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Featured researches published by Alpa V. Patel.


CA: A Cancer Journal for Clinicians | 2012

American Cancer Society guidelines on nutrition and physical activity for cancer prevention

Lawrence H. Kushi; Colleen Doyle; Marji McCullough; Cheryl L. Rock; Wendy Demark-Wahnefried; Elisa V. Bandera; Susan M. Gapstur; Alpa V. Patel; Kimberly S. Andrews; Ted Gansler

The American Cancer Society (ACS) publishes Nutrition and Physical Activity Guidelines to serve as a foundation for its communication, policy, and community strategies and, ultimately, to affect dietary and physical activity patterns among Americans. These Guidelines, published approximately every 5 years, are developed by a national panel of experts in cancer research, prevention, epidemiology, public health, and policy, and they reflect the most current scientific evidence related to dietary and activity patterns and cancer risk. The ACS Guidelines focus on recommendations for individual choices regarding diet and physical activity patterns, but those choices occur within a community context that either facilitates or creates barriers to healthy behaviors. Therefore, this committee presents recommendations for community action to accompany the 4 recommendations for individual choices to reduce cancer risk. These recommendations for community action recognize that a supportive social and physical environment is indispensable if individuals at all levels of society are to have genuine opportunities to choose healthy behaviors. The ACS Guidelines are consistent with guidelines from the American Heart Association and the American Diabetes Association for the prevention of coronary heart disease and diabetes, as well as for general health promotion, as defined by the 2010 Dietary Guidelines for Americans and the 2008 Physical Activity Guidelines for Americans. CA Cancer J Clin 2012.


American Journal of Epidemiology | 2010

Leisure Time Spent Sitting in Relation to Total Mortality in a Prospective Cohort of US Adults

Alpa V. Patel; Leslie Bernstein; Anusila Deka; Heather Spencer Feigelson; Peter T. Campbell; Susan M. Gapstur; Graham A. Colditz; Michael J. Thun

The obesity epidemic is attributed in part to reduced physical activity. Evidence supports that reducing time spent sitting, regardless of activity, may improve the metabolic consequences of obesity. Analyses were conducted in a large prospective study of US adults enrolled by the American Cancer Society to examine leisure time spent sitting and physical activity in relation to mortality. Time spent sitting and physical activity were queried by questionnaire on 53,440 men and 69,776 women who were disease free at enrollment. The authors identified 11,307 deaths in men and 7,923 deaths in women during the 14-year follow-up. After adjustment for smoking, body mass index, and other factors, time spent sitting (> or = 6 vs. <3 hours/day) was associated with mortality in both women (relative risk = 1.34, 95% confidence interval (CI): 1.25, 1.44) and men (relative risk = 1.17, 95% CI: 1.11, 1.24). Relative risks for sitting (> or = 6 hours/day) and physical activity (<24.5 metabolic equivalent (MET)-hours/week) combined were 1.94 (95% CI: 1.70, 2.20) for women and 1.48 (95% CI: 1.33, 1.65) for men, compared with those with the least time sitting and most activity. Associations were strongest for cardiovascular disease mortality. The time spent sitting was independently associated with total mortality, regardless of physical activity level. Public health messages should include both being physically active and reducing time spent sitting.


Nature Genetics | 2009

Genome-wide association study identifies variants in the ABO locus associated with susceptibility to pancreatic cancer

Laufey Amundadottir; Peter Kraft; Rachael Z. Stolzenberg-Solomon; Charles S. Fuchs; Gloria M. Petersen; Alan A. Arslan; H. Bas Bueno-de-Mesquita; Myron D. Gross; Kathy J. Helzlsouer; Eric J. Jacobs; Andrea Z. LaCroix; Wei Zheng; Demetrius Albanes; William R. Bamlet; Christine D. Berg; Franco Berrino; Sheila Bingham; Julie E. Buring; Paige M. Bracci; Federico Canzian; Françoise Clavel-Chapelon; Sandra Clipp; Michelle Cotterchio; Mariza de Andrade; Eric J. Duell; John W. Fox; Steven Gallinger; J. Michael Gaziano; Edward Giovannucci; Michael Goggins

We conducted a two-stage genome-wide association study of pancreatic cancer, a cancer with one of the lowest survival rates worldwide. We genotyped 558,542 SNPs in 1,896 individuals with pancreatic cancer and 1,939 controls drawn from 12 prospective cohorts plus one hospital-based case-control study. We conducted a combined analysis of these groups plus an additional 2,457 affected individuals and 2,654 controls from eight case-control studies, adjusting for study, sex, ancestry and five principal components. We identified an association between a locus on 9q34 and pancreatic cancer marked by the SNP rs505922 (combined P = 5.37 × 10−8; multiplicative per-allele odds ratio 1.20; 95% confidence interval 1.12–1.28). This SNP maps to the first intron of the ABO blood group gene. Our results are consistent with earlier epidemiologic evidence suggesting that people with blood group O may have a lower risk of pancreatic cancer than those with groups A or B.


The Lancet | 2016

Body-mass index and all-cause mortality: Individual-participant-data meta-analysis of 239 prospective studies in four continents.

Emanuele Di Angelantonio; Shilpa N. Bhupathiraju; David Wormser; Pei Gao; Stephen Kaptoge; Amy Berrington de Gonzalez; Benjamin J Cairns; Rachel R. Huxley; Chandra L. Jackson; Grace Joshy; Sarah Lewington; JoAnn E. Manson; Neil Murphy; Alpa V. Patel; Jonathan M. Samet; Mark Woodward; Wei Zheng; Maigen Zhou; Narinder Bansal; Aurelio Barricarte; Brian Carter; James R. Cerhan; Rory Collins; George Davey Smith; Xianghua Fang; Oscar H. Franco; Jane Green; Jim Halsey; Janet S Hildebrand; Keum Ji Jung

Summary Background Overweight and obesity are increasing worldwide. To help assess their relevance to mortality in different populations we conducted individual-participant data meta-analyses of prospective studies of body-mass index (BMI), limiting confounding and reverse causality by restricting analyses to never-smokers and excluding pre-existing disease and the first 5 years of follow-up. Methods Of 10 625 411 participants in Asia, Australia and New Zealand, Europe, and North America from 239 prospective studies (median follow-up 13·7 years, IQR 11·4–14·7), 3 951 455 people in 189 studies were never-smokers without chronic diseases at recruitment who survived 5 years, of whom 385 879 died. The primary analyses are of these deaths, and study, age, and sex adjusted hazard ratios (HRs), relative to BMI 22·5–<25·0 kg/m2. Findings All-cause mortality was minimal at 20·0–25·0 kg/m2 (HR 1·00, 95% CI 0·98–1·02 for BMI 20·0–<22·5 kg/m2; 1·00, 0·99–1·01 for BMI 22·5–<25·0 kg/m2), and increased significantly both just below this range (1·13, 1·09–1·17 for BMI 18·5–<20·0 kg/m2; 1·51, 1·43–1·59 for BMI 15·0–<18·5) and throughout the overweight range (1·07, 1·07–1·08 for BMI 25·0–<27·5 kg/m2; 1·20, 1·18–1·22 for BMI 27·5–<30·0 kg/m2). The HR for obesity grade 1 (BMI 30·0–<35·0 kg/m2) was 1·45, 95% CI 1·41–1·48; the HR for obesity grade 2 (35·0–<40·0 kg/m2) was 1·94, 1·87–2·01; and the HR for obesity grade 3 (40·0–<60·0 kg/m2) was 2·76, 2·60–2·92. For BMI over 25·0 kg/m2, mortality increased approximately log-linearly with BMI; the HR per 5 kg/m2 units higher BMI was 1·39 (1·34–1·43) in Europe, 1·29 (1·26–1·32) in North America, 1·39 (1·34–1·44) in east Asia, and 1·31 (1·27–1·35) in Australia and New Zealand. This HR per 5 kg/m2 units higher BMI (for BMI over 25 kg/m2) was greater in younger than older people (1·52, 95% CI 1·47–1·56, for BMI measured at 35–49 years vs 1·21, 1·17–1·25, for BMI measured at 70–89 years; pheterogeneity<0·0001), greater in men than women (1·51, 1·46–1·56, vs 1·30, 1·26–1·33; pheterogeneity<0·0001), but similar in studies with self-reported and measured BMI. Interpretation The associations of both overweight and obesity with higher all-cause mortality were broadly consistent in four continents. This finding supports strategies to combat the entire spectrum of excess adiposity in many populations. Funding UK Medical Research Council, British Heart Foundation, National Institute for Health Research, US National Institutes of Health.


JAMA Internal Medicine | 2015

Leisure Time Physical Activity and Mortality: A Detailed Pooled Analysis of the Dose-Response Relationship

Hannah Arem; Steven C. Moore; Alpa V. Patel; Patricia Hartge; Amy Berrington de Gonzalez; Kala Visvanathan; Peter T. Campbell; Michal Freedman; Elisabete Weiderpass; Hans-Olov Adami; Martha S. Linet; I.-Min Lee; Charles E. Matthews

IMPORTANCE The 2008 Physical Activity Guidelines for Americans recommended a minimum of 75 vigorous-intensity or 150 moderate-intensity minutes per week (7.5 metabolic-equivalent hours per week) of aerobic activity for substantial health benefit and suggested additional benefits by doing more than double this amount. However, the upper limit of longevity benefit or possible harm with more physical activity is unclear. OBJECTIVE To quantify the dose-response association between leisure time physical activity and mortality and define the upper limit of benefit or harm associated with increased levels of physical activity. DESIGN, SETTING, AND PARTICIPANTS We pooled data from 6 studies in the National Cancer Institute Cohort Consortium (baseline 1992-2003). Population-based prospective cohorts in the United States and Europe with self-reported physical activity were analyzed in 2014. A total of 661,137 men and women (median age, 62 years; range, 21-98 years) and 116,686 deaths were included. We used Cox proportional hazards regression with cohort stratification to generate multivariable-adjusted hazard ratios (HRs) and 95% CIs. Median follow-up time was 14.2 years. EXPOSURES Leisure time moderate- to vigorous-intensity physical activity. MAIN OUTCOMES AND MEASURES The upper limit of mortality benefit from high levels of leisure time physical activity. RESULTS Compared with individuals reporting no leisure time physical activity, we observed a 20% lower mortality risk among those performing less than the recommended minimum of 7.5 metabolic-equivalent hours per week (HR, 0.80 [95% CI, 0.78-0.82]), a 31% lower risk at 1 to 2 times the recommended minimum (HR, 0.69 [95% CI, 0.67-0.70]), and a 37% lower risk at 2 to 3 times the minimum (HR, 0.63 [95% CI, 0.62-0.65]). An upper threshold for mortality benefit occurred at 3 to 5 times the physical activity recommendation (HR, 0.61 [95% CI, 0.59-0.62]); however, compared with the recommended minimum, the additional benefit was modest (31% vs 39%). There was no evidence of harm at 10 or more times the recommended minimum (HR, 0.69 [95% CI, 0.59-0.78]). A similar dose-response relationship was observed for mortality due to cardiovascular disease and to cancer. CONCLUSIONS AND RELEVANCE Meeting the 2008 Physical Activity Guidelines for Americans minimum by either moderate- or vigorous-intensity activities was associated with nearly the maximum longevity benefit. We observed a benefit threshold at approximately 3 to 5 times the recommended leisure time physical activity minimum and no excess risk at 10 or more times the minimum. In regard to mortality, health care professionals should encourage inactive adults to perform leisure time physical activity and do not need to discourage adults who already participate in high-activity levels.


Cancer Epidemiology, Biomarkers & Prevention | 2007

Body Mass Index, Weight Change, and Risk of Prostate Cancer in the Cancer Prevention Study II Nutrition Cohort

Carmen Rodriguez; Stephen J. Freedland; Anusila Deka; Eric J. Jacobs; Marjorie L. McCullough; Alpa V. Patel; Michael J. Thun; Eugenia E. Calle

Background: Obesity has been associated with aggressive prostate cancer. The extent of this association, which varies by stage and grade, remains unclear. The role of recent weight change had not been previously examined. Methods: We examined body mass index (BMI) and weight change in relation to incident prostate cancer by disease stage and grade at diagnosis among 69,991 men in the Cancer Prevention Study II Nutrition Cohort. Participants provided information on height and weight in 1982, and again at enrollment in 1992. During follow-up through June 30, 2003 (excluding the first 2 years of follow-up), we documented 5,252 incident prostate cancers. Cox proportional hazards models were used to estimate rate ratios (RR) and 95% confidence intervals (95% CI). Results: The association between BMI in 1992 and risk of prostate cancer differed by stage and grade at diagnosis. BMI was inversely associated with risk of nonmetastatic low-grade prostate cancer (RR, 0.84; 95% CI, 0.66-1.06), but BMI was positively associated with risk of nonmetastatic high-grade prostate cancer (RR, 1.22; 95% CI, 0.96-1.55) and risk of metastatic or fatal prostate cancer (RR, 1.54; 95% CI, 1.06-2.23). Compared with weight maintenance, men who lost >11 pounds between 1982 and 1992 were at a decreased risk of nonmetastatic high-grade prostate cancer (RR, 0.58; 95% CI, 0.42-0.79). Conclusion: Obesity increases the risk of more aggressive prostate cancer and may decrease either the occurrence or the likelihood of diagnosis of less-aggressive tumors. Men who lose weight may reduce their risk of prostate cancer. (Cancer Epidemiol Biomarkers Prev 2007;16(1):63–9)


PLOS Medicine | 2012

Leisure time physical activity of moderate to vigorous intensity and mortality: a large pooled cohort analysis.

Steven C. Moore; Alpa V. Patel; Charles E. Matthews; Amy Berrington de Gonzalez; Yikyung Park; Hormuzd A. Katki; Martha S. Linet; Elisabete Weiderpass; Kala Visvanathan; Kathy J. Helzlsouer; Michael J. Thun; Susan M. Gapstur; Patricia Hartge; I-Min Lee

Analyzing data from over 650,000 individuals, Dr. Steven Moore and colleagues report that greater amounts of leisure-time physical activity were associated with higher life expectancy across a wide range of activity levels and body mass index groups.


Cancer Causes & Control | 2000

Predictors of pancreatic cancer mortality among a large cohort of United States adults

Steven S. Coughlin; Eugenia E. Calle; Alpa V. Patel; Michael J. Thun

AbstractObjectives: Cigarette smoking is considered an important risk factor for pancreatic cancer, but other purported risk factors are less well established. To learn more about the epidemiology of this important cause of mortality we examined associations with a variety of possible risk factors for death from pancreatic cancer in a large, prospective study of United States adults. Methods: We used proportional hazards models to obtain adjusted estimates of relative risks (hazards ratios). During 14 years of follow-up, 3751 persons died of pancreatic cancer in a cohort of 483,109 men and 619,199 women who had no reported history of cancer at enrollment in 1982. Results: Cigarette smoking at baseline was associated with fatal pancreatic cancer among men (multivariate relative risk [RR] = 2.1, 95% confidence interval [CI] 1.9–2.4) and among women (RR = 2.0, 95% CI 1.8–2.3). A trend in risk was observed with increasing number of cigarettes smoked per day among current smokers at baseline. With several variables included in separate models for men and women, we found additional factors to be predictive of pancreatic cancer mortality, including family history of pancreatic cancer, black race, diabetes, and increased body mass index. History of gallstones was predictive of pancreatic cancer among men. An inverse association with vegetable consumption was observed among men, that was not statistically significant. Conclusion: Our findings confirm that cigarette smoking is an important predictor of pancreatic cancer mortality, and identify several other factors that may contribute to increased risk.


Cancer Epidemiology, Biomarkers & Prevention | 2005

Obesity, Recreational Physical Activity, and Risk of Pancreatic Cancer In a Large U.S. Cohort

Alpa V. Patel; Carmen Rodriguez; Leslie Bernstein; Ann Chao; Michael J. Thun; Eugenia E. Calle

Background: Obesity and physical activity, in part through their effects on insulin sensitivity, may be modifiable risk factors for pancreatic cancer. Methods: The authors analyzed data from the American Cancer Society Cancer Prevention Study II Nutrition Cohort to examine the association between measures of adiposity, recreational physical activity, and pancreatic cancer risk. Information on current weight and weight at age 18, location of weight gain, and recreational physical activity were obtained at baseline in 1992 via a self-administered questionnaire for 145,627 men and women who were cancer-free at enrollment. During the 7 years of follow-up, 242 incident pancreatic cancer cases were identified among these participants. Cox proportional hazards modeling was used to compute hazard rate ratios (RR) and to adjust for potential confounding factors including personal history of diabetes and smoking. Results: We observed an increased risk of pancreatic cancer among obese [body mass index (BMI) ≥ 30] men and women compared with men and women of normal BMI [<25; RR, 2.08; 95% confidence interval (95% CI), 1.48-2.93, Ptrend = 0.0001]. After adjustment for between BMI, risk of pancreatic cancer was independently increased among men and women who reported a tendency for central weight gain compared with men and women reporting a tendency for peripheral weight gain (RR, 1.45; 95% CI, 1.02-2.07). We observed no difference in pancreatic cancer incidence rates between men and women who were most active (>31.5 metabolic equivalent hours per week) at baseline compared with men and women who reported no recreational physical activity (RR, 1.20; 95% CI, 0.63-2.27). Conclusion: This study, along with several recent studies, supports the hypothesis that obesity and central adiposity are associated with pancreatic cancer risk.


JAMA Internal Medicine | 2010

Anthropometric Measures, Body Mass Index and Pancreatic Cancer: a Pooled Analysis from the Pancreatic Cancer Cohort Consortium (PanScan)

Alan A. Arslan; Kathy J. Helzlsouer; Charles Kooperberg; Xiao-Ou Shu; Emily Steplowski; H. Bas Bueno-de-Mesquita; Charles S. Fuchs; Myron D. Gross; Eric J. Jacobs; Andrea Z. LaCroix; Gloria M. Petersen; Rachael Z. Stolzenberg-Solomon; Wei Zheng; Demetrius Albanes; Laufey Amundadottir; William R. Bamlet; Aurelio Barricarte; Sheila Bingham; Heiner Boeing; Marie-Christine Boutron-Ruault; Julie E. Buring; Stephen J. Chanock; Sandra Clipp; J. Michael Gaziano; Edward Giovannucci; Susan E. Hankinson; Patricia Hartge; Robert N. Hoover; David J. Hunter; Amy Hutchinson

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, > or = 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; P(trend) < .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; P(trend) < .03), and in women it was 1.34 (95% CI, 1.05-1.70; P(trend) = .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; P(trend) = .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.

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Leslie Bernstein

Beckman Research Institute

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