Recreational physical activity and risk of postmenopausal breast cancer in a large cohort of US women

Due to its potential effects on ovarian hormone production, physical activity has been proposed as a modifiable risk factor for breast cancer. The authors analyzed data from the American Cancer Society Cancer Prevention Study II (CPS-II) Nutrition Cohort to examine the association between various measures of physical activity and postmenopausal breast cancer risk. Information on physical activity was obtained in 1992 via a self-administered questionnaire for 72,608 postmenopausal female participants who were cancer-free. During the five year prospective follow-up, 1520 incident breast cancer cases were identified among these women. Cox proportional hazards modeling was used to compute hazard rate ratios (RR) and to adjust for potential confounding factors including mammography. Women who were most physically active (>42.0 MET-h/week) at baseline had 29% lower incidence rates than active women with the least activity (>0–7.0 MET-h/week) (95% CI, 0.49–1.02). The difference in risk was largest for localized breast cancer, and for women who did not use hormone replacement therapy (HRT) at enrollment. Our findings are consistent with other studies that show lower risk of postmenopausal breast cancer associated with regular physical activity.     

Cholesterol-lowering drugs and advanced prostate cancer incidence in a large U.S. cohort.

BACKGROUND: 3-Hydroxy-3-methylglutaryl CoA reductase inhibitors, commonly known as statins, account for the great majority of cholesterol-lowering drug use in the United States. Long-duration statin use was associated with substantially reduced risk of advanced prostate cancer in a recent large prospective study. METHODS: We examined the association between use of cholesterol-lowering drugs and prostate cancer incidence by disease stage and grade among 55,454 men in the Cancer Prevention Study II Nutrition Cohort. Proportional hazards modeling was used to calculate RRs. RESULTS: During follow-up from 1997 to 2003, we identified 3,413 cases of incident prostate cancer, including 317 cases of advanced prostate cancer. After adjustment for age, history of prostate-specific antigen testing, and other potential prostate cancer risk factors, current use of cholesterol-lowering drugs for 5 or more years was not associated with overall prostate cancer incidence (multivariate adjusted rate ratio, 1.06; 95% confidence interval, 0.93-1.20), but was associated with a marginally statistically significant reduction in risk of advanced prostate cancer (rate ratio, 0.60; 95% confidence interval, 0.36-1.00). CONCLUSION: These results provide some support for the hypothesis that long-term statin use is associated with reduced risk of advanced prostate cancer.     

Dietary patterns and risk of prostate cancer in U.S. men.

We prospectively investigated the associations between dietary patterns and risk of prostate cancer in the Health Professionals Follow-up Study. Between 1986 and 2000, 3,002 incident prostate cancer cases were identified in our cohort. Using factor analysis, two major dietary patterns were identified, a prudent and a western dietary pattern. Dietary patterns were not appreciably associated with risk of total prostate cancer. For the highest versus the lowest quintiles, the multivariable relative risk (RR) for the prudent pattern was 0.94 [95% confidence interval (CI), 0.83-1.06], and for the western pattern, the multivariable RR was 1.03 (95% CI, 0.92-1.17). Neither were these associated with risk of advanced prostate cancer [highest versus lowest quintile, prudent pattern (RR, 1.01; 95% CI, 0.68-1.49); western pattern (RR, 1.13; 95% CI, 0.77-1.67)]. Higher western pattern scores were suggestively associated with a greater risk of advanced prostate cancer among older men [highest versus lowest quintile (RR, 1.35; 95% CI, 0.97-1.90)], but not after adding processed meat to the model [highest versus lowest quintile (RR, 1.11; 95% CI, 0.75-1.65)]. We did not find any evidence for a protective association between prudent pattern and risk of prostate cancer. The lack of association between a western dietary pattern as identified by factor analysis in our cohort and prostate cancer risk suggests that dietary risk factors for prostate cancer are likely to differ from those for other conditions, such as cardiovascular disease and type 2 diabetes, that have been associated with a western dietary pattern in this cohort.     

Obesity, recreational physical activity, and risk of pancreatic cancer in a large U.S. Cohort.

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, P(trend) = 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.     

Vitamin E supplements and risk of prostate cancer in U.S. men.

Supplementation with alpha-tocopherol (a form of vitamin E) was associated with decreased risk of prostate cancer in a randomized trial among Finnish smokers. We examined the association between vitamin E supplement use and prostate cancer incidence in the Cancer Prevention Study II Nutrition Cohort. Participants in the study completed a detailed questionnaire at enrollment in 1992-1993. Historical information was also available from a questionnaire completed in 1982 at enrollment in a previous cohort. Through August 31, 1999, we documented 4,281 cases of incident prostate cancer among 72,704 men. Multivariate-adjusted rate ratios (RRs) were calculated using Cox Proportional Hazards models. Regular vitamin E supplement use (>/=4 times per week) was not associated with overall risk of prostate cancer or with risk of advanced prostate cancer at diagnosis. No trend was seen with increasing dose of vitamin E. Men who reported regular vitamin E use in both 1982 and in 1992-1993 were not at lower risk of prostate cancer. Among current smokers, there was a suggestion of slightly reduced risk with regular vitamin E supplement use [RR = 0.87, 95% confidence interval (CI) = 0.67-1.11]. Our results do not support an important role for vitamin E supplements in prostate cancer prevention.     

Supplemental vitamin E intake and prostate cancer risk in a large cohort of men in the United States.

A clinical trial of vitamin E and beta-carotene supplementation for lung cancer prevention among male smokers in Finland recently reported an unexpected, strong protective effect of vitamin E against prostate cancer incidence and mortality. Our objective was to prospectively examine supplemental vitamin E intake and prostate cancer risk in a distinct U.S. population. In 1986, we identified 47,780 U.S. male health professionals, free from diagnosed cancer, who completed a dietary and lifestyle questionnaire; supplemental vitamin E and prostate cancer incidence were updated biennially through 1996. We estimated relative risks (RRs) from multivariate pooled logistic regression models. There were 1896 total (non-stage A1), 522 extraprostatic, and 232 metastatic or fatal incident prostate cancer cases diagnosed between 1986-1996. Men consuming at least 100 IU of supplemental vitamin E daily had multivariate RRs of 1.07 (95% confidence interval [CI], 0.95-1.20) for total and 1.14 (95% CI, 0.82-1.59) for metastatic or fatal prostate cancer compared with those consuming none. Current use, dosage, and total duration of use of specific vitamin E supplements or multivitamins were not associated with risk. However, among current smokers and recent quitters, those who consumed at least 100 IU of supplemental vitamin E per day had a RR of 0.44 (95% CI, 0.18-1.07) for metastatic or fatal prostate cancer compared with nonusers. Thus, supplemental vitamin E was not associated with prostate cancer risk generally, but a suggestive inverse association between supplemental vitamin E and risk of metastatic or fatal prostate cancer among current smokers and recent quitters was consistent with the Finnish trial among smokers and warrants further investigation.     

Recreational physical activity and risk of epithelial ovarian cancer

Background

Physical activity may influence ovarian cancer risk through hormonal, inflammatory, or immune-mediated processes or by suppressing ovulation. In a population-based case–control study of epithelial ovarian cancer, we assessed risk associated with recreational physical activity with a focus on characterizing risk within histologic subtypes.

Methods

Information was collected during in-person interviews with 812 women with ovarian cancer diagnosed in western Washington State from 2002–2005 and 1,313 controls. Logistic regression was used to calculate odds ratios (ORs) and 95% confidence intervals (CIs). Exercise was assessed according to the average hours and metabolic equivalent (MET)-hours per week and the number of years in which regular recreational activity occurred.

Results

Relative to women who reported no regular exercise throughout adulthood, the overall risk of invasive, but not borderline, ovarian cancer was reduced among more active women. Reductions in risk of invasive disease were most evident among women with the greatest frequency of high-intensity activity during adulthood. For serous invasive cancer, women in the uppermost category of MET-hours per week of recreational activity in adulthood had 60% the risk of inactive women (95% CI 0.4–0.9), whereas this level of activity was associated with more than a doubling in risk of endometrioid and clear cell invasive tumors.

Conclusions

Our findings are compatible with an overall reduction in risk of invasive epithelial ovarian cancer associated with recreational activity but suggest that this association may differ in women with different histologic types of disease. Inconsistent findings across studies that have considered histologic type indicate that this issue is not yet resolved.     

Occupational physical activity and risk for prostate cancer in a nationwide cohort study in Sweden

We investigated effects of occupational physical activity on relative risk for prostate cancer. From Swedish nationwide censuses in 1960 and 1970, we defined two cohorts of men whose occupational titles allowed classification of physical activity levels at work in 1960 (n=1,348,971) and in 1970 (n=1,377,629). A third cohort included only men whose jobs required a similar level of physical activity in both 1960 and 1970 (n=673,443). The incidence of prostate cancer between 1971 and 1989 was ascertained through record linkage to the Swedish Cancer Register. A total of 43,836, 28,702, and 19,670 prostate cancers, respectively, occurred in the three cohorts. In all three cohorts, the relative risk for prostate cancer increased with decreasing level of occupational physical activity (P<0.001), using Poisson regression. Among men with the same physical activity levels in 1960 and 1970, the rate ratio was 1.11 for men with sedentary jobs as compared with those whose jobs had very high/high activity levels after adjustment for age at follow-up, calendar year of follow-up and place of residence (95% CI 1.05-1.17; P for trend <0.001). There was no association between occupational activity and prostate cancer mortality. Since we had no data on other potential risk factors the observed associations for both incidence and mortality might have been confounded. Further studies are needed to better understand the potential role of physical activity for prostate cancer.     

Obesity, physical activity and the risk of pancreatic cancer in a large Japanese cohort

It is unclear whether body mass index (BMI) and physical activity are associated with the risk of pancreatic cancer in Asian populations. We examined these associations in the Japanese Collaborative Cohort Study for Evaluation of Cancer Risk. Our cohort study included 110,792 Japanese men and women at enrollment (1988-1990). Data on height, body weight (at baseline and at age 20 years) and physical activity were obtained from a questionnaire. Cox proportional hazards models were used to estimate the relative risks of pancreatic cancer mortality. We observed a total of 402 pancreatic cancer deaths during the follow-up period. Men with a BMI of 30 or more at age 20 years had a 3.5-fold greater risk compared with men with a normal BMI. Women with a BMI of 27.5-29.9 at baseline had approximately 60% increased risk compared with women with a BMI of 20.0-22.4. In men, weight loss of 5 kg or more between 20 years of age and baseline age was associated with an increased risk of pancreatic cancer death. In contrast, women with weight loss of 5 kg or more over the same period had a decreased risk. Physical activity was not associated with pancreatic cancer risk in either men or women. Obesity in young adulthood may be associated with an increased risk of death from pancreatic cancer in Japanese men. The risk of pancreatic cancer in relation to BMI seems to differ according to sex and the period over which BMI was measured.     

Age‐specific physical activity and prostate cancer risk among white men and black men

BACKGROUND:

The relation of physical activity across the lifespan to risk of prostate cancer has not been thoroughly investigated, particularly among black men. The authors investigated physical activity, including activity during different age periods and of various intensities, in relation to prostate cancer incidence among white men and black men.

METHODS:

In total, 160,006 white men and 3671 black men ages 51 years to 72 years who were enrolled in the National Institutes of Health‐AARP Diet and Health Study reported their time spent per week engaging in physical activity during ages 15 to 18 years, 19 years to 29 years, 35 years to 39 years, and during the past 10 years. Cox regression models were used to examine physical activity, categorized by intensity (moderate or vigorous, light, and total), in relation to prostate cancer risk.

RESULTS:

During 7 years of follow‐up, 9624 white men and 371 black men developed prostate cancer. Among white men, physical activity had no association with prostate cancer regardless of age period or activity intensity. Among black men, engaging in ≥4 hours of moderate/vigorous intensity physical activity versus infrequent activity during ages 19 years to 29 years was related to a 35% lower risk of prostate cancer (relative risk, 0.65; 95% confidence interval [95% CI], 0.43‐0.99 [P_trend = .01]). Frequent moderate/vigorous physical activity at ages 35 years to 39 years also potentially was related to reduced prostate cancer risk (relative risk, 0.59; 95% CI, 0.36‐0.96 [P_trend = .15]).

CONCLUSIONS:

Regular physical activity may reduce prostate cancer risk among black men, and activity during young adulthood may yield the greatest benefit. This novel finding needs confirmation in additional studies. Cancer 2009. Published 2009 by the American Cancer Society.     

Lifetime physical activity and prostate cancer risk

The purpose of our study was to investigate the relation in between physical activity in different periods of life at work and in leisure-time and prostate cancer risk. We conducted a case-control study on prostate cancer in Italy between 1991 and 2002, which included 1,294 incident cases of histologically confirmed prostate cancer below 75 years of age and 1,451 controls, who were admitted to hospital for acute nonneoplastic conditions. Odds ratios (OR) of prostate cancer according to physical activity in different periods of life were obtained by unconditional multiple logistic regression models, including terms for age, study centre, education, social class, body mass index, energy intake, family history and other selected covariates. Compared to the lowest level of occupational physical activity, the multivariate ORs for prostate cancer for the highest level were 0.94 (95% confidence interval, CI, 0.75-1.17) at age 15-19, 0.78 (95% CI, 0.63-0.97) at age 30-39 and 0.75 (95% CI, 0.61-0.93) at age 50-59. A significant inverse trend in risk was found for activity at work at ages 30-39 and 50-59. The inverse associations were consistent in strata of age at diagnosis, body mass index, education and social class. No significant association was found for leisure-time physical activity. The inverse association between occupational physical activity and prostate cancer risk may reflect favorable hormonal correlates of physical activity, but residual confounding by socioeconomic covariates cannot be excluded.     

Risk of cancer in a large cohort of U.S. veterans with diabetes

Prior studies of cancer risk among diabetic men have reported inconsistent findings. The aim of this study was to assess the risk of cancer among a large cohort (n = 4,501,578) of black and white U.S. veterans admitted to Veterans Affairs hospitals. The cancer risk among men with diabetes (n = 594,815) was compared to the risk among men without diabetes (n = 3,906,763). Poisson regression was used to estimate adjusted relative risks (RRs) and 95% confidence intervals (CIs). Overall, men with diabetes had a significantly lower risk of cancer (RR = 0.93, 95%CI = 0.93–0.94). Men with diabetes, however, had increased risks of cancers of the liver (RR = 1.95, 95%CI = 1.82–2.09), pancreas (RR = 1.50, 95%CI = 1.42–1.59), biliary tract (RR = 1.41, 95%CI = 1.22–1.62), colon (RR = 1.20, 95%CI = 1.16–1.25), rectum (RR = 1.12, 95%CI = 1.07–1.18), and kidney (RR = 1.09, 95%CI = 1.03–1.16), as well as leukemia (RR = 1.14, 95%CI = 1.08–1.21) and melanoma (RR = 1.13, 95%CI = 1.03–1.24). In contrast, men with diabetes had decreased risks of cancers of the prostate (RR = 0.89, 95%CI = 0.87–0.91), brain (RR = 0.91, 95% CI = 0.82–0.99), buccal cavity (RR = 0.85, 95%CI = 0.82–0.89), lung (RR = 0.79, 95%CI = 0.77–0.80), esophagus (RR = 0.77, 95%CI = 0.72–0.82), and larynx (RR = 0.76, 95%CI = 0.71–0.80). These findings indicate that black and white men with diabetes are at significantly lower risk of total cancer and of two of the most common cancers among U.S. males; lung and prostate cancers. These decreased risks were offset, however, by increased risks of cancer at several sites. Hyperinsulinemia may explain the increased risks of the digestive cancers, while lower testosterone levels, in the case of prostate cancer, and higher BMI, in the case of lung cancer, may explain the decreased risks of those tumors.     

Meat mutagens and risk of distal colon adenoma in a cohort of U.S. men.

Cooking meats at high temperatures and for long duration produces heterocyclic amines and other mutagens. These meat-derived mutagenic compounds have been hypothesized to increase risk of colorectal neoplasia, but prospective data are unavailable. We examined the association between intakes of the heterocyclic amines 2-amino-3,8-dimethylimidazo[4,5,-f]quinoxaline (MeIQx), 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP), 2-amino-3,4,8-trimethylimidazo[4,5,-f]quinoxaline (DiMeIQx), and meat-derived mutagenicity (MDM) and risk of distal colon adenoma using a cooking method questionnaire administered in 1996 in the Health Professionals Follow-up Study cohort. Between 1996 and 2002, 581 distal colon adenoma cases were identified. Higher intake of MDM was marginally associated with increased risk of distal adenoma [fourth versus lowest quintile: odds ratio (OR), 1.39; 95% confidence interval (95% CI), 1.05-1.84; highest versus lowest quintile: OR, 1.29; 95% CI, 0.97-1.72; P(trend) = 0.08]. Adjusting for total red meat or processed meat intake did not explain those associations. Our data also suggested a positive association between higher MeIQx (highest versus lowest quintile: OR, 1.28; 95% CI, 0.95-1.71; P(trend) = 0.22) and risk of adenoma, but this association was attenuated after adjusting for processed meat intake. DiMeIQx and PhIP did not seem to be associated with risk of adenoma. In conclusion, higher consumption of mutagens from meats cooked at higher temperature and longer duration may be associated with higher risk of distal colon adenoma independent of overall meat intake. Because mutagens other than heterocyclic amines also contribute to MDM, our results suggest that mutagens other than heterocyclic amines in cooked meats may also play a role in increasing the risk of distal adenoma.     

Use of multivitamins and prostate cancer mortality in a large cohort of US men

Objective: To assess the association between the use of multivitamins and prostate cancer mortality.Methods: A total of 5585 deaths from prostate cancer were identified during 18 years of follow-up of 475,726 men who were cancer-free and provided complete information on multivitamin use at enrollment in the Cancer Prevention Study II (CPS-II) cohort in 1982. Cox proportional hazards modeling was used to measure the association between multivitamin use at baseline and death from prostate cancer and to adjust for potential confounders.Results: The death rate from prostate cancer was marginally higher among men who took multivitamins regularly (≥15 times/month) compared to non-users (multivariate rate ratio=1.07, 95% CI: 0.99–1.15); this risk was statistically significant only for those multivitamin users who used no additional (vitamin A, C, or E) supplements (multivariate rate ratio=1.15, 95% CI: 1.05–1.26). In addition, risk was greatest during the initial four years of follow-up (1982–1986, multivariate rate ratio=1.12, 95 CI: 0.87–1.46).Conclusions: Regular multivitamin use was associated with a small increase in prostate cancer death rates in our study, and this association was limited to a subgroup of users.     

Physical activity and the risk of prostate and testicular cancer: a cohort study of 53,000 Norwegian men

The associations between recreational and occupational physical activity and the subsequent risk of prostate and testicular cancer were examined in a population-based cohort study of 53,242 men in Norway. Age at study entry was 19 to 50 years. Information on physical activity was based on questionnaire responses and a brief clinical examination. A total of 220 prostate and 47 testicular cancer cases were recorded in the Cancer Registry of Norway during a mean follow-up time of 16.3 years. We found a nonsignificant, reduced, adjusted relative risk (RR) of prostate cancer with increased level of physical activity at work and among those men with the greatest recreational physical activity. When occupational and recreational physical activity were combined, a reduced adjusted risk of prostate cancer was observed among men who walked during occupational hours and performed either moderate recreational activity (RR-0.61, 95 percent confidence interval [CI]=0.36 to 1.01) or regular recreational training (RR=0.45, CI=0.20 to 1.01) relative to sedentary men (test for trend,P=0.03). Physically active men who were older than 60 years of age at diagnosis showed a reduced adjusted RR of borderline significance, while no association was observed for younger men. No evidence was found for any association between physical activity and testicular cancer regardless of physical activity at work and recreation.This project is funded by the Norwegian Cancer Society.     

Endometriosis and risk of ovarian and endometrial cancers in a large prospective cohort of U.S. nurses

Purpose

Endometriosis is associated with ovarian cancer, but the relation with endometrial cancer is unclear. Prior studies generally were retrospective and had potential limitations, including use of self-reported endometriosis, failure to account for delays between symptom onset and endometriosis diagnosis, and changes in risk factors post-endometriosis diagnosis. We evaluated whether these limitations obscured a weak association with endometrial cancer and the extent to which these limitations impacted associations with ovarian cancer.

Methods

Cox proportional hazards regression models were used to assess associations between endometriosis and cancer risk, evaluating the impacts of self-reported vs. laparoscopically confirmed endometriosis, delayed diagnosis, and post-endometriosis diagnosis changes in risk factor exposures on relative risk estimates.

Results

Over 18 years of follow-up, we identified 228 ovarian and 166 endometrial cancers among 102,025 and 97,109 eligible women, respectively. Self-reported endometriosis was associated with ovarian cancer [relative risk (RR): 1.81; 95% confidence interval (CI): 1.26–2.58]; this association was stronger for laparoscopically confirmed endometriosis (HR: 2.14; 95% CI 1.45–3.15). No association was observed with endometrial cancer (self-report RR: 0.78; 95% CI 0.42–1.44; laparoscopic-confirmation RR: 0.76; 95% CI 0.35–1.64). Accounting for diagnosis delays or post-endometriosis diagnosis changes in risk factors had a little impact.

Conclusions

This study adds to the evidence that endometriosis is not strongly linked to endometrial cancer risk and that the association with ovarian cancer is robust to misclassification, diagnostic delay, and changes in exposures post-endometriosis diagnosis. Our analysis suggests that confounding and misclassification do not obscure a weak association for endometrial cancer risk, although our results should be replicated.

     

A review of physical activity and prostate cancer risk

Objectives: The purpose was to review the etiologic role and the possible biologic mechanisms for physical activity in the primary prevention of prostate cancer and to identify future research priorities. Methods: We conducted literature searches and systematically reviewed all the epidemiologic studies of physical activity and prostate cancer and the literature on the underlying biologic mechanisms. Results: Among 24 previously conducted studies, 14 studies suggested an inverse association of physical activity on prostate cancer; however, no overall association was found in six studies and an increased risk of prostate cancer was observed amongst the most physically active men in four other studies. The methodologic limitations in these studies include variations in detection of latent disease and possible outcome misclassification, crude assessments of physical activity, inadequate control for confounding, and incomplete examination of effect modification. Conclusions: Physical activity may have an inverse association with prostate cancer risk; however, the epidemiologic evidence is currently inconsistent and the magnitude of the risk reduction observed is small. These inconsistent results could be attributable, in part, to methodologic limitations of previous studies. Hence, further investigation of the etiologic role of physical activity is needed before more definitive conclusions can be made. Specifically, research studies should be designed to measure all types and parameters of physical activity throughout lifetimes. Furthermore, a better understanding of the biologic mechanisms and etiologically relevant time periods in prostate carcinogenesis when physical activity may be operative is needed, so that these studies can be properly designed.     

Micronutrient intake and risk of prostate cancer in a cohort of middle-aged, Danish men

Purpose

Micronutrients may protect against prostate cancer. However, few studies have had high-quality assessment of both dietary and supplemental consumption of micronutrients, rendering possible different source-specific effects difficult to discern. This study evaluates associations between intake of vitamin C, E, folate, and beta-carotene and prostate cancer risk, focusing on possible different effects of dietary, supplemental, or total intake and on potential effect modification by alcohol intake and BMI.

Methods

Danish prospective cohort study of 26,856 men aged 50–64 years with questionnaire-based information on diet, supplements, and lifestyle. Hazard ratios (HRs) for prostate cancer associated with micronutrient intake were calculated using Cox proportional hazard analyses.

Results

During follow-up (1993–2010), 1,571 prostate cancer cases were identified. Supplemental folic acid was inversely associated with prostate cancer risk, notably on a continuous scale [HR 0.88 (95 % CI 0.79–0.98) per 100 μg increase/day]. The risk reduction was largely confined to non-aggressive tumors [HR 0.71 (0.55–0.93) per 100 μg increase/day]. No influence on prostate cancer risk was observed for dietary folate or for the other studied micronutrients, regardless of source. We found no significant effect modification by alcohol intake and BMI in relation to any micronutrient.

Conclusion

Our study may indicate an inverse association between folic acid and prostate cancer; however, the inverse association was confined to supplemental folic acid and non-aggressive prostate cancer and may thus be a chance finding. Further studies are warranted to evaluate our findings.     

Interrelation of energy intake, body size, and physical activity with prostate cancer in a large prospective cohort study

Energy restriction reduces prostate tumor growth in transplantable tumor models in rodents, which suggests that excessive energy intake may contribute to the risk of prostate cancer. The association of total energy intake across the normal range with prostate cancer has not been consistent in epidemiological studies. We prospectively evaluated the joint associations of energy intake and body size or physical activity with prostate cancer. Participants were 46786 male health professionals ages 40-75 years at baseline in 1986 who were free of cancer diagnosis. Between 1986 and 2000, we documented 2896 incident prostate cancer cases (excluding stage T1a) by review of medical records and histopathology reports. Of these, 339 were metastatic or fatal cases. We used Cox proportional hazards regression to estimate the multivariate relative risk (RR) of prostate cancer associated with energy intake measured using a food frequency questionnaire, overall and stratified by body mass index, waist size, physical activity, as well as by age and family history of prostate cancer. There was no association between energy intake and total prostate cancer incidence. However, a modest increased risk of metastatic or fatal disease with energy intake was suggested [RR comparing extreme quintiles: 1.38, 95% confidence interval (CI) 0.96-1.98, P(trend) = 0.06]. This association was most pronounced in men with a lower body mass index (in stratum < 24 kg/m(2): RR = 1.76, 95% CI 0.92-3.39; P(interaction) = 0.04), smaller waist size [in stratum or= median: RR = 1.74, 95% CI 0.93-3.26; P(interaction) = 0.09]. Also, the association of energy intake with metastatic and fatal prostate cancer was restricted to men who were younger [in stratum 相似文献