Cigarette Smoking, Alcohol Consumption, and Endometrial Cancer Risk: A Population-based Study in Sweden

Objective: To assess effects of cigarette smoking and alcohol consumption on the risk of endometrial cancer among postmenopausal women. Methods: We performed a nationwide population-based case–control study among postmenopausal women aged 50–74 years in Sweden, including 709 incident endometrial cancer cases and 3368 controls. Results: Compared to never smokers, recent/current smokers had a decreased risk of endometrial cancer (multivariate OR 0.61, 95% CI 0.47–0.80), but former smokers presented no substantial difference in risk (multivariate OR 0.90, 95% CI 0.72–1.14). We observed a decreased risk of endometrial cancer for postmenopausal smoking, but there was no clear impact on risk for premenopausal smoking. The inverse association of smoking with risk was not explained by differences in body mass index between smokers and nonsmokers. Alcohol consumption was not clearly associated with risk of endometrial cancer. The multivariate OR for women consuming up to 1.6 g of alcohol per day was 1.12 (95% CI 0.88–1.44), and 0.92 (95% CI 0.70–1.20) for women consuming more than 4 g per day (p for trend over categories=0.44). Conclusions: Current cigarette smoking reduces the risk of postmenopausal endometrial cancer, but the inverse association dissipates after smoking cessation. Premenopausal smoking might not affect risk of postmenopausal endometrial cancer. Alcohol consumption is not materially associated with risk.     

Diet,alcohol, and smoking and the occurrence of hyperplastic polyps of the colon and rectum (United States)

Hyperplastic polyps of the colon reveal a geographic distribution similar to that of colorectal cancer and adenomatous polyps. However, unlike adenomas—known precursors of colorectal cancer—little is known about the etiology or clinical significance of the hyperplastic polyp. In this prospective study, we set out to determine the main dietary and other lifestyle factors in the United States that might be associated with this lesion. Hyperplastic polyps of the distal colon and rectum were diagnosed in 219 of 12,922 men of the Health Professionals Follow-up Study having had an endoscopic procedure between 1986 and 1992, and 175 of 15,339 women of the Nurses' Health Study who had undergone an endoscopy for a variety of reasons between 1980 and 1990. After adjusting for age, family history of colon cancer, history of previous endoscopy, and total energy intake using multiple logistic regression, those consuming 30 g or more of alcohol per day were at increased risk relative to nondrinkers among men (relative risk [RR]=1.69; 95 percent confidence interval [CI]=1.01–2.80) and women (RR=1.79, CI=1.02–3.15). Current smoking also was found to be associated strongly positively with hyperplastic polyps in men (RR=2.45, CI=1.59–3.75) and women (RR=1.96, CI=1.16–2.86). High intake of folate was associated inversely with risk in both men (RR=0.74, CI=0.49–1.11, between high and low intakes of folate) and women (RR=0.45, CI=0.28–0.74, between high and low intakes of folate). Among macronutrients, a suggestive increase in risk existed with intake of animal fat, although this was attenuated in the full multivariate model (RR[men]=1.48, CI=0.94–2.41, and RR [women]=1.22, CI=0.77–1.94) between high and low quantities of animal fat intake. These prospective data provide evidence of associations between low folate intake, alcohol consumption, and current cigarette smoking, and risk of hyperplastic polyps of the distal colon and rectum. These same factors also have been found to be related to adenoma and cancer of the colon. The hyperplastic polyp is an indicator of populations at high risk for colorectal carcinoma, and it also may serve as a marker for factors that influence neoplastic evolution.Drs Giovannucci, Stampfer, Colditz, and Willett are with the Channing Laboratory, Department of Medicine, Harvard Medical School and Brigham and Women's Hospital, Boston, MA, USA. Authors also are affiliated with: the Department of Nutrition, Harvard School of Public Health, Boston, MA (Drs Kearney, Rimm, Stampfer, Ascherio, and Willett); the Department of Epidemiology, Harvard School of Public Health (Drs Rimm, Stampfer, Colditz, Ascherio, and Willett); and the Department of Surgery, New England Deaconess Hospital, Boston, MA (Dr Bleday). Address correspondence to Dr Giovannucci, Channing Laboratory, 180 Longwood Avenue, Boston, MA 02115, USA. This project was supported by research grants number CA 55075 and HL 35464 from the National Institutes of Health and Special Institution Grant No. 18 from the American Cancer Society. Dr Colditz. was supported by a Faculty Research Award (FRA-398) from the American Cancer Society.     

Smoking,alcohol, coffee,tea, caffeine,and theobromine: risk of prostate cancer in Utah (United States)

Data from a population-based study of newly diagnosed cases of prostate cancer (n=362) and age-matched controls (n=685) conducted in Utah (United States) between 1983 and 1986 were used to determine if cigarette smoking, alcohol, coffee, tea, caffeine, and theobromine were associated with prostate cancer risk. These factors were examined since their use differs in the Utah population, which is comprised predominantly of members of the Church of Jesus Christ of Latter-day Saints (LDS or Mormon), from most other populations. Pack-years of cigarettes smoked, alcohol intake, and consumption of alcohol, coffee, tea, and caffeine were not associated with prostate cancer risk. Compared with men with very low levels of theobromine intake, older men consuming 11 to 20 and over 20 mg of theobromine per day were at increased risk of prostate cancer (odds ratio [OR] for all tumors = 2.06, 95 percent confidence interval [CI]=1.33–3.20, and OR=1.47, CI=0.99–2.19, respectively; OR for aggressive tumors = 1.90, CI=0.90–3.97, and OR=1.74, CI=0.91–3.32, respectively). We present biological mechanisms for a possible association between prostate cancer and theobromine. This finding needs further exploration in studies with a wider range of theobromine exposures and more men with aggressive tumors.Dr Slattery is with the University of Utah School of Medicine, Salt Lake City, UT, USA. Dr West is with the Northerm California Cacer Center, Alameda, CA, USA. Address correspondence to Dr Slattery, Department of Family and Preventive Medicine, University of Utah School of Medicine, 50 North Medical Drive, Salt Lake City, UT 84132, USA. This study was supported in part by grant number CA 34804 from the US National Cancer Institute.     

Second primary tumors in patients with upper aerodigestive tract cancers: joint effects of smoking and alcohol (United States)

Objective: This study evaluated the joint effects of tobacco smoking and alcohol consumption on the risk of second primary tumors (SPT) in patients with early-stage head and neck squamous cell carcinoma (HNSCC). Methods: Data are presented for 1181 patients enrolled in a placebo-controlled chemoprevention trial of 13-cis-retinoic acid. Nearly 17% of patients presented with a SPT. The log rank test and Cox proportional hazards model were used to examine risk factors for SPT development. Results: After adjusting for the time from the index diagnosis to randomization, age at diagnosis, stage, and site of the primary cancer, the factors that emerged as simultaneous predictors of SPT development were continued smoking and alcohol intake after the index diagnosis. Increased SPT risk was associated with older age (RR = 2.1; 95% CI 1.5–2.8); stage II diagnosis (RR = 1.5; 95% CI 1.1–2.1); index diagnosis of pharyngeal cancer (RR = 1.6; 95% CI 1.1–2.5); current smoking at registration (RR = 2.1; 95% CI 1.3–3.6) and continued alcohol consumption post-diagnosis (RR = 1.3; 95% CI 1.0–1.7). Conclusion: Important associations exist between SPT development and continued smoking and alcohol consumption after treatment for HNSCC.     

Risk factors for prostate cancer: results from the Canadian National Enhanced Cancer Surveillance System

Objectives: To evaluate the relationship between prostate cancer and several potential lifestyle risk factors.Methods: We analyzed data obtained from a population-based case–control study conducted in eight Canadian provinces. Risk estimates were generated by applying multivariate logistic regression methods to 1623 histologically confirmed prostate cancer cases and 1623 male controls aged 50–74.Results: Cases were more likely to have a first-degree relative with a history of cancer, particularly prostate cancer (OR = 3.1, 95% CI = 1.8–5.4). Reduced risks of prostate cancer were observed among those of Indian descent (OR = 0.2, 95% CI = 0.1–0.5) or any Asian descent (OR = 0.3, 95% CI = 0.2–0.6) relative to those of western European descent. Total fat consumption, tomato and energy intake, were not associated with prostate cancer. The risk of prostate cancer was inversely related to the number of cigarettes smoked daily (p = 0.06) and cigarette pack-years (p < 0.01), while no association was observed between the total number of smoking years or the number of years since smoking cessation. Anthropometric measures and moderate and strenuous levels of leisure time physical activity were not strongly related to prostate cancer. In contrast, strenuous occupational activities at younger ages appeared protective.Conclusions: Our analyses are limited by the absence of data related to tumor severity and screening history. Further studies are needed to investigate the relationship between behavioral risk factors and prostate cancer screening practices.     

Smoking and the risk of prostate cancer in the European Prospective Investigation into Cancer and Nutrition

Background:

Smoking is not associated with prostate cancer incidence in most studies, but associations between smoking and fatal prostate cancer have been reported.

Methods:

During 1992 and 2000, lifestyle information was assessed via questionnaires and personal interview in a cohort of 145 112 European men. Until 2009, 4623 incident cases of prostate cancer were identified, including 1517 cases of low-grade, 396 cases of high grade, 1516 cases of localised, 808 cases of advanced disease, and 432 fatal cases. Multivariable Cox proportional hazards regression models were used to examine the association of smoking status, smoking intensity, and smoking duration with the risk of incident and fatal prostate cancer.

Results:

Compared with never smokers, current smokers had a reduced risk of prostate cancer (RR=0.90, 95% CI: 0.83–0.97), which was statistically significant for localised and low-grade disease, but not for advanced or high-grade disease. In contrast, heavy smokers (25+ cigarettes per day) and men who had smoked for a long time (40+ years) had a higher risk of prostate cancer death (RR=1.81, 95% CI: 1.11–2.93; RR=1.38, 95% CI: 1.01–1.87, respectively).

Conclusion:

The observation of an increased prostate cancer mortality among heavy smokers confirms the results of previous prospective studies.     

A prospective study of lifestyle factors and the risk of pancreatic cancer in Nord-Trøndelag, Norway

Objectives: Cancer of the pancreas is highly fatal and, despite extensive scrutiny, only cigarette smoking stands out as a likely causal agent in epidemiological studies. To explore to what extent different lifestyle factors are associated with the risk of pancreatic cancer, data from a large health screening survey in a county in Norway were analyzed. Methods: Our study included 31,000 men and 32,374 women initially free from any diagnosed cancer, and during 12 years of follow-up, 166 incident cases of pancreatic cancer were diagnosed at the Cancer Registry. Results: Compared with never smokers, we found a two-fold increased risk among current smokers, and a dose–response association with number of cigarettes (p for trend = 0.02 for both men and women) and with number of pack-years (p for trend = 0.02 for men and 0.01 for women). The risk among former smokers quitting more than 5 years before study entry was close to the risk of never smokers. Compared with persons who reported never or infrequently to be physically worn out after a day's work, the relative risk (RR) among those who nearly always became worn out was 2.9 (95% confidence interval (CI) = 1.4–5.8) for men and 3.8 (95% CI = 1.6–9.2) for women. Divorced or separated men had a risk of 3.1 (95% CI = 1.3–7.2) compared with married men. We observed a higher risk among women in occupations of high socioeconomic status (RR = 2.5; 95% CI = 1.2–5.2), and among men occupied in farming, agriculture or forestry (RR = 2.1; 95% CI = 1.1–4.0), compared with persons in occupations of low socioeconomic status. Conclusions: Our results confirm the findings of previous studies that indicate a causal role of cigarette smoking in pancreatic cancer. Moreover, we found that the risk of former smokers may approach the risk of never smokers within a few years subsequent to quitting.     

Alcohol and smoking and subsequent risk of prostate cancer in Japanese men: The Japan Public Health Center‐based prospective study

Although alcohol and smoking have not been established as risk factors for prostate cancer, they are important risk factors for other human cancers and potentially major avoidable factors. Alcohol drinkers and smokers might be less likely to get screening, which might lead to attenuation of the positive association. Here, we investigated the association of alcohol drinking and smoking and prostate cancer according to stage, as well as prostate cancer detected by subjective symptoms, in a large prospective study among Japanese men. The Japan Public Health Center‐based prospective study (JPHC study) was established in 1990 for Cohort I and in 1993 for Cohort II. Subjects were 48,218 men aged 40–69 years who completed a questionnaire, which included their alcohol and smoking habits at baseline, and who were followed until the end of 2010. During 16 years of follow‐up, 913 men were newly diagnosed with prostate cancer; of whom 248 had advanced cases, 635 were organ‐localized and 30 were of an undetermined stage. Alcohol consumption was dose‐dependently associated with advanced prostate cancer [nondrinkers: reference, 0–150 g/week: hazard ratio (HR) = 1.23, 95% confidence interval (CI) = 0.83–1.82; 150–300 g/week: HR = 1.51, 95% CI = 1.04–2.19; ≥300 g/week: HR = 1.41, 95% CI = 0.97–2.05, p for trend = 0.02]. The positive association was not substantially changed among cancers detected by subjective symptoms. Smoking was inversely associated with prostate cancer among total subjects, but tended to increase the risk of advanced prostate cancer detected by subjective symptoms. In conclusion, abstinence from alcohol and prohibition of smoking might be important factors in the prevention of advanced prostate cancer.     

Risk factors for renal cell carcinoma in Denmark. I. Role of socioeconomic status,tobacco use,beverages, and family history

Risk factors for renal cell carcinoma were examined in a population based case-control study in Denmark. A total of 368 cases and 396 age- and gender-matched controls were interviewed in their homes. Increased risk was associated with low socioeconomic status. For men, an increasing risk with decreasing socioeconomic status was seen (odds ratio [OR]=2.2, 95 percent confidence interval [CI]=1.0–4.6 for men in the lowest socioeconomic stratumcf the highest). For women, the risk was lower in the highest socioeconomic stratum compared with the rest (OR=2.4, CI=0.9–5.9 for the lowest stratacf the highest). Cigarette smoking was a risk factor in men with an OR=2.3 (CI=1.1–5.1) for cigarette smokers with a total consumption of more than 40 pack-years compared with nonsmokers. Family history of kidney cancer was associated with an increased risk in both genders (for men, OR=4.1, CI=1.1–14.9; for women, OR=4.8, CI=1.0–23). Observations were inconsistent regarding coffee and alcohol consumption, and we found no association with tea drinking. The association with socioeconomic status remained after adjustment for other factors.     

Are Coffee, Tea, and Total Fluid Consumption associated with Bladder Cancer Risk? Results from the Netherlands Cohort Study

Objectives: Coffee, tea, and fluid consumption have been thought to influence bladder cancer incidence. In a large prospective study, these associations were investigated. Methods: In 1986, cohort members (55–69 years) completed a questionnaire on cancer risk factors. Follow-up was established by linkage to cancer registries until 1992. The multivariable case–cohort analysis was based on 569 bladder cancer cases and 3123 subcohort members. Results: The incidence rate ratios (RR) for men consuming <2 cups of coffee/day was 0.89 (95% CI 0.51–1.5) using the median consumption category (4–<5 cups/day) as reference. This RR increased to 1.3 (95% CI 0.94–1.9) for men consuming 7 cups/day, although no clear dose–response association was found. The RRs decreased from 1.2 (95% CI 0.56–2.7) for women consuming <2 cups of coffee/day to 0.36 (95% CI 0.18–0.72) for women consuming 5 cups/day compared to the median consumption category (3–<4 cups/day). Men and women who abstained from drinking tea had a RR of 1.3 (95% CI 0.97–1.8) compared to those consuming 2–<3 cups of tea per day (median consumption category). The RR for men and women comparing highest to lowest quintile of total fluid consumption was 0.87 (95% CI 0.63–1.2). Conclusion: The data suggest a possible positive association between coffee consumption and bladder cancer risk in men and a probable inverse association in women. Tea consumption was inversely associated with bladder cancer. Total fluid consumption did not appear to be associated with bladder cancer.     

Marijuana use and cancer incidence (California, United States)

The purpose of this retrospective cohort study was to examine therelationship of marijuana use to cancer incidence. The study populationconsisted of 64,855 examinees in the Kaiser Permanente multiphasic healthcheckup in San Francisco and Oakland (California, United States), between1979-85, aged 15 to 49 years, who completed self-ad-ministered questionnairesabout smoking habits, including marijuana use. Follow-up for cancer incidencewas conducted through 1993 (mean length 8.6 years). Compared withnonusers/experimenters (lifetime use of less than seven times), ever- andcurrent use of marijuana were not associated with increased risk of cancer ofall sites (relative risk [RR] = 0.9, 95 percent confidence interval [CI] =0.7-1.2 for ever-use in men; RR = 1.0, CI = 0.8-1.1 in women) in analysesadjusted for sociodemographic factors, cigarette smoking, and alcohol use.Marijuana use also was not associated with tobacco-related cancers or withcancer of the following sites: co lorectal, lung, melanoma, prostate, breast,cervix. Among nonsmokers of tobacco cigarettes, ever having used marijuanawas associated with increased risk of prostate cancer (RR = 3.1, CI =1.0-9.5) and nearly significantly increased risk of cervical cancer (RR =1.4, CI = 1.0-2.1). We conclude that, in this relatively young study cohort,marijuana use and cancer were not associated in overall analyses, but thatassociations in nonsmokers of tobacco cigarettes suggested that marijuana usemight affect certain site-specific cancer risks.     

Alcohol Consumption, Smoking and Risk of Gastric Cancer: Case—Control Study from Moscow, Russia

Objectives: To examine the risk of gastric cancer associated with alcohol consumption and smoking in men and women in Moscow, Russia. Materials and methods: A case-control study which includes 448 cases and 610 controls was conducted. Cases consisted of patients with newly diagnosed histologically confirmed gastric cancer. Controls were patients admitted during the study period to the hospital with diagnoses other than cancer and/or gastrointestinal diseases. Information on demographic variables, smoking, alcohol consumption and diet was collected from all subjects. Venous blood was drawn from 361 cases and 441 controls. A serological test for Helicobacter pylori immunoglobulin G was performed. Results: Alcohol consumption, particularly vodka consumption, was found to increase the risk of gastric cancer. In men the effect of hard liquor drinking was stronger for cancer of the cardia (OR = 3.4, CI = 1.2–10.2), while in women the effect was stronger for cancer of sites other than gastric cardia (OR = 1.5, CI = 1.0–2.3). Smoking increased the risk of developing gastric cancer in men, but not in women. In men a dose-response relationship between mean number of cigarettes smoked per day (p = 0.03), pack-years of cigarettes smoked (p = 0.01) duration of smoking (p = 0.08) and the risk of cancer of gastric cardia was observed. Further statistical analysis revealed interactions between effect of smoking and alcohol consumption and between smoking and H. pylori infection status. Conclusions: The findings further support the role of alcohol consumption and smoking in the etiology of gastric cancer.     

Oral cavity cancer risk in relation to tobacco chewing and bidi smoking among men in Karunagappally, Kerala, India: Karunagappally cohort study

The Karunagapally cohort in Kerala, India was established in the 1990s. The present study examined oral cancer risk among 66,277 men aged 30-84 years in the cohort, using Poisson regression analysis of grouped data, stratified on attained age, calendar time, education, and family income. By the end of 2005, 160 oral cancer cases were identified by the Karunagapally Cancer Registry. Tobacco chewing increased oral cancer risk (P < 0.001). Particularly increased was the risk of cancers of the gum and mouth (relative risk [RR] = 4.7; 95% confidence interval [CI] = 2.8-7.9), which increased with higher daily frequencies (P < 0.001) and longer duration (P < 0.001) of tobacco chewing. Alcohol drinking was not significantly related to oral cancer risk regardless of tobacco chewing. Bidi smoking significantly increased oral cancer risk (RR = 2.6; 95%CI = 1.4-4.9) only among men without tobacco chewing habits. The risk increased with higher daily consumption (P < 0.001), longer duration (P = 0.001), and younger age at start of bidi smoking (P = 0.007). In location-specific analysis, bidi smoking was significantly associated with cancer of the gum and mouth (RR = 3.6; 95%CI = 1.1-12.1), and its risk significantly increased with larger daily consumption of bidis (P = 0.013) and younger age at the start of smoking (P = 0.044). Tongue cancer risk was significantly increased among men who smoked bidis for 30 years or longer, and men started bidi smoking at 18 years old or younger. The present study is the first cohort study showing that tobacco chewing increases cancers of the gum and mouth among men keeping chewing tobacco in the cheek, and that bidi smoking strongly increased oral cancer risk among men without a tobacco chewing habit.     

A prospective study on active and environmental tobacco smoking and bladder cancer risk (The Netherlands)

Objective: In a prospective cohort study among 120,852 adult subjects the authors investigated the associations between cigarette, cigar, pipe, environmental tobacco smoking (ETS), and bladder cancer. Methods: In 1986 all subjects completed a questionnaire on cancer risk factors. Follow-up for incident bladder cancer was established by linkage to cancer registries until 1992. The case–cohort analysis was based on 619 cases and 3346 subcohort members. Results: Compared with lifelong non-smokers the age- and sex-adjusted incidence rate ratios (RR) for ex- and current cigarette smokers were 2.1 (95% CI 1.5–3.0) and 3.3 (95% CI 2.4–4.6), respectively. The RR for smoking duration was 1.03 (95% CI: 1.02–1.04) per 1-year increment. The RR per 10 cigarettes/day was 1.3 (95% CI 1.2–1.4). Tar and nicotine exposure increased bladder cancer risk only weakly. It appeared that associations of cigarette smoking characteristics with bladder cancer risk were largely attributable to cigarette smoking duration only. Smoking cessation, age at first exposure, filter-tip usage, cigar and pipe smoking, and ETS were no longer associated with bladder cancer risk after adjustment for frequency and duration of smoking. Conclusions: The authors conclude that current cigarette smokers have a three-fold higher bladder cancer risk than non-smokers. Ex-smokers experience a two-fold increased risk. About half of male bladder cancer and one-fifth of female bladder cancer was attributable to cigarette smoking. Other smoking types (cigar, pipe, or ETS) were not associated with increased risks.     

Meat consumption among Black and White men and risk of prostate cancer in the Cancer Prevention Study II Nutrition Cohort.

Previous epidemiologic studies have suggested that intake of red meat may be associated with increased risk of prostate cancer. Few studies, however, have examined these associations by race. We examined intake of red meat, processed meat, and poultry in relation to incident prostate cancer among Black and White men in the Cancer Prevention Study II Nutrition Cohort. Participants in the study completed a detailed questionnaire on diet, medical history, and lifestyle in 1992 to 1993. After excluding men with a history of cancer and incomplete dietary information, 692 Black and 64,856 White men were included in the cohort. During follow-up through August 31, 2001, we documented 85 and 5,028 cases of incident prostate cancer among Black and White men, respectively. Cox proportional hazards models were used to estimate rate ratios (RR) and 95% confidence intervals (95% CI). No measure of meat consumption was associated with risk of prostate cancer among White men. Among Black men, total red meat intake (processed plus unprocessed red meat) was associated with higher risk of prostate cancer (RR, 2.0; 95% CI, 1.0-4.2 for highest versus lowest quartile; P(trend) = 0.05); this increase in risk was mainly due to risk associated with consumption of cooked processed meats (sausages, bacon, and hot dogs; RR, 2.7; 95% CI, 1.3-5.3 for highest versus lowest quartile; P(trend) = 0.008). This study suggests that high consumption of cooked processed meats may contribute to prostate cancer risk among Black men in the United States.     

Height and Body Mass Index in Relation to Colorectal and Gallbladder Cancer in Two Million Norwegian Men and Women

Objectives: The present study aimed at exploring the relations between BMI and stature and colorectal and gallbladder cancer in a huge Norwegian cohort with measured height and weight.Material and methods: Height and weight were measured in two million Norwegian men and women aged 20–74 during 1963–2001. During follow-up, 47,117 colorectal and 1715 gallbladder cancer cases were registered. Relative risks (RRs) of colorectal and gallbladder cancer were estimated using Cox proportional hazards regression.Results: The risk of colon cancer increased with increasing BMI in men; the RR of colon cancer per unit increase in BMI was 1.04 (95% CI: 1.04–1.05). For mucinous colorectal adenocarcinomas, the risk increased to a larger extent with increasing BMI in both sexes. The RR of colorectal cancer associated with 10 cm increase in height was 1.14 (95% CI: 1.11–1.16) in men and 1.17 (95% CI: 1.14–1.20) in women. The risk of gallbladder cancer increased with increasing BMI in women; the overall RR associated with one unit increase in BMI was 1.06 (95% CI: 1.04–1.07). There was no association between height and gallbladder cancer in either sex.Conclusion: The risk of colon cancer increased with increasing BMI in men, and the risk of gallbladder cancer increased with increasing BMI in women. In both sexes, the risk of colon cancer increased with increasing height.     

Vasectomy, cigarette smoking, and age at first sexual intercourse as risk factors for prostate cancer in middle-aged men

A population-based case-control study was conducted in men aged 60 or less to assess the risk of prostate cancer associated with vasectomy and other factors. Data were obtained from 216 case-control pairs by telephone interviews; this number represented 55% of all eligible cases. The matched pairs relative risk (RR) for vasectomy in ever married men was 1.4 with a 95% confidence interval (CI) of 0.9-2.3. There was a positive association between the number of years since vasectomy and prostate cancer risk (1-sided P = 0.01). Early age at first sexual intercourse was associated with increased prostate cancer risk (age less than 17 vs. 21+, RR = 2.3, 95% CI = 1.3, 4.0) but there were no consistent associations with number of sexual partners or frequency of sexual intercourse. Cigarette smoking was also associated with increased risk of prostate cancer (RR = 1.9, 95% CI = 1.2, 3.0) and there was a positive dose-response relationship with years of smoking (1-sided P = 0.001). We discuss the possible implication of the low response rate on each of these findings. To determine whether the association with vasectomy might have a hormonal basis, we compared levels of testosterone (T) and testosterone binding globulin-binding capacity (TeBG-bc) in 33 of the vasectomized control men with levels in 33 non-vasectomized controls of the same age, weight and height. T levels were higher in vasectomized than in non-vasectomized controls (1-sided P = 0.06). The ratio of T to TeBG-bc (an index of bioavailable T) was 13.5% higher in vasectomized men (1-sided P = 0.03).     

Daily aspirin use and prostate cancer risk in a large,multiracial cohort in the US

Objective: To examine the relationship between daily aspirin use and risk of prostate cancer in a large, racially diverse cohort of men followed for up to 32 years. Methods: The study population included 90,100 male subscribers to the Kaiser Permanente Medical Care Program who had received one or more multiphasic health checkups between 1964 and 1973. This general health checkup included a self-completed questionnaire that requested men to record if they took more than six aspirin almost every day during the previous year. Subjects were followed for the development of prostate cancer using the local tumor registry. Cox regression was used to estimate relative risks (RR) and 95% confidence intervals (CI). Results: A total of 2574 men developed prostate cancer. Of these, 1617 had local stage disease and 719 had either regional or distant disease at diagnosis. A total of 2466 men (2.7%) reported taking more than six aspirin almost every day during the past year at one or more health checkups. After adjusting for birth year, education, race, and the number of health checkups, the relative risk of prostate cancer associated with this amount of aspirin use was 0.76 (95% CI 0.60–0.98). Relative risks did not differ by race and were similar for both local stage and regional or distant stage prostate cancer. Conclusion: Results from our large, multiracial cohort study support a modest inverse relationship between daily consumption of more than six aspirin and prostate cancer risk.     

Jewish ethnicity and prostate cancer mortality in two large US cohorts

Objective: To investigate prospectively the relationship between Jewish ethnicity and prostate cancer mortality. Methods: Men were selected from white male participants in two large American Cancer Society cohorts: Cancer Prevention Studies I (CPS-I) (enrolled in 1959 and followed through 1972) and II (CPS-II) (enrolled in 1982 and followed through 1996). During the follow-up periods there were 1751 prostate cancer deaths among 417,018 men in CPS-I and 3594 deaths among 447,780 men in CPS-II. Cox proportional hazards modeling was used to compute rate ratios (RR) and to adjust for known and suspected risk factors for prostate cancer. Results: Prostate cancer death rates were substantially lower among Jewish men than other white men in both cohorts (multivariate adjusted rate ratios (RR) = 0.54, 95% CI = 0.38–0.77 in CPS-I; RR = 0.72, 95% CI = 0.61–0.86 in CPS-II). Factors such as tobacco avoidance and measured dietary patterns did not account for this difference. Lower prostate cancer death rates were observed among Jewish men regardless of place of birth of the participants or their parents. Conclusions: Prostate cancer death rates are lower among Jewish men in the US and in Israel than among non-Jewish US white men. This may reflect persistent differences in unknown environmental risk factors or possible genetic susceptibility.     

Calcium,vitamin D,dairy products,and risk of colorectal cancer in the Cancer Prevention Study II Nutrition Cohort (United States)

Objective: Calcium, vitamin D, and dairy product intake may reduce the risk of colorectal cancer. We therefore examined the association between these factors and risk of colorectal cancer in a large prospective cohort of United States men and women. Methods: Participants in the Cancer Prevention Study II Nutrition Cohort completed a detailed questionnaire on diet, medical history, and lifestyle in 1992–93. After excluding participants with a history of cancer or incomplete dietary information, 60,866 men and 66,883 women remained for analysis. During follow-up through 31 August 1997 we documented 421 and 262 cases of incident colorectal cancers among men and women, respectively. Multivariate-adjusted rate ratios (RR) were calculated using Cox proportional hazards models. Results: Total calcium intake (from diet and supplements) was associated with marginally lower colorectal cancer risk in men and women (RR = 0.87, 95% CI 0.67–1.12, highest vs lowest quintiles, p trend = 0.02). The association was strongest for calcium from supplements (RR = 0.69, 95% CI 0.49–0.96 for 500 mg/day vs none). Total vitamin D intake (from diet and multivitamins) was also inversely associated with risk of colorectal cancer, particularly among men (RR = 0.71, 95% CI 0.51–0.98, p trend = 0.02). Dairy product intake was not related to overall risk. Conclusions: Our results support the hypothesis that calcium modestly reduces risk of colorectal cancer. Vitamin D was associated with reduced risk of colorectal cancer only in men.