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Articles by J. E Buring
Total Records ( 10 ) for J. E Buring
  A. A Arslan , K. J Helzlsouer , C Kooperberg , X. O Shu , E Steplowski , H. B Bueno de Mesquita , C. S Fuchs , M. D Gross , E. J Jacobs , A. Z LaCroix , G. M Petersen , R. Z Stolzenberg Solomon , W Zheng , D Albanes , L Amundadottir , W. R Bamlet , A Barricarte , S. A Bingham , H Boeing , M. C Boutron Ruault , J. E Buring , S. J Chanock , S Clipp , J. M Gaziano , E. L Giovannucci , S. E Hankinson , P Hartge , R. N Hoover , D. J Hunter , A Hutchinson , K. B Jacobs , P Kraft , S. M Lynch , J Manjer , J. E Manson , A McTiernan , R. R McWilliams , J. B Mendelsohn , D. S Michaud , D Palli , T. E Rohan , N Slimani , G Thomas , A Tjonneland , G. S Tobias , D Trichopoulos , J Virtamo , B. M Wolpin , K Yu , A Zeleniuch Jacquotte and A. V. Patel
 

Background  Obesity has been proposed as a risk factor for pancreatic cancer.

Methods  Pooled data were analyzed from the National Cancer Institute Pancreatic Cancer Cohort Consortium (PanScan) to study the association between prediagnostic anthropometric measures and risk of pancreatic cancer. PanScan applied a nested case-control study design and included 2170 cases and 2209 control subjects. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using unconditional logistic regression for cohort-specific quartiles of body mass index (BMI [calculated as weight in kilograms divided by height in meters squared]), weight, height, waist circumference, and waist to hip ratio as well as conventional BMI categories (underweight, <18.5; normal weight, 18.5-24.9; overweight, 25.0-29.9; obese, 30.0-34.9; and severely obese, ≥35.0). Models were adjusted for potential confounders.

Results  In all of the participants, a positive association between increasing BMI and risk of pancreatic cancer was observed (adjusted OR for the highest vs lowest BMI quartile, 1.33; 95% CI, 1.12-1.58; Ptrend < .001). In men, the adjusted OR for pancreatic cancer for the highest vs lowest quartile of BMI was 1.33 (95% CI, 1.04-1.69; Ptrend < .03), and in women it was 1.34 (95% CI, 1.05-1.70; Ptrend = .01). Increased waist to hip ratio was associated with increased risk of pancreatic cancer in women (adjusted OR for the highest vs lowest quartile, 1.87; 95% CI, 1.31-2.69; Ptrend = .003) but less so in men.

Conclusions  These findings provide strong support for a positive association between BMI and pancreatic cancer risk. In addition, centralized fat distribution may increase pancreatic cancer risk, especially in women.

  D. A Schaumberg , R Dana , J. E Buring and D. A. Sullivan
 

Objective  To estimate the prevalence and risk factors for dry eye disease (DED) among US men.

Methods  Cross-sectional prevalence survey among male participants 50 years and older in the Physicians' Health Studies I (N = 18 596) and II (N = 6848). We defined DED as the presence of clinically diagnosed dry eye or severe symptoms (both dryness and irritation constantly or often). We calculated the age-standardized prevalence of DED adjusted to the age distribution of US men in 2004 and projected estimates forward to 2030. We compared DED prevalence with a similar cohort of women and examined associations with possible risk factors.

Results  The prevalence of DED increased with age, from 3.90% among men aged 50 to 54 years to 7.67% among men 80 years and older (P for trend <.001). High blood pressure (odds ratio, 1.28; 95% confidence interval, 1.12-1.45) and benign prostatic hyperplasia (odds ratio, 1.26; 95% confidence interval, 1.09-1.44) were associated with a higher risk of DED. Use of antidepressants, antihypertensives, and medications to treat benign prostatic hyperplasia were also associated with increased risk of DED. The age-standardized prevalence of DED was 4.34%, or 1.68 million men 50 years and older, and is expected to affect more than 2.79 million US men by 2030.

Conclusions  Dry eye disease is prevalent and increases with age, hypertension, benign prostatic hyperplasia, and antidepressant use.

  W. G Christen , R. J Glynn , H. D Sesso , T Kurth , J MacFadyen , V Bubes , J. E Buring , J. E Manson and J. M. Gaziano
 

Objective  To test whether supplementation with alternate-day vitamin E or daily vitamin C affects the incidence of age-related cataract in a large cohort of men.

Methods  In a randomized, double-masked, placebo-controlled trial, 11 545 apparently healthy US male physicians 50 years or older without a diagnosis of cataract at baseline were randomly assigned to receive 400 IU of vitamin E or placebo on alternate days and 500 mg of vitamin C or placebo daily.

Main Outcome Measure  Incident cataract responsible for a reduction in best-corrected visual acuity to 20/30 or worse based on self-report confirmed by medical record review.

Application to Clinical Practice  Long-term use of vitamin E and C supplements has no appreciable effect on cataract.

Results  After 8 years of treatment and follow-up, 1174 incident cataracts were confirmed. There were 579 cataracts in the vitamin E–treated group and 595 in the vitamin E placebo group (hazard ratio, 0.99; 95% confidence interval, 0.88-1.11). For vitamin C, there were 593 cataracts in the treated group and 581 in the placebo group (hazard ratio, 1.02; 95% confidence interval, 0.91-1.14).

Conclusion  Long-term alternate-day use of 400 IU of vitamin E and daily use of 500 mg of vitamin C had no notable beneficial or harmful effect on the risk of cataract.

Trial Registration  clinicaltrials.gov Identifier: NCT00270647

  J. E Lee , S Mannisto , D Spiegelman , D. J Hunter , L Bernstein , P. A van den Brandt , J. E Buring , E Cho , D. R English , A Flood , J. L Freudenheim , G. G Giles , E Giovannucci , N Hakansson , P. L Horn Ross , E. J Jacobs , M. F Leitzmann , J. R Marshall , M. L McCullough , A. B Miller , T. E Rohan , J. A Ross , A Schatzkin , L. J Schouten , J Virtamo , A Wolk , S. M Zhang and S. A. Smith Warner
 

Fruit and vegetable consumption has been hypothesized to reduce the risk of renal cell cancer. We conducted a pooled analysis of 13 prospective studies, including 1,478 incident cases of renal cell cancer (709 women and 769 men) among 530,469 women and 244,483 men followed for up to 7 to 20 years. Participants completed a validated food-frequency questionnaire at baseline. Using the primary data from each study, the study-specific relative risks (RR) were calculated using the Cox proportional hazards model and then pooled using a random effects model. We found that fruit and vegetable consumption was associated with a reduced risk of renal cell cancer. Compared with <200 g/d of fruit and vegetable intake, the pooled multivariate RR for ≥600 g/d was 0.68 [95% confidence interval (95% CI) = 0.54-0.87; P for between-studies heterogeneity = 0.86; P for trend = 0.001]. Compared with <100 g/d, the pooled multivariate RRs (95% CI) for ≥400 g/d were 0.79 (0.63-0.99; P for trend = 0.03) for total fruit and 0.72 (0.48-1.08; P for trend = 0.07) for total vegetables. For specific carotenoids, the pooled multivariate RRs (95% CIs) comparing the highest and lowest quintiles were 0.87 (0.73-1.03) for -carotene, 0.82 (0.69-0.98) for β-carotene, 0.86 (0.73-1.01) for β-cryptoxanthin, 0.82 (0.64-1.06) for lutein/zeaxanthin, and 1.13 (0.95-1.34) for lycopene. In conclusion, increasing fruit and vegetable consumption is associated with decreasing risk of renal cell cancer; carotenoids present in fruit and vegetables may partly contribute to this protection. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1730–9)

  L Djousse , I M Lee , J. E Buring and J. M. Gaziano
 

Background— Although an association between moderate alcohol consumption and decreased cardiovascular disease (CVD) and death has been reported, limited data are available on potential mediating mechanisms. We examined the association between alcohol and CVD and death in 26 399 women and estimated the proportion of reduced risk of CVD/death explained by a series of intermediate factors.

Methods and Results— Alcohol consumption was self-reported at baseline, and CVD events and deaths were ascertained via follow-up questionnaires and medical records. Baseline levels of hemoglobin A1c, inflammatory markers, hemostatic factors, and lipids were measured. Blood pressure and hypercholesterolemia and treatment for lipids were self-reported. During a mean follow up of 12.2 years, 1039 CVD events and 785 deaths (153 CVD deaths) occurred. There was a J-shaped relation between alcohol consumption and incident CVD and total and CVD deaths in a multivariable model. Compared with abstainers, alcohol intake of 5 to 14.9 g/d was associated with 26%, 35%, and 51% lower risk of CVD, total death, and CVD death, respectively, in a multivariable model. For CVD risk reduction, lipids made the largest contribution to the lower risk of CVD (28.7%), followed by hemoglobin A1c/diabetes (25.3%), inflammatory/hemostatic factors (5%), and blood pressure factors (4.6%). All these mediating factors together explained 86.3%, 18.7%, and 21.8% of the observed lower risk of CVD, total death, and CVD death, respectively.

Conclusions— These data suggest that alcohol effects on lipids and insulin sensitivity may account for a large proportion of the lower risk of CVD/death observed with moderate drinking under the assumption that the alcohol-CVD association is causal.

  D Conen , U. B Tedrow , N. R Cook , J. E Buring and C. M. Albert
 

Background— Few if any studies have assessed the relationship between birth weight and incident atrial fibrillation (AF).

Methods and Results— From 1993 to 2009, we prospectively followed 27 982 women who were >45 years of age and free of cardiovascular disease and AF at baseline. Information on birth weight was categorized into 5 different categories: <2.5, 2.5 to 3.2, 3.2 to 3.9, 3.9 to 4.5, and >4.5 kg. The primary outcome was time to incident AF. During 14.5 years of follow-up, 735 AF events occurred. Age-adjusted incidence rates for incident AF from the lowest to the highest birth weight category were 1.45, 1.82, 1.88, 2.57, and 2.55 events per 1000 person-years of follow-up. After multivariable adjustment, hazard ratios for incident AF across increasing birth weight categories were 1.0, 1.30 (95% confidence interval [CI], 0.96 to 1.75), 1.28 (95% CI, 0.96 to 1.69), 1.70 (95% CI, 1.23 to 2.37), and 1.71 (95% CI, 1.12 to 2.61) (P for linear trend=0.002). Adding body mass index, blood pressure, and diabetes mellitus at study entry did not have a large effect on these estimates (P for linear trend=0.004). In contrast, including height in the multivariable model substantially attenuated the relationship between birth weight and AF (P for linear trend=0.17), and additional adjustment for maximum weight in young adulthood further attenuated this association (multivariable-adjusted hazard ratio across birth weight categories, 1.0, 1.27 [95% CI, 0.94 to 1.71], 1.10 [95% CI, 0.83 to 1.46], 1.41 [95% CI, 1.01 to 1.96], and 1.29 [95% CI, 0.84 to 1.98]; P for linear trend=0.23).

Conclusions— Birth weight is significantly associated with incident AF among women, suggesting that early life determinants may play an important role in the pathogenesis of AF.

Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT00000479.

  C. M Albert , C. A MacRae , D. I Chasman , M VanDenburgh , J. E Buring , J. E Manson , N. R Cook and C. Newton Cheh
  Background—

Rare variants in cardiac ion channel genes are associated with sudden cardiac death in rare primary arrhythmic syndromes; however, it is unknown whether common variation in these same genes may contribute to sudden cardiac death risk at the population level.

Methods and Results—

We examined the association between 147 single nucleotide polymorphisms (SNPs) (137 tag, 5 noncoding SNPs associated with QT interval duration, and 5 nonsynonymous SNPs) in 5 cardiac ion channel genes, KCNQ1, KCNH2, SCN5A, KCNE1, and KCNE2, and sudden and/or arrhythmic death in a combined nested case-control analysis among 516 cases and 1522 matched control subjects of European ancestry enrolled in 6 prospective cohort studies. After accounting for multiple testing, 2 SNPs (rs2283222 located in intron 11 in KCNQ1 and rs11720524 located in intron 1 in SCN5A) remained significantly associated with sudden/arrhythmic death (false discovery rate=0.01 and 0.03, respectively). Each increasing copy of the major T-allele of rs2283222 or the major C-allele of rs1172052 was associated with an odds ratio of 1.36 (95% confidence interval, 1.16 to 1.60; P=0.0002) and 1.30 (95% confidence interval, 1.12 to 1.51; P=0.0005), respectively. Control for cardiovascular risk factors and/or limiting the analysis to definite sudden cardiac death did not significantly alter these relationships.

Conclusion—

In this combined analysis of 6 prospective cohort studies, 2 common intronic variants in KCNQ1 and SCN5A were associated with sudden cardiac death in individuals of European ancestry. Further study in other populations and investigation into the functional abnormalities associated with noncoding variation in these genes may lead to important insights into predisposition to lethal arrhythmias.

  S Mora , P. R Kamstrup , N Rifai , B. G Nordestgaard , J. E Buring and P. M. Ridker
  BACKGROUND:

Previous studies have demonstrated that cardiovascular risk is higher with increased lipoprotein(a) [Lp(a)]. Whether Lp(a) concentration is related to type 2 diabetes is unclear.

METHODS:

In 26 746 healthy US women (mean age 54.6 years), we prospectively examined baseline Lp(a) concentrations and incident type 2 diabetes (n = 1670) for a follow-up period of 13 years. We confirmed our findings in 9652 Danish men and women with prevalent diabetes (n = 419). Analyses were adjusted for risk factors that included age, race, smoking, hormone use, family history, blood pressure, body mass index, hemoglobin A1c (Hb A1c), C-reactive protein, and lipids.

RESULTS:

Lp(a) was inversely associated with incident diabetes, with fully adjusted hazard ratios (HRs) and 95% CIs for quintiles 2–5 vs quintile 1 of 0.87 (0.75–1.01), 0.80 (0.68–0.93), 0.88 (0.76–1.02), and 0.78 (0.67–0.91); P for trend 0.002. The association was stronger in nonfasting women, for whom respective HRs were 0.79 (0.58–1.09), 0.78 (0.57–1.08), 0.66 (0.46–0.93), and 0.56 (0.40–0.80); P for trend 0.001; P for interaction with fasting status 0.002. When we used Lp(a) ≥10 mg/L and Hb A1c <5% as reference values, the adjusted HRs were 1.62 (0.91–2.89) for Lp(a) <10 mg/L and Hb A1c <5%, 3.50 (3.06–4.01) for Lp(a)≥10 mg/L and Hb A1c 5%–<6.5%, and 5.36 (4.00–7.19) for Lp(a) <10 mg/L and Hb A1c 5%–<6.5%. Results were similar in nonfasting Danish men and women, for whom adjusted odds ratios were 0.75 (0.55–1.03), 0.64 (0.46–0.88), 0.74 (0.54–1.01), and 0.58 (0.42–0.79) for Lp(a) quintiles 2–5 vs quintile 1; P for trend 0.002.

CONCLUSIONS:

Our results indicated that Lp(a) was associated inversely with risk of type 2 diabetes independently of risk factors, in contrast to prior findings of positive associations of Lp(a) with cardiovascular risk.

  D Conen , R. J Glynn , P. M Ridker , J. E Buring and M. A. Albert
  Aims

The aim of this study was to examine the association between socioeconomic status, blood pressure (BP) progression, and incident hypertension.

Methods and results

We included 27 207 female health professionals free of hypertension and cardiovascular disease at baseline. Participants were classified into five education and six income categories. The main outcome variables were BP progression at 48 months of follow-up and incident hypertension during the entire study period. At 48 months, 48.1% of women had BP progression. The multivariable adjusted relative risks [95% confidence intervals (CIs)] for BP progression were 1.0 (referent), 0.96 (0.92–1.00), 0.92 (0.88–0.96), 0.90 (0.85–0.94), and 0.84 (0.78–0.91) (P for trend <0.0001) across increasing education categories and 1.0 (referent), 1.01 (0.94–1.08), 0.99 (0.93–1.06), 0.97 (0.91–1.04), 0.96 (0.90–1.03), and 0.89 (0.83–0.96) across increasing income categories (P for trend = 0.0001). During a median follow-up of 9.8 years, 8248 cases of incident hypertension occurred. Multivariable adjusted hazard ratios (95% CI) were 1.0 (referent), 0.92 (0.86–0.99), 0.85 (0.79–0.92), 0.87 (0.80–0.94), and 0.74 (0.65–0.84) (P for trend <0.0001) across increasing education categories and 1.0 (referent), 1.07 (0.95–1.21), 1.07 (0.95–1.20), 1.06 (0.94–1.18), 1.04 (0.93–1.16), and 0.93 (0.82–1.06) (P for trend 0.08) across increasing income categories. In joint analyses, education but not income remained associated with BP progression and incident hypertension.

Conclusion

Socioeconomic status, as determined by education but not by income, is a strong independent predictor of BP progression and incident hypertension in women.

 
 
 
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