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Objectives. To quantify disparities in health and economic burdens of cancer attributable to suboptimal diet among US adults. Methods. Using a probabilistic cohort state-transition model, we estimated the number of new cancer cases and cancer deaths, and economic costs of 15 diet-related cancers attributable to suboptimal intake of 7 dietary factors (a low intake of fruits, vegetables, dairy, and whole grains and a high intake of red and processed meats and sugar-sweetened beverages) among a closed cohort of US adults starting in 2017. Results. Suboptimal diet was estimated to contribute to 3.04 (95% uncertainty interval [UI] = 2.88, 3.20) million new cancer cases, 1.74 (95% UI = 1.65, 1.84) million cancer deaths, and $254 (95% UI = $242, $267) billion economic costs among US adults aged 20 years or older over a lifetime. Diet-attributable cancer burdens were higher among younger adults, men, non-Hispanic Blacks, and individuals with lower education and income attainments than other population subgroups. The largest disparities were for cancers attributable to high consumption of sugar-sweetened beverages and low consumption of whole grains. Conclusions. Suboptimal diet contributes to substantial disparities in health and economic burdens of cancer among young adults, men, racial/ethnic minorities, and socioeconomically disadvantaged groups. (Am J Public Health. 2021;111(11):2008–2018. https://doi.org/10.2105/AJPH.2021.306475) [ABSTRACT FROM AUTHOR]

Background: The Mediterranean and Dietary Approaches to Stop Hypertension (DASH) diets are characterized by higher intake of fruit, vegetables, whole grains, and unsaturated fatty acids. All of these foods and nutrients may affect cholesterol, inflammation, the development of atherosclerosis, and, therefore, risk of cardiac death. Objective: Our objective was to examine the association between the Mediterranean and DASH dietary patterns and risk of sudden cardiac death (SCD) in women. Design: We used a prospective cohort of 93,122 postmenopausal women enrolled in the Women's Health Initiative study between 1993 and 1998 and followed for an average of 10.5 y. Women completed a food-frequency questionnaire (FFQ) twice during follow-up. We scored their diets according to how closely the reported diet resembled each dietary pattern. SCD was defined as death that occurred within 1 h of symptom onset. Results: A higher Mediterranean diet score was associated with lower risk of SCD (HR: 0.64; 95% CI: 0.43, 0.94) when women in the highest quintile were compared with women in the lowest quintile after adjustment for age, total energy, race, income, smoking, and physical activity. After adjustment for potential mediators, the association was similar (HR: 0.67; 95% CI: 0.46, 0.99). A higher DASH diet score was not associated with risk of SCD. However, sodium intake, which is a crucial component of the DASH dietary pattern, was not well characterized by the FFQ. Conclusion: The Mediterranean dietary pattern may be associated with lower risk of SCD in women. This trial was registered at clinicaltrials.gov as NCT00000611. [ABSTRACT FROM AUTHOR]

It has been hypothesized that high fluid intake may reduce contact time between carcinogens and bladder epithelium and consequently reduce carcinogenesis. Epidemiologic studies examining fluid intake and bladder cancer have been extremely inconsistent, ranging from strong inverse to strong positive associations. The authors reevaluated the association between fluid intake and bladder cancer among 47,909 participants in the prospective Health Professionals Follow-up Study over a period of 22 years. During follow-up (1986–2008), 823 incident bladder cancer cases were diagnosed. Information on fluid intake was collected by using the food frequency questionnaire at baseline and every 4 years thereafter. Cox proportional hazard regression analysis was used to adjust for risk factors for bladder cancer. Total fluid intake was inversely associated with bladder cancer when the analysis was based on the baseline diet (relative risk = 0.76, 95% confidence interval: 0.60, 0.97), comparing the highest total daily fluid intake quintile (>2,531 mL/day) with the lowest quintile (<1,290 mL/day) (Ptrend = 0.01). However, no association was detected when the analysis was based on recent diet or cumulative updated diet. The updated analysis for total fluid intake and bladder cancer was attenuated compared with the original findings from the first 10-year follow-up period. [ABSTRACT FROM AUTHOR]

Many studies have investigated the relation between magnesium and iron intake and diabetes and, separately, between diabetes and pancreatic cancer. However, no known study has examined the direct association of magnesium and iron intake with pancreatic cancer risk. The authors obtained magnesium and iron intake data using food frequency questionnaires from the US male Health Professionals Follow-up Study, which began in 1986. During 851,476 person-years and 20 years of follow-up, 300 pancreatic cancer cases were documented. Cox proportional hazards models were used to estimate relative risks, adjusting for age, smoking, and body mass index. No associations were observed between magnesium or iron intake and pancreatic cancer (highest vs. lowest quintile: relative risk (RR) = 0.94, 95% confidence interval (CI): 0.66, 1.32 and RR = 0.93, 95% CI: 0.65, 1.34, respectively). Similarly, iron or magnesium supplement use was not related to pancreatic cancer. A statistically significant inverse relation was noted between magnesium and pancreatic cancer for subjects with a body mass index of ≥25 kg/m2 (RR = 0.67, 95% CI: 0.46, 0.99; P-trend = 0.04). Although, overall, no relation between magnesium or iron intake and pancreatic cancer was observed in this cohort of men, an inverse association with magnesium was suggested among overweight individuals, which should be examined in other studies. [ABSTRACT FROM PUBLISHER]

In 1995–1996, the authors mailed a food frequency questionnaire to 3.5 million American Association of Retired Persons members who were aged 50–69 years and who resided in one of six states or two metropolitan areas with high-quality cancer registries. In establishing a cohort of 567,169 persons (340,148 men and 227,021 women), the authors were fortunate in that a less-than-anticipated baseline response rate (threatening inadequate numbers of respondents in the intake extremes) was offset by both a shifting and a widening of the intake distributions among those who provided satisfactory data. Reported median intakes for the first and fifth intake quintiles, respectively, were 20.4 and 40.1 (men) and 20.1 and 40.0 (women) percent calories from fat, 10.3 and 32.0 (men) and 8.7 and 28.7 (women) g per day of dietary fiber, 3.1 and 11.6 (men) and 2.8 and 11.3 (women) servings per day of fruits and vegetables, and 20.7 and 156.8 (men) and 10.5 and 97.0 (women) g per day of red meat. After 5 years of follow-up, the cohort is expected to yield nearly 4,000 breast cancers, more than 10,000 prostate cancers, more than 4,000 colorectal cancers, and more than 900 pancreatic cancers. The large size and wide intake range of the cohort will provide ample power for examining a number of important diet and cancer hypotheses. [ABSTRACT FROM PUBLISHER]

Data derived from laboratory investigations suggest that a number of dietary variables may contribute to bladder carcinogenesis. Although bladder cancer is the fourth leading cause of cancer in men in the United States, dietary studies are few. The authors examined the relations between intakes of macro- and micronutrients and the risk of bladder cancer among men in the prospective Health Professionals Follow-Up Study. Each participant completed a 131-item food frequency questionnaire in 1986 and in 1990, from which nutrient intakes were calculated. During 12 years of follow-up, 320 cases of bladder cancer were diagnosed. No association was observed for total caloric or macronutrient intake and bladder cancer risk. Similarly, we found no relation for dietary intake of potassium, sodium, calcium, magnesium, phosphorus, iron, or water-soluble vitamins and bladder cancer risk. Total vitamin E intake and vitamin E supplements were inversely associated with risk. In addition, a dose-response relation was observed for duration of vitamin E supplement use. A suggestive inverse association was seen with dose of vitamin C supplement use. More studies are needed to determine the role of vitamins E and C supplement intake in bladder carcinogenesis. [ABSTRACT FROM PUBLISHER]

Background Diet is an important risk factor for cancer that is amenable to intervention. Estimating the cancer burden associated with diet informs evidence-based priorities for nutrition policies to reduce cancer burden in the United States. Methods Using a comparative risk assessment model that incorporated nationally representative data on dietary intake, national cancer incidence, and estimated associations of diet with cancer risk from meta-analyses of prospective cohort studies, we estimated the annual number and proportion of new cancer cases attributable to suboptimal intakes of seven dietary factors among US adults ages 20 years or older, and by population subgroups. Results An estimated 80 110 (95% uncertainty interval [UI] = 76 316 to 83 657) new cancer cases were attributable to suboptimal diet, accounting for 5.2% (95% UI = 5.0% to 5.5%) of all new cancer cases in 2015. Of these, 67 488 (95% UI = 63 583 to 70 978) and 4.4% (95% UI = 4.2% to 4.6%) were attributable to direct associations and 12 589 (95% UI = 12 156 to 13 038) and 0.82% (95% UI = 0.79% to 0.85%) to obesity-mediated associations. By cancer type, colorectal cancer had the highest number and proportion of diet-related cases (n = 52 225, 38.3%). By diet, low consumption of whole grains (n = 27 763, 1.8%) and dairy products (n = 17 692, 1.2%) and high intake of processed meats (n = 14 524, 1.0%) contributed to the highest burden. Men, middle-aged (45–64 years) and racial/ethnic minorities (non-Hispanic blacks, Hispanics, and others) had the highest proportion of diet-associated cancer burden than other age, sex, and race/ethnicity groups. Conclusions More than 80 000 new cancer cases are estimated to be associated with suboptimal diet among US adults in 2015, with middle-aged men and racial/ethnic minorities experiencing the largest proportion of diet-associated cancer burden in the United States. [ABSTRACT FROM AUTHOR]

Background: African Americans have the highest pancreatic cancer incidence of any racial/ethnic group in the United States. The oral microbiome was associated with pancreatic cancer risk in a recent study, but no such studies have been conducted in African Americans. Poor oral health, which can be a cause or effect of microbial populations, was associated with an increased risk of pancreatic cancer in a single study of African Americans., Methods: We prospectively investigated the oral microbiome in relation to pancreatic cancer risk among 122 African-American pancreatic cancer cases and 354 controls. DNA was extracted from oral wash samples for metagenomic shotgun sequencing. Alpha and beta diversity of the microbial profiles were calculated. Multivariable conditional logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for associations between microbes and pancreatic cancer risk., Results: No associations were observed with alpha or beta diversity, and no individual microbial taxa were differentially abundant between cases and control, after accounting for multiple comparisons. Among never smokers, there were elevated ORs for known oral pathogens: Porphyromonas gingivalis (OR = 1.69, 95% CI: 0.80-3.56), Prevotella intermedia (OR = 1.40, 95% CI: 0.69-2.85), and Tannerella forsythia (OR = 1.36, 95% CI: 0.66-2.77)., Conclusions: Previously reported associations between oral taxa and pancreatic cancer were not present in this African-American population overall., (© 2021. The Author(s), under exclusive licence to Springer Nature Limited.)

Importance: Obesity-associated cancer burdens are increasing in the US. Nutrition policies, such as the Nutrition Facts added-sugar labeling, may reduce obesity-associated cancer rates., Objective: To evaluate the cost-effectiveness of Nutrition Facts added-sugar labeling and obesity-associated cancer rates in the US., Design, Setting, and Participants: A probabilistic cohort state-transition model was used to conduct an economic evaluation of added-sugar labeling and 13 obesity-associated cancers among 235 million adults aged 20 years or older by age, sex, and race/ethnicity over a median follow-up of 34.4 years. Policy associations were considered in 2 scenarios: with consumer behaviors and with additional industry reformulation. The model integrated nationally representative population demographics, diet, and cancer statistics; associations of policy intervention with diet, diet change and body mass index, and body mass index with cancer risk; and policy and health-related costs from established sources. Data were analyzed from January 8, 2019, to May 6, 2020., Main Outcomes and Measures: Net costs and incremental cost-effectiveness ratio were estimated from societal and health care perspectives. Probabilistic sensitivity analyses incorporated uncertainty in input parameters and generated 95% uncertainty intervals (UIs)., Results: Based on consumer behaviors, the policy was associated with a reduction of 30 000 (95% UI, 21 600-39 300) new cancer cases and 17 100 (95% UI, 12 400-22 700) cancer deaths, a gain of 116 000 (95% UI, 83 800-153 000) quality-adjusted life-years, and a saving of $1600 million (95% UI, $1190 million-$2030 million) in medical costs associated with cancer care among US adults over a lifetime. The policy was associated with a savings of $704 million (95% UI, $44.5 million-$1450 million) from the societal perspective and $1590 million (95% UI, $1180 million-$2020 million) from the health care perspective. Additional industry reformulation to reduce added-sugar amounts in packaged foods and beverages would double the impact. Greater health gains and cost savings were expected among young adults, women, and non-Hispanic Black individuals than other population subgroups., Conclusions and Relevance: These findings suggest that the added-sugar labeling is associated with reduced costs and lower rates of obesity-associated cancers. Policymakers may consider and prioritize nutrition policies for cancer prevention in the US.

Increasing evidence supports a positive association between periodontal disease and total cancer risk. We evaluated the association of clinically assessed periodontal disease and a consequence, edentulism with total cancer mortality in participants without a prior cancer diagnosis in a U.S. nationally representative population. Included were 6,034 participants aged ≥40 years without a prior cancer diagnosis who participated in the National Health and Nutrition Examination Survey III. Periodontal health was measured by trained dentists. Cancer deaths (n = 702) were ascertained during a median of 21.3 years of follow-up. Cox proportional hazards regression was used to estimate the association of periodontal disease and edentulism with total cancer mortality using no periodontal disease/dentate as the reference and adjusting for potential demographic, lifestyle including smoking and social factor confounders. Fifteen percent had periodontitis and 17% were edentulous. Periodontitis was not statistically significantly associated with risk of total cancer death after multivariable adjustment. Edentulism was associated with an increased risk of cancer mortality (hazard ratio = 1.50, 95% confidence interval = 1.12-2.00) after multivariable adjustment, including in men and women and in each racial/ethnic group studied. The positive association was observed in overweight/obese participants but not participants with normal body mass index, more strongly in prediabetic/diabetic participants than in participants without diabetes and in ever cigarette smokers but not in never cigarette smokers. In this U.S. nationally representative population, those with edentulism, but not periodontal disease, had a higher risk of total cancer death, especially in those with shared risk factors for periodontal disease and cancer., (© 2020 UICC.)

Introduction: Processed meats are associated with increased risk of colorectal and stomach cancers, but health and economic impacts of policies to discourage processed meats are not well established. This paper aims to evaluate the cost effectiveness of implementing tax and warning labels on processed meats., Methods: A probabilistic cohort-state transition model was developed in 2018, including lifetime and short-term horizons, healthcare, and societal perspectives, and 3% discount rates for costs and health outcomes. The model simulated 32 subgroups by age, gender, and race/ethnicity from the U.S. adult population and integrated nationally representative 2011-2014 data on processed meat consumption, with etiologic effects of processed meat consumption on cancer incidence, medical and indirect societal costs, and policy costs., Results: Over a lifetime, the 10% excise tax would prevent 77,000 cases of colorectal cancer (95% uncertainty interval=56,800, 107,000) and 12,500 cases of stomach cancer (95% uncertainty interval=6,880, 23,900), add 593,000 quality-adjusted life years (95% uncertainty interval=419,000, 827,000), and generate net savings of $2.7 billion from a societal perspective, including $1.1 billion healthcare costs saved. The warning label policy would avert 85,400 cases of colorectal cancer (95% uncertainty interval=56,600, 141,000) and 15,000 cases of stomach cancer (95% uncertainty interval=6,860, 34,500), and add 660,000 quality-adjusted life years (95% uncertainty interval=418,000, 1,070,000), with net savings of $4.5 billion from a societal perspective, including $1.3 billion healthcare costs saved. In subgroup analyses, greater health and economic benefits accrued to (1) younger subpopulations, (2) subpopulations with greater cancer risk, and (3) those with higher baseline processed meat consumption., Conclusions: The model shows that implementing tax or warning labels on processed meats would be a cost-saving strategy with substantial health and economic benefits. The findings should encourage policy makers to consider nutrition-related policies to reduce cancer burden., (Copyright © 2019 American Journal of Preventive Medicine. Published by Elsevier Inc. All rights reserved.)

Background: The incidence of melanoma is rising faster than that of any other preventable cancer in the United States. The American Academy of Dermatology has sponsored free skin cancer education and screenings conducted by volunteer dermatologists in the United States since 1985., Objective: We aimed to assess the American Academy of Dermatology's national skin cancer screening program from 1986 to 2014 by analyzing the risk factor profile, access to dermatologic services, and examination results., Methods: We conducted several detailed statistical analyses of the screening population., Results: From 1986 to 2014, records were available for 2,046,531 screenings, 1,963,141 (96%) of which were subjected to detailed analysis. Men comprised 38% of all participants. The number of annual screenings reached approximately 100,000 in 1990 and remained relatively stable thereafter. From 1991 to 2014 (data for 1995, 1996 and 2000 were unavailable), clinical diagnoses were rendered for 20,628 melanomas, 156,087 dysplastic nevi, 32,893 squamous cell carcinomas, and 129,848 basal cell carcinomas. Only 21% of screenees had a regular dermatologist. Those with a clinical diagnosis of skin cancer were more likely than the general screening population to be uninsured., Limitations: Inability to verify clinical diagnoses histopathologically., Conclusion: Our findings suggest that the SPOTme program has detected thousands of skin cancers that may have gone undetected or experienced a delay in detection., (Copyright © 2018 American Academy of Dermatology, Inc. Published by Elsevier Inc. All rights reserved.)

Purpose: Oral and pharyngeal cancer patients diagnosed at an advanced stage experience increased morbidity and mortality relative to those with localized disease. The aim of this study was to assess the impact of dental insurance status and regularity of dental visits on early detection of oral and pharyngeal cancer., Methods: We examined the relationship of dental insurance and frequency of dental visits with stage at diagnosis among 441 oral and pharyngeal cancer cases from a population-based study of head and neck cancer. Ordinal logistic regression models were used to assess the association with stage, and tumor (T) and nodal (N) classification., Results: Never or rarely going to the dentist was associated with being diagnosed at higher stage for oral and pharyngeal cancer (cumulative OR = 2.28, 95 % CI: 1.02-5.10) and oral cancer (cumulative OR = 9.17, 95 % CI: 2.70-31.15) compared to those going to the dentist at least annually. Oral and pharyngeal cancer patients who went to the dentist infrequently (cumulative OR = 1.82, 95 % CI: 1.09-3.05) or rarely/never (cumulative OR = 3.24, 95 % CI: 1.59-6.57) were diagnosed with a higher T classification compared with those who went at least annually., Conclusions: Receipt of regular dental examinations at least annually may reduce the public health burden of oral and pharyngeal cancer by facilitating earlier detection of the disease.

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.

Background & Aims: Peptic ulcer disease has been associated with an increased risk of pancreatic cancer, but findings on this topic are inconsistent. We investigated the association between pancreatic cancer and the occurrence of gastric or duodenal ulcer in a large US cohort., Methods: We analyzed data collected from 51,529 male health professionals in a prospective cohort study. History of peptic ulcer disease was assessed at baseline in 1986 and updated biennially thereafter. Relative risks (RRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models adjusting for smoking, body mass index, diabetes, and physical activity., Results: During 18 years of follow-up evaluation, we observed 274 incident pancreatic cancer cases. Compared with those with report of no peptic ulcer disease, men with gastric ulcer had an increased risk of pancreatic cancer (RR, 1.83; 95% CI, 1.13-2.97). Although the risk was highest for those with a diagnosis of gastric ulcer that was close in time to the cancer diagnosis (RR, 3.66; 95% CI, 1.45-9.24), the risk remained significantly increased 10-19 years after the gastric ulcer diagnosis (RR, 2.89; 95% CI, 1.26-6.64). In contrast, duodenal ulcer was not associated with pancreatic cancer risk (RR, 1.15; 95% CI, 0.78-1.71)., Conclusions: Gastric ulcer increases the risk of pancreatic cancer, whereas there does not appear to be an association between duodenal ulcers and pancreatic cancer.

Background: Although it has been hypothesized that hyperglycemia, hyperinsulinemia, and insulin resistance are involved in the development of pancreatic cancer, results from epidemiologic studies of added sugar intake are inconclusive., Objective: Our objective was to investigate whether the consumption of total added sugar and sugar-sweetened foods and beverages is associated with pancreatic cancer risk., Design: In 1995 and 1996, we prospectively examined 487 922 men and women aged 50-71 y and free of cancer and diabetes. Total added dietary sugar intake (in tsp/d; based on the US Department of Agriculture's Pyramid Servings Database) was assessed with a food-frequency questionnaire. Relative risks (RRs) and 95% CIs were calculated with adjustment for total energy and potential confounding factors., Results: During an average 7.2 y of follow-up, 1258 incident pancreatic cancer cases were ascertained. The median intakes for the lowest and highest quintiles of total added sugar intake were 12.6 (3 tsp/d) and 96.2 (22.9 tsp/d) g/d, respectively. No overall greater risk of pancreatic cancer was observed in men or women with high intake of total added sugar or sugar-sweetened foods and beverages. For men and women combined, the multivariate RRs of the highest versus lowest intake categories were 0.85 (95% CI: 0.68, 1.06; P for trend = 0.07) for total added sugar, 1.01 (0.82,1.23; P for trend = 0.58) for sweets, 0.98 (0.82,1.18; P for trend = 0.49) for dairy desserts, 1.12 (0.91,1.39; P for trend = 0.35) for sugar added to coffee and tea, and 1.01 (0.77,1.31; P for trend = 0.76) for regular soft drinks., Conclusion: Our results do not support the hypothesis that consumption of added sugar or of sugar-sweetened foods and beverages is associated with overall risk of pancreatic cancer.

Background: Studies suggest that tooth loss and periodontal disease might increase the risk of developing various cancers; however, smoking might have confounded the reported associations. We aimed to assess whether periodontal disease or tooth loss is associated with cancer risk., Methods: The analysis was done in a prospective study (the Health Professionals Follow-Up Study [HPFS]), which was initiated in 1986 when US male health professionals aged 40-75 years responded to questionnaires posted by the Department of Nutrition, Harvard University School of Public Health, Boston, MA, USA. In addition to the baseline questionnaires, follow-up questionnaires were posted to all living participants every 2 years and dietary questionnaires every 4 years. At baseline, participants were asked whether they had a history of periodontal disease with bone loss. Participants also reported number of natural teeth at baseline and any tooth loss during the previous 2 years was reported on the follow-up questionnaires. Smoking status and history of smoking were obtained at baseline and in all subsequent questionnaires. Additionally at baseline, participants reported their mean frequency of food intake over the previous year on a 131-item semiquantitative food-frequency questionnaire. Participants reported any new cancer diagnosis on the follow-up questionnaires. Endpoints for this study were risk of total cancer and individual cancers with more than 100 cases. Multivariate hazard ratios (HRs) and 95% CIs were calculated by use of Cox proportional hazard models according to periodontal disease status and number of teeth at baseline., Findings: In the main analyses, 48 375 men with median follow-up of 17.7 years (1986 to Jan 31, 2004) were eligible after excluding participants diagnosed with cancer before 1986 (other than non-melanoma skin cancer, n=2076) and those with missing data on periodontal disease (n=1078). 5720 incident cancer cases were documented (excluding non-melanoma skin cancer and non-aggressive prostate cancer). The five most common cancers were colorectal (n=1043), melanoma of the skin (n=698), lung (n=678), bladder (n=543), and advanced prostate (n=541). After adjusting for known risk factors, including detailed smoking history and dietary factors, participants with a history of periodontal disease had an increased risk of total cancer (HR 1.14 [95% CI 1.07-1.22]) compared with those with no history of periodontal disease. By cancer site, significant associations for those with a history of periodontal disease were noted for lung (1.36 [1.15-1.60]), kidney (1.49 [1.12-1.97]), pancreas (1.54 [1.16-2.04]; findings previously published), and haematological cancers (1.30 [1.11-1.53]). Fewer teeth at baseline (0-16) was associated with an increase in risk of lung cancer (1.70 [1.37-2.11]) for those with 0-16 teeth versus those with 25-32 teeth. In never-smokers, periodontal disease was associated with significant increases in total (1.21 [1.06-1.39]) and haematological cancers (1.35 [1.01-1.81]). By contrast, no association was noted for lung cancer (0.96 [0.46-1.98])., Interpretation: Periodontal disease was associated with a small, but significant, increase in overall cancer risk, which persisted in never-smokers. The associations recorded for lung cancer are probably because of residual confounding by smoking. The increased risks noted for haematological, kidney, and pancreatic cancers need confirmation, but suggest that periodontal disease might be a marker of a susceptible immune system or might directly affect cancer risk.

Increased body size and lack of physical activity are associated with increased risk of several cancers, but the relations of body mass index (BMI) and physical activity to bladder cancer are poorly understood. We investigated the associations between BMI, physical activity, and bladder cancer in the NIH-AARP Diet and Health Study, a prospective cohort of 471,760 U.S. men and women, followed from 1995 to 2003. During 3,404,642 person-years of follow-up, we documented 1,719 incident cases of bladder cancer. Compared with normal weight, obesity was associated with an up to 28% increased risk for bladder cancer. The multivariate relative risks of bladder cancer for BMI values of 18.5 to 24.9 (reference), 25.0 to 29.9, 30.0 to 34.9, and >or=35 kg/m2 were 1.0, 1.15, 1.22, and 1.28 (95% confidence interval, 1.02-1.61; P trend = 0.028). The association between BMI and bladder cancer was consistent among subgroups defined by gender, education, smoking status, and other potential effect modifiers. In contrast, physical activity showed no statistically significant relation with bladder cancer. After multivariate adjustment, including BMI, the relative risks of bladder cancer for increasing frequency of physical activity [0 (reference), <1, 1-2, 3-4, and >or=5 times a week] were 1.0, 0.85, 0.89, 0.91, and 0.87 (95% confidence interval, 0.74-1.02; P trend = 0.358), respectively. In conclusion, these findings provide support for a modest adverse effect of adiposity on risk for bladder cancer. In contrast, our results do not suggest a relation between physical activity and bladder cancer.

Obesity and lack of physical activity have been inconsistently associated with pancreatic cancer. Using data from a self-administered baseline questionnaire (1995-1996), the authors investigated the association between adiposity and physical activity and pancreatic cancer in 495,035 participants of the National Institutes of Health-AARP Diet and Health Study who were aged 50-71 years. To avoid the influence of subclinical disease, follow-up time started 1 year after baseline, and subjects with a body mass index (BMI) of <18.5 kg/m(2) were excluded. A subcohort (n = 302,060) completed a second questionnaire with information about physical activity and waist and hip circumference. During follow-up though 2000, 654 pancreatic cancer cases were identified. The authors used Cox proportional hazard models to generate adjusted hazard ratios and 95% confidence intervals. Compared with those with a BMI of 18.5-<25, those with a BMI of >/=35 had a 45% greater pancreatic cancer risk (95% confidence interval (CI): 1.04, 2.02; p(trend) = 0.02). Significant positive associations for BMI were observed among nonsmokers (for BMI > or =35: hazard ratio = 1.70, 95% CI: 1.14, 2.53; p(trend) = 0.004) but not recent smokers (p(interaction) = 0.08). Waist circumference was positively associated with pancreatic cancer (fourth vs. first quartile: hazard ratio = 2.53, 95% CI: 1.13, 5.65; p(trend) = 0.04) in women but not men. The authors observed no association with physical activity. Their results suggest a positive association between adiposity and pancreatic cancer.

Background: Nutrients in dietary fruit and vegetables have been hypothesized to lower the risk of glioma by reducing the endogenous formation of N-nitroso compounds. Studies examining fruit and vegetable consumption and brain tumors have relied on case-control study designs, with one exception, and results have been inconsistent., Objective: We prospectively examined the relation between consumption of fruit and vegetables (and specifically carotenoids) and the risk of glioma among men and women in 3 large US cohort studies: the Health Professionals Follow-Up Study (HPFS), the Nurses' Health Study I (NHS I), and NHS II., Design: Dietary intake was assessed by food-frequency questionnaires obtained at baseline and updated every 4 y through 2002 (HPFS and NHS I) or 2003 (NHS II). We identified 296 incident adult gliomas during 3 669 589 person-years of follow-up. Cox proportional hazard models were used to estimate incidence rate ratios (RR) and 95% CIs between intake of fruit, vegetables, and carotenoids and glioma risk, with adjustment for age and total caloric intake., Results: Updated average consumption of total fruit and vegetables was not significantly associated with glioma risk in the men and women (pooled multivariate RR in a comparison of the highest with the lowest quintile: 1.12; 95% CI: 0.74, 1.69). Other fruit and vegetable subgroups, individual fruit and vegetables, and 5 major carotenoids were not significantly associated with risk of glioma., Conclusion: Our findings suggest that fruit, vegetable, and carotenoid consumption is not likely associated strongly with the risk of adult glioma.

Two previous cohort studies reported positive associations between tooth loss or periodontitis and pancreatic cancer risk. Data on periodontal disease were obtained at baseline and every other year thereafter in a cohort of 51,529 male health professionals aged 40-75 years. A total of 216 patients were diagnosed with incident pancreatic cancer during 16 years of follow-up. Multivariable relative risks (RRs) and 95% confidence intervals (CIs) were estimated using Cox proportional hazards models controlling for potential confounders, including detailed smoking history. All statistical tests were two-sided. Compared with no periodontal disease, history of periodontal disease was associated with increased pancreatic cancer risk (overall, multivariable RR = 1.64, 95% CI = 1.19 to 2.26; P = .002; crude incidence rates: 61 versus 25 per 100,000 person-years; among never smokers, multivariable RR = 2.09, 95% CI = 1.18 to 3.71; P = .01; crude incidence rates: 61 versus 19 per 100,000 person-years). In contrast, baseline number of natural teeth and cumulative tooth loss during follow-up were not strongly associated with pancreatic cancer. The association between periodontal disease and increased risk of pancreatic cancer may occur through plausible biologic mechanisms, but confirmation of this association is necessary.

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 > or =30 kg/m(2) to a BMI of 18-22.9 kg/m(2) [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.

Objective: To evaluate prospectively the association between intakes of fish, marine fatty acids, and bladder cancer risk in two ongoing cohorts, the Health Professionals Follow-up Study and the Nurses' Health Study., Methods: During 16 and 18 years of follow-up, 501 and 235 incident cases of bladder cancer were diagnosed among men and women, respectively. Cox proportional hazard models were used to estimate incidence rate ratios (RR) and 95% confidence intervals (CI) between fish intake and bladder cancer risk adjusting for age, total caloric intake, pack-years of cigarette smoking, and current smoking., Results: We observed no significant overall association between total fish intake and bladder cancer risk, even when we compared >/=1 servings of fish per day to fish intake /=1 total fish servings per day compared to

Objective: To examine the relation between fruits and vegetables, carotenoids, folate, and vitamins A, C, E and the risk of bladder cancer in a prospective study of women., Methods: A total of 237 incident bladder cancer cases were documented during 20 years of follow-up among 88,796 women enrolled in the Nurses' Health Study. Dietary intake was assessed by food-frequency questionnaires every two to four years and incident diagnosis of bladder cancer was ascertained every two years. Cox proportional hazard models were used to estimate incidence rate ratios (RR) and 95% confidence intervals (CI) for bladder cancer risk, adjusting for age, pack-years of smoking, current smoking, and total caloric intake., Results: Consumption of total fruits and vegetables was not associated with bladder cancer risk (RR = 1.08, 95% CI = 0.70-1.65, for > 5.5 compared to < 2.5 servings per day). Similarly, dietary intakes of carotenoids, folate, and vitamins A, C, E, were not related to bladder cancer risk. No association was observed between supplemental intake of multivitamins, vitamins A, C, E and bladder cancer risk., Conclusions: We did not observe any association for fruit and vegetable consumption or vitamin intake and bladder cancer risk among women.

Background: Diabetes appears to be associated with the development of pancreatic cancer. Three large prospective cohort studies observed a statistically significant relation between obesity and pancreatic cancer risk. Dietary patterns have been associated with fasting insulin levels and risk of diabetes. To determine whether dietary patterns are associated with pancreatic cancer risk, we analyzed data from two large prospective cohort studies., Methods: We combined data for men and women to obtain a total of 366 cases of incident pancreatic cancer from a total of 124,672 eligible participants. Dietary data were obtained from food frequency questionnaires in 1986 for men and in 1984 for women. We identified two major dietary patterns, prudent and western, by factor analysis. The prudent pattern was characterized by high fruit and vegetable intake; the western pattern was characterized by high meat and high fat intakes. Multivariable relative risks (RRs) were adjusted for potential confounders, including smoking and body mass index., Results: In the pooled analysis of men and women, no associations were observed between the prudent pattern (RR = 1.32, 95% confidence interval [CI] = 0.66 to 2.63, for highest versus lowest quintile) or the western pattern (RR = 0.91, 95% CI = 0.57 to 1.47, for highest versus lowest quintile) and the risk of pancreatic cancer. Stratifying by body mass index or physical activity did not change the associations., Conclusion: Dietary patterns were not associated with the risk of pancreatic cancer in two large cohort studies of men and women.

Background: Laboratory studies have shown that n-3 fatty acids inhibit and n-6 fatty acids stimulate prostate tumor growth, but whether the dietary intake of these fatty acids affects prostate cancer risk in humans remains unclear., Objective: We prospectively evaluated the association between intakes of alpha-linolenic (ALA; 18:3n-3), eicosapentaenoic (EPA; 20:5n-3), docosahexaenoic (DHA; 22:6n-3), linoleic (LA; 18:2n-6), and arachidonic (AA; 20:4n-6) acids and prostate cancer risk., Design: A cohort of 47 866 US men aged 40-75 y with no cancer history in 1986 was followed for 14 y., Results: During follow-up, 2965 new cases of total prostate cancer were ascertained, 448 of which were advanced prostate cancer. ALA intake was unrelated to the risk of total prostate cancer. In contrast, the multivariate relative risks (RRs) of advanced prostate cancer from comparisons of extreme quintiles of ALA from nonanimal sources and ALA from meat and dairy sources were 2.02 (95% CI: 1.35, 3.03) and 1.53 (0.88, 2.66), respectively. EPA and DHA intakes were related to lower prostate cancer risk. The multivariate RRs of total and advanced prostate cancer from comparisons of extreme quintiles of the combination of EPA and DHA were 0.89 (0.77, 1.04) and 0.74 (0.49, 1.08), respectively. LA and AA intakes were unrelated to the risk of prostate cancer. The multivariate RR of advanced prostate cancer from a comparison of extreme quintiles of the ratio of LA to ALA was 0.62 (0.45, 0.86)., Conclusions: Increased dietary intakes of ALA may increase the risk of advanced prostate cancer. In contrast, EPA and DHA intakes may reduce the risk of total and advanced prostate cancer.

Background: In vitro experiments and limited animal studies suggest that aspirin and nonsteroidal anti-inflammatory drugs may inhibit pancreatic carcinogenesis. Because few studies have examined the association between aspirin use and pancreatic cancer in humans and the results have been inconsistent, we examined the relationship between aspirin use and the development of pancreatic cancer in the Nurses' Health Study., Methods: Among 88 378 women without cancer at baseline, we documented 161 cases of pancreatic cancer during 18 years of follow-up. Aspirin use was first assessed at baseline in 1980 and updated biennially thereafter. All statistical tests were two-sided., Results: Participants were classified according to history of aspirin use. In a multivariable analysis, the risk of pancreatic cancer was not associated with current regular aspirin use (defined as two or more standard tablets per week; relative risk [RR] = 1.20, 95% confidence interval [CI] = 0.87 to 1.65), compared with use of fewer than two tablets per week. Increasing duration of regular aspirin use, compared with non-use, was associated with a statistically significant increase in risk: Women who reported more than 20 years of regular aspirin use had an increased risk of pancreatic cancer (RR = 1.58, 95% CI = 1.03 to 2.43; P(trend) =.01). Among women who reported aspirin use on at least two of three consecutive biennial questionnaires compared with consistent non-users of aspirin, the risk increased with dose (one to three tablets per week: RR = 1.11, 95% CI = 0.70 to 1.76; four to six tablets per week: RR = 1.29, 95% CI = 0.70 to 2.40; seven to 13 tablets per week: RR = 1.41, 95% CI = 0.76 to 2.61; and > or = 14 tablets per week: RR = 1.86, 95% CI = 1.03 to 3.35) (P(trend) =.02)., Conclusion: Extended periods of regular aspirin use appear to be associated with a statistically significantly increased risk of pancreatic cancer among women.

Incidence rates for pancreatic cancer are consistently lower in women than in men. Previous studies suggest that reproductive factors, particularly parity, may reduce pancreatic cancer risk in women. We examined parity, breast feeding history, age at first birth, menstrual factors, and exogenous hormone use in relation to pancreatic cancer risk in a prospective cohort study of women. Information on parity and other reproductive factors was assessed by questionnaires in 1976 and updated biennially. Multivariate relative risks were adjusted for cigarette smoking, body mass index, diabetes, and height. During 22 years of follow-up (1976-1998), 115,474 women contributed 2.4 million years of person time, and 243 cases of pancreatic cancer were identified. Compared with nulliparous women, the relative risk of pancreatic cancer was 0.86 [95% confidence interval (CI), 0.55-1.36] for women with 1-2 births, 0.75 (95% CI, 0.48-1.17) for 3-4 births, and 0.58 (95% CI, 0.34-0.98) for those with >/=5 births after adjusting for other factors. An analysis for linear trend indicates a 10% reduction in risk for each birth (P(trend) = 0.008). Other reproductive factors and exogenous hormone use were not significantly related to pancreatic cancer risk. In this large prospective cohort of women, parity was associated significantly with a reduced risk of pancreatic cancer. Additional studies should examine the physiological or hormonal changes underlying pregnancy or childbirth that may explain this finding.