; Aron S. Buchman; Eric Boerwinkle; David Couper; Philip L. De Jager; Denis A. Evans; Tamara B. Harris; Wolfgang Hoffmann; Albert Hofman; David Karasik; Douglas P. Kiel; Thomas Kocher; Maris Kuningas; Lenore J. Launer; Kurt Lohman; Pamela L. Lutsey
Human longevity and healthy aging show moderate heritability (20%-50%). We conducted a meta-analysis of genome-wide association studies from 9 studies from the Cohorts for Heart and Aging Research in Genomic Epidemiology Consortium for 2 outcomes: (1) all-cause mortality, and (2) survival free of major disease or death. No single nucleotide polymorphism (SNP) was a genome-wide significant predictor of either outcome (p < 5 × 10(-8)). We found 14 independent SNPs that predicted risk of death, and 8 SNPs that predicted event-free survival (p < 10(-5)). These SNPs are in or near genes that are highly expressed in the brain (HECW2, HIP1, BIN2, GRIA1), genes involved in neural development and function (KCNQ4, LMO4, GRIA1, NETO1) and autophagy (ATG4C), and genes that are associated with risk of various diseases including cancer and Alzheimers disease. In addition to considerable overlap between the traits, pathway and network analysis corroborated these findings. These findings indicate that variation in genes involved in neurological processes may be an important factor in regulating aging free of major disease and achieving longevity.
American Journal of Public Health | 2008
Pamela L. Lutsey; Ana V. Diez Roux; David R. Jacobs; Gregory L. Burke; Jane Harman; Steven Shea; Aaron R. Folsom
OBJECTIVES We assessed whether markers of acculturation (birthplace and number of US generations) and socioeconomic status (SES) are associated with markers of subclinical cardiovascular disease-carotid artery plaque, internal carotid intima-media thickness, and albuminuria-in 4 racial/ethnic groups. METHODS With data from the Multi-Ethnic Study of Atherosclerosis (n = 6716 participants aged 45-84 years) and race-specific binomial regression models, we computed prevalence ratios adjusted for demographics and traditional cardiovascular risk factors. RESULTS The adjusted US- to foreign-born prevalence ratio for carotid plaque was 1.20 (99% confidence interval [CI] = 0.97, 1.39) among Whites, 1.91 (99% CI = 0.94, 2.94) among Chinese, 1.62 (99% CI = 1.28, 2.06) among Blacks, and 1.23 (99% CI = 1.15, 1.31) among Hispanics. Greater carotid plaque prevalence was found among Whites, Blacks, and Hispanics with a greater number of generations with US residence (P < .001) and among Whites with less education and among Blacks with lower incomes. Similar associations were observed with intima-media thickness. There was also evidence of an inverse association between albuminuria and SES among Whites and Hispanics. CONCLUSIONS Greater US acculturation and lower SES were associated with a higher prevalence of carotid plaque and greater intima-media thickness but not with albuminuria. Maintenance of healthful habits among recent immigrants should be encouraged.
American Journal of Epidemiology | 2011
Daniel Duprez; David R. Jacobs; Pamela L. Lutsey; David A. Bluemke; Lyndia C. Brumback; Joseph F. Polak; Carmen A. Peralta; Philip Greenland; Richard A. Kronmal
Functional biomarkers like large artery elasticity (LAE) and small artery elasticity (SAE) may predict cardiovascular disease (CVD) events beyond blood pressure. The authors examined the prognostic value of LAE and SAE for clinical CVD events among 6,235 Multi-Ethnic Study of Atherosclerosis participants who were initially aged 45-84 years and without symptomatic CVD. LAE and SAE were derived from diastolic pulse contour analysis. During a median 5.8 years of follow-up between 2000 and 2008, 454 adjudicated CVD events occurred, including 256 cases of coronary heart disease (CHD), 93 strokes, and 126 heart failures (multiple diagnoses were possible). After adjustment for age, race/ethnicity, sex, clinic, height, heart rate, body mass index, systolic and diastolic blood pressure, use of antihypertensive and cholesterol-lowering medications, smoking, total cholesterol, high density lipoprotein cholesterol, triglycerides, diabetes, and high-sensitivity C-reactive protein, the hazard ratio for any CVD per standard-deviation increase in SAE was 0.71 (95% confidence interval: 0.61, 0.83; P < 0.0001). The lowest (stiffest) SAE quartile had a hazard ratio of 2.28 (95% confidence interval: 1.55, 3.36) versus the highest (most elastic) quartile. The net reclassification index, conditional on base risk, was 0.11. SAE was significantly associated with future CHD, stroke, and heart failure. After adjustment, LAE was not significantly related to CVD. In asymptomatic participants free of overt CVD, lower SAE added prognostic information for CVD, CHD, stroke, and heart failure events.