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Health Professionals Follow-up Study (health + professional_follow-up_study)
Selected AbstractsFamily history of colorectal cancer: A determinant of advanced adenoma stage or adenoma multiplicity?INTERNATIONAL JOURNAL OF CANCER, Issue 2 2009Petra A. Wark Abstract A family history of colorectal cancer may increase colorectal cancer risk by influencing adenoma growth or enhancing the formation of new lesions. Data of men from the prospective Health Professionals Follow-Up Study who underwent an endoscopy between 1986 and 2004 were used to evaluate whether a family history of colorectal cancer is associated with adenoma multiplicity or advanced adenoma stage (,1 cm, histology with villous component or carcinoma in situ). 21.4% of the 3,881 adenoma patients and 13.9% of the 24,959 adenoma-free men had a first-degree relative with colorectal cancer. Thousand four hundred and ninety-six men were classified as having advanced and 1,507 as having nonadvanced adenomas. Six hundred and twenty-two men had multiple and 1,985 had single adenomas in the distal colon and rectum. A family history of colorectal cancer was similarly associated with advanced and nonadvanced adenomas [multivariable odds ratio (OR) (95% confidence interval): advanced vs. nonadvanced, 0.98 (0.82,1.17), advanced vs. adenoma-free: 1.67 (1.47,1.91), nonadvanced vs. adenoma-free: 1.70 (1.49,1.94)], although potential differences according to adenoma location were seen. A family history of colorectal cancer was more strongly associated with multiple distally located adenomas [odds ratio (95% confidence interval): multiple vs. single, 1.35 (1.09,1.68), multiple vs. no distally located adenomas: 2.02 (1.67,2.44), single vs. no distally located adenomas: 1.49 (1.32,1.68)]. The number of adenomas was also positively associated with a family history of colorectal cancer. Our findings suggest that at the population level, heritable factors may be more important in earlier stages of adenoma formation than at stages of adenoma advancement for at least distally located adenomas. © 2009 UICC [source] Risk factors for prostate cancer incidence and progression in the health professionals follow-up studyINTERNATIONAL JOURNAL OF CANCER, Issue 7 2007Edward Giovannucci Abstract Risk factors for prostate cancer could differ for various sub-groups, such as for "aggressive" and "non-aggressive" cancers or by grade or stage. Determinants of mortality could differ from those for incidence. Using data from the Health Professionals Follow-Up Study, we re-examined 10 factors (cigarette smoking history, physical activity, BMI, family history of prostate cancer, race, height, total energy consumption, and intakes of calcium, tomato sauce and ,-linolenic acid) using multivariable Cox regression in relation to multiple subcategories for prostate cancer risk. These were factors that we previously found to be predictors of prostate cancer incidence or advanced prostate cancer in this cohort, and that have some support in the literature. In this analysis, only 4 factors had a clear statistically significant association with overall incident prostate cancer: African,American race, positive family history, higher tomato sauce intake (inversely) and ,-linolenic acid intake. In contrast, for fatal prostate cancer, recent smoking history, taller height, higher BMI, family history, and high intakes of total energy, calcium and ,-linolenic acid were associated with a statistically significant increased risk. Higher vigorous physical activity level was associated with lower risk. In relation to these risk factors, advanced stage at diagnosis was a good surrogate for fatal prostate cancer, but high-grade (Gleason , 7 or Gleason , 8) was not. Only for high calcium intake was there a close correspondence for associations among high-grade cancer, advanced and fatal prostate cancer. Tomato sauce (inversely) and ,-linolenic acid (positively) intakes were strong predictors of advanced cancer among those with low-grade cancers at diagnosis. Although the proportion of advanced stage cancers was much lower after PSA screening began, risk factors for advanced stage prostate cancers were similar in the pre-PSA and PSA era. The complexity of the clinical and pathologic manifestations of prostate cancer must be considered in the design and interpretation of studies. © 2007 Wiley-Liss, Inc. [source] Nonsteroidal antiinflammatory drug use and risk of bladder cancer in the health professionals follow-up studyINTERNATIONAL JOURNAL OF CANCER, Issue 10 2007Jeanine M. Genkinger Abstract Nonsteroidal antiinflammatory drugs (NSAIDs) use, particularly aspirin, may lower the risk of several cancers, including bladder. NSAIDs may reduce development of bladder tumors by decreasing inflammation, inhibiting cycloxygenase-2, inhibiting proliferation and inducing apoptosis of cancer cells. However, acetaminophen, a major metabolite of phenacetin, may be positively associated with bladder cancer risk. Results from case-control studies on NSAIDs and acetaminophen use and bladder cancer risk are inconsistent. We investigated the association between NSAID and acetaminophen use and bladder cancer risk in a large cohort of US males. Among 49,448 men in the Health Professionals Follow-Up Study, 607 bladder cancer cases were confirmed during 18 years of follow-up. Relative risks (RR) and 95% confidence intervals (CI) were calculated by Cox proportional hazards models. Multivariate RR were adjusted for age, current smoking status, pack years, geographic region and fluid intake. No significant associations were observed for regular aspirin (,2 tablets per week), (RR = 0.99, 95% CI 0.83,1.18), ibuprofen (RR = 1.11, 95% CI 0.81,1.54), acetaminophen (RR = 0.96, 95% CI 0.67,1.39) or total NSAID use (not including acetaminophen; RR = 1.01, 95% CI 0.85,1.20) and bladder cancer risk compared with nonuse. Consistent use (over 6 years) of aspirin, ibuprofen, acetaminophen and total NSAIDs, compared to nonuse, was not associated with bladder cancer risk. No association was observed between aspirin frequency and dose and bladder cancer risk. We observed no effect-modification by smoking, age or fluid intake. Our results suggest that regular NSAID or acetaminophen use has no substantial impact on bladder cancer risk among men. © 2007 Wiley-Liss, Inc. [source] Prospective study of body mass index, height, physical activity and incidence of bladder cancer in US men and womenINTERNATIONAL JOURNAL OF CANCER, Issue 1 2007Crystal N. Holick Abstract We evaluated prospectively the association between body mass index (BMI), height, recreational physical activity and the risk of bladder cancer among US adults. Data were used from 2 ongoing cohorts, the Health Professionals Follow-up Study and the Nurses' Health Study, with 3,542,012 years of follow-up and 866 incident bladder cancer cases (men = 507; women = 359) for the anthropometric analysis and 1,890,476 years of follow-up and 706 incident bladder cancer cases (men = 502; women = 204) for the physical activity analysis. Cox proportional hazard models were used to estimate incidence rate ratios (RR) and 95% confidence intervals (CI) between BMI, height, physical activity and bladder cancer risk adjusting for age, pack-years of cigarette smoking and current smoking. Estimates from each cohort were pooled using a random-effects model. We observed no association between baseline BMI and bladder cancer risk, even when we compared a BMI of ,30 kg/m2 to a BMI of 18,22.9 kg/m2 [pooled multivariate (MV) RR, 1.16; 95% CI: 0.89,1.52]. A weak, but statistically significant, association was observed for the same comparison after excluding bladder cancer cases diagnosed within the first 4 years of follow-up (pooled MV RR, 1.33; 95% CI: 1.01,1.76). Height was not related to bladder cancer risk (pooled MV RR, 0.82; 95% CI: 0.65,1.03, top vs. bottom quintile). Total recreational physical activity also was not associated with the risk of bladder cancer (pooled MV RR, 0.97; 95% CI: 0.77,1.24, top vs. bottom quintile). Our findings do not support a role for BMI, height or physical activity in bladder carcinogenesis. © 2006 Wiley-Liss, Inc. [source] A prospective study of cardiovascular risk factors and incident hearing loss in men,,THE LARYNGOSCOPE, Issue 9 2010Josef Shargorodsky MD Abstract Objectives/Hypothesis: Hearing loss is the most common sensory disorder in the United States, affecting more than 36 million people. Cardiovascular risk factors have been associated with the risk of hearing loss in cross-sectional studies, but prospective data are currently lacking. Study Design: Prospective cohort study. Methods: We prospectively evaluated the association between diagnosis of hypertension, diabetes mellitus, hypercholesterolemia, smoking, or body mass index (BMI) and incident hearing loss. Participants were 26,917 men in the Health Professionals Follow-up Study, aged 40 to 74 years at baseline in 1986. Study participants completed questionnaires about lifestyle and medical history every 2 years. Information on self-reported professionally diagnosed hearing loss and year of diagnosis was obtained from the 2004 questionnaire, and cases were defined as hearing loss diagnosed between 1986 and 2004. Multivariable-adjusted hazard ratios (HRs) were calculated using Cox proportional hazards regression models. Results: A total of 3,488 cases of hearing loss were identified. History of hypertension (HR 0.96; 95% confidence interval [CI], 0.88-1.03), diabetes mellitus (HR 0.92; 95% CI, 0.78,1.08), or obesity (HR 1.02; 95% CI, 0.90,1.15 for BMI ,30 compared to normal range of 19,24.9) was not significantly associated with hearing-loss risk. Hypercholesterolemia (HR 1.10; 95% CI, 1.02,1.18) and past smoking history (HR 1.09; 95% CI, 1.01,1.17) were associated with a significantly increased risk of hearing loss after multivariate adjustment. Conclusions: A history of hypertension, diabetes mellitus, or obesity is not associated with increased risk of hearing loss; a history of past smoking or hypercholesterolemia has a small but statistically significant association with increased risk of hearing loss in adult males. Laryngoscope, 2010 [source] Vitamin D receptor (VDR) gene polymorphisms and haplotypes, interactions with plasma 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, and prostate cancer riskTHE PROSTATE, Issue 9 2007Bahar Mikhak Abstract BACKGROUND The vitamin D receptor (VDR) is required for actions of vitamin D. The binding of 1,25-dihydroxyvitamin D to the VDR on prostatic epithelial cells prompts the regulation of cancer-related genes. METHODS We conducted a nested case-control study in the Health Professionals Follow-up Study to investigate the role of the VDR Cdx2, Fok1, and Bsm1 gene polymorphisms and associated haplotypes and their interaction with plasma vitamin D metabolites in relation to prostate cancer (PC) risk. RESULTS No association was found between these SNPs or their associated haplotypes and all PC subtypes except that haplotype 2 (A-f-b) with Cdx2 A, Fok1 f, and Bsm1 b alleles and haplotype 3 (A-F-B) with Cdx2 A, Fok1 F and Bsm1 B alleles compared to the most common haplotype (A-F-b), were associated with reduced risk of aggressive PC (high stage or Gleason sum ,7; P,=,0.02), both with two alleles suspected of being low risk. Carriers of the variant Cdx2 A allele who were deficient in plasma 25-hydroxyvitamin D (,15 ng/ml) compared to non-carriers with normal 25-hydroxyvitamin D, had a lower risk of total and poorly differentiated PCs (Gleason sum ,7) (P for interaction,=,0.02 and 0.04, respectively). Plasma 1,25-dihydroxyvitamin D deficiency (,26 pg/ml) was associated with a threefold risk of poorly differentiated PC (P for interaction,=,0.01) when comparing carriers of the Cdx2 A allele to non-carriers with normal 1,25-dihydroxyvitamin D. CONCLUSION In this population of men, none of the VDR polymorphisms studied was associated with susceptibility to PC. Prostate 67: 911,923, 2007. © 2007 Wiley-Liss, Inc. [source] Genetic determinants of hair color and parkinson's disease risk,ANNALS OF NEUROLOGY, Issue 1 2009Xiang Gao MD Objective A history of melanoma is associated with increased risks for Parkinson's disease (PD). We examined whether hair color, one of the most important phenotypes of pigmentation and a risk factor for melanoma, was associated with PD risk in the Health Professionals Follow-up Study (HPFS; 1986,2002) and the Nurses' Health Study (NHS; 1980,2002). Methods We included 38,641 men and 93,661 women who were free of PD at baseline. Information on natural hair color in early adulthood (age 18,21 years) was assessed via a questionnaire. We also conducted a case,control study (298 PD cases) nested in these two cohorts to examine the association between the melanocortin1-receptor Arg151Cys polymorphism and PD risk. Relative risks (RRs) were estimated using Cox proportional hazards models in the cohort analyses and conditional logistic regression in the nested case,control study. Results PD risk increased with decreasing darkness of hair color. Pooled RRs for PD were 1 (reference), 1.40, 1.61, and 1.93 (95% confidence interval, 1.1,3.4) for black, brown, blond, and red hair, respectively, after adjusting for age, smoking, ethnicity, and other covariates. The associations between hair color and PD were particularly strong for relative younger onset of PD (<70 yr) (adjusted RR for red vs black hair = 3.83; 95% confidence interval, 1.7,8.7). In the case,control study, participants with Cys/Cys genotype, which was associated with red hair, had a greater PD risk, relative to the Arg/Arg genotype (adjusted RR, 3.15; 95% confidence interval, 1.1,9.4). Interpretation These findings suggest a potential role of pigmentation in PD. Ann Neurol 2009;65:76,82 [source] Prospective study of caffeine consumption and risk of Parkinson's disease in men and womenANNALS OF NEUROLOGY, Issue 1 2001Alberto Ascherio MD, DrPH Results of case-control studies and of a prospective investigation in men suggest that consumption of coffee could protect against the risk of Parkinson's disease, but the active constituent is not clear. To address the hypothesis that caffeine is protective against Parkinson's disease, we examined the relationship of coffee and caffeine consumption to the risk of this disease among participants in 2 ongoing cohorts, the Health Professionals' Follow-Up Study (HPFS) and the Nurses' Health Study (NHS). The study population comprised 47,351 men and 88,565 women who were free of Parkinson's disease, stroke, or cancer at baseline. A comprehensive life style and dietary questionnaire was completed by the participants at baseline and updated every 2,4 years. During the follow-up (10 years in men, 16 years in women), we documented a total of 288 incident cases of Parkinson's disease. Among men, after adjustment for age and smoking, the relative risk of Parkinson's disease was 0.42 (95% CI: 0.23,0.78; p for trend < 0.001) for men in the top one-fifth of caffeine intake compared to those in the bottom one-fifth. An inverse association was also observed with consumption of coffee (p for trend = 0.004), caffeine from noncoffee sources (p for trend < 0.001), and tea (p for trend = 0.02) but not decaffeinated coffee. Among women, the relationship between caffeine or coffee intake and risk of Parkinson's disease was U-shaped, with the lowest risk observed at moderate intakes (1,3 cups of coffee/day, or the third quintile of caffeine consumption). These results support a possible protective effect of moderate doses of caffeine on risk of Parkinson's disease. [source] | ||||||||||