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Dive into the research topics where Lisa B. Rafalson is active.

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Featured researches published by Lisa B. Rafalson.


Journal of Hypertension | 2010

A population-based study of reduced sleep duration and hypertension: the strongest association may be in premenopausal women.

Saverio Stranges; Joan Dorn; Francesco P. Cappuccio; Richard P. Donahue; Lisa B. Rafalson; Kathleen M. Hovey; Jo L. Freudenheim; Ngianga-Bakwin Kandala; Michelle A. Miller; Maurizio Trevisan

Objectives Recent evidence indicates that reduced sleep duration may be associated with an increased risk of hypertension with possibly stronger effects among women than men. We therefore examined cross-sectional sex-specific associations of sleep duration with hypertension in a large population-based sample from the Western New York Health Study (1996<2001). Methods Participants were 3027 white men (43.5%) and women (56.5%) without prevalent cardiovascular disease (median age 56 years). Hypertension was defined as blood pressure at least 140 or at least 90&mmHg or regular use of antihypertensive medication. Multivariate logistic regression analyses were performed to estimate odds ratios (ORs) of hypertension comparing less than 6&h of sleep per night versus the reference category (&6&h) while accounting for a number of potential confounders. Results In multivariate analyses, less than 6&h of sleep was associated with a significant increased risk of hypertension compared to sleeping at least 6&h per night, only among women [OR&=&1.66 (1.09 to 2.53)]. No significant association was found among men [OR&=&0.93 (0.62 to 1.41)]. In subgroup analyses by menopausal status, the effect was stronger among premenopausal women [OR&=&3.25 (1.37 to 7.76)] than among postmenopausal women [OR&=&1.49 (0.92 to 2.41)]. Conclusion Reduced sleep duration, by increasing the risk of hypertension, may produce detrimental cardiovascular effects among women. The association is independent of socioeconomic status, traditional cardiovascular risk factors, and psychiatric comorbidities, and is stronger among premenopausal women. Prospective and mechanistic evidence is necessary to support causality.


Diabetes Care | 2007

Sex Differences in Endothelial Function Markers Before Conversion to Pre-Diabetes: Does the Clock Start Ticking Earlier Among Women?: The Western New York Study

Richard P. Donahue; Karol Rejman; Lisa B. Rafalson; Jacek Dmochowski; Saverio Stranges; Maurizio Trevisan

OBJECTIVE—We examined whether biomarkers of endothelial function, fibrinolysis/thrombosis and adiponectin, predict the progression from normal to pre-diabetes more strongly among women than men over 6 years of follow-up from the Western New York Health Study. RESEARCH DESIGN AND METHODS—In 2002–2004, 1,455 participants from the Western New York Health Study, who were free of type 2 diabetes and cardiovascular disease at baseline (1996–2001), were selected for reexamination. An incident case of pre-diabetes was defined as fasting glucose <100 mg/dl at the baseline examination and ≥100 and <126 mg/dl at the follow-up examination. Biomarkers of endothelial function (E-selectin and soluble intracellular adhesion molecule-1 [sICAM-1]), fibrinolysis/thrombosis (plasminogen activator inhibitor-1 [PAI-1]), and fasting insulin, adiponectin, and inflammation (high-sensitivity C-reactive protein) were measured in frozen (−190°C) baseline samples. RESULTS—Multivariate analyses revealed higher adjusted mean values of biomarkers of endothelial dysfunction (E-selectin and sICAM-1) and fibrinolysis (PAI-1) and lower mean values of adiponectin only among women who developed pre-diabetes compared with control subjects. Formal tests for interaction between sex and case/control status were statistically significant for E-selectin (P = 0.042), PAI-1 (P = 0.001), sICAM-1 (P = 0.011), and frequency of hypertension (P < 0.001). CONCLUSIONS—These results support the concept that women who progressed from normoglycemia to pre-diabetes have greater endothelial dysfunction than men as well as more hypertension and a greater degree of fibrinolysis/thrombosis. Whether this relates to the higher risk of heart disease among diabetic women awaits further study.


Annals of Epidemiology | 2010

SHORT SLEEP DURATION IS ASSOCIATED WITH THE DEVELOPMENT OF IMPAIRED FASTING GLUCOSE: THE WESTERN NEW YORK HEALTH STUDY

Lisa B. Rafalson; Richard P. Donahue; Saverio Stranges; Michael J. LaMonte; Jacek Dmochowski; Joan Dorn; Maurizio Trevisan

PURPOSE To examine whether sleep duration was associated with incident-impaired fasting glucose (IFG) over 6 years of follow-up in the Western New York Health Study. METHODS Participants (N = 1,455, 68% response rate) who were free of type 2 diabetes and known cardiovascular disease at baseline (1996-2001) were reexamined in the period 2003-2004. A nested case-control study was conducted. Cases had fasting plasma glucose (FPG) less than 100 mg/dL at baseline and 100 to 125 mg/dL at follow-up: controls (n = 272) had FPG less than 100 mg/dL at both exams. Cases (n = 91) were individually matched to three controls (n = 272) on sex, race, and year of study enrollment. Average sleep duration was categorized as short (<6 hours), mid-range (6 to 8 hours), and long (>8 hours). RESULTS In multivariate conditional logistic regression after adjustment for several diabetes risk factors, the odds ratio (OR) of IFG among short sleepers was 3.0 (95% confidence limit [CL]: 1.05, 8.59) compared to mid-range sleepers. There was no association between long sleep and IFG: OR 1.6 (95% CL: 0.45, 5.42). Adjustment for insulin resistance attenuated the association only among short sleepers: OR 2.5 (95% CL: 0.83, 7.46). CONCLUSIONS Short sleep duration was associated with an elevated risk of IFG. Insulin resistance appears to mediate this association.


Diabetes Care | 2007

Elevated cystatin C concentration and progression to pre-diabetes: the Western New York study.

Richard P. Donahue; Saverio Stranges; Karol Rejman; Lisa B. Rafalson; Jacek Dmochowski; Maurizio Trevisan

OBJECTIVE— We conducted a nested case-control investigation to examine whether elevated baseline concentrations of cystatin C predicted progression from normoglycemia to pre-diabetes over 6 years of follow-up from the Western New York Health Study. RESEARCH DESIGN AND METHODS— In 2002–2004, 1,455 participants from the Western New York Health Study, who were free of type 2 diabetes and known cardiovascular disease at baseline (1996–2001), were reexamined. An incident case of pre-diabetes was defined as an individual with fasting glucose <100 mg/dl at the baseline examination and ≥100 and ≤125 mg/dl at the follow-up examination, thereby eliminating individuals with prevalent pre-diabetics. All case patients (n = 91) were matched 1:3 to control participants based on sex, race/ethnicity, and year of study enrollment. All control subjects had fasting glucose levels <100 mg/dl at both baseline and follow-up examinations. Cystatin C concentrations and the urinary albumin-to-creatinine ratio were measured from frozen (−196°C) baseline blood and urine samples. Serum creatinine concentrations were available from the baseline examination only. RESULTS— Multivariate conditional logistic regression analyses adjusted for age, baseline glucose level, homeostasis model assessment of insulin resistance, BMI, hypertension, estimated glomerular filtration rate, cigarette smoking, and alcohol use revealed a significantly increased risk of progression to pre-diabetes among those with elevated baseline concentrations of cystatin C (odds ratio 3.28 [95% CI 1.43–7.54]) (upper quintile versus the remainder). Results of secondary analyses that considered high-sensitivity C-reactive protein, interleukin-6, E-selectin, or soluble intercellular adhesion molecule-1 did not alter these results. CONCLUSIONS— These results suggest that cystatin C was associated with a threefold excess risk of progression to pre-diabetes in this population.


Archive | 2007

Elevated cystatin-C concentration is associated with progression to prediabetes: the Western New York Study

Richard P. Donahue; Saverio Stranges; Karol Rejman; Lisa B. Rafalson; Jacek Dmochowski; Maurizio Trevisan

OBJECTIVE— We conducted a nested case-control investigation to examine whether elevated baseline concentrations of cystatin C predicted progression from normoglycemia to pre-diabetes over 6 years of follow-up from the Western New York Health Study. RESEARCH DESIGN AND METHODS— In 2002–2004, 1,455 participants from the Western New York Health Study, who were free of type 2 diabetes and known cardiovascular disease at baseline (1996–2001), were reexamined. An incident case of pre-diabetes was defined as an individual with fasting glucose <100 mg/dl at the baseline examination and ≥100 and ≤125 mg/dl at the follow-up examination, thereby eliminating individuals with prevalent pre-diabetics. All case patients (n = 91) were matched 1:3 to control participants based on sex, race/ethnicity, and year of study enrollment. All control subjects had fasting glucose levels <100 mg/dl at both baseline and follow-up examinations. Cystatin C concentrations and the urinary albumin-to-creatinine ratio were measured from frozen (−196°C) baseline blood and urine samples. Serum creatinine concentrations were available from the baseline examination only. RESULTS— Multivariate conditional logistic regression analyses adjusted for age, baseline glucose level, homeostasis model assessment of insulin resistance, BMI, hypertension, estimated glomerular filtration rate, cigarette smoking, and alcohol use revealed a significantly increased risk of progression to pre-diabetes among those with elevated baseline concentrations of cystatin C (odds ratio 3.28 [95% CI 1.43–7.54]) (upper quintile versus the remainder). Results of secondary analyses that considered high-sensitivity C-reactive protein, interleukin-6, E-selectin, or soluble intercellular adhesion molecule-1 did not alter these results. CONCLUSIONS— These results suggest that cystatin C was associated with a threefold excess risk of progression to pre-diabetes in this population.


Annals of Epidemiology | 2009

Cigarette smoking is associated with conversion from normoglycemia to impaired fasting glucose: the Western New York Health Study.

Lisa B. Rafalson; Richard P. Donahue; Jacek Dmochowski; Karol Rejman; Joan Dorn; Maurizio Trevisan

PURPOSE To determine whether cigarette smoking is associated with the conversion from normoglycemia to impaired fasting glucose (IFG). METHODS During the years 2003 and 2004, 1,455 participants (mean age, 56.5 years; range, 35-79 years) from the Western New York Health Study who were free of type 2 diabetes and known cardiovascular disease at baseline (1996-2001) were reexamined (68% response rate). Incident IFG was defined as a subject whose baseline fasting plasma glucose was <100mg/dL (normoglycemic) and between 100 and 125 mg/dL at follow-up. Prevalent IFG (n=528) was excluded. Baseline smoking status was categorized as never, former, or current. RESULTS Of the 1,455 participants, 924 were normoglycemic at baseline: 101/924 converted to IFG over 6 years. Compared with those who remained normoglycemic, converters to IFG were at baseline older, had a larger body mass index, more likely to be hypertensive, currently smoke, and have a family history of type 2 diabetes mellitus (all p<0.05). Multivariate logistic regression demonstrated that compared with subjects who remained normoglycemic, the odds ratio of incident IFG among former and current smokers (vs. never) was 1.68 (95% confidence interval: 0.99-2.80) and 2.35 (95% confidence interval: 1.17-4.72) (p trend=0.008), respectively. CONCLUSION Smoking was positively associated with incident IFG after accounting for several putative risk factors.


Obesity | 2008

Additional Contribution of Emerging Risk Factors to the Prediction of the Risk of Type 2 Diabetes: Evidence From the Western New York Study

Saverio Stranges; Lisa B. Rafalson; Jacek Dmochowski; Karol Rejman; Russell P. Tracy; Maurizio Trevisan; Richard P. Donahue

Objective: To examine whether several biomarkers of endothelial function and inflammation improve prediction of type 2 diabetes over 5.9 years of follow‐up, independent of traditional risk factors.


Obesity | 2013

The association between acanthosis nigricans and dysglycemia in an ethnically diverse group of eighth grade students

Lisa B. Rafalson; Trang Pham; Steven M. Willi; Marsha D. Marcus; Ann Jessup; Tom Baranowski

The purpose of this study was to describe the prevalence of acanthosis nigricans (AN) and to quantify its association with dysglycemia in an ethnically diverse group of eighth‐grade students.


Clinical Pediatrics | 2011

Screening Obese Students for Acanthosis Nigricans and Other Diabetes Risk Factors in the Urban School-Based Health Center

Lisa B. Rafalson; Jill Eysaman; Teresa Quattrin

Objective. To determine the prevalence of acanthosis nigricans (AN) and other diabetes risk factors in urban school health clinics. Methods. During the period 2006-2009 nurse practitioners (NPs) screened students who had a BMI ≥ 95th percentile and 1 additional diabetes risk factor. Blood glucose (BG) was measured by finger stick. NPs were trained on how to ascertain the presence of AN on the neck area. Results. NPs screened 854 students (mean age 11.4 years, 60.5% female, and 73.3% black). AN and elevated BG were found among 26% and 6.4% of students, respectively. Females and minorities were respectively 50% and 4 times more likely to have AN. Youth with AN were twice as likely to have elevated glucose. Conclusion. AN can be easily identified by trained health care professionals even in busy school-based clinic settings. Checking for AN and appropriate education and counseling should become a routine part of electronic documentation in overweight youth.


European Journal of Preventive Cardiology | 2009

Vitality and recurrent event risk in acute myocardial infarction survivors

Brent A. Williams; Joan Dorn; Richard P. Donahue; Kathleen M. Hovey; Lisa B. Rafalson; Maurizio Trevisan

Background Low vitality, characterized by fatigue and lack of energy, is common among survivors of acute myocardial infarction (AMI) and has been shown to be associated with increased risk of primary and secondary cardiac events. The goal of this study was to determine whether an association between vitality and recurrent cardiac events (nonfatal MI, cardiac death) among acute MI survivors persists after controlling for possible physiological and psychological confounders. Design and methods Incident AMI survivors (n = 1328) from Erie and Niagara (New York) county hospitals were enrolled and followed up to 9 years. Vitality was measured by the Short Form-36 on a 0–100 scale approximately 4 months post-AMI. Cox proportional hazards models were developed to assess the vitality-recurrent event association controlling for traditional cardiovascular disease risk factors, index MI severity, and psychological correlates of vitality. Results Low-vitality individuals at baseline were more likely females, of higher BMI, smoking, diabetic, less physically active, and to have worse depression scores. Vitality was not strongly associated with MI severity markers. Lower vitality scores were associated with increased risk of recurrent cardiac events: adjusted hazard ratios (95% CI) for vitality scores 51–79, 21–50, and ≤ 20 (compared with ≥ 80) were 1.2 (0.8, 1.8), 1.4 (0.9, 2.2), and 2.9 (1.5, 5.4), respectively (P trend = 0.005). Conclusion Low vitality was associated with increased risk of recurrent cardiac events among AMI survivors after controlling for physiological and psychological confounders. Mechanistic links with vitality should be sought as interventional targets.

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Jacek Dmochowski

University of North Carolina at Charlotte

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Saverio Stranges

University of Western Ontario

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Joan Dorn

Centers for Disease Control and Prevention

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Saverio Stranges

University of Western Ontario

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Ann Jessup

University of North Carolina at Chapel Hill

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